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Medscape
7 days ago
- Health
- Medscape
Taurine: From Energy Drink Darling to Cancer Suspect?
Taurine enjoys a strong reputation for boosting both physical and mental performance and has long been a staple ingredient in many energy drinks. A 2023 study in Science even suggested that supplementing this amino sulfonic acid — which the body can produce endogenously — could extend life span, at least in mice and monkeys. That research, led by Parminder Singh, PhD, of the Buck Institute in Novato, California, also observed that taurine levels in human blood appear to decline with age. These findings helped fuel a rise in over-the-counter taurine supplement sales. But new evidence suggests that the antiaging effects may be overstated — and that high intake of taurine could even pose risks, including a possible increase in blood cancer susceptibility for some individuals. Poor Fit as Aging Biomarker A more recent Science study casts further doubt on taurine's longevity promise. Maria Emilia Fernandez, PhD, and colleagues at the National Institute on Aging, Baltimore, found that taurine does not serve as a reliable biomarker of biological aging. Unlike the earlier cross-sectional study, their longitudinal research repeatedly measured taurine levels in participants over time. The results showed no consistent age-related decline. In many cases, taurine concentrations increased with age. The researchers concluded that individual variability far outweighed any patterns linked to aging. No Reliable Reference Ranges 'There are no reliable reference values for taurine that could be applied broadly to the general population,' Kristina Norman, MD, head of the Department of Nutrition and Gerontology at the German Institute of Human Nutrition in Potsdam-Rehbrücke, Nuthetal, Germany, told Medscape's German edition . Still, she noted that the study doesn't rule out the possibility that taurine may have beneficial effects in specific contexts — such as for cardiometabolic health. 'That was not the question Fernandez and her colleagues set out to explore,' said Norman, who is also the deputy director of the Research Group in Geriatrics at the Charite Universitätsmedizin Berlin, Berlin, Germany. 'There are a number of interventional studies on taurine supplementation,' Norman added, 'but the results have been inconsistent, which makes interpretation difficult.' Currently, the effects of taurine appear highly dependent on individual factors, including a person's age and underlying health status. As such, Norman advised that taurine supplementation should neither be broadly recommended nor discouraged at this stage. Taurine in the Diet — and in the Data According to the European Food Safety Authority, the maximum safe daily intake of taurine is 100 mg/kg of body weight — about 7 g for a 70-kg adult. European regulations limit taurine in energy drinks to no more than 4 g/L. Taurine also occurs naturally as a breakdown product of the amino acids cysteine and methionine, particularly in meat, fish, seafood, and dairy products. Fernandez's study analyzed data from three human cohorts (973 participants in total) as well as blood samples from rhesus monkeys and mice. The researchers found no evidence of age-related declines in circulating taurine levels among healthy individuals — in fact, levels were often stable or increased with age. Diet, rather than age, showed a stronger correlation with taurine concentrations. Moreover, they found no association between taurine levels and physical parameters such as muscle strength or body weight. 'These findings challenge the prevailing hypothesis that taurine declines with age and contributes to aging,' Norman said. Linked With Leukemia Cell Growth A second study, recently published in Nature , has raised new concerns about potential risks associated with high taurine intake. Researchers led by Sonali Sharma, PhD, from the Department of Biomedical Genetics at the Wilmot Cancer Institute, University of Rochester Medical Center, Rochester, New York, found elevated taurine concentrations in the microenvironment of leukemia cells. They also identified taurine transporters on the cell membranes, which facilitated the uptake of taurine into the cells, where it appeared to support glycolysis. According to Sharma's team, taurine may play a role in both the development and progression of leukemia. 'It's still unclear whether this potential risk applies broadly or only to certain individuals — such as those with a personal or family history of blood cancer,' said Norman. She also noted that it remains uncertain whether orally supplemented taurine even reaches the tumor microenvironment. Nevertheless, she added, the findings open up new therapeutic possibilities — namely, targeting taurine transporters in malignant cells as a novel approach to leukemia treatment. Benefit for Longevity or Performance The Nature study also reinforces the need to re-evaluate taurine's use as a dietary supplement. 'Individuals at increased risk of leukemia should probably avoid taurine supplementation,' Norman advised. More broadly, she noted there is currently no strong evidence to support taurine's use for enhancing physical or cognitive performance or slowing the aging process. 'We simply don't have high-quality data confirming whether taurine works — or at what dose,' Norman said. She also cautioned that taurine's side-effect profile remains poorly understood. 'Taurine could potentially offer benefits in some clinical contexts,' she acknowledged. 'But right now, I would discourage people from taking it on their own 'just in case.''
Yahoo
08-07-2025
- Health
- Yahoo
Surprise Discovery Could Rewrite What We Know About Alzheimer's
A new study just uncovered a surprising link between how brain cells manage sugar and the progression of Alzheimer's disease—and the implications could reshape future treatments. Researchers at the Buck Institute for Research on Aging have discovered that stored glucose, in the form of glycogen, may not be the passive energy reserve scientists once assumed. Instead, it may actively contribute to the buildup of tau proteins, a hallmark of Alzheimer's and other neurodegenerative diseases. Tauopathies like Alzheimer's are characterized by toxic tangles of tau inside neurons. But this study, published in Nature Metabolism, found that those tangles may form, at least in part, because of disruptions in how glycogen is processed in the brain. 'Stored glycogen doesn't just sit there in the brain,' said Buck Institute biologist Pankaj Kapahi. 'It is involved in pathology.' Using fruit fly models and postmortem brain cells from people with Alzheimer's, scientists found elevated levels of both tau and glycogen. The buildup appeared to be driven by a breakdown in how glycogen is metabolized, specifically through the enzyme glycogen phosphorylase (GlyP), which normally helps convert glycogen into usable fuel. When researchers increased GlyP activity in the flies, they saw significant benefits. Brain cells reduced oxidative stress, protected themselves better, and even lived longer. The team also tested whether a low-protein diet, already linked to improved brain health, might produce similar effects. It did. Fruit flies fed this restricted diet showed fewer signs of damage and extended lifespans, suggesting that dietary changes could naturally shift brain metabolism in a protective direction. Even more intriguing, the researchers developed a drug that mimicked the effect of dietary restriction. It worked. And they noted potential crossover with medications like Ozempic, which may also support brain health by targeting glycogen-related pathways. 'By discovering how neurons manage sugar,' said lead researcher Sudipta Bar, 'we may have unearthed a novel therapeutic strategy—one that targets the cell's inner chemistry to fight age-related decline.' If future studies replicate these results in humans, this could mark a turning point in our understanding and treatment of Alzheimer' Discovery Could Rewrite What We Know About Alzheimer's first appeared on Men's Journal on Jul 7, 2025
Yahoo
08-07-2025
- Health
- Yahoo
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years
Yahoo
08-07-2025
- Health
- Yahoo
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years
Yahoo
06-07-2025
- Health
- Yahoo
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight loss, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years
