new research on taurine

Taurine may be a key to longer and healthier life

A deficiency of taurine -- a nutrient produced in the body and found in many foods -- is a driver of aging in animals, according to a new study led by Columbia researchers and involving dozens of aging researchers around the world.

The same study also found that taurine supplements can slow down the aging process in worms, mice, and monkeys and can even extend the healthy lifespans of middle-aged mice by up to 12%.

The study was published June 8 in Science .

"For the last 25 years, scientists have been trying to find factors that not only let us live longer, but also increase healthspan, the time we remain healthy in our old age," says the study's leader, Vijay Yadav, PhD, assistant professor of genetics & development at Columbia University Vagelos College of Physicians and Surgeons.

"This study suggests that taurine could be an elixir of life within us that helps us live longer and healthier lives."

Anti-aging molecules within us

Over the past two decades, efforts to identify interventions that improve health in old age have intensified as people are living longer and scientists have learned that the aging process can be manipulated.

Many studies have found that various molecules carried through the bloodstream are associated with aging. Less certain is whether these molecules actively direct the aging process or are just passengers going along for the ride. If a molecule is a driver of aging, then restoring its youthful levels would delay aging and increase healthspan, the years we spend in good health.

Taurine first came into Yadav's view during his previous research into osteoporosis that uncovered taurine's role in building bone. Around the same time, other researchers were finding that taurine levels correlated with immune function, obesity, and nervous system functions.

"We realized that if taurine is regulating all these processes that decline with age, maybe taurine levels in the bloodstream affect overall health and lifespan," Yadav says.

Taurine declines with age, supplementation increases lifespan in mice

First, Yadav's team looked at levels of taurine in the bloodstream of mice, monkeys, and people and found that the taurine abundance decreases substantially with age. In people, taurine levels in 60-year-old individuals were only about one-third of those found in 5-year-olds.

"That's when we started to ask if taurine deficiency is a driver of the aging process, and we set up a large experiment with mice," Yadav says.

The researchers started with close to 250 14-month-old female and male mice (about 45 years old in people terms). Every day, the researcher fed half of them a bolus of taurine or a control solution. At the end of the experiment, Yadav and his team found that taurine increased average lifespan by 12% in female mice and 10% in males. For the mice, that meant three to four extra months, equivalent to about seven or eight human years.

Taurine supplements in middle age improves health in old age

To learn how taurine impacted health, Yadav brought in other aging researchers who investigated the effect of taurine supplementation on the health and lifespan in several species.

These experts measured various health parameters in mice and found that at age 2 (60 in human years), animals supplemented with taurine for one year were healthier in almost every way than their untreated counterparts.

The researchers found that taurine suppressed age-associated weight gain in female mice (even in "menopausal" mice), increased energy expenditure, increased bone mass, improved muscle endurance and strength, reduced depression-like and anxious behaviors, reduced insulin resistance, and promoted a younger-looking immune system, among other benefits.

"Not only did we find that the animals lived longer, we also found that they're living healthier lives," Yadav says.

At a cellular level, taurine improved many functions that usually decline with age: The supplement decreased the number of "zombie cells" (old cells that should die but instead linger and release harmful substances), increased survival after telomerase deficiency, increased the number of stem cells present in some tissues (which can help tissues heal after injury), improved the performance of mitochondria, reduced DNA damage, and improved the cells' ability to sense nutrients.

Similar health effects of taurine supplements were seen in middle-aged rhesus monkeys, which were given daily taurine supplements for six months. Taurine prevented weight gain, reduced fasting blood glucose and markers of liver damage, increased bone density in the spine and legs, and improved the health of their immune systems.

Randomized clinical trial needed

The researchers do not know yet if taurine supplements will improve health or increase longevity in humans, but two experiments they conducted suggest taurine has potential.

In the first, Yadav and his team looked at the relationship between taurine levels and approximately 50 health parameters in 12,000 European adults aged 60 and over. Overall, people with higher taurine levels were healthier, with fewer cases of type 2 diabetes, lower obesity levels, reduced hypertension, and lower levels of inflammation. "These are associations, which do not establish causation," Yadav says, "but the results are consistent with the possibility that taurine deficiency contributes to human aging."

The second study tested if taurine levels would respond to an intervention known to improve health: exercise. The researchers measured taurine levels before and after a variety of male athletes and sedentary individuals finished a strenuous cycling workout and found a significant increase in taurine among all groups of athletes (sprinters, endurance runners, and natural bodybuilders) and sedentary individuals.

"No matter the individual, all had increased taurine levels after exercise, which suggests that some of the health benefits of exercise may come from an increase in taurine," Yadav says.

Only a randomized clinical trial in people will determine if taurine truly has health benefits, Yadav adds. Taurine trials are currently underway for obesity, but none are designed to measure a wide range of health parameters.

Other potential anti-aging drugs -- including metformin, rapamycin, and NAD analogs -- are being considered for testing in clinical trials.

"I think taurine should also be considered," Yadav says. "And it has some advantages: Taurine is naturally produced in our bodies, it can be obtained naturally in the diet, it has no known toxic effects (although it's rarely used in concentrations used ), and it can be boosted by exercise.

"Taurine abundance goes down with age, so restoring taurine to a youthful level in old age may be a promising anti-aging strategy."

• Healthy Aging
• Medical Topics
• Teen Health
• Genetically Modified
• Calorie restricted diet
• Health science
• Ketone bodies
• Epidemiology
• General fitness training
• Antioxidant

Story Source:

Materials provided by Columbia University Irving Medical Center . Note: Content may be edited for style and length.

Journal Reference :

• Parminder Singh, Kishore Gollapalli, Stefano Mangiola, Daniela Schranner, Mohd Aslam Yusuf, Manish Chamoli, Sting L. Shi, Bruno Lopes Bastos, Tripti Nair, Annett Riermeier, Elena M. Vayndorf, Judy Z. Wu, Aishwarya Nilakhe, Christina Q. Nguyen, Michael Muir, Michael G. Kiflezghi, Anna Foulger, Alex Junker, Jack Devine, Kunal Sharan, Shankar J. Chinta, Swati Rajput, Anand Rane, Philipp Baumert, Martin Schönfelder, Francescopaolo Iavarone, Giorgia di Lorenzo, Swati Kumari, Alka Gupta, Rajesh Sarkar, Costerwell Khyriem, Amanpreet S. Chawla, Ankur Sharma, Nazan Sarper, Naibedya Chattopadhyay, Bichitra K. Biswal, Carmine Settembre, Perumal Nagarajan, Kimara L. Targoff, Martin Picard, Sarika Gupta, Vidya Velagapudi, Anthony T. Papenfuss, Alaattin Kaya, Miguel Godinho Ferreira, Brian K. Kennedy, Julie K. Andersen, Gordon J. Lithgow, Abdullah Mahmood Ali, Arnab Mukhopadhyay, Aarno Palotie, Gabi Kastenmüller, Matt Kaeberlein, Henning Wackerhage, Bhupinder Pal, Vijay K. Yadav. Taurine deficiency as a driver of aging . Science , 2023; 380 (6649) DOI: 10.1126/science.abn9257

Cite This Page :

Explore More

• Otters Use Tools to Survive a Changing World
• Monogamy in Mice: Newly Evolved Type of Cell
• Sustainable Electronics, Doped With Air
• Male Vs Female Brain Structure
• Breeding 'Carbon Gobbling' Plants
• Why Do We Overindulge?
• Jelly Sea Creatures and Underwater Robotics
• Teeth of Sabre-Toothed Tigers
• Robotic 'SuperLimbs' Could Help Moonwalkers
• Solving Quantum Many-Body Problems

Trending Topics

Strange & offbeat.

Can Taurine Slow Aging? Here’s What the Latest Science Says

A nti-aging supplements become popular based more on hype than hard evidence—but researchers are starting to investigate some of the more promising ones to add some scientific rigor to the claims.

The latest is the amino acid taurine: a familiar ingredient in energy drinks and one that scientists have been studying for decades, albeit for reasons other than aging. In a paper published June 8 in Science , researchers report on encouraging results that show taurine can slow aging in a number of animal species, including worms, mice, and monkeys. In people, the team also reports that taurine levels decline with age and can be boosted with exercise.

Taurine is a far cry from a fountain of youth, but the findings suggest that it may be hold promise as a supplement that could help certain body systems function better and act “younger” again.

More from TIME

Humans make taurine naturally in the body, mostly in the brain, heart, and reproductive organs. We can also get it through diet by eating meat, fish, and eggs. Athletes have long known that taurine can improve energy and performance, and it’s also been part of obesity treatments. But its role in aging wasn’t clear until now.

Read More : Pre-Workout Powders Are Gaining Popularity. Do They Work?

What is especially intriguing about the findings, the authors said during a briefing, is that taurine appears to not only slow aging and extend lifespan, but also improve health span—meaning that the animals didn’t just live longer, but healthier.

In a series of experiments that extended over 11 years, the team, led by Vijay Yadav from the National Institute of Immunology in New Delhi, India, first documented that circulating levels of taurine in the blood of mice declined with age. Next, they fed older animals taurine supplements to restore these levels to what they were when the mice were younger, and found that the supplemented mice lived on average 10% to 12% longer than old mice who hadn’t received taurine supplements.

The longer lifespan was also a healthier one for the animals. “Whatever we checked, the taurine-supplemented mice were healthier and appeared younger than controls,” Yadav said. “Taurine made the animals live healthier and longer lives because it was affecting all the major hallmarks of aging.”

Yadav found similar life-extending and health-promoting effects of taurine supplementation in worms and monkeys, the latter of which most closely resemble people.

Read More : Magnesium Supplements Are a Buzzy New Sleep and Anxiety Aid. Do They Work?

“It’s almost too good to be true,” said his collaborator Henning Wackerhage, professor of exercise biology at the Technical University of Munich in Germany. Wackerhage built off of Yadav’s work in the various animal species and looked at how taurine levels might be related to aging in people. He took advantage of an earlier, large study of 12,000 people in which other scientists had collected blood from the participants and therefore had data on a variety of metabolites, including taurine. The study also included data on people’s health outcomes and showed that people with higher taurine levels tended to be healthier—with lower levels of blood glucose, cholesterol, and inflammation, all of which are associated with aging—compared to those with lower taurine levels. “That showed taurine levels in the blood are associated with disease,” he said.

Wackerhage then investigated how taurine levels are affected by exercise. After a group of people in the large data set were asked to cycle on a stationary bike to exhaustion, their taurine levels rose.

Taken together, the data all point to the possibility that taurine can play a role in slowing aging—or, at the very least, in making animals healthier as they get older. They also suggest that restoring depleted levels through supplements, or possibly even exercise, is possible.

However, taurine’s effect on aging needs to be verified in human studies, said Yadav and Wackerhage. “We do not recommend buying off-the-shelf taurine or drinking energy drinks,” said Yadav. “We need to wait for human clinical trials to be completed, and the decision to supplement or not to supplement with taurine should be based on comparing the benefits and risks, which may depend on age and the population. It’s not going to be a straightforward answer.”

Those studies will join other trials that are currently exploring whether other supplements, including rapamycin , a compound that suppresses the immune system, and metformin , a diabetes drug, can slow aging processes in the body.

More Must-Reads from TIME

• The New Face of Doctor Who
• Putin’s Enemies Are Struggling to Unite
• Women Say They Were Pressured Into Long-Term Birth Control
• Scientists Are Finding Out Just How Toxic Your Stuff Is
• Boredom Makes Us Human
• John Mulaney Has What Late Night Needs
• The 100 Most Influential People of 2024
• Want Weekly Recs on What to Watch, Read, and More? Sign Up for Worth Your Time

Contact us at [email protected]

Skip to content

• Health Insights

Health Insights is your guide to wellness and medicine, informed by clinicians from Columbia University Irving Medical Center.

Specialties

• Treatments & Conditions

Find a Doctor

For patients.

Search for a provider by specialty, expertise, location and insurance. Schedule an appointment online.

Taurine May Be a Key to Longer and Healthier Life

A deficiency of taurine—a nutrient produced in the body and found in many foods—is a driver of aging in animals, according to a new study led by Columbia researchers and involving dozens of aging researchers around the world.

The same study also found that taurine supplements can slow down the aging process in worms, mice, and monkeys and can even extend the healthy lifespans of middle-aged mice by up to 12%.

The study was published June 8 in Science .

“For the last 25 years, scientists have been trying to find factors that not only let us live longer, but also increase healthspan, the time we remain healthy in our old age,” says the study’s leader, Vijay Yadav, PhD, assistant professor of genetics & development at Columbia University Vagelos College of Physicians and Surgeons.

“This study suggests that taurine could be an elixir of life within us that helps us live longer and healthier lives.”

Anti-aging molecules within us

Over the past two decades, efforts to identify interventions that improve health in old age have intensified as people are living longer and scientists have learned that the aging process can be manipulated.

Many studies have found that various molecules carried through the bloodstream are associated with aging. Less certain is whether these molecules actively direct the aging process or are just passengers going along for the ride. If a molecule is a driver of aging, then restoring its youthful levels would delay aging and increase healthspan, the years we spend in good health.

Taurine first came into Yadav’s view during his previous research into osteoporosis that uncovered taurine’s role in building bone. Around the same time, other researchers were finding that taurine levels correlated with immune function, obesity, and nervous system functions.

“We realized that if taurine is regulating all these processes that decline with age, maybe taurine levels in the bloodstream affect overall health and lifespan,” Yadav says.

Taurine declines with age, supplementation increases lifespan in mice

First, Yadav’s team looked at levels of taurine in the bloodstream of mice, monkeys, and people and found that the taurine abundance decreases substantially with age. In people, taurine levels in 60-year-old individuals were only about one-third of those found in 5-year-olds.

“That’s when we started to ask if taurine deficiency is a driver of the aging process, and we set up a large experiment with mice,” Yadav says.

The researchers started with close to 250 14-month-old female and male mice (about 45 years old in people terms). Every day, the researcher fed half of them a bolus of taurine or a control solution. At the end of the experiment, Yadav and his team found that taurine increased average lifespan by 12% in female mice and 10% in males. For the mice, that meant three to four extra months, equivalent to about seven or eight human years.

Taurine supplements in middle age improve health in old age

To learn how taurine impacted health, Yadav brought in other aging researchers who investigated the effect of taurine supplementation on the health and lifespan in several species.

These experts measured various health parameters in mice and found that at age 2 (60 in human years), animals supplemented with taurine for one year were healthier in almost every way than their untreated counterparts.

The researchers found that taurine suppressed age-associated weight gain in female mice (even in “menopausal” mice), increased energy expenditure, increased bone mass, improved muscle endurance and strength, reduced depression-like and anxious behaviors, reduced insulin resistance, and promoted a younger-looking immune system, among other benefits.

“Not only did we find that the animals lived longer, we also found that they’re living healthier lives,” Yadav says.

At a cellular level, taurine improved many functions that usually decline with age: The supplement decreased the number of “zombie cells” (old cells that should die but instead linger and release harmful substances), increased survival after telomerase deficiency, increased the number of stem cells present in some tissues (which can help tissues heal after injury), improved the performance of mitochondria, reduced DNA damage, and improved the cells‘ ability to sense nutrients.

Similar health effects of taurine supplements were seen in middle-aged rhesus monkeys, which were given daily taurine supplements for six months. Taurine prevented weight gain, reduced fasting blood glucose and markers of liver damage, increased bone density in the spine and legs, and improved the health of their immune systems.

Randomized clinical trial needed

The researchers do not know yet if taurine supplements will improve health or increase longevity in humans, but two experiments they conducted suggest taurine has potential.

In the first, Yadav and his team looked at the relationship between taurine levels and approximately 50 health parameters in 12,000 European adults aged 60 and over. Overall, people with higher taurine levels were healthier, with fewer cases of type 2 diabetes, lower obesity levels, reduced hypertension, and lower levels of inflammation. “These are associations, which do not establish causation,” Yadav says, “but the results are consistent with the possibility that taurine deficiency contributes to human aging.”

The second study tested if taurine levels would respond to an intervention known to improve health: exercise. The researchers measured taurine levels before and after a variety of male athletes and sedentary individuals finished a strenuous cycling workout and found a significant increase in taurine among all groups of athletes (sprinters, endurance runners, and natural bodybuilders) and sedentary individuals.

“No matter the individual, all had increased taurine levels after exercise, which suggests that some of the health benefits of exercise may come from an increase in taurine,” Yadav says.

Only a randomized clinical trial in people will determine if taurine truly has health benefits, Yadav adds. Taurine trials are currently underway for obesity, but none are designed to measure a wide range of health parameters.

Other potential anti-aging drugs—including metformin, rapamycin, and NAD analogs—are being considered for testing in clinical trials.

“I think taurine should also be considered,” Yadav says. “And it has some advantages: Taurine is naturally produced in our bodies, it can be obtained naturally in the diet, it has no known toxic effects (although it’s rarely used in concentrations used in this study), and it can be boosted by exercise.

“Taurine abundance goes down with age, so restoring taurine to a youthful level in old age may be a promising anti-aging strategy.”

More information

The study, titled “ Taurine deficiency as a driver of aging ,” was published in Science on June 8, 2023.  

All authors: Parminder Singh, Kishore Gollapalli, Stefano Mangiola, Daniela Schranner, Mohd Aslam Yusuf, Manish Chamoli, Sting L. Shi, Bruno Lopes Bastos, Tripti Nair, Annett Riermeier, Elena M. Vayndorf, Judy Z. Wu, Aishwarya Nilakhe, Christina Q. Nguyen, Michael Muir, Michael G. Kiflezghil, Anna Foulger, Alex Junker, Jack Devine, Kunal Sharan, Shankar J. Chinta, Swati Rajput, Anand Rane, Philipp Baumert, Martin Schönfelder, Francescopaolo lavarone, Giorgia di Lorenzo, Swati Kumari, Alka Gupta, Rajesh Sarkar, Costerwell Khyriem, Amanpreet S. Chawla, Ankur Sharma, Nazan Sarper, Naibedya Chattopadhyay, Bichitra K. Biswal, Carmine Settembre, Perumal Nagarajan, Kimara L. Targoff, Martin Picard, Sarika Gupta, Vidya Velagapudi, Anthony T. Papenfuss, Alaattin Kaya, Miguel Godinho Ferreiral, Brian K. Kennedy, Julie K. Andersen, Gordon J. Lithgow, Abdullah Mahmood Ali, Arnab Mukhopadhyay, Aarno Palotie, Gabi Kastenmiller, Matt Kaeberlein, Henning Wackerhage, Bhupinder Pal, Vijay K. Yadav.

This work was funded by the Nathan Shock Center of Excellence in the Basic Biology of Aging Project; National Institutes of Health (R01HD107574, P30AG013280, T32AG066574); Wellcome (098051); Deutsche Forschungsgemeinschaft (450149205-TRR333/1); Institut National Du Cancer (PLBIO21-228 ); Science and Engineering Research Board (STR/2019/00064); Department of Biotechnology (BT/PR40325/BTIS/137/1/2020); a Longevity Impetus Grant; Academy of Finland Center of Excellence in Complex Disease Genetics (312074, 336824, and 352793); The Sigrid Juselius Foundation; a Larry L. Hillblom Foundation Fellowship; Victorian Cancer Agency (ECRF21036 and MCRF21002); and a DBT Ramalingaswamy Fellowship.  

Columbia University has filed provision patent applications on which Vijay Yadav is listed as an inventor. The remaining authors declare no competing interests.  

• Alzheimer's disease & dementia
• Arthritis & Rheumatism
• Attention deficit disorders
• Autism spectrum disorders
• Biomedical technology
• Diseases, Conditions, Syndromes
• Endocrinology & Metabolism
• Gastroenterology
• Gerontology & Geriatrics
• Health informatics
• Inflammatory disorders
• Medical economics
• Medical research
• Medications
• Neuroscience
• Obstetrics & gynaecology
• Oncology & Cancer
• Ophthalmology
• Overweight & Obesity
• Parkinson's & Movement disorders
• Psychology & Psychiatry
• Radiology & Imaging
• Sleep disorders
• Sports medicine & Kinesiology
• Vaccination
• Breast cancer
• Cardiovascular disease
• Chronic obstructive pulmonary disease
• Colon cancer
• Coronary artery disease
• Heart attack
• Heart disease
• High blood pressure
• Kidney disease
• Lung cancer
• Multiple sclerosis
• Myocardial infarction
• Ovarian cancer
• Post traumatic stress disorder
• Rheumatoid arthritis
• Schizophrenia
• Skin cancer
• Type 2 diabetes
• Full List »

share this!

June 8, 2023

This article has been reviewed according to Science X's editorial process and policies . Editors have highlighted the following attributes while ensuring the content's credibility:

fact-checked

peer-reviewed publication

trusted source

Taurine may be a key to longer and healthier life

by Columbia University Irving Medical Center

A deficiency of taurine—a nutrient produced in the body and found in many foods—is a driver of aging in animals, according to a new study led by Columbia researchers and involving dozens of aging researchers around the world.

The same study also found that taurine supplements can slow down the aging process in worms, mice, and monkeys and can even extend the healthy lifespans of middle-aged mice by up to 12%. The study was published June 8 in Science .

"For the last 25 years, scientists have been trying to find factors that not only let us live longer, but also increase health span, the time we remain healthy in our old age," says the study's leader, Vijay Yadav, Ph.D., assistant professor of genetics & development at Columbia University Vagelos College of Physicians and Surgeons.

"This study suggests that taurine could be an elixir of life within us that helps us live longer and healthier lives."

Anti-aging molecules within us

Over the past two decades, efforts to identify interventions that improve health in old age have intensified as people are living longer and scientists have learned that the aging process can be manipulated.

Many studies have found that various molecules carried through the bloodstream are associated with aging. Less certain is whether these molecules actively direct the aging process or are just passengers going along for the ride. If a molecule is a driver of aging, then restoring its youthful levels would delay aging and increase healthspan, the years we spend in good health.

Taurine first came into Yadav's view during his previous research into osteoporosis that uncovered taurine's role in building bone. Around the same time, other researchers were finding that taurine levels correlated with immune function, obesity, and nervous system functions.

"We realized that if taurine is regulating all these processes that decline with age, maybe taurine levels in the bloodstream affect overall health and lifespan," Yadav says.

Taurine declines with age, supplementation increases lifespan in mice

First, Yadav's team looked at levels of taurine in the bloodstream of mice, monkeys, and people and found that the taurine abundance decreases substantially with age. In people, taurine levels in 60-year-old individuals were only about one-third of those found in five-year-olds.

"That's when we started to ask if taurine deficiency is a driver of the aging process , and we set up a large experiment with mice," Yadav says.

The researchers started with close to 250 14-month-old female and male mice (about 45 years old in people terms). Every day, the researcher fed half of them a bolus of taurine or a control solution. At the end of the experiment, Yadav and his team found that taurine increased average lifespan by 12% in female mice and 10% in males. For the mice, that meant three to four extra months, equivalent to about seven or eight human years.

Taurine supplements in middle age improves health in old age

To learn how taurine impacted health, Yadav brought in other aging researchers who investigated the effect of taurine supplementation on the health and lifespan in several species.

These experts measured various health parameters in mice and found that at age two (60 in human years), animals supplemented with taurine for one year were healthier in almost every way than their untreated counterparts.

The researchers found that taurine suppressed age-associated weight gain in female mice (even in "menopausal" mice), increased energy expenditure, increased bone mass, improved muscle endurance and strength, reduced depression-like and anxious behaviors, reduced insulin resistance, and promoted a younger-looking immune system, among other benefits.

"Not only did we find that the animals lived longer, we also found that they're living healthier lives," Yadav says.

At a cellular level , taurine improved many functions that usually decline with age: The supplement decreased the number of "zombie cells" (old cells that should die but instead linger and release harmful substances), increased survival after telomerase deficiency, increased the number of stem cells present in some tissues (which can help tissues heal after injury), improved the performance of mitochondria, reduced DNA damage, and improved the cells' ability to sense nutrients.

Similar health effects of taurine supplements were seen in middle-aged rhesus monkeys, which were given daily taurine supplements for six months. Taurine prevented weight gain, reduced fasting blood glucose and markers of liver damage, increased bone density in the spine and legs, and improved the health of their immune systems.

Randomized clinical trial needed

The researchers do not know yet if taurine supplements will improve health or increase longevity in humans, but two experiments they conducted suggest taurine has potential.

In the first, Yadav and his team looked at the relationship between taurine levels and approximately 50 health parameters in 12,000 European adults aged 60 and over. Overall, people with higher taurine levels were healthier, with fewer cases of type 2 diabetes, lower obesity levels, reduced hypertension, and lower levels of inflammation. "These are associations, which do not establish causation," Yadav says, "but the results are consistent with the possibility that taurine deficiency contributes to human aging."

The second study tested if taurine levels would respond to an intervention known to improve health: exercise. The researchers measured taurine levels before and after a variety of male athletes and sedentary individuals finished a strenuous cycling workout and found a significant increase in taurine among all groups of athletes (sprinters, endurance runners, and natural bodybuilders) and sedentary individuals.

"No matter the individual, all had increased taurine levels after exercise, which suggests that some of the health benefits of exercise may come from an increase in taurine," Yadav says.

Only a randomized clinical trial in people will determine if taurine truly has health benefits, Yadav adds. Taurine trials are currently underway for obesity, but none are designed to measure a wide range of health parameters.

Other potential anti-aging drugs—including metformin, rapamycin, and NAD analogs—are being considered for testing in clinical trials.

"I think taurine should also be considered," Yadav says. "And it has some advantages: Taurine is naturally produced in our bodies, it can be obtained naturally in the diet, it has no known toxic effects (although it's rarely used in concentrations used ), and it can be boosted by exercise.

"Taurine abundance goes down with age, so restoring taurine to a youthful level in old age may be a promising anti-aging strategy."

The study, titled "Taurine deficiency as a driver of aging," is published in Science .

Joseph McGaunn et al, Taurine linked with healthy aging, Science (2023). DOI: 10.1126/science.adi3025 , www.science.org/doi/10.1126/science.adi3025

Explore further

Feedback to editors

A long-term ketogenic diet accumulates aged cells in normal tissues, new study shows

11 hours ago

Gut bacteria enhance cancer immunotherapy in mouse study

Research finds the protein VISTA directly blocks T cells from functioning in immunotherapy

Study opens the door to designing therapies to improve lung development in growth-restricted fetuses

13 hours ago

Researchers make strides in microbiome-based cancer therapies via iron deprivation in the tumor microenvironment

Study reveals that the brain modulates visual signals according to internal states

Limiting certain light exposure has potential to prevent inherited retinal dystrophy

Researchers reveal molecular mechanisms of different donor arteries for coronary artery bypass grafting

Cell types and molecules usually associated with autoimmune diseases found to be normal components of gut immunity

14 hours ago

Key protein behind brain asymmetry uncovered by scientists

Related stories.

New study shows taurine supplements may improve performance recovery

Nov 13, 2017

Red Bull additive taurine improves symptoms of young people suffering first episode psychosis

Oct 20, 2016

Scientists identify nutrient that helps prevent bacterial infection

Jan 15, 2021

Study shows that the amino acid taurine could be used in anti-aging therapy

Jul 20, 2022

Taurine deficiency in sperm causes male infertility, study finds

May 14, 2018

Hunting dogs may benefit from antioxidant boost in diet

May 8, 2018

Recommended for you

Discovery of a master neuron that controls movement in worms has implications for human disease

May 16, 2024

Study investigates cardiac cell regeneration in search of novel therapeutics

Study finds astrocytic pH regulator can repair blood-brain barrier, reverse brain damage caused by ischemic stroke

May 15, 2024

The doctor is in… but what's behind them? Study reveals impacts of telehealth background settings

Researchers develop innovative platform for modeling human muscle diseases in worms

Study paves the way for an active agent against hepatitis E

Let us know if there is a problem with our content.

Use this form if you have come across a typo, inaccuracy or would like to send an edit request for the content on this page. For general inquiries, please use our contact form . For general feedback, use the public comments section below (please adhere to guidelines ).

Please select the most appropriate category to facilitate processing of your request

Thank you for taking time to provide your feedback to the editors.

Your feedback is important to us. However, we do not guarantee individual replies due to the high volume of messages.

E-mail the story

Your email address is used only to let the recipient know who sent the email. Neither your address nor the recipient's address will be used for any other purpose. The information you enter will appear in your e-mail message and is not retained by Medical Xpress in any form.

Newsletter sign up

Get weekly and/or daily updates delivered to your inbox. You can unsubscribe at any time and we'll never share your details to third parties.

More information Privacy policy

Donate and enjoy an ad-free experience

We keep our content available to everyone. Consider supporting Science X's mission by getting a premium account.

E-mail newsletter

Advertisement

Taurine supplements extend lifespan and health in old age in mammals

Mice had longer lives and monkeys stayed healthier as they aged when given taurine supplements  

8 June 2023

Further research is required, but taurine supplements could have potential in prolonging people’s longevity

photo_gonzo/Alamy

We lose levels of the amino acid taurine as we age, with experiments in mice and monkeys suggesting that supplements could reverse this loss to keep us healthy and potentially even extend our lifespan.

A new class of anti-ageing drugs has arrived – which ones really work?

Found in many animals, including humans, taurine is naturally synthesised in the pancreas, but can also be obtained by eating animal products. Previous studies have found that taurine deficiencies in early life impair the skeletal muscle and central nervous system in mice , as well as causing retinal degeneration in mice and cats , but little is known about the amino acid’s potential role in ageing.

To learn more, Vijay Yadav at Columbia University in New York and his colleagues measured taurine concentrations in the blood of mice, monkeys and humans, finding that its levels declined as they all aged. Among the human participants, those aged around 65 had taurine levels that were more than 80 per cent lower than those of the study’s infant participants. In a separate analysis of nearly 12,000 60-year-olds, higher taurine levels correlated with various markers of better health, including a lower prevalence of type 2 diabetes and reduced inflammation.

Next, the researchers wanted to see if reversing taurine’s decline could improve the animals’ health as they aged and potentially extend their lifespan. They therefore gave daily taurine supplements to 14-month-old mice, the equivalent age of a person between 45 and 50 years old.

On average, these mice lived up to 12 per cent longer than those that weren’t given taurine. They also had lower hallmarks of ageing , such as reduced DNA damage and mitochondrial dysfunction. “They were leaner, had improved bone density and muscle strength and had a younger-looking immune system, among other benefits,” says Yadav.

Sign up to our Health Check newsletter

Get the most essential health and fitness news in your inbox every Saturday.

In the monkeys, the researchers didn’t assess the effect of the supplements on their lifespan, but did link them to a healthier liver, body mass, immune system and bone density. “In other words, supplements made monkeys healthier for longer,” says Yadav.

The researchers hope to repeat their experiment in people, but in the meantime, they don’t recommend that people take taurine supplements in the hope of living longer. “We need to wait for a large-scale, randomised-controlled taurine intervention before taurine supplementation can be safely recommended for people,” says Yadav.

“Although more clinical studies are still needed, this study provides relevant scientific support that taurine supplementation may have a positive impact on promoting healthy longevity in humans,” says Cláudia Cavadas at the University of Coimbra in Portugal. “However, it is important to never forget that a healthy lifestyle is essential for achieving a healthy lifespan.”

Journal reference:

Science DOI: 10.1126/science.abn9257

Sign up to our weekly newsletter

Receive a weekly dose of discovery in your inbox! We'll also keep you up to date with New Scientist events and special offers.

More from New Scientist

Explore the latest news, articles and features

A daily multivitamin could keep your memory sharp as you age

Which dietary supplements actually work and which should you take.

Subscriber-only

Can probiotics and supplements really improve your gut microbiome?

Popular articles.

Trending New Scientist articles

Higher taurine levels help slow aging in animals, new research shows

Taurine, an amino acid found in meat and shellfish, is a popular supplement added to energy drinks that are touted to promote sharper brain function. While those claims are unproven, new research suggests the nutrient may help with healthy aging.

Low levels of taurine can speed the aging process in several species of animals. Now scientists report that supplementing with the nutrient may slow that process down, leading to longer, healthier lives in animals — and maybe humans, too — an international group of researchers reported Thursday in Science.

“This is a really exciting time,” said study co-author Vijay Yadav, an assistant professor of genetics and development at the Vagelos College of Physicians and Surgeons, the medical school for Columbia University in New York City.

That’s because researchers are now exploring specific molecules, such as taurine, that might improve health and lead to longer life, Yadav said.

Yadav and his colleagues showed that taurine levels declined dramatically with age in mice, monkeys and humans. No one knows yet why levels of the nutrient decline as much as 80% with age, Yadav said.

In experiments with mice and monkeys, the researchers found that supplementing middle-age animals led to better health.

In mice, the supplementation led to less weight gain, increased bone density, improved muscle endurance and strength, reduced insulin resistance, a better-functioning immune system and a 10% longer lifespan, which in humans would be about seven or eight years.

In monkeys, supplementation prevented age-related weight gain, improved fasting blood sugar levels, increased bone density and led to healthier livers and improved immune system function.

Yadav was quick to point out that it doesn’t look like supplementation is reversing the effects of aging.

“It’s hitting the brakes on aging, not putting things in reverse gear,” he said at a news briefing Tuesday.

While there haven’t yet been trials in humans, data suggests that the findings in animals might be applicable.

Examining data from the University of Cambridge's EPIC-Norfolk study — which from 1993 to 1998 tracked health, diet and physical activity of 30,000 men and women ages 40 to 79 — the researchers found that, overall, people with higher taurine levels were healthier, had lower levels of inflammation and were less likely to have Type 2 diabetes or high blood pressure or to be obese.  

Exercise may boost taurine

In another intriguing finding, the researchers discovered an association between the amount people exercise and their taurine levels. Scrutinizing data from the EPIC-Norfolk study, the researchers discovered that taurine levels rise with exercise.

The next step is to run a clinical trial to determine whether similar benefits can be seen when humans receive taurine supplements, Yadav said, adding that he couldn’t recommend that people try to boost their taurine levels without such data.

Fortunately, the European Food Safety Authority has deemed doses of taurine in humans similar to what was given to the mice to be safe, said Henning Wackerhage, a co-author of the study and a professor of exercise biology at the Technical University of Munich.

Levels of taurine added to energy drinks would be safe, but Wackerhage expressed concern about the levels of caffeine in the beverages.

As for higher doses, Yadav said no one knows whether there would be safety issues.

Foods high in taurine

While the human body can make small amounts of taurine, an amino acid, people mostly get it through food .

Shellfish, as well as dark chicken and turkey meat, contain the highest levels of taurine. Other meats contain moderate amounts of taurine, while dairy products, such as milk and ice cream, also have taurine, although less of it.

One of the first hints that taurine might be an important but underappreciated nutrient came in the 1970s, when scientists discovered that a rash of cases of blindness in cats could be explained by the lack of the amino acid in popular cat foods. Cats can’t make taurine on their own. When pet food manufacturers changed their formulations to include higher levels of the nutrient, the problems resolved.

A short time after, researchers discovered that the lack of taurine in pet food was also causing a severe heart problem called dilated cardiomyopathy in cats.

Since then, researchers have associated taurine deficiency with a host of age-related diseases in humans.

Is it safe to take taurine supplements?

Neuroscientist Charles Mobbs called the research “extraordinarily thorough.”  

“It’s very credible and is consistent with many of the things we already know about taurine and aging,” said Mobbs, who specializes in endocrinology and geriatrics at the Icahn School of Medicine at Mount Sinai in New York. “This research brings it to the next level.”

Mobbs would like to see future research explaining why taurine levels decline with age and how the nutrient works.

“Because the study is so thorough, it’s likely that the results will be replicated,” said Mobbs, who wasn’t involved in the new research.

When it comes to giving people taurine as a supplement, Dr. Toren Finkel, a cardiologist, is concerned that “if you scale the dose given to the mice to a human dose, it would be 5 to 6 grams per day.”

“Many pills people take are 100 milligrams,” said Finkel, the director of the Aging Institute of the University of Pittsburgh and UPMC. “A dose of 5 grams would be 50 times that. So that’s a lot.”  

The equivalent of 5 grams would be about 1 teaspoon.

“One really nice part of the study is that they saw declines in taurine in multiple species,” said Finkel, who isn’t part of the study. “And if you intervene with taurine supplements, it appears to reverse a lot of aging issues in multiple species. These are very intriguing results.”

The new study “provides one more piece of evidence that dietary alterations can have an impact on aging and aging-related pathologies,” said Dr. Douglas Vaughan, the chair of medicine at the Northwestern University Feinberg School of Medicine, who isn’t associated with the new research.

While the researchers used supplements to boost taurine levels, people can reach the same goal by consuming foods that are high in the nutrient, Vaughan said.

The research was funded by the National Institutes of Health and the Nathan Shock Centers of Excellence. Columbia University has applied for patents for medical uses of taurine, a spokesperson for the university said in an email.

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." 

• Share full article

Advertisement

Supported by

From Energy Drinks to Extending Life? Supplement Slows Aging in Mice and Monkeys

Taurine helped stave off death in laboratory animals, but researchers cautioned that the supplement is not a magic elixir.

By Elie Dolgin

A dietary supplement taken by fitness buffs could hold the key to a longer and healthier life, suggests a new study of mice, monkeys and worms. Researchers found that a high daily dose of taurine, an amino acid commonly added to energy drinks and naturally found in various foods, helped to delay death and mitigate against the biological ravages of aging.

Strength, memory and metabolism improved in the lab animals, according to the new study, published on Thursday in Science. Inflammation and DNA damage were kept at bay. And middle-aged mice that regularly took taurine supplements lived significantly longer than those that did not.

“There’s something here, and if it works in humans it’s going to be a terrific thing,” said Dr. Nir Barzilai, the director of the Institute for Aging Research at the Albert Einstein College of Medicine, who was not involved in the study.

But Dr. Barzilai and other longevity researchers cautioned against viewing taurine as a magic elixir for life extension. They said people should consume the supplement with prudence, particularly when considering high dosage levels similar to those administered to the mice and monkeys.

Taurine — a nutrient produced by the body and obtained from animal-based foods like shellfish and turkey — has a long track record of safety, they said. But when ingested in large amounts it could cause digestive problems, kidney strain and potentially harmful interactions with medications.

Its effectiveness in promoting healthy aging in people is yet to be established — and other once-hyped anti-aging drugs that showed initial promise in mice and monkeys have not always panned out in human testing.

One small clinical trial in Brazil found that four months of low-dose taurine supplementation had positive antioxidant effects in older women , with no toxicity concerns. But larger and longer studies are needed to gauge the effectiveness of other doses of taurine, researchers said.

Human studies on taurine supplementation have generally tested low doses, typically around 1.5 grams per day. The mice and monkeys in the new study were given a dose equivalent to about three to six grams a day for humans — a level deemed safe by European regulators, but still on the higher end of the spectrum.

“The bottom line is that clinical trials need to be done,” said Vijay Yadav, a longevity researcher at Columbia University Irving Medical Center, who led the study.

Taurine got its name in the 1820s from the Latin word “taurus,” meaning bull, after German scientists first isolated the amino acid from the bile of an ox.

Dr. Yadav didn’t know anything about taurine, however, until around a decade ago, when he found that the supplement helped promote bone development in young mice born to vitamin-deficient mothers.

Studies on humans had already linked low taurine levels to poor heart health, cognitive performance and muscle function. Some research also points to taurine underpinning the extraordinary longevity of people living on the Japanese island of Okinawa .

But whether taurine deficiency was a driver of aging, or simply a byproduct of the aging process, remained unclear.

Dr. Yadav, together with colleagues at the National Institute of Immunology in New Delhi, first measured taurine levels in people’s blood and found a steady decline with age. In 60-year-olds, taurine levels were about one-third of those in small children.

His team then gave high-dose taurine supplements to middle-aged mice and rhesus monkeys and compared their health outcomes to animals that did not get the amino acid boost. Six months of treatment were enough to see improvements in bone density, sugar metabolism and immune function in the monkeys, while the mice showed these benefits and more.

The mice gained less weight, had stronger muscles, were less anxious and showcased multiple improvements on a cellular level, including a reduction in the number of so-called zombie cells , old cells that stop dividing but continue to wreak havoc on neighboring tissues‌. Taurine also increased the average life span of the mice by 12 percent for females and 10 percent for males. The supplement had a similar impact on worm longevity.

The researchers also found supporting evidence for the anti-aging potential of taurine in people by analyzing two data sets. One, involving nearly 12,000 middle-aged individuals living in eastern England, showed a connection between low taurine levels and diseases such as obesity, diabetes and hypertension. The other, involving athletes from Germany, found that high-intensity exercise could naturally enhance taurine levels — which could account for some of the anti-aging benefits of physical activity.

What taurine does inside the body isn’t yet clear. Experiments in mice and worms point to a role for taurine in maintaining the health of mitochondria, energy-producing factories inside each cell. But more work is needed, noted Christy Carter, a health scientist administrator at the National Institute on Aging. “We are not sure how it’s working,” she said.

Biohackers and longevity seekers aren’t likely to wait for those scientific insights before adding taurine to their supplement stacks.

“This paper is very thorough and convincing,” said Nick Engerer, the founder of the Longevity Blog , who is based in Byron Bay, Australia. “This makes taurine a lead contender for something you might try at home for your own longevity.”

But most clinicians and longevity scientists urged against guzzling energy drinks or adding taurine powder to protein shakes until more well-controlled human data are available. “I’m constantly telling people: Hold fire until we do the clinical trials,” said Dr. James Kirkland, a geriatrician at the Mayo Clinic, who is leading anti-aging studies with other compounds .

David Sinclair, a longevity researcher at Harvard Medical School, is more open to self-experimentation outside of a trial protocol. On his podcast and in his 2019 book, he regularly discusses his own cocktail of anti-aging supplements .

Dr. Sinclair said he had dabbled with taurine in the past. But based on the new paper, he said he would likely add high doses of taurine to his regimen — with regular blood testing for possible side effects. “My caution and heartfelt concern, really, is that people will just take it and not monitor their bodies,” he said.

Dr. Yadav, for his part, declined to say whether he takes taurine supplements. “I don’t want to be an influencer,” he said.

A Guide to Supplements

Surveys suggest that more than half of americans use some kind of supplement. but how effective are all those pills, powders and tinctures.

Several companies are now selling bovine colostrum as a supplement for humans, claiming several health benefits. Here’s what experts say .

Research suggests that a daily multivitamin can improve cognition. But that doesn’t mean everyone should take one .

Proponents of castor oil claim it can improve vision, reduce wrinkles, boost hair growth and more. Can it really do all that ?

Some manufacturers claim that certain supplements can help you focus. Here is what the experts say .

Melatonin tricks your body into feeling like it’s time for bed, but it isn’t a sleeping pill. Here’s how to use it  and why it might be tricky for regular users to fall asleep without it .

Can you distinguish the good supplements from the harmful or useless ones? Take our quiz .

New Study Says Taurine Could Be Key to Living Longer, Healthier Life

New animal research has some surprising findings around the dietary supplement.

We may earn commission from links on this page, but we only recommend products we back. Why Trust Us?

• New research on animals and humans finds taurine levels decline with age.
• The study also discovered that mice and monkeys meet healthier markers after taking taurine for a set period of time.
• A lot of taurine research is on animals—not humans.

Many people have a goal of leading a long, healthy life. But the factors that lead to aging are complex and researchers are still learning about what drives it. Now, a new study suggests that the nutrient taurine may be a factor.

The researchers first looked at levels of taurine in the blood of mice, monkeys, and people, and found that levels decrease with age. In humans, for example, the taurine levels in 60-year-olds were about a third of those in 5-year-olds.

The researchers then took 250 14-month old mice (which are about 45 years old in people years) and fed them either a bolus of taurine or a control solution daily. The researchers discovered that the female mice given taurine had a 12% higher lifespan and the male mice had a lifespan that increased 10%. (That translated to three to four extra months in mice and about seven or eight years in humans.)

Other experiments on mice found that, at age two—which is about 60 human years—animals that took taurine for a year were healthier in nearly every way than those who didn’t take the supplement.

There were similar results in middle-aged monkeys that were given taurine supplements every day for six months. The nutrient prevented weight gain, reduced fasting blood glucose and markers of liver damage, increased bone density in the spine and legs, and improved the health of their immune systems.

It’s important to note that the research was largely done on animals—not humans. “These studies suggest that taurine abundance is a regulator of health in old age and its supplementation may have beneficial effects as well,” says study co-author Vijay Yadav, Ph.D., an assistant professor of genetics and development at Columbia University. “Our next goal is to perform a controlled trial in humans.”

This raises a lot of questions about taurine and its uses. Here’s what you need to know.

What is taurine?

Taurine is an amino acid that occurs naturally in foods with protein, like meat or fish, says Jessica Cording, R.D., author of The Little Book of Game-Changers .

Your body uses taurine for actions in cells, including energy production, according to the Mayo Clinic . Taurine also helps your body process bile acid and balance the fluids, salts, and minerals in your body.

“Unlike many other amino acids, taurine is not used in the construction of proteins,” says Scott Keatley, R.D., co-owner of Keatley Medical Nutrition Therapy . “It is considered a semi-essential micronutrient because the body can produce some amount of taurine, but not always enough. Hence, dietary intake is sometimes needed especially in times of stress.”

Taurine is found “abundantly” in the brain, retina, heart, and blood cells called platelets, Keatley says.

Worth noting, per Cording: Taurine is “very commonly” added to energy drinks.

The potential benefits of taurine

There are not a lot of studies on the impact of taurine on humans. However, research has shown that it’s involved in several brain processes. “It’s an important nutrient for brain function,” Cording says.

It’s also sometimes discussed as an important nutrient for heart health, Cording says. Research has shown that taurine has an anti-inflammatory effect on the body, may help regulate blood pressure, and can even protect against coronary disease.

“Prior to this study, taurine was already recognized for various potential health benefits,” Keatley says. “It may help in managing diabetes by improving glucose control and reducing insulin resistance. Taurine may also have antioxidant properties, potentially helping to fight inflammation and protect the body’s cells from damage.”

Cording notes this important point: “We don’t really have any clear guidelines around taurine.” Meaning, there’s no official recommendation for all Americans to have a certain amount of taurine every day. Still, Keatley says that “athletes take taurine for improved performance, while others might use it to help manage conditions such as heart disease, liver disease, cystic fibrosis, and even to improve mentally.”

“But most of the potential benefits of taking taurine have been associated with animal and in-vitro studies, not with humans,” says Keri Gans, R.D., author of The Small Change Diet . “More research is needed in clinically-controlled human trials to confirm any health benefits.”

Are there risks to taking taurine?

Taurine is “generally considered safe” when it’s taken in moderation, Keatley says. However, having too much of it can lead to side effects, including:

• Stomach discomfort

“People with kidney problems should avoid taurine supplements, as their kidneys may not be able to remove it effectively, leading to accumulation in the body,” Keatley says.

Foods that contain taurine

You can get taurine from certain foods. Keatley says these are the biggest sources:

• Seafood : Shellfish, salmon, and mackerel are high in taurine.
• Meat : Chicken, beef, and pork contain taurine, with darker meat typically containing more than white meat.
• Dairy products : Milk and other dairy products like cheese and yogurt contain taurine.
• Energy drinks : Many energy drinks contain taurine. “It’s worth noting that these drinks often also contain high levels of caffeine and sugar, which might not align with all healthful diets,” Keatley says.

The bottom line

While there has been some research in taurine, there still is a lot to be explored. “Most of the research we have on taurine is in animals,” Cording says. “We need more human studies to have a better understand of this is something that should be recommended for humans.”

She suggests focusing on food sources of taurine. Gans agrees. “At this time, I am not sure there is enough clinical evidence to suggest taking taurine,” she says. “The majority of people can get adequate amounts from their daily diet, along with what their body produces.”

Worth noting: Yadav also does not recommend taking a taurine supplement. “We do not recommend taurine supplementation in humans as of now,” he says. “We need to first test it in different groups and populations.”

If you’re still interested in taking a taurine supplement, Keatley recommends talking to your doctor first. “If someone is interested in taking taurine, they should consult with a healthcare professional first,” he says. “This is especially important for people with existing health conditions or those who are pregnant or breastfeeding.”

Keatley also stresses that the recent study that tied taurine to anti-aging is mostly based on mice, monkeys, and worms. “More research, specifically well-controlled human trials, is needed to establish the anti-aging effects of taurine in humans,” he says.

How to Tell If You Have a Spider Bite

Olivia Munn's Hysterectomy, Fertility Preservation

Ozempic May Impact Fertility: Here’s How

Wait... Do Cicadas Bite?

13 Causes That May Be the Root of Lower Back Pain

Let’s Talk About Bone Health

Oprah Apologized for Her Role in 'Diet Culture'

What a Hormone Specialist Wants You to Know

9 Best Shoes for Neuropathy, According to Experts

Michael Strahan Shares Rare IG Post With Daughters

What Is Gaslighting? Know the Signs

The Protective Effects of Taurine, a Non-essential Amino Acid, Against Metals Toxicities: A Review Article

• Published: 13 May 2024

Cite this article

• Karim Naraki 1 , 4 ,
• Majid Keshavarzi 1 ,
• Bibi Marjan Razavi 1 , 3 &
• Hossein Hosseinzadeh   ORCID: orcid.org/0000-0002-3483-851X 1 , 2  

33 Accesses

Explore all metrics

Taurine is a non-proteinogenic amino acid derived from cysteine. It is involved in several phenomena such as the regulation of growth and differentiation, osmoregulation, neurohormonal modulation, and lipid metabolism. Taurine is important because of its high levels in several tissues such as the central nervous system (CNS), heart, skeletal muscles, retinal membranes, and platelets. In this report, we present the functional properties of taurine indicating that it has potential effects on various metal toxicities. Therefore, a comprehensive literature review was performed using the Scopus, PubMed, and Web of Science databases. According to the search keywords, 61 articles were included in the study. The results indicate that taurine protects tissues against metal toxicity through enhancement of enzymatic and non-enzymatic antioxidant capacity, modulation of oxidative stress, anti-inflammatory and anti-apoptotic effects, involvement in different molecular pathways, and interference with the activity of various enzymes. Taken together, taurine is a natural supplement that presents antitoxic effects against many types of compounds, especially metals, suggesting public consumption of this amino acid as a prophylactic agent against the incidence of metal toxicity.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price includes VAT (Russian Federation)

Instant access to the full article PDF.

Rent this article via DeepDyve

Institutional subscriptions

Similar content being viewed by others

On the Mechanisms of Heavy Metal-Induced Neurotoxicity: Amelioration by Plant Products

The modulatory potential of herbal antioxidants against oxidative stress and heavy metal pollution: plants against environmental oxidative stress

The Use of N-Acetylcysteine as a Chelator for Metal Toxicity

Data availability.

All data generated or analyzed during this study are included in this published article.

Abbreviations

δ-aminolevulinic acid dehydratase

Alanine aminotransferase

Alendronate

Alkaline phosphatase

Aspartate aminotransferase

Activating transcription factor-6

Azathioprine

Bronchoalveolar lavage fluid

bcl-2-like protein 4

B-cell lymphoma 2

Blood urine nitrogen

C/EBP homologous protein

creatine kinase

Cyclooxygenase-2

C-reactive protein

Cytochrome P450

Dibromoacetonitrile

Depotentiation

Endoplasmic reticulum

Excitatory postsynaptic potential

Extracellular regulated protein kinases

Fructose 1,6-bisphosphatase

Follicle stimulating

Glucose 6-phosphate dehydrogenase

gamma-Aminobutyric acid

Glutathione peroxidase

Glutathione

Glutathione disulfide

Glutathione-S-transferase

Hydrogen peroxide

Hexabromocyclododecane

Homocysteine

High-density lipoprotein

Heme oxygenase-1

Intercellular adhesion molecule-1

Intercellular cell adhesion molecule-1

Interlukin-1β

Interleukin

Inducible nitric oxide synthase

Inositol-requiring enzyme 1 alpha

Isoproterenol

c-Jun N-terminal kinases

Potassium bromate

Lactate dehydrogenase

Low-density lipoprotein

Luteinizing

Lipid hydroperoxides

Lectin-type oxidized LDL receptor 1

Lipid peroxidase

Lipopolysaccharide

Long-term potentiation

Left ventricular ejection fraction

Malate dehydrogenase

Mean cell hemoglobin

Mean cell hemoglobin concentration

Monocyte chemoattractant protein-1

Malondialdehyde

Malic enzyme

Methamphetamine

Myeloperoxidase

Mammalian target of rapamycin

N-acetyl-b-D-glucosaminidase

Nuclear factor kappa‐β

Pyrin domain-containing 3

Nitric oxide

NADPH-quinone oxidoreductase

Nuclear factor erythroid 2–related factor 2

Poly (ADP-ribose) polymerase

Parkinson’s disease

Protein kinase RNA-like ER kinase

Reactive oxygen system

Superoxide dismutase

Thiobarbituric acid reactive substances

Triglycerides

Tumor necrosis factor-alpha

Triorthocresyl phosphate

Vascular cell adhesion molecule-1

White blood cells

Zinc protoporphyrin

Inam UL et al (2018) Ameliorative effects of taurine against diabetes: a review. Amino Acids 50(5):487–502

Article   Google Scholar  

Ripps H, Shen W (2012) Review: taurine: a “very essential” amino acid. Mol Vis 18:2673–86

CAS   PubMed   PubMed Central   Google Scholar  

Han X et al (2006) The taurine transporter: mechanisms of regulation. Acta Physiol (Oxf) 187(1–2):61–73

Article   CAS   PubMed   Google Scholar  

Zulli A (2011) Taurine in cardiovascular disease. Curr Opin Clin Nutr Metab Care 14(1):57–60

Yamori Y et al (2010) Taurine in health and diseases: consistent evidence from experimental and epidemiological studies. J Biomed Sci 17(Suppl 1):S6

Article   PubMed   PubMed Central   Google Scholar  

L’Amoreaux WJ et al (2010) Taurine regulates insulin release from pancreatic beta cell lines. J Biomed Sci 17(Suppl 1):S11

Schmidt SY, Berson EL, Hayes KC (1976) Retinal degeneration in cats fed casein I. Taurine deficiency. Invest Ophthalmol 15(1):47–52

CAS   PubMed   Google Scholar  

Gupta RC (2006) Taurine analogues and taurine transport: therapeutic advantages. Adv Exp Med Biol 583:449–67

Kulthinee S et al (2017) Taurine supplementation ameliorates the adverse effects of perinatal taurine depletion and high sugar intake on cardiac ischemia/reperfusion injury of adult female rats. Adv Exp Med Biol 975(Pt 2):741–755

Miyazaki T, Matsuzaki Y (2014) Taurine and liver diseases: a focus on the heterogeneous protective properties of taurine. Amino Acids 46(1):101–10

Sirdah MM (2015) Protective and therapeutic effectiveness of taurine in diabetes mellitus: a rationale for antioxidant supplementation. Diabetes Metab Syndr 9(1):55–64

Article   PubMed   Google Scholar  

Lerdweeraphon W et al (2013) Perinatal taurine exposure affects adult oxidative stress. Am J Physiol Regul Integr Comp Physiol 305(2):R95-7

Ghosh J et al (2009) Taurine prevents arsenic-induced cardiac oxidative stress and apoptotic damage: role of NF-kappa B, p38 and JNK MAPK pathway. Toxicol Appl Pharmacol 240(1):73–87

Kim C, Cha Y-N (2014) Taurine chloramine produced from taurine under inflammation provides anti-inflammatory and cytoprotective effects. Amino Acids 46(1):89–100

Ommati MM et al (2022) Taurine mitigates the development of pulmonary inflammation, oxidative stress, and histopathological alterations in a rat model of bile duct ligation. Naunyn-Schmiedeberg’s Archives of Pharmacology 395(12):1557–1572

Khlifi R, Hamza-Chaffai A (2010) Head and neck cancer due to heavy metal exposure via tobacco smoking and professional exposure: a review. Toxicol Appl Pharmacol 248(2):71–88

Gilbert SG (2004) A small dose of toxicology: The health effects of common chemicals. 1st Edition edn. CRC Press. https://doi.org/10.1201/9780203461730

Seiler H, Sigel A, Sigel H (1994) Handbook on metals in clinical and analytical chemistry. 1st Edition edn. CRC Press

Egorova KS, Ananikov VP (2017) Toxicity of metal compounds: knowledge and myths. Organometallics 36(21):4071–4090

Article   CAS   Google Scholar  

El-Sayed WM, Al-Kahtani MA, Abdel-Moneim AM (2011) Prophylactic and therapeutic effects of taurine against aluminum-induced acute hepatotoxicity in mice. J Hazard Mater 192(2):880–886

Feng T et al (2016) Combination of DFP and taurine counteracts the aluminum-induced alterations in oxidative stress and ATPase in cortex and blood of rats. Biol Trace Elem Res 174(1):142–149

Qiao M et al (2015) Potential protection of taurine on antioxidant system and ATPase in brain and blood of rats exposed to aluminum. Biotechnol Lett 37(8):1579–84

Wenting L et al (2014) Therapeutic effect of taurine against aluminum-induced impairment on learning, memory and brain neurotransmitters in rats. Neurol Sci 35(10):1579–84

Abdulkadir TS et al (2021) Taurine and camel milk modulate neurobehavioral and biochemical changes in aluminum chloride-induced Alzheimer’s disease in rats. J Alzheimer’s Dis 84(1):291–302

Al Kahtani MA, Abdel-Moneim AM, El-Sayed WM (2014) The influence of taurine pretreatment on aluminum chloride induced nephrotoxicity in Swiss albino mice

Khalaf HA et al (2022) Endoplasmic reticulum stress and mitochondrial injury are critical molecular drivers of AlCl3-induced testicular and epididymal distortion and dysfunction: protective role of taurine. Histochem Cell Biol 158(1):97–121

Article   CAS   PubMed   PubMed Central   Google Scholar  

Zheng Y et al (2017) Protection of taurine against arsenic-induced DNA damage of mice kidneys. Adv Exp Med Biol 975(Pt 2):917–927

Zhang C et al (2017) Taurine normalizes the levels of Se, Cu, Fe in mouse liver and kidney exposed to arsenic subchronically. In: Taurine 10. Springer

Roy A, Manna P, Sil PC (2009) Prophylactic role of taurine on arsenic mediated oxidative renal dysfunction via MAPKs/NF-κ B and mitochondria dependent pathways. Free radic res 43(10):995–1007

Guan H et al (2017) Protection of taurine against impairment in learning and memory in mice exposed to arsenic. Adv Exp Med Biol 975(Pt 1):255–269

Li S et al (2017) Taurine ameliorates arsenic-induced apoptosis in the hippocampus of mice through intrinsic pathway. Adv Exp Med Biol 975(Pt 1):183–192

Das J et al (2009) Arsenic-induced oxidative cerebral disorders: protection by taurine. Drug Chem Toxicol 32(2):93–102

Das J et al (2010) Protective role of taurine against arsenic-induced mitochondria-dependent hepatic apoptosis via the inhibition of PKCdelta-JNK pathway. PLoS One 5(9):e12602

Flora SJ et al (2008) Combined administration of taurine and monoisoamyl DMSA protects arsenic induced oxidative injury in rats. Oxid Med Cell Longev 1(1):39–45

 Li S et al (2017) Taurine protects mouse liver against arsenic-induced apoptosis through JNK pathway. Adv Exp Med Biol 975 Pt 2:855–862. https://doi.org/10.1007/978-94-024-1079-2_67

Pei P et al (2019) Inorganic arsenic induces pyroptosis and pancreatic β cells dysfunction through stimulating the IRE1α/TNF-α pathway and protective effect of taurine. Food Chem Toxicol 125:392–402

Sinha M, Manna P, Sil PC (2007) Taurine, a conditionally essential amino acid, ameliorates arsenic-induced cytotoxicity in murine hepatocytes. Toxicol In Vitro 21(8):1419–28

Wang Z et al (2019) Taurine protected As2O3-induced the activation of hepatic stellate cells through inhibiting PPARα-autophagy pathway. Chem Biol Interact 300:123–130

Gao N et al (2019) Taurine improves low-level inorganic arsenic-induced insulin resistance by activating PPARγ-mTORC2 signalling and inhibiting hepatic autophagy. J Cell Physiol 234(4):5143–5152

Bai J et al (2016) Taurine protects against As2O3-induced autophagy in livers of rat offsprings through PPARγ pathway. Sci Rep 6(1):27733

Bai J et al (2016) Taurine protects against As2O3-induced autophagy in pancreas of rat offsprings through Nrf2/Trx pathway. Biochim 123:1–6. https://doi.org/10.1016/j.biochi.2016.01.002

Qiu T et al (2018) Taurine attenuates arsenic-induced pyroptosis and nonalcoholic steatohepatitis by inhibiting the autophagic-inflammasomal pathway. Cell Death Dis 9(10):946

Ghosh J et al (2009) Taurine prevents arsenic-induced cardiac oxidative stress and apoptotic damage: Role of NF-κB, p38 and JNK MAPK pathway. Toxicol Appl Pharmacol 240(1):73–87

Kumar P et al (2009) Ascorbic acid, garlic extract and taurine alleviate cadmium-induced oxidative stress in freshwater catfish (Clarias batrachus). Sci Total Environ 407(18):5024–30

Manna P, Sinha M, Sil PC (2009) Taurine plays a beneficial role against cadmium-induced oxidative renal dysfunction. Amino Acids 36:417–428

Hwang D-F, Wang L (2001) Effect of taurine on toxicity of cadmium in rats. Toxicol 167(3):173–180

Zheng J et al (2023) Hepatoprotective effects of taurine against cadmium-induced liver injury in female mice. Biol Trace Elem Res 201(3):1368–1376

Hano T et al (2017) Effect of taurine supplementation on hepatic metabolism and alleviation of cadmium toxicity and bioaccumulation in a marine teleost, red sea bream Pagrus major. Fish Physiol Biochem 43(1):137–152

Manna P, Sinha M, Sil PC (2008) Amelioration of cadmium-induced cardiac impairment by taurine. Chem Biol Interact 174(2):88–97

Choi K-S et al (2013) Effects of taurine on cadmium exposure in muscle, gill, and bone tissues of Carassius auratus. Nutr Res Pract 7(1):22–25

Abalaka SE et al (2021) Effects of Moringa oleifera leaves extract, vitamin C, and taurine co-exposures on calcium and metallothionein levels, oxidative stress, and gill histopathological changes in Clarias gariepinus exposed to sub-lethal cadmium. Environ Sci Pollut Res 28(37):52258–52271

Chen N et al (2022) Cadmium induces placental glucocorticoid barrier damage by suppressing the cAMP/PKA/Sp1 pathway and the protective role of taurine. Toxicol Appl Pharmacol 440:115938

Manna P, Sinha M, Sil PC (2008) Cadmium induced testicular pathophysiology: prophylactic role of taurine. Reprod Toxicol 26(3–4):282–291

Sinha M, Manna P, Sil PC (2008) Cadmium-induced neurological disorders: prophylactic role of taurine. J Appl Toxicol 28(8):974–986

Hwang D-F, Wang L, Cheng H (1998) Effect of taurine on toxicity of copper in rats. Food Chem Toxicol 36(3):239–244

Husain N, Mahmood R (2020) Taurine attenuates Cr(VI)-induced cellular and DNA damage: an in vitro study using human erythrocytes and lymphocytes. Amino Acids 52(1):35–53

Boşgelmez II, Söylemezoğlu T, Güvendik G (2008) The protective and antidotal effects of taurine on hexavalent chromium-induced oxidative stress in mice liver tissue. Biol Trace Elem Res 125(1):46-58

Boşgelmez İİ, Güvendik G (2019) Beneficial effects of N-acetyl-L-cysteine or taurine pre-or post-treatments in the heart, spleen, lung, and testis of hexavalent chromium-exposed mice. Biol Trace Elem Res 190(2):437–445

Boşgelmez II, Güvendik G (2004) Effects of taurine on oxidative stress parameters and chromium levels altered by acute hexavalent chromium exposure in mice kidney tissue. Biol Trace Elem Res 102:209–225

Lakshmi Devi S, Anuradha CV (2010) Mitochondrial damage, cytotoxicity and apoptosis in iron-potentiated alcoholic liver fibrosis: amelioration by taurine. Amino Acids 38(3):869-79

Zhang Z et al (2014) Taurine supplementation reduces oxidative stress and protects the liver in an iron-overload murine model. Mol Med Rep 10(5):2255–62

Oudit GY et al (2004) Taurine supplementation reduces oxidative stress and improves cardiovascular function in an iron-overload murine model. Circulation 109(15):1877–1885

Devi SL, Viswanathan P, Anuradha CV (2009) Taurine enhances the metabolism and detoxification of ethanol and prevents hepatic fibrosis in rats treated with iron and alcohol. Environ Toxicol Pharmacol 27(1):120–126

Feng X et al (2022) Taurine ameliorates iron overload-induced hepatocyte injury via the Bcl-2/VDAC1-mediated mitochondrial apoptosis pathway. Oxid Med Cell Longev 2022

Dawson R et al (2000) Taurine inhibition of metal-stimulated catecholamine oxidation. Neurotox Res 2:1–15

Gürer H et al (2001) Antioxidant effect of taurine against lead-induced oxidative stress. Arch Environ Contam Toxicol 41(4):397–402

Flora SJ et al (2004) Combined administration of taurine and meso 2,3-dimercaptosuccinic acid in the treatment of chronic lead intoxication in rats. Hum Exp Toxicol 23(4):157–66

Zhu DM et al (2005) Protection by a taurine supplemented diet from lead-induced deficits of long-term potentiation/depotentiation in dentate gyrus of rats in vivo. Neuroscience 134(1):215–24

Neuwirth LS et al (2022) Taurine-derived compounds produce anxiolytic effects in rats following developmental lead exposure. Taurine 12: a conditionally essential amino acid. Springer, pp 445–460

Chapter   Google Scholar  

Akande M et al (2014) Taurine mitigates cognitive impairment induced by chronic co-exposure of male Wistar rats to chlorpyrifos and lead acetate. Environ Toxicol Pharmacol 37(1):315–325

Aglan HS et al (2021) Developmental toxicity of lead in rats after gestational exposure and the protective role of taurine. 35(8):e22816

Ommati MM et al (2023) Taurine improves sperm mitochondrial indices, blunts oxidative stress parameters, and enhances steroidogenesis and kinematics of sperm in lead-exposed mice. Reprod Sci 30(6):1891–1910

Lu C-L et al (2014) Taurine improves the spatial learning and memory ability impaired by sub-chronic manganese exposure. J Biomed Sci 21(1):1–8

Xu Z et al (2010) Effects of MK-801, taurine and dextromethorphan on neurotoxicity caused by manganese in rats. Toxicol Ind Health 26(1):55–60

Ahmadi N et al (2018) Taurine prevents mitochondrial membrane permeabilization and swelling upon interaction with manganese: implication in the treatment of cirrhosis-associated central nervous system complications. J Biochem Mol Toxicol 32(11):e22216

Ommati MM et al (2019) Taurine treatment provides neuroprotection in a mouse model of manganism. Biol Trace Elem Res 190(2):384–395

Agha FE et al (2014) Nephroprotective potential of selenium and taurine against mercuric chloride induced nephropathy in rats. Ren Fail 36(5):704–16

Jagadeesan G, Pillai SS (2007) Hepatoprotective effects of taurine against mercury induced toxicity in rat. J Environ Biol 28(4):753

Xu S et al (2015) The neuroprotective effects of taurine against nickel by reducing oxidative stress and maintaining mitochondrial function in cortical neurons. Neurosci Lett 590:52–7

Yeh YH et al (2011) Dietary taurine reduces zinc-induced toxicity in male Wistar rats. J Food Sci 76(4):T90–T98

Abdoli N et al (2021) Taurine mitigates bile duct obstruction-associated cholemic nephropathy: effect on oxidative stress and mitochondrial parameters. Clin Exp Hepatol 7(1):30–40

Mousavi K et al (2020) Taurine mitigates cirrhosis-associated heart injury through mitochondrial-dependent and antioxidative mechanisms. Clin Exp Hepatol 6(3):207–219

Niknahad H et al (2023) Cirrhosis-induced oxidative stress in erythrocytes: the therapeutic potential of taurine. Clin Exp Hepatol 9(1):79–93

Ommati MM et al (2019) Taurine enhances skeletal muscle mitochondrial function in a rat model of resistance training. PharmaNutrition 9:100161

Klotz K et al (2017) The health effects of aluminum exposure. Dtsch Arztebl Int 114(39):653–659

PubMed   PubMed Central   Google Scholar  

Barabasz W et al (2002) Ecotoxicology of aluminium. Pol J Environ Stud 11(3):199–204

CAS   Google Scholar  

Olaniran AO, Balgobind A, Pillay B (2013) Bioavailability of heavy metals in soil: impact on microbial biodegradation of organic compounds and possible improvement strategies. Int J Mol Sci 14(5):10197–10228

Vardar F, Ünal M (2007) Aluminum toxicity and resistance in higher plants

Shayan M et al (2023) The protective effect of natural or chemical compounds against arsenic-induced neurotoxicity: Cellular and molecular mechanisms. Food Chem Toxicol 175:113691. https://doi.org/10.1016/j.fct.2023.113691

Costa M (2019) Review of arsenic toxicity, speciation and polyadenylation of canonical histones. Toxicol Appl Pharmacol 375:1–4

Susan A et al (2019) An overview of plant-based interventions to ameliorate arsenic toxicity. Biomed Pharmacother 109:838–852

Yarmohammadi F et al (2023) Melatonin ameliorates arsenic-induced cardiotoxicity through the regulation of the Sirt1/Nrf2 pathway in rats. Biofactors 49(3):620–635

Yang L et al (2019) Taurine protects against arsenic trioxide-induced insulin resistance via ROS-Autophagy pathway in skeletal muscle. Int J Biochem Cell Biol 112:50–60

Yang H, Shu Y (2015) Cadmium transporters in the kidney and cadmium-induced nephrotoxicity. Int J Mol Sci 16(1):1484–94

Rani A et al (2014) Cellular mechanisms of cadmium-induced toxicity: a review. International journal of environmental health research 24(4):378–399

Patrick L (2003) Toxic metals and antioxidants: Part II. The role of antioxidants in arsenic and cadmium toxicity. Altern Med Rev 8(2)

Ahmadian R et al (2023) Alpha-mangostin protects PC12 cells against neurotoxicity induced by cadmium and arsenic. Biol Trace Elem Res 201(8):4008–4021

Joseph P (2009) Mechanisms of cadmium carcinogenesis. Toxicol Appl Pharmacol 238(3):272–279

Rahimzadeh MR et al (2017) Cadmium toxicity and treatment: an update. Caspian J Intern Med 8(3):135–145. https://doi.org/10.22088/cjim.8.3.135

Balarastaghi S et al (2022) Melatonin improves arsenic-induced hypertension through the inactivation of the Sirt1/autophagy pathway in rat. Biomed Pharmacother 151:113135

Keshavarzi M et al (2019) Hormesis effects of nano-and micro-sized copper oxide. Iran J Pharm Res: IJPR 18(4):2042

Gaetke LM, Chow-Johnson HS, Chow CK (2014) Copper: toxicological relevance and mechanisms. Arch Toxicol 88:1929–1938

Hasan NM, Lutsenko S (2012) Regulation of copper transporters in human cells. Curr Top Membr 69:137–161

Tian X et al (2009) Copper–taurine (CT): a potential organic compound to facilitate infected wound healing. Med Hypotheses 73(6):1048–1050

Costello RB, Dwyer JT, Bailey RL (2016) Chromium supplements for glycemic control in type 2 diabetes: limited evidence of effectiveness. Nutr Rev 74(7):455–68

Dayan A, Paine A (2001) Mechanisms of chromium toxicity, carcinogenicity and allergenicity: review of the literature from 1985 to 2000. Hum Exp Toxicol 20(9):439–451

DesMarias TL, Costa M (2019) Mechanisms of chromium-induced toxicity. Curr Opin Toxicol 14:1–7

Hershko C (2007) Mechanism of iron toxicity. Food Nutr Bull 28(4_suppl4): S500-S509

Rouault TA (2016) Mitochondrial iron overload: causes and consequences. Curr Opin Genet Dev 38:31–37

Pasantes-Morales H, Wright C, Gaull G (1985) Taurine protection of lymphoblastoid cells from iron-ascorbate induced damage. Biochem Pharmacol 34(12):2205–2207

Mitra P et al (2017) Clinical and molecular aspects of lead toxicity: an update. Crit Rev Clin Lab Sci 54(7–8):506–528

Nemsadze K et al (2009) Mechanisms of lead-induced poisoning. Georgian Med News 172–173:92–96

Google Scholar  

Dzugkoev S, Dzugkoeva F, Margieva O (2022) Mechanisms of lead toxicity and their pathogenetic correction. J Evol Biochem Phys 58(3):807–814

Neuwirth LS et al (2019) Early neurodevelopmental exposure to low lead levels induces fronto-executive dysfunctions that are recovered by taurine co-treatment in the rat attention set-shift test: implications for taurine as a psychopharmacotherapy against neurotoxicants. Taurine 11. Springer, pp 821–846

Cruz GB et al (2022) Developmental lead exposure in rats causes sex-dependent changes in neurobiological and anxiety-like behaviors that are improved by taurine co-treatment. Taurine 12: a conditionally essential amino acid. Springer, pp 461–479

Caudle WM (2015) Occupational exposures and parkinsonism. Handb Clin Neurol 131:225–239

Cappelletti S et al (2019) Mercuric chloride poisoning: symptoms, analysis, therapies, and autoptic findings. A review of the literature. Crit Rev Toxicol 49(4):329-341

Yang L et al (2020) Toxicity of mercury: molecular evidence. Chemosphere 245:125586

Das KK et al (2018) Primary concept of nickel toxicity - an overview. J Basic Clin Physiol Pharmacol 30(2):141–152

Macomber L, Hausinger RP (2011) Mechanisms of nickel toxicity in microorganisms. Metallomics 3(11):1153–1162

Agnew UM, Slesinger TL (2020) Zinc toxicity

Download references

Author information

Authors and affiliations.

Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

Karim Naraki, Majid Keshavarzi, Bibi Marjan Razavi & Hossein Hosseinzadeh

Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

Hossein Hosseinzadeh

Targeted Drug Delivery Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

Bibi Marjan Razavi

Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran

Karim Naraki

You can also search for this author in PubMed   Google Scholar

Contributions

HH contributed to the study conception, design, and supervision of the research. Data collection and analysis were performed by KN and MK. A critical revision of the paper was conducted by BMR. The first draft of the manuscript was written by KN and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Hossein Hosseinzadeh .

Ethics declarations

Ethical approval.

This article does not contain any studies with human participants or animals performed by the author.

Competing Interests

The authors declare no competing interests.

Additional information

Publisher's note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and permissions

About this article

Naraki, K., Keshavarzi, M., Razavi, B.M. et al. The Protective Effects of Taurine, a Non-essential Amino Acid, Against Metals Toxicities: A Review Article. Biol Trace Elem Res (2024). https://doi.org/10.1007/s12011-024-04191-8

Download citation

Received : 24 February 2024

Accepted : 16 April 2024

Published : 13 May 2024

DOI : https://doi.org/10.1007/s12011-024-04191-8

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

• Protective effects
• Toxicity, Antidot
• Find a journal
• Publish with us
• Track your research

The Protective Effects of Taurine, a Non-essential Amino Acid, Against Metals Toxicities: A Review Article

Affiliations.

• 1 Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
• 2 Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran.
• 3 Targeted Drug Delivery Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
• 4 Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. [email protected].
• 5 Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran. [email protected].
• PMID: 38735894
• DOI: 10.1007/s12011-024-04191-8

Taurine is a non-proteinogenic amino acid derived from cysteine. It is involved in several phenomena such as the regulation of growth and differentiation, osmoregulation, neurohormonal modulation, and lipid metabolism. Taurine is important because of its high levels in several tissues such as the central nervous system (CNS), heart, skeletal muscles, retinal membranes, and platelets. In this report, we present the functional properties of taurine indicating that it has potential effects on various metal toxicities. Therefore, a comprehensive literature review was performed using the Scopus, PubMed, and Web of Science databases. According to the search keywords, 61 articles were included in the study. The results indicate that taurine protects tissues against metal toxicity through enhancement of enzymatic and non-enzymatic antioxidant capacity, modulation of oxidative stress, anti-inflammatory and anti-apoptotic effects, involvement in different molecular pathways, and interference with the activity of various enzymes. Taken together, taurine is a natural supplement that presents antitoxic effects against many types of compounds, especially metals, suggesting public consumption of this amino acid as a prophylactic agent against the incidence of metal toxicity.

Keywords: Metals; Protective effects; Taurine; Toxicity, Antidot.

© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Publication types

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List

Review: Taurine: A “very essential” amino acid

Harris ripps.

1 Departments of Ophthalmology and Visual Science, Anatomy and Cell Biology, Physiology and Biophysics, University of Illinois College of Medicine, Chicago, IL

2 The Marine Biological Laboratory, Woods Hole, MA

3 Department of Biomedical Science, College of Medicine, Florida Atlantic University, 777 Glades Road, Boca Raton, FL

Taurine is an organic osmolyte involved in cell volume regulation, and provides a substrate for the formation of bile salts. It plays a role in the modulation of intracellular free calcium concentration, and although it is one of the few amino acids not incorporated into proteins, taurine is one of the most abundant amino acids in the brain, retina, muscle tissue, and organs throughout the body. Taurine serves a wide variety of functions in the central nervous system, from development to cytoprotection, and taurine deficiency is associated with cardiomyopathy, renal dysfunction, developmental abnormalities, and severe damage to retinal neurons. All ocular tissues contain taurine, and quantitative analysis of ocular tissue extracts of the rat eye revealed that taurine was the most abundant amino acid in the retina, vitreous, lens, cornea, iris, and ciliary body. In the retina, taurine is critical for photoreceptor development and acts as a cytoprotectant against stress-related neuronal damage and other pathological conditions. Despite its many functional properties, however, the cellular and biochemical mechanisms mediating the actions of taurine are not fully known. Nevertheless, considering its broad distribution, its many cytoprotective attributes, and its functional significance in cell development, nutrition, and survival, taurine is undoubtedly one of the most essential substances in the body. Interestingly, taurine satisfies many of the criteria considered essential for inclusion in the inventory of neurotransmitters, but evidence of a taurine-specific receptor has yet to be identified in the vertebrate nervous system. In this report, we present a broad overview of the functional properties of taurine, some of the consequences of taurine deficiency, and the results of studies in animal models suggesting that taurine may play a therapeutic role in the management of epilepsy and diabetes.

Introduction

The impetus for this review dates back more than a few decades, having originated with a curious malady, i.e., the severe headaches that were often suffered by diners who had ingested monosodium glutamate, a common food additive in general use in homes and restaurants. It came to be known by a variety of names, the most common being the “The Chinese Restaurant Syndrome” because of its perhaps excessive use in wonton soup. The cause remained a mystery until 1969, when John Olney and his colleagues unequivocally demonstrated the neurotoxic effects of monosodium glutamate. In an impressive series of papers, they showed that when applied topically or by injection, glutamate and its analogs (aspartate, kainate, N-methyl-d-aspartate [NMDA], α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid [AMPA]) were cytotoxic to nerve cells in every part of the central nervous system (CNS) [ 1 - 3 ]. The issue is of more than academic interest, since glutamate-triggered neuronal damage is known to occur when the glutamate concentration of interstitial fluids reaches abnormally high levels as a result of hypoxia, ischemia, or brain trauma.

A striking curiosity was seen when Olney’s studies were extended to the visual system. In the neonatal mouse retina, for example, he reported that a 30 min exposure to parenterally administered glutamate (1 mM) produced a histopathological lesion characterized by swollen cell bodies in the ganglion cell layer, the proximal half of the inner nuclear layer, and extending to the inner plexiform layer. Even after washing and transferring the excised retina to glutamate-free medium, Olney found that the lesion had progressed further, particularly in cells within the inner half of the inner nuclear layer, [ 2 ]. It is noteworthy that although the retina had been bathed in glutamate, only the inner layers were seriously affected.

Why had the nerve cells in the distal layers been spared? Neurons and glia have been shown to sequester glutamate via high-affinity uptake systems. These transport mechanisms, regarded as responsible for clearing L-glutamate from the synaptic cleft [ 4 , 5 ] and for terminating the excitatory signal [ 6 ], represent the first step in the recycling of the transmitter through the “glutamine cycle” [ 7 , 8 ]. Glutamate uptake undoubtedly plays a cytoprotective role, but it is clearly inadequate to spare the inner retina when exposed to toxic levels of glutamate. Rather, it seems likely that there are one or more endogenous substances that serve to protect the outer retina from the typically severe reaction to glutamate. We suggest that one of the most effective endogenous agents protecting the distal retina from the application of toxic levels of glutamate is the amino acid taurine .

Other cytoprotectants

Before considering further some of the biochemical and physiological features of taurine, as well as the broad range of conditions in which taurine has been shown to be beneficial, we must acknowledge that the retina may be exposed to several other survival-promoting agents under normal conditions. Many that have been shown to be effective, e.g., brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), and basic fibroblast growth factor (bFGF) were identified and extensively investigated by LaVail and coworkers [ 9 - 12 ]. These and other members of the transforming growth factor-β family help to protect retinal neurons from ischemia, free radical formation, light damage, and related forms of neuronal insult. Although levels of some of these factors are upregulated in response to injury [ 11 , 13 ], these agents, even when applied exogenously, primarily tend to slow the cell death process. Treatment with combinations of antioxidants has also proven to effectively rescue photoreceptors in an animal model (rd1) of retinal degeneration [ 14 ], but here too the agents were applied exogenously. We suggest that the high concentration of endogenous taurine throughout the retina can better serve the role of neuroprotectant against glutamate-induced excitotoxicity.

Some Functional Properties

A broad-spectrum cytoprotective agent.

Taurine (2-aminoethane- sulfonic acid), an organic osmolyte involved in cell volume regulation, provides a substrate for the formation of bile salts, and plays a role in the modulation of intracellular free calcium concentration [ 15 , 16 ]. Taurine is one of the most abundant amino acids in the brain and spinal cord, leukocytes, heart and muscle cells, the retina, and indeed almost every tissue throughout the body. It was first identified and isolated from the bile of the ox ( Bos taurus ), from which it derives its name [ 17 , 18 ]. The chemical structure of taurine, shown in Figure 1A , reveals that it lacks the carboxyl group typical of other amino acids, but does contain a sulfonate group. The major route for the biosynthesis of taurine, shown in Figure 1B is from methionine and cysteine via cysteinesulfinic acid decarboxylase (CSD), and typically requires oxidation of hypotaurine to taurine as the final step [ 19 ].

Structure and formation of taurine. A : The chemical formula of taurine is C 2 H 7 NO 3 S MW=125.15. B : This oversimplified diagram shows the main steps in the conversion of L-cysteine to taurine. The enzyme cysteine dioxygenase (CDO) catalyzes the conversion of L-cysteine to cysteine sulfinate, and the oxidation of hypotaurine (2-aminoethane sulfinate) results in taurine.

CSD was initially cloned and identified in the liver as the rate-limiting enzyme in the biosynthesis of taurine [ 20 ], and was later shown to be present in the kidney as well as the brain, where it is localized in glial cells. CSD levels are very low in cats, as well as humans and other primates, but the ingestion of meat and seafood—or taurine supplements—helps to maintain normal tissue concentrations of taurine. As Sinwell and Gorodischer [ 21 ] have shown, there is an increased incidence of pediatric problems in children being raised on the totally vegetarian diets of vegan communities. Aside from the retina, every region of the brain that has been tested contains or takes up taurine; this includes the pineal [ 22 , 23 ], pons medulla [ 24 ], hypothalamus [ 25 ], striatum [ 26 ], and cerebellum [ 27 , 28 ]. At each of these sites, there is evidence of taurine’s ability to ameliorate certain forms of neuropathology.

Because it is one of the few amino acids not used in protein synthesis, taurine is often referred to as a “nonessential” amino acid, or more generously as a “conditionally essential” amino acid. Considering its broad distribution, its many cytoprotective attributes [ 29 , 30 ], and its functional significance in cell development, nutrition, and survival [ 31 , 32 ], these are clearly misnomers. Taurine is undoubtedly one of the most essential substances in the body. Moreover, there is ever-increasing evidence that taurine depletion leads to a wide range of pathological conditions, including severe cardiomyopathy [ 33 ], renal dysfunction [ 34 ], pancreatic β cell malfunction [ 35 ], and loss of retinal photoreceptors [ 36 ]. The close relationship between taurine levels and nutritionally induced degeneration is supported further in that taurine supplementation can inhibit light-induced lipid peroxidation, and thereby protect isolated rod outer segments from photic damage [ 37 , 38 ].

There is a long list of diseases that are impacted by taurine, although the precise biochemical mechanism of action is often not entirely clear. A case in point is its role in diabetes. Numerous studies have indicated that taurine plays a significant role in overcoming insulin resistance and other risk factors in animal models of Type 1 and Type 2 diabetes [ 39 - 47 ]. More specifically, taurine administration has been shown to prevent high glucose-induced microangiopathy, i.e., vascular endothelial cell apoptosis [ 48 ], and in fructose-fed rats, it has been found to restore glucose metabolizing enzyme activities and improve insulin sensitivity by modifying the postreceptor events of insulin action [ 49 ]. The suggestion that nitric oxide (NO) may be implicated in the pathogenesis of diabetes prompted a study to determine whether endogenous NO synthesis or local reactivity to endogenous NO might be impaired in patients with Type 1 insulin-dependent diabetes mellitus [ 50 ]. The results showed that either NO- synthase activity is increased or NO sensitivity is decreased in Type 1 patients, a good indication that the L-arginine–NO system is involved in the pathophysiology of diabetes and its sequelae, e.g., diabetic retinopathy. Subsequently, the elevated levels of NO were shown to cause upregulation of the taurine transporter gene and a concomitant increase in taurine uptake in human retinal pigment epithelial cells [ 51 ].

Taurine’s effect on renal function [ 52 ], particularly as it relates to streptozotocin-induced diabetic animal models, is also noteworthy. As Trachtman et al. (1995) have shown, taurine ameliorates diabetic nephropathy by decreasing lipid peroxidation and lessening the accumulation of advanced glycation end-products in the kidney [ 39 ]. However, whether the findings from animal models of diabetes translate to an effective therapy in the management of diabetes in humans is an open question. In this connection, it is important to note that taurine was shown to reduce insulin secretion by β cells in vitro [ 53 ]. Moreover, contrary to the results from animal experiments, a study of 20 obese human subjects with a genetic predisposition for Type 2 diabetes demonstrate that taurine supplementation (1.5 g for 8 weeks) had no effect on insulin secretion or sensitivity [ 54 ]. In short, these findings do not support the view that dietary supplementation with taurine can be used to prevent the development of Type 2 diabetes. However, it should be noted that this study was clearly too small and of too short a duration to have any clinical significance. Further experimental and clinical studies will be of importance in evaluating taurine’s therapeutic potential in the management of diabetes in humans [ 45 ].

Similar issues have clouded the relationship between taurine and epilepsy, although there is little doubt that taurine has antiepileptic activity in experimental animals. The efficacy of taurine has been demonstrated in both naturally occurring and drug-induced epilepsy in cats [ 55 ], mice [ 56 ], rats [ 57 ], and dogs [ 58 ], and evidence that taurine blocks dentato-hippocampal synapses, a locus of importance in epileptogenesis, indicates a specific action in epilepsy. Indeed, preliminary experiments in human epileptic subjects confirm the anticonvulsive effect of taurine, but the effects are not robust, nor are they consistent [ 59 ]. This may be because taurine does not readily cross the blood-brain barrier, and several taurine analogs that do are currently under investigation for their therapeutic potential [ 60 ].

Taurine in the eye

It has long been known that all ocular tissues, both neural and nonneural, contain taurine [ 61 , 62 ], prompting a host of studies to identify its cellular distribution [ 63 - 66 ]. Quantitative analysis of whole ocular tissue extracts of the rat eye revealed that taurine was the most abundant amino acid in the retina, vitreous, lens, cornea, iris, and ciliary body [ 67 ]. The highest level of taurine was, of course, in the vertebrate retina, and an ingenious experiment involving a judicious selection of normal and diseased mouse retinas enabled Cohen and coworkers [ 68 ] to quantify the distribution of taurine and other amino acids across the layers of retinal cells ( Figure 2 ). Note that in the normal (control) retina, taurine exceeds the concentration of each of the other amino acids by tenfold or more, whereas in the photoreceptorless C3H mouse, its concentration is about one-third of its value in the control retina. Note also that destruction of the inner retina by glutamate has little effect on taurine concentration. It is apparent, therefore, that taurine is highly concentrated in the outermost layers of the vertebrate retina. This is consistent with the findings that animals (e.g., cats, monkeys, man) that do not produce adequate levels of taurine experience severe degenerative changes in their photoreceptors and retinal pigment epithelium (RPE) when deprived of dietary taurine [ 36 , 69 - 75 ].

Chemical and genetic fractionation of the retina. A: Juxtaposed images of histological sections comparing the retinas of a normal (control) mouse, with one whose inner retina has been damaged by glutamate, and another that was taken from a C3H mouse suffering the loss of the distal retina. B: The concentrations of five amino acids in each preparation. The latter values represent the averages from six different groups of dark-adapted animals. (Modified from Cohen et al., 1973, with the permission of the publishers).

The selective distribution of taurine within the retinal laminas, as well as in other tissues, is attributable to the presence of both high and low affinity Na + - and Cl - - dependent taurine transporters [ 66 , 76 , 77 ]. At the cellular level, the taurine content is determined primarily by the sum of three processes: (i) its synthesis from methionine/cysteine, (ii) its active uptake by the taurine transporter, and (iii) its release via a volume-sensitive leak pathway [ 78 ]. The principal transport protein is the saturable, high-affinity TauT transporter (K m =18 μM), a member of the neurotransmitter transporter family that includes the transporters for serotonin, creatine, and gamma amino-butyric acid (GABA) [ 79 ]. All members of this family have 12 membrane-spanning helices, with the N- and C-terminal ends exposed to the cytosol [ 80 ]. The cytosolic domains contain several highly conserved serine, tyrosine, and threonine residues that provide sites for phosphorylation. In terms of its stoichiometry, the active uptake of one molecule of taurine requires two to three sodium ions and one chloride ion [ 78 ], and only guanidinoethyl sulfonate (GES) and other close analogs of taurine, e.g., β-alanine, GABA, are inhibitors of taurine uptake. Interestingly, both a GABA transporter and a taurine transporter are active at apical membrane vesicles from bovine RPE; they both require Na + and Cl - and exhibit a similar stoichiometry. An analysis of taurine uptake at this site showed that uptake was severely depressed in the presence of GABA, and conversely, GABA uptake was suppressed by the presence of taurine [ 81 ].

Depletion of taurine in rats treated with GES leads to a marked and progressive reduction in the amplitude of the electroretinogram [ 82 ] and severe degenerative changes in photoreceptors and the RPE [ 83 ], effects that can be reversed by intravenous infusion of taurine [ 84 ]. A precipitous loss of taurine is also seen after genetic disruption of TauT in mice. In this model, there is severe photoreceptor degeneration 2–4 weeks after birth, and this spreads to the inner retinal neurons after 4 weeks [ 85 ]. Clearly, endogenous taurine is crucial for preventing retinal neurodegeneration. Findings such as these, although difficult to interpret precisely, add to an appreciation of the importance of taurine in the cell biology of the retina.

Taurine and cytoprotection

Photoreceptors are considerably richer in taurine than other retinal neurons, but all retinal cells from the outer and inner nuclear layers to the ganglion cell layer, and seemingly the radial glia (Müller cells) as well [ 86 ], take up taurine from the extracellular milieu [ 66 , 87 - 91 ]. Therefore, it is not surprising that depleting endogenous taurine by the genetic knockout of TauT or by blocking the taurine transporter with GES has been shown to cause ganglion cell loss, along with degenerative changes in the distal retina [ 75 , 85 ]. It is apparent that taurine serves a neuroprotective role in ganglion cells, as well as in photoreceptors. On the other hand, it was surprising to learn that the early in vivo experiments on the active transport of taurine through the frog RPE showed the main flux to be in the retina to choroid direction [ 92 ]. However, the ship was righted with evidence of bidirectional transport [ 93 ], and the demonstration of taurine transport from the blood to retina direction [ 94 ]. In addition, passive diffusion of such a small molecule as taurine would allow it to traverse the plasma membrane of retinal cells without the aid of an active transport mechanism, and there is experimental evidence that both path length and matrix components (collagen and elastic tissue) influence the diffusion of taurine across human and bovine tissues comprised of Bruch’s membrane–choroid [ 95 ].

Perhaps the most exhaustive body of experimental work on the neuroprotective properties of taurine was performed by Wu and colleagues [ 29 , 30 , 96 - 98 ]. These innovative studies provide convincing evidence that there are several avenues by which taurine exerts its protective role. Using primary neuronal cultures from the fetal rat brain, these researchers showed that taurine suppresses glutamate-induced toxicity through several pathways: (i) it inhibits calcium influx through L-, N- and P/Q-type voltage-gated calcium channels, (ii) it prevents the downregulation of Bcl-2 and the upregulation of Bax, the protein products of which otherwise would translocate to the mitochondria and result in the release of the highly toxic cytochrome C (cyC), (iii) it protects neurons from oxidative stress, and (iv) it inhibits glutamate-induced calpain activation, thereby preventing the cleavage of Bcl-2 (see also [ 99 ]).

There is obviously a broad array of mechanisms by which taurine serves its cytoprotective role, but the molecular identity of a taurine-selective receptor remains a mystery. Several studies have implicated a metabotropic GABA B -binding site as mediating the action of taurine, particularly in the brain regions of the mouse and rat [ 100 , 101 ], as well as in the mammalian retina [ 75 ]. However, the pathway linking the GABA B receptor to its physiologic action has yet to be identified, and there is a high level of uncertainty regarding the existence or nature of a taurine-specific receptor (see below).

An experimental study

One of the many experiments demonstrating the cytoprotective action of taurine is based on the now well-established fact that when cells die, they tend to generate toxic substances. These toxins can pass through gap junctions to kill their neighbors, a process referred to as “bystander” cell death [ 102 - 104 ]. Because RPE cells are extensively interconnected via gap junctions [ 105 ], a human RPE cell line (ARPE-19) expressing Cx43 and Cx46 was chosen to conduct an experiment that directly tested the efficacy of taurine in the prevention of cell death [ 106 ]. Using a very fine blade, a small incision was made in the monolayer of ARPE-19 cells, and a solution of the potent cytotoxin cyC was applied to the site of the cut. Since cyC (molecular mass ~12 kDa) cannot pass through the cell wall, nor can it traverse gap junctions, entry was confined to the narrow row of injured cells. However, not only did cyC induce the death of cells along the scrape, but it also caused apoptosis in cells remote from the site of injury. In contrast, when the cells were preincubated in taurine, or the gap junctions were blocked with octanol, cell death was confined to those cells that were injured by the scrape. To ensure that the taurine effect was not due to the blockage of gap junctions, voltage clamp recordings from electrically coupled Xenopus oocytes transfected with Cx43 showed that junctional communication was not affected by taurine [ 106 ].

We should stress that experimentally induced cell death by cyC (as used in the foregoing study) simply bypasses the usual mitochondrial pathway to apoptosis. In more physiological circumstances, pathological conditions often lead to mitochondrial dysfunction, triggering the release of cyC, activation of a downstream caspase cascade, and eventual nuclear disruption. How taurine interferes with this process is unclear, although the results of experiments by Takatani et al. [ 107 ] suggest that taurine inhibits apoptosis by preventing the formation of the Apaf-1/caspase 9 apoptosome, a key stage in the mitochondrial pathway to cell death. However, this finding has not been independently confirmed, nor as we have already mentioned is it likely to be its sole mode of action.

Its role in development

In addition to its protective and therapeutic actions, taurine has proven essential for normal development [ 85 , 108 ], and the genetic TauT knockout mouse has been valuable in this regard. Without appropriate taurine uptake, cell degeneration is inevitable, and this mouse line experiences birth defects in their mitochondria, and in myocardial and skeletal muscle development, e.g., increased ventricular wall thickness and cardiac atrophy.

Taurine also plays a critical role in brain development. Taurine deficiency leads to a delay in cell differentiation and migration in cerebellum, pyramidal cells, and visual cortex in cats and monkeys [ 109 - 113 ]. Moreover, Hernandez-Benitez et al. [ 114 ] have shown that taurine promotes neural development not only in embryonic brain, but also in adult brain regions. Of particular interest is the fact that within the subventricular zone of the cultured adult mouse brain, taurine activates stem cells and neural precursor cells to differentiate into neurons rather than astrocytes. The subventricular zone is one of the few regions in the brain in which neurogenesis continues throughout adulthood, and the cells from this region can proliferate and migrate via the rostral migratory stream to the olfactory bulb where they differentiate into neurons [ 115 ]. Considering the high taurine content in the adult olfactory bulb, it is likely that taurine is an important factor for neurogenesis. It should also be noted that the actions of taurine on adult subventricular stem cells and progenitor cells are not mimicked by glycine, GABA, or alanine [ 114 ].

The importance of taurine in retinal development was revealed in many of the earlier studies in which endogenous taurine was depleted by the taurine transport inhibitor GES, or by feeding mothers and their newborn taurine-free diets. The findings showed that taurine deficiency during the early stages of retinal development leads to impaired photoreceptor development, loss of ganglion cell axons, a higher frequency of fetal resorption, and stillbirth [ 109 , 110 , 116 - 119 ]. Perhaps even more relevant are the striking results from the Cepko laboratory, where it was shown that taurine stimulates rod development when added to media containing rat retinal cultures [ 120 ]. Interestingly, taurine uptake could be blocked without inhibiting its ability to stimulate rod production, evidence that the mechanism of action is neither osmoregulatory nor nutritive. Subsequent studies have implicated the ligand-gated glycine α2 receptor in photoreceptor development [ 121 ], since mice with targeted deletion of this receptor no longer experienced proper normal photoreceptor development. However, the spotlight focused once again on taurine when a genome-wide analysis identified a noncoding RNA expressed in the developing retina, taurine upregulated gene 1, and that its knockdown with RNA interference resulted in malformed or nonexistent photoreceptor outer segments [ 122 ].

Further evidence for the involvement of taurine in retinal development was provided in a recent study showing that under defined culture conditions, taurine (and certain growth factors) can efficiently promote the in vitro generation of putative rod and cone photoreceptors from mouse, monkey, and human embryonic stem cells [ 123 ]. The suggestion that taurine’s ability to promote photoreceptor development may be mediated by GlyRα2 subunit-containing glycine receptors [ 124 ] is apparently at odds with the evidence that neither the addition of glycine nor GABA to the media had the same effect as taurine [ 125 ].

Taurine and oxidative stress

It has become increasingly apparent that oxidative stress plays a major role in a broad range of human diseases. The overproduction of reactive oxygen specie and the body’s inability to stem the accumulation of highly reactive free radicals have been implicated in cardiovascular disease [ 126 ], diabetes-induced renal injury [ 127 ], inflammatory disease [ 128 ], light-induced lipid peroxidation in photoreceptors [ 38 ], reperfusion injury [ 129 ], and several of the major disorders of the CNS [ 130 , 131 ]. In each case, taurine, by virtue of its antioxidant activity, has been shown to play a crucial role as a cytoprotectant and in the attenuation of apoptosis. Despite this diversity of pathophysiology in so varied a group of seemingly unrelated disorders, there is a growing consensus that oxidative stress is linked to mitochondrial dysfunction [ 127 , 130 - 133 ], and that the beneficial effects of taurine are a result of its antioxidant properties [ 126 , 128 , 129 ], as well as its ability to improve mitochondrial function by stabilizing the electron transport chain and inhibiting the generation of reactive oxygen species [ 134 , 135 ].

This mode of action has been described by Schaffer and coworkers [ 135 ] in cases of diabetes. They find that in this condition, there occurs a decline in the levels of endogenous taurine, and suggest that this taurine deficiency reduces the expression of the respiratory chain components required for normal translation of mitochondrial-encoded proteins. They propose that the dysfunctional respiratory chain accumulates electron donors, thereby diverting electrons from the respiratory chain to oxygen, and forming superoxide anion in the process. Increasing taurine levels restores respiratory chain activity and increases the synthesis of ATP at the expense of superoxide anion production.

Taurine and neurotransmission

Perhaps the most enigmatic question regarding taurine is whether it is a neurotransmitter. The structural resemblance between γ-aminobutyric acid and taurine, the similar distributions of these amino acids and their synthesizing enzymes in various regions of the brain, and the evidence that taurine, when applied to CNS neurons, exerts an inhibitory effect on their firing rate [ 136 ] have all contributed to the view that taurine is indeed a neurotransmitter. Adding to this is the fact that there is a rapid calcium-dependent efflux of taurine after electrical stimulation of cortical slices of rat brain, and the presence of uptake mechanisms to terminate its action [ 137 - 139 ]. Nevertheless, the issue is far from resolved, and the effects of taurine on the responses of retinal neurons have served to highlight some of the difficulties.

In their initial studies on the action of taurine on neuronal pathways in the rabbit retina, Cunningham and Miller [ 140 ] showed that taurine was able to separate the ‘On’ and ‘Off’ channels of the parallel pathways identified in recordings of the electroretinogram, the proximal negative response of amacrine cells [ 141 ], and the spontaneous activity of ganglion cells. Without detailing the findings in this paper, it is noteworthy that application of 20 μM strychnine blocked the neuronal effects of taurine, suggesting that taurine was acting on receptors that were also responsive to glycine. Subsequent studies by these authors on the actions of both of these agents revealed that the same concentrations of either amino acid had similar effects on intra- and extracellular recordings from retinal neurons and Müller (glial) cells [ 142 , 143 ]. The fact that this array of responses to both taurine and glycine were blocked by strychnine suggests that a single glycinergic receptor may be sensitive to both agents. However, there is some evidence to the contrary. For example, the inhibitory actions of both glycine and taurine on the frog spinal cord are blocked by strychnine, but the hyperpolarizing effect of taurine could be blocked by a strychnine concentration of 100 μM, which had no effect on the response to glycine [ 144 ]. In addition, the taurine antagonist TAG (6-aminomethyl-3-methyl-4H,1,2,4-benzothiadiazine-1,1-dioxide) blocks spinal cord depolarization without affecting the similar response to glycine [ 145 ]. Thus, although the actions of glycine and taurine overlap at similar receptors, there is reason to suspect that the receptor populations are not the same [ 146 ].

A similar situation arose with the inhibitory neurotransmitter GABA, another ω-amino acid whose molecular structure is strikingly similar to that of glycine and taurine. Once again it was difficult to clearly distinguish between their neuronal actions. Electrical stimulation significantly enhanced both the formation and efflux of GABA and taurine in isolated synaptosomes from the mouse brain, and the kinetic parameters for their high affinity uptake were almost identical [ 147 ]. Moreover, equivalent amounts of taurine and GABA depressed the firing rate of brainstem neurons almost equally [ 148 ], and similar specific, carrier-mediated transport systems are known to operate at brain cell membranes [ 149 , 150 ]. However, unlike the findings with glycine, there are significant differences between taurine and GABA. Both in retina and isolated synaptosomes, strychnine suppressed the action of taurine but not that of GABA, whereas the GABA antagonist bicuculline had no effect on the inhibitory action of taurine, but blocked the depressant action of GABA. In sum, these observations suggest that taurine and GABA are acting on different receptors, and thus, there is no convincing evidence that the electrophysiological actions of taurine are mediated via binding to an ionotropic GABA receptor.

Criteria that define a neurotransmitter

Uncertainties as to whether a molecule is a neurotransmitter have led to the establishment of various criteria (some more essential than others) for inclusion. These are as follows:

(i) Evidence that the substance, together with the enzymes and related chemical machinery required for its synthesis are present within the presynaptic neurons;

(ii) Evidence that the substance is released by a calcium-dependent mechanism in response to presynaptic depolarization, and that it exerts an effect on postsynaptic cells;

(iii) The presence of a mechanism to terminate the action of the transmitter (e.g.., degradation, high-affinity uptake), and the availability of a relatively specific antagonist; and

(iv) The presence on postsynaptic cells of a receptor that specifically binds the putative neurotransmitter.

Studies too numerous to cite here have shown that agents such as GABA, glutamate, acetylcholine, and glycine satisfy these criteria, and studies already cited show that taurine satisfies all but one of the above criteria. Thus, although taurine is released after electrical stimulation, and at physiologic concentrations it exerts a powerful inhibitory effect on the bioelectric activity of the retina and on synaptic transmission in retinotectal pathways, the one crucial criterion that has not yet been met is the presence of a taurine-specific receptor on postsynaptic cells .

There is no shortage of publications claiming to have detected one or more putative taurine receptors. Results obtained by Kudo et al. [ 151 ] on the effects of taurine in the frog spinal cord were interpreted as revealing two taurine receptor subtypes. This conclusion was based on their observation that the application of 10 mM taurine caused a biphasic response consisting of a hyperpolarization followed by a slow onset depolarization. The former was selectively depressed by low concentrations of bicuculline that had no significant effect on the antagonizing action of GABA, whereas the hyperpolarizing component was selectively reduced by a strychnine concentration that had no effect on the response to glycine. Clearly these findings are highly suggestive, but cannot be considered definitive evidence of the presence of taurine-specific receptors. Other studies purporting to have detected taurine receptors in rabbit brain [ 152 ] and in RPE cells in culture [ 153 ] have been similarly inconclusive. In contrast, the kinetics and pharmacology of a receptor prepared from mammalian brain are consistent with what one might expect of a taurine-specific receptor, i.e., the binding of 3 H-taurine was highly specific, and not affected by agonists or antagonists of receptors for glutamate, glycine, benzodiazepine, and GABA B , nor by monovalent or divalent cations [ 154 ]. The binding was completely abolished by 0.1 mM cobalt, zinc, or mercury, suggesting the presence of free sulfhydryl groups near or at the ligand-binding site.

Another study examining proteins that interact with taurine used the cross-linker bis-(sulfosuccinimidyl) suberate (BS3) to covalently bind 3 H-taurine to cell surface proteins on membranes from the olfactory organ of the spiny lobster [ 155 ]. In their inhibition studies, only taurine inhibited the crosslinkage of 3 H-taurine to the membrane, and the taurine-evoked behavioral search response was significantly reduced following treatment of their antennules with BS3 + taurine as compared with animals treated with BS3 alone. This suggests that the taurine-labeled binding proteins include taurine receptor proteins involved in the first stage of olfactory transduction. However, neither of these studies attempted to determine the molecular structure of a taurine receptor at the respective sites.

Currently, perhaps the best hope for establishing the molecular structure of a taurine receptor stems from the elegant work of Anderson and Trapido-Rosenthal [ 156 ], who discovered a unique taurine receptor candidate at a fast excitatory synapse in the motor nerve net (MNN) of the jellyfish Cyanea capillata . Intracellular recording from these relatively large cells in the MNN showed that only taurine (a β-sulfonic acid) and β-alanine (a β-carboxylic acid), both of which are present in the neurons and released on depolarization, produced responses consistent with those of the normal excitatory post-synaptic potentials (EPSPs) in these cells. They tested the effects of 28 candidate neurotransmitters including glycine, GABA, dopamine, epinephrine, acetylcholine, and a variety of neuropeptides and nucleotides. Although a very small response was elicited with GABA, the most effective agents were taurine and β-alanine, both of which produced large depolarizations that varied in amplitude with membrane potential. Either or both of these amino acids, or a closely related unidentified compound, is likely to be the neurotransmitter at this fast chemical synapse. The magnitude of the changes they elicited was exceeded only by the taurine analog homotaurine (3-aminopropane-sulfonic acid), although the time course of the response decay was much slower. As the authors noted, while it is evident that glycine is not a transmitter at the MNN synapse, the features of the taurine response are unlike that typically seen in mammalian preparations, i.e., a hyperpolarizing, inhibitory response. The slow, long-lasting nature of these depolarizing responses suggests that they may be mediated by metabotropic receptors rather than the ionotropic receptors acting at the fast excitatory synapses of the MNN. It remains to be seen whether cloning and expression of the proteins of the MNN neurons will yield a taurine-specific receptor.

Summary and Final Thoughts

In this brief review, we have described several conditions, both normal and pathological, i n which taurine has been shown to exert a significant effect. More inclusive reviews can be found in excellent accounts by Huxtable [ 157 ], Lombardini [ 158 ], Timbrell et al. [ 159 ], Schaffer et al. [ 134 ], and Yamori et al. [ 34 ]. In addition, the reader may wish to consult the many insightful studies on the effects of taurine on intercellular communication (cf. [ 160 - 163 ]), the axonal transport of taurine in the retina and CNS [ 25 , 164 - 166 ], and a comprehensive review devoted solely to the actions of taurine in the retina [ 167 ].

Taurine plays an important role as a basic factor for maintaining cellular integrity in the heart, muscle, retina, and throughout the CNS. As we have attempted to show, this ubiquitous amino acid is a potent cytoprotective agent; moreover, it is considered to be a neurotransmitter candidate, is clearly a modulator of neuronal activity, and is a molecule that deserves significantly more attention than it has received thus far. It is likely that the multiple functions of taurine we have described are mediated at different loci on both extracellular sites (e.g., to participate in neuronal activity, stimulate rod production) and intracellular targets (e.g., to fulfill its role in development and cytoprotection).

Although there is considerable evidence that, in specific circumstances, taurine can interact with GABA B receptors to activate a metabotropic pathway, neither the intracellular link nor a taurine-specific receptor has yet to be identified at the molecular level. However, the quest may end before too long. Although there is no shortage of nonhuman neuronal systems in which taurine is a prominent component, e.g., the squid giant axon [ 168 ], the mollusk Aplysia [ 169 ], and the migratory locust [ 170 ], results obtained from the jellyfish motor nerve net suggest that a taurine-specific receptor may be present in this unusual beast [ 156 ]. If it could be described at the molecular level, this would be a major achievement, and a significant step toward unraveling the pathway(s) by which taurine provides cytoprotection, osmoregulation, neuromodulation, and the myriad of important functions it serves in humans and animals.

In the preface to the second edition of their fine text on Molecular Cell Biology [ 171 ], James Darnell, Harvey Lodish, and David Baltimore state that the quest in all biologic disciplines is the same: “to discover proteins that could carry out specific biologically important tasks.” A rephrasing of that statement might well include all molecules that engage in such tasks, even the “nonessential” amino acid taurine, which participates in so many vital biological functions.

Acknowledgments

The preparation of this review was supported by grants from the National Eye Institute (EY14161, WS) and the National Science Foundation (IOS 1,021,646, WS). The authors are extremely grateful to Dr. Thoru Pederson (University of Massachusetts Medical School) for a critical reading of the manuscript, and the many helpful suggestions that have been incorporated in the text. Co-corresponding author: Dr. Wen Shen is co-corresponding author, and her email address: [email protected].

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

• View all journals
• Explore content
• About the journal
• Publish with us
• Sign up for alerts
• 09 June 2023

Taurine supplement makes animals live longer — what it means for people is unclear

• Myriam Vidal Valero

You can also search for this author in PubMed   Google Scholar

Ageing mice, worms and monkeys can live longer or healthier lives when fed large amounts of taurine, a common ingredient in health supplements and energy drinks, a study suggests.

Access options

Access Nature and 54 other Nature Portfolio journals

Get Nature+, our best-value online-access subscription

24,99 € / 30 days

cancel any time

Subscribe to this journal

Receive 51 print issues and online access

185,98 € per year

only 3,65 € per issue

Rent or buy this article

Prices vary by article type

Prices may be subject to local taxes which are calculated during checkout

doi: https://doi.org/10.1038/d41586-023-01910-4

Singh, P. et al. Science 380 , eabn9257 (2023).

Article   PubMed   Google Scholar  

Marcinkiewicz, J. & Kontny, E. Amino Acids 46 , 7–20 (2014).

Wu, J.-Y. & Prentice, H. J. Biomed. Sci. 17 , S1 (2010).

Download references

Reprints and permissions

Related Articles

• Molecular biology

Release of a ubiquitin brake activates OsCERK1-triggered immunity in rice

Article 15 MAY 24

The temperature sensor TWA1 is required for thermotolerance in Arabidopsis

Structural mechanism of angiogenin activation by the ribosome

Article 08 MAY 24

Dual-action obesity drug rewires brain circuits for appetite

News & Views 15 MAY 24

Temporal dynamics of the multi-omic response to endurance exercise training

Article 01 MAY 24

Obesity drugs aren’t always forever. What happens when you quit?

News Feature 16 APR 24

How to kill the ‘zombie’ cells that make you age

News Feature 15 MAY 24

Hacking the immune system could slow ageing — here’s how

News Feature 07 MAY 24

Could a rare mutation that causes dwarfism also slow ageing?

News 26 APR 24

Postdoc in CRISPR Meta-Analytics and AI for Therapeutic Target Discovery and Priotisation (OT Grant)

APPLICATION CLOSING DATE: 14/06/2024 Human Technopole (HT) is a new interdisciplinary life science research institute created and supported by the...

Human Technopole

Research Associate - Metabolism

Houston, Texas (US)

Baylor College of Medicine (BCM)

Postdoc Fellowships

Train with world-renowned cancer researchers at NIH? Consider joining the Center for Cancer Research (CCR) at the National Cancer Institute

Bethesda, Maryland

NIH National Cancer Institute (NCI)

Faculty Recruitment, Westlake University School of Medicine

Faculty positions are open at four distinct ranks: Assistant Professor, Associate Professor, Full Professor, and Chair Professor.

Hangzhou, Zhejiang, China

Westlake University

PhD/master's Candidate

PhD/master's Candidate    Graduate School of Frontier Science Initiative, Kanazawa University is seeking candidates for PhD and master's students i...

Kanazawa University

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Quick links

• Explore articles by subject
• Guide to authors
• Editorial policies

Taurine may slow ageing process, research suggests

Taurine – a nutrient found in foods with protein such as meat or fish – may slow down the ageing process, scientists have said.

A team of international researchers found that taurine supplements slow ageing in mice and monkeys – extending life and health in middle-aged mice by up to 12%.

The scientists said their findings, published in the journal Science, make the case for further studies with human trials.

Study leader Vijay Yadav, assistant professor of genetics and development at Columbia University Vagelos College of Physicians and Surgeons, said: “Human society is ageing.

“It is associated with changes in molecular composition within us.”

He added: “For the last 25 years, scientists have been trying to find factors that not only let us live longer, but also increase healthspan, the time we remain healthy in our old age.

“This study suggests that taurine could be an elixir of life within us that helps us live longer and healthier lives.”

Taurine is an amino acid found in meat, fish and eggs, and plays an important role in supporting immune health, nervous system function and energy production.

Some energy drinks have taurine added to them, due to its hypothesised effect on mental and athletic performance.

This study suggests that taurine could be an elixir of life within us that helps us live longer and healthier lives

Previous research has shown taurine deficiency to be associated with ageing but Prof Yadav said it was not clear whether it actively directs the ageing process or is just a passenger going along for the ride.

For the study, the researchers looked at blood samples and measured the taurine concentrations at different ages in mice, monkeys, and humans.

They tested nearly 250 female and male mice around 14 months old, about 45 years of age in people terms, giving half of them a taurine supplement and the other half a control solution.

The team found that consuming taurine supplements increased average lifespan by 12% in female mice and 10% in males.

This translates to three to four extra months for mice, equivalent to about seven or eight human years, the researchers said.

The team also found that daily intake of 500 and 1000 milligrams of taurine supplement per kilogram of body weight was also associated with improvements in strength, coordination, and cognitive functions in the rodents.

Prof Yadav said: “Not only did we find that the animals lived longer, we also found that they’re living healthier lives.”

These are associations, which do not establish causation but the results are consistent with the possibility that taurine deficiency contributes to human ageing

The team then tested the effects of taurine supplements in middle-aged monkeys and found that those taking it every day for six months also showed improvements in their immune systems, bone density and overall metabolic health.

The researchers then looked at data from a study involving 12,000 European adults aged 60 and over.

They found that people with higher taurine levels were healthier, with fewer cases of type 2 diabetes, lower obesity levels, and lower levels of inflammation.

Prof Yadav said: “These are associations, which do not establish causation but the results are consistent with the possibility that taurine deficiency contributes to human ageing.”

Lastly, the researchers measured taurine levels of male athletes and sedentary people who took part in a strenuous cycling workout, before and after the activity.

They said a “significant increase” in taurine levels was seen in both athletes – such as sprinters and endurance runners – and sedentary people.

Prof Yadav said: “No matter the individual, all had increased taurine levels after exercise, which suggests that some of the health benefits of exercise may come from an increase in taurine.”

Based on their findings, the researchers said anti-ageing human clinical trials, which are already investigating drugs such as metformin and rapamycin, should also include taurine.

Prof Yadav said: “Taurine abundance goes down with age, so restoring taurine to a youthful level in old age may be a promising anti-ageing strategy.”

Register now for one of the Evening Standard’s newsletters. From a daily news briefing to Homes & Property insights, plus lifestyle, going out, offers and more. For the best stories in your inbox, click here .

• Search the site GO Please fill out this field.
• Newsletters
• Vitamins and Supplements

Health Benefits of Magnesium Taurate

Dr. Dorwart has a Ph.D. from UC San Diego and is a health journalist interested in mental health, pregnancy, and disability rights.

Magnesium taurate is a common dietary supplement. This chemical complex is made up of the mineral magnesium and taurine, an amino acid.  

There is some evidence that magnesium taurate can help treat various health conditions, such as hypertension (high blood pressure), cataracts, diabetes, and anxiety. It may also help to protect overall eye, heart, and brain health. However, research about the benefits of magnesium taurate is limited and ongoing.

The available evidence about the benefits of magnesium taurate comes primarily from animal studies. It suggests that magnesium taurate may help to lower blood pressure, improve heart health, regulate insulin sensitivity, prevent and treat cataracts, lower anxiety, and help manage the effects of a traumatic brain injury (TBI).

Design by Health

Lowers Blood Pressure

Magnesium is known to regulate blood pressure . Many people with hypertension take magnesium supplements and/or try to increase their intake of magnesium-rich foods, such as avocados, nuts, and fatty fish.  

Some people prefer to take magnesium taurate rather than magnesium alone because it’s more easily absorbed and causes fewer side effects, such as diarrhea. A 2019 animal study found that magnesium taurate significantly reduced blood pressure when administered to rats with hypertension.

Improves Heart Health

In addition to reducing blood pressure, magnesium taurate may have an overall cardioprotective effect—meaning that it may protect heart health. This could be due to its antioxidant properties, or its ability to reduce cell damage caused by oxidative stress. 

Magnesium supplements, including magnesium taurate, have been found to prevent and treat high cholesterol, cardiac arrhythmias (irregular heartbeats), stroke, and heart disease . They may also help to reduce the overall damage after experiencing a myocardial infarction (heart attack).

Improves Insulin Sensitivity

People with type 2 diabetes and other metabolic disorders often have impaired insulin sensitivity, also known as insulin resistance . This refers to how your body regulates blood sugar (glucose) levels. 

Taurine has been found to lower blood sugar and regulate insulin sensitivity. Meanwhile, magnesium deficiency has been linked to a higher risk of type 2 diabetes . There is some preliminary evidence that magnesium taurate can help to improve the way your body responds to insulin, which may in turn work to reduce your diabetes risk.

Prevents Cataracts

Cataracts, an eye condition characterized by blurry vision and cloudiness in the lens of the eye, is one of the world’s leading causes of blindness. Magnesium supplementation may help to prevent cataracts and stop them from getting worse, possibly because high blood pressure is a key risk factor for developing the condition. 

One 2016 animal study found that magnesium taurate was effective in halting the progression of cataractogenesis, or the process by which cataracts form. In addition to lowering subjects’ blood pressure, magnesium taurate worked to decrease the levels of oxidative damage in their eyes. This may be due to taurine’s antioxidant properties.

May Help Treat Traumatic Brain Injuries (TBIs)

Early research indicates that magnesium taurate may help to improve cognitive functioning and treat certain neurological disorders. 

For example, a 2020 animal study found that magnesium taurate helped with recovery after a traumatic brain injury (TBI). Supplementation with magnesium taurate sped up the tissue healing process and improved several aspects of the study subjects’ brain structure and functioning, including the ability to show empathy , after head trauma.

May Lower Anxiety

Many people take magnesium supplements to reduce tension, decrease anxiety , and relieve stress. In a 2019 study, magnesium taurate was found to be especially effective in reducing anxiety when compared with other magnesium compounds.

How To Take Magnesium Taurate

Magnesium taurate isn’t regulated by the U.S. Food and Drug Administration (FDA). It’s typically available as an over-the-counter (OTC) dietary supplement , to be taken orally. You can often find it at pharmacies, drugstores, online retailers, and health food stores.

Since it’s not FDA-regulated, there’s no specific recommended dosage of magnesium taurate. However, the U.S. Food and Nutrition Board (FNB) has established the upper recommended daily limit for magnesium supplements as 350 milligrams (mg) for adults. Most magnesium taurate supplements are available in doses of 100-500 mg.

Is Magnesium Taurate Safe?

Magnesium taurate is typically safe and well-tolerated for most people. Many people choose to take it because it often causes fewer side effects than other supplements that contain magnesium .

However, magnesium taurate may cause side effects if taken in excess. It can also potentially interact with other supplements and medications. This can lead to adverse reactions and/or make your treatment less effective. Before trying magnesium taurate, it’s important to let your healthcare provider know about any other medications you’re currently taking.

Potential Drug Interactions

Magnesium supplements can interact with the following drugs:

• Blood pressure medications: Magnesium supplements can lower blood pressure, which means they can cause hypotension (low blood pressure) if taken with other blood pressure medicines.
• Antibiotics: Taking magnesium supplements at the same time as antibiotics like doxycycline can make them less effective in fighting infections. 
• Diuretics: Lasix ( furosemide ) and certain other diuretics may make magnesium supplements less effective.
• Proton pump inhibitors (PPIs): Some PPIs, such as Prevacid (lansoprazole), can dangerously lower your serum magnesium levels. Magnesium supplements may not work as well if you take them as well as PPIs.
• Osteoporosis medications: Certain medicines prescribed to treat osteoporosis , such as Fosamax (alendronate), are less effective when taken alongside magnesium supplements.  

Taurine may also interact with:

• Caffeine: Taurine is often used as an ingredient in energy drinks that contain caffeine. In large amounts, it may increase certain side effects of caffeine, such as a rapid heart rate.  
• Insulin: Because taurine can decrease blood sugar levels, it can lead to hypoglycemia (dangerously low blood sugar) among people who also take insulin.

Can You Take Too Much Magnesium Taurate?

Taking more than 350 mg of magnesium per day in supplement form may cause side effects. 

In rare cases, you may develop magnesium toxicity if your serum (blood) levels of magnesium become very high. This may occur if you take more than 5,000 mg of magnesium at one time. Symptoms of magnesium toxicity may include:

• Hypotension (low blood pressure)
• Inability to urinate
• Facial flushing
• Irregular heartbeat
• Difficulty breathing
• Muscle weakness

It’s more likely to experience symptoms of magnesium toxicity if you have a renal (kidney) condition because your kidneys typically flush out excessive magnesium from your body. Very rarely, untreated magnesium toxicity can be fatal.

Side Effects of Magnesium Taurate

Possible side effects of magnesium supplements include:

• Stomach pain

Taurine hasn’t been found to cause many side effects. Because it’s a naturally occurring amino acid , taking a supplement that contains it usually doesn’t lead to adverse health outcomes. However, some people who have taken taurine in a multivitamin or mineral supplement drink have reported gastrointestinal side effects, such as nausea and vomiting. It can also cause excessive urination.

A Quick Review

Magnesium taurate is a nutritional supplement with several potential health benefits. Research suggests that it may help to reduce blood pressure, regulate blood sugar, lower anxiety, and protect against damage caused by cataracts, heart disease, and TBIs.

While magnesium taurate is generally safe, it can cause side effects like diarrhea and stomach cramps. Talk to your healthcare provider about any concerns, such as potential drug interactions and adverse reactions.

Shrivastava P, Choudhary R, Nirmalkar U, et al. Magnesium taurate attenuates progression of hypertension and cardiotoxicity against cadmium chloride-induced hypertensive albino rats . J Tradit Complement Med . 2018;9(2):119-123. doi:10.1016/j.jtcme.2017.06.010

Curran CP, Marczinski CA. Taurine, caffeine, and energy drinks: Reviewing the risks to the adolescent brain . Birth Defects Res . 2017;109(20):1640-1648. doi:10.1002/bdr2.1177

National Institutes of Health: Office of Dietary Supplements. Magnesium .

Houston M. The role of magnesium in hypertension and cardiovascular disease . J Clin Hypertens (Greenwich) . 2011;13(11):843-7. doi:10.1111/j.1751-7176.2011.00538.x

Tao X, Zhang Z, Yang Z, Rao B. The effects of taurine supplementation on diabetes mellitus in humans: A systematic review and meta-analysis . Food Chem (Oxf) . 2022;4:100106. doi:10.1016/j.fochms.2022.100106

Vormann J. Magnesium: Nutrition and homoeostasis . AIMS Public Health . 2016;3(2):329-340. doi:10.3934/publichealth.2016.2.329

National Eye Institute. Cataracts .

Choudhary R, Bodakhe SH. Magnesium taurate prevents cataractogenesis via restoration of lenticular oxidative damage and ATPase function in cadmium chloride-induced hypertensive experimental animals . Biomed Pharmacother . 2016;84:836-844. doi:10.1016/j.biopha.2016.10.012

Hosgorler F, Koc B, Kizildag S, et al. Magnesium acetyl taurate prevents tissue damage and deterioration of prosocial behavior related with vasopressin levels in traumatic brain injured rats . Turk Neurosurg . 2020;30(5):723-733. doi:10.5137/1019-5149.JTN.29272-20.1

Uysal N, Kizildag S, Yuce Z, et al. Timeline (bioavailability) of magnesium compounds in hours: Which magnesium compound works best? . Biol Trace Elem Res . 2019;187(1):128-136. doi:10.1007/s12011-018-1351-9

Maleki V, Alizadeh M, Esmaeili F, Mahdavi R. The effects of taurine supplementation on glycemic control and serum lipid profile in patients with type 2 diabetes: A randomized, double-blind, placebo-controlled trial . Amino Acids . 2020;52(6-7):905-914. doi:10.1007/s00726-020-02859-8

McGurk KA, Kasapi M, Ware JS. Effect of taurine administration on symptoms, severity, or clinical outcome of dilated cardiomyopathy and heart failure in humans: a systematic review . Wellcome Open Res . 2022;7:9. doi:10.12688/wellcomeopenres.17505.3

Related Articles

Click through the PLOS taxonomy to find articles in your field.

For more information about PLOS Subject Areas, click here .

Loading metrics

Open Access

Peer-reviewed

Research Article

Study of correlations between serum taurine, thyroid hormones and echocardiographic parameters of systolic function in clinically healthy Golden retrievers fed with commercial diet

Roles Conceptualization, Data curation, Formal analysis, Funding acquisition, Investigation, Methodology, Validation, Writing – original draft, Writing – review & editing

Affiliations Department of veterinary Medicine and Animal Science, University of Milan, Lodi, Italy, Cardiology Unit, Anicura Clinica Veterinaria Malpensa, Samarate, VA, Italy

Roles Formal analysis, Investigation, Validation, Writing – review & editing

Affiliation Department of veterinary Medicine and Animal Science, University of Milan, Lodi, Italy

Roles Data curation, Formal analysis, Investigation, Supervision, Writing – review & editing

* E-mail: [email protected]

Roles Formal analysis, Investigation, Supervision, Writing – review & editing

Roles Supervision, Writing – review & editing

Roles Funding acquisition, Investigation, Project administration, Supervision, Writing – review & editing

Affiliation Cardiology Unit, Anicura Clinica Veterinaria Orobica, Bergamo, Italy

Roles Data curation, Writing – review & editing

Roles Conceptualization, Investigation, Resources, Writing – review & editing

Roles Data curation, Investigation, Writing – original draft, Writing – review & editing

Roles Data curation, Investigation, Visualization, Writing – review & editing

Roles Conceptualization, Funding acquisition, Project administration, Resources, Supervision, Validation, Writing – review & editing

• Mara Bagardi, 
• Sara Ghilardi, 
• Giulietta Minozzi, 
• Eleonora Fusi, 
• Chiara Locatelli, 
• Paolo Luigi Ferrari, 
• Giulia Drago, 
• Michele Polli, 
• Elisa Lorenzi, 

• Published: May 16, 2024
• https://doi.org/10.1371/journal.pone.0297811
• Peer Review
• Reader Comments

Taurine deficiency predisposes to the development of nutritional dilated cardiomyopathy and is widespread in dogs fed with non-traditional diets. However, Golden retrievers show lower plasma taurine concentration and an impaired systolic function compared to breeds of the same size and morphotype. For these reasons, it can be difficult to classify a subject from a cardiological point of view, with the risk of considering as pathological characteristics that can be completely normal in this breed. This is a cross-sectional multicenter study. The aims were 1) to identify breed-specific range of serum taurine concentration, 2) to describe a correlation between serum taurine concentration and echocardiographic parameters of systolic function in clinically healthy Golden retrievers fed with traditional diet, 3) to identify a correlation between thyroid hormones, serum taurine concentration and echocardiographic indices. Sixty clinically healthy Golden retrievers (33% males, 67% females) were included. Fifty-three dogs were fed with traditional diets and their range of serum taurine concentration was 398.2 (31.8–430) nmol/ml. Serum taurine concentration was found to be negatively correlated to systolic internal diameter of the left ventricle and systolic and diastolic left ventricular indices and volumes obtained with different methods, whereas was positively correlated to the left ventricle ejection and shortening fractions but difference was not statistically significative. A weak but significant correlation between serum taurine and T4 was demonstrated. Serum taurine median values in dogs with normal systolic function were higher than in dogs with impaired systolic function. A cut-off of serum taurine concentration of 140.6 nmol/ml had a moderate sensitivity and specificity in the identification of an impaired left ventricular systolic function (AUC 0.6, Se 78%, Sp 44%). This study showed that the median serum taurine concentration was significantly lower in dogs with impaired systolic function. Therefore, echocardiographic monitoring is recommended in all dogs with serum taurine concentration lower than 140.6 nmol/ml.

Citation: Bagardi M, Ghilardi S, Minozzi G, Fusi E, Locatelli C, Ferrari PL, et al. (2024) Study of correlations between serum taurine, thyroid hormones and echocardiographic parameters of systolic function in clinically healthy Golden retrievers fed with commercial diet. PLoS ONE 19(5): e0297811. https://doi.org/10.1371/journal.pone.0297811

Editor: Vincenzo Lionetti, Scuola Superiore Sant’Anna, ITALY

Received: January 14, 2024; Accepted: April 10, 2024; Published: May 16, 2024

Copyright: © 2024 Bagardi et al. 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 credited.

Data Availability: All relevant data are within the paper and its supporting information files.

Funding: The project has been approved by the Anicura Scientific Council in 2022 and the Authors received funding for this project.

Competing interests: The authors have declared that no competing interests exist.

Introduction

Canine dilated cardiomyopathy (DCM) is the second most common acquired heart disease in dogs [ 1 ]. Multiple aetiologies have been identified [ 1 ]. While DCM of genetic origins have been described in some breeds based upon discovered mutations or observed heritability and pattern of inheritance, determining the aetiology of DCM when observed outside of these breeds is challenging [ 1 , 2 ]. Nutritionally mediated DCM (NDCM) has been identified in a lot of species, including dog, and is related to taurine deficiency [ 3 – 5 ]. Recent peer reviewed research on DCM in breeds that were not previously known to have a genetic predisposition for the disease has raised concern about the relationship between diets with certain characteristics and the development of NDCM [ 6 – 8 ]. The Food and Drug Administration (FDA) issued a warning and subsequently released data that identified dietary characteristics which were over-represented in some pet food [ 9 ]. These data are supported by similar findings from researchers at many institutions and suggest that diets which are grain-free or contain legume or potato ingredients should be study to further elucidate their possible role in the causation of DCM [ 7 – 10 ]. When evaluated, the FDA data also identify an inverse relationship/correlation between the size of a company in terms of worldwide sales and the number of reported cases of DCM (smaller companies have the highest reported cases) [ 9 ]. The Golden retriever (GR) is the breed that is most frequently reported to be affected by NDCM in the FDA report [ 9 ]. If compared to other breeds eating similar diets, the role of taurine deficiency in this breed appears of great interest. The over-representation of GRs is interesting as there is no literature to support any familial relationship or genetic aetiology for classic DCM in this breed. In 2005 an autosomal recessive and/or polygenic transmission has been supposed, but this theory has not been confirmed in subsequent studies [ 11 ]. In 1999, a survey conducted on 1400 GRs belonging to the same breed club showed that the incidence of cardiomyopathy is less than 0.7% [ 12 ]. Additionally, a large study on heart diseases in insured dogs identified GRs as a low-risk breed for all cardiac claims and reported that they have a lower cardiac mortality rate than the pooled study population [ 13 ]. Thus, the investigators sought to examine the relationship between diet and nutritional elements with NDCM without or with taurine deficiency. Several studies have reported that GRs may be more susceptible to taurine deficiency, supporting the hypothesis that the GRs are particularly sensitive to dietary taurine deficiency, and probably, this breed has a greater requirement of this amino acid than others [ 14 , 15 ]. These findings are supported by the assessment of lower blood taurine reference ranges in the GRs compared to other breeds: the taurine ranges on whole blood and plasma are respectively 214–377 nmol/ml and 63–194 nmol/ml in healthy GRs against the ranges of 261–271 nmol/ml and 75–79 nmol/ml in healthy dogs of different breeds [ 15 ]. Golden retrievers fed with diets that directly or indirectly affect taurine blood concentration (e.g., grain-free diets, low protein and amino acid diets, high fibre, or legume content) often appear to present hypotaurinemia and more easily develop forms of DCM [ 14 , 15 ]. The authors have previously reported a serum taurine plasma concentration in 10 GRs that was lower than the value reported in another large breed (German pointer, not reported as predisposed to taurine deficiency) in a pilot study carried out in 2021 [ 16 ]. Moreover, it has been demonstrated that this breed normally tends to have higher ventricular volumes, lower sphericity index, and lower ejection fraction when compared to the general canine population [ 16 ]. These breed-specific echocardiographic features should be taken into consideration for an accurate echocardiographic interpretation and screening every time the cardiologist must evaluate one of these subjects. The clinician must also keep in mind that this breed is predisposed to an increased risk of developing hypothyroidism, for which an association with an impaired left ventricular systolic function has not yet been completely demonstrated [ 17 – 20 ]. This introduces new doubts on myocardial disease with DCM echocardiographic phenotype in GRs. For all these reasons, the presence of an association between taurine deficiency, thyroid hormones, diet and dietary ingredients and the left ventricular systolic function in the myocardial disease process in this breed must be investigated to avoid the risk of interpreting as abnormal something that could be normal for the breed. In addition, to gain some insight into the possible cause of DCM in a not genetically predisposed breed, a detailed study on the mode of inheritance, also including the inbreeding evaluation, need to be considered.

The hypothesises of this study are that: 1) Clinically healthy GRs with decreased systolic function have lower serum taurine concentration, 2) GRs with lower serum taurine concentration have higher inbreeding and kinship scores.

Therefore, the aims of this study are: 1) To identify the relationship between serum taurine concentration, T4 and TSH assessment and echocardiographic indices of systolic function in clinically healthy GRs, 2) To establish a cut-off of serum taurine concentration that can discriminate between healthy GRs and GRs with systolic dysfunction, 3) To perform an inbreeding and kinship check through the pedigree evaluation.

Materials and methods

Golden retrievers were recruited for this cross-sectional multicenter study from the populations of the cardiovascular breed screening examinations at the Cardiac Unit of the University veterinary teaching hospital in Lodi—University of Milan—Italy and at Anicura Clinica Veterinaria Orobica in Bergamo—Italy between July 2022 and June 2023. The possibility to take part on this research has been presented to the owners of the dogs recognized as possible participants. The study was approved by the Anicura Committee and all study participants provided written informed consent.

Inclusion criteria were an unchanged diet history for at least 3 months prior to enrolment, a complete echocardiographic examination without any pharmacological restraint, and a complete diet history. All included GRs were subjected to a complete physical examination, systemic blood pressure measurement via Doppler method, electrocardiogram, and echocardiography. Dogs were considered healthy basing on the absence of prior clinical conditions/abnormalities documented by the owners and unremarkable physical examination, blood analysis, and cardiovascular assessment. Blood samples were processed (complete blood count, biochemical profile, complete thyroid profile, urinary analysis, and troponin I concentration) and considered normal according to the laboratory reference ranges. Dogs with congenital heart diseases were excluded from the study, as well as dogs aged <18 months because of the possible influence of young age on the serum taurine concentration.

Diet history

Traditional diets (TD) were required to meet the following criteria: kibble diets which are grain-inclusive and not include legumes or potatoes in the top 5 ingredients listed. Non-traditional diets (NTD) had to contain kibble or raw food diets that are grain-free or include legumes or potatoes [ 9 ]. Body condition score was assessed by the veterinary nutritionist (EF) and recorded using a validated 9-point scale [ 21 ]. Dogs with diet histories not meeting the defined categories were excluded (i.e., dogs eating a mix from the TD and NTD group, etc.). Dogs with incomplete diet histories that could not be elucidated through a contact with the owner were excluded. Dogs that did not have a consistent diet history for >3 months were excluded. Dogs receiving dietary supplements containing taurine, methionine or L-carnitine have been excluded.

Blood analysis

Venous blood samples were obtained for complete blood count, complete biochemical analysis, serum thyroid profile (T 4 and TSH), serum taurine concentration measurements, and plasma troponin (cTnI). Fasting was required before blood sampling, even if fasting status does not impact taurine level in dogs; however, it impacts biochemical analysis [ 22 ] and cTnI concentration [ 23 ]. Complete blood count (CBC), associated with the evaluation of the blood smear and the biochemical analysis, was performed at the internal laboratory of the University Veterinary Teaching Hospital of the University of Milan (Lodi) with the automated hematology analyzer Sysmex XT-2000iV (Sysmex, Kobe, Japan). Biochemical analyses were carried out with the automated spectrophotometer BT3500 (Biotecnica Instruments, Rome, Italy). The dosage of serum taurine was performed at the San Marco veterinary laboratory (Padova—Italy) by liquid chromatography with a non-contact mass spectrophotometer (LC-MS/MS, liquid chromatography-mass Spectrometry), a method developed and validated by the certified laboratory itself. Evaluation of the thyroid profile was conducted at the Idexx laboratory through chemiluminescent immunoassay and enzyme immunoassay for TSH and T4 respectively. Measurement of cTnI was carried out using the Immulite (EuroDPC, Gwynedd, Wales) according to the manufacturer’s recommended methods. The manufacturer’s quoted imprecision was 8.4–6.1% (0.8–86 μg/L). The detection limit of the assay was 0.1 μg/L, the 99th centile of a reference population was 0.2 μg/L, and the upper measurement upper limit was 180 μg/L. The total imprecision of the assay was evaluated using NCCLS protocol EP-5A and compared with the manufacturers claims of 8.4–6.1% across the range 0.8–34 μg/L [ 24 ].

Urine analysis

All urine samples were collected through cystocentesis and were immediately refrigerated. Within 8 h, standard urinalysis was performed by dipstick chemistry test and refractometer (for USG evaluation); all samples were then immediately centrifugated at 1250 rpm for 5 min and the supernatant was stored at − 20 °C. The supernatant underwent urinary protein (UP) and urinary creatinine (UC) evaluation by Pyrogallol Red Method and UP/UC was calculated (values < 0.5 were considered normal [ 25 ]).

Echocardiography

All dogs received an echocardiogram by an experienced echocardiographer or a cardiologist resident in training, both blinded to diet history and assigned diet group, using three ultrasonographic units equipped with two different multifrequency phased array probes (Esaote MyLab TM 30 Gold, Esaote MyLab TM Omega, Mindray M9). Images were also stored for off-line analysis. All echocardiographic scans were carried out on conscious dogs in right and left lateral recumbency, in accordance with previous published standards [ 26 , 27 ]. All measurements were taken from three consecutive cardiac cycles, and the mean was recorded. Echocardiographic measures recorded for the study included LA/Ao measured in 2D-mode using the Hansson’s method [ 28 ] from the right parasternal short axis view, measurement of left ventricular internal diameter in diastole (LVIDd), left ventricular internal diameter in systole (LVIDs) and calculated percent fractional shortening (SF) and the ejection fraction (EF). Left ventricular measurements were performed from the right parasternal short-axis view with M-mode of the left ventricle at the level of the papillary muscles with the leading edge to leading edge method. Fractional shortening was calculated according to the equation: (LVIDd-LVIDs)/LVIDd x 100. Ejection fraction was calculated from M-mode and B-mode measurements using the Teichholz method to determine chamber volumes as previously published [ 29 ]. End diastolic volume index (EDVI) and end-systolic volume index (ESVI) were also calculated by dividing the end-systolic or end-diastolic volumes in millilitres by body surface area in squared meters as previously described [ 30 ]. Body surface area was calculated by the formula 0.101 x body weight (kg) 2/3 . Normalized left ventricular end-diastolic and end-systolic internal diameters (LVIDNd and LVIDNs) were obtained using the allometric equation, as previously described [ 31 ]. LVIDd was considered increased when >51 mm [ 32 ], and LVIDs was considered increased when >35 mm [ 32 ]. The fractional shortening was recorded as low when <25% [ 31 , 32 ]. E-point septal separation (EPSS) was obtained from M-mode measurements in the right parasternal short axis view at the mitral valve level [ 33 ]. The mitral and tricuspid annular plane systolic excursion (MAPSE and TAPSE) were measured according to the literature form the left apical four chambers view with M-mode [ 34 , 35 ]. End-systolic and end-diastolic left ventricle volumes (LVVs e LVVd) were obtained from B-mode measurements by the Simpson method and by the area-length method in the right parasternal long axis view. Left ventricle sphericity index (SI) was calculated from B-mode measurements in the left parasternal apical 4-chambers view [ 36 ]. Fractional area change (FAC%) of the left ventricle was calculated from B-mode measurements in the right parasternal short axis view at the papillary muscles level. Left ventricular diastolic diameter to aorta ratio (LVIDd/Ao) was obtained from B-mode measurements in the right parasternal long axis view. Transmitral flow (E peak velocity, A peak velocity, E peak velocity-to-A peak velocity ratio) was measured using pulsed-wave Doppler from the left four chamber apical view. Aortic and pulmonary flows were also evaluated from the subxiphoid view and from the right parasternal short axis view at the base of the heart, respectively. The chosen cut-off values were based on previously published data and on breed-specific reference intervals to maintain consistency with prior publications [ 13 , 31 , 32 , 37 ].

Systolic function evaluation.

The subjects were classified as dogs affected by impaired systolic function according to the following criteria: 1) LVVd >101.6 cm 2 and LVIDNd >1.7 or LVVd >101.6 cm 2 and sphericity index <1.65 or LVIDNd >1.7 and sphericity index <1.65; 2) at least two of these parameters: EF <40%, LVVs >45.6 cm 2 , SF <20%, FAC < 35%, EPSS > 0.7 cm. Dogs with normal systolic function presented: LVVd and LVVs included in the normal reference ranges for weight (41.1–106.1 cm 2 and 18.4–45.6 cm 2 ), LVIDNd ≤1.7, sphericity index ≥1.65, EF ≥40%, FS ≥35%, FAC ≥35% and EPSS ≤0.7 cm. All dogs with echocardiographic characteristics that did not meet these criteria were not included in the analysis of the assessment of systolic function.

Pedigree analysis

Pedigree information were used to estimated inbreeding coefficients on the entire cohort. Data handling and calculations were performed in the R statistical environment [ 38 ], version 4.1.3 with the “OptiSel” package [ 39 ]. The “prePed” function of the “OptiSel” package was used to prepare the pedigree file. The function “summary.Pedig” was used to calculate the pedigree inbreeding coefficient of all individuals that had pedigree information, the number of fully traced generations and the number of maximum generations traced [ 40 , 41 ]. The analysis was conducted both on the entire cohort and subsequently means of inbreeding were given only on the animals with impaired systolic function.

Statistical analysis

Statistical analysis was performed using SPSS 28 (IBM, SPSS, USA). Data were tested for normality using the Shapiro–Wilk test. Normally distributed data were presented as mean ± standard deviation (SD) and compared by the two-sided Student’s t-test and non-normally distributed data were presented as median and interquartile range (IQR) and compared by the median test. Correlation was tested by the Pearson rho (ρ) correlation coefficient, with the following interpretation: ≤ 0.3 weak correlation, > 0.3 and ≤ 0.7 moderate correlation, > 0.7 strong correlation. Requiring 80% power, weak correlations less than 0.35 were considered for descriptive purposes only.

Multiple linear regression was performed, and the backward method was used. Only an R square value greater than 0.1 (P<0.05) was considered suitable.

Receiver operating characteristic (ROC) analysis was performed. The area under the ROC curve (AUC) was used to assess the diagnostic accuracy and to quantify the predictive value of serum taurine concentration for systolic dysfunction, as suggested by Šimundić in 2009 [ 42 ]; the degree of diagnostic accuracy was interpreted as follows: non informative test (AUC = 0.5); inaccurate test (0.5 < AUC ≤ 0.7), accurate test (0.7 < AUC <1), perfect test (AUC = 1) [ 43 ]. A cut-off value was found by maximizing the Youden index. Statistical significance was accepted at p-value ≤ 0.05.

The study included 60 Golden Retrievers, 40 females (66.7%), 3 spayed (5%), and 20 males (33.3%), 2 neutered (3.3%). The mean age was 4.2±2.8 years and the mean weight was 30.2±4.7 Kg. The mean heart rate, systolic, diastolic, and mean blood pressure were 101.3±14.4 bpm, 136.0±17.3 mmHg, 79.4±19.9 mmHg and 101.1±15.9 mmHg, respectively. All the pressure data were considered normal according to the guidelines for dogs and cats. The mean BCS was 5.2±0.8 points. Fifty-three (88.3%) dogs were fed with TD, 5 (8.3%) with GF diet, and 2 (3.4%) with NTD. Furthermore, forty-five of these diets were gluten free. The echocardiographic data of the included population are reported in Table 1 .

• PPT PowerPoint slide
• PNG larger image
• TIFF original image

https://doi.org/10.1371/journal.pone.0297811.t001

Dogs with normal systolic function were 34 (56.7%), while 14 (23.3%) presented impaired systolic function (8–13.3%–according to the first criterion and 7–11.7%–to the second one). The other 12 (20%) dogs presented a systolic function not strictly classifiable according to the criteria reported in the materials and methods section and therefore were not considered for the analysis.

The urinalysis was normal for all included dogs, including the UP/UC ratio. The median serum taurine concentration in the overall population was 121.1 (78.2–171.9) nmol/ml. There were no statistical differences in the serum taurine concentrations of dogs with different sex and weight.

The serum taurine concentration levels of the 48 subjects meeting the inclusion criteria for the analysis of the systolic function were related to the echocardiographic parameters. A negative weak to moderate correlation with LVIDs (ρ = -0.345; P = 0.009), EDVI (ρ = -0.273; P = 0.042), ESVI (ρ = -0.361; P = 0.006), EPSS (ρ = -0.277; P = 0.040), LVVd, and LVVs (ρ = -0.406; P = 0.003 and ρ = -0.385; P = 0.006, respectively) was described. Whereas, between taurine, EF (ρ = 0.360; P = 0.006) and SF (ρ = 0.352; P = 0.008) a positive moderate correlation was found. Fig 1 shows the scatter plots of echocardiographic variables whose correlation absolute value with serum taurine was stronger than 0.35.

A-C Scatter plots showing the negative moderate correlation between serum taurine concentration and ESVI, LVVd, and LVVs, respectively. D-E Scatter plots showing the positive moderate correlation between serum taurine concentration and EF and SF.

https://doi.org/10.1371/journal.pone.0297811.g001

In addition, the study of normality allowed to identify dogs with echocardiographic parameters of impaired systolic function as having a lower median serum taurine concentration compared to normal dogs (100.88 versus 131.36 nmol/ml), however the result was not statistically proved (P>0.05). The diagnostic accuracy of optimal serum taurine concentration cut-off (140.6 nmol/ml) for prediction of the reduction of systolic function was reported, as well as sensitivity (78%) and specificity (44%) (AUC = 0.60) ( Fig 2 ).

https://doi.org/10.1371/journal.pone.0297811.g002

By reducing the serum taurine cut-off (124.85 nmol/ml), the sensitivity decreased (71%) and the specificity increased (59%).

Regarding the thyroid profile, none of the included subjects presented hypothyroidism. The median TSH was 0.09 (0.07–0.13) ng/ml and the mean T4 was 1.63±0.63 μg/ml. Although a weak correlation between serum taurine concentration and T4 was found (ρ = 0.3; P = 0.05), no correlation with TSH was proved. The T4 was not statistically different in subjects with impaired systolic function.

Results of the complete blood count (CBC) and biochemical analysis are shown in the S1 Table . All the results were within reference ranges. The statistical analysis was performed to evaluate the correlation between CBC, biochemical analysis, and serum taurine concentration, but no statistical significance was identified (P>0.05). The same was observed for the correlation between blood results and echocardiographic parameters suggestive of impaired systolic function (P>0.05).

Results of the pedigree analysis shown in the S2 Table have been estimated on 50 of the 60 animals in the study. Ten dogs were not included as no pedigree information was available. The mean inbreeding coefficient of the 50 dogs was 0.031±0.058, while the highest value was 0.298 and the lowest value was 0. Subsequently estimates were calculated only on the 14 dogs with altered systolic function. Inbreeding coefficients were available only for 13 of them due to pedigree availability. The mean inbreeding of this group was estimated to be 0.043 ± 0.076, with highest value 0.289 and lowest value 0.001. However, inbreeding coefficient in the two groups did not differ significantly (P = 0.278).

Among the canine DCM etiologies, the literature reports the blood taurine deficiency [ 1 – 5 ]. The Golden retriever is the most represented breed affected by this peculiar form of DCM, despite this breed is not predisposed to the development of the hereditary form of DCM [ 9 , 11 – 13 ]. Furthermore, the literature reports that the Golden Retriever has lower basal taurine levels compared to the other breeds and for this reason it could be more sensitive to an additional deficiency state [ 13 – 15 ]. Some studies reported the reference ranges for plasma, and whole blood taurine in this breed [ 13 – 15 ]. The present study confirmed the lower taurine levels compared to serum concentration reported for other breeds, showing a median serum taurine concentration of 121 (78.2–171.9) nmol/ml. Since the concentration of taurine varies greatly depending on the substrate analyzed, further studies on the evaluation of a breed-specific reference range are needed, because the literature focused on the evaluation of plasma and whole blood ranges, limiting the data regarding the serum concentration. A cause of hypotaurinemia in Golden Retrievers has not yet been clarified. A hereditary-genetic basis has been supposed [ 10 ]. However, it is also suspected that the low taurine level is not a primary condition but could be due to other typical alterations of this breed, such as intestinal dismicrobism. An altered intestinal microbiome can cause an absorption modification of this amino acid, thus hesitating in a deficiency state. Further studies are required to confirm this supposition in this breed.

However, it is also suspected that the taurine metabolism could be altered due to intestinal dysbiosis. It is well known that taurine is processed by intestinal bacteria via bile salt hydroxylase enzymes and dehydroxylation to yield secondary bile acids. Dogs affected by IBD showed higher faecal concentrations of primary bile acids that have been correlated with a lower expression of apical sodium-dependent bile acid transporter proteins in the ileum [ 44 ]. Moreover, in their study on human pro-carcinogenic gut microbiota Yang and co-authors (2023) evidenced a reduction of serum taurine associated with the increase in Desulfovibrionaceae and the decrease in Lactobacillus in the intestinal community [ 45 ].

This study demonstrated that sex and body weight were not related to taurine concentration. To the author knowledge, no studies reported the correlation between serum taurine concentration and echocardiographic data, in particular those measurements describing the left ventricular systolic function. This study focused on the evaluation of these parameters and found a significant correlation between serum taurine concentration and LVIDs, ESVI and EDVI, LVVs and LVVd obtained with Simpson method of discs, EPSS, EF and SF. Only EF and FS showed a positive correlation with taurine. These correlations suggest that low serum taurine concentration is associated to impaired systolic function in clinically healthy Golden Retrievers. The included subjects were classified into two subpopulations basing on systolic function indices (normal vs subjects with impaired systolic function). These two populations had a different median and distribution of serum taurine concentration. The group with impaired systolic function showed a lower median taurine concentration compared to the other group (100.88 nmol/ml vs 131.36 nmol/ml). It is interesting to underline how the taurine distribution in dogs with decreased systolic function showed a decreasing trend, with data more focused on the lower limits of the group range, whereas in the group of normal dogs the taurine concentration focused more on the mean value. Therefore, the obtained results agree with studies reporting a relationship between taurine deficiency and the development of DCM [ 3 – 8 ]. Based on this, it is possible to emphasize the importance of a correct and thorough dietary history in subjects suspected of DCM to set a correction of the diet and an oral integration of this amino acid. This study has also defined, through the evaluation of a ROC curve, a cut-off of serum taurine concentration that can be clinically useful for the identification of a systolic function reduction (a cut-off of 140.6 nmol/ml showed a sensitivity of 78% and a specificity of 44%). Although in the literature it has been shown that a state of hypotaurinemia is related with the intake of specific diets, such as NTD, grain free diets or diets containing legumes and potatoes [ 9 ], this study was not able to demonstrate it, since the population was too small and only few subjects were fed constantly with one of the diets listed above. This study also focused on the evaluation of the thyroid profile, as a reduction of thyroid hormones is reported in the literature as an additional possible etiology of DCM [ 1 , 16 ].

In addition, the Golden Retriever is described as one of the breeds predisposed to the development of hypothyroidism [ 16 ]. The subjects included in the study were not hypothyroid. The results showed a weak correlation between serum taurine concentration and T4, but no significant correlation with TSH. Therefore, this study did not demonstrate a real correlation between hypotaurinemia and changes in the thyroid profile. These results are part of a heterogeneous literature describing an effective correlation between hypothyroidism and DCM development. Although this link is proven in humans, in veterinary medicine the results are still confusing. Some of them reported an improvement in the systolic function after thyroxine intake, while others showed that, although hypothyroid subjects show cardiac changes, a specific correlation between systolic dysfunction and hypothyroidism is not demonstrable, clarifying that the described cardiac modifications are not able to determine an overt DCM [ 17 – 20 ].

Furthermore, as pedigree information of the dogs was available, estimates of inbreeding coefficients have been produced. There was no significant difference in the mean of the inbreeding coefficient between the dogs with healthy or impaired systolic function. However, the two groups were not homogenous and further analysis should be conducted on a more balanced cohort.

This study had some limitations. The first is the lack of the evaluation of intra and inter-operator variability of echocardiographic measurements. The different level of experience and the use of different ultrasound machines may have introduced some analytical errors, not estimated. However, the Osservatorio Veterinario Italiano Cardiopatie (OVIC) accredited veterinarians as well as operators working at the University Veterinary teaching hospital, have an intra-operator and inter-operator variability ≤8 and ≤12% respectively, depending on the echocardiographic measurement, as demonstrated by previous variability tests. Another limit is the inclusion of a population with a small number of subjects fed with grain free and with NTD. This did not permit to assess if the serum taurine concentration in these subjects was lower compared to dogs fed with TD, thus confirming an already suggested correlation between taurine level and type of diet. Moreover, the sample was very homogeneous in terms of age, with predominantly young-adult subjects. This may have affected the levels of thyroid hormones, that were within the normal range for the included population, as endocrine diseases are mostly related to senility. This may have affected the lack of a correlation between serum taurine levels and thyroid hormones. Finally, an important limitation was the lack of the follow-up of the included dogs. For this reason, the possible development of systolic dysfunction and DCM are not known.

The results of this study showed a correlation between serum taurine concentration and echocardiographic parameters of left ventricular systolic function. Lower serum taurine concentrations are related to larger left ventricle diameters and volumes (both systolic and diastolic), as well as greater EPSS, and lower ejection and shortening fractions. This demonstrated that low serum taurine concentration was associated with impaired left ventricular systolic function. The results of this study suggest that the evaluation of the serum taurine concentration should be performed in normal (or healthy) GRs with impaired systolic function at the echocardiographic examination. For this reason, the results of this study suggest that an echocardiographic examination when serum taurine concentration is lower than the proposed cut-off of 140.6 nmol/ml should be performed. Finally, the study showed a weak correlation between echocardiographic indices of systolic function and T4, but not with TSH. No difference in thyroid profile was observed in normal subjects compared to those with impaired systolic function. Basing on the obtained results, it would be interesting to evaluate the correlation between serum taurine concentration, echocardiographic indices of left ventricular systolic function and thyroid profile in a larger sample of dogs, with greater variability in terms of age, including older subjects, more likely affected by an alteration of the thyroid profile. A study with a larger number of subjects fed with NTD is also desirable to further investigate the correlation between hypotaurinemia and the type of diet. In addition, research is already in progress to trace a possible link between serum taurine deficiency associated with intestinal dysbiosis: an alteration of the intestinal microbiome may be the cause of a lack of absorption of taurine in GRs, generating a deficiency state. Since there are no previous studies on a possible predisposition of the Golden Retriever to intestinal dysbiosis, it remains to clarify whether the hypotaurinemia is a primary condition and is related to the breed or if it is secondary to other pathological condition of the GR. Since DCM has proven strong hereditary bases in different large breed dogs, its prevalence is also linked to the degree of inbreeding within a population. In this study, for 45 subjects a pedigree analysis was available, and a very limited inbreeding coefficient was found, evidence that the obtained results were not affected by consanguinity.

Supporting information

S1 table. results of the complete blood count and biochemical analysis of the dogs included in the study..

https://doi.org/10.1371/journal.pone.0297811.s001

S2 Table. Inbreeding data, the number of complete generations, and the number of incomplete (1 parent) generations in the animals under study.

https://doi.org/10.1371/journal.pone.0297811.s002

Acknowledgments

The authors would like to thank all the colleagues of the Osservatorio Veterinario Italiano Cardiopatie, and Doctor Luisa Ginoulhiac (Maple Tree breeding) for contributing to the collection of data presented in this study.

• View Article
• PubMed/NCBI
• Google Scholar
• 30. Knight DH. No Title. In: Feldman SJE and EC, editor. Textbook of Veterinary Internal Medicine. 5th ed. Philadelphia, PA, USA; 1995. pp. 844–867.
• 38. R Core Team., 2022. R: A language and environment for statistical computing. R Foundation for Statistical Computing, Vienna, Austria. https://www.R-project.org/ . (accessed 05/11/2023).

• Skip to main content
• Keyboard shortcuts for audio player

Influx of deadly street fentanyl reaching the U.S. continues to grow, research shows

Two new reports show the fentanyl crisis isn't easing, as drug cartels continue to flood U.S. communities with the deadly illicit opioid often disguised as fake prescription pills.

Copyright © 2024 NPR. All rights reserved. Visit our website terms of use and permissions pages at www.npr.org for further information.

NPR transcripts are created on a rush deadline by an NPR contractor. This text may not be in its final form and may be updated or revised in the future. Accuracy and availability may vary. The authoritative record of NPR’s programming is the audio record.