category
stringclasses 191
values | search_query
stringclasses 434
values | search_type
stringclasses 2
values | search_engine_input
stringclasses 748
values | url
stringlengths 22
468
| title
stringlengths 1
77
| text_raw
stringlengths 1.17k
459k
| text_window
stringlengths 545
2.63k
| stance
stringclasses 2
values |
|---|---|---|---|---|---|---|---|---|
Holistic Health | Can detox diets help in weight loss? | yes_statement | "detox" "diets" can "help" in "weight" "loss".. "weight" "loss" can be achieved through "detox" "diets". | https://www.anxiety.org/nutrition/detox/how-to-detox-your-body-to-lose-weight-different-ways-tips-risks | Detox Your Body To Lose Weight - Expert Tips & Infos 2023 | How To Detox Your Body To Lose Weight? – Different Ways, Tips & Risks For Weight Loss With Detox 2023
Detoxification as a means of weight loss and improved well-being has experienced a surge in popularity. In today’s fast-paced, toxin-laden environment, more and more people are eagerly seeking ways to cleanse their systems of harmful substances and begin their weight loss efforts.
While experts continue to debate the merits and efficacy of detox diets, incorporating certain practices can potentially enhance the body’s natural detoxification processes and facilitate the shedding of unwanted pounds. By understanding the basic principles of detoxification and adopting these strategies, achieving a healthier physique and weight loss goals may become more attainable.
The role of detoxification in facilitating weight loss
Detoxification has emerged as a potential catalyst for weight loss through several mechanisms. First, detoxification diets typically advocate the consumption of whole, nutrient-dense foods while limiting processed foods and added sugars[1]. This dietary shift is of paramount importance as excessive consumption of processed foods, particularly those with added sugars, has been linked to excess body weight, obesity and several health conditions.
By shifting to a healthier and more balanced diet, individuals can reduce their overall calorie consumption, thereby promoting weight loss. In addition, detoxification encourages the intake of water and fibre-rich foods, which promotes a sense of satiety and curbs the tendency to overeat.
In addition, the process of detoxification can optimise the body’s natural detoxification mechanisms, such as liver function and the elimination processes mediated by the kidneys and digestive system. By strengthening these vital systems, the efficient removal of toxins and waste products becomes possible, potentially contributing to improved metabolism and more effective weight management.
In conclusion, detoxification holds great promise as an adjunct to weight loss. By emphasising healthier dietary choices and promoting the body’s detoxification processes, it can help individuals achieve their weight loss goals and promote better overall health.
A comprehensive guide to detoxifying your body for weight loss
In the pursuit of weight loss, a detoxification programme that focuses on maintaining healthy habits proves to be essential in facilitating the elimination of toxins and optimising the body's internal processes. There are many effective ways to detoxify and rid the body of harmful substances, all of which contribute to achieving a holistic sense of wellbeing.
Hydration: Drinking plenty of water plays a key role in flushing toxins from the system. Staying well hydrated supports the body's detoxification mechanisms and helps promote overall bodily functions.
Regular exercise: Regular physical activity not only promotes weight loss, but also stimulates sweating and improves circulation. Sweating helps to eliminate toxins through the skin, further aiding the detoxification process.
High Fibre Foods: Eating a diet rich in fibre, including fruits, vegetables and whole grains, is essential for proper digestion. Fibre helps remove toxins and waste from the body, contributing to a more efficient detoxification process.
Prioritise sleep: Adequate and restorative sleep allows the body to repair and rejuvenate itself. During sleep, the body undergoes essential detoxification processes, making it essential for effective weight loss and overall health.
Stress reduction: Adopting stress-reduction techniques is essential for overall wellbeing and detoxification. Chronic stress can negatively impact the body's ability to detoxify, so it is imperative to incorporate practices such as meditation or yoga to reduce stress.
Optimizing Detoxification for Weight Loss: Simple Steps to Follow
Detoxing for weight loss transcends the mere adoption of specialized juices and fad diets. True detoxification involves incorporating straightforward yet effective healthy routines that enable the body to reach its full potential. By integrating uncomplicated measures, such as consuming nutritious foods, increasing water intake, engaging in regular exercise, and ensuring sufficient sleep, weight loss objectives can be achieved. Here are some effective ways to detox for weight loss:
Embrace a Nutritious Diet
While adopting a healthier diet is beneficial for overall well-being, focusing on antioxidant-rich foods during detoxification provides enhanced protection for cells against damage. Including foods like berries, nuts, and vegetables helps foster detoxification. Furthermore, fiber-rich foods can aid in weight loss by promoting satiety, and the inclusion of bananas in the diet can be particularly helpful for weight management.
Amplify Water Consumption
Water plays a pivotal role in eliminating toxins and waste products from the body. Additionally, it supports vital organs like the liver and kidneys, which are actively involved in the detoxification process. Thus, maintaining proper hydration is a primary key to successful detoxification.
Reduce Alcohol and Caffeine Intake
The liver, responsible for metabolizing alcohol, can face adverse effects due to excessive drinking, potentially leading to alcoholic liver disease (ALD)[2]. Restricting or abstaining from alcohol allows the liver to function optimally, facilitating proper detoxification.
Engage in Regular Exercise
Participating in physical activity is a laudable approach to detoxifying the body. Not only does exercise help reduce the likelihood of chronic diseases such as diabetes and heart disease, but it also plays a key role in reducing inflammation[3] in the body. Consequently, this reduction in inflammatory processes[4] greatly facilitates the body’s detoxification process. By incorporating more consistent physical activity into your daily routine, you can ensure that your body is working at its best.
Prioritize Adequate Sleep
Sleep is a crucial factor in detoxification[6]. Sufficient rest allows the body to recharge and maintain optimal functioning, effectively eliminating waste products and reducing the risk of neurological issues like Alzheimer’s disease. Aim for 7 to 9 hours of sleep per night, adhering to a consistent sleep schedule and limiting screen time before bedtime.
Incorporating these straightforward yet powerful practices into daily life can substantially support the body’s detoxification processes, facilitating weight loss and promoting overall health. By embracing these holistic approaches to detoxification, individuals can embark on a transformative journey towards improved well-being and weight management.
Potential Hazards to Consider While Detoxing for Weight Loss
Engaging in a detox regimen for weight loss holds promise for numerous benefits, but it is crucial to be cognizant of certain risks[7]. Before embarking on any detox program, it is advisable to seek counsel from a healthcare professional or registered dietitian to ascertain its safety and suitability according to your unique requirements. Their expert guidance can pave the way for adopting healthy and sustainable weight loss methods.
Electrolyte Imbalance
Certain detox programs advocate excessive fluid intake or employ diuretic substances, potentially leading to electrolyte imbalances. These imbalances, in turn, may manifest as symptoms such as dizziness, fatigue, and irregular heartbeats. To safeguard against adverse effects, it is essential to monitor hydration levels diligently and promptly seek advice from a healthcare professional if any concerning symptoms arise.
Nutritional Deficiencies
One must exercise caution with detox diets that impose restrictions on specific food groups or severely curtail calorie intake, as these practices may result in nutrient deficiencies if prolonged. To meet the body’s nutritional demands, it becomes imperative to incorporate a diverse array of nutrient-dense foods into the detox plan.
Emotional Toll
The stringent nature of detox diets can exact a toll on one’s mental and emotional well-being, potentially evoking sensations of deprivation, frustration, or guilt. Approaching detoxing with a healthy mindset and being mindful of its potential emotional impact are vital considerations for a well-rounded approach to weight loss.
In conclusion, while detoxing for weight loss can hold allure, it is crucial to tread cautiously and remain informed about the potential risks. Seeking professional advice, maintaining a nutritionally balanced approach, and being attuned to both physical and emotional well-being can foster a safer and more successful detox journey.
Sluggish Metabolism
Extreme detox diets, which drastically slash calorie consumption, can force the body into a state of starvation, thereby slowing down metabolism. This effect poses challenges to achieving long-term weight loss objectives and sustaining the achieved weight loss after the detox period concludes.
Frequently Asked Questions
Can Detoxing Enhance Metabolism?
Detoxing holds the potential to support liver function and the body’s natural elimination processes, which may have a positive impact on metabolism. However, the degree of influence on metabolism can vary among individuals.
Indeed, detoxing may yield rapid weight loss initially, primarily due to the reduction of water weight. However, for sustainable weight loss, long-term lifestyle changes are fundamental.
Is Detoxing Essential for Weight Loss?
Detoxing, while not an obligatory component of weight loss, can play a supportive role by fostering healthier eating habits and facilitating the removal of toxins from the body.
Are Detox Diets Safe?
In the short term, detox diets can be deemed safe, but caution should be exercised with prolonged or extreme detox programs as they might lack essential nutrients and trigger adverse effects. It is advisable to seek guidance from a healthcare professional before embarking on such regimens.
Nonetheless, it is imperative to perceive detoxing as a transient approach rather than a sole, enduring solution for long-term weight management, as protracted reliance on it may prove detrimental to the body. Therefore, before embarking on any detox program, seeking counsel from a healthcare professional becomes a prudent step to ascertain its compatibility with one’s specific needs and aspirations.
In summary, when employed judiciously and as part of a comprehensive weight loss strategy, detoxing can be a supportive ally in achieving a healthier and fitter self.
Ashley Bujalski is a second year clinical psychology doctoral student at William Paterson University. She holds a MA in Forensic Mental Health Counseling from John Jay College, and has worked as a mental health clinician at Riker’s Island Correctional Facility and Crossroads Juvenile Detention Center. At present, she is a graduate assistant at the William Paterson University Women’s Center, where she implements programs to raise awareness on campus and in the community about prevention of violence against women. Her research interests include trauma and posttraumatic stress disorder in forensic populations and among those who have been victimized by interpersonal violence.
Claire Galloway is a post-doctoral fellow at Emory University. She received her Bachelor of Science in psychology from Georgia State University in 2011, her Master of Arts in psychology from Emory University in 2013, and her Doctor of Philosophy in psychology (neuroscience and animal behavior program) from Emory University in 2017. Claire studies the nature of hippocampal dysfunction in Alzheimer’s disease and how brain regions important for memory, the amygdala and hippocampus, interact during memory tasks.
Our content does not constitute medical advice and is for informational purposes only. Consult a licensed health care professional for medical advice/diagnosis.
Anxiety.org is a website that aims to provide comprehensive education on various health topics and help people navigate the overwhelming information overload. It presents the latest medical knowledge in a clear and accessible way, based on evidence-based sources. | How To Detox Your Body To Lose Weight? – Different Ways, Tips & Risks For Weight Loss With Detox 2023
Detoxification as a means of weight loss and improved well-being has experienced a surge in popularity. In today’s fast-paced, toxin-laden environment, more and more people are eagerly seeking ways to cleanse their systems of harmful substances and begin their weight loss efforts.
While experts continue to debate the merits and efficacy of detox diets, incorporating certain practices can potentially enhance the body’s natural detoxification processes and facilitate the shedding of unwanted pounds. By understanding the basic principles of detoxification and adopting these strategies, achieving a healthier physique and weight loss goals may become more attainable.
The role of detoxification in facilitating weight loss
Detoxification has emerged as a potential catalyst for weight loss through several mechanisms. First, detoxification diets typically advocate the consumption of whole, nutrient-dense foods while limiting processed foods and added sugars[1]. This dietary shift is of paramount importance as excessive consumption of processed foods, particularly those with added sugars, has been linked to excess body weight, obesity and several health conditions.
By shifting to a healthier and more balanced diet, individuals can reduce their overall calorie consumption, thereby promoting weight loss. In addition, detoxification encourages the intake of water and fibre-rich foods, which promotes a sense of satiety and curbs the tendency to overeat.
In addition, the process of detoxification can optimise the body’s natural detoxification mechanisms, such as liver function and the elimination processes mediated by the kidneys and digestive system. By strengthening these vital systems, the efficient removal of toxins and waste products becomes possible, potentially contributing to improved metabolism and more effective weight management.
In conclusion, detoxification holds great promise as an adjunct to weight loss. By emphasising healthier dietary choices and promoting the body’s detoxification processes, it can help individuals achieve their weight loss goals and promote better overall health.
| yes |
Holistic Health | Can detox diets help in weight loss? | yes_statement | "detox" "diets" can "help" in "weight" "loss".. "weight" "loss" can be achieved through "detox" "diets". | https://www.nccih.nih.gov/health/detoxes-and-cleanses-what-you-need-to-know | “Detoxes” and “Cleanses”: What You Need To Know | NCCIH | âDetoxesâ and âCleansesâ: What You Need To Know
What are âdetoxesâ and âcleansesâ?
A variety of âdetoxificationâ diets, regimens, and therapiesâsometimes called âdetoxesâ or âcleansesââhave been suggested as ways to remove toxins from your body, lose weight, or promote health.
âDetoxificationâ programs may involve a single process or a variety of approaches. These include:
These programs may be advertised commercially, offered at health centers, or part of naturopathic treatment.
Some âdetoxificationâ programs can be unsafe and falsely advertised. For more information on safety, see the âWhat about safety?â section below.
(The Centers for Disease Control and Prevention recommends chelation therapy, a type of chemical detoxification procedure, for removing toxic metals from the body in some specific serious cases. This page does not address that type of detoxification.)
What does the research say about âdetoxesâ and âcleansesâ?
There have been only a small number of studies on âdetoxificationâ programs in people. While some have had positive results on weight and fat loss, insulin resistance, and blood pressure, the studies themselves have been of low qualityâwith study design problems, few participants, or lack of peer review (evaluation by other experts to ensure quality).
A 2015 review concluded that there was no compelling research to support the use of âdetoxâ diets for weight management or eliminating toxins from the body. A 2017 review said that juicing and âdetoxâ diets can cause initial weight loss because of low intake of calories but that they tend to lead to weight gain once a person resumes a normal diet. There have been no studies on long-term effects of âdetoxificationâ programs.
What about safety?
The U.S. Food and Drug Administration (FDA) and Federal Trade Commission (FTC) have taken action against several companies selling detox/cleansing products because they (1) contained illegal, potentially harmful ingredients; (2) were marketed using false claims that they could treat serious diseases; or (3) in the case of medical devices used for colon cleansing, were marketed for unapproved uses.
Some juices used in âdetoxesâ and âcleansesâ that havenât been pasteurized or treated in other ways to kill harmful bacteria can make people sick. The illnesses can be serious in children, elderly people, and those with weakened immune systems.
Some juices are made from foods that are high in oxalate, a naturally occurring substance. Two examples of high-oxalate foods are spinach and beets. Drinking large quantities of high-oxalate juice can increase the risk for kidney problems.
People with diabetes should follow the eating plan recommended by their health care team. If you have diabetes, consult your health care providers before making major changes in your eating habits, such as going on a âdetoxâ diet or changing your eating patterns.
Diets that severely restrict calories or the types of food you eat usually donât lead to lasting weight loss and may not provide all the nutrients you need.
Colon cleansing procedures may have side effects, some of which can be serious. Harmful effects are more likely in people with a history of gastrointestinal disease, colon surgery, severe hemorrhoids, kidney disease, or heart disease.
âDetoxificationâ programs may include laxatives, which can cause diarrhea severe enough to lead to dehydration and electrolyte imbalances.
Drinking large quantities of water and herbal tea and not eating any food for days in a row could lead to dangerous electrolyte imbalances.
Take charge of your healthâtalk with your health care providers about any complementary health approaches you use, including any âdetoxesâ or âcleanses.â Together, you and your health care providers can make shared, well-informed decisions.
Are all fasting programs considered âdetoxesâ and âcleansesâ?
Although some fasting programs are advertised with âdetoxificationâ claims, other fasting programsâincluding intermittent fasting and periodic fastingâare being researched for health promotion, disease prevention, improved aging, and in some cases weight loss. But there are no firm conclusions about their effects on human health. Also, fasting can cause headaches, fainting, weakness, and dehydration.
For More Information
NCCIH Clearinghouse
The NCCIH Clearinghouse provides information on NCCIH and complementary and integrative health approaches, including publications and searches of Federal databases of scientific and medical literature. The Clearinghouse does not provide medical advice, treatment recommendations, or referrals to practitioners.
Know the Science
NCCIH and the National Institutes of Health (NIH) provide tools to help you understand the basics and terminology of scientific research so you can make well-informed decisions about your health. Know the Science features a variety of materials, including interactive modules, quizzes, and videos, as well as links to informative content from Federal resources designed to help consumers make sense of health information.
This publication is not copyrighted and is in the public domain. Duplication is encouraged.
NCCIH has provided this material for your information. It is not intended to substitute for the medical expertise and advice of your health care provider(s). We encourage you to discuss any decisions about treatment or care with your health care provider. The mention of any product, service, or therapy is not an endorsement by NCCIH. | These include:
These programs may be advertised commercially, offered at health centers, or part of naturopathic treatment.
Some âdetoxificationâ programs can be unsafe and falsely advertised. For more information on safety, see the âWhat about safety?â section below.
(The Centers for Disease Control and Prevention recommends chelation therapy, a type of chemical detoxification procedure, for removing toxic metals from the body in some specific serious cases. This page does not address that type of detoxification.)
What does the research say about âdetoxesâ and âcleansesâ?
There have been only a small number of studies on âdetoxificationâ programs in people. While some have had positive results on weight and fat loss, insulin resistance, and blood pressure, the studies themselves have been of low qualityâwith study design problems, few participants, or lack of peer review (evaluation by other experts to ensure quality).
A 2015 review concluded that there was no compelling research to support the use of âdetoxâ diets for weight management or eliminating toxins from the body. A 2017 review said that juicing and âdetoxâ diets can cause initial weight loss because of low intake of calories but that they tend to lead to weight gain once a person resumes a normal diet. There have been no studies on long-term effects of âdetoxificationâ programs.
What about safety?
The U. | no |
Holistic Health | Can detox diets help in weight loss? | yes_statement | "detox" "diets" can "help" in "weight" "loss".. "weight" "loss" can be achieved through "detox" "diets". | https://www.muhealth.org/our-stories/detox-diets-do-they-really-work | Detox Diets: Do They Really Work? | Main More
Breadcrumb
Detox Diets: Do They Really Work?
Feeling sluggish? Want to lose weight? Worried about toxins in your body? There are plenty of pills, potions and concoctions that promise to boost energy, shed pounds and eliminate poisons.
Many do-it-yourself cleanses call for fasting followed by a regimen of vegetables, fruits, juices and water, in addition to taking herbs and other supplements.
The thought of wiping the slate clean is appealing, but is there proof to back these claims?
“There is little evidence that detox diets eliminate toxins from the body,” said Matthew Bechtold, MD, a gastroenterologist at MU Health Care. “Detox programs may help in weight loss by eliminating or reducing high-calorie, low-nutrition foods and by reducing water weight for the period of the detox.”
Matthew Bechtold, MD
After the detox, though, the water weight quickly comes back. If people return to their unhealthy eating habits, those pounds also pile back on, Bechtold said.
So why do so many people extol detoxing benefits? They may feel better during the period when they eliminated highly processed foods and sugary treats, both of which have nothing to do with a magic pill.
What about cleanses that purport to remove toxins and impurities from organs such as the colon or liver? Bechtold said our bodies have all the detox mechanisms needed for optimal health.
“The colon collects, concentrates and removes toxins from the body in the form of stools,” he said. “The liver also removes toxins that are absorbed through the gut by the portal vein. This is how the body protects us against ingested toxins.”
While the body naturally eliminates toxins, cleanses claiming to clean colons that use laxatives, such as enemas, can have adverse effects on the body and overall health.
“Patients must be wary of cleanses with laxatives because they can result in bloating, cramping, nausea and possibly dehydration if used in a period of fasting. Furthermore, laxatives may affect the good bacteria in the colon that protects us from bad bacteria,” Bechtold said.
One of the most popular cleanses involves consuming a mixture of lemon juice, water, maple syrup and cayenne for a week to 10 days. At the same time, dieters take laxatives every night and gulp salt water every morning to encourage a bowel movement.
This laxative regimen can cause the same problems as those with the colon cleanse, Bechtold said, but with prolonged use during fasting, it can also cause depletion of electrolytes and impairment of normal bowel function. Although weight loss is common because no food is eaten during this plan, the pounds typically return after the fast.
If you’re looking to reverse the effects of a bad diet, the prescription to better health is a lot less splashy, but as Bechtold points out, it’s safe, sustainable and simple.
“Eat a healthy diet, exercise regularly and limit treats to small portions and special occasions,” he said. | Main More
Breadcrumb
Detox Diets: Do They Really Work?
Feeling sluggish? Want to lose weight? Worried about toxins in your body? There are plenty of pills, potions and concoctions that promise to boost energy, shed pounds and eliminate poisons.
Many do-it-yourself cleanses call for fasting followed by a regimen of vegetables, fruits, juices and water, in addition to taking herbs and other supplements.
The thought of wiping the slate clean is appealing, but is there proof to back these claims?
“There is little evidence that detox diets eliminate toxins from the body,” said Matthew Bechtold, MD, a gastroenterologist at MU Health Care. “Detox programs may help in weight loss by eliminating or reducing high-calorie, low-nutrition foods and by reducing water weight for the period of the detox.”
Matthew Bechtold, MD
After the detox, though, the water weight quickly comes back. If people return to their unhealthy eating habits, those pounds also pile back on, Bechtold said.
So why do so many people extol detoxing benefits? They may feel better during the period when they eliminated highly processed foods and sugary treats, both of which have nothing to do with a magic pill.
What about cleanses that purport to remove toxins and impurities from organs such as the colon or liver? Bechtold said our bodies have all the detox mechanisms needed for optimal health.
“The colon collects, concentrates and removes toxins from the body in the form of stools,” he said. “The liver also removes toxins that are absorbed through the gut by the portal vein. This is how the body protects us against ingested toxins.”
While the body naturally eliminates toxins, cleanses claiming to clean colons that use laxatives, such as enemas, can have adverse effects on the body and overall health.
| yes |
Holistic Health | Can detox diets help in weight loss? | yes_statement | "detox" "diets" can "help" in "weight" "loss".. "weight" "loss" can be achieved through "detox" "diets". | https://www.nebraskamed.com/weight-loss/why-summer-crash-diets-dont-work | How to spot a fad diet to avoid | Nebraska Medicine Omaha, NE | How to spot a fad diet to avoid
Breadcrumb
With a new year of resolutions upon us, you may once again wish to eliminate unwanted pounds once and for all.
The problem is, most crash diets being pitched are simply quick - and often temporary - fixes for a long-term problem. Crash diets often involve unhealthy calorie restrictions without making true lifestyle behavior changes. So not only are you not getting to the root of the problem, but your weight loss may not be sustainable.
Crash diets also can back fire, causing you to lose muscle, not fat. In addition, if you are trying to lose weight by excessively restricting your calories only, your body will adjust by slowing its metabolism, which decreases the amount of calories you need. Not only will this eventually stall your weight loss, but once you go off your diet, you are more likely to regain the weight and more, as your body has adjusted to living off fewer calories.
How to spot a fad diet:
How can you tell if it’s a fad diet?
Be honest with yourself. If it sounds too good to be true, it probably is.
The sales pitch is "quick weight loss."
The diet is extremely restrictive. Like the grapefruit diet, these diets are not sustainable over the long-term and you likely will be missing out on important vitamins and nutrients.
No real, statistically valid studies back up the diet. Watch for words like "clinically proven."
The diet lists “good” and “bad” foods. Eating healthy is about making smart choices and eating in moderation. If you eat in moderation, you shouldn’t have to completely eliminate any types of foods.
Detox diets for example, are often advertised as quick fix ways to flush toxins out of your system to help with weight loss. Detoxing isn’t necessary because the body filters and detoxes naturally through the liver, kidneys and its immune system. Restricting yourself too much to “detox” can leave you extremely hungry, causing you to overeat once you do eat normally again, resulting in weight gain. Instead, strive for following a well-balanced eating plan with adequate amounts of fluid and fiber to promote regular bowel movements.
What does a good diet look like?
The best weight loss plan is based on a well-rounded diet that focuses on lean proteins, non-starchy vegetables and fruits, whole grains and low-fat dairy while limiting your intake of foods high in saturated fat and sugar. Regular, intentional exercise should also be a part of your regimen with a goal of getting about 150 minutes a week that includes a combination of cardio and weight training. This can be obtained by exercising at least 30 minutes a day, five times a week. For long-term weight maintenance, studies show that those who have lost more than 10 percent of their body weight and are trying to maintain that weight loss, can best achieve that by striving for 300 minutes of exercise per week.
Consider these additional tricks for losing weight:
Eat your meals on a salad plate
Portion out snacks ahead of time in small bags to avoid overeating
Share an entrée when eating out
Self monitor your food intake with an app or food journal. Research shows that people who record their eating habits are more successful at losing weight and keeping it off
Avoid beverages that are calorie-filled and full of added sugars
Limit eating out excessively
Focus on eating three meals a day and not skipping meals
Avoid yo-yo dieting, which can cause your metabolism to drop, making weight loss more difficult
Be careful where you are getting your nutrition and weight loss information. If it is on the internet, make sure it is from a reputable and reliable source
Remember, there’s no quick fix to losing and maintaining weight loss. It’s about adopting healthy behaviors that you can maintain over the long-term.
Note: Weight loss results vary depending on the individual. No guarantee of weight loss is provided or implied. | The sales pitch is "quick weight loss. "
The diet is extremely restrictive. Like the grapefruit diet, these diets are not sustainable over the long-term and you likely will be missing out on important vitamins and nutrients.
No real, statistically valid studies back up the diet. Watch for words like "clinically proven. "
The diet lists “good” and “bad” foods. Eating healthy is about making smart choices and eating in moderation. If you eat in moderation, you shouldn’t have to completely eliminate any types of foods.
Detox diets for example, are often advertised as quick fix ways to flush toxins out of your system to help with weight loss. Detoxing isn’t necessary because the body filters and detoxes naturally through the liver, kidneys and its immune system. Restricting yourself too much to “detox” can leave you extremely hungry, causing you to overeat once you do eat normally again, resulting in weight gain. Instead, strive for following a well-balanced eating plan with adequate amounts of fluid and fiber to promote regular bowel movements.
What does a good diet look like?
The best weight loss plan is based on a well-rounded diet that focuses on lean proteins, non-starchy vegetables and fruits, whole grains and low-fat dairy while limiting your intake of foods high in saturated fat and sugar. Regular, intentional exercise should also be a part of your regimen with a goal of getting about 150 minutes a week that includes a combination of cardio and weight training. This can be obtained by exercising at least 30 minutes a day, five times a week. For long-term weight maintenance, studies show that those who have lost more than 10 percent of their body weight and are trying to maintain that weight loss, can best achieve that by striving for 300 minutes of exercise per week.
| no |
Holistic Health | Can detox diets help in weight loss? | yes_statement | "detox" "diets" can "help" in "weight" "loss".. "weight" "loss" can be achieved through "detox" "diets". | https://www.healthifyme.com/blog/detox-diet-plan-benefits-recipes/ | Detox Diet Plan - Benefits And Recipes - HealthifyMe | The Ultimate Guide to Detox Diet Plan
Detox diets are short term changes in eating habits which seek to remove excess toxins present in the body through the consumption of juices, fruits, and vegetables. They usually span across 3 to 7 days.
These diets aim to improve circulation, boost immunity, clear your skin, and increase energy. The juices involved in a detox diet are generally blends of many different kinds of fresh fruit and vegetables.
Detox diets have a good number of benefits. The most important one is that such a diet will definitely improve your idea of food and your eating habits for the better; regardless of whether you receive the other benefits.
Detox diets are said to bring about changes not just physically, but also mentally by bringing about focus and clarity.
What is a Detox Diet?
This hustle culture of today may bring in a lot of excitement and rush into a person’s life. However; one cannot neglect the poor lifestyle choices that one might make due to this, such as drinking a lot of coffee or eating outside. This fast-paced life can sometimes lead to the negligence of one’s health and well-being.
It is said that over time, due to poor food choices, exposure to harmful chemicals, and various forms of pollution, several toxins accumulate within the body.
A detox diet aims to remove unwanted substances present in the body and also the increase absorption of vitamins and minerals.
Such a diet generally consists of drinking a lot of fluids, eating whole foods, or even fasting for a few days or sometimes even a week.
Types of detox diets
Detox diets vary significantly from each other in terms of practice as well as intensity.
1. Master Cleanse
The most intense of all is the Master Cleanse which involves making a concoction of lemon juice, maple syrup, cayenne pepper and water which is consumed for at least ten days.
2. Juice Diet
Perhaps one of the most popular detox diets is the juice cleanse wherein one consumes only fruit or vegetable juices through the duration of the diet.
Liver cleansing diets are also followed, which essentially involve drinking a lot of water, vegetable/fruit juices as well as controlling potassium consumption.
Why should I do a detox diet?
A detox diet has several advantages, physically and mentally.
In addition to cleansing the body of toxins, a detox diet also has positive effects on mental health. According to the experiences shared by a number of people who followed this diet, a detox brings about a sense of calm, freshness, and peace within the body. Others have also reported feeling rejuvenated and energized.
On a closer look, one can also find instances of fasting in many cultures which are said to bring about this feeling of serenity but also build discipline.
Hence, the idea of fasting or limiting diet for specific kinds of food at specific times of the day is not completely alien.
These detox diets are mainly used for weight-loss, to decrease consumption of substances like alcohol, tobacco or coffee, to overcome ailments such as headaches or joint pain and even to just improve one’s eating habits.
Detox Diet Benefits
Indeed, there are several tangible benefits that one can supposedly get from such a diet apart from just mental peace. These include:
1. Promoting healthy skin and hair
Removing toxins leads to healthy, glowing skin. It may also decrease acne and clear your skin, making detox diets good for the skin.
These diets are said to make hair shinier and also make them grow longer. This is due to the removal of toxins at the follicles, which could have been hampering the hair growth, leading to brittle, lifeless hair.
2. Supporting the digestive system and weight loss
The removal of toxins aids the absorption of vitamins and other nutrients. Furthermore, detox diets are said to alter metabolism leading to long term weight management
3. Boost in the immune system
Since greater amounts of vitamins and minerals are absorbed, and vital organs begin to get healthier, a boost in immunity results.
4. Improved mental state
Detox diets are also to aid in sleep, focus, and clarity. Thus, they play a role in improving any individual’s mental state. In addition to that, these diets also help in delaying or decrease the visible signs of aging.
5. Antioxidant content
Fruits contain a lot of antioxidant-rich substances such as Vitamins A, C, E, etc. Hence, a detox diet increases the antioxidant content in the body. These antioxidants further improve blood circulation.
6. Promotes mindful eating
Whether a detox diet works in your favor or not, your relationship with food will certainly improve for the better. This is because you become extremely aware of what you are putting inside your body.
Therefore, the idea of a detox builds a healthier lifestyle. You begin to appreciate your body more than ever. You become cautious about what you eat as you know what effect it has on your body. Moreover, it brings balance into your life.
How to begin a detox diet?
We’ve worked across why one should take on such a diet. The following steps might help in beginning your detox diet:
The first thing to do before starting is to consult a nutritionist or a doctor. Ensure that following this diet will not cause any detrimental effects on your health.
Prepare to give up stimulants such as caffeine, alcohol, or tobacco. Replace them with lemon water, infused or herbal tea, or simply water.
Choose a type of detox diet that suits you the best. The diet varies from person to person based on their physique and general calorie intake.
Removal of toxins can cause symptoms like nausea, headaches, and vomiting, which are temporary and occur in the initial stages. Prepare yourself for such situations.
Plan your detox such that you don’t completely stop eating solid food. This is because; a pure detox diet does not contain carbohydrates or proteins which your body needs. So, make sure that you are getting enough nutrition but in a healthier way.
Prepare for headaches, tiredness, and nausea, which usually occur in the initial stages.
Avoid exercise during a detox. Your body has a decreased calorie intake, so, exercising is not beneficial during the course of this diet. It can cause tiredness and fatigue.
It is possible that during this diet, your tongue may get coated. Use a tongue scraper to remove this layer of bacteria.
You can definitely consume fruit and vegetables if you are looking to improve gut health as such foods contain fiber.
After the detox is over, and if you have not consumed solid foods during the course, ensure that you re-introduce it slowly but surely. If you suddenly begin eating solid food, your system will be disturbed.
For a juice diet:
Try to use organic fruits and vegetables.
Try to make your juices at home rather than buying packaged ones as they may contain preservatives and excess sugar, which goes against the purpose of your diet.
Try to use the whole fruit, including the peel while juicing. This is because; the peel also contains a lot of nutrients and minerals which are beneficial for the body.
Try to consume all your juice immediately after you have made them. Storing juices is not recommended.
Furthermore, consume fruits that are low on the glycemic index, i.e., use low sugar fruits. Although you may not like the taste of some green vegetables, those contain the most nutrients.
You can certainly try to improve the taste of your juices by adding flavorsome herbs or other spices.
Moreover, try your best to use locally grown produce to enjoy good taste and even better nutrition.
Ensure that you are hydrated throughout your diet. It is absolutely necessary to drink lots of water as it flushes out toxins.
Detox Diet Plan
Anyone looking to follow a detox diet plan must consult a nutritionist before getting started on it. The following plan is an example of what can be followed on the first day of a 3-day diet plan.
While a detox diet can prove to be extremely useful for one’s health, it is ideal to follow a balanced diet. You can find the best Indian diet plan for weight loss here.
Detox Diet Recipes
1. Cucumber and Ginger Detox Smoothie
This smoothie with ginger and cucumber is great for your digestive system! It also contains oranges which is a great source of vitamin C.
Ingredients required
30g spinach
1 cucumber
1 orange
1/2 avocado
1/2 inch ginger
1 cup of water
1 cup ice
Preparation
Chop the cucumbers and the ginger.
Peel the oranges
Cut the avocado in half and scoop it out.
Wash the spinach leaves thoroughly and roughly chop them
Add all the ingredients into a blender along with water
Blend the ingredients together until there are no lumps. Serve
Yellow Turmeric Ginger Smoothie
This smoothie has the detoxifying properties of both turmeric and ginger! This also contains squash which is a great source of iron, magnesium, and folate!
Ingredients
1 yellow squash
1 orange
1/2 tsp turmeric
1/2 inch ginger
1 tbsp hemp seed
1 cup of water
1 cup ice
Preparation
Chop the squash into small pieces.
Peel the orange and chop the ginger
Add all the ingredients into a blender
Add water and blend until smooth. Serve.
Juices and smoothies are great during a detox. Apart from this, salads and soups are also recommended. However, the best way to achieve a detox is to eat food whole. Eat fruits whole, including the peel! (Eat the peel only for some fruit like sapota or mango, not all fruit)
Detox Diet Side Effects
The apparent benefits of a detox diet do seem to be plentiful and desirable. However, these are just theoretical, and no empirical scientific evidence exists to support the science behind these benefits.
1. Natural detox mechanisms
The body itself has numerous ways of removing toxins on its own. The body eliminates its toxins through urine, through sweat, through the kidneys, the liver, the immune system, and the respiratory system.
Therefore, these mechanisms of the body render the idea of detoxification to be completely redundant. The body does not allow toxins to get accumulated, so there is nothing to “de-toxify,” which the diet claims to do.
2. Weight loss results
The weight loss that people report could mainly be just due to a decrease in calorie intake and also due to fluid loss resulting from the intake of laxatives.
Hence, after the duration of the diet is complete, you are likely to gain all the weight back leading to no actual progress. During the course of the diet, metabolism rates come down and hence, when a normal diet is resumed, rapid weight gain results.
3. Toxin removal
The body might accumulate toxins such as heavy metals or organic solvents which cannot be removed by natural metabolism, but, these cannot be removed by a detox diet either.
Therefore, if the body does have accumulated toxins, detoxing may not the way to solve the issue.
A Word of Caution
Anybody who wants to take such a diet up must consult a dietician before starting. This diet involves a massive change in eating habits and must not be done without appropriate guidance. If you are diabetic or pregnant or have an eating disorder, do not follow this diet. It may cause harm to your body.
Anybody who wishes to follow this diet must note that it may not always work in the way that it is theorized. You may experience nausea, giddiness, or feel drained out due to a decrease in calorie intake. Never take on this diet without consultation.
Summary
If you desire to cleanse your body, eat mindfully, and eat light, you can opt for a detox diet after consulting with your nutritionist. While they do have their benefits, it is necessary to understand if a detox diet suits your requirements.
Frequently Asked Questions(FAQs)
Q. What do you eat when you are detoxing?
A: Eating whole foods such as fruits and raw vegetables along with juices will help you detox.
Q. Can you lose weight while detoxing?
A: Yes, you can lose weight while detoxing. However, the detox diet requires proper planning in order to achieve the desired results. It is best to consult a nutritionist in order to ensure that your diet is balanced well.
Q. Is detox healthy for weight loss?
A: While detox diet is healthy, it does not necessarily lead to weight loss. Detox diets mainly helps in cleansing the body in order to better the functionality of the body’s system. However, it is not ideal to follow a detox diet regularly since it can lead to nutrient and calorie deficiency in the body. These diets must be followed only under professional guidance.
Q. How do you detox fast?
A: Detox can be achieved faster by fasting, drinking juices or smoothies, or eating only fruits, etc. However, such quick detoxes may not provide the same results that you may yield from a week-long detox.
About the Author
Ritu, who battled weight issues, acne and other health issues as an adolescent, managed to overcome these problems through changes in diet and lifestyle. Her success prompted her to pursue the subject professionally, leading her to a BSc in Home Science followed by an MSc in Food and Nutrition from Lady Irwin College, Delhi University. Ritu completed a training programme with All India Institute of Medical Science (AIIMS) before working with Fortis Hospital, and the Nutrition Foundation of India. Serving as a Sr. Nutritionist at HealthifyMe, she aims to help her clients to make small changes in their lifestyle that will positively impact their health. | Therefore, these mechanisms of the body render the idea of detoxification to be completely redundant. The body does not allow toxins to get accumulated, so there is nothing to “de-toxify,” which the diet claims to do.
2. Weight loss results
The weight loss that people report could mainly be just due to a decrease in calorie intake and also due to fluid loss resulting from the intake of laxatives.
Hence, after the duration of the diet is complete, you are likely to gain all the weight back leading to no actual progress. During the course of the diet, metabolism rates come down and hence, when a normal diet is resumed, rapid weight gain results.
3. Toxin removal
The body might accumulate toxins such as heavy metals or organic solvents which cannot be removed by natural metabolism, but, these cannot be removed by a detox diet either.
Therefore, if the body does have accumulated toxins, detoxing may not the way to solve the issue.
A Word of Caution
Anybody who wants to take such a diet up must consult a dietician before starting. This diet involves a massive change in eating habits and must not be done without appropriate guidance. If you are diabetic or pregnant or have an eating disorder, do not follow this diet. It may cause harm to your body.
Anybody who wishes to follow this diet must note that it may not always work in the way that it is theorized. You may experience nausea, giddiness, or feel drained out due to a decrease in calorie intake. Never take on this diet without consultation.
Summary
If you desire to cleanse your body, eat mindfully, and eat light, you can opt for a detox diet after consulting with your nutritionist. While they do have their benefits, it is necessary to understand if a detox diet suits your requirements.
Frequently Asked Questions(FAQs)
Q. What do you eat when you are detoxing?
A: Eating whole foods such as fruits and raw vegetables along with juices will help you detox.
| no |
Holistic Health | Can detox diets help in weight loss? | yes_statement | "detox" "diets" can "help" in "weight" "loss".. "weight" "loss" can be achieved through "detox" "diets". | https://www.stylecraze.com/articles/guide-for-detox-diet-plans/ | 3-day & 7-day Detox Diet Plan For Weight Loss That Really Work | Dr. Jill Carnahan is a functional medicine expert and dual board-certified in Family Medicine (ABFM) and Integrative Holistic Medicine (ABIHM) with 12 years of experience. She was also part of the first 100+ healthcare practitioners to be c... more
Dr. Jill Carnahan is a functional medicine expert and dual board-certified in Family Medicine (ABFM) and Integrative Holistic Medicine (ABIHM) with 12 years of experience. She was also part of the first 100+ healthcare practitioners to be c... more
Charushila is an ISSA certified Fitness Nutritionist and a Physical Exercise Therapist. Over a span of 6 years, she has authored more than 400 articles on diet, lifestyle, exercises, healthy food, and... more
Charushila is an ISSA certified Fitness Nutritionist and a Physical Exercise Therapist. Over a span of 6 years, she has authored more than 400 articles on diet, lifestyle, exercises, healthy food, and... more
The detox diet is a dietary strategy to flush out toxins from the body. It is a great way to cleanse and rejuvenate your system. The 3-day and 7-day detox diet plans work great for everyone. It may help you lose weight and improve your skin and hair by reducing free radicalsiXAn atom or molecule with an unpaired electron that has the potential to start a chain of events that might be harmful to cells. and inflammation.
You can go on a detox diet every 2 months because the harmful toxins from trans fats-loaded food and an unhealthy lifestyle lead to chronic low-grade inflammationiXA continuous swelling, redness, or discomfort in the body as a response to illnesses, wounds, or pathogens.. This may lead to weight gain (1). Moreover, the toxin build-up may cause hair loss, acne breakouts, constipationiXWhen stools become challenging to pass and bowel movements become less frequent (less than 3 per week)., and indigestion.
A detox diet plan may help boost metabolismiXAll chemical processes necessary to turn food into energy and maintain the organism's existing state in the cells., enhance cognitive function, aid weight loss, and make your skin glow and your hair smooth and shiny. Read on to know everything about the 3-day cleanse and 7-day cleanse diet plans for weight loss.
Why This Works
According to the British Dietetic Association, a detox diet helps the liver to detoxify and get rid of the persistent organic pollutants present in the body (2).
This 3-day meal plan is designed in a way that you can easily prepare it at home. All the ingredients are available at the supermarket, and they are low-calorie but highly nutritious. You will be concentrating on foods that are rich in vitamins, minerals, dietary fiber, protein, and complex carbs and follow cooking methods that harm the nutrients the least (3). These foods boost digestion and improve metabolism (4).
According to the American Society for Nutrition, a 3-day juice cleanse may help individuals lose weight and boost heart health (5).
Quick Tip
You can also include colorful fruits in your detox diet as they are rich in phytonutrients that are beneficial for the body (6).
Though your diet has been taken care of, you should also flush toxins off your mind. Here is what you should do.
3-Day Detox Yoga Plan
Image: Shutterstock
Neck rotations (clockwise and anticlockwise) – 1 set of 10 reps
Shoulder rotations (clockwise and anticlockwise)- 1 set of 10 reps
Full arm rotations (clockwise and anticlockwise) – 1 set of 10 reps
Wrist rotation (clockwise and anticlockwise) – 1 set of 10 reps
Waist rotation (clockwise and anticlockwise) – 1 set of 10 reps
Ankle rotation (clockwise and anticlockwise) – 1 set of 10 reps
Tadasana
Padmasana
Urdhva Mukha Savasana
Savasana
How You Will Feel By The End Of The 3-Day Detox Diet
By the end of the 3-day detox diet plan, you may feel healthier. Although there is no scientific evidence to prove it, some believe this could be due to improved gut health. Anecdotal evidence also suggests that detox diets may treat hair problems. To be precise, you may notice fewer breakouts and your hair regaining its luster. It makes you feel refreshed and improves overall wellness.
While you may love to continue being on this detox diet plan after seeing the results, instead of following this 3-day detox diet plan, over and over again, you may give the 7-day detox diet plan a try. Here is all you need to know about it.
The 7-Day Detox Diet Plan
Image: Shutterstock
The 7-day detox follows the same plan as the 3-day detox but stretches for a week. Just like the 3-day detox, the emphasis is on healthy eating of natural foods to cleanse the body of toxins and eliminate free radicals (6). You must also drink a lot of water for body cleanse. Start your morning with a glass of morning detox water to get your digestive juices going. Make sure to drink this before you have your breakfast.
Why The 7-Day Detox Diet Plan Works
The 7-day detox diet plan is designed in a way to allow those on a diet to eat foods that are organic and nutritious. The fruits and vegetables included in the 7-day diet plan may help your body get rid of the accumulated toxins, which, in turn, may improve your skin, hair, gut, and liver health (7), (8).
As you will be drinking at least 8 glasses of water throughout the day, you may not experience constipation, dehydration, and flaky skin. Improving hydration may also improve your brain function and concentration, regulate blood pressure, reduce anxiety and depression (9), (10). Mary Sabat, MS, RDN, LD, says, “Typically, in the first week, people drop the most weight as they are also dropping some fluid. When we start to lose weight, we also lose fluid as the glycogen stores that are used up first carry water. As we get into our fat stores, the fluid weight decreases, and it’s more fat that is burned, so the weight loss is slower. I would say people could lose up to 7 lbs. In week 1 and with a 21-day detox, possibly up to 16 lbs.”
Along with taking care of what you eat, you should also take care of your body by exercising regularly. Here is a 7-day detox yoga plan for you.
Tip: If you are someone who likes cardio and strength training, you can hit the gym or do cardio at home. You can also do simple exercises, such as running up the stairs, brisk walking, jogging, rope jumping, biking, swimming, dancing, etc.
How You Will Feel After the 7-Day Detox Diet
You may notice a difference in how your body and mind respond to various internal and external stimuli. You would be surprised how all your health problems may start diminishing. Most importantly, you may feel rejuvenated and fresh.
While you are on the detox diet plan, you should avoid eating foods that may cause a toxic build-up in your system. Here is a list of foods that you should avoid.
How Many Days Should You Be On The Detox Diet?
It is recommended to follow the detox diet for at least 24 days. After 24 days, it may become a habit to eat nutritious foods and snack wisely. You may also learn to take care of your physical and mental health. It would not feel like a “diet” anymore.
The next most common question that may pop into your head is, what should you do if you are on medication? Here is what you should do.
Should You Be On The Detox Diet If You Are On Medication?
A detox diet is all about eating clean and incorporating healthy habits to promote better health. Hence, you can be on a detox diet while you are on medication. But always check with your doctor before starting the diet plan.
Other Ways To Detox
Traditional saunas cause more sweating than infrared saunas, making them more efficient in removing toxic elements from the body (11).
Things To Keep In Mind
Before you start your detox and cleanse program, keep these pointers in mind and make this a daily habit. You will make the most of the 3-day detox plan and 7-day detox plan.
Make sure you drink at least 8 oz of warm water in the morning. Add freshly squeezed lemon juice to it to ensure your body gets vitamin C, which will spur the production of digestive juices. Katherine Gomez, RDN, says, “Lemon water can help you feel fuller, stay hydrated, enhance your metabolism, and lose weight. However, lemon water is no better than plain water for weight loss. You can reduce weight by drinking two glasses of warm lemon water each morning and evening.”
Along with the consumption of fresh fruit juices, such as apple, orange, and pineapple, make sure you also drink at least 8 glasses of water throughout the day. Juicing makes it easier for the body to absorb the nutrients in fruits and vegetables.
During the 3-day detoxification process, it is necessary to flush out your kidneys and liver. Drink dandelion or chamomile tea as they are effective natural remedies for liver detoxification. Drinking fresh fruit and veggie juices can also help.
Daily exercise is a must. This can be in the form of jogging, brisk walking, or aerobics.
Sleep is important, so make sure you get about 8 hours of sleep every night. If possible, take a short nap of 30 minutes in the afternoon.
If you do not follow these tips and the diet plan properly, you might experience a few side effects.
Potential Risks Of A Detox Diet
Sudden changes to your eating habits may cause your body to react in certain ways. The first few days of the diet may seem challenging because of the following issues:
Headache
Tiredness
Sleepiness
Restlessness
Stomach troubles
Muscle aches
Irritability
Nausea
These are some of the risks associated with detox diets. However, these improve with proper hydration and nutrition. Your body will also get used to the changes in a day or two. However, consult your doctor if these side effects persist.
Infographic: Signs Your Body Needs A Detox
As per anecdotal evidence, a detox diet can flush out all toxins from the body and help you lose weight and improve skin health. However, some signs may suggest the presence of toxins in your body. You need to rejuvenate your skin and cleanse your body as soon as possible if you observe these symptoms. Check out the infographic below to learn about the signs that show your body needs a detox.
The detox diet aims at flushing out toxins from your body and cleansing your whole internal system. This may reflect in your improved skin and hair health along with a boost in your immunity levels. You may opt for a 3-day or 7-day detox diet plan and further supplement with relevant yoga asanas to make the most of this cleansing period. Most food options included in the detox diet plan are rich in essential vitamins and minerals to help boost digestion and improve your metabolism. Including clean eating habits and balanced meal options would help you feel better in and out in a matter of days.
Frequently Asked Questions
Does detox make you lose belly fat?
The detox diet takes care of your nutritional intake while cleansing your gut and intestines of toxic build-up. Though the research is limited, the diet is also believed to improve your metabolism and make losing stubborn belly fat easier. However, sticking to a healthy balanced diet and regular workout is essential to find any visible difference.
Sources
Articles on StyleCraze are backed by verified information from peer-reviewed and academic research papers, reputed organizations, research institutions, and medical associations to ensure accuracy and relevance. Read our editorial policy to learn more.
High intake of fruit and vegetables is related to low oxidative stress and inflammation in a group of patients with type 2 diabetes Scandinavian Journal of Food & Nutrition US National Library of Medicine National Institutes of Health. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2606994/
Related
Dr. Jill Carnahan is a functional medicine expert and dual board-certified in Family Medicine (ABFM) and Integrative Holistic Medicine (ABIHM) with 12 years of experience. She was also part of the first 100+ healthcare practitioners to be certified in Functional Medicine through the Institute of Functional Medicine (IFMCP). Dr. Carnahan completed her residency at the University of Illinois Program in...more
Charushila is an ISSA certified Fitness Nutritionist and a Physical Exercise Therapist. Over a span of 6 years, she has authored more than 400 articles on diet, lifestyle, exercises, healthy food, and fitness equipment. She strives to inform, educate, and motivate her readers via authentic, straightforward, and fact-checked information. After completing her master's in biotechnology from Vellore Institute of Technology,...more
Mary SabatMS, RDN, LD
Mary Sabat, MS, RDN, LD, is a registered dietitian and a certified in personal training by the American Council of Exercise. She has 30 years of experience in nutrition education, wellness coaching, fitness training, holistic health, and weight loss coaching. She obtained her bachelor's degree in Dietetics and Nutrition from the University of Delaware and master’s degree in Human Nutrition with an emphasis on Exercise Science from Rutgers University.
Mary Sabat, MS, RDN, LD, is a registered dietitian and a certified in personal training by the American Council of Exercise. She has 30 years of experience in nutrition education, wellness coaching, fitness training, holistic health, and weight loss coaching. She obtained her bachelor's degree in Dietetics and Nutrition from the University of Delaware and master’s degree in Human Nutrition with an emphasis on Exercise Science from Rutgers University.
StyleCraze provides content of general nature that is designed for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Click here for additional information. | It is a great way to cleanse and rejuvenate your system. The 3-day and 7-day detox diet plans work great for everyone. It may help you lose weight and improve your skin and hair by reducing free radicalsiXAn atom or molecule with an unpaired electron that has the potential to start a chain of events that might be harmful to cells. and inflammation.
You can go on a detox diet every 2 months because the harmful toxins from trans fats-loaded food and an unhealthy lifestyle lead to chronic low-grade inflammationiXA continuous swelling, redness, or discomfort in the body as a response to illnesses, wounds, or pathogens.. This may lead to weight gain (1). Moreover, the toxin build-up may cause hair loss, acne breakouts, constipationiXWhen stools become challenging to pass and bowel movements become less frequent (less than 3 per week)., and indigestion.
A detox diet plan may help boost metabolismiXAll chemical processes necessary to turn food into energy and maintain the organism's existing state in the cells., enhance cognitive function, aid weight loss, and make your skin glow and your hair smooth and shiny. Read on to know everything about the 3-day cleanse and 7-day cleanse diet plans for weight loss.
Why This Works
According to the British Dietetic Association, a detox diet helps the liver to detoxify and get rid of the persistent organic pollutants present in the body (2).
This 3-day meal plan is designed in a way that you can easily prepare it at home. All the ingredients are available at the supermarket, and they are low-calorie but highly nutritious. You will be concentrating on foods that are rich in vitamins, minerals, dietary fiber, protein, and complex carbs and follow cooking methods that harm the nutrients the least (3). | yes |
Holistic Health | Can detox diets help in weight loss? | yes_statement | "detox" "diets" can "help" in "weight" "loss".. "weight" "loss" can be achieved through "detox" "diets". | https://health.clevelandclinic.org/are-you-planning-a-cleanse-or-detox-read-this-first/ | Do Detoxes and Cleanses Actually Work? – Cleveland Clinic | Looking for health + wellness advice?
Do Detoxes and Cleanses Actually Work?
You hear a lot about the supposed health benefits of cleanses and detoxes. These quick fixes supposedly remove toxins from your body and make you healthier — like the TikTok Detox drink or the much-hyped “internal shower.”
We talked to registered dietitian Kate Patton, MEd, RD, CSSD, LD, to get the low down on detoxes and cleanses and whether they’re all they’re cracked up to be.
What you may not realize, Patton says, is that our bodies naturally detox. Every day, your digestive tract, liver, kidneys and skin break down toxins and eliminate them through your urine, stool and sweat. So, that celery juice you’ve been downing? Probably not doing what you think it is.
What is a detox cleanse?
“That supposedly gives your digestive system a break, allowing it to heal and better absorb nutrients in the future,” explains Patton. “Most of the time, the ingredients suggested in a cleanse aren’t necessarily bad for you. They’re just not likely to do what they say.”
Types of detoxes and cleanses
Detox diets and cleanses often suggest replacing solid foods with drinks like special water, tea or fruit and vegetable juices. While popular on social media, the effects of detoxes and cleanses haven’t been backed up by any substantial scientific research.
Good stuff, that green tea. Does that mean you should drink it by the gallon to cleanse your whole system and make you radiant? Not exactly.
“Green tea is caffeinated, so you want to be careful about not overdoing it,” Patton says. “Also, drinking an excessive quantity of green tea or taking high dosages of green tea supplements is linked to upset stomachs, liver disease, bone disorders and other issues.”
Juice cleanses
An entire industry has been built around the notion of cleaning out your system with a series of juices. The idea is that all those vitamins and minerals can kick-start your system by purging toxins and giving you a clean slate.
At least one study shows that because “juicing” is commonly associated with a low consumption of calories, it can lead to some quick weight loss. But the effects aren’t likely to last. And those little juice bottles can be costly.
Detox water
Some people claim that drinking water laced with lemon, apple cider, cayenne pepper or other additives will do amazing things for you. Clearer skin! Weight loss! Better poops!
OK, nothing wrong with drinking water. Water makes up 60% of your body and is super important for your body to function properly.
A water detox drink? Eh. It’s probably not going to do much for you in reality. If flavoring your water with a little cucumber — or vinegar for that matter — is your thing, go for it. Just don’t expect any miracles.
Careful, too, not to drink excessive amounts of water. If you drink so much your pee is constantly clear you’re overdoing it and could be losing out on electrolytes and salt your body needs, Patton says. The basic rule of thumb is to aim for drinking 64 ounces of fluid a day to keep your system operating at peak efficiency.
Do detoxes actually work?
Unless you have a digestive disorder such as Crohn’s disease or gastroparesis, there’s no conclusive medical evidence that detoxes or cleanses will benefit your digestive tract.
“Solid foods are helpful and important to a healthy diet,” Patton says.
Sure, you may lose a few pounds if you replace food with water, but it’s unlikely to last.
“Cleanses aren’t effective for long-term weight loss,” she continues. “The weight you lose from a cleanse is a result of losing water, carbohydrate stores and stool, which all return after you resume a regular diet.”
For athletes, losing carbohydrate stores means losing your body’s preferred fuel source during exercise. So, a cleanse isn’t appropriate while training for any sport. If you choose to do a cleanse or detox, do so for no more than two days during a recovery week when you are doing little to no exercise.
Should you try a detox or cleanse?
Before you decide to cleanse and spend big bucks on a magic drink or pounds of freshly juiced fruits and vegetables, Patton says to be sure to weigh the benefits and drawbacks.
Pros
Cons
You can benefit from an increased intake of vitamins and minerals either naturally from juiced fruits and veggies or supplemented from drinks.
Cleanse and detox diets are low in calories, which will leave you with little energy to exercise and may disrupt your metabolism and blood sugar levels.
Cleansing and detoxing can help you identify food sensitivities by eliminating certain foods for several days, then gradually reintroducing potential trigger foods.
You may experience gastrointestinal distress and frequent bowel movements.
Detox diets are low in protein, which is an important food group to support your hair, skin, nails and muscles.
Whatever you decide, remember that your body is designed to detox itself, so sipping on lemon water with maple syrup — or whatever your detox of choice may be — likely won’t lead to any long-term health gains.
“A balanced diet of whole foods such as vegetables, fruit, whole grains and legumes is healthy for your entire body,” Patton says. “Your body is built to take care of business, and fueling it with healthy foods will help you achieve the results you’re looking for.” | The basic rule of thumb is to aim for drinking 64 ounces of fluid a day to keep your system operating at peak efficiency.
Do detoxes actually work?
Unless you have a digestive disorder such as Crohn’s disease or gastroparesis, there’s no conclusive medical evidence that detoxes or cleanses will benefit your digestive tract.
“Solid foods are helpful and important to a healthy diet,” Patton says.
Sure, you may lose a few pounds if you replace food with water, but it’s unlikely to last.
“Cleanses aren’t effective for long-term weight loss,” she continues. “The weight you lose from a cleanse is a result of losing water, carbohydrate stores and stool, which all return after you resume a regular diet.”
For athletes, losing carbohydrate stores means losing your body’s preferred fuel source during exercise. So, a cleanse isn’t appropriate while training for any sport. If you choose to do a cleanse or detox, do so for no more than two days during a recovery week when you are doing little to no exercise.
Should you try a detox or cleanse?
Before you decide to cleanse and spend big bucks on a magic drink or pounds of freshly juiced fruits and vegetables, Patton says to be sure to weigh the benefits and drawbacks.
Pros
Cons
You can benefit from an increased intake of vitamins and minerals either naturally from juiced fruits and veggies or supplemented from drinks.
Cleanse and detox diets are low in calories, which will leave you with little energy to exercise and may disrupt your metabolism and blood sugar levels.
Cleansing and detoxing can help you identify food sensitivities by eliminating certain foods for several days, then gradually reintroducing potential trigger foods.
You may experience gastrointestinal distress and frequent bowel movements.
Detox diets are low in protein, which is an important food group to support your hair, skin, nails and muscles.
Whatever you decide, remember that your body is designed to detox itself, | no |
Holistic Health | Can detox diets help in weight loss? | yes_statement | "detox" "diets" can "help" in "weight" "loss".. "weight" "loss" can be achieved through "detox" "diets". | https://timesofindia.indiatimes.com/life-style/health-fitness/weight-loss/do-you-think-detox-diets-can-help-in-weight-loss-heres-the-truth-behind-the-same/articleshow/63218159.cms | Do you think detox diets can help in weight loss? Here's the truth ... | To understand if a detox diet can help you lose weight, first what we need to understand is what a detox diet is? Detoxification is a process where you get rid of toxins from your body by following a proper diet regimen. A detox diet encourages you to drink plenty of water and eat fruits and veggies. Though detoxifying your body once in a while is important but some detox diets have harmful effects just like fad diets. Detoxification may help you lose weight but it does not lead to permanent weight loss.
What is detox diet? There are many types of detox diets, some include not eating at all and being on a liquid diet for some time. While some encourage you to have only fruits. Some also include enema. Laxatives are also a part of the detoxification process. It is said detoxification process can help to get one rid of toxins.
What are toxins? Toxins, as the name suggests are the chemicals have the potential to cause harm to your body. These toxins are everywhere, in the food you eat, where you work, in your car, on your sofa and everywhere. Toxins, once when they enter your body are processed through organs like kidneys and liver and then later are eliminated through urination, perspiration and bowel movements. Does detoxification actually help you to get rid of toxins?
Itâs true that these toxins do not leave our body completely through the natural process of perspiration and urination. These toxins linger in our digestive and lymph systems. These toxins can make you sick. So, detoxification means stop eating foods that may contain toxins in them. Talking about the positive effects of detox diet, people who have tried it say that following it increases your energy level and in some cases, it also prevents and even cures certain health conditions. Read here : Have You Tried Atkins diet for Weight loss? Detox diet and weight loss As detox plans are so much in fashion, you can surely see some your friend at office carrying a water bottle with cucumber and carrots in it. If you restrict yourself from eating certain foods for some time and also do portion control, it obviously helps you lose weight. But detox diet is not one of the best methods when it comes to permanent weight loss. These diets may also not suit everyone as it includes giving up an entirely. During the detox process, what you lose is water weight and not fat weight. That is the reason once you stop doing it, you gain back the lost amount of weight. Detox diet can also lead to muscle loss. And muscle loss is not a great thing if you want to lose weight permanently. Muscles help you burn calories even if you do not do anything. Your muscles burn a certain number of calories just to remain in your body. Metabolism Metabolism is directly proportional to weight loss. The higher the metabolism the more you lose weight. And much to your surprise detox diet slows down your metabolism. And thus making it hard for you to lose weight in future. Who should not do detox diets? Pregnant women, diabetics, teenagers, children, people suffering from a heart disease and any other serious medical condition should not follow a detox diet. Even people with any sort of eating disorder should not follow detox plans. People playing sports or those who have very demanding jobs should not follow detox diet as it will leave them deficient in nutrients and thus energy. So, before starting any detox diet which involves any food restriction or eating any particular food, it is important to consult your doctor | To understand if a detox diet can help you lose weight, first what we need to understand is what a detox diet is? Detoxification is a process where you get rid of toxins from your body by following a proper diet regimen. A detox diet encourages you to drink plenty of water and eat fruits and veggies. Though detoxifying your body once in a while is important but some detox diets have harmful effects just like fad diets. Detoxification may help you lose weight but it does not lead to permanent weight loss.
What is detox diet? There are many types of detox diets, some include not eating at all and being on a liquid diet for some time. While some encourage you to have only fruits. Some also include enema. Laxatives are also a part of the detoxification process. It is said detoxification process can help to get one rid of toxins.
What are toxins? Toxins, as the name suggests are the chemicals have the potential to cause harm to your body. These toxins are everywhere, in the food you eat, where you work, in your car, on your sofa and everywhere. Toxins, once when they enter your body are processed through organs like kidneys and liver and then later are eliminated through urination, perspiration and bowel movements. Does detoxification actually help you to get rid of toxins?
Itâs true that these toxins do not leave our body completely through the natural process of perspiration and urination. These toxins linger in our digestive and lymph systems. These toxins can make you sick. So, detoxification means stop eating foods that may contain toxins in them. Talking about the positive effects of detox diet, people who have tried it say that following it increases your energy level and in some cases, it also prevents and even cures certain health conditions. Read here : Have You Tried Atkins diet for Weight loss? Detox diet and weight loss As detox plans are so much in fashion, you can surely see some your friend at office carrying a water bottle with cucumber and carrots in it. | yes |
Holistic Health | Can detox diets help in weight loss? | no_statement | "detox" "diets" cannot "help" in "weight" "loss".. "weight" "loss" cannot be achieved through "detox" "diets". | https://www.advanceer.com/resources/blog/2019/may/detox-side-effects-the-hidden-dangers-of-detox-p/ | Detox Side Effects | Dangers of Detox Pills & Diets | Detox Side Effects: The Hidden Dangers of Detox Products
The Dangers of Detox Pills, Detox Diets and More
Detox diets, pills, and other products are all the rage right now, but are they as safe and effective as advertised? Here’s your guide to detox side effects.
If you're interested in losing weight, there are a lot of options available to you.
Some people use exercise as their main way to lose weight. Others rely on altering their eating habits and may follow a diet like keto. But there's one new weight loss trend that seems to be growing in popularity: detox diets.
It seems like everyone from Instagram models to celebrities is talking about the benefits of detox teas, smoothies, and pills.
Detox diets may be popular, but are they safe? Some people trying these may have never considered detox side effects.
If you're considering doing a detox diet, don't make any decisions before you read this post.
Contact the professionals at Advance ER today to learn more about the hidden dangers of detox pills, detox diets and more.
What Is Detoxing?
Detoxing, also known as detoxification, is the practice of ridding the body of toxic or harmful substances.
Detox diets and products may be popular now, but the concept of detoxifying the body isn't new. People have been looking for ways to "purify" the human body for thousands of years.
Saunas and sweat lodges have been used as ways to detoxify the body. Some people believe that sweat is one of the best ways to get rid of body impurities.
Others have used other more extreme methods to purify their bodies. Enemas, fasting, and even bloodletting have all been viewed as ways to rid the body of toxins.
Why Do People Detox?
People that live in today's world have legitimate concerns about the chemicals we put into our bodies.
Some people are concerned about how environmental pollutants could be affecting their bodies. Others may be focused on chemicals and hormones we get from the dairy and meat we eat each day.
Many people believe that toxins are responsible for a variety of ailments in their lives. Toxins have been blamed for nearly everything from headaches and fatigue to obesity and other chronic health conditions.
Detox diets also usually offer positive side effects that go beyond weight loss. Some diets and pills claim to give people more energy, heal skin conditions like psoriasis, and even help improve mental health.
All of these concerns and wanted benefits are legitimate, but detox diets may not be the best way to address them.
The "Benefits" of Detox Diets
There are some legitimate benefits that come from some of the practices that surround detox diets.
The average American diet is very high in processed, high-calorie foods that don't have a lot of nutritional value. A lot of detox diets will focus on cutting out those foods and replacing them with lean meats, whole grains, fruits, and veggies.
Improving your diet is always helpful. The added vitamins and minerals you could get from detox products could also positively affect your diet. But in all fairness, you could get these helpful benefits by just improving your diet and not "detoxing".
What Does A Detox Pill Do To Your Body?
It is important for the body to be able to rid itself of toxins, but the likelihood of a detox pill or diet doing that is very low. The truth is that the human body already has very effective ways to deal with detoxing itself.
Your liver and kidneys are designed to filter out harmful substances in your body. To some extent, even your skin and lungs can do work to protect the body from harmful toxins.
If your organs are functioning normally and your body is healthy, you don't need to do anything else to help your body detoxify itself. Eating right, exercising, and taking care of yourself are far more effective detoxing methods.
On the off chance that your body does have something dangerous or toxic inside of it, you'd need help from a doctor or medical professional. A green drink or detox pills can't help you fight truly toxic substances.
Dangerous Detox Side Effects
At best, detox products and diets won't largely affect people's wellbeing and could give them some minor positive benefits. At worst, detox products can do some serious harm to the body.
One of the problems around the detox craze is that methods are largely unregulated and untested. You could easily buy something that could end up being harmful to the body.
If you're thinking about doing a detox diet, you may change your mind after you learn about the negative ways they could affect your body.
Dehydration
It isn't uncommon for some detox diets to use laxatives or diuretics so people use the bathroom more.
When those medications are given by doctors and taken over a short period of time they're safe. But when people take them over long periods of time it could lead to severe dehydration.
Dehydration is more than just needing more fluids. Overtime dehydration could do serious damage to major organs or could lead to more serious health problems like seizures.
Stomach Problems
Detox pills and diets can use a variety of substances to "purge" the body of toxins. The laxatives, supplements, and even the "helpful" bacteria used in some of these products can cause severe gastrointestinal issues.
Some people on detox diets and cleanses can have problems with diarrhea, nausea, and vomiting.
Nutrient Deficiencies
A lot of detox diets have people eliminate certain foods that are believed to cause the buildup of toxins.
Plenty of people cut meat and dairy out of their diets with no problem, but that's usually paired with changing their diets to make up for the lack of nutrients.
Many of these detox diets involve cutting important nutrients out of your diet without having a safe way to replace them. You could be missing out on crucial vitamins and minerals if you follow detox diets.
The Bottom Line
Your body is already doing a great job of filtering toxins out of your system. The detox side effects you could get from diets and products are severe enough to make anyone think twice about doing them.
We encourage everyone that's interested in losing weight and "purifying" their body to eat right and exercise. That's more than enough to help your body and improve your health.
Do you have any questions or concerns about diets? Contact us today so we can give you the answers you need.
The information on this website is for general information purposes only.
Nothing on this site should be taken as medical advice for any individual
case or situation. This information is not intended to create, and receipt
or viewing does not constitute, a doctor-patient relationship. | Toxins have been blamed for nearly everything from headaches and fatigue to obesity and other chronic health conditions.
Detox diets also usually offer positive side effects that go beyond weight loss. Some diets and pills claim to give people more energy, heal skin conditions like psoriasis, and even help improve mental health.
All of these concerns and wanted benefits are legitimate, but detox diets may not be the best way to address them.
The "Benefits" of Detox Diets
There are some legitimate benefits that come from some of the practices that surround detox diets.
The average American diet is very high in processed, high-calorie foods that don't have a lot of nutritional value. A lot of detox diets will focus on cutting out those foods and replacing them with lean meats, whole grains, fruits, and veggies.
Improving your diet is always helpful. The added vitamins and minerals you could get from detox products could also positively affect your diet. But in all fairness, you could get these helpful benefits by just improving your diet and not "detoxing".
What Does A Detox Pill Do To Your Body?
It is important for the body to be able to rid itself of toxins, but the likelihood of a detox pill or diet doing that is very low. The truth is that the human body already has very effective ways to deal with detoxing itself.
Your liver and kidneys are designed to filter out harmful substances in your body. To some extent, even your skin and lungs can do work to protect the body from harmful toxins.
If your organs are functioning normally and your body is healthy, you don't need to do anything else to help your body detoxify itself. Eating right, exercising, and taking care of yourself are far more effective detoxing methods.
On the off chance that your body does have something dangerous or toxic inside of it, you'd need help from a doctor or medical professional. | yes |
Holistic Health | Can detox diets help in weight loss? | no_statement | "detox" "diets" cannot "help" in "weight" "loss".. "weight" "loss" cannot be achieved through "detox" "diets". | https://www.cnn.com/2017/06/09/health/sugar-detox-food-drayer/index.html | One-month sugar detox: A nutritionist explains how and why | CNN | Story highlights
Reducing sugar in your diet can help you drop pounds and improve your health
CNN
—
If you’ve read about the latest wellness trends, you may have entertained the idea of a diet detox.
But whether you’ve considered juicing, fasting or cleansing in an effort to lose weight or improve your well-being, you’re probably aware that drastically cutting out foods is not effective as a long-term lifestyle approach to healthy eating.
But there is one kind of sustainable detox that is worthwhile, according to some experts. Reducing sugar in your diet can help you drop pounds, improve your health and even give you more radiant skin.
“Sugar makes you fat, ugly and old,” said Brooke Alpert, a registered dietitian and co-author of “The Sugar Detox: Lose the Sugar, Lose the Weight – Look and Feel Great.” “What we’ve discovered in the last couple of years is that sugar is keeping us overweight. It’s also a leading cause of heart disease; it negatively affects skin, and it leads to premature aging.”
Sugar addiction
Here’s more bad news: We can’t stop consuming sugar. “People have a real dependency – a real addiction to sugar,” Alpert said. “We have sugar, we feel good from it, we get (the feeling of) an upper, and then we crash and need to reach for more.”
About 10% of the US population are true sugar addicts, according to Robert Lustig, professor of pediatrics and member of the Institute for Health Policy Studies at the University of California, San Francisco. What’s more, research suggests that sugar induces rewards and cravings that are similar in magnitude to those induced by addictive drugs.
One of the biggest concerns is the amount of added sugars in our diets, which are often hidden in foods. Although ice cream cake is an obvious source of sugar, other foods that may not even taste sweet – such as salad dressings, tomato sauces and breads – can be loaded with the white stuff.
How to sugar detox: Going cold turkey for three days
The good news is that even if you’re not a true sugar “addict,” by eliminating sugar from your diet, you can quickly lose unwanted pounds, feel better and have a more radiant appearance.
“There is no one person who wouldn’t benefit by eliminating added sugars from their diets,” Lustig said.
Children can benefit, too. Lustig’s research revealed that when obese children eliminated added sugars from their diets for just nine days, every aspect of their metabolic health improved – despite no changes in body weight or total calories consumed.
“Early on in my practice, when I would notice that people had real addiction to sugar, we’d start trying to wean them of sugar or limit their intake or eat in moderation … but the word ‘moderation’ is so clichéd and not effective,” Alpert said. “It was just ineffective to ask people to eat less of something when they’re struggling with this bad habit. You wouldn’t ask an alcoholic to just drink two beers.
“What was so successful in getting my clients to kick their sugar habit was to go cold turkey. When they would go cold turkey, I wasn’t their favorite person – but the number one positive effect was that it recalibrated their palate,” she said. “They could now taste natural sugars in fruits, vegetables and dairy that they used to be so dulled to.”
So for the first three days on a sugar detox, Alpert recommends no added sugars – but also no fruits, no starchy vegetables (such as corn, peas, sweet potatoes and butternut squash), no dairy, no grains and no alcohol. “You’re basically eating protein, vegetables and healthy fats.”
For example, breakfast can include three eggs, any style; lunch can include up to 6 ounces of poultry, fish or tofu and a green salad, and dinner is basically a larger version of lunch, though steamed vegetables such as broccoli, kale and spinach can be eaten in place of salad. Snacks include an ounce of nuts and sliced peppers with hummus. Beverages include water, unsweetened tea and black coffee.
Though they don’t contribute calories, artificial sweeteners are not allowed on the plan, either. “These little pretty colored packets pack such a punch of sweetness, and that’s how our palates get dulled and immune and less reactive to what sweetness really is,” Alpert said.
Consuming artificial sweeteners causes “you not only (to) store more fat,” Lustig explained, “you also end up overeating later on to compensate for the increased energy storage.”
How to sugar detox: When an apple tastes like candy
Once the first three days of the sugar detox are completed, you can add an apple.
Starting with day four, you can add one apple and one dairy food each day. Dairy, such as yogurt or cheese, should be full-fat and unsweetened. “Fat, fiber and protein slow the absorption of sugar, so taking out fat from dairy will make you absorb sugar faster,” Alpert said.
You can also add some higher-sugar vegetables such as carrots and snow peas, as well as a daily serving of high-fiber crackers. Three glasses of red wine in that first week can be added, too.
During week two, you can add a serving of antioxidant-rich berries and an extra serving of dairy. You can also add back starchy vegetables such as yams and winter squash.
For week three, you can add grains such as barley, quinoa and oatmeal, and even some more fruit including grapes and clementines. You can also have another glass of red wine during the week and an ounce of dark chocolate each day.
“Week three should be quite livable,” Alpert said.
Week four is the home stretch, when you can enjoy two starches per day, including bread and rice, in addition to high-fiber crackers. Wine goes up to five glasses per week.
“You can have a sandwich in week four, which just makes things easier,” Alpert said. “I want people living. Week four is the way to do it.”
Week four defines the maintenance part of the plan – though intentional indulgences are allowed, such as ice cream or a piece of cake at a birthday party. “Because the addictive behavior is gone, having ice cream once or twice will not send you back to square one,” Alpert said. Additionally, no fruit is off-limits once you’ve completed the 31 days.
“The whole purpose is to give people control and ownership and a place for these foods in our life,” Alpert said.
Benefits and cautions with slashing sugar
Detoxing from sugar can help you lose weight quickly. “We had over 80 testers from all over the country, and they lost anywhere between 5 to 20 pounds during the 31 days, depending on their weight or sugar addiction,” Alpert said. “Many also noticed that a lot of the weight was lost from their midsection. Belts got looser!”
Participants also reported brighter eyes, clearer skin and fewer dark circles. They also had more energy and fewer mood swings.
“I have lost approximately 40 pounds following the sugar detox,” said Diane, who preferred not to share her last name. She has been on the plan for approximately two years.
“I thought I was educated on weight loss, but like many, I was miseducated, and by reducing fat, I was really just adding sugar. With the elimination of sugar, including artificial sweeteners, it is incredible how sweet foods tastes.”
Diane added back some healthy fats into her diet, which keeps her feeling satisfied. And her sugar cravings disappeared. “This is probably the longest I have remained on a plan, and I don’t feel like this will change. It just feels natural and normal.”
There are challenges and medical considerations before starting, though. Since the first few days of a sugar detox can be challenging, it’s important to pick three days during which your schedule will be supportive.
“Depending on how intense your addiction is, you can experience withdrawal symptoms, such as brain fog, crankiness and fatigue,” Alpert said. Lustig found that the children in his study experienced anxiety and irritability during the first five days of eliminating sugar and caffeine, though it eventually subsided.
“If you feel bad, stop and have a piece of fruit. But if you can push through and stay well-hydrated, you can really break your cycle of sugar addiction,” Alpert said.
Follow CNN Health on Facebook and Twitter
See the latest news and share your comments with CNN Health on Facebook and Twitter.
It’s important to note that the plan may not be appropriate for diabetics, extreme athletes or anyone taking medication to control blood sugar. It is also not recommended for pregnant women.
Finally, before starting a sugar detox, enlist the help of friends and/or family members for support. “You need people around you to help you be successful,” Lustig said. “The whole family has to do it together.” | Story highlights
Reducing sugar in your diet can help you drop pounds and improve your health
CNN
—
If you’ve read about the latest wellness trends, you may have entertained the idea of a diet detox.
But whether you’ve considered juicing, fasting or cleansing in an effort to lose weight or improve your well-being, you’re probably aware that drastically cutting out foods is not effective as a long-term lifestyle approach to healthy eating.
But there is one kind of sustainable detox that is worthwhile, according to some experts. Reducing sugar in your diet can help you drop pounds, improve your health and even give you more radiant skin.
“Sugar makes you fat, ugly and old,” said Brooke Alpert, a registered dietitian and co-author of “The Sugar Detox: Lose the Sugar, Lose the Weight – Look and Feel Great.” “What we’ve discovered in the last couple of years is that sugar is keeping us overweight. It’s also a leading cause of heart disease; it negatively affects skin, and it leads to premature aging.”
Sugar addiction
Here’s more bad news: We can’t stop consuming sugar. “People have a real dependency – a real addiction to sugar,” Alpert said. “We have sugar, we feel good from it, we get (the feeling of) an upper, and then we crash and need to reach for more.”
About 10% of the US population are true sugar addicts, according to Robert Lustig, professor of pediatrics and member of the Institute for Health Policy Studies at the University of California, San Francisco. What’s more, research suggests that sugar induces rewards and cravings that are similar in magnitude to those induced by addictive drugs.
One of the biggest concerns is the amount of added sugars in our diets, which are often hidden in foods. Although ice cream cake is an obvious source of sugar, other foods that may not even taste sweet – such as salad dressings, tomato sauces and breads – can be loaded with the white stuff.
| yes |
Veterinary Science | Can dogs understand human language? | yes_statement | "dogs" can "understand" "human" "language".. "human" "language" can be understood by "dogs". | https://vcahospitals.com/know-your-pet/eavesdropping-dogsdo-dogs-understand-our-conversations | Eavesdropping Dogs: Do Dogs Understand Our Conversations ... | Eavesdropping Dogs...Do Dogs Understand Our Conversations?
Well trained dogs oblige their masters. They sit, stay, and come when asked. Our faithful companions respond when we speak directly to them. Do they also understand when we talk to other people? Do they grasp our private telephone conversations? Do they comprehend our dinner table discussions? Are our dogs eavesdropping on us?
Canine Language Capabilities
Most dog owners will agree that their dogs understand familiar words. Say, “Sit” and your dog will collapse upon his haunches. Say “Let’s go for a walk” and he’ll run to the door and grab his leash. Say, “It’s time to eat” and he’ll head for the food bowl. It appears that they understand the words sit, walk, and eat leading us to believe that dogs learn to associate specific words with specific actions or objects.
Our dogs may get what we say, but what we say is only part of the equation. How we say it impacts how much a dog comprehends. Dogs interpret human spoken language as well as human body language in their effort to understand us. There are debates regarding just how much each factor (what we say and how we say it) plays in canine communication.
How
Some people think how we say something can be more important than what we say. Dogs read more into our tone and body language than our actual words. They focus on us and observe our physical clues to determine what we want them to do or not do. They watch our facial expressions, posture, and body movements. They listen to the tone of our voice. They combine all of these observations to determine our meaning.
"Some people think how we say something can be more important than what we say."
If you smile and excitedly say “Let’s go for a walk!”, your dog will likely wag his tail and prance around enthusiastically. If you utter those very same words in a gruff voice with a scowl on your face, he may cower and whine.
Making these observations led many scientists to feel that dogs respond much like human infants in understanding our language. In fact, dogs may have basically the same cognitive ability as a 6-12-month-old human infant. Think about this. Both a dog and a human baby quickly grasp the meaning of “NO!” when grabbing a crumb from the floor and trying to pop it in their mouths. Do they really know the difference between “yes” and “no” or do they respond to our commanding tone of voice and anxious body language?
Could it be a combination of learned vocabulary and observation of body language and tone? With repetition, both dogs and babies will associate certain words with certain objects or actions. That’s why we say, “Sit” over and over while prompting the dog to actually sit. Eventually he associates the word with the action. It’s also why we say “dog” to our baby while pointing to the dog. Eventually the little human understands that this furry creature is called “dog”.
"Body language, tone, and words are all involved in effective canine communication."
Even though many scientists agree that dogs understand specific words, some believe they don’t comprehend full sentences. They feel that saying “trees, birds, grass, walk” invokes the same meaning as, “let’s go for a walk”. While the dog may not understand every word in the sentence, he gets “walk”. And if you say those words with enthusiasm in a sweet voice, your dog will bolt for the front door! Body language, tone, and words are all involved in effective canine communication.
Despite a limited vocabulary, dogs and babies communicate with us. They may not be verbal creatures, but they manage to “speak” back to us. Even without an extensive vocabulary, they make us understand their whines, cries, and coos especially when combined with their own special body language.
What
Now let’s focus on what we say. Some scientists believe that dogs understand the actual meaning of many words unrelated to the tone in which they are delivered. Here’s how this theory took root.
Researchers trained dogs to lie in an MRI machine. The scientists monitored the dogs’ brain activity while speaking to them. They learned that dogs process language much like humans do. The left side of the brain processes word meaning while the right side interprets intonation. Dogs, like humans, integrate the function of both sides of the brain to arrive at a clearer meaning.
"Some scientists believe that dogs understand the actual meaning of many words unrelated to the tone in which they are delivered."
Some dogs fully activate the brain’s left side learning words regardless of how they are spoken. Case in point—Rico. A border collie named Rico was featured in a 2004 article in Science Magazine because he could “fast map” new words. Rico learned the names of over 200 different items. He could grasp a word’s meaning after hearing it only once, much like young children during their years of language development. Rico also retained the meaning of the words 4 weeks after learning them. This illustrates the dog’s uncanny ability to learn words independent of intonation.
How and What Together
Like most opposing theories, the truth may lie somewhere in the middle. Dogs use both left and right sides of the brain. They read our body language and listen to our tone. They combine all this data to understand us.
In another study with MRI screening, the dog’s left and right sides of the brain were activated when the researcher said “good boy” in a praising tone. The same words spoken in a neutral tone stimulated only the left side of the brain and the dog didn’t always grasp what was said. Furthermore, when study dogs heard random words like “however” in a sweet tone, the right side of the brain was active, while the left was not. This led scientists to believe that dogs understand better when both sides of the brain are in play simultaneously. In other words, what words are said and how they are said are both critical to understanding.
The study also showed that the reward center of the brain that responds to pleasurable sensations like affection, playing, or eating was only activated when the dogs heard words they understood in a tone they liked! So praising your dog is nice, but it’s nicer if you say it sweetly!
What does this mean?
All this research is a good first step in understanding how our dogs interpret our speech. It’s interesting to learn how the canine brain works, but we don’t need scientific studies to know that our dogs understand us. Humans and dogs have lived side by side for generations. The survival of our canine companions is due, in part, to their ability to communicate with their protectors and providers, i.e., us. Spending that much time with anyone should lead to better communication, right?
With that in mind, research may help us have more respect for our dog’s ability to understand not just our words, but also how we say them. The canine ability to comprehend human body language and intonation is amazing. Our dogs know more than just “Sit” or “Stay” or “Walk”. They can learn the meaning of many words and can grasp that meaning even better when we say those words in an appropriate tone. We can talk to our dogs and feel gratified that they “get” us.
But what about eavesdropping? Do we need to speak softly on the phone so our dog doesn’t overhear our private conversations? Do we need to go in the yard to have an argument? Who are we kidding??? Our dogs witness almost everything in our lives, so what’s one more conversation? And even if they understand us, we can rest assured that they won’t repeat a single word! | Eavesdropping Dogs...Do Dogs Understand Our Conversations?
Well trained dogs oblige their masters. They sit, stay, and come when asked. Our faithful companions respond when we speak directly to them. Do they also understand when we talk to other people? Do they grasp our private telephone conversations? Do they comprehend our dinner table discussions? Are our dogs eavesdropping on us?
Canine Language Capabilities
Most dog owners will agree that their dogs understand familiar words. Say, “Sit” and your dog will collapse upon his haunches. Say “Let’s go for a walk” and he’ll run to the door and grab his leash. Say, “It’s time to eat” and he’ll head for the food bowl. It appears that they understand the words sit, walk, and eat leading us to believe that dogs learn to associate specific words with specific actions or objects.
Our dogs may get what we say, but what we say is only part of the equation. How we say it impacts how much a dog comprehends. Dogs interpret human spoken language as well as human body language in their effort to understand us. There are debates regarding just how much each factor (what we say and how we say it) plays in canine communication.
How
Some people think how we say something can be more important than what we say. Dogs read more into our tone and body language than our actual words. They focus on us and observe our physical clues to determine what we want them to do or not do. They watch our facial expressions, posture, and body movements. They listen to the tone of our voice. They combine all of these observations to determine our meaning.
"Some people think how we say something can be more important than what we say. "
If you smile and excitedly say “Let’s go for a walk!”, your dog will likely wag his tail and prance around enthusiastically. If you utter those very same words in a gruff voice with a scowl on your face, he may cower and whine.
Making these observations led many scientists to feel that dogs respond much like human infants in understanding our language. In fact, dogs may have basically the same cognitive ability as a 6-12-month-old human infant. Think about this. | yes |
Veterinary Science | Can dogs understand human language? | yes_statement | "dogs" can "understand" "human" "language".. "human" "language" can be understood by "dogs". | https://www.nbcnews.com/health/health-news/dogs-understand-foreign-language-brain-scans-show-rcna11074 | Dogs understand foreign language, brain scans show | Dogs understand foreign language, brain scans show
Our canine pets are such good social learners that they can detect speech and distinguish languages without any explicit training.
Kun-kun with earphones.Raúl Hernández
Jan. 6, 2022, 10:33 AM UTC / Updated Jan. 6, 2022, 5:30 PM UTC
By Linda Carroll
Just like you, your dog knows when someone is speaking your native tongue or a foreign language, Hungarian researchers reported.
Brain scans from 18 dogs showed that some areas of the pups’ brains lit up differently depending on whether the dog was hearing words from a familiar language or a different one, according to a report published in NeuroImage.
“Dogs are really good in the human environment,” said study author Laura Cuaya, a postdoctoral researcher at the Neuroethology of Communication Lab at Eötvös Loránd University in Budapest, Hungary.
“We found that they know more than I expected about human language,” Cuaya said. “Certainly, this ability to be constant social learners gives them an advantage as a species — it gives them a better understanding of their environment.”
Dogs appear to recognize their owners’ native language based on how it sounds overall, since the experiments did not use words the dogs would have been familiar with, Cuaya said in an email.
“We found that dogs’ brains can detect speech and distinguish languages without any explicit training,” she added. “I think this reflects how much dogs are tuned to humans.”
Cuaya was inspired to do the research when she and her dog Kun-kun moved from Mexico to Hungary. Cuaya had previously only spoken to Kun-kun in Spanish and wondered if he “noticed that people in Budapest talk a different language,” she said. “Then, happily, this question fitted with the Neuroethology of Communication Lab goals.”
Our results show that dogs learn from their social environments, even when we don’t teach them directly.
Laura Cuaya, Eötvös Loránd University
To take a closer look at whether dogs have the same kind of innate ability to differentiate between languages that human infants do, the researchers turned to a group of pet dogs ranging in age from 3 to 11 — five golden retrievers, six border collies, two Australian shepherds, one labradoodle, one cocker spaniel and three of mixed breed — who had previously been trained to remain still in an MRI scanner. The native language of 16 of the dogs was Hungarian and Spanish for the other two.
In their experiments, Cuaya and her colleagues had a native Hungarian speaker and a native Spanish speaker read sentences from Chapter 21 of “The Little Prince” while the dogs were in the scanner. The text and the readers were unknown to all the dogs.
When Cuaya and her colleagues compared the fMRI scans from the readings in the two languages, the researchers found different activity patterns in two areas of the brain that have been associated in both humans and dogs with deciphering the meaning of speech and whether its emotional content is positive or negative: the secondary auditory cortex and the precruciate gyrus. The differences were more pronounced in older dogs and dogs with longer snouts.
The dogs' brain scans were compared during readings in two languages, Hungarian and Spanish.Enikő Kubinyi
Cuaya suspects the older dogs had a different result because they had more years listening to the native language of their owners. She wasn’t sure why dogs with longer snouts did better at distinguishing the languages.
What should owners take from this study?
“As many owners already know, dogs are social beings interested in what is happening in their social world,” Cuaya said. “Our results show that dogs learn from their social environments, even when we don’t teach them directly. So, just continue involving your dogs in your family, and give them opportunities to continue learning.”
The findings were a surprise to Dr. Katherine Houpt, the James Law Professor Emeritus in the section of behavior medicine at the Cornell University College of Veterinary Medicine.
“I didn’t know that they would respond differently to different languages, particularly because I thought voice intonation would mean more than the words,” Houpt said. “This shows they know when you are not speaking the language they learned. Knowing the difference between languages might be important to dogs as part of their guard dog duties. [When on alert] the dog is more likely to be suspicious of people speaking a different language.”
It’s possible, she added, that the explanation for longer-snouted dogs might be that head shape is common among sheep dogs, who have to be able to understand what a shepherd is saying to the dog.
Linda Carroll
Linda Carroll is a regular health contributor to NBC News. She is coauthor of "The Concussion Crisis: Anatomy of a Silent Epidemic" and "Out of the Clouds: The Unlikely Horseman and the Unwanted Colt Who Conquered the Sport of Kings." | Dogs understand foreign language, brain scans show
Our canine pets are such good social learners that they can detect speech and distinguish languages without any explicit training.
Kun-kun with earphones. Raúl Hernández
Jan. 6, 2022, 10:33 AM UTC / Updated Jan. 6, 2022, 5:30 PM UTC
By Linda Carroll
Just like you, your dog knows when someone is speaking your native tongue or a foreign language, Hungarian researchers reported.
Brain scans from 18 dogs showed that some areas of the pups’ brains lit up differently depending on whether the dog was hearing words from a familiar language or a different one, according to a report published in NeuroImage.
“Dogs are really good in the human environment,” said study author Laura Cuaya, a postdoctoral researcher at the Neuroethology of Communication Lab at Eötvös Loránd University in Budapest, Hungary.
“We found that they know more than I expected about human language,” Cuaya said. “Certainly, this ability to be constant social learners gives them an advantage as a species — it gives them a better understanding of their environment.”
Dogs appear to recognize their owners’ native language based on how it sounds overall, since the experiments did not use words the dogs would have been familiar with, Cuaya said in an email.
“We found that dogs’ brains can detect speech and distinguish languages without any explicit training,” she added. “I think this reflects how much dogs are tuned to humans.”
Cuaya was inspired to do the research when she and her dog Kun-kun moved from Mexico to Hungary. Cuaya had previously only spoken to Kun-kun in Spanish and wondered if he “noticed that people in Budapest talk a different language,” she said. “Then, happily, this question fitted with the Neuroethology of Communication Lab goals.”
Our results show that dogs learn from their social environments, even when we don’t teach them directly.
| yes |
Veterinary Science | Can dogs understand human language? | yes_statement | "dogs" can "understand" "human" "language".. "human" "language" can be understood by "dogs". | https://www.cbc.ca/news/science/dogs-language-1.3740980 | Dogs really do understand human language, study suggests | CBC ... | They found that dogs processed words with the left hemisphere, while intonation was processed with the right hemisphere — just like humans.
Researchers in Hungary scanned the brains of dogs as they were listening to their trainer speaking to determine which parts of the brain they were using. (Vilja & Vanda Molnár)
What's more, the dogs only registered that they were being praised if the words and intonation were positive; meaningless words spoken in an encouraging voice, or meaningful words in a neutral tone, didn't have the same effect.
"Dog brains care about both what we say and how we say it," said lead researcher Attila Andics, a neuroscientist at Eotvos Lorand University in Budapest. "Praise can work as a reward only if both word meaning and intonation match."
Lead researcher Attila Andics said the findings suggest that the mental ability to process language evolved earlier than previously believed and that what sets humans apart from other species is the invention of words. (Enikő Kubinyi)
Andics said the findings suggest that the mental ability to process language evolved earlier than previously believed and that what sets humans apart from other species is the invention of words.
Brain language abilities not uniquely human
"The neural capacities to process words that were thought by many to be uniquely human are actually shared with other species," he said. "This suggests that the big change that made humans able to start using words was not a big change in neural capacity."
While other species probably also have the mental ability to understand language like dogs do, their lack of interest in human speech makes it difficult to test, said Andics.
All of the dogs were awake, unrestrained and happy during the tests, researchers said. (Eniko Kubinyi)
Dogs, on the other hand, have socialized with humans for thousands of years, meaning they are more attentive to what people say to them and how.
Researchers imaged the brains of 13 dogs using a technique called functional MRI, or fMRI, which records brain activity.
The dogs— six border collies, five golden retrievers, a German shepherd and a Chinese crested — were trained to lie motionless in the scanner for seven minutes during the tests. The dogs were awake and unrestrained as they listened to their trainer's voice through headphones.
Andics noted that all of the dogs were awake, unrestrained and happy during the tests. "They participated voluntarily," he said.
While dog owners may find the results unsurprising, from a scientific perspective, it's a "shocker" that word meaning seems to be processed in the left hemisphere of the brain, said Brian Hare, associate professor of evolutionary anthropology at Duke University, who had no role in the research.
Emory University neuroscientist Gregory Berns cautioned that the study involved a small number of dogs. Before concluding it's a smoking gun for word processing, "they should have looked for other evidence in the brain," he said in an email. | They found that dogs processed words with the left hemisphere, while intonation was processed with the right hemisphere — just like humans.
Researchers in Hungary scanned the brains of dogs as they were listening to their trainer speaking to determine which parts of the brain they were using. (Vilja & Vanda Molnár)
What's more, the dogs only registered that they were being praised if the words and intonation were positive; meaningless words spoken in an encouraging voice, or meaningful words in a neutral tone, didn't have the same effect.
"Dog brains care about both what we say and how we say it," said lead researcher Attila Andics, a neuroscientist at Eotvos Lorand University in Budapest. "Praise can work as a reward only if both word meaning and intonation match. "
Lead researcher Attila Andics said the findings suggest that the mental ability to process language evolved earlier than previously believed and that what sets humans apart from other species is the invention of words. (Enikő Kubinyi)
Andics said the findings suggest that the mental ability to process language evolved earlier than previously believed and that what sets humans apart from other species is the invention of words.
Brain language abilities not uniquely human
"The neural capacities to process words that were thought by many to be uniquely human are actually shared with other species," he said. "This suggests that the big change that made humans able to start using words was not a big change in neural capacity. "
While other species probably also have the mental ability to understand language like dogs do, their lack of interest in human speech makes it difficult to test, said Andics.
All of the dogs were awake, unrestrained and happy during the tests, researchers said. (Eniko Kubinyi)
Dogs, on the other hand, have socialized with humans for thousands of years, meaning they are more attentive to what people say to them and how.
Researchers imaged the brains of 13 dogs using a technique called functional MRI, or fMRI, which records brain activity.
| yes |
Veterinary Science | Can dogs understand human language? | yes_statement | "dogs" can "understand" "human" "language".. "human" "language" can be understood by "dogs". | https://www.thewildest.com/dog-behavior/do-dogs-understand-words | Do Dogs Understand Our Words? · The Wildest | share article
Sign up for product updates, offers, and learn more about The Wildest, and other Mars Petcare brands. Must be over 16 years to sign up.
See our privacy statement to find out how we collect and use your data, to contact us with privacy questions or to exercise your personal data rights.
What do words mean to dogs? Do you sound like Charlie Brownâs teacherâjust a series of âwah wah wahsââor does your dog genuinely understand your words? Are dogs on the same page as us, or even in the same book? This article will explore dogs and their understanding of human language.
Some dogs like Chaser (the dog who knows 1,000+ words) are celebrated for their panache for human language. The news media hails them as âsuper smart,â and after meeting Chaser, astrophysicist Neil deGrasse Tyson exclaimed, âWho would have thought that animals are capable of this much display of intellect?â So, what are these dogs doing with words?
Letâs look at the types of words that dogs understand.
Objects
Dogs can learn the names of many, many, many different objects. Julia Fischer, group leader at the German Primate Centerâs Cognitive Ethology Lab, heard that a Border Collie named Rico knew the names of 70 individual objects, and she wanted to know how Rico mapped specific human words to particular objects. âI contacted the owners, and they let us visit their home and start a study of Rico,â explains Fischer. This culminated in 2004 with an article in Science, reporting that Rico knew the names of over 200 different objects.
Seven years later, Chaser, a Border Collie in South Carolina, took the gold medal when Alliston Reid and John Pilley of Wofford College reported that Chaser knew the distinct names of 1,022 objects â more than 800 cloth animals, 116 balls, 26 Frisbees, and 100 plastic items. This is not merely a story about Border Collies, however. Thereâs also Bailey, a 12-year-old Yorkshire Terrier, that researchers found knew the names of about 120 toys.
Dogs also win praise for their ability to learn and retain the names of new objects. When presented with a group of toys, all of which were familiar except one, both Chaser and Rico could retrieve the unknown toy when asked to fetch using an unfamiliar word. In essence, the dogs were pairing a novel object with an unfamiliar name after a single association and then remembering the name of that new object in subsequent trials. In children, this is called âfast mapping,â and it was thought to be uniquely human. Pilley notes, âThis research shows that this understanding occurs on a single trial. However, Chaser needed additional rehearsal in order to transfer this understanding or learning into long-term memory.â
Actions
But life is not only about knowing the names of oneâs stuffies and Frisbees. Humans often use verbs such as come, sit, down and off to get dogs to alter their behavior. After controlling for external contextual cues, researchers found that dogs could still understand that specific words map to specific physical actions. Chaser showed an incredible amount of flexibility with actions â performing âtake,â âpaw,â and ânoseâ toward different objects.
âThatâs just training,â you might say, but this suggests that some dogs show a cognitively advanced skill where actions are understood as independent from objects. Reid and Pilley found that Chaser did not interpret âfetch sockâ as one single word, like âfetchsock.â Instead, she could perform a number of different fetch actions flexibly toward a number of different objects. Daniela Ramos, a veterinary behaviorist in São Paulo, discovered that a mutt named Sofia could also differentiate object names from action commands, suggesting these dogs attend to the individual meaning of each word.
Categories
Chaser could assign objects to different categories based on their physical properties; some are âtoys,â others are âFrisbeesâ and, of course, there are âballs.â Chaser takes her cue from Alex, Irene Pepperbergâs African Grey Parrot, who also learned categories like color, shape, and material and differentiated which trait was the same or different.
New Dog Training Program
Try these free training programs from our friends at Dogo to help with new dog life and basic obedience.
Is it training or something more?
This all seems quite extraordinary, but nothing comes free of controversy. Do dogs understand words the same way humans do or are they merely well-trained? For example, some researchers are not certain that dogs actually âfast mapâ; dogs might be doing something that simply looks like âfast mappingâ from the outside. Regardless, it does seem as though these dogs have a conception of objects and actions.
Patricia McConnell, PhD, Certified Applied Animal Behaviorist, agrees. âUnderstanding requires that we share the same reference â that we have the same construct of an object or an action. For some dogs, it seems like they do.â Pilley concurs. âWhen an object, such as a toy, is held before Chaser and a verbal label is given to that object, Chaser understands that the verbal label refers to that object.â
In her book Inside of a Dog, Alexandra Horowitz reminds us that even if these are the only dogs in the world capable of using words this way, it allows us to see that a âdogâs cognitive equipment is good enough to understand language in the right context.â This body of research indicates what is possible, not necessarily what most dogs do every day.
How does your dog stack up?
Whether you have a genius in your home might largely depend on you. As Fischer explains, âA dogâs use of human language depends very much on the willingness of the owner to establish a verbal relationship, to establish links between words and particular meanings.â Fischer is referring to motivation in both the human and the dog.
Ramos and her colleagues trained and tested Sofia two to three times a day, three to six times a week. When Pilley, who doubled as researcher and Chaserâs parent, began training Chaser to identify objects at five months of age, Pilley repeated object names 20 to 40 times each session to make sure she got it.
Like Rocky Balboa preparing for his climactic showdown, these dogs are highly motivated. Fischer notes, âRico was eager and hard working. Youâd have to tell him, âThatâs enough. Get something to drink. Take a rest.ââ
Denise Fenzi, a professional dog trainer from Woodside, Calif., who specializes in a variety of dog sports, reminds us that this type of motivation is not necessarily the norm. âNot all dogs share this attention to words. Even in my dogs [all of whom are the same breed], there is a huge difference in the ability to verbally process. I didnât train them differently. Itâs just easier for one to quickly get words.â
How you train your dog matters.
The way dogs learn words might be the biggest piece of the puzzle. McConnell finds, âWord learning might depend upon how words are first introduced. People who explicitly differentiate words, teaching, âGet your Greenie! Get your ball,â often have the dogs with big vocabularies. On the other hand, my dog Willie was given verbal cues for years that stood for actions rather than objects. When I tried to teach him that words could refer to objects, he was completely confused.â
What dogs are able to do with language could also be explained by their tutelage. If dogs donât learn to attach a variety of different actions to a variety of objects, it might be harder for them in the long run to be flexible with human language. Susanne Grassmann, a developmental psychologist and psycholinguist at the University of Groningen in the Netherlands explains, âChaser was trained to do different things with different objects, and she differentiates between what is the object label and what is the action command, meaning what to do with that object.â
Ramos notes that Sofiaâs relationship with certain objects was a bit different. âThroughout the training, we always paired âstickâ with âpoint.â As a result, it was difficult for her to perform any other action toward the stick besides âpoint.â If we had trained her âstick: sit,â âstick: pointâ and âstick: fetch,â she would have learned that multiple actions can be directed toward the stick, and her response would probably be different. For example, when presented with a novel object, such as a toy bear, she could direct a number of different actions toward the bear, but there was a reluctance to change her action towards the stick, which could have to do with the rigidity of training.â
And even if you do explicitly teach that different words have different meanings, it can be challenging. Ramos found that learning the names of objects is not always easy for dogs. âIt was hard for Sofia to learn to discriminate the names of her first two objects, but after the initial discrimination, it was like she learned to learn. It became easier,â recalls Ramos. âBecause this type of learning can be challenging, service dogs [who have little margin for error] are taught a limited, but instrumental, set of words,â explains Kate Schroer-Shepord, a qualified guide dog instructor at Guiding Eyes for the Blind in Yorktown Heights, N.Y.
Pilley found that dogsâ success at object learning depended upon the training method used. âWhen we put two objects on the floor and asked dogs to retrieve each object by name, they couldnât do it; simultaneous discrimination wasnât working. Instead, Chaser was able to learn the names of objects through successive discrimination. She would play with one object in each training session, and through play, the object assumed value. Weâd name the object, hide it and ask her to find it. Discrimination testing between the names of different objects occurred later.â
Do dogs understand the words or the melody?
Are these just âtype-Aâ dogs whose accomplishments cannot easily be replicated? After all, most dogs arenât explicitly taught words as described above, yet they interact with us talkers in ways that make us feel like weâre on the same page. âDinnertime!â âWanna go for a walk?â âWhereâs Dad?â elicit an appropriate âbouncing dogâ response. But are most dogs attending to our actual words, or are other factors at play?
Dogs derive an enormous amount of information from contextual cues, particularly our body movements as well as tone and âprosodyâ â the rhythm, stress, and intonation of our speech. âWhen people talk to dogs, dogs pay attention to the melody and the mood to predict what is happening or what will happen next,â explains Fischer.
Fenzi says that dogs can just as easily respond to gibberish as to real English words; âI could go through every level of AKC obedience from the bottom to the top saying, âKaboola,â and the dog could succeed.â In many cases, dogs may be understanding tone rather than individual words.
âOne of the most notable differences between novices and professional trainers is the ability to modulate the prosodic features of their speech,â notes McConnell. âThe pros learn to keep problematic emotions out of their verbal cues, like nervousness in a competition, and to use prosody to their advantage when itâs advantageous, for example, to calm a dog down or to motivate them to speed up.â
In another study, Ramos explored whether dogs knew the words relating to toys they were thought to know when taken out of context. Most did not, much to the surprise of the people. When the verbal skills of Fellow, a performing German Shepherd from the 1920s, were tested outside their customary contexts, Fellow knew only some of the words and actions that his person thought he understood.
While many pet parents deem their dogs to be word-savvy, their reports tell a different story. The Pongrácz survey found that many words and phrases were executed only in contextually adequate situations (for example, saying âbedtimeâ when itâs dark and youâre in your pajamas rather than at noon when youâre in your work clothes). As with Fellow, this suggests dogs might not be attending to only words themselves.
Put words to the test.
Does your dog understand your words as you intend them, or do they have a different understanding? If you always use a word in the same context, itâs easy to assume that you and your dog define it identically. Changing the context in some way offers a better understanding of what the dog perceives.
McConnell initially thought Willie knew the name of her partner, Jim. âTo teach my dog to find them, I would say, âWhereâs Jim?â and Jim would call Willie over. When Willie consistently went to Jim, Iâd say it as Jim was driving up, and Willie would run to the window. One day, Jim was sitting on the couch, and I said, âWhereâs Jim?â and Willie ran to the window, all excited. This difference in definitions is more common than people realize â dogs donât have the exact same concept of words that we do.â
While there is no question dogs can understand verbs, their definitions might differ from ours. McConnell shares a classic example that she learned from Ian Dunbar, founder of the Association of Pet Dog Trainers. âWhat do dogs think âsitâ means? We think âsitâ means this posture we call âsitting,â but if you ask a dog who is sitting to âsit,â they will very often lie down. To them, âsitâ might mean get lower, go down toward the ground.â
Many people tend to overestimate their dogsâ ability with words and assume that dogs and humans have a shared understanding. Because a dog responds in one context and not in another doesnât mean they are being disobedient. As Tom Brownlee, master trainer with the American Society of Canine Trainers and instructor in Carroll Collegeâs anthrozoology program, candidly advises owners, âIf a dogâs not getting âitâ â whatever âitâ may be â then you are doing something wrong. Itâs our job to help them understand.â
When you talk to your dog, consider that the words you speak might not carry the same meaning for both of you. Instead, other aspects of the communication might be more relevant. Maybe the real lesson is that context, prosody and tone â rather than dictionary definitions of words â are vitally important for human communication, too.
Pongrácz, P., et al. 2001. Ownersâ beliefs on the ability of their pet dogs to understand human verbal communication: A case of social understanding. Current Psychology of Cognition 20 (1/2): 87â107.
Warden, C.J., and L.H. Warner. 1928. The sensory capacities and intelligence of dogs, with a report on the ability of the noted dog âFellowâ to respond to verbal stimuli. Quarterly Review of Biology 3 (1): 1â28. | Must be over 16 years to sign up.
See our privacy statement to find out how we collect and use your data, to contact us with privacy questions or to exercise your personal data rights.
What do words mean to dogs? Do you sound like Charlie Brownâs teacherâjust a series of âwah wah wahsââor does your dog genuinely understand your words? Are dogs on the same page as us, or even in the same book? This article will explore dogs and their understanding of human language.
Some dogs like Chaser (the dog who knows 1,000+ words) are celebrated for their panache for human language. The news media hails them as âsuper smart,â and after meeting Chaser, astrophysicist Neil deGrasse Tyson exclaimed, âWho would have thought that animals are capable of this much display of intellect?â So, what are these dogs doing with words?
Letâs look at the types of words that dogs understand.
Objects
Dogs can learn the names of many, many, many different objects. Julia Fischer, group leader at the German Primate Centerâs Cognitive Ethology Lab, heard that a Border Collie named Rico knew the names of 70 individual objects, and she wanted to know how Rico mapped specific human words to particular objects. âI contacted the owners, and they let us visit their home and start a study of Rico,â explains Fischer. This culminated in 2004 with an article in Science, reporting that Rico knew the names of over 200 different objects.
Seven years later, Chaser, a Border Collie in South Carolina, took the gold medal when Alliston Reid and John Pilley of Wofford College reported that Chaser knew the distinct names of 1,022 objects â more than 800 cloth animals, 116 balls, 26 Frisbees, and 100 plastic items. This is not merely a story about Border Collies, however. | yes |
Veterinary Science | Can dogs understand human language? | yes_statement | "dogs" can "understand" "human" "language".. "human" "language" can be understood by "dogs". | https://www.ajc.com/news/world/dogs-may-understand-humans-better-than-thought-according-researchers/tpE7Z2WT9VEjf9679QKdiM/ | Here's how much dogs can understand humans, researchers say | Researchers from Emory University recently conducted a study, published in Frontiers in Neuroscience, to explore how pups understand human words.
"Many dog owners think that their dogs know what some words mean, but there really isn't much scientific evidence to support that," coauthor Ashley Prichard said in a statement. "We wanted to get data from the dogs themselves — not just owner reports."
For the assessment, the team evaluated 12 dogs of varying breeds, who were trained by their owners to retrieve two different objects − one with a soft texture like a stuffed animal and one with a rougher texture like rubber. The canines were successfully trained when they could distinguish between the two objects by consistently fetching the one requested by the owner when presented with both.
After the training, the scientists then examined the pooches by administering fMRI scans. During the procedure, the doggy’s owner stood directly in front of the dog at the opening of the machine, calling out the name of the toys at set intervals and then holding up the corresponding toys. They also said gibberish words to their dogs and showed them something they hadn’t seen before as a control.
After analyzing the results, the researchers found that regions of the dogs’ brains responsible for auditory processing were more activated when hearing gibberish words. They believe their findings mean dogs can tell the difference between human words they’ve previously heard and words they haven’t.
“We expected to see that dogs neurally discriminate between words that they know and words that they don’t,” Prichard said. “What’s surprising is that the result is opposite to that of research on humans — people typically show greater neural activation for known words than novel words.”
The researchers said the dogs’ brains are more activated by the novel terms, “because they sense their owners want them to understand what they are saying, and they are trying to do so,” the team wrote.
The researchers did note their findings do not mean spoken words are the most effective way for an owner to communicate with a dog. They acknowledged previous studies that show the effectiveness of visual and scent clues.
“When people want to teach their dog a trick, they often use a verbal command because that’s what we humans prefer,” Prichard concluded. “From the dog’s perspective, however, a visual command might be more effective, helping the dog learn the trick faster.”
Najja Parker is the Newsletter Coach for The Atlanta Journal-Constitution. She manages the newsroom’s free and premium newsletters. Parker also co-curates Unapologetically ATL, a newsletter about Atlanta's Black culture, and produces and hosts “ATL Closeup,” a things to do series featuring local influencers. | Researchers from Emory University recently conducted a study, published in Frontiers in Neuroscience, to explore how pups understand human words.
"Many dog owners think that their dogs know what some words mean, but there really isn't much scientific evidence to support that," coauthor Ashley Prichard said in a statement. "We wanted to get data from the dogs themselves — not just owner reports. "
For the assessment, the team evaluated 12 dogs of varying breeds, who were trained by their owners to retrieve two different objects − one with a soft texture like a stuffed animal and one with a rougher texture like rubber. The canines were successfully trained when they could distinguish between the two objects by consistently fetching the one requested by the owner when presented with both.
After the training, the scientists then examined the pooches by administering fMRI scans. During the procedure, the doggy’s owner stood directly in front of the dog at the opening of the machine, calling out the name of the toys at set intervals and then holding up the corresponding toys. They also said gibberish words to their dogs and showed them something they hadn’t seen before as a control.
After analyzing the results, the researchers found that regions of the dogs’ brains responsible for auditory processing were more activated when hearing gibberish words. They believe their findings mean dogs can tell the difference between human words they’ve previously heard and words they haven’t.
“We expected to see that dogs neurally discriminate between words that they know and words that they don’t,” Prichard said. “What’s surprising is that the result is opposite to that of research on humans — people typically show greater neural activation for known words than novel words.”
The researchers said the dogs’ brains are more activated by the novel terms, “because they sense their owners want them to understand what they are saying, and they are trying to do so,” the team wrote.
The researchers did note their findings do not mean spoken words are the most effective way for an owner to communicate with a dog. They acknowledged previous studies that show the effectiveness of visual and scent clues.
“When people want to teach their dog a trick, they often use a verbal command because that’s what we humans prefer,” | yes |
Veterinary Science | Can dogs understand human language? | yes_statement | "dogs" can "understand" "human" "language".. "human" "language" can be understood by "dogs". | https://www.petvet.lk/can-dogs-understand-human-speech/ | Can Dogs Understand Human Speech? – PetVet Clinic ~ Full ... | Can Dogs Understand Human Speech?
Dog and man have lived side by side for thousands of years, and despite not understanding each other’s language, have established a bond so deep that they are labeled our best friends.
Pet parents across the world will proudly admit that they spend countless hours talking to their fur-children. They miss you the most when you leave, and are the most excited when you get back, so naturally, you’d want to speak to them. You may often catch yourself in the middle of asking them who wants dinner, not expecting a reply entirely, and then stop and think, “does my dog understand me?”.
Seeing that they can neither speak back nor understand the vastness of human language, this common question can leave you feeling a little ridiculous- so we’re here to answer it. In short, yes, dogs can understand what we say, but to a certain extent. Allow us to break it down for you.
When it comes to effective communication, there are 2 factors at play:
Linguistic content – what is being said
Emotional content – how it’s being said
Linguistic content
As defined by a vocable, words are essentially just sounds if you take away their meaning, and while dogs may not be able to comprehend all of them, they certainly can set apart a few when they are used frequently.
This is why it’s possible to train your dog to respond to commands like “sit” and “paw”- they hear the different words, and they know the appropriate action. Thus, in a certain way, they are able to understand its meaning.
Similarly, you may notice that your dog tends to favour certain words; perhaps “dinner” or “walk” or “treat”. They have associated these frequently used words with the situations that follow, and are able to remember the different things that each one entails. Give it a try with your own dog and watch how they respond.
In fact, research has shown that the vocabulary of a dog can hold up to 165 words on average, and is quite similar to that of a 2-3 year old in terms of what they can understand.
This being said, your dog does not understand any particular human language, it is merely able to remember vocables and attach meaning to them. This also means that your dog could respond to multiple languages spoken in your home- which is quite a common occurrence, especially in Sri Lankan households.
Emotional content
It’s a commonly known theory that your tone has everything to do with how dogs perceive what you’re trying to say, and many of us are guilty of testing it by calling them “silly” in honey-like voices or yelling “You’re such a good boy!” aggressively.
Most of the time, it works. Dogs seem to have no idea what you’re saying, and merely get excited or upset by the way you say it.
However, as aforementioned, research has proven that dogs do in fact understand words to a certain extent, regardless of its packaging. In fact, another study carried out in Budapest showed that dogs still responded positively to praise, even when it was spoken in a neutral tone- proving that it is not the only determinant. Nevertheless, tone still plays a vital role in what they can gather from our speech.
Think about it this way; if you came across someone speaking in a language you didn’t understand, you would instinctively turn to their tone in an attempt to decipher what they are trying to convey. Do they sound happy or sad? Should you run or stand?
Dogs think the same way. When they cannot understand what you are saying, they turn to how you are saying it, and act accordingly.
They decode the emotion in your voice based on determinants like intonation and inflection, and may even pair this with your body language. For example, your dog most likely notices the difference in what you are feeling when you move from a calm disposition to flailing your arms around violently- they’ll see the shift in emotion, and respond by looking excited or alarmed.
So while your dog may not be able to understand the depth of your sentences, it is a combination of both linguistic and emotional content that makes it possible for them to grasp what you’re trying to say, and the feeling with which you are saying it.
Thus, it’s a misconception that dogs can merely understand tone and not language, when in fact they can comprehend both. Although their capacity for communication is limited in comparison to that of humans, your dog does understand you to some extent, therefore speaking to them does have value.
So go ahead, tell them you love them, use their favourite vocables and talk to your dog- maybe let them get a word in too. | Can Dogs Understand Human Speech?
Dog and man have lived side by side for thousands of years, and despite not understanding each other’s language, have established a bond so deep that they are labeled our best friends.
Pet parents across the world will proudly admit that they spend countless hours talking to their fur-children. They miss you the most when you leave, and are the most excited when you get back, so naturally, you’d want to speak to them. You may often catch yourself in the middle of asking them who wants dinner, not expecting a reply entirely, and then stop and think, “does my dog understand me?”.
Seeing that they can neither speak back nor understand the vastness of human language, this common question can leave you feeling a little ridiculous- so we’re here to answer it. In short, yes, dogs can understand what we say, but to a certain extent. Allow us to break it down for you.
When it comes to effective communication, there are 2 factors at play:
Linguistic content – what is being said
Emotional content – how it’s being said
Linguistic content
As defined by a vocable, words are essentially just sounds if you take away their meaning, and while dogs may not be able to comprehend all of them, they certainly can set apart a few when they are used frequently.
This is why it’s possible to train your dog to respond to commands like “sit” and “paw”- they hear the different words, and they know the appropriate action. Thus, in a certain way, they are able to understand its meaning.
Similarly, you may notice that your dog tends to favour certain words; perhaps “dinner” or “walk” or “treat”. They have associated these frequently used words with the situations that follow, and are able to remember the different things that each one entails. Give it a try with your own dog and watch how they respond.
In fact, research has shown that the vocabulary of a dog can hold up to 165 words on average, and is quite similar to that of a 2-3 year old in terms of what they can understand.
This being said, your dog does not understand any particular human language, it is merely able to remember vocables and attach meaning to them. | no |
Veterinary Science | Can dogs understand human language? | yes_statement | "dogs" can "understand" "human" "language".. "human" "language" can be understood by "dogs". | https://animals.howstuffworks.com/animal-facts/can-animals-understand-human-language.htm | Can animals understand human language? | HowStuffWorks | Can animals understand human language?
""
Do animals really understand what we're saying to them or are they royally duping us?
Mike Watson Images/Thinkstock
Humans have a special relationship with house pets, and a full 62 percent claim that their pets understand the words that they speak [source: USA Today]. While there's no way to know exactly how much Fido gets what you're saying, scientists have proven that some dogs, apes and even dolphins can understand spoken language.
In one study, a border collie named Rico demonstrated that he knew the name of more than 200 objects, and could fetch these items on command [source: Science]. A similar study conducted on another border collie named Chaser went even further; not only could Chaser distinguish the names of at least 1,022 objects, he could also infer the names of new objects [source: Hecht]. For example, if asked to fetch Mr. Monkey -- a toy he had never seen before -- he could locate Mr. Monkey through the process of elimination when the monkey was placed near toys he was familiar with.
Advertisement
Perhaps even more exciting, Chaser was able to repeat this process of locating unfamiliar toys by name a full month later, after only being exposed to the new items once before. He was also able to understand verbs and objects used in different contexts; for example, Chaser demonstrated that he could put his nose to a ball, fetch, touch or take the ball depending on the command given.
Just so you don't think that border collies have an edge, a Yorkshire terrier demonstrated his understanding of more than 120 words in a separate study [source: Hecht].
But what about other animals who don't have such a close relationship with humans? Consider the case of Kanzi, a bonobo ape. Through years of work with his trainer, Kanzi was able to demonstrate his understanding of more than 3,000 English words [source: Raffaele]. A researcher would speak the words from a separate room to avoid giving any contextual clues, and Kanzi would listen through headphones and point to the symbol represented by the word on his special keyboard. The ape was also able to respond appropriately to commands, such as, "Put the soap in the water."
Perhaps even more interesting is the case of a pair of bottlenose dolphins, who demonstrated that they were able to understand full sentences in a 1984 study. Trainers used computer-generated sounds and hand signals to communicate with the dolphins, who were able to follow instructions ranging from two to five words in length. The dolphins could also locate objects placed in the tank with them a full 30 seconds after commands were given, or report to their trainers when commands given were impossible to execute [source:Herman et al].
As for the mighty housecat -- studies indicate that cats can easily distinguish their owner's voice from other voices calling their name [source: Saito and Shinozuka]. While they send signals demonstrating they know exactly what's going on, they also make it clear they don't care all that much and really aren't listening to exactly what you're saying. Seems only fitting behavior for the independent cat. | Can animals understand human language?
""
Do animals really understand what we're saying to them or are they royally duping us?
Mike Watson Images/Thinkstock
Humans have a special relationship with house pets, and a full 62 percent claim that their pets understand the words that they speak [source: USA Today]. While there's no way to know exactly how much Fido gets what you're saying, scientists have proven that some dogs, apes and even dolphins can understand spoken language.
In one study, a border collie named Rico demonstrated that he knew the name of more than 200 objects, and could fetch these items on command [source: Science]. A similar study conducted on another border collie named Chaser went even further; not only could Chaser distinguish the names of at least 1,022 objects, he could also infer the names of new objects [source: Hecht]. For example, if asked to fetch Mr. Monkey -- a toy he had never seen before -- he could locate Mr. Monkey through the process of elimination when the monkey was placed near toys he was familiar with.
Advertisement
Perhaps even more exciting, Chaser was able to repeat this process of locating unfamiliar toys by name a full month later, after only being exposed to the new items once before. He was also able to understand verbs and objects used in different contexts; for example, Chaser demonstrated that he could put his nose to a ball, fetch, touch or take the ball depending on the command given.
Just so you don't think that border collies have an edge, a Yorkshire terrier demonstrated his understanding of more than 120 words in a separate study [source: Hecht].
But what about other animals who don't have such a close relationship with humans? Consider the case of Kanzi, a bonobo ape. Through years of work with his trainer, Kanzi was able to demonstrate his understanding of more than 3,000 English words [source: Raffaele]. A researcher would speak the words from a separate room to avoid giving any contextual clues, and Kanzi would listen through headphones and point to the symbol represented by the word on his special keyboard. | yes |
Veterinary Science | Can dogs understand human language? | yes_statement | "dogs" can "understand" "human" "language".. "human" "language" can be understood by "dogs". | https://www.independent.co.uk/news/science/dogs-can-understand-human-speech-scientists-say-a7216481.html | Dogs can understand human speech, scientists discover | The ... | Recommended
While this was only the dogs’ “word-meaning representation”, it still shows they had an idea of what message the specific sound of an individual human word was designed to convey.
Lead researcher Dr Attila Andics, of Eötvös Loránd University, Budapest, said: “During speech processing, there is a well-known distribution of labour in the human brain.
“It is mainly the left hemisphere’s job to process word meaning, and the right hemisphere’s job to process intonation. The human brain not only separately analyses what we say and how we say it, but also integrates the two types of information, to arrive at a unified meaning.
This country has opened its first-ever dog beach
“Our findings suggest that dogs can also do all that, and they use very similar brain mechanisms.”
During the brain scans, the researchers spoke words like “good boy” and “well done” spoken with a praising intonation, the same words in a neutral voice and also words that were meaningless to them, like “however”, in both intonations.
The scans showed the dogs left brain tended to be activated when they heard words that were meaningful to them. This did not happen when they heard words they did not understand. The right hemisphere activated when they heard a praising intonation.
But the reward centre of their brains – which responds to pleasurable sensations like being petted, having sex and eating nice food – was only activated when they heard praising words spoken in a praising intonation.
“It shows that for dogs, a nice praise can very well work as a reward, but it works best if both words and intonation match,” Dr Andics said.
“So dogs not only tell apart what we say and how we say it, but they can also combine the two, for a correct interpretation of what those words really meant.
“This is very similar to what human brains do.”
The dogs from Instagram
Show all 6
1/6The dogs from Instagram
The dogs from Instagram
Noodle the Dachshund is just over a year old and comes with her own hashtag (#OodlesOfNoodle)
The dogs from Instagram
Three-year-old Staffie Ramsey was malnourished when he was adopted as a puppy but is now big and boisterous with ripped muscles and a cheeky grin
The dogs from Instagram
Winny the Welsh Corgi has been credited with the breed's upsurge in popularity
The dogs from Instagram
Bruno the miniature Dachshund has 66,700 followers
The dogs from Instagram
Mika the Husky has 58,900 followers
The dogs from Instagram
Elle the French Bulldog has 8,868 followers
This appears to contradict the idea that dogs only understand tone of voice and do not have an idea of the words actual meaning.
While they might respond tentatively to a praising tone using words they do not understand – or even insults – they are only genuinely happy when they understand the praise they are receiving.
The researchers described their work as a first step towards understanding how dogs interpret human speech.
A statement about the study said the researchers believed their results could “help to make communication and cooperation between dogs and humans even more efficient”. | Recommended
While this was only the dogs’ “word-meaning representation”, it still shows they had an idea of what message the specific sound of an individual human word was designed to convey.
Lead researcher Dr Attila Andics, of Eötvös Loránd University, Budapest, said: “During speech processing, there is a well-known distribution of labour in the human brain.
“It is mainly the left hemisphere’s job to process word meaning, and the right hemisphere’s job to process intonation. The human brain not only separately analyses what we say and how we say it, but also integrates the two types of information, to arrive at a unified meaning.
This country has opened its first-ever dog beach
“Our findings suggest that dogs can also do all that, and they use very similar brain mechanisms.”
During the brain scans, the researchers spoke words like “good boy” and “well done” spoken with a praising intonation, the same words in a neutral voice and also words that were meaningless to them, like “however”, in both intonations.
The scans showed the dogs left brain tended to be activated when they heard words that were meaningful to them. This did not happen when they heard words they did not understand. The right hemisphere activated when they heard a praising intonation.
But the reward centre of their brains – which responds to pleasurable sensations like being petted, having sex and eating nice food – was only activated when they heard praising words spoken in a praising intonation.
“It shows that for dogs, a nice praise can very well work as a reward, but it works best if both words and intonation match,” Dr Andics said.
“So dogs not only tell apart what we say and how we say it, but they can also combine the two, for a correct interpretation of what those words really meant.
“This is very similar to what human brains do.”
| yes |
Veterinary Science | Can dogs understand human language? | no_statement | "dogs" cannot "understand" "human" "language".. "human" "language" is not "understandable" by "dogs". | https://www.allsortsdogtraining.co.nz/blog/how-can-you-influence-your-dog-without-saying-a-word | Influencing your dog without saying a word - Allsorts Dog Training | BLOG SPOT
If we learnt more about how to communicate in 'dog language' rather than expecting them to understand human language, then surely we'd all have more social and well mannered dogs?
If we learnt more about how to communicate in 'dog language' rather than expecting them to understand human language, then surely we'd all have more social and well mannered dogs?
DOGS DON'T SPEAK ENGLISH (or any other human language) Studies at the University of Arizona have found that humans speak on average, over 16,000 words in a single day. It’s understandable that dogs are simply overwhelmed by the cacophony of sound coming from our mouths every day. Perhaps this is why so many owners tell me their dog has 'selective hearing' or 'deaf ears'.
THE SILENT TREATMENT I urge you to take a moment and to just sit with your dog without saying a word. I can assure you that you are still communicating with your dog but in a very different way, through body language. Are you relaxed, excited, frustrated or angry? Is your dog’s demeanor influenced or can you influence it, by your mood? In future, keep in mind what your body language says when you speak to your dog, as it can have a profound effect on the response.
YOUR WISH IS MY COMMAND Telling a dog what to do by saying a command word, when it has no clue what that is, must be very frustrating to a dog. Just because you say a word like 'stay' doesn't mean it miraculously understands what it is you are asking it to do. Imagine walking into a room with no clue what is expected of you, the only way of knowing you’ve done the right thing is someone saying “Good Dog”.
For example, I see people say the ‘stay command’ over and over again and then get upset with the dog when it breaks the stay. There's several reasons for this;
The dog has not been shown repeatedly what the owner wants it to do successfully, before applying a command word to the action
The expectation on time and distance is too much too soon, small milestones with big rewards makes for more consistent results.
The owner may be inadvertently teaching their dog 'learnt disobedience', so instead of repeatedly teaching the correct action they are teaching the wrong action.
The dog, in it's moment of confusion, seeks the owners help and reassurance by moving towards them and is then commonly reprimanded
I guarantee the body language from the owner is probably all wrong; ask yourself, are you smiling because your dog is correctly staying in position or are you serious and assertive?
HOW CAN YOU COMMUNICATE MORE POSITIVELY WITH YOUR DOG? It's simple, become aware of what your body language is portraying. Use attention and affection as your primary reward (within 2 seconds of the desired behaviour) and most importantly, always show your dog what it is you want them to do by guiding them step-by-step through the process first before using a command signal or word. This ensures they understand every actionable element of the 'command'. Only then can you apply a ‘word command’. Less is truly more!
Comments are closed.
Authors
Articles created by the team at Allsorts Dog Training, Bay of Plenty, New Zealand | BLOG SPOT
If we learnt more about how to communicate in 'dog language' rather than expecting them to understand human language, then surely we'd all have more social and well mannered dogs?
If we learnt more about how to communicate in 'dog language' rather than expecting them to understand human language, then surely we'd all have more social and well mannered dogs?
DOGS DON'T SPEAK ENGLISH (or any other human language) Studies at the University of Arizona have found that humans speak on average, over 16,000 words in a single day. It’s understandable that dogs are simply overwhelmed by the cacophony of sound coming from our mouths every day. Perhaps this is why so many owners tell me their dog has 'selective hearing' or 'deaf ears'.
THE SILENT TREATMENT I urge you to take a moment and to just sit with your dog without saying a word. I can assure you that you are still communicating with your dog but in a very different way, through body language. Are you relaxed, excited, frustrated or angry? Is your dog’s demeanor influenced or can you influence it, by your mood? In future, keep in mind what your body language says when you speak to your dog, as it can have a profound effect on the response.
YOUR WISH IS MY COMMAND Telling a dog what to do by saying a command word, when it has no clue what that is, must be very frustrating to a dog. Just because you say a word like 'stay' doesn't mean it miraculously understands what it is you are asking it to do. Imagine walking into a room with no clue what is expected of you, the only way of knowing you’ve done the right thing is someone saying “Good Dog”.
For example, I see people say the ‘stay command’ over and over again and then get upset with the dog when it breaks the stay. There's several reasons for this;
The dog has not been shown repeatedly what the owner wants it to do successfully, before applying a command word to the action
The expectation on time and distance is too much too soon, small milestones with big rewards makes for more consistent results.
| no |
Diabetology | Can drinking coffee prevent type 2 diabetes? | yes_statement | "drinking" "coffee" can "prevent" "type" "2" "diabetes".. "coffee" consumption can lower the risk of developing "type" "2" "diabetes". | https://www.healthline.com/health/coffee-s-effect-diabetes | Coffee and Diabetes: Prevention, Effects on Glucose and Insulin ... | Coffee was once condemned as being bad for your health. Yet, there’s growing evidence that it may protect against certain kinds of cancers, liver disease, and even depression.
There’s also compelling research to suggest that increasing your coffee intake may actually lower your risk for developing type 2 diabetes. This is good news for those of us who can’t face the day until we get in our cup of java.
However, for those who already have type 2 diabetes, coffee could have adverse effects.
Whether you’re trying to lower your risk, you already have diabetes, or you just can’t go without your cup of joe, learn about coffee’s effects on diabetes.
Diabetes is a disease that affects how your body processes blood glucose. Blood glucose, also known as blood sugar, is important because it’s what fuels your brain and gives energy to your muscles and tissues.
If you have diabetes, that means that you have too much glucose circulating in your blood. This happens when your body becomes insulin resistant and is no longer able to efficiently uptake glucose into the cells for energy.
Excess glucose in the blood can cause serious health concerns. There are a number of different factors that can cause diabetes.
Researchers at Harvard tracked over 100,000 people for about 20 years. They concentrated on a four-year period, and their conclusions were later published in this 2014 study.
They found that people who increased their coffee intake by over one cup per day had an 11 percent lower risk of developing type 2 diabetes.
However, people who reduced their coffee intake by one cup per day increased their risk of developing diabetes by 17 percent. There was no difference in those drinking tea.
It’s not clear why coffee has such an impact on the development of diabetes.
Thinking caffeine? It may not be responsible for those good benefits. In fact, caffeine has been shown in the short term to increase both glucose and insulin levels.
In one small study involving men, decaffeinated coffee even showed an acute rise in blood sugar. Right now there are limited studies and more research needs to be done on the effects of caffeine and diabetes.
While coffee could be beneficial for protecting people against diabetes, some studies have shown that your plain black coffee may pose dangers to people who already have type 2 diabetes.
Caffeine, blood glucose, and insulin (pre- and post-meal)
One 2004 study showed that taking a caffeine capsule before eating resulted in higher post-meal blood glucose in people with type 2 diabetes. It also showed an increase in insulin resistance.
According to a recent 2018 study, there may be a genetic proponent involved. Genes may play a role in caffeine metabolism and how it affects blood sugar. In this study, people who metabolized caffeine slower showed higher blood sugar levels than those who genetically metabolized caffeine quicker.
Of course, there’s a lot more in coffee other than caffeine. These other things may be what’s responsible for the protective effect seen in the 2014 study.
Drinking caffeinated coffee over a long period of time may also change its effect on glucose and insulin sensitivity. Tolerance from long-term consumption may be what causes the protective effect.
A more recent study from 2018 showed that long-term effects of coffee and caffeine may be linked to lowering risk of prediabetes and diabetes.
Fasting blood glucose and insulin
Another study in 2004 looked at a “mid-range” effect on people without diabetes who had been either drinking 1 liter of regular paper-filtered coffee a day, or who had abstained.
At the end of the four-week study, those who consumed more coffee had higher amounts of insulin in their blood. This was the case even when fasting.
If you have type 2 diabetes, your body is unable to use insulin effectively to manage blood sugar. The “tolerance” effect seen in long-term coffee consumption takes a lot longer than four weeks to develop.
Habitual coffee drinking
There’s a clear difference in how people with diabetes and people without diabetes respond to coffee and caffeine. A 2008 study had habitual coffee drinkers with type 2 diabetes continuously monitor their blood sugar while doing daily activities.
During the day, it was shown that right after they drank coffee, their blood sugar would soar. Blood sugar was higher on days that they drank coffee than it was on days they didn’t.
If you don’t have diabetes but are concerned about developing it, be careful before increasing your coffee intake. There may be a positive effect from coffee in its pure form. However, the benefits aren’t the same for coffee drinks with added sweeteners or dairy products.
Daily diabetes tip
Coffee may be more popular than ever, but drinking it on a regular basis isn’t the best way to manage diabetes — even if (believe it or not) there’s growing evidence that it could help prevent diabetes.
Was this helpful?
Creamy, sugary drinks found at cafe chains are often loaded with unhealthy carbs. They’re also very high in calories.
The impact of the sugar and fat in a lot of coffee and espresso drinks can outweigh the good from any protective effects of the coffee.
The same can be said about sugar-sweetened and even artificially sweetened coffee and other beverages. Once sweetener is added, it increases your risk of developing type 2 diabetes. Consuming too many added sugars is directly linked to diabetes and obesity.
Having coffee drinks that are high in saturated fat or sugar on a regular basis can add to insulin resistance. It can eventually contribute to type 2 diabetes.
No food or supplement offers total protection against type 2 diabetes. If you have prediabetes or are at risk for getting diabetes, losing weight, exercising, and consuming a balanced, nutrient-dense diet is the best way to reduce your risk.
Taking up drinking coffee in order to stave off diabetes won’t guarantee you a good result. But if you already drink coffee, it may not hurt.
Try reducing the amount of sugar or fat you drink with your coffee. Also talk with your doctor about diet options, exercise, and the effects that drinking coffee might have.
Q:
A:
Answers represent the opinions of our medical experts. All content is strictly informational and should not be considered medical advice.
Was this helpful?
Last medically reviewed on November 9, 2018
How we reviewed this article:
Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations. We avoid using tertiary references. You can learn more about how we ensure our content is accurate and current by reading our editorial policy. | ’s a clear difference in how people with diabetes and people without diabetes respond to coffee and caffeine. A 2008 study had habitual coffee drinkers with type 2 diabetes continuously monitor their blood sugar while doing daily activities.
During the day, it was shown that right after they drank coffee, their blood sugar would soar. Blood sugar was higher on days that they drank coffee than it was on days they didn’t.
If you don’t have diabetes but are concerned about developing it, be careful before increasing your coffee intake. There may be a positive effect from coffee in its pure form. However, the benefits aren’t the same for coffee drinks with added sweeteners or dairy products.
Daily diabetes tip
Coffee may be more popular than ever, but drinking it on a regular basis isn’t the best way to manage diabetes — even if (believe it or not) there’s growing evidence that it could help prevent diabetes.
Was this helpful?
Creamy, sugary drinks found at cafe chains are often loaded with unhealthy carbs. They’re also very high in calories.
The impact of the sugar and fat in a lot of coffee and espresso drinks can outweigh the good from any protective effects of the coffee.
The same can be said about sugar-sweetened and even artificially sweetened coffee and other beverages. Once sweetener is added, it increases your risk of developing type 2 diabetes. Consuming too many added sugars is directly linked to diabetes and obesity.
Having coffee drinks that are high in saturated fat or sugar on a regular basis can add to insulin resistance. It can eventually contribute to type 2 diabetes.
No food or supplement offers total protection against type 2 diabetes. If you have prediabetes or are at risk for getting diabetes, losing weight, exercising, and consuming a balanced, nutrient-dense diet is the best way to reduce your risk.
Taking up drinking coffee in order to stave off diabetes won’t guarantee you a good result. | no |
Diabetology | Can drinking coffee prevent type 2 diabetes? | yes_statement | "drinking" "coffee" can "prevent" "type" "2" "diabetes".. "coffee" consumption can lower the risk of developing "type" "2" "diabetes". | https://www.hsph.harvard.edu/nutritionsource/food-features/coffee/ | Coffee | The Nutrition Source | Harvard T.H. Chan School of Public ... | Coffee
Coffee lovers around the world who reach for their favorite morning brew probably aren’t thinking about its health benefits or risks. And yet this beverage has been subject to a long history of debate. In 1991 coffee was included in a list of possible carcinogens by the World Health Organization. By 2016 it was exonerated, as research found that the beverage was not associated with an increased risk of cancer; on the contrary, there was a decreased risk of certain cancers among those who drink coffee regularly once smoking history was properly accounted for. Additional accumulating research suggests that when consumed in moderation, coffee can be considered a healthy beverage. Why then in 2018 did one U.S. state pass legislation that coffee must bear a cancer warning label? Read on to explore the complexities of coffee.
Source Of
Plant chemicals: polyphenols including chlorogenic acid and quinic acid, and diterpenes including cafestol and kahweol
One 8-ounce cup of brewed coffee contains about 95 mg of caffeine. A moderate amount of coffee is generally defined as 3-5 cups a day, or on average 400 mg of caffeine, according to the Dietary Guidelines for Americans.
Coffee and Health
Coffee is an intricate mixture of more than a thousand chemicals. [1] The cup of coffee you order from a coffee shop is likely different from the coffee you brew at home. What defines a cup is the type of coffee bean used, how it is roasted, the amount of grind, and how it is brewed. Human response to coffee or caffeine can also vary substantially across individuals. Low to moderate doses of caffeine (50–300 mg) may cause increased alertness, energy, and ability to concentrate, while higher doses may have negative effects such as anxiety, restlessness, insomnia, and increased heart rate. [2] Still, the cumulative research on coffee points in the direction of a health benefit. [3,4] Does the benefit stem from the caffeine or plant compounds in the coffee bean? Is there a certain amount of coffee needed a day to produce a health benefit?
Cancer
Coffee may affect how cancer develops, ranging from the initiation of a cancer cell to its death. For example, coffee may stimulate the production of bile acids and speed digestion through the colon, which can lower the amount of carcinogens to which colon tissue is exposed. Various polyphenols in coffee have been shown to prevent cancer cell growth in animal studies. Coffee has also been associated with decreased estrogen levels, a hormone linked to several types of cancer. [5] Caffeine itself may interfere with the growth and spread of cancer cells. [6] Coffee also appears to lower inflammation, a risk factor for many cancers.
The 2018 uproar in California due to warning labels placed on coffee products stemmed from a chemical in the beverage called acrylamide, which is formed when the beans are roasted. Acrylamide is also found in some starchy foods that are processed with high heat like French fries, cookies, crackers, and potato chips. It was classified in the National Toxicology Program’s 2014 Report on Carcinogens, as “reasonably anticipated to be a human carcinogen” based on studies in lab animals. However, there is not yet evidence of a health effect in humans from eating acrylamide in food. Regardless, in March 2018 a California judge ruled that all California coffee sellers must warn consumers about the “potential cancer risk” from drinking coffee, because coffee-selling companies failed to show that acrylamide did not pose a significant health risk. California’s law Proposition 65, or The Safe Drinking Water and Toxic Enforcement Act of 1986, fueled the ruling, which requires a warning label to be placed on any ingredient from a list of 900 confirmed or suspected carcinogens.
However, many cancer experts disputed the ruling, stating that the metabolism of acrylamide differs considerably in animals and humans, and the high amount of acrylamide used in animal research is not comparable to the amount present in food. They cited the beneficial health effects of coffee, with improved antioxidant responses and reduced inflammation, both factors important in cancer prevention. Evidence from the American Institute for Cancer Research concludes that drinking coffee may reduce risk for endometrial and liver cancer, and based on a systematic review of a large body of research, it is not a risk for the cancers that were studied.
In June 2018, the California Office of Environmental Health Hazard Assessment (OEHHA) proposed a new regulation exempting coffee from displaying cancer warnings under Proposition 65. This proposal was based on a review of more than 1,000 studies published by the World Health Organization’s International Agency for Research on Cancer that found inadequate evidence that drinking coffee causes cancer. In January 2019, OEHHA completed its review and response to comments and submitted the regulation to the Office of Administrative Law (OAL) for final review.
Type 2 Diabetes
Although ingestion of caffeine can increase blood sugar in the short-term, long-term studies have shown that habitual coffee drinkers have a lower risk of developing type 2 diabetes compared with non-drinkers. The polyphenols and minerals such as magnesium in coffee may improve the effectiveness of insulin and glucose metabolism in the body.
In a meta-analysis of 45,335 people with type 2 diabetes followed for up to 20 years, an association was found with increasing cups of coffee and a lower risk of developing diabetes. Compared with no coffee, the decreased risk ranged from 8% with 1 cup a day to 33% for 6 cups a day. Caffeinated coffee showed a slightly greater benefit than decaffeinated coffee. [7]
Another meta-analysis of prospective cohort studies showed similar associations. When comparing the highest intake of coffee (up to 10 cups a day) with the lowest (<1 cup), there was a 30% decreased risk of type 2 diabetes in those drinking the highest amounts of coffee and caffeine and a 20% decreased risk when drinking decaffeinated coffee. Further analysis showed that the incidence of diabetes decreased by 12% for every 2 extra cups of coffee a day, and 14% for every 200 mg a day increase in caffeine intake (up to 700 mg a day). [8]
Heart health
Caffeine is a stimulant affecting the central nervous system that can cause different reactions in people. In sensitive individuals, it can irritate the stomach, increase anxiety or a jittery feeling, and disrupt sleep. Although many people appreciate the temporary energy boost after drinking an extra cup of coffee, high amounts of caffeine can cause unwanted heart palpitations in some.
Unfiltered coffee, such as French press and Turkish coffees, contains diterpenes, substances that can raise bad LDL cholesterol and triglycerides. Espresso coffee contains moderate amounts of diterpenes. Filtered coffee (drip-brewed coffee) and instant coffee contain almost no diterpenes as the filtering and processing of these coffee types removes the diterpenes.
Among 83,076 women in the Nurses’ Health Study, drinking 4 or more cups of coffee each day was associated with a 20% lower risk of stroke compared with non-drinkers. Decaffeinated coffee also showed an association, with 2 or more cups daily and a 11% lower stroke risk. The authors found no such association with other caffeinated drinks such as tea and soda. These coffee-specific results suggest that components in coffee other than caffeine may be protective. [9]
A large cohort of 37,514 women concluded that moderate coffee drinking of 2-3 cups a day was associated with a 21% reduced risk of heart disease. [10]
In addition, a meta-analysis of 21 prospective studies of men and women looking at coffee consumption and death from chronic diseases found a link between moderate coffee consumption (3 cups per day) and a 21% lower risk of cardiovascular disease deaths compared with non-drinkers. [11]
Another meta-analysis of 36 studies including men and women reviewed coffee consumption and risk of cardiovascular diseases (including heart disease, stroke, heart failure, and deaths from these conditions). It found that when compared with the lowest intakes of coffee (average 0 cups), a moderate coffee intake of 3-5 cups a day was linked with a 15% lower risk of cardiovascular disease. Heavier coffee intake of 6 or more cups daily was neither associated with a higher nor a lower risk of cardiovascular disease. [12]
Depression
Naturally occurring polyphenols in both caffeinated and decaffeinated coffee can act as antioxidants to reduce damaging oxidative stress and inflammation of cells. It may have neurological benefits in some people and act as an antidepressant. [13] Caffeine may affect mental states such as increasing alertness and attention, reducing anxiety, and improving mood. [14] A moderate caffeine intake of less than 6 cups of coffee per day has been associated with a lower risk of depression and suicide. However in a few cases of sensitive individuals, higher amounts of caffeine may increase anxiety, restlessness, and insomnia. Suddenly stopping caffeine intake can cause headache, fatigue, anxiety, and low mood for a few days and may persist for up to a week. [15]
A prospective cohort study following 263,923 participants from the National Institutes of Health and American Association of Retired Persons found that those who drank 4 or more cups of coffee a day were almost 10% less likely to become depressed than those who drank none. [15]
In a meta-analysis of observational studies including 330,677 participants, the authors found a 24% reduced risk of depression when comparing the highest (4.5 cups/day) to lowest (<1 cup) intakes of coffee. They found an 8% decreased risk of depression with each additional cup of coffee consumed. There was also a 28% reduced risk of depression comparing the highest to lowest intakes of caffeine, with the greatest benefit occurring with caffeine intakes between 68 and 509 mg a day (about 6 oz. to 2 cups of coffee). [16]
A review looking at three large prospective cohorts of men and women in the U.S. found a decreasing risk of suicide with increasing coffee consumption. When compared with no-coffee drinkers, the pooled risk of suicide was 45% lower among those who drank 2-3 cups daily and 53% lower among those who drank 4 or more cups daily. There was no association between decaffeinated coffee and suicide risk, suggesting that caffeine was the key factor, rather than plant compounds in coffee. [17]
Neurodegenerative diseases
Parkinson’s disease (PD) is mainly caused by low dopamine levels. There is consistent evidence from epidemiologic studies that higher consumption of caffeine is associated with lower risk of developing PD. The caffeine in coffee has been found in animal and cell studies to protect cells in the brain that produce dopamine.
A systematic review of 26 studies including cohort and case-control studies found a 25% lower risk of developing PD with higher intakes of caffeinated coffee. It also found a 24% decreased risk with every 300 mg increase in caffeine intake. [18]
A Finnish cohort study tracked coffee consumption and PD development in 6,710 men and women over 22 years. In that time, after adjusting for known risks of PD, those who drank at least 10 cups of coffee a day had a significantly lower risk of developing the disease than non-drinkers. [19]
A large cohort of men and women were followed for 10 and 16 years, respectively, to study caffeine and coffee intake on PD. The results showed an association in men drinking the most caffeine (6 or more cups of coffee daily) and a 58% lower risk of PD compared with men drinking no coffee. Women showed the lowest risk when drinking moderate intakes of 1-3 cups coffee daily. [20]
Alzheimer’s disease: In the CAIDE (Cardiovascular Risk Factors, Aging and Dementia) study, drinking 3-5 cups of coffee a day at midlife (mean age 50 years) was associated with a significantly decreased risk of Alzheimer’s disease later in life compared with low coffee drinkers after 21 years of follow-up. [2]
However, three systematic reviews were inconclusive about coffee’s effect on Alzheimer’s disease due to a limited number of studies and a high variation in study types that produced mixed findings. Overall the results suggested a trend towards a protective effect of caffeine against late-life dementia and Alzheimer’s disease, but no definitive statements could be made. The authors stated the need for larger studies with longer follow-up periods. Randomized controlled trials studying a protective effect of coffee or caffeine on the progression of Alzheimer’s disease and dementia are not yet available. [21-23]
Gallstones
There are various proposed actions of caffeine or components in coffee that may prevent the formation of gallstones. The most common type of gallstone is made of cholesterol. Coffee may prevent cholesterol from forming into crystals in the gallbladder. It may stimulate contractions in the gallbladder and increase the flow of bile so that cholesterol does not collect. [24]
A study of 46,008 men tracked the development of gallstones and their coffee consumption for 10 years. After adjusting for other factors known to cause gallstones, the study concluded that men who consistently drank coffee were significantly less likely to develop gallstones compared to men who did not. [24] A similar large study found the same result in women. [25]
Mortality
In a large cohort of more than 200,000 participants followed for up to 30 years, an association was found between drinking moderate amounts of coffee and lower risk of early death. Compared with non-drinkers, those who drank 3-5 cups of coffee daily were 15% less likely to die early from all causes, including cardiovascular disease, suicide, and Parkinson’s disease. Both caffeinated and decaffeinated coffee provided benefits. The authors suggested that bioactive compounds in coffee may be responsible for interfering with disease development by reducing inflammation and insulin resistance. [26]
In a large prospective cohort of more than 500,000 people followed for 10 years, an association was found between drinking higher amounts of coffee and lower rates of death from all causes. Compared with non-drinkers, those drinking 6-7 cups daily had a 16% lower risk of early death. [26] A protective association was also found in those who drank 8 or more cups daily. The protective effect was present regardless of a genetic predisposition to either faster or slower caffeine metabolism. Instant and decaffeinated coffee showed a similar health benefit.
The bottom line: A large body of evidence suggests that consumption of caffeinated coffee does not increase the risk of cardiovascular diseases and cancers. In fact, consumption of 3 to 5 standard cups of coffee daily has been consistently associated with a reduced risk of several chronic diseases. [4] However, some individuals may not tolerate higher amounts of caffeine due to symptoms of jitteriness, anxiety, and insomnia. Specifically, those who have difficulty controlling their blood pressure may want to moderate their coffee intake. Pregnant women are also advised to aim for less than 200 mg of caffeine daily, the amount in 2 cups of coffee, because caffeine passes through the placenta into the fetus and has been associated with pregnancy loss and low birth weight. [3, 27] Because of the potential negative side effects some people experience when drinking caffeinated coffee, it is not necessary to start drinking it if you do not already or to increase the amount you currently drink, as there are many other dietary strategies to improve your health. Decaffeinated coffee is a good option if one is sensitive to caffeine, and according to the research summarized above, it offers similar health benefits as caffeinated coffee. It’s also important to keep in mind how you enjoy your brew. The extra calories, sugar, and saturated fat in a coffee house beverage loaded with whipped cream and flavored syrup might offset any health benefits found in a basic black coffee.
What about iced coffee?
Types
Coffee beans are the seeds of a fruit called a coffee cherry. Coffee cherries grow on coffee trees from a genus of plants called Coffea. There are a wide variety of species of coffee plants, ranging from shrubs to trees.
Type of bean.There are two main types of coffee species, Arabica and Robusta. Arabica originates from Ethiopia and produces a mild, flavorful tasting coffee. It is the most popular type worldwide. However, it is expensive to grow because the Arabica plant is sensitive to the environment, requiring shade, humidity, and steady temperatures between 60-75 degrees Fahrenheit. The Robusta coffee plant is more economical to grow because it is resistant to disease and survives in a wider range of temperatures between 65-97 degrees Fahrenheit. It can also withstand harsh climate changes such as variations in rainfall and strong sunlight.
Type of roast.Coffee beans start out green. They are roasted at a high heat to produce a chemical change that releases the rich aroma and flavor that we associate with coffee. They are then cooled and ground for brewing. Roasting levels range from light to medium to dark. The lighter the roast, the lighter the color and roasted flavor and the higher its acidity. Dark roasts produce a black bean with little acidity and a bitter roasted flavor. The popular French roast is medium-dark.
Type of grind. A medium grind is the most common and used for automatic drip coffee makers. A fine grind is used for deeper flavors like espresso, which releases the oils, and a coarse grind is used in coffee presses.
Decaffeinated coffee. This is an option for those who experience unpleasant side effects from caffeine. The two most common methods used to remove caffeine from coffee is to apply chemical solvents (methylene chloride or ethyl acetate) or carbon dioxide gas. Both are applied to steamed or soaked beans, which are then allowed to dry. The solvents bind to caffeine and both evaporate when the beans are rinsed and/or dried. According to U.S. regulations, at least 97% of the caffeine must be removed to carry the decaffeinated label, so there may be trace residual amounts of caffeine. Both methods may cause some loss of flavor as other naturally occurring chemicals in coffee beans that impart their unique flavor and scent may be destroyed during processing.
Watch out for hidden calories in coffee drinks
A plain “black” cup of coffee is a very low calorie drink—8 ounces only contains 2 calories! However, adding sugar, cream, and milk can quickly bump up the calorie counts. A tablespoon of cream contains 52 calories, and a tablespoon of whole milk contains 9 calories. While 9 calories isn’t a lot, milk is often poured into coffee without measuring, so you may be getting several servings of milk or cream in your coffee. A tablespoon of sugar contains 48 calories, so if you take your coffee with cream and sugar, you’re adding over 100 extra calories to your daily cup.
However, the real caloric danger occurs in specialty mochas, lattes, or blended ice coffee drinks. These drinks are often super-sized and can contain anywhere from 200-500 calories, as well as an extremely large amount of sugar. With these drinks, it’s best to enjoy them as a treat or dessert, and stick with plain, minimally sweetened coffee on a regular basis
Store
Place beans or ground coffee in an airtight opaque container at room temperature away from sunlight. Inside a cool dark cabinet would be ideal. Exposure to moisture, air, heat, and light can strip coffee of its flavor. Coffee packaging does not preserve the coffee well for extended periods, so transfer larger amounts of coffee to airtight containers.
Coffee can be frozen if stored in a very airtight container. Exposure to even small amounts of air in the freezer can lead to freezer burn.
Make
Follow directions on the coffee package and your coffee machine, but generally the ratio is 1-2 tablespoons of ground coffee per 6 ounces of water.
For optimal coffee flavor, drink soon after brewing. The beverage will lose flavor with time.
Use ground coffee within a few days and whole beans within two weeks.
Did You Know?
It is a myth that darker roasts contain a higher level of caffeine than lighter roasts. Lighter roasts actually have a slightly higher concentration!
Coffee grinds should not be brewed more than once. Brewed grinds taste bitter and may no longer produce a pleasant coffee flavor.
While water is always the best choice for quenching your thirst, coffee can count towards your daily fluid goals. Although caffeine has a mild diuretic effect, it is offset by the total amount of fluid from the coffee.
Related
Caffeine
Caffeine is naturally found in the fruit, leaves, and beans of coffee, cacao, and guarana plants. It is also added to beverages and supplements. Learn about sources of caffeine, and a review of the research on this stimulant and health.
Terms of Use
The contents of this website are for educational purposes and are not intended to offer personal medical advice. You should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The Nutrition Source does not recommend or endorse any products. | Evidence from the American Institute for Cancer Research concludes that drinking coffee may reduce risk for endometrial and liver cancer, and based on a systematic review of a large body of research, it is not a risk for the cancers that were studied.
In June 2018, the California Office of Environmental Health Hazard Assessment (OEHHA) proposed a new regulation exempting coffee from displaying cancer warnings under Proposition 65. This proposal was based on a review of more than 1,000 studies published by the World Health Organization’s International Agency for Research on Cancer that found inadequate evidence that drinking coffee causes cancer. In January 2019, OEHHA completed its review and response to comments and submitted the regulation to the Office of Administrative Law (OAL) for final review.
Type 2 Diabetes
Although ingestion of caffeine can increase blood sugar in the short-term, long-term studies have shown that habitual coffee drinkers have a lower risk of developing type 2 diabetes compared with non-drinkers. The polyphenols and minerals such as magnesium in coffee may improve the effectiveness of insulin and glucose metabolism in the body.
In a meta-analysis of 45,335 people with type 2 diabetes followed for up to 20 years, an association was found with increasing cups of coffee and a lower risk of developing diabetes. Compared with no coffee, the decreased risk ranged from 8% with 1 cup a day to 33% for 6 cups a day. Caffeinated coffee showed a slightly greater benefit than decaffeinated coffee. [7]
Another meta-analysis of prospective cohort studies showed similar associations. When comparing the highest intake of coffee (up to 10 cups a day) with the lowest (<1 cup), there was a 30% decreased risk of type 2 diabetes in those drinking the highest amounts of coffee and caffeine and a 20% decreased risk when drinking decaffeinated coffee. | yes |
Diabetology | Can drinking coffee prevent type 2 diabetes? | yes_statement | "drinking" "coffee" can "prevent" "type" "2" "diabetes".. "coffee" consumption can lower the risk of developing "type" "2" "diabetes". | https://www.diabetes.co.uk/food/coffee-and-diabetes.html | Coffee and Diabetes - Benefits of Coffee & Effect on Blood Sugar | Coffee and Diabetes
The effect of coffee on diabetes, when presented in the media can often be confusing.
News stories can in the same week tout the benefits coffee can have on diabetes and shoot down coffee as being unhelpful for blood sugar levels.
This doesn’t mean the articles are contradictory though.
Put slightly more simply, coffee contains different chemicals, some of which have beneficial effects whereas others can have a less beneficial effect, such as caffeine which can impair insulin in the short term.
Caffeine and blood sugar levels
Whilst the researchers found a relationship between higher coffee consumption and lower sensitivity to insulin, they recognised that the rapid transition to having more coffee may have produced an atypical or emphasised response by the body.
Coffee contains polyphenols, which are a molecule that anti-oxidant properties which are widely believed to help prevent inflammatory illnesses, such as type 2 diabetes, and anticarcinogenic (anti-cancer) properties.
As well as polyphenols, coffee contains the mineral magnesium and chromium. Greater magnesium intake has been linked with lower rates of type 2 diabetes.
The blend of these nutrients can be helpful for improving insulin sensitivity, which may help to offset the opposite effects of caffeine.
Coffee and prevention of diabetes
Coffee and its effect on risks of developing type 2 diabetes have been studied a number of times and has indicated a notably lower risk of type 2 diabetes being associated with coffee drinkers.
Decaffeinated coffee and blood glucose
So whilst caffeine may hamper insulin sensitivity, other properties in coffee have the opposite effect.
It is therefore believed that decaffeinated coffee may present the best option for people with diabetes as researchers find it includes the benefits of coffee with some of negative effects that are associated with caffeine.
Lattes and syrups in coffee
Some varieties of coffee need to be approached with caution by those of us with diabetes. Coffees with syrup have become a much more popular variety of coffee within the 21st Century but could be problematic for people either with or at risk of, diabetes.
If you have diabetes or are at risk of diabetes, it is advisable to reduce your exposure to too much sugar. If you wish to enjoy a syrupy coffee from time to time, pick the smaller sized cups and drink slowly to better appreciate the taste without dramatically raising your blood glucose levels.
Another modern trend in coffee is in the popularity of lattes, very milky coffees. Lattes present two considerations: the number of calories in the latte and the amount of carbohydrate in them.
Whilst skinny lattes are usually made with skimmed milk, some of them may be sweetened which will raise their calories. Milk, whether full fat or skimmed, tends to have around 5g of carbs per 100g. A regular, unsweetened skinny latte can typically contain anywhere between 10 and 15g of carbohydrate. | Coffee and Diabetes
The effect of coffee on diabetes, when presented in the media can often be confusing.
News stories can in the same week tout the benefits coffee can have on diabetes and shoot down coffee as being unhelpful for blood sugar levels.
This doesn’t mean the articles are contradictory though.
Put slightly more simply, coffee contains different chemicals, some of which have beneficial effects whereas others can have a less beneficial effect, such as caffeine which can impair insulin in the short term.
Caffeine and blood sugar levels
Whilst the researchers found a relationship between higher coffee consumption and lower sensitivity to insulin, they recognised that the rapid transition to having more coffee may have produced an atypical or emphasised response by the body.
Coffee contains polyphenols, which are a molecule that anti-oxidant properties which are widely believed to help prevent inflammatory illnesses, such as type 2 diabetes, and anticarcinogenic (anti-cancer) properties.
As well as polyphenols, coffee contains the mineral magnesium and chromium. Greater magnesium intake has been linked with lower rates of type 2 diabetes.
The blend of these nutrients can be helpful for improving insulin sensitivity, which may help to offset the opposite effects of caffeine.
Coffee and prevention of diabetes
Coffee and its effect on risks of developing type 2 diabetes have been studied a number of times and has indicated a notably lower risk of type 2 diabetes being associated with coffee drinkers.
Decaffeinated coffee and blood glucose
So whilst caffeine may hamper insulin sensitivity, other properties in coffee have the opposite effect.
It is therefore believed that decaffeinated coffee may present the best option for people with diabetes as researchers find it includes the benefits of coffee with some of negative effects that are associated with caffeine.
Lattes and syrups in coffee
Some varieties of coffee need to be approached with caution by those of us with diabetes. | yes |
Diabetology | Can drinking coffee prevent type 2 diabetes? | yes_statement | "drinking" "coffee" can "prevent" "type" "2" "diabetes".. "coffee" consumption can lower the risk of developing "type" "2" "diabetes". | https://www.hsph.harvard.edu/nutritionsource/disease-prevention/diabetes-prevention/preventing-diabetes-full-story/ | Simple Steps to Preventing Diabetes | The Nutrition Source ... | Simple Steps to Preventing Diabetes
Keeping weight in check, being active, and eating a healthy diet can help prevent most cases of type 2 diabetes.
Overview
If type 2 diabetes were an infectious disease, passed from one person to another, public health officials would say we’re in the midst of an epidemic. This difficult disease is striking an ever-growing number of adults, and with the rising rates of childhood obesity, it has become more common in youth, especially among certain ethnic groups (learn more about diabetes, including the other types and risk factors).
The good news is that prediabetes and type 2 diabetes are largely preventable. About 9 in 10 cases in the U.S. can be avoided by making lifestyle changes. These same changes can also lower the chances of developing heart disease and some cancers. The key to prevention can be boiled down to five words: Stay lean and stay active.
What if I already have diabetes?
Guidelines for preventing or lowering your risk of developing type 2 diabetes are also appropriate if you currently have a diabetes diagnosis. Achieving a healthy weight, eating a balanced carbohydrate-controlled diet, and getting regular exercise all help to improve blood glucose control. If you are taking insulin medication, you may need more or less carbohydrate at a meal or snack to ensure a healthy blood glucose range. There may also be special dietary needs for exercise, such as bringing a snack so that your blood glucose does not drop too low. For specific guidance on scenarios such as these, refer to your diabetes care team who are the best resources for managing your type of diabetes.
Simple steps to lowering your risk
Control your weight
Excess weight is the single most important cause of type 2 diabetes. Being overweight increases the chances of developing type 2 diabetes seven-fold. Being obese makes you 20 to 40 times more likely to develop diabetes than someone with a healthy weight. [1]
Losing weight can help if your weight is above the healthy-weight range. Losing 7-10% of your current weight can cut your chances of developing type 2 diabetes in half.
Get moving—and turn off the television
Inactivity promotes type 2 diabetes. [2] Working your muscles more often and making them work harder improves their ability to use insulin and absorb glucose. This puts less stress on your insulin-making cells. So trade some of your sit-time for fit-time.
Long bouts of hot, sweaty exercise aren’t necessary to reap this benefit. Findings from the Nurses’ Health Study and Health Professionals Follow-up Study suggest that walking briskly for a half hour every day reduces the risk of developing type 2 diabetes by 30%. [3,4] More recently, The Black Women’s Health Study reported similar diabetes-prevention benefits for brisk walking of more than 5 hours per week. [5] This amount of exercise has a variety of other benefits as well. And even greater cardiovascular and other advantages can be attained by more, and more intense, exercise.
Television-watching appears to be an especially-detrimental form of inactivity: Every two hours you spend watching TV instead of pursuing something more active increases the chances of developing diabetes by 20%; it also increases the risk of heart disease (15%) and early death (13%). [6] The more television people watch, the more likely they are to be overweight or obese, and this seems to explain part of the TV viewing-diabetes link. The unhealthy diet patterns associated with TV watching may also explain some of this relationship.
Tune Up Your Diet
Four dietary changes can have a big impact on the risk of type 2 diabetes.
There is convincing evidence that diets rich in whole grains protect against diabetes, whereas diets rich in refined carbohydrates lead to increased risk [7]. In the Nurses’ Health Studies I and II, for example, researchers looked at the whole grain consumption of more than 160,000 women whose health and dietary habits were followed for up to 18 years. Women who averaged 2-3 servings of whole grains a day were 30% less likely to have developed type 2 diabetes than those who rarely ate whole grains. [8] When the researchers combined these results with those of several other large studies, they found that eating an extra two servings of whole grains a day decreased the risk of type 2 diabetes by 21%.
Whole grains don’t contain a magical nutrient that fights diabetes and improves health. It’s the entire package—elements intact and working together—that’s important. The bran and fiber in whole grains make it more difficult for digestive enzymes to break down the starches into glucose. This leads to lower, slower increases in blood sugar and insulin, and a lower glycemic index. As a result, they stress the body’s insulin-making machinery less, and so may help prevent type 2 diabetes. [9] Whole grains are also rich in essential vitamins, minerals, and phytochemicals that may help reduce the risk of diabetes.
In contrast, white bread, white rice, mashed potatoes, donuts, bagels, and many breakfast cereals have what’s called a high glycemic index and glycemic load. That means they cause sustained spikes in blood sugar and insulin levels, which in turn may lead to increased diabetes risk. [9] In China, for example, where white rice is a staple, the Shanghai Women’s Health Study found that women whose diets had the highest glycemic index had a 21% higher risk of developing type 2 diabetes, compared with women whose diets had the lowest glycemic index. [10] Similar findings were reported in the Black Women’s Health Study. [11]
More recent findings from the Nurses Health Studies I and II and the Health Professionals Follow-Up Study suggest that swapping whole grains for white rice could help lower diabetes risk: Researchers found that women and men who ate the most white rice—five or more servings a week—had a 17% higher risk of diabetes than those who ate white rice less than one time a month. People who ate the most brown rice—two or more servings a week—had an 11% lower risk of diabetes than those who rarely ate brown rice. Researchers estimate that swapping whole grains in place of even some white rice could lower diabetes risk by 36%. [12]
2. Skip the sugary drinks, and choose water, coffee, or tea instead.
Like refined grains, sugary beverages have a high glycemic load, and drinking more of this sugary stuff is associated with increased risk of diabetes. In the Nurses’ Health Study II, women who drank one or more sugar-sweetened beverages per day had an 83% higher risk of type 2 diabetes, compared with women who drank less than one sugar-sweetened beverage per month. [13]
Combining the Nurses’ Health Study results with those from seven other studies found a similar link between sugary beverage consumption and type 2 diabetes. For every additional 12-ounce serving of sugary beverage that people drank each day, their risk of type 2 diabetes rose 25%. [14] Studies also suggest that fruit drinks— powdered drinks, fortified fruit drinks, or juices—are not the healthy choice that food advertisements often portray them to be. Women in the Black Women’s Health study who drank two or more servings of fruit drinks a day had a 31% higher risk of type 2 diabetes, compared with women who drank less than one serving a month. [15]
How do sugary drinks lead to this increased risk? Weight gain may explain the link. In both the Nurses’ Health Study II and the Black Women’s Health Study, women who drank more sugary drinks gained more weight than women who cut back on sugary drinks. [13,15] Several studies show that children and adults who drink soda or other sugar-sweetened beverages are more likely to gain weight than those who don’t. [15-17] and that switching from these to water or unsweetened beverages can reduce weight. [18] Even so, weight gain caused by sugary drinks may not completely explain the increased diabetes risk. There is mounting evidence that sugary drinks contribute to chronic inflammation, high triglycerides, decreased “good” (HDL) cholesterol, and increased insulin resistance, all of which are risk factors for diabetes. [19]
What to drink in place of the sugary stuff? Water is an excellent choice. Coffee and tea are also good calorie-free substitutes for sugared beverages (as long as you don’t load them up with sugar and cream). And there’s convincing evidence that coffee may help protect against diabetes; [20,21] emerging research suggests that tea may hold diabetes-prevention benefits as well, but more research is needed.
There’s been some controversy over whether artificially sweetened beverages are beneficial for weight control and, by extension, diabetes prevention. [22] Some studies have found that people who regularly drink diet beverages have a higher risk of diabetes than people who rarely drink such beverages, [23,24] but there could be another explanation for those findings. People often start drinking diet beverages because they have a weight problem or a family history of diabetes; studies that don’t adequately account for these other factors may make it wrongly appear as though the diet soda led to the increased diabetes risk. A long-term analysis on data from 40,000 men in the Health Professionals Follow-up Study found that drinking one 12-ounce serving of diet soda a day did not appear to increase diabetes risk. [25] So, in moderation diet beverages can be a sugary-drink alternative for adults.
3. Choose healthy fats.
The types of fats in your diet can also affect the development of diabetes. Healthful fats, such as the polyunsaturated fats found in liquid vegetable oils, nuts, and seeds can help ward off type 2 diabetes. [26] Trans fats do just the opposite. [1,27] These harmful fats were once found in many kinds of margarine, packaged baked goods, fried foods in most fast-food restaurants, and any product that listed “partially hydrogenated vegetable oil” on the label. Eating polyunsaturated fats from fish—also known as “long chain omega 3” or “marine omega 3” fats—does not protect against diabetes, even though there is much evidence that these marine omega 3 fats help prevent heart disease. [28] If you already have diabetes, eating fish can help protect you against a heart attack or dying from heart disease. [29]
The evidence is growing stronger that eating red meat (beef, pork, lamb) and processed red meat (bacon, hot dogs, deli meats) increases the risk of diabetes, even among people who consume only small amounts. A meta-analysis combined findings from the Nurses’ Health Studies I and II, the Health Professionals Follow-up Study, and six other long-term studies. The researchers looked at data from roughly 440,000 people, about 28,000 of whom developed diabetes during the course of the study. [30] They found that eating just one 3-ounce serving of red meat daily—say, a steak that’s about the size of a deck of cards—increased the risk of type 2 diabetes by 20%. Eating even smaller amounts of processed red meat each day—just two slices of bacon, one hot dog, or the like—increased diabetes risk by 51%.
The good news from this study: Swapping out red meat or processed red meat for a healthier protein source, such as nuts, low-fat dairy, poultry, or fish, or for whole grains lowered diabetes risk by up to 35%. Not surprisingly, the greatest risk reductions came from ditching processed red meat.
How meat is cooked may matter too. A study of three large cohorts followed for 12-16 years—including more than 289,000 men and women from the Nurses’ Health Studies and the Health Professionals Follow-up Study—found that participants who most frequently ate meats and chicken cooked at high temperatures were 1.5 times more likely to develop type 2 diabetes, compared with those who ate the least. [31] An increased risk of weight gain and developing obesity in the frequent users of high-temperature cooking methods may have contributed to the development of diabetes.
Why do these types of meat appear to boost diabetes risk? It may be that the high iron content of red meat diminishes insulin’s effectiveness or damages the cells that produce insulin. The high levels of sodium and nitrites (preservatives) in processed red meats may also be to blame. Red and processed meats are a hallmark of the unhealthful “Western” dietary pattern, which seems to trigger diabetes in people who are already at genetic risk. [32]
Furthermore, a related body of research has suggested that plant-based dietary patterns may help lower type 2 diabetes risk, and more specifically, those who adhere to predominantly healthy plant-based diets may have a lower risk of developing type 2 diabetes than those who follow these diets with lower adherence:
A 2019 meta-analysis that included health data from 307,099 participants with 23,544 cases of type 2 diabetes examined adherence to an “overall” predominantly plant-based diet (which could include a mix of healthy plant-based foods such as fruits, vegetables, whole grains, nuts, and legumes, but also less healthy plant-based foods such as potatoes, white flour, and sugar, and modest amounts of animal products). The researchers also looked at “healthful” plant-based diets, which were defined as those emphasizing healthy plant-based foods, with lower consumption of unhealthy plant-based foods. They found that people with the highest adherence to overall predominantly plant-based diets had a 23% lower risk of type 2 diabetes compared to those with weaker adherence to the diets. The researchers also found that the association was strengthened for those who ate healthful plant-based diets [41]
Don’t smoke
Add type 2 diabetes to the long list of health problems linked with smoking. Smokers are roughly 50% more likely to develop diabetes than nonsmokers, and heavy smokers have an even higher risk. [33]
Light to moderate alcohol consumption
Evidence has consistently linked moderate alcohol consumption with reduced risk of heart disease. The same may be true for type 2 diabetes. Moderate amounts of alcohol—up to a drink a day for women, up to two drinks a day for men—increases the efficiency of insulin at getting glucose inside cells. And some studies indicate that moderate alcohol consumption decreases the risk of type 2 diabetes. [1, 34-39], but excess alcohol intake actually increases the risk. If you already drink alcohol, the key is to keep your consumption in the moderate range, as higher amounts of alcohol could increase diabetes risk. [40] If you don’t drink alcohol, there’s no need to start—you can get the same benefits by losing weight, exercising more, and changing your eating patterns.
Beyond individual behavior
Type 2 diabetes is largely preventable by taking several simple steps: keeping weight under control, exercising more, eating a healthy diet, and not smoking. Yet it is clear that the burden of behavior change cannot fall entirely on individuals. Families, schools, worksites, healthcare providers, communities, media, the food industry, and government must work together to make healthy choices easy choices. For links to evidence-based guidelines, research reports, and other resources for action, visit our diabetes prevention toolkit.
Terms of Use
The contents of this website are for educational purposes and are not intended to offer personal medical advice. You should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The Nutrition Source does not recommend or endorse any products. | There is mounting evidence that sugary drinks contribute to chronic inflammation, high triglycerides, decreased “good” (HDL) cholesterol, and increased insulin resistance, all of which are risk factors for diabetes. [19]
What to drink in place of the sugary stuff? Water is an excellent choice. Coffee and tea are also good calorie-free substitutes for sugared beverages (as long as you don’t load them up with sugar and cream). And there’s convincing evidence that coffee may help protect against diabetes; [20,21] emerging research suggests that tea may hold diabetes-prevention benefits as well, but more research is needed.
There’s been some controversy over whether artificially sweetened beverages are beneficial for weight control and, by extension, diabetes prevention. [22] Some studies have found that people who regularly drink diet beverages have a higher risk of diabetes than people who rarely drink such beverages, [23,24] but there could be another explanation for those findings. People often start drinking diet beverages because they have a weight problem or a family history of diabetes; studies that don’t adequately account for these other factors may make it wrongly appear as though the diet soda led to the increased diabetes risk. A long-term analysis on data from 40,000 men in the Health Professionals Follow-up Study found that drinking one 12-ounce serving of diet soda a day did not appear to increase diabetes risk. [25] So, in moderation diet beverages can be a sugary-drink alternative for adults.
3. Choose healthy fats.
The types of fats in your diet can also affect the development of diabetes. Healthful fats, such as the polyunsaturated fats found in liquid vegetable oils, nuts, and seeds can help ward off type 2 diabetes. [26] Trans fats do just the opposite. | yes |
Diabetology | Can drinking coffee prevent type 2 diabetes? | yes_statement | "drinking" "coffee" can "prevent" "type" "2" "diabetes".. "coffee" consumption can lower the risk of developing "type" "2" "diabetes". | https://www.rush.edu/news/health-benefits-coffee | Health Benefits of Coffee | RUSH | Turns out that coffee's good for more than jump-starting our mornings or keeping us awake during meetings. A lot of recent research suggests that coffee offers a host of potential health benefits.
Every day, Americans drink 400 million cups of this incredibly complex beverage, which contains more than 1,000 compounds that can affect the body. The most commonly studied are caffeine (a nervous-system stimulant that's known to have positive cognitive effects) and polyphenols (antioxidants that can help slow or prevent cell damage).
What health benefits does coffee offer?
Though researchers don't always know exactly which of coffee's ingredients are responsible for producing their studies' health-boosting results, there's evidence that drinking coffee may help do the following:
1. Improve overall health.
An analysis of nearly 220 studies on coffee, published in the BMJ in 2017, found that coffee drinkers may enjoy more overall health benefits than people who don't drink coffee.
The analysis found that during the study period, coffee drinkers were 17% less likely to die early from any cause, 19% less likely to die of heart disease and 18% less likely to develop cancer than those who don't drink coffee.
2. Protect against Type 2 diabetes.
A 2014 study by Harvard researchers published in the journal Diabetologica tracked nearly 124,000 people for 16 to 20 years.
Those who increased their coffee intake by more than a cup a day over a four-year period had an 11% lower risk of developing Type 2 diabetes; those who decreased their intake by one cup per day had a 17% higher risk of developing the disease.
The reason may be the antioxidants in coffee, which reduce inflammation (inflammation contributes to your Type 2 diabetes risk).
If you already have Type 2 diabetes, however, you should avoid caffeinated products, including coffee. Caffeine has been shown to raise both blood sugar and insulin levels in people with the disease.
3. Control Parkinson's disease symptoms.
A number of studies have suggested that consuming caffeine can reduce your risk of developing Parkinson's disease — and research published in 2012 in the journal of the American Academy of Neurology showed that a daily dose of caffeine equivalent to that found in two eight-ounce cups of black coffee can help to control the involuntary movements of people who already have the disease. (You'd have to drink nearly eight cups of brewed black tea to get the same amount of caffeine.)
4. Slow the progress of dementia.
In a 2012 study published in the Journal of Alzheimer's Disease, Florida researchers tested the blood levels of caffeine in older adults with mild cognitive impairments, which can be a precursor to severe dementia, including Alzheimer's disease.
When the researchers re-evaluated the subjects two to four years later, those whose blood levels contained caffeine amounts equivalent to about three cups of coffee were far less likely to have progressed to full-blown dementia than those who had consumed little or no caffeine.
5. Safeguard the liver.
Several studies published in respected journals have found that coffee drinking has beneficial effects on the liver, including reducing the risk of death from liver cirrhosis, decreasing harmful liver enzyme levels and limiting liver scarring in people who have hepatitis C.
6. Promote heart health.
According to a study published in 2021 in the American Heart Association journal Circulation: Heart Failure, drinking one or more daily cups of plain, caffeinated coffee was associated with a significant reduction in a person's long-term risk of heart failure.
The study looked at the original data from three well-known heart disease studies: the Framingham Heart Study, the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study.
Although there's not enough evidence to support prescribing coffee to lower your risk of heart disease risk, this recent revelation seems to strengthen previous findings that coffee is, in fact, good for heart health.
In 2013, the journal Epidemiology and Prevention published a review of studies analyzing the correlation between coffee consumption and cardiovascular disease. Data from 36 different studies showed that people who drink three to five cups of coffee per day had a lower risk of heart disease than those who drink no coffee or more than five cups per day.
While the reason isn't clear, one possibility is that coffee helps to improve blood vessels' control over blood flow and blood pressure.
7. Reduce melanoma risk.
A 2015 study appearing in the Journal of the National Cancer Institute looked at the coffee-drinking habits of more than 447,000 people over 10 years. The researchers found that those who drank four or more cups of caffeinated coffee each day had a 20% lower risk of developing melanoma than people who drank decaffeinated coffee or no coffee.
8. Lower mortality risk
Your morning coffee could help lower your risk of death. A 2022 study in The Annals of Internal Medicine has shown that moderate consumption of unsweetened and sugar-sweetened coffee was associated with a reduced risk of mortality. The research shows that those who drank 1.5 to 3.5 cups of coffee per day, including with sugar, had a 30% less lower risk of death from any cause during the study.
Advice for coffee drinkers
While he's never gone so far as to prescribe a daily dose of java for any of his patients, he says, "I'm certainly familiar with a lot of research showing that coffee has a mildly beneficial effect in protecting against issues like stroke, diabetes and cardiovascular problems."
He offers a few caveats, however:
Bottom line? Enjoy a daily cup or two of coffee, but don't use it as a substitute for other healthy behaviors.
Don't doctor up your drink.
"Keep in mind that the research focuses on the benefits of black coffee, which we're still learning about," Rothschild says. "But we definitely know the harms associated with the fat and sugar you find in a lot of coffee drinks."
A Starbucks Venti White Chocolate Mocha, for instance, has 580 calories, 22 grams of fat (15 of which are saturated) and 75 grams of sugar. A plain cup of brewed coffee? Two calories, no fat and zero carbs.
If you can't drink it black, stick with low-calorie, low-fat add-ins, such as skim milk or almond milk.
Coffee is for grownups only.
"It's not true that coffee will stunt kids' growth, as parents used to be fond of saying," Rothschild says. But there are a few good reasons for kids not to drink coffee or other caffeinated drinks (e.g., colas and energy drinks).
One study, published in 2014 in the journal Pediatrics, showed that even small amounts of caffeine, equivalent to one cup of coffee, increased children's blood pressure and — to compensate for the rise in blood pressure — slowed heart rates.
Beyond that, Rothschild says, he'd be concerned about sleep disruption and behavioral issues that might result from ingesting a stimulant.
Switch to decaf if you have acid reflux ...
"Caffeine causes the gastroesophageal sphincter to relax, which allows acid to enter the esophagus," Rothschild explains.
... or insomnia ...
"People who have trouble sleeping can get into a vicious cycle: They sleep badly, increase their caffeine intake the next day to compensate, then sleep badly again, and on and on," he says, suggesting that people with insomnia avoid all caffeine after noon.
"There's some evidence showing that moderate to high coffee consumption — more than four cups per day — is linked with calcium loss and fractures," says Rothschild.
But if you do drink decaf, definitely limit your consumption. That study in Circulation: Heart Failure found that decaffeinated coffee was actually associated with an increased risk for heart failure.
Enjoy coffee in moderation.
Bottom line? Enjoy a daily cup or two of coffee, Rothschild says, but don't use it as a substitute for other healthy behaviors. "Unless you have a condition like reflux, it's fine to keep drinking a reasonable amount of coffee," he says.
But you can also try other healthy ways to get some of the benefits you might attribute to coffee.
"For instance, if you rely on coffee to fight after-lunch sluggishness every day, you might think about getting outside and going for a 10 to 20 minute walk," Rothschild suggests. "It'll not only wake you up, but you'll also get a lot of benefits in terms of bone health and cardiovascular health."
All physicians featured on this website are on the medical faculty of RUSH University Medical Center, RUSH Copley Medical Center or RUSH Oak Park Hospital. Some of the physicians featured are in private practice and, as independent practitioners, are not agents or employees of RUSH University Medical Center, RUSH Copley Medical Center or RUSH Oak Park Hospital. | 7% less likely to die early from any cause, 19% less likely to die of heart disease and 18% less likely to develop cancer than those who don't drink coffee.
2. Protect against Type 2 diabetes.
A 2014 study by Harvard researchers published in the journal Diabetologica tracked nearly 124,000 people for 16 to 20 years.
Those who increased their coffee intake by more than a cup a day over a four-year period had an 11% lower risk of developing Type 2 diabetes; those who decreased their intake by one cup per day had a 17% higher risk of developing the disease.
The reason may be the antioxidants in coffee, which reduce inflammation (inflammation contributes to your Type 2 diabetes risk).
If you already have Type 2 diabetes, however, you should avoid caffeinated products, including coffee. Caffeine has been shown to raise both blood sugar and insulin levels in people with the disease.
3. Control Parkinson's disease symptoms.
A number of studies have suggested that consuming caffeine can reduce your risk of developing Parkinson's disease — and research published in 2012 in the journal of the American Academy of Neurology showed that a daily dose of caffeine equivalent to that found in two eight-ounce cups of black coffee can help to control the involuntary movements of people who already have the disease. (You'd have to drink nearly eight cups of brewed black tea to get the same amount of caffeine.)
4. Slow the progress of dementia.
In a 2012 study published in the Journal of Alzheimer's Disease, Florida researchers tested the blood levels of caffeine in older adults with mild cognitive impairments, which can be a precursor to severe dementia, including Alzheimer's disease.
| yes |
Diabetology | Can drinking coffee prevent type 2 diabetes? | yes_statement | "drinking" "coffee" can "prevent" "type" "2" "diabetes".. "coffee" consumption can lower the risk of developing "type" "2" "diabetes". | https://www.sciencedaily.com/releases/2015/04/150430191138.htm | Replacing one serving of sugary drink per day by water or ... | Replacing one serving of sugary drink per day by water or unsweetened tea or coffee cuts risk of type 2 diabetes, study shows
Date:
April 30, 2015
Source:
Diabetologia
Summary:
Replacing the daily consumption of one serving of a sugary drink with either water or unsweetened tea or coffee can lower the risk of developing diabetes by between 14 percent and 25 percent, concludes new research.
New research published in Diabetologia (the journal of the European Association for the Study of Diabetes) indicates that for each 5% increase of a person's total energy intake provided by sweet drinks including soft drinks, the risk of developing type 2 diabetes may increase by 18%. However, the study also estimates that replacing the daily consumption of one serving of a sugary drink with either water or unsweetened tea or coffee can lower the risk of developing diabetes by between 14% and 25%.
This research is based on the large EPIC-Norfolk study which included more than 25,000 men and women aged 40-79 years living in Norfolk, UK. Study participants recorded everything that they ate and drank for 7 consecutive days covering weekdays and weekend days, with particular attention to type, amount and frequency of consumption, and whether sugar was added by the participants. During approximately 11 years of follow-up, 847 study participants were diagnosed with new-onset type 2 diabetes.
Lead scientist Dr Nita Forouhi, of the UK Medical Research Council (MRC) Epidemiology Unit, University of Cambridge, said: "By using this detailed dietary assessment with a food diary, we were able to study several different types of sugary beverages, including sugar-sweetened soft drinks, sweetened tea or coffee and sweetened milk drinks as well as artificially sweetened beverages (ASB) and fruit juice, and to examine what would happen if water, unsweetened tea or coffee or ASB were substituted for sugary drinks."
In an analysis that accounted for a range of important factors including total energy intake the researchers found that there was an approximately 22% increased risk of developing type 2 diabetes per extra serving per day habitually of each of soft drinks, sweetened milk beverages and ASB consumed, but that consumption of fruit juice and sweetened tea or coffee was not related to diabetes. After further accounting for body mass index and waist girth as markers of obesity, there remained a higher risk of diabetes associated with consumption of both soft drinks and sweetened milk drinks, but the link with ASB consumption no longer remained, likely explained by the greater consumption of ASB by those who were already overweight or obese.
This new research with the greater detail on types of beverages adds to previous research published in Diabetologia by the authors in 2013 which collected information from food frequency questionnaires across 8 European countries. That previous work indicated that habitual daily consumption of sugar sweetened beverages (defined as carbonated soft drinks or diluted syrups) was linked with higher risk of type 2 diabetes, consistent with the current new findings.
In this new study, the authors also found that if study participants had replaced a serving of soft drinks with a serving of water or unsweetened tea or coffee, the risk of diabetes could have been cut by 14%; and by replacing a serving of sweetened milk beverage with water or unsweetened tea or coffee, that reduction could have been 20%-25%. However, consuming ASB instead of any sugar-sweetened drink was not associated with a statistically significant reduction in type 2 diabetes, when accounting for baseline obesity and total energy intake.
Finally, they found that each 5% of higher intake of energy (as a proportion of total daily energy intake) from total sweet beverages (soft drinks, sweetened tea or coffee, sweetened milk beverages, fruit juice) was associated with a 18% higher risk of diabetes. The authors estimated that if study participants had reduced the energy they obtained from sweet beverages to below 10%, 5% or 2% of total daily energy, 3%, 7% or 15% respectively of new-onset diabetes cases could have been avoided.
Dr Forouhi said: "The good news is that our study provides evidence that replacing a daily serving of a sugary soft drink or sugary milk drink with water or unsweetened tea or coffee can help to cut the risk of diabetes, offering practical suggestions for healthy alternative drinks for the prevention of diabetes."
The authors acknowledge limitations of dietary research which relies on asking people what they eat, but their study was large with long follow-up and had detailed assessment of diet that was collected in real-time as people consumed the food/drinks, rather than relying on memory. They concluded that their study helps to provide evidence with a robust method within the currently available methods and with detailed attention to accounting for factors that could distort the findings.
Commenting on the wider implications of these results, Dr Forouhi concluded: "Our new findings on the potential to reduce the burden of diabetes by reducing the percentage of energy consumed from sweet beverages add further important evidence to the recommendation from the World Health Organization to limit the intake of free sugars in our diet."
Diabetologia. "Replacing one serving of sugary drink per day by water or unsweetened tea or coffee cuts risk of type 2 diabetes, study shows." ScienceDaily. ScienceDaily, 30 April 2015. <www.sciencedaily.com/releases/2015/04/150430191138.htm>.
Diabetologia. (2015, April 30). Replacing one serving of sugary drink per day by water or unsweetened tea or coffee cuts risk of type 2 diabetes, study shows. ScienceDaily. Retrieved August 14, 2023 from www.sciencedaily.com/releases/2015/04/150430191138.htm
Diabetologia. "Replacing one serving of sugary drink per day by water or unsweetened tea or coffee cuts risk of type 2 diabetes, study shows." ScienceDaily. www.sciencedaily.com/releases/2015/04/150430191138.htm (accessed August 14, 2023).
Apr. 10, 2022 New research finds that the consumption of healthy plant-based foods, including fruits, vegetables, nuts, coffee, and legumes, is associated with a lower risk of developing type 2 diabetes (T2D) in ...
May 13, 2020 In a study of female California teachers, drinking one or more sugary beverages daily was associated with nearly a 20% higher risk of having cardiovascular disease when compared to those who rarely ...
Dec. 19, 2019 Coffee can help reduce the risk of developing type 2 diabetes -- but only filtered coffee, rather than boiled coffee. New research show that the choice of preparation method influences the health ... | Replacing one serving of sugary drink per day by water or unsweetened tea or coffee cuts risk of type 2 diabetes, study shows
Date:
April 30, 2015
Source:
Diabetologia
Summary:
Replacing the daily consumption of one serving of a sugary drink with either water or unsweetened tea or coffee can lower the risk of developing diabetes by between 14 percent and 25 percent, concludes new research.
New research published in Diabetologia (the journal of the European Association for the Study of Diabetes) indicates that for each 5% increase of a person's total energy intake provided by sweet drinks including soft drinks, the risk of developing type 2 diabetes may increase by 18%. However, the study also estimates that replacing the daily consumption of one serving of a sugary drink with either water or unsweetened tea or coffee can lower the risk of developing diabetes by between 14% and 25%.
This research is based on the large EPIC-Norfolk study which included more than 25,000 men and women aged 40-79 years living in Norfolk, UK. Study participants recorded everything that they ate and drank for 7 consecutive days covering weekdays and weekend days, with particular attention to type, amount and frequency of consumption, and whether sugar was added by the participants. During approximately 11 years of follow-up, 847 study participants were diagnosed with new-onset type 2 diabetes.
Lead scientist Dr Nita Forouhi, of the UK Medical Research Council (MRC) Epidemiology Unit, University of Cambridge, said: "By using this detailed dietary assessment with a food diary, we were able to study several different types of sugary beverages, including sugar-sweetened soft drinks, sweetened tea or coffee and sweetened milk drinks as well as artificially sweetened beverages (ASB) and fruit juice, and to examine what would happen if water, unsweetened tea or coffee or ASB were substituted for sugary drinks. | yes |
Diabetology | Can drinking coffee prevent type 2 diabetes? | yes_statement | "drinking" "coffee" can "prevent" "type" "2" "diabetes".. "coffee" consumption can lower the risk of developing "type" "2" "diabetes". | https://www.diabetes.org.uk/diabetes-the-basics/types-of-diabetes/type-2/preventing/ten-tips-for-healthy-eating | 10 tips for healthy eating | Type 2 diabetes risk | Diabetes UK | Breadcrumb
Savefor later Page saved! You can go back to this later in your Diabetes and MeClose
10 tips for healthy eating if you are at risk of type 2 diabetes
Lots of factors can contribute to someone being at risk of or diagnosed with type 2 diabetes. There are some things that you can change and some you can’t. Our tips on healthy eating could help reduce your risk of developing type 2 diabetes.
Things like your age, ethnicity and family history can all contribute to your overall risk. We also know that having obesity is the most significant risk factor. If you know you have obesity, losing weight is one way you can prevent type 2 diabetes.
And eating a healthy, balanced diet is way great way to manage your weight. Any amount of weight loss can help, research shows losing even 1kg can help to reduce your risk. There are so many different ways to lose weight, so it’s important to find out what works best for you.
We know that not everyone who is at risk or living with diabetes type 2 diabetes is carrying extra weight. But whether you need to lose weight or not, it is still important to make healthier food choices. Research tells us that there are even certain foods that are linked to reducing the risk of type 2 diabetes.
Here are our top tips for healthier food choices you can make, to reduce your risk of type 2 diabetes.
1. Choose drinks without added sugar
We know there is a link between having full sugar fizzy and energy drinks, and an increased risk of type 2 diabetes. Cutting down on these can help to reduce your risk and support keeping your weight down. Evidence also shows that drinking unsweetened tea and coffee is associated with a reduced risk. If you are finding it hard to cut down, look out for diet or low calorie versions of soft drinks and check there’s no added sugar. Try not to replace sugary drinks with fruit juices or smoothies as these still contain a high amount of free sugar. Try plain water, plain milk, tea or coffee without added sugar, as replacements.
2. Choose higher fibre carbs
Eating white bread, white rice and sugary breakfast cereals known as refined carbs are linked with an increased risk of type 2 diabetes. But wholegrains such as brown rice, wholewheat pasta, wholemeal flour, wholegrain bread and oats and linked to a reduced risk so choose these instead. When you’re out shopping remember to check food labels to see if a food is high fibre. Compare different foods to find the ones with the most fibre in them.
Other healthy sources of carbs include:
fruit and vegetables
pulses such has chickpeas, beans and lentils
dairy like unsweetened yoghurt and milk
Having more fibre is also associated with lower risk of other serious conditions such as obesity, heart diseases and certain types of cancers. It’s also important to think about your carbohydrate portion sizes.
3. Cut down on red and processed meat
Having more red and processed meats like bacon, ham, sausages, pork, beef and lamb are all associated with an increased risk of type 2 diabetes. They also have links to heart problems and certain types of cancer.
Try to get your protein from healthier foods like:
pulses such as beans and lentils
eggs
fish
chicken and turkey
unsalted nuts
Fish is really good for us and oily fish like salmon and mackerel are rich in omega-3 oil which helps protect your heart. Try to have at least one portion of oily fish each week and one portion of white fish.
Becoming educated on food labelling, which appears on all food packets was massive benefit as we were able to identify highly processed foods and those with high levels of sugar, fat and salt which has helped us make much healthier food choices.
Pat, who reduced his risk of type 2 diabetes.
4. Eat plenty of fruit and veg
Including more fruit and vegetables in your diet is linked with a reduced risk of type 2 diabetes. But did you know there are also certain types of fruit and veg that have been specifically associated with a reduced risk?
These are:
apples
grapes
berries
green leafy veg such as spinach, kale, watercress, rocket.
It doesn’t matter whether they are fresh or frozen, try to find ways to include these in your diet. Try having them as snacks or an extra portion of veg with your meals.
It can be confusing to know whether you should eat certain types of fruit, because they contain sugar. The good news is the natural sugar in whole fruit is not the type of added (or free) sugar we need to cut down on. But drinks like fruit juices and smoothies do contain free sugar, so eat the whole fruit and veg instead.
5. Choose unsweetened yogurt and cheese
Yogurt and cheese are fermented dairy products and they have been linked with a reduced risk of type 2 diabetes. You might be wondering whether to choose full fat or low fat? When it comes to dairy and risk of type 2 diabetes, the amount of fat from these dairy foods is not as important. What is more important is that you choose unsweetened options like plain natural or Greek yoghurt and plain milk.
Having three portions of dairy each day also helps you to get the calcium your body needs. A portion of dairy is:
200ml (1/3 pint) milk
30g cheese
125g yoghurt
6. Be sensible with alcohol
Drinking too much alcohol is linked with an increased risk of type 2 diabetes. As it is also high in calories, drinking lots can make it difficult if you are trying to lose weight. Current guidelines recommend not regularly drinking more than 14 units per week and that these units should be spread evenly over 3-4 days. Try to have a few days per week without any alcohol at all).
Drinking heavily on one or two days per week, known as binge drinking, will also increase the risk of other health conditions such as certain types of cancer.
7. Choose healthier snacks
If you want a snack, go for things like:
unsweetened yoghurts
unsalted nuts
seeds
fruits and vegetables
instead of crisps, chips, biscuits, sweets and chocolates. But watch your portions as it’ll help you keep an eye on your weight.
8. Include healthier fats in your diet
It’s important to have some healthy fat in our diets because it gives us energy. The type of fat we choose can affect our health. Some saturated fats can increase the amount of cholesterol in your blood, increasing your risk of heart problems. These are mainly found in animal products and prepared food like:
red and processed meat
butter
lard
ghee
biscuits, cakes, sweets, pies and pastries.
If you are at risk of type 2 diabetes, you are likely to be at an increased risk of heart problems so try to reduce these foods.
Healthier fats are found in foods like:
unsalted nuts
seeds
avocados
olive oil, rapeseed oil, sunflower oil.
We also know that the type of fat found in oily fish like salmon and mackerel is linked with a reduced risk, especially if you are from a South Asian background.
9. Cut down on salt
Eating lots of salt can increase your risk of high blood pressure, which can lead to an increased risk of heart disease and stroke. Having high blood pressure has also been linked to an increased risk of type 2 diabetes.
Try to limit yourself to a maximum of one teaspoonful (6g) of salt a day. Lots of pre-packaged foods like bacon, sausages, crisps, ready meals already contain salt. So remember to check food labels and choose those with less salt in them. Cooking from scratch will help you keep an eye on how much salt you’re eating. Instead of adding extra salt to your food try out different herbs and spices to add in extra flavour.
10. Getting vitamins and minerals from food instead of tablets
You might have heard that certain vitamins and supplements can reduce your risk of type 2 diabetes. Currently we don’t have evidence to say this is true. So, unless you’ve been told to take something by your healthcare team, like folic acid for pregnancy, you don’t need to take supplements. It’s better to get all your vitamins and minerals by eating a mixture of different foods.
Recipe ideas to help reduce your risk of type 2 diabetes
You've read the tips, now time to start cooking. The recipes we have picked out below make the most of the healthy eating tips, to help you on the way to making healthier choices and reducing your risk of type 2 diabetes.
The Virgin Mojito is great alternative to alcohol, ideal for parties and celebrations. | Breadcrumb
Savefor later Page saved! You can go back to this later in your Diabetes and MeClose
10 tips for healthy eating if you are at risk of type 2 diabetes
Lots of factors can contribute to someone being at risk of or diagnosed with type 2 diabetes. There are some things that you can change and some you can’t. Our tips on healthy eating could help reduce your risk of developing type 2 diabetes.
Things like your age, ethnicity and family history can all contribute to your overall risk. We also know that having obesity is the most significant risk factor. If you know you have obesity, losing weight is one way you can prevent type 2 diabetes.
And eating a healthy, balanced diet is way great way to manage your weight. Any amount of weight loss can help, research shows losing even 1kg can help to reduce your risk. There are so many different ways to lose weight, so it’s important to find out what works best for you.
We know that not everyone who is at risk or living with diabetes type 2 diabetes is carrying extra weight. But whether you need to lose weight or not, it is still important to make healthier food choices. Research tells us that there are even certain foods that are linked to reducing the risk of type 2 diabetes.
Here are our top tips for healthier food choices you can make, to reduce your risk of type 2 diabetes.
1. Choose drinks without added sugar
We know there is a link between having full sugar fizzy and energy drinks, and an increased risk of type 2 diabetes. Cutting down on these can help to reduce your risk and support keeping your weight down. Evidence also shows that drinking unsweetened tea and coffee is associated with a reduced risk. If you are finding it hard to cut down, look out for diet or low calorie versions of soft drinks and check there’s no added sugar. Try not to replace sugary drinks with fruit juices or smoothies as these still contain a high amount of free sugar. Try plain water, plain milk, tea or coffee without added sugar, as replacements.
| yes |
Evolution | Can evolution explain the existence of 'junk DNA'? | yes_statement | "evolution" can "explain" the "existence" of '"junk" dna'. the "existence" of '"junk" dna' can be "explained" by "evolution" | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5804262/ | Selfish genetic elements and the gene's-eye view of evolution - PMC | Share
RESOURCES
As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with,
the contents by NLM or the National Institutes of Health.
Learn more:
PMC Disclaimer
|
PMC Copyright Notice
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
Abstract
During the last few decades, we have seen an explosion in the influx of details about the biology of selfish genetic elements. Ever since the early days of the field, the gene’s-eye view of Richard Dawkins, George Williams, and others, has been instrumental to make sense of new empirical observations and to the generation of new hypotheses. However, the close association between selfish genetic elements and the gene’s-eye view has not been without critics and several other conceptual frameworks have been suggested. In particular, proponents of multilevel selection models have used selfish genetic elements to criticize the gene’s-eye view. In this paper, I first trace the intertwined histories of the study of selfish genetic elements and the gene’s-eye view and then discuss how their association holds up when compared with other proposed frameworks. Next, using examples from transposable elements and the major transitions, I argue that different models highlight separate aspects of the evolution of selfish genetic elements and that the productive way forward is to maintain a plurality of perspectives. Finally, I discuss how the empirical study of selfish genetic elements has implications for other conceptual issues associated with the gene’s-eye view, such as agential thinking, adaptationism, and the role of fitness maximizing models in evolution.
Introduction
Historically, the predominant view of genomes was one of a highly coordinated network, with all parts playing fair, working together to produce individual organisms. This view is challenged by the existence of stretches of DNA that can promote their own transmission at the expense of other genes in the genome, but have no or a negative effect on organismal fitness. These days, we usually refer to such stretches of DNA as selfish genetic elements, but over the years they have also been known by a variety of names including parasitic DNA, selfish DNA, ultra selfish genes, genomic outlaws, and self-promoting elements (reviewed in, e.g., Werren et al. 1988; Hurst et al. 1996; Burt and Trivers 2006; Werren 2011). Although foreshadowed by Weisman’s “germinal selection” (Weismann 1903), proper discussions of selfish genetic elements began in earnest a couple of decades later. Haldane (1932) discussed several examples of conflict between different levels in the biological hierarchy, including how pollen competition could lead to the spread of traits that were deleterious to the individual organism. In 1945, the Swedish botanist and cytogeneticist Gunnar Östergren’s argument that supernumerary (i.e., non-vital) B chromosomes were best perceived as parasitic provided the first clear articulation of what we know refer to as selfish genetic elements (Östergren 1945). Östergren’s work coincided with several other similar empirical observations, particularly in plants (Ågren and Wright 2015). For example, female meiotic drive was first reported in maize (Rhoades 1942), and Lewis (1941) presented evidence that cytoplasmic male sterility in plants was due to the conflict between the organellar and nuclear genes. However, such cases were typically considered to be genetic oddities with few implications for evolutionary theory (Burt and Trivers 2006; Werren 2011). It would take several decades until selfish genetic elements in general, and their evolutionary implications in particular, became widely appreciated.
A conceptual development that coincided with and contributed to the raised status of selfish genetic elements was the arrival of the gene’s-eye view on evolution. Introduced in George Williams’ (1966)Adaptation and Natural Selection and more forcefully in Richard Dawkins’ (1976)The Selfish Gene, the gene’s-eye view, or selfish gene theory, can be defined as the idea that the gene is the ultimate beneficiary of selection. Whereas organisms and their phenotypes are unique occurrences, each a product of the genome and its environment at a particular time, genes are the only units passed on intact and thus survive across generations. The gene is therefore the fundamental unit of selection.
Although the gene’s-eye view was instrumental in the development of the study of selfish genetic elements, the framework has been criticized and various other models have been suggested. Given that the central role of selfish genetic element in evolutionary biology is increasingly being recognized (Lisch 2013; Rice 2013), it is important to explore how to make sense of new empirical observations. Reciprocally, studying selfish genetic elements under different frameworks will also aid in building a unified theory of conflict and cooperation (Keller 1999; Michod 1999; Queller and Strassmann 2009; Bourke 2011; Foster 2011; Ågren 2014; West et al. 2015). In this paper, I discuss this relationship between the empirical study of selfish genetic elements and the gene’s-eye view as a conceptual model of evolution. I begin by outlining the historical origins of both the study of selfish genetic elements and the gene’s-eye view. After discussing the extent to which their histories are intertwined, I examine how the association between the study of selfish genetic elements and the gene’s-eye view holds up in face of alternative models of selfish genetic element evolution. In particular, I focus on the critique from proponents of multilevel selection models. Often these models are not mutually exclusive and my aim is not to argue in favor of one framework, nor to suggest how the various models can be morphed into one unifying framework. Instead, using on examples from transposable elements and the major transitions, I show how different perspectives highlight distinctive aspects of the biology of selfish genetic elements. Finally, in the last section of the paper, I discuss 3 other conceptual issues that have been associated with arguments about the gene’s-eye view: agential thinking, adaptationism, and fitness maximizing models in evolution, and how selfish genetic elements can inform these debates.
Early connections between the gene’-eye view and selfish genetic elements
Selfish genetic elements played no role in the early developments of the gene’s eye view. Instead, Williams and Dawkins weaved together 2 strands of evolutionary theory. First, several assumptions can be traced back all the way to early days of population genetics and in particular to Fisher (1918, 1930). Although, Fisher never used the term “gene’s-eye” or “gene-centered”, the approach was nevertheless explicit in his writings (Okasha 2008a; Edwards 2014). Second, evolutionary biology was seeing a growing appreciation of conflict more generally in social evolution. Parker (1979) pioneered the study of sexual conflict and Trivers (1974) outlined the idea of parent–offspring conflict, which later inspired the kinship theory of genomic imprinting (Haig 2002). Finally, game theory models of conflict resolution were introduced to evolutionary biology, first by Lewontin (1961) and later to a broader audience by Maynard Smith and Price (1973). Most importantly, Hamilton’s inclusive fitness models provided a formal alternative to the prevailing group selection thinking of the time (Hamilton 1963, 1964).
In addition to the general conceptual shift to gene level thinking in evolutionary biology, Werren (2011) identified 2 other parallel historical developments as central to the origin of the study of selfish genetic elements. First, empirical work on genome structure reported that large chunks of eukaryotic genomes were made up of genetic material, such as repetitive DNA, with seemingly no connection to organismal function or fitness (e.g., Britten and Kohne 1968; Britten 1969). This helped shift the focus away from individual organisms and to the gene level. Moreover, while it was clear that genome size varied dramatically across species (we now know eukaryotes vary more than 60,000-fold; Elliot and Gregory 2015), there was no correlation between the amount of DNA of a species (C-value) and its perceived complexity. For example, the genome of single-celled amoeba is about 100 times the size of that of humans. This lack of correlation was termed the “C-value paradox” (Thomas 1971) and later the “C-value enigma” (Gregory 2001). These observations were central to 2 papers published back-to-back in Nature in 1980, both of which cited Dawkins’ writing as a key inspiration for their argument. Doolittle and Sapienza (1980) and Orgel and Crick (1980) independently argued that large parts of eukaryotic genomes can best be described as selfish DNA, with negative or neutral effects on organismal fitness. These papers resulted in a series of exchanges in the same journal (Cavalier-Smith 1980; Dover 1980; Dover and Doolittle 1980; Jain 1980; Orgel et al. 1980) representing the first high profile discussion of the implications of selfish genetic elements.
Second, empirical work in molecular genetics continued to provide new examples of selfish genetic elements. When Werren et al. (1988) published the first comprehensive review of all kinds of selfish genetic elements discovered at the time, their discussion covered examples ranging from meiotic drive and supernumerary B chromosomes to killer plasmids, selfish mitochondria, and transposable elements. We now know that selfish genetic elements are prominent features of the genomes of virtually all organisms (Hurst and Werren 2001; Burt and Trivers 2006; Werren 2011). In light of the growing evidence of the central role played by selfish genetic elements in all aspects of genome evolution, Rice (2013) recently argued that “nothing in genetics makes sense except in the light of genomic conflicts”.
In retrospect it is perhaps easy to see how the gene’s-eye view and selfish genetic elements came to be closely associated. Just consider the similarity in language in 2 key papers in each field, Hamilton’s little read 1963 note in the American Naturalist where he first introduced the concept of inclusive fitness and Östergren's (1945) paper on B chromosomes mentioned above:
Despite the principle of ‘survival of the fittest’ the ultimate criterion that determines whether [a gene for altruism] G will spread is not whether the behavior is to the benefit of the behaver but whether it is of benefit to the gene G. (Hamilton 1963)
In many cases these chromosomes have no useful function at all to the species carrying them, but that they often lead an exclusively parasitic existence … [B chromosomes] need not be useful for the plants. They need only be useful to themselves. (Östergren 1945)
A crucial conceptual insight in both papers is that in order to explain the phenomenon under study, the origin of altruism and the spread of B-chromosomes, respectively, the investigator is better off viewing the world from the perspective of the gene, rather than the individual organism. As such, this is the main strength of the gene’s-eye view. The evolutionary logic of selfish genetic elements is difficult to follow from an organismal perspective, but straightforward from a gene’s-eye view. Hamilton too was quick to make the connection between inclusive fitness and selfish genetic elements. In his 1967 paper on extraordinary sex ratios, he shows how asymmetries in transmission between autosomes and sex chromosomes will lead to conflict over the ideal sex ratio (Hamilton 1967).
Replicator and vehicles
Upon publication, The Selfish Gene (Dawkins 1976) received both enthusiastic praise (e.g., Hamilton 1977) and fierce criticism (e.g., Lewontin 1977). A common theme among critics was that the gene cannot be the unit of selection because selection cannot act on them directly, only via their effects on individual organisms (Gould 1977). The distinction between replicator and vehicles (Dawkins 1982a, 1982b; also known as interactors, Hull 1980) was introduced partly to address this issue. Under this model of evolution, natural selection requires 2 different units playing different roles in the evolutionary process (Godfrey-Smith 2000). Replicators are entities that faithfully produce copies of themselves that are transmitted across generations. In biological evolution, as far as we know, genes play this role. A vehicle is an entity that interacts with the environment, and whose phenotype has evolved to preserve the replicator that it carries. Since it is the differential survival and reproduction of vehicles that lead to the spread of replicators, selection can be said to act on replicators via their effects on the vehicles that house them. However, since individual organisms and groups are transient occurrences, vehicles cannot be a unit of selection. Genes, on the other hand, are units of selection because they are “potentially immortal” (Dawkins 1982a, p. 97; Bourke 2011).
To see how selfish genetic elements fit into the replicator/vehicle distinction, it is first worth noticing that Dawkins himself changed his mind slightly about the implications of the distinction (Sterelny and Kitcher 1988; Okasha 2008b). In The Selfish Gene (Dawkins 1976), he argues that the gene level offers a uniquely correct representation of the causal processes underlying evolutionary change. In The Extended Phenotype (Dawkins 1982a), however, he presents a weaker argument. Here, Dawkins argues that the gene’s-eye view and the traditional individual centered view as 2 different, equivalent perspectives of evolution—2 orientations of a Necker Cube, as he puts it. Whereas selfish genetic elements are easily accommodated by the first, stronger, argument, the equivalence of the individual and gene’s-eye view is more problematic. Selfish genetic elements are the textbook example of a phenomenon not explainable by the traditional individual-centered perspective. A way around this, as has been suggested multiple times (Sober and Wilson 1998; Reeve and Keller 1999; Okasha 2008b; Lloyd 2012), is to treat replicators that are selfish genetic elements also as vehicles. Thus, whereas all genes are replicators, and can only improve their chances of transmission by contributing to the fitness of the vehicle that houses them, selfish genetic elements play a dual role.
Hierarchical views of selfish genetic elements
The relationship between the gene’s-eye view as articulated by Williams and Dawkins and the study of selfish genetic elements may thus seem straightforward. The existence of selfish genetic elements has indeed often been seen as one of the strongest arguments for the approach (Okasha 2006), a point emphasized in recent commentary commemorating the 40th anniversary of The Selfish Gene (Ridley 2016). For example, when discussing the work of Eberhard (1980) and Cosmides and Tooby (1981) on the conflicts between the nuclear and organellar genomes, Dawkins (1982a) wrote:
Neither Eberhart nor Cosmides and Tooby explicitly justify or document the genes’-eye view of life: they simply assume it (…) These papers have what I can only describe as the flavour of post-revolutionary normal science.
We need only to turn to Williams’ Adaptation and Natural Selection (1966), the first articulation of the gene’s-eye view, to see why this is not the whole story. Williams discusses one example of a selfish genetic element, the t-allele in mice studied by Lewontin (1962; Lewontin and Dunn 1960). Ironically, however, the inability of the t-allele to spread to high frequencies is presented as the only convincing case of group selection in nature (Williams 1966, p. 117). The tension between selfish genetic elements and other levels of selection was also central to one of the strongest proponents of a hierarchical approach to evolutionary theory: Stephen Jay Gould. In his majestic final book, The Structure of Evolutionary Theory (2002), he wrote:
When future historians chronicle the interesting failure of exclusive gene selectionism (based largely on the confusion of bookkeeping with causality), and the growing acceptance of an opposite hierarchical model, I predict that they will identify a central irony in the embrace by gene selectionists of a special class of data [i.e. selfish genetic elements], mistakenly read as crucial support, but actually providing strong evidence of their central error.
Here, Gould is attacking the strongest version of the gene’s-eye view, the argument that a gene level perspective is the only true representation of evolution by natural selection. Gould never warmed to the term “selfish DNA” (as selfish genetic elements have often been called), which he thought privileged the individual organism in an inappropriate way, he did consider selfish genetic elements to be among the strongest evidence for the need of a hierarchical view of evolutionary biology (Gould 1983, 1984, 2002). This link between within-genome selection and hierarchy has later been picked up and expanded by several others (Vrba and Eldredge 1984; Doolittle 1989, 2013; Gregory 2001, 2004, 2005, 2013). The main argument of these papers is that explanations of selfish genetic elements must involve selection at both the level of the selfish genetic element and the level of the individual organism. Thus, like Dawkins and other gene proponents, Gould and his colleagues strive to demote the individual from the central position in evolutionary theory. However, since proponents of multilevel selection models are committed to the organism as one level of explanation they need to invoke an additional level to explain selfish genetic elements. This is in contrast to Dawkins who wants to remove the individual organism completely from evolutionary explanations, as he once put it: “I coined the vehicle not to praise it but to bury it” (Dawkins 1994).
In his account of hierarchy, Gould was greatly inspired by Lewontin (1970). In this formulation of the general principles of evolution by natural selection, which argued that evolution will occur in any population of entities, as long as the entities exhibit “heritable variation in fitness”. These basic principles of variation, heredity, and differential fitness are also key to the Price equation (Price 1970) as well as Godfrey-Smith’s ‘Darwinian populations’ concept (Godfrey-Smith 2009), which also allow us to partition out selection at multiple levels.
Multilevel selection and the gene’s-eye view in practice: genome size variation and the major transitions
The gene’s-eye view and multilevel selection models are often presented as rival conceptual frameworks. In reality, they highlight different aspects of the biology of selfish genetic elements. Depending on which perspective one adopts, different aspects of their biology stand out. A multilevel selection model shows how selection on one level will have fitness effects on other levels in the hierarchy and therefore comes in handy when we want to assess the importance phenotypic effects of selfish genetic elements. Taking a gene’s-eye view, on the other, offers a way to understand the strategic logic of selfish genetic elements. Two empirical examples that highlight the benefit of maintaining both perspectives are the role of transposable elements in genome size variation and the major transitions.
Transposable element and genome size variation
Genome size correlates with several traits relevant to organismal fitness, such as development and metabolic rate (Gregory 2005, 2013), but much of variation in genome size among closely related species is due to differential accumulation of selfish transposable elements (Ågren and Wright 2011). Thus, while selection at the gene level will push for an increased genome size, this will be counteracted by selection at the individual level (Kidwell and Lisch 2001). A full understanding of the mechanisms governing genome size variation can therefore only come by considering evolutionary processes operating at multiple levels (Gregory 2004, 2013; Gregory et al. 2016). In particular, a multilevel perspective allows us to partition out the strength of selection acting on transposons themselves contra the individual organism. Furthermore, if species with transposon-rich or transposon-poor genomes are formed and/or go extinct at different rates then species level selection may help us to understand why transposons are abundant in some species but not others (Brunet and Doolittle 2015). For other aspects of transposon biology a gene’s-eye view can be very helpful. For example, predictions about why transposons will be more common in sexually reproducing species, in groups with low effective population size, and in regions of the genome with low recombination are born out of (diploid) population genetic models. (Whether the gene’s-eye view and diploid genotypic models are equivalent is the subject of long and still ongoing debate in the philosophy of biology; see, e.g., the exchange between Brandon and Nijhout 2006; Weinberger 2011).
The major transitions
The study of the major transitions reinvigorated the levels of selection and it has been gathering plenty of interest recently as a way of unifying work on social evolution across the hierarchy of life (Maynard Smith and Szathmáry 1995; Michod 1999; Bourke 2011; Calcott and Sterelny 2011; West et al. 2015). Throughout evolutionary history, evolutionary transitions in individuality have occurred when units that were previously able to reproduce independently now could only do so as part of a new level of individuality (Buss 1987; Maynard Smith and Szathmáry 1995; Michod 1999). This is what has given life its hierarchical structure: genes in genomes, genomes in cells, cells in multicellular organisms, and multicellular organism in eusocial groups. One of the major achievements of the modern study of social evolution is therefore the insight that whatever level in this hierarchy we are interested in, regardless whether we are studying the origin and maintenance of fair meiosis or the policing of worker eggs in social insects, we are faced with similar conceptual issues (Queller 1997; Bourke 2011; West et al. 2015). Most importantly, what prevents selfish behavior at lower levels from disrupting the functionality of higher levels? Whereas early formulations of the debate took the existence of distinct levels as a given, the major transitions tradition shows that this hierarchy too has an evolutionary origin (Griesemer 2000; Okasha 2005). Thus, the challenge is to explain how selection may act at one or more levels now, and also how the levels evolved to begin with.
The major transitions view is often considered the best vindication of the view that multilevel selection models and the gene’s eye view are complementary (Queller 1997; Okasha 2006; Bourke 2011). For example, the pioneering major transitions models of Michod (e.g., 1997, 1999) are simultaneously multi-level and population genetic. In these hierarchical models, selection at lower levels comes out as transmission bias at higher levels and selfish genetic elements can therefore be treated as genetic entities with a systematic transmission bias (Michod 1999). Using the framework of the major transitions to understand the origin and maintenance of genome cooperation in face of selfish genetic elements has indeed been the theme of several recent papers (Durand and Michod 2010; Ågren 2014; Higgs and Lehman 2015).
Other conceptual consequences of selfish genetic elements
Selfish genetic elements have provided empirical ammunition in the disagreements between proponents of the gene’s-eye view and multilevel selectionists. Below I briefly touch on 3 other conceptual issues where selfish genetic elements may contribute: agential thinking, adaptationism, and fitness maximizing models.
In an infamous review of The Selfish Gene, Mary Midgley (1979) presented one of the more bizarre misunderstandings of the book:
Genes cannot be selfish or unselfish, any more than atoms can be jealous, elephants abstract or biscuits teleological.
Of course, no one seriously believes that the gene’s-eye view is committed to assigning emotions to genes. The heuristic of assigning agency to biological entities has a strong tradition (Dennett 1995, 2011; Wilson 2005). Thinking of genes as agents with the goal to maximize their own transmission is part of this strategy and has been popular especially for problems related to social behavior (Haig 1997, 2012; Queller 2011). A more serious critique of thinking about evolution as a competition between agents is that it may lead to what Francis (2004) in a memorable phrase referred to as “Darwinian paranoia”. Godfrey-Smith (2009), picking up on this theme, places the gene’s-eye view in the same explanatory family as demonic possessions and Freudian psychology. In each of these approaches, the world is explained by the presence and interaction between agents with competing or overlapping agendas. Moreover, both Francis (2004) and Godfrey-Smith (2009) warn that agential thinking may lead to an overreliance on adaptive explanations at the expense of other evolutionary explanations (although the latter is quick to point out that there is room for non-paranoid adaptationist thinking in evolutionary biology).
By fully accounting for the existence of selfish genetic elements some adaptationist thinking can be counteracted. The modern version of inclusive fitness theory tends to emphasize that individual organisms can be agents designed to maximize their inclusive fitness (West and Gardner 2013 and references therein). Although inclusive fitness can be useful in the study of selfish genetic elements and other forms of within-individual conflict (Grafen 2006; Bourke 2011), a key assumption in the individual centered models is usually that within-individual conflict can be safely ignored. As Gardner and Grafen (2009) put it “Mendelian outlaws are the exception rather than the rule, at least insofar as we are interested in understanding phenotypic evolution”. This argument can be difficult to stomach for those of us interested in the spread of selfish genetic elements and other examples of within-organism conflicts (Shelton and Michod 2014). Especially given the sheer abundance of evidence of phenotypic effects of selfish genetic elements that has become available by now (Werren 2011; Lisch 2013; Rice 2013). If nothing else, it begs the question of why internal conflicts do not get out of hand and the shorthand of the individual as a maximizer and the optimization programme works so well for many evolutionary questions. Indeed, an important lesson from both the gene’s-eye view and the study of selfish genetic elements is the value of downplaying the organism and pushes to explain how it can persist in face of internal conflicts. The very existence of individual organism is a “paradox” (Dawkins 1990) or an “adaptive compromise” (Haig 2006, 2014). Or, as Maynard Smith (1985) puts it:
How did it come about that most genes, most of the time, play fair, so that a gene’s fitness depends only on the success of the individual that carries it? (Maynard Smith 1985)
In general, selfish genetic elements can act as a counterweight to naïve kinds of adaptationist thinking. Given the growing appreciation of the phenotypic consequences of selfish genetic elements (Burt and Trivers 2006; Werren 2011; Ågren 2013; Lisch 2013; Rice 2013), it becomes more difficult to ignore the existence of competing genes within individuals, at least if our goal is to develop a general account of adaptation. As discussed above, the idea that individual organisms act to maximize their inclusive fitness is based on the assumption that all genes share the same fitness interests, or that when they do not such disagreements can be discarded (Haig 2014). Selfish genetic elements show that instead of being a cohesive fitness maximizer, the individual organism is a compromise of several fitness interests (Cosmides and Tooby 1981; Dawkins 1990; Hurst 1996; Haig 2014). Individuals will still appear to be well adapted to their environments, as maximizing individual fitness will serve the majority of the genes in the organism.
Although it is easy to recognize that the same conceptual problems of conflict and cooperation exist at all levels in the hierarchy, moving between levels is not without problems. For example, the population genetic models used in studies of transposable elements have been said to have little in common with the game theoretical approaches of researchers of parent–offspring conflict (Charlesworth 2000; but see, e.g., Haig 1992, 1996). The lack of similarity is expressed in several ways. For example, the fitness-maximizing approach of behavioral ecology has had tremendous empirical success (Davies et al. 2012), but the take-home message of modern population genetics is that fitness is rarely if ever maximized (Ewens 2004). Moreover, whereas traditional Hamiltonian models have been designed under assumptions of weak selection, selfish genetic elements cause strong selective effects so that the application of such models may be difficult (Hamilton 1995; Keller 1999; Wenseleers and Ratnieks 2001).
Is it a problem that our modeling frameworks are based on such fundamentally different assumptions? On the one hand, both population genetic and game theory frameworks have enjoyed great empirical success, which arguably is ultimately what matters for any theoretical framework. On the other hand, it can be unsatisfactory to have such fundamental disagreement at the heart of evolutionary theory. Addressing this is the goal of Alan Grafen’s admirable and ambitious Formal Darwinism Project (Grafen 1999, 2007, 2008, 2014). Making use of Grafen’s Formal Darwinism approach, Gardner and Welch (2011) developed a “gene as maximizing agent” analogy. This allowed them to link optimization models with the Price equation, thus providing a link between gene-level intentionality and the dynamic change in gene frequencies. Furthermore, several researchers have successfully taken modeling tools from behavioral ecology and applied them to selfish genetic elements (Bohl et al. 2014; Haig 2014). For example, Wenseleers and Ratnieks (2001) used a hawk and dove game theory approach to model meiotic drive, showing that insights from population genetics can be expressed in game theory terms. Similarly, Wagner (2006) used game theory to argue that there is little reason to expect transposable elements to cooperate. Finally, Haig and Grafen (1991) used game theory to model the evolution of recombination and fair meiosis as a defence against meiotic drive. Later, Haig (1996) showed how meiotic drive and parent–offspring conflict could be modeled with the same mathematical approach.
Concluding remarks
Close to a century of empirical advances mean that the days of considering selfish genetic elements as irrelevant oddities of limited evolutionary significance are long gone. Instead the last few decades has seen a rapid increase in our understanding of their biology. This review highlights how several alternative, but not necessarily mutually exclusive, concepts within the levels of selection tradition can be used to make sense of the evolutionary dynamics of selfish genetic elements. Most importantly, the gene’s-eye view helps us follow the strategic logic of selfish genetic elements, whereas focus on the levels of selection highlights how selection on selfish genetic elements will affect selection at other levels.
The gene’s-eye view and the multilevel selection models are not the only theoretical frameworks available. Additional conceptual insights to the biology of selfish genetic elements have also come from research on host–parasite interactions (Nee and Maynard Smith 1990; Brookfield 2011), political philosophy (Okasha 2012), epidemiology (Wagner 2009), and community ecology (Venner et al. 2009; Linquist et al. 2015). Different ways of modeling the same evolutionary process can often yield the same empirical prediction (Maynard Smith 1987; Waters 2005; Foster 2006). Occasionally some models may better represent the causal structure (Okasha 2015). Often, however, different models highlight different aspects of the phenomena in question and the empirical study of selfish genetic elements is better off keeping different conceptual approaches.
Acknowledgments
Many thanks to Andrew G. Clark, Tyler A. Elliott, David Haig, and Samir Okasha for comments and discussion. I am also grateful to 2 anonymous reviewers, Manus Patten, and Tom A.R. Price, who provided extensive comments on earlier versions that greatly improved the paper.
Lewis D, 1941.
Male sterility in natural populations of hermaphrodite plants: the equilibrium between females and hermaphrodites to be expected with different types of inheritance. New Phytol40:56–63. [Google Scholar] | 117). The tension between selfish genetic elements and other levels of selection was also central to one of the strongest proponents of a hierarchical approach to evolutionary theory: Stephen Jay Gould. In his majestic final book, The Structure of Evolutionary Theory (2002), he wrote:
When future historians chronicle the interesting failure of exclusive gene selectionism (based largely on the confusion of bookkeeping with causality), and the growing acceptance of an opposite hierarchical model, I predict that they will identify a central irony in the embrace by gene selectionists of a special class of data [i.e. selfish genetic elements], mistakenly read as crucial support, but actually providing strong evidence of their central error.
Here, Gould is attacking the strongest version of the gene’s-eye view, the argument that a gene level perspective is the only true representation of evolution by natural selection. Gould never warmed to the term “selfish DNA” (as selfish genetic elements have often been called), which he thought privileged the individual organism in an inappropriate way, he did consider selfish genetic elements to be among the strongest evidence for the need of a hierarchical view of evolutionary biology (Gould 1983, 1984, 2002). This link between within-genome selection and hierarchy has later been picked up and expanded by several others (Vrba and Eldredge 1984; Doolittle 1989, 2013; Gregory 2001, 2004, 2005, 2013). The main argument of these papers is that explanations of selfish genetic elements must involve selection at both the level of the selfish genetic element and the level of the individual organism. Thus, like Dawkins and other gene proponents, Gould and his colleagues strive to demote the individual from the central position in evolutionary theory. However, since proponents of multilevel selection models are committed to the organism as one level of explanation they need to invoke an additional level to explain selfish genetic elements. | yes |
Evolution | Can evolution explain the existence of 'junk DNA'? | yes_statement | "evolution" can "explain" the "existence" of '"junk" dna'. the "existence" of '"junk" dna' can be "explained" by "evolution" | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4014423/ | The Case for Junk DNA - PMC | Share
RESOURCES
As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with,
the contents by NLM or the National Institutes of Health.
Learn more:
PMC Disclaimer
|
PMC Copyright Notice
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
Overview
With the advent of deep sequencing technologies and the ability to analyze whole genome sequences and transcriptomes, there has been a growing interest in exploring putative functions of the very large fraction of the genome that is commonly referred to as “junk DNA.” Whereas this is an issue of considerable importance in genome biology, there is an unfortunate tendency for researchers and science writers to proclaim the demise of junk DNA on a regular basis without properly addressing some of the fundamental issues that first led to the rise of the concept. In this review, we provide an overview of the major arguments that have been presented in support of the notion that a large portion of most eukaryotic genomes lacks an organism-level function. Some of these are based on observations or basic genetic principles that are decades old, whereas others stem from new knowledge regarding molecular processes such as transcription and gene regulation.
Introduction
The search for function in the genome
It has been known for several decades that only a small fraction of the human genome is made up of protein-coding sequences and that at least some noncoding DNA has important biological functions. In addition to coding exons, the genome contains sequences that are transcribed into functional RNA molecules (e.g., tRNA, rRNA, and snRNA), regulatory regions that control gene expression (e.g., promoters, silencers, and enhancers), origins of replication, and repeats that play structural roles at the chromosomal level (e.g., telomeres and centromeres).
New discoveries regarding potentially important sequences amongst the nonprotein-coding majority of the genome are becoming more prevalent. By far the best-known effort to identify functional regions in the human genome is the recently completed Encyclopaedia of DNA Elements (ENCODE) project [1], whose authors made the remarkable claim that a “biochemical function” could be assigned to 80% of the human genome [2]. Reports that ENCODE had refuted the existence of large amounts of junk DNA in the human genome received considerable media attention [3], [4]. Criticisms that these claims were based on an extremely loose definition of “function” soon followed [5]–[8] (for a discussion of the relevant function concepts, see [9]), and debate continues regarding the most appropriate interpretation of the ENCODE results. Nevertheless, the excitement and subsequent backlash served to illustrate the widespread interest among scientists and nonspecialists in determining how much of the human genome is functionally significant at the organism level.
The origin of “junk DNA”
Although the term “junk DNA” was already in use as early as the 1960s [10]–[12], the term's origin is usually attributed to Susumu Ohno [13]. As Ohno pointed out, gene duplication can alleviate the constraint imposed by natural selection on changes to important gene regions by allowing one copy to maintain the original function as the other undergoes mutation. Rarely, these mutations will turn out to be beneficial, and a new gene may arise (“neofunctionalization”) [14]. Most of the time, however, one copy sustains a mutation that eliminates its ability to encode a functional protein, turning it into a pseudogene. These sequences are what Ohno initially referred to as “junk” [13], although the term was quickly extended to include many types of noncoding DNA [15]. Today, “junk DNA” is often used in the broad sense of referring to any DNA sequence that does not play a functional role in development, physiology, or some other organism-level capacity. This broader sense of the term is at the centre of most current debate about the quantity—or even the existence—of “junk DNA” in the genomes of humans and other organisms.
It has now become something of a cliché to begin both media stories and journal articles with the simplistic claim that most or all noncoding DNA was “long dismissed as useless junk.” The implication, of course, is that current research is revealing function in much of the supposed junk that was unwisely ignored as biologically uninteresting by past investigators. Yet, it is simply not true that potential functions for noncoding DNA were ignored until recently. In fact, various early commenters considered the notion that large swaths of the genome were nonfunctional to be “repugnant” [10], [16], and possible functions were discussed each time a new type of nonprotein-coding sequence was identified (including pseudogenes, transposable elements, satellite DNA, and introns; for a compilation of relevant literature, see [17]).
Importantly, the concept of junk DNA was not based on ignorance about genomes. On the contrary, the term reflected known details about genome size variability, the mechanism of gene duplication and mutational degradation, and population genetics theory. Moreover, each of these observations and theoretical considerations remains valid. In this review, we examine several lines of evidence—both empirical and conceptual—that support the notion that a substantial percentage of the DNA in many eukaryotic genomes lacks an organism-level function and that the junk DNA concept remains viable post-ENCODE.
Genome Size and “The Onion Test”
There are several key points to be understood regarding genome size diversity among eukaryotes and its relationship to the concept of junk DNA. First, genome size varies enormously among species [18], [19]: at least 7,000-fold among animals and 350-fold even within vertebrates. Second, genome size varies independently of intuitive notions of organism complexity or presumed number of protein-coding genes (Figure 1). For example, a human genome contains eight times more DNA than that of a pufferfish but is 40 times smaller than that of a lungfish. Third, organisms that have very large genomes are not few in number or outliers—for example, of the >200 salamander genomes analyzed thus far, all are between four and 35 times larger than the human genome [18]. Fourth, even closely related species with very similar biological properties and the same ploidy level can differ significantly in genome size.
Summary of haploid nuclear DNA contents (“genome sizes”) for various groups of eukaryotes.
This graph is based on data for about 10,000 species [18], [19]. There is a wide range in genome sizes even among developmentally similar species, and there is no correspondence between genome size and general organism complexity. Humans, which have an average-sized genome for a mammal, are indicated by a star. Note the logarithmic scale.
These observations pose an important challenge to any claim that most eukaryotic DNA is functional at the organism level. This logic is perhaps best illustrated by invoking “the onion test” [20]. The domestic onion, Allium cepa, is a diploid plant (2n = 16) with a haploid genome size of roughly 16 billion base pairs (16 Gbp), or about five times larger than humans. Although any number of species with large genomes could be chosen for such a comparison, the onion test simply asks: if most eukaryotic DNA is functional at the organism level, be it for gene regulation, protection against mutations, maintenance of chromosome structure, or any other such role, then why does an onion require five times more of it than a human? Importantly, the comparison is not restricted to onions versus humans. It could as easily be between pufferfish and lungfish, which differ by ∼350-fold, or members of the genus Allium, which have more than a 4-fold range in genome size that is not the result of polyploidy [21].
In summary, the notion that the majority of eukaryotic noncoding DNA is functional is very difficult to reconcile with the massive diversity in genome size observed among species, including among some closely related taxa. The onion test is merely a restatement of this issue, which has been well known to genome biologists for many decades [18].
Genome Composition
Another important consideration is the composition of eukaryotic genomes. Far from being composed of mysterious “dark matter,” the characteristics of the sequences constituting 98% or so of the human genome that is nonprotein-coding are generally well understood.
Transposable elements
By far the dominant type of nongenic DNA are transposable elements (TEs), including various well-described retroelements such as Short and Long Interspersed Nuclear Elements (SINEs and LINEs), endogenous retroviruses, and cut-and-paste DNA transposons. Because of their capacity to increase in copy number, transposable elements have long been described as “parasitic” or “selfish” [22], [23]. However, the vast majority of these elements are inactive in humans, due to a very large fraction being highly degraded by mutation. Due to this degeneracy, estimates of the proportion of the human genome occupied by TEs has varied widely, between one-half and two-thirds [24], [25]. Larger genomes, such as those of salamanders and lungfishes, almost certainly contain an even more enormous quantity of transposable element DNA [26], [27].
Many examples have been found in which TEs have taken on regulatory or other functional roles in the genome [28]. In recognition of the more complex interactions between transposable elements and their hosts, Kidwell and Lisch proposed an expansion of the “parasitism” framework where each TE can be classified along a spectrum from parasitism to mutualism [29]. Nevertheless, there is evidence of organism-level function for only a tiny minority of TE sequences. It is therefore not obvious that functional explanations can be extrapolated from a small number of specific examples to all TEs within the genome.
Highly repetitive DNA
Another large fraction of the genome consists of highly repetitive DNA. These regions are extremely variable even amongst individuals of the same population (hence their use as “DNA fingerprints”) and can expand or contract through processes such as unequal crossing over or replication slippage. Many repeats are thought to be derived from truncated TEs, but others consist of tandem arrays of di- and trinucleotides [30]. As with TEs, some highly repetitive sequences play a role in gene regulation (for example, [31]). Others, such as telomeric- and centromeric-associated repeats [32], [33], play critical roles in chromosomal maintenance. Despite this, there is currently no evidence that the majority of highly repetitive elements are functional.
Introns
According to Gencode v17, about 40% of the human genome is comprised of intronic regions; however, this figure is likely an overestimate as it includes all annotated events. It is also important to note that a large fraction of TEs and repetitive elements are found in introns. Although introns can increase the diversity of protein products by modulating alternative splicing, it is also clear that the vast majority of intronic sequence evolves in an unconstrained way, accumulating mutations at about the same rate as neutral regions. Although the median intron size in humans is ∼1.5 kb [30], data suggest that most of the constrained sequence is confined to the first and last 150 nucleotides [34].
Pseudogenes
The human genome is also home to a large number of pseudogenes. Estimates of the total number range from 12,600 to 19,700 [35]. These include both “classical” pseudogenes (direct duplicates, of the sort imagined by Ohno [13]) and “processed” pseudogenes, which are reverse transcribed from mRNA [36]. Once again, although some pseudogenes have been co-opted for organism-level function (for example see [37]), most are simply evolving without selective constraints on their sequences and likely have no function [38].
Conserved sequences
Several analyses of sequence conservation between humans and other mammals have found that about 5% of the genome is conserved [1], [39]–[42]. It is possible that an additional 4% of the human genome is under lineage-specific selection pressure [39]; however, this estimate appears to be somewhat questionable [43], [44] (also see [45]). Ignoring these problems, the idea that 9% of the human genome shows signs of functionality is actually consistent with the results of ENCODE and other large-scale genome analyses.
Besides protein-coding sequences (including associated untranslated regions), which make up 1.5%–2.5% of the human genome [24], data from ENCODE suggest that conserved long noncoding RNAs (lncRNAs) are generated from about 9,000 loci that add up to less than an additional 0.4% [46], [47]. Thus, even if a vast new untapped world of functional noncoding RNA is discovered, this will probably be transcribed from a small fraction of the human genome.
At first blush, sequences that are bound by transcription factors (TFs) appear to be very abundant, making up about 8.5% of the genome according to ENCODE [2]. This number, however, is an estimate of regions that are hypersensitive to DNase I treatment due to the displacement of nucleosomes by TFs. As pointed out by others [6], these regions are annotated as being several hundreds of nucleotides long and are thus much larger than the actual size of individual TF-binding motifs, which are typically 10 bp in length [48]. By ENCODE's own estimates, less than half of the nucleotide bases in these DNase I hypersensitivity regions contain actual TF recognition motifs [2], and only 60% of these are under purifying selection [49]. Others have found that weak and transient TF-binding events are routinely identified by chromatin IP experiments despite the fact that they do not significantly contribute to gene expression [50]–[53] and are poorly conserved [53]. Given that experiments performed in a diverse number of eukaryotic systems have found only a small correlation between TF-binding events and mRNA expression [54], [51], it appears that in most cases only a fraction of TF-binding sites significantly impacts local gene expression.
In summary, most of the major constituents of the genome have been well characterized. The majority of human DNA consists of repetitive, mutationally degraded sequences. There are unambiguous examples of nonprotein-coding sequences of various types having been co-opted for organism-level functions in gene regulation, chromosome structure, and other roles, but at present evidence from the published literature suggests that these represent a small minority of the human genome.
Evolutionary Forces
To understand the current state of the human genome, we need to examine how it evolved, and as Michael Lynch once wrote, “Nothing in evolution makes sense except in the light of population genetics” [55]. Unfortunately, concepts that have been generated by this field have not been widely recognized in other domains of the life sciences. In particular, what is underappreciated by many nonevolution specialists is that much of molecular evolution in eukaryotes is primarily the result of genetic drift, or the fixation of neutral mutations. This view has been widely appreciated by molecular evolutionary biologists for the past 35 years.
The nearly neutral theory of molecular evolution
An important development in the understanding of how various evolutionary forces shape eukaryotic genes and genomes came with the theories developed by Kimura, Ohta, King, and Jukes. They demonstrated that alleles that were slightly beneficial or deleterious behaved like neutral alleles, provided that the absolute value of their selection coefficient was smaller than the inverse of the “effective” population size [56]–[59]. In other words, it is important to keep in mind population size when thinking about whether deleterious mutations are subjected to purifying selection.
It is also important to realize that the “effective” population size is dependent on many factors and is typically much lower than the total number of individuals in a species [55]. For humans it has been estimated that the historical effective population size is approximately 10,000, and this is on the low side in comparison to most metazoans [60]. Given the overall low figures for multicellular organisms in general, we would expect that natural selection would be powerless to stop the accumulation of certain genomic alterations over the entirety of metazoan evolution. One type of mutation that fits this description is intergenic insertions, be they transposable elements, pseudogenes, or random sequence [55]. The creation and loss of TF-binding motifs or cryptic transcriptional start sites in these same intergenic regions will equally be invisible to natural selection, provided that these do not drastically alter the expression of any nearby genes or cause the production of stable toxic transcripts. Thus, a central tenet of the nearly neutral theory of molecular evolution is that extraneous DNA sequences can be present within genomes, provided that they do not significantly impact the fitness of the organism.
Genetic load
It has long been appreciated that there is a limit to the number of deleterious mutations that an organism can sustain per generation [61], [62]. The presence of these mutations is usually not harmful, because diploid organisms generally require only one functional copy of any given gene. However, if the rate at which these mutations are generated is higher than the rate at which natural selection can weed them out, then the collective genomes of the organisms in the species will suffer a meltdown as the total number of deleterious alleles increases with each generation [63]. This rate is approximately one deleterious mutation per generation. In this context it becomes clear that the overall mutation rate would place an upper limit to the amount of functional DNA. Currently, the rate of mutation in humans is estimated to be anywhere from 70–150 mutations per generation [64], [65]. By this line of reasoning, we would estimate that, at most, only 1% of the nucleotides in the genome are essential for viability in a strict sequence-specific way. However, more recent computational models have demonstrated that genomes could sustain multiple slightly deleterious mutations per generation [66]. Using statistical methods, it has been estimated that humans sustain 2.1–10 deleterious mutations per generation [66]–[68]. These data would suggest that at most 10% of the human genome exhibits detectable organism-level function and conversely that at least 90% of the genome consists of junk DNA. These figures agree with measurements of genome conservation (∼9%, see above) and are incompatible with the view that 80% of the genome is functional in the sense implied by ENCODE. It remains possible that large amounts of noncoding DNA play structural or other roles independent of nucleotide sequence, but it far from obvious how this would be reconciled with “the onion test.”
The evolution of the nucleus
When dealing with the evolution of any lineage, one must also keep in mind unique events, also known as historical contingencies, which constrain and shape subsequent evolutionary trajectories [69]. One of these key events in our own ancestry was the evolution of the eukaryotic nucleus. A further examination of why the nucleus evolved and how this altered cellular function may generate significant insights into the current shape of the eukaryotic genome.
One important event in early eukaryotic evolution was the development of a symbiotic relationship between the α-proteobacteria progenitor of mitochondria and an archaebacteria-like host [70], [71]. As with most endosymbiotically derived organelles [72], DNA was transferred from mitochondria to the host. In this way, Group II introns, which are still found in both mitochondria and α-proteobacteria [73], invaded the host genome. Group II introns are parasitic DNA fragments that replicate when they are transcribed, typically as part of a larger transcript. The intron then folds into a catalytic ribozyme that splices itself out of the precursor transcript and then reinserts itself at a new genomic locus by reversing the splicing reaction. Importantly, functional fragments of Group II introns can splice out inactive versions in a trans-splicing reaction [74], [75]. As described elsewhere, it is likely that Group II introns proliferated and evolved into two populations: inactivated copies that could be nonetheless spliced out in trans, and active fragments that promoted splicing of the former group. This latter group eventually evolved into the spliceosomal snRNAs [75]–[77]. This idea is supported by not only structural, catalytic, and functional similarities between Group II introns and snRNAs [78], [79] but also by the fact that expression of the U5 snRNA rescues the splicing of Group II introns that lack the corresponding U5-like region [80].
It is likely that the proliferation of trans-splicing triggered the spatial segregation of RNA processing (the nucleoplasm) from the translation machinery (the cytoplasm) [77]. This subdivision ensured that mRNAs were properly spliced before they encountered the translation machinery. Not only would this segregation prevent translating ribosomes from interfering with the splicing reaction (and vice versa) but would also prevent the translation of incompletely processed mRNAs, which often encode toxic proteins [81], [82]. Importantly, the segregation of translation from both transcription and RNA processing provided an opportunity for nuclear quality-control processes to eliminate misprocessed and spurious transcripts that did not meet the minimal requirements of “mRNA identity” (see below) before these RNAs ever encountered a ribosome. This in turn permitted intergenic DNA and cryptic transcriptional start sites to proliferate with minimal cost to the fitness of the organism. It should also be noted that the increase in ATP regeneration due to mitochondrial-derived metabolic pathways provided the surplus energy that is required to support an expansion not only in genome size and membranes [83], [84] but also wasteful transcription. Thus, by several independent mechanisms, the acquisition of mitochondria likely allowed the expansion of nonfunctional intergenic DNA and the evolution of a noisy transcriptional system.
Gene Expression in Eukaryotes
Eukaryotic transcription is inherently noisy
One of the most widely discussed discoveries of the past decade of transcriptome analysis is that much of the metazoan genome is transcribed at some level (although this, too, was already recognized in rough outline in the 1970s [15]). When nascent transcripts from mouse have been analyzed by deep sequencing, the total number of reads that map to intergenic loci is almost equivalent to the number mapping to exonic regions (Figure 2A, reproduced from reference [85]). This is consistent with the observation that a large fraction of the cellular pool of RNA Polymerase II is associated with intergenic regions [86] and that transcription can be initiated at random sequences (see Figure S4 in [87]) and nucleosome-free regions [88], [89]. Strikingly, when one examines the steady state level of polyadenylated RNA, very little maps to intergenic regions (Figure 2A, 2B, the latter reproduced from reference [46]; also see [85], [90]–[92]). In fact, when one eliminates the ∼9,000 transcript species that are thought to be derived from conserved lncRNA, then most of the annotated noncoding polyadenylated RNAs are present at levels below one copy per cell and are found exclusively in the nucleus (Figure 2B). The situation is no better in the unpolyadenylated pool, in which the amount of lncRNA and intergenic RNA is practically insignificant, especially in the cytoplasmic pool (Figure 2B). In aggregate, these data indicate that the majority of intergenic RNAs are degraded almost immediately after transcription. Consistent with this idea, the level of intergenic transcripts increase when RNA degradation machinery is inhibited [93]–[101]. Although pervasive transcription has been used as an argument against junk DNA [3], [4], it is in fact entirely in line with the idea that intergenic regions are evolving under little-to-no constraint, especially when one considers that this intergenic transcription is unstable.
(A) Analysis of nascent and total poly(A)+ RNA levels from mouse liver nuclei. Nascent (i.e., polymerase-associated) RNA and poly(A)+ RNA were isolated from mouse liver nuclei and analyzed by high-throughput sequencing. Individual reads were categorized by their source. Exonic and intronic are from known referenced genes (i.e., “RefSeq” genes), while intergenic originate from nonreferenced loci (i.e., “non-RefSeq”) in the mouse genome. Reproduced from [85]. (B) Empirical Cumulative Distribution Function (ECDF) of transcript expression in each cell compartment as determined by the ENCODE consortia. Results for RNA that either contain (“polyA+”) or lack (“polyA−”) a poly(A)-tail in the nucleus and cytosolic fractions are shown. Each human cell line that was analyzed is represented by three lines, one for each pool of RNA (red for protein-coding RNAs, blue for lncRNAs [“noncoding”], and green for intergenic transcripts [“novel intergenic”]). The lines indicate the cumulative fraction of RNAs in a given pool (y-axis) that are expressed at levels that are equal or less than the reads per kilobase per million mapped reads (RPKM) on the x-axis. Total numbers in each pool are as follows: reference protein coding genes: 20,679, loci producing lncRNAs: 9,277, and regions producing intergenic transcripts: 41,204. Transcripts with expression levels of 0 RPKM were adjusted to an artificial value of 10−6 RPKM so that the onset of each graph represents the fraction of nonexpressed genes or loci. Note that 1–4 RPKM is approximately equivalent to one copy per tissue culture cell [46], [129]. Using this figure, one can easily deduce that the vast majority of intergenic transcripts are present at levels less than one copy per cell. Reproduced with permission from [46].
Identifying mRNA from intergenic transcription
A common theme that has emerged from the study of mRNA synthesis is that various steps in RNA synthesis and processing are biochemically coupled. In other words, cellular machineries that participate in one biochemical activity also promote subsequent steps. For example, during the splicing of the 5′most intron, the spliceosome collaborates with the 5′cap binding complex to deposit nuclear export factors onto the 5′end of the processed transcript [102], [103], and this helps to explain why splicing enhances the nuclear export of mRNA [104]–[106]. Countless other examples of coupling exist (for reviews, see [107]–[111]).
The ultimate goal of these coupling reactions is to sort protein-coding RNAs (i.e. mRNA) from intergenic transcripts [111], [112]. Given that, on average, protein-coding genes have eight introns [30], while the majority of annotated ENCODE intergenic transcripts tend not to be spliced [46], introns help distinguish these two populations and thus serve as “mRNA identity” markers. These mRNA identity features activate coupling reactions, which in turn promote the further processing, nuclear export, and translation of a particular transcript. Likewise, other classes of functional RNAs (e.g., tRNAs and snRNAs) have their own identity elements [113]. In contrast, transcripts that lack identity elements are targeted for degradation. In agreement with this model, intronless RNA molecules that have a random sequence are poorly exported from the nucleus and have a very short half-life [114], [115]. In contrast, intronless mRNAs have specialized motifs that promote their nuclear export [105], [116]–[119].
In light of the fact that many functional lncRNAs serve a role in regulating chromatin structure or transcription, it is not surprising that most localise to the nucleoplasm [46]. One would predict that lncRNAs contain a differential set of identity elements that not only serve to prevent their decay but also retain them in the nucleus. This would especially be critical for lncRNAs that are spliced. Despite this, the elements that regulate the localization and stability of these RNAs have received little attention, but can be informed by the view that they may have their own identity markers.
It is also important to point out that eukaryotes have other mechanisms that either degrade aberrant mRNAs (e.g., nonsense-mediated decay) or limit the amount of intergenic transcription (e.g., heterochromatin). Nevertheless, eukaryotes appear to have evolved an intricate network of coupling reactions that are required to cope with a large burden of junk RNA. These findings are consistent with the idea that eukaryotic genomes are filled with junk DNA that is transcribed at a low level.
An alternative view of transcription and conservation?
In an attempt to counter the argument that sequence conservation is a prerequisite for functionality, it has been recently proposed that certain transcriptional events may serve some role in regulating cellular function, despite the fact that the sequence of the transcriptional product is unconstrained [120]. Indeed, this view is in line with the findings that the transcription of certain yeast genes is inhibited as a consequence of the production of cryptic unstable transcripts originating from upstream and/or downstream promoters (for a review see [121]). Other examples have linked the generation of cryptic unstable transcripts to chromatin modifications [101], [122], DNA methylation [123], and DNA stability [124]. However, it remains unclear whether the majority of unstable noncoding RNAs have any effect on DNA or chromatin, let alone contribute to the fitness of the organism. In the cases where cryptic unstable transcriptional events impact gene expression, they usually consist of short transcripts that are synthesized from regions around the transcriptional start sites or within the gene itself [121]. Indeed most of the available data are consistent with the fact that transcriptional start sites are promiscuous, often generating bidirectional transcription [100], [101], and that subsequent coupling processes, such as the interaction between promoter-associated complexes and 3′end processing factors, are required to enforce proper transcriptional directionality [125]. Other unstable transcripts function to promote or maintain heterochromatin formation in the vicinity of the transcriptional site, likely because these regions produce toxic transcripts [122]. Although this form of transcription has a function (viz., to maintain a repressive state), it is not clear that the elimination of these regions would have any effect on the organism [8]. The transcription of other short unstable transcripts, mostly produced from enhancer regions, has been shown to promote gene expression [126]; however, again these “enhancer RNAs” are transcribed from a small fraction of the total genome [127]. As stated by others [128], it is imperative that those who claim that the vast majority of intergenic transcription is functional test their hypotheses. In the absence of this evidence, the declaration that we are in the midst of a paradigm shift with regards to eukaryotic genomes and gene expression [120] seems premature.
Concluding Remarks
For decades, there has been considerable interest in determining what role, if any, the majority of the DNA in eukaryotic genomes plays in organismal development and physiology. The ENCODE data are only the most recent contribution to a long-standing research program that has sought to address this issue. However, evidence casting doubt that most of the human genome possesses a functional role has existed for some time. This is not to say that none of the nonprotein-coding majority of the genome is functional—examples of functional noncoding sequences have been known for more than half a century, and even the earliest proponents of “junk DNA” and “selfish DNA” predicted that further examples would be found. Nevertheless, they also pointed out that evolutionary considerations, information regarding genome size diversity, and knowledge about the origins and features of genomic components do not support the notion that all of the DNA must have a function by virtue of its mere existence. Nothing in the recent research or commentary on the subject has challenged these observations.
Acknowledgments
We would like to thank L. Moran, S. Eddy, D. Graur, R. Hardison, J. Wan, and A. Akef for helpful comments on the manuscript.
Funding Statement
This work was supported by a grant from the Canadian Institutes for Health Research (CIHR) to AFP and a Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery Grant to TRG. The funders had no role in the preparation of the article. | Rarely, these mutations will turn out to be beneficial, and a new gene may arise (“neofunctionalization”) [14]. Most of the time, however, one copy sustains a mutation that eliminates its ability to encode a functional protein, turning it into a pseudogene. These sequences are what Ohno initially referred to as “junk” [13], although the term was quickly extended to include many types of noncoding DNA [15]. Today, “junk DNA” is often used in the broad sense of referring to any DNA sequence that does not play a functional role in development, physiology, or some other organism-level capacity. This broader sense of the term is at the centre of most current debate about the quantity—or even the existence—of “junk DNA” in the genomes of humans and other organisms.
It has now become something of a cliché to begin both media stories and journal articles with the simplistic claim that most or all noncoding DNA was “long dismissed as useless junk.” The implication, of course, is that current research is revealing function in much of the supposed junk that was unwisely ignored as biologically uninteresting by past investigators. Yet, it is simply not true that potential functions for noncoding DNA were ignored until recently. In fact, various early commenters considered the notion that large swaths of the genome were nonfunctional to be “repugnant” [10], [16], and possible functions were discussed each time a new type of nonprotein-coding sequence was identified (including pseudogenes, transposable elements, satellite DNA, and introns; for a compilation of relevant literature, see [17]).
Importantly, the concept of junk DNA was not based on ignorance about genomes. On the contrary, the term reflected known details about genome size variability, the mechanism of gene duplication and mutational degradation, and population genetics theory. Moreover, each of these observations and theoretical considerations remains valid. | yes |
Evolution | Can evolution explain the existence of 'junk DNA'? | yes_statement | "evolution" can "explain" the "existence" of '"junk" dna'. the "existence" of '"junk" dna' can be "explained" by "evolution" | https://link.springer.com/article/10.1007/s10539-022-09854-1 | Not functional yet a difference maker: junk DNA as a case study ... | Abstract
It is often thought that non-junk or coding DNA is more significant than other cellular elements, including so-called junk DNA. This is for two main reasons: (1) because coding DNA is often targeted by historical or current selection, it is considered functionally special and (2) because its mode of action is uniquely specific amongst the other actual difference makers in the cell, it is considered causally special. Here, we challenge both these presumptions. With respect to function, we argue that there is previously unappreciated reason to think that junk DNA is significant, since it can alter the cellular environment, and those alterations can influence how organism-level selection operates. With respect to causality, we argue that there is again reason to think that junk DNA is significant, since it too (like coding DNA) is remarkably causally specific (in Waters’, in J Philos 104:551–579, 2007 sense). As a result, something is missing from the received view of significance in molecular biology—a view which emphasizes specificity and neglects something we term ‘reach’. With the special case of junk DNA in mind, we explore how to model and understand the causal specificity, reach, and corresponding efficacy of difference makers in biology. The account contains implications for how evolution shapes the genome, as well as advances our understanding of multi-level selection.
Working on a manuscript?
Introduction
How to understand biological function has long been a subject of both philosophical and scientific debate focused on evolutionary biology. Philosophical assessments of biological function have often focused on whether function needs to be understood as a past product of natural selection (Wimsatt 1972; Millikan 1984; Neander 1991) or is aptly described by just what biological causes presently do (Cummins 1975; Hinde 1975; Boorse 1976). The former style of “selected effects” approach is historical—or “etiological,” in philosopher-speak. The latter style of “causal role” approach is often ahistorical but—at least in current biological discourse—nevertheless typically assumes that natural selection should be operating on these entities in the present (Allen and Neal 2020).Footnote 1
In the philosophy of biology, there is also a notion of “actual difference makers” as special targets of biological explanation and investigation (Waters 2007). According to this approach, functional genomic entities like certain stretches of DNA are actual difference makers—since different actual “values” for these causal “variables” (i.e., different sequences of the “same” stretch of DNA among various organisms within a population) can and do generate different actual “values” for intervened-on “variables” (such as RNA and protein) in that population, which can sometimes lead to different actual phenotypic and even fitness “values” for the different organisms in that population.
Here we demonstrate that there is another class of actual difference makers in biology: one which has often been overlooked in discussions of function, role, and import (likely due to the commonly conjoined emphasis on fitness and selection). These are genomic entities whose presence or absence alters the character of the cell and are thus influential—despite that these entities may not have been selected for, and that mutations in these regions do not necessarily affect the fitness of the organism. The presence of these entities generates cellular work, and their complete deletion would likely decrease the fitness of the organism; but their alteration by the typical mutation does not often affect fitness—at least not to the extent that such mutations are detected, eliminated, and/or preserved by organism-level natural selection. One main difference between these genomic regions and typically coding DNAFootnote 2 is not their causal specificity but rather their reach (or lesser extent thereof) and hence their efficacy (both terms described in more detail later in the text). Our aim is to provide a characterization of these overlooked causal entities and relationships, using junk DNA as an illustrative case.
Junk DNA
It is widely agreed (Ponting and Hardison 2011; Rands et al. 2014; Ponting 2017) that approximately 90% of the human genome is not subject to purifying selection and hence—at least according to typical accounts of function in molecular biology—is not functional. Despite this, we argue that paradigmatically “non-functional” DNA, commonly referred to as junk DNA, is still a difference maker (in Waters’ [2007] sense). The fact that there are entities which matter (as they affect cell physiology), yet which are not necessarily sculpted by organism-level natural selection, has profound implications for the evolution of humans, and multicellular life in general.
Junk DNA represents a large fraction of all eukaryotic genomes. Its existence is due to the fact that eukaryotic genomes contain selfish DNA entities (also known as transposable elements), which have the ability to replicate themselves (Doolittle and Sapienza 1980; Orgel and Crick 1980). It is believed that transposable element activity fueled the expansion of the eukaryotic genome. In all eukaryotic genomes examined thus far most transposable elements have accumulated inactivating mutations, with only a minority still having the ability to replicate. These dead transposable elements are a vast graveyard that constitutes much junk DNA.
One critical factor that permitted the expansion of transposable elements, and thus junk DNA, is the nucleus (Martin and Koonin 2006; López-García and Moreira 2006; Palazzo and Gregory 2014). The nucleus effectively divides the cytoplasm into two distinct compartments: the nucleoplasm, where DNA is transcribed into premature messenger RNAs (pre-mRNAs), which are then spliced to form mature messenger RNAs (mRNAs); and the cytoplasm, where these fully processed mRNAs are translated into proteins.Footnote 3 The segregation of mRNA processing machinery away from mRNA translation machinery has two main effects. First, this segregation ensures that for any given mRNA, its splicing is completed before it is allowed to be exported from the nucleus to the cytoplasm (Martin and Koonin 2006). This, in-and-of-itself, has several advantages. It ensures that pre-mRNA is free of translating ribosomes, which would likely collide into—and interfere with—the splicing machinery, and it prevents unprocessed pre-mRNAs from being translated into proteins (many of which are toxic). Hence, this segregation of RNA processing and translation increases the efficiency and fidelity of these two processes. Second, the nucleus/cytoplasmic divide acts as a quality control device. In most eukaryotic systems studied, it has been observed that unprocessed pre-mRNAs and misprocessed mRNAs are not efficiently exported to the cytoplasm, but instead retained in the nucleus and degraded by dedicated RNA decay machinery (Palazzo and Lee 2018). This severely reduces the translation of misprocessed mRNAs, whose protein products are potentially toxic.
So, what does this have to do with junk DNA? Well, DNA in general is a non-specific substrate for RNA polymerase. As a result, intergenic DNA is transcribed at a low level into junk RNA, also known as ‘transcriptional noise’ (Struhl 2007; Palazzo and Gregory 2014; Palazzo and Lee 2015). Like misprocessed mRNAs, most of this junk RNA is retained in the nucleus and eliminated by RNA decay machinery. This makes sense, since if this transcriptional noise was not eliminated and instead allowed to be translated into junk protein, then it would become a significant burden on the organism (Palazzo and Lee 2015). The exposure of the ribosome to misprocessed mRNAs and intergenic RNAs is very toxic in tissue culture cells (Ogami et al. 2017). By retaining junk RNA in the nucleus, and promoting its decay, junk DNA becomes less of a liability. In a sense, the nucleus and all of its associated quality control machinery acts as a global mechanism to suppress the deleterious effects of rampant mRNA mis-processing and transcriptional noise that is inherently present in cells with large junky genomes (Warnecke and Hurst 2011; Rajon and Masel 2011, 2013; Koonin 2016).
Eukaryotic cells have additional mechanisms to reduce the deleteriousness of junk DNA. For example, excess DNA is usually packaged into heterochromatin, which prevents it from being transcribed robustly, thus further limiting the amount of junk RNA that is produced.
Overall, these many processes in eukaryotic cells buffer against the deleteriousness of junk DNA. But these buffering systems are a double-edged sword: by relieving the selection pressure on organisms to get rid of this excess DNA, they also permit junk DNA to accumulate. It is thus possible that the amount of junk and the efficiency of systems that render it less harmful could have arisen in parallel as a sort of evolutionary arms race.
In addition, it is likely that many of these buffering systems are somewhat tuned to the amount of junk DNA they must contend with. Cells with large amounts of junk DNA will likely acquire secondary adaptive changes to help their quality control systems to better deal with this increased load. In addition, these quality control systems have also been co-opted to regulate the functional portion of the genome. For example, RNA decay machinery is also required to properly trim precursor ribosomal RNA to its mature form (Zinder and Lima 2017). Thus, a certain level of junk DNA becomes necessary for the entire system to work properly. In the absence of a certain level of junk RNA, RNA decay machinery will likely start to degrade functional RNAs (Doma and Parker 2007; Garland and Jensen 2020; Wang and Cheng 2020). Similarly, in the absence of junk DNA, proteins that silence this junk by packing it into heterochromatin will likely start to silence functional DNA.
Note that, within this context, junk DNA neither historically evolved for a specific function; nor is it currently being selected for or against for organisms.Footnote 4 According to the predominant accounts of “function” in biology, junk DNA has no function (for the organism). Yet its presence matters for an historical and comparative understanding of evolution. For instance, this type of evolution—one not necessarily directed by natural selection—leads to real differences between diverse branches of the evolutionary tree. Over long stretches of evolutionary time, different organism types have accumulated diverse sets and amounts of these non-functional (yet influential) entities (Gregory et al. 2007). These different entities contribute to features which permit different cellular “life” styles, which can contribute to multi-level selection (Vinogradov 2004; Gregory 2005b). In sum, the existence of junk DNA changes many basic features of the cell. Since these features affect cell physiology, junk DNA is a difference maker. We elaborate on what this means in the next section.
Difference makers
In 2007, the philosopher of science C. Kenneth Waters identified the class of “actual difference makers” as the causes that actually make a difference (Waters 2007). Waters offered this contribution to the extensive literature on causality in order to resolve a stubborn puzzle from the historical study of causation. The puzzle is traditionally framed by asking the following question: when someone strikes a match (say, to light a fire), why do we attribute the cause of the fire-lighting-event to the striking of the match, as opposed to the availability of oxygen (or some other, equally crucial element of the causal situation)?
Prior to Waters’ (2007) contribution, the received philosophical view of this type of situation had been—since the 1843 publication of John Stuart Mill’s A System of Logic—one of causal parity. According to Mill, all causes are ontologically equal, or on a par (hence the term ‘parity’ for this sort of view). On Mill’s view, there is no substantial difference between the striking of the match and the availability of oxygen. This position is at odds with our common, intuitive sense that the actual cause of the lit fire is the match-striking-event, and that other elements such as the presence of oxygen are mere background conditions (or some such). Post-Millian philosophical attempts to explain our tendency to pick out one cause among many have tended, as Waters (2007) details, to point to our interests as the cause of our commonsense beliefs in causal priority rather than parity (Hart and Honoré 1959; Mackie 1974). Believing something like “sure, oxygen is in some sense a cause of the fire lighting, but striking the match is the real cause” is a view which attributes causal priority to one cause (striking the match) over others (such as the presence of oxygen). Here, one cause is being thought of as more significant than others (hence the term ‘priority’ for this sort of view).
Waters develops an account designed to pick out commonly emphasized biological causes, such as differences in the structure of DNA (when it varies in ways which generate variation in other variables such as RNA and other molecules). He then explains the perceived significance, or priority, of this DNA relative to other causal elements, such as the structure of accessory proteins (when these do not tend to vary in ways which generate corresponding variation in other variables). Waters accomplishes all this with the help of a trio of distinctions:
1 – potential difference makers (causes whose variables could vary in a population to make a difference in effect) versus actual difference makers (causes whose variables do vary in a population to make a difference in effect). For example: if there was variation within a population among the structures of one of its protein-folding accessory proteins, and that variation generated corresponding variation in protein conformation, then that protein-folding accessory protein would be an actual difference maker in that population. But in the absence of actual variation among the structures of that protein-folding accessory protein generating actual variation in protein expression within a population, that molecule is merely a potential rather than an actual difference maker in that population.
2 – an actual difference maker (working to generate population-based differences in effect, together with other actual difference-making causes) versus the actual difference maker (working to generate population-based differences in effect, without any other actual difference-making causes). Waters points to RNA synthesis in bacterial cells as an example of the latter kind of case—one in which only activated DNA segments act as the actual difference maker in this process, since only that “variable” takes on different “values” for different cells within the relevant population. Although accessory proteins like RNA polymerase are (of course) required for RNA synthesis in bacterial cells, RNA polymerase is not in this case a “variable” which takes on different “values” in this population, in the sense of individual bacterial cells expressing structurally distinct versions of RNA polymerase (or other protein-folding accessory proteins) which then correspondingly generate differences in synthesized RNA. (RNA polymerase is still a potential difference maker, though, since different bacterial cells within a population could presumably contain structurally distinct versions of RNA polymerase which could then presumably affect instances and rate of RNA synthesis.) Alternatively, Waters points to RNA synthesis in eukaryotic cells as an example of the former kind of case—one in which activated DNA segments act as an actual difference maker along with RNA polymerases, since in this more complicated context there are different kinds of RNA polymerases and “presumably, different accessory molecules are also associated with the synthesis of different RNA molecules” (Waters 2007, p. 574).
3 – causally specific difference makers (causal variables whose values can be distinctly many, variation among which corresponds to distinctly many values in effect-variable) versus causally non-specific difference makers (causal variables whose values are not distinctly many, or whose distinctly many values do not correspond to distinctly many values in effect-variable). Woodward (2010) explicates these notions with a contrast between fine-grained (or dial-like) and coarse-grained (or switch-like) control. To listen to a particular station on your radio, you need to both flip the on/off switch and turn the dial to the appropriate frequency. But only turning the dial gives you fine-grained control over which station you might receive, and there are distinctly many positions on that dial which each correspond to distinctly many stations to which you might listen. Obviously, moving the on/off switch to the correct position is required in order to listen, but “the switch is not causally specific with respect to which program is received” (Woodward 2010).
The upshot of all this conceptual machinery—for biology as it is being practiced, and even more specifically for genetics—is that it provides a potential justification for judgments of the causal priority of coding DNA. Therefore, according to Waters, “it makes sense for biologists to say that DNA is not on a causal par with many of the other molecules that play causally necessary roles in the synthesis of RNA and polypeptides” (2007, p. 579). This stance—that of assigning causal significance, or priority, to DNA over other molecules—is indeed a familiar one in biology. And it is explained, according to Waters (2007), by the fact that DNA is an actual as opposed to a merely potential difference maker. Additionally, although DNA is an actual difference maker, among several others (it is not the only actual difference maker), of those assorted actual difference makers, DNA is the causally specific one (its difference-making is not merely causally non-specific.Footnote 5
Junk DNA as an actual difference maker
A surprising thing about this account of causal priority is that it leaves all “activated” DNA on a par with one another—including junk DNA. Waters writes: “An important actual difference in cells is the difference in the nucleotide sequences of RNA molecules synthesized in a cell” (2007, p. 573). As discussed in the “Junk DNA” section, both coding and junk DNA are transcribed in cells; both make for actual differences in the nucleotide sequences of RNA molecules synthesized in cells; both generate causally specific differences in the sequences of RNA molecules synthesized in cells. Any stretch of transcribed DNA which varies among individuals within a population—transcription of which generates corresponding variation in the RNA synthesized among individuals in that population—is going to look, on Waters’ account, like an important actual difference maker in that population. Given what has recently been learned about widespread transcription activity, this includes junk DNA.
Ironically, since junk DNA is likely subject to less (or even zero) purifying selection relative to coding DNA, junk DNA will often tend to vary more among individuals in a population than does coding DNA, and thus junk DNA might even turn out to be more causally specific than coding DNA on Waters’ view. To apply Woodward’s toy example from above, if we think of a stretch of DNA like a radio dial that can be tuned to different stations (where each station is an instance of phenotypic variation existing in the population), then there are likely going to be more stations available for tuning to, on a dial corresponding to a stretch of junk DNA, than on one corresponding to a stretch of coding DNA. A stretch of junk DNA is a causal variable which is likely to take on more distinct values among individuals in a population than is a stretch of coding DNA, and to thereby correspond with more distinct values of the synthesized RNA effect-variable.
But—as discussed above, and contingently so—biologists and philosophers of biology do not typically view causally specific differences generated by actual differences in junk DNA as on a causal par with causally specific differences generated by actual differences in coding DNA. Although Waters’ account of causal specificity goes some way towards explaining why DNA has been causally elevated relative to other actual difference makers (such as RNA polymerase), it does not explain why coding DNA has been causally elevated relative to junk DNA. Junk DNA has the same two features which Waters has picked out as the distinguishing features of coding DNA: actual difference-making and causal specificity. Yet junk DNA is not on a causal par with coding DNA in biology.
Something is missing from Waters’ account; something related to causal specificity but involving additional concepts we hereby term ‘causal reach’ and ‘causal efficacy’.Footnote 6 One obvious, crucial difference between coding and junk DNA is that, although each of these causal variables generate both proximate and distal effects, not just the immediately proximate but also some of the rather more distal effects of coding DNA can be nonetheless quite causally specific. Although junk DNA has both proximate and distal effects, too—and junk DNA often has casually quite specific proximate effects—the more distal effects of junk DNA tend to be significantly reduced in causal specificity, compared with some of those of coding DNA. So, even taking on board much of Waters’ framework for comprehensively understanding the causal priority typically afforded coding DNA, we need to track not just the specificity of actual difference-making causes in biology, but also the extended (or not) reach of these causes, as well as the maintenance (or not) of that specificity throughout the reach of their effects—i.e., the complex combinatorial feature of causal efficacy.Footnote 7
See Fig. 1 for a conceptual depiction of various causes with distinct combinations of specificity, reach, and corresponding efficacy. Causal specificity has already been explained; causal reach has to do with how many effects a single, initiating cause generates.Footnote 8 These effects can: extend straightforwardly out in a linear chain from the initiating cause; scatter out in a burst from the initiating cause, or both scatter and extend in a cascade from the initiating cause. Explained in engineering terms, causal reach can occur via parallel processing (multiple effects radiating out from one causal node), in sequence (a series of proximate and distal effects), or by combination of these two modes.
Fig. 1
Various causes with distinct combinations of specificity, reach, and corresponding efficacy. Top left, an utterly inefficacious cause with no effects. Bottom right, an extremely efficacious cause—one that has both reach and specificity in terms of its effects. Reach is indicated by number of nodes—where each cause can have either unitary or multiple effects, both proximate and ultimate. Causal specificity is indicated by effect opacity—where each node can either transmit its full pigmentation or produced a faded node with increased transparency. Within rows, causes increase in specificity from left to right; within columns, causes increase in reach from top to bottom. Hence, top right has more specificity though less reach relative to bottom left, which has more reach though less specificity. Both are less efficacious than bottom right, but more efficacious than top left; neither are necessarily insignificant causes. (Prepared by Adam Streed using the matplotlib library for Python 3; all the code is his own)
Causal efficacy tracks interaction of the two prior notions of specificity and reach. This concept is required to monitor the effects a difference maker has—as the effects of that difference maker extend and cascade (or not) and given the causal specificity (or not) of those resulting effects. A causally abrupt, non-specific difference maker is by its nature not very efficacious. A difference maker with extensive reach can nonetheless be rather causally inefficacious if its many “reach” effects are mostly non-specific. Likewise, a highly causally specific difference maker can nonetheless be rather causally inefficacious if it does not have much reach in terms of its effects. A difference maker with both extensive reach and specificity in the effects it causes will be extremely efficacious.
See Fig. 2 for a conceptual depiction of various genetic causes with distinct combinations of specificity, reach, and corresponding efficacy. So, one likely reason coding DNA is considered causally so significant by biologists because it can have quite the causal reach, and not just its proximate but often also its more distal effects can be quite causally specific. Note, however, that not all causally specific changes to coding DNA are on a par with one another—in terms of their causal reach, corresponding efficacy and resulting effect on judgments of causal priority.Footnote 9
Fig. 2
Various genetic causes with distinct combinations of specificity, reach, and corresponding efficacy. a A synonymous, conservative mutation in any transcribed DNA—coding or junk. b A synonymous, semi-conservative mutation in coding DNA. c A non-synonymous, semi-conservative mutation in coding DNA—one that produces a change in protein amino acid sequence but no change in conformation. d A non-synonymous, non-conservative mutation in coding DNA—a genotypic change with phenotypic and other ultimate effects. e Insertion or deletion of a small “repeat” segment of junk DNA. f Insertion or deletion of a large “repeat” segment of junk DNA—one which ultimately produces an uptick in RNA decay machinery. g Insertion or deletion of a large, unique (not a repeat) segment of junk DNA—the size rather than uniqueness of which also produces an uptick in RNA decay machinery. h Insertion or deletion of another large, unique segment of junk DNA—one that produces in virtue of its size and uniqueness not just an uptick in RNA decay machinery but also other downstream, causally non-specific distal effects. Explication of these cases continues in the main text below (Prepared by Adam Streed using the matplotlib library for Python 3; all the code is his own)
A synonymous, conservative mutation in transcribed DNA (e.g., a change from a GGC codon to GGG), although it will produce a causally specific change in synthesized RNA, will not necessarily produce any further changes of note—even if protein synthesis occurs (since GGC and GGG both code for glycine; Fig. 2a).Footnote 10 However, even synonymous mutations in coding DNA can turn out to be not perfectly conservative (i.e., they can be productive of further, causally non-specific effects; Fig. 2b).Footnote 11 Non-synonymous mutations in coding DNA can also vary in terms of the (semi-) conservativeness of their effects. A replacement event which introduces one hydrophobic amino acid for another during protein expression, or one positively charged amino acid for another (Fig. 2c), is likely to be more conservative in its changes than those events which substitute a hydrophobic amino acid for a charged one, or a negatively charged amino acid for a positively charged one. A non-synonymous, non-conservative mutation in coding DNA which introduces a stop codon in a new place will likely affect more than just one amino acid of a protein’s primary sequence (it may cut off several) and could affect not just genotype but also phenotype (Fig. 2d). All these changes (Fig. 2a–d) are proximately causally specific, but they vary in reach, as well as in the specificity of their more distal effects (i.e., their causal efficacy). The fact that these changes also vary in perceived importance (ascending from a to d) shows that not just causal specificity but also causal reach and efficacy are features relevant to judgments of biological importance.Footnote 12
The relevance of causal reach and efficacy to judgments of biological importance becomes even more apparent when considering potential changes to junk DNA. Of course, many changes to junk DNA are unimportant from this point of view. Insertion or deletion of a small, “repeat” segment of junk DNA can fail—even when transcription occurs—to produce any causally specific effects. Such insertions or deletions are likely—if they alter anything at all—to change only the amount or proportion of various segments of junk RNA already synthesized in the cell (since they will neither introduce an entirely new kind of segment nor entirely remove any kind of previously-existing segment; Fig. 2e). To re-apply and extend the radio metaphor from Woodward (2010), this is something like turning up or down the volume on a station to which the cell is already tuned. Insertion or deletion of a larger but still “repeat” segment of junk DNA might produce additional causally non-specific effects further downstream, e.g., an uptick in RNA decay machinery (described in “Junk DNA” section), via sizable alteration of the amount of junk DNA transcribed in the cell (Fig. 2f). Alternatively, insertion or deletion of a large, unique (not a repeat) segment of junk DNA might have causally specific effects on the types of junk RNA that are synthesized in the cell (since its uniqueness means that it will, if that stretch of genome is transcribed, either introduce or eliminate expression of a segmentFootnote 13), but could also have causally non-specific distal effects on, e.g., the amount of RNA decay machinery, via its sizable alteration of the amount of junk RNA being synthesized (Fig. 2g). Finally, insertion or deletion of a large collection of junk DNA segments could have other cascading, causally non-specific distal effects—such as altered patterns of interaction with RNA decay machinery, changes in cellular size, or degradation of functional RNA (introduced in “Junk DNA” section, additional discussion in “Detecting the hidden significance of junk DNA” section; Fig. 2h). As before, these changes tend to vary in perceived biological significance (ascending from e to h).
Our presentation of these cases reflects the fact that the relative significance of junk DNA, when it is significant, does not usually stem from its occasional uniqueness (and corresponding causal specificity). The diagram also helps us to demonstrate, given the reduced causal specificity of this bottom set of cases (Fig. 2e–h) relative to the prior top set (Fig. 2a–d), why coding DNA is considered causally so significant by biologists—because it can have quite the causal reach, and not just its proximate but often also its more distal effects can be quite causally specific. Coding DNA can be a highly efficacious cause, and this reliably leads to judgements of elevated causal importance. But we can further see, given the significant causal reach of some of these cases (Fig. 2d and h) relative to others (Fig. 2a–c and e–g), how not just causal specificity but also reach might play a role in judgements of causal importance. Although junk DNA may rarely be a highly efficacious cause (due to its diminished distal causal specificity), it can still have reach. The conceptual machinery of causal specificity, reach, and corresponding efficacy gives us the tools to understand the utmost causal importance of certain kinds of changes in coding DNA, the relatively reduced in importance but still non-negligible role of certain other kinds of changes in junk DNA, and the common occurrence of trivial sorts of changes in either—even from a relatively restricted, emphasis-on-selection-at-the-level-of-the-organism style of view.
Obviously, we have not exhausted all the diverse ways that either coding or junk DNA can causally affect change (or fail to do so).Footnote 14 We posit that junk DNA, and other non-functional (in the selectionist sense) components of the cell, are a significant part of the evolutionary story of eukaryotes; low-efficacy causes can still be significant. We suspect that the diminished causal efficacy of these components has often made it difficult for either biologists or philosophers to appreciate and characterize their significance, despite their reach.
From the point of view of organism-level selection, junk DNA may have arrived in cells in a non-adaptive manner (at the organismal level), and typical mutations (such as small nucleotide polymorphisms) in a nucleotide sequence of junk DNA may not generally be selected for or against (at the organismal level), but mechanisms within the cell have generally adapted to its presence. In the context of this evolutionary interplay, the presence and potency of the total sum of junk DNA in the cell dictates the need for various cellular machineries of “quality control,” changing the resources required and expended by the cell, and committing the cell to particular strategies. Significant changes to either party (the junk DNA or the cellular clean-up crew) can produce causally significant though non-specific effects. We detail these possibilities, and how to detect them, in the next section.
Detecting the hidden significance of junk DNA
One way to illustrate the difference between significant but not functional (in the selections sense) and functional biological entities is to explore how these entities as a whole might affect the fitness of an organism: to explore their hypothetical, collective effect. In theory, this could be done. In practice, the amount of resources that would be required to carry out the full experiment may not be feasible. First, we would need to pick a genome. Next, we would need to unambiguously identify non-functional DNA by deleting small segments of the genome. If we chose to investigate the human genome, the deletion size that we would use would be similar to mutations that naturally occur in human populations, since it is precisely these types of mutations that are seen by natural selection. Any deletions that did not affect the number of offspring could be tagged for further investigation. Then, we would combine these deletions in increasing amounts and evaluate how these affect the number of offspring of the resulting organism.
Cataloguing functional versus non-functional roles
If given unlimited resources and time, we could in principle test whether each segment of the chosen genome is functional. Any region of DNA can play a causally specific, sequence-dependent role or a causally non-specific, sequence-independent role.
To test whether any given region of DNA has a sequence-dependent role, we could introduce nucleotide substitutions. However, this would not test whether the region in question has more non-specific roles that contribute to its reach. For example, it is known that 5′ untranslated regions have to be a minimal length—if they are any shorter than this minimum, the translational start site will not be reliably recognized and the mRNA will not be properly translated (Kozak 1991). Thus the 5′ untranslated region acts as a spacer, one that can be quite important—since even from a perspective that emphasizes organismal-level selection, it is a physical entity that contributes to the cellular environment.
To test whether any given region DNA has a sequence-independent role, we could systematically delete these regions.Footnote 15 Assessing the rate of insertions or deletions (indels) between organisms has been used to determine that most annotated non-coding transcripts produced in mammalian cells are non-functional, although these analyses are statistical in nature (Ponting 2017). To precisely assess each individual region, we would have to empirically test it. We would begin by deleting as much DNA as what occurs in natural mutations, since these alterations are the ones on which selection operates. The size of the average deletion can vary quite considerably, typically because those regions of the genome which contain repeat elements are quite prone to large alterations. In non-repeat regions it has been estimated that 96% of all deletions are smaller than 16 base pairs in length (Mullaney et al. 2010). In repeat regions, spontaneous deletions are more common and can be larger. Although very long deletions are rarer, they can accumulate in lineages over generations, and as a result the size of any given repeat region varies considerably in the human population, with many of these deletions being tens of thousands of base pairs in length (Jeffreys et al. 1985; Redon et al. 2006). With this in mind, we would begin our experiment by deleting ~ 100 base pair segments in parts of the genome that show no sequence conservation between humans and other mammals, which represents about 95% of the human genome. It is likely that some of this non-conserved DNA plays a lineage specific-role in humans (i.e., has been under selection in the human lineage but is not conserved between humans and related species, such as chimpanzees), although most estimates place this at less than 5% of the genome (Ward and Kellis 2012; Rands et al. 2014; Gulko et al. 2015; Ponting 2017).
To perform this experiment in an informative manner we would need to track the reproductive success of thousands of individuals having the same mutation under very controlled conditions to infer whether a given deletion was slightly deleterious. Thus, in practice, the effect of slight changes to fitness would be almost impossible to assess. Nevertheless, in theory, this experiment could be done.
Testing the boundary between non-functional and functional roles
With all the functional and non-functional DNA cataloged (though only from the organism-level-selection point of view), we could then move on, in a rather interesting way, to determining how consequential each region of so-called junk DNA might be. We could combine previously tested deletions of junk DNA together into unnatural mutations (i.e., mutations not typically seen in nature, and thus not subjected to selection pressures) and determine their effect on reproductive success.
To reiterate, this experiment would not test whether these sequences are functional (in the purifying selectionist sense), as selection would never encounter these types of combinatorial mutations. Instead, this would be one means of testing whether given regions of junk DNA are influential (i.e., whether they are difference makers). The degree to which deletion mutations would have to be combined before they affect fitness (i.e., reproductive success) might indicate how (in)efficacious these regions are as difference makers.
We expect that quite a large number of deletions must be combined before we would be able to detect any effect on fitness. Indeed, it has been seen that deleting 1.5 Megabases of non-coding DNA from the mouse genome (approximately 0.06% of the entire genome) had no measurable effect on the fitness of the animals (Nóbrega et al. 2004). How much of the junk DNA genome would need to be eliminated before measurable effects can be detected is hard to estimate at this time.
Nevertheless, there would likely come a point where the diffuse effects of deleting many junk DNA regions, when combined, would become detectable and significant—and that this would show the cumulative “difference making” effect of the presence of junk DNA (relative to its absence), along with the corresponding cellular adjustment to its usual presence (relative to its absence). We might expect that quite a sizable amount of junk DNA would need to be removed before we would be able to measure any effects on fitness.
Of course, in practice there would be additional complications. Different genomic regions may play redundant roles, thus elimination of one or the other may have little to no fitness effect, while deletion of both will have a large impact on fitness. This combination would not test the diffuse effects of junk DNA, but rather uncover much more specific effects that were previously hidden. Untangling these two possibilities may be almost impossible.
Non-functional yet significant roles for junk DNA
So, what would the massive elimination of junk DNA change? Alternatively, what non-functional roles does it normally play? Below we list some of the causally non-specific yet nonetheless significant effects which can make junk DNA consequential for the cell.
Cell size
It is well known that DNA content correlates with the size of the cell nucleus, which in turn correlates with the total cell size (Cavalier-Smith, 1978; Gregory, 2001). It has thus been inferred that DNA content affects cell size. Thus, massive reductions in the amount of junk DNA would lead to a reduction in cell size. This would fundamentally change many aspects of cell physiology. First, as cell size changes, surface areas and volumes do not scale with one another in a linear fashion. As cells become smaller, the ratio of surface area/volume increases. An increase in cell membrane/volume ratio would allow molecules to diffuse more rapidly into and out of cells, and thus allow for greater rates of metabolism. It is widely believed that the small genome size of both birds and bats, and the accompanying increase in metabolic rate, was a necessary prerequisite for the evolution of flight (Hughes and Hughes 1995; Gregory 2002). Indeed, even within birds, those which have the smallest genomes and have the most rapid metabolism are the hummingbirds and those with the largest genomes are flightless birds (Gregory et al. 2009). Interestingly, in the avian lineage it appears that genome size reduction happened before the evolution of flight as cell size estimates for closely related non-avian dinosaurs were found to be quite small (Organ 2007).This suggests that there was no initial selection pressure to reduce genomes due to metabolic constraints associated with flight, but rather that the organisms that happened to have small genomes had the metabolic prerequisites that were necessary to evolve flight. Subsequently, it appears that bird genomes have stayed small due to occasional large genomic deletions, which are possibly driven by positive selection (Kapusta et al. 2017).
The increase of surface area/volume as the genome contracts is true not only for the cell (cell plasma membrane/cell volume) but also for some of the organelles, for example the nucleus. Other organelles, such as mitochondria, would most probably remain the same. These alterations will have their own consequences. For example, in the nucleus, newly made mRNAs are known to randomly diffuse from their site of production to the nuclear pore (Shav-Tal et al. 2004), thus the larger the nucleus, the more time it will take for newly made mRNAs to reach the cytoplasm where they are translated into proteins. If we compare the nuclear export rate (t1/2; time it takes for half of the pool of mRNA to be exported from the nucleus to the cytosol) for the exact same mRNA (in this case the ftz reporter mRNA), it is 2 h in frog oocytes (Luo and Reed 1999), whose nuclei have a radius of 200 µm; but only 15 min in mammalian cells (Palazzo et al. 2007), whose nuclei have a radius of about 4 µm. Nuclear export rates (t1/2) are 3–5 times faster in yeast, whose nuclei have a radius that is smaller than a micrometer (Oeffinger and Zenklusen 2012). The nuclear export rate of mRNA is one of the main determinants of the lag time between gene activation and protein production, and can affect biological processes such as the timing of circadian rhythm as well as how cells respond to their environment (Hoyle and Ish-Horowicz 2013).
Besides gene expression timing, it is likely that other cellular processes would also be affected by cell size (Cavalier-Smith 1978). It is not entirely clear how drastic changes in cell size would affect the development and the proper function of tissues and organs, but it is reasonable to expect that many of these may become dysregulated. Note that we are not claiming that cell size could never undergo a drastic change due to these constraints. It is likely that if an organism gradually lost DNA over long periods of time, this would be accompanied by other adaptive changes which would compensate for these alterations in cell physiology. But it is likely that a drastic reduction of cell size, without all the accompanying adaptive changes, would lead to a fair number of problems.
As is the case with birds and bats, it is likely that drastic changes in cell size—and the accompanying adaptive changes to compensate for changes in cell physiology—could alter the organism in such a way that it could open up or limit the ability of the organism to occupy certain niches. In insects and vertebrates it has been documented that certain aspects of development and cell physiology are restricted to animals with a limited range of genome sizes (Gregory 2005b). It is also worth noting that in comparison to animals, plants—whose development and organ function appears to be more plastic—more often experience whole genome duplication events which effectively double their cell size. In animals, whole genome duplication events are rarer and seen most in amphibians (frogs, axolotls)—a class of animals that tend to have large genomes, and thus may have extensive buffering capacities. Again, this may indicate that drastic changes in cell size may only be compatible with certain types of cell physiology. The idea that genome size is consequential due to its effects on cell size has been advanced previously; however, unlike previous commentators (e.g. Cavalier-Smith 1978), we believe that the typical indel mutations that alter cell size are not subject to selection, as these indels are so small (see “Cataloguing functional versus non-functional roles” section) that each contributes negligibly to the overall dimensions of the cell. There may be some species that have enough variation in genome size for it to be under selection, but these appear to be the exceptions rather than the rule (Blommaert 2020).
Timing of cell division
It has been noted that cells with larger genomes take longer to divide. Superficially this makes sense as one would expect it would take more time to replicate the increased amount of DNA. However, this can easily be remedied by increasing the number of DNA polymerases in the cell, and also increasing the origins of replication which would allow all the extra polymerases to have access to the DNA. It thus remains unclear how genome size impacts cell division timing.
Regardless of the reasons, the timing of cell division will have drastic effects on the organism’s ability to grow, generate new tissue, and heal after injuries. It is not hard to see that changing this timing would have a major effect on how the organism develops and its overall fitness.
Providing excess substrates for cellular machineries
As we discussed in “Junk DNA” section, junk DNA also provides additional, non-specific substrates for enzymes in the cell to engage with. All enzymes have a preferred substrate, but they will act on non-optimal substrates as well, especially when subjected to non-adaptive evolutionary pressures (Khersonsky and Tawfik 2010; Bar-Even et al. 2011; Tawfik 2020; Copley 2020). Normally the amount of activity associated with these non-optimal substrates is negligible; however, when the amount of non-optimal substrate is in vast excess of the preferred substrate, non-optimal reactions can become substantial. This is true for RNA polymerase enzymes (Struhl 2007), which transcribe DNA into RNA. It is also true of DNA binding proteins (Villar et al. 2014), both those that recognize certain motifs to regulate gene activation, and those that package DNA non-specifically. The easiest solution to deal with an excess of non-optimal substrates is to increase the number of proteins so the excess substrate binding does not interfere with its normal selected activity. In other words, the amounts and activities of all these enzymes are under selection to be able to accomplish their job in a cellular environment filled with excess non-specific substrates: junk DNA and junk RNA.
For other enzymes, their preferred substrates are junk DNA and junk RNA. This is especially true for RNA decay enzymes, since these generally operate with a certain load of junk RNA that they must constantly eliminate. A drastic drop in junk RNA would mean that these enzymes would work more-and-more on their non-optimal substrates, in this case functional RNAs. This “kinetic competition” in RNA quality control systems has been well documented (Doma and Parker 2007; Garland and Jensen 2020; Wang and Cheng 2020). Other proteins that fall in this class are DNA binding proteins that package and silence junk DNA into heterochromatin.
It is possible that many of these enzymes are regulated by feedback loops that “sense” how much excess substrates there are. A large decrease in the number of excess substrates could lead to a decrease in the levels or activities of these enzymes. This, however, may severely impair the proper functioning of enzymes that have both junk RNA, and functional RNAs, as their optimal substrates. For example many RNA decay enzymes also help to trim ribosomal RNAs and other functional non-coding RNAs (Zinder and Lima 2017). Thus, a drastic reduction in junk RNA, if it activated a feedback loop to decrease total RNA decay capacity, may inadvertently diminish the cell’s ability to properly process functional RNAs.
Other (even) more speculative effects
There are possibly other general aspects of the cellular environment that would be altered if a substantial amount of junk DNA were removed.
In eukaryotic cells, long stretches of DNA that contain numerous genes adopt complicated loops, commonly referred to as “topological associated domains” (TADs). There has been much speculation about the importance of these structures (Szabo et al. 2019; Ghavi-Helm et al. 2019; Beagan and Phillips-Cremins 2020). In some cases, these are thought to bring together distant DNA regions, which allows one DNA regulatory element to influence how a distant gene is either turned on or off. In other cases, it is believed that the genes found in one of these loops are co-regulated. It is possible that elimination of large fractions of junk DNA could perturb these local architectural arrangements of the genome. It should be noted that the relative importance of TADs remains controversial. Moreover, it is unclear whether any given TAD would be disrupted if all of the junk within the TAD were to be removed. We understand even less about larger scale architectural features of the genome, how these are affected by junk DNA, and how these structures ultimately contribute to fitness. Nevertheless, effects on DNA architecture could arise, both at the local and global levels, if a genome were massively compacted.
Another aspect of cell physiology that could change is some of its biophysical properties. Recently, there has been a renewed interest in how certain biopolymers tend to form molecular condensates which phase separate from the bulk solution (Banani et al. 2017). Several recent reports suggest that large portions of the genome which are silenced—and normally referred to as heterochromatin—form these condensates (Larson and Narlikar 2018). Similarly, excess amounts of RNA can also form different condensates and these may constitute the matrix of many membrane-less organelles (Jain and Vale 2017; Treeck et al. 2018; Quinodoz et al. 2021). Removal of junk DNA and RNA may alter the amount of these condensates in the nucleus, and this could ultimately impact the biophysical properties of various subcellular regions. Again, it is unclear whether the presence or absence of these condensates would alter the cellular environment enough to impact how functional parts of the genome operate, but it remains possible.
It is likely that many other cell biological processes would be disrupted after large fractions of the junk DNA were to be eliminated. Our goal is not to provide a complete list, but simply to point out that there are many general aspects of the cellular environment that are likely affected by junk DNA.
Summary
Even from a selection-at-the-level-of-the-organism point of view, junk DNA impacts the environment of the cell in which the more traditionally “functional” parts of the genome operate. Normally these impacts are distal, non-specific, and difficult to detect. We can help ourselves conceive of and understand these impacts by imagining how the cell would react to or be changed by the sudden and drastic removal of large swaths of junk DNA. Note that we are not suggesting that these bits of junk DNA are necessarily functional in the traditional sense. Rather, we are suggesting that junk DNA has causal reach; that its presence more than its specificity affects the cell and by extension the organism. There would be significant effects on cell size, timing of cell division, cellular enzymatic activity—to say the least—if it were drastically altered. These are all features and activities of the cell for which junk DNA is, in a normal context, quite important—even though said junk is not subject to the normal processes of natural selection as paradigmatically understood.
Our analysis of junk DNA thus differs from some notable others: those who solely focus on how junk DNA lacks function at the level of the organism (Palazzo and Gregory 2014) as well as those who argue that junk DNA is functional after all (Cavalier-Smith 1978; ENCODE Project Consortium et al. 2012; Mattick and Dinger 2013; Freeling et al. 2015). Similarly, a more nuanced view could also extend to other biological difference makers which do not typically act as organism-level targets of natural selection. Carving out an intermediary role—not necessarily a functional one, but still significant—allows for the recognition of more complex and diffuse elements of cause and effect in biology.
Potential objections and replies
Here we briefly consider two potential objections to the view we have articulated, and offer a pair of pre-emptive replies.
Objection: junk DNA can be eliminated by natural selection—as evidenced in eukaryotic lineages that have undergone genome reduction—and thus its presence must have adaptive or maladaptive effects on cell physiology
Reply: We do not argue that the long-term elimination of junk DNA cannot happen. In the case of some eukaryotes, such as in certain species of Arabidopsis mustard greens (Hu et al. 2011) and Arachis peanuts (Ren et al. 2018), this has occurred within a relatively very short time span. As stated above, flying birds and bats have undergone numerous large deletions that have prevented their genomes from growing due to the periodic invasion of transposable elements in their genomes (Kapusta et al. 2017). Having said that, it is not clear that these genomic reductions were due to positive selection for smaller genomes. It is also possible that genomes could get smaller by non-adaptive mechanisms; for example, when the rate of DNA deletion surpasses the rate of insertion (Petrov 2002), as is likely the case in Fugu pufferfishes (Neafsey and Palumbi 2003). If these non-adaptive processes were ultimately responsible for reducing genome size, we would expect that said organisms also acquired secondary adaptive mutations—so that their cells could operate once their basic properties (such as cell size, timing of cell division, altered rate of molecule diffusion) have significantly changed. It remains possible that in certain organisms, size reductions (or increases) in the genome could be adaptive for a particular reason (Blommaert 2020). For example, it has been suggested that as mammalian lineages expanded after the extinction of the non-avian dinosaurs, mammalian genomes may have undergone a reduction in size due to an increase in the effective population sizes and an increased selection against transposable elements (Lynch et al. 2011). We would expect this to result in the streamlining of the genome only if the advantage that it conferred outweighed all of the negative side effects associated with smaller genomes. Moreover, these effects would not be expected to be linear. We anticipate that quite a sizeable fraction of the genome would have to be eliminated before any adverse effects would be felt. Once that level of depletion is reached, we would expect that these organisms would acquire secondary adaptive changes to counter any negative effects.
Objection: a lack of negative selection against junk DNA shows that it is a reservoir for future function
Reply: This teleological argument is commonly asserted by biologists (Makalowski 2000, 2003; Muotri et al. 2007)—despite the fact that it has been thoroughly rejected by philosophers of biology and evolutionary theorists (e.g., Hull, 1965). The increase or elimination of junk DNA by positive selection within a lineage is strictly subject to how this alteration impacts an organism’s immediate fitness level (not some future potential fitness level). Lineages that do gain properties due to a steady increase or decrease in junk after many generations (after all junk DNA is a difference maker, albeit a relatively inefficacious one) may outcompete other lineages. So, there may be selection on a higher level between lineages, as suggested elsewhere (Jablonski 2008; Brunet and Doolittle 2015). But this type of selection will not change the amount of junk DNA within a lineage; it will only impact whether one lineage is selected over another that differs in this difference maker. Junk DNA elements may also be co-opted by natural selection to produce new functional units. In some cases, new functions may also arise by constructive neutral evolution (i.e., non-adaptive processes). For example: the conversion of junk RNA to functional lncRNAs (Palazzo and Lee 2018; Palazzo and Koonin 2020). While the efficacy of a particular difference maker remains low, it will be subject to non-adaptive evolution.
From this standpoint, a fair question to ask is whether the future exaptation of junk DNA can ever make it (more or less) influential. In line with previous commentaries (Linquist et al. 2020), we think it is important to describe in what time frame we are speaking. Our arguments evaluate whether non-functional (traditionally understood) elements such as junk DNA are influential even from an organismic-level view and in the present. This entails an examination of their current effects, and how efficacious they are in affecting the organism’s phenotype. Of course, this could change in the future. Certain elements of junk could become more efficacious, especially if they acquire new properties, to the point that they transition from non-functional to functional, even on typically selectionist accounts of function. Other transitions are likely (see Graur et al., 2015).
Conclusions
Throughout molecular biology, as well as in the philosophy of biology, function has often been seen as binary in terms of both type and influence: entities are either functional, or not; and only the functional ones are significant. But there are non-functional (traditionally understood) yet significant entities in biology—entities such as junk DNA. According to the dominant accounts of function in biology, most junk DNA is a non-functional entity—since it is and never was a target of selection at the level of the organism. Nonetheless, junk DNA is often a significant entity in the cellular context, and we have adapted Waters’ (2007) account of DNA as an actual difference maker to account for the significance of junk DNA. Namely, junk DNA typically has causal specificity but only for a limited extent of its reach, and thereby it is a relatively inefficacious actual difference maker in cells. Our identification of this option within the conceptual landscape—that of causal reach with proximate, but not distal, causal specificity—allows us to characterize the importance of junk DNA, while maintaining and explaining why it might be assessed as of lesser significance when compared to (for instance) enduringly causally specific stretches of coding DNA.
On both our and Waters’ (2007) accounts, junk DNA is an actual difference maker, and a causally specific one (at least proximally), precisely because it tends to be involved in actual biological process (such as that of making defined RNAs), and because specific changes in it as a cause correspond with specific changes in its effects (e.g., changes in the nucleotide sequences of junk DNA generate specific changes in resultingly transcribed RNA). However, junk DNA is often quite causally inefficacious: despite that it can produce causally specific proximate effects, its cascading ultimate effects tend towards the non-specific. The constrained significance (for the organism) of junk DNA is not due to a total absence of causal specificity, but rather a limited reach for its causal specificity, and resulting limitations in its causal efficacy.
Junk DNA nonetheless contributes to the environment of the cell in which other, more traditionally functional entities exist. Total DNA levels control cell size, the amount of transcriptional noise, the number of transcription factor binding sites, the timing of cell division and likely many other aspects of the cellular environment. More paradigmatically functional entities of the cell have been tuned by natural selection to operate within this environment. This is especially true for quality control processes, which specifically evolve to deal with junk DNA and all its associated biochemical activity. On the one hand, and despite being an actual difference maker, junk DNA is not typically subject to organism-level natural selection. When non-functional DNA is mutated by natural processes, this does not alter the fitness of the organism sufficiently for natural selection to eliminate such mutations. For these reasons and given the way ‘function’ is predominantly understood in biology and philosophy of biology, junk DNA is typically conceived of as a non-functional entity. On the other hand, various components of cellular machinery exist precisely in order to deal with the effects of junk DNA, and the cellular workload is significantly affected by the need to (for instance) perform routine clean-up of the products of junk DNA transcription. If large swaths of junk DNA were eliminated, this would likely affect the fitness of the organism. Although such instances of widespread elimination of junk DNA are highly unlikely to naturally occur, such alterations could in principle could be performed in the lab. For these alternative reasons, and in our proposed terms, junk DNA is significant for the cell—despite its paradigmatically non-functional role.
Ultimately—since there are actual, causally-specific difference makers which shape and impact the cellular environment, but which are not typically subject to organism-level natural selection—our discussion demonstrates that for certain biological organisms, there can be influential features which nonetheless are non-functional in the selectionist sense, i.e., they are not shaped by natural selection. Indeed, in organisms for which drift dominates, it is possible for non-functional-yet-influential biological components to proliferate—especially when the production of these components is fueled by additional processes. The activity of transposable elements appears, in eukaryotes at least, to have driven the proliferation of junk DNA in just such a manner.
Notes
Linquist et al. (2020) argue that it is conceptually incoherent for molecular biologists to adopt “causal role” approaches to function in biology, while also inferring that said functions imply a contribution to fitness. The fact that such a position is inherently confused does not prohibit its presence or prevalence in the literature.
Although we primarily focus on coding DNA, our arguments apply equally to other unambiguously functional genomic elements, such as non-coding RNA genes and promoter regions.
It remains unclear whether the extensive RNA processing found in eukaryotic mRNAs pre-dated the evolution of the nucleus/cytosolic divide, or whether the evolution of the nucleus permitted RNA processing to evolve and proliferate (López-García and Moreira 2015). Despite this uncertainty, it does appear that the last eukaryotic common ancestor was intron-rich (Rogozin et al. 2003).
Although transposable elements are not being selected for within the species (and in many cases are selected against, as they are a mutational hazard), they are under selection pressure within the genome to become better at copying themselves. For more on how selection at different levels operates on transposable elements, see (Brunet and Doolittle 2015). In any case, active transposable elements make up only a small fraction of all junk DNA in most eukaryotes. Most junk DNA consists of either inactive TEs, small simple repeats, or other heterogeneous sequences of uncertain origin (Gregory 2005a).
Though see (Griffiths et al. 2015) for a persuasive challenge—one different from the trajectory followed in this manuscript—to the notion that causal specificity in combination with actual difference making can uniquely and consistently pick out DNA as the most special and important cause when it comes to transcription and translation across different genes and organisms.
Here we follow Woodward (2010) in the sense that we do not offer these concepts as strict criteria for causation, but rather as features which—although they might not be necessary conditions which must pertain for a relationship to be causal—can nonetheless “play important roles in particular scientific contexts” (p. 288).
If causal specificity and reach are first-order properties, then causal efficacy is a second-order property of reach in combination with specificity.
Our use of the term ‘causal specificity’ refers to what Woodward (2010) calls the fine-grained influence conception of causal specificity, a conception inspired by Lewis’s notion of influence (Lewis 2000). But there is another candidate conception of causal specificity, one Woodward (2010) calls the one to one conception of causal specificity. Whereas the fine-grained influence conception of causal specificity picks out those causal variables which take on many distinct values corresponding to many distinct values in effect, the one to one conception of causal specificity picks out those causal variables which have solitary effects—in an only-one-cause, only-one-effect manner. As Woodward (2010) stresses, causes which are specific in this one to one sense can be powerful targets for intervention, precisely because of how clean-cut and controlled the effects of intervening on these causes can be. Our concept of causal reach acts as something of a counterpart to this one-to-one sense of causal specificity, since causal reach picks out those causal variables with extended and possibly even cascading effects—in an only-one-cause, yet-many-effects manner. Causes which have reach in this one-to-many sense can also be powerful targets for intervention, because of how sweeping and far-reaching the effects of intervening on these causes can be. Just as there is more than one sense of causal specificity, so too is there more than one sense of causal power (where power is here understood as tracking a cause’s prospects for acting as a target for intervention).
This does not necessarily mean that such causes have absolutely zero further, downstream effects—that the causal reach of such a change is nil. Woodward (2010) discusses the issue of causal proportionality, which pertains to choices of explanatory level and extent. All causal representations offered here are necessarily, selectively representative; they depict some details and ignore others.
In some cases, common codons are more rapidly decoded than rare codons, and thus the presence of certain codons can affect the rate at which a particular mRNA is translated. In bacteria, codon choice can even be selected for, in order to optimize the rate of production for certain proteins (Ermolaeva 2001). Even in mammalian cells, the use of different synonymous codons in certain mRNAs can have profound effects. For example, in mammalian actin mRNAs, the presence of particular rare codons can slow down protein synthesis, leading to the modification of the nascent actin polypeptide at a particular amino acid (Zhang et al. 2010). In the absence of such rare codons, the actin protein is synthesized very quickly, allowing it to fold and bury the amino acid before it can be modified.
This is not to say that now we have completely explained judgements of biological significance. For instance, this critique is being offered from within the selectionist framework. If we stepped outside of that framework, effects on fitness might become markedly less interesting and important. If we cared more about molecular differentiation and diversity, we might prioritize different casual or even non-causal features over specificity, reach, and efficacy. We thank our reviewers for drawing attention to this limitation of the paper’s framing.
This is like adding or losing a station at the end of the tuning dial.
There are of course other functional and non-functional DNA elements, not discussed here, with distinct combinations of causal specificity, reach, and efficacy. For example: promoters, telomeres, origins of replication, and genes for RNA molecules that directly impact a cell biological process (e.g., tRNA, rRNA). Although these DNA elements do not specify proteins directly, they nevertheless have precise downstream causal effects that are specific and efficacious. Some, such as tRNA genes, are very analogous, as they are transcribed into tRNAs which have specific folds based on their sequence and have roles in decoding mRNAs into proteins. A base change in this gene would lead to a transcriptional product that had a corresponding base change. This altered tRNA would likely have a profound change in its ability to decode mRNA into proteins. Other DNA elements, such as promoters, are not themselves copied into RNA, and hence do not appear to have specific causal effects, but they nevertheless influence how often and under what conditions nearby DNA sequences are transcribed into RNA. Base changes in promoters may alter how much and under what conditions the nearby genes are transcribed, thus their effects are quite efficacious. Considerations of space necessitate some limit to the molecular variety we showcase here.
In principle the mutational analysis of putative junk DNA has already been done. Given the number of humans alive today (7 × 109), the size of the diploid genome (6 × 109), and the fact that each person carries on the order of 100 de novo mutations each generation (Ségurel et al. 2014; Sung et al. 2016), this means that every base in the human genome has been altered in approximately 100 humans (with the exception of those alterations that are lethal). About 80–90% of these mutations are single nucleotide polymorphisms, with the rest (about 10–20%) being indels (Mills et al. 2006, 2011; Mullaney et al. 2010; Sung et al. 2016). Thus, every base in the human genome has been deleted de novo in 5–10 humans. In addition, individuals will also have indels inherited from their parents, so the overall number of mutations that each individual harbors is quite high, numbering over a thousand (Agrawal and Whitlock 2012). Suffice to say that by sequencing the genomes of all humans alive, we could determine which parts of the human genome can allow for alterations without compromising viability. Having said that, humans are diploid, so compromising a putative functional element in one copy of the genome is often alleviated by the presence of a second wildtype copy of the same element. This likely explains why most individuals carry many inactivating mutations in essential genes yet do not display any problems, likely because they have a second fully functional version of these defective genes (MacArthur et al. 2012).
Acknowledgements
We would like to thank Stefan Linquist and Ford Doolittle for organizing and inviting us to their workshop, Evolutionary Roles of Transposable Elements: The Science and the Philosophy, held in Halifax, Nova Scotia in October of 2018. We would also like to thank the other participants at that workshop for their valuable contributions. We are grateful to Adam Streed for producing our graphics. Finally, we additionally thank Stefan and Ford for their efforts as editors and reviewers of this special issue.
Author information
Author notes
Joyce C. Havstad and Alexander F. Palazzo are Co-first authors.
Authors and Affiliations
Department of Philosophy, Clinical and Translational Science Institute, Office of Research Integrity and Compliance, University of Utah, Salt Lake City, UT, USA
Joyce C. Havstad
Department of Biochemistry, University of Toronto, Toronto, ON, Canada
Corresponding authors
Ethics declarations
Conflict of interest
Additional information
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rights and permissions
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. | However, junk DNA is often quite causally inefficacious: despite that it can produce causally specific proximate effects, its cascading ultimate effects tend towards the non-specific. The constrained significance (for the organism) of junk DNA is not due to a total absence of causal specificity, but rather a limited reach for its causal specificity, and resulting limitations in its causal efficacy.
Junk DNA nonetheless contributes to the environment of the cell in which other, more traditionally functional entities exist. Total DNA levels control cell size, the amount of transcriptional noise, the number of transcription factor binding sites, the timing of cell division and likely many other aspects of the cellular environment. More paradigmatically functional entities of the cell have been tuned by natural selection to operate within this environment. This is especially true for quality control processes, which specifically evolve to deal with junk DNA and all its associated biochemical activity. On the one hand, and despite being an actual difference maker, junk DNA is not typically subject to organism-level natural selection. When non-functional DNA is mutated by natural processes, this does not alter the fitness of the organism sufficiently for natural selection to eliminate such mutations. For these reasons and given the way ‘function’ is predominantly understood in biology and philosophy of biology, junk DNA is typically conceived of as a non-functional entity. On the other hand, various components of cellular machinery exist precisely in order to deal with the effects of junk DNA, and the cellular workload is significantly affected by the need to (for instance) perform routine clean-up of the products of junk DNA transcription. If large swaths of junk DNA were eliminated, this would likely affect the fitness of the organism. Although such instances of widespread elimination of junk DNA are highly unlikely to naturally occur, such alterations could in principle could be performed in the lab. | yes |
Evolution | Can evolution explain the existence of 'junk DNA'? | yes_statement | "evolution" can "explain" the "existence" of '"junk" dna'. the "existence" of '"junk" dna' can be "explained" by "evolution" | https://www.icr.org/home/resources/resources_tracts_scientificcaseagainstevolution/ | The Scientific Case Against Evolution | The Institute for Creation ... | The Scientific Case Against Evolution
by Henry M. Morris, Ph.D.
Belief in evolution is a remarkable phenomenon. It is a belief passionately defended by the scientific establishment, despite the lack of any observable scientific evidence for macroevolution (that is, evolution from one distinct kind of organism into another). This odd situation is briefly documented here by citing recent statements from leading evolutionists admitting their lack of proof. These statements inadvertently show that evolution on any significant scale does not occur at present, and never happened in the past, and could never happen at all.
Evolution Is Not Happening Now
First of all, the lack of a case for evolution is clear from the fact that no one has ever seen it happen. If it were a real process, evolution should still be occurring, and there should be many "transitional" forms that we could observe. What we see instead, of course, is an array of distinct "kinds" of plants and animals with many varieties within each kind, but with very clear and -- apparently -- unbridgeable gaps between the kinds. That is, for example, there are many varieties of dogs and many varieties of cats, but no "dats" or "cogs." Such variation is often called microevolution, and these minor horizontal (or downward) changes occur fairly often, but such changes are not true "vertical" evolution.
Evolutionary geneticists have often experimented on fruit flies and other rapidly reproducing species to induce mutational changes hoping they would lead to new and better species, but these have all failed to accomplish their goal. No truly new species has ever been produced, let alone a new "basic kind."
A current leading evolutionist, Jeffrey Schwartz, professor of anthropology at the University of Pittsburgh, has recently acknowledged that:
. . . it was and still is the case that, with the exception of Dobzhansky's claim about a new species of fruit fly, the formation of a new species, by any mechanism, has never been observed.1
The scientific method traditionally has required experimental observation and replication. The fact that macroevolution (as distinct from microevolution) has never been observed would seem to exclude it from the domain of true science. Even Ernst Mayr, the dean of living evolutionists, longtime professor of biology at Harvard, who has alleged that evolution is a "simple fact," nevertheless agrees that it is an "historical science" for which "laws and experiments are inappropriate techniques"2 by which to explain it. One can never actually see evolution in action.
Evolution Never Happened in the Past
Evolutionists commonly answer the above criticism by claiming that evolution goes too slowly for us to see it happening today. They used to claim that the real evidence for evolution was in the fossil record of the past, but the fact is that the billions of known fossils do not include a single unequivocal transitional form with transitional structures in the process of evolving.
Given that evolution, according to Darwin, was in a continual state of motion . . . it followed logically that the fossil record should be rife with examples of transitional forms leading from the less to the more evolved.3
Even those who believe in rapid evolution recognize that a considerable number of generations would be required for one distinct "kind" to evolve into another more complex kind. There ought, therefore, to be a considerable number of true transitional structures preserved in the fossils -- after all, there are billions of non-transitional structures there! But (with the exception of a few very doubtful creatures such as the controversial feathered dinosaurs and the alleged walking whales), they are not there.
Instead of filling in the gaps in the fossil record with so-called missing links, most paleontologists found themselves facing a situation in which there were only gaps in the fossil record, with no evidence of transformational intermediates between documented fossil species.4
The entire history of evolution from the evolution of life from non-life to the evolution of vertebrates from invertebrates to the evolution of man from the ape is strikingly devoid of intermediates: the links are all missing in the fossil record, just as they are in the present world.
With respect to the origin of life, a leading researcher in this field, Leslie Orgel, after noting that neither proteins nor nucleic acids could have arisen without the other, concludes:
And so, at first glance, one might have to conclude that life could never, in fact, have originated by chemical means.5
Being committed to total evolution as he is, Dr. Orgel cannot accept any such conclusion as that. Therefore, he speculates that RNA may have come first, but then he still has to admit that:
The precise events giving rise to the RNA world remain unclear. . . . investigators have proposed many hypotheses, but evidence in favor of each of them is fragmentary at best.6
Translation: "There is no known way by which life could have arisen naturalistically." Unfortunately, two generations of students have been taught that Stanley Miller's famous experiment on a gaseous mixture, practically proved the naturalistic origin of life. But not so!
Miller put the whole thing in a ball, gave it an electric charge, and waited. He found that amino acids and other fundamental complex molecules were accumulating at the bottom of the apparatus. His discovery gave a huge boost to the scientific investigation of the origin of life. Indeed, for some time it seemed like creation of life in a test tube was within reach of experimental science. Unfortunately, such experiments have not progressed much further than the original prototype, leaving us with a sour aftertaste from the primordial soup.7
Neither is there any clue as to how the one-celled organisms of the primordial world could have evolved into the vast array of complex multi-celled invertebrates of the Cambrian period. Even dogmatic evolutionist Gould admits that:
The Cambrian explosion was the most remarkable and puzzling event in the history of life.8
Equally puzzling, however, is how some invertebrate creature in the ancient ocean, with all its "hard parts" on the outside, managed to evolve into the first vertebrate -- that is, the first fish-- with its hard parts all on the inside.
Yet the transition from spineless invertebrates to the first backboned fishes is still shrouded in mystery, and many theories abound.9
Other gaps are abundant, with no real transitional series anywhere. A very bitter opponent of creation science, paleontologist, Niles Eldredge, has acknowledged that there is little, if any, evidence of evolutionary transitions in the fossil record. Instead, things remain the same!
It is a simple ineluctable truth that virtually all members of a biota remain basically stable, with minor fluctuations, throughout their durations. . . .10
So how do evolutionists arrive at their evolutionary trees from fossils of oganisms which didn't change during their durations?
Fossil discoveries can muddle over attempts to construct simple evolutionary trees -- fossils from key periods are often not intermediates, but rather hodge podges of defining features of many different groups. . . . Generally, it seems that major groups are not assembled in a simple linear or progressive manner -- new features are often "cut and pasted" on different groups at different times.11
As far as ape/human intermediates are concerned, the same is true, although anthropologists have been eagerly searching for them for many years. Many have been proposed, but each has been rejected in turn.
All that paleoanthropologists have to show for more than 100 years of digging are remains from fewer than 2000 of our ancestors. They have used this assortment of jawbones, teeth and fossilized scraps, together with molecular evidence from living species, to piece together a line of human descent going back 5 to 8 million years to the time when humans and chimpanzees diverged from a common ancestor.12
Anthropologists supplemented their extremely fragmentary fossil evidence with DNA and other types of molecular genetic evidence from living animals to try to work out an evolutionary scenario that will fit. But this genetic evidence really doesn't help much either, for it contradicts fossil evidence. Lewin notes that:
The overall effect is that molecular phylogenetics is by no means as straightforward as its pioneers believed. . . . The Byzantine dynamics of genome change has many other consequences for molecular phylogenetics, including the fact that different genes tell different stories.13
Summarizing the genetic data from humans, another author concludes, rather pessimistically:
Even with DNA sequence data, we have no direct access to the processes of evolution, so objective reconstruction of the vanished past can be achieved only by creative imagination.14
Since there is no real scientific evidence that evolution is occurring at present or ever occurred in the past, it is reasonable to conclude that evolution is not a fact of science, as many claim. In fact, it is not even science at all, but an arbitrary system built upon faith in universal naturalism.
Actually, these negative evidences against evolution are, at the same time, strong positive evidences for special creation. They are, in fact, specific predictions based on the creation model of origins.
Creationists would obviously predict ubiquitous gaps between created kinds, though with many varieties capable of arising within each kind, in order to enable each basic kind to cope with changing environments without becoming extinct. Creationists also would anticipate that any "vertical changes" in organized complexity would be downward, since the Creator (by definition) would create things correctly to begin with. Thus, arguments and evidences against evolution are, at the same time, positive evidences for creation.
The Equivocal Evidence from Genetics
Nevertheless, because of the lack of any direct evidence for evolution, evolutionists are increasingly turning to dubious circumstantial evidences, such as similarities in DNA or other biochemical components of organisms as their "proof" that evolution is a scientific fact. A number of evolutionists have even argued that DNA itself is evidence for evolution since it is common to all organisms. More often is the argument used that similar DNA structures in two different organisms proves common evolutionary ancestry.
Neither argument is valid. There is no reason whatever why the Creator could not or would not use the same type of genetic code based on DNA for all His created life forms. This is evidence for intelligent design and creation, not evolution.
The most frequently cited example of DNA commonality is the human/chimpanzee "similarity," noting that chimpanzees have more than 90% of their DNA the same as humans. This is hardly surprising, however, considering the many physiological resemblances between people and chimpanzees. Why shouldn't they have similar DNA structures in comparison, say, to the DNA differences between men and spiders?
Similarities -- whether of DNA, anatomy, embryonic development, or anything else -- are better explained in terms of creation by a common Designer than by evolutionary relationship. The great differences between organisms are of greater significance than the similarities, and evolutionism has no explanation for these if they all are assumed to have had the same ancestor. How could these great gaps between kinds ever arise at all, by any natural process?
The apparently small differences between human and chimpanzee DNA obviously produce very great differences in their respective anatomies, intelligence, etc. The superficial similarities between all apes and human beings are nothing compared to the differences in any practical or observable sense.
Nevertheless, evolutionists, having largely become disenchanted with the fossil record as a witness for evolution because of the ubiquitous gaps where there should be transitions, recently have been promoting DNA and other genetic evidence as proof of evolution. However, as noted above by Roger Lewin, this is often inconsistent with, not only the fossil record, but also with the comparative morphology of the creatures. Lewin also mentions just a few typical contradictions yielded by this type of evidence in relation to more traditional Darwinian "proofs."
The elephant shrew, consigned by traditional analysis to the order insectivores . . . is in fact more closely related to . . . the true elephant. Cows are more closely related to dolphins than they are to horses. The duckbilled platypus . . . is on equal evolutionary footing with . . . kangaroos and koalas.15
There are many even more bizarre comparisons yielded by this approach.
The abundance of so-called "junk DNA" in the genetic code also has been offered as a special type of evidence for evolution, especially those genes which they think have experienced mutations, sometimes called "pseudogenes."16 However, evidence is accumulating rapidly today that these supposedly useless genes do actually perform useful functions.
Enough genes have already been uncovered in the genetic midden to show that what was once thought to be waste is definitely being transmitted into scientific code.17
It is thus wrong to decide that junk DNA, even the socalled "pseudogenes," have no function. That is merely an admission of ignorance and an object for fruitful research. Like the socalled "vestigial organs" in man, once considered as evidence of evolution but now all known to have specific uses, so the junk DNA and pseudogenes most probably are specifically useful to the organism, whether or not those uses have yet been discovered by scientists.
At the very best this type of evidence is strictly circumstantial and can be explained just as well in terms of primeval creation supplemented in some cases by later deterioration, just as expected in the creation model.
The real issue is, as noted before, whether there is any observable evidence that evolution is occurring now or has ever occurred in the past. As we have seen, even evolutionists have to acknowledge that this type of real scientific evidence for evolution does not exist.
A good question to ask is: Why are all observable evolutionary changes either horizontal and trivial (so-called microevolution) or downward toward deterioration and extinction? The answer seems to be found in the universally applicable laws of the science of thermodynamics.
Evolution Could Never Happen at All
The main scientific reason why there is no evidence for evolution in either the present or the past (except in the creative imagination of evolutionary scientists) is because one of the most fundamental laws of nature precludes it. The law of increasing entropy -- also known as the second law of thermodynamics -- stipulates that all systems in the real world tend to go "downhill," as it were, toward disorganization and decreased complexity.
This law of entropy is, by any measure, one of the most universal, bestproved laws of nature. It applies not only in physical and chemical systems, but also in biological and geological systems -- in fact, in all systems, without exception.
No exception to the second law of thermodynamics has ever been found -- not even a tiny one. Like conservation of energy (the "first law"), the existence of a law so precise and so independent of details of models must have a logical foundation that is independent of the fact that matter is composed of interacting particles.18
The author of this quote is referring primarily to physics, but he does point out that the second law is "independent of details of models." Besides, practically all evolutionary biologists are reductionists -- that is, they insist that there are no "vitalist" forces in living systems, and that all biological processes are explicable in terms of physics and chemistry. That being the case, biological processes also must operate in accordance with the laws of thermodynamics, and practically all biologists acknowledge this.
Evolutionists commonly insist, however, that evolution is a fact anyhow, and that the conflict is resolved by noting that the earth is an "open system," with the incoming energy from the sun able to sustain evolution throughout the geological ages in spite of the natural tendency of all systems to deteriorate toward disorganization. That is how an evolutionary entomologist has dismissed W. A. Dembski's impressive recent book, Intelligent Design. This scientist defends what he thinks is "natural processes' ability to increase complexity" by noting what he calls a "flaw" in "the arguments against evolution based on the second law of thermodynamics." And what is this flaw?
Although the overall amount of disorder in a closed system cannot decrease, local order within a larger system can increase even without the actions of an intelligent agent.19
This naive response to the entropy law is typical of evolutionary dissimulation. While it is true that local order can increase in an open system if certain conditions are met, the fact is that evolution does not meet those conditions. Simply saying that the earth is open to the energy from the sun says nothing about how that raw solar heat is converted into increased complexity in any system, open or closed.
The fact is that the best known and most fundamental equation of thermodynamics says that the influx of heat into an open system will increase the entropy of that system, not decrease it. All known cases of decreased entropy (or increased organization) in open systems involve a guiding program of some sort and one or more energy conversion mechanisms.
Evolution has neither of these. Mutations are not "organizing" mechanisms, but disorganizing (in accord with the second law). They are commonly harmful, sometimes neutral, but never beneficial (at least as far as observed mutations are concerned). Natural selection cannot generate order, but can only "sieve out" the disorganizing mutations presented to it, thereby conserving the existing order, but never generating new order. In principle, it may be barely conceivable that evolution could occur in open systems, in spite of the tendency of all systems to disintegrate sooner or later. But no one yet has been able to show that it actually has the ability to overcome this universal tendency, and that is the basic reason why there is still no bona fide proof of evolution, past or present.
From the statements of evolutionists themselves, therefore, we have learned that there is no real scientific evidence for real evolution. The only observable evidence is that of very limited horizontal (or downward) changes within strict limits.
Evolution Is Religion -- Not Science
In no way does the idea of particles-to-people evolution meet the long-accepted criteria of a scientific theory. There are no such evolutionary transitions that have ever been observed in the fossil record of the past; and the universal law of entropy seems to make it impossible on any significant scale.
Evolutionists claim that evolution is a scientific fact, but they almost always lose scientific debates with creationist scientists. Accordingly, most evolutionists now decline opportunities for scientific debates, preferring instead to make unilateral attacks on creationists.
Scientists should refuse formal debates because they do more harm than good, but scientists still need to counter the creationist message.20
The question is, just why do they need to counter the creationist message? Why are they so adamantly committed to anti-creationism?
The fact is that evolutionists believe in evolution because they want to. It is their desire at all costs to explain the origin of everything without a Creator. Evolutionism is thus intrinsically an atheistic religion. Some may prefer to call it humanism, and "new age" evolutionists place it in the context of some form of pantheism, but they all amount to the same thing. Whether atheism or humanism (or even pantheism), the purpose is to eliminate a personal God from any active role in the origin of the universe and all its components, including man.
The core of the humanistic philosophy is naturalism -- the proposition that the natural world proceeds according to its own internal dynamics, without divine or supernatural control or guidance, and that we human beings are creations of that process. It is instructive to recall that the philosophers of the early humanistic movement debated as to which term more adequately described their position: humanism or naturalism. The two concepts are complementary and inseparable.21
Since both naturalism and humanism exclude God from science or any other active function in the creation or maintenance of life and the universe in general, it is very obvious that their position is nothing but atheism. And atheism, no less than theism, is a religion! Even doctrinaire-atheistic evolutionist Richard Dawkins admits that atheism cannot be proved to be true.
Of course we can't prove that there isn't a God.22
Therefore, they must believe it, and that makes it a religion.
The atheistic nature of evolution is not only admitted, but insisted upon by most of the leaders of evolutionary thought. Ernst Mayr, for example, says that:
Darwinism rejects all supernatural phenomena and causations.23
A professor in the Department of Biology at Kansas State University says:
Even if all the data point to an intelligent designer, such a hypothesis is excluded from science because it is not naturalistic.24
It is well known by almost everyone in the scientific world today that such influential evolutionists as Stephen Jay Gould and Edward Wilson of Harvard, Richard Dawkins of England, William Provine of Cornell, and numerous other evolutionary spokesmen are dogmatic atheists. Eminent scientific philosopher and ardent Darwinian atheist Michael Ruse has even acknowledged that evolution is their religion!
Evolution is promoted by its practitioners as more than mere science. Evolution is promulgated as an ideology, a secular religion -- a full-fledged alternative to Christianity, with meaning and morality . . . . Evolution is a religion. This was true of evolution in the beginning, and it is true of evolution still today.25
Another way of saying "religion" is "worldview," the whole of reality. The evolutionary worldview applies not only to the evolution of life, but even to that of the entire universe. In the realm of cosmic evolution, our naturalistic scientists depart even further from experimental science than life scientists do, manufacturing a variety of evolutionary cosmologies from esoteric mathematics and metaphysical speculation. Socialist Jeremy Rifkin has commented on this remarkable game.
Cosmologies are made up of small snippets of physical reality that have been remodeled by society into vast cosmic deceptions.26
They must believe in evolution, therefore, in spite of all the evidence, not because of it. And speaking of deceptions, note the following remarkable statement.
We take the side of science in spite of the patent absurdity of some of its constructs, . . . in spite of the tolerance of the scientific community for unsubstantiated commitment to materialism. . . . we are forced by our a priori adherence to material causes to create an apparatus of investigation and set of concepts that produce material explanations, no matter how counterintuitive, no matter how mystifying to the uninitiated. Moreover, that materialism is absolute, for we cannot allow a Divine Foot in the door.27
The author of this frank statement is Richard Lewontin of Harvard. Since evolution is not a laboratory science, there is no way to test its validity, so all sorts of justso stories are contrived to adorn the textbooks. But that doesn't make them true! An evolutionist reviewing a recent book by another (but more critical) evolutionist, says:
We cannot identify ancestors or "missing links," and we cannot devise testable theories to explain how particular episodes of evolution came about. Gee is adamant that all the popular stories about how the first amphibians conquered the dry land, how the birds developed wings and feathers for flying, how the dinosaurs went extinct, and how humans evolved from apes are just products of our imagination, driven by prejudices and preconceptions.28
A fascinatingly honest admission by a physicist indicates the passionate commitment of establishment scientists to naturalism. Speaking of the trust students naturally place in their highly educated college professors, he says:
And I use that trust to effectively brainwash them. . . . our teaching methods are primarily those of propaganda. We appeal -- without demonstration -- to evidence that supports our position. We only introduce arguments and evidence that supports the currently accepted theories and omit or gloss over any evidence to the contrary.29
Creationist students in scientific courses taught by evolutionist professors can testify to the frustrating reality of that statement. Evolution is, indeed, the pseudoscientific basis of religious atheism, as Ruse pointed out. Will Provine at Cornell University is another scientist who frankly acknowledges this.
As the creationists claim, belief in modern evolution makes atheists of people. One can have a religious view that is compatible with evolution only if the religious view is indistinguishable from atheism.30
Once again, we emphasize that evolution is not science, evolutionists' tirades notwithstanding. It is a philosophical worldview, nothing more.
(Evolution) must, they feel, explain everything. . . . A theory that explains everything might just as well be discarded since it has no real explanatory value. Of course, the other thing about evolution is that anything can be said because very little can be disproved. Experimental evidence is minimal.31
Even that statement is too generous. Actual experimental evidence demonstrating true evolution (that is, macroevolution) is not "minimal." It is nonexistent!
The concept of evolution as a form of religion is not new. In my book, The Long War Against God,32 I documented the fact that some form of evolution has been the pseudo-rationale behind every anti-creationist religion since the very beginning of history. This includes all the ancient ethnic religions, as well as such modern world religions as Buddhism, Hinduism, and others, as well as the "liberal" movements in even the creationist religions (Christianity, Judaism, Islam).
As far as the twentieth century is concerned, the leading evolutionist is generally considered to be Sir Julian Huxley, primary architect of modern neo-Darwinism. Huxley called evolution a "religion without revelation" and wrote a book with that title (2nd edition, 1957). In a later book, he said:
Evolution . . . is the most powerful and the most comprehensive idea that has ever arisen on earth.33
Later in the book he argued passionately that we must change "our pattern of religious thought from a God-centered to an evolution-centered pattern."34 Then he went on to say that: "The God hypothesis . . . is becoming an intellectual and moral burden on our thought." Therefore, he concluded that "we must construct something to take its place."35
That something, of course, is the religion of evolutionary humanism, and that is what the leaders of evolutionary humanism are trying to do today.
In closing this survey of the scientific case against evolution (and, therefore, for creation), the reader is reminded again that all quotations in the article are from doctrinaire evolutionists. No Bible references are included, and no statements by creationists. The evolutionists themselves, to all intents and purposes, have shown that evolutionism is not science, but religious faith in atheism. | The duckbilled platypus . . . is on equal evolutionary footing with . . . kangaroos and koalas.15
There are many even more bizarre comparisons yielded by this approach.
The abundance of so-called "junk DNA" in the genetic code also has been offered as a special type of evidence for evolution, especially those genes which they think have experienced mutations, sometimes called "pseudogenes. "16 However, evidence is accumulating rapidly today that these supposedly useless genes do actually perform useful functions.
Enough genes have already been uncovered in the genetic midden to show that what was once thought to be waste is definitely being transmitted into scientific code.17
It is thus wrong to decide that junk DNA, even the socalled "pseudogenes," have no function. That is merely an admission of ignorance and an object for fruitful research. Like the socalled "vestigial organs" in man, once considered as evidence of evolution but now all known to have specific uses, so the junk DNA and pseudogenes most probably are specifically useful to the organism, whether or not those uses have yet been discovered by scientists.
At the very best this type of evidence is strictly circumstantial and can be explained just as well in terms of primeval creation supplemented in some cases by later deterioration, just as expected in the creation model.
The real issue is, as noted before, whether there is any observable evidence that evolution is occurring now or has ever occurred in the past. As we have seen, even evolutionists have to acknowledge that this type of real scientific evidence for evolution does not exist.
A good question to ask is: Why are all observable evolutionary changes either horizontal and trivial (so-called microevolution) or downward toward deterioration and extinction? The answer seems to be found in the universally applicable laws of the science of thermodynamics.
Evolution Could Never Happen at All
The main scientific reason why there is no evidence for evolution in either the present or the past (except in the creative imagination of evolutionary scientists) is because one of the most fundamental laws of nature precludes it. | no |
Evolution | Can evolution explain the existence of 'junk DNA'? | yes_statement | "evolution" can "explain" the "existence" of '"junk" dna'. the "existence" of '"junk" dna' can be "explained" by "evolution" | https://wi.mit.edu/news/human-genome-project-ten-vignettes-stories-genomic-discovery | The Human Genome Project TEN VIGNETTES: Stories of Genomic ... | Secondary Menu
The Human Genome Project TEN VIGNETTES: Stories of Genomic Discovery
1. THE BREATHTAKING LANDSCAPE OF THE HUMAN GENOME
Like early explorers catching the first glimpse of a new and unexplored land, scientists are getting their first look at the uncharted territory of the human genome. But unlike their predecessors, these 21st century explorers have a distinct advantage — a bird’s-eye view of the entire landscape. The view, according to these genomic explorers, is no less than awe-inspiring!
"The distribution of genes on mammalian chromosomes is uneven, making for a striking appearance," said Bob Waterston, Director of the Genome Center at Washington University in St. Louis. "In some regions, genes are crowded together much like buildings in urban centers. In other areas, genes are spread over the vast expanses like farmhouses on the prairie. And then there are large tracts of desert, where only non-coding ‘junk DNA’ can be found. Each region tells a unique story about the history of our species and what makes us tick."
This landscape contrasts starkly with the genomes of many other organisms, such as the mustard weed, the worm, and the fly. Their genomes more closely resemble uniform, sprawling suburbs, with genes relatively evenly spaced along chromosomes.
The human genome’s gene-dense urban centers are predominantly composed of the DNA building blocks G and C and are called "GC-rich regions." In contrast, the junk-DNA deserts are AT rich. GC- and AT-rich regions can actually be seen through a microscope as light and dark bands on chromosomes.
On each human chromosome, there are large and noticeable swings in GC content; one stretch might have 60 percent while an adjacent stretch might have only 30 percent. These swings could never occur randomly and represent a definite organization of "neighborhoods" with local accents.
The urban centers contain a ten-fold higher density of genes than the deserts. "It is as though a détente has been established between genes and the long, repeating segments of junk DNA — a treaty whereby certain repeat elements have agreed to occupy the deserts, leaving the cities for the genes," says Eric Lander, the Director of the Whitehead Institute Center for Genome Research.
Another interesting feature is that so-called "HOX gene clusters," which play an important role in development, are never invaded by junk DNA. This suggests that evolution has a reason for retaining the integrity of these gene clusters.
Near the gene cities are neighboring regions of the dinucleotide CpG — stretches of up to 30,000 letters with only two bases, C and G, repeating over and over. Usually underrepresented throughout the genome, many CpG regions help regulate gene function.
2. THE BILLION-DOLLAR QUESTION: HOW MANY GENES ARE THERE?
Predictions regarding the number of genes in the human genome have been as variable as the biotech index in the NASDAQ, with estimates ranging anywhere from 20,000 to 120,000 genes.
Ending this decade-long period of wild speculation, the international consortium now reports that they have arrived at a more accurate and stable estimate. They have concluded that the genome contains between 30,000 and 35,000 genes. Although small gaps in the human genome sequence must be filled before scientists can arrive at an exact number, they now have almost all of the data they need to make an accurate projection.
This news represents a humbling reality check for those who have long harbored hubris about the number of genes in humans. The new estimate indicates that humans have only twice as many genes as the worm or the fly! How can human complexity be explained by a genome with such a paucity of genes? It turns out humans are very thrifty with their genes, able to do more with what they have than other species. Instead of producing only one protein per gene, human genes can produce several different proteins.
Humans use a process called "alternative splicing," in which different parts of a protein can be rearranged as needed–much like parts of tinker toys–to make different proteins from the same basic components. Alternative splicing is possible because human genes are spread out over large regions of genomic DNA, and regions that code for proteins are not necessarily continuous, allowing one gene to code for different parts of a protein. On the average, each human gene probably makes three proteins, more than worms and flies do.
Because genes comprise a tiny fraction of the human genome, they are the most challenging to identify in the genome sequence. Thus, the predicted genes and protein sets described by scientists are not final; they will continue to be fine- tuned as better gene-finding tools are developed.
The low number of genes comes as good news for scientists in academia and pharmaceutical companies. Gene hunters who want to compile a compendium of all genes, and pharmaceutical companies looking for finite numbers of drug targets, have just had their work, time, and expense cut significantly.
3. REINVENTING THE WHEEL
Why reinvent the wheel when you’ve got a strategy that works? Evolution certainly seems to operate that way, especially where human proteins are concerned.
The full set of proteins (the proteome) encoded by the human genome is more complex than those of invertebrates largely because vertebrates have rearranged old protein domains into a richer collection of new architectures. In other words,
Humans have achieved innovations by rearranging and expanding tried-and-true strategies from other species — not by developing novel strategies of their own. "The cheapest way to invent something new is to take a good invention and tweak it to suit a new purpose," says Sir John Sulston, Former Director of the Sanger Centre.
Another way we humans innovate is by expanding protein families. Scientists report that some 60 percent of protein families in humans are superfamilies, with more family members than in any of the other four sequenced organisms. This suggests that gene duplication has been a major evolutionary force during vertebrate evolution.
Many of the families that have undergone expansions in humans are involved in distinctive aspects of vertebrate physiology. One example is the family of immunoglobulin (Ig) domains, first identified in antibodies thirty years ago. Classic Ig domains are absent from the yeast and the mustard weed. In vertebrates, the Ig repertoire includes a wide range of immune functions and is a testament to the notion that a single family of proteins can be extremely versatile, mounting a multi-pronged, orchestrated response to infection.
Another example of a family that has proliferated in humans is epithelial proteins such as keratin. This protein family probably grew to support and line the various organs in humans, including the lining of the small intestine and cilia in the inner ear.
Finally, at least some families of genes in the human genome seem to be shrinking. More than half of our smell receptors seem to be broken. This is curious, given that smell receptors belong to one of the biggest gene families (with more than 1000 members). It seems that despite the high priority given to smell by our vertebrate ancestors, humans seem to have lost their dependence on it. Smell was key to survival in our vertebrate ancestors, but for us, vision is probably more important for survival.
4. YES, IT’S JUNK, BUT IT’S NOT GARBAGE
Only a tiny fraction, about 1.5 percent, of the human genome is comprised of protein-coding regions of the genome. The vast majority of the genome–more than 50 percent–consists of repetitive sequences, or "junk DNA," that have been hopping around the genome for 3 billion years.
Junk DNA has helped scientists come to terms with one of the human genome’s most perplexing paradoxes–that our genome is 200 times larger than that of baker’s yeast but 200 times smaller than that of amoeba! Scientists chalked up this discrepancy in genome sizes to the existence of junk DNA collecting in organisms and the lack of routine housecleaning. Even so, scientists didn’t fully appreciate the value of junk DNA–until now.
Junk DNA represents a rich fossil record of clues to our evolutionary past. It is possible to date groups of repeats to when in the evolutionary process they were "born" and to follow their fates in different regions of the genome or in different species. The HGP scientists used 3 million such elements as dating tools.
Based on such "DNA dating," scientists can build family trees of the repeats, showing exactly where they came from and when. These repeats have reshaped the genome by rearranging it, creating entirely new genes, and modifying and reshuffling existing genes.
Calculating the evolutionary age of the repeat elements in the human genome has turned up a wealth of interesting, shocking, and curious facts about the stuff that we are made of (see next two vignettes for details).
5. JUST BLAME IT ON OUR PACK-RAT MENTALITY
One of the most interesting aspects of the repeat elements is that as a species, we humans seem to have a tendency to be pack-rats–in stark contrast to other organisms. The amount of junk we’ve accumulated in our genome far exceeds those collected by our early evolutionary cousins (with the amoeba being a notable exception).
We have a greater percentage of repeats in our genomes–50 percent–than the mustard weed (11 percent), the worm (7 percent) or the fly (3 percent). Also, our repeat elements are much older–actually, really ancient–when compared to those found in the other organisms.
"This suggests that we haven’t been fastidious with our house-cleaning. We have been slow to clean out our drawers, closets, or attics," says Arian Smit, bioinformatics scientist at the Institute for Systems Biology. When we calculate the half-life of some of these elements, we find that while the fly did its last house-cleaning 12 million years ago, mammals last cleaned house 800 million years ago. These features of the human genome probably apply to all mammals.
6. THE SHOCKER: DRAMATIC DECREASE IN REPEATS
But one feature–shockingly–does not. It seems that there has been a dramatic decrease in repeats in the human genome over the past 50 million years. It’s as if we decided 50 million years ago to stop collecting junk. In contrast, there seems to be no such decline in repeats in rodents.
What’s more, it seems as though some of our really ancient junk is extinct and some other junk is teetering on the brink of extinction. But these extinct or near-extinct repeats --called DNA transposons and LTR retroposons, respectively--are alive and kicking in the mouse genome. The contrast between human and mouse genomes suggests that the extinction or near extinction of these repeat elements may be accounted for by some fundamental differences between hominids and rodents.
"Population structure and dynamics would seem to be likely suspects," says Eric Lander, Director, Whitehead Genome Center. "Rodents tend to have large populations, whereas hominid populations are typically small and may undergo frequent bottlenecks. Also responsible may be such factors as inbreeding and genetic drift, Lander continued." Scientists hope that further studies will shed more light on these differences.
7. SOLVED: MYSTERY OF THE ALU
And now comes the curious story about one repeat element, a phenomenon researchers call "the mystery of the Alu." This mystery revolves around how the repeat element SINE Alu, known to be a "second-class citizen" of the human genome, found its way into the fancy neighborhoods of the human genome.
Repeat elements, or junk DNA, in the human genome come in four varieties: the "extinct" type (DNA transposons), the near-extinct type (the LTR retroposons), and two other types that still are active in the human genome (LINE elements and SINE elements).
When researchers looked at the distribution of these elements by GC content (or gene-rich neighborhoods), they found a pattern that, at first glance, defied logic and baffled them.
Most repeat elements–second-class citizens in a kingdom where genes rule–wind up in less desirable neighborhoods in the genome–regions that are AT rich and GC poor. But SINE elements seem to have landed in the really fancy neighborhoods of the genome–the regions that are gene rich.
Scientists reckoned there were two possible explanations. One is that the wily SINEs somehow trick their way into the GC-rich neighborhoods. The other hypothesis is that most SINEs land in GC-poor neighborhoods to begin with, and evolution favors the SINEs that happened to land in GC-rich real estate.
The scientists used the draft genome sequence to investigate this mystery by comparing the proclivities of young, adolescent, middle-aged and old Alus. Strikingly, young Alus live in the AT-rich regions and progressively older Alus have a tendency to move up to the GC-rich neighborhoods.
As a result, the latter hypothesis that evolution cares about putting the SINEs near genes must be right. Over the years, SINE elements have acquired a bad reputation among scientists for what looked like parasitic behavior. But this reputation may be unjustified; it appears that SINE elements have remained in the genome over time because they are helpful symbiots that earn their keep in the genome.
8. FAST LIVING ON THE Y CHROMOSOME
The human genome sequence, with its large database of repeats elements, provides a powerful resource for addressing the unusual history of the Y chromosome.
By dating the 3 million repeat elements and examining the pattern of interspersed repeats on Y chromosome, scientists estimated the relative mutation rates in the X and the Y chromosomes and in the male and female germ lines. They found that there are twice as many mutations in males than in females.
To do this, scientists identified the repeat elements from recent subfamilies (effectively, birth cohorts dating from the past 50 million years) and measured the substitution rates for subfamily members on the X and the Y chromosomes. They found that the ratio of mutations in males versus female is 2:1.
Scientists point to several possible reasons for the higher mutation rate in the male germ line, including the fact that there are a greater number of cell divisions involved in the formation of sperm than eggs and the existence of different repair mechanisms in sperm and eggs.
9. HORIZONTAL TRANSFER: BACTERIA BEARING GIFTS
Using a molecular fossil dig of the human genome sequence, scientists have uncovered remnants of an ancient migration that occurred within our early vertebrate ancestors. These ancestors had few defense systems against invading parasites, so bacteria could take residence inside the vertebrate host. Some time during the cohabitation of host and parasite, ancient genes were exchanged between the two. Scientists speculate that the genes may have been left behind by the bacterial invaders or transported into the genome by viral intermediaries, although they can’t entirely rule out the possibility that bacteria stole genes from the vertebrate ancestors.
Scientists have identified more than 200 genes in the human genome whose closest relatives are in bacteria. Analogous genes are not found in invertebrates, such as the worm, fly, and yeast. This suggests that these genes were acquired at a more recent evolutionary moment, perhaps after the birth of vertebrates. Most probably, infections led to a transfer of DNA from bacteria to the chromosomes of a human ancestor. Scientists didn’t find any single bacterial source for the transferred genes, indicating that several independent gene transfers from different bacteria occurred.
This process, called horizontal transfer, is unlikely to happen today because human eggs and sperm, which pass DNA on to the next generation, are isolated from the outside world, and humans have highly developed immune systems to guard against foreign invaders.
But here’s the kicker! Many of the transferred genes are far from trivial and appear to be involved in important physiological functions, which may have provided a survival advantage for vertebrate ancestors. As a result, these genes have been maintained in the human genome over evolution. For instance, monoamine oxidase (MAO), an enzyme that is important in processing neurotransmitters, is involved in psychiatric disorders. Other important acquisitions include RAG1 and RAG2, enzymes critical to the immune system’s antibody response.
10. SNP MAP: COMPANION VOLUME TO THE BOOK OF LIFE
The Book of Life, the human genome sequence, is analogous to a basic parts list for the human species, because human beings are 99.9 percent similar. But that 0.1 percent difference–one in every 1,000 letters–contributes to our individuality, and taken as a whole, can explain the genetic basis of disease.
In a companion volume to the Book of Life, scientists have created a catalogue of 1.4 million single-letter differences, or single nucleotide polymorphisms (SNPs)–with their exact location in the human genome. This SNP map, the word’s largest publicly available catalogue of SNPs, promises to revolutionize both mapping diseases and tracing human history
Without the SNP map, scientists studying a disease gene had to go through a laborious, time consuming, and costly process of comparing the genomes of many individuals and finding a set of SNPs within the gene of interest. . Now, a scientist studying a disease gene can first turn to the SNP map to find the gene variations. Since the average gene is about 30,000 letters long, many SNPs can be identified in a typical gene in one short computer session.
"We are using the SNP map in everyday science already. Last month, we were able to ask, ‘does a gene that affects how much testosterone is produced by the body affect prostate cancer risk?’ We pulled 15 SNPs off the web, and typed them in our patients. The 15 SNPs came in only four combinations. So that gene can now be reduced to four flavors. The whole process took about two weeks, whereas before it would have been a massive project, costly project," explains David Altshuler, a Research Scientist at the Whitehead Genome Center.
The SNP map goes beyond being a reference for disease genes and answers questions about the history of human populations. It supports an existing population- genetics model that postulates that a very small number of people expanded rapidly to populate the whole earth in the last 10,000 to 100,000 years.
Supporting the prediction, scientists report that SNPs aren’t evenly distributed and concentrations vary widely throughout the human genome. Some areas of the genome are SNP deserts without a single SNP, while others have a great number. Areas with few SNPs may result from evolution selecting one form of a gene to be maintained throughout time. For example, little variation is seen in the X chromosome. But the HLA region, which codes for proteins on the surface of blood cells that elicit the strongest immune response, has a lot of diversity.
The current SNP map results from the combined efforts of International Human Genome Sequencing Consortium and The SNP Consortium. The SNPs Consortium is an unusual public/private partnership between academic institutions, pharmaceutical companies, and charities, to create a map that would be available to the public without charge. The consortium has far outperformed its original goal of discovering 300,000 SNPs by April of 2001. The catalogue of 1.4 million SNPs is not a complete set of all the SNPs in the genome, but it is more than enough to enable genetic studies that were not possible before.
THE GENOME ANALYSIS GROUP
In April of 1999, the Human Genome Project put together a group called the hard-core analysis group. Chaired by Eric Lander, Director of the Whitehead Institute Center for Genome Research, this group was composed of 40 analysts, including experts in a diverse array of genomic topics, such as proteins, genes, gene assembly, evolution, and repeat elements.
The group pored over the sequence data for six solid months, and over weekly conference calls and meetings at Whitehead and in Philadelphia, began to conduct the initial analysis of the human genome sequence. Meanwhile, a group at the University of Santa Cruz assembled the genome sequence into a "goldenpath"–a tongue-in—cheek reference to the fact that this was still an imperfect sequence.
The genome analysis group represented the largest group of sequence analysts pulled together for any task. E-mails flew back and forth–5,000 in all–across three continents and seven countries. By Thanksgiving of 2000, the group had its analysis together.
The group began writing the Nature paper in October and submitted it in December. Lander compares the task to writing a travel guide to the U.S. for which the editor needed to pull together a diverse set of experts. They needed some who, in essence, could write authoritatively about white water rafting on the Colorado River and others who knew the ins and outs of clubbing in Greenwich Village, in New York.
"We needed someone to describe the history of Route 66 and others to talk about cruising Sixth Avenue. We needed someone to paint the big picture descriptions of topographic features like the Rocky Mountains, and also someone to give us food reviews of hole-in-the-wall restaurants in San Francisco," says Lander, Director, Whitehead Genome Center. "It was a challenge, but it was also a heck of a lot of fun."
For a complete list of the Genome Analysis Group members, refer to the Nature paper.
Scientists turned cutting-edge CRISPR and single-cell sequencing tools on human cytomegalovirus, which affects around half of all adults, illuminating interactions between viral and host genes and adding to the list of possible drug targets.
A new screening method from the labs of Whitehead Institute Member Jonathan Weissman, Britt Adamson at Princeton University, and Editas Medicine provides a deeper look at how cells repair DNA damage. The method could help researchers assess the action of new gene editing methods. | 4. YES, IT’S JUNK, BUT IT’S NOT GARBAGE
Only a tiny fraction, about 1.5 percent, of the human genome is comprised of protein-coding regions of the genome. The vast majority of the genome–more than 50 percent–consists of repetitive sequences, or "junk DNA," that have been hopping around the genome for 3 billion years.
Junk DNA has helped scientists come to terms with one of the human genome’s most perplexing paradoxes–that our genome is 200 times larger than that of baker’s yeast but 200 times smaller than that of amoeba! Scientists chalked up this discrepancy in genome sizes to the existence of junk DNA collecting in organisms and the lack of routine housecleaning. Even so, scientists didn’t fully appreciate the value of junk DNA–until now.
Junk DNA represents a rich fossil record of clues to our evolutionary past. It is possible to date groups of repeats to when in the evolutionary process they were "born" and to follow their fates in different regions of the genome or in different species. The HGP scientists used 3 million such elements as dating tools.
Based on such "DNA dating," scientists can build family trees of the repeats, showing exactly where they came from and when. These repeats have reshaped the genome by rearranging it, creating entirely new genes, and modifying and reshuffling existing genes.
Calculating the evolutionary age of the repeat elements in the human genome has turned up a wealth of interesting, shocking, and curious facts about the stuff that we are made of (see next two vignettes for details).
5. JUST BLAME IT ON OUR PACK-RAT MENTALITY
One of the most interesting aspects of the repeat elements is that as a species, we humans seem to have a tendency to be pack-rats–in stark contrast to other organisms. | yes |
Evolution | Can evolution explain the existence of 'junk DNA'? | yes_statement | "evolution" can "explain" the "existence" of '"junk" dna'. the "existence" of '"junk" dna' can be "explained" by "evolution" | https://www.frontiersin.org/articles/10.3389/fgene.2015.00002 | Non-coding RNA: what is functional and what is junk? - Frontiers | HYPOTHESIS AND THEORY article
Non-coding RNA: what is functional and what is junk?
Department of Biochemistry, University of Toronto, Toronto, ON, Canada
The genomes of large multicellular eukaryotes are mostly comprised of non-protein coding DNA. Although there has been much agreement that a small fraction of these genomes has important biological functions, there has been much debate as to whether the rest contributes to development and/or homeostasis. Much of the speculation has centered on the genomic regions that are transcribed into RNA at some low level. Unfortunately these RNAs have been arbitrarily assigned various names, such as “intergenic RNA,” “long non-coding RNAs” etc., which have led to some confusion in the field. Many researchers believe that these transcripts represent a vast, unchartered world of functional non-coding RNAs (ncRNAs), simply because they exist. However, there are reasons to question this Panglossian view because it ignores our current understanding of how evolution shapes eukaryotic genomes and how the gene expression machinery works in eukaryotic cells. Although there are undoubtedly many more functional ncRNAs yet to be discovered and characterized, it is also likely that many of these transcripts are simply junk. Here, we discuss how to determine whether any given ncRNA has a function. Importantly, we advocate that in the absence of any such data, the appropriate null hypothesis is that the RNA in question is junk.
At present, the distinction between functional ncRNAs and junk RNA appears to be quite vague. There has been, however, some effort to differentiate between these two groups, based on various criteria ranging from their expression levels and splicing to conservation. Ultimately these efforts have failed to bring consensus to the field.
A similar problem has plagued the investigation of whether transposable elements (TEs), which make up a significant proportion of most vertebrate genomes, have been exapted for the benefit of the host organism. Although some have claimed that many TEs are functional, a few groups have offered a much more balanced view that is in line with our current understanding of molecular evolution (de Souza et al., 2013; Elliott et al., 2014).
In this article we explain several concepts that researchers must keep in mind when evaluating whether a given ncRNA has a function at the organismal level. Importantly, the presence of low abundant non-functional transcripts is entirely consistent with our current understanding of how eukaryotic gene expression works and how the eukaryotic genome is shaped by evolution. With this in mind, researchers should take the approach that an uncharacterized non-coding RNA likely has no function, unless proven otherwise. This is the null hypothesis. If a given ncRNA has supplementary attributes that would not be expected to be found in junk RNA, then this would provide some evidence that this transcript may be functional.
The Amount of Various RNA Species in the Typical Eukaryotic Cell
As is evident from a number of sources, almost all of the human genome is transcribed. However, one must not confuse the number of different types of transcripts with their abundance in a typical cell. Many of the putative functional ncRNAs are present at very low levels and thus unlikely to be of any importance with respect to cell or organismal physiology. Importantly, the abundance of an ncRNA species roughly correlates with its level of conservation (Managadze et al., 2011), which is a good proxy for function (Doolittle et al., 2014; Elliott et al., 2014; however, see below); thus, determining the relative abundance of a given ncRNA in the relevant cell type is an important piece of information. However, one should keep in mind that if the ncRNA has catalytic activity or if it acts as a scaffold to regulate chromosomal architecture near its site of transcription, the RNA may not need to be present at very high levels to be able to perform its task.
At steady state, the vast majority of human cellular RNA consists of rRNA (∼90% of total RNA for most cells, see Table 1 and Figure 1). Although there is less tRNA by mass, their small size results in their molar level being higher than rRNA (Figure 1). Other abundant RNAs, such as mRNA, snRNA, and snoRNAs are present in aggregate at levels that are about 1–2 orders of magnitude lower than rRNA and tRNA (Table 1 and Figure 1). Certain small RNAs, such as miRNA and piRNAs can be present at very high levels; however, this appears to be cell type dependent.
TABLE 1
TABLE 1. Estimates of total RNA content in mammalian cells.
FIGURE 1
FIGURE 1. Estimate of RNA levels in a typical mammalian cell. Proportion of the various classes of RNA in mammalian somatic cells by total mass (A) and by absolute number of molecules (B). Total number of RNA molecules is estimated at roughly 107 per cell. Other ncRNAs in (A) include snRNA, snoRNA, and miRNA. Note that due to their relatively large sizes, rRNA, mRNA, and lncRNAs make up a larger proportion of the mass as compared to the overall number of molecules.
By general convention, most other ncRNAs longer than 200 nucleotides, regardless of whether or not they have a known function, have been lumped together into a category called “long non-coding RNAs” (lncRNAs). As a whole, these are present at levels that are two orders of magnitude less than total mRNA (Table 1). Although the estimated number of different types of human lncRNAs has ranged from 5,400 to 53,000 (Table 2), only a small fraction have been found to be present at levels high enough to suggest that they have a function. According to ENCODE’s own estimates, fewer than 1,000 lncRNAs are present at greater than one copy per cell in the typical human tissue culture cell line (Djebali et al., 2012; Palazzo and Gregory, 2014), although some other estimates have determined that the levels may be substantially higher (Hangauer et al., 2013). One caveat with the data collected thus far is that some of these lncRNAs may have a very restricted expression pattern; therefore until the relevant cell type is tested, we may not be in a position to judge whether it is expressed at a sufficient level to provide evidence of functionality. It is also worthwhile noting that certain annotated lncRNAs may actually encode short functional peptides (Ingolia et al., 2011, 2014; Magny et al., 2013; Bazzini et al., 2014), although in general lncRNAs are poorly translated (Bánfai et al., 2012; Guttman et al., 2013; Hangauer et al., 2013). Finally, it is also worth pointing out that a significant fraction of these lncRNAs may actually be misannotated untranslated regions of known mRNAs (Miura et al., 2013).
TABLE 2
TABLE 2. Estimate number of human ncRNAs from various sources.
Other short ncRNAs have been lumped into several groups, depending on their attributes. For example, several regions of the human genome that are believed to be enhancers, are transcribed into short enhancer RNAs (eRNAs). These are thought to act as scaffolds that regulate the 3D architecture of chromosomes in the vicinity of their transcription site (Lai et al., 2013). eRNAs are typically present at even lower levels than lncRNAs (Djebali et al., 2012; Andersson et al., 2014); however, if these play a localized structural role, then they would be expected to be present at only a few copies per cell.
In addition to all of the mentioned species, ENCODE and other groups have found transcripts that map to the rest of the genome termed “intergenic RNA” (Djebali et al., 2012). Most of these transcripts are present at levels that are significantly below one copy per cell (Djebali et al., 2012; Palazzo and Gregory, 2014). Again this arbitrary division of ncRNAs has led to much confusion. It is unclear why these transcripts are considered to be intergenic if they are also functional (as in 80% of the genome is functional); after all, if a region of DNA that is transcribed into a functional product is called a gene, then the term intergenic would automatically imply that these regions have no function.
Regardless of these concerns, it is clear that most of the ncRNAs in question (lncRNAs, eRNAs, circular RNAs, intergenic RNAs, etc.) are typically present at very low levels when compared to known functional RNAs. These observations are consistent with the idea that the eukaryotic genome produces a vast amount of spurious transcripts.
Where Do All These ncRNAs Come From?
As of spring 2014, the LNCipedia website1 (Volders et al., 2013) has compiled a list of ∼21,000 human lncRNAs, with an average length of about 1 kb (Table 2). These would originate from <1% of the human genome. Needless to say, this is a very small fraction of the total. Even if we compiled all of the putative lncRNAs using the most optimistic analysis (Managadze et al., 2013), all the putative lncRNAs would still be transcribed from at most 2% of the genome (Table 2). Thus far, only a small minority of lncRNAs have been shown to be important for organismal development, cell physiology, and/or homeostasis. As of December 2014, the LncRNA Database2, a repository of lncRNAs “curated from evidence supported by the literature,” lists only 166 biologically validated lncRNAs in humans (Quek et al., 2014). Additionally there are so called eRNAs, which according to FANTOM5 come from an additional 43,000 loci. However, at an average length of ∼250 nucleotides they would be made from ∼0.34% of the human genome (Andersson et al., 2014). Again, these are very small numbers.
In summary, our best candidates for novel functional ncRNAs (lncRNAs, eRNAs) arise from only a minute fraction of the genome. Again it appears that the vast majority of the genome that falls outside of these loci is transcribed into junk RNA that is present at very low levels at steady state.
Biochemical Support for Junk RNA
It is important to recognize that the pervasive transcription associated with the human genome is entirely consistent with our understanding of biochemistry. Although RNA polymerases prefer to start transcription at promoter regions, they do have a low probability of initiating transcription on any accessible DNA (Struhl, 2007; Tisseur et al., 2011). Indeed it has been observed that most nucleosome-free DNA is transcribed in vivo (Cheung et al., 2008) and that many random pieces of DNA can promote transcription by recruiting transcription factors [TFs; see figure S4 in White et al. (2013)].
Of course eukaryotic cells limit the amount of inappropriate transcription by packaging intergenic regions into heterochromatin. This shields the DNA from both RNA polymerases and TFs which can bind to DNA and activate adjacent cryptic transcriptional start sites. The formation of these heterochromatic regions is largely dictated by a complicated array of DNA elements that initiate and restrict chromatin packing. However, there is quite a bit of data that supports the notion that heterochromatin formation is not always strictly regulated or enforced. For example, it has been shown that many heterochromatic regions are transcriptionally active, albeit at a low level (Moazed, 2009), suggesting that either heterochromatin is periodically loosened, or that under certain circumstances RNA polymerases can transcribe these tightly packed regions. Another line of evidence that suggests that heterochromatin formation is not strictly regulated comes from the investigation of TF binding sites. In particular, it has been observed that most TF binding sites which are occupied by TF proteins are not conserved between highly related species (Paris et al., 2013) and that many TF binding events have little to no impact on the expression of nearby genes (Li et al., 2008; Biggin, 2011; Lickwar et al., 2012; Paris et al., 2013). In other words, many putative TF binding sites are created and destroyed by neutral evolution and do not appear to contribute to the expression of functional parts of the genome. These TF binding sites are nonetheless accessible to TF proteins, and thus are not found in heterochromatin.
From the above discussion it is clear that there are many sources for cryptic transcription in eukaryotic genomes. Consistent with this idea, it was found that nascent RNA polymerase II transcripts from mouse liver cells generate a fair amount of transcripts that map to unannotated genomic regions (Menet et al., 2012). When these nascent transcripts were analyzed by next generation sequencing, the number of reads that mapped to intergenic regions (i.e., unannotated parts of the genome) was equal to those mapping to known exonic regions (Menet et al., 2012). Thus it appears that transcription in mammalian cells is quite non-specific.
Thus it appears that transcription in eukaryotes is very messy, but that much of the junk RNA is removed by quality control mechanisms. This view is completely in line with what is known about the biochemistry underlying eukaryotic gene expression.
Evolutionary Support for Junk RNA
Ultimately to understand how TF binding sites, heterochromatin domains, and transcriptional start sites are created and destroyed within the genome, one needs to take into consideration certain concepts that have been derived from the field of population genetics.
One of the most fundamental discoveries in population genetics came from the work of Kimura, Ohta, King and Jukes. They showed that the ability of natural selection to weed out slightly deleterious mutations depends on the size of the breeding population in a given species (Kimura, 1968, 1984; King and Jukes, 1969; Ohta, 1973). The higher the number of individuals, the more powerful natural selection is at identifying slightly deleterious mutations and eliminating them. Due to certain aspects of population dynamics, the effective population size is far smaller than the number of individuals [for a more detailed discussion see (Lynch, 2007)]. For modern humans, the effective population size has been calculated to be 10,000 throughout most of its history, which is typical for mammals (Charlesworth, 2009). Indeed there exists an inverse linear correlation between the effective population size and how deleterious a mutation has to be before it can be effectively eliminated from a population by natural selection. In the absence of selection pressure, some neutral and slightly deleterious mutations will reach fixation due solely to genetic drift [for an extensive examination of this process see (Lynch, 2007)]. It is also important to realize that this relationship also applies to slightly beneficial mutations – there is an inverse correlation between the effective population size and how beneficial a mutation has to be before it can be effectively selected for by natural selection. Thus when one observes some genetic alteration, it is critical that we keep in mind how the alteration affects the fitness of the organism and whether this change can be acted on by selection (either positively or negatively) given the size of the population.
Given that the displacement of a few nucleosomes can promote transcription initiation (Cheung et al., 2008), that TF binding sites and transcriptional start sites are made up of small degenerate sequences (Stewart et al., 2012), and that many random pieces of DNA can activate transcription (White et al., 2013), we would expect that a large number of random mutations would create fortuitous transcriptional start sites. Importantly, natural selection will be powerless to prevent the appearance of these sites, as long as the resulting RNA is not too deleterious to the organism. Conversely, a transcriptional event needs to provide a substantial advantage before natural selection can act to preserve this alteration in future generations. Most of the data on eukaryotic genomes support the view that the fixation of most genomic alterations are due to drift, while few can be ascribed to positive selection (Lynch, 2007).
Thus the presence of a certain level of junk RNA is not only compatible with our understanding of evolution, but would be expected. Nevertheless, it still remains unclear how much junk RNA a eukaryote could tolerate before natural selection would begin to eliminate it.
The Dangers of Hyperadaptationism
The overreliance on adaptationist “just-so stories” in the field of evolutionary biology has been openly criticized since the 1970s. Famously, Gould and Lewontin (1979) compared such thinking to the ideology espoused by Pangloss, the fictional professor from Voltaire’s novel Candide who used just-so stories to prove that we lived in the best of all possible worlds. Unfortunately hyperadaptionalism, or the belief that the vast majority of traits found in an organism (including its DNA) are present due to some selective force, has plagued much of molecular biology as well (Sarkar, 2014). The proclamation that a biochemical activity is equivalent to function (ENCODE Project Consortium et al., 2012) is just another example of this ideology. Using this logic we would state that any transcribed DNA is functional, but would this mean that the transcript (or transcriptional process) is functional by virtue of its mere existence? To resolve this paradox, we would either have to state that (1) although the DNA is functional, its output, the RNA (or the act of transcription) is not; or (2) that all RNAs are de facto functional. Obviously both of these nonsensical conclusions have their roots in hyperadaptionalist thinking and an abuse of the concept of biological function. To resolve this, we need to install a more rigorous definition of function. However, this can only be accomplished if we properly define the null hypothesis.
Throwing Down the Gauntlet: The Hypothetical Example of a Non-Functional ncRNA
To determine the degree to which a process is adaptive, it is important to establish how the exact same events would evolve by non-adaptive mechanisms. Selection should only be invoked when non-adaptive explanations do not suffice. This viewpoint has been used to determine the contribution of selection to alternative splicing, RNA editing and in determining the lengths of UTRs and introns (Lynch, 2007; Huang and Niu, 2008; Wang et al., 2014; Xu and Zhang, 2014). Here, we would like to introduce the example of a hypothetical non-functional ncRNA as a useful null hypothesis. Again, adaptation (and hence function) should only be invoked if an ncRNA has more attributes than our hypothetical non-functional ncRNA. Using principles of biochemistry and population genetics, we will describe its attributes.
Expression Levels
This putative non-functional ncRNA would be present at levels that would not be a burden to the cell. There are three considerations to take into account when considering the level at which a ncRNA is present.
First the mere presence of the ncRNA may act as a burden. The typical mammalian tissue culture cell has on the order of 500,000 mRNA molecules. Other RNAs with unknown function (i.e., “intergenic” RNA and lncRNA) are at levels between 1 and 4% those of mRNA (Mortazavi et al., 2008; Ramsköld et al., 2009; Menet et al., 2012) and thus present on the order of about 10,000 total copies per cell (Table 1). Therefore if a hypothetical ncRNA were present at 10 copies per cell at steady state, they would increase the pool of intergenic/lncRNAs by 0.1%, and would increase the total pool of RNA by a negligible amount (Figure 1).
Second, there is a cost to synthesizing the RNA. One study that investigated the energetics of synthesizing long introns has estimated that for an mRNA that is expressed at a level of 30 copies per cell and a half-life of 1 h (resulting in the generation of 360 new RNA molecules/cell per day), an intron would have to be roughly 83,000 nucleotides long for it to be a significant burden, given the effective population size of humans (Huang and Niu, 2008). Using these figures, we can estimate that in humans a non-functional ncRNA that is 1 kb in length and is ubiquitously expressed throughout the body would have to be synthesized at a rate of almost 30,000 copies per cell per day before it would be eliminated by natural selection. Of course if the ncRNA was spliced from a longer transcript, this number would be less.
Third, the ncRNA may have some associated activity that may be deleterious. Most often the major concern is whether it will be translated into short random peptides (see point 3, below). Although ncRNAs are poorly translated, most studies have found that they can be engaged by the ribosome at low levels (Guttman et al., 2013). This can be further mitigated by subcellular localization (see below). Thus as long as the putative ncRNA does not have some activity that negatively impacts some cellular function or the organism in general, our guess would be that if a ncRNA was present even at a level of 10 copies per cell, this small increase in the ncRNA burden would be tolerable (i.e., not deleterious enough to be subjected to negative selection).
Expression Profiles
We might imagine that our putative non-functional RNA was transcribed due to the fortuitous action of one or more TF binding events. As described above, it is likely that many such sites exist in the mammalian genome as the number of active transcriptional start sites exceed the number of protein-coding genes by an order of magnitude (Carninci et al., 2006). Since the majority of TFs are expressed in a developmentally or spatially regulated manner, it follows that our hypothetical ncRNA will also be expressed in a manner that appears to be under some sort of precise regulatory control. Some researchers have tried to claim tissue-specific expression patterns provide some proof of functionality (Ponting et al., 2009; Hangauer et al., 2013; Mattick and Dinger, 2013); however, such a restricted expression of the ncRNA is entirely consistent with a lack of function.
Distribution of the ncRNA in the Cell
In determining how our putative non-functional RNA would be distributed intracellularly, there are several facts to take into account. First, if this RNA were to be exported to the cytoplasm, it is reasonable to believe that it would be a substrate for the translational machinery, as long as the RNA is free of extensive secondary structures. Second, this RNA would be translated into a random polypeptide. Unlike nucleic acids, unstructured polypeptides have a high tendency to aggregate and activate cellular stress (West et al., 1999; Chi et al., 2003). Lastly, a single RNA molecule can be used to generate many polypeptides, thus amplifying any potential deleterious effects. For these reasons, we believe that non-functional RNAs are much more likely to promote cellular stress if they are present in the cytoplasm where they can be translated by ribosomes. Indeed, it is likely that the nucleo-cytoplasmic division evolved in part to prevent ribosomes from translating misprocessed mRNAs and aberrant RNA transcripts (Martin and Koonin, 2006; Akef et al., 2013; Palazzo and Gregory, 2014). This may be the reason that features associated with mRNAs tend to promote their nuclear export (Palazzo and Akef, 2012), while problems during translation will promote the degradation of the RNA by processes such as non-sense mediated decay (Baker and Parker, 2004). These reasons may explain why most lncRNAs are nuclear (Derrien et al., 2012; Djebali et al., 2012) and not significantly translated (Guttman et al., 2013). By this same logic we would expect that our putative ncRNA would not likely be present in the cytoplasm, although we do not yet have any hard data about what level of cytoplasmic ncRNA would be tolerable.
From this discussion it makes sense that our non-functional ncRNA would be nuclear, but what about its localization to a specific sub-nuclear compartment? Again, some have used localization to sub-nuclear loci as proof of functionality (Mattick et al., 2010; Kapusta and Feschotte, 2014). In experiments performed in our lab we have documented how reporter RNAs with an essentially random sequence are indeed localized to discrete nuclear foci. In some cases these colocalize with known nuclear structures, such as nuclear speckles (Akef et al., 2013); in other instances these RNAs form discrete nuclear puncta that are of unknown nature (Lee and Palazzo, unpublished observations). These observations suggest that even sub-nuclear compartmentalization cannot be used as evidence to support functionality for any ncRNA.
Processing
We would expect that the non-functional ncRNA would lack strong processing signals, as these regions would be expected to be under strong purifying selection only in functional spliced transcripts. For example in most mRNAs, introns are not only flanked by splicing donor and acceptor sites but are also defined by location of intronic and exonic splicing elements (Blencowe, 2000; Wang et al., 2012). However, to our knowledge, no one has systematically studied the splicing of randomly generated RNAs. Despite this we can still estimate the prevalence of splicing signals computationally. For example, the occurrence of consensus donor and acceptor splice sites in essentially random human DNA sequences are one every 3 and 10 kb, respectively (Shepard et al., 2009). Because the spliceosome requires suboptimal sequences to initiate splicing, it is likely that the actual number of potential donor and acceptor sites is much higher. Thus if the primary transcript of our non-functional RNA is long enough, it will probably be spliced to a certain extent. As for smaller transcripts, a small but significant number are also likely to be spliced. However, since splicing helps to stabilize the RNA (Palazzo and Akef, 2012), it is likely that a non-functional ncRNA would only be present at detectable levels by virtue of the fact that it is spliced. In other words, although a lack of processing would lead to the instability of many functionless RNAs, we would expect that a small minority of junk RNAs would be spliced and hence stabilized, and it is precisely these ncRNAs that would be under investigation.
Polyadenylation signals are also likely to be present in our putative junk RNA. These sites are quite abundant – to the extent that many of these sites are present in introns but are normally suppressed by the action of the spliceosome. These cryptic 3′cleavage sites become quite heavily used in cells with reduced U1 snRNA levels (Kaida et al., 2010). As with splicing, polyadenylation promotes mRNA stability (Akef et al., 2013); thus many junk RNAs that would be present at detectable levels are likely present by the very fact that they are polyadenylated. In summary, the fact that a given ncRNA is spliced and polyadenylated is entirely consistent with it not having any function.
Certain groups, such as the HUGO Gene Nomenclature Committee (Wright and Bruford, 2011), have defined lncRNAs as being “spliced, capped and polyadenylated,” with the clear implication that these processes are more likely to be found in functional RNAs than stable junk RNA. We disagree with this view on three counts. First, some non-functional RNAs may be processed [as described above, and by others (Ulitsky and Bartel, 2013)]. Second, many known functional ncRNAs lack all of these processing steps, one example being 7SL (Walter and Blobel, 1982; Ullu and Weiner, 1984). Third, although the goal of this nomenclature is presumably to identify functional non-coding RNAs, as is implied by the term “lncRNA,” these groups never come out and categorically state whether they consider these RNAs functional (although we assume that they do). If the term lncRNA does not imply function, then what exactly does it mean? Is it a meaningless term?
The important distinction between functional and non-functional RNAs is that processing signals are under a high level of selection pressure in the former but not in the latter. Thus, although non-functional ncRNAs may be processed, they will likely have weak signals. Interestingly, introns in lncRNAs tend to be spliced post-transcriptionally, while those in mRNAs tend to be removed co-transcriptionally (Derrien et al., 2012; Tilgner et al., 2012). This may suggest that many lncRNA introns have weak signals due to a lack of selection pressure. Of course a paucity of hard data about the processing of random RNA polymers prevents us from making firmer conclusions. Perhaps studies such as the random genome project (Eddy, 2013) would help us identify how often spliced non-functional ncRNAs would occur purely by chance from a given stretch of DNA.
Conservation
It has been demonstrated for the last 50 years that sequence conservation is a reliable indicator of function. In line with this thinking, many commentators have declared that conservation should be the only criterion for identifying functional genomic loci (Doolittle et al., 2014). In agreement with this, we would expect that our non-functional ncRNA would accumulate mutations at a rate consistent with genetic drift. Indeed some groups have tried to restrict their definition of lncRNAs by using conservation (Guttman et al., 2009).
There are, however, various circumstances that may give the appearance of conservation. For example, the transcribed loci may also contain some conserved functional element, such as a critical TF binding site. If the region of conservation is confined to a pseudogene or TE sequences, one may simply be detecting these entities, which are typically non-functional.
The other problem with relying exclusively on sequence conservation to define functionality is that we know of many genomic loci which have sequence-independent roles. In many cases these regions serve as spacers. Thus natural selection may conserve the presence of any sequence, but not a precise sequence. For example, 5′UTRs and introns need to have a minimal length in order to promote robust translation initiation (Kozak, 1991) and splicing (Wieringa et al., 1984), respectively. Other examples include centromeric-associated repeats, which serve as sequence-independent scaffolds for kinetochore assembly (Torras-Llort et al., 2009). It is also possible that certain ncRNAs may act as a sequence-independent scaffold for protein-binding, as likely is the case of the regulation of HP1 by transcripts produced from heterochromatic regions of the Saccharomyces cerevisiae genome (Keller et al., 2012). Some evidence exists supporting the idea that certain eRNAs may recruit the Mediator complex to form DNA-loops, and this may require very little sequence specificity in the RNA itself (Lai et al., 2013; Andersson et al., 2014; Shibayama et al., 2014). Other times, the act of transcription, and not the resulting ncRNA, may play a role in regulating the expression of nearby genes. Presumably, the initiation of these putative regulatory transcription events are due to the activity of transcriptional start sites and/or other critical cis-acting elements that do display some degree of conservation. However, in practice, these promoters may be hard to identify solely by sequence analysis.
There has also been much talk about human-specific functional ncRNAs, which have generated considerable interest since they could potentially help explain differences between us and related species (Wu et al., 2013). Although these ncRNAs would not be conserved between species, they could in principle be distinguished from non-functional ncRNA by the analysis of numerous human genomes. We would predict that non-functional ncRNA would diverge between individuals within the species at a rate comparable with genetic drift. In contrast, loci producing functional ncRNAs would be conserved. This calculation would depend on when the region in question became fixed and how fast it spread in the population. Unfortunately determining these parameters is not straight forward as it requires a large number of human genomes to be sequenced. Further, complicating the issue is the possibility that the ncRNA locus in question might be located near a genomic region that was under positive selection. The spread of neutral loci by riding on the coattails of nearby positive mutations is known as hitchhiking or draft and may be quite common (Gillespie, 2000). For these reasons, sorting lineage-specific functional ncRNA genes from non-functional ncRNAs is not trivial. Even when one turns to protein-coding genes, many of those that were once thought to be human-specific may not code for proteins after all and may indeed be non-functional (Ezkurdia et al., 2014). It is useful to keep in mind that if our ability to spot lineage-specific coding genes is problematic and fraught with error, the identification of functional human-specific ncRNAs would be even more difficult.
Causal Roles
As stated above, certain commentators have championed selection as the primary arbiter of whether a genomic locus is functional. These same individuals have dismissed any evidence that is based on causal roles, which is defined as “the way(s) in which a component contributes to a stated capacity of some predefined system of which it is a part: what it in fact does” (Doolittle et al., 2014). The problem with defining functionality with causal roles, according to these commentators, is that this concept can be easily misappropriated. For example, a given genetic locus may be transcribed (i.e., caused the production of an RNA), but this event may not necessarily contribute to the fitness of the organism. Only if this activity was important, then natural selection would act to conserve it. Thus in the absence of any evidence of selection, regions of the genome that display some sort of causal role are likely not functional. This is not an absolute statement. As we point out in the previous section, certain functional RNAs may have a critical role that is sequence-independent. In other circumstances, the act of transcription, and not the ncRNA (or presumably its sequence), plays some critical role.
In light of these problems, the question clearly becomes, can a non-functional ncRNA be distinguished from one that is functional, simply on the basis of an experiment that demonstrates a “causal role”? In our opinion the answer is yes, as long as the appropriate causal role is chosen. By definition, elimination of functional ncRNAs should affect homeostasis, development or other important biological processes that would impact the fitness of the organism. In contrast, other causal role events that could potentially be associated with non-functional ncRNAs would be insufficient to qualify as evidence of functionality.
There are some problems with relying on causal roles to determine function, in that it is not always clear whether an activity could occur by chance with an RNA with a random sequence. For example, if the overexpression of an ncRNA promotes oncogenesis, would this provide evidence of functionality? This hypothetical ncRNA could simply be sequestering an RNA binding protein that has a pro-apoptotic function, and in this instance this type of evidence would be weak. If, on the other hand, the ncRNA in question acted as a ribozyme that generated free radicals which caused DNA damage, this would then be much stronger evidence, as this activity would not be expected from a random RNA. Other evidence, such as the association of lncRNAs with certain protein complexes [e.g., the polycomb repressive complex (Khalil et al., 2009)], seems unclear. How often would such an association occur with a random non-functional nuclear RNA?
Ultimately, the ideal experiment is to determine whether the elimination of an ncRNA affects a biological process that is required for the proper development or homeostasis of the organism. This has become more feasible with the advent of CRISPR/Cas9 technology (Doudna and Charpentier, 2014). One serious problem with this approach is that the elimination of a given ncRNA may only have a small impact on the biological process being assessed and thus results in a small reduction in fitness, for example, reducing the number of offspring by 0.1%. Such small effects would be hard to detect in a laboratory setting but would be strongly selected against in the wild, and would indicate that the RNA has a function. In this case it might be beyond our current experimental abilities to obtain causal evidence for certain functional ncRNAs.
Building a Case for Function
To date, projects such as ENCODE, LNCipedia and the HUGO Gene Nomenclature Committee have distinguished lncRNAs from junk RNA primarily based on expression levels and RNA-processing. In contrast, we believe that researchers need to evaluate whether any putative functional ncRNAs have properties that are beyond what one would expect from a non-functional ncRNA, given our knowledge of biochemistry, genomic evolution and current empirical data. Evidence for function can consist of expression levels that are very high (i.e., imposing a significant cost on the organism), a high degree of conservation, and/or experimental evidence that the ncRNA is required for some important biological process. Importantly, ncRNAs should be evaluated on a case-by-case basis. In the absence of sufficient evidence, a given ncRNA should be provisionally labeled as non-functional. Subsequently, if the ncRNA displays features/activities beyond what one would expect for the null hypothesis, then we can reclassify the ncRNA in question as being functional.
Conclusion
It is clear that the human genome contains a large number of functional ncRNAs. Indeed it is likely that the list of biologically validated ncRNAs, as listed in the LncRNA Database (Quek et al., 2014), will continue to grow. As others have pointed out, even if 10% of current lncRNAs prove to be functional, this would represent a wealth of new biology. However, given our current understanding of biochemistry and evolution, it is likely that most of the RNAs generated from the low levels of pervasive transcription, and likely a substantial number of currently annotated “lncRNAs,” are non-functional.
Conflict of Interest Statement
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Acknowledgments
We would like to thank L. Moran and J. Wan for feedback on the manuscript. This work was supported by a grant from the Canadian Institutes of Health Research to Alexander F. Palazzo (FRN 102725). The funding sponsors had no role in the design of the study, in the collection, analyses, or interpretation of data, in the writing of the manuscript, and in the decision to publish the results.
Torras-Llort, M., Moreno-Moreno, O., and Azorín, F. (2009). Focus on the centre: the role of chromatin on the regulation of centromere identity and function. EMBO J. 28, 2337–2348. doi: 10.1038/emboj.2009.174 | Thus the presence of a certain level of junk RNA is not only compatible with our understanding of evolution, but would be expected. Nevertheless, it still remains unclear how much junk RNA a eukaryote could tolerate before natural selection would begin to eliminate it.
The Dangers of Hyperadaptationism
The overreliance on adaptationist “just-so stories” in the field of evolutionary biology has been openly criticized since the 1970s. Famously, Gould and Lewontin (1979) compared such thinking to the ideology espoused by Pangloss, the fictional professor from Voltaire’s novel Candide who used just-so stories to prove that we lived in the best of all possible worlds. Unfortunately hyperadaptionalism, or the belief that the vast majority of traits found in an organism (including its DNA) are present due to some selective force, has plagued much of molecular biology as well (Sarkar, 2014). The proclamation that a biochemical activity is equivalent to function (ENCODE Project Consortium et al., 2012) is just another example of this ideology. Using this logic we would state that any transcribed DNA is functional, but would this mean that the transcript (or transcriptional process) is functional by virtue of its mere existence? To resolve this paradox, we would either have to state that (1) although the DNA is functional, its output, the RNA (or the act of transcription) is not; or (2) that all RNAs are de facto functional. Obviously both of these nonsensical conclusions have their roots in hyperadaptionalist thinking and an abuse of the concept of biological function. To resolve this, we need to install a more rigorous definition of function. However, this can only be accomplished if we properly define the null hypothesis.
Throwing Down the Gauntlet: The Hypothetical Example of a Non-Functional ncRNA
To determine the degree to which a process is adaptive, it is important to establish how the exact same events would evolve by non-adaptive mechanisms. | yes |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4356734/ | Fish do not feel pain and its implications for understanding ... | Share
RESOURCES
As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with,
the contents by NLM or the National Institutes of Health.
Learn more:
PMC Disclaimer
|
PMC Copyright Notice
Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
Abstract
Phenomenal consciousness or the subjective experience of feeling sensory stimuli is fundamental to human existence. Because of the ubiquity of their subjective experiences, humans seem to readily accept the anthropomorphic extension of these mental states to other animals. Humans will typically extrapolate feelings of pain to animals if they respond physiologically and behaviourally to noxious stimuli. The alternative view that fish instead respond to noxious stimuli reflexly and with a limited behavioural repertoire is defended within the context of our current understanding of the neuroanatomy and neurophysiology of mental states. Consequently, a set of fundamental properties of neural tissue necessary for feeling pain or experiencing affective states in vertebrates is proposed. While mammals and birds possess the prerequisite neural architecture for phenomenal consciousness, it is concluded that fish lack these essential characteristics and hence do not feel pain.
Introduction
There is a belief in some scientific and lay communities that because fish respond behaviourally to noxious stimuli, then ipso facto, fish feel pain. Sneddon (2011) clearly articulates the logic by stating: “to explore the possibility of pain perception in nonhumans we use indirect measures similar to those used for human infants who cannot convey whether they are in pain. We measure physiological responses (e.g., cardiovascular) and behavioral changes (e.g. withdrawal) to assess whether a tissue-damaging event is painful to an animal”. In some cases, the inference that fish have affective states arises because of conflation of nociception with pain (Demski 2013; Kittilsen 2013; Malafoglia et al. 2013). Interestingly, sometimes the difference between nociception and pain is recognized but it is still considered safer to err on the side of caution and accept that fish feel pain (Jones 2013). Unfortunately, endowing fish with the subjective ability to experience pain is typically undertaken without reference to its neurophysiological bases (Rose 2002, 2007; Browman and Skiftesvik 2011).
Before interrogating the issue of fish feeling pain and its implications for phenomenal consciousness, I will briefly define several key terms. When I refer to fish it is with the knowledge that this is a highly diverse paraphyletic group consisting of ~30,000 species. Since most of the behavioural and neuroanatomical investigations discussed here have been undertaken only on a small number of ray-finned fish, there is considerable extrapolation involved when I use the generic term fish. A noxious stimulus is one that is considered to be physically harmful to an animal without reference to feelings. For example, excessive heat, a skin incision, toxic chemical exposure and extreme mechanical pressure are all stimuli that can perturb normal tissue morphology, and are hence considered to be noxious. Nociception is referred to as the neurobiological processes associated with the activation of peripheral sensory neurons and their upstream neural pathways by noxious stimuli in the absence of conscious feeling. In contrast, pain is the subjective experience of feeling a noxious stimulus (however, in certain central neuropathies in humans it can arise without external stimuli). The subjective “feeling” associated with a sensory stimulus is also referred to as a “quale” or “phenomenal consciousness” (Kanai and Tsuchiya 2012). Given the above, I acknowledge the tautology in the manuscript’s title since the word “pain” is already defined as “to feel a noxious stimuli”. However, the phrase “feel pain” within the title was chosen to over-emphasize the subjective or qualitative nature of pain.
One of the main proponents in the literature of the thesis that fish do not feel pain has been John D. Rose. In a series of comprehensive articles (Rose 2002, 2007; Rose et al. 2014) it was argued that fish do not experience the sensation of pain. Anthropomorphism was considered as a hindrance to understanding the underlying causes of behavioural responses of animals to sensory stimuli (Rose 2002, 2007). Rose advocated attention to the evolution, development and organization of the nervous system in order to understand fish behaviour. He initially drew attention to three key issues (Rose 2002). First, behavioural responses to sensory stimuli must be distinguished from psychological experiences. Second, the cerebral cortex in humans is fundamental for the awareness of sensory stimuli. Third, fish lack a cerebral cortex or its homologue and hence cannot experience pain or fear. In 2007, Rose highlighted the problems of anthropomorphic thinking in respect to fish behaviour and how it influenced welfare issues. He stressed that pain and emotion were not primitive feelings that arose early in vertebrate evolution but were rather more recent acquisitions, associated with the emergence of the cerebral cortex (Rose 2007). In 2014, Rose et al. (2014) rebutted experimental evidence supposedly supporting claims that fish feel pain. They demonstrated deficiencies in methodological approaches and highlighted problems in concluding pain experience from behavioural responses. Moreover, they recognized that teleosts typically lack nociceptors responsible for transmission of pain but instead have an abundance of A-delta fibres that are most likely subserving escape and avoidance responses rather than the experience of pain.
Despite the work of Rose et al. (Rose 2002, 2007; Rose et al. 2014) there remains a strong trend in the literature to bestow fish with the ability to feel pain and to experience fear and other emotions. The alternate view that fish do not feel pain or experience affective states needs more careful consideration, particularly as it has consequences for understanding the neuroanatomical basis of phenomenal consciousness. Here I consolidate the arguments for why fish are believed to feel pain into six main reasons. By undertaking a deeper analysis of the behavioural observations in the light of our understanding of neurophysiology and neuroanatomy, I subsequently propose that it is more plausible and probable to reason that fish do not feel pain. Concluding that fish do not feel pain affords an opportunity to define the basic architectural properties of the neural circuitry necessary for phenomenal consciousness through comparisons of fish and mammalian neuroanatomies. These properties then provide a simple tool for assessing the likelihood that a vertebrate animal will experience “feelings” such as pain.
What are the reasons for the anthropomorphic view that fish feel pain?
There are six principal reasons that account for why some people believe that fish feel pain. One, fish demonstrate behaviours consistent with the way humans might react to noxious stimuli that cause pain. For example, fish will either attempt to rapidly escape or display anomalous behaviour (Reilly et al. 2008) in response to noxious stimuli, such as electric shock or a chemical irritant. Two, medicating fish with an analgesic (a drug that attenuates pain in humans) reduces the escape response to electric shock (Sneddon 2003; Sneddon et al. 2003; Jones et al. 2012). Three, fish display classic physiological indicators of stress such as increased ventilation and heart rate and elevated blood levels of the stress hormone cortisol during and after exposure to supposedly stressful stimuli (Reilly et al. 2008; Filk et al. 2006; Wolkers et al. 2013). Four, fish have nociceptive nerve fibres and have increased neural activity in the spinal cord, hindbrain and pallium that is specifically associated with a noxious stimulus (Dunlop and Laming 2005). Five, fish can be trained to associate a neutral signal with an impending noxious stimulus and so learn to escape prior to experiencing the noxious stimuli (Dunlop et al. 2006). Six, it is evolutionarily advantageous to feel pain in order to prevent body injury.
Behavioural responses to noxious stimuli are not necessarily evidence of pain
It is common to attribute inner mental states or feelings to organisms or even inanimate objects on the basis of observed behavior. When a noxious stimulus is applied either to the plantar surface of the human foot, or directly to the nerves innervating this region, there is a reflex withdrawal of the lower limb involving contraction of the hip and knee flexors, and relaxation of the extensors. This reflex is protective and enables the rapid removal of the limb from a harmful stimulus. Complete spinal cord injury patients, who lack sensations arising from the lower limb, continue to exhibit the withdrawal flexion reflex (Dimitrijevic and Nathan 1968). Thus, reflexes are neither good evidence for, nor a measure of feeling pain. Nonetheless, simple reflex behaviours in response to noxious stimuli continue to be inappropriately used to suggest that fish feel pain.
Fish exhibit behavioural responses to somatosensory stimulation from a very early stage of development. For example, within the first few days of fertilisation, zebrafish embryos response to touch by initially exhibiting a twitch of their tail, and then slightly later in development, by a few strokes of their tail that elicits a short burst of swimming. While it is tempting to attribute feelings to these embryos, it must be remembered that the telencephalon is not yet morphologically distinct when the touch response first appears at around 21 h post-fertilisation (Hjorth and Key 2001; Saint-Amant 2006). Moreover, a lesion to the anterior spinal cord, that isolates the cord from the brain, does not affect the execution of the touch-induced swimming escape response (Pietri et al. 2009). Thus, simple reflex escape behaviours of fish that can be activated by somatosensory stimuli are best not used as evidence for fish experiencing phenomenal consciousness.
It is important here to draw attention to the fact that pain in humans arises in the forebrain, and is distinct from unconscious behavioural responses mediated by lower brain levels. The forebrain also plays an essential role in pain perception in other mammals. This is elegantly illustrated in a rat model of pain that uses injection of a dilute solution of formalin into the paw. This chemical irritant induces a variety of body movements such as paw shaking, licking and grooming. Animals also exhibit a protective response and attempt to reduce contact of the affected limb with the floor. These behaviours are sometimes considered as indicators of pain. However, rats continued to exhibit such behavioural responses following surgical decerebration (Matthies and Franklin 1992, 1995). One interpretation of these results is that pain is actually experienced in the brainstem, and not in the forebrain in rats. However, this is most unlikely given that systemic administration of an analgesic (morphine) does not attenuate behavioural responses to formalin in decerebrated animals. Morphine was only effective in inhibiting behaviours when connections between the forebrain and brainstem were left intact in sham-operated rats (Matthies and Franklin 1992). Moreover, local application of morphine into either the somatosensory, prefrontal orbital or agranular insular cortices attenuates behavioural responses in the formalin pain model in rats (Soto-Moyano et al. 1988; Xie et al. 2004). Thus, morphine is active in the rat forebrain, which is consistent with it modulating the subjective experience of the noxious stimuli, as in humans (Jones et al. 1991; Taylor et al. 2013).
Fish are known to swim away from noxious electric shock and this behavioural response has been used to indicate that these animals feel pain. However, this interpretation is simplistic and can be dismissed given the extensive evidence that fish continue to exhibit escape behaviour following ablation of the entire telencephalon (Hainsworth et al. 1967; Davis et al. 1976). Forebrainless fish display no clear evidence of deficits in normal behaviours. For example, forebrainless fish continue to flee from capture by a small fish net with similar locomotor agility as their unoperated counterparts (Kaplan and Aronson 1967). The ability to escape or respond to an electric shock is unaffected by removal of either the forebrain or telencephalon in goldfish (Hainsworth et al. 1967; Savage 1969; Portavella et al. 2004a, b) or telencephalon in Tilapia mossambica (Overmier and Gross 1974).
In summary, the idea that fish flee noxious stimuli because they experience phenomenal consciousness (feel pain) is not the best explanation for this behaviour. It is more probable that fish demonstrate these behaviours because they have evolved innate reflexes associated with specific spinal and sub-telencephalic neural circuits.
Modification of behaviour with drugs does not necessarily demonstrate pain
It has been proposed that if an animal’s behavioural response to a noxious stimulus is attenuated following administration of a drug known to be an analgesic in humans, then it is likely that the animal can feel pain. However, it needs to be pointed out that analgesics can be active at multiple sites in the neuroanatomical pathways associated with noxious stimuli. If an analgesic blocks or reduces neural activity in the spinal cord (Yaksh and Rudy 1976) it can subsequently attenuate neural responses in the brainstem and telencephalon. Similarly, if an analgesic works at the level of the brainstem it can modulate both brainstem and higher-order brain responses (Pert and Yaksh 1975). If an analgesic is active at the level of the telencephalon and reduces behavioural responses (Xie et al. 2004) then the animal, at least, has the possibility of feeling a noxious stimulus as painful (however this interpretation is dependent first, on the behaviour being non-reflexive and second, on the existence of the necessary neural hardware; see below). At present, the inference that fish feel pain because behavioural responses to noxious stimuli are attenuated following systemic administration of morphine (Sneddon 2003) is weak, particularly given that both the site of action as well as the physiological role of this drug in fish are unknown.
Physiological stress is not pain
Physiological stress as determined by plasma cortisol levels and opercula beat rate have been used as indicators of feeling pain by fish (Chandroo et al. 2004; Braithwaite and Boulcott 2007; Scott Weber 2011). The underlying assumption in these cases is that if a fish is exposed to a stimulus that triggers both increased cortisol and behavioural responses, then that fish must be consciously feeling that stimulus as a mental state such as fear and/or pain. If pain was felt by a fish exposed to a physiological stressor, and cortisol was an indicator of the level of discomfort that fish experienced, then one would predict increased cortisol levels in fish as a noxious stimulus was increased. However, this does not appear to be the case. There is no relationship between the apparent “stressful” stimulus and the level of cortisol in fish (Roques et al. 2010). Even when the stimulus causes increased behavioural responses there was no relationship to the level of plasma cortisol. The cortisol response to increased stress seems to be highly variable (Fatira et al. 2014; Quillet et al. 2014) and context specific (Manek et al. 2014). Surprisingly, exposure to multiple stressors simultaneously can lead to decreased rather than an expected increase in cortisol levels (Manek et al. 2014). Thus, changes in cortisol levels in fish are better explained by autonomic responses to external environmental stresses rather than by internally generated mental states such as fear or pain.
Brain activity in response to noxious activity is not equivalent to pain
It has been proposed that fish can feel pain both because they have peripheral nociceptors and because neural responses to noxious stimuli have been recorded in the spinal cord, cerebellum, tectum and telencephalon of fish (Sneddon 2004; Dunlop and Laming 2005). Nordgreen et al. (2007) reported neural activity in the telencephalon following electrical stimulation of the tail of Atlanic salmon. While these authors indicated that this activity is a necessary prerequisite for feeling pain, they realised that it does not necessarily provide evidence for the ability of fish to feel pain. Unfortunately, the neuroanatomical localisation of electrical activity recorded in the telencephalon has not been described. If activity was recorded in the dorsal pallium (homologous to the neocortex; Mueller and Wullimann 2009; Mueller et al. 2011) of the telencephalon, it would, at least, provide some phylogenetic insight into neural pathways underlying nociception. It would not, however, be evidence of pain or emotion.
Associative learning using noxious stimuli is possible without feeling pain
Considering the problems with using simple behavioural responses to noxious stimuli as a measure of pain sensation, avoidance learning has instead been adopted as a means for assessing pain in animals. Rats can easily learn to avoid locations in a cage where electric shocks are delivered and to push a lever that terminates the shock. This learning is viewed as requiring the animal to initially decipher the stimulus (i.e. feeling the stimulus as painful and assessing the intensity using the cerebral cortex; Baastrup et al. 2010) and then to plan and perform a relatively complex motor task (Vierck 2006). Higher-level brain activity (involving the cerebrum) is essential for avoidance learning since decerebrate rats fail to learn to avoid electric shock (Vierck 2006). Interestingly, rats exhibit an escape response substantially faster than a brainstem reflex (such as paw licking or jumping) in response to a noxious stimulus (Vierck 2006). In addition, the rat threshold for escape response from cold temperatures is approximately 16 °C whereas the threshold for brainstem reflexes is <5 °C (Vierck 2006). These comparisons between brainstem reflexes and higher-level escape responses suggest that the cerebrum quickly perceives noxious stimuli as potentially harmful before they are actually physically damaging. Taken together, these results are consistent with rats feeling pain.
Operant conditioning with negative reinforcement demonstrates that fish can also learn to associate a conditioned stimulus (light cue) with an impending unconditioned stimulus (electric shock) administered in one chamber of a two-chamber holding tank (Hurtado-Parrado 2010). Fish typically learn to terminate their exposure to the electric shock by escaping to the chamber where the shock is not present. With more and more trials, the fish learn to associate the light stimulus with the temporally delayed electric shock and hence begin to escape prior to the delivery of the shock. However, as pointed out above, the escape response in fish is a reflex behaviour and does not equate to the more complex escape routines used in rodent models of pain (Cain et al. 2010). Thus, the better explanation is that fish reflexively associate the stimulus with the shock.
It has been reasoned that if a behavioural response was modifiable under different circumstances, then it was not a reflex. This vague distinction between reflex and non-reflexive (or flexible) behaviours in fish relies on the notion that higher-level brain activity was associated with the latter and not the former (Dunlop et al. 2006; Braithwaite et al. 2013). Evidence for this activity was purported to come from numerous observations that telencephalon ablation perturbed avoidance learning in fish. However, it has been consistently reported that although avoidance learning by fish is perturbed by full or partial forebrain ablations, these animals continue to exhibit escape responses (and many continue to learn to avoid) as a result of electric shock (Hainsworth et al. 1967; Kaplan and Aronson 1967; Savage 1968; Overmier and Gross 1974; Flood et al. 1976; Overmier and Papini 1985; Portavella et al. 2003, 2004a, b; Portavella and Vargas 2005; Vargas et al. 2009). Thus, forebrainless fish are still able to either escape from, or learn (albeit more slowly) to avoid, an electric shock. Fish with, or without, the forebrain had similar latencies of escape. Escape latency was the time taken for a fish to escape from the chamber once it received a shock. Clearly, the forebrain was not needed for fish to exhibit escape behaviour, but it was important for learning the association between the light and the unconditioned stimulus (shock).
Taken together, the above results demonstrate that the escape responses used in the avoidance learning paradigms for fish involve sub-forebrain regions associated with instinctive and/or reflexive behaviours. Thus, the avoidance learning paradigms typically used in fish studies are more informative about learning processes in fish, then about the sensation of pain experienced by these animals. It is most likely that the sorts of avoidance learning exhibited to date in fish studies is better explained by innate neural circuitry mediating reflex behaviour.
Pain is not essential for reducing injury
The idea that nociception has an evolutionary survival advantage for animals is well established in the scientific literature (Kavaliers 1988). However, the significance of feeling pain in animals is less well understood since the nociception-pain axis has not been carefully interrogated. It has been assumed that pain enables animals to adopt longer-term protective behaviours in order to facilitate tissue repair and to prevent compounding injuries (Bolles and Faneslow 1980).
If fish were to feel pain then one would, at least, expect them to exhibit a longer-term protective response to injury. The fins of fish are densely innervated by sensory axons and are one of the most highly sensitive regions of the fish body surface to noxious stimulation (Chervova 1997). If fish were experiencing pain, and if pain was serving a protective function, then fish should respond to fin injury either by not using that fin or by altering swimming behaviour until the injury was repaired. However, after either partial or complete tail fin amputation, fish show no evidence of protecting their fins by reducing their swimming behaviour; they are instead quite capable of swimming continuously against a current (Fu et al. 2013). These observations are also consistent with the normal behaviour of fish with bacterial tail or fin rot. This disease causes progressive erosion of the affected fins/tail and yet these fish swim and eat normally. The consensus in the fish welfare literature is that fin rot, despite its ability to cause loss of most of the tail fin, does not affect the behaviour of fish. These animals continue to eat and swim like their healthy counterparts (Ellis et al. 2008). The most plausible interpretation of these observations is that fish do not modulate long-term behaviour in order to allow injury repair. This conclusion is more consistent with fish not feeling pain.
What is the neural basis of pain?
I have suggested above that the behavioural responses of fish to noxious stimuli is best explained by sub-telencephalic reflexes mediated by innate neural circuits rather then by fish experiencing phenomenal consciousness. By accepting this argument it now becomes possible to better address the necessary anatomical prerequisites underlying phenomenal consciousness. All chordates possess a central nervous system consisting of an enlarged anterior end and a posterior cord-like structure. The differences in neuroanatomy that have emerged during evolution within this phylum reflect specialised functions (Butler 2000). While the posterior cord has typically preserved a simple morphology that subserves basic locomotor behaviours, the rostral nervous system has instead undergone extensive structural modifications that have led to devise functional consequences. For instance, the evolution of the neocortex in humans has allowed us to experience our environment through subjective mental states such as pain, smell, hearing and vision. By understanding how our environment subjectively “feels” it has become possible for humans to appreciate and predict how other people would respond in certain situations. Consequently by manipulating our environment we are able to affect the behaviour of others to achieve specific outcomes. The human neocortex is particularly adept at this function and it is clearly an important driving force in our cultural evolution.
What is so unique about the cortex that enables inner mental states? First, the cortex is parcellated into discrete anatomically structures or cortical areas that process information related to specific functions. It is estimated that there are about 200 cortical areas in humans (Kaas 2012). For instance, the cortical visual system consists of over a dozen distinct regions with diverse subfunctions that are strongly interconnected by reciprocal axon pathways. One of the defining features of these subregions is that they become simultaneously active. Both recurrent activity and binding of neural activity across cortical regions are believed to be essential prerequisites for the subjective experience of vision (Sillito et al. 2006; Pollen 2011; Koivisto and Silvanto 2012). It has been shown that when neural processing of recurrent signalling from higher cortical regions entering the V1 visual cortex is perturbed by transcranial magnetic stimulation, the subjective awareness of a visual stimulus is disrupted (Koivisto et al. 2010, 2011; Jacobs et al. 2012; Railo and Koivisto 2012; Avanzini et al. 2013).
The subregionalisation of the neocortex also allows the formation of spatial maps of the sensory world, such as those associated with the representations of the surface of the body or the visual field. These topographical maps are important for the multiscale processing of sensory information (Kaas 1997; Thivierge and Marcus 2007). Variation in the size of the maps alters the sensitivity of responses to stimuli while spatial segregation of neurons responding to selective parts of a stimulus allows for finer perceptual discrimination. Painful and non-painful somatosensory stimuli are topographically mapped to overlying regions in the primary somatosensory cortex (SI) in humans (Mancini et al. 2012). These results are consistent with the known point-to-point topography from the body surface to SI (called somatotopy) that underlies spatial acuity. However, by using high resolution mapping in the squirrel monkey SI (sub-millimetre level) it was revealed that there were slight differences in the localisation of different somatosensory modalities (Chen et al. 2001). This slight physical separation of cortical neurons responding to different peripheral stimuli suggests that differences in the subjective quality of somatosensory sensations may arise as early as in SI. Somatotopic maps for painful stimuli are also present in the human SII and insular cortices (Baumgartner et al. 2010). Interestingly, different qualities of painful stimuli (such as heat and pinprick) are more distinctly mapped topographically to different regions of SII and the insular cortex than in SI. Similarly, painful and non-painful stimuli are mapped to separate regions in human SII (Torquati et al. 2005). This separation of cortical processing of heat and tactile stimuli within different cortical areas has also been observed in non-human primates (Chen et al. 2011). These multiple neural maps suggests that SII and the insular cortex play important roles in discriminating differences in the subjective quality of somatosensory stimuli, particularly painful from non-painful (Tommerdahl et al. 1996; Baumgartner et al. 2010; Chen et al. 2011; Mazzola et al. 2012). This idea is supported by evidence from direct electrical stimulation of discrete areas in the human insular cortex (Afif et al. 2010).
Second, the cortex is a laminated structure that enables the efficient processing and integration of different types of neural information by unique subpopulations of neurons (Schubert et al. 2007; Maier et al. 2010; Larkum 2013). Lamination appears to facilitate complex wiring patterns during development. If two populations of neurons were randomly distributed within a specific brain region and incoming axons were required to synapse with only one subpopulation, then those axons would need to rely on stochastic and hence error-prone searching to complete wiring. On the other hand, when similar neurons are partitioned together in a single lamina then a small set of molecular cues is able to guide axons with high precision to their appropriate post-synaptic target. Two principal afferent inputs (from the neocortex itself, and the thalamus) enter the neocortex and separately innervate distinct layers (Nieuwenhuys 1994). The main thalamic fibres terminate densely in layer IV (called the granular layer) while the neocortical fibres innervate different pyramidal neurons in layers I–III (supragranular layers) (Opris 2013). By selectively ablating Pax6, a developmentally significant patterning gene, in the cortex of mice it is possible to disrupt the laminar organisation of this structure (Tuoc et al. 2009). This altered cortical layering causes neurological deficits that are similar to those observed in humans with Pax6 haploinsufficiency (Tuoc et al. 2009) and provides strong experimental evidence of the importance of lamination to cortical function. A number of human brain disorders involve defects in cortical lamination that are detrimental to brain function (Guerrini et al. 2008; Guerrini and Parrini 2010; Bozzi et al. 2012).
Third, lamination facilitates the economical establishment of microcircuitry between neurons processing different properties of the stimulus. A vertical canonical microcircuit is established which leads to the emergence of functionally interconnected columns and minicolumns of neurons (Mountcastle 1997). For example, a hexagonal column in the primate somatosensory cortex is about 400 μm in width and contains populations of neurons that respond to the same stimulus (e.g. light touch or joint stimulation) arising from a specific topographical zone of the body. Columns can be associated with processing information related to a specific function (e.g. “visual tracking” and “arm reach” columns in the parietal cortex; Kass 2012). Each column itself consists of minicolumns (80–100 neurons) that are ~30–50 μm in diameter and interconnected by short-range horizontal processes (Buxhoeveden and Casanova 2002). While columns are most clearly distinguished in the sensory and motor cortices of primates, minicolumns appear to be ubiquitous in all animals with a neocortex (Kaas 2012). Minicolumns have a small receptive field within the larger receptive field of the column. The correlated activity in the fine-scale networks of minicolumns produces concentrated bursts of neural activity that may enable the cortex to transmit signals in the face of background noise (Ohiorhenuan et al. 2010). The function of the cortex seems to depend on the ability of canonical circuitry within the minicolumns to rapidly switch from feedforward to feedback processing between layers. During learned tasks in responses to cues in the awake monkey, information flows from layer 4 to layer 2/3 and then down to layer 5 in a feedforward loop in the temporal neocortex (Takeuchi et al. 2011; Bastos et al. 2012). This is followed shortly afterwards by a feedback loop from layer 5 to layer 2/3. Correlated firing of layer 2/3 and layer 5 neurons in minicolumns occurs during decision making in the monkey prefrontal cortex, an area responsible for executive control in primates (Opris et al. 2012). The accuracy of error-prone tasks was increased when layer 5 neurons were artificially stimulated by activity recorded during successful task execution. These results provide evidence for the role of the minicolumn as the fundamental processing unit of the neocortex associated with higher order behaviour (Bastos et al. 2012; Opris et al. 2012).
In summary, the unique morphology of the mammalian cortex facilitates multiscale processing of sensory information. Initially there is course scaling at the level of gross anatomical cortical regions specialising, for example, in processing of visual or somatosensory information. Some of these regions are then topographically mapped in order to preserve spatial relationships and facilitate selective processing of specific sensory features. Importantly, to preserve the holistic quality of a sensory stimulus, these subregions are strongly interconnected via axon pathways that create synchronized re-entrant loops of neural activity. Cortical regions are laminated which supports finer scale sensitivity in the processing of specific features. Finally, canonical microcircuits (minicolumns) bridge across layers to enhance signal contrast (Casanova 2010). Local connectivity between minicolumns enables the lowest level of stimulus binding that contributes to the holistic nature of the stimulus (Buxhoeveden and Casanova 2002).
I propose that only animals possessing the above neuroanatomical features (i.e. discrete cortical sensory regions, topographical maps, multiple cortical layers, columns/minicolumns and strong local and long-range interconnections), or their functionally analogous counterparts, have the necessary morphological prerequisites for experiencing subjective inner mental states such as pain. It has been argued that since the avian pallium is non-laminated, and yet these animals exhibit high levels of cognitive ability and behaviours rivalling those of primates, that lamination is not an essential prerequisite for consciousness (Gunturkun 2005; Kirsch et al. 2008; Gunturkun 2012; Veit and Nieder 2013). However, the classic view of the organisation of the avian telencephalon has been revised and previous subpallial regions are now recognised as pallial in nature (Shimizu 2009). Careful examination of pallial neuroanatomy has further revealed that distinct regions of the avian pallium act like layers of the neocortex (Dugas-Ford et al. 2012). Moreover, columnar processing units appear to operate across these brain regions in the processing of sensory and motor information (Jarvis et al. 2013). When this is combined with complex parcellation, the presence of topographical maps and strong interconnectivity in the avian pallium (Shimizu et al. 1995; Shimizu and Bowers 1999; Bingman and Able 2002; Manger et al. 2002; Nguyen et al. 2004; Watanabe and Masuda 2010), it appears that birds possess the necessary neural machinery for phenomenal consciousness.
The pallium of fish is non-laminated. It is partitioned into five broad nuclear regions (dorsomedial, dorsolateral, dorsodorsal, dorsoposterior and ventral; Northcutt 2011). While the dorsodorsal pallium is believed to be homologous to the neocortex there remains some controversy as to the definitive homology between these structures (Echleter and Saidel 1981; Northcutt 2008; Braford 2009; Northcutt 2011). There is converging evidence from electrophysiological recordings (Precht et al. 1998; Saidel et al. 2001; Northcutt et al. 2004) and neuroanatomical tracing (Yamamoto and Ito 2008) that, unlike in the neocortex, sensory information such as visual input, is diffusely processed across the fish dorsal pallium, and certainly not localised to multiple interconnected areas that are topographically mapped (Giassi et al. 2012). Evidence is also lacking for canonical microcircuitry subserving fine scale processing of sensory information in the dorsal pallium. This lack of contrast in signal processing does not support the ability of the fish pallium to differentiate sensory modalities with sufficient resolution to allow the emergence of distinct feelings for different sensory modalities.
It has been suggested that sub-forebrain structures in fish may somehow take over the function of phenomenal consciousness in the neocortex. While parcellated sensory processing, laminated cytoarchitecture and columnar-like modules are present in the mid- and hindbrains of some fish (Meek 1983; Krahe and Maler 2014), these structures lack the necessary local and long-range feedforward and recurrent pathways associated with information binding underlying phenomenal consciousness (Baars et al. 2013). Instead, the vertebrate midbrain optic tectum has conserved structural features across a variety of species such as fish, frogs, birds and mammals that subserve common functionalities (e.g. orienting, direction-sensitivity, and spatial relationships; Ingle 1973). Furthermore, while ablation of the tecta perturbs visual function, startle responses in tectumless fish are preserved (Yager et al. 1977; Roeser and Naier 2003). Thus, the tectum is not needed to respond to somatosensory stimuli and certainly does not possess novel circuitry responsible for pain. On the basis of our current understanding of the structure and function of the “fish” brain, it most likely that fish do not have the necessary neural machinery for phenomenal consciousness.
In summary, I have demonstrated how misleading it is to infer that fish have feelings on the basis of behavioural responses to sensory stimulation. It is essential that our anthropomorphic tendencies to bestow animals with feelings does not hinder the progress of scientific enquiry into the evolution of phenomenal consciousness. I propose that there are a number of fundamental neural building blocks that are necessary prerequisites for phenomenal consciousness in the vertebrate lineage. The possession of this hardware sets the minimal requirements for the sensation of noxious stimuli as painful. The idea that other neural architectures that have been specifically wired for fundamentally different functions in vertebrates (such as the mid- and hindbrains) could also subserve pain in fish is incongruent with evolutionary biology and neuroscience. While there is some degree of plasticity of function in the mammalian neocortex (Kupers and Pitto 2013), the very notion that either the fish tectum as well as the mid- and hindbrain reticular formations (that are reciprocally interconnected with the tectum; Perez-Perez et al. 2003; Luque et al. 2005) has some hidden neural circuitry that allows for the processing of somatosensory inputs into discrete feelings of pinprick, heat, cold, scratch, cutting and stabbing is difficult to defend.
Conflict of interest
The author states that he has not been paid for this work and has no conflict of interest.
Meek J. Functional anatomy of the tectum mesencephala of the goldfish. An explorative analysis of the functional implications of the laminar structural organization of the tectum. Brain Res. 1983;287:247–297. [PubMed] [Google Scholar] | While mammals and birds possess the prerequisite neural architecture for phenomenal consciousness, it is concluded that fish lack these essential characteristics and hence do not feel pain.
Introduction
There is a belief in some scientific and lay communities that because fish respond behaviourally to noxious stimuli, then ipso facto, fish feel pain. Sneddon (2011) clearly articulates the logic by stating: “to explore the possibility of pain perception in nonhumans we use indirect measures similar to those used for human infants who cannot convey whether they are in pain. We measure physiological responses (e.g., cardiovascular) and behavioral changes (e.g. withdrawal) to assess whether a tissue-damaging event is painful to an animal”. In some cases, the inference that fish have affective states arises because of conflation of nociception with pain (Demski 2013; Kittilsen 2013; Malafoglia et al. 2013). Interestingly, sometimes the difference between nociception and pain is recognized but it is still considered safer to err on the side of caution and accept that fish feel pain (Jones 2013). Unfortunately, endowing fish with the subjective ability to experience pain is typically undertaken without reference to its neurophysiological bases (Rose 2002, 2007; Browman and Skiftesvik 2011).
Before interrogating the issue of fish feeling pain and its implications for phenomenal consciousness, I will briefly define several key terms. When I refer to fish it is with the knowledge that this is a highly diverse paraphyletic group consisting of ~30,000 species. Since most of the behavioural and neuroanatomical investigations discussed here have been undertaken only on a small number of ray-finned fish, there is considerable extrapolation involved when I use the generic term fish. A noxious stimulus is one that is considered to be physically harmful to an animal without reference to feelings. | no |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://www.sciencedaily.com/releases/2013/08/130808123719.htm | Do fish feel pain? Not as humans do, study suggests -- ScienceDaily | Do fish feel pain? Not as humans do, study suggests
Fish do not feel pain the way humans do, according to a team of neurobiologists, behavioral ecologists and fishery scientists. The researchers conclude that fish do not have the neuro-physiological capacity for a conscious awareness of pain.
Fish do not feel pain the way humans do. That is the conclusion drawn by an international team of researchers consisting of neurobiologists, behavioural ecologists and fishery scientists. One contributor to the landmark study was Prof. Dr. Robert Arlinghaus of the Leibniz Institute of Freshwater Ecology and Inland Fisheries and of the Humboldt University in Berlin.
On July 13th a revised animal protection act has come into effect in Germany. But anyone who expects it to contain concrete statements regarding the handling of fish will be disappointed. Legislators seemingly had already found their answer to the fish issue. Accordingly, fish are sentient vertebrates who must be protected against cruel acts performed by humans against animals. Anyone in Germany who, without due cause, kills vertebrates or inflicts severe pain or suffering on them has to face penal consequences as well as severe fines or even prison sentences. Now, the question of whether or not fish are really able to feel pain or suffer in human terms is once again on the agenda.
A final decision would have far-reaching consequences for millions of anglers, fishers, aquarists, fish farmers and fish scientists. To this end, a research team consisting of seven people has examined all significant studies on the subject of fish pain. During their research the scientists from Europe, Canada, Australia and the USA have discovered many deficiencies. These are the authors’ main points of criticism: Fish do not have the neuro-physiological capacity for a conscious awareness of pain. In addition, behavioural reactions by fish to seemingly painful impulses were evaluated according to human criteria and were thus misinterpreted. There is still no final proof that fish can feel pain.
This is how it works for humans
To be able to understand the researchers’ criticism you first have to comprehend how pain perception works for humans. Injuries stimulate what is known as nociceptors. These receptors send electrical signals through nerve-lines and the spinal cord to the cerebral cortex (neocortex). With full awareness, this is where they are processed into a sensation of pain. However, even severe injuries do not necessarily have to result in an experience of pain. As an emotional state, pain can for example be intensified through engendering fear and it can also be mentally constructed without any tissue damage. Conversely, any stimulation of the nociceptors can be unconsciously processed without the organism having an experience of pain. This principle is used in cases such as anaesthesia. It is for this reason that pain research distinguishes between a conscious awareness of pain and an unconscious processing of impulses through nociception, the latter of which can also lead to complex hormonal reactions, behavioural responses as well as to learning avoidance reactions. Therefore, nociceptive reactions can never be equated with pain, and are thus, strictly speaking, no prerequisite for pain.
Fish are not comparable to humans in terms of anatomy and physiology
Unlike humans fish do not possess a neocortex, which is the first indicator of doubt regarding the pain awareness of fish. Furthermore, certain nerve fibres in mammals (known as c-nociceptors) have been shown to be involved in the sensation of intense experiences of pain. All primitive cartilaginous fish subject to the study, such as sharks and rays, show a complete lack of these fibres and all bony fish – which includes all common types of fish such as carp and trout – very rarely have them. In this respect, the physiological prerequisites for a conscious experience of pain are hardly developed in fish. However, bony fish certainly possess simple nociceptors and they do of course show reactions to injuries and other interventions. But it is not known whether this is perceived as pain.
advertisement
There is often a lack of distinction between conscious pain and unconscious nociception
The current overview-study raises the complaint that a great majority of all published studies evaluate a fish’s reaction to a seemingly painful impulse - such as rubbing the injured body part against an object or the discontinuation of the feed intake - as an indication of pain. However, this methodology does not prove verifiably whether the reaction was due to a conscious sensation of pain or an unconscious impulse perception by means of nociception, or a combination of the two. Basically, it is very difficult to deduct underlying emotional states based on behavioural responses. Moreover, fish often show only minor or no reactions at all to interventions which would be extremely painful to us and to other mammals. Pain killers such as morphine that are effective for humans were either ineffective in fish or were only effective in astronomically high doses that, for small mammals, would have meant immediate death from shock. These findings suggest that fish either have absolutely no awareness of pain in human terms or they react completely different to pain. By and large, it is absolutely not advisable to interpret the behaviour of fish from a human perspective.
What does all this mean for those who use fish?
In legal terms it is forbidden to inflict pain, suffering or harm on animals without due cause according to §1 of the German Animal Protection Act. However, the criteria for when such acts are punishable are exclusively tied to the animal’s ability to feel pain and suffering in accordance with § 17 of the very same Act. The new study severely doubts that fish are aware of pain as defined by human terms. Therefore, it should actually no longer constitute a criminal offence if, for example, an angler releases a harvestable fish at his own discretion instead of eating it. However, at a legal and moral level, the recently published doubts regarding the awareness of pain in fish do not release anybody from their responsibility of having to justify all uses of fishes in a socially acceptable way and to minimise any form of stress and damage to the fish when interacting with it.
Jan. 12, 2022 A team of researchers has shown for the first time that decisions feel right to us if we have compared the options as attentively as possible -- and if we are conscious of having done so. This ...
Mar. 29, 2021 When humans look out at a visual landscape like a sunset or a beautiful overlook, we experience something -- we have a conscious awareness of what that scene looks like. This awareness of the visual ...
Aug. 8, 2019 We are all familiar with the common myth that fish have poor memory, but it turns that their DNA has the capacity to hold much more memory than that of humans. Rwesearchers report that memory in the ... | Do fish feel pain? Not as humans do, study suggests
Fish do not feel pain the way humans do, according to a team of neurobiologists, behavioral ecologists and fishery scientists. The researchers conclude that fish do not have the neuro-physiological capacity for a conscious awareness of pain.
Fish do not feel pain the way humans do. That is the conclusion drawn by an international team of researchers consisting of neurobiologists, behavioural ecologists and fishery scientists. One contributor to the landmark study was Prof. Dr. Robert Arlinghaus of the Leibniz Institute of Freshwater Ecology and Inland Fisheries and of the Humboldt University in Berlin.
On July 13th a revised animal protection act has come into effect in Germany. But anyone who expects it to contain concrete statements regarding the handling of fish will be disappointed. Legislators seemingly had already found their answer to the fish issue. Accordingly, fish are sentient vertebrates who must be protected against cruel acts performed by humans against animals. Anyone in Germany who, without due cause, kills vertebrates or inflicts severe pain or suffering on them has to face penal consequences as well as severe fines or even prison sentences. Now, the question of whether or not fish are really able to feel pain or suffer in human terms is once again on the agenda.
A final decision would have far-reaching consequences for millions of anglers, fishers, aquarists, fish farmers and fish scientists. To this end, a research team consisting of seven people has examined all significant studies on the subject of fish pain. During their research the scientists from Europe, Canada, Australia and the USA have discovered many deficiencies. These are the authors’ main points of criticism: Fish do not have the neuro-physiological capacity for a conscious awareness of pain. In addition, behavioural reactions by fish to seemingly painful impulses were evaluated according to human criteria and were thus misinterpreted. There is still no final proof that fish can feel pain.
This is how it works for humans
To be able to understand the researchers’ criticism you first have to comprehend how pain perception works for humans. Injuries stimulate what is known as nociceptors. | no |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://hakaimagazine.com/features/fish-feel-pain-now-what/ | Fish Feel Pain. Now What? | Hakai Magazine | Authored by
Wordcount
Share this article
Stream or download audio For this article
This article is also available in audio format. Listen now, download, or subscribe to “Hakai Magazine Audio Edition” through your favorite podcast app.
Article body copy
When Culum Brown was a young boy, he and his grandmother frequented a park near her home in Melbourne, Australia. He was fascinated by the park’s large ornamental pond wriggling with goldfish, mosquitofish, and loaches. Brown would walk the perimeter of the pond, peering into the translucent shallows to gaze at the fish. One day, he and his grandmother arrived at the park and discovered that the pond had been drained—something the parks department apparently did every few years. Heaps of fish flapped upon the exposed bed, suffocating in the sun.
Brown raced from one trash can to another, searching through them and collecting whatever discarded containers he could find—mostly plastic soda bottles. He filled the bottles at drinking fountains and corralled several fish into each one. He pushed other stranded fish toward regions of the pond where some water remained. “I was frantic, running around like a lunatic, trying to save these animals,” recalls Brown, who is now a marine biologist at Macquarie University in Sydney. Ultimately, he managed to rescue hundreds of fish, about 60 of which he adopted. Some of them lived in his home aquariums for more than 10 years.
As a child, I too kept fish. My very first pets were two goldfish, bright as newly minted pennies, in an unornamented glass bowl the size of a cantaloupe. They died within a few weeks. I later upgraded to a 40-liter tank lined with rainbow gravel and a few plastic plants. Inside I kept various small fish: neon tetras with bands of fluorescent blue and red, guppies with bold billowing tails like solar flares, and glass catfish so diaphanous they seemed nothing more than silver-crowned spinal columns darting through the water. Most of these fish lived much longer than the goldfish, but some of them had a habit of leaping in ecstatic arcs straight through the gaps in the tank’s cover and onto the living room floor. My family and I would find them flopping behind the TV, cocooned in dust and lint.
Should we care how fish feel? In his 1789 treatise An Introduction to the Principles of Morals and Legislation, English philosopher Jeremy Bentham—who developed the theory of utilitarianism (essentially, the greatest good for the greatest number of individuals)—articulated an idea that has been central to debates about animal welfare ever since. When considering our ethical obligations to other animals, Bentham wrote, the most important question is not, “Can they reason? nor, Can they talk? but, Can they suffer?” Conventional wisdom has long held that fish cannot—that they do not feel pain. An exchange in a 1977 issue of Field & Stream exemplifies the typical argument. In response to a 13-year-old girl’s letter about whether fish suffer when caught, the writer and fisherman Ed Zern first accuses her of having a parent or teacher write the letter because it is so well composed. He then explains that “fish don’t feel pain the way you do when you skin your knee or stub your toe or have a toothache, because their nervous systems are much simpler. I’m not really sure they feel any pain, as we feel pain, but probably they feel a kind of ‘fish pain.’” Ultimately, whatever primitive suffering they endure is irrelevant, he continues, because it’s all part of the great food chain and, besides, “if something or somebody ever stops us from fishing, we’ll suffer terribly.”
Such logic is still prevalent today. In 2014, BBC Newsnight invited Penn State University biologist Victoria Braithwaite to discuss fish pain and welfare with Bertie Armstrong, head of the Scottish Fishermen’s Federation. Armstrong dismissed the notion that fish deserve welfare laws as “cranky” and insisted that “the balance of scientific evidence is that fish do not feel pain as we do.”
That’s not quite true, Braithwaite says. It is impossible to definitively know whether another creature’s subjective experience is like our own. But that is beside the point. We do not know whether cats, dogs, lab animals, chickens, and cattle feel pain the way we do, yet we still afford them increasingly humane treatment and legal protections because they have demonstrated an ability to suffer. In the past 15 years, Braithwaite and other fish biologists around the world have produced substantial evidence that, just like mammals and birds, fish also experience conscious pain. “More and more people are willing to accept the facts,” Braithwaite says. “Fish do feel pain. It’s likely different from what humans feel, but it is still a kind of pain.”
At the anatomical level, fish have neurons known as nociceptors, which detect potential harm, such as high temperatures, intense pressure, and caustic chemicals. Fish produce the same opioids—the body’s innate painkillers—that mammals do. And their brain activity during injury is analogous to that in terrestrial vertebrates: sticking a pin into goldfish or rainbow trout, just behind their gills, stimulates nociceptors and a cascade of electrical activity that surges toward brain regions essential for conscious sensory perceptions (such as the cerebellum, tectum, and telencephalon), not just the hindbrain and brainstem, which are responsible for reflexes and impulses.
Fish also behave in ways that indicate they consciously experience pain. In one study, researchers dropped clusters of brightly colored Lego blocks into tanks containing rainbow trout. Trout typically avoid an unfamiliar object suddenly introduced to their environment in case it’s dangerous. But when scientists gave the rainbow trout a painful injection of acetic acid, they were much less likely to exhibit these defensive behaviors, presumably because they were distracted by their own suffering. In contrast, fish injected with both acid and morphine maintained their usual caution. Like all analgesics, morphine dulls the experience of pain, but does nothing to remove the source of pain itself, suggesting that the fish’s behavior reflected their mental state, not mere physiology. If the fish were reflexively responding to the presence of caustic acid, as opposed to consciously experiencing pain, then the morphine should not have made a difference.
In another study, rainbow trout that received injections of acetic acid in their lips began to breathe more quickly, rocked back and forth on the bottom of the tank, rubbed their lips against the gravel and the side of the tank, and took more than twice as long to resume feeding as fish injected with benign saline. Fish injected with both acid and morphine also showed some of these unusual behaviors, but to a much lesser extent, whereas fish injected with saline never behaved oddly.
Testing for pain in fish is challenging, so researchers often look for unusual behavior and physiological responses. In one study, rainbow trout given injections of acetic acid in their lips responded by rubbing their lips on the sides and bottom of their tank and delaying feeding. Photo by Alex Mustard/2020Vision/Minden Pictures
Several years ago, Lynne Sneddon, a University of Liverpool biologist and one of the world’s foremost experts on fish pain, began conducting a set of particularly intriguing experiments; so far, only some of the results have been published. In one test, she gave zebrafish the choice between two aquariums: one completely barren, the other containing gravel, a plant, and a view of other fish. They consistently preferred to spend time in the livelier, decorated chamber. When some fish were injected with acid, however, and the bleak aquarium was flooded with pain-numbing lidocaine, they switched their preference, abandoning the enriched tank. Sneddon repeated this study with one change: rather than suffusing the boring aquarium with painkiller, she injected it straight into the fish’s bodies, so they could take it with them wherever they swam. The fish remained among the gravel and greenery.
The collective evidence is now robust enough that biologists and veterinarians increasingly accept fish pain as a reality. “It’s changed so much,” Sneddon says, reflecting on her experiences speaking to both scientists and the general public. “Back in 2003, when I gave talks, I would ask, ‘Who believes fish can feel pain?’ Just one or two hands would go up. Now you ask the room and pretty much everyone puts their hands up.” In 2013, the American Veterinary Medical Association published new guidelines for the euthanasia of animals, which included the following statements: “Suggestions that finfish responses to pain merely represent simple reflexes have been refuted. … the preponderance of accumulated evidence supports the position that finfish should be accorded the same considerations as terrestrial vertebrates in regard to relief from pain.”
Yet this scientific consensus has not permeated public perception. Google “do fish feel pain” and you plunge yourself into a morass of conflicting messages. They don’t, says one headline. They do, says another. Other sources claim there’s a convoluted debate raging between scientists. In truth, that level of ambiguity and disagreement no longer exists in the scientific community. In 2016, University of Queensland professor Brian Key published an article titled “Why fish do not feel pain” in Animal Sentience: An Interdisciplinary Journal on Animal Feeling. So far, Key’s article has provoked more than 40 responses from scientists around the world, almost all of whom reject his conclusions.
Key is one of the most vociferous critics of the idea that fish can consciously suffer; the other is James D. Rose, a professor emeritus of zoology at the University of Wyoming and an avid fisherman who has written for the pro-angling publication Angling Matters. The thrust of their argument is that the studies ostensibly demonstrating pain in fish are poorly designed and, more fundamentally, that fish lack brains complex enough to generate a subjective experience of pain. In particular, they stress that fish do not have the kind of large, dense, undulating cerebral cortices that humans, primates, and certain other mammals possess. The cortex, which envelops the rest of the brain like bark, is thought to be crucial for sensory perceptions and consciousness.
Some of the critiques published by Key and Rose are valid, particularly on the subject of methodological flaws. A few studies in the growing literature on fish pain do not properly distinguish between a reflexive response to injury and a probable experience of pain, and some researchers have overstated the significance of these flawed efforts. At this point, however, such studies are in the minority. Many experiments have confirmed the early work of Braithwaite and Sneddon.
Moreover, the notion that fish do not have the cerebral complexity to feel pain is decidedly antiquated. Scientists agree that most, if not all, vertebrates (as well as some invertebrates) are conscious and that a cerebral cortex as swollen as our own is not a prerequisite for a subjective experience of the world. The planet contains a multitude of brains, dense and spongy, globular and elongated, as small as poppy seeds and as large as watermelons; different animal lineages have independently conjured similar mental abilities from very different neural machines. A mind does not have to be human to suffer.
Despite the evidence of conscious suffering in fish, they are not typically afforded the kind of legal protections given to farm animals, lab animals, and pets in many countries around the world. The United Kingdom has some of the most progressive animal welfare legislation, which typically covers all nonhuman vertebrates. In Canada and Australia, animal welfare laws are more piecemeal, varying from one state or province to another; some protect fish, some don’t. Japan’s relevant legislation largely neglects fish. China has very few substantive animal welfare laws of any kind. And in the United States, the Animal Welfare Act protects most warm-blooded animals used in research and sold as pets, but excludes fish, amphibians, and reptiles. Yet the sheer number of fish killed for food and bred for pet stores dwarfs the corresponding numbers of mammals, birds, and reptiles. Annually, about 70 billion land animals are killed for food around the world. That number includes chickens, other poultry, and all forms of livestock. In contrast, an estimated 10 to 100 billion farmed fish are killed globally every year, and about another one to three trillion fish are caught from the wild. The number of fish killed each year far exceeds the number of people who have ever existed on Earth.
“We have largely thought of fish as very alien and very simple, so we didn’t really care how we killed them,” Braithwaite says. “If we look at trawl netting, that’s a pretty gruesome way for fish to die: the barometric trauma of getting ripped from the ocean into open air, and then slowly suffocating. Can we do that more humanely? Yes. Should we? Probably, yes. We’re mostly not doing it at the moment because it’s more expensive to kill fish humanely, especially in the wild.”
There are no regulations on how fish should be killed; techniques include a swift blow to the head, suffocation, freezing, poisoning, and electric shock. Photo by Michelle Howell/Alamy Stock Photo
In some countries, such as the United Kingdom and Norway, fish farms have largely adopted humane slaughter methods. Instead of suffocating fish in air—the easiest and historically the most common practice—or freezing them to death in ice water, or poisoning them with carbon dioxide, they render fish unconscious with either a quick blow to the head or strong electrical currents, then pierce their brains or bleed them out. In Norway, Hanne Digre and her colleagues at the research organization SINTEF have brought these techniques onto commercial fishing vessels on a trial basis to investigate whether humane slaughter is feasible out at sea.
In a series of experiments, Digre and her colleagues tested different open-sea slaughter methods on a variety of species. They found that cod and haddock stored in dry bins on ships after harvest remained conscious for at least two hours. An electric shock delivered immediately after bringing fish onto a ship could knock them unconscious, but only if the current was strong enough. If the electric shock was too weak, the fish were merely immobilized. Some species, such as saithe, tended to break their spines and bleed internally when shocked; others, such as cod, struggled much less. Some fish regained consciousness about 10 minutes after being stunned, so the researchers recommend cutting their throats within 30 seconds of an electric shock.
In the United States, two brothers are pioneering a new kind of humane fishing. In fall of 2016, Michael and Patrick Burns, both longtime fishermen and cattle ranchers, launched a unique fishing vessel named Blue North. The 58-meter boat, which can carry about 750 tonnes and a crew of 26, specializes in harvesting Pacific cod from the Bering Sea. The crew works within a temperature-controlled room in the middle of the boat, which houses a moon pool—a hole through which they haul up fish one at a time. This sanctuary protects the crew from the elements and gives them much more control over the act of fishing than they would have on an ordinary vessel. Within seconds of bringing a fish to the surface, the crew moves it to a stun table that renders the animal unconscious with about 10 volts of direct current. The fish are then bled.
The Burns brothers were initially inspired by groundbreaking research on humane slaughter facilities for livestock conducted by Colorado State University animal science professor and internationally renowned autism spokesperson Temple Grandin. By considering the perspectives of the animals themselves, Grandin’s innovative designs greatly reduced stress, panic, and injury in cattle being herded toward an abattoir, while simultaneously making the whole process more efficient for ranchers. “One day it occurred to me, why couldn’t we take some of those principles and apply them to the fishing industry? Michael recalls. Inspired by moon pools on Norwegian fishing vessels, and the use of electrical stunning in various forms of animal husbandry, they designed Blue North. Michael thinks his new ship is one of perhaps two vessels in the world to consistently use electrical stunning on wild-caught fish. “We believe that fish are sentient beings, that they do experience panic and stress,” he says. “We have come up with a method to stop that.”
Right now, the Burns brothers export the cod they catch to Japan, China, France, Spain, Denmark, and Norway. The fact that the fish are humanely harvested has not been a big draw for their main buyers, Michael says, but he expects that will change. He and his team have been speaking with various animal welfare organizations to develop new standards and certifications for humanely caught wild fish. “It will become more common,” Michael says. “A lot of people out there are concerned with where their food comes from and how it’s handled.”
Meanwhile, the vast majority of the trillions of fish slaughtered annually are killed in ways that likely cause them immense pain. The truth is that even the adoption of humane slaughter methods in more progressive countries has not been entirely or even primarily motivated by ethics. Rather, such changes are driven by profit. Studies have shown that reducing stress in farmed and caught fish, killing them swiftly and efficiently with minimal struggle, improves the quality of the meat that eventually makes it to market. The flesh of fish killed humanely is often smoother and less blemished. When we treat fish well, we don’t really do it for their sake; we do it for ours.
“I’ve always had a natural empathy for animals and had no reason to exclude fish,” Brown says. “At that park [in Melbourne], they didn’t have any concern that there were fish in there and they might need some water. There was no attempt to save them or house them whatsoever. I was shocked by that at that age, and I still see that kind of callous disregard for fish in people today in all sorts of contexts. In all the time since we discovered the first evidence for pain in fish, I don’t think public perception has moved an ounce.”
Lately, I’ve been spending a lot of time at my local pet stores, watching the fish. They move restlessly, noiselessly—leglessly pacing from one side of their tanks to another. Some hang in the water, heads tilted up, as though caught on an invisible line. A glint of scales draws my attention; an unexpected swatch of color. I try to look one in the eye—a depthless disc of obsidian. Its mouth moves so mechanically, like a sliding door stuck in a loop. I look at these fish, I enjoy looking at them, I do not wish them any harm; yet I almost never wonder what they are thinking or feeling. Fish are our direct evolutionary ancestors. They are the original vertebrates, the scaly, stubby-limbed pioneers who crawled still wet from the sea and colonized the land. So many gulfs separate us now: geographical, anatomical, psychological. We can understand, rationally, the overwhelming evidence for fish sentience. But the facts are not enough. Genuinely pitying a fish seems to require an Olympian feat of empathy.
Perhaps, though, our typical interactions with fish—the placid pet in a glass puddle, or the garnished filet on a plate—are too circumscribed to reveal a capacity for suffering. I recently learned of a culinary tradition, still practiced today, known as ikizukuri: eating the raw flesh of a living fish. You can find videos online. In one, a chef covers a fish’s face with a cloth and holds it down as he shaves off its scales with something like a crude cheese grater. He begins to slice the fish lengthwise with a large knife, but the creature leaps violently from his grasp and somersaults into a nearby sink. The chef reclaims the fish and continues slicing away both its flanks. Blood as dark as pomegranate juice spills out. He immerses the fish in a bowl of ice water as he prepares the sashimi. The whole fish will be served on a plate with shaved daikon and shiso leaves, rectangular chunks of its flesh piled neatly in its hollowed side, its mouth and gills still flapping, and the occasional shudder rippling across the length of its body. | He then explains that “fish don’t feel pain the way you do when you skin your knee or stub your toe or have a toothache, because their nervous systems are much simpler. I’m not really sure they feel any pain, as we feel pain, but probably they feel a kind of ‘fish pain.’” Ultimately, whatever primitive suffering they endure is irrelevant, he continues, because it’s all part of the great food chain and, besides, “if something or somebody ever stops us from fishing, we’ll suffer terribly.”
Such logic is still prevalent today. In 2014, BBC Newsnight invited Penn State University biologist Victoria Braithwaite to discuss fish pain and welfare with Bertie Armstrong, head of the Scottish Fishermen’s Federation. Armstrong dismissed the notion that fish deserve welfare laws as “cranky” and insisted that “the balance of scientific evidence is that fish do not feel pain as we do.”
That’s not quite true, Braithwaite says. It is impossible to definitively know whether another creature’s subjective experience is like our own. But that is beside the point. We do not know whether cats, dogs, lab animals, chickens, and cattle feel pain the way we do, yet we still afford them increasingly humane treatment and legal protections because they have demonstrated an ability to suffer. In the past 15 years, Braithwaite and other fish biologists around the world have produced substantial evidence that, just like mammals and birds, fish also experience conscious pain. “More and more people are willing to accept the facts,” Braithwaite says. “Fish do feel pain. It’s likely different from what humans feel, but it is still a kind of pain.”
At the anatomical level, fish have neurons known as nociceptors, which detect potential harm, such as high temperatures, intense pressure, and caustic chemicals. Fish produce the same opioids—the body’s innate painkillers—that mammals do. | yes |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://www.understandinganimalresearch.org.uk/news/do-fish-feel-pain | Do fish feel pain? | Do fish feel pain?
For a long time, fish were thought incapable of feeling pain. The common belief was that the biology of a fish was far too simple to process pain. Indeed, fish brains don’t seem to have an equivalent structure to the part of the human brain capable of processing pain.
But claiming that fish don't feel pain due to the absence of brain regions equivalent to those found in humans is like concluding they can't swim because they don't have arms and legs.
“Before 2002, no one thought that fish even had nociceptors. These are the nerve endings that detect potentially painful stimuli, such as high temperatures, intense pressure, and caustic chemicals,” explains Lynne Sneddon, director of bioveterinary science at Liverpool University.
Sneddon published the first study to prove that fish do indeed have pain-sensing receptors in their brains. “It was quite a paradigm shifting event. Up until then there was no pain in fish. And then suddenly, there was a possibility. My research has since shown that fish have a strikingly similar neuronal system to mammals.”
Sneddon found that pinching and pricking fish activates the same nerve types that, in humans, detect painful stimuli. Nerves are not proof that fish experience pain, but the study showed that fish have the necessary anatomical hardware.
The software comes in the form of brain chemicals called neurotransmitters that carry the information. Mammals and fish often share those neurotransmitters too. Fish also produce the same opioids — the body’s innate painkillers — that mammals do.
Fish also exhibit behavioral responses to pain.
“Stimuli that cause pain in humans also affect fish,” explains Lynne Sneddon. A painful injection will cause fish to breath faster and rub the injection site. Furthermore, fish in pain don’t respond to fear-causing situations and do not show normal anti-predator behaviour, just like humans do tasks less well when they are in pain. Drugs like aspirin, lidocaine and morphine, make these pain symptoms disappear. “If fish don’t experience pain,” adds Sneddon, “then the analgesic drugs don’t have any effect.”
Of course, it is impossible to know for certain whether another creature’s subjective experience is like our own. We don’t know for sure whether mice, cats, dogs, chickens and lab animals feel pain the way we do too. Yet, we still afford them legal protections because they have demonstrated an ability to suffer.
When considering our ethical obligations to other animals, English philosopher Jeremy Bentham wrote in 1789 that the most important question is not, “Can they reason? nor, Can they talk? but, Can they suffer?” That idea has been central to debates about animal welfare ever since. Asking whether fish suffer means asking what our fundamental obligations to fish might be.
“I think people now generally accept that fish do experience pain and we should do something about it,” says Seddon. “I’ve seen fish welfare massively change, especially over the last 10 years, because of it. Although I always think we are 10 years behind mammals in terms of progress, but we are getting there.”
At the moment about half a million fish a year are used in laboratory procedures. They are subject to experiments ranging from very mild behavioural studies through to major surgery. It is important that they are given the care that they deserve, and that includes pain management.
“The home office in the UK is asking to put pain relief in experimental methods where possible,” adds Sneddon. “It would be inconceivable to do surgery in mammals without providing pain relief. Yet we had been doing it to fish for a long time. This has now changed.”
The United Kingdom has some of the most progressive animal welfare legislation in the world, which typically covers all non-human vertebrates.
Fish models are used in many biomedical research fields including studies looking at heart and spinal regeneration, but also Alzheimer’s disease, visual impairments and even cancer. They remain crucial for therapeutic breakthroughs and it is important that welfare standards are adequate to their ability to feel. | Do fish feel pain?
For a long time, fish were thought incapable of feeling pain. The common belief was that the biology of a fish was far too simple to process pain. Indeed, fish brains don’t seem to have an equivalent structure to the part of the human brain capable of processing pain.
But claiming that fish don't feel pain due to the absence of brain regions equivalent to those found in humans is like concluding they can't swim because they don't have arms and legs.
“Before 2002, no one thought that fish even had nociceptors. These are the nerve endings that detect potentially painful stimuli, such as high temperatures, intense pressure, and caustic chemicals,” explains Lynne Sneddon, director of bioveterinary science at Liverpool University.
Sneddon published the first study to prove that fish do indeed have pain-sensing receptors in their brains. “It was quite a paradigm shifting event. Up until then there was no pain in fish. And then suddenly, there was a possibility. My research has since shown that fish have a strikingly similar neuronal system to mammals.”
Sneddon found that pinching and pricking fish activates the same nerve types that, in humans, detect painful stimuli. Nerves are not proof that fish experience pain, but the study showed that fish have the necessary anatomical hardware.
The software comes in the form of brain chemicals called neurotransmitters that carry the information. Mammals and fish often share those neurotransmitters too. Fish also produce the same opioids — the body’s innate painkillers — that mammals do.
Fish also exhibit behavioral responses to pain.
“Stimuli that cause pain in humans also affect fish,” explains Lynne Sneddon. A painful injection will cause fish to breath faster and rub the injection site. Furthermore, fish in pain don’t respond to fear-causing situations and do not show normal anti-predator behaviour, just like humans do tasks less well when they are in pain. Drugs like aspirin, lidocaine and morphine, make these pain symptoms disappear. | yes |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://www.peta.org/issues/animals-used-for-food/factory-farming/fish/fish-feel-pain/ | Fish Feel Pain | PETA | Fish Feel Pain
In her book Do Fish Feel Pain?, biologist Victoria Braithwaite says that “there is as much evidence that fish feel pain and suffer as there is for birds and mammals.”
Fish don’t audibly scream when they’re impaled on hooks or grimace when the hooks are ripped from their mouths, but their behavior offers evidence of their suffering—if we’re willing to look. For example, when Braithwaite and her colleagues exposed fish to irritating chemicals, the animals behaved as any of us might: They lost their appetite, their gills beat faster, and they rubbed the affected areas against the side of the tank.
Neurobiologists have long recognized that fish have nervous systems that comprehend and respond to pain. Fish, like “higher vertebrates,” have neurotransmitters such as endorphins that relieve suffering—the only reason for their nervous systems to produce these painkillers is to alleviate pain. Researchers have created a detailed map of more than 20 pain receptors, or “nociceptors,” in fish’s mouths and heads—including those very areas where an angler’s barbed hook would penetrate a fish’s flesh. As Dr. Stephanie Yue wrote in her position paper on fish and pain, “Pain is an evolutionary adaptation that helps individuals survive . . . . [A] trait like pain perception is not likely to suddenly disappear for one particular taxonomic class.”
Even though fish don’t have the same brain structures that humans do—fish do not have a neocortex, for example—Dr. Ian Duncan reminds us that we “have to look at behaviour and physiology,” not just anatomy. “It’s possible for a brain to evolve in different ways,” he says. “That’s what is happening in the fish line. It’s evolved in some other ways in other parts of the brain to receive pain.”
Numerous studies in recent years have demonstrated that fish feel and react to pain. For example, when rainbow trout had painful acetic acid or bee venom injected into their sensitive lips, they stopped eating, rocked back and forth on the tank floor, and rubbed their lips against the tank walls. Fish who were injected with a harmless saline solution didn’t display this abnormal behavior.
Trout are “neophobic,” meaning that they actively avoid new objects. But those who were injected with acetic acid showed little response to a brightly colored Lego tower that was placed in their tank, suggesting that their attention was focused instead on the pain that they were experiencing. In contrast, trout injected with saline—as well as those who were given painkillers following the painful acid injection—displayed the usual degree of caution regarding the new object. Similar results have been demonstrated in human patients suffering from painful medical conditions: Medical professionals have long known that pain interferes with patients’ normal cognitive abilities.
A study in the journal Applied Animal Behaviour Science found that fish who are exposed to painful heat later show signs of fear and wariness—illustrating that fish both experience pain and can remember it.
A study by scientists at Queen’s University Belfast proved that fish learn to avoid pain, just like other animals. Rebecca Dunlop, one of the researchers, said, “This paper shows that pain avoidance in fish doesn’t seem to be a reflex response, rather one that is learned, remembered and is changed according to different circumstances. Therefore, if fish can perceive pain, then angling cannot continue to be considered a non-cruel sport.”
Similarly, researchers at the University of Guelph in Canada concluded that fish feel fear when they’re chased and that their behavior is more than simply a reflex. The “fish are frightened and … they prefer not being frightened,” said Dr. Duncan, who headed the study.
In a 2014 report, the Farm Animal Welfare Committee (FAWC), an advisory body to the British government, stated, “Fish are able to detect and respond to noxious stimuli, and FAWC supports the increasing scientific consensus that they experience pain.”
Dr. Culum Brown of Macquarie University, who reviewed nearly 200 research papers on fish’s cognitive abilities and sensory perceptions, believes that the stress that fish experience when they’re pulled from the water into an environment in which they cannot breathe may even exceed that of a human drowning. “[U]nlike drowning in humans, where we die in about 4–5 minutes because we can’t extract any oxygen from water, fish can go on for much longer. It’s a prolonged slow death most of the time,” he says.
Anglers may not want to think about it, but fishing is nothing more than a cruel blood sport. When fish are impaled on an angler’s hook and yanked out of the water, it’s not a game to them. They are scared, in pain, and fighting for their lives. Michael Stoskopf, professor of aquatics, wildlife, and zoologic medicine and of molecular and environmental toxicology at North Carolina University, said, “It would be an unjustified error to assume that fish do not perceive pain in these situations merely because their responses do not match those traditionally seen in mammals subjected to chronic pain.”
As a result of his research, Dr. Culum Brown concludes that “it would be impossible for fish to survive as the cognitively and behaviorally complex animals they are without a capacity to feel pain” and “the potential amount of cruelty” that we humans inflict on fish “is mind-boggling.”
Get PETA Updates
Stay up to date on the latest vegan trends and get breaking animal rights news delivered straight to your inbox!
E-Mail Address
Sign me up for the following e-mail:
Membership Updates PETA News
Current subscribers: You will continue to receive e-mail unless you explicitly opt out by clicking here.
By submitting this form, you are agreeing to our collection, storage, use, and disclosure of your personal info in accordance with our privacy policy as well as to receiving e-mails from us.
“Almost all of us grew up eating meat, wearing leather, and going to circuses and zoos. We never considered the impact of these actions on the animals involved. For whatever reason, you are now asking the question: Why should animals have rights?” READ MORE | Fish Feel Pain
In her book Do Fish Feel Pain?, biologist Victoria Braithwaite says that “there is as much evidence that fish feel pain and suffer as there is for birds and mammals.”
Fish don’t audibly scream when they’re impaled on hooks or grimace when the hooks are ripped from their mouths, but their behavior offers evidence of their suffering—if we’re willing to look. For example, when Braithwaite and her colleagues exposed fish to irritating chemicals, the animals behaved as any of us might: They lost their appetite, their gills beat faster, and they rubbed the affected areas against the side of the tank.
Neurobiologists have long recognized that fish have nervous systems that comprehend and respond to pain. Fish, like “higher vertebrates,” have neurotransmitters such as endorphins that relieve suffering—the only reason for their nervous systems to produce these painkillers is to alleviate pain. Researchers have created a detailed map of more than 20 pain receptors, or “nociceptors,” in fish’s mouths and heads—including those very areas where an angler’s barbed hook would penetrate a fish’s flesh. As Dr. Stephanie Yue wrote in her position paper on fish and pain, “Pain is an evolutionary adaptation that helps individuals survive . . . . [A] trait like pain perception is not likely to suddenly disappear for one particular taxonomic class.”
Even though fish don’t have the same brain structures that humans do—fish do not have a neocortex, for example—Dr. Ian Duncan reminds us that we “have to look at behaviour and physiology,” not just anatomy. “It’s possible for a brain to evolve in different ways,” he says. “That’s what is happening in the fish line. It’s evolved in some other ways in other parts of the brain to receive pain.”
Numerous studies in recent years have demonstrated that fish feel and react to pain. | yes |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://en.wikipedia.org/wiki/Pain_in_fish | Pain in fish - Wikipedia | Fish fulfill several criteria proposed as indicating that non-human animals may experience pain. These fulfilled criteria include a suitable nervous system and sensory receptors, opioid receptors and reduced responses to noxious stimuli when given analgesics and local anaesthetics, physiological changes to noxious stimuli, displaying protective motor reactions, exhibiting avoidance learning and making trade-offs between noxious stimulus avoidance and other motivational requirements.
Whether fish feel pain similar to humans or differently is a contentious issue. Pain is a complex mental state, with a distinct perceptual quality but also associated with suffering, which is an emotional state. Because of this complexity, the presence of pain in an animal, or another human for that matter, cannot be determined unambiguously using observational methods, but the conclusion that animals experience pain is often inferred on the basis of likely presence of phenomenal consciousness which is deduced from comparative brain physiology as well as physical and behavioural reactions.[1]
The possibility that fish and other non-human animals may experience pain has a long history. Initially, this was based around theoretical and philosophical argument, but more recently has turned to scientific investigation.
The idea that non-human animals might not feel pain goes back to the 17th-century French philosopher, René Descartes, who argued that animals do not experience pain and suffering because they lack consciousness.[2][3][4] In 1789, the British philosopher and social reformist, Jeremy Bentham, addressed in his book An Introduction to the Principles of Morals and Legislation the issue of our treatment of animals with the following often quoted words: "The question is not, Can they reason? nor, Can they talk? but, Can they suffer?"[5]
Charles Darwin said that "The lower animals, like man, manifestly feel pleasure and pain, happiness and misery."[6]
Peter Singer, a bioethicist and author of Animal Liberation published in 1975, suggested that consciousness is not necessarily the key issue: just because animals have smaller brains, or are 'less conscious' than humans, does not mean that they are not capable of feeling pain. He goes on further to argue that we do not assume newborn infants, people suffering from neurodegenerative brain diseases or people with learning disabilities experience less pain than we would.[7]
Bernard Rollin, the principal author of two U.S. federal laws regulating pain relief for animals, writes that researchers remained unsure into the 1980s as to whether animals experience pain, and veterinarians trained in the U.S. before 1989 were taught to simply ignore animal pain.[8] In his interactions with scientists and other veterinarians, Rollin was regularly asked to "prove" that animals are conscious, and to provide "scientifically acceptable" grounds for claiming that they feel pain.[8]
Continuing into the 1990s, discussions were further developed on the roles that philosophy and science had in understanding animal cognition and mentality.[9] In subsequent years, it was argued there was strong support for the suggestion that some animals (most likely amniotes) have at least simple conscious thoughts and feelings[10] and that the view animals feel pain differently to humans is now a minority view.[2]
The absence of a neocortex does not appear to preclude an organism from experiencing affective states. Convergent evidence indicates that non-human animals have the neuroanatomical, neurochemical, and neurophysiological substrates of conscious states along with the capacity to exhibit intentional behaviors. Consequently, the weight of evidence indicates that humans are not unique in possessing the neurological substrates that generate consciousness. Non-human animals, including all mammals and birds, and many other creatures, including octopuses, also possess these neurological substrates.[11]
In the 20th and 21st centuries, there were many scientific investigations of pain in non-human animals.
Dr Lynne Sneddon, with her colleagues, Braithwaite, and Gentle, were the first to discover nociceptors (pain receptors) in fish. She stated that fish demonstrate pain-related changes in physiology and behaviour, that are reduced by painkillers, and they show higher brain activity when painfully stimulated.[12] Professor Victoria Braithwaite, in her book, Do Fish Feel Pain?, wrote that, fish, like birds and mammals, have a capacity for self-awareness, and can feel pain.[13]Donald Broom, Professor of Animal Welfare, Cambridge University, England, said that most mammalian pain systems are also found in fish, who can feel fear and have emotions which are controlled in the fish brain in areas anatomically different but functionally very similar to those in mammals.[14]
The American Veterinary Medical Association accepts that fish feel pain saying that the evidence supports the position that fish should be accorded the same considerations as terrestrial vertebrates concerning relief from pain.[15]
The Royal Society for the Prevention of Cruelty to Animals, in Britain, commissioned in 1980 an independent panel of experts. They concluded that it was reasonable to believe that all vertebrates are capable of suffering to some degree or another.[16]RSPCA Australia more recently added that evidence that fish are capable of experiencing pain and suffering has been growing for some years.[17]
The European Union Panel on Animal Health and Welfare European Food Safety Authority said that the balance of evidence indicates that some fish species can experience pain.[18] The British Farm Animal Welfare Committee 2014's report, Opinion on the Welfare of Farmed Fish, said that the scientific consensus is that fish can detect and respond to noxious stimuli, and experience pain.[19]
In 2001 studies were published showing that arthritic rats self-select analgesic opiates.[20]
In 2014, the veterinary Journal of Small Animal Practice published an article on the recognition of pain which started – "The ability to experience pain is universally shared by all mammals..."[21] and in 2015, it was reported in the science journal Pain, that several mammalian species (rat, mouse, rabbit, cat and horse) adopt a facial expression in response to a noxious stimulus that is consistent with the expression of pain in humans.[22]
At the same time as the investigations using arthritic rats, studies were published showing that birds with gait abnormalities self-select for a diet that contains carprofen, a human analgesic.[23] In 2005, it was written "Avian pain is likely analogous to pain experienced by most mammals"[24] and in 2014, "...it is accepted that birds perceive and respond to noxious stimuli and that birds feel pain"[25]
Veterinary articles have been published stating both reptiles[26][27][28] and amphibians[29][30][31] experience pain in a way analogous to humans, and that analgesics are effective in these two classes of vertebrates.
Arguing by analogy, Varner claims that any animal which exhibits the properties listed in the table could be said to experience pain. On that basis, he concludes that all vertebrates, including fish, probably experience pain, but invertebrates apart from cephalopods probably do not experience pain.[32][37]
Crustaceans
Some studies however find crustaceans do show responses consistent with signs of pain and distress.[38]
Although there are numerous definitions of pain, almost all involve two key components.
First, nociception is required.[39] This is the ability to detect noxious stimuli which evoke a reflex response that rapidly moves the entire animal, or the affected part of its body, away from the source of the stimulus. The concept of nociception does not imply any adverse, subjective "feeling" – it is a reflex action. An example in humans would be the rapid withdrawal of a finger that has touched something hot – the withdrawal occurs before any sensation of pain is actually experienced.
The second component is the experience of "pain" itself, or suffering – the internal, emotional interpretation of the nociceptive experience. Again in humans, this is when the withdrawn finger begins to hurt, moments after the withdrawal. Pain is therefore a private, emotional experience. Pain cannot be directly measured in other animals, including other humans; responses to putatively painful stimuli can be measured, but not the experience itself. To address this problem when assessing the capacity of other species to experience pain, argument-by-analogy is used. This is based on the principle that if an animal responds to a stimulus in a similar way to ourselves, it is likely to have had an analogous experience.
Nociception: The reflex arc of a dog with a pin in her paw. Note there is no communication to the brain, but the paw is withdrawn by nervous impulses generated by the spinal cord. There is no conscious interpretation of the stimulus by the dog.
Nociception usually involves the transmission of a signal along a chain of nerve fibers from the site of a noxious stimulus at the periphery to the spinal cord and brain. This process evokes a reflex arc response generated at the spinal cord and not involving the brain, such as flinching or withdrawal of a limb. Nociception is found, in one form or another, across all major animal taxa.[39] Nociception can be observed using modern imaging techniques; and a physiological and behavioral response to nociception can often be detected. However, nociceptive responses can be so subtle in prey animals that trained (human) observers cannot perceive them, whereas natural predators can and subsequently target injured individuals.[40]
Sometimes a distinction is made between "physical pain" and "emotional" or "psychological pain". Emotional pain is the pain experienced in the absence of physical trauma, for example, the pain experienced by humans after the loss of a loved one, or the break-up of a relationship. It has been argued that only primates and humans can feel "emotional pain", because they are the only animals that have a neocortex – a part of the brain's cortex considered to be the "thinking area". However, research has provided evidence that monkeys, dogs, cats and birds can show signs of emotional pain and display behaviours associated with depression during or after a painful experience, specifically, a lack of motivation, lethargy, anorexia, and unresponsiveness to other animals.[7]
The nerve impulses of the nociception response may be conducted to the brain thereby registering the location, intensity, quality and unpleasantness of the stimulus. This subjective component of pain involves conscious awareness of both the sensation and the unpleasantness (the aversive, negative affect). The brain processes underlying conscious awareness of the unpleasantness (suffering), are not well understood.
There have been several published lists of criteria for establishing whether non-human animals experience pain, e.g.[41][42] Some criteria that may indicate the potential of another species, including fishes, to feel pain include:[42]
The adaptive value of nociception is obvious; an organism detecting a noxious stimulus immediately withdraws the limb, appendage or entire body from the noxious stimulus and thereby avoids further (potential) injury. However, a characteristic of pain (in mammals at least) is that pain can result in hyperalgesia (a heightened sensitivity to noxious stimuli) and allodynia (a heightened sensitivity to non-noxious stimuli). When this heightened sensitisation occurs, the adaptive value is less clear. First, the pain arising from the heightened sensitisation can be disproportionate to the actual tissue damage caused. Second, the heightened sensitisation may also become chronic, persisting well beyond the tissues healing. This can mean that rather than the actual tissue damage causing pain, it is the pain due to the heightened sensitisation that becomes the concern. This means the sensitisation process is sometimes termed maladaptive. It is often suggested hyperalgesia and allodynia assist organisms to protect themselves during healing, but experimental evidence to support this has been lacking.[43][44]
In 2014, the adaptive value of sensitisation due to injury was tested using the predatory interactions between longfin inshore squid (Doryteuthis pealeii) and black sea bass (Centropristis striata) which are natural predators of this squid. If injured squid are targeted by a bass, they began their defensive behaviours sooner (indicated by greater alert distances and longer flight initiation distances) than uninjured squid. If anaesthetic (1% ethanol and MgCl2) is administered prior to the injury, this prevents the sensitisation and blocks the behavioural effect. The authors claim this study is the first experimental evidence to support the argument that nociceptive sensitisation is actually an adaptive response to injuries.[40]
The question has been asked, "If fish cannot feel pain, why do stingrays have purely defensive tail spines that deliver venom? Stingrays' ancestral predators are fish. And why do many fishes possess defensive fin spines, some also with venom that produces pain in humans?"[45]
Rainbow trout have nociceptors on the face, eyes, snout and other areas of the body
Primitive fish such as lampreys (Petromyzon marinus) have free nerve endings in the skin that respond to heat and mechanical pressure. However, behavioural reactions associated with nociception have not been recorded, and it is also difficult to determine whether the mechanoreceptors in lamprey are truly nociceptive-specific or simply pressure-specific.[46]
Nociceptors in fish were first identified in 2002.[47][48] The study was designed to determine whether nociceptors were present in the trigeminal nerve on the head of the trout and to observe the physiological and behavioural consequences of prolonged noxious stimulation. Rainbow trout lips were injected with acetic acid, while another group were injected with bee venom. These substances were chosen because protons of the acid stimulate nociceptive nerves in mammals and frogs,[49] while venom has an inflammatory effect in mammals[50] and both are known to be painful in humans. The fish exhibited abnormal behaviours such as side-to-side rocking and rubbing of their lips along the sides and floors of the tanks. Their respiration rate increased, and they reduced the amount of swimming. The acid group also rubbed their lips on the gravel. Rubbing an injured area to ameliorate pain has been demonstrated in humans and in mammals.[51] Fifty-eight receptors were located on the face and head of the rainbow trout. Twenty-two of these receptors could be classified as nociceptors, as they responded to mechanical pressure and heat (more than 40 °C). Eighteen also reacted to acetic acid. The response of the receptors to mechanical, noxious thermal and chemical stimulation clearly characterised them as polymodal nociceptors. They had similar properties to those found in amphibians, birds[52][53] and mammals, including humans.[54] Trout that were injected with venom or acid took approximately 3 hours to resume eating, whereas the saline and control groups took approximately 1 hour. This may be guarding behaviour, where animals avoid using a painful limb, preventing continuing pain and harm being caused to the area.[52]
Rainbow trout (Oncorhynchus mykiss) have polymodal nociceptors on the face and snout that respond to mechanical pressure, temperatures in the noxious range (> 40 °C), and 1% acetic acid (a chemical irritant). Cutaneous receptors overall were found to be more sensitive to mechanical stimuli than those in mammals and birds, with some responding to stimuli as low 0.001g. In humans at least 0.6 g is required. This may be because fish skin is more easily damaged, necessitating nociceptors to have lower thresholds.[47][55][56][57] Further studies found nociceptors to be more widely distributed over the bodies of rainbow trout, as well as those of cod and carp. The most sensitive areas of the body are around the eyes, nostrils, fleshy parts of the tail, and pectoral and dorsal fins.[13][58]
Rainbow trout also have corneal nociceptors. Out of 27 receptors investigated in one study, seven were polymodal nociceptors and six were mechanothermal nociceptors. Mechanical and thermal thresholds were lower than those of cutaneous receptors, indicating greater sensitivity in the cornea.[59]
Bony fish possess nociceptors that are similar in function to those in mammals.[12]
There are two types of nerve fibre relevant to pain in fish. Group C nerve fibres are a type of sensory nerve fibre which lack a myelin sheath and have a small diameter, meaning they have a low nerve conduction velocity. The suffering that humans associate with burns, toothaches, or crushing injury are caused by C fibre activity. A typical human cutaneous nerve contains 83% Group C nerve fibres.[60]A-delta fibres are another type of sensory nerve fibre, however, these are myelinated and therefore transmit impulses faster than non-myelinated C fibres. A-delta fibres carry cold, pressure and some pain signals, and are associated with acute pain that results in "pulling away" from noxious stimuli.
Bony fish possess both Group C and A-delta fibres representing 38.7% (combined) of the fibres in the tail nerves of common carp and 36% of the trigeminal nerve of rainbow trout. However, only 5% and 4% of these are C fibres in the carp and rainbow trout, respectively.[60][61]
In fish, similar to other vertebrates, nociception travels from the peripheral nerves along the spinal nerves and is relayed through the spinal cord to the thalamus. The thalamus is connected to the telencephalon by multiple connections through the grey matter pallium, which has been demonstrated to receive nerve relays for noxious and mechanical stimuli.[64][65]
The major tracts that convey pain information from the periphery to the brain are the spinothalamic tract (body) and the trigeminal tract (head). Both have been studied in agnathans, teleost, and elasmobranch fish (trigeminal in the common carp,
spinothalamic tract in the sea robin, Prionotus carolinus).[66]
If sensory responses in fish are limited to the spinal cord and hindbrain, they might be considered as simply reflexive. However, recordings from the spinal cord, cerebellum, tectum and telencephalon in both trout and goldfish (Carassius auratus) show these all respond to noxious stimuli. This indicates a nociceptive pathway from the periphery to the higher CNS of fish.[67]
Somatosensory evoked potentials (SEPs) are weak electric responses in the CNS following stimulation of peripheral sensory nerves. These further indicate there is a pathway from the peripheral nociceptors to higher brain regions. In goldfish, rainbow trout, Atlantic salmon (Salmo salar) and Atlantic cod (Gadus morhua), it has been demonstrated that putatively non-noxious and noxious stimulation elicit SEPs in different brain regions, including the telencephalon[70] which may mediate the co-ordination of pain information.[71] Moreover, multiple functional magnetic resonance imaging (fMRI) studies with several species of fishes have shown that when suffering from putative pain, there is profound activity in the forebrain which is highly reminiscent of that observed in humans and would be taken as evidence of the experience of pain in mammals.[72][73]
Therefore, "higher" brain areas are activated at the molecular, physiological, and functional levels in fish experiencing a potentially painful event. Sneddon stated "This gives much weight to the proposal that fish experience some form of pain rather than a nociceptive event".[74]
Teleost fish have a functional opioid system which includes the presence of opioid receptors similar to those of mammals.[75][76]
Opioid receptors were already present at the origin of jawed vertebrates 450 million years ago.[77] All four of the main opioid receptor types (delta, kappa, mu, and NOP) are conserved in vertebrates, even in primitive jawless fishes (agnathastoma).[64]
The same analgesics and anaesthetics used in humans and other mammals, are often used for fish in veterinary medicine. These chemicals act on the nociceptive pathways, blocking signals to the brain where emotional responses to the signals are further processed by certain parts of the brain found in amniotes ("higher vertebrates").[78][79]
Pre-treatment with morphine (an analgesic in humans and other mammals) has a dose-dependent anti-nociceptive effect[80] and mitigates the behavioural and ventilation rate responses of rainbow trout to noxious stimuli.
When acetic acid is injected into the lips of rainbow trout, they exhibit anomalous behaviours such as side-to-side rocking and rubbing their lips along the sides and floors of the tanks, and their ventilation rate increases. Injections of morphine reduce both the anomalous, noxious-stimulus related behaviours and the increase in ventilation rate.[81] When the same noxious stimulus is applied to zebrafish (Danio rerio), they respond by decreasing their activity. As with the rainbow trout, morphine injected prior to the acid injection attenuates the decrease in activity in a dose-dependent manner.[71]
Injection of acetic acid into the lips of rainbow trout causes a reduction in their natural neophobia (fear of novelty); this is reversed by the administration of morphine.[13]
In goldfish injected with morphine or saline and then exposed to unpleasant temperatures, fish injected with saline acted with defensive behaviours indicating anxiety, wariness and fear, whereas those given morphine did not.[82]
Different analgesics have different effects on fish. In a study on the efficacy of three types of analgesic, buprenorphine (an opioid), carprofen (a non-steroidal anti-inflammatory drug) and lidocaine (a local anaesthetic), ventilation rate and time to resume feeding were used as pain indicators. Buprenorphine had limited impact on the fish's response, carprofen ameliorated the effects of noxious stimulation on time to resume feeding, however, lidocaine reduced all the behavioural indicators.[84] Administration of aspirin prevents behavioural change caused by acetic acid.[85]
Tramadol also increases the nociceptive threshold in fish, providing further evidence of an anti-nociceptive opioid system in fish.[13][86]
Naloxone is an μ-opioid receptor antagonist which, in mammals, negates the analgesic effects of opioids. Both adult and five-day-old zebrafish larvae show behavioural responses indicative of pain in response to injected or diluted acetic acid. The anti-nociceptive properties of morphine or buprenorphine are reversed if adults,[71] or larvae,[87] are co-treated with naloxone. Both naloxone and prolyl-leucyl-glycinamide (another opiate antagonist in mammals) reduced the analgesic effects of morphine to electric shocks received by goldfish, indicating they can act as an opiate antagonist in fish.[88][89]
Noxiously stimulated common carp show anomalous rocking behaviour and rub their lips against the tank wallsNoxiously stimulated zebrafish reduce their frequency of swimming and increase their ventilation rateNoxiously stimulated Atlantic cod display increased hovering close to the bottom of the tank and reduced use of shelterPredator fish learn to avoid sticklebacks with spines
When acetic acid or bee venom is injected into the lips of rainbow trout, they exhibit an anomalous side-to-side rocking behaviour on their pectoral fins, rub their lips along the sides and floors of the tanks[91] and increase their ventilation rate.[90] When acetic acid is injected into the lips of zebrafish, they respond by decreasing their activity. The magnitude of this behavioural response depends on the concentration of the acetic acid.[71]
The behavioural responses to a noxious stimulus differ between species of fish. Noxiously stimulated common carp (Cyprinus carpio) show anomalous rocking behaviour and rub their lips against the tank walls, but do not change other behaviours or their ventilation rate. In contrast, zebrafish (Danio rerio) reduce their frequency of swimming and increase their ventilation rate but do not display anomalous behaviour. Rainbow trout, like the zebrafish, reduce their frequency of swimming and increase their ventilation rate.[92]Nile tilapia (Oreochromis niloticus), in response to a tail fin clip, increase their swimming activity and spend more time in the light area of their tank.[93]
Since this initial work, Sneddon and her co-workers have shown that rainbow trout, common carp and zebrafish experiencing a noxious stimulation exhibit rapid changes in physiology and behavior that persist for up to 6 hours and thus are not simple reflexes.[66]
Five-day-old zebrafish larvae show a concentration dependent increase in locomotor activity in response to different concentrations of diluted acetic acid. This increase in locomotor activity is accompanied by an increase in cox-2 mRNA, demonstrating that nociceptive pathways are also activated.[87]
Fish show different responses to different noxious stimuli, even when these are apparently similar. This indicates the response is flexible and not simply a nociceptive reflex. Atlantic cod injected in the lip with acetic acid, capsaicin, or piercing the lip with a commercial fishing hook, showed different responses to these three types of noxious stimulation. Those cod treated with acetic acid and capsaicin displayed increased hovering close to the bottom of the tank and reduced use of shelter. However, hooked cod only showed brief episodes of head shaking.[90]
Early experiments provided evidence that fish learn to respond to putatively noxious stimuli. For instance, toadfish (Batrachoididae) grunt when they are electrically shocked, but after repeated shocks, they grunt simply at the sight of the electrode.[94][95] More recent studies show that both goldfish and trout learn to avoid locations in which they receive electric shocks. Sticklebacks receive some protection from predator fish through their spines. Researchers found pike and perch initially snapped them up but then rejected them. After a few experiences, the pike and perch learned to avoid the sticklebacks altogether. When the stickleback spines were removed, their protection disappeared.[96] Furthermore, this avoidance learning is flexible and is related to the intensity of the stimulus.[86][97][98][99]
Goldfish make trade-offs between their motivation to feed or avoid an acute noxious stimulus
A painful experience may change the motivation for normal behavioural responses.
In a 2007 study, goldfish were trained to feed at a location of the aquarium where subsequently they would receive an electric shock. The number of feeding attempts and time spent in the feeding/shock zone decreased with increased shock intensity and with increased food deprivation the number and the duration of feeding attempts increased as did escape responses as this zone was entered. The researchers suggested that goldfish make a trade-off in their motivation to feed with their motivation to avoid an acute noxious stimulus.[98]
Rainbow trout naturally avoid novelty (i.e. they are neophobic). Victoria Braithwaite describes a study in which a brightly coloured Lego brick is placed in the tank of rainbow trout. Trout injected in the lip with a small amount of saline strongly avoided the Lego brick, however, trout injected with acetic acid spent considerably more time near the Lego block. When the study was repeated but with the fish also being given morphine, the avoidance response returned in those fish injected with acetic acid and could not be distinguished from the responses of saline injected fish.[13][100]
To explore the possibility of a trade-off between responding to a noxious stimulus and predation, researchers presented rainbow trout with a competing stimulus, a predator cue. Noxiously stimulated fish cease showing anti-predator responses, indicating that pain becomes their primary motivation. The same study investigated the potential trade-off between responding to a noxious stimulus and social status. The responses of the noxiously treated trout varied depending on the familiarity of the fish they were placed with. The researchers suggested the findings of the motivational changes and trade-offs provide evidence for central processing of pain rather than merely showing a nociceptive reflex.[100][101]
Zebrafish given access to a barren, brightly lit chamber or an enriched chamber prefer the enriched area. When these fish are injected with acetic acid or saline as a control they still choose the same enriched chamber. However, if an analgesic is dissolved in the barren, less-preferred chamber, zebrafish injected with noxious acid lose their preference and spend over
half their time in the previously less-favourable, barren chamber. This suggests a trade-off in motivation and furthermore, they are willing to pay a cost to enter a less preferred environment to access pain relief.[41]
The learning abilities of fish demonstrated in a range of studies indicate sophisticated cognitive processes that are more complex than simple associative learning. Examples include the ability to recognise social companions, avoidance (for some months or years) of places where they encountered a predator or were caught on a hook and forming mental maps.[83]
It has been argued that although a high cognitive capacity may indicate a greater likelihood of experiencing pain, it also gives these animals a greater ability to deal with this, leaving animals with a lower cognitive ability a greater problem in coping with pain.[102]
Scientists have also proposed that in conjunction with argument-by-analogy, criteria of physiology or behavioural responses can be used to assess the possibility of non-human animals perceiving pain. The following is a table of criteria suggested by Sneddon et al.[41]
Given that some have interpreted the existing scientific information to suggest that fish may feel pain,[103] it has been suggested that precautionary principles should be applied to commercial fishing, which would likely have multiple consequences.[103]
Both scientists and animal protection advocates have raised concerns about the possible suffering (pain and fear) of fish caused by angling.[104][105][106]
Other societal implications of fish experiencing pain include acute and chronic exposure to pollutants, commercial and sporting fisheries (e.g. injury during trawling, tagging/fin clipping during stock assessment, tissue damage, physical exhaustion and severe oxygen deficit during capture, pain and stress during slaughter, use of live bait), aquaculture (e.g. tagging/fin clipping, high stocking densities resulting in increased aggression, food deprivation for disease treatment or before harvest, removal from water for routine husbandry, pain during slaughter), ornamental fish (e.g. capture by sub-lethal poisoning, permanent adverse physical states due to selective breeding), scientific research (e.g. genetic-modification) may have detrimental effects on welfare, deliberately-imposed adverse physical, physiological and behavioural states, electrofishing, tagging, fin clipping or otherwise marking fish, handling procedures which may cause injury.[46][107]
Browman et al.[108] suggest that if the regulatory environment continues on its current trajectory (adding more aquatic animal taxa to those already regulated), activity in some sectors could be severely restricted, even banned. They further argue that extending legal protection to aquatic animals is a societal choice, but they emphasize that choice should not be ascribed to strong support from a body of research that does not yet exist, and may never exist, and the consequences of making that decision must be carefully weighed.
In the UK, the legislation protecting animals during scientific research, the "Animals (Scientific Procedures) Act 1986", protects fish from the moment they become capable of independent feeding.[109] The legislation protecting animals in most other circumstances in the UK is "The Animal Welfare Act, 2006" which states that in the Act, " "animal" means a vertebrate other than man",[110] clearly including fish.
In the US, the legislation protecting animals during scientific research is "The Animal Welfare Act".[111] This excludes protection of "cold-blooded" animals, including fish.[112]
The 1974 Norwegian Animal Rights Law states it relates to mammals, birds, frogs, salamander, reptiles, fish, and crustaceans.[113]
A 2018 article by Howard Browman and colleagues provides an overview of what different perspectives regarding fish pain and welfare mean to in the context of aquaculture, commercial fisheries, recreational fisheries, and research.[108]
It has been argued that fish can not feel pain because they do not have a sufficient density of appropriate nerve fibres. A typical human cutaneous nerve contains 83% GroupC nerve fibres,[114] however, the same nerves in humans with congenital insensitivity to pain have only 24–28% C-type fibres.[114] Based on this, James Rose, from the University of Wyoming, has argued that the absence of C-type fibres in cartilagenous sharks and rays indicates that signalling leading to pain perception is likely to be impossible, and the low numbers for bony fish (e.g. 5% for carp and trout) indicate this is also highly unlikely for these fish.[114] A-delta-type fibres, believed to trigger avoidance reactions, are common in bony fish, although they have not been found in sharks or rays.[114] Rose concludes that fish have survived well in an evolutionary sense without the full range of nociception typical of humans or other mammals.[114] Professor Culum Brown of Macquarie University, Sydney, states that evidence has been used as evidence of lack; a fundamental misinterpretation of the scientific method, and has been taken to suggest that sharks and rays cannot feel pain. He asserts that the fact that nociception occurs in jawless fish,[115] as well as in bony fish,[116] suggests the most parsimonious explanation is that sharks do have these capacities but that we have yet to understand that the receptors or the fibres we have identified operate in a novel manner. He points out that the alternative explanation is that elasmobranchs have lost the ability of nociception, and one would have to come up with a very convincing argument for the adaptive value of such a loss in a single taxon in the entire animal kingdom.[117] Professor Broom of Cambridge University, submits that feeling pain gives active complex vertebrates a selective advantage through learning and responding, allowing them to survive in their environment. Pain and fear systems are phylogenetically extremely ancient and so are unlikely to have suddenly appeared in mammals or humans.[118]
In 2002, Rose published reviews arguing that fish cannot feel pain because they lack a neocortex in the brain.[119][120] This argument would also rule out pain perception in most mammals, and all birds and reptiles.[52][72] However, in 2003, a research team led by Lynne Sneddon concluded that the brains of rainbow trout fire neurons in the same way human brains do when experiencing pain.[121][122] Rose criticized the study, claiming it was flawed, mainly because it did not provide proof that fish possess "conscious awareness, particularly a kind of awareness that is meaningfully like ours".[123]
Rose, and more recently Brian Key[124][125] from The University of Queensland, argue that because the fish brain is very different from the human brain, fish are probably not conscious in the manner humans are, and while fish may react in a way similar to the way humans react to pain, the reactions in the case of fish have other causes. Studies indicating that fish can feel pain were confusing nociception with feeling pain, says Rose. "Pain is predicated on awareness. The key issue is the distinction between nociception and pain. A person who is anaesthetised in an operating theatre will still respond physically to an external stimulus, but he or she will not feel pain."[126] According to Rose and Key, the literature relating to the question of consciousness in fish is prone to anthropomorphisms and care is needed to avoid erroneously attributing human-like capabilities to fish.[127] However, no other animal can directly communicate how it feels and thinks, and Rose and Key have not published experimental studies to show that fish do not feel pain.[128] Sneddon suggests it is entirely possible that a species with a different evolutionary path could evolve different neural systems to perform the same functions (i.e. convergent evolution), as studies on the brains of birds have shown.[129] Key agrees that phenomenal consciousness is likely to occur in mammals and birds, but not in fish.[124] Animal behaviouralist Temple Grandin argues that fish could still have consciousness without a neocortex because "different species can use different brain structures and systems to handle the same functions."[122] Sneddon proposes that to suggest a function suddenly arises without a primitive form defies the laws of evolution.[130]
Other researchers also believe that animal consciousness does not require a neocortex, but can arise from homologoussubcortical brain networks.[11] It has been suggested that brainstem circuits can generate pain. This includes research with anencephalic children who, despite missing large portions of their cortex, express emotions. There is also evidence from activation studies showing brainstem mediated feelings in normal humans and foetal withdrawal responses to noxious stimulation but prior to development of the cortex.[131]
In papers published in 2017 and 2018, Michael Woodruff[132][133] summarized a significant number of research articles that, in contradiction to the conclusions of Rose and Key, strongly support the hypothesis that the neuroanatomical organization of the fish pallium and its connections with subpallial structures, especially those with the preglomerular nucleus and the tectum, are complex enough to be analogous to the circuitry of the cortex and thalamus assumed to underlie sentience in mammals. He added neurophysiological and behavioral data to these anatomical observations that also support the hypothesis that the pallium is an important part of the hierarchical network proposed by Feinberg and Mallatt to underlie consciousness in fishes.[134]
Work by Sneddon characterised behavioural responses in rainbow trout, common carp and zebrafish.[66] However, when these experiments were repeated by Newby and Stevens without anaesthetic, rocking and rubbing behaviour was not observed, suggesting that some of the alleged pain responses observed by Sneddon and co-workers were likely to be due to recovery of the fish from anaesthesia. But, Newby and Stevens, in an attempt to replicate research conducted by Sneddon's laboratory, used a different protocol to the one already published. The lack of abnormal rubbing behaviours and resumption of feeding in the Newby and Stevens experiment can be attributed to them injecting such a high concentration of acid. If no nociceptive information is being conducted to the central nervous system then no behavioural changes will be elicited. Sneddon states that this demonstrates the importance of following experimental design of published studies to get comparable results.[135][136][137]
Several researchers argue about the definition of pain used in behavioural studies, as the observations recorded were contradictory, non-validated and non-repeatable by other researchers.[60] In 2012, Rose argued that fishes resume "normal feeding and activity immediately or soon after surgery".[60] But Stoskopf suggested that fish may respond to chronic stimuli in subtle ways. These include colour changes, alterations in posture and different utilization of the water column, and that these more nuanced behaviours, may be missed, while Wagner and Stevens said that further testing examining more behaviours is needed.[138][139]
Nordgreen said that the behavioural differences they found in response to uncomfortable temperatures showed that fish feel both reflexive and cognitive pain.[140] "The experiment shows that fish do not only respond to painful stimuli with reflexes, but change their behavior also after the event," Nordgreen said. "Together with what we know from experiments carried out by other groups, this indicates that the fish consciously perceive the test situation as painful and switch to behaviors indicative of having been through an aversive experience."[140] In 2012, Rose and others reviewed this and further studies which concluded that pain had been found in fish. They concluded that the results from such research are due to poor design and misinterpretation, and that the researchers were unable to distinguish unconscious detection of injurious stimuli (nociception) from conscious pain.[60]
In 2018, Sneddon, Donald Broom, Culum Brown and others, published a paper that found that despite the empirical proof, sceptics still deny anything beyond reflex responses in fishes and state that they are incapable of complex cognitive abilities. Recent studies[141][142] on learning have shown that cleaner wrasse fish, as well as parrots, perform better than chimpanzees, orangutans or capuchin monkeys in a complex learning task in which they have to learn to discriminate reliable food sources from unreliable ones. Goldfish learn to avoid an area where they have received an electric shock. Even when food has been previously provided in this area and the fish are strongly motivated to spend time there, they avoid it for three days, at which time they trade off their hunger with the risk of receiving another shock. This shows complex decision-making beyond simple reflexes.[128] | They concluded that it was reasonable to believe that all vertebrates are capable of suffering to some degree or another.[16]RSPCA Australia more recently added that evidence that fish are capable of experiencing pain and suffering has been growing for some years.[17]
The European Union Panel on Animal Health and Welfare European Food Safety Authority said that the balance of evidence indicates that some fish species can experience pain.[18] The British Farm Animal Welfare Committee 2014's report, Opinion on the Welfare of Farmed Fish, said that the scientific consensus is that fish can detect and respond to noxious stimuli, and experience pain.[19]
In 2001 studies were published showing that arthritic rats self-select analgesic opiates.[20]
In 2014, the veterinary Journal of Small Animal Practice published an article on the recognition of pain which started – "The ability to experience pain is universally shared by all mammals..."[21] and in 2015, it was reported in the science journal Pain, that several mammalian species (rat, mouse, rabbit, cat and horse) adopt a facial expression in response to a noxious stimulus that is consistent with the expression of pain in humans.[22]
At the same time as the investigations using arthritic rats, studies were published showing that birds with gait abnormalities self-select for a diet that contains carprofen, a human analgesic.[23] | yes |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://www.bonappetit.com/story/do-fish-feel-pain | Do Fish Feel Pain? | Bon Appétit | Do Fish Feel Pain?
InToo Afraid to Ask, we’re answering the food-related questions you may or may not be avoiding. Today: Do fish feel pain?
With their blank stares, cold blood, and gaping mouths, it’s easy to assume fish don’t feel pain. That’s long been the dominant narrative in the US, one that’s kept us layering bagels with fleshy slices of cured salmon or buying sushi rolls stuffed with jewel-toned bites of fresh tuna. It’s also a script that a dedicated cohort of scientists has spent the past two decades trying to rewrite.
While most livestock producers in the US have to abide by ethical slaughter and animal handling regulations, the welfare of fish caught for food has largely been ignored. In many ways, it’s unsurprising: Humans rarely interact with fish, who can’t vocalize or make the same sorts of facial expressions that many mammals can. And research shows that we’re less likely to show empathy to species we have little in common with, evolutionarily speaking. It’s also because researchers have been slow to answer the question: Do fish feel pain?
Studying the subjective experiences of animals, who cannot scream “ouch!” when poked and prodded, is a fraught endeavor. Yet, since the early 2000s, scientists have developed a body of compelling evidence that pushes back on old ideas about pain in fish. Various studies have found that they behave differently when they’re injured, just like us, and actively seek out pain relief. Still, despite mounting research, some people remain unconvinced, claiming that fish don’t have the brains for pain. So, which camp is right?
The research
According to Paula Droege, a philosopher who researches animal consciousness at Pennsylvania State University, “the best indicator that fish feel pain is the way their behavior changes when injured.”
In 2002, Lynne Sneddon, a biologist at Sweden’s University of Gothenburg and one of the first scientists to study pain in fish, injected bee venom or acetic acid (the stuff responsible for vinegar’s sting) into the lips of rainbow trout. Soon after, the fish started breathing faster, and Sneddon and her colleagues noticed profound changes in their actions. Typically eager to eat, the fish took, on average, almost three hours to start nibbling at food. They swam around far less than normal, rocked from side to side while resting at the bottom of the tank, and rubbed their lips into the gravel and against the glass walls. And when Sneddon gave the trout a hit of morphine, these abnormal behaviors significantly reduced.
At the time it was published, the groundbreaking research was the first of its kind to challenge long-standing assumptions. Sneddon was convinced that what she’d observed couldn’t possibly be a mere reflex, which is known scientifically as nociception and is different from pain. “If you touch something hot, you instantly remove your hand,” she tells me—that’s nociception. “But if you don’t get cold water on the burn area it starts to throb, it really hurts, and you might cradle your hand”—that’s pain, which includes both the “sensory damage and the negative affective or psychological state.”
Various researchers have since made similar discoveries. In 2006, Rebecca Dunlop, Sarah Millsopp, and Peter Laming, researchers from the Queen’s University in Belfast, Northern Ireland, published a study demonstrating that fish can also learn to avoid painful experiences. They gave eight goldfish an electric shock. All of them darted away, but more surprisingly, the fish didn’t immediately return to the area where the incident took place—even when food was present. The scientists concluded that the response to the initial shock might have been instinctual, but the decision to stay away indicated more complex pain responses.
Looks can be deceiving. Though they appear alien, fish share some important anatomical similarities with mammals, who have long been thought to experience pain. In response to noxious stimuli, fish bodies produce the same opioids (like natural painkillers) that are present across the animal kingdom. And when they’re injured, parts of the brain considered essential for conscious sensory perception light up like glow sticks at a rave, just as they do in terrestrial animals.
Sneddon says the biological function of pain is virtually universal to the living creatures that experience it. “It’s an alarm system to warn you about injury,” she says. “If it was not a horrible psychological experience, animals would not learn to avoid painful stimuli and would just go about their lives hurting themselves continually.”
The skeptics
Others argue that fish aren’t capable of experiencing pain, and that any recorded behavioral responses are more likely unconscious reactions to negative stimuli. In other words, they believe fish can instinctually detect harm to their bodies, without any suffering.
James Rose, an avid angler and professor emeritus of zoology at the University of Wyoming, has claimed fish don’t possess a human-like capacity for pain because our nociceptors—neural cells that transmit pain reflexively—are different. Those in fish, he and his peers wrote in a 2012 paper, more likely trigger instinctual escape responses than signal injury.
Two years later, BBCNewsnight interviewed Bertie Armstrong, head of the Scottish Fishermen’s Federation. He argued that scientists haven’t adequately proven that fish feel pain, and said that marine animals shouldn’t have the same welfare protections as those grown on land. Alternative slaughter methods, Armstrong said, could be cost prohibitive for the fishing industry.
Then, in 2016, Brian Key, a biomedical scientist from Australia’s University of Queensland, argued that fish lack the neurological architecture to feel pain. The squishy neocortex that sits atop a human brain is like a city: Various neighborhoods, connected by neural highways, work together to produce vivid experiences of pain. The crux of Key’s argument is that, because fish brains lack that same organized neocortex, they aren’t able to consciously experience hurt as we do.
The rebuttal
Droege and colleagues have countered Rose’s argument. They’ve found homologous structures in fish that may play the same role as elements of the human brain—arguing that our own pain, in fact, tells us very little about that of animals.
On the BBC program, the late Pennsylvania State University biologist Victoria Braithwaite (who wrote the 2010 book, Do Fish Feel Pain?) countered Armstrong, saying that fish undeniably don’t have the same pain response as humans, but that they likely feel it similar to other land animals: If “we extend birds and mammals welfare, then logically, why not fish?” She went on to argue that the protection of fish doesn’t have to be mutually exclusive with viable commercial fishing outcomes—there are probably some innovations that could be made to decrease suffering.
Pushing back on Key’s idea that animal brains should be comparable to human ones in order to feel pain, Ed Yong, a science reporter for The Atlantic, has argued that it’s “grossly anthropomorphic.” Expecting to find identical human traits in animals is flawed logic. He writes in his 2022 book, An Immense World: How Animal Senses Reveal the Hidden Realms Around Us: “It blithely assumes that the neocortex must be necessary for pain in all animals, since that’s the case in humans.”
We have ample evidence that dogs, cats, and birds all feel hurt, yet if we accept Key’s thesis, “then no animals except primates can experience pain,” adds Sneddon. Yong poked other holes in Key’s argument: The neocortex is also essential to learning, attention, and sight in humans. So if fish don’t have one, then surely they should be lacking those skills too—which they clearly are not.
Sneddon also points out that none of the critics who deny that fish feel pain have published conflicting studies of their own. “They write reviews on the subject,” she says. “So this is their opinion and not scientific fact.”
What it all means for fish
As of 2019, the US was the world’s second largest market for fish, consuming 6.3 billion pounds that year. While the Humane Methods of Slaughter Act, which was first introduced federally in 1958, mandates that food animals (such as cows and pigs) are treated ethically and killed quickly, fish are notably excluded. “There are currently no national welfare standards for fish or other aquatic animals raised for food,” says Stephanie Showalter-Otts, the Director of the National Sea Grant Law Center, which reports on various aquatic issues to educate policy makers.
At the state level, some governments include fish in their animal cruelty laws. But they’re limited. “Those that do usually exempt permitted fishing and enforcement is rarely prioritized, even where fish are subjected to illegal treatment,” says Christopher Berry, the managing attorney at the Animal Legal Defense Fund, which files high-impact lawsuits to protect animals from harm.
Globally, between 787 billion to 2.3 trillion fish are killed for food each year. Weighted nets are trawled along the ocean floor, collecting hundreds of thousands of fish at once. Some spend hours on deck slowly suffocating, an experience that’s prolonged when they’re put on ice, while others are gutted alive. Unlike cows, chickens, and pigs, very few fish are stunned before slaughter. Conditions are even worse for farmed fish, which now make up the majority of those we buy at supermarkets in the US. Tanks are often overcrowded, meaning animals could suffer for months (even years) before they’re killed, live in poor quality water (from their own waste and antibiotics), and are more susceptible to disease and injury.
Though there are still no legal incentives for killing fish as painlessly as possible, some private companies are voluntarily tackling the problem. US-based brothers Michael Burns and Patrick Burns launched a fishing vessel in 2016 called F/V Blue North, which was specially designed to harvest Pacific cod from the Bering Sea, a stretch of ocean between Alaska and Russia. Fish are hauled into a temperature-controlled room one by one, stunned unconscious within seconds, and quickly killed.
Another company, Shinkei Systems, has developed a machine that uses AI technology to replicate a traditional Japanese slaughter process called ike-jime: Fish are pierced in the brain using a sharp spike, which supposedly prevents suffering, kills them instantly, and makes the flesh taste better (because they aren’t releasing stress chemicals). Shinkei has automated the process, and the company claims it can kill at least four fish per minute.
Findings around fish feeling pain have also informed the work done by animal welfare organizations. Mercy For Animals has covertly documented conditions at fish farms in the US, and the Aquatic Life Institute formed in 2019 to increase welfare standards for all marine animals.
It’s impossible to fully understand the subjective experience of another animal. Still, apart from “a very small number of scientists who are skeptical,” Sneddon thinks most people are starting to shift their opinions around this topic. In a survey of more than 9,000 Europeans, 73% said they thought that fish do feel pain.
Laws still haven’t caught up with public opinion. But Berry argues that we have enough evidence to extend welfare protections to marine animals. “There is no good justification for treating fish differently than other animals,” he says. | She went on to argue that the protection of fish doesn’t have to be mutually exclusive with viable commercial fishing outcomes—there are probably some innovations that could be made to decrease suffering.
Pushing back on Key’s idea that animal brains should be comparable to human ones in order to feel pain, Ed Yong, a science reporter for The Atlantic, has argued that it’s “grossly anthropomorphic.” Expecting to find identical human traits in animals is flawed logic. He writes in his 2022 book, An Immense World: How Animal Senses Reveal the Hidden Realms Around Us: “It blithely assumes that the neocortex must be necessary for pain in all animals, since that’s the case in humans.”
We have ample evidence that dogs, cats, and birds all feel hurt, yet if we accept Key’s thesis, “then no animals except primates can experience pain,” adds Sneddon. Yong poked other holes in Key’s argument: The neocortex is also essential to learning, attention, and sight in humans. So if fish don’t have one, then surely they should be lacking those skills too—which they clearly are not.
Sneddon also points out that none of the critics who deny that fish feel pain have published conflicting studies of their own. “They write reviews on the subject,” she says. “So this is their opinion and not scientific fact.”
What it all means for fish
As of 2019, the US was the world’s second largest market for fish, consuming 6.3 billion pounds that year. While the Humane Methods of Slaughter Act, which was first introduced federally in 1958, mandates that food animals (such as cows and pigs) are treated ethically and killed quickly, fish are notably excluded. | yes |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://www.theguardian.com/news/2018/oct/30/are-we-wrong-to-assume-fish-cant-feel-pain | Are we wrong to assume fish can't feel pain? | Fish | The Guardian | I have cast my rod into the tidal current flowing around Montauk Point in New York and my lure is chugging across the surface when a bluefish swirls and fails to grab it. There is a heavier swirl. On a third appearance, the fish grabs. The hook pierces. The fish swims one way and abruptly changes direction. It darts deep. Comes up. The fish is struggling. I have never seen a free-swimming fish leap and wriggle as if to dislodge something. But this fish suddenly bursts through the surface, shaking its head energetically. It works. My lure goes flying. The line goes slack. The fish vanishes; escaped.
Was that fish feeling pain? Fear? If a sociopath is someone who disregards the pain of others, and if someone who ignores evidence is in denial, what does that make me? Such questions plague me. I cast again.
The impression that fish are insensate, short of memory and, therefore, can be caught, killed and eaten without guilt, is being revisited. Angling, the so-called “gentle art”, derives enjoyment from the struggles of its quarry. Up to 2.7tn wild fish are caught worldwide every year; a third of which are ground into feed for chickens, pigs and other fish. The ethics of all this depend on what fish do or do not experience. It is a question dividing the science community; forced to reassess in light of new evidence.
Their battle rages. In 2016, the journal Animal Sentience published Australian neuroscientist Brian Key’s essay Why Fish Do Not Feel Pain. Key had earlier written that “it doesn’t feel like anything to be a fish”. Now he argued thus: mammals feel things, and only mammal brains have a structure called the neocortex; ergo fish, lacking a neocortex, feel nothing.
But that is like saying that because we travel using legs, then fish, who have no legs, cannot travel. Key’s essay triggered more than three dozen opposing scientific responses, pressing new evidence that fish are aware; of pain, of anxiety, of pleasures.
A diver and a dusky grouper off Corsica in the Mediterranean. Photograph: Alamy
Mine was first among the responses. I have devoted my career to conservation and to fish as wild animals. When I was a child on Long Island, I would hear toadfish croaking through the thin hull of my aluminum rowboat. Sea-robins have often grunted when I have caught one. To human sensibilities, their grunts do not sound like growling, or screaming – but what if they are just that? Even when we hear them, we don’t hear them. When you are a fish, no one can hear you scream.
Fish have honed their skills for hundreds of millions of years; humans are just making their acquaintance. Research has shown that various fish show long-term memory, social bonding, parenting, learned traditions, tool use, and even inter-species cooperation. Compared to those, pain and fear are primitive and basic.
Although aquatic farms in a handful of countries, including the UK and Norway, must follow humane slaughter guidelines, there are no standards for considering the tens of thousands of wild fish caught every second. In an essay titled Fish Intelligence, Sentience and Ethics, the Australian researcher Culum Brown suggests that the sheer scale of the global fishing industry makes the idea of legislating for the humane treatment of fish “too daunting to consider”.
But I do not have that excuse. Trying to catch just one wild fish, I have time to consider all the implications.
Asking whether fish suffer means asking whether fish possess the ability to feel at all. Brains offer only circumstantial evidence. Even behaviour can mislead. Yes, my fish jerked from the hook’s jab, but that could be merely reflexive. Yet by examining fish brains and behaviours, then comparing them to a species universally acknowledged to feel pain and pleasure – humans – we can look for clues.
Fish were ancestors to all other vertebrates; their brains were the template for our own brains’ evolution. Lynne Sneddon, director of bioveterinary science at Liverpool University, was the first scientist to discover that fish possess nerves known to convey pain. In 2002, she identified in fish the same nerve types that, in humans, detect painful stimuli. We call such nerves “pain receptors”. Sneddon showed that pinching and pricking fish activates these nerve fibres. “My research has shown that fish have a strikingly similar neuronal system to mammals,” she told me, adding that until 2002, “it was generally believed fish did not have feelings”. Nerves are not proof that fish experience pain – but Sneddon showed that fish have the necessary hardware.
The software to match this comes in the form of brain chemicals called neurotransmitters. Mammals and fish share many identical neurotransmitters including dopamine and serotonin. In humans these are involved in pain, hunger, thirst and fear, and include opiate-like chemicals that reduce pain.
Tuna fish off the coast of Turkey. Photograph: Getty
Putting the hardware and software together and watching behaviour in experiments creates strong evidence. When Sneddon’s team gave trout an injection of acetic acid or bee venom – both of which cause pain in humans – the fish began breathing faster and rubbed the injection site on gravel. “Stimuli that would cause pain to us also affect fish,” said Sneddon. “When humans are in pain, we do other tasks less well. Fish consumed by pain do not respond to fear-causing situations and do not show normal anti-predator behaviour.” Yet when Sneddon’s team administered drugs such as aspirin, lidocaine and morphine, the drugs made the pain symptoms disappear. “If fish did not experience pain,” Sneddon pointed out, “then analgesic drugs would have no effect.”
In other experiments, zebrafish injected with pain-inducers swam to a normally avoided barren, brightly lit chamber of their tank if a painkiller was added there. With no painkiller to swim to, the zebrafish remained in a chamber of their tank that had hiding places and low light. When I asked Jonathan Balcombe, author of What a Fish Knows, for his take on their behavioural choices, he said: “This shows that fish will incur risk to get pain relief.”
‘How could they not feel?” fumed famed oceanographer Sylvia Earle indignantly when we spoke. “Fish have had a few hundred million years to figure things out. We’re newcomers. I find it astonishing that many people seem shocked at the idea that fish feel. The way I see it, some people have wondrous fish-like characteristics – they can think and feel!”
Fish sometimes recognise particular divers or keepers and approach them to be stroked. Earle calls groupers “Labrador retrievers of the sea”. Her daughter, Liz Taylor, now president of submarine maker DOER Marine, added that at San Francisco’s Steinhart Aquarium, “Ulysses the giant grouper would lay on his side and open his huge mouth to be petted – by certain people. He distinctly disliked some people and would blast them with water. One woman got soaked repeatedly and refused to even pass his pool. She swore ‘he knew’ she was coming. I always got a warm welcome, with eye contact. Such a good fish.”
Seafood sustainability expert Shelley Dearhart recalled “a huge grouper at the Bermuda Aquarium who would squirt water at anyone on the dock if they did not give his head a little rub – no food involved.” She showed me photos of herself obliging his desire for a rub. Pleasure; it implies a capacity for pain.
An angler using pliers to remove hook from a mackerel. Photograph: UIG via Getty
When we ask if they can feel what a human feels, we imply that that is the best a fish might aspire to. But as Earle said, fish “have senses we humans can only dream about. Try to imagine having taste buds all along your body. Or the ability to sense the electricity of a hiding fish. Or eyes of a deep sea shark.” Many fish see four major colours; humans only see three. Some see polarised light, some see ultraviolet. Some, such as flounders, move their eyes independently, processing two image fields. Archerfish and “four-eyed fish” see above and below water simultaneously, processing four images. Groupers and others signal with changing skin-colour patterns.
The long-held myth that a fish is a naturally unintelligent animal, with no memory, has no basis in research. Bob Wicklund, marine expert and author of Eyes in the Sea, told me he calls the Nassau grouper the “Einstein of the reef”. He has watched a grouper using its tail to wash bait to the edge of a fish trap where they could take a bite. Each bite pushed the bait back to the centre of the trap, whereupon the grouper repeatedly “swept” it back into reach.
Some fish learn by watching. Archerfish squirt water at bugs on leaves overhanging water. When naive archerfish watch fish already skilled at hitting moving targets, they more often hit their target on their first attempt, compared to those who never observed others hunt. How does one explain that unless fish can hold a mental image in their mind’s eye?
Some wrasses use rocks to bash urchins open. Such work cannot be reflexive. They must know when they have accomplished their mission.
Shelley Dearhart, who had bonded with a grouper, also worked at the South Carolina Aquarium, where “a huge, incredibly old cobia – apparently blind – would rest on the bottom of our largest tank,” she says. “At feeding time, a smaller, younger cobia would venture down and nudge the older one up to the surface to feed. They would swim in tandem until feeding time ended. Then the younger fish would take the older one back to the bottom. It happened daily. Seeing a relationship between two fish gave me an entirely new appreciation for the complexity of their world.”
Twenty metres deep off Cuba in 2017, I was amazed to watch several Nassau groupers closely attending two moray eels flowing in and out of coral crevices. They moved together, the eels actively hunting, the groupers expecting that a prey fish might flee its cover so they might grab it. The groupers certainly seemed to understand what they were doing, with the goal in mind.
More impressively, researchers in the Red Sea in 2002 and 2004 watched groupers and morays hunting cooperatively on numerous occasions. After one grouper chased a fish into a crevice, the grouper swam 15 metres to a cave, fetched a moray back to the hiding prey, then used posture to indicate the hiding fish. Such communication is so rarified that before this study only ravens, chimpanzees and humans were known to use “referential gesturing”. It indicates that a grouper knows that a moray, too, can know. That is “theory of mind”, and it is a big deal. Flexibile behaviour shows understanding, reflecting conscious awareness. Biologists at the University of Cambridge and the University of Neuchâtel in Switzerland wrote that groupers “perform at an ape-like level”. (But groupers came first, so we could say that apes perform at a grouper-like level.) Behavioural flexibility is the strongest evidence that – however their brains accomplish it – being a fish certainly feels like something.
Fish anatomy, neurochemistry and behaviour all indicate that fish experience sensations including wellbeing and pain. And fear. Wicklund, who dives regularly, told me about being in the middle of a massive herring school. “Suddenly, all the fish turned. Soon they were pelting us like hail stones.” Based on the time it took for the divers to see that a pack of large bluefish was on the attack, Wicklund estimated that the small fish “were communicating danger and panic throughout the school from as far as a mile away”.
Fish act as though they remember fear. Earle recalled five cobia who were acclimated to scientific divers around an underwater lab. After spearfishermen killed three of the fish, the remaining two were – understandably – “strikingly wary”. After experimenters used a fake predator to frighten fish crossing the centre of an apparatus, fish avoided the centre. If they did cross, they sprinted, indicating a memory of feeling fear.
Undersea photographer David Doubilet, on a shoot in the Gulf of St Lawrence off Newfoundland, wanted to capture the fish’s perspective inside a herring trap. “At first the fish were swimming in slow, calm circles as I floated above them,” he said. Then the net began to rise. Tailbeats (movement in the tails) and breathing rates increased. “Chaos ensued as they lost the space between them,” Doubliet recalled. “Fish searching in vain for an exit slammed into each other.” Doubilet himself was engulfed in panic. The net tightened, concentrating the fish until, from the look in their eyes, “I could see and feel resignation set in as they stopped struggling and awaited their fate. I slipped out of the net.”
My lure and another fish have found each other. The fish tries everything it can to shake or break the connection. I work the fish alongside, and hoist it into the air. I slide the fish into an ice slurry that near-instantly chills it to stillness.
My fish has not died the way it was supposed to die. But the fish lived as it was supposed to live, by catching its own food. So if the fish could comprehend anything about me, my killing to eat might be the one thing the fish could understand.
My fish would not understand a life lived in a pen, crammed to the gills by the thousands. Most pen-raised animals – in water or air – are forced to live far worse than they are made to die.
A fisherman spears a grouper fish off the coast of Qalamun in northern Lebanon. Photograph: AFP/Getty
In cold-flowing water, I have stood watching salmon returning to their birth streams from 1,000 miles away, negotiating rapids and falls, feeding bears and eagles, and people too, their life profound, nourishing and metaphorically potent.
But I once dived 20 metres into a salmon-farm pen. Their life, one slow cyclone, seemed divorced from instincts, devoid of experience. Repeatedly I was hit head-on by slow-motion salmon in a seeming stupor who made no effort to avoid bumping my face-mask or body. All senses blunted, their existence appeared robbed of meaning. It was not that their lives were over; it was as if they had never lived. Zombies.
I have been in open water hand-feeding 400kg bluefin tuna who rocketed past to snatch my handouts, yet never brushed me with a fin-tip. But I have also been on deck as one of these giants, exhausted by a long struggle with the line, was brought alongside, its eye swivelling as the gaff hook sank and its warm blood spread upon the sea. And I have watched nets that strain the sea hauled up, their strings loosened to dump the condemned on to the deck where they writhed to stillness, and only then were the desired sorted from the unwanted dead. I have seen mighty swordfish during moments of peace in warm sunlight, dozing, fin out of the water, then suddenly struck by the harpoon and shooting down, down and away while hundreds of metres of rope emptied from the baskets. A flagged buoy followed, and after dragging that rope and a length of chain for hours, the fish died 200 metres down.
Is this the relationship we want with our food? Is this the kind of people we want to be? Must we even all agree that fish suffer, when there are so many reasons to treat them better? The pain question aside, animal health specialist Ben Diggles says fish farmers “need to avoid stress at all stages to optimise health, growth and post-slaughter product quality”. He adds that “recreational angling stress can be minimised using best-practice guidelines”. But he also acknowledges that “there may be intractable issues around the inability to control injury and slaughter humanely while taking large numbers of fish in nets”.
Nerves, brain structure, brain chemistry and behaviour – all evidence indicates that, to varying degrees, fish can feel pain, fear and psychological stress. Must we insist on denying them even that paltry acknowledgment? If we do insist, let us be honest about why: it is too painful to contemplate. Fish feel pain because we refuse to.
Follow the Long Read on Twitter at @gdnlongread, or sign up to the long read weekly email here. | We call such nerves “pain receptors”. Sneddon showed that pinching and pricking fish activates these nerve fibres. “My research has shown that fish have a strikingly similar neuronal system to mammals,” she told me, adding that until 2002, “it was generally believed fish did not have feelings”. Nerves are not proof that fish experience pain – but Sneddon showed that fish have the necessary hardware.
The software to match this comes in the form of brain chemicals called neurotransmitters. Mammals and fish share many identical neurotransmitters including dopamine and serotonin. In humans these are involved in pain, hunger, thirst and fear, and include opiate-like chemicals that reduce pain.
Tuna fish off the coast of Turkey. Photograph: Getty
Putting the hardware and software together and watching behaviour in experiments creates strong evidence. When Sneddon’s team gave trout an injection of acetic acid or bee venom – both of which cause pain in humans – the fish began breathing faster and rubbed the injection site on gravel. “Stimuli that would cause pain to us also affect fish,” said Sneddon. “When humans are in pain, we do other tasks less well. Fish consumed by pain do not respond to fear-causing situations and do not show normal anti-predator behaviour.” Yet when Sneddon’s team administered drugs such as aspirin, lidocaine and morphine, the drugs made the pain symptoms disappear. “If fish did not experience pain,” Sneddon pointed out, “then analgesic drugs would have no effect.”
In other experiments, zebrafish injected with pain-inducers swam to a normally avoided barren, brightly lit chamber of their tank if a painkiller was added there. With no painkiller to swim to, the zebrafish remained in a chamber of their tank that had hiding places and low light. | yes |
Ichthyology | Can fish feel pain like humans? | yes_statement | "fish" can "feel" "pain" "like" "humans".. "fish" have the ability to experience "pain" similar to "humans". | https://www.uq.edu.au/news/article/2015/01/grey-matter-matters-when-it-comes-feeling-pain | Grey matter matters when it comes to feeling pain - UQ News - The ... | “Fish don’t have complex brain structures,” said Professor Key, who has published new research on the mechanics of pain.
“They do not have ‘grey matter’, the thin outer layer of brain cells that enables humans and other mammals to carry out functions such as reasoning or imagining.”
Professor Key said the new study was significant in helping to understand pain processes in humans with damaged grey matter, and people in comas or semi-conscious states.
“The ability of humans and other animals to experience pain is due to the complex wiring and structure of our brains,” he said.
“Fish have evolved from our ancient ancestors without developing grey matter or any other region of the brain that has a similar structure or function.”
“The research indicates that the simple structure of a fish brain renders them unable to respond to stimuli or feel pain in the same way that humans do.”
Professor Key, a neurobiologist, said there had been much debate between different branches of science on the topic.
Some comparative psychologists who focused on fish behaviour were not convinced by the neuroscience research indicating that fish could not feel pain.
“It’s controversial, there’s no denying it,” Professor Key said. “But neither will I resile from what the research indicates.”
“This research shows it is probable that fish do not ‘feel’ pain.
“Inductive reasoning tells us this is what’s happening – but of course the assessment is not absolute.”
“We suspect that some humans who have suffered strokes that damage their grey matter cannot feel pain.
“This would indicate that fish – with no grey matter – also do not feel pain.”
“When a fish is flapping about on the deck of a boat, humans respond emotionally,” Professor Key said.
“It’s an anthropomorphic response – we are mentally transposing the human experience – presuming that the fish has the same emotions and feelings as a human.”
“However, the fact that a fish will continue to struggle with a hook in its mouth would indicate it doesn’t feel pain in the same way that we do.”
Professor Key said although it was unlikely that fish could ‘feel’ pain, harmful stimuli still caused stress to their bodies.
“Fish secrete stress hormones,” he said.
“This research should not be interpreted as meaning that we do not need to care for their welfare.
“Fish must be kept in conditions which ensure their health and natural behaviour can be maintained.”
Professor Key noted that the term “fish” referred to a highly diverse group consisting of about 30,000 species.
“The scientific investigations referenced in my paper have been undertaken on only a small number of fish, so there is considerable extrapolation involved when we use the generic term ‘fish’,” he said.
“It is also important to remember that whales and dolphins are not fish, they are ‘marine mammals’ with lots of grey matter.” | “Fish don’t have complex brain structures,” said Professor Key, who has published new research on the mechanics of pain.
“They do not have ‘grey matter’, the thin outer layer of brain cells that enables humans and other mammals to carry out functions such as reasoning or imagining.”
Professor Key said the new study was significant in helping to understand pain processes in humans with damaged grey matter, and people in comas or semi-conscious states.
“The ability of humans and other animals to experience pain is due to the complex wiring and structure of our brains,” he said.
“Fish have evolved from our ancient ancestors without developing grey matter or any other region of the brain that has a similar structure or function.”
“The research indicates that the simple structure of a fish brain renders them unable to respond to stimuli or feel pain in the same way that humans do.”
Professor Key, a neurobiologist, said there had been much debate between different branches of science on the topic.
Some comparative psychologists who focused on fish behaviour were not convinced by the neuroscience research indicating that fish could not feel pain.
“It’s controversial, there’s no denying it,” Professor Key said. “But neither will I resile from what the research indicates.”
“This research shows it is probable that fish do not ‘feel’ pain.
“Inductive reasoning tells us this is what’s happening – but of course the assessment is not absolute.”
“We suspect that some humans who have suffered strokes that damage their grey matter cannot feel pain.
“This would indicate that fish – with no grey matter – also do not feel pain.”
“When a fish is flapping about on the deck of a boat, humans respond emotionally,” Professor Key said.
“It’s an anthropomorphic response – we are mentally transposing the human experience – presuming that the fish has the same emotions and feelings as a human.”
“However, the fact that a fish will continue to struggle with a hook in its mouth would indicate it doesn’t feel pain in the same way that we do.”
Professor Key said although it was unlikely that fish could ‘feel’ pain, harmful stimuli still caused stress to their bodies.
| no |
Aging | Can gene therapy reverse the aging process? | yes_statement | "gene" "therapy" has the potential to "reverse" the "aging" "process".. the "aging" "process" can be "reversed" through "gene" "therapy". | https://www.news-medical.net/news/20230119/Partial-genetic-reprogramming-might-extend-lifespan-and-reverse-aging-in-old-mice.aspx | Partial genetic reprogramming might extend lifespan and reverse ... | *Important notice: bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
Background
The rapidly growing world population is increasing the societal burden. Moreover, aging raises the threat of contracting several fatal human diseases. Thus, it is urgent and crucial to identify anti-aging interventions to reverse or defer the aging process.
Although longevity, i.e., increasing the ‘lifespan,’ is a feasible goal, whose golden standard biomarker is time to death. However, it does not improve their quality of life or health span.
On the contrary, age reversal could restore the aging effects at the genetic level and increase health and lifespan. Another issue with anti-aging interventions is cycle time, which requires waiting for a living being to die. Even in mice, testing anti-aging interventions can take six months to three years.
Takahashi and Yamanaka in 2006 showed that somatic cells could go back to a pluripotent state, thereby shaking off the paradigm of unidirectional differentiation. In the 4F-progeroid mouse model, doxycycline induced partial reprogramming of the OSK cassette. A reverse tetracycline transactivator (rtTA) drove this process and extended the lifespan of 4F-progeroid mice. Furthermore, this study showed a correlation between the epigenetic profile of tissues and improved function. The researchers, Horvath and Raj, assessed this using epigenetic methylation clocks.
About the study
In the present study, researchers generated a two-component AAV9 vector system having doxycycline-inducible OSK, of which one vector carried rtTa and the other a polycistronic OSK expression cassette. They also selected AAV9 capsid for maximal distribution of vectors to most mouse tissues. For these experiments, the team used 124-week-old wild-type C57BL6/J mice, equivalent to ~77 years in human age, who they retro-orbitally (RO) injected with phosphate buffer saline (PBS) or 1E12 vector genomes (vg) of each AAV9 system. The total dosage for each test animal was ~6E13 vg/kg. After a day, the team induced both mouse groups with doxycycline, alternating weekly on/off cycles till the animal lived.
Clinicians widely use a frailty index (FI) to measure aging-related increased susceptibility to adverse health outcomes, where higher scores indicate age-related health deficits or a frail state. The researchers used a similar index for FI measurements in mice. Methylation patterns of genomic deoxyribonucleic acid (DNA) or epigenetic age is a renowned aging biomarker. They decouple chronological age from the functionality of cells and tissues, concomitantly reflecting aging and health deficits in an individual.
Finally, the team expressed OSK in HEK001 keratinocytes retrieved from the scalp of a 65-year-old patient. They used immunoblotting to assess the exogenous OSK in these keratinocytes transduced with a lentivirus.
Study findings
The researchers observed an extraordinary 109% extension in average remaining life due to OSK expression. Accordingly, control and TRE-OSK mice had 8.86 and 18.5 weeks of extended remaining lives, respectively. Further, the researchers noted a median lifespan of ~133 and 142.5 weeks for doxycycline-treated control and TRE-OSK mice, respectively. Since there was no substantial change in the median survival of mice, it suggested that doxycycline had no adverse or beneficial effects.
Furthermore, the reduction in the FI for doxycycline-treated control mice was 7.5 points, and for TRE-OSK mice was six points, indicating that an increased lifespan represented better health. Furthermore, the DNA isolated from heart and liver tissue pointed at reduced epigenetic age of test animals per the Lifespan Uber Clock (LUC). Most importantly, the researchers observed no teratoma formation in their cyclically induced OSK paradigm.
While aging cannot currently be prevented, its impact on life and healthspan can be minimized by interventions that aim to return gene expression networks to optimal function. The study results suggest that partial reprogramming could be a potential treatment in the elderly for reversing age-associated diseases and could extend human lifespan.”
Conclusions
Together, the study data suggested that AAV-mediated gene therapy delivered OSK increased lifespan in mice, other health parameters, and reversed epigenetic aging biomarkers in human cells. The authors advocated for follow-up monitoring studies in large animals to assess the safety and effectiveness of partial genetic reprogramming studies. The results of these studies would determine whether therapeutic rejuvenation in aging humans in specific age-related diseases and health and lifespan extension would be feasible and safe.
*Important notice: bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
Neha is a digital marketing professional based in Gurugram, India. She has a Master’s degree from the University of Rajasthan with a specialization in Biotechnology in 2008. She has experience in pre-clinical research as part of her research project in The Department of Toxicology at the prestigious Central Drug Research Institute (CDRI), Lucknow, India. She also holds a certification in C++ programming.
Other Useful Links
News-Medical.Net provides this medical information service in accordance
with these terms and conditions.
Please note that medical information found
on this website is designed to support, not to replace the relationship
between patient and physician/doctor and the medical advice they may provide. | *Important notice: bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
Background
The rapidly growing world population is increasing the societal burden. Moreover, aging raises the threat of contracting several fatal human diseases. Thus, it is urgent and crucial to identify anti-aging interventions to reverse or defer the aging process.
Although longevity, i.e., increasing the ‘lifespan,’ is a feasible goal, whose golden standard biomarker is time to death. However, it does not improve their quality of life or health span.
On the contrary, age reversal could restore the aging effects at the genetic level and increase health and lifespan. Another issue with anti-aging interventions is cycle time, which requires waiting for a living being to die. Even in mice, testing anti-aging interventions can take six months to three years.
Takahashi and Yamanaka in 2006 showed that somatic cells could go back to a pluripotent state, thereby shaking off the paradigm of unidirectional differentiation. In the 4F-progeroid mouse model, doxycycline induced partial reprogramming of the OSK cassette. A reverse tetracycline transactivator (rtTA) drove this process and extended the lifespan of 4F-progeroid mice. Furthermore, this study showed a correlation between the epigenetic profile of tissues and improved function. The researchers, Horvath and Raj, assessed this using epigenetic methylation clocks.
About the study
In the present study, researchers generated a two-component AAV9 vector system having doxycycline-inducible OSK, of which one vector carried rtTa and the other a polycistronic OSK expression cassette. They also selected AAV9 capsid for maximal distribution of vectors to most mouse tissues. | yes |
Aging | Can gene therapy reverse the aging process? | yes_statement | "gene" "therapy" has the potential to "reverse" the "aging" "process".. the "aging" "process" can be "reversed" through "gene" "therapy". | https://fortune.com/well/2023/07/18/harvard-scientists-chemical-cocktail-may-reverse-aging-process-in-one-week/ | 'Chemical cocktail' may reverse aging in just 1 week | Fortune Well | Harvard scientists have identified a drug combo that may reverse aging in just one week: ‘A step towards affordable whole-body rejuvenation’
Harvard geneticist David Sinclair finds a group of “chemical cocktails” reversed aging in a one-week animal study, but experts say the results are preliminary.
Getty Images
Harvard researchers found a “chemical cocktail” that helped reverse aging in mice within a week by rejuvenating old cells within muscles, tissues, and some organs.
Aging and longevity expert David Sinclair, who is a researcher in the department of genetics and codirector of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School, announced the findings on Twitter.
“We’ve previously shown age reversal is possible using gene therapy to turn on embryonic genes,” Sinclair tweeted in a thread with over 1 million engagements. “Now we show it’s possible with chemical cocktails, a step towards affordable whole-body rejuvenation.”
In research over the course of three years, Sinclair and his team at Harvard observed mice taking six “chemical cocktails” that can reverse key hallmarks of aging by rejuvenating senescent or older, deteriorating cells “without erasing cellular identity,” according to the study.
“Studies on the optic nerve, brain tissue, kidney, and muscle have shown promising results, with improved vision and extended lifespan in mice and, recently, in April of this year, improved vision in monkeys,” Sinclair tweeted.
In a press release, Sinclair said, “This new [hotlink]discovery ignore=true[/hotlink] offers the potential to reverse aging with a single pill, with applications ranging from improving eyesight to effectively treating numerous age-related diseases.”
Is a “chemical cocktail” the answer to living longer?
The cocktail consists of a variety of molecules, including valproic acid, which is an anti-seizure medication used for migraine and mood disorders, and a drug used for cancer with anti-aging properties.
To Sinclair, we may be close to a reverse-aging concoction to restore youthfulness, but longevity experts have their concerns. It’s too early to interpret these results for humans, Dr. Luigi Fontana, author of Manual of Healthy Longevity & Wellbeing and the director of the Healthy Longevity Research and Clinical Program at the University of Sydney, tells Fortune.
“These are just preclinical data that must be validated in well-designed and adequately powered human randomized clinical trials,” he says. “It is essential to rely on rigorous scientific research and evidence-based studies before drawing conclusions about the effects of such molecules on human health.”
Dr. Neil Paulvin, a New York–based regenerative and functional medicine doctor, says the study does not prove there’s one pill to extend life span. Top of mind for him in the aging space is addressing inflammation and mitochondrial issues, which are integral to extending health span.
“Some of the cocktail may have potential for aging 15, 20, 50 years from now,” Paulvin tells Fortune, although people should not assume “that there’s something coming tomorrow that’s going to help them live another 10 years.”
Additionally, all of the components of the cocktail must be rigorously tested in humans to ensure they don’t cause an increased risk of cancer, for example.
Sinclair says the team is preparing for human cellular trials using gene therapy for reverse aging, per his Twitter account, and he responded to a question confirming human trials will be available within a decade.
“There’s a race between many groups to show chemicals can rejuvenate cells like gene therapy can,” Sinclair tweeted. He adds, “We envision a future where age-related diseases can be effectively treated, injuries can be repaired more efficiently, and the dream of whole-body rejuvenation becomes a reality.”
Subscribe to Well Adjusted, our newsletter full of simple strategies to work smarter and live better, from the Fortune Well team. Sign up today. | Harvard scientists have identified a drug combo that may reverse aging in just one week: ‘A step towards affordable whole-body rejuvenation’
Harvard geneticist David Sinclair finds a group of “chemical cocktails” reversed aging in a one-week animal study, but experts say the results are preliminary.
Getty Images
Harvard researchers found a “chemical cocktail” that helped reverse aging in mice within a week by rejuvenating old cells within muscles, tissues, and some organs.
Aging and longevity expert David Sinclair, who is a researcher in the department of genetics and codirector of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School, announced the findings on Twitter.
“We’ve previously shown age reversal is possible using gene therapy to turn on embryonic genes,” Sinclair tweeted in a thread with over 1 million engagements. “Now we show it’s possible with chemical cocktails, a step towards affordable whole-body rejuvenation.”
In research over the course of three years, Sinclair and his team at Harvard observed mice taking six “chemical cocktails” that can reverse key hallmarks of aging by rejuvenating senescent or older, deteriorating cells “without erasing cellular identity,” according to the study.
“Studies on the optic nerve, brain tissue, kidney, and muscle have shown promising results, with improved vision and extended lifespan in mice and, recently, in April of this year, improved vision in monkeys,” Sinclair tweeted.
In a press release, Sinclair said, “This new [hotlink]discovery ignore=true[/hotlink] offers the potential to reverse aging with a single pill, with applications ranging from improving eyesight to effectively treating numerous age-related diseases.”
Is a “chemical cocktail” the answer to living longer?
| yes |
Aging | Can gene therapy reverse the aging process? | yes_statement | "gene" "therapy" has the potential to "reverse" the "aging" "process".. the "aging" "process" can be "reversed" through "gene" "therapy". | https://hsci.harvard.edu/news/reversing-aging-eye | Reversing aging in the eye | Harvard Stem Cell Institute (HSCI) | Harvard Stem Cell Institute (HSCI) scientists are part of a team that has successfully restored vision in mice by turning back the clock in aged eye cells in the retina to recapture youthful gene function.
The team’s work, published in the journal Nature, is the first demonstration that it may be possible to safely reprogram complex tissues, such as the nerve cells of the eye, to an earlier age. The researchers also successfully reversed vision loss in animals with a condition mimicking human glaucoma, a leading cause of blindness around the world. The achievement represents the first successful attempt to reverse glaucoma-induced vision loss, rather than merely stem its progression.
If replicated through further studies, the approach could pave the way for therapies to promote tissue repair across various organs and reverse age-related diseases in humans.
“Our study demonstrates that it’s possible to safely reverse the age of complex tissues such as the retina and restore its youthful biological function,” said co-senior author David Sinclair, professor of genetics in the Blavatnik Institute at Harvard Medical School (HMS). “If affirmed through further studies, these findings could be transformative for the care of age-related vision diseases like glaucoma and to the fields of biology and medical therapeutics for disease at large.”
Other co-senior authors of the study include HSCI Principal Faculty member Zhigang He, HSCI Affiliate Faculty member Bruce Ksander, and Meredith Gregory-Ksander.
Gene trio
The team’s approach is based on a new theory about why we age. Most cells in the body contain the same DNA molecules but have widely diverse functions. To achieve this degree of specialization, these cells must read only genes specific to their type. This regulatory function is the purview of the epigenome, a system of turning genes on and off in specific patterns without altering the basic underlying DNA sequence of the gene.
This theory postulates that changes to the epigenome over time cause cells to read the wrong genes and malfunction — giving rise to diseases of aging. One of the most important changes to the epigenome is DNA methylation, a process by which methyl groups are tacked onto DNA. Patterns of DNA methylation are laid down during embryonic development to produce the various cell types. Over time, youthful patterns of DNA methylation are lost, and genes inside cells that should be switched on get turned off and vice versa, resulting in impaired cellular function. Some of these DNA methylation changes are predictable and have been used to determine the biologic age of a cell or tissue.
Yet, whether DNA methylation drives age-related changes inside cells has remained unclear. In the current study, the researchers hypothesized that if DNA methylation does indeed control aging, then erasing some of its footprints might reverse the age of cells inside living organisms and restore them to their earlier, more youthful state.
Lead study author Yuancheng Lu developed a gene therapy based on the Nobel Prize-winning discovery of Shinya Yamanaka, who identified the four transcription factor proteinsthat can erase epigenetic markers on cells and return them to their embryonic state, from which they can develop into any other type of cell.
Subsequent studies, however, showed two important setbacks. First, when used in adult mice, the four Yamanaka factors could also induce tumor growth, rendering the approach therapeutically unsafe. Second, the factors could reset the cellular state to the most primitive cell state, thus completely erasing a cell’s identity.
Lu and colleagues circumvented these hurdles by slightly modifying the approach and delivering only three factors. The modified approach successfully reversed cellular aging without fueling tumor growth or losing cellular identity.
Applying gene therapy to optic nerve regeneration
The researchers tested their approach on cells in the central nervous system because it is the first part of the body affected by aging. After birth, the ability of the central nervous system to regenerate declines rapidly.
To test whether the regenerative capacity of young animals could be imparted to adult mice, the researchers delivered the modified three-gene combination into retinal ganglion cells of adult mice with optic nerve injury.
For the work, Lu and Sinclair collaborated with Zhigang He, HMS professor of neurology and of ophthalmology at Boston Children’s Hospital, who studies optic nerve and spinal cord development and regeneration.
The treatment resulted in a two-fold increase in the number of surviving retinal ganglion cells after the injury and a five-fold increase in nerve regrowth.
“At the beginning of this project, many of our colleagues said our approach would fail or would be too dangerous to ever be used,” said Lu. “Our results suggest this method is safe and could potentially revolutionize the treatment of the eye and many other organs affected by aging.”
Reversal of glaucoma and age-related vision loss
Following the encouraging findings in mice with optic nerve injuries, the team collaborated with colleagues at Schepens Eye Research Institute of Massachusetts Eye and Ear: Bruce Ksander, HMS associate professor of ophthalmology, and Meredith Gregory-Ksander, HMS assistant professor of ophthalmology. They planned two sets of experiments: one to test whether the three-gene cocktail could restore vision loss due to glaucoma, and another to see whether the approach could reverse vision loss stemming from normal aging.
In a mouse model of glaucoma, the treatment led to increased nerve cell electrical activity and a notable increase in visual acuity, as measured by the animals’ ability to see moving vertical lines on a screen. Remarkably, it did so after the glaucoma-induced vision loss had already occurred.
“Regaining visual function after the injury occurred has rarely been demonstrated by scientists,” Ksander said. “This new approach, which successfully reverses multiple causes of vision loss in mice without the need for a retinal transplant, represents a new treatment modality in regenerative medicine.”
The treatment worked similarly well in elderly, 12-month-old mice with diminishing vision due to normal aging. Following treatment, the gene expression patterns and electrical signals of the optic nerve cells in elderly mice were similar to young mice and vision was restored.
When the researchers analyzed molecular changes in treated cells, they found reversed patterns of DNA methylation—an observation suggesting that DNA methylation is not a mere marker or a bystander in the aging process, but rather an active agent driving it.
“What this tells us is the clock doesn’t just represent time — it is time,” said Sinclair. “If you wind the hands of the clock back, time also goes backward.”
The researchers said that if their findings are confirmed in further animal studies, they could initiate clinical trials within two years to test the efficacy of the approach in people with glaucoma. Thus far, the outlook is encouraging — in the current study, a one-year, whole-body treatment of mice with the three-gene approach showed no negative side effects.
Read more
This story was originally published on the HMS website on December 2, 2020, under the title “Vision Revision.”
This work was supported in part by an HMS Epigenetics Seed Grant and Development Grant, The Glenn Foundation for Medical Research, Edward Schulak, the National Institutes of Health, and the St. Vincent de Paul Foundation. | Harvard Stem Cell Institute (HSCI) scientists are part of a team that has successfully restored vision in mice by turning back the clock in aged eye cells in the retina to recapture youthful gene function.
The team’s work, published in the journal Nature, is the first demonstration that it may be possible to safely reprogram complex tissues, such as the nerve cells of the eye, to an earlier age. The researchers also successfully reversed vision loss in animals with a condition mimicking human glaucoma, a leading cause of blindness around the world. The achievement represents the first successful attempt to reverse glaucoma-induced vision loss, rather than merely stem its progression.
If replicated through further studies, the approach could pave the way for therapies to promote tissue repair across various organs and reverse age-related diseases in humans.
“Our study demonstrates that it’s possible to safely reverse the age of complex tissues such as the retina and restore its youthful biological function,” said co-senior author David Sinclair, professor of genetics in the Blavatnik Institute at Harvard Medical School (HMS). “If affirmed through further studies, these findings could be transformative for the care of age-related vision diseases like glaucoma and to the fields of biology and medical therapeutics for disease at large.”
Other co-senior authors of the study include HSCI Principal Faculty member Zhigang He, HSCI Affiliate Faculty member Bruce Ksander, and Meredith Gregory-Ksander.
Gene trio
The team’s approach is based on a new theory about why we age. Most cells in the body contain the same DNA molecules but have widely diverse functions. To achieve this degree of specialization, these cells must read only genes specific to their type. This regulatory function is the purview of the epigenome, a system of turning genes on and off in specific patterns without altering the basic underlying DNA sequence of the gene.
This theory postulates that changes to the epigenome over time cause cells to read the wrong genes and malfunction — giving rise to diseases of aging. | yes |
Aging | Can gene therapy reverse the aging process? | yes_statement | "gene" "therapy" has the potential to "reverse" the "aging" "process".. the "aging" "process" can be "reversed" through "gene" "therapy". | https://scitechdaily.com/age-reversal-breakthrough-harvard-mit-discovery-could-enable-whole-body-rejuvenation/ | Age Reversal Breakthrough: Harvard/MIT Discovery Could Enable ... | Scientists from Harvard Medical School, the University of Maine, and MIT have published a groundbreaking study revealing a chemical method to reprogram cells to a more youthful state. This technique offers a potential alternative to gene therapy for reversing aging. The implications of this research are vast, with potential applications in regenerative medicine, treatment of age-related diseases, and whole-body rejuvenation.
In a pioneering study, researchers from Harvard Medical School, University of Maine, and MIT have introduced a chemical method for reversing cellular aging. This revolutionary approach offers a potential alternative to gene therapy for age reversal. The findings could transform treatments for age-related diseases, enhance regenerative medicine, and potentially lead to whole-body rejuvenation.
Groundbreaking Discovery in Aging Reversal
In a monumental study, a team of researchers has revealed a novel approach to combating aging and age-related diseases. This work, undertaken by scientists at Harvard Medical School, introduces the first chemical method to rejuvenate cells, bringing them to a more youthful state. Prior to this, only powerful gene therapy could achieve this feat.
Mice in the Sinclair lab have been engineered to age rapidly to test the effectiveness of therapies to reverse the aging process. The mouse on the right has been aged to 150% that of its sibling on the left by disrupting its epigenome. Photo credit: D. Sinclair, Harvard Medical School. Credit: 2023 Yang et al.
Exploring the Methodology
This discovery builds on the finding that the expression of specific genes, known as Yamanaka factors, can transform adult cells into induced pluripotent stem cells (iPSCs). This breakthrough, which earned a Nobel Prize, prompted scientists to question if cellular aging could be reversed without pushing cells to become too young and potentially cancerous.
Rejuvenation and age reversal of senescent human skin cells by chemical means. Cells in the right two panels have restored compartmentalization of the red fluorescent protein in the nucleus, a marker of youth that was used to find the cocktails, before the scientists confirmed they were younger, based on how genes were expressed. Image credit: J. -H. Yang, Harvard Medical School. Credit: 2023 Yang et al.
In this recent study, the scientists probed for molecules that could, in tandem, revert cellular aging and refresh human cells. They designed advanced cell-based assays to differentiate between young and old, as well as senescent cells. The team employed transcription-based aging clocks and a real-time nucleocytoplasmic protein compartmentalization (NCC) assay. In a significant development, they identified six chemical combinations that could return NCC and genome-wide transcript profiles to youthful states, reversing transcriptomic age in less than a week.
Relevance and Potential Applications
The Harvard team has previously shown the possibility of reversing cellular aging without causing unregulated cell growth. This was done by inserting specific Yamanaka genes into cells using a viral vector. Studies on various tissues and organs like the optic nerve, brain, kidney, and muscle have yielded encouraging results, including improved vision and extended lifespan in mice. Additionally, recent reports have documented improved vision in monkeys.
These findings have profound implications, paving the way for regenerative medicine and potentially full-body rejuvenation. By establishing a chemical alternative to gene therapy for age reversal, this research could potentially transform the treatment of aging, injuries, and age-related diseases. The approach also suggests the possibility of lower development costs and shorter timelines. Following successful results in reversing blindness in monkeys in April 2023, plans for human clinical trials using the lab’s age reversal gene therapy are currently underway.
Views from the Research Team
“Until recently, the best we could do was slow aging. New discoveries suggest we can now reverse it,” said David A. Sinclair, A.O., Ph.D., Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School and lead scientist on the project. “This process has previously required gene therapy, limiting its widespread use.”
The team at Harvard envisions a future where age-related diseases can be effectively treated, injuries can be repaired more efficiently, and the dream of whole-body rejuvenation becomes a reality. “This new discovery offers the potential to reverse aging with a single pill, with applications ranging from improving eyesight to effectively treating numerous age-related diseases,” Sinclair said.
YEP. Promises! Promises! All the way back to the Egyptian Pharaohs and their “cost-intensive” bid for immortality. If one skips the fancy Jar and storage in a Mausoleum, it “more affordable”. It certainly won’t matter to the Dead. As such, memory and some photos will do.
If science is able to eliminate death control via senescence and apoptosis, and this technology spreads to everyone regardless of affordability, then birth control will become even more critical, in fact essential, to keep the human race from overpopulating into mass disaster. But it would also mean the end of natural human evolution, and the advent of taking our evolution into our own hands via genetic modification, because it would also mean the end of children, who are evolution’s natural mutation-testing petri dish, in the name of preserving terrestrial space for the survival of the glut of already living and henceforth virtually immortal adults.
1. Reversing methylation doesn’t cure aging. Even if we can control senescent cells, extend telomeres, restore healthy mitochondria, and restore the thymus gland. None of the aging scientists have a plan for repairing DNA errors. We incur 10,000 to 100,000 DNA breaks in each cell every day. 99%+ are repaired correctly, but some are not. Those mistakes carry over to future cell generations. Most DNA is junk, other genes are not important to the tissue damaged, so every mistake is not crucial. There are genetic variants that do a better job of repair and are more represented in the population of centenarians. And there are other things that accumulate like glucosepane, forms of amyloid plaques like misfolded transthyretin, genetically damaged mitochondria (they burn fuel inefficiently making wastes like lipofuscin which is the brown stuff in age spots, and these lipofuscin accumulations are not just on the skin. They are in muscle, heart, liver, kidneys, and the brain). We accumulate scar tissue. Accumulated latent infections often promote diseases, quite possibly schizophrenia, Alzheimer’s, and others. 2. The Earth can handle 500x current human population provided we develop technology to directly manufacture food from atoms, recycle everything, live in greater density, and in more diverse locations, like under domes in Antarctica, on the oceans, underground, on stilts above the surface of the land, without interfering with the land. And we can build large space stations and inhabit the Moon, Mars, asteroids… The Solar System can support many trillions of humans while dramatically improving the Earth environment. 3. Machines and tech that allow food surplus and some tech like contact lenses and braces, limit selection pressure, but it remains. We can and should reduce genetic birth defects through genetic surgery at the zygote or blastocyst stage. But there will always be natural births that are not repaired. We can fix some of this, but the repairs will be limited.
Were we playing God, when we developed fire? Clothing? Shoes? The plow? Antibiotics? Anesthesia? Eyeglasses? Scuba gear? Airplanes? Spaceships? If you haven’t noticed, life expectancy has tripled from the time of the Romans. If it doubles or triples again, how is that any different? I am not saying this treatment will double it. I would find that highly unlikely, but in combination with other advances, it is not inconceivable. It is very unlikely you will be kept alive, if you sign a do not resuscitate will, and have a copy in your wallet, or on a metal wristband. Certainly, no one will force you to take some elixir of life or anything like that. Seems exceedingly unlikely, anyway.
This would be extremely dangerous to try. It may be justified for some very important tissue like the retina to restore vision or the “hair” cells in the cochlea to restore stop maddening ear ringing, or to attempt to reverse spinal injuries. For whole body, there are many steps to go to insure safety. They have to test on normal mice, perhaps dogs, then monkeys, then people with some unusual condition where methylation aging is accelerated, then probably the very old, with little to lose. Probably with a very modest dose, at first. Probably a good 15 years, before they get to ordinary 40-70-year-olds. Maybe millionaires will get it in some Latin American country in 5 or 10 years. But that would be very risky. I would try gene therapy, way before I would try this.
There have been other successful attempts to correct fast aging mice. The type of fast aging mice are well-chosen, or engineered exactly for the test. Something of a parlor trick. But it has a purpose. It verifies what has gone wrong and that it can be fixed. But it gives the impression that you can just apply this to people with decent chance of success. Unless and until they dramatically increase the life expectancy of normal mice, they have not proven anything. That takes a few years. Hopefully, they already started a couple of years ago because doing something dramatic, like doubling average lifespan, will take 5 or 6 years to finish. There are many things which change during aging. This will not correct the other dozen, even if it worked perfectly in humans with no side effects. And that is a big “if” because it may restore senescent cells, which can be very dangerous. There is also the risk that cells will regress too far and forget what they are and create tumors. If you talk to aging scientists, they will likely emphasize the aspect of aging they are working on, and mostly ignore the others. Methylation may be upstream of some of these, but not all of them. Various types of accumulations with age are unlikely to be addressed. Things like the accumulation of genetic damage. Each cell’s DNA is broken 10,000-100,000 times a day. And most of the time correctly repaired, but not all the time. Errors are carried over to the next generation of cells. And there is this stuff called Glucosepane which accumulates between cells making the tissues stiff, especially arteries, and is implicated in a number of aging diseases. Neither our bodies nor scientists have figured out how to reverse this. There are also the accumulations of misfolded proteins called amyloid. And there are 30 kinds, not just the 1 involved in Alzheimer’s, like Wild-type ATTR Amyloidosis, which may be near certain over 110 years of age. That stiffens the heart, and make exertion very difficult.
How much reverse aging are we talking about? The paper as I understand it spoke of age reversal of only a few years. Also how long will this “pill” remain in effect? Will there be a rebound or is the effect permanent? Much remains to be done but still a groundbreaking paper even if the results don’t lead to an anti-aging pill. | These findings have profound implications, paving the way for regenerative medicine and potentially full-body rejuvenation. By establishing a chemical alternative to gene therapy for age reversal, this research could potentially transform the treatment of aging, injuries, and age-related diseases. The approach also suggests the possibility of lower development costs and shorter timelines. Following successful results in reversing blindness in monkeys in April 2023, plans for human clinical trials using the lab’s age reversal gene therapy are currently underway.
Views from the Research Team
“Until recently, the best we could do was slow aging. New discoveries suggest we can now reverse it,” said David A. Sinclair, A.O., Ph.D., Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School and lead scientist on the project. “This process has previously required gene therapy, limiting its widespread use.”
The team at Harvard envisions a future where age-related diseases can be effectively treated, injuries can be repaired more efficiently, and the dream of whole-body rejuvenation becomes a reality. “This new discovery offers the potential to reverse aging with a single pill, with applications ranging from improving eyesight to effectively treating numerous age-related diseases,” Sinclair said.
YEP. Promises! Promises! All the way back to the Egyptian Pharaohs and their “cost-intensive” bid for immortality. If one skips the fancy Jar and storage in a Mausoleum, it “more affordable”. It certainly won’t matter to the Dead. As such, memory and some photos will do.
If science is able to eliminate death control via senescence and apoptosis, and this technology spreads to everyone regardless of affordability, then birth control will become even more critical, in fact essential, to keep the human race from overpopulating into mass disaster. | yes |
Aging | Can gene therapy reverse the aging process? | yes_statement | "gene" "therapy" has the potential to "reverse" the "aging" "process".. the "aging" "process" can be "reversed" through "gene" "therapy". | https://www.medicalnewstoday.com/articles/harvard-scientists-reverse-aging-in-mice-is-it-possible-in-humans | Scientists reversed aging in mice: Is it possible in humans? | For many years, most researchers have believed changes to a body’s DNA — called mutations — are a leading cause of aging.
Now a team led by researchers from Harvard Medical School finds support for an alternative hypothesis: it is the changes that affect the expression of the DNA — called epigenetics — that affect aging. Scientists demonstrated this via a mouse model where changes in epigenetic information caused mice to first age and then reverse aging.
Gene activity, the “switch on” and “switch off” of genes, is associated with epigenetic changes, chemical changes in the DNA that do not alter the DNA sequence. Epigenetics studies how the environment can modify how genes work without actually changing the genes themselves.
This study is not the first time researchers have used epigenetics to study aging. For example, previous research shows epigenetics provides a biological clock for the body, helping scientists measure a person’s aging rate.
Medical News Today spoke with Dr. David Sinclair, a professor in the Department of Genetics and co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School, and senior author of this study.
Dr. Sinclair said the research team decided to study epigenetics as a potential driver for the aging process based on previous research he had been involved with in the 1990s that showed lifespan is under the control of epigenetic regulators called sirtuins.
“We have discovered that if you turn on three “Yamanaka” genes that normally switch on during embryogenesis, you can safely reverse the aging process by more than 50%,” he explained to MNT. “These genes initiate a program that is not well understood, but the outcome is age reversal and restoration of tissue function. For example, we can reverse the age of optic nerves to restore the vision of all mice.”
During this study, researchers created temporary, fast-healing “cuts” in the DNA of mice. These cuts imitated the effect of certain lifestyle and environmental effects on the DNA’s epigenetic pattern.
Researchers found the cuts caused the mice’s epigenetic pattern to change and eventually malfunction, causing the mice to begin looking and acting older. These mice also had increased biomarkers indicating aging.
Scientists then gave these mice gene therapy to reverse the epigenetic changes, which they said “reset” the mice’s epigenetic program and ultimately reversed the aging the mice had experienced.
“We hope these results are seen as a turning point in our ability to control aging,” Sinclair says. “This is the first study showing that we can have precise control of the biological age of a complex animal; that we can drive it forwards and backward at will.”
MNT also spoke about this study with Dr. Santosh Kesari, a neurologist at Providence Saint John’s Health Center in Santa Monica, CA, and Regional Medical Director for the Research Clinical Institute of Providence Southern California.
Dr. Kesari said this was a “very exciting study,” opening up the understanding of how aging occurs and how we can measure it at the DNA level.
“And it turns out it’s not just that we accumulate mutations in the DNA, which is we think is one of the main factors that cause age-related disorders, … but more of how the DNA is read that is really contributing to aging,” Dr. Kesari explained. “And as we age, the reading of the DNA is affected in a big way. (This) really opens up a new way of thinking about aging, but also a new way to think about targeting aging by developing drugs that affect how the cell reads the DNA.”
As this study was conducted in an animal model, Dr. Kesari said the next question and challenge would be to understand how individual humans age in the real world — what tests are required, and how scientists can monitor for bad aging.
“And then doing really smart studies to look at biomarkers that give you a signal that you’re actually affecting aging in a positive way,” he continued. “What are those markers? What drugs can we do to test that?”
“Certainly, we don’t want to wait (for) 10, 20, or 30 years to do aging studies, so the challenge is really identifying markers in humans, … testing drugs, and then having short-term biomarkers that tell us whether a drug is working or not and affecting age-related disorders,” Dr. Kesari concluded. | Dr. Sinclair said the research team decided to study epigenetics as a potential driver for the aging process based on previous research he had been involved with in the 1990s that showed lifespan is under the control of epigenetic regulators called sirtuins.
“We have discovered that if you turn on three “Yamanaka” genes that normally switch on during embryogenesis, you can safely reverse the aging process by more than 50%,” he explained to MNT. “These genes initiate a program that is not well understood, but the outcome is age reversal and restoration of tissue function. For example, we can reverse the age of optic nerves to restore the vision of all mice.”
During this study, researchers created temporary, fast-healing “cuts” in the DNA of mice. These cuts imitated the effect of certain lifestyle and environmental effects on the DNA’s epigenetic pattern.
Researchers found the cuts caused the mice’s epigenetic pattern to change and eventually malfunction, causing the mice to begin looking and acting older. These mice also had increased biomarkers indicating aging.
Scientists then gave these mice gene therapy to reverse the epigenetic changes, which they said “reset” the mice’s epigenetic program and ultimately reversed the aging the mice had experienced.
“We hope these results are seen as a turning point in our ability to control aging,” Sinclair says. “This is the first study showing that we can have precise control of the biological age of a complex animal; that we can drive it forwards and backward at will.”
MNT also spoke about this study with Dr. Santosh Kesari, a neurologist at Providence Saint John’s Health Center in Santa Monica, CA, and Regional Medical Director for the Research Clinical Institute of Providence Southern California.
Dr. Kesari said this was a “very exciting study,” opening up the understanding of how aging occurs and how we can measure it at the DNA level.
| yes |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://poolscouts.com/why-hair-turns-green-in-the-pool-and-9-ways-to-fix-it/ | Why Hair Turns Green In The Pool And 9 Ways To Fix It! - Pool Scouts | Blog
Why Hair Turns Green In The Pool And 9 Ways To Fix It!
All you blondes out there are probably dealing with similar struggles this summer. If your hair turns green after taking a splash in the pool, you’re certainly not alone. Green hair can be an irritating setback during a season expected to be fun and free, so we are here to explain the mystery and solve the problem!
At some point in time, you’ve probably heard that blonde hair turns green after a swim-session because of the chlorine in pool water. You most likely believed chlorine to be the culprit from that point on. You’re not completely wrong, but the truth is, copper is actually the main factor at fault. Copper is a metal found in water. Even tap water with a high copper content can give your hair a green tint! However, the green color is more likely to show up after swimming in the pool because pool water contains chlorine. Chlorine and copper bond together to form a film that sticks to the proteins in each strand of hair, causing the hair to turn green.
How to Prevent and/or Fix Green Hair
We know this is an annoyance, even while knowing it isn’t permanent. Whether you’re hoping to prevent green hair before it appears or trying to wash the green out of your hair after a swim, here are a few solutions to test.
Leave-in conditioner – If you apply a leave-in conditioner before swimming, the pool water won’t stick to your hair as easily.
Wet hair – Don’t get in the pool with dry hair. If you start with wet hair, chlorine and copper won’t hang onto your hair as tightly.
Always, always, always wash your hair as soon as you are done swimming for the day.
V8/Tomato Juice – Coat your hair with tomato juice or V8 and let it sit for 5-10 minutes. Wash and condition as normal when you are finished.
Ketchup – Coat your hair in ketchup. Either wrap it in up tinfoil or put on a swim cap and let it sit for about 30 minutes before shampooing and conditioning.
Aspirin – Crush 6-8 aspirin tablets inside a bowl, add warm water to it, and let it dissolve. Put the aspirin-water mixture into your hair and let it sit for about 15-20 minutes. Rinse it out with clean water, then shampoo and condition normally.
Baking soda – Use ¼ – ½ a cup of baking soda and mix water with it in order to make a paste. Massage the paste into green hair and rinse it out with clean water, then wash and condition normally. The amount of times this needs to be done will depend on the intensity of the green color.
Lemon juice – Saturate your hair with lemon juice and let it sit for 5-10 minutes before shampooing and conditioning as normal.
Lemon Kool-Aid – Mix the Kool-Aid with water and apply it to the green areas in the hair and let it sit for several minutes. Shampoo and condition normally.
Try these tricks on yourself or your kids. You’ll finally be able to enjoy a pool day without having to worry about losing those gorgeous golden locks! Good luck!
Get on the Schedule
Give your local Pool Scouts a call at 844-775-2742 for all of your pool service needs! Or fill out the form to the right for a free estimate. We’ll keep your backyard oasis cannonball ready at all times. Your hair might turn green, but your pool certainly won’t be. Perfect Pools, Scout’s Honor.
Request a Quote
By submitting this form you agree to receive recurring, automated marketing text messages from Pool Scouts at the number provided. Reply HELP for help and STOP to cancel. Msg frequency varies. Msg & data rates may apply. | Blog
Why Hair Turns Green In The Pool And 9 Ways To Fix It!
All you blondes out there are probably dealing with similar struggles this summer. If your hair turns green after taking a splash in the pool, you’re certainly not alone. Green hair can be an irritating setback during a season expected to be fun and free, so we are here to explain the mystery and solve the problem!
At some point in time, you’ve probably heard that blonde hair turns green after a swim-session because of the chlorine in pool water. You most likely believed chlorine to be the culprit from that point on. You’re not completely wrong, but the truth is, copper is actually the main factor at fault. Copper is a metal found in water. Even tap water with a high copper content can give your hair a green tint! However, the green color is more likely to show up after swimming in the pool because pool water contains chlorine. Chlorine and copper bond together to form a film that sticks to the proteins in each strand of hair, causing the hair to turn green.
How to Prevent and/or Fix Green Hair
We know this is an annoyance, even while knowing it isn’t permanent. Whether you’re hoping to prevent green hair before it appears or trying to wash the green out of your hair after a swim, here are a few solutions to test.
Leave-in conditioner – If you apply a leave-in conditioner before swimming, the pool water won’t stick to your hair as easily.
Wet hair – Don’t get in the pool with dry hair. If you start with wet hair, chlorine and copper won’t hang onto your hair as tightly.
Always, always, always wash your hair as soon as you are done swimming for the day.
V8/Tomato Juice – Coat your hair with tomato juice or V8 and let it sit for 5-10 minutes. Wash and condition as normal when you are finished.
Ketchup – Coat your hair in ketchup. Either wrap it in up tinfoil or put on a swim cap and let it sit for about 30 minutes before shampooing and conditioning. | yes |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://pooltroopers.com/blog/get-green-out-of-blond-hair/ | How To Get Green Out Of Blonde Hair After The Pool | How To Get Green Out Of Blonde Hair After The Pool ?
Have you ever taken a swim only to later notice that your hair has a green tinge? This is a common issue among those with light hair, blonde or gray, that swim in any body of water, but most frequently noticed in salt and freshwater pools. The key to addressing this issue is proper chemical treatment of the pool and a few preventative steps taken by the swimmer to prevent their hair from turning green. Has your hair already turned green? There are some things that you can do to restore your hair to its normal color, and many of these solutions are items found in your own kitchen cupboard or pantry. For pool treatment and cleaning services, call the professionals at Pool Troopers, serving customers that live either Florida, Texas, or Arizona.
How to get green out of blonde hair after the pool? Here is what you need to know:
Copper
The root cause of why blonde and other light-colored hair turns green after swimming in a pool is copper. This metal is found in the water of most pools, whether fresh or saltwater varieties. Since chlorine is commonly found in all swimming pools, it serves to oxidize the copper, and other hard water metals, which then saturates hair, turning it a green color. So, basically, the green color is the presence of metals in your hair; to restore your hair color, you must remove these metals.
Know that copper and other metals like manganese and iron are in municipal water systems, and the tap or well water that people widely drink. Hair is porous so it is particularly vulnerable to the effects of these hard metals; think of hair as a ‘catchall’ for whatever happens to be in the water that you saturate it with. The reason that it turns green is that this is the resulting patina of the oxidation process, just like an old copper penny that has been subjected to the elements.
Algae
Another explanation for your hair turning green when you use the pool is algae; or rather, it is caused by algaecide, another common element found in many pools. Copper is often in these commercial algaecide products that homeowners buy to treat their pool with and prevent the green growth of algae in and around their pools. If you are vigilant about keeping the pool filtered, cleaned, and treated, you may not need to use an algaecide product to eliminate this residue from the pool. However, if you do use these treatments, there is a higher chance that your hair will turn green from the copper comprising many of these additives.
Testing
The first thing to do is to test the pool water. Use testing strips or the services of a pool professional to determine if there is copper in your pool’s water. Sometimes, you can take a sample of your pool water to your pool servicing company and have them test and address the situation for you. Also, keep chemicals and minerals out of the water as much as you can by using a hose filter when you initially fill or when you add water to your pool. This helps to keep these minerals, including copper, out in the first place.
Hair and Highlights
While all hair is at risk of turning green, blonde hair is more vulnerable simply due to the light hue and obvious effects of discoloration. All hair is prone to oxidation and green tinge; if you have darker hair with highlights, you may notice discoloring primarily on your lighter strands. Whether your hair is blonde, brown, black, red, or gray, use the same precautions and measures to prevent your hair from turning green during and after a swim.
Prevention
Take the bull by the horns and use a leave-in conditioner after swimming or between time spent in the pool. Make sure to wash your hair well first to remove any residue from the water and look for nourishing hair products that contain beneficial ingredients like Argan oil, which can help protect hair from the rigors of chlorine and the rays of the sun.
Protection
The best protection for preventing discoloration is to block access to your porous hair, such as by wearing a swim cap. Swim caps are simple to don and cheap to buy; they are perhaps the most effective way at avoiding the fallout and repercussions of swimming in water with minerals and additives. Plus, wearing a cap prevents the common drying out impact of chlorine on hair. If you swim frequently, a cap makes good sense is available at discount, drug, and retail venues in most regions.
Tips and Tactics
Make an effort to find alternative ways to prevent discoloration when swimming; many of these solutions involve simple items found in your own kitchen.
Some tips and tactics include these suggestions:
Try treating your hair with ordinary Baking Soda, which costs pennies per application. Make a paste from a cup of baking soda and warm water, massage it into the areas of your hair that have been discolored. Pay special attention to the areas that are the most- green; rinse it well and go ahead and shampoo/condition as normal.
Use and leave deep conditioner on your hair for a minimum of 15-minutes, at least once weekly. Use cold water to rinse away after the time is up. Not sure what to use for a conditioner? Try regular coconut oil, also very inexpensive and likely something in your kitchen already. Rinse well after treating.
Try using tomato ketchup to get rid of the green tinge; that’s right: ketchup! This practice is based on color theory and how red and green are opposite shades on the universal color wheel. Massage the ketchup into your affected hair and then wrap your head in aluminum wrap or tinfoil for 30 minutes; rinse, wash, and condition as you normally would. The red ketchup can reverse and alter the greenish color of hair in most cases.
Try saturating your hair with lemon juice after you swim to reduce the impact of copper and chlorine on your hair. Soak your hair with lemon and let it sit for a few minutes before you rinse, wash, and condition, as normal. You can use fresh lemons or a bottled lemon juice for this procedure; make sure to deep condition your hair later as lemon juice can be very drying. .
Try rinsing your hair with plain apple cider vinegar before you get in the pool. The acidic vinegar makes it harder for the minerals, primarily copper, to infiltrate the hair strands and discolor the hair. Keep some in a spray bottle to easily spritz and saturate hair before a swim.
Another effective approach is to wash your hair as soon as you are done swimming; do not allow it to naturally dry first. This can curb the damage and discoloration done during your swim!
Talk to your hairstylist or barber for recommendations and specific products designed to prevent discoloration of your distinct hair type from the elements, pollutants, or swimming.
If you own a pool in Arizona, Florida, or Texas, call on the industry professionals at Pool Troopers for your full-service pool maintenance services. Tired of doing the work on your own? Hire a reputable company with decades of experience in serving residential pool owners widely. Our team at Pool Troopers will keep you informed of and on top of trends, tips, and tricks for swimming pool maintenance and an optimal swim experience. | How To Get Green Out Of Blonde Hair After The Pool ?
Have you ever taken a swim only to later notice that your hair has a green tinge? This is a common issue among those with light hair, blonde or gray, that swim in any body of water, but most frequently noticed in salt and freshwater pools. The key to addressing this issue is proper chemical treatment of the pool and a few preventative steps taken by the swimmer to prevent their hair from turning green. Has your hair already turned green? There are some things that you can do to restore your hair to its normal color, and many of these solutions are items found in your own kitchen cupboard or pantry. For pool treatment and cleaning services, call the professionals at Pool Troopers, serving customers that live either Florida, Texas, or Arizona.
How to get green out of blonde hair after the pool? Here is what you need to know:
Copper
The root cause of why blonde and other light-colored hair turns green after swimming in a pool is copper. This metal is found in the water of most pools, whether fresh or saltwater varieties. Since chlorine is commonly found in all swimming pools, it serves to oxidize the copper, and other hard water metals, which then saturates hair, turning it a green color. So, basically, the green color is the presence of metals in your hair; to restore your hair color, you must remove these metals.
Know that copper and other metals like manganese and iron are in municipal water systems, and the tap or well water that people widely drink. Hair is porous so it is particularly vulnerable to the effects of these hard metals; think of hair as a ‘catchall’ for whatever happens to be in the water that you saturate it with. The reason that it turns green is that this is the resulting patina of the oxidation process, just like an old copper penny that has been subjected to the elements.
Algae
Another explanation for your hair turning green when you use the pool is algae; or rather, it is caused by algaecide, another common element found in many pools. | yes |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://www.swimuniversity.com/hair-green-pool/ | Why Blond Hair Turns Green in the Pool and How to Fix It | Why Blond Hair Turns Green in the Pool and How to Fix It
We’re willing to be that being blonde during the summer isn’t so fun if you go swimming and your hair turns green from the pool. These days, lots of people dye their hair green on purpose, but those are usually lush, vibrant colors, not the dull, watery green that results from the pool.
You’ve probably heard that chlorine is the culprit. And if that’s true, there may be no way to avoid green hair since most pools are sanitized with chlorine. But we have good news: It’s not chlorine’s fault. Well, not totally. The key to fixing green hair is to understand why it happens. And that will also help you prevent it from happening again.
Why Does Hair Turn Green From the Pool?
The answer is simple: copper.
You know how an old penny starts to turn green after years and years of being handled? Well, maybe not if you pay for everything with cards instead of cash. OK, here’s a better example.
You know the Statue of Liberty is green, right? Well, it wasn’t always. The statue actually has a copper exterior. When it was new, it was coppery and shiny. But after years of exposure to sea water and the elements, the copper oxidized and gained its famous green patina.
The same thing happens when copper is present in pool water. It oxidizes, and can turn certain things—the walls, the floor, your hair—green.
How Does Copper End Up in Pool Water?
It usually happens in one of three ways, or some combination thereof.
Your Water Source
If the water you use to fill your pool has a high copper content, you’ll also have copper in your pool. This happens most often with well water, but some municipal water sources can also have high mineral concentrations.
Algaecide
Copper is a well-known algae killer, so it’s often the active ingredient in algaecide. If you’re keeping your pool properly clean and sanitized, you shouldn’t have to worry about using an algaecide. But if you do, the potential for green hair is increased.
If you click this link and make a purchase, we earn a commission at no additional cost to you.
08/09/2023 09:51 pm GMT
Mineral Sanitizers
Chlorine isn’t the only sanitizer that can cause your hair to turn green from the pool. One of the active ingredients in a pool mineral sanitizer is copper, precisely for its algicidal properties.
Have any or all of these factors going on in your pool, and … hello green hair!
But How Does it Turn Hair Green?!
When the metal is exposed to the water and chlorine, it oxidizes. This is why you may sometimes end up with pool stains of a greenish color.
That oxidized metal then binds to the proteins in hair strands. So really, all hair can end up with oxidized copper in it. It’s just that it won’t show in darker hair colors. Because blond hair is so light, the green of the oxidized metal is visible.
Will Blond Hair Turn Green in a Saltwater Pool?
Yes. Salt water pools still use chlorine to sanitize the water, it’s just made from salt by a chlorine generator instead of being added manually as tablets or a powder.
If there’s copper in the water, and the chlorine created by the salt oxidizes it, your hair may turn green from the pool, just like it would in a regular chlorine pool.
How to Keep Your Hair from Turning Green Hair in the Pool
To keep the oxidized copper out of your hair, you’ll need to keep the copper out of the pool.
Test your water source. Use test strips or a water testing kit to determine whether your water source contains copper. You can also take a water sample to your local pool store and have them test it for you.
Use a hose filter. If there is copper in your water source, use a hose filter when filling your pool to keep as many minerals out as possible.
Use a metal sequestrant. This water additive doesn’t remove metal from the water. It simply binds with the metal and prevents it from oxidizing. If you use a mineral sanitizer, you may want to skip the sequestrant. It may reduce the effectiveness of the copper component of the sanitizer. Check the manufacturers’ instructions for both the sequestrant and the sanitizer.
Use a copper-free algaecide. If your pool develops an algae infestation, and you decide to use an algaecide during the treatment process, use one that doesn’t have copper as its active ingredient.
Frustrated by adding chemicals and trying to keep your pool clear all the time?
We cut out all the confusion of pool maintenance in this easy-to-read illustrated ebook and video course. It'll help you save $100 right away on pool care!
But what if you swim in someone else’s pool? Or a public pool? You don’t have any control over the water or chemicals there, so you’ll need to protect your hair.
Wear a swim cap. OK, so they may not be the most attractive things in the world, but it’s the easiest and most effective way to protect your hair from turning green in the pool. It will also protect your hair from harsh pool chemicals.
Use a leave-in conditioner. Applying this to your hair before you go swimming will coat your hair shaft, and make it more difficult for the copper to attach itself to your hair.
Use apple cider vinegar. Rinsing your hair with this before you swim seals the hair cuticle, which can also make it more difficult for copper to attach itself and turn your hair green.
Wash your hair immediately. As soon as you get out of the pool, wash your hair. Don’t let it dry first.
Use swimmer’s shampoo. Take washing your hair an extra step by using a shampoo with a chelating agent in it.
Use a hot oil treatment. After shampooing, before you go swimming, apply hot oil to your hair. It will seal the hair cuticle, protecting it from metals, and from drying chlorine.
How to Fix Green Hair
If your hair has already turned green from the pool, don’t worry. You don’t have to cut it or wait for it to grow out. You can try a few remedies.
Use that swimmer’s shampoo. This is better as a preventive treatment, but if you weren’t able to wash your hair right after swimming, using a chelating shampoo on green hair may take some of the tint out.
Use lemon juice. Citric acid is often used to clean copper pots and kitchen utensils. It gets rid of oxidation, and makes them shine again. Rinsing your hair with lemon juice may do the same thing for it.
Use apple cider vinegar. Acetic acid is also used to clean copper, and it’s found in vinegar. Give your hair a good rinse with it, and you may see some, if not all of that green come out.
Use ketchup. No, really. It’s not a joke. Ketchup contains both vinegar and acetic acid, so it’s a double whammy on that oxidized copper in your hair. But you can’t exactly rinse with it. Instead:
Apply it as you would conditioner, working it through every strand of your hair.
Cover your hair with a shower cap.
Let it sit for 30 minutes.
Thoroughly wash your hair. Then wash it again to make sure all the ketchup—and the copper—is gone.
Apply conditioner.
Rinse thoroughly.
Caution: You may develop an intense craving for french fries during this procedure. We recommend a healthy dose of fries to alleviate this.
Use tomato juice. It works on the same principle as ketchup, but is a little weaker, so you may need to do it more than once.
Use baking soda. Don’t have any lemon juice or ketchup on hand? Mix ¼ to ½ a cup of baking soda with water to make a thick paste. Apply it to your hair, and massage it through every strand. Rinse it out, then wash and condition your hair. Baking soda isn’t as strong as acids, so you may need to do it more than once.
Use aspirin. Not Tylenol (acetaminophen). Not Advil or Motrin (ibuprofen). And not Aleve (naproxen sodium). Just plain ol’ aspirin (Bayer).
Crush six to eight tablets in a bowl. Better yet, in a mortar and pestle, if you have one.
Add enough warm water to rinse your hair—less for short, more for long—and allow the aspirin powder to dissolve fully, stirring if necessary.
Apply it to your wet hair, and let it sit for 15 to 20 minutes.
Rinse, shampoo and condition as you normally would.
It’s Not Easy Having Green Hair
If all else fails, and your hair’s still a sickly green color, you always do have the last resort of cutting your hair and letting healthy blond hair grow back in its place. But with all of these precautions and home remedies, we’re thinking you won’t have to go that far.
Just remember to stock up on swimmer’s shampoo, lemon juice and ketchup at the beginning of the summer, and you’ll be fine.
Happy Swimming!
Matt Giovanisci is the founder of Swim University® and has been in the pool and spa industry since 1995. Since then, his mission is to make pool and hot tub care easy for everyone. And each year, he continues to help more people with water chemistry, cleaning, and troubleshooting. | Why Blond Hair Turns Green in the Pool and How to Fix It
We’re willing to be that being blonde during the summer isn’t so fun if you go swimming and your hair turns green from the pool. These days, lots of people dye their hair green on purpose, but those are usually lush, vibrant colors, not the dull, watery green that results from the pool.
You’ve probably heard that chlorine is the culprit. And if that’s true, there may be no way to avoid green hair since most pools are sanitized with chlorine. But we have good news: It’s not chlorine’s fault. Well, not totally. The key to fixing green hair is to understand why it happens. And that will also help you prevent it from happening again.
Why Does Hair Turn Green From the Pool?
The answer is simple: copper.
You know how an old penny starts to turn green after years and years of being handled? Well, maybe not if you pay for everything with cards instead of cash. OK, here’s a better example.
You know the Statue of Liberty is green, right? Well, it wasn’t always. The statue actually has a copper exterior. When it was new, it was coppery and shiny. But after years of exposure to sea water and the elements, the copper oxidized and gained its famous green patina.
The same thing happens when copper is present in pool water. It oxidizes, and can turn certain things—the walls, the floor, your hair—green.
How Does Copper End Up in Pool Water?
It usually happens in one of three ways, or some combination thereof.
Your Water Source
If the water you use to fill your pool has a high copper content, you’ll also have copper in your pool. This happens most often with well water, but some municipal water sources can also have high mineral concentrations.
Algaecide
Copper is a well-known algae killer, so it’s often the active ingredient in algaecide. If you’re keeping your pool properly clean and sanitized, you shouldn’t have to worry about using an algaecide. But if you do, the potential for green hair is increased. | no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://blog.hayward-pool.com/maintenance/blonde-hair-can-turn-green-swimming/ | Why Blonde Hair Can Turn Green from Swimming - Hayward ... | Why Blonde Hair Can Turn Green from Swimming
There are many myths floating around about the topic of hair turning green from swimming. We’re pretty sure what we’re about to share, is not what you think is the cause.
Myths: Some urban myths base hair turning green after swimming on dirty pools, pools with an algae problem, some blame the types of hair shampoos and conditioners used, and the most talked about myth is chlorine turns hair green.
Truth:
The truth of the matter is, hair turning green post swimming is very avoidable and it has to do with the way you’re managing your chemistry. Simply: the cause of green hair is improperly balanced water.
When your pool’s water is not properly balanced and the pH, total alkalinity and calcium hardness fall below recommended levels, the water becomes corrosive. In this state, your water can etch you pool’s plaster, stain and wrinkle vinyl liners, most definitely irritate swimmers’ eyes and skin, turn hair green and worst of all, improperly balanced water can corrode and damage your pool equipment.
Factory-produced Chlorine and Salt Chlorine Generators are NOT to blame!
Corrosive Water: Corrosive water caused from allowing pH, Alkalinity and calcium hardness to fall out of range can also eat away at the copper in your pool equipment. Copper then dissolves into the pool water, and this…copper, turns blonde hair green.
Green hair can be a nuisance for sure, but you will have much bigger problems if your corrosive water damages your pool equipment, finishes and plumbing. Damaged equipment caused by chemistry issues will void your pool warranty, that’s a big price to pay for regular water chemistry management.
How to avoid damage to your equipment, finishes and hair Properly filtering and sanitizing your pool and spa water, and keeping your water in balance is very important – for swimmer comfort and safety, and to protect your pool and spa finishes and equipment. Water out of balance can cause more issues than red eyes and dry skin; it can actually damage your equipment and surfaces if scale or corrosion occurs so balanced water is important in that it prevents corrosion to metal parts as well as scaling on pool surfaces.
Test your water often
Also check out our easy-to-use online Chemistry Calculator. The calculator is based on the requirements and recommended levels of The Center for Disease Control (CDC), The Association of Pool & Spa Professionals (APSP) and the National Swimming Pool Foundation (NSPF). It makes managing your pool water fool proof and incredibly easy. Also, enlist the help of a Pro. Many dealers offer a free water testing service – to find a pool dealer or servicer in your area, use our Dealer Locator. The simplest way to silky hair
Continuously balanced water will save your hair! Salt Chlorine Generators turn ordinary salt into Chlorine automatically, day in, day out. This continuous chlorination will help minimize the formation of Combined Chlorine, and, it’s as easy on your hair, as it is on your wallet. Chlorine produced from a Hayward salt cell will save you 50% or more over the chlorine you buy today and the salinity of your pool’s water is similar to that of a human tear… which means, it won’t irritate your eyes or turn hair green. The addition of Chemistry Automation to your Hayward Salt Chlorinator will manage pH for you. | Why Blonde Hair Can Turn Green from Swimming
There are many myths floating around about the topic of hair turning green from swimming. We’re pretty sure what we’re about to share, is not what you think is the cause.
Myths: Some urban myths base hair turning green after swimming on dirty pools, pools with an algae problem, some blame the types of hair shampoos and conditioners used, and the most talked about myth is chlorine turns hair green.
Truth:
The truth of the matter is, hair turning green post swimming is very avoidable and it has to do with the way you’re managing your chemistry. Simply: the cause of green hair is improperly balanced water.
When your pool’s water is not properly balanced and the pH, total alkalinity and calcium hardness fall below recommended levels, the water becomes corrosive. In this state, your water can etch you pool’s plaster, stain and wrinkle vinyl liners, most definitely irritate swimmers’ eyes and skin, turn hair green and worst of all, improperly balanced water can corrode and damage your pool equipment.
Factory-produced Chlorine and Salt Chlorine Generators are NOT to blame!
Corrosive Water: Corrosive water caused from allowing pH, Alkalinity and calcium hardness to fall out of range can also eat away at the copper in your pool equipment. Copper then dissolves into the pool water, and this…copper, turns blonde hair green.
Green hair can be a nuisance for sure, but you will have much bigger problems if your corrosive water damages your pool equipment, finishes and plumbing. Damaged equipment caused by chemistry issues will void your pool warranty, that’s a big price to pay for regular water chemistry management.
How to avoid damage to your equipment, finishes and hair Properly filtering and sanitizing your pool and spa water, and keeping your water in balance is very important – for swimmer comfort and safety, and to protect your pool and spa finishes and equipment. | no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://waterandhealth.org/healthy-pools/exposing-roots-green-hair-chlorine-myth/ | Green Hair Caused by Copper, Not Chlorine — Myth Busted – Water ... | Healthy Pools
Green Hair Caused by Copper, Not Chlorine — Myth Busted
Swimmers, especially blondes, may be surprised – and even horrified – to discover that frequent pool use imparts a greenish hue to their hair. Typically chlorine in pool water is named as the culprit, sending the green-haired swimmer in search of products to remove the unwanted color or at least in search of a swim cap.
The green hair-chlorine connection is a firmly embedded myth: Almost half of respondents to our 2012 swimmer survey agreed that chlorine in the pool can turn hair green. We would like to expose this urban legend at its roots and offer an explanation of how it might have grown.
Copper, Not Chlorine, is Responsible for Green Hair
Green hair is caused by the presence of copper, not chlorine, in swimming pool water. Copper sulfate, for example, is added to pools to help control algae. Tiny particles of this greenish-blue compound can turn blonde or white hair green. Copper may also be leached into pool water from metal plumbing or from copper ionizer equipment and form copper sulfate in the water. One research study titled “The Green Hair Problem1” concluded that hair that had been extensively damaged–either by harsh cosmetic treatment or by exposure to sun and weathering–showed the highest degree of green coloration from absorbed copper.
To avoid an unwanted green tint:
Wear a swim cap, or
Use a shampoo formulated to help remove copper (yes, they exist) after swimming.
We suggest there could be a semantic reason for the chlorine/green hair linkage. The root “chloro” is Greek for “green.” Chlorophyll, for example, is the organic compound in plants that absorbs sunlight and lends a green color to leaves. In 1810 the chemical element chlorine was named for the greenish color of its gas. Nevertheless, chlorine does not impart a green color to pool water.
Chlorine is added to pool water to destroy bacteria, viruses and parasites in water that would otherwise put swimmers at risk for disease. Most chlorine is added to pool water in the form of compounds of chlorine that are either white solids or colorless liquids. Although some pools are designed to bubble chlorine gas into the water, the greenish chlorine gas reacts quickly with pool water to produce dissolved “free chlorine,” which is colorless.
Chlorine is a well-known pool chemical and its name implies the color “green.” We think it is conceivable that those two factors together helped shape a myth linking chlorine and green hair. Hopefully we have helped expose the roots of this myth and untangled the truth. Happy swimming!
MORE FROM HEALTHY POOLS
Interactive spray fountains, splash parks and splash pads are popular summertime venues where kids can cool off and have fun in “zero-depth” or very shallow water. Many urban areas feature these venues; families discover they can beat the heat inexpensively without leaving the city. They are also found in amusement parks and as part of...
Read More »
WASHINGTON DC -- With summer right around the corner, a new survey finds an overwhelming majority of parents are concerned that electronic devices are interfering with traditional family activities, including swimming, and see potential negative health and social consequences as a result....
Read More » | Healthy Pools
Green Hair Caused by Copper, Not Chlorine — Myth Busted
Swimmers, especially blondes, may be surprised – and even horrified – to discover that frequent pool use imparts a greenish hue to their hair. Typically chlorine in pool water is named as the culprit, sending the green-haired swimmer in search of products to remove the unwanted color or at least in search of a swim cap.
The green hair-chlorine connection is a firmly embedded myth: Almost half of respondents to our 2012 swimmer survey agreed that chlorine in the pool can turn hair green. We would like to expose this urban legend at its roots and offer an explanation of how it might have grown.
Copper, Not Chlorine, is Responsible for Green Hair
Green hair is caused by the presence of copper, not chlorine, in swimming pool water. Copper sulfate, for example, is added to pools to help control algae. Tiny particles of this greenish-blue compound can turn blonde or white hair green. Copper may also be leached into pool water from metal plumbing or from copper ionizer equipment and form copper sulfate in the water. One research study titled “The Green Hair Problem1” concluded that hair that had been extensively damaged–either by harsh cosmetic treatment or by exposure to sun and weathering–showed the highest degree of green coloration from absorbed copper.
To avoid an unwanted green tint:
Wear a swim cap, or
Use a shampoo formulated to help remove copper (yes, they exist) after swimming.
We suggest there could be a semantic reason for the chlorine/green hair linkage. The root “chloro” is Greek for “green.” Chlorophyll, for example, is the organic compound in plants that absorbs sunlight and lends a green color to leaves. In 1810 the chemical element chlorine was named for the greenish color of its gas. Nevertheless, chlorine does not impart a green color to pool water.
| no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://babesinhairland.com/tips-and-tricks/5-easy-ways-to-get-rid-of-green-swimmers-hair/ | 5 Easy Ways to Get Rid of Green Swimmer's Hair - Babes In Hairland | Despite my girls having lighter hair (especially Bee) we’ve not had too many issues with green hair. However, as I mentioned in our post from last week, we bought a big above the ground pool this year, which means they’ll be swimming a lot more than normal. So I’m all about prevention – or at least being educated on what I can do if green starts to creep into their hair. So hopefully this post will help you as much as it does me.
I’ve searched all over online, and got tips from my friends who were life guards and on the swim team as well as my sister who is a stylist to compile these different ways to get rid of green hair.
The “science” behind why your hair can turn green:
First things first. I’m sure you’re aware, but our hair is like a sponge. It is very porous. Contrary to popular belief, the greening of hair from swimming pools is not caused by the chlorine in pool water or by the water reacting to your hair if you color it. Your hair turns green from the presence of hard metals (copper, iron, and manganese, in particular) in the pool water. Think old pennies and the Statue of Liberty. The metals are oxidized by the chlorine and then they stick to your hair and turning it green or making your hair color look extremely dull or ashy. That’s one reason why in our previous post one of the ways to try fight green hair is to completely soak your hair with clean water before entering the pool preventing your hair from sucking up the chlorinated water.
Easy Cheap Home Remedies
Baking Soda
This is probably the cheapest and easiest method since most everyone has baking soda at home. If not – grab some HERE from Amazon! (It’s got so many other household uses, so you’ll always use it!
In a bowl take a 1/4 to 1/2 cup of baking soda and mix enough water to form a paste. Coat green areas with the paste and massage it around in the hair. Rinse with clean water. Shampoo and conditioner as normal once all baking soda is rinsed out. Depending on how green your hair is, you may have to repeat the process a few times.
You can also mix baking soda into your shampoo for a similar outcome, but it’s easier to just make a paste with the water and baking soda first.
Lemon Juice
Saturate your hair with lemon juice (fresh or from a bottle) for about 5 minutes. Then wash & condition as normal. In a post I did years ago, one of our readers said her stylist told her to use lemon Kool-Aid. She mixed it with water and applied it to the areas that were green in her daughter’s hair and that removed the green.
Tomato Juice, V8, or Ketchup
As with the lemon juice, saturate your hair with tomato juice or V8 and let it sit for several minutes. Then wash and condition as normal. If you use ketchup massage it through the effected areas and then wrap in tin foil for about 30 minutes. Then wash and condition like normal.
Aspirin
Crush about 8 Aspirin in a bowl and then mix with water until it dissolves. Wash your hair with the aspirin water and let it sit in your hair for about 15 minutes. Rinse hair with water and then wash and condition your hair normally.
Coke or Club Soda
I’m sure you’re all familiar with soaking a penny in Coke, or cleaning rust off something with Coke right? Well that’s the same reason you can use it to get rid of the copper in your hair. Saturate your hair with Coke or club soda and massage it through the green areas. Rinse with clean water and then wash and condition like normal.
Other Options and Products
As I mentioned in our post on 10 Ways to Protect Your Hair from the Sun & Chlorine using a clarifying shampoo after you’ve been swimming can be helpful, but you need to use them sparingly to prevent further damage to your hair. We also mentioned treating your hair with a leave in conditioner before entering the pool. That will also help keep the water from sucking up into your hair.
And I also mentioned in that last post SwimSpray Chlorine Removal Spray – 4 oz has been said to be great for removing chemicals from your hair and is said to remove the green as well, although I have yet to try it.
I read inthis post that Trader Joe’s sells something called “Vitamin C Crystals” and if you dissolve them in water and spray them on your hair and skin it can help get rid of the chlorine smell as well as if you’ve got green in your hair. I imagine it works similar to lemon juice due to the acidity. Just be sure to always use a good conditioner afterward.
Have you had to deal with green hair after swimming? What tips or tricks have you found work best? We’d love to hear what’s worked for you.
Disclaimer: This post contains affiliate links but all opinions are 100% mine.
Comments
Thanks for posting this advice. I went to the hairdresser for a trim today and…wow. The great lighting in those places really brought out the green in my hair. 😉 I’m going to try that baking soda tip one and see what happens!
Side note – I LOVE your name and logo!!
Welcome
Hi! I'm Becky and welcome to Hairland! Some would say I'm obsessed with hair...I'm ok with that! I have 3 beautiful daughters with amazing hair, and over the years doing their hair has become our bonding time. Whether you're doing your own hair, or someone else's hair, you're in the right place! So pull up a chair, grab a comb, and let's do some hair! | Despite my girls having lighter hair (especially Bee) we’ve not had too many issues with green hair. However, as I mentioned in our post from last week, we bought a big above the ground pool this year, which means they’ll be swimming a lot more than normal. So I’m all about prevention – or at least being educated on what I can do if green starts to creep into their hair. So hopefully this post will help you as much as it does me.
I’ve searched all over online, and got tips from my friends who were life guards and on the swim team as well as my sister who is a stylist to compile these different ways to get rid of green hair.
The “science” behind why your hair can turn green:
First things first. I’m sure you’re aware, but our hair is like a sponge. It is very porous. Contrary to popular belief, the greening of hair from swimming pools is not caused by the chlorine in pool water or by the water reacting to your hair if you color it. Your hair turns green from the presence of hard metals (copper, iron, and manganese, in particular) in the pool water. Think old pennies and the Statue of Liberty. The metals are oxidized by the chlorine and then they stick to your hair and turning it green or making your hair color look extremely dull or ashy. That’s one reason why in our previous post one of the ways to try fight green hair is to completely soak your hair with clean water before entering the pool preventing your hair from sucking up the chlorinated water.
Easy Cheap Home Remedies
Baking Soda
This is probably the cheapest and easiest method since most everyone has baking soda at home. If not – grab some HERE from Amazon! (It’s got so many other household uses, so you’ll always use it!
In a bowl take a 1/4 to 1/2 cup of baking soda and mix enough water to form a paste. Coat green areas with the paste and massage it around in the hair. Rinse with clean water. Shampoo and conditioner as normal once all baking soda is rinsed out. | no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://www.yahoo.com/lifestyle/why-swimming-pools-turn-hair-green-its-not-the-120191345902.html | Why Swimming Pools Turn Hair Green (It's Not the Chlorine!) | Why Swimming Pools Turn Hair Green (It's Not the Chlorine!)
Chlorine is commonly assumed to be the culprit behind Kermit-colored hair. But the truth is, another compound designed to keep the pool clean may actually be what’s turning your hair green.
Copper sulfate is often added to swimming pools to combat algae, according to the authors of a 2014 case study about a 15-year-old girl whose blonde hair was turning progressively green. “Copper compounds in the water bind to the protein on the surface of the hair shaft and deposit their color,” the researchers explain. (This can also occur if your home has new copper piping.)
Although blonde hair is the most likely shade to go green, “it happens to other colors also,” says Steve Pullan, a trichologist at the Philip Kingsley hair clinic in New York City. “You just don’t notice it as much.” As a hair scientist, he sees green-haired goddesses all summer long — and has noticed a trend among these clients: They’ve often bleached their tresses.
“Even natural hair can become green,” Pullan tells Yahoo Health. But coloring your hair — especially when bleach is involved — makes the shaft of each strand more porous, allowing your locks to absorb the pool chemicals more easily. In fact, in a study called “The Green Hair Problem,” conducted way back in 1979, researchers found that hair treated with peroxide or damaged by the sun was more likely to suck up copper.
To shield your strands, soak them with fresh water before diving into the pool. That way, “the hair is already wet, like a sponge,” says Pullan. The result? It’s less likely to absorb the copper-tinged pool water. Even better, wet your hair and coat it with conditioner before swimming. Pullan recommends Philip Kingsley’s Swimcap Cream, originally developed for the U.S. Olympic synchronized swimming team — it contains sunscreen to shield your hair from UV rays, while also creating a protective barrier against copper. Afterward, rinse off in the pool shower to eliminate any lingering chemicals.
Still have a green-hair mishap? You may be able to mask the funky hue with a shampoo formulated to prevent gray and blonde hair from going brassy, says Pullan. In addition, “we deep-condition to lift out impurities and cleanse the scalp very thoroughly,” he says. You can also try a chelating shampoo — that is, one capable of stripping away mineral-build-up — such as Redken Hair Cleansing Cream Shampoo. | Why Swimming Pools Turn Hair Green (It's Not the Chlorine!)
Chlorine is commonly assumed to be the culprit behind Kermit-colored hair. But the truth is, another compound designed to keep the pool clean may actually be what’s turning your hair green.
Copper sulfate is often added to swimming pools to combat algae, according to the authors of a 2014 case study about a 15-year-old girl whose blonde hair was turning progressively green. “Copper compounds in the water bind to the protein on the surface of the hair shaft and deposit their color,” the researchers explain. (This can also occur if your home has new copper piping.)
Although blonde hair is the most likely shade to go green, “it happens to other colors also,” says Steve Pullan, a trichologist at the Philip Kingsley hair clinic in New York City. “You just don’t notice it as much.” As a hair scientist, he sees green-haired goddesses all summer long — and has noticed a trend among these clients: They’ve often bleached their tresses.
“Even natural hair can become green,” Pullan tells Yahoo Health. But coloring your hair — especially when bleach is involved — makes the shaft of each strand more porous, allowing your locks to absorb the pool chemicals more easily. In fact, in a study called “The Green Hair Problem,” conducted way back in 1979, researchers found that hair treated with peroxide or damaged by the sun was more likely to suck up copper.
To shield your strands, soak them with fresh water before diving into the pool. That way, “the hair is already wet, like a sponge,” says Pullan. The result? It’s less likely to absorb the copper-tinged pool water. Even better, wet your hair and coat it with conditioner before swimming. Pullan recommends Philip Kingsley’s Swimcap Cream, originally developed for the U.S. Olympic synchronized swimming team — it contains sunscreen to shield your hair from UV rays, while also creating a protective barrier against copper. | no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://allenpoolatlanta.com/chlorine-can-turn-hair-green/ | Myth or Truth: Chlorine Can Turn Hair Green | Allen Pool Atlanta | Myth or Truth: Chlorine Can Turn Hair Green
It’s one of the most common refrains we hear every summer – beware of the chlorine in the pool, it’ll turn your hair green! But will it, really? Yes, no, and maybe. As your Atlanta pool maintenance team, we get this question a lot. The answer is, it really depends on a few different factors, so let’s dive in!
Is Chlorine to Blame?
Whenever the discussion around green hair in the pool arises, chlorine is always the first thing to get called out. However, chlorine is only half of the green-hair equation, here. The real tint-changer behind it all is copper. And copper not only exists in pool water but tap water too (though rarely in high enough concentrations to affect your hair). Copper is the actual agent that’s creating the reaction that causes your hair to turn green. But the thing is, it rarely happens outside of the pool for one very important reason. And that reason is, you guessed it – chlorine. Chlorine and copper bond together to form a film that sticks to the proteins in your hair, coating each strand and making it that much easier for it to turn green.
Blondes are Susceptible
Unfortunately for all those golden-locked beauties out there, blondes are the ones most susceptible to this chemical reaction. Because the hair is already light, the green tint is far more easily apparent. Alas, it’s true! The same thing that makes blondes a great candidate for hair color success also makes them the first to fall to the follies of the copper-chlorine greens. However, that doesn’t mean they are the only ones susceptible. Really, the chemical reaction can occur on anyone that takes a swim in chlorinated water. For those with colored hair, you might see a change in the tint or tone of your hair even if it’s dyed dark because the process of coloring your hair opens the cuticle on each strand, making it more susceptible to a range of damage.
Precautions
There are a few things you can do to slow down or prevent the reaction from getting your hair green, but if you’re a frequent swimmer, the best precaution we can recommend is a well-fitted swim cap. If you’re not feeling that swim cap life, give these few ideas a shot:
Leave-in conditioner (it makes it more difficult for the film to stick to those strands)
Pre-wet your hair
Shower and wash your hair as soon as you’re done swimming
Those are your three best defenses against the copper-chlorine film. If you end up with green hair regardless, there are a number of things you can try to return your hair to its rightful golden hue, but we’ll save that for another blog. | Myth or Truth: Chlorine Can Turn Hair Green
It’s one of the most common refrains we hear every summer – beware of the chlorine in the pool, it’ll turn your hair green! But will it, really? Yes, no, and maybe. As your Atlanta pool maintenance team, we get this question a lot. The answer is, it really depends on a few different factors, so let’s dive in!
Is Chlorine to Blame?
Whenever the discussion around green hair in the pool arises, chlorine is always the first thing to get called out. However, chlorine is only half of the green-hair equation, here. The real tint-changer behind it all is copper. And copper not only exists in pool water but tap water too (though rarely in high enough concentrations to affect your hair). Copper is the actual agent that’s creating the reaction that causes your hair to turn green. But the thing is, it rarely happens outside of the pool for one very important reason. And that reason is, you guessed it – chlorine. Chlorine and copper bond together to form a film that sticks to the proteins in your hair, coating each strand and making it that much easier for it to turn green.
Blondes are Susceptible
Unfortunately for all those golden-locked beauties out there, blondes are the ones most susceptible to this chemical reaction. Because the hair is already light, the green tint is far more easily apparent. Alas, it’s true! The same thing that makes blondes a great candidate for hair color success also makes them the first to fall to the follies of the copper-chlorine greens. However, that doesn’t mean they are the only ones susceptible. Really, the chemical reaction can occur on anyone that takes a swim in chlorinated water. For those with colored hair, you might see a change in the tint or tone of your hair even if it’s dyed dark because the process of coloring your hair opens the cuticle on each strand, making it more susceptible to a range of damage.
Precautions
There are a few things you can do to slow down or prevent the reaction from getting your hair green, but if you’ | yes |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://lizearlewellbeing.com/beauty-advice/beauty-diy/green-swimming-pool-hair/ | How to avoid green swimming pool hair - Liz Earle Wellbeing | How to avoid green swimming pool hair
Trying to avoid your hair going green after being in the swimming pool? It’s a common issue, especially for regular swimmers and as the summer holidays roll around.
Even a short summer break spent in and out of a swimming pool can leave post-holiday tresses with a distinctly greenish tinge. Hairdressers often nod sagely and say “see how the chlorine has turned your hair green” but this is not actually the case. It isn’t the chlorine that turns hair luminous lime, but traces of metals in a swimming pool purification system. The better pools have a well-balanced pool pH, but some are overloaded with heavy metals. The chief culprit is copper. Used as an algicide to prevent green slime forming in a pool, it unfortunately often results in green swimming pool hair instead.
Chlorine does play a part by oxidizing metals (such as copper) in purified pool water, causing a kind of rusting and turning these minerals green. It’s the constant immersion in the pool water itself that damages hair. It dries out the protective cuticle shaft wrapped around each hair strand. This protective sheath is made up of lots of tiny scales and when they dry they start to peel apart. This allows copper deposits to lodge in the cracks of the scaly outer coating of each strand. The resulting green tinge is most noticeable in blonde hair, but all hair colours take up the copper deposits – they’re just less visible on darker hair.
How to prevent green swimming pool hair
The good news is we don’t need to buy expensive ‘swimmer’ shampoos to cure the problem. Wetting hair with (clean) water before swimming helps. It saturates the hair so it doesn’t absorb as much pool water – so don’t dive in with dry hair. The next single most useful thing we can do is to rinse hair thoroughly with a pool-side shower as soon as we get out of the pool. Follow this with a proper shampoo as soon as is practical. This goes a long way to removing the oxidized metal deposits before they have much chance to fix themselves into damaged hair cuticles. Keeping hair well conditioned also helps by sealing and protecting hair cuticles. This in turn makes them less likely to peel apart and harder for molecules of metals to penetrate.
Another simple tip is to comb through a dab of hair conditioner before each swim to give hair a light waterproof coating. Leave-in conditioners are useful for this and you can easily make your own by mixing a small amount of regular hair conditioner with water in a spray bottle and keeping this in your poolside bag. Want additional protection? We love Phillip Kingsley’s Swimcap Mask to protect hair before swimming.
Use a wide-toothed comb and work gently into wet hair to prevent damaging the hair cuticles you’re aiming to protect. You can also sport a tightly fitting swimming cap – perhaps not the most stylish option, unless you can carry off a wonderfully retro floral version! A swimming cap is actually a very useful barrier and something for all blondes to consider – especially bleached blondes who already have damaged hair cuticles.
After swimming
Use a gentle SLS-free shampoo (avoid sodium lauryl and laureate sulphates, especially important if washing hair daily), followed by plenty of conditioner. Comb with a wide-tooth comb, pat dry instead of scrunching in a towel and minimise the use of hot hairdryers. Leave to air-dry naturally whenever possible.
How to treat green swimming pool hair
Finally, if all else fails and you end up going green, a treatment using citric acid will help release the copper compounds from hair shafts. The old wives tales of a vinegar or lemon juice hair rinse can help here. Alternatively, try a tomato puree hair-pack left on for twenty minutes to help remove copper oxide.
Professional hair colourists can use more sophisticated chemicals to reduce a green tinge, but keep in mind it’s likely to return if you swim again in the same pool. Lastly, at least a green hue is only a temporary tinge – and the shade soon fades
Would you like more exclusive content like this?
Sign up to our email newsletter and each week you’ll receive the most sensational recipes, expert beauty advice, wellbeing wisdom and interviews, plus plenty of tips to help you look and feel your radiant best from the inside out. Along with exclusive online content, our latest offers and competitions, and a personal letter from Liz each month, we’ll make sure that you never miss a thing.
I agree to sign up to the Liz Earle Wellbeing newsletter. I understand I have the option to unsubscribe at any time. | How to avoid green swimming pool hair
Trying to avoid your hair going green after being in the swimming pool? It’s a common issue, especially for regular swimmers and as the summer holidays roll around.
Even a short summer break spent in and out of a swimming pool can leave post-holiday tresses with a distinctly greenish tinge. Hairdressers often nod sagely and say “see how the chlorine has turned your hair green” but this is not actually the case. It isn’t the chlorine that turns hair luminous lime, but traces of metals in a swimming pool purification system. The better pools have a well-balanced pool pH, but some are overloaded with heavy metals. The chief culprit is copper. Used as an algicide to prevent green slime forming in a pool, it unfortunately often results in green swimming pool hair instead.
Chlorine does play a part by oxidizing metals (such as copper) in purified pool water, causing a kind of rusting and turning these minerals green. It’s the constant immersion in the pool water itself that damages hair. It dries out the protective cuticle shaft wrapped around each hair strand. This protective sheath is made up of lots of tiny scales and when they dry they start to peel apart. This allows copper deposits to lodge in the cracks of the scaly outer coating of each strand. The resulting green tinge is most noticeable in blonde hair, but all hair colours take up the copper deposits – they’re just less visible on darker hair.
How to prevent green swimming pool hair
The good news is we don’t need to buy expensive ‘swimmer’ shampoos to cure the problem. Wetting hair with (clean) water before swimming helps. It saturates the hair so it doesn’t absorb as much pool water – so don’t dive in with dry hair. The next single most useful thing we can do is to rinse hair thoroughly with a pool-side shower as soon as we get out of the pool. Follow this with a proper shampoo as soon as is practical. | no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://saloninvi.com/chlorine-hair/ | Chlorine and Your Hair: Everything You Need to Know | Salon Invi | Chlorine and Your Hair: Everything You Need to Know
Most people already know that if they regularly expose their hair to the chlorine found in swimming pools, it can do some serious damage. Whether your hair has become dry and brittle, lifeless, or even turned green, learning more about the effects of chlorine on your hair and how you can prevent them will help you look your best without having to avoid the pool this summer.
What Does Chlorine Do to Hair?
Chlorine is a disinfectant that’s used to kill bacteria as well as to remove contaminants like dirt and oil from pools. Because it is so very good at its job, it also strips the protective natural oils from your hair, which leaves it especially prone to damage from heat and the sun. What’s more, it can cause the otherwise smooth cuticle of the hair to become porous, which makes hair very brittle.
Does Chlorine Turn Your Hair Green?
Anyone who has blonde color-treated hair (or even blonde highlights) can attest that swimming in a chlorinated pool has the potential to turn it from a platinum or golden blonde to a very unflattering green. Chlorine cannot turn your hair green; this is a very common misconception. The oxidized metals in the water are responsible for this greenish hue, and copper is the biggest culprit. As copper oxidizes, it develops a greenish patina that is desirable in many situations, and it’s this very same reaction that causes hair to turn green in a pool. Particles of oxidized copper bind with the protein in your hair shaft and turn it green.
What are the Risk Factors for Chlorine Damaged Hair?
Some people are more prone to hair damage and discoloration when swimming in chlorinated pools. Pay special care if you have:
Color-treated hair. Chemically lightened hair is most likely to experience damage due to chlorine in pools.
Dry, thin, or fine hair. It is important to remember that if your hair is already thinning, especially fine, or overly dry, chlorine in a swimming pool will exacerbate this.
Damaged hair. If your hair has been damaged for any reason – especially if it is overly processed, this is a significant risk.
Permed or relaxed hair. Though perms and straightening treatments make your hair look amazing, they also weaken it a great deal and leave it susceptible to damage.
Tips for Damage Prevention
If any of the risk factors above apply to you, or if you simply want to protect your already healthy hair as much as you possibly can, there are several things you can do.
Wear a swim cap. Though this is the most obvious solution, it’s also the best one. When your hair is in a swim cap, the chlorine cannot affect it.
Saturate your hair with water before entering the pool. Just use tap water to wet your hair before you take a dip. This will prevent your hair from absorbing the chlorine-laden water.
Rinse your hair immediately after swimming. As soon as you step out of the pool, rinse your hair very well in lukewarm water. This will help to remove chlorinated water.
Use a sulfate free shampoo. Finally, as soon as you have finished swimming, use a sulfate free shampoo to remove any residual chlorine without over-drying your hair.
Though it may sound like the enemy – at least to your hair – chlorine is a vital component in swimming pools. Without it, they’d be cesspools of bacteria that can cause far worse than dry, damaged, or even green hair. Fortunately, you can follow the tips and advice above to minimize the damage as much as possible. | Chlorine and Your Hair: Everything You Need to Know
Most people already know that if they regularly expose their hair to the chlorine found in swimming pools, it can do some serious damage. Whether your hair has become dry and brittle, lifeless, or even turned green, learning more about the effects of chlorine on your hair and how you can prevent them will help you look your best without having to avoid the pool this summer.
What Does Chlorine Do to Hair?
Chlorine is a disinfectant that’s used to kill bacteria as well as to remove contaminants like dirt and oil from pools. Because it is so very good at its job, it also strips the protective natural oils from your hair, which leaves it especially prone to damage from heat and the sun. What’s more, it can cause the otherwise smooth cuticle of the hair to become porous, which makes hair very brittle.
Does Chlorine Turn Your Hair Green?
Anyone who has blonde color-treated hair (or even blonde highlights) can attest that swimming in a chlorinated pool has the potential to turn it from a platinum or golden blonde to a very unflattering green. Chlorine cannot turn your hair green; this is a very common misconception. The oxidized metals in the water are responsible for this greenish hue, and copper is the biggest culprit. As copper oxidizes, it develops a greenish patina that is desirable in many situations, and it’s this very same reaction that causes hair to turn green in a pool. Particles of oxidized copper bind with the protein in your hair shaft and turn it green.
What are the Risk Factors for Chlorine Damaged Hair?
Some people are more prone to hair damage and discoloration when swimming in chlorinated pools. Pay special care if you have:
Color-treated hair. Chemically lightened hair is most likely to experience damage due to chlorine in pools.
Dry, thin, or fine hair. | no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://www.formswim.com/blogs/all/9-tips-to-protect-your-hair-from-chlorine | 9 Tips on How to Protect Your Hair from Chlorine Water Damage ... | 9 Tips to Protect Your Hair from Chlorine
The feeling of gliding through the water can feel serene until you remember the damage that the chlorinated water is likely doing to your beautiful hair. Daily pool swimming can wreak havoc on hair due to the harsh chlorine found in pools; however, it's possible to protect your hair from chlorine exposure and its damaging effects.
In this article, we're going to look at how chlorine damages your hair, share our expert tips for minimizing or preventing chlorine damage, and provide a few ways to fix chlorine-damaged hair.
How does chlorine damage your hair?
Chlorinated water can make your hair dry and weak, which can cause breakage. While regular tap water contains chlorine, it usually doesn't contain enough to be a problem for regular showers. But the increased amount found in pools can have damaging effects on your hair and skin with more frequent exposure.
Casual swimmers don't often see the effects of chlorinated water—for example, a dip in the pool once a year on holiday won't make a massive difference to your hair's health. But it doesn't matter if you swim once a month or once a day; people with specific hair types are more susceptible to chlorine damage than others. This includes people with:
Thin or fine hair
Color-treated hair
Bleached hair
Chemical-treated hair
Dry hair
Thin of fine hair
Hair with existing damage
Whether you're a regular or daily pool swimmer, you need to know how to protect your hair from chlorine damage, regardless of your natural color or hair type.
How do swimmers keep their hair healthy?
If you only swim occasionally, there's not much you need to do to keep your hair healthy, except wearing a swim cap to avoid getting your hair wet with chlorinated water.
If you're in the pool daily or even several times a week, it's important to put a little more care and attention into protecting your skin and hair from chlorine damage.
How can I protect my hair from chlorine water damage?
Here are our top picks for the best ways to protect hair from chlorine. These tips should reduce the damaging effects of chlorinated pool water:
1. Rinse and wet hair before and after swimming.
Lap swim etiquette is the spoken and unspoken "rules" of the pool that help keep everyone safe and healthy. For example, there's an important reason the pool staff tells you to shower before going into the pool. This is a crucial step to remove any dirt and oils from your body, so they don't end up on the bottom of the pool, but it's also helpful to prevent chlorine damage to your hair.
When you pre-soak your hair with clean tap water or non-chlorinated water before entering the pool, your hair strands absorb that water, minimizing the amount of chlorine that is absorbed.
Likewise, it's always a good idea to rinse your hair thoroughly with clean water after swimming. You can apply some clarifying shampoo to give it a deeper clean.
2. Apply coconut oil, olive oil, and other natural oils to your hair.
If you're a frequent swimmer or have hair that's more prone to chlorine damage, consider applying a leave-in chlorine protectant on your hair. Natural oils, including coconut oil, olive oil, and jojoba act as a protective layer to prevent chlorine and other pool chemicals from being absorbing into your hair strands. For added protection, use a deep conditioning mask or leave-in conditioner, too.
3. Use Swim Spray.
If you have blond hair and are especially worried about the effects of chlorine on your light-colored hair, you can purchase a swim spray product to apply to your hair to help block chlorine from penetrating your strands. This product works for all hair types.
4. Use gentle shampoos.
We recommend using a gentle, sulfate-free shampoo and following with a conditioner after swimming, regardless of your hair type. This helps wash away any remnants of chlorine from your hair.
5. Wear a swim cap.
If you're a competitive swimmer, you likely already wear a swim cap on your head for swim practice. Swim caps are great to prevent chlorine from reaching your hair in the first place. For the best protection, wear it correctly so that all your hair is inside. Don't forget to wear your swim cap over wet hair to help it fit easier over your head. Keeping a couple of spare swim caps in your swim bag in case one tears isn't a bad idea either.
6. Put long hair in a ponytail.
If you have long hair and don't have a swim cap, tie your hair back in a ponytail, braid, or tight bun. This will minimize contact with chlorine.
7. Swim in outdoor pools.
When possible, swimming in outdoor pools is best. In outdoor pools, chlorine gas from the water evaporates into the air faster, reducing the concentration in the water and, ultimately, the amount of chlorine that could end up absorbed in your hair and skin.
8. Adopt these post-swim hair care routines.
Perhaps the most critical time to prevent chlorine-damaged hair is when you exit the water. Your post-swim shower and hair routine will help remove chlorine before it penetrates too deeply into your strands.
You probably have a pretty detailed post-swim regime if you swim regularly, including cleaning and care for your swim goggles. In addition to your existing post-swim routine, here are our recommended hair care tips for immediately after swimming:
Let your hair completely air dry while you get changed. Resist the temptation to use blow dryers, as they will dry your hair out more. If your hair needs additional drying after air drying, use a microfibre towel to dry any dripping or excess water from your hair gently.
Brush gently and remove tangles with a detangling brush designed for wet hair.
How can I fix chlorine-damaged hair?
The first step is knowing how to recognize chlorine damage. Chlorine-damaged hair usually appears very dry, frizzy, and constantly tangled. If you think your hair is damaged from the chlorine in the pool, talk to your hairstylist, who can likely assess the severity of the damage and help you protect your hair further while swimming.
Then, try these at-home remedies to reverse the damage or ease any dryness and itchiness:
Use a hair clarifier wash and natural conditioner to remove chlorine and any lingering harsh chemicals currently in your hair. You can make one using baking soda and apple cider vinegar.
Moisturize your scalp. If your head is dry or flaky, talk to your doctor or hairstylist for products to help restore and maintain moisture. Otherwise, coconut oil can help moisturize any dry skin.
To reverse significant damage from chlorine and prevent further damage, use a deep conditioner twice a week and apply natural oils like argan oil to protect the hair and scalp.
How to fix green hair
Chlorine bonds with copper, manganese, iron, and other hard metals in swimming pool water, which can tint your hair a shade of dull, ashy green—especially if you have lighter-colored hair. It's not-so-lovingly known as "Swimmers Hair."
Of course, your best defense is to protect your hair so it doesn't turn green in the first place.
Depending on the severity of the damage, it may take time to fully repair your beautiful hair to its original shine and volume, so be patient and seek professional help if needed. In the meantime, continue protecting your hair with regular shampoo and conditioner washes.
Keeping your hair and eyes healthy in chlorine water
Don't worry! It's possible to keep your hair healthy, even if you swim daily in chlorinated water. Follow our tips to protect your hair from chlorine so you can keep enjoying your swims.
If the chlorine burns your eyes while you're in the water, consider protecting them with FORM swimming goggles. Not only do they protect your eyes from chlorine, but they help you become a better swimmer. Our integrated augmented reality display shows you real-time swim metrics like distance, time, and pace. It's an excellent tool for measuring your performance as you train for a swimming competition or race. | Then, try these at-home remedies to reverse the damage or ease any dryness and itchiness:
Use a hair clarifier wash and natural conditioner to remove chlorine and any lingering harsh chemicals currently in your hair. You can make one using baking soda and apple cider vinegar.
Moisturize your scalp. If your head is dry or flaky, talk to your doctor or hairstylist for products to help restore and maintain moisture. Otherwise, coconut oil can help moisturize any dry skin.
To reverse significant damage from chlorine and prevent further damage, use a deep conditioner twice a week and apply natural oils like argan oil to protect the hair and scalp.
How to fix green hair
Chlorine bonds with copper, manganese, iron, and other hard metals in swimming pool water, which can tint your hair a shade of dull, ashy green—especially if you have lighter-colored hair. It's not-so-lovingly known as "Swimmers Hair. "
Of course, your best defense is to protect your hair so it doesn't turn green in the first place.
Depending on the severity of the damage, it may take time to fully repair your beautiful hair to its original shine and volume, so be patient and seek professional help if needed. In the meantime, continue protecting your hair with regular shampoo and conditioner washes.
Keeping your hair and eyes healthy in chlorine water
Don't worry! It's possible to keep your hair healthy, even if you swim daily in chlorinated water. Follow our tips to protect your hair from chlorine so you can keep enjoying your swims.
If the chlorine burns your eyes while you're in the water, consider protecting them with FORM swimming goggles. Not only do they protect your eyes from chlorine, but they help you become a better swimmer. Our integrated augmented reality display shows you real-time swim metrics like distance, time, and pace. | yes |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://woodfieldoutdoors.com/why-does-blonde-hair-turn-green-swimming-pool/ | Why Does Blonde Hair Turn Green From A Swimming Pool ... | Why Does Blonde Hair Turn Green From A Swimming Pool?
Share This
The old saying goes, “Blondes have more fun.” But there’s nothing fun about green hair from a pool. So we ask the pressing question: Why does blonde hair turn green from a swimming pool? It’s a legitimate question. If your hair is turning green, or your children suddenly have green hair instead of that cute tow-headed look, you want answers.
Your first guess would be that chlorine in the pool turns blonde hair green. But chlorine is not the main culprit. Copper is. The chlorine in your pool oxidizes the copper, and the copper then binds to the protein in hair strands. The metal will then produce a green tint in the hair. It happens to everyone if there is high copper content. It’s just way more noticeable in blonde hair.
How Does Copper Get in Your Pool Water?
There are a number of ways copper gets into your pool. Much of our municipality water and well water has dissolved metals and minerals in it. Your water supply very possibly has more copper in it than is healthy for your pool or your hair.
In fact, the Environmental Protection Agency (EPA) regulates the level of copper in drinking water to no more than 1.3 ppm (parts-per-million). That’s more than six times the maximum recommended level of copper (0.2 ppm) for your pool water! So if you’re anywhere near the maximum level allowed, your pool water is going to gain copper.
You can find out the level of copper in your water by checking the water analysis report put out by your municipal water company.
How to Prevent Green Hair From a Pool
The good news is, you don’t have to risk green hair. There are things you can do to prevent the problem from occurring – in your own pool that is.
Pool Water Testing
The first thing you can do to prevent green hair from your pool is to do pool water testing regularly. This can tell you if levels of copper or other chemicals or minerals are too high or too low. Then you can take steps to regulate the levels.
Stop Using Copper-Based Algaecides
Nobody wants algae in their swimming pool. But you don’t want to get an algae-free pool if it means swimmers get green hair. If you need to use an algaecide, opt for a non-copper formula.
Protect Your Hair from Copper
You may be wondering not only why does blonde hair turn green from a swimming pool, but how to prevent it. Of course, you could wear a swim cap, but who wants to do that? You can also protect your hair from turning green from copper by using a leave-in conditioner diving in. Also, wash and rinse your hair as soon as you get out of the pool. This is where a outdoor shower comes in really handy. Otherwise, shower and shampoo as soon as you go inside.
Your hair salon may be able to help you as well. You can ask for a “seal coat” or a “gloss coat” that seals many cuticles on the hair. This will prevent the copper from attaching to the hair strands and turning it green.
How to Get Rid of Green Hair From a Pool
If you or a family member already has green hair, don’t panic. There are a number of ways to get rid of the green tint. These include:
Wash your hair with a shampoo formulated for swimmers. It will contain chelating ingredients that help break down and remove metals from your hair. Once the green is gone, resume using your regular shampoo.
Comb a half cup of vinegar or lemon juice through your hair, and let it sit for ten minutes. Ketchup also works. The acidity will help remove the copper oxide. The rinse, and shampoo your hair as normal.
Create a baking soda paste and massage it into your hair. Rinse, and shampoo as normal. You may need to repeat the process.
So there you have it – the science behind why blonde hair turns green from a swimming pool, and what you can do about it. | Why Does Blonde Hair Turn Green From A Swimming Pool?
Share This
The old saying goes, “Blondes have more fun.” But there’s nothing fun about green hair from a pool. So we ask the pressing question: Why does blonde hair turn green from a swimming pool? It’s a legitimate question. If your hair is turning green, or your children suddenly have green hair instead of that cute tow-headed look, you want answers.
Your first guess would be that chlorine in the pool turns blonde hair green. But chlorine is not the main culprit. Copper is. The chlorine in your pool oxidizes the copper, and the copper then binds to the protein in hair strands. The metal will then produce a green tint in the hair. It happens to everyone if there is high copper content. It’s just way more noticeable in blonde hair.
How Does Copper Get in Your Pool Water?
There are a number of ways copper gets into your pool. Much of our municipality water and well water has dissolved metals and minerals in it. Your water supply very possibly has more copper in it than is healthy for your pool or your hair.
In fact, the Environmental Protection Agency (EPA) regulates the level of copper in drinking water to no more than 1.3 ppm (parts-per-million). That’s more than six times the maximum recommended level of copper (0.2 ppm) for your pool water! So if you’re anywhere near the maximum level allowed, your pool water is going to gain copper.
You can find out the level of copper in your water by checking the water analysis report put out by your municipal water company.
How to Prevent Green Hair From a Pool
The good news is, you don’t have to risk green hair. There are things you can do to prevent the problem from occurring – in your own pool that is.
Pool Water Testing
The first thing you can do to prevent green hair from your pool is to do pool water testing regularly. This can tell you if levels of copper or other chemicals or minerals are too high or too low. Then you can take steps to regulate the levels.
| no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://xlpools.com/blondes-green-hair-swimming/ | Why Do Blondes Get Green Hair in Swimming Pools? - Pool Guides | 01233 840336
Why Do Blondes Get Green Hair in Swimming Pools?
Share This Post
Blondes have more fun, according to Rod Stewart. However, when they exit a swimming pool, blondes have more trouble too: green hair! I’m sure you’ve heard it before – swimming pools can turn blonde hair green. Most people are under the false impression that chlorine is to blame. The truth is, chlorine is not the main enemy here.
What Turns Blonde Hair Green in A Swimming Pool?
The answer is: copper!
Copper is a metal that is found in some swimming pools, particularly ones that are filled using well water. Copper can also enter the pool water from certain copper-based algaecides.
So how does copper in pool water turn your hair green?
The copper in the water is oxidized by chlorine, which then binds to the proteins in the hair strands. The metal will produce a green tint in the hair.
Will Blonde Hair Turn Green in a Saltwater Pool?
Short answer: yes.
Saltwater pools are chlorine-based pools. However, instead of adding chlorine manually with tablets or powder, salt is added to the water, which runs through an electrically charged generator, turning the salt into chlorine.
If you have copper in the water, and the chlorine created by the salt oxidizes it, it may turn your hair green just like a regular chlorine swimming pool.
3 Ways To Prevent Green Hair From a Pool
As a pool owner, you can start by getting your pool checked for metals, especially copper. You can use test strips at home or take a sample of your water to us to have it professionally checked.
1. Stop Using Copper-Based Algaecides
Some algaecides contain copper, and are very effective in killing algae, but they can also cause staining and, of course, green hair.
Look for non-copper algaecides to use in your pool as an annual algae preventative. Or don’t use algaecide at all and just keep your chlorine level in check.
2. Remove The Metals In The Water
If you have metals in your water, be sure to remove them by using a chemical that removes metals in the water or a pre-filter that you can attach to your garden hose.
3. Hair Conditioner and Other Treatments
You can also protect your hair by using a leave-in conditioner before swimming. Also, wash and rinse your hair as soon as you get out of the pool.
You can visit your regular hair salon and ask for a “seal coat” or a “gloss coat” that seals many cuticles on the hair. This will prevent the copper from attaching to the hair strands and turning it green.
At home, you can use a “hot oil” treatment that you can pick up at a local beauty shop.
These simple techniques will protect your hair from the metal in the water however they will affect the water chemistry of the pool with the products you are diluting into the water so the last and probably the simplest solution is to wear a swimming cap!
We hope this article helps if you have ever suffered from green hair and clears up the myths around the reason why it happens. As always, if you have any questions, our team are always happy to help.
The Swimming Pool Installation Guide
Buying a pool is an investment, so we have written this guide to help you understand the process. This guide covers building a pool and how we minimise disruption to get your pool built in as little time as possible. | 01233 840336
Why Do Blondes Get Green Hair in Swimming Pools?
Share This Post
Blondes have more fun, according to Rod Stewart. However, when they exit a swimming pool, blondes have more trouble too: green hair! I’m sure you’ve heard it before – swimming pools can turn blonde hair green. Most people are under the false impression that chlorine is to blame. The truth is, chlorine is not the main enemy here.
What Turns Blonde Hair Green in A Swimming Pool?
The answer is: copper!
Copper is a metal that is found in some swimming pools, particularly ones that are filled using well water. Copper can also enter the pool water from certain copper-based algaecides.
So how does copper in pool water turn your hair green?
The copper in the water is oxidized by chlorine, which then binds to the proteins in the hair strands. The metal will produce a green tint in the hair.
Will Blonde Hair Turn Green in a Saltwater Pool?
Short answer: yes.
Saltwater pools are chlorine-based pools. However, instead of adding chlorine manually with tablets or powder, salt is added to the water, which runs through an electrically charged generator, turning the salt into chlorine.
If you have copper in the water, and the chlorine created by the salt oxidizes it, it may turn your hair green just like a regular chlorine swimming pool.
3 Ways To Prevent Green Hair From a Pool
As a pool owner, you can start by getting your pool checked for metals, especially copper. You can use test strips at home or take a sample of your water to us to have it professionally checked.
1. Stop Using Copper-Based Algaecides
Some algaecides contain copper, and are very effective in killing algae, but they can also cause staining and, of course, green hair.
Look for non-copper algaecides to use in your pool as an annual algae preventative. | no |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | http://scienceline.ucsb.edu/getkey.php?key=495 | UCSB Science Line | Does blonde hair turn green in chlorinated water
because chlorine is green?
Question Date: 2003-12-18
Answer 1:
Any color hair can take on a greenish tinge
after a lot of exposure to swimming pool water,
it's just that the greenish tinge is easier to see
on light-colored hair than on dark-colored hair.
Chlorine is not green, and it's actually
not the chlorine that causes the color, although
the chlorine may help indirectly. Here's what I
mean by that:
The green color is caused by certain heavy
metals, mostly copper, that lodge in cracks
in the scaly outer covering of your hair shaft.
This outer covering is called the cuticle,
and it normally protects your hair. Swimming a lot
can damage your cuticle, allowing the copper and
other metals to get it and stick there. Once
there, they oxidize (kind of like rusting), and
oxidized copper is green. (Incidentally, that's
why the Statue of Liberty is green, and why old
pennies are sometimes green--the copper in them
has oxidized.) Chlorine's role in this is that it
helps damage your hair's cuticle. So, although the
green you see is not chlorine, the chlorine
probably helped the copper get in and stick there.
The copper then oxidizes, and voila! Green hair.
Answer 2:
Many people have experienced blonde hair going
green after prolonged exposure to chlorine in
swimming pools. Sometimes darker hair can also
develop a green tint to it. The problem is due to
high concentrations of copper compounds
dissolved in the pool water. This can
chemically interact with chlorine and the
resulting chemical compound readily binds to the
hair. It has also been reported that high levels
of copper in tap water can also turn hair green.
Chlorine in swimming pool water may affect the
general appearance of the hair. After a swim in
chlorinated water most people's hair looks very
dull and dry. This is usually due to removal of
oils that coat the hair to give it a shiny look
and certainly chlorine is a very powerful remover
of hair lipids.
So the short answer is, no, it is not because
chlorine is green. In fact, it is because the
copper compounds, which are also in pools, are
greenish. When that reacts with the chlorine it
can bind to hair causing it to look green. You can
see this for yourself... take a clean copper penny
and put it in a little chlorine bleach overnight
and see what happens! The penny needs to be shiny
clean, not dark looking. Also, please be sure
to do this with an adult because chlorine bleach
is a dangerous chemical. | Does blonde hair turn green in chlorinated water
because chlorine is green?
Question Date: 2003-12-18
Answer 1:
Any color hair can take on a greenish tinge
after a lot of exposure to swimming pool water,
it's just that the greenish tinge is easier to see
on light-colored hair than on dark-colored hair.
Chlorine is not green, and it's actually
not the chlorine that causes the color, although
the chlorine may help indirectly. Here's what I
mean by that:
The green color is caused by certain heavy
metals, mostly copper, that lodge in cracks
in the scaly outer covering of your hair shaft.
This outer covering is called the cuticle,
and it normally protects your hair. Swimming a lot
can damage your cuticle, allowing the copper and
other metals to get it and stick there. Once
there, they oxidize (kind of like rusting), and
oxidized copper is green. (Incidentally, that's
why the Statue of Liberty is green, and why old
pennies are sometimes green--the copper in them
has oxidized.) Chlorine's role in this is that it
helps damage your hair's cuticle. So, although the
green you see is not chlorine, the chlorine
probably helped the copper get in and stick there.
The copper then oxidizes, and voila! Green hair.
Answer 2:
Many people have experienced blonde hair going
green after prolonged exposure to chlorine in
swimming pools. Sometimes darker hair can also
develop a green tint to it. The problem is due to
high concentrations of copper compounds
dissolved in the pool water. This can
chemically interact with chlorine and the
resulting chemical compound readily binds to the
hair. It has also been reported that high levels
of copper in tap water can also turn hair green.
Chlorine in swimming pool water may affect the
general appearance of the hair. | yes |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://hairpros.edu/chlorine-hair-what-happens/ | How to Prevent and Reduce Chlorine Damage | Hair Professionals ... | Chlorine and Hair: How to Prevent and Reduce Damage
If you’ve gone swimming at all this summer or in the past, you’ve probably experienced the distinct smell of chlorine on your clothes, skin, and hair. Chlorine is used in swimming pools to kill unwanted bacteria and keep swimmers safe from infections and disease from the water. While there isn’t enough chlorine in swimming pools to cause permanent damage, it can leave your hair dry and your skin irritated and red.
Curious about what chlorine actually does to your hair and skin? Keep reading for tips on how to prevent and reduce damage!
What Chlorine Does to Your Hair and Skin
Chlorine sucks the natural oils from your hair and skin, leaving them dry, rough, and damaged. Your hair needs some of its natural oil to remain smooth and healthy, and chlorine removes those oils. Chlorine can also cause chemical reactions in your hair, changing the natural color of your hair, weakening each hair strand, and causing split ends. The oils removed from the skin can leave your skin red and irritated depending on the sensitivity of your skin.
Does Chlorine Turn Your Hair Green?
Some swimmers find that their hair turns green after swimming. The green color is not actually from the chlorine, but instead from copper that has been oxidized by chlorine. The chlorine with the oxidized copper is absorbed in your hair, which can leave your hair looking slightly green.
4 Ways to Prevent Chlorine Damage
While you can’t completely prevent damage from chlorine, especially if you go swimming often, you can prevent some of the damage by doing one of the following before jumping in.
Wet your hair first
Your hair soaks in liquid fast. If you get your hair wet before you step in the pool, you can prevent some of the water with chlorine or damaging salts from being absorbed.
Wear a swim cap
The best way to prevent chlorine damage is to prevent your hair from getting wet in the first place. A swim cap is a great way to enjoy the pool without subjecting your hair to a lot of chlorine. You can even wet your hair before putting on the cap to create a tighter seal that prevents even more chlorinated water from being absorbed.
Use a leave-in conditioner before entering the pool
Applying a little conditioner before you enter the pool can help prevent some of the chlorine from being absorbed. Using a leave-in conditioner with a cap can not only help prevent chlorine from being absorbed but can also moisturize your hair while swimming!
Apply oil
Applying an oil like coconut oil and wearing a swim cap is a great way to prevent chlorine from damaging your hair. The oil repels water and prevents your hair from absorbing the chlorine.
3 Ways To Repair Chlorine Damage
Damage from chlorine doesn’t have to be permanent. There are ways to reduce the damage and go back to healthy, soft hair in no time. Here are a few ways you can repair damage from chlorine:
Rinse your hair immediately
To reduce the damage and get your hair on the road to recovery, rinse your hair immediately after swimming. Don’t let the chlorine, salt, or other contaminants sit in your hair. If you’re really worried about damage, use a special shampoo formulated to remove chlorine from your hair.
Comb gently
Wet hair has a tendency to tangle, and brushing with a brush is more likely to damage your hair. Use a wide-toothed comb to gently detangle and smooth wet hair.
Clarify your hair
A hair clarifier can remove any harsh chemicals from your hair. While you can buy a clarifying shampoo, you can also use an apple cider vinegar rinse to remove any unwanted chlorine.
Whether you go swimming every week, once a month, or once a year, chlorine can do damage to your hair. Check out our salon services to find a hair treatment that can pamper you and your hair this summer! All of our students perform services under the supervision of licensed cosmetologists to make sure you are in good hands.
If the chemistry behind hair is something that interests you, a career in cosmetology might be the right choice for you! You can learn all about hair, skin, and nail science so that you can provide the best services for your clients. If you’re interested in learning more about what a career in cosmetology can do for you, contact Hair Professionals Career College. We have campuses in Sycamore, Palos Hills, and Oswego. You can also text us at 630-884-5554 for more information. | Chlorine and Hair: How to Prevent and Reduce Damage
If you’ve gone swimming at all this summer or in the past, you’ve probably experienced the distinct smell of chlorine on your clothes, skin, and hair. Chlorine is used in swimming pools to kill unwanted bacteria and keep swimmers safe from infections and disease from the water. While there isn’t enough chlorine in swimming pools to cause permanent damage, it can leave your hair dry and your skin irritated and red.
Curious about what chlorine actually does to your hair and skin? Keep reading for tips on how to prevent and reduce damage!
What Chlorine Does to Your Hair and Skin
Chlorine sucks the natural oils from your hair and skin, leaving them dry, rough, and damaged. Your hair needs some of its natural oil to remain smooth and healthy, and chlorine removes those oils. Chlorine can also cause chemical reactions in your hair, changing the natural color of your hair, weakening each hair strand, and causing split ends. The oils removed from the skin can leave your skin red and irritated depending on the sensitivity of your skin.
Does Chlorine Turn Your Hair Green?
Some swimmers find that their hair turns green after swimming. The green color is not actually from the chlorine, but instead from copper that has been oxidized by chlorine. The chlorine with the oxidized copper is absorbed in your hair, which can leave your hair looking slightly green.
4 Ways to Prevent Chlorine Damage
While you can’t completely prevent damage from chlorine, especially if you go swimming often, you can prevent some of the damage by doing one of the following before jumping in.
Wet your hair first
Your hair soaks in liquid fast. If you get your hair wet before you step in the pool, you can prevent some of the water with chlorine or damaging salts from being absorbed.
Wear a swim cap
The best way to prevent chlorine damage is to prevent your hair from getting wet in the first place. | yes |
Trichology | Can hair really turn green from chlorine in swimming pools? | yes_statement | "hair" can "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" can cause "hair" to "turn" "green". | https://www.milkshakehair.com/blogs/news/how-to-protect-your-blonde-hair-from-turning-green-in-the-pool | How to protect your blonde hair from turning green in the pool ... | How to protect your blonde hair from turning green in the pool
Does blonde hair really turn green in the pool? Will saltwater dry out your hair? Are UV rays responsible for hair color fading? These are some of the most-asked summer hair care questions that salon pros around the country tackle as soon as the temperatures start to rise.
There are three things in life that you can absolutely count on: death, taxes, and an irresistible urge to go blonde in the summertime. One of the biggest fears when considering going lighter for summer is how your color will stand up to all of your fun summer activities. Kicking it poolside and having a beach day are great for our mental health, not so much for the health of our hair. Fortunately, there are ways to prevent and even reverse damage to your new summer blonde.
Does blonde hair turn green in the pool?
Yes and no. Contrary to popular belief, chlorine is not the culprit when it comes to blonde hair turning greenish after a swim. Chlorine actually works to lighten hair, which sets the stage for the real menace to step in: copper. Copper is a common ingredient in algaecide, which is used to control algae growth in swimming pools. When copper oxidizes (aka, is exposed to the air) it turns from a shiny orange hue to a dull green. While chlorine may not be responsible for turning your blonde hair green, it can cause hair color to fade more quickly and lose its sheen. Highly porous hair is especially susceptible to losing moisture and shine, and lightening your hair increases its porosity.
How to treat it:
If your blonde hair has already started to turn green due to copper exposure, see your hair colorist. There are treatments that can be done to remove metal deposits; however, they are best handled by a professional. Remember that hair that has been chemically lightened is more fragile and removing any additional additives can cause further damage.
How to prevent it:
The single best thing that you can do for your hair after swimming is to use a deep cleansing shampoo. milk_shake deep cleansing shampoo gently removes product build-up and chlorine from the hair. Our formula is SLES-free, to gently remove styling product residue and chlorine from hair. Our deep cleansing shampoo also contains fruit and honey extracts and milk proteins, to cleanse hair deeply but gently, maintaining its moisture balance.
Product Rx After a Day at the Pool:
Cleanse with Deep Cleansing Shampoo
Moisturize with Sun & More Beauty Mask
Protect with Sun & More Incredible milk
Will going to the beach ruin my hair?
The combination of sun and salt is like a one-two punch to your hair’s hydration. Swimming in the ocean can quickly lead to dry, crunchy hair if you don’t care for it properly afterwards. Believe it or not, the salt in ocean water attracts more water to your hair, forming salt crystals. These salt crystals give your hair extra body (think natural, beachy waves) however, they also pull moisture away. This is what leads to that dry, brittle feeling. This goes double for chemically treated hair. | How to protect your blonde hair from turning green in the pool
Does blonde hair really turn green in the pool? Will saltwater dry out your hair? Are UV rays responsible for hair color fading? These are some of the most-asked summer hair care questions that salon pros around the country tackle as soon as the temperatures start to rise.
There are three things in life that you can absolutely count on: death, taxes, and an irresistible urge to go blonde in the summertime. One of the biggest fears when considering going lighter for summer is how your color will stand up to all of your fun summer activities. Kicking it poolside and having a beach day are great for our mental health, not so much for the health of our hair. Fortunately, there are ways to prevent and even reverse damage to your new summer blonde.
Does blonde hair turn green in the pool?
Yes and no. Contrary to popular belief, chlorine is not the culprit when it comes to blonde hair turning greenish after a swim. Chlorine actually works to lighten hair, which sets the stage for the real menace to step in: copper. Copper is a common ingredient in algaecide, which is used to control algae growth in swimming pools. When copper oxidizes (aka, is exposed to the air) it turns from a shiny orange hue to a dull green. While chlorine may not be responsible for turning your blonde hair green, it can cause hair color to fade more quickly and lose its sheen. Highly porous hair is especially susceptible to losing moisture and shine, and lightening your hair increases its porosity.
How to treat it:
If your blonde hair has already started to turn green due to copper exposure, see your hair colorist. There are treatments that can be done to remove metal deposits; however, they are best handled by a professional. Remember that hair that has been chemically lightened is more fragile and removing any additional additives can cause further damage.
How to prevent it:
The single best thing that you can do for your hair after swimming is to use a deep cleansing shampoo. | no |
Trichology | Can hair really turn green from chlorine in swimming pools? | no_statement | "hair" cannot "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" does not cause "hair" to "turn" "green". | https://www.glam.com/995572/fix-green-hued-blond-hair-after-day-pool/ | 11 Ways To Fix Blond Hair That's Turned Green From Swimming In ... | If you have blond hair and love spending your time in the pool, chances are you've noticed that pool water often gives your hair a green tint. While this can happen to any hair color, the lighter your hair is, the more visible the green will be. If you do have lighter hair, you may be tempted to bleach the green out of your strands. However, this can cause further damage, especially if you've recently bleached your hair — and you definitely want to avoid that.
Instead, there are several ways to remove the green tint from your hair without causing more damage. Additionally, there are tricks you can try to prevent your hair from turning green in the first place (and no — we're not talking about rocking a swimming cap). However, keep in mind that everyone's hair is different, which is why a home remedy that works for one person may not work for another. Luckily, though, there are many options available for removing that green tint from your hair.
Why does hair turn green in the pool?
PeopleImages.com - Yuri A/Shutterstock
Before we get into the remedies and ways to prevent your hair from turning green, let's dive into why the hair becomes green in the first place. Most people think chlorine on its own is the culprit. But what's really to blame? Copper! Some pools have a high copper content in the water itself, especially if the water is from the tap. Another common source is copper-based algaecides, which are used to prevent the growth of algae and help the pool maintain a swim-worthy blue hue.
But that doesn't mean the chlorine in the pool isn't doing its part to damage the hair and give it a green tint. "Chlorine damages porous hair by drying it out and rendering it susceptible to external aggressors," celebrity hairstylist Nick Stenson tells Makeup.com. "But copper oxidizing in the hair is actually the culprit for delivering shades of green."
What happens is that the chlorine oxidizes the copper creating copper ions, which then bind to the proteins in the hair, creating a green tint. Apart from getting a green tint, chlorine is also very damaging to the hair, and those who swim in pools frequently will notice that their hair is very porous (and may be frizzy, dry, and prone to damage). And hair with high porosity absorbs the copper ions much quicker.
Before you try home remedies, wash your hair with a clarifying shampoo
Mystockimages/Getty Images
If you notice that your hair looks green after the pool, your first step should always be to wash it thoroughly with a clarifying shampoo. Since they are designed to remove any product buildup, clarifying shampoos act as a detox for your scalp and are effective at removing other impurities from the hair, including the copper ions that cause the hair to turn green.
However, keep in mind that a clarifying shampoo can also strip your hair of the natural oils that it needs, which is why it's super important to nourish it with a moisturizing conditioner or a hair mask afterward. If you're lucky, the clarifying shampoo will remove all of the green from your hair.
Although a clarifying shampoo is an effective first step in removing the green tint from your hair, the truth is that it may take a few washes to completely remove it. However, we don't recommend using a clarifying shampoo too often, as it can over-strip your hair and leave it dry. If there is still some green left, there are a couple of other hacks you can use to get rid of it safely.
Rinse your hair with apple cider vinegar
Kazmulka/Getty Images
Many people use apple cider vinegar in their daily routines. Not only is it one of the most well-known home remedies, but it has many uses in beauty too. In fact, an apple cider vinegar rinse has been known to be beneficial for hair as it helps balance the pH of your scalp and makes your strands shiny and soft. Apart from that, apple cider vinegar is excellent for removing any buildup, which is why it can also help with getting rid of the copper ions that turn the hair green.
For the rinse, mix 1 cup of apple cider vinegar and 2 cups of water. Then, rinse your hair with it after you've already shampooed and conditioned. Let the apple cider vinegar water sit on your hair for five to 10 minutes, and after that, rinse it out with just water. Since this method isn't harmful to your hair, it's the second thing your should try — right after washing your hair with a clarifying shampoo.
Remove the green with the help of baking soda
Marcus Chung /Getty Images
Baking soda can be a helpful remedy to eliminate the green tint caused by swimming in chlorinated water. Since baking soda has color-lifting properties, it can help rid the hair of any green tones and restore your hair's color.
We recommend mixing about 1/2 cup of baking soda with water to make a thick, toothpaste-like consistency. Apply the paste to your hair and massage it thoroughly, focusing on any green areas. Leave the paste on for a few minutes to allow the baking soda to do its magic. After that, rinse the paste out and shampoo and condition your hair as usual.
You might need to repeat this process several times, depending on how green your hair is. However, you may want to wait at least a day between the treatments to ensure you don't over-strip your hair and damage it. While baking soda is a safe and rather cheap solution, using it too frequently can dry out your hair.
Saturate your hair in lemon juice
Courtneyk/Getty Images
Lemon juice is another home remedy that can help remove the green pigment from your hair. The acid in the lemon not only breaks down the green but can also lighten your hair — so beware of that if you don't want your hair any lighter.
To use lemon juice, saturate your hair in it. We recommend diluting the lemon juice in water or wetting your hair before applying pure lemon juice. If you want to simultaneously lighten your strands, it's best to either sit in the sun for a bit or apply some heat to your hair with a blow dryer, as the heat is what kicks off the lightening process.
After five to 10 minutes, rinse the lemon out and shampoo and condition your hair as always. Since lemon can dry your hair out, using a deep conditioning treatment or a leave-in product is best. Again, we don't recommend repeating this process immediately if some of the green is still in your hair. Instead, wait at least 24 hours to give your hair some time to recover.
Soak the green strands in Coke
Delphix/Shutterstock
As Coca-Cola contains phosphoric acid, it is known to help remove rust — and a similar principle also works when you apply it to your hair. This compound helps remove the green tint in your hair, as it strips the copper buildup that causes it.
To use it, saturate your hair in Coke and massage it through the green areas for a couple of minutes, ensuring any green spots are generously covered. After that, leave it on for a couple of minutes to allow the Coke to penetrate the hair and break down the copper buildup.
Rinse your hair with water and shampoo and condition it, ensuring you use a nourishing hair treatment. Again, while this will help lift some of the green, you might need to redo it again in a couple of days. While using Coke to remove the green tint in hair can be effective, it shouldn't be used as a regular hair treatment as it can strip the hair of its essential oils.
Ketchup works as a toner that neutralizes the green
Sergeyryzhov/Getty Images
If you know anything about color theory, you're probably aware that the color red neutralizes green since the two are opposite of each other on the color wheel. Because of this, ketchup has become a popular at-home remedy for neutralizing the post-pool green tint that can happen in blond hair. Since ketchup is acidic, it also helps stop the hair from turning greener — and the red color helps tone it to remove the green that is already visible.
If you want to use ketchup, ensure your hair is wet before you apply it. Then add a generous amount of ketchup to the green areas of your hair and let it sit for 10 to 20 minutes. After that, rinse it out and wash your hair as usual. If you have blond hair, chances are, you're familiar with a purple toner that neutralizes any brassy and yellow color that appears. Ketchup essentially works the same way by canceling out any green tones that appear in your hair.
Add aspirin to your shampoo
Kim Kuperkova/Shutterstock
Aspirin — which contains salicylic acid — is another home remedy that can help you get rid of any green hues in your hair. The salicylic acid in the aspirin breaks down and dissolves the copper buildup, thereby removing the green tint from your hair.
The easiest way to apply aspirin to your hair is to simply take a couple of tablets, crush them into a powder and mix them with your shampoo (the shampoo you squeezed into your hand, not the entire bottle, of course). Once you have an even paste, shampoo your hair with it, focusing on the spots where the green is most prominent.
Since it is acidic, aspirin can also harm your hair, so make sure you apply a moisturizing product to your hair afterward. The amount of aspirin tablets you should use depends on your hair thickness as well as how strong the green tint is. However, we recommend starting with only a few, and if they don't give you the result you were hoping for, repeat the process after at least 24 hours to ensure the damage to your hair is minimal.
Use Kool-Aid to brighten the hair
Lisa Holder/Shutterstock
Kool-Aid can actually be used as a temporary hair dye, and it works particularly well on lighter hair colors. Because of this, you can use pink or red Kool-Aid to neutralize the green and tone your hair. Lemon Kool-Aid may also be a great idea if you are worried about the red staining your strands too much.
Depending on your hair length and thickness, mix one to three packs of Kool-Aid with a bit of water to create a paste. Apply the paste evenly to your hair and massage it in. Check on your hair every few minutes by removing some of the paste from a strand. Since Kool-Aid is very vibrant, you won't need to keep it on your hair for too long. Once you notice that the green is being neutralized, you can rinse your hair and clean it with a gentle shampoo, making sure you're not overwashing it.
If your hair ends up looking a bit too red or pink, don't stress — the color should wash out after a few more washes. However, since Kool-Aid works as a temporary hair tint, you might notice green peeking through once the Kool-Aid washes out. If this is the case, one of the other methods might be more beneficial.
Use a red-boosting hair product
Simonskafar/Getty Images
As we already established, one way to counteract the green in your hair is by simply adding some red to it. If ketchup and Kool-Aid sound too intimidating for you, you can always opt for a red-boosting hair product. However, those are not as easily found as purple shampoos and conditioners, which you can pick up at most drugstores.
If you struggle to find a red hair product in the form of a shampoo or conditioner, consider opting for a temporary red hair dye which you can add to your favorite hair mask and apply evenly to any green spots. Of course, make sure you only add a bit of the color to your mask since you want to avoid having your hair look red after — you only want to cancel out the green. We recommend doing a patch test before going all in and applying it to your whole head.
Get a professional chlorine-removing shampoo
Aleksandargeorgiev/Getty Images
Home remedies can be great, but they can also be inefficient, especially if the green in your hair is very vibrant. If you have blond hair and spend a lot of time in pools, consider investing in a chlorine-removing shampoo which will help eliminate the chlorine and copper ions from the hair immediately. One product with plenty of great reviews is Malibu C Swimmers Wellness Hair Remedy, specifically designed to help restore your hair's health while removing its green hues.
"My daughter's hair went from silky white to crunchy and neon green in like 20 minutes of swimming!!!!! I tried three different swim shampoos, and none of them did a thing! My hairdresser recommended this to me, so I figured I'd give one more product a shot. This is literally a miracle product! I saw the green disappearing before my eyes," a satisfied buyer raves in their Amazon review. Definitely reach for a product like this if you spend a lot of time in pools and want to keep your hair healthy.
Visit your hairstylist for a professional result
Miljko/Getty Images
While you can try home remedies if your hair is healthy, if you have brittle, dry, and damaged hair, the best thing you can do is visit a professional and see what they can do to remove the green from it.
A good hairstylist will approach each case individually, but most commonly, they will wash the hair with a clarifying or chlorine-removing shampoo, after which they might go in with a toner to cover up any leftover green. Additionally, a hairstylist may also suggest a deep conditioning treatment that will help restore the hair's moisture, as your hair has most likely been dehydrated by the pool water.
Of course, this is the most expensive solution, but it is also the one that will give you the best results, as a professional will provide you with a custom solution to counteract the green, taking into account your hair type and health.
Prevention tip: Pre-wet your hair before you go into the pool
Robert Daly/Getty Images
We can all agree that preventing the green from happening is much better than looking for a way to get rid of it once it's already there. One of the easiest ways you can ensure your hair doesn't turn green is to wet your hair with clean water before you enter the pool. This small step only takes seconds but can save you a lot of hassle in the long run.
Hair already saturated with non-chlorinated water won't absorb as much of the pool water, meaning that it also can't absorb as many copper ions. Of course, this doesn't mean your hair won't turn green at all — but it will certainly turn way more green if you dive in the pool with dry hair. Additionally, wetting your hair before going in the pool can also help prevent chlorine damage which is why this trick is useful for everyone and not just those with blond hair.
Prevention tip: Apply oil or conditioner to your hair before you go into the pool
Emilija Randjelovic/Getty Images
While saturating your hair in non-chlorinated water before going into the pool is great, an even better prevention hack is to apply a conditioner or coconut oil to your hair before jumping into a chlorinated pool. This will help protect your hair from the water while also nourishing it so that it doesn't get stripped of its natural oils.
Since oil and water don't mix, once your hair absorbs the oil, it won't allow the pool water to penetrate your hair strands. For this, you can use any oil you like, whether it's a specific hair oil or simply something you already have at home, like coconut or olive oil.
"However, you have to keep your head covered, as oil will also cook your hair in the hot sun," celebrity hairstylist Scott Fontana told StyleCaster. So, reach for a swim cap, or at the very least, put your hair in a protective hairstyle such as a bun or a braid. Once you get out of the pool, wash your hair as always, and you will immediately notice that your hair doesn't have any additional damage at all — and most importantly, there won't be any green hues in it.
Prevention tip: Rinse your hair as soon as possible after swimming
Skynesher/Getty Images
One prevention tip that seems very obvious, yet many tend to forget about it, is to immediately rinse your hair once you leave the pool. If you're someone who loves to chill by the pool after swimming, read a book, and even let your hair dry completely before you wash it — you definitely need to change that.
Now, we're not saying you need to shampoo and condition your hair immediately, but you do need to rinse the hair with non-chlorinated water to ensure there is no time for the green tint to form on your hair. The chlorine and copper particles in the pool water can bond with your hair quickly, which is why it's essential to act fast to remove them. If there is no shower available to you immediately, a good tip is to always have a bottle of water with you, which you can use to quickly rinse your hair. | If you have blond hair and love spending your time in the pool, chances are you've noticed that pool water often gives your hair a green tint. While this can happen to any hair color, the lighter your hair is, the more visible the green will be. If you do have lighter hair, you may be tempted to bleach the green out of your strands. However, this can cause further damage, especially if you've recently bleached your hair — and you definitely want to avoid that.
Instead, there are several ways to remove the green tint from your hair without causing more damage. Additionally, there are tricks you can try to prevent your hair from turning green in the first place (and no — we're not talking about rocking a swimming cap). However, keep in mind that everyone's hair is different, which is why a home remedy that works for one person may not work for another. Luckily, though, there are many options available for removing that green tint from your hair.
Why does hair turn green in the pool?
PeopleImages.com - Yuri A/Shutterstock
Before we get into the remedies and ways to prevent your hair from turning green, let's dive into why the hair becomes green in the first place. Most people think chlorine on its own is the culprit. But what's really to blame? Copper! Some pools have a high copper content in the water itself, especially if the water is from the tap. Another common source is copper-based algaecides, which are used to prevent the growth of algae and help the pool maintain a swim-worthy blue hue.
But that doesn't mean the chlorine in the pool isn't doing its part to damage the hair and give it a green tint. "Chlorine damages porous hair by drying it out and rendering it susceptible to external aggressors," celebrity hairstylist Nick Stenson tells Makeup.com. "But copper oxidizing in the hair is actually the culprit for delivering shades of green. "
What happens is that the chlorine oxidizes the copper creating copper ions, which then bind to the proteins in the hair, creating a green tint. | yes |
Trichology | Can hair really turn green from chlorine in swimming pools? | no_statement | "hair" cannot "turn" "green" from "chlorine" in "swimming" "pools".. "chlorine" in "swimming" "pools" does not cause "hair" to "turn" "green". | https://glazehair.co/blogs/news/tips-to-care-for-your-blonde-hair-this-summer | Tips to Care for Your Blonde Hair This Summer – Glaze | Tips to Care for Your Blonde Hair This Summer
Blonde is our favorite summer hair color. However, it’s the shade that can take on the most damage from summery conditions. Harmful UV rays can fry blonde hair and chlorine from swimming pools can even change the tone, turning our beautiful blonde locks green.
But having blonde hair doesn’t mean that you’ll have to avoid the sun all summer long. With our blonde hair care tips, you can get out to enjoy the warm weather and show off your luscious locks.
Use SPF for your hair
We all know that we need to wear SPF on our skin. But did you know you can get SPF for your hair? There’s a huge range of UV-protection products specifically designed to keep our hair safe from UV. An SPF hair mist will not only shield your locks but also your scalp, helping to prevent it from burning. Without proper protection, UV rays can make hair brittle and dry, and it can also cause blonde hair to fade in vibrancy. If you’re planning a day at the beach or by the pool, look for a water-resistant UV-defense spray.
Use a hair gloss treatment
It’s super important to keep your blonde hair hydrated throughout the warm summer months. Hydration is key to keeping your hair sleek and healthy, so you should aim to use a hair gloss treatment at least once a week. Hair gloss will smooth the cuticle of the hair, reducing frizz and adding shine. Our Glaze Super Gloss is available in a range of shades, so you can get a mirror glaze shine for your hair whilst also boosting the vibrancy of the color. We have a Super Gloss for beach blondes and a Super Gloss for pearl blondes, so you can find the right shade for your hair and banish brassiness. Our Super Gloss is enriched with Babassu Oil to deeply nourish, and contains no parabens, sulfates, silicones or ammonia.
Reduce how much you shampoo
If you have colored blonde hair, you should always avoid shampooing too much, as this can cause the color to fade quicker. This is even more important in the summer months when you’re battling damage from the sun as well. Shampooing too often will strip your hair of its natural oils, which will cause it to dry out. Instead, you can rinse your hair with water and use a light conditioner to get out any sweat and dirt from the day. However, you should always use shampoo if you’ve been swimming in a pool with chlorine, as leaving the chemical in can cause your blonde locks to turn green.
Use the right hair care products
When choosing a shampoo and conditioner you should look for hydrating and restorative formulas. These will help to repair the hair after a day in the sun, and will get it looking healthy and nourished again.
Formulas that contain keratin and collagen are great for preparing hair to deal with the effects of summertime. You should avoid any hair care products that contain sulfates. Sulfates are commonly used in shampoos to create a sudsy lather, but they will dry your hair out and cause even more damage. Make sure to always read the labels closely to ensure you’re not adding any harmful chemicals to your hair.
You should also be careful when using hair oils. Whilst many hair oils can help to hydrate hair, oils with yellow or orange tints can actually stain platinum and white-blonde hair. Look for lightweight, clear oils instead, as these won’t carry any risk of affecting your hair color.
Protect your hair when swimming
If you’re heading to a pool party or the beach, you should make sure to rinse your hair in fresh water before you go swimming. This will help prevent the chlorine or salt water from getting into the hair strands and drying it out. You should rinse your hair again with fresh water when you finish swimming, and wash with shampoo to get the chlorine out.
Use a shower head filter
Swimming pools aren’t the only place where you should be wary of chlorine. The water you use to shower can also contain chlorine, as well as other minerals, fluoride and iron that can all turn your beautiful blonde hair brassy. A shower filter will work to ensure the water you wash your hair with has minimal chemicals that can affect your hair color, ensuring it stays bright and vibrant.
Ditch the heat styling tools
You’ll want to minimize the heat that’s applied to your hair throughout the summer, so you should ditch the heat styling tools to prevent any further damage. Use a microfiber towel to blot your hair dry and then leave it to finish drying naturally. Use a salt spray for beachy waves and texture, or a smoothing serum or oil to tame any frizz. | This is even more important in the summer months when you’re battling damage from the sun as well. Shampooing too often will strip your hair of its natural oils, which will cause it to dry out. Instead, you can rinse your hair with water and use a light conditioner to get out any sweat and dirt from the day. However, you should always use shampoo if you’ve been swimming in a pool with chlorine, as leaving the chemical in can cause your blonde locks to turn green.
Use the right hair care products
When choosing a shampoo and conditioner you should look for hydrating and restorative formulas. These will help to repair the hair after a day in the sun, and will get it looking healthy and nourished again.
Formulas that contain keratin and collagen are great for preparing hair to deal with the effects of summertime. You should avoid any hair care products that contain sulfates. Sulfates are commonly used in shampoos to create a sudsy lather, but they will dry your hair out and cause even more damage. Make sure to always read the labels closely to ensure you’re not adding any harmful chemicals to your hair.
You should also be careful when using hair oils. Whilst many hair oils can help to hydrate hair, oils with yellow or orange tints can actually stain platinum and white-blonde hair. Look for lightweight, clear oils instead, as these won’t carry any risk of affecting your hair color.
Protect your hair when swimming
If you’re heading to a pool party or the beach, you should make sure to rinse your hair in fresh water before you go swimming. This will help prevent the chlorine or salt water from getting into the hair strands and drying it out. You should rinse your hair again with fresh water when you finish swimming, and wash with shampoo to get the chlorine out.
Use a shower head filter
Swimming pools aren’t the only place where you should be wary of chlorine. The water you use to shower can also contain chlorine, as well as other minerals, fluoride and iron | yes |
Hematology | Can hemophilia be cured? | yes_statement | "hemophilia" can be "cured".. there is a "cure" for "hemophilia". | https://hhma.org/can-hemophilia-be-cured/ | Can Hemophilia Be Cured? | Tufts Medical Center Community Care | Can Hemophilia Be Cured?
Can Hemophilia Be Cured?
Hemophilia is a bleeding disorder that is inherited, or passed down from parent to child. It is characterized by a deficiency of certain proteins known as “clotting factors,” leading to blood that doesn’t clot well and excessive or spontaneous bleeding. Hemophilia may develop after birth in extremely rare cases.
A cure for hemophilia has not yet been discovered. However, there are several treatment options available to help individuals with this condition manage their symptoms, prevent complications and live a normal life.
Each patient’s best course of treatment will depend on what type of hemophilia is present:
Hemophilia A – The most common type, hemophilia A can be treated with desmopressin—a prescription hormone that is injected into a vein to help activate blood clotting factors.
Hemophilia B – Also known as Christmas disease, hemophilia B can be treated by infusing blood with clotting factors from a donor or in synthetic form.
Hemophilia C – The rarest type, hemophilia C can be treated through plasma infusions that work to stop excessive bleeding following trauma or injury.
Self-Care Measures for Hemophilia
People with hemophilia can also take self-care measures to help manage their symptoms, prevent bleeding episodes and improve overall health. Many physicians recommend:
What Are the Symptoms of Hemophilia?
According to the Centers for Disease Control and Prevention (CDC), the most common signs and symptoms of hemophilia include:
Frequent and difficult-to-stop nosebleeds
Bleeding after having vaccinations or immunizations
Bleeding into the joints (often the elbows, knees and ankles) that can cause swelling and pain
Easy bruising and bruises that are large or unexplained
Frequent hematomas, or a collection of blood outside of a blood vessel
Blood in urine or stools
Frequent bleeding in the mouth and gums, especially after losing a tooth
The frequency and severity of hemophilia symptoms will depend on the amount of clotting factors in the blood. The lower the level of clotting factors, the more significant symptoms will likely be.
Hemophilia Treatment at Tufts Medical Center Community Care
For hemophilia treatment and specialized hematology services, residents of north suburban Boston can turn to Tufts Medical Center Community Care. Our multispecialty medical group features more than 120 clinicians, including primary care physicians and hematologists who assist patients with all types of hemophilia.
Receive the specialized hemophilia treatment you need at Tufts Medical Center Community Care. With multiple easily accessible locations and better-than-average appointment availability, we make it simple to find the right doctor for your needs. Plus, our practice is in-network with most health insurance providers, including Medicare, Medicaid and Tricare. Contact our friendly professionals today to schedule an appointment.
Find a Provider
Patient Portal
myTuftsMed is our new online patient portal that provides you with access to your medical information in one place. MyTuftsMed can be accessed online or from your mobile device providing a convenient way to manage your health care needs from wherever you are.
With myTuftsMed, you can:
View your health information including your medications, test results, scheduled appointments, medical bills even if you have multiple doctors in different locations.
Make appointments at your convenience, complete pre-visit forms and medical questionnaires and find care or an emergency room. | Can Hemophilia Be Cured?
Can Hemophilia Be Cured?
Hemophilia is a bleeding disorder that is inherited, or passed down from parent to child. It is characterized by a deficiency of certain proteins known as “clotting factors,” leading to blood that doesn’t clot well and excessive or spontaneous bleeding. Hemophilia may develop after birth in extremely rare cases.
A cure for hemophilia has not yet been discovered. However, there are several treatment options available to help individuals with this condition manage their symptoms, prevent complications and live a normal life.
Each patient’s best course of treatment will depend on what type of hemophilia is present:
Hemophilia A – The most common type, hemophilia A can be treated with desmopressin—a prescription hormone that is injected into a vein to help activate blood clotting factors.
Hemophilia B – Also known as Christmas disease, hemophilia B can be treated by infusing blood with clotting factors from a donor or in synthetic form.
Hemophilia C – The rarest type, hemophilia C can be treated through plasma infusions that work to stop excessive bleeding following trauma or injury.
Self-Care Measures for Hemophilia
People with hemophilia can also take self-care measures to help manage their symptoms, prevent bleeding episodes and improve overall health. Many physicians recommend:
What Are the Symptoms of Hemophilia?
| no |
Hematology | Can hemophilia be cured? | yes_statement | "hemophilia" can be "cured".. there is a "cure" for "hemophilia". | https://sheba-global.com/breakthrough-study-hemophilia-cure-achieved-within-months/ | Hemophilia Breakthrough: New Gene Therapy Offers Rapid Cure | Breakthrough Study: Hemophilia Cure Achieved Within Months
A groundbreaking trial which included Sheba researchers revealed that hemophilia patients, who suffer from a chronic genetic disease, can be cured in just a few months, by successfully replacing the defective gene.
Hemophilia is a bleeding disorder which is usually inherited. It results from a genetic mutation or alteration in one of the genes that provide instructions for producing clotting factor proteins essential for forming blood clots. Individuals with hemophilia suffer from spontaneous bleeding as well as excessive bleeding following injury or surgery.
The severity of hemophilia is determined by the amount of clotting factor present, with lower levels resulting in a higher likelihood of bleeding and potentially serious health complications. Individuals with a severe form of hemophilia are at high risk of experiencing internal bleeding, particularly in their knees, ankles, and elbows, which can cause damage to organs and tissues and pose a life-threatening risk.
Hemophilia can be treated with preventative or on-demand approaches. Most cases of hemophilia are severe and require preventative treatment, which involves regular clotting factor injections to prevent bleeding and joint/muscle damage. Patients receiving preventative treatment require ongoing monitoring and usually continue treatment for life. On-demand treatment is used to treat prolonged bleeding as needed.
In the global effort to eradicate hemophilia, innovative treatments based on genetic engineering are emerging. Israel has gained recognition for early detection of hemophilia, and Sheba is breaking new ground in the treatment of the disease.
In a groundbreaking study in the fight against hemophilia, Sheba researchers played a pivotal role in replacing the defective gene responsible for the disorder’s severe effects.
The experiment, which included 50 medical centers across 30 countries, and was conducted by BioMarin, involved 134 elderly patients who were suffering from hemophilia, including five individuals from Israel. The findings, published in The New England Journal of Medicine, reveal that researchers were able to successfully insert a healthy gene into the liver of the participants using a virus.
At the time of the trial, patients had to undergo repeated transfusions to replace the missing factor in their blood, which was administered frequently to prevent severe bleeding and resulting disability. According to Prof. Gili Kenet, director of the Israel National Hemophilia Center and Thrombosis Institute at Sheba, “We were able to cure a person suffering from a serious genetic disease within just a few months.”
According to Prof. Kenet, all Israeli participants were cured of the disease, exhibiting normal blood clotting and no signs of bleeding. Although six patients still experienced moderate hemophilia, their bleeding had significantly decreased. She emphasized the significance of the experiment, noting that what was once considered science fiction is now a reality.
The successful study offers new hope in the fight against the disease that affects over 400,000 individuals worldwide, and could potentially reduce the need for frequent transfusions and prevent severe bleeding and disability.
More Posts
Sheba Pandemic Research Institute (SPRI) has joined a groundbreaking collaboration with the National Institutes of Health (NIH)’s Vaccine Research Center, the Walter Reed Army Institute of Research, and pharmaceutical giant Sanofi. Researchers aim to develop booster vaccines that can provide comprehensive protection against multiple coronavirus variants, including SARS-CoV-2, revolutionizing virus care worldwide. Sheba’s COVID-19 research program, which involves over 9,000 healthcare workers, will serve as the framework for the design of the pan-coronavirus vaccine.
In today’s unpredictable world, hospitals play a critical role in responding to public health emergencies, be it natural disasters, disease outbreaks, or terrorist attacks. Below are five reasons why hospitals must prioritize emergency preparedness to ensure the safety and wellbeing of patients and healthcare professionals.
Useful Information
We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits. By clicking “Accept”, you consent to the use of ALL the cookies. However you may visit Cookie Settings to provide a controlled consent.
Privacy Overview
This website uses cookies to improve your experience while you navigate through the website. Out of these cookies, the cookies that are categorized as necessary are stored on your browser as they are essential for the working of basic functionalities of the website. We also use third-party cookies that help us analyze and understand how you use this website. These cookies will be stored in your browser only with your consent. You also have the option to opt-out of these cookies. But opting out of some of these cookies may have an effect on your browsing experience. | Breakthrough Study: Hemophilia Cure Achieved Within Months
A groundbreaking trial which included Sheba researchers revealed that hemophilia patients, who suffer from a chronic genetic disease, can be cured in just a few months, by successfully replacing the defective gene.
Hemophilia is a bleeding disorder which is usually inherited. It results from a genetic mutation or alteration in one of the genes that provide instructions for producing clotting factor proteins essential for forming blood clots. Individuals with hemophilia suffer from spontaneous bleeding as well as excessive bleeding following injury or surgery.
The severity of hemophilia is determined by the amount of clotting factor present, with lower levels resulting in a higher likelihood of bleeding and potentially serious health complications. Individuals with a severe form of hemophilia are at high risk of experiencing internal bleeding, particularly in their knees, ankles, and elbows, which can cause damage to organs and tissues and pose a life-threatening risk.
Hemophilia can be treated with preventative or on-demand approaches. Most cases of hemophilia are severe and require preventative treatment, which involves regular clotting factor injections to prevent bleeding and joint/muscle damage. Patients receiving preventative treatment require ongoing monitoring and usually continue treatment for life. On-demand treatment is used to treat prolonged bleeding as needed.
In the global effort to eradicate hemophilia, innovative treatments based on genetic engineering are emerging. Israel has gained recognition for early detection of hemophilia, and Sheba is breaking new ground in the treatment of the disease.
In a groundbreaking study in the fight against hemophilia, Sheba researchers played a pivotal role in replacing the defective gene responsible for the disorder’s severe effects.
The experiment, which included 50 medical centers across 30 countries, and was conducted by BioMarin, involved 134 elderly patients who were suffering from hemophilia, including five individuals from Israel. The findings, published in The New England Journal of Medicine, reveal that researchers were able to successfully insert a healthy gene into the liver of the participants using a virus.
At the time of the trial, | yes |
Hematology | Can hemophilia be cured? | yes_statement | "hemophilia" can be "cured".. there is a "cure" for "hemophilia". | https://www.healthline.com/health-news/hemophilia-may-not-be-lifelong-disease-soon | Hemophilia and Gene Therapy Treatments | “Puberty for me went off like a bomb. I started my period when I was 11 years old. The periods would last for weeks and weeks and I’d eventually be hospitalized each month. Eventually I developed ovarian cysts, which ruptured and bled in my abdomen. I was in excruciating pain,” Radford told Healthline.
Radford is one of the 20,000 people in the United States living with hemophilia, a genetic bleeding disorder that prevents blood from clotting normally.
For many with hemophilia, daily life consists of trying to avoid cuts and bruises. There are treatments but many are expensive and not effective for everybody.
However, new research is providing hope for people with this potentially dangerous disease.
Advances in gene therapy are showing enough promise that some experts say one day hemophilia may no longer be a lifelong ailment.
Hemophilia is more common in males, but females can also be affected by the disorder.
Girls and young women can experience heavy menstrual bleeding lasting more than seven days as well as hemorrhaging after childbirth.
Radford received a diagnosis at 7 months old when a small contusion on her head turned into a large bump.
She spent nine months in the hospital while doctors attempted to reach a diagnosis. Hospitalization was to become a recurring theme for Radford.
When she began menstruating, she was hospitalized for an extended period of time.
“I was airlifted to the children’s hospital in St. Johns Newfoundland and spent a year there. I turned 13 in the hospital while doctors pumped me full of blood and pain meds to try and stop the bleeding. Eventually a high-dose birth control worked and I’ve been able to manage my periods like that,” she said.
Hemophilia is caused by a decrease in one of the blood clotting factors, either factor VIII or factor IX.
The disorder can cause uncontrolled and spontaneous bleeding without an obvious injury. The level of bleeding risk is dependent on the level of clotting factor decrease.
Bleeds can occur both externally from cuts or trauma as well as internally in the spaces around the joints and muscles. If left untreated, the bleeding can cause permanent damage.
There’s currently no cure for hemophilia, but patients can be treated with an intravenous clotting factor.
“In hemophilia, patients are missing a single clotting factor protein, either factor VIII or IX, which arrests the progress of the clot formation putting patients at risk for serious bleeding, particularly recurrent bleeding into joints with subsequent development of crippling arthritis,” Dr. Steven Pipe, chair of the Medical and Scientific Advisory Committee of the National Hemophilia Foundation, told Healthline.
“To prevent this pathology, they administer ‘replacement therapy’ by infusing the factor VIII or IX proteins on a regular basis – typically every other day for factor VIII and 2 to 3 times per week for factor IX,” Pipe said.
Replacement therapies have revolutionized outcomes for those with hemophilia, but the treatment is not without its problems.
“When patients born with no expression of factor VIII or IX at birth are exposed to replacement proteins of factor VIII or IX, their immune system can mount a response to what it perceives as a foreign protein,” Pipe said. “These antibodies can inactivate the protein such that it will no longer treat or prevent their bleeding. This happens in up to 30 percent or more of patients with severe hemophilia A (factor VIII deficiency). These inhibitors require alternative but less effective treatments and lead to poorer outcomes for patients.”
In most individuals with hemophilia, regular treatment from infusions can prevent the vast majority of bleeding. But it comes at a heavy cost for both patients and caregivers.
Treatment for infants can begin at 1 year of age or earlier. Parents must learn how to administer treatments that can be as frequent as every second day.
“This comes at a tremendous cost to patients, families, and health systems. We know that joint disease can still appear in young adults and annualized bleeding rates are still not zero. There’s still room for new interventions that could improve patient outcomes even further,” Pipe said.
One of the interventions for hemophilia currently being explored is gene therapy.
This works by providing patients with hemophilia a new “working copy” of the genes for either factor VIII or factor IX.
The goal is to put the genes into cells in the body that are capable of making proteins. The most suitable organ for this is the liver.
“At present, all of the hemophilia gene therapy trials are using a virus called AAV (adeno-associated virus) to get the gene into the body,” Dr. Jonathan Ducore, director of the Hemophilia Treatment Center at the University of California Davis told Healthline.
“The AAV types used are ones which go to the liver and insert the gene (either factor VIII or factor IX) into liver cells. The viruses don’t divide and, so far, haven’t made people sick. Most researchers don’t believe that the virus will interfere with the normal liver genes and feel that the risk of causing severe liver damage or cancer is very low,” Ducore said.
With the genes enabling the person’s own liver to make the necessary proteins, plasma increases to a level that’s stable enough to eliminate bleeding risk.
Although there are still multiple trials taking place around the world, results have been life-changing for some of the participants.
“Subjects from the earlier trials who had good responses have successfully come off prophylactic factor replacement therapy, and have had dramatic reductions in bleeding, many with complete cessation of bleeding,” said Pipe, who is a lead investigator of a clinical trial conducted by the biotech company BioMarin. “Some of these clinical trial participants are approaching 10 years out from their treatment and still showing persistent expression. In several recent trials, the clotting factor levels achieved in many of the subjects have been within the normal range for factor VIII and IX,” Pipe said.
“This gives promise for a durable — if not lifelong — correction of the hemophilia. The biggest promise from gene therapy is to liberate patients from the burden and cost of prophylactic therapy,” Pipe added.
In studies with dogs, the clotting factor has successfully been produced for decades, but human trials haven’t been conducted enough to know how long the factor can be produced.
Researchers don’t yet know whether young people can be treated with gene therapy as current trials require all patients to be 18 years or older.
“There are questions about administering these viruses to younger children with growing livers. We don’t know if the liver is the best organ to target for the gene therapy. Factor IX is normally made in the liver, but factor VIII isn’t. We know that people will have immune reactions to the virus and that this can cause mild liver reactions and decrease the amount of factor produced. We don’t know the best way to treat this,” Ducore said.
Grant Hiura, 27, was diagnosed with severe hemophilia A at birth.
He self-infuses every second day. Despite the promising results of gene therapy trials, he’s apprehensive about the potential consequences on the blood disorders community.
“Whenever gene therapy comes up in the world of hemophilia, I always get cautious because that discussion inevitably ends in this very question of ‘ridding’ people of hemophilia,” Hiura told Healthline. “Given how tight knit the bleeding disorders community is, I think there’s a much bigger discussion that needs to be had about how this potential transition from being ‘born with hemophilia’ to being ‘genetically cured of hemophilia’ would play out within the community.”
“What happens if only a select portion of the community is able to access gene therapy?” he added. “How would we view those who have received gene therapy versus those who haven’t?”
Gene therapy, if successful, would provide a clinical cure, but not alter the genetic defect itself. As such, the reproductive inheritance of hemophilia in subsequent generations wouldn’t change.
Ducore says we’ll know more about how effective current gene therapies are for hemophilia in the next five or more years. We should also know whether they can create a better lifelong solution for those living with the disorder.
“Those patients volunteering for these trials are, in many ways, pioneers,” he said. “They’re exploring parts unknown, risking hardships — only some of which are known and only partially understood — in search of a better life, free from frequent injections and restrictions on their activities. We’re learning a lot from these pioneers and believe that the future will be better because of them.” | If left untreated, the bleeding can cause permanent damage.
There’s currently no cure for hemophilia, but patients can be treated with an intravenous clotting factor.
“In hemophilia, patients are missing a single clotting factor protein, either factor VIII or IX, which arrests the progress of the clot formation putting patients at risk for serious bleeding, particularly recurrent bleeding into joints with subsequent development of crippling arthritis,” Dr. Steven Pipe, chair of the Medical and Scientific Advisory Committee of the National Hemophilia Foundation, told Healthline.
“To prevent this pathology, they administer ‘replacement therapy’ by infusing the factor VIII or IX proteins on a regular basis – typically every other day for factor VIII and 2 to 3 times per week for factor IX,” Pipe said.
Replacement therapies have revolutionized outcomes for those with hemophilia, but the treatment is not without its problems.
“When patients born with no expression of factor VIII or IX at birth are exposed to replacement proteins of factor VIII or IX, their immune system can mount a response to what it perceives as a foreign protein,” Pipe said. “These antibodies can inactivate the protein such that it will no longer treat or prevent their bleeding. This happens in up to 30 percent or more of patients with severe hemophilia A (factor VIII deficiency). These inhibitors require alternative but less effective treatments and lead to poorer outcomes for patients.”
In most individuals with hemophilia, regular treatment from infusions can prevent the vast majority of bleeding. But it comes at a heavy cost for both patients and caregivers.
Treatment for infants can begin at 1 year of age or earlier. Parents must learn how to administer treatments that can be as frequent as every second day.
“This comes at a tremendous cost to patients, families, and health systems. We know that joint disease can still appear in young adults and annualized bleeding rates are still not zero. There’s still room for new interventions that could improve patient outcomes even further,” Pipe said.
| no |
Hematology | Can hemophilia be cured? | yes_statement | "hemophilia" can be "cured".. there is a "cure" for "hemophilia". | https://www.ucsfbenioffchildrens.org/conditions/hemophilia | Hemophilia | Conditions | UCSF Benioff Children's Hospitals | Hemophilia
Overview
Hemophilia is a disorder that prevents blood from clotting properly, resulting in bruising and bleeding. Caused by a defective gene, it affects about one in 5,000 boys born in the United States. Although hemophilia typically is inherited, a third of cases may result from a new genetic mutation. In children with hemophilia, one of the 11 blood clotting factors — proteins that help stop bleeding — is missing or reduced.
The most common type of hemophilia, caused by a lack of clotting factor VIII, is called Hemophilia A or classic hemophilia. The second most common type is caused by a lack of clotting factor IX and is called Hemophilia B or Christmas disease, named for Stephen Christmas, the first person diagnosed with the factor IX deficiency. Hemophilia A and B almost always occur in boys. A third, very rare type of hemophilia, called Hemophilia C, is caused by a lack of clotting factor XI and can occur in both girls and boys.
Hemophilia is caused by a mutation in the gene for factor VIII or factor IX. This occurs on the X chromosome, the chromosome inherited from the mother. If there is a family history of hemophilia, the mother is a carrier and her son will have the same type of hemophilia as her relatives. If there is no family history of hemophilia, the child's hemophilia is due to a new mutation and the mother may or may not be a carrier.
At UCSF Benioff Children's Hospital, the pediatric Hemophilia Treatment Center offers the most comprehensive care for children with hemophilia throughout Northern California. Through our research, we also provide the latest advances in treating complications of the disease. UCSF is also a federally designated Hemophilia Comprehensive Care Center, designated by the Centers for Disease Control and Prevention, that cares for both adult and pediatric patients.
Children with hemophilia may qualify for coverage of medical expenses through California Children's Services and the Genetically Handicapped Persons' Program, and if severely disabled, for financial support from the Social Security Administration. A social worker at the Hemophilia Treatment Center can refer you to the appropriate resources.
Contact us
To request an appointment, give us a call.
Forms of hemophilia
Hemophilia may occur in mild, moderate and severe forms, based on both the child's symptoms and the level or amount of clotting factor in the blood.
Mild Hemophilia — A child with mild hemophilia has 6 percent to 49 percent factor level and usually has problems with bleeding only after serious injury, trauma or surgery. In many cases, mild hemophilia is not discovered until a major injury, surgery or tooth extraction results in unusual bleeding. The first episode may not occur until adulthood.
Moderate Hemophilia — A child with moderate hemophilia has 1 percent to 5 percent factor level and has bleeding episodes after injuries, major trauma or surgery. He also may experience occasional bleeding without obvious cause. These are called spontaneous bleeding episodes.
Severe Hemophilia — A child with severe hemophilia has less than 1 percent factor level and has bleeding following an injury or surgery, and may have frequent spontaneous bleeding episodes into the joints and muscles.
A person's severity of hemophilia does not change over time. If a person's cells cannot make clotting factor during childhood, they will not have the ability to make clotting factor during adulthood.
Signs & symptoms
The most common symptom of hemophilia is bleeding, especially into the joints and muscles. When a child with hemophilia is injured, he does not bleed faster than a child without hemophilia. He bleeds longer. He may also start bleeding again several days after an injury or surgery. Small cuts or surface bruises usually are not a problem, but deeper injuries may result in bleeding episodes that can cause serious problems and lead to permanent disability unless treated promptly.
Symptoms of hemophilic bleeding depend on where the bleeding occurs. Infants may have bleeding from their mouth when they are cutting teeth, bite their tongue or tear tissue in their mouth. Toddlers and older children commonly have bleeding into muscles and joints. Symptoms of bleeding include pain, swelling, loss of range of motion and an inability to move or use the affected arm or leg. Usually there is no bruising or discoloration of the skin to indicate that the swelling and pain are due to blood.
Another symptom of hemophilia is easy bruising. Children with hemophilia may have many bruises of different sizes all over their bodies. Other symptoms of bleeding may be a prolonged nosebleed or vomiting of blood.
Diagnosis
The diagnosis of hemophilia is made by blood tests to determine if clotting factors are missing or at low levels, and which ones are causing the problem. If you have a family history of hemophilia, it is important to tell your child's doctors which clotting factor your relatives are missing, since your child will be missing the same one.
If you know you are a carrier, the diagnosis of hemophilia can be made in your newborn soon after birth. Tests to determine if your baby has hemophilia can be run on blood obtained from the umbilical cord or drawn from the newborn's vein. You will be advised to delay some procedures, such as circumcision, until after you learn whether your child has hemophilia.
Some families with a history of hemophilia may want to request prenatal testing, or testing before birth. This testing can be done early in pregnancy, allowing your family to make informed decisions and preparations. UCSF Benioff Children's Hospital has genetic counselors who are available to help you make family planning decisions and arrange for prenatal testing, if desired.
If you are pregnant and think you could be a carrier, or if you have a child diagnosed with hemophilia and you are expecting another child, it is important that you tell your obstetrician that you are at risk for having a child with hemophilia. There are three ways to test if you are a carrier:
Family Tree — Review your family tree. If you have a son with hemophilia and have another son, brother, father, uncle, cousin or grandfather with the disorder, then you are a carrier. No additional tests are needed.
Clotting Factor — Measure clotting factor level in your blood. If it is below 50 percent of normal, you probably are a carrier and have mild hemophilia. If the clotting factor level is above 50 percent, you still may be a carrier, since other conditions can elevate the factor level. Another test may be necessary.
DNA Test — Conduct a DNA test to look for the mutation that caused hemophilia in your son or another relative. It is necessary to obtain samples of blood from your son or relative with hemophilia.
Treatment
The present goal of therapy is to raise factor levels, decrease the frequency and severity of bleeding episodes and prevent the complications of bleeding. This is done by injecting the missing clotting factor into your child's vein soon after he has injury or shows signs of bleeding.
Clotting factor concentrate, also called "factor," is a dried powder form of the clotting factor. It is mixed with water to form a liquid before it is given. Some clotting factor products, called plasma-derived factor, are made from donated human blood plasma. Others, called recombinant factor, are made in a laboratory and do not use human blood proteins. Because recombinant products do not contain human blood, they are much safer since they avoid potential transmission of a virus from donated blood.
When clotting factor is administered, it immediately circulates in the blood so the body can use it to form a blood clot. Once the blood clot is established and the bleeding has stopped, the body begins to reabsorb the blood that has leaked into the tissues and joints.
If your child does not receive prompt treatment, extra blood can pool in the joint or soft tissue and cause pain and swelling that takes longer to go away. Over time, repeated bleeding into a joint can lead to severe joint damage and arthritis. Early treatment will minimize the risk of joint damage.
At first, your child may only need to be treated episodically for bleeding disorders, that is, each time he or she experiences a bleeding episode. However, as the child gets older and becomes more active, the frequency of bleeding episodes may increase. Doctors may recommend giving factor replacement treatments every other day, a therapy regimen called prophylaxis, to prevent most bleeding. Prophylaxis reduces the number of bleeds, but does not prevent all bleeding. The goal of prophylaxis is to make a person with severe hemophilia reach factor VIII or factor IX levels similar to patients with moderate hemophilia, about 1 percent to 5 percent.
Treatments include home therapy, over-the-counter medications and gene therapy.
Home Therapy
All factor treatments are infused or injected intravenously into a child's vein. At first, a child will be treated at a hemophilia treatment center, his doctor's office or an emergency room. Later, parents may be taught how to give the factor at home. Devices, called ports, can be surgically inserted under the skin in the chest area to make it easier to administer clotting factor products.
At first, it is helpful to have your child evaluated and treated for each bleed by your doctor. As your child grows, especially if he has severe hemophilia and bleeds frequently, you may want to learn how to give the factor-replacement treatments at home. Most families find home therapy a fast, easy way to treat a child with frequent bleeds. Moreover, most children who receive treatment at home eventually learn how to do the infusions for themselves. If you have questions or would like to try home therapy, talk to your doctor.
Whether or not your child is on home treatment, you should always have factor concentrate at home to take to the emergency room when your child needs a treatment. If the decision is made to infuse factor to treat your child's bleeding episode, the most important thing you can do is to give it as soon as possible. If there is a delay, however, you can apply ice to help shrink the size of the leaking blood vessels, limit the amount of bleeding into joints or tissues and prevent a small bleed from becoming a larger one. To avoid ice burn, place a cloth, such as a washcloth or a clean diaper, between your child's skin and the ice.
After your child receives factor treatment for a joint bleed, "rest, ice, compression and elevation" or RICE is required. Your child may also benefit from support devices, such as crutches, following a bleed into the knee or ankle or a sling following a bleed into a muscle or joint in the arm. Depending on the site of the bleed, your child may have to limit his activities for a few days after a bleed. Our health care team can help you decide what is right for your child.
Over-the-Counter Medications
Acetaminophen, sold under the brand names Tempra and Tylenol, is recommended as a safe pain reliever for children with hemophilia. Follow the directions carefully and be sure to give your child only the recommended amount of the medicine.
However, never give your child any product with aspirin, or acetylsalicylic acid, in it. Aspirin can interfere with clotting. Many common household remedies, such as Alka-Seltzer, contain aspirin, so read labels very carefully before you give your child any medication. Ibuprofen, such as Advil, Aleve and Motrin, also may interfere with clotting and should not be used by your child. If you have any questions about what is or is not safe for your child to take, talk to your doctor or hemophilia medical staff.
In addition, if your child has a head injury or symptoms of a head injury, do not give him any pain medicine unless your doctor instructs you to do so. Pain medicine can mask symptoms and make it difficult for the doctor to make a diagnosis about the seriousness of the injury.
Gene Therapy
With modern treatment, children born with hemophilia can expect to live a long, full life. Until the 1990s, this was not necessarily the case. But with safe recombinant clotting factors and with the prospect of gene therapy on the horizon, children born today can expect to live into their 70s or 80s.
Unfortunately, there is not yet a cure for hemophilia, though new developments may make a cure possible in the next five to 10 years. Technically, hemophilia can be cured through a liver transplant, but the risks involved in the surgery and the requirement for lifelong medications to prevent rejection of the new liver may outweigh the benefits.
Researchers are currently working on a way to insert the factor VIII or factor IX gene into the cells of patients with hemophilia to produce some clotting factor. People treated with this gene therapy should have fewer bleeding episodes. The present goal of gene therapy is to raise factor levels enough to decrease the frequency and severity of bleeding episodes and to prevent the complications of bleeding. Gene therapy does not replace the altered factor VIII or IX gene on the male's X chromosome. So, the daughters of a man with hemophilia still will be carriers, even if he is treated with gene therapy.
UCSF Benioff Children's Hospitals medical specialists have reviewed this information. It is for educational purposes only and is not intended to replace the advice of your child's doctor or other health care provider. We encourage you to discuss any questions or concerns you may have with your child's provider.
Where to get care (1)
2
Hemophilia Treatment Center
Hemophilia Treatment Center
San Francisco / Oakland
Support services
Child Life
Certified child life specialists ease the stress and anxiety of childhood illness through therapeutic play, schooling and family-focused support.
Family Amenities
Family-friendly amenities help you relax and take care of yourself while staying close to your child. We offer lounges, kitchens, showers, breastfeeding rooms and more.
Family Resource Center
We help families cope with the challenges of childhood illness and hospitalization in a relaxing environment where parents can get a much-needed break.
Individual Playtime & Instruction
If your child can't be around other kids for medical reasons, you can sign up for private sessions in our activity and school rooms. Find out how.
Interpreter Services & Communication Assistance
Interpreter services in many languages and TDDs are available for families that need help communicating with care teams. Here's how to access them.
Music Therapy Program
Board-certified music therapists help kids cope with illness and the feelings that come with it. Find out about group activities and bedside therapy.
Patient Relations
Patient relations reps and nursing supervisors are here to answer questions and address concerns. Learn about your rights, how to reach us and more.
School Program
Our schoolroom services and individual learning programs help children hospitalized at UCSF continue their education and get ready to return to school. | Pain medicine can mask symptoms and make it difficult for the doctor to make a diagnosis about the seriousness of the injury.
Gene Therapy
With modern treatment, children born with hemophilia can expect to live a long, full life. Until the 1990s, this was not necessarily the case. But with safe recombinant clotting factors and with the prospect of gene therapy on the horizon, children born today can expect to live into their 70s or 80s.
Unfortunately, there is not yet a cure for hemophilia, though new developments may make a cure possible in the next five to 10 years. Technically, hemophilia can be cured through a liver transplant, but the risks involved in the surgery and the requirement for lifelong medications to prevent rejection of the new liver may outweigh the benefits.
Researchers are currently working on a way to insert the factor VIII or factor IX gene into the cells of patients with hemophilia to produce some clotting factor. People treated with this gene therapy should have fewer bleeding episodes. The present goal of gene therapy is to raise factor levels enough to decrease the frequency and severity of bleeding episodes and to prevent the complications of bleeding. Gene therapy does not replace the altered factor VIII or IX gene on the male's X chromosome. So, the daughters of a man with hemophilia still will be carriers, even if he is treated with gene therapy.
UCSF Benioff Children's Hospitals medical specialists have reviewed this information. It is for educational purposes only and is not intended to replace the advice of your child's doctor or other health care provider. We encourage you to discuss any questions or concerns you may have with your child's provider.
Where to get care (1)
2
Hemophilia Treatment Center
Hemophilia Treatment Center
San Francisco / Oakland
Support services
Child Life
Certified child life specialists ease the stress and anxiety of childhood illness through therapeutic play, schooling and family-focused support.
| no |
Hematology | Can hemophilia be cured? | yes_statement | "hemophilia" can be "cured".. there is a "cure" for "hemophilia". | https://www.forbes.com/sites/matthewherper/2017/12/09/scientists-could-cure-hemophilia-with-gene-therapy-for-real/ | Excitement Builds Around Gene Therapy Cures For Hemophilia | The New England Journal of Medicine declares a cure for hemophilia is near.
The New England Journal Of Medicine
How enthralled are scientists by the prospects for gene therapy in hemophilia, the deadly disease of uncontrolled bleeding? Ask the usually staid New England Journal of Medicine, which just ran this headline: “A Cure for Hemophilia [is] within Reach.”
It would be one of medicine's holy grails – and they are the talk of the annual meeting of the American Society of Hematology here in Atlanta.
The New England Journal headline – which would have seemed fantasy just a few years ago – is a harbinger of a revolution in hemophilia treatment. A new drug, from Roche, could transform the way many patients are treated. But it’s being followed by gene therapy treatments that use viruses to implant new genes into patients’ cells, potentially making it so they no longer need any treatment. It’s a revolution that’s been a long time coming: The World Health Organization forecast that hemophilia gene therapy was imminent in 1994, and doctors made similar claims to Bloomberg News in 1999. Widespread internet use, the iPhone, and reality TV all happened in the interim. A cure for hemophilia didn’t.
Today's excitement is driven by a study of a gene therapy for the most common form of hemophilia, developed by BioMarin of Notaro, Calif., published in the New England Journal and presented at ASH today, and another of a gene therapy treatment, from Spark Therapeutics and Pfizer, for a less common form of hemophilia, that the journal published last week. Other companies are following those leaders. Says Christiana Bardon, a manager at the venture capital firm MPM Capital and the hedge fund Burrage Capital: “The gene therapy data are looking phenomenal.”
How good were the gene therapy results? “The easiest thing to say is that we were absolutely blown away by them,” says K. John Pasi, of Barts Health NHS Trust and the London School of Medicine and Dentistry, who led the BioMarin study, of 9 patients. The patients all stopped using clotting factors to treat their hemophilia, yet their annualized bleeding rate fell from 16 episodes a year to just one. “Their bleeding rates collapsed to zero or nearly zero and we’ve improved their quality of life beyond recognition,” Pasi says. For the Spark gene therapy, bleeding rates were reduced from 11.1 bleeding events per year to 0.4 bleeding events per year.
Glenn Pierce found that his hemophilia was cured by a liver transplant.
Glenn Pierce, a pharmaceutical researcher who helped design the BioMarin study, says that the change those patients experienced is profound. He knows first hand. He had hemophilia, but was cured by a liver transplant he received because of hepatitis C he’d contracted decades ago. The new liver started making the missing clotting factor, resulting in a surprise cure.
“It’s a remarkable gift to be able to go from thinking about hemophilia every minute of every day to no longer worrying,” Pierce says. “If I stand up from this chair and I feel a little pain in my ankle, I know it is arthritis from all my bleeding episodes. It’s not bleeding. It’s a remarkable change in outlook, in independence, in freedom, to be able to now function without having to think of my hemophilia. That’s what a cure will mean for individuals who are able to achieve that through gene therapy.”
Hemophilia has long been a terrifying disease. Even small cuts and bruises can be deadly, and routine movement can lead patients to bleed into their joints, destroying them. This is the disease that so terrified the last Russian Tsarina that she sought the care of a strange mystic, Rasputin, to care for her son, Alexei. Her faith in a strange mystic helped undermine faith in the royal family, helping lead to the revolution that led to their deaths.
Scientists now know there are two forms of hemophilia, caused by defective genes for two different clotting factors needed to allow blood to coagulate. Both occur almost entirely in men. The more common form, hemophilia A, results from low levels of Factor VIII. It afflicts 16,000 men in the U.S., and more than 320,000 globally, according to the National Hemophilia Foundation. Hemophilia B, caused by a deficiency of clotting factor IX, afflicts about 4,000 Americans and 80,000 men globally. The BioMarin gene therapy treats hemophilia A; the Spark’s results on Thursday were for hemophila B.
Care of hemophiliacs has been transformed by the ability of companies to derive Factor VIII and Factor IX from blood products, and through genetic engineering. These have become multibillion-dollar products, sold by Shire, Novo-Nordisk, and Bioverativ.
One of the problems with these products is that some patients develop antibodies to their clotting factors. These can cause allergic reactions. It also means the clotting factors no longer work. These antibodies are called ‘inhibitors’, and 30% of hemophilia A patients develop them at some point. The usual treatment is to give clotting factor more often, to basically blow past the B cells that are producing the antibodies. This usually works, but in 5% to 10% of patients, other medicines must be used. The annual cost of factors for most hemophilia patients is $400,000 a year, according to Cowen & Co., but for inhibitor patients it is $1 million per patient. This summer, an Iowa insurer blamed its exit from the exchanges run under the Affordable Care Act on a teen with hemophilia whose treatment was costing $1 million a year.
On Nov. 16, the FDA approved Hemlibra, an antibody drug, to treat hemophilia A patients who have antibodies against factor VIII. Its annual list price: $482,000. Factor VIII’s job is to bind together two other clotting factors: factor X and factor IXa. Hemlibra doesn’t resemble factor VIII at all, but mimics this function. The drug is approved for these patients already. Roche also said in November that Hemlibra was superior to factor VIII in patients with hemophilia A whether they had antibodies or not, but the company has yet to approve these results.
If there is a gene therapy revolution about to hit, these patients with inhibitors will have to wait in a long line. The BioMarin study, aside from only including adult patients, did not allow any patients with inhibitors. The reason is that one worry about gene therapy is that it will create antibodies. So far, it hasn’t. But there’s a question of whether gene therapy will work in these patients. It might. After all, says Pierce, the current treatment is to give more factor VIII. “Let’s just build a little bioreactor in the body and build constant amounts of Factor VIII,” he says, “and that would be an excellent way to tolerize a patient to gene therapy.”
But no company is likely to take that step until a product is approved for patients without inhibitors, Pierce says. BioMarin says it conduct two trials of its hemophilia A gene therapy, using slightly different doses. One will begin late this year, and a second early next, with both taking 52 weeks. After that, the company plans to ask for regulatory approval. Analysts think a competing hemophilia A gene therapy from Spark is just six months to a year behind. | It’s not bleeding. It’s a remarkable change in outlook, in independence, in freedom, to be able to now function without having to think of my hemophilia. That’s what a cure will mean for individuals who are able to achieve that through gene therapy.”
Hemophilia has long been a terrifying disease. Even small cuts and bruises can be deadly, and routine movement can lead patients to bleed into their joints, destroying them. This is the disease that so terrified the last Russian Tsarina that she sought the care of a strange mystic, Rasputin, to care for her son, Alexei. Her faith in a strange mystic helped undermine faith in the royal family, helping lead to the revolution that led to their deaths.
Scientists now know there are two forms of hemophilia, caused by defective genes for two different clotting factors needed to allow blood to coagulate. Both occur almost entirely in men. The more common form, hemophilia A, results from low levels of Factor VIII. It afflicts 16,000 men in the U.S., and more than 320,000 globally, according to the National Hemophilia Foundation. Hemophilia B, caused by a deficiency of clotting factor IX, afflicts about 4,000 Americans and 80,000 men globally. The BioMarin gene therapy treats hemophilia A; the Spark’s results on Thursday were for hemophila B.
Care of hemophiliacs has been transformed by the ability of companies to derive Factor VIII and Factor IX from blood products, and through genetic engineering. These have become multibillion-dollar products, sold by Shire, Novo-Nordisk, and Bioverativ.
One of the problems with these products is that some patients develop antibodies to their clotting factors. These can cause allergic reactions. It also means the clotting factors no longer work. These antibodies are called ‘inhibitors’, and 30% of hemophilia A patients develop them at some point. | yes |
Hematology | Can hemophilia be cured? | yes_statement | "hemophilia" can be "cured".. there is a "cure" for "hemophilia". | https://www.hemophilia.on.ca/resources/faqs/ | FAQs - Hemophilia Ontario | What is hemophilia?
Hemophilia is an inherited bleeding disorder caused by little or no clotting factor in the blood. Clotting factors are proteins that are vital to stop bleeding when it occurs. Deficiency of clotting factors results in prolonged bleeding. Top ↑
What are the different types of hemophilia?
There are several types of clotting factor. Based on the clotting factor affected, there are three main types of hemophilia:
Hemophilia A is caused by missing or defective clotting factor VIII Hemophilia B is caused by the deficiency of clotting factor IX Hemophilia C is caused by the defective or missing clotting factor XI Top ↑
What is acquired hemophilia?
Acquired hemophilia is a rare type of autoimmune condition in which the body mistakenly attacks its own clotting factors. It usually develops later in life and often resolves with proper treatment. Top ↑
How is hemophilia inherited?
Humans have 22 pairs of chromosomes called the autosomes that are identical in men and women. One pair of chromosomes, called the sex chromosome, determines a person’s gender.
The inheritance pattern of hemophilia depends on which chromosome the affected gene is located on.
The genes affected in hemophilia A and B are located on the X-chromosome. Therefore, they are inherited in an X-linked pattern. Men are at a higher risk of developing hemophilia A and B because they only have one X chromosome.
Hemophilia C is caused by a mutation in a gene located on chromosome 4, an autosome. Therefore, both men and women have the same risk of inheriting the mutation and being affected by hemophilia C. Top ↑
What is the life expectancy?
The life expectancy of people with hemophilia depends on the severity of the condition and whether or not the patient receives adequate treatment. With proper care, the life expectancy of people with hemophilia is about 10 years less than those without the disease. Top ↑
What are the symptoms?
The most common symptoms of hemophilia are excessive bleeding and easy bruising due to internal bleeding. Bleeding can affect different parts of the body and can be seen as:
Frequent nose bleeds Heavy bleeding after an injury Large bruises Blood in the urine and stool due to kidney, bladder, or intestinal bleeding Bleeding in the joints, causing joint tightness with or without pain Bleeding in the brain, known as brain hemorrhage or brain stroke, which can cause headache, vomiting, stiff neck, blurred vision, and loss of muscle coordination. The type and severity of the symptoms vary from person to person. Top ↑
How is hemophilia diagnosed?
Hemophilia is diagnosed using a blood test to measure the levels of clotting factors and their activity in the blood.
Prenatal genetic testing can help diagnose hemophilia in cases in which parents are known to be carriers of the condition. Chorionic villus sampling can be done between nine and 11 weeks of pregnancy, and fetal blood sampling at 19 weeks or more. Top ↑
How is hemophilia treated?
The primary treatment for hemophilia is replacement therapy, in which the missing clotting factor is administered to the body through injection. Other approved treatments include hormone therapy — such as desmopressin — that stimulate the production of clotting factors and bypassing agents in cases in which the body develops antibodies against clotting factors. Several experimental treatments also are under evaluation. Top ↑
Can hemophilia be cured?
There currently is no cure for hemophilia. However, the condition can be managed effectively with proper treatment. Top ↑
How is the severity of hemophilia determined?
The level of clotting factor in the blood determines the severity of hemophilia. The lower the levels, the more severe the condition.
In mild hemophilia, clotting factor levels are between 5% and 40% (0.05-0.40 IU/ml). In moderate hemophilia, clotting factor levels are between 1% and 5% (0.01-0.05 IU/ml). In severe hemophilia, clotting factor levels are less than 1% (0.01 IU/ml). The rate of bleeding differs based on the severity of the condition. People with severe hemophilia bleed frequently and for no specific reason. Those with moderate hemophilia bleed less frequently and spontaneously and usually only as a result of injury. In cases of mild hemophilia, excessive bleeding usually occurs only as a result of surgery or a major injury. Top ↑
Is hemophilia contagious?
No. Hemophilia is an inherited condition and cannot be spread through physical contact. Top ↑
Are there any medication that patients should avoid?
People with hemophilia should not take aspirin or any other blood thinner. Aspirin prevents blood cells called platelets from clumping together and forming blood clots. It can make bleeding worse in hemophilia patients. Top ↑
Is it safe to exercise?
Sports and exercise can help strengthen the muscles and prevent bleeding. Therefore, individuals with hemophilia are encouraged to incorporate frequent exercise in their routine. Sports with a high risk of injuries, such as boxing, football, or rugby are not recommended, however. People with hemophilia should consider the severity of their disease when planning their exercise routine and choosing a sport. Top ↑
Where can I find more information?
Comprehensive information about hemophilia and its different treatment options, as well as news about research and ongoing clinical trials, can be found on this website.
What does it mean to be a carrier of Hemophilia?
Women can be carriers of the hemophilia gene. Some women may know they are carriers while others may not. Women can experience bleeding symptoms as carriers of hemophilia, even though they may think they do not have a bleeding disorder. If you think you might be a carrier of the hemophilia gene, talk with your doctor about being tested. If you are a carrier of the hemophilia gene, feel free to contact us to gain support and education from our community. Top ↑
What is von Willebrand Disease (vWD)?
Women can be carriers of the hemophilia gene. Some women may know they are carriers while others may not. Women can experience bleeding symptoms as carriers of hemophilia, even though they may think they do not have a bleeding disorder. If you think you might be a carrier of the hemophilia gene, talk with your doctor about being tested. If you are a carrier of the hemophilia gene, feel free to contact us to gain support and education from our community. Top ↑
What is a Platelet Function Disorder?
Bleeding symptoms in women can also be attributed to platelet function disorders. Platelet function disorders can be inherited or acquired and they occur when the platelets do not function properly and cause bleeding issues. Top ↑ | Other approved treatments include hormone therapy — such as desmopressin — that stimulate the production of clotting factors and bypassing agents in cases in which the body develops antibodies against clotting factors. Several experimental treatments also are under evaluation. Top ↑
Can hemophilia be cured?
There currently is no cure for hemophilia. However, the condition can be managed effectively with proper treatment. Top ↑
How is the severity of hemophilia determined?
The level of clotting factor in the blood determines the severity of hemophilia. The lower the levels, the more severe the condition.
In mild hemophilia, clotting factor levels are between 5% and 40% (0.05-0.40 IU/ml). In moderate hemophilia, clotting factor levels are between 1% and 5% (0.01-0.05 IU/ml). In severe hemophilia, clotting factor levels are less than 1% (0.01 IU/ml). The rate of bleeding differs based on the severity of the condition. People with severe hemophilia bleed frequently and for no specific reason. Those with moderate hemophilia bleed less frequently and spontaneously and usually only as a result of injury. In cases of mild hemophilia, excessive bleeding usually occurs only as a result of surgery or a major injury. Top ↑
Is hemophilia contagious?
No. Hemophilia is an inherited condition and cannot be spread through physical contact. Top ↑
Are there any medication that patients should avoid?
People with hemophilia should not take aspirin or any other blood thinner. Aspirin prevents blood cells called platelets from clumping together and forming blood clots. It can make bleeding worse in hemophilia patients. Top ↑
Is it safe to exercise?
Sports and exercise can help strengthen the muscles and prevent bleeding. Therefore, individuals with hemophilia are encouraged to incorporate frequent exercise in their routine. | no |
Hematology | Can hemophilia be cured? | yes_statement | "hemophilia" can be "cured".. there is a "cure" for "hemophilia". | http://scienceline.ucsb.edu/getkey.php?key=5767 | UCSB Science Line | It would be great if there were a simple cure for
hemophilia. As you know, people with hemophilia
have blood that does not clot well. They can
have severe bleeding, even from a small injury.
Some diseases can be cured by killing the bacteria
that causes them. Some diseases can be prevented
with vaccines against viruses. But Hemophilia
is not caused by a germ.
Hemophilia is caused by a small problem in the
DNA (mutation). There are many proteins
involved in making our blood clot. If the recipe
for even one of these proteins is changed,
clotting may be slow, or less effective, or not
happen at all.There are actually many types of
hemophilia depending on which protein recipe
(gene) has a mutation. Safely giving a person
a missing gene is not easy. The gene has to get to
the right kind of cells without damaging the cells
and causing other problems, like cancer. No one
has found a solution to that problem yet.
Right now, there are only treatments, not
cures. A person with hemophilia might need
platelets or proteins called clotting
factors. Platelets are pieces of special blood
cells. They help to plug up a wound. Clotting
factors work with the platelets to make a better
plug. One treatment takes clotting factors from
the plasma of healthy people and gives them to
people with hemophilia. Clotting factors can also
be produced by other animals and given to people.
Other times, people get platelets from donors.
I am a platelet donor. Once every few weeks, I go
to our local blood center and spend an hour or two
reading while a machine takes my blood, separates
out the platelets, and returns the rest of the
blood to my vein. Some of the people who get my
platelets have hemophilia. Some have cancer.
Some may have had an accident or surgery that used
up all of their own platelets. Others have other
blood diseases. Sometimes they take plasma too.
They can get clotting factors from my plasma.
Most of the genes that help with clotting are on
the X chromosome. This means that males are much
more likely than females to have hemophilia.Can
you figure out why?
You may want to study physiology or genetics to
learn more about hemophilia.
Thanks for asking,
Answer 2:
Hemophilia is a blood disease that is caused
by a mutation in DNA. DNA or
deoxyribonucleic acid is the genetic code
found in almost all the cells in your body and
provides the information needed for your body to
function. One of these functions is the ability to
clot blood when you get a cut. Mutations
are changes that happen in the DNA letters A, T,
G, and C that make up the DNA code.
For example, a mutation might result in an A
instead of a G. A lot of times this is not a
problem but sometimes it can cause lots of
problems and result in a disease like
hemophilia.
Since the cause of hemophilia is an actual
change in your DNA it is not an easy fix. We
can treat people with hemophilia by giving them
medicine that helps them clot blood but right
now there is no cure. We would have to change
the genetic sequence of the person to permanently
cure them. We would need to introduce a non-
mutated, "correct" form of the specific gene that
is causing the hemophilia in order to cure
someone. There are also different forms of
hemophilia that result from mutations in different
genes.
Fortunately scientists have been developing
different ways to be able to help people with
problems with their DNA. They will hopefully
be able to replace mutated genes with healthy ones
in the future.
Answer 3:
This is a really complicated question because the
biology of diseases is naturally complex. Human
bodies are never totally isolated and always have
multiple factors that determine how they react
when something goes wrong. Hemophilia cannot be
cured because it is a genetic disorder. This
means that the problem comes from an error in a
person’s DNA. Since every single cell in a
person’s body has their own copy of DNA, every
single cell has the same disorder. Repairing
broken or incorrect DNA is really hard for
scientists because DNA is protected and guarded in
the cell’s nucleus. Although scientists have a
few ways to alter or rewrite DNA, the technique
isn’t perfect enough to be used on humans yet.
Furthermore, it would be almost impossible to edit
every single cell in a person’s body to eliminate
the disorder entirely. This idea is really
complicated but considering ideas like these are
the first steps to becoming scientist! Thank
you for the question!
Answer 4:
It's genetic. People with hemophilia lack a
protein that causes blood to clot. Their
bodies cannot make this protein because the copy
of the gene that they carry and which is
responsible for this protein is defective. Because
it's not possible currently to alter a person's
DNA in a controlled fashion, hemophilia is
incurable.
In the future, it may be possible to insert a
working copy of the gene onto a virus and then use
the virus to implant the working gene into the
patient's genome. This would cure hemophilia and a
number of other bad genetic diseases.
Answer 5:
Hemophilia is a genetic disease that results
in uncontrolled bleeding after an injury.
Usually when someone gets a cut, the blood vessel
will get blocked which is called clotting.
This stops the blood from flowing out of the cut.
Blood clotting is a very complex process that
involves a lot of parts. In hemophilia, one of
those parts doesn’t work right so the entire
clotting process doesn’t work. To treat people,
you can give them the broken parts of the clotting
process, but they need to be given really
often. People are generally born with hemophilia
and get it from their parents. The best way to
prevent hemophilia is to fertilize the embryo
outside the body, check it for hemophilia, and
then implant it in a women’s uterus. This is not
generally how children are conceived so for the
most part the disease can’t be prevented.
The only way to cure the disease would be to
teach the body how to make the right parts of the
clotting process. This is called gene
therapy and involves genetically engineering a
person. Gene therapy is not generally used since
it’s still being developed and some people don’t
like the idea of changing a person’s genes.
Although, someday many genetic diseases may be
cured with gene therapy. | We would have to change
the genetic sequence of the person to permanently
cure them. We would need to introduce a non-
mutated, "correct" form of the specific gene that
is causing the hemophilia in order to cure
someone. There are also different forms of
hemophilia that result from mutations in different
genes.
Fortunately scientists have been developing
different ways to be able to help people with
problems with their DNA. They will hopefully
be able to replace mutated genes with healthy ones
in the future.
Answer 3:
This is a really complicated question because the
biology of diseases is naturally complex. Human
bodies are never totally isolated and always have
multiple factors that determine how they react
when something goes wrong. Hemophilia cannot be
cured because it is a genetic disorder. This
means that the problem comes from an error in a
person’s DNA. Since every single cell in a
person’s body has their own copy of DNA, every
single cell has the same disorder. Repairing
broken or incorrect DNA is really hard for
scientists because DNA is protected and guarded in
the cell’s nucleus. Although scientists have a
few ways to alter or rewrite DNA, the technique
isn’t perfect enough to be used on humans yet.
Furthermore, it would be almost impossible to edit
every single cell in a person’s body to eliminate
the disorder entirely. This idea is really
complicated but considering ideas like these are
the first steps to becoming scientist! Thank
you for the question!
Answer 4:
It's genetic. People with hemophilia lack a
protein that causes blood to clot. Their
bodies cannot make this protein because the copy
of the gene that they carry and which is
responsible for this protein is defective. Because
it's not possible currently to alter a person's
DNA in a controlled fashion, hemophilia is
incurable.
| no |
Hematology | Can hemophilia be cured? | no_statement | "hemophilia" cannot be "cured".. there is no "cure" for "hemophilia". | https://ashpublications.org/bloodadvances/article/2/20/2780/16101/Implementing-emicizumab-in-hemophilia-inhibitor | Implementing emicizumab in hemophilia inhibitor management ... | Hemophilia is an X-linked bleeding disorder characterized by deficiency of factor VIII (FVIII), known as hemophilia A, or FIX, known as hemophilia B, which left untreated results in early death and permanent disability. Currently, patients receiving clotting factor replacement concentrates (CFCs) can expect to have healthy joints and a normal life expectancy.1 Unfortunately, a common complication of CFCs is the development of neutralizing antibodies (inhibitors), which render factor therapy ineffective. For inhibitor patients, bleeding can be treated either episodically or prophylactically with bypassing agents (activated prothrombin complex concentrates [APCC; FEIBA, Shire, Dublin, Ireland] or recombinant activated factor VII [rFVIIa; Novoseven, Novo Nordisk, Bagsvaerd, Denmark]); however, these agents are not as effective as replacing the missing factor with CFCs.2 As such, patients with inhibitors have both worse morbidity3,4 and mortality.5 Thus, the major goal for such patients is eradicating the inhibitor. The only known effective approach to achieve this involves repeated injections of CFCs, a treatment modality called immune tolerance induction (ITI). Considering the subject of this debate, the remainder of the discussion will be restricted to inhibitors in hemophilia A. More specifically, this therapy involves daily or every-other-day injection of CFC, and as ITI is usually conducted in young children, a central venous catheter (CVC) is often required, and the treatment burden and costs are very high. Finally, this approach is effective in ∼70% of cases but is lower (∼40%) in an intention-to-treat analysis demonstrating the difficulty of adhering to ITI.6 Although achieving a higher success rate is an important goal for the future, ITI, nevertheless, remains the most effective way to eradicate inhibitors.
Recently, a novel bispecific antibody (emicizumab-kxwh, Hemlibra; Roche, Basel, Switzerland) was licensed in the United States and Europe for the prevention of bleeding in hemophilia A patients with inhibitors. This agent has demonstrated remarkable reductions in bleeding episodes in adolescents/adults in the HAVEN 1 study7 and even more dramatic results in the ongoing pediatric HAVEN 2 study.8 Prior to the availability of this drug, a debate such as this would not even be considered, and it is quite remarkable that the mere idea of not recommending ITI to all patients is even being discussed and a testament to the efficacy demonstrated in the emicizumab clinical trials.
With this in mind, there are several arguments, however, in favor of continuing to recommend ITI (Table 1). First, the mortality of inhibitor patients remains higher than those without inhibitors and is directly attributed to bleeding events.5 Second, treatment of breakthrough bleeding episodes in patients with emicizumab has resulted in serious adverse events, problems not encountered in noninhibitor patients treated with CFCs. Third, patients with inhibitors are not eligible for gene therapy trials, and when commercialized, the presence of an inhibitor may disqualify a patient from a potentially curative therapy. Finally, with such a novel therapy as emicizumab, there remains uncertainty regarding the long-term outcomes of patients who would be left with lifelong (no ITI) inhibitors.
Table 1.
Pros and cons of ITI vs emicizumab without ITI
.
Pros
.
Cons
.
Mortality
Patients with inhibitors have increased mortality.
Data regarding mortality predate the licensure of emicizumab and may not apply with emicizumab available.
Breakthrough bleeding treatment
Treatment of breakthrough bleeding is much simpler, safer, and less costly with factor replacement than with bypassing agents.
Emicizumab is a novel agent, and only ∼400 patients have ever received it. It is always possible that unforeseen adverse events could occur. Treatment with factor replacement is known to be very safe (with the exception of inhibitor formation).
The mechanism of action of substituting for FVIIIa suggests nonthrombotic-type events should not occur or be rare. Monoclonal antibodies have been in widespread use for several decades, and unforeseen side effects are uncommon.
Gene therapy
Gene therapy when it becomes available may not be effective in patients with active inhibitors but could be effective in patients who have been tolerized.
Some animal data suggest that gene therapy could lead to tolerization when active inhibitors are present.
.
Pros
.
Cons
.
Mortality
Patients with inhibitors have increased mortality.
Data regarding mortality predate the licensure of emicizumab and may not apply with emicizumab available.
Breakthrough bleeding treatment
Treatment of breakthrough bleeding is much simpler, safer, and less costly with factor replacement than with bypassing agents.
Emicizumab is a novel agent, and only ∼400 patients have ever received it. It is always possible that unforeseen adverse events could occur. Treatment with factor replacement is known to be very safe (with the exception of inhibitor formation).
The mechanism of action of substituting for FVIIIa suggests nonthrombotic-type events should not occur or be rare. Monoclonal antibodies have been in widespread use for several decades, and unforeseen side effects are uncommon.
Gene therapy
Gene therapy when it becomes available may not be effective in patients with active inhibitors but could be effective in patients who have been tolerized.
Some animal data suggest that gene therapy could lead to tolerization when active inhibitors are present.
With respect to mortality, a number of studies have evaluated this important issue in inhibitor patients with mixed results9-12; however, the largest and most recent study was conducted in the United States utilizing the Centers for Disease Control Surveillance system.5 More than 7000 males with hemophilia were included in this retrospective analysis including 432 deaths. Importantly, patients who were tolerized were not considered as inhibitor patients in this study. In the multivariate analysis, inhibitor patients had a 70% higher likelihood of dying, and bleeding as a cause of death was more than threefold higher than for noninhibitor patients. Perhaps this alone is sufficient evidence to warrant that every new inhibitor patient undergo ITI.
As described, emicizumab has demonstrated remarkable efficacy at preventing bleeding in inhibitor patients with reductions of 87% and 79% compared with episodic and prophylactic bypassing agent therapy, respectively.7 Perhaps even more relevant is the 99% reduction in bleeding seen in HAVEN 2 as this pediatric study more closely reflects the patient population that would undergo ITI.8 Nevertheless, breakthrough bleeding, surgical procedures, and episodes of trauma will occur necessitating treatment with bypassing agents, and when bypassing agents (particularly APCC) were administered to patients on the HAVEN 1 trial, serious thrombotic events occurred in 2 subjects, and thrombotic microangiopathy (TMA) occurred in 3 subjects approximating 5% of the study population. It should be noted that these events occurred when APCC was used at relatively high doses (>100 IU/kg per day) for >24 hours. There have been no known occurrences of TMA when treating noninhibitor (or tolerized) patients for bleeding with CFCs. Furthermore, although thrombosis has occurred in hemophilia patients, it is exceedingly rare and generally provoked by CVCs or surgical procedures. In essence, treatment with CFCs in noninhibitor patients is extremely safe, whereas treatment of bleeding in inhibitor patients either with bypassing agents or, in particular, with bypassing agents concomitantly with emicizumab carries with it a thrombotic risk. Accordingly, it should be noted that APCC and rFVIIa both carry black box warnings for the risk of thrombosis, and emicizumab has a black box warning regarding thrombosis and TMA when it is combined with APCC. As such, avoiding bypassing agents (with or without emicizumab) is an important goal in the management of inhibitor patients, and this can only be accomplished if ITI is performed successfully.
The next reason to pursue ITI is perhaps more theoretical currently but involves the potential for a future phenotypic cure of hemophilia. Recently, noteworthy results from early clinical trials for a FVIII gene therapy approach were reported whereby 13 subjects treated with the 2 highest doses achieved sustained normal factor levels; that is, they were cured of hemophilia.13 This trial excluded patients both with current and a history of inhibitors. Assuming this therapy becomes commercially available (possibly in the next 5 years), adult patients with hemophilia A without inhibitors could opt for this curative approach. Although animal studies have suggested that gene therapy could lead to immune tolerance in dogs with inhibitors,14 the prospect that this will occur in humans is entirely unclear. Until such data are demonstrated in humans (and this will take years to generate), the safest assumption is that gene therapy will not be made available to patients with active inhibitors. Thus, pursuing ITI for all inhibitor patients should remain the goal so as not to end up with a cohort of young men who could be ineligible to be cured of hemophilia.
Finally, we are left with what could be called “unknown unknowns,” that is, the uncertainty that emicizumab may result in unexpected and unintended harmful consequences. Taking the extensive preclinical data, the mechanism of action, and the fact that >200 inhibitor patients have been treated (some for >2 years), it is entirely possible, if not likely, that emicizumab will not lead to unexpected untoward effects, but only several years more of data can entirely remove this uncertainty inherent to all new technologies. Thus, until such data are generated, the prospect of abandoning ITI in favor of emicizumab alone should be undertaken with this, albeit, theoretical concern.
For those patients who do undergo ITI and are successful, we are, unfortunately, left with a quandary. In the current situation, all patients who are tolerized continue on FVIII therapy in the form of prophylaxis with the express goal of bleed prevention; however, this ongoing exposure to FVIII is also achieving the goal of maintaining tolerance. Little to nothing is known about the consequences of achieving tolerance and then purposefully abandoning FVIII prophylaxis. In other words, once tolerance is achieved, is it lifelong, or will inhibitors recur in the absence of continued exposure to FVIII? At this time and given the available information, one cannot recommend to simply use emicizumab alone in tolerized patients, meaning that patients will still need to continue FVIII therapy. The research questions that must be addressed in order to inform decision making in the future include an understanding of first whether continued, regular exposure to FVIII is necessary, and if so, what is the least burdensome way this can be achieved? How infrequent could it be done? Can a subcutaneous approach be used solely for the maintenance of tolerance?
Although I have argued in favor of continuing to pursue ITI in new inhibitor patients rather than treating them exclusively with emicizumab, it should be pointed out that these 2 approaches are not mutually exclusive. Although patients on ITI were excluded from HAVEN 1 and HAVEN 2, the labeled indication does not exclude concomitant treatment with ITI and emicizumab. Importantly, such therapy should be safe given the mechanism of action of emicizumab and CFCs.15 In fact, considering the high risk for bleeding during ITI as has been demonstrated6 and the joint damage that such bleeds can result in, an entirely new approach to ITI makes perfect sense. The International ITI study demonstrated equal efficacy for the success of ITI between a high-dose daily regimen and a low-dose every-other-day regimen.6 The study was discontinued early because of a higher bleeding rate in the low-dose arm; however, the low-dose arm is less burdensome and far less expensive as it utilizes only 12.5% of the factor needed in the high-dose regimen. Furthermore, the low-dose regimen could potentially avoid the use of CVCs. Thus, low-dose ITI coupled with emicizumab could result in successful tolerization while preventing bleeding and preserving joint function. Based on the cost of ITI in the United States, this combined approach would be less expensive than the high-dose ITI approach. Alternatively, emicizumab alone could ultimately reduce the cost of care for inhibitor patients in general including those for whom ITI is not performed because the overall costs of ITI while not formally studied in comparison with emicizumab alone are likely substantially higher.
In summary, inhibitor eradication remains the most important goal of the management of inhibitor patients given the higher mortality, risks associated with treating breakthrough bleeding, and preserving the prospect for gene therapy. Prevention of bleeding during the long course of ITI is also important such that tolerized patients do not emerge from ITI with permanently damaged joints. Emicizumab has shown a remarkable ability to prevent bleeding particularly in the younger age group, the same age group that presents with inhibitors. Thus, moving forward, novel approaches to achieve tolerance, perhaps with even lower doses or alternative administration routes, in combination with emicizumab to prevent bleeding should be a goal for future research.
Acknowledgments
The author thanks Steven Pipe and Rolf Ljung, both of whom contributed to the ideas in this opinion piece. These ideas emerged during a debate the 3 of us participated in regarding the future of ITI during a scientific meeting held in March 2018.
Authorship
Contribution: G.Y. wrote the paper.
Conflict-of-interest disclosure: G.Y. has received honoraria and consulting fees from Genentech/Roche, Novo Nordisk, and Shire, all of whose products are discussed in the manuscript. | Hemophilia is an X-linked bleeding disorder characterized by deficiency of factor VIII (FVIII), known as hemophilia A, or FIX, known as hemophilia B, which left untreated results in early death and permanent disability. Currently, patients receiving clotting factor replacement concentrates (CFCs) can expect to have healthy joints and a normal life expectancy.1 Unfortunately, a common complication of CFCs is the development of neutralizing antibodies (inhibitors), which render factor therapy ineffective. For inhibitor patients, bleeding can be treated either episodically or prophylactically with bypassing agents (activated prothrombin complex concentrates [APCC; FEIBA, Shire, Dublin, Ireland] or recombinant activated factor VII [rFVIIa; Novoseven, Novo Nordisk, Bagsvaerd, Denmark]); however, these agents are not as effective as replacing the missing factor with CFCs.2 As such, patients with inhibitors have both worse morbidity3,4 and mortality.5 Thus, the major goal for such patients is eradicating the inhibitor. The only known effective approach to achieve this involves repeated injections of CFCs, a treatment modality called immune tolerance induction (ITI). Considering the subject of this debate, the remainder of the discussion will be restricted to inhibitors in hemophilia A. More specifically, this therapy involves daily or every-other-day injection of CFC, and as ITI is usually conducted in young children, a central venous catheter (CVC) is often required, and the treatment burden and costs are very high. Finally, this approach is effective in ∼70% of cases but is lower (∼40%) in an intention-to-treat analysis demonstrating the difficulty of adhering to ITI.6 Although achieving a higher success rate is an important goal for the future, ITI, nevertheless, remains the most effective way to eradicate inhibitors.
| no |
Hematology | Can hemophilia be cured? | no_statement | "hemophilia" cannot be "cured".. there is no "cure" for "hemophilia". | https://www.chula.ac.th/en/highlight/95180/ | “Hemophilia” – a Disease that May Not Be Cured But Opportunities ... | News & Updates
Knowledge
“Hemophilia” – a Disease that May Not Be Cured But Opportunities for a Good Life Are Still Possible
22 December 2022
Writer Kanitha Chancharoen
Patients suffering from Hemophilia, a genetic disease that lasts throughout one’s lifetime and has no long-term cure can still expect a quality of life. A Chula medical specialist recommends preventive replacement factor treatment that uses an application to record abnormal bleeding along with regular communication with one’s physician.
Bleeding when one is wounded is a common occurrence for everyone. Yet there are cases where a person experiences bleeding without having had any cuts or wounds. There can also be instances of bleeding without any wounds or only a slight injury and the bleeding shows no sign of stopping especially in the joints or muscles. These symptoms shouldn’t be ignored since they might mean that a person has Hemophilia.
Dr. Chatphatai Moonla, General Medicine Instructor, General Practitioner in Hematologic Diseases, Division of General Medicine, King Chulalongkorn Memorial Hospital explains that “Hemophilia is a genetic disease that is found only in males. Out of a population of ten to twenty thousand, one hemophiliac might be found. This disease is caused by a genetic disorder that impairs the body’s ability to make blood clot. Patients usually display abnormal bleeding patterns from the time of their birth while in some cases they are found in their childhood or adolescence if they experience joint bleeds or easy bruising during the motor development process.”
At present, around 1,800 people suffer from Hemophilia but it is hoped that more patients can be diagnosed, especially those displaying only mild symptoms. This would require more awareness among the public and medical professionals in all areas to realize the importance of detecting this disease.
What causes Hemophilia
Hemophilia is caused by a disorder of the gene that creates the coagulation factor which is called factor for short. There are two important factors: factor VIII and factor IX. Those lacking factor VIII have hemophilia A and those without factor IX have hemophilia B. In 2020, Thailand had 1,600 patients with hemophilia A and 200 with hemophilia B.
Dr. Chatphatai explained that hemophilia A and B are both X-linked recessive disorders which is why it affects males who acquire the X hemophiliac chromosome from their mothers while females with the hemophiliac gene are carriers but asymptomatic.
How much bleeding indicates that it’s hemophilia?
Characteristic symptoms for hemophilia vary according to severity. 80-100 percent of the bleeding is joint bleeding whereas 10-20% is muscle bleeding that happens after an accident or collision such as in a sports tournament. The severity of the disease depends on the level of factor VII or factor IX and can be divided into 3 levels as follow:
Severe hemophilia symptoms (factor level less than 1 percent)
usually show signs of bruising on their bodies from the time they are very young, and experience joint or muscle bleeding without having had an accident or collision.
Moderate hemophilia symptoms (factor level of 1-5 percent)
will experience joint or muscle bleeding after only a slight accident. In only some cases will they experience joint bleeds on their own.
Slight hemophilia symptoms (factor level between 5-40 percent)
usually don’t bleed on their own but will find it hard to stop the bleeding after an accident or surgical procedure like tooth extraction, for example.
Easy bleeding makes life difficult.
Patients with hemophilia have to be extra cautious in avoiding crashes and collisions. This affects their way of life, especially for those in their childhood where active fun and games are a part of their physical development and learning process.
“Active kids who take part in strenuous physical activities that affect their muscles and joints may encounter situations of bleeding. Many need to refrain from such activities and some need to be absent from school whenever they start bleeding and require treatment. Those who fail to receive treatment when they are young will go through osteoarthritis or joint impairments that adversely affect their way of life and put them in need of caregiver’s assistance and worse yet, disabilities leading to them being crippled.”
Diagnosis of hemophilia
Dr. Chatphatai advises male babies born to families with a history of hemophilia to be tested for the disease by way of assessing their blood clot ability and factor levels of factor VII and IX from the time of their birth or during infancy.
“A family with a child who shows abnormal bleeding in the joints or muscles or has bleeding marks on the skin after only a small bump should bring the baby to his pediatrician for assessment.”
“Patients showing slight or moderate signs who encounter bruising or bleeding in the joints or muscles, or those who continue to bleed after a tooth extraction or surgery should make sure to see their physician for further diagnosis as well.”
Forms of treatment to ensure a better quality of life
We have yet to find a cure for hemophilia but there are two forms of treatment available – treatment and prevention of bleeding episodes.
“Prevention is the best form of treatment which is done by replacing the missing blood clotting factors 2-3 or more times a week. Here in Thailand, there are still some limitations based on budgetary concerns whereas in some foreign countries, factors could be given every other day to prevent abnormal bleeding and successfully delay joint osteoarthritis.”
Since care for hemophilia patients needs to be done continuously throughout the patient’s lifetime, systems and technologies have therefore been developed to help both the patients and their doctors to follow up on their symptoms and provide extended care. Various applications such as the HemMobile recommended by King Chulalongkorn Memorial Hospital have been tested on patients. The application works like a personal assistant for the patient recording all instances of abnormal bleeding and factor injections onto the application that will process that data onto the physician to observe the patient’s bleeding patterns leading to greater accuracy and appropriate treatment.”
“Care for a hemophiliac is a lifelong process. The patient and his family must understand the disease as well as the treatment. The team of doctors treating the patient must be knowledgeable and engage in a close relationship with the patient. This will ensure that the patient will receive appropriate care in the long run and be able to live with hemophilia while enjoying a good quality of life, especially for children who should be able to grow up with a strong life and with the least occurrences of osteoarthritis.” Dr. Chatphatai concluded. | News & Updates
Knowledge
“Hemophilia” – a Disease that May Not Be Cured But Opportunities for a Good Life Are Still Possible
22 December 2022
Writer Kanitha Chancharoen
Patients suffering from Hemophilia, a genetic disease that lasts throughout one’s lifetime and has no long-term cure can still expect a quality of life. A Chula medical specialist recommends preventive replacement factor treatment that uses an application to record abnormal bleeding along with regular communication with one’s physician.
Bleeding when one is wounded is a common occurrence for everyone. Yet there are cases where a person experiences bleeding without having had any cuts or wounds. There can also be instances of bleeding without any wounds or only a slight injury and the bleeding shows no sign of stopping especially in the joints or muscles. These symptoms shouldn’t be ignored since they might mean that a person has Hemophilia.
Dr. Chatphatai Moonla, General Medicine Instructor, General Practitioner in Hematologic Diseases, Division of General Medicine, King Chulalongkorn Memorial Hospital explains that “Hemophilia is a genetic disease that is found only in males. Out of a population of ten to twenty thousand, one hemophiliac might be found. This disease is caused by a genetic disorder that impairs the body’s ability to make blood clot. Patients usually display abnormal bleeding patterns from the time of their birth while in some cases they are found in their childhood or adolescence if they experience joint bleeds or easy bruising during the motor development process.”
At present, around 1,800 people suffer from Hemophilia but it is hoped that more patients can be diagnosed, especially those displaying only mild symptoms. This would require more awareness among the public and medical professionals in all areas to realize the importance of detecting this disease.
What causes Hemophilia
Hemophilia is caused by a disorder of the gene that creates the coagulation factor which is called factor for short. There are two important factors: factor VIII and factor IX. Those lacking factor VIII have hemophilia A and those without factor IX have hemophilia B. | no |
Diabetology | Can honey be a safe sugar substitute for diabetics? | yes_statement | "honey" can be a "safe" "sugar" "substitute" for "diabetics".. "diabetics" can "safely" use "honey" as a "sugar" "substitute". | https://mantracare.org/diabetes/diet/honey-and-diabetes/ | Honey And Diabetes: Is Honey Good for You?- MantraCare | Honey And Diabetes
People with diabetes use honey as both food and medicine. It has many health benefits for many diseases like diabetes, tuberculosis, etc. It is much healthier than sugar. This is so because it contains fewer calories as compared to sugar. For diabetics, honey is the best alternative component to use instead of sugar.
Honey is another type of sugar. It is a natural sweetness that comes from nectar by honeybees. It is made up of water and a mixture of two sugars: fructose and glucose, In which, glucose contains sugar up to 30 to 35 percent, and fructose contains sugar for about 40 percent.
Also, it presents a small amount (approximately 0.5 percent) of vitamins, minerals, and other antioxidants. This makes honey nutritious. Honey has roughly 17 grams of carbs and 60 calories per tablespoon.
On the other hand, traditional white sugar, often known as sucrose, is 50 percent glucose and 50 percent fructose. For about one tablespoon of white sugar, there are 13 grams of carbohydrates with no vitamins or minerals. This shows that honey is healthier than white sugar. But, a diabetic should always have a controlled hand on honey too.
Types of Honey
There are mainly two types of honey, that vary according to the source of nectar that affects the taste of honey and its color.
Raw Honey
Unfiltered honey is another name for raw honey. This honey comes from a beehive. It is then filtered to remove toxins. Earlier, raw honey was used as a folk treatment for centuries. It also has a wide range of health and medical benefits.
It’s even utilized as wound therapy in some hospitals. Moreover, it is a good source of many antioxidants. Raw honey has antibacterial and antifungal properties. This type of honey not only helps in digestive issues but also helps in healing wounds.
Processed Honey
Processed honey is over pasteurized for a thin consistency. This type of honey is filtered and structured many times. It gives honey a transparent and presentable structure.
The process includes heating, filtration, ultrasonication, creaming, microwave radiation, gamma radiation, and also helps in eliminating all the impurities from honey.
Processed honey has fewer benefits as compared to raw honey. However, most people prefer buying processed ones to use at home.
Difference Between Honey And Other Sweeteners
As honey contains less GI value than sugar, you can use honey as an alternative to it. Due to this, it is capable of offering various other areas of difference as compared to other sweeteners:
Because of its low GI value, it does not raise blood sugar levels and proves itself to be better than other sweeteners.
It is sweeter than sugar which implies that intake of honey should be limited. For diabetic people, honey is the healthier option in substitute for sugar.
There is no actual benefit of replacing honey with sugar. For those trying to optimize their insulin levels, honey, in some way, can benefit them, while other sweeteners fail to do so.
Moreover, it is to note that overconsumption of both honey and other sweeteners can create major health problems. While honey can be the better option for diabetics as it contains more nutrients than other sweeteners. The flavours and textures of commonly used sweeteners that is honey and sugar are vastly different.
You probably prefer the tenderness of honey on your morning toast over the molasses flavour and moisture of brown sugar in baking. Experiment with each while keeping track of how much you use, to see which is best for you.
Although honey has more benefits, both honey and sugar can be harmful to your health if taken in excess. If you have diabetes or heart disease, or if you want to lose weight, talk to your doctor and a nutritionist about your dietary requirements. They can collaborate with you to come up with the ideal dietary strategy for your betterment.
Benefits Of Honey For Diabetic
In a study, it is found that people with type 2 diabetes can use honey. Honey has the potential to raise your insulin levels. This also helps you to control your blood sugar. It is a source of antioxidants and has anti-inflammatory qualities which help in replacing sugar with honey.
Nutritive Value
Honey contains many nutritive values such as vitamins, minerals, and some other antioxidants. It also has no fibre, fat, or proteins. Rather it contains more energy and water.
Hence, contains fewer risk factors as compared to sugar for diabetics. Antioxidant-rich foods contain honey that can help your body to digest it effectively.
Health Benefits
Honey contains many antioxidants that will help in lowering your blood pressure, improves cholesterol levels, triglycerides levels, and improves other heart-related diseases.
Besides this, it also helps in curing diseases like dizziness, fatigue, tuberculosis, eye diseases, healing of ulcers and wounds. Also, honey will help you in decreasing the risks of metabolic diseases.
Moreover, researchers also found that honey helps in fighting inflammatory processes. These inflammatory processes occur due to diabetes, atherosclerosis, and cardiovascular diseases.
All these diseases are the features of metabolic syndrome. However, combining diabetes medications with honey may also benefit you in many ways. But these findings still need to be confirmed.
Ways To Use Honey Safely
Honey is considered an added sugar in the diet, even though it is natural. However, diabetics can safely enjoy honey when consumed in moderation. Thus, you may also prefer fibre-rich foods such as vegetables, fruit, whole grains, nuts, seeds, and legumes that can help with blood sugar management.
Any meal or snack containing honey needs to be balanced with other healthful, low-carbohydrate items. Here are some of the ways by which you can use honey safely:
Use of Honey With Yogurt
To keep your blood sugar levels under control, eat pure honey with yoghurt first thing in the morning. Repeat this every day for a month, and witness the gradual drop in your blood sugar levels.
Honey And Cinnamon
This popular combination is a three-in-one diabetes cure. It increases metabolism, decreases cholesterol, and helps in weight loss. In addition to managing an increase in blood sugar levels.
Honey, Ginger And Lemon Tea
Tea made with honey and ginger, with a touch of lemon has antibacterial and antioxidant qualities. It helps to promote digestion and immunity. Lemons are high in vitamin C and potassium, which help to strengthen the immune system and purify the body of disease-causing free radicals.
Effect of Honey on Diabetic Factors
It is advisable to monitor the effect of honey or any other sweetener with care. In the forthcoming sections, you will see the effect of honey on two major diabetic factors: insulin and blood sugar.
Honey And Insulin
Insulin is a hormone produced by the pancreas that helps in blood sugar regulation. When blood sugar levels begin to rise, the pancreas receives a signal to release insulin. It then functions as a key, unlocking cells and allowing glucose to flow from the bloodstream into cells where it can be used for energy. Blood sugar levels are reduced as a result of the whole procedure.
Moreover, honey is already proven in certain studies to generate a stronger insulin response than other sugars. As a result, some people have theorized that honey is beneficial to diabetics and may even prevent diabetes.
People with diabetes can either no longer generate insulin (type 1) or can no longer use insulin correctly (type 2). When type 1 diabetes does not have enough insulin or it does not use as correctly by the body, then glucose (sugar) stays in the bloodstream. This resulting in high blood sugar levels (hyperglycemia).
Honey and Blood Sugar
Honey is different from white sugar because sugar does not have many vitamins and minerals. If you have diabetes, honey is not likely to benefit you but affects your blood sugar in many ways. Honey has a lower glycemic index than sugar, too. The glycemic index measures how quickly carbohydrates raise blood sugar levels.
Honey has a GI value of 58, whereas sugar has a GI value of 60. That means honey (like all carbohydrates) raises blood sugar quickly, but not quite as fast as sugar. Hence, not making a big difference. It can negatively affect your blood sugar and your ability to take the right amount of insulin.
Replacing Honey With Sugar
Honey can be used to replace refined sugars like white sugar, turbinado sugar, cane sugar, and powdered sugar. People should, however, use it in moderation. It, too, can cause blood sugar levels to rise. Especially when used in place of another sugar.
Some producers make honey that isn’t 100% pure and may contain added sugars or syrups. It’s also worth noting that raw honey may contain a toxin that might induce botulism or be harmful to infants under the age of one year.
Moreover, honey provides nutrients to other foods like fresh fruits and vegetables that are greater sources of the nutrients, as well as provides more fibre and water, which helps to keep blood sugar levels in check. Diabetics should consume sweeteners of any kind frequently. It is because frequent use of sweeteners will cause less spike in blood sugar levels.
Risks Of Honey For Diabetics
Honey has some nutrients that are beneficial to your health. You would have to take a bit more than honey to obtain any major benefit from it. A significant quantity of honey is not worth consuming. This is only to obtain additional vitamins and minerals.
As other sources of these nutrients will have far less impact on blood sugar levels. You only need a small amount of honey to replace sugar. Following are some of the risks factors that honey causes to diabetics:
Impact Of Honey On Blood Sugar
Diabetics should avoid honey and other sweeteners until diabetes is under control as it can impact blood sugar. It should only be taken in little amounts. Before using it as a sweetener, consult your healthcare professional. Pregnant women and adults with weak immune systems, on the other hand, are at risk.
Impact Of Honey In Baby Botulism
Another risk factor of honey includes infants under the age of 12 months. This is due to the danger of baby botulism. It can transmit from both raw and pasteurized honey. However, it is safe for anyone over the age of one. Botulism of the intestine in adults is extremely rare. That’s why honey causes fewer indications of diabetes in them.
Prevention of Diabetes With Honey
No study has yet not found supporting honey as a diabetes prevention factor. However, the fact is that honey enhances insulin levels and assists diabetics to control their blood sugar. According to researchers, honey also reduces glycemic index values.
When compared to sugar, honey had a lower glycemic effect on all participants in a study of 50 persons with type 1 diabetes. On the other hand, 30 people without type 1 diabetes have lower glycemic effects. It also increases C-peptide, a chemical released into the bloodstream when the body manufactures insulin. Moreover, a normal C-peptide means your body is making sufficient insulin.
A Word From Mantra Care
Hence, substituting honey in place of sugar gives no advantage to your diabetes eating plan. As honey contains few more calories and carbohydrates than granulated sugar. It is why honey should be used in limit. Though, many types of research are still going on to find out whether honey can prevent diabetes or can provide treatments for diabetes.
Here at Mantra Care, we have an incredibly skilled team of healthcare professionals and coaches who will be happy to answer any questions and provide further information so you know what’s best for your unique needs. | Moreover, honey provides nutrients to other foods like fresh fruits and vegetables that are greater sources of the nutrients, as well as provides more fibre and water, which helps to keep blood sugar levels in check. Diabetics should consume sweeteners of any kind frequently. It is because frequent use of sweeteners will cause less spike in blood sugar levels.
Risks Of Honey For Diabetics
Honey has some nutrients that are beneficial to your health. You would have to take a bit more than honey to obtain any major benefit from it. A significant quantity of honey is not worth consuming. This is only to obtain additional vitamins and minerals.
As other sources of these nutrients will have far less impact on blood sugar levels. You only need a small amount of honey to replace sugar. Following are some of the risks factors that honey causes to diabetics:
Impact Of Honey On Blood Sugar
Diabetics should avoid honey and other sweeteners until diabetes is under control as it can impact blood sugar. It should only be taken in little amounts. Before using it as a sweetener, consult your healthcare professional. Pregnant women and adults with weak immune systems, on the other hand, are at risk.
Impact Of Honey In Baby Botulism
Another risk factor of honey includes infants under the age of 12 months. This is due to the danger of baby botulism. It can transmit from both raw and pasteurized honey. However, it is safe for anyone over the age of one. Botulism of the intestine in adults is extremely rare. That’s why honey causes fewer indications of diabetes in them.
Prevention of Diabetes With Honey
No study has yet not found supporting honey as a diabetes prevention factor. However, the fact is that honey enhances insulin levels and assists diabetics to control their blood sugar. According to researchers, honey also reduces glycemic index values.
When compared to sugar, honey had a lower glycemic effect on all participants in a study of 50 persons with type 1 diabetes. | no |
Diabetology | Can honey be a safe sugar substitute for diabetics? | yes_statement | "honey" can be a "safe" "sugar" "substitute" for "diabetics".. "diabetics" can "safely" use "honey" as a "sugar" "substitute". | https://www.healthycanning.com/sugars-role-in-home-canning/ | Sugar's role in home canning - Healthy Canning | Summary
Preserving the “appeal” of the food: the quality of the food in terms of texture, colour, taste,and appearance.
In the quantities used in home canning, sugar has texture and colour preserving properties, but not food-safety preserving properties.
Sweetness plays a role not just in jams, jellies and fruits: it also plays a flavour role in savoury items such relishes and pickles. Sweetener helps to make the food product more palatable by masking the tartness and sourness of the acidity. Without sweetness, some pickled products might just be inedible to many people’s tastes.
Linda Ziedrich, author of the Joy of Pickling, says,
as Extension agents explain, the purpose of the sugar in such recipes isn’t to ensure safety but to balance the sharpness of the vinegar.” [1]Ziedrich, Linda. Gardener’s Table blog. “Rice vinegar for home canning.” 2 June 2012. https://agardenerstable.com/2012/06/02/rice-vinegar-for-home-canning/
Sugar, as a carbohydrate, can also act as a thickener, binding up free water.
Some recipes claiming to be sugar free are in fact merely free sugar in its refined white form. They will swap in other forms of free sugars such as honey, maple syrup or agave nectar. Such recipes are not helpful for diabetics, people with sugar sensitivity, or people wanting to lose or manage their weight.
Sugar’s role in safety
The experts say that sugar does not always play a safety role in home canning. (Note: there are a few recipes where it does.)
Barb Ingham at Wisconsin Extension says, “You can omit or reduce the sugar when freezing fruits, and when making pickles, salsas and sauces” [2] Ingham, Barb. Safe Preserving: Using Splenda. University of Wisconsin Cooperative Extension. 9 September 2013. Accessed March 2013 at https://fyi.uwex.edu/safepreserving/2013/09/09/safe-preserving-using-splenda/
Michigan State University Extension says, “All fruits can be safely canned or frozen without sugar… Sugar is not needed to prevent spoilage and that is why water or fruit juice can be substituted for sugarless home-canning. If you are on a special diet or are just watching your calories you may want to try canning without sugar; it is a good option.” [3] Nichols, Jeannie. Home canning without sugar. Michigan State University Extension. 14 August 2012.
Angela Fraser at Clemson University says, “Canning fruits and vegetables without adding sugar or salt does not affect the processing time or the safety of the product.”
Angela Fraser at Clemson University says, “Canning fruits and vegetables without adding sugar or salt does not affect the processing time or the safety of the product.” [5] Fraser, Angela. Associate Professor/Food Safety Education Specialist. How Canning Preserves Food. Clemson University, Clemson, SC. Accessed March 2015 at https://www.foodsafetysite.com/consumers/resources/canning.html
Virginia Cooperative Extension says, “Sugar is primarily added to improve flavor, help stabilize color, and retain the shape of the fruit. Fruits canned without sugar will be softer in texture than those canned with sugar.” [6] Boyer, Renee R. Boiling Water Bath Canning. Virginia Cooperative Extension. Publication 348-594. 2013. Accessed March 2015 at https://pubs.ext.vt.edu/348/348-594/348-594_pdf.pdf Page 3.https://pubs.ext.vt.edu/348/348-594/348-594_pdf.pdf
Brent Fountain at Mississippi State University Extension Service says, “Q: Is it safe to can without salt and sugar? A. Salt and sugar are not necessary for safe processing of fruits and vegetable.” [7] Fountain, Brent. Home Canning: Questions and Answers. Mississippi State University Extension Service. Publication 99. Accessed March 2015 at https://msucares.com/pubs/publications/p0993.pdf
The National Center for Home Food Preservation (NCHFP) says, “Sugar is not needed for safety because the heat used in canning is what kills microorganism and preserves the product.” [8] National Center for Home Food Preservation Self Study Course. Module 3. Canning Acid Foods: Canning Liquids for Fruits. Accessed March 2015. [Ed: Here they are discussing canning low-acid products. pH is as important as heat when it comes to water-bathed or steam-canned products.]
Note that it is possible to affect the safety of a home-canned good by using too much sugar. Sugar is, after all, a carbohydrate, and carbs impact the density of foods. Elizabeth Andress, head of the NCHFP says, “The following slow down heat penetration: – Extra sugar or fat.” [9]Andress, E.L. 2008. Pressure canning & canning low-acid foods at home (slides). Athens, GA: The University of Georgia, Cooperative Extension.. Accessed August 2016
Sugar’s role in quality
Even though sugar has no impact one way or the other on the aspect of food safety, it can often play a role in preserving texture and colour.
“The texture and color preserving aspects of a sugar syrup will not be provided. The result would be like canning in water ….. The USDA fruit canning directions do allow for canning in water (i.e., without a sugar syrup), as there is adequate preservation for safety from the heat of proper canning.” [10] National Center for Home Food Preservation: Can Splenda® (sucralose) be used in preserving food? In: Frequently Asked General Preservation Questions. Accessed March 2015 at https://nchfp.uga.edu/questions/FAQ_general.html#3
For some recipes that call for extremely heavy amounts of sugar, if you are going to get the same time length of shelf stability, the water bath processing times seem to require 5 to 10 minutes added onto them:
“…for shelf stability…..Sugar is required for the preservation of these syrupy fruit preserves as published, with very short boiling water canner processes. Without that heavy amount of sugar, these products become fruit pieces canned in water or lighter sugar syrups, and the usual (and longer) fruit canning process times and preparation directions would need to be used.” [11] National Center for Home Food Preservation: Can Splenda® (sucralose) be used in preserving food? In: Frequently Asked General Preservation Questions. Accessed March 2015 at https://nchfp.uga.edu/questions/FAQ_general.html#3
Note that the above advice relates to long-term shelf quality, rather than a safety issue. But then again, the USDA also now advises us not to store for more than a year anyway.
Georgia Lauritzen at Utah State says,
Sweeteners are considered an essential ingredient of most of the products of the canning industry, except vegetables. They act as preservatives and maintain desirable appearance, flavor, color and body in the products. Altering the type and amount of sugar in standardized preservation recipes will alter these characteristics. The principal sweeteners used in canning are sugar (sucrose), and corn syrup……
The addition of sugar to canned fruit aids in retaining the shape, texture, color, appearance, and flavor of the original product. When sugar is not used or reduced in canning, there will be slight changes in these characteristics. When canning fruit without the addition of sugar, or at reduced levels, follow the tested directions for the product being preserved.” [12] Lauritzen, Georgia C. Reduced Sugar and Sugar-free Food Preservation. Utah State University Cooperative Extension. FN209. 1992. Accessed March 2015 at https://extension.usu.edu/files/publications/publication/FN_209.pdf
William Schafer with the University of Minnesota Extension Service wrote,
The high cost of commercially canned, special diet food often prompts interest in preparing these products at home. Some low-sugar and low-salt foods may be easily and safely canned at home. However, the color, flavor, and texture of these foods may be different than expected and be less acceptable.” [13] William Schafer. Canning Basics 10: Canning Foods for Special Diets. University of Minnesota Extension Service. 2010. Accessed January 2015 at https://www.extension.umn.edu/food/food-safety/preserving/canning/canning-basics-10/
The following advice is from an extension agent in Mississippi. He doesn’t want you to reduce sugar in recipes, but he does clarify that his concern relates to quality, not safety:
Q: Is it safe to can without salt and sugar? A. The salt in recipes for pickled products and sugar in jams, preserves, and jellies should not be reduced, since the measures given are needed to provide good quality.” [14] Fountain, Brent. Home Canning: Questions and Answers. Mississippi State University Extension Service. Publication 99. Accessed March 2015 at https://msucares.com/pubs/publications/p0993.pdf
Patricia Kendall, Professor and Extension Specialist at Colorado State University, essentially says you can try sugar-free relish and pickle recipes, but says that (in her experience) the quality can be uneven:
Sweet relish and pickle recipes do not adapt as well to sugar-free canning as do plain fruits. Try recipes that call for artificial sweeteners, but don’t be too discouraged if some batches are disappointing. Finished products often are mushy or have an unsuitable flavor. When canning pickles and relishes, use the boiling water bath method and processing times that are adjusted for altitude.” [15] Kendall, P. Canning Fruits. Colarado State University Extension. No. 9.347. June 2013. Accessed March 2015 at https://www.ext.colostate.edu/pubs/foodnut/09347.html
But finally, some practical wartime advice from a time when backing up a dump truck full of sugar and emptying it into your preserves was simply not an option, owing to rationing:
Sugar customarily used in canning fruits does improve their texture, flavor and color, but it does not prevent age, according to Mrs. Madge Little, of the home economics extension staff, University of Illinois College of Agriculture. When sugar is scarce, appearance and flavor take second place. Saving the fruit is the important thing, and this can be done with little or no sugar, provided the proper methods of sterilization are followed and a perfect seal is accomplished.” [16] SUGAR ALLOWANCE SHOULD BE USED WISELY IN CANNING. Farmers’ Weekly Review, 30 June 1943. Joliet, Illinois. Page 1.
Old fears about sugar substitutes in canning
Experts were opposed to sugar substitutes in home canning because of quality issues. HealthyCanning.com feels that this general advice is now dated — it dates from testing almost a generation ago, when what they had to test was saccharin or aspartame based, and modern alternatives such as sucralose and stevia were only just coming on the market.
In the interest of thoroughness, however, it’s important to acknowledge that concern and bring it forward.
We’ve seen the concern expressed as early as 1942 by the USDA:
Housewives often ask about using saccharine instead, of sugar in canning and preserving. Saccharine is not a food but a coal-tar product with an extremely sweet flavor, often used in diabetic diets. You can’t use saccharine in canning because heating makes it bitter.” [17]USDA Homemakers Chat. Stretching your sugar in canning. 17 April 1942. Page 3.
The University of Missouri Extension recorded this advice back in 1989 from Dr Gerald Kuhn: “While both Equal (aspartame) and saccharin-based sweeteners are safe to use, the quality of any pickled product made with either of these sweeteners is poor. Equal quickly loses its sweetness when heated while saccharin-based sweeteners become bitter.” Source: Personal communication with Dr. Gerald Kuhn, Food Scientist, Penn State University, June 1989. [18]Accessed August 2017 at https://missourifamilies.org/quick/foodsafetyqa/qafs556.htm
Kuhn may have been the last one who actually had the resources to test sweeteners, back in the 1980s, using what was on the market back then. At that time, North Americans had only just discovered olive oil and hadn’t discovered kale yet.
Since then as far as we’re aware, there’s not been resources for much if any testing, and the advice from that era is just repeated.
Colorado State University Extension says, “Saccharin-based sweeteners can turn bitter during processing. Aspartame-based sweeteners lose their sweetening power during processing.” [19] Kendall, Pat. Canning Fruits. Colorado State University Extension. No. 9.347. June 2013. Accessed March 2015 at https://www.ext.colostate.edu/pubs/foodnut/09347.html
Penn State says, “In general, non-nutritive (artificial) sweeteners are not recommended for canning. Aspartame containing sweeteners such as Equal or NutraSweet degrade with heat and lose their sweetening power. Saccharine-based sweeteners such as Sweet’N Low, Sugar Twin, or Sweet 10 become bitter when exposed to canning temperatures and should be added after the canned fruit is opened. Sucralose or Splenda is a new artificial sweetener derived from sugar molecules and will not produce an aftertaste when heated.” [21] Penn State Extension. Canning With Artificial Sweeteners . Accessed January 2015 at https://extension.psu.edu/food/preservation/faq/canning-with-artificial-sweeteners
Michigan State says, “You may want to stay away from using saccharin- and aspartame-based sweeteners when canning. Saccharin-based sweeteners turn bitter when processed. Aspartame-based sweeteners lose their sweetening power during processing. ” [22] Nichols, Jeannie. Home canning without sugar. Michigan State University Extension. 14 August 2012.
The National Center says, “Saccharin or aspartame-based artificial sweeteners in canned fruits are best added just before serving. Sucralose (e.g., Splenda) is a newer sugar substitute that can be added prior to canning.” [24] National Center for Home Food Preservation Self Study Course. Module 3. Canning Acid Foods: Canning Liquids for Fruits. Accessed March 2015.
Summary of sugar concerns to be addressed
We have now seen that:
There is no food safety concern about sugar-free home canning;
There are concerns about sugar-free products not being as high quality in terms of long-lasting texture and colour; and
There are concerns that some sugar substitutes are to be avoided because they don’t perform well in canning. Those sweeteners were, to be precise, saccharin or aspartame based.
Let’s try therefore now to address points (2) and (3).
Compensating for lack of sugar in sugar-free home canned products
Sweetness
Even for those who may say they don’t necessarily have a sweet tooth, sweetness is often necessary in some pickled items, even, in order to take the edge off from the harsh, white vinegar used in canning.
HealthyCanning.com uses both Splenda and stevia as non-caloric sweeteners. When it comes to stevia, we use liquid stevia for purity of taste, ease of use, and for the quality results it delivers in home canning.
Firming and crisping
“Sugar helps to firm the vegetables in a relish.” [25] Penn State Extension. Relishes. September 26 2012. Accessed January 2015 at https://extension.psu.edu/food/preservation/news/2012/relishes
Sugar can help in achieving and maintaining a firmer texture in fruits and vegetables. To compensate, we could simply use a few pinches of Pickle Crisp ® (aka calcium chloride) per jar.
Really, though, the crispness of your pickle is going to absolutely depend on how long it was since your cucumbers were picked, and once they lose that crisp snap, nothing you can add to the jar — not sugar, not Pickle Crisp, not grape leaves — can restore it.
Colour
Sugar can help the colour of some foods to stay sharper for longer. Ascorbic acid, citric acid and Vitamin C are other elements that can help improve the staying power of colour.
Utah State University Cooperative Extension says, “Noncaloric sweeteners do not help retain color or texture in home preserved fruits. The use of an antioxidant such as ascorbic acid will result in better color when no sugar is used.” [26] Lauritzen, Georgia C. Reduced Sugar and Sugar-free Food Preservation. Utah State University Cooperative Extension. FN209. 1992. Accessed March 2015 at https://extension.usu.edu/files/publications/publication/FN_209.pdf
Colorado State University Extension says, “If ascorbic acid products are not used in the pretreatment of cut fruit, they may be added to the canning juices or liquids before processing. This will help keep the fruit from darkening during storage. Use ¼ to ½ teaspoon crystalline ascorbic acid or 750 to 1,500 mg crushed vitamin C tablets per quart of fruit. Commercial ascorbic and citric acid mixtures also may be used according to manufacturer’s directions.” [27] Kendall, P. Canning Fruits. Colorado State University Extension. No. 9.347. June 2013. Accessed March 2015 at https://www.ext.colostate.edu/pubs/foodnut/09347.html
Consistency
Sugar can act as a thickener to provide body. In recipes using no sugar needed pectins, the pectin takes care of the body. Other than that, HealthyCanning.com hasn’t yet found a need to compensate directly on the “body” issue in any of the recipes posted on the site.
Penn State Extension says, “Most pickles and relishes and jams and jellies still need sugar for the proper consistency, but a few new recipes have been developed for low or no sugar products.” [28] Penn State Extension. Canning with Less Sugar . 17 September 2012. Accessed January 2015 at https://extension.psu.edu/food/preservation/news/2012/canning-with-less-sugar
They go on to say: “You can use Splenda® and other non-heat sensitive artificial sweeteners in jam or jelly made with no-sugar needed pectin. Package inserts with commercial pectins tell you when you should add artificial sweeteners. Artificial sweeteners do not provide the properties of sugar needed to jell traditional long cook jams and jellies though.” [29] Penn State Extension. Canning with Less Sugar . 17 September 2012. Accessed January 2015 at https://extension.psu.edu/food/preservation/news/2012/canning-with-less-sugar
Processing times
In general, the presence or absence of sugar does not influence processing times one way or the other.
That being said, the National Center for Home Food Preservation advises that a few recipes on its site (fig, peach and pear fruit preserves in thick sugar syrup) would require the longer normal canning times for those fruits if sugar is left out:
“Splenda® cannot be used in several traditional Southern preserves we have on this website or in the University of Georgia Extension publications. These are whole or uniform pieces of fruit in a very thick sugar syrup, usually made with figs, peaches or pears. (These preserves are not jam or pectin gel products.) Sugar is required for the preservation of these syrupy fruit preserves as published, with very short boiling water canner processes. Without that heavy amount of sugar, these products become fruit pieces canned in water or lighter sugar syrups, and the usual (and longer) fruit canning process times and preparation directions would need to be used.” [31] National Center for Home Food Preservation. Can Splenda® (sucralose) be used in preserving food? Accessed June 2015 at https://nchfp.uga.edu/questions/FAQ_general.html
What are the results of sugar-free canning like?
Some of the home canning experts are really down on the idea; and you get the impression that they just wish the whole topic would go away.
They say, as you’ve seen, that while there is no safety concern, that the quality is not desirable.
Here at HealthyCanning.com, our findings have been the exact polar opposite, and we consequently have to respectfully but firmly disagree.
We’ve had absolutely fantastic results in terms of quality and taste — using the canning experts’ own tested, quality recipes.
National Center for Home Food Preservation: Can Splenda® (sucralose) be used in preserving food? In: Frequently Asked General Preservation Questions. Accessed March 2015 at https://nchfp.uga.edu/questions/FAQ_general.html#3
National Center for Home Food Preservation: Can Splenda® (sucralose) be used in preserving food? In: Frequently Asked General Preservation Questions. Accessed March 2015 at https://nchfp.uga.edu/questions/FAQ_general.html#3
William Schafer. Canning Basics 10: Canning Foods for Special Diets. University of Minnesota Extension Service. 2010. Accessed January 2015 at https://www.extension.umn.edu/food/food-safety/preserving/canning/canning-basics-10/
National Center for Home Food Preservation. Can Splenda® (sucralose) be used in preserving food? Accessed June 2015 at https://nchfp.uga.edu/questions/FAQ_general.html
Reader Interactions
Comments
Sheila
May 21, 2023 at 3:54 pm
The only caution in making a reduced or no-sugar jelly is when making jellies with low-acid fruits and vegetables like peppers. Sugar *does* reduce water activity, and also when using low/no sugar pectins, you *must* follow a tested recipe to have the correct acidification, as these modified pectins will set at higher pH levels. When using a traditional pectin, you won’t get a gel unless the pH is approximately 3.2 which is more than enough to prevent botulism spores from forming.
Hi Bruce, I’ve not read a lot about the effect of pressure cooking or canning on carbs, but I have seen that there is some research emerging about the beneficial effect of them on the starch in potatoes: https://www.hippressurecooking.com/pressure-cooker-potato-nutrition/ For a better answer to your question, ask Laura, the woman who runs that same site, hippressurecooking.
I wrote a homesteading blog, and have been meaning to tackle a piece on home canning vs canning for sale (I’m licensed to sell jams in the state of Washington), but not pickled products. The difference, by our local laws is that one is naturally a low enough pH to be safe, vs having to add vinegar to make it safe, what they consider an “acidified” product. Just wanted to let you know I LOVE your approach to this question, with lots of references from valid reputable sources. NICE work!
Thank you SOOOOO much for this information!
It answers all my questions about the need for sugar in canning.
I hope I am reading it rightly… I can develop my own chutney or
relish recipe without ‘having’ to use sugar.
The experts recommend that you freeze or refrigerate recipes that you develop for yourself. Otherwise, for canning purposes, the recommendation is to only use tested recipes from reputable sources. Though sugar and salt don’t play a critical safety role in most home canning recipes with exceptions cited on this site from experts, there are other factors in home canning chutney and relish recipes which are important. (1) An overall low enough pH that any botulism spores can never germinate; (2) maintaining a density that isn’t too thick to allow complete heat penetration to every “corner” of the jar, to kill off other nasties such as listeria, salmonella, moulds, etc; (3) a tested processing time that ensures that the jar is exposed to heat long enough to ensure that (2) happens, and also to guarantee a quality shelf-life period. If you want to safely tweak recipes, look for the page on this site on that topic to see what tweaking the experts say can be done. Hope that helps.
If you need FAST or relatively immediate canning help or answers, please try one of these Master Food Preserver groups; they are more qualified than we are and have many hands to help you. Many of them even operate telephone hotlines in season. | /rice-vinegar-for-home-canning/
Sugar, as a carbohydrate, can also act as a thickener, binding up free water.
Some recipes claiming to be sugar free are in fact merely free sugar in its refined white form. They will swap in other forms of free sugars such as honey, maple syrup or agave nectar. Such recipes are not helpful for diabetics, people with sugar sensitivity, or people wanting to lose or manage their weight.
Sugar’s role in safety
The experts say that sugar does not always play a safety role in home canning. (Note: there are a few recipes where it does.)
Barb Ingham at Wisconsin Extension says, “You can omit or reduce the sugar when freezing fruits, and when making pickles, salsas and sauces” [2] Ingham, Barb. Safe Preserving: Using Splenda. University of Wisconsin Cooperative Extension. 9 September 2013. Accessed March 2013 at https://fyi.uwex.edu/safepreserving/2013/09/09/safe-preserving-using-splenda/
Michigan State University Extension says, “All fruits can be safely canned or frozen without sugar… Sugar is not needed to prevent spoilage and that is why water or fruit juice can be substituted for sugarless home-canning. If you are on a special diet or are just watching your calories you may want to try canning without sugar; it is a good option.” [3] Nichols, Jeannie. Home canning without sugar. Michigan State University Extension. 14 August 2012.
Angela Fraser at Clemson University says, “Canning fruits and vegetables without adding sugar or salt does not affect the processing time or the safety of the product.”
Angela Fraser at Clemson University says, “Canning fruits and vegetables without adding sugar or salt does not affect the processing time or the safety of the product.” [5] Fraser, Angela. Associate Professor/Food Safety Education Specialist. How Canning Preserves Food. | no |
Diabetology | Can honey be a safe sugar substitute for diabetics? | yes_statement | "honey" can be a "safe" "sugar" "substitute" for "diabetics".. "diabetics" can "safely" use "honey" as a "sugar" "substitute". | https://tastyhoney.com/blogs/news/comparing-honey-and-table-sugar-for-calories-and-glycemic-index-gi | Comparing honey and table sugar for calories and glycemic Index ... | Comparing honey and table sugar for calories and glycemic Index (GI)
Honey is often used as a substitute for sugar, both in cooking, in desserts and in drinks like tea or coffee. And many consumers believe honey, as a wholly natural product, is healthier or better for you than table sugar.
Of course, honey is itself mostly sugar and indeed is typically composed of around 80% natural sugars (mostly fructose and sucrose). The other 20% of honey is mostly water, with a tiny amount of fat, salt and traces of fibre, protein and minerals.
However there are significant differences between table sugar and honey which are very important in a health context, and particularly as regards diabetes
1.1 Honey and Calories
Honey has less calories than the equivalent amount of sugar. According to a report published some years back at foodwatch.com.au 100gms of white sugar has 1700kJ/406Cals whereas 100g of honey has 1400kJ/334Cals.
But according to nutritionist Catherine Saxelby, the comparison is deceiving because we tend to eat and measure out honey with a spoon “,,,[F]ew of us eat honey by weight” she said adding that “We’re much more likely to use a teaspoon or tablespoon here and there, so measure for measure, honey has more kilojoules/Calories. That’s because honey is denser and 1 tablespoon weighs 28g, whereas a tablespoon of sugar weighs only 16g.”
So if counting calories is an important part of your health regime, don’t forget that a spoonful of honey has more calories than a spoonful of sugar.
1.2 Honey and Diabetes
Most of the table sugar sold in Australian supermarkets, known as white sugar, is refined from sugar cane juice, and what chemists would call a polysaccharide, and specifically, sucrose.
But from a chemical standpoint, sucrose is actually a combination of two disaccharides – glucose and fructose (other types of disaccharides include maltose, dextrose, lactose etc)
This is important, because the body needs to break down sucrose into its constituent parts before they can be digested and absorbed. Honey is like, sucrose, comprised mostly of glucose and fructose.
But whereas white sugar typically breaks down into half glucose and half fructose, most standard honey blends have more glucose than fructose.
Some of the varietal honeys (such as yellow box honey or redgum honey etc) may have higher proportions of fructose.
For diabetics, fructose is a lesser concern than glucose because glucose is so readily absorbed into the bloodstream.
So eating honeys with a majority of fructose is arguably, better for those who, like diabetics, have to manage their sugar intake. Some nutritionists even suggest that it may be OK for diabetics to eat small amounts of high fructose honeys.
However the reality is that both table sugar and honey are relatively simple sugar compounds, quickly absorbed by the body and both generally not recommended for diabetics.
1.3 Honey and GI
Many diabetics, and others, rely upon the so-called glycaemic index (i.e. GI) ratings to decide what they can safely eat. GI is essentially an indicator of how readily the human body absorbs particular carbohydrates, and so how quickly they increase natural blood sugar levels.
Ratings less than 55 are generally considered good, and indicate that that particular food or product is relatively safe to consume for diabetics and /or others with blood sugar issues.
The GI index tops out at 100, and surprisingly, table sugar has a GI of only around 60, and only marginally higher than most honeys. (Quickly digested carbohydrates such as potatoes or white bread have typically higher GI ratings than either sugar or honey)
Unfortunately, there isn’t a single official testing method for determining GI ratings. So, for example, the University of Sydney’s GI index (at www.glycemicindex.com) reports ratings as low as 35 for a yellow box honey with high fructose levels, 58 for a pure honey, and a whopping 78 for an unspecified honey with high glucose levels.
Other GI testing methods give higher levels for honey. So whilst GI numbers may be useful information for diabetics, they should only form part of the information used to make dietary decisions. | This is important, because the body needs to break down sucrose into its constituent parts before they can be digested and absorbed. Honey is like, sucrose, comprised mostly of glucose and fructose.
But whereas white sugar typically breaks down into half glucose and half fructose, most standard honey blends have more glucose than fructose.
Some of the varietal honeys (such as yellow box honey or redgum honey etc) may have higher proportions of fructose.
For diabetics, fructose is a lesser concern than glucose because glucose is so readily absorbed into the bloodstream.
So eating honeys with a majority of fructose is arguably, better for those who, like diabetics, have to manage their sugar intake. Some nutritionists even suggest that it may be OK for diabetics to eat small amounts of high fructose honeys.
However the reality is that both table sugar and honey are relatively simple sugar compounds, quickly absorbed by the body and both generally not recommended for diabetics.
1.3 Honey and GI
Many diabetics, and others, rely upon the so-called glycaemic index (i.e. GI) ratings to decide what they can safely eat. GI is essentially an indicator of how readily the human body absorbs particular carbohydrates, and so how quickly they increase natural blood sugar levels.
Ratings less than 55 are generally considered good, and indicate that that particular food or product is relatively safe to consume for diabetics and /or others with blood sugar issues.
The GI index tops out at 100, and surprisingly, table sugar has a GI of only around 60, and only marginally higher than most honeys. (Quickly digested carbohydrates such as potatoes or white bread have typically higher GI ratings than either sugar or honey)
Unfortunately, there isn’t a single official testing method for determining GI ratings. | no |
Diabetology | Can honey be a safe sugar substitute for diabetics? | no_statement | "honey" is not a "safe" "sugar" "substitute" for "diabetics".. "diabetics" should not use "honey" as a "sugar" "substitute". | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5817209/ | Honey and Diabetes: The Importance of Natural Simple Sugars in ... | Share
RESOURCES
As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with,
the contents by NLM or the National Institutes of Health.
Learn more:
PMC Disclaimer
|
PMC Copyright Notice
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Diabetes is a metabolic disorder with multifactorial and heterogeneous etiologies. Two types of diabetes are common among humans: type 1 diabetes that occurs when the immune system attacks and destroys insulin and type 2 diabetes, the most common form, that may be caused by several factors, the most important being lifestyle, but also may be determined by different genes. Honey was used in folk medicine for a long time, but the health benefits were explained in the last decades, when the scientific world was concerned in testing and thus explaining the benefits of honey. Different studies demonstrate the hypoglycemic effect of honey, but the mechanism of this effect remains unclear. This review presents the experimental studies completed in the recent years, which support honey as a novel antidiabetic agent that might be of potential significance for the management of diabetes and its complications and also highlights the potential impacts and future perspectives on the use of honey as an antidiabetic agent.
1. Introduction
Diabetes mellitus is one of the top diseases in modern times, with more than 285 million people estimated in 2010 and about 438 million people predicted for 2030 in all over the world [1]. Diabetes prevalence may be genetically determined or can be developed during lifetime at any age. This disease takes no account of age for example, but scientific studies reveal that it is more common in developing countries than in the rest of the world (developed countries and third world countries) [1]. The increasing incidence may be due to demographic changes and undesirable result of risk factors such as obesity and sedentary life.
What is in fact diabetes mellitus? Diabetes is a metabolic disorder with multifactorial and heterogeneous etiologies. The high blood sugar level is the “symptom” known for diabetes, but other symptoms should not be ignored: increased thirst and hunger, unexplained fatigue, increased urination, blurred vision, and unexpected weight loss. Two types of diabetes are common among humans: type 1 diabetes that occurs when the immune system attacks and destroys insulin. This type of diabetes is believed to be genetically determined but also environmental factors are important in the determination of the disease. The symptoms of this type of diabetes generally start quickly, in a matter of weeks. Type 2 diabetes, the most common form, may be caused by several factors, the most important being lifestyle, but also it may be determined by different genes. This type of disease is developed during several years, and the symptoms are also not noticeable; for this reason, many people find themselves with diabetes without specific or unusual symptoms. Type 2 diabetes is most of the time related to overweight or obese state.
Although diabetes mellitus is a chronic disease of endocrine diagnosis and remains the major cause of mortality worldwide [2–5], it is not a death sentence.
Nowadays, the medical world is turning more and more on the health benefits of natural products, medicinal herbs, and also honey, in the management of this illness. Together with classic medical treatment, using recipes of traditional medicine, including the use of apicultural products (i.e., honey), the diabetic patients can maintain the normal level of insulin in the blood and also their overall health condition.
Honey composition comprises more than 200 components, with fructose, glucose, and water as main substances. Honey was used in folk medicine back in time at the beginning of our era, but their health benefits were based only on eye observations, without having any basis for scientific support. Only in the last decades, the scientific world was concerned in testing and explaining the benefits of honey. These research studies explain to a large extent many medicinal effects of honey such as antioxidant [6–11], hepatoprotective [12–14], cardioprotective [15–17], antibacterial [18–23], anti-inflammatory [24–26], or antitumor [27–30].
For a long time, there has been a myth that honey could not be used in diabetic patient's diet, due to the high content of carbohydrates from its chemical composition. Considering the background of the research team that has been working on characterization of different types of honey from Romania and worldwide and the determination of its biological properties for a long period, we considered being appropriate to gather in a review, literature studies that may answer the question: is honey a good substitute for sugar in diabetic diet? Are natural simple sugars important in preventing and treating diabetes mellitus?
Therefore, the present study acknowledged different scientific studies, demonstrating the use of honey in diabetes mellitus: preclinical and clinical studies, animal model studies, and human studies that demonstrate the potential impact of honey on this complex disease.
2. Fructose and the Hypoglycemic Effect of Honey
Fructose content of honey varies from 21 to 43% and the fructose/glucose ratio from 0.4 to 1.6 or even higher [31–34]. Although fructose is the sweetest naturally occurring sweetener, it has a glycemic index of 19, compared to glucose which has 100 or sucrose (refined sugar) with 60 [35]. Different studies reveal the hypoglycemic effect of honey, but the mechanism of this effect remains unclear. It was suggested that fructose, selective mineral ions (selenium, zinc, copper, and vanadium), phenolic acids, and flavonoids might have a role in the process [10, 11, 31, 33, 36, 37].
There is evidence that fructose tends to lower blood glucose in animal models of diabetes [38, 39]. Mechanisms involved in this process may include reduced rate of intestinal absorption [40], prolongation of gastric emptying time [41, 42], and reduced food intake [43, 44]. Fructose stimulates glucokinase in hepatocytes, which plays an important role in the uptake and storage of glucose as glycogen by the liver. Glucose on the other hand, which is present beside fructose in honey, enhances the absorption of fructose and promotes its hepatic actions through its enhanced delivery to the liver [45, 46].
The pancreas is an important organ in diabetes, because it secrets two glucose-regulating hormones—insulin and glucagon—and honey might protect this organ against oxidative stress and damage with its antioxidant molecules, this being another potential mechanism of hypoglycemic effect of honey [32, 47].
Different studies were made on the effect of fructose on glycemic control, glucose-regulating hormones, appetite-regulating hormones, body weight, food intake, and oxidation of carbohydrates or energy expenditure [38, 44, 48–61].
Fructose administrated alone or as part of sucrose molecule in normal rats improved glucose homeostasis and insulin response compared to rats which received glucose [62]. Other studies show that fructose supplementation in normal or type 2 model of diabetic rats produced lower levels of plasma insulin and glucose, more than other administrated sugars [38].
3. Animal Model Experiments
Different animal models were used to study the possible hypoglycemic effect of honey. The most used experimental tool for inducing type 1 and type 2 diabetes is streptozotocin and alloxan of appropriate doses [63–66].
A study of six weeks [67] on healthy nondiabetic rats fed with a honey-containing diet exhibits good results: weight was reduced statistically significant, but no significant decreasing for glycosylated hemoglobin or food intake was observed.
Long-term honey feeding in Sprague-Dawley rats (52 weeks) produces a significant decrease of HbA1c levels but increases HDL cholesterol [68]. In sucrose-fed and sugar-free diet-fed rats, in the same experiment, HDL cholesterol levels were decreased and no other differences were observed for other lipids. Weight gain was similar for honey and sugar-free diet-fed rats but less compared to sucrose-fed rats.
If honey was demonstrated to have hypoglycemic effect in healthy animals, the same beneficial effect was observed in induced diabetic animals. A very important observation regarding honey and diabetes is that honey augments the antihyperglycemic effect of standard antidiabetic drugs in induced diabetes [10, 33].
Rabbits with diabetes induced by alloxan were used in one experiment, and three types of sweeteners were used for feeding the animals [65]. Pure honey of Apis florea and Apis dorsata and adulterated honey were given in different doses in a rabbit's diet, and a dose-dependent rise in blood glucose was registered.
Another study [66] of alloxan-induced diabetic rats fed with honey and healthy rats fed with fructose shows different results: glucose decreased significantly in alloxan-induced diabetic rats and not significantly in fructose-fed rats. Body weight increased in healthy fructose-fed rats, and hypoglycemic effect and also the same effect were found for streptozotocin-induced diabetic rats [71]. Table 1 summarizes the preclinical studies on healthy and induced diabetic animals, using honey solution or other sweeteners in their diet.
8 groups of rabbits (6 animals/group); groups I to IV were normal and healthy (nondiabetic) and groups V to VIII were diabetic induced by alloxan monohydrate
Group I: untreated control received 20 ml of water orally. Groups II–IV treated orally with 5, 10, and 15 mg/kg BW honey diluted up to 20 ml/kg with distilled water. Groups V–VI treated with tolbutamide (250 mg and 500 mg). Group V: diabetic control, treated with 20 ml of water. Groups VI–VIII treated orally with 5, 10, and 15 ml/kg BW of honey diluted to 20 ml with distilled water
Oral administration of pure honeys in 5 ml/kg/doses could not produce a significant (P > 0.05) increase in glucose levels in normal and alloxan-diabetic rabbits whereas the adulterated honey significantly raised the blood glucose levels in normal and hyperglycemic rabbits even at this low dosage.
Group 1a: control had standard rat chow for 3 weeks. Group 1b: fed with honey along with standard rat chow for 3 weeks. Group 2a: alloxan-induced diabetes and standard rat chow for 3 weeks. Group 2b: alloxan-induced diabetes, fed with honey and standard rat chow. Group 3a: standard rat chow and fructose for 3 weeks. Group 3b: standard rat chow fructose for three weeks than honey along with standard rat chow and fructose for 3 weeks
At the end of three weeks, it was found that daily ingestion of honey for 3 weeks progressively and effectively reduced blood glucose level in rats with alloxan-induced diabetes. Honey also caused a reduction in hyperglycemia induced by long-term ingestion of fructose, albeit to a lesser degree than its effect on alloxan-induced hyperglycemia. Honey could not reduce blood glucose in controlled rats that received neither alloxan treatment nor fructose ingestion, even though it caused an increase in body weight, irrespective of other substances concomitantly administered to the rats.
Weight gain was substantially reduced in honey-fed rats compared with those given a sucrose-based diet; the finding that consuming honey increases HDL cholesterol levels is still a significant result though. There have been strong associations seen between low HDL cholesterol levels and the increased risk of cardiovascular disease.
4. Honey versus Sugars in Human Clinical Trials
Human diet must have all types of nutrients required in the metabolic transformations and life support. Water, proteins, lipids, carbohydrates, vitamins, minerals, amino acids, and bioactive compounds are needed by the human body, and all of these compounds are taken from the diet. Maintaining a healthy life, equilibrate diet, and intake of each and every one of these nutrients is the key factor of health in general. Different diseases have as a starting point unbalances in metabolism, because of lack or excess of one or more nutrients.
Diabetes, as stated before, represents the high level of blood sugars due to low or no insulin production in the body. Experimental studies on animals suggest the beneficial effects of honey as a diet supplement and encouraging results on control of diabetes mellitus and additional complications are presented in medical studies; the experiments and reports on humans (healthy or diabetic) are rather sparse.
The published studies present favourable effects of honey in both healthy and diabetic subjects [16, 31, 72–76]. Since oxidative stress is implicated and mainly responsible for diabetes development, the antioxidant effects of honey are very important in this disease management [77].
The study of Al-Waili [78] on healthy, diabetic, or patients with hypertriglyceridemia shows promising results, when honey was used in their diet, compared with dextrose and sucrose. Thus, lipid profile was improved, normal and elevated C-reactive protein was lowered, and also homocysteine value and triacylglycerol were decreased in patients with hypertriglyceridemia. In diabetic patients, honey compared with dextrose caused a significantly lower rise of plasma glucose level (PGL). Honey caused greater elevation of insulin compared to sucrose; after different time of consumption, it reduces blood lipids, homocysteine, and CRP in normal subjects. The conclusion was that honey compared with dextrose and sucrose caused lower elevation of PGL in diabetics. This experimental study on healthy, diabetic, and hyperlipidemic human subjects demonstrates the different intake rate of refined sugar and honey, the raising of blood sugar and also raising their insulin levels.
Sugar is a refined product, obtained from different natural sources, but follows a technological process, leading to an almost pure substance—sucrose—highly used in modern life in the food industry.
Honey, on the other hand, being also a natural sweet product, has a complex composition, but compared to sugar, it has a lower glycemic index and energetic value. When we talk about refined sugar, it is easy to state the exact chemical composition, very simple actually, but talking about honey, many aspects should be considered regarding its composition. Botanical and geographical origins determine the specific composition and properties of all types of honeys.
∗Values specified for honey represent an average of floral and honeydew honey.
The fact that refined sugar is almost 100% sucrose, and very small amounts of other components compared to honey, makes the last one, an important sweetener, with almost 80% simple sugars from the total chemical composition (35–40% fructose and 30–35% glucose).
Even though the exact mechanism by which honey may have beneficial effects upon blood glucose is not very clear; from comparative experiments, some conclusions about the importance of fructose in honey are available. Fructose is known to stimulate glucokinase in hepatocytes, which plays an important role in the uptake and storage of glucose as glycogen by the liver [79], the amount of fructose in honey being very important for its hypoglycemic effects.
A study on humans [80] evaluated for a large period of time wherein a group of twenty adult patients with type 2 diabetes volunteered to stop their medication and use honey as treatment for their disease. This nonrandomized, open clinical trial aiming to study the safety and efficiency of honey as unique treatment revealed interesting results (Table 3).
12 healthy subjects receive inhalation with distilled water for 10 min; after one week, they received inhalation of honey solution (60% wt/v) for 10 min. 12 healthy subjects received inhalation of 10% dextrose for 10 min
Blood glucose and plasma insulin were measured at zero time and then at 15, 30, 60, 90, and 120 min after the meal. Counting the blood glucose increase after glucose as 100%, the corresponding increases in glycemia for other carbohydrates were fructose, 81.3%; lactose, 68.6%; apples, 46.9%; potatoes, 41.4%; bread, 36.3%; rice, 33.8%; honey, 32.4%; and carrots, 16.1%.
20 young type I diabetic patients in the experimental group; 10 healthy nondiabetics in the control group
Calculated amount of glucose, sucrose, and honey (amount = weight of the subject in kg × 1.75 with a maximum of 75 g/patient)
Honey, compared to sucrose, had lower GI and PII in both patients and control groups. In the patient group, the increase in the level of C-peptide after using honey was not significant when compared with glucose or sucrose.
30 individuals with a proven parental (mother or father) history of type II diabetes mellitus
Glucose diet supplementation Honey diet supplementation
The plasma glucose levels in response to honey peaked at 30–60 minutes and showed a rapid decline as compared to that of glucose. Significantly, the high degree of tolerance to honey was recorded in subjects with diabetes as well, indicating a lower glycemic index of honey.
20 adult patient volunteers suffering from type 2 DM and its associated metabolic disorders from 30 to 65 years and both sexes
Honey dose of 2 g/kg BW/day, (i) 50 ml (60 g) honey was dissolved in water (ratio of 1 : 3) and given before meals twice daily; (ii) the remaining 25 ml (30 g) was used for sweetening purposes
Honey consumption resulted in more hyperglycemia in these patients but without diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar state (HHS). Longer-term honey consumption resulted also in weight reduction in all the patients, and control of the blood pressure in the patients, who had hypertension before the honey intervention. The cardiovascular status improved in the patients, who had coronary heart disease (CHD) before the intervention.
The GI and PII of either sucrose or honey did not differ significantly between patients and controls. Both the GI and PII of honey were significantly lower when compared with sucrose in patients and controls. In both patients with diabetes and controls, the increase in the level of C-peptide after the honey was significant when compared with either glucose or sucrose.
Besides glycemic index (GI), peak incremental index (PII) is used to assess the glycemic effect (the effect on blood glucose level after ingestion of various foods) [81].
C-peptide is considered a good marker of insulin secretion, being cosecreted with insulin by the pancreatic cells as a by-product, with no biological activity of its own [82], of the enzymatic cleavage of proinsulin to insulin. Scientific studies regarding the effects of honey on insulin and C-peptide levels are controversial in healthy and diabetic patients [54, 83, 84].
A study made in the National Institute of Diabetes in Cairo, Egypt, on twenty diabetic young patients and ten healthy nondiabetic ones try to elucidate this controversy [73]. Glucose, sucrose, and honey were administrated diluted with 200 ml water, according to the patient's weight (amount of sugar/honey = weight of the subject in kg × 1.75, with a maximum of 75 g). The diluted sugars and honey were ingested in the morning by every participant, one week apart for each sugar type, the whole test lasting for three weeks. Blood tests were made before ingestion and after every 30 min postprandial of sugars, until 120 min (2 hours). Serum C-peptide level and glucose assay were measured for all blood samples.
The glycemic index and peak incremental index were lower both in patients and control group, when honey was used compared to glucose and fructose, but the level of C-peptide was different in patients and control group.
Honey causes a postprandial rise of plasma C-peptide levels compared to sucrose and glucose in nondiabetic patients, suggesting that honey might have a direct stimulatory effect on the healthy beta cells of the pancreas [73].
Although honey has lower GI than sugar (Table 2), an average value for honey is presented [85], according to fructose/glucose ratio, and GI value of different honeys is also different [86].
Twenty healthy subjects from Erciyes University, Kayseri, Turkey, were subjected voluntarily to a test of ingesting 50 g of pure glucose in 250 ml water and an amount of honey that corresponds to 50 g glucose (accordingly to the physicochemical analysis of honey used in the test). Capillary blood samples were taken from the finger in the next morning after sugar consumption and again every 15 minutes after second ingestion of sugars in the next day, until 120 minutes. Serum glucose and serum insulin level decreased after 2 hours of honey intake, and C-peptide level increased slightly 2 hours after honey intake. This study demonstrates how different types of honey, having different GI values, influence the parameters usually measured for diabetes control in a different manner [85].
Sixty healthy subjects aged 18 to 30 years, enrolled in one experiment in Isfahan University of Medical Science, Iran [87], receive 80 g of honey and 80 g sucrose dissolved in 250 ml water once a day for six weeks. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and fasting blood sugar (FBS) were determined from each participant at the beginning and in the end of the study. No significant change was registered in SBP and DBP in both groups at the beginning and in the end of the study, but FBS registered a significant reduction in the honey group at the end of the study, compared to the sucrose group [87].
Different studies mentioned before show that honey consumption reduces body weight but also blood glucose in healthy and diabetic patients compared to sugar intake. A study on type 2 diabetic patients consuming natural honey shows that body weight may be reduced and blood lipids and glucose as well [31]. The study consists of 58 patients with type 2 diabetes, with fasting blood sugar of 110–220 mg/dl, with same oral hypoglycemic drugs, but no insulin treatment. The experimental group (n = 25) receives natural honey for eight weeks following an experimental scheme, and the control group (n = 23) did not receive honey or other sweeteners. The participants continued their usual diet over the study period. The body weight and fast blood sugar were measured every 2 weeks, and constant decreasing was registered [31]. Scientific studies reviewed by Erejuwa et al. [12, 33] demonstrate that fructose and oligosaccharides from honey contribute to its hypoglycemic effect. In addition to lowering oxidative stress and hyperglycemia, honey consumption ameliorates other metabolic disorders associated with diabetes, such as reduced levels of hepatic transaminases, triglycerides, and glycosylated hemoglobin (HbA1c) and increased HDL cholesterol [12, 31].
Several honey types from different parts of the world ameliorate metabolic abnormalities in type 1 and type 2 diabetic patients [36, 73, 88]. These studies investigate the acute effects of honey on hyperglycemia and metabolic disorders, because the diabetic parameters were measured postprandial in studies which last from two to eight weeks. Table 3 summarizes the clinical studies on humans, applied treatment, and the main obtained results.
5. Honey in Diabetic Wound Healing
Besides the health benefits of ingesting honey in diabetes, another important use of honey could be in managing diabetic wounds [89]. These wounds are not like typical wounds, they are slower in healing or they do not heal at all, leading to complications that conventional medications do not work.
Honey was used in alternative medicine for healing different wounds since ancient times, the use of honey in diabetic wound management being more recent. Diabetic patients sometimes suffer from different complications such as arterial disease, vascular problems, ulcerations, and foot complications [90, 91].
Even if diabetic wounds are similar to wounds from normal patients, the healing process in the former is very slow and problematic and the medical costs are extremely high. Honey is a potential candidate to be used in these treatments because it is available, natural, and not expensive. But how can honey work at the wound site? The honey diluted with water or different body fluids forms hydroxyl radicals and hypochlorite anions at the wound site. The antioxidants present in the honey act through two different mechanisms in a wound: first, antioxidants fight against microorganisms and lower the infection in the wound [75, 92, 93]; second, the same antioxidants reduce the reactive oxygen species and inflammation caused by the wound, helping in the healing process [94–96].
The antimicrobial activity of honey is due to acidic pH, osmotic effect, hydrogen peroxide, and nitric oxide. The presence of nitric oxide metabolites in honey as well as the production of NO products by honey in different body fluids improves the healing process [74, 80, 97].
Debridement, wound odor, scar formation, and inflammation control are very important in diabetic wound management [89]. The slow healing process in diabetic wounds is due to the peripheral arterial diseases and peripheral neuropathy that occur with diabetes; the blood vessels tend to shrink, reducing blood circulation in the respective areas. The nerves do not receive enough blood (nutrients) and may become damaged and more vulnerable to injury. The stimulating tissue growth when honey is used is due to the chemical composition, the presence of assimilable sugars, vitamins, amino acids, and phenolics that increases oxygen and nutrients in the wound area [98, 99].
Numerous studies show evidence of successful honey treatments against diabetic wounds all over the world [100–105]. Honey applications reduce wound ulcer pain and size and deodorization of the wound, and reduction of healing time and are safe and there are no side effects.
A recent study [106] brings new evidence in demonstrating the effects of Manuka honey in wound healing. The results reported by the authors, based on the capacity of this type of honey to improve the responsiveness to oxidative damage, as well as stimulation of cell proliferation, could help to understand how Manuka honey develops its healing effect on wounds.
Although, some guidelines for honey applications must be used such as natural unheated honey should be used in treatments and stored in dark glass bottles in cool places. Different medical grade honey with standardized antibacterial activity for use in wound treatments are known, such as Apiban (Apimed: Cambridge, New Zealand), Woundcare 18+ (Comvita: Te Puke, New Zealand), and Medihoney (Capilano: Richmonds, Queensland, Australia) [99]. If these honeys are not available, any dark honey with high antibacterial activity may be used.
6. Conclusions
Considerable evidence from experimental studies shows that the honey may provide benefits in the management of diabetes mellitus. The benefits could be a better control of the hyperglycemic state, limiting other metabolic disorders and diminishing the deleterious effects on different organs that may produce diabetic complications. Anyway, there are some data and literature with contrary discussions regarding the use of honey in diabetic diseases.
Animal models of diabetes were employed chemically (streptozotocin or alloxan), and this may not entirely reflect the development of type 2 diabetes in humans. More studies on animals are necessary but following other animal models, closer than human type 2 diabetes.
Optimal doses for human consumption must be established, and longer period experiments must be developed, due to the fact that diabetes mellitus is a chronic disease.
Answering the main question of the study, it is true that honey may be used as a potential antidiabetic agent that has the potential to reduce the complications of diabetes, long-term studies using honey as an alternative or a complementary therapy in human subjects suffering from type 2 diabetes mellitus are needed, with a larger number of patients, randomized clinical trials set up with different levels of diabetes, treated with different doses of honey, following both short-term and long-term treatment.
As stated recently [107], “The use of honey in diabetic patients still has obstacles and challenges and needs more large sample sized, multicenter clinical controlled studies to reach better conclusions.”
Abbreviations
ALT:
Alanine aminotransferase
AST:
Aspartate aminotransferase
BW:
Body weight
CAT:
Catalase
CHD:
Coronary heart disease
CRP:
C-reactive protein
DBP:
Diastolic blood pressure
DKA:
Diabetic ketoacidosis
DM:
Diabetes mellitus
FBG:
Fasting blood glucose
FBS:
Fasting blood sugar
FPG:
Fasting plasma glucose
GI:
Glycemic index
GPx:
Glutathione peroxidase
GR:
Glutathione reductase
GSH:
Reduced glutathione
GSSP:
Oxidized glutathione
GST:
Glutathione-S-transferase
HbA1C:
Glycated hemoglobin
HDL:
High-density lipoproteins
HHS:
Hyperglycemic hyperosmolar state
MDA:
Malondialdehyde
NO:
Nitric oxide
PII:
Peak incremental index
PGL:
Plasma glucose level
SBP:
Systolic blood pressure
SGOT:
Serum glutamic oxaloacetic transaminase
SGPT:
Serum glutamate pyruvate transaminase
SOD:
Superoxide dismutase
STZ:
Streptozotocin
TAS:
Total antioxidant status
TBARS:
Thiobarbituric acid reactive substances
TC:
Total cholesterol
TG:
Triglyceride
VLDL:
Very low-density lipoprotein.
Conflicts of Interest
The authors declare that there are no conflicts of interest regarding the publication of this paper.
46. Ushijima K., Riby J. E., Fujisawa T., Kretchmer N. Absorption of fructose by isolated small intestine of rats is via a specific saturable carrier in the absence of glucose and by the disaccharide-related transport system in the presence of glucose. The Journal of Nutrition. 1995;125(8):2156–2164. [PubMed] [Google Scholar] | 12–14], cardioprotective [15–17], antibacterial [18–23], anti-inflammatory [24–26], or antitumor [27–30].
For a long time, there has been a myth that honey could not be used in diabetic patient's diet, due to the high content of carbohydrates from its chemical composition. Considering the background of the research team that has been working on characterization of different types of honey from Romania and worldwide and the determination of its biological properties for a long period, we considered being appropriate to gather in a review, literature studies that may answer the question: is honey a good substitute for sugar in diabetic diet? Are natural simple sugars important in preventing and treating diabetes mellitus?
Therefore, the present study acknowledged different scientific studies, demonstrating the use of honey in diabetes mellitus: preclinical and clinical studies, animal model studies, and human studies that demonstrate the potential impact of honey on this complex disease.
2. Fructose and the Hypoglycemic Effect of Honey
Fructose content of honey varies from 21 to 43% and the fructose/glucose ratio from 0.4 to 1.6 or even higher [31–34]. Although fructose is the sweetest naturally occurring sweetener, it has a glycemic index of 19, compared to glucose which has 100 or sucrose (refined sugar) with 60 [35]. Different studies reveal the hypoglycemic effect of honey, but the mechanism of this effect remains unclear. It was suggested that fructose, selective mineral ions (selenium, zinc, copper, and vanadium), phenolic acids, and flavonoids might have a role in the process [10, 11, 31, 33, 36, 37].
There is evidence that fructose tends to lower blood glucose in animal models of diabetes [38, 39]. | yes |
Diabetology | Can honey be a safe sugar substitute for diabetics? | no_statement | "honey" is not a "safe" "sugar" "substitute" for "diabetics".. "diabetics" should not use "honey" as a "sugar" "substitute". | https://diabetesstrong.com/how-natural-artificial-sweeteners-affect-blood-sugar/ | The Best Sweeteners for People with Diabetes - Diabetes Strong | The Best Sweeteners for People with Diabetes
I am often asked about what the best sweeteners are for people with diabetes and what can be used as a replacement for sugar that won’t raise blood sugar. That’s why I have created this in-depth guide to natural and artificial sweeteners for people with diabetes.
I get a little frustrated when reading or hearing outright incorrect claims and marketing spin about how some of the natural and artificial sweeteners affect your blood sugar.
As a person with diabetes, I want to know exactly what will happen to my blood sugar when I eat or drink something, and I don’t take kindly to half-true marketing claims.
I’ve decided to focus on which natural and artificial sweeteners are good for people with diabetes as it relates to impact on blood sugar, rather than on whether they are healthy choices in general since I think that is somewhat out of my domain and because plenty of others have already covered that.
What are natural & artificial sweeteners?
The FDA defines sweeteners as: “…commonly used as sugar substitutes or sugar alternatives because they are many times sweeter than sugar but contribute only a few or no calories when added to foods”.
This means that regular sugar, honey, and Agave nectar/syrup don’t fall into the sweetener category. However, I do want to address these quickly before moving on to the real natural and artificial sweeteners, since I’ve seen claims of how honey and agave won’t impact blood sugar in the same way as sugar.
Sugar substitutes that are NOT blood sugar friendly
Honey
Let’s start with honey because, let’s face it, it’s sugar in liquid form (82% of honey is sugar, the rest is water and small amounts of pollen, etc.).
It’s delicious, but a 2015 study in the Journal of Nutrition found that when subjects were given honey, cane sugar, or high-fructose corn syrup, they saw no notable difference in blood sugar increase.
The only benefit of honey over regular table sugar from a blood sugar perspective is that honey is slightly sweeter so you can use a little bit less of it and achieve the same sweetness. But that still doesn’t make it a good option for people with diabetes!
Agave nectar may have a lower glycemic index than sugar or honey, but it’s still up to 90 percent liquid fructose.
At the end of the day, sugar is sugar. Honey or agave nectar may be slightly better for you than pure white sugar from an overall nutrition perspective, but don’t get tricked into thinking that they are blood sugar-friendly alternatives.
Natural & artificial sweeteners that won’t affect blood sugar
None of the natural and artificial sweeteners I list below will affect your blood sugar in their raw form, but you have to make sure that the manufacturer hasn’t added anything else to the product such as fillers or flavors.
With the exception of aspartame, none of the sweeteners can actually be broken down by the body, which is why they won’t affect your blood sugar. Instead, they’ll pass through your systems without being digested, so they provide no extra calories.
Natural Sweeteners
New natural low-calorie and low-carb sweeteners have come to market in recent years, which is exciting if you’re looking to reduce your carb intake but still enjoy something sweet.
Here we’ll talk about 3 different natural sweeteners that will have little to no impact on your blood sugar
So, what is Stevia? Stevia is a completely natural sweetener since it’s simply an extract from the leaves of the plant species Stevia Rebaudiana. Most grocery stores carry it and you can purchase it as a powder, extract, or flavored drops.
In its purest processed form, Stevia is about 300 times sweeter than regular table sugar but the products available on the market have varying degrees of sweetness so it’s important to know the sweetness of the product you use.
Stevia powder: I used to buy the standard supermarket brand Stevia powder until I realized that they mix it with fillers (primarily dextrose) to make it behave more like sugar. This actually has some calorie impact as well as a minimal effect on your blood sugar if you use large amounts.
The nutritional label will claim that it’s a zero-calorie food, but that’s only because the FDA allows all food with less than 0.5 g sugar per serving to be categorized as having zero calories.
All that being said, I do still use powdered Stevia as a sugar replacement for baking as it reacts well to heat. If you use a brand like Stevia in the Raw, it substitutes one-for-one to sugar and I just acknowledge that it might have a minimal/neglectable impact on blood sugars.
The extract has a more intense flavor but you’ll get the sweetness without any calories or blood sugar impact whatsoever. To me, that’s a winner if you want a natural sweetener to sweeten up your morning coffee or oatmeal. I use the NOW brand Stevia Extract.
Flavored Stevia drops: If you have a hard time drinking enough water (or just think plain water is boring), you have to try Sweet Leaf’s Liquid Stevia Drops. You simply squirt a few drops into your water and it tastes like lemonade, but without the blood sugar impact.
Monk fruit
Monk fruit is another good choice for people with diabetes since it’s a natural sweetener that won’t affect your blood sugar.
I’ve tried it, but it’s not a product I really use simply because I prefer the taste of Stevia (monk fruit has a slightly fruity aftertaste). But that’s a personal preference, many people really like monk fruit.
It’s a good alternative if you are looking for a natural sweetener but don’t like the taste of Stevia.
Always carefully read the nutrition label when buying monk fruit extract as some brands combine the monk fruit with sweeteners like Erythritol or even sugar and molasses. I recommend the brand Monk Fruit in the Raw.
Allulose
Allulose is a simple sugar (monosaccharide) and should not affect blood sugars as it’s not metabolized by the body.
It’s a naturally occurring sweetener and can be found in small quantities in different foods such as maple syrup, brown sugar, wheat, and fruits (e.g., raisins, dried figs). However, whereas those foods will impact blood sugars and add calories to what you eat or drink, allulose won’t and is nearly calorie-free.
Allulose is 70% as sweet as regular sugar so you need to use slightly more if you are replacing regular sugar in a recipe or if you’re just sweetening your tea or coffee.
The FDA has reviewed allulose and determined that it’s a very low-calorie sweetener (i.e., no more than 0.4 kcal/g). The carbs in allulose are included on the nutrition label of foods that contain allulose (in contrast to many other low-carb sweeteners where the carbs aren’t included) but that is only because the FDA determines carb counts based on chemical markup rather than blood sugar impact.
What’s exciting about allulose, and what sets it apart from other natural sweeteners, is that clinical studies have shown that it can potentially help with blood sugar management. The studies were very small, but they showed that when people not living with diabetes as well as people living with pre-diabetes ate allulose together with carbohydrates, the blood sugar impact wasn’t as big as when allulose wasn’t included.
Artificial Sweeteners (FDA approved only)
The list below covers the FDA-approved artificial sweeteners and their brand names.
None of them should affect your blood sugar but there is a lot of controversy about whether or not they have long-term health implications. I won’t go into that in this post, but my personal preference is to stick to the natural stuff. I mean, if it pretty much tastes the same, why take the chance?
Acesulfame potassium (also called acesulfame K) – Sunett & Sweet One
Aspartame – Equal & Nutrasweet
Saccharin – Sweet ‘N Low, Sweet Twin & Sugar Twin
Sucralose – Splenda
Neotame – NA
Advantame – A Sweet Leaf, Sun Crystals, Steviva, Truvia & PureVia
Low-calorie alternatives
Other sweeteners, which are often used in diet foods, food labeled as “sugar-free”, and sugar-free gum, are sugar alcohols.
Per the American Society for Nutrition: “Sugar alcohols are slightly lower in calories than sugar and do not promote tooth decay or cause a sudden increase in blood glucose.”
The most common sugar alcohols are Maltitol, Sorbitol, Xylitol, Erythritol, and Isomalt (that’s a lot of names to remember, so I generally just categorize them as the ‘ols’).
They do indeed affect your blood sugar less than regular sugar, but their main problem is that they also work as laxatives. This means that they most likely will give you gas or cause bloating. I can eat some of them in small amounts but my body reacts badly to Xylitol.
Sugar alcohols give you about 2.5 calories/gram versus 4 calories/gram for regular sugar so if you can stomach them (pun intended), you can reduce the blood sugar impact by 50% by using any of these sweeteners. To me, this is not really worth the potential health issues and side effects.
So what are the best sweeteners for people with diabetes?
In general, there is no reason not to choose one of the natural sweeteners that don’t affect blood sugar – Stevia, monk fruit, or allulose. They are all great for people with diabetes and you can choose whichever one you think tastes the best. For baking, Stevia in the Raw is my preferred sweetener as it retains its taste and acts the most like sugar when heated.
Artificial sweeteners and sugar alcohols are not terrible, but they do potentially have side effects, the most common of which is digestive issues. I, therefore, see no reason to use them when natural and safe alternatives are available.
Sugar substitutes such as honey and agave nectar are essentially identical to normal sugar when it comes to blood sugar impact. I do keep both sugar and honey in the house for the rare occasions where I want to bake something really decadent (like a birthday cake), but I try to use it as little as possible.
About Christel Oerum
Christel is the founder of Diabetes Strong. She is a Certified Personal Trainer specializing in diabetes. As someone living with type 1 diabetes, Christel is particularly passionate about helping others with diabetes live active healthy lives. She’s a diabetes advocate, public speaker, and author of the popular diabetes book Fit With Diabetes.
Reader Interactions
Comments
I have had type 1 for 38 yrs now and have seen the progression of sweeteners and for most of us stevia is the best substitute . Why do so many places carry only sweet& low which to me is rat poison, you go into maybe a well established coffee shop sit down and all you see is some old hard & stained packets of this. Really ruins the whole coffee vibe and I live in Seattle where coffee is every where.
We used to buy stevia crystals but suddenly they’ve changed them from 3:1 amount of sweetness to 1.1: 1 and that’s enough to taste the stevia in tea rather than just adding sweetness and it is disgusting. as well as being a hidden price rise of almost 3 times, I am very unhappy. I tried stevia powder but there was no sweetness in that at all, it was a waste of money. I bought through WholeFoods which was the only firm I could find available in the UK. I will consider trying the brand you suggest, but so far as i can see, it’s a way of paying a tax for being diabetic.
My better half can’t have artificial sweetener because it gives him migraine headaches, or having mood swings, and he tried to use truvia and all it does is give him bad cases of bouts of sitting on the toilet. He has to have regular sugar as a sweetener or he won’t eat anything that needs it. He has type two diabetes, and he can’t stand the tast of coffee on its own. He needs to at least have creamer with his coffee, or none at all. He is more of a soda drinker, and he’s not too fond of teas at all either. Pure white sugar is 100% all natural, either comes from sugar beet or cane sugar. Either one he can have with no issues. But all others, forget it. So some one needs to rethink of how some diabetics needs regular sugar, over all of the artificial stuff. Some people can’t handle any artificial sweeteners at all, and my man is one of them. He started taking 1000mg of metformin, and the results was messy. 4 to 5 times a day on the toilet, now he is suffering from hemorrhoids for the past year. I even tried to use truvia, and it also made me go to the toilet on the 2nd day of using it. No thanks, but we are both going to stay with sugar!
This was a great article so thank you.
I can’t tolerate any sugar alcohols but manage PURE STEVIA quite well but the issue I have is baking with it .Most recipe say to be successful you need to add apple sauce to stabilise the cake etc . That would defeat the purpose of being type 2 diabetic & low carb . Do you have information on how you would use pure Stevia in recipe’s & the quantity you would use
Thanks Kathleen | The Best Sweeteners for People with Diabetes
I am often asked about what the best sweeteners are for people with diabetes and what can be used as a replacement for sugar that won’t raise blood sugar. That’s why I have created this in-depth guide to natural and artificial sweeteners for people with diabetes.
I get a little frustrated when reading or hearing outright incorrect claims and marketing spin about how some of the natural and artificial sweeteners affect your blood sugar.
As a person with diabetes, I want to know exactly what will happen to my blood sugar when I eat or drink something, and I don’t take kindly to half-true marketing claims.
I’ve decided to focus on which natural and artificial sweeteners are good for people with diabetes as it relates to impact on blood sugar, rather than on whether they are healthy choices in general since I think that is somewhat out of my domain and because plenty of others have already covered that.
What are natural & artificial sweeteners?
The FDA defines sweeteners as: “…commonly used as sugar substitutes or sugar alternatives because they are many times sweeter than sugar but contribute only a few or no calories when added to foods”.
This means that regular sugar, honey, and Agave nectar/syrup don’t fall into the sweetener category. However, I do want to address these quickly before moving on to the real natural and artificial sweeteners, since I’ve seen claims of how honey and agave won’t impact blood sugar in the same way as sugar.
Sugar substitutes that are NOT blood sugar friendly
Honey
Let’s start with honey because, let’s face it, it’s sugar in liquid form (82% of honey is sugar, the rest is water and small amounts of pollen, etc.).
It’s delicious, but a 2015 study in the Journal of Nutrition found that when subjects were given honey, cane sugar, or high-fructose corn syrup, they saw no notable difference in blood sugar increase.
| no |
Diabetology | Can honey be a safe sugar substitute for diabetics? | no_statement | "honey" is not a "safe" "sugar" "substitute" for "diabetics".. "diabetics" should not use "honey" as a "sugar" "substitute". | https://indianexpress.com/article/lifestyle/health-specials/sweeteners-sugar-free-diabetes-health-tips-8230228/ | Artificial sweetener as sugar substitute: is it good for you? Which is ... | Artificial sweetener as sugar substitute: is it good for you? Which is best for diabetics?
Premium
Artificial sweetener as sugar substitute: is it good for you? Which is best for diabetics?
Using artificial sweeteners may provoke a sense of complacency and drive us to eat other high-calorie food more liberally. It is common to see people digging into their brownies and pizzas but taking extra care to order only diet colas. It has been suggested that these intensely sweet substances may alter how our brains respond to signals, making less sweet substances like fruits unappealing to our senses, says Dr Ambrish Mithal, Chairman and Head, Endocrinology and Diabetes, Max Healthcare
With the growing awareness of the ill effects of sugar, particularly for those with diabetes, the quest to satisfy our sweet tastebuds without causing harmful effects has picked up pace.
The mention of the word “sweet” always conjures up visions of goodness, happiness and pleasure. Honey, sugar or sweetheart are popular terms of endearment. Sweet-tempered or sweet-natured people are always preferable to those who are bitter. Yet we all know that sugar is now blamed for many of our ills, including obesity, diabetes, heart disease and even cancer. Indians were the first to use cane sugar crystals (around 400 BCE) which they called sharkara (gravel). The word sugar itself is derived from sharkara.
With the growing awareness of the ill effects of sugar, particularly for those with diabetes, the quest to satisfy our sweet tastebuds without causing harmful effects has picked up pace. People commonly substitute sugar with brown sugar, honey and jaggery in the mistaken belief that they are safer whereas in terms of calorie content they are the same as sugar (a gram of sugar has 4 calories). Similarly many feel that fruit juice is a good substitute for colas but actually their calorie content is almost the same.
Natural sources, therefore, don’t give us many healthy options to satisfy our sweet cravings. Undoubtedly, sugar substitutes help in reducing calorie intake, since many of them have close to zero calories. A 500 ml can of a cola has approximately 12 spoons of added sugar, almost 220 calories. A can of diet cola has zero calories! Theoretically, therefore, sugar substitutes are a very attractive proposition.
Types of sugar substitutes
There are two common types of sugar substitutes — artificial sweeteners and sugar alcohols. Artificial sweeteners are synthetic substitutes and include saccharin, cyclamate, aspartame, sucralose, acesulfame and neotame. Stevia is a separate category, described as a “natural” sweetener since it is derived from plant sources.
The other variety of sugar substitutes comprises plant-derived sugar alcohols (they don’t contain alcohol!) like erythritol, mannitol and sorbitol. In addition to sweetness, they add some texture to food. The sweetness of sugar alcohols varies from 25-100 per cent as compared to sugar. Eating high quantities of sugar alcohols can cause bloating, loose stools or diarrhoea. Over a period of time, tolerance usually develops to these effects.
Sugar substitutes are widely used in processed foods, including soft drinks, jams and dairy products. Some, like sucralose, can be used in baking or cooking. It is important to check what kind of sweetener a product contains. A “sugar free” label on a product can be misleading—we then tend to consume excess amounts, considering it to be totally safe, not realising that it could be laden with fat or might contain sugar alcohols. A typical bar of sugar-free chocolate contains about 60 per cent of the calories of a regular slab.
Can sugar substitutes reverse diabetes?
Notwithstanding their commercial popularity, sugar substitutes have always attracted controversy. Other than improvement in dental health, it remains unclear if replacement of dietary sugar with artificially sweetened products can reverse the health consequences (like obesity, diabetes, and heart disease) of sugar over-consumption. In some studies, artificial sweeteners have been shown to increase the risk of diabetes and obesity, although others have not found such evidence. The WHO 2022 report on the health effects of artificial sweeteners observed modest associations between consumption of beverages with artificial sweeteners to cholesterol abnormalities and high blood pressure.
Advertisement
Using artificial sweeteners may provoke a sense of complacency and drive us to eat other high-calorie food more liberally. It is common to see people digging into their brownies and pizzas but taking extra care to order only diet colas. It has been suggested that these intensely sweet substances may alter how our brains respond to signals, making less sweet substances like fruits unappealing to our senses. Some scientists feel that the use of these products may lead us to crave more sweets.
Saccharine was once linked to cancer in rats, and aspartame to brain tumours without much evidence. Concerns like adverse impact on kidneys, memory loss, dementia and stroke are unproven. It has also been suggested that use of these sweeteners may alter our gut flora, potentially leading to a greater risk of weight gain and diabetes. The mixing of alcohol with artificially sweetened beverages increases blood alcohol levels and increases chances of intoxication.
A population-based study from France, published in September this year, involving more than 100,000 participants, followed up for more than 10 years, showed a potential association between artificial sweeteners (especially aspartame, acesulfame, sucralose) intake and cardiac disease, stroke and cancer. Since it was an association study, it cannot be regarded as definitive, but certainly suggests the need for caution in using the products.
Advertisement
Children should not consume sweeteners over long periods as the risks may be greater. Adults who consume large amounts of sweet beverages can use artificially sweetened beverages temporarily and gradually try to taper the consumption, replacing them with water. Artificial sweetener use can only help if the overall calorie intake is reduced. Those with bowel disorders and who have bariatric procedures should also avoid them completely.
How to control intake of sweeteners
What then should those of us trying to lose weight or control diabetes do? Try and give up sugar completely. If your sweet cravings are persistent, it is safe to consume sweeteners in small amounts. Adding a sweetener to your morning tea or evening coffee or to an occasional low-fat dessert is fine. | Artificial sweetener as sugar substitute: is it good for you? Which is best for diabetics?
Premium
Artificial sweetener as sugar substitute: is it good for you? Which is best for diabetics?
Using artificial sweeteners may provoke a sense of complacency and drive us to eat other high-calorie food more liberally. It is common to see people digging into their brownies and pizzas but taking extra care to order only diet colas. It has been suggested that these intensely sweet substances may alter how our brains respond to signals, making less sweet substances like fruits unappealing to our senses, says Dr Ambrish Mithal, Chairman and Head, Endocrinology and Diabetes, Max Healthcare
With the growing awareness of the ill effects of sugar, particularly for those with diabetes, the quest to satisfy our sweet tastebuds without causing harmful effects has picked up pace.
The mention of the word “sweet” always conjures up visions of goodness, happiness and pleasure. Honey, sugar or sweetheart are popular terms of endearment. Sweet-tempered or sweet-natured people are always preferable to those who are bitter. Yet we all know that sugar is now blamed for many of our ills, including obesity, diabetes, heart disease and even cancer. Indians were the first to use cane sugar crystals (around 400 BCE) which they called sharkara (gravel). The word sugar itself is derived from sharkara.
With the growing awareness of the ill effects of sugar, particularly for those with diabetes, the quest to satisfy our sweet tastebuds without causing harmful effects has picked up pace. People commonly substitute sugar with brown sugar, honey and jaggery in the mistaken belief that they are safer whereas in terms of calorie content they are the same as sugar (a gram of sugar has 4 calories). Similarly many feel that fruit juice is a good substitute for colas but actually their calorie content is almost the same.
Natural sources, therefore, don’t give us many healthy options to satisfy our sweet cravings. | no |
Diabetology | Can honey be a safe sugar substitute for diabetics? | no_statement | "honey" is not a "safe" "sugar" "substitute" for "diabetics".. "diabetics" should not use "honey" as a "sugar" "substitute". | https://naomedical.com/info/good-sugar-substitute-for-diabetics.html | What Is a Good Sugar Substitute for Diabetics? - Nao Medical - Nao ... | What Is a Good Sugar Substitute for Diabetics?
Living with diabetes means making conscious choices about what you eat and drink. One of the biggest challenges for diabetics is finding alternatives to sugar that won't spike blood sugar levels. In this blog post, we will explore the best sugar substitutes for diabetics and provide you with valuable information to help you make healthier choices.
Why Do Diabetics Need Sugar Substitutes?
Diabetes is a condition that affects the body's ability to regulate blood sugar levels. Consuming too much sugar can lead to a rapid increase in blood glucose levels, which can be dangerous for diabetics. Therefore, finding suitable sugar substitutes is crucial for managing diabetes effectively.
Best Sugar Substitutes for Diabetics
1. Stevia
Stevia is a natural sweetener derived from the leaves of the Stevia rebaudiana plant. It has zero calories and does not raise blood sugar levels, making it an excellent choice for diabetics. Stevia is available in both liquid and powdered forms and can be used in various recipes.
2. Monk Fruit
Monk fruit, also known as Luo Han Guo, is another popular sugar substitute for diabetics. It contains natural compounds called mogrosides, which provide sweetness without affecting blood sugar levels. Monk fruit sweeteners are available in granulated and liquid forms and can be used in baking and cooking.
3. Erythritol
Erythritol is a sugar alcohol that occurs naturally in some fruits and fermented foods. It has a sweet taste but does not raise blood sugar levels or contribute to tooth decay. Erythritol is available in granulated and powdered forms and can be used as a one-to-one replacement for sugar in recipes.
4. Xylitol
Xylitol is another sugar alcohol that is commonly used as a sugar substitute. It has a similar sweetness to sugar but has fewer calories and does not raise blood sugar levels significantly. Xylitol is often used in chewing gums, candies, and oral care products.
How to Choose the Right Sugar Substitute
When selecting a sugar substitute, it's essential to consider factors such as taste, texture, and cooking properties. Some sugar substitutes may have a slightly different taste or texture compared to sugar, so it's a good idea to experiment and find the one that suits your preferences.
Frequently Asked Questions
Q: Can diabetics consume artificial sweeteners?
A: Yes, diabetics can consume artificial sweeteners in moderation. However, it's important to choose sweeteners that do not raise blood sugar levels.
Q: Are sugar alcohols safe for diabetics?
A: Sugar alcohols like erythritol and xylitol are generally safe for diabetics when consumed in moderation. However, they may cause digestive issues in some individuals.
Q: Can diabetics use honey as a sugar substitute?
A: While honey is a natural sweetener, it still contains sugar and can raise blood glucose levels. It's best for diabetics to choose sugar substitutes with minimal impact on blood sugar.
Conclusion
Finding a good sugar substitute for diabetics is essential for managing blood sugar levels and overall health. Stevia, monk fruit, erythritol, and xylitol are excellent alternatives that provide sweetness without the negative effects of sugar. Remember to choose a sugar substitute that suits your taste preferences and dietary needs. Take control of your health today by making informed choices and exploring the wide range of sugar substitutes available. For more information and comprehensive healthcare solutions, visit Medical Health Authority.
Please note that this blog post is for informational purposes only and should not replace professional medical advice. Always consult with your healthcare provider before making any changes to your diet or treatment plan.
Discover the Best Sugar Substitutes for Diabetics and Take Control of Your Health Today!
Disclaimer: The content in this article is provided for general informational purposes only. It may not be accurate, complete, or up-to-date and should not be relied upon as medical, legal, financial, or other professional advice. Any actions or decisions taken based on this information are the sole responsibility of the user. Medical Health Authority expressly disclaims any liability for any loss, damage, or harm that may result from reliance on this information. Please note that this article may contain affiliate endorsements and advertisements. The inclusion of such does not indicate an endorsement or approval of the products or services linked. Medical Health Authority does not accept responsibility for the content, accuracy, or opinions expressed on any linked website. When you engage with these links and decide to make a purchase, we may receive a percentage of the sale. This affiliate commission does not influence the price you pay, and we disclaim any responsibility for the products or services you purchase through these links. | Some sugar substitutes may have a slightly different taste or texture compared to sugar, so it's a good idea to experiment and find the one that suits your preferences.
Frequently Asked Questions
Q: Can diabetics consume artificial sweeteners?
A: Yes, diabetics can consume artificial sweeteners in moderation. However, it's important to choose sweeteners that do not raise blood sugar levels.
Q: Are sugar alcohols safe for diabetics?
A: Sugar alcohols like erythritol and xylitol are generally safe for diabetics when consumed in moderation. However, they may cause digestive issues in some individuals.
Q: Can diabetics use honey as a sugar substitute?
A: While honey is a natural sweetener, it still contains sugar and can raise blood glucose levels. It's best for diabetics to choose sugar substitutes with minimal impact on blood sugar.
Conclusion
Finding a good sugar substitute for diabetics is essential for managing blood sugar levels and overall health. Stevia, monk fruit, erythritol, and xylitol are excellent alternatives that provide sweetness without the negative effects of sugar. Remember to choose a sugar substitute that suits your taste preferences and dietary needs. Take control of your health today by making informed choices and exploring the wide range of sugar substitutes available. For more information and comprehensive healthcare solutions, visit Medical Health Authority.
Please note that this blog post is for informational purposes only and should not replace professional medical advice. Always consult with your healthcare provider before making any changes to your diet or treatment plan.
Discover the Best Sugar Substitutes for Diabetics and Take Control of Your Health Today!
Disclaimer: The content in this article is provided for general informational purposes only. It may not be accurate, complete, or up-to-date and should not be relied upon as medical, legal, financial, or other professional advice. Any actions or decisions taken based on this information are the sole responsibility of the user. Medical Health Authority expressly disclaims any liability for any loss, damage, or harm that may result from reliance on this information. | no |
Diabetology | Can honey be a safe sugar substitute for diabetics? | no_statement | "honey" is not a "safe" "sugar" "substitute" for "diabetics".. "diabetics" should not use "honey" as a "sugar" "substitute". | https://www.wholesomeyum.com/sugar-substitutes/ | Sugar Substitutes: Best Healthy & Keto Sweeteners - Wholesome Yum | Wholesome Yum is a food blog for healthy recipes and keto recipes. Here you will find simple, healthy dishes made with whole food ingredients, as well as gluten-free, low carb meals -- all with 10 ingredients or less.
It’s here: the ultimate guide to sugar substitutes for baking, cooking, keto desserts, beverages, and everything in between! I get a lot of questions from people asking about the best sugar alternatives, the right keto sweeteners to use for a low carb lifestyle or diabetes, or simply how to cut refined sugar for better health or avoiding weight gain. Most of the keto options make excellent sweeteners for diabetics as well.
Not sure which keto sweetener to try first? I highly recommend starting with Besti Monk Fruit Allulose Blend! It tastes and bakes just like sugar, but unlike other brands of monk fruit, it also dissolves and browns like sugar as well.
Types Of Sugar Substitutes
For when you want that sweet taste without resorting to white sugar, there are many types of sugar substitutes to choose from. Below is an overview of all the different kinds, and we’ll cover the properties, pros, and cons of each in this article.
Powdered Sugar Substitutes – Any of the above ground to a fine powder.
One of the most significant measuring tools for sugar alternatives is glycemic index (GI), which measures how much they increase blood sugar levels. The lower, the better, but there are other factors outlined below.
Sugar Alcohol Sugar Substitutes: Erythritol & Xylitol
Sugar alcohols are sugar substitutes that can occur naturally in fruits and vegetables, or be produced by fermenting plant sugars. Because the body either does not absorb or metabolize them, they contain fewer calories (some of them have none — making them “non-nutritive sweeteners”) and have a smaller effect on blood glucose levels than sugar does.
Erythritol Sweetener
Erythritol sweetener is my favorite of the sugar alcohols and a very popular keto sweetener. It has very little aftertaste, aside from a slight cooling sensation if used in large quantities. It’s 70% as sweet as sugar.
Erythritol is naturally occurring in many fruits, but the granulated kind is made by fermenting glucose, usually from corn. (Wholesome Yum Erythritol comes from non-GMO corn.) However, because of how fermentation works, there is no corn remaining in the end product.
Erythritol has a glycemic index of 0, meaning it does not spike insulin. In comparison, xylitol has a glycemic index of 7, maltitol has a glycemic index of 35, and sucrose (table sugar) has a glycemic index of 65. The higher the number, the worse they are as sweeteners for diabetics.
Is Erythritol Keto?
Yes, absolutely! Because it is not metabolized, erythritol is keto and suitable for low carb diets. It has 0 grams net carbs.
Where To Buy Erythritol
Erythritol is available at some grocery stores, but sometimes it may be GMO. Wholesome Yum brand erythritol is always non-GMO:
Xylitol Sweetener
Xylitol is another popular natural sugar alcohol, made by fermenting corn (in the same way as erythritol) or birch.
Is Xylitol Keto?
Yes, xylitol is keto friendly, but less so than other sugar substitutes. Our bodies don’t absorb most of it, but since its glycemic index is 7 (not zero like many other sugar alternatives), it can still spike blood glucose and insulin slightly.
Other Sugar Alcohols
There are many other sugar alcohols, but they have less desirable qualities. Maltitol, sorbitol, mannitol, and isomalt are the most common ones used in commercially packaged “sugar-free” products. Unfortunately, these can actually have a substantial effect on blood sugar. They also cause stomach upset and diarrhea more often than erythritol and xylitol do. I recommend avoiding them.
Benefits Of Erythritol & Xylitol:
Erythritol – Since this sugar substitute has no calories, no carbs, no sugar, does not raise blood glucose levels, and tastes great, that makes it an almost perfect low carb sugar substitute. As a bonus, it can reduce absorption of fructose, which is not good for us. Erythritol also has anti-oxidant properties and can remove free radicals in the bloodstream [*].
Xylitol – One of the biggest advantages of xylitol is that it measures 1:1 like sugar in terms of sweetness. Unlike erythritol, it has no aftertaste (or cooling effect) and tastes closer to sugar. Toothpaste often contains xylitol, because it can actually help prevent tooth decay [*].
Plant-Based Keto Sweeteners: Monk Fruit & Stevia
Plant-based healthy sweeteners are derived from plants like monk fruit, stevia, and chicory root. Their sweetness comes from extracts or prebiotic fibers. These are natural sweeteners and are not artificial, but watch for additives on ingredient labels.
Pure monk fruit and stevia sugar substitutes (with no added ingredients) have a very concentrated sweetness, hundreds of times as sweet as sugar. This is why they are often called high-intensity sweeteners. They can be bitter on their own and are difficult to use in baking in their concentrated form. Because of this, most brands blend them with other ingredients, such as erythritol (good), maltodextrin or dextrose (not good — these are other names for sugar), or allulose (great — and this is what Besti Monk Fruit Sweetener contains).
Monk Fruit Sweetener
Monk fruit, also known as luo han guo, is a round green melon native to central Asia. Traditional Chinese medicine has used it for at least hundreds of years, with applications including treatment of diabetes and respiratory illnesses [*]. For our purposes, monk fruit makes a wonderful sugar substitute.
Monk fruit keto sweetener is collected from the monk fruit itself. After removing the skin and seeds, the fruit is crushed and the juice inside is collected. The end result is very concentrated, up to 400 times as sweet as sugar. From here, it can be suspended in liquid, dried into a pure powder, or blended with other sugar alternatives to make a more suitable sugar substitute for baking and cooking.
Is Monk Fruit Keto?
Yes, monk fruit is keto friendly. It has a glycemic index of 0. However, watch for hidden sugars on ingredient labels for monk fruit.
Mogroside V In Monk Fruit:
Different brands of monk fruit extract come with different levels of Mogroside V, which is the component in monk fruit extract that makes it sweet. This affects how sweet they are and whether they have any aftertaste, as lower concentrations are actually more bitter.
The highest grade is 50% Mogroside V, but most brands use lower grades for cost savings (if they don’t specify, it’s usually 30%). Most brands also blend the monk fruit with erythritol. This can lead to a cooling aftertaste and sometimes stomach upset (see the Side Effects section below).
Where To Buy Monk Fruit
This is why I recommend Besti Monk Fruit Allulose Blend as the best brand of monk fruit sweetener. It has the highest grade of Mogroside V (50%), is non-GMO, and is blended with allulose (not erythritol), which bakes well (see the Comparison Of Sugar Substitutes For Baking section below!), has no aftertaste, and no side effects. You can check the Wholesome Yum Foods store locator for a store near you, or buy it online:
Stevia Sweetener
Some cultures have used stevia leaves have been used as a natural sugar substitute for over a thousand years. Steviol glycosides are the active compounds derived from the stevia rebaudiana plant. They can be up to 150 times as sweet as sugar.
To make stevia sugar substitute, the leaves are dried, then steeped in hot water, like tea. Next, there is a filtering process to achieve concentration and purity. Stevia extract can be dried into a powder or suspended in liquid form.
The main issue with stevia is that it can have a bitter aftertaste, which is worse when using larger quantities. Blending it with other sweeteners, like erythritol, can help. The bitterness can also vary among brands, or even among batches from the same brand, because the age of the stevia plant leaves plays a role. Younger leaves have less bitterness, so how and when they are harvested will impact the aftertaste that results.
Is Stevia Keto?
Yes, stevia is keto friendly, if you can get past the bitter aftertaste. It has a glycemic index of 0. However, watch for hidden sugars on ingredient labels. Many brands of stevia use maltodextrin or dextrose (sugars) as a filler.
Chicory Root & Inulin Sweetener
Chicory root is the root of the Belgian endive plant and has long been used as a coffee substitute. It contains soluble fibers called inulin and fructooligosaccharides (FOS), both of which are responsible for sweetening [*]. Inulin and oligosaccharides are also found in other plants, but are most concentrated in chicory root.
Is Chicory Root Keto?
Inulin is a carbohydrate that human digestive enzymes cannot break down. Since we cannot digest it, it is a low carb keto sweetener and has zero net carbs.
Benefits Of Plant-Based Sweeteners:
Monk Fruit – The mogrosides in monk fruit have been used as treatment for sore throats, remove inflammation, and can help with diabetes and even cancer [*].
The Best Sugar Substitute: Allulose
Allulose is a relatively new natural, healthy sugar substitute with incredible benefits for cooking and baking. Even though it’s plant based, it’s neither a sugar alcohol nor an extract — it’s actually a rare type of sugar that we can’t absorb, which puts it in its own category. Despite being the same family as sugar, allulose has a glycemic index of 0 and 0 net carbs, too. Like erythritol, allulose is 70% as sweet as sugar.
Being in the same family as sugar makes allulose totally different from other keto sugar substitutes. (That’s why it ends with “ose”, just like glucose, fructose, or lactose do.) The difference from other sugars is that we can’t metabolize allulose [*]. That means it tastes and behaves like sugar without the problems of sugar. In April 2019, the FDA ruled that sugar counts on nutrition labels do not need to include allulose [*].
Even though using allulose as a packaged keto sweetener is relatively new, it has been around for a long time, because it’s naturally occurring in fruit, maple syrup, and other plants. Unfortunately, the amounts in fruit are small and difficult to extract. For this reason, allulose for us to consume is made just like erythritol, via a natural fermentation process.
Is Allulose Keto?
Allulose Benefits:
The biggest benefits of allulose are how it behaves when you cook with it — much closer to sugar than other sugar alternatives. Being in the same family, it bakes, tastes, browns, and dissolves just like sugar does. (See the Comparison Of Sugar Substitutes For Baking section below for more details.) In addition, allulose has numerous health benefits:
Allulose has a glycemic index of zero and does not impact blood sugar levels [*].
Studies on rats show that allulose may help reduce body fat, including belly fat [*, *].
Studies link allulose consumption to a reduction in fat storage in the liver [*, *]. This condition that can otherwise lead to insulin resistance and diabetes.
Where To Buy Allulose
I highly recommend Besti Monk Fruit Allulose Blend for an allulose-based sweetener that measures just like sugar. It still has all the benefits and baking properties of allulose. You can also buy plain allulose:
Liquid Healthy Sweeteners: Syrups With Natural Sugar
Many people use honey, maple syrup, or agave as healthy sweetener alternatives to sugar, and they are also paleo friendly. This can work if you don’t need a keto sweetener and they fit your lifestyle, and they do have benefits…
Benefits:
Honey – Honey is very high in antioxidants [*]. Its chemical structure also makes it a natural antimicrobial [*] and cough suppressant [*]. It has even been linked to reduction of cancer cells in lab tests [*].
Agave – Agave has a lower glycemic index than other liquid healthy sweeteners like maple syrup and honey, but fewer benefits beyond that.
Drawbacks:
Unfortunately, these sweeteners also have their drawbacks compared to some of the other sugar alternatives, particularly if used as sweeteners for diabetics:
Glycemic Index – Maple syrup has a glycemic index of 54, honey clocks in at 59, and agave comes in at a more moderate 19. This means that despite their benefits, all of them will spike blood sugar and insulin. They are not suitable sweeteners for diabetics or for a low carb lifestyle. Considering that many of the other substitutes on this page have a glycemic index of zero, there are much better options.
Calories – Even though honey, maple syrup, and agave are healthy sweeteners compared to table sugar, they are still high in calories: 60 for honey, 52 for maple syrup, and 62 for agave — and that’s in just one tablespoon [*, *, *].
Fructose – In particular, agave is higher in fructose than many sweeteners, which is linked to insulin resistance [*]. Fructose is almost entirely metabolized in the liver. With too much fructose, liver will start converting it to fat, which some research suggests could lead to fatty liver disease [*, *]. Honey also has a moderate amount of fructose (40%), wile maple syrup doesn’t have much.
Where To Buy Keto Honey & Maple Syrup
If you need keto sweeteners that will taste and behave like honey and maple syrup, try Wholesome Yum’s sugar-free versions. They are naturally sweetened with Besti (monk fruit with allulose), naturally flavored from real honey and maple, measure 1:1, and have the same consistency — but without the sugar, calories, and insulin spike. You can check the Wholesome Yum Foods store locator for a store near you, or buy them online:
Granulated Sugar Alternatives: Date & Coconut Sugar
Coconut sugar and date sugar are common paleo sugar substitutes. People not following the diet also use them as a natural healthy sweetener option.
Coconut Sugar – Coconut sugar is made from coconut palm sap, which is dehydrated to make granulated coconut sugar. It does retain a small amount of nutrients from the sap, and has a small amount of inulin, which can support gut health and slow down blood sugar spikes [*]. However, it still has a high glycemic index of 54 and is as high in calories as conventional table sugar.
Date Sugar – Date sugar is one of the least processed sweeteners. It’s the ground-up equivalent of whole, dried dates, so it retains a lot of the vitamins, fiber, and other nutrients of the dried fruit. It has a glycemic index of 42, which is lower than many nutritive healthy sweeteners, but still fairly high. On the negative side, date sugar does not melt or dissolve, and has a strong date taste that doesn’t work well in all recipes.
Both of these options are more natural and better than white table sugar. However, they do not make suitable keto sweeteners for diabetics.
Artificial Sweeteners & Why To Avoid Them
Sometimes people call monk fruit, stevia, allulose, and erythritol “artificial sweeteners”, but they are not. They are simply natural sugar substitutes. Yes, there is some processing involved to achieve the granulated keto sweeteners you can purchase for home use. But this is no less natural than the processing needed for coconut sugar, maple syrup, or white table sugar.
On the other hand, there are several truly artificial sweeteners (not found in nature) and each has potential health concerns:
Asparatame
Asparatame is known under the brand names Equal and Nutrasweet. It’s also the most common sweetener in diet sodas. It has been linked to cancer in rats and kidney strain [*, *]. It also contains phenylalanine, which can be dangerous for people with phenylketonuria (a rare disorder that causes sensitivity to this amino acid), and can affect certain medications. Neotame, a newer artificial sugar substitute derived from asparatame, has been linked to disruption of gut flora [*].
Finally, asparatame is 200 times sweeter than sugar and loses sweetness when heated. For these reasons, it’s not the best sugar substitute for baking.
Saccharin
Created in 1879, saccharin is the oldest artificial sugar substitute, often recognized by the brand name Sweet’N’Low. For many years, it was touted as the best sweetener for diabetics.
However, a 2019 study suggested that long-term consumption increases the risk of obesity, diabetes, liver and renal impairment, and even brain cancer [*]. Saccharin also has a bitter aftertaste.
Sucralose
Most well known under the brand name Splenda, sucralose has been approved by the FDA in 1998. (You can read more about sucralose here.) By FDA standards, the acceptable daily intake for a 132-pound person is 23 packets of sucralose per day [*].
Rumors have circulated that sucralose causes cancer. But, the biggest study supporting this claim involved feeding rats an amount of artificial sweetener that no human would reasonably consume (equal to hundreds of cans of diet soda a day) [*]. Other studies linking sucralose and cancer show that exposing it to higher temperatures, along with glycerol (found in fats), produced cancer-causing compounds [*]. This could mean that baking with sucralose isn’t a great idea.
In addition, a more clear issue with sucralose is that it can impact digestion and immunity by altering gut flora. A study in rats showed a reduced amount of “good bacteria” in the gut after consuming sucralose [*].
Acesulfame Potassium
Acesulfame potassium, also known as Ace-K, is an artificial sweetener that has been used in foods since 1988. Its chemical structure is similar to saccharin. A 2017 study in mice found that this sugar substitute affects the gut microbiome and can lead to weight gain [*].
Conclusion About Artificial Sugar Substitutes:
All of these artificial sugar alternatives do have zero calories and a glycemic index of zero. But, I wouldn’t call them healthy sweeteners or even keto sweeteners (except maybe for dirty keto). In addition to the specific issues above, my biggest concern with them is time. The amount of time we’ve had to observe their effects on humans is much smaller, compared to the time that people have been exposed to natural sweeteners found in plants. With so many natural choices available, it’s not worth the risk.
Best & Worst Sweeteners For Diabetics Or Keto
Whether you have diabetes or are following a keto diet, the best sugar substitutes for you to use will be the same — those with zero glycemic index. Most people following a low carb lifestyle for health reasons would also want natural sweeteners.
Best Keto Sweeteners:
Natural Granulated Keto Sweeteners – Monk fruit, stevia, or allulose. You can also use these in their powdered or brown forms.
Even though some people consider these healthy sweeteners and they may contain nutritive qualities, they are all simple sugars from a chemistry standpoint. While the ratios between glucose and fructose can vary, they will all spike blood sugar.
Side Effects Of Sugar Substitutes & How To Avoid Them
The natural sugar substitutes in this article are pretty mild in side effects, but they are possible:
Side Effects Of Sugar Alcohols:
Because sugar alcohols are not absorbed well, they can cause stomach upset, bloating, or diarrhea. Their impact on blood sugar and potential for side effects varies depending on the type of sugar alcohol.
Erythritol – Although it’s in the sugar alcohol family, erythritol does not raise blood glucose like some polyols do [*]. It is also less likely to cause gastrointestinal distress, because most of it gets absorbed in the small intestine (but is poorly metabolized [*]) and is later excreted unchanged into the urine. All other sugar alcohols reach the large intestine instead, which is why they are more likely to cause stomach upset. Still, erythritol can cause stomach issues for some people. Erythritol can also create a cooling aftertaste in cooking and baking.
Xylitol – Unlike erythritol, xylitol does not get absorbed in the small intestine. Instead, it proceeds to the large intestine, and the reaction between the natural bacteria there and the xylitol is what can cause distress. How much varies from person to person. People with dogs in the house may want to avoid keeping xylitol around, because even a small accidentally ingested amount can be lethal for a dog [*].
Side Effects Of Monk Fruit, Stevia, & Chicory Root:
Side effects with monk fruit and stevia are rare. However, since monk fruit and stevia are very concentrated in sweetness, most brands blend it with other sugar substitutes to make them measure like sugar does (check those labels!). And these other food additives can have other side effects in addition to the below.
Monk Fruit – There are no reported side effects of monk fruit sweetener. Although the Food & Drug Administration only approved it in 2010, Eastern cultures have used it for hundreds of years.
Stevia – Because the stevia plant is in the ragweed family, people with ragweed allergies can be allergic to stevia as well, leading to headaches. It’s not dangerous, but unpleasant, so if this affects you, try other sugar substitutes instead.
Chicory Root – Oligosaccharides, including inulin, do not cause stomach upset in most people, when used in reasonable amounts. However, like any fiber, they can cause stomach upset if you consume too much. Like stevia, chicory root is also in the ragweed family, so is best avoided for those with ragweed allergies. A study also showed that people allergic to birch should avoid chicory root [*].
Allulose Side Effects:
Many keto sweeteners contain erythritol (which can cause gas and bloating) or bulking agents (which can spike your blood sugar). Compared to other alternative sweeteners, allulose does not cause gas or bloating [*], and side effects are minimal.
Tips For Minimizing Side Effects:
Introduce slowly – Start with consuming just a little bit of sweetener to see how you react. Often times, you may be able to gradually increase the amount once your body gets used to it.
Use blends – Using a low carb sweetener blend can help reduce side effects because you aren’t getting too much of any one sweetener. If you notice a reaction to a particular type, try another.
Consider eliminating all sugar alcohols – If you have a sensitive stomach, it’s best to avoid xylitol and possibly erythritol (or any monk fruit or stevia blends containing them).
Be cautious with fibers – Prebiotic fiber syrups can cause bloating and gas for those sensitive to too much fiber.
Skip stevia and chicory for ragweed allergies – Stevia and chicory root may cause headaches for people that are allergic to ragweed, birch, and similar plants. Chicory root may cause other allergic reactions as well.
The keto sweetener with the least side effects is allulose (or monk fruit allulose blend), because it’s chemically most similar to sugar — without the sugar spike, of course!
Baking Sweetener Considerations
There are many factors that go into choosing sugar substitutes for baking. Their properties vary, and most don’t behave exactly like sugar does.
The number one question I get in baking recipes is people asking if they can use a different sweetener. You can use the sweetener conversion calculator here, but before you do, consider these factors when making substitutions:
Ratio of wet to dry ingredients: People often ask if they can replace a liquid sweetener with a granulated one, or vice versa. Another common question is wanting to replace a granulated sweetener, like erythritol, with a very concentrated one, like pure stevia. The answer is usually no. The problem with these swaps is that it alters the ratio between wet and dry ingredients. If that ratio changes, the end result won’t have the same texture or consistency. It could be too dense, too wet, too dry, or fall apart. Therefore, it’s best to substitute sweeteners with similar volumes and consistencies.
Function as a bulking agent: This issue is similar to the above. If you are reducing bulk by using a more concentrated sweetener than a recipe calls for, you will need to replace it with something else (such as more flour). Then, balance out the sweetness accordingly. If you increase bulk by using a less concentrated sweetener, add more wet ingredients to absorb the extra dry sweetener.
Level of sweetness: This is the easiest one. Different sugar substitutes have different levels of sweetness. So, you can’t just replace one with another in the same quantity. If you do, your end result could be too sweet, not sweet enough, or worse, have an awful aftertaste. This is where the conversion chart below can help. It doesn’t address differences in wet/dry ingredients or bulk, but it does help you convert sweetness levels as a starting point.
Browning & Caramelization: Allulose-based sweeteners brown more readily and quickly than other types. Often times, the baking temperature or time may be lower for recipes using Besti compared to other sweeteners. Further, erythritol-based sweeteners will hardly caramelize at all, so an allulose-based sweetener is best for this purpose.
Dissolving: Any sweetener that contains erythritol (whether plain or a blend) will not easily dissolve. This can lead to a gritty texture compared to liquid or allulose-based sweeteners.
Moisture: Allulose-based sweeteners lock in moisture (read: more moist baked goods, which is a great thing!), sugar alcohols tend to be drying, and other sugar substitutes are mostly neutral in this area. If you make a substitution, this can affect how dry the end result turns out.
If you ever wonder about options for sugar substitutes in one of my keto recipes, ask in the comments on that post.
Comparison Of Sugar Substitutes For Baking
Because different regular and keto sweeteners vary in consistency, volume, and level of sweetness, they will behave differently in baking.
Erythritol In Baking:
Erythritol is about 70% as sweet as sugar, so the correct conversion would indicate to use a little more compared to sugar (about 1.3 times more). However, many people use it as a 1:1 replacement for sugar without noticing a difference.
In most situations, baking with erythritol is similar to baking with sugar. You can mix it with dry ingredients or cream butter with it. However, there are several main differences when baking with erythritol instead of sugar:
Erythritol does not dissolve quite as well as sugar. It’s still possible, just a little more difficult. For any uses where a smooth texture is important, use a powdered (or confectioners) version instead for a good end result.
Erythritol can cause a cooling sensation, similar to mint. This is the only type of aftertaste that it might have, and is more prevalent when using larger quantities.
Erythritol does not caramelize. Depending on what you are trying to make, you would need to find an alternate way to achieve the same result.
Erythritol may crystallize. Like it sounds, crystallization means that crystals can form when storing foods made with erythritol (especially sauces, frostings, etc.) The result is a crunchy, gritty texture instead of a smooth one. Using the powdered form can help reduce this phenomenon, but does not fully eliminate it.
Some erythritol brands, like Swerve, add other ingredients to make them measure 1:1 with sugar, but the issues above will still exist.
Monk Fruit In Baking:
Monk fruit extract by itself (either as a powder or liquid drops) is very concentrated. This makes it difficult to use as a sugar substitute in its pure form. It’s hard to get the right amount, an aftertaste is common, and you don’t get the bulking function of regular sugar.
It’s easier to use a monk fruit blend that contains another, less concentrated sweetener or bulking agent, like allulose or erythritol. Most brands labeled “monk fruit” are actually blends for this reason, and can replace sugar 1:1 in recipes.
The way a monk fruit sugar substitute behaves in baking will be similar to the bulking agent it contains. Most brands of monk fruit will behave the same way as erythritol above, whereas Besti Monk Fruit Allulose Blend will have the advantages of allulose below.
Stevia In Baking:
If you use pure stevia powder or drops, their concentration can make it difficult to use them recipes, for the same reasons as monk fruit above. With stevia, the exact conversion amount for concentrated varieties can vary widely by brand.
There are also stevia blends, much like monk fruit, that combine stevia with erythritol to offer a product that measures 1:1 like sugar. These will have the same problems in baking as erythritol above.
Regardless of brand or blend, one thing to note is that stevia in baking does not work very well with foods that are already naturally bitter. An example of this is dark chocolate, which can sometimes amplify any stevia aftertaste. However, in many other applications, it works great.
Allulose In Baking:
Allulose-based sweeteners are my top choice for keto baking — you can use them pretty much the same way you would sugar! It’s particularly great for soft baked goods, such as cookies, muffins, cakes, pancakes, etc.
Plain allulose is about 70% as sweet as sugar, so the correct conversion would indicate to use a little more compared to sugar (about 1.3 times more). However, just like erythritol, many people use it as a 1:1 replacement for sugar without noticing a difference.
However, allulose has these additional benefits over erythritol:
Allulose creates more moist, soft baked goods. While erythritol is good for a little crunch, allulose locks in moisture beautifully, which is far more often desirable.
Allulose browns, caramelizes and dissolves like sugar. Other sugar substitutes don’t do this.
Allulose doesn’t crystallize. Erythritol can crystallize in certain situations, while allulose does not.
Chicory Root Fiber In Baking:
Chicory root fiber can be used cup-for-cup like sugar. However, it can have an aftertaste, so is best when blended with other sweeteners.
Artificial Sweeteners In Baking:
Artificial sweeteners, including sucralose, asparatame, and others, can vary widely in sweetness. Sucralose generally makes a decent 1:1 sugar substitute, whereas asparatame is sweeter and more bitter. However, I don’t recommend any of them, as there are much better natural healthy sweeteners to choose from.
Liquid Sweeteners In Baking:
Liquid sweeteners, including maple syrup (regular or zero sugar maple syrup), honey (regular or zero sugar honey), agave, and liquid inulin-based sweeteners require recipes developed for a liquid sweetener. This is because they would drastically alter the batter consistency in a baking recipe that calls for any granulated sugar or sugar alternative.
Coconut Sugar & Date Sugar In Baking:
You can use coconut sugar and date sugar in baking in the same way you’d use regular sugar. However, keep in mind that they will affect the flavor of your baked goods.
Summary Comparison Chart:
The chart below is a good summary of the most common sugar substitutes for baking. Some are keto sweeteners and some are not.
If you are on a mobile device, swipe the table below to the right to see all the info!
Sugar Substitute
Natural
Glycemic Index
Net Carbs Per Tbsp
Sweetness Compared To Sugar
Key Baking Properties
Monk Fruit (concentrated)
Yes
0
0g
150-400X
Too concentrated to use easily in pure form.
Stevia (concentrated)
Yes
0
0g
100-300X
Can be bitter. Too concentrated to use easily in pure form.
Allulose (including blends)
Yes
0
0g
0.7X plain, 1X blends
Locks in moisture in baked goods. Dissolves and caramelizes like sugar. Browns more quickly than erythritol, so may need reduced baking time or temp. Does not crystallize.
Erythritol (including blends)
Yes
0
0g
0.7X plain, 1-2X blends
Can be drying in baked goods, but good for crispy results. Does not dissolve or caramelize well. May crystallize.
Xylitol
Yes
7
3g (assumes 1/4 carbs absorbed)
1X
Can be drying in baked goods, but less than erythritol. Good for crispy results.
Browns and caramelizes, and imparts mild honey flavor. Locks in moisture in baked goods. Liquid form requires special recipes.
Zero Sugar Honey (Wholesome Yum)
Yes
0
0g
1X
Like regular honey.
Agave
Yes
19
15g
1.5X
Browns and caramelizes. Liquid form requires special recipes.
Coconut Sugar
Yes
54
12g
1X
Browns, dissolves and caramelizes like sugar, but can be more drying in comparison. Burns at a lower temp.
Date Sugar
Yes
42
6g
1.5X
Does not melt or dissolve. Has a strong date flavor.
Aspartame, Saccharin, & Acesulfame Potassium
No
0
0g
200-400X
Typically in packets or food products, not for baking. Asparatame loses sweetness when heated.
Table Sugar
Yes
65
12g
1X
Behaves like what you’d expect from sugar.
Brown Sugar Substitutes
Use brown sugar substitutes when you need to replace brown sugar to achieve the desired flavor and texture. Most of these are erythritol-based, even when they are labeled monk fruit or stevia.
Where To Buy The Best Brown Sugar Substitute
Besti Brown Monk Fruit Allulose Blend will give you the closest result to real brown sugar. It has similar moisture content and doesn’t dry out baked goods the way erythritol-based brown sweeteners do. It’s also available on Amazon.
Powdered Sugar Substitutes
Most needs for powdered sugar alternatives arise when you need a smooth consistency, for things like drinks, sauces, dressings, frosting, glaze, etc.
Unfortunately, one big difference between most keto sweeteners and sugar is their ability to dissolve. While there are many powdered sugar substitutes, most of them use erythritol as a base. Granulated versions will definitely yield a gritty texture, but even powdered ones can have this issue. Besides, erythritol can crystallize, making the problem worse. So while powdered erythritol is an okay choice for these applications, it’s not the best one.
Where To Buy The Best Powdered Sugar Substitute
To substitute powdered sugar 1-to-1, the best option is Besti Powdered Monk Fruit Allulose Blend. It dissolves easily and completely, for a silky smooth texture. It’s the only allulose-based sweetener in the world right now that is ground as fine as real powdered sugar. It’s also available on Amazon. The only other options that will come out as smooth are liquid keto sweeteners, but these will only work when the bulking aspect doesn’t matter.
Conclusion: Using Sugar Alternatives
As you can see, there are many sugar substitutes (for baking and more) to choose from! Hopefully, you are now armed with the information you need for choosing the best keto sweeteners, sweeteners for diabetics, or simply sugar alternatives that fit your lifestyle.
FREE PRINTABLE: SWEETENER CONVERSION CHART
Join 300,000+ others to get a FREE printable conversion chart for keto sweeteners!
8 Comments
This is great info. My husband has had blood sugar issues for several years, but never realized how bad it was until he got one of those monitors. Now we are both doing sugar-free and low carb eating, because I figured it would be good for me as well. I started using monk fruit/erythritol and we have been happy with its taste. Neither of us like the bitter aftertaste of stevia or other common sugar substitutes. I want to do some baking, so am happy to know about what works and what to use in place of brown sugar. Thank you for this info.
Wow.! You must work hard to put all this together. Thanks for all the hard work. Do you have a list of restaurants that serve meals without sugar.? Specifically, using the keto friendly sweeteners such as Monk Fruit, Agave, Allulose, etc.?
Hey, I'm Maya!
I create easy healthy recipes your whole family will love, as well as gluten-free keto recipes that taste just as delicious — all with 10 ingredients or less. I also wrote a couple of cookbooks. Learn more about me here or at MayaKrampf.Com. | This means that despite their benefits, all of them will spike blood sugar and insulin. They are not suitable sweeteners for diabetics or for a low carb lifestyle. Considering that many of the other substitutes on this page have a glycemic index of zero, there are much better options.
Calories – Even though honey, maple syrup, and agave are healthy sweeteners compared to table sugar, they are still high in calories: 60 for honey, 52 for maple syrup, and 62 for agave — and that’s in just one tablespoon [*, *, *].
Fructose – In particular, agave is higher in fructose than many sweeteners, which is linked to insulin resistance [*]. Fructose is almost entirely metabolized in the liver. With too much fructose, liver will start converting it to fat, which some research suggests could lead to fatty liver disease [*, *]. Honey also has a moderate amount of fructose (40%), wile maple syrup doesn’t have much.
Where To Buy Keto Honey & Maple Syrup
If you need keto sweeteners that will taste and behave like honey and maple syrup, try Wholesome Yum’s sugar-free versions. They are naturally sweetened with Besti (monk fruit with allulose), naturally flavored from real honey and maple, measure 1:1, and have the same consistency — but without the sugar, calories, and insulin spike. You can check the Wholesome Yum Foods store locator for a store near you, or buy them online:
Granulated Sugar Alternatives: Date & Coconut Sugar
Coconut sugar and date sugar are common paleo sugar substitutes. People not following the diet also use them as a natural healthy sweetener option.
| no |
Diabetology | Can honey be a safe sugar substitute for diabetics? | no_statement | "honey" is not a "safe" "sugar" "substitute" for "diabetics".. "diabetics" should not use "honey" as a "sugar" "substitute". | https://www.thehindu.com/sci-tech/health/diet-and-nutrition/hey-honey/article4977836.ece | Hey honey! - The Hindu | Hey honey!
Once used by the ancient Egyptians to anoint their gods, honey has a long history of healing and medicinal properties that have been documented in cultures and holistic practices across the world. But is it really a healthier alternative to sugar? Here are some honeyed truths and myths…
It's rich golden hue and intense sweetness awakens the senses. As you spoon it into your beverages, bake it into your cakes or slide it over bread, you vaguely recall that there may be some healthful properties. A popular home remedy even recommends that you take a spoonful of honey in water, first thing in the morning to facilitate weight loss, but these are just one of the many honey myths that abound. You will not lose weight this way and if you've opted for honey as a sugar substitute, you may be disappointed, say experts.
Not ideal for weight watchers, diabetics
"Honey for weight watchers or diabetics is not as good as it is believed to be," says nutritionist Neelanjana Singh, Heinz Nutri Life Clinic in New Delhi. "It is a myth that it does not add fat to your body. Honey has just as much carbohydrates as sugar so it is best to restrict its use, especially if you're trying to lose weight or are diabetic. Since honey has some vitamins, minerals and antioxidants, nutritionally, it is a better option when compared to sugar."
Essentially, honey is a mixture of glucose and fructose, both forms of simple sugar. And much like ordinary sugar, it is absorbed fairly quickly into your blood stream and has almost the same effect on your body. "Honey has a glycemic index value of 55 and sugar has a glycemic index of 68 which is much higher. Foods with a higher glycemic index lead to a higher rise in blood sugar levels which causes the body to keep releasing insulin from the pancreas to process all that sugar. High insulin levels in the blood have been linked to obesity, type 2 diabetes and other chronic conditions. While honey is (slightly) better than sugar in this regard, moderate use is the key," says clinical dietician Ruhi Alware who practices at Niron and Guru Nanak hospitals, Mumbai.
Keep in mind that while it gives you instant energy, the calories in honey can quickly add up. In fact, a spoonful of honey will have slightly more calories (22 calories) than an equal amount of sugar (20 calories), simply because honey is denser. However, honey does have some intrinsic healing properties.
Sweet healing
History has it that before the discovery of antibiotics, honey was widely used in healing. "Honey has been in use since ancient times, both as a food and in medicine," says Ruhi Alware. "The Ph of honey is acidic which prevents the growth of many bacteria. It also contains powerful antioxidants with antiseptic and anti-bacterial properties. It has been known to boost the immune system, providing energy as well as aiding in digestion." However, raw honey (that which has been directly collected from the honey comb and has not been processed and packaged) is found to be a far more effective anti-bacterial agent than the processed kind. The quality of honey--which is determined largely by the bee itself and the kind of flowers from which it partakes of its nectar--matters too. "Different kinds of honey have differing levels of hydrogen peroxide and this is what provides honey with its antiseptic value," explains Neelanjana Singh. "There is a special kind of honey called Manuka honey. This has very potent antiseptic properties and can be compared to powerful antiseptics such as phenol and carbolic; this honey has been used to treat wounds in diabetic patients and has aided the healing of (severe) pressure sores and leg ulcers."
The presence of substances called phytonutrients also provides honey with its medicinal qualities, in particular, its ability to prevent colon and other cancers. Unfortunately, when raw honey is subjected to excessive heat and preservatives during the pasteurization process, the benefits of these phytonutrients are largely lost. If you're interested in reaping rich nutritional benefits from honey, purchase only organic, fresh honey that is 100% pure. Also, read food labels carefully to ensure that the honey you purchase does not contain any other food additives/ingredients. It should not have a strong odour either nor should it have fermented.
No honey for your honey!
Paediatricians around the world strictly advise against feeding honey to infants and children below one year. According to the American Academy of Paediatrics' Committee on Nutrition and the US Department of Health and Human Services, honey contains spores from a certain kind of bacteria called botulism, which find their way in from dust and soil. While these spores have no effect on adults, for children, they can be fatal or can cause paralysis, especially since the immune system of infants has not matured. So though your grandparents might ask you to feed your infant honey in order to prevent cough and cold, develop a sweet voice or give him/her glowing skin, realize that real dangers can often lurk behind propagating these myths.
So should one avoid honey completely during childhood? Not necessarily, says experts. If your child is above one year, honey is perfectly safe and can even offer lasting relief from chronic cough. In a study conducted by the Penn State College of Medicine in the US, it was established that a spoonful of buckwheat honey (a variety that is available in India) before bedtime helped ease cough in children over one year. The home remedy worked better than treatment with dextromethorphan (DM), an ingredient found in many cough syrups. When taken at the right time and in moderation, honey can offer the sweet relief of nature's bounty.
Get notified by email for early access to discounts & offers on our products
Comments
Comments have to be in English, and in full sentences. They cannot be abusive or personal. Please abide by our community guidelines for posting your comments.
We have migrated to a new commenting platform. If you are already a registered user of The Hindu and logged in, you may continue to engage with our articles. If you do not have an account please register and login to post comments. Users can access their older comments by logging into their accounts on Vuukle. | Hey honey!
Once used by the ancient Egyptians to anoint their gods, honey has a long history of healing and medicinal properties that have been documented in cultures and holistic practices across the world. But is it really a healthier alternative to sugar? Here are some honeyed truths and myths…
It's rich golden hue and intense sweetness awakens the senses. As you spoon it into your beverages, bake it into your cakes or slide it over bread, you vaguely recall that there may be some healthful properties. A popular home remedy even recommends that you take a spoonful of honey in water, first thing in the morning to facilitate weight loss, but these are just one of the many honey myths that abound. You will not lose weight this way and if you've opted for honey as a sugar substitute, you may be disappointed, say experts.
Not ideal for weight watchers, diabetics
"Honey for weight watchers or diabetics is not as good as it is believed to be," says nutritionist Neelanjana Singh, Heinz Nutri Life Clinic in New Delhi. "It is a myth that it does not add fat to your body. Honey has just as much carbohydrates as sugar so it is best to restrict its use, especially if you're trying to lose weight or are diabetic. Since honey has some vitamins, minerals and antioxidants, nutritionally, it is a better option when compared to sugar. "
Essentially, honey is a mixture of glucose and fructose, both forms of simple sugar. And much like ordinary sugar, it is absorbed fairly quickly into your blood stream and has almost the same effect on your body. "Honey has a glycemic index value of 55 and sugar has a glycemic index of 68 which is much higher. Foods with a higher glycemic index lead to a higher rise in blood sugar levels which causes the body to keep releasing insulin from the pancreas to process all that sugar. High insulin levels in the blood have been linked to obesity, type 2 diabetes and other chronic conditions. | no |
Veterinary Science | Can horses vomit? | yes_statement | "horses" are capable of "vomiting".. "vomiting" is possible for "horses". | https://equusmagazine.com/horse-care/qa-horses-vomit-28006/ | Q&A: Why can't horses vomit? | Q&A: Why can’t horses vomit?
Q: Most horsepeople know that horses can’t throw up. But when my young daughter asked me why not, I didn’t have an answer. So, why can other species like cats, dogs and people vomit but not horses?
A: This question actually breaks down into two parts: Why is it physically impossible (or at least very difficult) for horses to vomit? And why should that be?
Horses have a number of key physiological differences to ensure that any food they ingest takes only a one-way trip.
Vomiting (emesis) is a complex physiological event that requires a closely coordinated sequence of reflexive motions. When you are going to throw up, you draw a deep breath, your vocal cords close, your larynx rises, and the soft palate shifts to close off your airways. Then your diaphragm contracts downward, which loosens pressure on the lower esophagus and the sphincter where it enters the stomach. Next, the muscles of the abdominal wall contract spasmodically, which puts sudden pressure on the stomach. With the upward “doors” open, the contents have a clear exit pathway. All of these separate actions happen involuntarily, of course, controlled by distinct “vomiting centers” in the brain.
Horses, however, have a number of key physiological differences to ensure that any food they ingest takes only a one-way trip. For example, the muscles of the equine lower esophageal sphincter are much stronger than in other animals, making it nearly impossible to open that valve under backward pressure from the stomach. Also, the equine esophagus joins the stomach at a much lower angle than in many animals, so when the stomach is distended, as with gas, it presses against the valve in such a way that holds it even more tightly closed. And, located deep within the rib cage, the equine stomach cannot be readily squeezed by the abdominal muscles. Finally, horses have a weak vomiting reflex—in other words, the neural pathways that control that activity in other animals are poorly developed in horses, if they exist at all.
All that said, however, vomiting in horses has occasionally been reported. But it’s possible that some of these cases may actually have been choke—the “vomited material” may have been ejected from a blockage in the esophagus, not from the stomach. It’s also possible that under certain circumstances, a seriously ill horse could regurgitate, which is different than vomiting. Vomiting is a reflexive, muscular action that expels material under great pressure. Regurgitation is passive. If the esophageal muscles go flaccid, ingested food may ooze from the nose and mouth.
Nearly every vertebrate we know of vomits. Vomiting has been observed in fish, amphibians, reptiles and birds as well as most mammals. Horses are a notable exception—as are rats, mice, rabbits and most other rodents. Usually, vomiting is a defensive action, to remove ingested toxic substances from the body, for example, but some animals have more specialized reasons for bringing food back out of their stomachs. Ruminants, like cows, regurgitate food to chew the cud. Wolves and other wild canine species may swallow food in large chunks, then carry it back to their dens to be vomited up to feed their pups.
So why did horses evolve this way? We can only speculate. At some point, the need to retain food in the stomach must have been a more important survival mechanism than the need to eject toxins. Because horses are built to graze—to take in very small portions at a time as they feed throughout the day—and because they are fairly fussy about the plants they browse, it’s possible that they never needed to vomit because they would consume toxic doses only rarely.
Another clue may come from how horses run. When a horse gallops, his intestines shift forward and back like a piston, which hammers the stomach. In any other species, that would produce vomiting. Perhaps the horse evolved such a powerful lower esophageal sphincter to prevent him from vomiting as he eluded predators. | Q&A: Why can’t horses vomit?
Q: Most horsepeople know that horses can’t throw up. But when my young daughter asked me why not, I didn’t have an answer. So, why can other species like cats, dogs and people vomit but not horses?
A: This question actually breaks down into two parts: Why is it physically impossible (or at least very difficult) for horses to vomit? And why should that be?
Horses have a number of key physiological differences to ensure that any food they ingest takes only a one-way trip.
Vomiting (emesis) is a complex physiological event that requires a closely coordinated sequence of reflexive motions. When you are going to throw up, you draw a deep breath, your vocal cords close, your larynx rises, and the soft palate shifts to close off your airways. Then your diaphragm contracts downward, which loosens pressure on the lower esophagus and the sphincter where it enters the stomach. Next, the muscles of the abdominal wall contract spasmodically, which puts sudden pressure on the stomach. With the upward “doors” open, the contents have a clear exit pathway. All of these separate actions happen involuntarily, of course, controlled by distinct “vomiting centers” in the brain.
Horses, however, have a number of key physiological differences to ensure that any food they ingest takes only a one-way trip. For example, the muscles of the equine lower esophageal sphincter are much stronger than in other animals, making it nearly impossible to open that valve under backward pressure from the stomach. Also, the equine esophagus joins the stomach at a much lower angle than in many animals, so when the stomach is distended, as with gas, it presses against the valve in such a way that holds it even more tightly closed. And, located deep within the rib cage, the equine stomach cannot be readily squeezed by the abdominal muscles. | no |
Veterinary Science | Can horses vomit? | yes_statement | "horses" are capable of "vomiting".. "vomiting" is possible for "horses". | http://www.vivo.colostate.edu/hbooks/pathphys/digestion/stomach/vomiting.html | Physiology of Vomiting | Physiology of Vomiting
Vomiting is the forceful expulsion of contents of the stomach and often, the proximal small intestine. It is a manifestation of a large number of conditions, many of which are not primary disorders of the gastrointestinal tract. Regardless of cause, vomiting can have serious consequences, including acid-base derangments, volume and electrolyte depletion, malnutrition and aspiration pneumonia.
The Act of Vomiting
Vomiting is usually experienced as the finale in a series of three events, which everyone reading this has experienced:
Nausea is an unpleasant and difficult to describe psychic experience in humans and probably animals. Physiologically, nausea is typically associated with decreased gastric motility and increased tone in the small intestine. Additionally, there is often reverse peristalsis in the proximal small intestine.
Retching ("dry heaves") refers to spasmodic respiratory movements conducted with a closed glottis. While this is occurring, the antrum of the stomach contracts and the fundus and cardia relax. Studies with cats have shown that during retching there is repeated herniation of the abdominal esophagus and cardia into the thoracic cavity due to the negative pressure engendered by inspiratory efforts with a closed glottis.
Emesis or vomition is when gastric and often small intestinal contents are propelled up to and out of the mouth. It results from a highly coordinated series of events that could be described as the following series of steps (don't practice these in public):
A deep breath is taken, the glottis is closed and the larynx is raised to open the upper esophageal sphincter. Also, the soft palate is elevated to close off the posterior nares.
The diaphragm is contracted sharply downward to create negative pressure in the thorax, which facilitates opening of the esophagus and distal esophageal sphincter.
Simultaneously with downward movement of the diaphragm, the muscles of the abdominal walls are vigorously contracted, squeezing the stomach and thus elevating intragastric pressure. With the pylorus closed and the esophagus relatively open, the route of exit is clear.
The series of events described seems to be typical for humans and many animals, but is not inevitable. Vomition occasionally occurs abruptly and in the absense of premonitory signs - this situation is often referred to as projectile vomiting. A common cause of projectile vomiting is gastric outlet obstruction, often a result of the ingestion of foreign bodies.
An activity related to but clearly distinct from vomiting is regurgitation, which is the passive expulsion of ingested material out of the mouth - this often occurs even before the ingesta has reached the stomach and is usually a result of esophageal disease. Regurgitation also is a normal component of digestion in ruminants.
There is also considerable variability among species in the propensity for vomition. Rats reportedly do not vomit. Cattle and horses vomit rarely - this is usually an ominous sign and most frequently a result of acute gastric distension. Carnivores such as dogs and cats vomit frequently, often in response to such trivial stimuli as finding themselves on a clean carpet. Humans fall between these extremes, and interestingly, rare individuals have been identified that seem to be incapable of vomiting due to congenital abnormalities in the vomition centers of the brainstem.
Control of Vomition
The complex, almost sterotypical set of activities that culminate in vomiting suggest that control is central, which indeed has been shown to be true. Within the brainstem are two anatomically and functionally distinct units that control vomiting:
Bilateral vomition centers in the reticular formation of the medulla integrate signals from a large number of outlying sources and their excitement is ultimately what triggers vomition. Electric stimulation of these centers induces vomiting, while destruction of the vomition centers renders animals very resistant to emetic drugs. The vomition centers receive afferent signals from at least four major sources:
The chemoreceptor trigger zone (see below)
Visceral afferents from the gastrointestinal tract (vagus or sympathetic nerves) - these signals inform the brain of such conditions as gastrointestinal distention (a very potent stimulus for vomition) and mucosal irritation.
Visceral afferents from outside the gastrointestinal tract - this includes signals from bile ducts, peritoneum, heart and a variety of other organs. These inputs to the vomition center help explain how, for example, a stone in the common bile duct can result in vomiting.
Afferents from extramedullary centers in the brain - it is clear that certain psychic stimuli (odors, fear), vestibular disturbances (motion sickness) and cerebral trauma can result in vomition.
The chemoreceptor trigger zone is a bilateral set of centers in the brainstem lying under the floor of the fourth ventricle. Electrical stimulation of these centers does not induce vomiting, but application of emetic drugs does - if and only if the vomition centers are intact. The chemoreceptor trigger zones function as emetic chemoreceptors for the vomition centers - chemical abnormalities in the body (e.g. emetic drugs, uremia, hypoxia and diabetic ketoacidosis) are sensed by these centers, which then send excitatory signs to the vomition centers. Many of the antiemetic drugs act at the level of the chemoreceptor trigger zone.
To summarize, two basic sets of pathways - one neural and one humoral - lead to activation of centers in the brain that initiate and control vomition. Think of the vomition centers as commander in chief of vomition, who makes the ultimate decision. This decision is based on input from a battery of advisors, among whom the chemoreceptor trigger zone has considerable influence. This straighforward picture is almost certainly oversimplified and flawed in some details, but helps to explain much of the physiology and pharmacology of vomition.
Causes and Consequences of Vomiting
The myriad causes of vomiting are left as an exercise - come up with a list based on personal experience and your understanding of the control of vomition. An important point, however, is that many cases of vomiting are due to diseases outside of the gastrointestinal tract.
Simple vomiting rarely causes problems, but on occasion, can lead to such serious consequences as aspiration pneumonia. Additionally, severe or repetitive vomition results in disturbances in acid-base balance, dehydration and electrolyte depletion. In such cases, the goal is to rapidly establish a definitive diagnosis of the underlying disease so that specific therapy can be instituted. This is often not easy and in many cases, it is advantageous to administer antiemetic drugs in order to suppress vomition and reduce its sequelae. | With the pylorus closed and the esophagus relatively open, the route of exit is clear.
The series of events described seems to be typical for humans and many animals, but is not inevitable. Vomition occasionally occurs abruptly and in the absense of premonitory signs - this situation is often referred to as projectile vomiting. A common cause of projectile vomiting is gastric outlet obstruction, often a result of the ingestion of foreign bodies.
An activity related to but clearly distinct from vomiting is regurgitation, which is the passive expulsion of ingested material out of the mouth - this often occurs even before the ingesta has reached the stomach and is usually a result of esophageal disease. Regurgitation also is a normal component of digestion in ruminants.
There is also considerable variability among species in the propensity for vomition. Rats reportedly do not vomit. Cattle and horses vomit rarely - this is usually an ominous sign and most frequently a result of acute gastric distension. Carnivores such as dogs and cats vomit frequently, often in response to such trivial stimuli as finding themselves on a clean carpet. Humans fall between these extremes, and interestingly, rare individuals have been identified that seem to be incapable of vomiting due to congenital abnormalities in the vomition centers of the brainstem.
Control of Vomition
The complex, almost sterotypical set of activities that culminate in vomiting suggest that control is central, which indeed has been shown to be true. Within the brainstem are two anatomically and functionally distinct units that control vomiting:
Bilateral vomition centers in the reticular formation of the medulla integrate signals from a large number of outlying sources and their excitement is ultimately what triggers vomition. Electric stimulation of these centers induces vomiting, while destruction of the vomition centers renders animals very resistant to emetic drugs. | yes |
Veterinary Science | Can horses vomit? | yes_statement | "horses" are capable of "vomiting".. "vomiting" is possible for "horses". | https://equinehelper.com/can-horses-throw-up/ | Can Horses Throw Up? What You Need To Know | 09 Jul Can Horses Throw Up? What You Need To Know
Are Horses Capable of Throwing Up?
As an equestrian, it is important to acquaint yourself with the normal behaviors and reactions of horses. Familiarizing yourself with potential signs of injury or illness allows you to get timely help from a professional veterinarian that could save your horses’ life. One area that is especially important to educate yourself on is the digestive health of your horse.
Can horses throw up? The way a horse’s digestive system is designed makes it nearly impossible for them to throw up, even if they are in extreme intestinal distress. In the rare occurrence that a horse vomits, it is almost always fatal, although there are a few instances where a horse has reached a full recovery after this unlikely event.
With vomiting being such a common reaction for both humans and other animals, it seems odd that a horse would not have this ability. However, there are several reasons why the horse was designed in this way.
In this post, we will discuss some of the nitty-gritty details surrounding your horse’s digestive system as well as some of the signs that they may be experiencing a form of intestinal distress.
Understanding Why Horses Rarely Vomit
Several scientific reasons explain why horses simply cannot vomit. A horse’s digestive system is comprised of several different parts, similar to that of a human. As they swallow their food, it travels down their esophagus where it eventually joins the stomach.
Located at this intersection is the esophageal sphincter muscle. This muscle relaxes when a horse is eating, allowing food to enter the stomach. Although humans also possess this muscle, it is much stronger in a horse. The strength of the esophageal sphincter muscle, along with the position of the stomach, prevents the valve from opening backward.
The angle at which the esophagus of a horse joins the stomach is much lower than that of other animals. When your horse experiences indigestion and bloating, the stomach presses up against the valve causing it to remain closed. Because of this, vomiting is nearly impossible for horses.
Instances When a Horse Might Vomit
While the design of the digestive tract of a horse makes it nearly impossible for them to throw up, there are rare instances where vomiting may occur. Unfortunately, pressure caused by a severely distended stomach may eradicate the valve that prevents vomiting.
Once again, this is highly unlikely, stomach distension in a horse must be extreme to result in vomiting. Extreme stomach pressure caused by food or gas most often leads to the rupturing of the stomach walls. This, of course, typically leads to infection of the abdomen lining, a condition that is usually fatal.
There have been a handful of cases where a horse has recovered after vomiting. However, it is imperative that you contact an emergency veterinarian immediately following any type of severe illness such as this.
Reasons Why Horses Do Not Have the Ability to Throw Up
We know the scientific reasoning behind a horse’s inability to throw up. But, why were horses created this way while other animals vomit frequently? Isn’t vomiting, after all, a defense mechanism against poison and toxic foods?
While we may never know the actual reasoning behind this design, there are many reasons why the design of a horse’s digestive system is optimal for their daily life.
In the wild, horses are known as prey for many other animals. Because of this, they frequently have to run, often in the middle of grazing. This would create severe intestinal distress for humans or other animals, resulting in vomiting. Horses, however, can run away at a moment’s notice, no matter what they were snacking on.
More often than not, a horse is found grazing with their head down. Without the strong esophageal sphincter that prevents vomiting, gravity may work against the horse, causing them to lose their meal. Since horses graze throughout the day, they must have a digestive system that supports consistent digestion without interruption.
The Dangers of a Horse Not Being Able to Throw Up
Although a horse’s inability to throw up has many benefits, there are dangers to this design. As an equestrian, it is important to understand these dangers so that you are prepared to intervene if necessary.
Throwing up is a natural response to anything that is toxic or causes discomfort. Without the ability to throw up, your horse is not able to deal with discomfort or intestinal pain. Unfortunately, they are left to simply wait it out, in hopes that the indigestion is relieved over time.
Your horse could experience intestinal discomfort as a result of eating something that is toxic to them. However, they can also have a negative reaction due to overeating. Because of this, it is your responsibility as their primary caretaker to protect them from foods that could cause discomfort or illness.
If your horse accidentally ingests something that is toxic to their system or simply eats too much food, it is important to contact your veterinarian as soon as possible.
Choking Hazard
Throwing up is also one of the ways that most animals recover after they choke. Horses do not have a good way of doing this. Most often, horses choke because they are eating too quickly.
Unlike humans, it can be hard to tell if your horse is choking. They may even seem to be breathing normally. However, if your horse is choking, they will likely begin to appear weak, depressed, and even unwilling to eat. Some horses may begin to panic or aggressively stretch their neck in attempts to clear the blockage.
You may be able to feel along the neck of your horse for any strange bumps that shouldn’t be there. At the first sign of your horse choking, remove any food from their reach and contact your veterinarian. Do your best to keep your horse calm until a professional can remove any obstruction from their throat, eliminating the danger of choking.
How to Handle Issues With Your Horse’s Digestive Tract
Because your horse does not have a great way to deal with indigestion, it is important to take care of their digestive tract to prevent issues before they arise.
Provide Your Horse With Appropriate Feed
If your horse seems uncomfortable regularly, it is wise to reach out to your veterinarian for advice on your horse’s dietary needs. You may find that changing your feed, feeding schedule, location, or calorie intake will eliminate any digestive issues your horse is experiencing.
Supplement Your Horse’s Dietary Needs
Just like humans, some horses are not able to get proper nutrients from grass or normal feeds. Fortunately, there are many equine supplements available to ensure that your horse remains in great health. It is important to consult with an equine nutritionist or veterinarian before adding supplements to your horse’s diet.
If your horse suffers from regular digestive issues, you may want to consider a digestive supplement that can help calm their digestive tract and prevent gastric ulcers. Antacids, fiber, collagen, aloe, and licorice are often used to improve the digestive health of horses.
Many equestrians also give their horse probiotics to support proper digestion and prevent colic. If your horse is a picky eater, they may refuse to eat if they taste add supplements. There are, however, many ways to disguise supplements and train your horse to eat their supplements without hesitation.
Eliminate Potential Hazards For Your Horse
This should go without saying but as a horse owner, it is your responsibility to eliminate potential hazards in your horse’s environment. Certain plants, nightshades, and even seemingly harmless treats can cause intense intestinal distress and even death.
You can learn more about different plants that are poisonous for horses in the article I wrote here.
Provide Your Horse With Plenty of Exercise
Movement and exercise will help encourage optimal digestion. It is important to make sure that you are providing your horse with enough exercise to maintain a healthy system. Even as little as 20 minutes a day in a pen or riding area will help to prevent gas buildup and indigestion. Here’s my guide for some of my favorite ways to exercise a horse.
Look for Signs of Discomfort
Your horse will know when they are experiencing indigestion and intestinal discomfort. It is your responsibility as the owner to notice the signs they are sending and intervene as needed. Agitation, loss of appetite, resistance to exercise, or any change in attitude could be signs that your horse is experiencing indigestion. As you begin to learn the normal behaviors and patterns of your horse, you will be able to more clearly recognize signs of illness or injury.
Final Thoughts
As a horse owner for many years, I’ve experienced a wide range of illnesses and injuries with my horses. Learning more about their normal responses to these unfortunate events allows me to intervene and provide relief when necessary by contacting a veterinarian.
Timely intervention during indigestion or other health scares is crucial to the overall health and wellbeing of your equine companion. If you are ever questioning the health or condition of your horse, it is important to contact a professional equine nutritionist or veterinarian for advice. After all, your horse is relying on you to provide them with the best quality care available. Owning a horse is a privilege and a gift, it is important to treat it as such.
P.S. Thank you for reading! If you got any value from this article, there are a couple of ways you can support me. 1: Share this article using one of the buttons below! 2: Subscribe to my YouTube Channel here where I’m sharing new videos every week. Thank you!
I’m a lifelong horse trainer and horseback rider who’s passionate about teaching others about the things I’ve learned. I grew up competing in numerous English horseback riding disciplines and am now a certified equine massage therapist. I currently own three horses.
About Us
Hi! I’m Carmella. My husband and I started Equine Helper to share what we’ve learned about owning and caring for horses. I’ve spent my whole life around horses, and I currently own a POA named Tucker. You can learn morehere. Thank you for reading, and happy trails!
Legal Information
This site is owned and operated by Wild Wire Media LLC. Equinehelper.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com. This site also participates in other affiliate programs and is compensated for referring traffic and business to these companies. | 09 Jul Can Horses Throw Up? What You Need To Know
Are Horses Capable of Throwing Up?
As an equestrian, it is important to acquaint yourself with the normal behaviors and reactions of horses. Familiarizing yourself with potential signs of injury or illness allows you to get timely help from a professional veterinarian that could save your horses’ life. One area that is especially important to educate yourself on is the digestive health of your horse.
Can horses throw up? The way a horse’s digestive system is designed makes it nearly impossible for them to throw up, even if they are in extreme intestinal distress. In the rare occurrence that a horse vomits, it is almost always fatal, although there are a few instances where a horse has reached a full recovery after this unlikely event.
With vomiting being such a common reaction for both humans and other animals, it seems odd that a horse would not have this ability. However, there are several reasons why the horse was designed in this way.
In this post, we will discuss some of the nitty-gritty details surrounding your horse’s digestive system as well as some of the signs that they may be experiencing a form of intestinal distress.
Understanding Why Horses Rarely Vomit
Several scientific reasons explain why horses simply cannot vomit. A horse’s digestive system is comprised of several different parts, similar to that of a human. As they swallow their food, it travels down their esophagus where it eventually joins the stomach.
Located at this intersection is the esophageal sphincter muscle. This muscle relaxes when a horse is eating, allowing food to enter the stomach. Although humans also possess this muscle, it is much stronger in a horse. The strength of the esophageal sphincter muscle, along with the position of the stomach, prevents the valve from opening backward.
The angle at which the esophagus of a horse joins the stomach is much lower than that of other animals. When your horse experiences indigestion and bloating, the stomach presses up against the valve causing it to remain closed. | no |
Veterinary Science | Can horses vomit? | yes_statement | "horses" are capable of "vomiting".. "vomiting" is possible for "horses". | https://www.reconnectwithnature.org/news-events/the-buzz/nature-curiosity-why-dont-squirrels-throw-up/ | Nature curiosity: Why don't squirrels throw up? | Forest Preserve ... | The Buzz
Nature curiosity: Why don't squirrels throw up?
Vomiting is one of the most universally dreaded human behaviors. Some people even fear it, a condition called emetophobia. And while vomiting is despised by most, it can be useful in helping rid our bodies of dangerous substances that could otherwise harm us or make us sick.
Scientists have long known that rodents aren't able to vomit, but the reason behind it has only more recently been understood, according to Smithsonian. In particular, a study into why rodents don't vomit has focused on their brains as well as the anatomy of their digestive systems.
A 2013 study by University of Pittsburgh neurobiologists on rodents and their inability to vomit investigated their brain stems by giving rodents substances that are known to trigger nausea and vomiting in other animals. The rodents in the study did not exhibit any of the mouth, throat, shoulder and nerve activity normally associated with throwing up, so the researchers concluded the rodents' brains do not have the neurological circuits that allow for vomiting.
The anatomy of their abdominal area and digestive tract also contributes to the inability to vomit. For example, their diaphragms are weaker than those of other species, and their stomachs are not designed in a way that allows the contents to easily move up through the esophagus, according to the study.
The inability to vomit isn't necessarily beneficial. In fact, it's precisely the reason rat poison is effective for rodent control. Most mammals, after ingesting a poisonous or toxic substance, will vomit. Rats and rodents cannot, so the poison then quickly kills the animals.
While most mammals are able to vomit, rodents aren't the only exception. Horses don't throw up either. The reasons they can't are related to their physiology and anatomy as well. First, the esophageal sphincter is much stronger in horses than in most other animals, making it difficult for it to open under backward pressure from the stomach, according to Equus magazine. Horses also have a weak gag reflex. And finally, their anatomy, with the stomach and esophagus joined at a lower angle than in many animals, would make it difficult for vomit to travel up and out of a horse.
Support the Forest Preserve District by making a donation to the Nature Foundation of Will County. Your donation will go toward enhancing the Forest Preserve's education, conservation and recreation programs. | The Buzz
Nature curiosity: Why don't squirrels throw up?
Vomiting is one of the most universally dreaded human behaviors. Some people even fear it, a condition called emetophobia. And while vomiting is despised by most, it can be useful in helping rid our bodies of dangerous substances that could otherwise harm us or make us sick.
Scientists have long known that rodents aren't able to vomit, but the reason behind it has only more recently been understood, according to Smithsonian. In particular, a study into why rodents don't vomit has focused on their brains as well as the anatomy of their digestive systems.
A 2013 study by University of Pittsburgh neurobiologists on rodents and their inability to vomit investigated their brain stems by giving rodents substances that are known to trigger nausea and vomiting in other animals. The rodents in the study did not exhibit any of the mouth, throat, shoulder and nerve activity normally associated with throwing up, so the researchers concluded the rodents' brains do not have the neurological circuits that allow for vomiting.
The anatomy of their abdominal area and digestive tract also contributes to the inability to vomit. For example, their diaphragms are weaker than those of other species, and their stomachs are not designed in a way that allows the contents to easily move up through the esophagus, according to the study.
The inability to vomit isn't necessarily beneficial. In fact, it's precisely the reason rat poison is effective for rodent control. Most mammals, after ingesting a poisonous or toxic substance, will vomit. Rats and rodents cannot, so the poison then quickly kills the animals.
While most mammals are able to vomit, rodents aren't the only exception. Horses don't throw up either. The reasons they can't are related to their physiology and anatomy as well. | no |
Veterinary Science | Can horses vomit? | no_statement | "horses" cannot "vomit".. vomiting is not a natural ability for "horses". | https://www.horsesandus.com/why-cant-horses-vomit/ | Why can't horses vomit? Surprising Facts | Why can’t horses vomit? Surprising Facts
Vomiting is an essential survival mechanism for many animals, including us. It is a way to get toxic substances out of the body before they can cause harm. Surprisingly, horses do not have this ability.
Horses can’t vomit because their digestive tract is designed to move food in only one direction. The main reason is that their cardiac sphincter squeezes so tightly that pressure from the stomach cannot open it. Under extreme pressure, it is more likely that the stomach wall will burst.
There are other characteristics of the horse’s digestive system that do not allow the horse to vomit. We will explain them in this article and also the reasons why the horse was designed this way.
Why it is physically impossible for horses to vomit
The horse is adapted to eat small and frequent portions of food. Thus its digestive system has a series of one-way passages (sphincters) to keep the food constantly moving in a one-way direction along the digestive tract. This prevents the horse from being able to vomit the food.
There are 3 main reasons why the horse can’t vomit.
1 – The muscles of the esophagus contract in only one direction
The esophagus is a muscular tube, approximately 1.5 m (60 inches) long. It moves the food from the mouth to the stomach through a series of rippling muscular contractions called peristaltic waves.
In a horse, these contractions work in only one direction, from the mouth to the stomach. This means that the horse cannot bring the food back up the esophagus to vomit.
Other animals (the ones that can vomit) have the ability to reverse these muscle contractions in the opposite direction so that vomiting can be possible.
2 – The cardiac sphincter is very strong
A muscular ring called the cardiac sphincter, also known as the lower esophageal sphincter (LES), connects the esophagus to the stomach. This sphincter acts like a valve that relaxes to let the food into the stomach, and afterward, it closes by squeezing down the opening.
In a horse, this sphincter is very strong. Once it closes, it is almost impossible to open under the pressure made when the horse’s stomach becomes bloated with either gas or food.
In other animals (those that can vomit), this sphincter is a two-way valve. It lets the food travel normally into the stomach. But also, when pressure builds in the stomach, it opens to allow food or gas to move back into the esophagus and out of the mouth.
3 – The Esophagus joins The Stomach At A Sharp Angle
In horses, the esophagus joins the stomach at a sharp angle. So when the stomach is distended with gas or food, the stomach wall will press against the cardiac sprinter, closing it even more tightly.
The cardiac sphincter’s strength and the angle between the esophagus and the stomach explain why a horse’s stomach would actually explode before he could vomit.
However, occasionally it is reported that a horse has vomited. But most likely, these are cases of horses choking rather than actually vomiting.
If it is, in fact, a case of vomiting, then the stomach is probably ruptured, and the horse will die. However, there have been very rare cases of horses that actually vomited and survived.
Why horses were designed To Not Vomit
Certainly nature designed horses this way because it brought them an advantage for survival.
We do not know for certain why the horse evolved this way, but we can identify some reasons why this may be beneficial for them.
Advantages of horses not being able to vomit
1. Not Vomiting When Running
Studies have shown that when horses are running, the abdominal muscles’ contraction forces the food into the upper part of the stomach. This is the area of the stomach that connects to the esophagus.
If the cardiac sphincter did not block the passage to the esophagus, the food would also flow into the esophagus and most probably out of the mouth.
This would result in the vomiting of food every time a predator chased the horse, which would have the following consequences:
more vulnerable to being caught by the predator.
loss of nutrients
This would obviously put at risk the survival of the horse. So not being able to vomit will eliminate this risk.
2. Protect the Esophagus From Acidic Stomach Liquid
Horses produce a very acidic gastric liquid to quickly break down the food and move it into the intestine.
However, they continuously produce gastric acid even when they are not eating, which means that acidic liquid is always present in their stomach. Horses can produce up to 16 gallons/60 liters of acidic gastric liquid per day.
Because of the cardiac sphincter’s impossibility to open, this acidic fluid will not be able to flow into the esophagus and damage it.
So not being able to vomit protects the esophagus from being damaged by the acidic stomach liquid.
How Horses Compensate the Inability to Vomit
Since horses cannot vomit, they developed instead their first defense line, which prevents them from needing to vomit.
1. Horses Will Usually Avoid Food That can Make Them Sick
Horses are very instinctive and are naturally picky about what they eat. They continuously sift through the vegetation and only pick what they like most. They will usually avoid food that can cause them to become sick. Toxic food is normally not tasteful for them, and they will reject it.
So when horses are in their natural environment, they usually do not need to vomit to expel toxic substances. This is because they adapted to strengthen instead their first line of defense to avoid foods that can be toxic.
2. Horses Do Not Eat Excess Food That Would Need to Be Expeled
Horses are continuous grazers rather than gorgers. They eat many small meals during the day because they have a small stomach (approx 8 – 12 liters capacity). Also, the food moves quickly through the stomach (sometimes it only takes 15min).
Thus, the horse’s stomach does not tend to get full of food (because the meals are small) nor with gas (because the food moves quickly out of the stomach).
So when horses are in their natural environment, they usually do not need to vomit or burp to expel excess food or gas.
The danger of horses not being able to vomit
Since horses can’t vomit, they have no way to get rid of the harmful substances. These will remain inside the body and put their health at risk and, in some cases, can even lead to death.
Domestic Horses are more exposed to harmful substances.
As we have mentioned earlier in this article, when horses are in their natural environment, they will rarely need to vomit.
But this is not the case with most horses today because they are exposed to toxic substances that would usually not exist in their natural environment.
Following are some of the risks to which horses are exposed nowadays.
Animal feed that is intended for other species and contaminated with substances that are toxic to horses, such as cacao by-products or antibiotic additives.
Poisonous plants, like, for example, oleander and yew.
Pesticides in the stables and herbicides in the fields.
Rotting hay and moldy corn.
Everyone who takes care of horses should know about these risks and make sure they don’t exist in their environment.
When to Call the Veterinarian
If you notice your horse is not feeling well and suspect that he has ingested something toxic, you should not try to solve this on your own. This is an emergency, and you should call your veterinarian immediately.
Meanwhile, until the veterinarian arrives, you should keep the horse away from the toxic substance and make sure he has fresh water available to drink.
You should never give your horse anything to make him vomit because this will cause major stomach spasms, which can lead to death.
How The Vet Can Help The Horse Expel Harmful Substances
When the veterinarian arrives, he will ask you to describe what happened and examine the horse to evaluate the situation’s severity.
He may take the following actions:
Do a gastric lavage with a nasal tube to remove the toxic substance from the stomach. The vet will pass the tube through the nose, down the esophagus, through the cardiac sphincter, and finally into the stomach.
But since the food passes quickly through the stomach, the poison may have already passed the pyloric sphincter and moved into the intestines. So, in this case:
The vet can use oral substances that can reach the intestines to help absorb the toxins, like activated charcoal.
He may administer laxatives or mineral oil to speed up the intestinal transit so that the toxic substance can leave the body as soon as possible.
These actions may save the horse, and the key to success is to do an intervention as soon as possible.
Choking may be confused with vomiting
If a horse has a greenish or brownish foamy liquid with food particles coming out of his mouth and nose and is snorting, coughing, stretching his neck, and shaking his head… it may look like he is vomiting.
But since a horse cannot vomit, he is most probably choking.
Choking in horses may look alarming, but it is different from choking in humans. Unlike humans, horses that choke do not have difficulty breathing because the problem is not in the trachea but instead in the esophagus.
What Can Cause A Horse To Choke
Horses will choke when something gets stuck in the esophagus such as:
Food that is too dry or coarse (hay or straw)
Food that was not completely chewed (apples, carrots, etc.)
Food that swells quickly after being chewed (sugar beet)
Any item not intended for eating but which a curious horse may have swallowed.
If you think that your horse is choking, you should immediately call your vet and remove all food and water from his reach.
The horse will be distressed, so try to keep him calm until help arrives.
How The Vet Can Help A Choking Horse
When the vet arrives, he will assess the situation and try to remove the obstruction from the esophagus.
He may sedate the horse to relax him so that the esophagus can dilate and allow the horse to swallow and remove the obstruction.
He may pass a tube from the nose to the stomach to remove the obstruction.
In severe cases, surgery may be necessary to remove the obstruction.
Can Horses Burp?
Horses cannot burp for the same reason they cannot vomit. The cardiac sphincter does not allow anything to move out of the stomach into the esophagus: neither food (vomit) nor gas (burp).
In humans, the cardiac sphincter can relax and allow gas to escape from the stomach in the form of a burp.
In horses, gas can only move in a one-way direction. So when the stomach fills with gas, the only way out is to move through the intestines and escape through the anus.
However, you may have heard from your horse a noise similar to burping. But this is air being released from the esophagus as a result of cribbing and wind sucking.
Cribbing and wind sucking force air down the esophagus, making a burping noise when it comes back out. | So when horses are in their natural environment, they usually do not need to vomit or burp to expel excess food or gas.
The danger of horses not being able to vomit
Since horses can’t vomit, they have no way to get rid of the harmful substances. These will remain inside the body and put their health at risk and, in some cases, can even lead to death.
Domestic Horses are more exposed to harmful substances.
As we have mentioned earlier in this article, when horses are in their natural environment, they will rarely need to vomit.
But this is not the case with most horses today because they are exposed to toxic substances that would usually not exist in their natural environment.
Following are some of the risks to which horses are exposed nowadays.
Animal feed that is intended for other species and contaminated with substances that are toxic to horses, such as cacao by-products or antibiotic additives.
Poisonous plants, like, for example, oleander and yew.
Pesticides in the stables and herbicides in the fields.
Rotting hay and moldy corn.
Everyone who takes care of horses should know about these risks and make sure they don’t exist in their environment.
When to Call the Veterinarian
If you notice your horse is not feeling well and suspect that he has ingested something toxic, you should not try to solve this on your own. This is an emergency, and you should call your veterinarian immediately.
Meanwhile, until the veterinarian arrives, you should keep the horse away from the toxic substance and make sure he has fresh water available to drink.
You should never give your horse anything to make him vomit because this will cause major stomach spasms, which can lead to death.
How The Vet Can Help The Horse Expel Harmful Substances
When the veterinarian arrives, he will ask you to describe what happened and examine the horse to evaluate the situation’s severity.
| no |
Veterinary Science | Can horses vomit? | no_statement | "horses" cannot "vomit".. vomiting is not a natural ability for "horses". | https://thehorse.com/165668/motion-sickness-trailer-loading-troubles-and-your-horse/ | Motion Sickness, Trailer Loading Troubles, and Your Horse – The ... | Q.My 11-year-old gelding is somewhat high strung and becomes nervous when hauled. I would like help in managing his nervousness, especially when trailering and, of course, safety is important! In the four years I’ve owned him, we’ve worked with various trainers and he is easier to load, but still scrambles constantly and lathers with sweat when hauled, even over short distances. I think he might have motion sickness. Do horses get motion sickness and what can I do?
—Via e-mail
A.Some horses do suffer from motion sickness, but not much is known about it or how common it is. Transporting horses involves a number of challenges, including loading, confinement, restraint, environment (e.g., road noise), and movement.1 Researchers Santurtun and Phillips investigated the effect of vehicle motion on a few livestock species, including horses.2 Some animals experienced clinical signs consistent with motion sickness, including: salivation and licking/chewing, gastrointestinal (GI) symptoms and frequent defecation, eating or chewing on nonfood items (pica), elevated heart rate, stress behaviors, teeth grinding, pawing, and stepping back and forth to maintain balance. Emesis (vomiting) is also a GI sign of motion sickness, but horses can’t vomit.
A video you shared shows that your gelding was relatively easy to load but his behavior problems began as soon as the trailer started to move. He scrambled, leaned against the trailer wall and divider, raised his head and pulled back against the lead rope, dropped his hindquarters with legs splayed, and shifted position frequently. After a few minutes he was lathered in sweat. These behaviors suggest that he is struggling to maintain balance, even though the trailer is moving slowly and has nonskid flooring. The balance challenges and possible motion sickness would understandably also make your horse nervous.
Why do animals get motion sickness?
Experts don’t know exactly why some animals get motion sickness. A leading theory is that it’s caused by conflicting sensory input from the visual system (eyes), vestibular system (ears), and proprioceptors (joints). One sensory system is telling the horse that its moving, but another system is telling the horse that its standing still; the contradictory signals to the brain cause motion sickness. This would be similar to becoming carsick.
A second theory is that motion sickness is caused by vehicle movement and the resulting postural instability. This would be like standing up in a small boat on rough seas. Santurtun and Phillips found evidence supporting the second theory2; livestock with motion sickness made persistent efforts to control and stabilize their balance during transport. A horse needs to make adjustments to stay standing upright in a moving vehicle, because the “ground” is unstable. They’ll typically brace themselves by splaying their legs and raising their heads and necks1, which describes your horse’s stance exactly. Heart rate increases during trailering, so not only are these horses unbalanced, they also appear to be stressed out.
How is motion sickness managed?
To manage motion sickness, an important first step is to reduce vehicle movement. A skilled transport driver will avoid rough roads, refrain from sudden braking and acceleration, and take smooth, slow turns around corners.3 Leaning against something in the trailer—such as other animals and fixtures—can also help the horse stay balanced during transport. They also need enough room to step back and forth, adopt a splayed stance, and raise and lower their head. A few studies2,4 have found that horses loaded facing backward (opposite the direction of travel) are less likely to lose their balance and have lower heart rates than horses facing forward, but other research has found that a horse’s orientation in the trailer has little or no effect on its ability to balance.5 A camera installed in the trailer will allow you to look for any signs of distress or problems your horse may have maintaining balance.
Can medication help reduce motion sickness?
Dogs, and especially puppies, often become sick when riding in a moving vehicle. Veterinary treatment for motion sickness in dogs is relatively advanced and prescription and nonprescription medications are available to reduce nausea, drooling, and vomiting. By contrast, few veterinary treatment options are available to relieve signs of motion sickness in horses. Management (described above) and nonprescription supplements calming supplements might be recommended by veterinarians and behaviorists to reduce anxiety related to transport. I contacted several equine veterinarians and thoroughly searched the literature, but to the best of my knowledge a veterinary protocol for horses that includes medication for treating motion sickness is not yet available.
Take-Home Message
Some horses with suspected trailer loading problems are probably suffering from motion sickness, which can’t be fully resolved through management and behavior modification techniques alone. During transport these animals struggle with balance, suffer GI distress, and become anxious. Horses might also anticipate this unpleasant experience and become reluctant to trailer load. As someone who suffers from motion sickness and relies on a Scopolamine patch for relief, I have great empathy for these horses and look forward to the improved welfare and reduced transport-related problems that will come with advances in our understanding and treatment of equine motion sickness.
About The Author
Robin Foster, PhD, CAAB, IAABC-Certified Horse Behavior Consultant, is a research professor at the University of Puget Sound in Seattle, Washington, and an affiliate professor at the University of Washington. She holds a doctorate in animal behavior and has taught courses in animal learning and behavior for more than 20 years. Her research looks at temperament, stress, and burn-out as they relate to the selection, retention, and welfare of therapy horses. She also provides private behavior consultations and training services in the Seattle area. | Emesis (vomiting) is also a GI sign of motion sickness, but horses can’t vomit.
A video you shared shows that your gelding was relatively easy to load but his behavior problems began as soon as the trailer started to move. He scrambled, leaned against the trailer wall and divider, raised his head and pulled back against the lead rope, dropped his hindquarters with legs splayed, and shifted position frequently. After a few minutes he was lathered in sweat. These behaviors suggest that he is struggling to maintain balance, even though the trailer is moving slowly and has nonskid flooring. The balance challenges and possible motion sickness would understandably also make your horse nervous.
Why do animals get motion sickness?
Experts don’t know exactly why some animals get motion sickness. A leading theory is that it’s caused by conflicting sensory input from the visual system (eyes), vestibular system (ears), and proprioceptors (joints). One sensory system is telling the horse that its moving, but another system is telling the horse that its standing still; the contradictory signals to the brain cause motion sickness. This would be similar to becoming carsick.
A second theory is that motion sickness is caused by vehicle movement and the resulting postural instability. This would be like standing up in a small boat on rough seas. Santurtun and Phillips found evidence supporting the second theory2; livestock with motion sickness made persistent efforts to control and stabilize their balance during transport. A horse needs to make adjustments to stay standing upright in a moving vehicle, because the “ground” is unstable. They’ll typically brace themselves by splaying their legs and raising their heads and necks1, which describes your horse’s stance exactly. Heart rate increases during trailering, so not only are these horses unbalanced, they also appear to be stressed out.
How is motion sickness managed?
To manage motion sickness, an important first step is to reduce vehicle movement. | no |
Astronomy | Can humans live on Mars? | yes_statement | "humans" can "live" on mars.. it is possible for "humans" to "live" on mars. | https://www.swissinfo.ch/eng/business/we-will-never-live-on-mars--or-anywhere-else-besides-earth/46510576 | We will never live on Mars, or anywhere else besides Earth - SWI ... | Search function
We will never live on Mars, or anywhere else besides Earth
Following a groundbreaking year for exploration of the Red Planet, University of Geneva astrophysicist Sylvia Ekström and designer Javier Nombela argue that our trips to Mars should and will remain the job of robots.
This content was published on April 7, 2021 - 15:12April 7, 2021 - 15:12
Sylvia Ekström has been a doctor in astrophysics since 2008, specialising in stellar physics. She is responsible for communications at the Department of Astronomy at the University of Geneva.
Javier G. Nombela is a graphic designer specialising in the visual representation of time. He is also the author of numerous popular works in the field of astronomy.
Can humans handle a trip to Mars?
The human body has been shaped by millions of years of evolution on Earth. It is therefore perfectly adapted to an environment subject to a certain gravity and pressure value and protected from solar and galactic radiation by the dual protection of the Earth's atmosphere and magnetosphere. If it leaves this environment, it is subjected to great physiological stress.
Loss of muscle mass: life is too easy for our muscles in zero gravity and they melt away;
Weakening of the heart: with less effort to make, it becomes weaker and rounder;
Fluids (blood, lymphatic system) flow upwards to the upper parts of the body. Our entire vascular system is designed to fight gravity and pump upwards, which it continues to do even when gravity is gone;
Risk of thrombosis: as a result of the above two points, the blood circulates less quickly and can clot;
Disturbance of the inner ear: our balance organ functions thanks to the weight of small crystals on hair cells, and without gravity that is lost.
The loss of muscle mass and the weakening of the heart can be partially countered by a strict discipline of daily exercise. On the ISS, astronauts do two hours of intense fitness (cardio and weight training) per day, and yet they are very weak when they return to Earth. Bone decalcification is also slowed down by weight training but remains one of the most worrying issues for the health of potential Martian astronauts, as a fracture could prove fatal on Mars. Vascular problems are also considered extremely dangerous.
The limits of artificial gravity, radiation and the human psyche
Could gravity be recreated on the Mars spacecraft? It is known that in a rotating system, the centrifugal force produces an acceleration that can be used to recreate an equivalent of gravity. Unfortunately, there is not enough room on a spacecraft to incorporate a centrifuge in which cosmonauts could spend a few hours a week, which would be sufficient to reduce the physiological damage of microgravity.
Could the spacecraft itself be rotated? In Hollywood, yes, it's easy! But in real life, it's a different story. Given that a spinning spacecraft would solve all the problems associated with weightlessness, the fact that no space agency is banking on such a development shows that it is totally out of our reach conceptually, technically and financially.
The second major problem faced by potential future Mars-bound astronauts is that of radiation in space. The Earth's double protection (atmosphere and magnetosphere) partially blocks or deflects UV rays and totally blocks X-rays and gamma rays as well as solar wind particles and cosmic rays. This protection has been compared to the equivalent of a 30-metre-thick concrete wall, or one made of 80 centimetres of lead. Once they leave this natural barrier, it is essential that the astronauts be protected in other ways, by means of the spaceship's insulation and/or individual shields. Despite these protections, it is estimated that Martian astronauts would receive the maximum accepted radiation for an astronaut's entire career over the course of their mission, with just over half of this occurring during the outward and return journeys.
A third major problem identified by the space agencies is human psychology. French astronaut Thomas Pesquet cites a good example of the psychological pressure astronauts face on the ISS: you know there will inevitably be problems during your stay, but you don't want to be the one to cause them. The pressure on a Mars-bound crew would be infinitely greater, as there would be no help available to them in the event of a major problem. On the ISS, astronauts can be returned to Earth within three hours. The Martian astronauts would be left to their own devices for the two-and-a-half years of their mission, knowing that the slightest error or failure, whether technical or human, could result in the death of the entire crew. It is impossible to test such a psychological situation on Earth. The Mars 500 psychological isolation experiment conducted by the European Space Agency developed methods of conflict resolution, but it is in no way representative of the real conditions of a voyage to Mars.
Can humans cope with a stay on Mars?
Mars is not a habitable planet. This is not an exaggerated statement, but rather a reflection of the impossibility of a normal life for organisms like ours on the Red Planet. The main problem is the weak atmosphere on Mars: it has 0.6% of the Earth's pressure at sea level, which is equivalent to the Earth's pressure at an altitude of 35 kilometres (22 miles). This means that water cannot be found in a liquid state on Mars. The surface layer of the planet's soil is covered with regolith (rock dust), which was recently discovered to be contaminated with perchlorates, which are very harmful to living organisms.
In order to survive in such conditions, a habitable bubble would have to be built that could perform a number of functions: recreate a viable atmosphere with the correct level of oxygenation, maintain a pressure that preserves the integrity of human bodies, protect against radiation and provide for daily needs.
The size of the bubble would depend on the number of people and the length of the stay. At minimum, astronauts would need a pressurised spacesuit which allows for the survival of one person for a few hours (such as for a spacewalk outside the ISS or on the moon). For several people over a duration of several months, the bubble must be the size of a complete dwelling (including a kitchen, rest areas, sanitary facilities, etc.) and must have an air and water recycling system as well as food and equipment reserves. The larger the bubble, the more complex the technical challenges would become and the more expensive it would be, to the point of becoming prohibitive.
What's the point of going to Mars?
Nothing? One of the arguments for sending humans to Mars is that they are more efficient on the ground than a robot and could therefore learn more about the planet. However, the progress made over successive generations of robotic probes shows that despite their limitations, the knowledge they provide is progressing rapidly. The indisputable advantage of robotic probes is that they do not need to eat or drink, nor do they need to operate under Earth’s pressure conditions. Minimal protection of their electronics is sufficient. The estimated cost of a single human mission would be equivalent to that of 40 robotic missions like Perseverance.
Moreover, these probes can be sterilised on departure from Earth according to the standards of the Planetary Protection Act, which aims to avoid contamination of places we visit in the solar system. This is impossible with humans: by placing a few individuals from our species on Mars, we are also depositing billions of bacteria from Earth. Even if their chance of survival on Mars is infinitesimal, it is not zero and risks confusing the answer to the main question that motivates our study of Mars: could life have developed there in the early stages of its evolution?
Sylvia EkströmExternal link has been a doctor in astrophysics since 2008, specialising in stellar physics. She is responsible for communications at the Department of Astronomy at the University of Geneva. Javier G. Nombela is a graphic designer specialising in the visual representation of time. He is also the author of numerous popular works in the field of astronomy. | On the ISS, astronauts can be returned to Earth within three hours. The Martian astronauts would be left to their own devices for the two-and-a-half years of their mission, knowing that the slightest error or failure, whether technical or human, could result in the death of the entire crew. It is impossible to test such a psychological situation on Earth. The Mars 500 psychological isolation experiment conducted by the European Space Agency developed methods of conflict resolution, but it is in no way representative of the real conditions of a voyage to Mars.
Can humans cope with a stay on Mars?
Mars is not a habitable planet. This is not an exaggerated statement, but rather a reflection of the impossibility of a normal life for organisms like ours on the Red Planet. The main problem is the weak atmosphere on Mars: it has 0.6% of the Earth's pressure at sea level, which is equivalent to the Earth's pressure at an altitude of 35 kilometres (22 miles). This means that water cannot be found in a liquid state on Mars. The surface layer of the planet's soil is covered with regolith (rock dust), which was recently discovered to be contaminated with perchlorates, which are very harmful to living organisms.
In order to survive in such conditions, a habitable bubble would have to be built that could perform a number of functions: recreate a viable atmosphere with the correct level of oxygenation, maintain a pressure that preserves the integrity of human bodies, protect against radiation and provide for daily needs.
The size of the bubble would depend on the number of people and the length of the stay. At minimum, astronauts would need a pressurised spacesuit which allows for the survival of one person for a few hours (such as for a spacewalk outside the ISS or on the moon). For several people over a duration of several months, the bubble must be the size of a complete dwelling (including a kitchen, rest areas, sanitary facilities, etc.) and must have an air and water recycling system as well as food and equipment reserves. | no |
Astronomy | Can humans live on Mars? | yes_statement | "humans" can "live" on mars.. it is possible for "humans" to "live" on mars. | https://www.skyatnightmagazine.com/space-science/could-we-live-on-mars | Could we really live on Mars? - BBC Sky at Night Magazine | Could we really live on Mars?
At the moment there seems to be a general feeling that the programme of crewed space research has been put on hold.
The International Space Station is beset with problems, and by no means all authorities are in favour of it; no astronauts have been to the Moon for over 30 years, and all the emphasis has been on the exploration of space by robotic probes.
The Space Shuttle fleet needs to be replaced and there is talk of destroying the Hubble Space Telescope – a proposal that has angered and alarmed scientists all over the world.
So what lies ahead for the foreseeable future?
Establishing a lunar base is by no means out of the question within the next couple of decades, provided that we do not indulge in any more senseless wars.
Mars. A future home for human beings? Credit: Emirates Mars Mission
After that it will be time to start looking toward Mars, and President George W Bush of the United States has already given a preliminary timescale.
Cynics (such as myself) suggest that he may be trying to ape President Kennedy's announcement of landing men on the Moon before 1970, but sooner or later Mars must be reached.
Could humans survive the journey to Mars?The problems are immense, one of the worst being the danger from solar radiation during the journey. A violent solar storm would be disastrous, and even Mr Bush cannot control the Sun.
Mars is not exactly welcoming, but it is less unlike the Earth than any other body in the Solar System. One trouble is that from our point of view, the atmosphere is of little use.
It is painfully thin, and it is made up almost entirely of carbon dioxide.
After the astronauts have landed there will be a prolonged delay before Earth and Mars are suitably placed for a return journey.
Establishing a permanent base on Mars
An artist’s impression of the first astronauts and human habitats on Mars. Credit: NASA
The first Martian bases will be far from luxurious, but if all goes well they will be made much more comfortable once we are sure that permanent bases really can be established.
At least there are no hidden dangers, so far as we know, and though dust storms will be common, they will have relatively little force in that thin atmosphere.
Neither is there likely to be any trouble from Marsquakes; the great volcanoes are quiet, and are not likely to erupt again.
Yet the fact remains that the astronauts will be unable to live on Mars except in very restricted conditions; they will have to stay inside their capsules, inside a base or inside their space suits. Mars is not suited to human visitors.
But can we change this?
Terraforming Mars
Could we terraform Mars and make it like Earth? Credit: Mark Stevenson/Stocktrek Images
Much has been heard about ‘terraforming’: ending up with a Mars on which conditions are much the same as they are on Earth.
Arthur C Clarke has written about a future Mars with blue skies, extensive oceans, widespread forests and breathable air.
Even if this can be achieved, it will take centuries, and the problems involved are only too clear.
For example, we must thicken the atmosphere, changing its composition and making certain that it does not leak away, as the first atmosphere presumably did (remember that the escape velocity of Mars is only just over three miles per second).
We must also raise the surface temperature, perhaps by introducing greenhouse gases or by melting the polar ice caps.
Persuading plants to grow on the surface of the terraformed Mars will be difficult, but can probably be done.
Eventually we will end up with a Mars where there are large cities, supporting a population of thousands or even millions.
Should we colonise Mars?
But... if we could achieve all this, are we sure that it is the right thing to do?
If there were advanced life forms on Mars it is tempting to say that the answer would have to be no, because the introduction of Earth-type beings would unquestionably mean that the indigenous Martians would be doomed.
However, there are no indigenous Martians, and certainly nothing nearly as intelligent as a beetle, which removes the most serious moral objections.
On the other hand we must agree that Mars would be irreversibly contaminated, and any organisms there would become extinct very quickly, even before scientists had had the time to examine them properly.
The risk may be low, but many people regard it as unjustifiable.
We may have contaminated Mars even now, despite all our efforts to sterilise the vehicles landing there.
There is also the purely practical aspect.
A terraforming programme would be vastly expensive by any standards, and would strain the resources of even a wholly united Earth.
What would be the benefits? Mars is not likely to contain any materials unobtainable at home.
When we consider our future on Mars, we must also consider our future on Earth. Credit: NASA / Toby Ord
The counter-argument here is that a terraforming programme could not be started except by a world in a state of permanent peace, with mutual friendship and trust between all nations.
This may be a Utopian dream in 2005, but perhaps things will be better in, say, 3005.
A terraformed Mars will have to become self- supporting, and will not have to depend upon help from Earth.
This means a well-regulated system ofgovernment, which will have to be global and will have to work better than ours does at themoment.
Of course, recreation will be an important part of life on Mars, but we may well hope that there will be noriots and no arrests at the end of a game of football between, say Syrtis Major United and Hellas Rovers!
We always have to reckon with the defects in human nature; has it ever struck you that the only creatures that wage organised war on each other are humans and ants?
There are bound to be calls of: "Leave Mars alone; we have done enough harm on Earth."
Terraforming, it is claimed, will be not only a criminal waste of money, but will also have adverse effects upon our way of life on Earth.
In any case, what right have we to interfere with the evolution of another planet?
Personally, I would like nothing better than to have the opportunity to visit Mars, but I admit that I would not be at all keen to exchange my Selsey home for a des res on the slopes of Olympus Mons.
This article originally appeared in the October 2005 issue of BBC Sky at Night Magazine.
Share this article
Sir Patrick Moore (1923–2012) presented The Sky at Night on BBC TV from 1957–2012. He was the Editor Emeritus of BBC Sky at Night Magazine, President of the British Astronomical Association and Society for Popular Astronomy, and a researcher and writer of over 70 books.
This website is owned and published by Our Media Ltd (an Immediate Group Company). www.ourmedia.co.uk | Neither is there likely to be any trouble from Marsquakes; the great volcanoes are quiet, and are not likely to erupt again.
Yet the fact remains that the astronauts will be unable to live on Mars except in very restricted conditions; they will have to stay inside their capsules, inside a base or inside their space suits. Mars is not suited to human visitors.
But can we change this?
Terraforming Mars
Could we terraform Mars and make it like Earth? Credit: Mark Stevenson/Stocktrek Images
Much has been heard about ‘terraforming’: ending up with a Mars on which conditions are much the same as they are on Earth.
Arthur C Clarke has written about a future Mars with blue skies, extensive oceans, widespread forests and breathable air.
Even if this can be achieved, it will take centuries, and the problems involved are only too clear.
For example, we must thicken the atmosphere, changing its composition and making certain that it does not leak away, as the first atmosphere presumably did (remember that the escape velocity of Mars is only just over three miles per second).
We must also raise the surface temperature, perhaps by introducing greenhouse gases or by melting the polar ice caps.
Persuading plants to grow on the surface of the terraformed Mars will be difficult, but can probably be done.
Eventually we will end up with a Mars where there are large cities, supporting a population of thousands or even millions.
Should we colonise Mars?
But... if we could achieve all this, are we sure that it is the right thing to do?
If there were advanced life forms on Mars it is tempting to say that the answer would have to be no, because the introduction of Earth-type beings would unquestionably mean that the indigenous Martians would be doomed.
However, there are no indigenous Martians, and certainly nothing nearly as intelligent as a beetle, which removes the most serious moral objections.
| no |
Astronomy | Can humans live on Mars? | yes_statement | "humans" can "live" on mars.. it is possible for "humans" to "live" on mars. | https://www.nationalgeographic.com/science/article/elon-musk-spacex-exploring-mars-planets-space-science | Elon Musk: A Million Humans Could Live on Mars By the 2060s | Elon Musk: A Million Humans Could Live on Mars By the 2060s
The SpaceX plan for building a Mars settlement includes refueling in orbit, a fleet of passenger ships, and the biggest rocket ever made.
ByNadia Drake
Published September 27, 2016
• 14 min read
GUADALAJARA, MexicoIn perhaps the most eagerly anticipated aerospace announcement of the year, SpaceX founder Elon Musk has revealed his grand plan for establishing a human settlement on Mars.
In short, Musk thinks it’s possible to begin shuttling thousands of people between Earth and our smaller, redder neighbor sometime within the next decade or so. And not too long after that—perhaps 40 or a hundred years later, Mars could be home to a self-sustaining colony of a million people.
“This is not about everyone moving to Mars, this is about becoming multiplanetary,” he said on September 27 at the International Astronautical Congress in Guadalajara, Mexico. “This is really about minimizing existential risk and having a tremendous sense of adventure.”
“I think the technical outline of the plan is about right. He also didn’t pretend that it was going to be easy and that they were going to do it in ten years,” says Bobby Braun, NASA’s former chief technologist who’s now at Georgia Tech University. “I mean, who’s to say what’s possible in a hundred years?”
National Geographic Channel is currently in production on MARS, a global event series set to premiere November 14. Join the journey at MakeMarsHome.com. #CountdownToMars
And for those wondering whether we should go at all, the reason for Musk making Mars an imperative is simple.
“The future of humanity is fundamentally going to bifurcate along one of two directions: Either we’re going to become a multiplanet species and a spacefaring civilization, or we’re going be stuck on one planet until some eventual extinction event,” Musk told Ron Howard during an interview for National Geographic Channel’s MARS, a global event series that premieres worldwide on November 14.
“For me to be excited and inspired about the future, it’s got to be the first option. It’s got to be: We’re going to be a spacefaring civilization.”
Mars Fleet
Though he admitted his exact timeline is fuzzy, Musk thinks it’s possible humans could begin flying to Mars by the mid-2020s. And he thinks the plan for getting there will go something like this:
SpaceX Interplanetary Transport System
Watch an animation of Elon Musk's vision for how to send humans to Mars.
It starts with a really big rocket, something at least 200 feet tall when fully assembled. In a simulation of what SpaceX calls its Interplanetary Transport System, a spacecraft loaded with astronauts will launch on top of a 39-foot-wide booster that produces a whopping 28 million pounds of thrust. Using 42 Raptor engines, the booster will accelerate the assemblage to 5,374 miles an hour.
Overall, the whole thing is 3.5 times more powerful than NASA’s Saturn V, the biggest rocket built to date, which carried the Apollo missions to the moon. Perhaps not coincidentally, the SpaceX rocket would launch from the same pad, 39A, at Kennedy Space Center in Cape Canaveral, Florida.
The rocket would deliver the crew capsule to orbit around Earth, then the booster would steer itself toward a soft landing back at the launch pad, a feat that SpaceX rocket boosters have been doing for almost a year now. Next, the booster would pick up a fuel tanker and carry that into orbit, where it would fuel the spaceship for its journey to Mars.
Once en route, that spaceship would deploy solar panels to harvest energy from the sun and conserve valuable propellant for what promises to be an exciting landing on the Red Planet.
As Musk envisions it, fleets of these crew-carrying capsules will remain in Earth orbit until a favorable planetary alignment brings the two planets close together—something that happens every 26 months. “We’d ultimately have upward of a thousand or more spaceships waiting in orbit. And so the Mars colonial fleet would depart en masse,” Musk says.
The key to his plan is reusing the various spaceships as much as possible. “I just don’t think there’s any way to have a self-sustaining Mars base without reusability. I think this is really fundamental,” Musk says. “If wooden sailing ships in the old days were not reusable, I don’t think the United States would exist.”
Musk anticipates being able to use each rocket booster a thousand times, each tanker a hundred times, and each spaceship 12 times. At the beginning, he imagines that maybe a hundred humans would be hitching a ride on each ship, with that number gradually increasing to more than 200.
By his calculations, then, putting a million people on Mars could take anywhere from 40 to a hundred years after the first ship launches.
And, no, it would not necessarily be a one-way trip: “I think it’s very important to give people the option of returning,” Musk says.
Colonizing Mars
After landing a few cargo-carrying spacecraft without people on Mars, starting with the Red Dragon capsule in 2018, Musk says the human phase of colonization could begin.
For sure, landing a heavy craft on a planet with a thin atmosphere will be difficult. It was tough enough to gently lower NASA’s Curiosity rover to the surface, and at 2,000 pounds, that payload weighed just a fraction of Musk’s proposed vessels. For now, Musk plans to continue developing supersonic retrorockets that can gradually and gently lower a much heavier spacecraft to the Martian surface, using his reusable Falcon 9 boosters as a model.
And that’s not all these spacecraft will need: Hurtling through the Martian atmosphere at supersonic speeds will test even the most heat-tolerant materials on Earth, so it’s no small task to design a spacecraft that can withstand a heated entry and propulsive landing—and then be refueled and sent back to Earth so it can start over again.
The first journeys would primarily serve the purpose of delivering supplies and establishing a propellant depot on the Martian surface, a fuel reservoir that could be tapped into for return trips to Earth. After that depot is set up and cargo delivered to the surface, the fun can (sort of) begin. Early human settlers will need to be good at digging beneath the surface and dredging up buried ice, which will supply precious water and be used to make the cryo-methane propellant that will power the whole enterprise.
As such, the earliest interplanetary spaceships would probably stay on Mars, and they would be carrying mostly cargo, fuel, and a small crew: “builders and fixers” who are “the hearty explorer type,” Musk said to Howard. “Are you prepared to die? If that’s OK, then you’re a candidate for going.”
While there will undoubtedly be intense competition and lots of fanfare over the first few seats on a Mars-bound mission, Musk worries that too much emphasis will be placed on those early bootprints.
“In the sort of grander historical context, what really matters is being able to send a large number of people, like tens of thousands if not hundreds of thousands of people, and ultimately millions of tons of cargo,” he says. “I actually care much more about that than, say, the first few trips.”
In short, his vision for establishing a settlement on Mars is more an endurance sport than a sprint.
Rocket Man
But Musk is used to that. In 2001, he founded SpaceX with one goal in mind: put humans on Mars. At the time, he recalls, he found himself thinking about why, after the successful Apollo missions to the moon, humans hadn’t visited Mars—or reached very far into space at all.
“It always seemed like we should have gone there by now, and we should have had a base on the moon, and we should have had space hotels and all these things,” he said to Howard. “I’d assumed that it was a lack of will … it was not a lack of will.”
I think what we want to avoid is a replay of Apollo.
ByElon MuskSpaceX
Instead, resources devoted to space exploration were scarce, and government spaceflight programs couldn’t assume the kind of risk that a private endeavor could tolerate. With an accumulated fortune from his time at Paypal, Musk founded a company dedicated to building rockets and vastly improving the vehicles that form the foundation of an interplanetary journey.
Contracts with private clients and the U.S. government followed, and now SpaceX is working on a version of its Dragon capsule that can send humans to the International Space Station.
Over the years, the company has had many high-profile successes—including landing the first suborbital reusable rocket stages on land and at sea—and its share of failures, with rockets exploding on the launch pad or en route to orbit.
That’s no surprise for any big technology development. But putting humans on Mars is a completely different challenge from sending humans into orbit, or even to the moon, especially when the goal isn’t just a few casual trips.
“I think what we want to avoid is a replay of Apollo,” Musk says. “We don’t want to send a few people, a few missions to Mars and then never go there again. That that will not accomplish the multiplanetary goal.”
Funding Muskville
Musk’s ultimate vision of a second, self-sustaining habitat for humans in the solar system is grand and lofty, but by no means unique. What makes Musk’s plan stand out from centuries of science fiction is that he might actually be able to make it happen—if he can bring costs down to his ideal levels.
“Entrepreneurs are able to look at questions that we think about, but we’re not quite ready to go there yet, things like supersonic retrograde propulsion,” said NASA administrator Charlie Bolden during a panel at the IAC.
"I think we can quibble over the numbers and the dollars and the timeframes and all, but we shouldn’t lose the fact that this guy went out on the international stage today and just laid it all out on the line," Braun adds. "I found it refreshing."
But for Mars to be a viable destination, Musk says the cost of the trip needs to come down to about $200,000, or the average price of a house in the United States. Trouble is, that’s a significant decrease from current cost estimates.
Musk doesn’t anticipate being able to do all of this on his own and said to Howard that some sort of synergistic relationship between governments and private industry will be crucial.
Elon Musk at the Dragon 2 unveiling in May 2014.
Photograph by Jae C. Hong, AP
Please be respectful of copyright. Unauthorized use is prohibited.
“I think we want to try to get as much in the way of private resources dedicated to the cause, and then get as much as possible in the way of government resources, so that if one of those funding sources disappears, things continue.”
But combining different management styles, abilities to assume risk, sources of funding, and working with old institutional road maps will be a challenge, to say the least.
How might that all work? “With difficulty,” says space policy expert John Logsdon, professor emeritus at The George Washington University. “It will involve breaking things.”
For instance, reaching Mars in the 2020s will require a bit of a kick in the pants for SpaceX on the technology front. The massive rocket featured in the simulation is much more powerful than anything in the company’s current arsenal. The first iteration of that futuristic rocket, a gargantuan stepping stone known as the Falcon Heavy, has already been delayed for years.
These types of delays are one of the reasons why space policy experts are skeptical about the timing of Musk’s plan, which he acknowledges is murky at best.
“Based on past performance, I don’t know how you could say, well, yeah he’s missed all these other deadlines, but this time he’s gonna do it,” Logsdon says. “So I think the reasonable posture is that I’ll believe it when he does it.”
If humans do manage to touch down on Mars, Musk thinks the momentum from such an achievement will propel additional developments, just as early explorers searching for glory, gold, and spices drove improvements in ship technology and global industry.
Ultimately, Musk believes this kind of endeavor will bring Mars out of the realm of science fiction and transform it from a world fraught with difficulty and danger to one that humans might actually enjoy living on—including Musk.
“I think that Mars is gonna be a great place to go,” he says. “It will be the planet of opportunity.” | Elon Musk: A Million Humans Could Live on Mars By the 2060s
The SpaceX plan for building a Mars settlement includes refueling in orbit, a fleet of passenger ships, and the biggest rocket ever made.
ByNadia Drake
Published September 27, 2016
• 14 min read
GUADALAJARA, MexicoIn perhaps the most eagerly anticipated aerospace announcement of the year, SpaceX founder Elon Musk has revealed his grand plan for establishing a human settlement on Mars.
In short, Musk thinks it’s possible to begin shuttling thousands of people between Earth and our smaller, redder neighbor sometime within the next decade or so. And not too long after that—perhaps 40 or a hundred years later, Mars could be home to a self-sustaining colony of a million people.
“This is not about everyone moving to Mars, this is about becoming multiplanetary,” he said on September 27 at the International Astronautical Congress in Guadalajara, Mexico. “This is really about minimizing existential risk and having a tremendous sense of adventure.”
“I think the technical outline of the plan is about right. He also didn’t pretend that it was going to be easy and that they were going to do it in ten years,” says Bobby Braun, NASA’s former chief technologist who’s now at Georgia Tech University. “I mean, who’s to say what’s possible in a hundred years?”
National Geographic Channel is currently in production on MARS, a global event series set to premiere November 14. Join the journey at MakeMarsHome.com. #CountdownToMars
And for those wondering whether we should go at all, the reason for Musk making Mars an imperative is simple.
“The future of humanity is fundamentally going to bifurcate along one of two directions: Either we’re going to become a multiplanet species and a spacefaring civilization, or we’re going be stuck on one planet until some eventual extinction event,” Musk told Ron Howard during an interview for National Geographic Channel’s MARS, a global event series that premieres worldwide on November 14. | yes |
Astronomy | Can humans live on Mars? | yes_statement | "humans" can "live" on mars.. it is possible for "humans" to "live" on mars. | https://qz.com/536483/why-its-compeltely-ridiculous-to-think-that-humans-could-live-on-mars | It's completely ridiculous to think that humans could live on Mars | It’s completely ridiculous to think that humans could live on Mars
Our 12-year-old daughter who, like us, is a big fan of The Martian by Andy Weir, said, “I can’t stand that people think we’re all going to live on Mars after we destroy our own planet. Even after we’ve made the Earth too hot and polluted for humans, it still won’t be as bad as Mars. At least there’s plenty of water here, and the atmosphere won’t make your head explode.”
What makes The Martian so wonderful is that the protagonist survives in a brutally hostile environment, against all odds, by exploiting science in clever and creative ways. To nerds like us, that’s better than Christmas morning or a hot fudge sundae. (One of us is nerdier than the other—I’m not naming any names, but his job title is “Captain of Moonshots.”) The idea of using our ingenuity to explore other planets is thrilling. Our daughter has a good point about escaping man-made disaster on Earth by colonizing Mars, though. It doesn’t make a lot of sense.
Advertisement
Mars has almost no surface water; a toxic atmosphere that is too thin for humans to survive without pressure suits; deadly solar radiation; temperatures lower than Antarctica; and few to none of the natural resources that have been critical to human success on Earth. Smart people have proposed solutions for those pesky environmental issues, some of which are seriously sci-fi, like melting the polar ice caps with nuclear bombs. But those aren’t even the real problems.
The real problems have to do with human nature and economics. First, we live on a planet that is perfect for us, and we seem to be unable to prevent ourselves from making it less and less habitable. We’re like a bunch of teenagers destroying our parents’ mansion in one long, crazy party, figuring that our backup plan is to run into the forest and build our own house. We’ll worry about how to get food and a good sound system later. Proponents of Mars colonization talk about “terraforming” Mars to make it more like Earth, but in the meantime, we’re “marsforming” Earth by making our atmosphere poisonous and annihilating our natural resources. We are also well on our way to making Earth one big desert, just like Mars.
Maybe a silver lining is that we have already proven ourselves capable of one aspect of terraforming Mars—heating up the planet. We have been warming Earth at a good clip by dumping enormous amounts of carbon dioxide into the atmosphere. On the other hand, the atmosphere of Mars is already 95% carbon dioxide, and despite centuries of vigorous efforts to deforest our planet and burn all of the fossil fuel we can lay our hands on, humans have raised carbon dioxide levels by a paltry 0.01% on Earth. It may be enough to cook us all to death, but staging a second industrial revolution on Mars—or exploding a few nuclear bombs (we’ve tried that here)—probably won’t raise those chilly temperatures much.
A second problem presented by human nature is that we don’t enjoy prolonged periods of extreme duress, and we don’t function particularly well under those conditions. It seems romantic to grow potatoes in a “hab” on Mars, but when you look at harsh environments on Earth, a different picture emerges. Antarctica has the closest temperatures to the red planet, an average of -56°F (-49°C) compared to an average of -67°F (-55°C) on Mars. Despite having a completely breathable atmosphere and plenty of fresh water, Antarctica has no permanent residents. Nobody wants to live there. Scientists who work at Antarctic bases suffer from a mental health disorder called Winter-Over syndrome, characterized by symptoms such as depression, irritability, aggressive behavior, insomnia, memory deficits, and the occurrence of mild fugue states known as the “antarctic stare.” Since it must be a bit like living with a colony of zombies, it’s no wonder that they want to stay drunk all winter (pdf). Living on Mars would be way, way more miserable than living in Antarctica. Imagine how much more expensive it would be to stay drunk for your entire life on Mars.
Advertisement
This brings us to the economic problem with colonizing Mars. It is extraordinarily expensive to ship goods to Mars, and at least right now, Mars has nothing to offer in return. There are no cod, no beavers to make hats from, no gold, no forests, none of the treasures that drew Europeans to colonize new continents. The wealth required to fund the colonies would need to come exclusively from here. We haven’t even colonized the Sahara desert, the bottom of the oceans or the moon, because it makes no economic sense. It would be far, far easier and cheaper to “terraform” the deserts on our own planet than to terraform Mars. Yet we can’t afford it. What makes us think that we could afford to colonize a barren rock 250 million miles (402 million km) away after we have used up all of our local resources?
Astro spends his days evaluating audacious ideas at X, Alphabet’s (formerly Google’s) “moonshot factory.” About six months ago, an ex-DARPA (Defense Advanced Research Projects Agency) program manager pitched a moonshot proposal: he wanted to set up a permanent manned colony on Mars. Astro suggested that for the amount of money and creativity necessary to set up a colony on Mars, we could help thousands of times as many people here on Earth. Sadly, this scientist wasn’t interested in projects on Earth. He said that he was a “space cadet,” and that nothing that didn’t have to do with space exploration interested him.
There is nothing wrong with being excited about exploring space. There’s nothing wrong with dreaming about setting up colonies in space either. But a colony on Mars would need to be a nearly perfectly self-contained, resource neutral system that harvests energy from the sun and is rarely or never re-supplied. That is currently beyond the reach of science and human ingenuity. Yet we are hurtling through a vast emptiness right now on a giant space station, and we won’t survive unless we learn to live in a resource neutral way. Our space station is way less boring than Mars—it is teeming with fascinating life forms and covered with mind-blowing geographic features. It even comes equipped with snacks that aren’t freeze-dried. The problems our space station faces aren’t boring either. To quote Mark Watney from The Martian, to avoid catastrophe, we’re going to have to science the shit out of this. Maybe if we got excited enough to treat Earth as though it were Mars, some of the energy currently pointed towards the stars could be repurposed to doing something even more audacious—ensure that the space station we already have can take us into the next millennium. | It’s completely ridiculous to think that humans could live on Mars
Our 12-year-old daughter who, like us, is a big fan of The Martian by Andy Weir, said, “I can’t stand that people think we’re all going to live on Mars after we destroy our own planet. Even after we’ve made the Earth too hot and polluted for humans, it still won’t be as bad as Mars. At least there’s plenty of water here, and the atmosphere won’t make your head explode.”
What makes The Martian so wonderful is that the protagonist survives in a brutally hostile environment, against all odds, by exploiting science in clever and creative ways. To nerds like us, that’s better than Christmas morning or a hot fudge sundae. (One of us is nerdier than the other—I’m not naming any names, but his job title is “Captain of Moonshots.”) The idea of using our ingenuity to explore other planets is thrilling. Our daughter has a good point about escaping man-made disaster on Earth by colonizing Mars, though. It doesn’t make a lot of sense.
Advertisement
Mars has almost no surface water; a toxic atmosphere that is too thin for humans to survive without pressure suits; deadly solar radiation; temperatures lower than Antarctica; and few to none of the natural resources that have been critical to human success on Earth. Smart people have proposed solutions for those pesky environmental issues, some of which are seriously sci-fi, like melting the polar ice caps with nuclear bombs. But those aren’t even the real problems.
The real problems have to do with human nature and economics. First, we live on a planet that is perfect for us, and we seem to be unable to prevent ourselves from making it less and less habitable. We’re like a bunch of teenagers destroying our parents’ mansion in one long, crazy party, figuring that our backup plan is to run into the forest and build our own house. We’ll worry about how to get food and a good sound system later. Proponents of Mars colonization talk about “terraforming” Mars to make it more like Earth, but in the meantime, we’ | no |
Astronomy | Can humans live on Mars? | yes_statement | "humans" can "live" on mars.. it is possible for "humans" to "live" on mars. | https://interestingengineering.com/science/becoming-interplanetary-how-can-humans-live-on-mars | The Science of Becoming "Interplanetary": How Can Humans Live ... | Stay ahead of your peers in technology and engineering - The Blueprint
Welcome back to our ongoing "Interplanetary Series." In our previous installments, we looked at what it would take to live on Mercury, Venus, and the Moon. Today, we look at "Earth's Twin," the fiery red planet known as Mars! For over a century, scientists have wondered if life could exist on Mars (or may once have).
The idea that humans may one-day travel to Mars and create an outpost of civilization there has also been enduringly popular. Today, we are getting close to the point where human-rated missions to the Red Planet are possible, which has led to a renewed interest in creating permanent settlements there.
See Also
Perhaps, someday soon, people could be traveling to Mars regularly in the same way tourists travel to different countries. Those visiting the Red Planet might even be treated to messages like this:
"Good morning, all, and welcome to Mars! The time is twelve fifty hours, Standard Martian Time, the month is Khumba, and the day is the fifteenth. Ambient temperatures on this beautiful day around the equator are a balmy twenty degrees celsius (68 deg. F). If this is your first time to the Red Planet, congratulations on booking accommodations that coincide with Martian Spring!
"Yes, that means that the Dust Storm season is now behind us, and we can all look forward to the many sunny months ahead. It also means that those who have booked the "Red Planet Adventure Tour" will have the chance to conduct surface walks with clear and unobstructed views of the Martian surface.
"We hope you are enjoying the view of our fair world as we descend to the surface. A reminder that we offer a full suite of accommodations here aboard the MarsLift. Since you'll be with us for a few days before we touch down, we recommend you take full advantage of our facilities. Our velocity has been adjusted to ensure you enjoy the sensation of Martian gravity for the entire descent.
"In the meantime, we invite you to take a look up at the Martian landscape using the ARES app. Prominent features and the story of how they were discovered will be indicated in your heads-up display. If you cannot access this app via neural link, we provide display glasses for just this purpose.
"This includes Valles Marineris and Olympus Mons, the two largest features of their kind in the Solar System. Just think: in a few days, you could be exploring these locations in person!"
Historically, Mars has gone by many names. Auqakuh, to the Inca; Al-Qahira, to the ancient Arabs; Huǒxīng, to ancient Chinese astronomers; Horus, to the ancient Egyptians; Kasei, in Japan; Ma'adim, to the ancient Hebrew, Mangala, to the ancient Hindu astronomers, and Girunugal to the Mesopotamians (Sumerians).
Western astronomical traditions are drawn from the ancient Romans, who derived their traditions from the ancient Greeks, who adopted some of theirs from the Babylonians and Sumerians. What was Girunugal to the Sumerians was Nergal to the Babylonians, Ares to the Greeks, and Mars to Rome. While the names have changed through time, the association with war, strife, blood, and fire — thanks to Mars' red appearance — have remained fixed throughout.
Astronomers often refer to Mars as "Earth's Twin" because of the similarities this celestial neighbor has with Earth. For starters, it is the second most-habitable planet in the Solar System, at least by our standards. Like Earth, it has polar caps, evidence of surface and subsurface water, a daily cycle that lasts close to 24 hours, and a tilted axis that causes seasonal variations.
Beyond that, the contrasts between our two planets are pretty extreme. Mars is an extremely cold, desiccated body with a very thin atmosphere compared to Earth. Its surface is drier than the driest deserts on Earth, water can only exist on its surface in ice form, and the level of irradiation it receives is enough to kill off most species of terrestrial plants and animals.
Yet, humans could establish a permanent human presence on the Red Planet with the right kind of hard work and technology. And with a LOT of hard work, the planet could be ecologically transformed (aka. terraformed) to the point that it could be "Earth's Twin" in just about every sense of the word.
Thin, cold, and toxic
Unlike Earth, Mars has no planetary magnetic field (or "magnetosphere.") On Earth, this field is believed to result from action in the planet's interior. This consists of the molten outer core revolving around a solid inner core (in the opposite direction of Earth's rotation), which creates a dynamo effect that generates a magnetic field.
According to multiple scientific investigations, Mars had a magnetic field about 4 billion years ago. However, its lower mass and density caused it to cool faster, leading the outer core to solidify while the inner core remained molten. This arrested Mars' interior's dynamo effect and its magnetic field disappeared.
Consequently, Mars' once-dense atmosphere was slowly stripped away by solar wind over the next few hundred million years. While it is replenished by outgassing, the atmospheric pressure today is less than 1% that of Earth's. And what little atmosphere it has is a toxic plume, composed predominantly of carbon dioxide, argon, and nitrogen, with traces of methane and water vapor.
The atmosphere is not only unbreathable, but also incredibly thin. Measured on the surface, the air pressure averages about 0.636 kPa, roughly 0.6% that of Earth's at sea level. And whereas Earth's atmosphere is composed of 78% nitrogen and 21% oxygen, Mars' atmosphere is a toxic plume composed of 96% carbon dioxide, 2.6% molecular nitrogen, 1.9% argon,carbon monoxide, and water vapor.
Because Mars is about 50% further from the Sun, it receives much less solar radiation and heat from our Sun. Another factor is Mars' thin, tenuous atmosphere, which cannot absorb much heat from the Sun. As a result, the average surface temperature on Mars is a frigid -82 °F (-63 °C), but this ranges considerably based on location and the time of year.
During a Martian summer, temperatures can reach as high as 95 °F (35 °C) around the equator at midday. During winter, temperatures plummet to as low as -233 °F (-135 °C) in the polar regions. But even when temperatures are at their warmest, the very thin atmosphere ensures that most of the heat is lost just a few inches from the surface.
To illustrate, if it were possible for a person to stand naked on the surface of Mars, their body would feel some severe temperature differences. While sand would feel very warm beneath their toes, everything above their ankles would be freezing. Above the waistline, temperatures could get low enough to freeze them cryogenically.
Radiation and dust storms
Then there's the small matter of all the radiation people would be exposed to. On Earth, human beings in developed nations are exposed to an average of 0.62 rads (6.2 mSv) per year. Because Mars has a very thin atmosphere and no protective magnetosphere, its surface receives about 24.45 rads (244.5 mSv) per year — more when a solar event occurs.
NASA has established an upper limit of 500 mSv per year for astronauts, and studies have shown that the human body can withstand a dose of up to 200 rads (2000 mSv) a year without permanent damage. However, prolonged exposure to the kinds of levels detected on Mars would dramatically increase the risk of acute radiation sickness, cancer, genetic damage, and even death.
Dust storms are a regular occurrence on Mars and happen whenever the lower atmosphere heats up, causing air currents to pick up dust and circulate it around the planet. This can occur when Mars is at the closest point in its orbit to the Sun (perihelion) and can also be exacerbated due to variations in temperature between the hemispheres — i.e. when one is in summer.
At times, dust storms on Mars can grow to the point that they encompass the entire planet. These are known as Martian Global Dust Storms (GDS), and they occur only in the latter half of the Martian year. Other than that, dust storms are temperamental and happen with every passing "dust storm season," which coincides with winter in each hemisphere.
Martian gravity
And then there's the matter of Martian gravity, which is roughly 38% that of Earth's (3.72 m/s2 or 0.379 g). While scientists do not yet know what effects long-term exposure to this level of gravity would have on the human body, multiple studies have been conducted into the long-term effects of microgravity — and the results are not encouraging.
This includes NASA's seminal Twins Study, which investigated the health of astronauts Scott and Mark Kelly after the former spent a year aboard the International Space Station (ISS). In addition to muscle and bone density loss, these studies showed that long-duration missions to space led to diminished organ function, eyesight, and even genetic changes.
It is fair to say that long-term exposure to around 1/3rd of Earth-normal gravity would have similar effects. Like astronauts serving aboard the ISS, these effects could be mitigated with a robust exercise and health monitoring regiment. But the possibility of living under these conditions, and children being born in them, raises a whole lot of unknowns.
But enough of the bad news! When it comes right down to it, there are several ways to overcome these challenges so that people can lead comfortable lives on Mars!
Regolith and ice
An absolute must for missions destined for the Moon, Mars, and other destinations in deep-space is the ability to be as self-sufficient as possible. This is known as In-Situ Resource Utilization (ISRU), and it entails using local resources to provide the necessities — like propellant, oxygen, water, building materials, and energy.
For starters, much of Mars is covered in silicate mineral dust and sand (aka. regolith) resulting from wind and (past) water erosion. This dust could be combined with bonding agents to create "Martian concrete," or bombarded with microwaves and printed as molten ceramic. The resulting shell would provide radiation protection, while a flexible inner structure would serve as the main habitat.
Another possible method would be to harvest local ice, which is plentiful in Mars' northern lowlands near the polar ice cap. This ice could then be combined with aerogel or other bonding agents and used to create "ice houses" that would protect against the radiation and the elements while also ensuring a view of the landscape.
The availability of water ice is also crucial and requires that landing sites be selected and scouted well in advance. The Northern Lowlands, which sit just south of the northern polar ice cap, have abundant supplies of water in the form of permafrost and subterranean ice. Recent observations also indicated that Valles Marineris (Mars' massive canyon system) has lots of ice just a few feet (1 meter) from the surface.
Yet another possibility would be to build habitats inside caves and stable lava tubes, many of which have been observed in Mars' Tharsis region. Much like the lava tubes on the Moon, these tubes could be accessed through collapsed sections (aka. "skylights"). These subterranean cave systems would provide natural radiation shielding and could be sealed and pressurized.
Recent studies have shown that there may be plenty of subsurface ice in these tubes, many of which are located in the equatorial region of Mars. This region is far more amenable to human settlement than the poles because it experiences warmer temperatures. Thanks to Mars' lower gravity, these lava tubes are significantly larger than similar features on Earth.
In terms of energy, solar arrays and wind farms are the most obvious means of providing electricity in the Martian environment. However, the thin nature of the atmosphere and the fact that Mars receives less light than Earth means that these methods will not be enough on their own. During the Dust Storm season, solar arrays will become effectively useless, and may even need to be taken down to prevent damage.
Luckily, NASA and China are developing compact nuclear reactors for long-duration missions off-world. NASA's current Fission Surface Power (FSB) concept, which began as the Kilopower project, will reportedly generate 40 kilowatts of power for ten years. China is seeking to create something even more powerful, allegedly 100 times as much!
Regardless, a combination of wind, solar, nuclear, fuel cells, and even biomass reactors will ensure that habitats on Mars (and their inhabitants) will have all the electricity they need to live, work, and thrive on Mars.
"The Greening of Mars"
Terraforming Mars comes down to three major steps: warming the surface, thickening the atmosphere, and altering the environment to something Earth-like. Luckily, these three tasks are interconnected and mutually beneficial.
Thickening the atmosphere will warm the surface and reduce the amount of radiation the planet receives. Similarly, warming the surface will melt the polar ice caps, releasing frozen CO2 and water vapor that will further thicken and warm the atmosphere. Introducing terrestrial microbes, lichens, plants, and animals will help stabilize the environment, create oxygen through photosynthesis, and establish a life cycle on the planet that will ensure long-term habitability.
With the right kind of commitment and resources, messages of welcome for people traveling to Mars could sound like this someday:
"Good morning, all, and welcome to Mars, humanity's home away from Earth. The time is oh-eight-thirty hours, Standard Martian Time, on this beautiful day of Sagittarius the third. Today's average temperature is a balmy 73 degrees Fahrenheit (23 deg. Celsius) in the northern hemisphere, while the south continues to experience a cool winter, with an average temperature of minus thirty.
"As we make our descent into the great city of Nergal, we encourage you to enjoy the view of Oceanus Borealis, the largest surface ocean in the Solar System. If you peer straight down, you'll see the great river valley of Valles Marineris and its Outflow Channels emptying into Chryse Mare. Look to your left, and you will see the Tharsis region and its prominent mountains still standing tall. From north to south, these massive features are Ascraeus, Pavonis, and Arsia Mons.
"To the left of them, you will see Olympus Mons, the tallest planetary mountain in the Solar System. Today, this feature towers at the edge of the warm water shallows of Amazonis Mare. For those who do not use ocular implants, the magnification app in the display glass will show you the dense jungles that surround the base of this behemoth and the beautiful sandy beaches and turquoise waters just beyond.
"As the Carriage comes about during our descent, you will get a chance to see the Southern Highlands. Things to be on the lookout for include the Thousand Lakes region, which is bordered on either side by the Great Lakes of Mars — Argyre and Hellas Mare. Those destined for this area are sure to enjoy the endless shorefronts, hot springs, and fishing retreats.
"We remind you that Martian flora and fauna are adapted to the local environment and that the export of local species is strictly prohibited by interplanetary law. All travels coming to and leaving from the surface will be subject to bioscans to determine if they are carrying harmful microbes or biota.
The first step is to trigger a greenhouse effect on Mars. There are several proposed methods for doing this. For one, "super greenhouse gases" like ammonia, methane, or chlorofluorocarbons (CFCs) could be introduced into the Martian atmosphere. This would thicken the atmosphere, raise global temperatures, and melt the polar ice caps.
There's also the possibility of using orbital mirrors to concentrate solar radiation and direct it toward the Martian surface. Positioned near the poles, these mirrors would sublimate the ice sheets and contribute to global warming. Once the atmosphere is thickened and warmed, conditions will be stable enough for water to flow on the surface again.
This will also require drilling into the ground to release additional pockets of methane and water. Over time, this will lead to precipitation and the gradual disappearance of dust storms. The introduction of microbes, lichens, plants, and eventually animals will help stabilize and enrich the soil with organic nutrients and create a complete life cycle on the planet.
In time, the atmosphere will become warm and breathable to the point that humans can wander around outside without a pressure suit. To ensure long-term stability, it will also be necessary to introduce an artificial magnetic field to prevent Mars' new atmosphere from being stripped away (and offer more radiation protection).
Several options for this have been proposed over the years, some that are smaller in scale and some that involve megascale engineering. At the smaller end of things, research has shown that electromagnetic toruses could be built around surface bases that would generate artificial magnetic fields. Another idea is to use Phobos, the larger of Mars' two moons, to generate a plasma torus around Mars.
Since Phobos orbits Mars every eight hours, generating this torus would be as simple as ejecting matter from the surface and using electromagnetic and plasma waves to drive a current strong enough to create a planetary magnetic field. A similar idea (but bolder!) is to build a series of planet-encircling superconducting rings to generate an artificial magnetic field.
An even more ambitious suggestion is to restore geological activity so that Mars will generate its own magnetic field again. Once again, there are many potential options available. One way would be to detonate a series of thermonuclear warheads to melt the outer core. The second involves running a massive electric current through the planet to heat the metallic outer core and melt it again.
However, there are limits to how much we can alter Mars to suit our needs. With only 38% of Earth's gravity, Mars would likely retain less than the 101.325 kilopascals (kPa) of air, which we are used to on Earth. Given its distance from the Sun, Mars would always receive about 40% of the solar radiation Earth does, limiting how warm outside temperatures get.
Then again, the magnetic shield mentioned earlier could help out with that. If the shield could polarize itself as needed, it could block out harmful radiation while enhancing the parts of the spectrum where photosynthesis occurs. This includes the yellow-red part of the spectrum (565-750 nanometers) and the yellow-green (500-590 nm) part for purple plants.
While adapting to Martian gravity will always be a challenge, there are strategies for dealing with this as well. In the long run, rotating pinwheel stations could be built in orbit that simulate Earth gravity (9.8 m/s2) and Martian gravity (3.721 m/s2). While the "Earth wheel" could offer gravity therapy, the Martian wheel could service visitors looking to adapt to Martian gravity.
Future Martian residents will need to commit to a health regimen that includes lots of exercise, healthy eating, radiation checks, and regular examinations in the short term. Future medicines and bioenhancements may also exist to help people mediate the long-term effects of living in lower gravity.
The challenges for living on Mars are certainly massive in scope! But there are solutions, and all that's required is the right kind of commitment and sense of adventure! Once we establish a foothold on Mars, the first generations of "Martians" will soon follow. On that day, the nickname "Earth's Twin" will take on a new meaning!
"Welcome to Nergal spaceport! For those departing our fair planet, please ensure that you have submitted to all pre-departure screenings. We would hate to think you would be taking more home from Mars than a few keepsakes and some precious memories! Speaking of which, be sure to check out the Duty-Free gift shop on your way out.
"If there's one thing we enjoy sending home with our visitors, it is the fine work of some of our planet's more prominent artists! And be sure to pick up a bottle of Mangala or Foche Estate late harvest ice wine made from the finest harvests in the lowlands. Or, if you're feeling more adventurous, try a bottle of Invierno Burya, Mars' premier brand of vodka!
"Those destined for Earth are reminded to include a brief stopover at Hóngsè Station, where you will spend the next few days in extreme comfort. See the 'Red Planet,' as it was once known, from space as you spent time readjusting to Earth-normal gravity. Though you may miss the feeling of having that extra spring in your step, it is important for your health and safety once your return home.
"We are sad to see you leave, but hope to see you again soon! Or as we say on Mars, 'Dukhee hai kàn dào depart, pero nous aasha kàn dào di revoir pronto¹!" | Stay ahead of your peers in technology and engineering - The Blueprint
Welcome back to our ongoing "Interplanetary Series." In our previous installments, we looked at what it would take to live on Mercury, Venus, and the Moon. Today, we look at "Earth's Twin," the fiery red planet known as Mars! For over a century, scientists have wondered if life could exist on Mars (or may once have).
The idea that humans may one-day travel to Mars and create an outpost of civilization there has also been enduringly popular. Today, we are getting close to the point where human-rated missions to the Red Planet are possible, which has led to a renewed interest in creating permanent settlements there.
See Also
Perhaps, someday soon, people could be traveling to Mars regularly in the same way tourists travel to different countries. Those visiting the Red Planet might even be treated to messages like this:
"Good morning, all, and welcome to Mars! The time is twelve fifty hours, Standard Martian Time, the month is Khumba, and the day is the fifteenth. Ambient temperatures on this beautiful day around the equator are a balmy twenty degrees celsius (68 deg. F). If this is your first time to the Red Planet, congratulations on booking accommodations that coincide with Martian Spring!
"Yes, that means that the Dust Storm season is now behind us, and we can all look forward to the many sunny months ahead. It also means that those who have booked the "Red Planet Adventure Tour" will have the chance to conduct surface walks with clear and unobstructed views of the Martian surface.
"We hope you are enjoying the view of our fair world as we descend to the surface. A reminder that we offer a full suite of accommodations here aboard the MarsLift. Since you'll be with us for a few days before we touch down, we recommend you take full advantage of our facilities. Our velocity has been adjusted to ensure you enjoy the sensation of Martian gravity for the entire descent.
"In the meantime, we invite you to take a look up at the Martian landscape using the ARES app. | yes |
Astronomy | Can humans live on Mars? | yes_statement | "humans" can "live" on mars.. it is possible for "humans" to "live" on mars. | https://www.theguardian.com/commentisfree/2017/jul/26/can-humans-live-on-mars-asked-google | Can humans live on Mars? You asked Google – here's the answer ... | Can humans live on Mars? You asked Google – here’s the answer
Every day millions of internet users ask Google life’s most difficult questions, big and small. Our writers answer some of the commonest queries
Ian Sample is the Guardian’s science editor
Wed 26 Jul 2017 03.00 EDTLast modified on Wed 14 Feb 2018 16.34 EST
Wanted: men and women to leave the birthplace of humanity and the only safe haven in the solar system for an interminable voyage in a cramped container with people you will probably learn to hate. Destination: the freezing, airless, highly irradiated and irredeemable wasteland we call Mars. Must be willing to live in a pressurised pod, drink crewmates’ recycled urine and endure disgraceful broadband service.
Hollywood has a knack for bringing excitement to Mars, but the foundation of any tension invariably lies in the fact that anyone who goes wants to come back, because it’s downright hostile and Earth was never that bad, that dangerous, or that doomed in the first place. Visionaries such as Stephen Hawking and Elon Musk want us to colonise other planets to safeguard the future of the species. They have a point. But if we can’t survive on the planet we evolved to live on – the only life-nurturing planet we know – it’s hard to see us making a great fist of it elsewhere. Another hitch: we’re nowhere near ready to leave.
As the crow flies, the shortest distance from Earth to Mars is 55m km, but Mars missions fail as often as they succeed. In the past, spacecraft have crashed into the surface, burned up in the atmosphere or barrelled on by. Instead of taking the shortest route, they typically follow more efficient trajectories that take about eight months one-way. That’s a long time to be cooped up with a bunch of strangers.
Aware of the potential for things to go wrong, space agencies have run several simulated missions to Mars by locking would-be spacefarers into pretend spaceships and watching how they cope. A 520-day European Space Agency simulation found that some men developed sleep problems, particularly on the long “return” leg, despite having plenty of music, books, DVDs and computer games for entertainment. It didn’t help that communications to the outside world have a 30- to 40-minute delay. But it’s the boredom that hurts the most, apparently. In Mary Roach’s Packing for Mars, a retired cosmonaut confesses to the mind-numbing boredom of space station life. “I wanted to hang myself,” he said. Which, he goes on to point out, isn’t that easy in weightless conditions.
Life on Earth is protected against the intense radiation of the solar wind and cosmic rays by the planet’s magnetic field. Once Mars-bound travellers pass through the field, they must be shielded by other means. Some of the most harmful radiation is in the form of high-energy protons, which can be stopped by hydrogen-rich substances, such as water and polyethylene. In principle, a spacecraft’s water tanks – topped up with filtered urine – and even the crew’s waste food packaging could be used as shielding in transit. But more sophisticated materials are on the horizon. Nasa is developing hydrogenated boron nitride nanotubes that can be woven into threads, potentially to make suits that absorb the damaging particles. They are an ever-present danger that would cause radiation sickness and cancer in those exposed.
The first humans to set foot on Mars will likely stay for a month or so. For such short visits, living and working spaces could be lightweight, pressurised inflatable shelters that can be deployed and covered with Martian soil to beef up radiation shielding. Once inside, people could ditch their space suits and breathe the air. As with the space station, more modules could be added over time to give people more room to move around and mingle. For brief spells, it would do.
Nasa’s latest plans for hurling humans to Mars involve testing the agency’s Orion spacecraft in lunar orbit before slating the first Mars missions in the 2030s. The best contender in the private sector is Elon Musk’s SpaceX, which is banking on its Interplanetary Transport System to ferry people straight to Mars as early as the next decade. Other private missions have been proposed but do not inspire much confidence: Mars One is a reality TV-based venture described in an Massachusetts Institute of Technology report as “not feasible”. Meanwhile Dennis Tito, the world’s first space tourist, wants to slingshot a married couple around Mars and bring them home without ever touching down. Both will need to buy rockets made by others.
Before humans can spend years on the red planet, they must invent a suite of new machines to take them there. Nasa opened a competition in 2015 for companies to come up with ways to 3D print Martian habitats from crew waste and Martian materials. But more serious breakthroughs are needed for Mars settlers to be self-sufficient. A colony would need equipment to extract water from subsurface ice, and oxygen from carbon dioxide in the thin Martian atmosphere. Mars is farther from the sun than Earth is and the temperature can plunge to -125ºC in the winter, calling for large fields of solar arrays to capture enough of the sun’s rays to generate electricity for power and heating.
In The Martian, Matt Damon opts for bags of human poo to grow potatoes in, and after analysing the red planet’s soil with its long-defunct Phoenix lander, Nasa agreed that some kind of fertiliser would probably be necessary to farm plants on Mars. Any crops would have to be grown indoors, however, to protect them from radiation, and under lamps, to make up for the feeble sunlight that reaches the surface. From first footfalls, it could take many decades to establish a functioning colony on Mars. And even if it became self-sufficient, it would still be reliant on supplies from Earth for equipment and parts: a colony can only do so much.
What would become of humans on Mars? Without a hefty exercise regime, they would become weak and feeble. Mars is a small planet with only one third the gravity of Earth. To stand would take less leg muscle; to pump blood to the brain, less heart. And what about the politics? At the outset, the first settlers would doubtless be revered as brave pioneers. Would that attitude hold as the novelty wore off? Or might Mars settlers find themselves out of sight and out of mind; resented for their need of support? Isaac Asimov anticipated as much in The Martian Way.
Humans on Mars would be the first to be neither on Earth nor able to see the planet as a life-sustaining marble in the blackness of space. Astronauts have found the view back to Earth enormously helpful for their mental wellbeing. What happens when, as seen from Mars, the Earth appears insignificant, no more than a tiny pale dot?
So, yes, given the right technology, humans can live on Mars. The question is do we want to? | Can humans live on Mars? You asked Google – here’s the answer
Every day millions of internet users ask Google life’s most difficult questions, big and small. Our writers answer some of the commonest queries
Ian Sample is the Guardian’s science editor
Wed 26 Jul 2017 03.00 EDTLast modified on Wed 14 Feb 2018 16.34 EST
Wanted: men and women to leave the birthplace of humanity and the only safe haven in the solar system for an interminable voyage in a cramped container with people you will probably learn to hate. Destination: the freezing, airless, highly irradiated and irredeemable wasteland we call Mars. Must be willing to live in a pressurised pod, drink crewmates’ recycled urine and endure disgraceful broadband service.
Hollywood has a knack for bringing excitement to Mars, but the foundation of any tension invariably lies in the fact that anyone who goes wants to come back, because it’s downright hostile and Earth was never that bad, that dangerous, or that doomed in the first place. Visionaries such as Stephen Hawking and Elon Musk want us to colonise other planets to safeguard the future of the species. They have a point. But if we can’t survive on the planet we evolved to live on – the only life-nurturing planet we know – it’s hard to see us making a great fist of it elsewhere. Another hitch: we’re nowhere near ready to leave.
As the crow flies, the shortest distance from Earth to Mars is 55m km, but Mars missions fail as often as they succeed. In the past, spacecraft have crashed into the surface, burned up in the atmosphere or barrelled on by. Instead of taking the shortest route, they typically follow more efficient trajectories that take about eight months one-way. That’s a long time to be cooped up with a bunch of strangers.
Aware of the potential for things to go wrong, space agencies have run several simulated missions to Mars by locking would-be spacefarers into pretend spaceships and watching how they cope. | no |
Astronomy | Can humans live on Mars? | yes_statement | "humans" can "live" on mars.. it is possible for "humans" to "live" on mars. | https://theconversation.com/could-people-breathe-the-air-on-mars-180504 | Could people breathe the air on Mars? | Authors
Disclosure statement
Phylindia Gant is a student collaborator on the M2020 rover. She receives funding through the University of Central Florida's NASA Florida Space Grant Consortium. She is a first year Geology PhD student at the University of Florida.
Amy J. Williams receives relevant funding from NASA's Mars Science Laboratory rover and M2020 rover Participating Scientist Programs, as well as through the University of Central Florida's NASA Florida Space Grant Consortium and Space Florida, and the Florida Space Institute. She is an assistant professor of Earth & Planetary Science at the University of Florida.
The air on Mars
The Martian atmosphere is thin – its volume is only 1% of the Earth’s atmosphere. To put it another way, there’s 99% less air on Mars than on Earth.
That’s partly because Mars is about half the size of Earth. Its gravity isn’t strong enough to keep atmospheric gases from escaping into space.
And the most abundant gas in that thin air is carbon dioxide. For people on Earth, that’s a poisonous gas at high concentrations. Fortunately, it makes up far less than 1% of our atmosphere. But on Mars, carbon dioxide is 96% of the air!
Meanwhile, Mars has almost no oxygen; it’s only one-tenth of one percent of the air, not nearly enough for humans to survive.
If you tried to breathe on the surface of Mars without a spacesuit supplying your oxygen – bad idea – you would die in an instant. You would suffocate, and because of the low atmospheric pressure, your blood would boil, both at about the same time.
Billions of years ago, Mars’ Jezero Crater hosted an ancient lake.
Life without oxygen
So far, researchers have not found any evidence of life on Mars. But the search is just beginning; our robotic probes have barely scratched the surface.
But plenty of organisms on Earth survive extreme environments. Life has been found in the Antarctic ice, at the bottom of the ocean and miles below the Earth’s surface. Many of those places have extremely hot or cold temperatures, almost no water and little to no oxygen.
That’s one of the goals of NASA’s Mars Perseverance rover mission – to look for signs of ancient Martian life. That’s why Perseverance is searching within the Martian rocks for fossils of organisms that once lived – most likely, primitive life, like Martian microbes.
Do-it-yourself oxygen
Among the seven instruments on board the Perseverance rover is MOXIE, an incredible device that takes carbon dioxide out of the Martian atmosphere and turns it into oxygen.
If MOXIE works the way that scientists hope it will, future astronauts will not only make their own oxygen; they could use it as a component in the rocket fuel they’ll need to fly back to Earth. The more oxygen people are able to make on Mars, the less they’ll need to bring from Earth – and the easier it becomes for visitors to go there. But even with “homegrown” oxygen, astronauts will still need a spacesuit.
Right now, NASA is working on the new technologies needed to send humans to Mars. That could happen in the next decade, perhaps sometime during the late 2030s. By then, you’ll be an adult – and maybe one of the first to take a step on Mars.
See what a human mission to Mars would be like.
Hello, curious kids! Do you have a question you’d like an expert to answer? Ask an adult to send your question to CuriousKidsUS@theconversation.com. Please tell us your name, age and the city where you live.
And since curiosity has no age limit – adults, let us know what you’re wondering, too. We won’t be able to answer every question, but we will do our best. | Fortunately, it makes up far less than 1% of our atmosphere. But on Mars, carbon dioxide is 96% of the air!
Meanwhile, Mars has almost no oxygen; it’s only one-tenth of one percent of the air, not nearly enough for humans to survive.
If you tried to breathe on the surface of Mars without a spacesuit supplying your oxygen – bad idea – you would die in an instant. You would suffocate, and because of the low atmospheric pressure, your blood would boil, both at about the same time.
Billions of years ago, Mars’ Jezero Crater hosted an ancient lake.
Life without oxygen
So far, researchers have not found any evidence of life on Mars. But the search is just beginning; our robotic probes have barely scratched the surface.
But plenty of organisms on Earth survive extreme environments. Life has been found in the Antarctic ice, at the bottom of the ocean and miles below the Earth’s surface. Many of those places have extremely hot or cold temperatures, almost no water and little to no oxygen.
That’s one of the goals of NASA’s Mars Perseverance rover mission – to look for signs of ancient Martian life. That’s why Perseverance is searching within the Martian rocks for fossils of organisms that once lived – most likely, primitive life, like Martian microbes.
Do-it-yourself oxygen
Among the seven instruments on board the Perseverance rover is MOXIE, an incredible device that takes carbon dioxide out of the Martian atmosphere and turns it into oxygen.
If MOXIE works the way that scientists hope it will, future astronauts will not only make their own oxygen; they could use it as a component in the rocket fuel they’ll need to fly back to Earth. The more oxygen people are able to make on Mars, the less they’ll need to bring from Earth – and the easier it becomes for visitors to go there. But even with “homegrown” oxygen, astronauts will still need a spacesuit.
Right now, NASA is working on the new technologies needed to send humans to Mars. | no |
Astronomy | Can humans live on Mars? | yes_statement | "humans" can "live" on mars.. it is possible for "humans" to "live" on mars. | https://www.universetoday.com/111462/how-can-we-live-on-mars/ | How Can We Live on Mars? - Universe Today | The Dragn Crew capsule is more than a modernized Apollo capsule. It will land softly and at least on Earth will be reusable while Musk and SpaceX dream of landing Falcon Crew on Mars. (Photo Credits: SpaceX)
How Can We Live on Mars?
Why live on Earth when you can live on Mars? Well, strictly speaking, you can’t. Mars is a completely hostile environment to human life, combining extreme cold with an unbreathable atmosphere and intense radiation. And while it is understood that the planet once had an atmosphere and lots of water, that was billions of years ago!
And yet, if we want to expand into the Solar System, we’ll need to learn how to live on other planets. And Mars is prime real-estate, compared to a lot of other bodies. So despite it being a challenge, given the right methods and technology, it is possible we could one day live on Mars. Here’s how we’ll do it.
Reasons To Go:
Let’s face it, humanity wants (and needs) to go Mars, and for several reasons. For one, there’s the spirit of exploration, setting foot on a new world and exploring the next great frontier – like the Apollo astronauts did in the late 60s and early 70s.
We also need to go there if we want to create a backup location for humanity, in the event that life on Earth becomes untenable due to things like Climate Change. We could also go there to search for additional resources like water, precious metals, or additional croplands in case we can no longer feed ourselves.
In that respect, Mars is the next, natural destination. There’s also a little local support, as Mars does provide us some raw materials. The regolith, the material which covers the surface, could be used to make concrete, and there are cave systems which could be converted into underground habitats to protect citizens from the radiation.
Elon Musk has stated that the goal of SpaceX is to help humans get to Mars, and they’re designing rockets, landers and equipment to support that. Musk would like to build a Mars colony with about 1 million people. Which is a good choice, as its probably the second most habitable place in our Solar System. Real estate should be pretty cheap, but the commute is a bit much.
And then there’s the great vistas to think about. Mars is beautiful, after a fashion. It looks like a nice desert planet with winds, clouds, and ancient river beds. But maybe, just maybe, the best reason to go there is because it’s hard! There’s something to be said about setting a goal and achieving it, especially when it requires so much hard work and sacrifice.
Reasons NOT To Go:
Yeah, Mars is pretty great… if you’re not made of meat and don’t need to breathe oxygen. Otherwise, it’s incredibly hostile. It’s not much more habitable than the cold vacuum of space. First, there’s no air on Mars. So if you were dropped on the surface, the view would be spectacular. Then you’d quickly pass out, and expire a couple minutes later from a lack of oxygen.
There’s also virtually no air pressure, and temperatures are incredibly cold. And of course, there’s the constant radiation streaming from space. You also might want to note that the soil is toxic, so using it for planting would first require that it be put through a decontamination process.
Assuming we can deal with those issues, there’s also the major problem of having limited access to spare parts and medical supplies. You can’t just go down to the store when you’re on Mars if your kidney gives out or if your sonic screwdriver breaks.
There will need to be a constant stream of supplies coming from Earth until the Martian economy is built up enough to support itself. And shipping from Earth will be very expensive, which will mean long period between supply drops.
One more big unknown is what the low gravity will do to the human body over months and years. At 40% of Earth normal, the long-term effects are not something we currently have any information on. Will it shorten our lifespan or lengthen it? We just don’t know.
There’s a long list of these types of problems. If we intend to live on Mars, and stay there permanently, we’ll be leaning pretty hard on our technology to keep us alive, never mind making us comfortable!
Possible Solutions:
In order to survive the lack of air pressure and the cold, humans will need pressurized and heated habitats. Martians, the terrestrial kind, will also need a spacesuit whenever they go outside. Every hour they spend outside will add to their radiation exposure, not to mention all the complications that exposure to radiation brings.
Artist’s concept of a habitat for a Mars colony. Credit: NASA
For the long term, we’ll need to figure out how to extract water from underground supplies, and use that to generate breathable air and rocket fuel. And once we’ve reduced the risk of suffocation or dying of dehydration, we’ll need to consider food sources, as we’ll be outside the delivery area of everyone except Planet Express. Care packages could be shipped up from Earth, but that’s going to come with a hefty price tag.
We’ll need to produce our own food too, since we can’t possible hope to ship it all in on a regular basis. Interestingly, although toxic, Martian soil can be used to grow plants once you supplement it and remove some of the harsher chemicals. NASA’s extensive experience in hydroponics will help.
To thrive on Mars, the brave adventurers may want to change themselves, or possibly their offspring. This could lead to genetic engineering to help future generations adapt to the low gravity, higher radiation and lower air pressure. And why stop at humans? Human colonists could also adapt their plants and animals to live there as well.
Finally, to take things to the next level, humanity could make a few planetary renovations. Basically, we could change Mars itself through the process of terraforming. To do this, we’ll need to release megatons of greenhouse gasses to warm the planet, unleashing the frozen water reserves. Perhaps we’ll crash a few hundred comets into the planet to deliver water and other chemicals too.
This might take thousands, or even millions of years. And the price tag will be, for lack of a better word, astronomical! Still, the technology required to do all this is within our current means, and the process could restore Mars to a place where we could live on it even without a spacesuit.
And even though we may not have all the particulars worked out just yet, there is something to be said about a challenge. As history has shown, there is little better than a seemingly insurmountable challenge to bring out the best in all of us, and to make what seems like an impossible dream a reality.
To quote the late, great John F. Kennedy, who addressed the people of the United States back when they was embarking on a similarly difficult mission:
We choose to go to the Moon! … We choose to go to the Moon in this decade and do the other things, not because they are easy, but because they are hard; because that goal will serve to organize and measure the best of our energies and skills, because that challenge is one that we are willing to accept, one we are unwilling to postpone, and one we intend to win
What do you think? Would you be part of the Mars terraforming expedition? Tell us in the comments below.
4 Replies to “How Can We Live on Mars?”
Short Term…
Bring hydrogen. React with CO2 to produce methane CH4 to power rockets and land vehicles and O2. All this should be done before colonists land. Hopefully our Martian cylons will not revolt.
With nukes, disassociate Martian water into hydrogen (see above) and oxygen.
Later, get nitrogen (a big problem) from inner belt asteroids.
By the time humans go to Mars maybe in the 2030s, medical nanotech should help us with the radiation cell damage issues.
3-D printer tech 20 years from now should prove invaluable for making stuff needed. Issue will be raw materials (see nitrogen above).
We really do need to send another HiRise or next gen. camera, this time with a powerful ground penetrating radar attached, to orbit Mars. Yes.. lets look for volcanic tubes or subsurface aquafirs/hot mineral springs? Especially in the Hellas Planitia region…
Isn’t it true that “strictly speaking” we can’t live on many places on Earth? The South Pole?
On the other hand it is rather absurdly hyperbolic to then say we might need a backup location to live in case Climate Change makes Earth inhabitable. What on Earth?!?!?!
As for terraforming… on the one hand people have suggested seeding Mars well before we try to live there in numbers. On the other hand there’s loosing significant scientific value as we do as much more change as the asteroid heavy bombardment even if by side affect.
Don’t forget that we have “The Martian” novel coming to the big screen. The story of a Martian castaway explores the ways, one person could survive on the planet until rescuers arrive. Its relevant to the questions of permanent settlement but not covering all problems. The story is essentially is a remake of “Robinson Crusoe on Mars” (1964).
A few months back I watched it again – the old movie. Last time was when I was about 10 years old. It is amazing how one’s mind saves recall of old memories. My images, quite vivid, are pretty spectacular vistas on Mars and profiles of a person struggling to survive in a cavern and harsh environment. My images were upgraded and far better than the original movie. The science of that movie was not bad but not perfect. Innovative for its time which I would guess “The Martian” is as well (haven’t read it). Special effects in 1964 for what was probably a “B” class sci-fi movie are modest, but still very cool as in the illustrations from that era.
I’ve woken up in Martian-like landscapes on Earth but there was a trip in the Sierras in which I woke up about 2 AM. Well above tree line, I woke up in my bag, no tent, in a small clearing surrounded by granite blocks, the terrain rising behind me. The silhouette of adjacent ridges stood in sight with a setting waxing moon. As the moon was disappearing, a wind rose up, a frigid dark sky was above and I was not on the Earth but somewhere alien. I and others have imagined ourselves in such moments, on Mars. | The Dragn Crew capsule is more than a modernized Apollo capsule. It will land softly and at least on Earth will be reusable while Musk and SpaceX dream of landing Falcon Crew on Mars. (Photo Credits: SpaceX)
How Can We Live on Mars?
Why live on Earth when you can live on Mars? Well, strictly speaking, you can’t. Mars is a completely hostile environment to human life, combining extreme cold with an unbreathable atmosphere and intense radiation. And while it is understood that the planet once had an atmosphere and lots of water, that was billions of years ago!
And yet, if we want to expand into the Solar System, we’ll need to learn how to live on other planets. And Mars is prime real-estate, compared to a lot of other bodies. So despite it being a challenge, given the right methods and technology, it is possible we could one day live on Mars. Here’s how we’ll do it.
Reasons To Go:
Let’s face it, humanity wants (and needs) to go Mars, and for several reasons. For one, there’s the spirit of exploration, setting foot on a new world and exploring the next great frontier – like the Apollo astronauts did in the late 60s and early 70s.
We also need to go there if we want to create a backup location for humanity, in the event that life on Earth becomes untenable due to things like Climate Change. We could also go there to search for additional resources like water, precious metals, or additional croplands in case we can no longer feed ourselves.
In that respect, Mars is the next, natural destination. There’s also a little local support, as Mars does provide us some raw materials. The regolith, the material which covers the surface, could be used to make concrete, and there are cave systems which could be converted into underground habitats to protect citizens from the radiation.
Elon Musk has stated that the goal of SpaceX is to help humans get to Mars, and they’re designing rockets, landers and equipment to support that. Musk would like to build a Mars colony with about 1 million people. | yes |
Astronomy | Can humans live on Mars? | no_statement | "humans" cannot "live" on mars.. it is not feasible for "humans" to "live" on mars. | https://www.nhm.ac.uk/discover/news/2018/july/its-official-we-cant-terraform-mars.html | It's official: we can't terraform Mars | Natural History Museum | Accept cookies?
We use cookies to give you the best online experience. We use them to improve our website and content, and to tailor our digital advertising on third-party platforms. You can change your preferences at any time.Â
Martian sand dunes near the central pit of a 35-kilometer-wide impact crater. This image was acquired by the High Resolution Imaging Science Experiment (HiRISE) instrument aboard MRO on April 27, 2009, at 15:16 local Mars time. Image: NASA/JPL/University of Arizona.
It's official: we can't terraform Mars
Would you wave goodbye to Earth and live out the rest of your days on Mars?
At first glance, our neighbouring planet doesn't seem particularly homely: Mars has an average temperature of -62°C and an atmosphere so thin that if you stood on it unprotected, your saliva would boil away to nothing.
There's no liquid water at the surface of Mars, and so far experts have found no signs of life.
It's clear that if humans ever wanted to walk on Mars in large numbers, there would be some work to do to make it liveable.
Yet some people, including business magnate and engineer Elon Musk, still hold out hope that one day a colony of humans could live on the planet, and some have contemplated the possibility of terraforming.Â
What is terraforming?
Terraforming means changing a planet or moon's atmosphere or surface to make it more habitable for organisms that live on Earth.
Terraforming could theoretically result in a temperate, correctly pressurised environment for a colony of thousands of humans and other organisms from Earth to live safely.
But Bruce Jakosky at the University of Colorado and Christopher Edwards at Northern Arizona University have done the maths, and concluded that the idea is beyond the realms of possibility - or at least not using the technology we have currently available to us.
A new paper, published in Nature Astronomy, declared that there is not enough carbon dioxide on Mars to make it a viable prospect for terraforming.
Zach Dickeson, a PhD Researcher at the Museum, is investigating ancient sources of liquid water on Mars.
Commenting on the study, he says, 'It's a fascinating paper. I think a lot of people know about the idea of terraforming from science fiction, and perhaps held out hope that it might be possible on Mars.
'However, even though this paper definitively concludes that humans can't yet change the climate of Mars, there are plenty of other discoveries going on at the moment that are really exciting, including planned sample return missions and the recently discovered body of liquid water.'
Why would we want to live on Mars?
It's a backup plan for the human race should a planet-wide disaster happen on Earth. Potentially deadly threats include nuclear destruction, asteroid impacts and pandemic.
Colonising other planets could ensure the continuation of humanity, should the worst happen.Â
Could we live on Mars?
The first step towards making Mars habitable would be raising the temperature and atmospheric pressure enough for Earth's organisms to survive.
Mars's atmosphere (the envelope of gases that surround a planet) is very thin. Pressure on the planet is so low that liquid water cannot exist at the surface, although it has been found beneath the planet's ice caps. Water is either ice in cold temperatures, or steam in warm ones.
Zach explains, 'If a human were dropped onto the surface of Mars right now, their saliva would boil away from their mouth. They also would not have enough oxygen to breathe. If we wanted to live there, we would have to wear a pressurised suit.
'To successfully walk on the Martian surface unaided, humans would need to create an atmosphere similar in composition and thickness to that of Earth.'
Carbon dioxide and other greenhouse gases would be vital to keep Mars warm enough.
Greenhouse gases trap heat in the atmosphere. Although there is too much of this warming effect happening on Earth, a little bit of a greenhouse effect is nonetheless necessary. Earth's blanket of gases protects us from the radiation of the Sun and keeps our climate within a liveable range.
Some have suggested that there is enough carbon dioxide locked away in Mars's ice and rocks to heat the planet and thicken the atmosphere, if only we could release it.
So can we do it?
The short answer is no. Using data from rovers and spacecrafts that have been monitoring Mars, the team in the study identified all of the planet's possible reservoirs of carbon dioxide and their potential contributions to the atmosphere. The researchers also took into account the continuous leaking of atmospheric CO2 into space.
The study concludes that at best, the readily accessible carbon dioxide could only triple Mars's atmospheric pressure, which is only one fiftieth of the change needed to make Mars habitable. It would increase the surface temperature by less than 10°C.
The authors conclude, 'Even if enough CO2 were to be available, it would not be feasible to mobilise it; doing so would require processing a major fraction of the surface to release it into the atmosphere, which is beyond present-day technology.'
Mars also can't support a thick enough atmosphere for humans because it doesn't have the same magnetic field as Earth does.
Earth's molten core creates a magnetic field surrounding our planet that helps to protect the atmosphere from the Sun. Harmful rays from the Sun are deflected by the magnetic field, so they don't hit the atmosphere and damage it.
It's thought that Mars once also had a molten core and a magnetic field, but lost it billions of years ago.
Now Mars is unprotected from the solar wind, a stream of particles from the Sun into space. This means that gas in Mars's thin atmosphere is constantly leaking into space.
Recent missions to Mars have shown that the majority of the planet's ancient, potentially habitable atmosphere has been lost to space, stripped away by solar wind and radiation.
The authors say, 'Once gas is lost it will very quickly become ionised and carried away by the solar wind. Once lost, it is gone and unable to come back.'
This research was supported in part by NASA through the MAVEN and Mars Odyssey THEMIS (Thermal Emission Imaging System) projects.
Don't miss a thing
Receive email updates about our news, science, exhibitions, events, products, services and fundraising activities. We may occasionally include third-party content from our corporate partners and other museums. We will not share your personal details with these third parties. You must be over the age of 13. Privacy notice. | Yet some people, including business magnate and engineer Elon Musk, still hold out hope that one day a colony of humans could live on the planet, and some have contemplated the possibility of terraforming. Â
What is terraforming?
Terraforming means changing a planet or moon's atmosphere or surface to make it more habitable for organisms that live on Earth.
Terraforming could theoretically result in a temperate, correctly pressurised environment for a colony of thousands of humans and other organisms from Earth to live safely.
But Bruce Jakosky at the University of Colorado and Christopher Edwards at Northern Arizona University have done the maths, and concluded that the idea is beyond the realms of possibility - or at least not using the technology we have currently available to us.
A new paper, published in Nature Astronomy, declared that there is not enough carbon dioxide on Mars to make it a viable prospect for terraforming.
Zach Dickeson, a PhD Researcher at the Museum, is investigating ancient sources of liquid water on Mars.
Commenting on the study, he says, 'It's a fascinating paper. I think a lot of people know about the idea of terraforming from science fiction, and perhaps held out hope that it might be possible on Mars.
'However, even though this paper definitively concludes that humans can't yet change the climate of Mars, there are plenty of other discoveries going on at the moment that are really exciting, including planned sample return missions and the recently discovered body of liquid water.'
Why would we want to live on Mars?
It's a backup plan for the human race should a planet-wide disaster happen on Earth. Potentially deadly threats include nuclear destruction, asteroid impacts and pandemic.
Colonising other planets could ensure the continuation of humanity, should the worst happen. Â
Could we live on Mars?
The first step towards making Mars habitable would be raising the temperature and atmospheric pressure enough for Earth's organisms to survive.
Mars's atmosphere (the envelope of gases that surround a planet) is very thin. | no |
Astronomy | Can humans live on Mars? | no_statement | "humans" cannot "live" on mars.. it is not feasible for "humans" to "live" on mars. | https://medium.com/@julianawright511/why-we-cannot-allow-the-colonization-of-humans-and-life-mars-4559e12944b6 | Why we cannot allow the colonization of humans and life Mars. | by ... | Why we cannot allow the colonization of humans and life Mars.
Humans cannot live on Mars. This is a scientifically proven fact: humans cannot survive in a Martian environment or with that atmosphere. We can actually live nowhere, other than Earth, sustainably, and even that is up in the air. Human bodies are not suited for Mars; they will collapse and die instantly without support. Childhood hero Bill Nye said, “it’s not reasonable because it’s so cold. And there is hardly any water. There’s absolutely no food, and the big thing, I just remind these guys, there’s nothing to breathe” (Carbone). Mars is somewhat comparable to what Earth would have been like during the Ice age, but way worse and way more deadly. The surface of Mars will boil every ounce of liquid in a human body in seconds: the heat and radiation on the surface of Mars is infinitely more deadly than any natural exposure here on Earth (Stoner). Evidently, this is not a suitable environment for animals or even bacteria; humans should not try and risk a life in an environment that cannot provide for even the simplest of creatures (Carbone). Growing food or living on Mars would require confinement to domes. Having to step from one domain to another, it would be like living inside, never experiencing the outdoors, which does not seem like an ideal way to live (especially considering we have a perfect environment that can sustain humans at the moment). It is important that humans recognize this colossal risk: Mars is not habitable and never will be naturally, without human interference.
Living in endless domes
Going to Mars would be messy to say the least when the politics behind doing so are taken into full account. Accomplishing a massive mission like this would take international efforts, and even putting a team together would call for the incorporation of government agencies, private companies, environmental programs, and many others. Because of the numerous groups involved, it would be difficult to distribute the claims on land, stocks, and shares among them. Each group is going for very different reasons, for the governments, it would be to gain popularity among citizens, for private organizations it is to “broaden horizons” and develop human exploration (Azam). Consider that the Earth has already been divided into plots of land for different peoples and different needs; there is conflict over resources, governmental ties, and allegiances of people. To incorporate all of what is currently happening while trying to maintain a new civilization far from help or aid seems impractical if not impossible. With a project that fundamentally involves all aspects of life, one must consider the societal impacts that this will cause globally overtime. Each time humans do something extraordinary or revolutionary, there are impacts. For example, with the introduction of nuclear power, people became fearful and did not trust one another or the government. How will something like this make an impact on media, advertising, sports, technology, and overall culture? This will set up a new set of ideals and there is no way to know or prepare for how this might affect humans and relationships (Azam).
Broadly, when all is taken in to account, three things must happen in order for a project like this to even be conceivable. It needs international cooperation, economic growth and stable funding for resources, and enabling technologies (Azam). Technology seems to be a small concern seeing as humans are steadily progressing further to keep people safe, transport people, and live outside of a terrestrial environment. If it is not yet advanced enough, it probably will be in the near future. However, regarding economic growth, we are decades away from being in a position where humans and the world are able to maintain a stable economy long enough to pool resources from it that can provide equipment, food, and aid to those living on Mars. Additionally, tensions are currently rising among international counterparts. At this point, no one can commit to political ties strong enough to cooperate peacefully and unselfishly in this project. Additionally, financially, who is really going to be reaping the benefits of making it to Mars? If all Americans are paying taxes that are going into a space travel fund, how many of them will be able to travel to space and be a part of this? If we are leaving to have a fresh start and create a new society, then who is involved in this process, who gets to say who is more worthy to participate in this “escape” (Stemwedel)? Even if humans do colonize Mars, it will not be for much, much longer, for society is far from ready for the commitments it would entail.
Prospective mining on the moon
One of the most appealing aspects of colonizing Mars is to utilize it’s natural resources: things like natural gasses, iron, titanium, nickel, the list goes on. Not only are these valuable, but they are also extraordinarily easy to harvest. This is because they are not trapped in the bottom of gravity wells like most planets, but they are on the surface and accessible (Stoner). This, although seemingly beneficial, does not give a reason as to why humans must actually colonize Mars in order to benefit from its resources. It would be more efficient, energetically and financially, to set up a mining system that does not require full colonization. Finally, the same resources found on Mars are found on our moon (also Earth, although most of the resources here have been expended), where it would be easier, cheaper, and safer to instead harvest them. Why, then, is this not being taken into account as a viable, perhaps much better, alternative? Even though humans can take from their moon, many people have qualms about digging into such an important aspect of their life. Will disrupting the moon affect human life on Earth? These precautions are taken very seriously because it is easy to see the effects doing so may have on human life. However, when considering digging into Mars, humans lack an understanding of its direct and indirect effects on the Earth, and therefore disregard those same worries that they feel for digging into the moon (Stoner). Although there are benefits to mining and harvesting resources are Mars, it appears to be unwise to focus the efforts on an entire colonization in place of a system for mere extraction of minerals.
In a system where there are no lifeforms, attempting to colonize or even transport objects into space would introduce mass amounts of bacteria and microbes that contaminate this space. When Elon Musk first announced his SpaceX project, introducing a formal plan for what a colonization on Mars would look like, he launched a car and a test dummy into the atmosphere, a feat named by scientists as the “largest load of earthly bacteria to ever enter space” (Bharmal). A few issues arise when considering this, one being that we will then be changing the biosphere in which this bacteria is living and growing, which may lead to a number of mutations that could be uncontrollable. We have no way of knowing how our impacts will create long term effects on the plants and animals introduced on Mars. Even exposing living things to radiation or other extreme conditions can change its cells, neurons, and many other biological aspects (Bharma). With that, going to an entirely new environment could have repercussions that we cannot know or even predict at this time. Can humans really risk contaminating space for personal gain? An additional biological concern is that humans may be stunting the development of Mars. We currently have no proof that life currently exists, but with the newfound discovery of water, it is likely that indigenous life could survive there. If it has not yet happened, the biome may soon working towards supporting and growing life forms (Stemwedel). If humans step in during this process, we will be destroying what has been set up naturally. It would be nearly impossible to distinguish what is indigenous to Mars and what is from Earth, or even what has mutated from Earth to Mars and vice versa. Humans would be distributing a natural cycle and possible developing ecosystem. It would be a travesty to know that humans ruined any chance of self-forming, natural, life forms on Mars, even if it is only bacteria.
Our planet has been sustaining life for billions and billions of years, must we take the first flight out of here and abandon the ultimate benefactress? Humans must accept that they have caused significant harm to the planet and work to resolve our current issues. We cannot use Mars as an escape route or a second chance. Elon Musk argued that humans must have a plan in case of asteroids or intense danger that requires humans to leave. This means people are choosing between fixing the planet that we already live on and working towards a new planet that currently cannot support human life. Humans feel they have an obligation to provide long term survival of this species in case an asteroid hits us, like the dinosaurs before us, or in the event that we face environmental destruction (Stoner). Being on Mars will actually bring us closer to deadly nearby supernovae and the risk of being hit by an asteroid is just as high, if not higher. We could protect the human race by taking significant measures here on Earth to save us from radiation, asteroids, or other significant dangers (Stoner). It would take trillions of dollars to colonize Mars, but if we instead channelled that into what we already are capable of living on, we would be resolving more current and pressing issues. Humans would be safer in large underground bunkers on Earth than being transported to a planet that we do not even know if it can sustain life (Bharmal). Is it fair for humans to escape the damage that they provided to this planet? With the oncoming evidences of environmental destruction, humans are beginning to fear for the future, however, few are working to make a significant difference. Leaving Earth would be like taking a shortcut that would lead us to a dead end, literally. Without learning any different, what will stop humans from destroying the Martian environment, will anything make them any different from how we treat Earth? Like in Wall-E, humans would leave their planet of trash, avoiding fixing their problems, only to later return to a planet of filth. Colonizing Mars would lead to a legacy of cowardness and the inability to accept and resolve massive issues.
In attempting to colonize Mars, humans would have to pool international resources into a politically and economically charged project, potentially eradicate a developing biosphere, and garner an excuse to neglect the environmental impacts on Earth today. Instead, it would be wiser to work on current issues such as creating a stable economy and cooperating with other nations. We should focus on living on this planet and work to improve quality of life here instead of funding research projects to allow life on Mars. Attention and technology should instead be improving with the efforts of creating a more sustainable life and governments should be enforcing the growth of our planet, not its deterioration. Whatever source you believe in, whether that is fate, God or Gods, divinity, chance and coincidence, or even just science, it brought humanity to Earth: a planet that is sufficient and loving to our needs. By denying this, we are denying a much larger deity or idea. Mars does not need to be colonized, instead, let us continue to colonize the world we currently live in and on. | Why we cannot allow the colonization of humans and life Mars.
Humans cannot live on Mars. This is a scientifically proven fact: humans cannot survive in a Martian environment or with that atmosphere. We can actually live nowhere, other than Earth, sustainably, and even that is up in the air. Human bodies are not suited for Mars; they will collapse and die instantly without support. Childhood hero Bill Nye said, “it’s not reasonable because it’s so cold. And there is hardly any water. There’s absolutely no food, and the big thing, I just remind these guys, there’s nothing to breathe” (Carbone). Mars is somewhat comparable to what Earth would have been like during the Ice age, but way worse and way more deadly. The surface of Mars will boil every ounce of liquid in a human body in seconds: the heat and radiation on the surface of Mars is infinitely more deadly than any natural exposure here on Earth (Stoner). Evidently, this is not a suitable environment for animals or even bacteria; humans should not try and risk a life in an environment that cannot provide for even the simplest of creatures (Carbone). Growing food or living on Mars would require confinement to domes. Having to step from one domain to another, it would be like living inside, never experiencing the outdoors, which does not seem like an ideal way to live (especially considering we have a perfect environment that can sustain humans at the moment). It is important that humans recognize this colossal risk: Mars is not habitable and never will be naturally, without human interference.
Living in endless domes
Going to Mars would be messy to say the least when the politics behind doing so are taken into full account. Accomplishing a massive mission like this would take international efforts, and even putting a team together would call for the incorporation of government agencies, private companies, environmental programs, and many others. Because of the numerous groups involved, it would be difficult to distribute the claims on land, stocks, and shares among them. Each group is going for very different reasons, for the governments, it would be to gain popularity among citizens, for private organizations it is to “broaden horizons” and develop human exploration (Azam). | no |
Astronomy | Can humans live on Mars? | no_statement | "humans" cannot "live" on mars.. it is not feasible for "humans" to "live" on mars. | https://www.slashgear.com/811194/bill-nyes-5-reasons-we-cant-live-on-mars/ | Bill Nye's 5 Reasons We Can't Live On Mars | Bill Nye's 5 Reasons We Can't Live On Mars
At an event promoting the new National Geographic Channel's series "Mars," scientist and science educator Bill Nye spoke about the Red Planet's future. While he's all about the idea that astronauts travel to Mars and explore Mars and possibly even mine Mars, he's pretty much against the idea that humans could live on Mars. "This whole idea of terraforming Mars," said Nye, "As respectful as I can be, are you guys high?"
1. We're already killing our own planet
Bill Nye made remarks this week in an interview this week with USA Today. "We can't even take care of this planet where we live," said Nye, "and we're perfectly suited for it, let alone another planet." He's not wrong. Have a peek at this recent heat study to see what sort of shape we're in with regard to climate change.
2. Not many people live in Antarctica
"Nobody goes to Antarctica to raise a family," said Nye. "You don't go there and build a park, there's just no such thing." Scientists visit Antarctica for relatively short periods of time, but no human lives there permanently. That's mostly because it's extremely cold. According to the CIA in the USA, in Antarctica the following is true: "[There are] no indigenous inhabitants, but there are both permanent and summer-only staffed research stations."
And also they get absolutely no cable TV or internet coverage up there – what kind of life is that?
3. Mars is cold
"Nobody's gonna go settle on Mars and raise a family and have generations of Martians," said Nye. "It's not reasonable because it's so cold." You'd have to wear protective gear whenever you weren't inside a protective structure. While parts of Mars can get up to 70 degrees F (20 degrees C), most of the time the whole planet's closer to well below zero.
The above image comes from an All About Mars Facts page at NASA where a whole bunch of Mars Facts can be found. So many Mars Facts you won't know what to do with the lot!
Let's say you DID somehow, for whatever reason, find reason enough to live on Mars. Whenever you wanted to get from one human-made structure to another, you'd need to wear a space suit and/or use a vehicle something like what we got a test drive in back in 2015 – the Mars rover, aka Space Exploration Vehicle, as seen in the video below.
4. There's very little water and absolutely no food
"There is hardly any water," said Nye, "[and] there's absolutely no food." That is unless you are Matt Damon in The Martian and you use a little bit of magic to grow the bare minimum amount of potatoes to survive several months, of course.
In our most recent visit to NASA, Vickie Kloeris Manager, Space Food Systems Laboratory was asked if Damon's potato-growing adventure was realistic. At that time, Kloeris said, "I certainly think that given the right infrastructure, you'd be able to do it." So... maybe?
5. Oxygen is lacking
"And the big thing, I just remind these guys," said Nye, "There's nothing to breathe." For the moment there's most certainly not enough oxygen on Mars for human beings to breathe. Barring any sort of futuristic not-yet-invented means to terraform Mars with an artificial atmosphere and one massive amount of oxygen, we're not realistically headed for Mars long-term.
But exploration is a must!
Dimitrios Kambouris/Getty Images
"We would send people there to make discoveries. To explore, that's the big idea," said Nye. "I want to find evidence of life on another world in my lifetime, so Mars in the next logical place to look." | Scientists visit Antarctica for relatively short periods of time, but no human lives there permanently. That's mostly because it's extremely cold. According to the CIA in the USA, in Antarctica the following is true: "[There are] no indigenous inhabitants, but there are both permanent and summer-only staffed research stations. "
And also they get absolutely no cable TV or internet coverage up there – what kind of life is that?
3. Mars is cold
"Nobody's gonna go settle on Mars and raise a family and have generations of Martians," said Nye. "It's not reasonable because it's so cold." You'd have to wear protective gear whenever you weren't inside a protective structure. While parts of Mars can get up to 70 degrees F (20 degrees C), most of the time the whole planet's closer to well below zero.
The above image comes from an All About Mars Facts page at NASA where a whole bunch of Mars Facts can be found. So many Mars Facts you won't know what to do with the lot!
Let's say you DID somehow, for whatever reason, find reason enough to live on Mars. Whenever you wanted to get from one human-made structure to another, you'd need to wear a space suit and/or use a vehicle something like what we got a test drive in back in 2015 – the Mars rover, aka Space Exploration Vehicle, as seen in the video below.
4. There's very little water and absolutely no food
"There is hardly any water," said Nye, "[and] there's absolutely no food." That is unless you are Matt Damon in The Martian and you use a little bit of magic to grow the bare minimum amount of potatoes to survive several months, of course.
In our most recent visit to NASA, Vickie Kloeris Manager, Space Food Systems Laboratory was asked if Damon's potato-growing adventure was realistic. At that time, Kloeris said, "I certainly think that given the right infrastructure, you'd be able to do it." So... maybe?
5. Oxygen is lacking
"And the big thing, | no |
Gerontology | Can humans live to be over 150 years old? | yes_statement | "humans" can "live" to be over "150" "years" "old".. it is possible for "humans" to "live" beyond "150" "years" of age. | https://nypost.com/2022/03/27/humans-could-live-up-to-150-years-according-to-new-study/ | Humans could live up to 150 years, new study claims | Humans could live until the ripe old age of 150 years according to recent research – and scientists are racing to work out how.
Harvard geniuses, biohackers and internet billionaires are all looking for ways that humans can crack the code on aging.
WaitButWhy blogger Tim Urban writes “the human body seems programmed to shut itself down somewhere around the century mark, if it hasn’t already”.
And Urban is right! There are no verified cases of a person living to be older than 122, though the oldest living person is on their way at age 119.
Researchers at GERO.AI concluded the “absolute limit” of the human lifespan to be between 100 and 150 – they came to this conclusion by analyzing 70,000 participants up to age 85 based on their ability to fight disease, risk of heart conditions and cognitive impairment.
The Conversation reported that not a single participant showed the biological resiliency to live to 150 – but notes the study is limited by today’s medical standards.
Will improvements in medicine, environment and technology to drastically lengthen the average lifespan and make 150 a reality?
Humans could live until the age of 150, according to a new study.Shutterstock
Brutal biology
The human body is made up of about 30 trillion cells. Cells are constantly dying and being replaced by replicants.
Within the cell body there are chromosomes – these are DNA strands with the code written for humans within them.
At the end of a DNA strand is a microscopic bundle of non-crucial DNA, so that none of the important stuff gets snipped off when the cell divides.
A cell can divide itself about 50 times before it’s lost its ability to replicate.
As more and more cells become ineffective and die, the signs of aging start to show in gray hair, weaker bones and vision loss.
Some theorize this process can be stopped or reversed.
There are no verified cases of a person living to be older than 122.Shutterstock
Researchers at Harvard’s Sinclair Lab write: “If DNA is the digital information on a compact disc, then aging is due to scratches. We are searching for the polish.”
Dr David Sinclair, the founder of the lab and one of the foremost scientists working on anti-aging technologies, led an experiment that restored the vision of elderly mice.
The team injected the mice with a serum of genes that affected the DNA of the cells in the eye.
“Our study demonstrates that it’s possible to safely reverse the age of complex tissues such as the retina and restore its youthful biological function,” Sinclair said.
Some people are fighting age not with tests on mice, but on themselves.
Dave Asprey wearing his iconic blue-light glasses which he theorizes will protect him from rays emitted by screens.Mike Coppola/Getty Images
Dave Asprey is an author and entrepreneur who predicts he’ll live to 180 based on his method of ‘biohacking’.
Asprey, 49, has invested over $2million in technologies he believes will alter his biology including stem cell injections and cryotherapy chambers.
Asprey was quoted as saying “The things I am working to pioneer, some of them are expensive, some of them are free like fasting. This will be like cell phones, everyone has cell phones – everyone will have anti-ageing. Change can happen rapidly in society.”
But even visionaries like Elon Musk are wary of immortality, and the billionaire theorizes it could lead to an elderly population with stagnated ideas.
Some people are fighting age not with tests on mice, but on themselves.Getty Images
Digital consciousness
Although the body shuts down, there is a line of thinking that if just our consciousnesses could be preserved, maybe humans could live longer not just 150 years but forever.
Our capacity to get the brain to interface with a computer is currently low – we’ve applied chips that communicate with just a few hundred of the 86 billion neurons – but a Russian billionaire is aiming to duplicate our entire consciousness and upload it onto a computer where it can live forever as a robot or hologram.
In the 2045 Initiative’s manifesto, Dmitry Itskov writes “People will make independent decisions about the extension of their lives and the possibilities for personal development in a new body after the resources of the biological body have been exhausted.”
A Russian billionaire is aiming to duplicate our entire consciousness and upload it onto a computer where it can live forever as a robot or hologram.Shutterstock
Of course, if this idea were to be achieved, you would have to exit your current body in favor of your “new body.”
Is that, on some level, a form of death? Do you restart at age zero once your consciousness has been duplicated? Do you age at all while living inside a computer?
These are biomedical ethics questions that are sure to be debated as the search for a prolonged lifespan carries on both in the hospital and the computer lab.
This story originally appeared on The Sun and has been reproduced here with permission. | Humans could live until the ripe old age of 150 years according to recent research – and scientists are racing to work out how.
Harvard geniuses, biohackers and internet billionaires are all looking for ways that humans can crack the code on aging.
WaitButWhy blogger Tim Urban writes “the human body seems programmed to shut itself down somewhere around the century mark, if it hasn’t already”.
And Urban is right! There are no verified cases of a person living to be older than 122, though the oldest living person is on their way at age 119.
Researchers at GERO.AI concluded the “absolute limit” of the human lifespan to be between 100 and 150 – they came to this conclusion by analyzing 70,000 participants up to age 85 based on their ability to fight disease, risk of heart conditions and cognitive impairment.
The Conversation reported that not a single participant showed the biological resiliency to live to 150 – but notes the study is limited by today’s medical standards.
Will improvements in medicine, environment and technology to drastically lengthen the average lifespan and make 150 a reality?
Humans could live until the age of 150, according to a new study. Shutterstock
Brutal biology
The human body is made up of about 30 trillion cells. Cells are constantly dying and being replaced by replicants.
Within the cell body there are chromosomes – these are DNA strands with the code written for humans within them.
At the end of a DNA strand is a microscopic bundle of non-crucial DNA, so that none of the important stuff gets snipped off when the cell divides.
A cell can divide itself about 50 times before it’s lost its ability to replicate.
As more and more cells become ineffective and die, the signs of aging start to show in gray hair, weaker bones and vision loss.
Some theorize this process can be stopped or reversed.
| no |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.