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Earlier this month, a study published in the prestigious journal Science heralded the arrival of a new contender in the anti-aging game. Mainstream news outlets and social media had a field day when the researchers reported that supplementation with the amino acid taurine could slow a variety of aging processes and extend lifespan, but such media frenzies – and often, the researchers themselves – have a way of inflating the importance of results and blurring the lines between fact and fiction. So what can we believe? Is taurine truly “an elixir of life,” as study author Dr. Vijay Yadav has suggested it could be? Or is it just the latest brand of snake oil?
What is taurine?
Though not one of the twenty canonical amino acids used as building blocks for protein synthesis, taurine is nevertheless one of the most abundant amino acids in mammalian tissues and is thought to have a range of physiological effects. In addition to its antioxidant properties, taurine is an organic osmolyte involved in regulating cell volume and other aspects of the body’s fluid dynamics. It is essential for normal neural and skeletomuscular development, and taurine deficiency has been associated with a number of cardiometabolic and kidney impairments.
Although various tissues are capable of synthesizing taurine from other amino acids, the level of such biosynthesis in humans is low. Thus, dietary intake – particularly from seafood and other animal meats – is the body’s primary source of taurine.
What did the study show?
Previous studies have demonstrated that taurine levels in various tissues decrease with age, possibly contributing to deterioration in metabolic and renal health and other age-related dysfunctions. Thus, Yadav and his colleagues sought to determine whether low taurine levels can indeed drive aging processes and whether supplementation might therefore slow or reverse these processes and extend lifespan.
The researchers showed dramatic age-associated declines in serum taurine in mice, rhesus monkeys, and humans. They then conducted experiments in mice and other non-human species on the effects of taurine supplementation on lifespan and health, ultimately reporting a 10-12% increase in median lifespan among mice treated with taurine relative to placebo-treated controls. (Importantly, controls demonstrated normal lifespans, so this effect was not due to control mice having unusually short lives). Taurine supplementation was associated with reduced body weight (~10%) relative to placebo, evidently due to an increase in energy expenditure. Supplemented mice also demonstrated increased bone strength, grip strength, and endurance, as well as decreased anxiety and depressive symptoms, among other findings. The authors provided evidence that taurine also reduced inflammatory markers, enhanced stem cell counts, and improved mitochondrial function, potentially demonstrating the underlying mechanisms for lifespan effects.
Yadav et al. also conducted a handful of taurine supplementation experiments in rhesus monkeys, finding that results in this species followed a similar pattern to those in mice. Supplementation resulted in lower fat gain, improved bone mineral density, decreased inflammatory markers, and reduced signs of oxidative damage.
What about humans?
While the authors did not conduct intervention experiments in humans, they analyzed human data from the EPIC-Norfolk study and reported that levels of taurine or taurine metabolites are inversely related to body mass index, diabetes incidence, inflammation, and liver dysfunction. They also noted a modest increase in taurine levels post-exercise relative to pre-exercise and suggested that this might be indicative of a role for taurine in mediating the health and longevity benefits of exercise. However, given the observational nature of these data and lack of randomized studies, we can make very little of these human data and must focus instead on the investigators’ animal studies.
In general, it’s important to keep in mind that animal data don’t necessarily generalize to humans, but in the case of taurine, we have reason for more than the usual level of skepticism on this point. As shown in the authors’ own data, typical circulating taurine levels in mice and rhesus monkeys greatly exceed levels in humans by as much as ten-fold. While it’s unclear why mice and other animals have higher taurine levels than humans, the existence of such a large discrepancy raises the likelihood that this compound has divergent functions, effects, and regulation across species.
Further, since mice and monkeys also consume far less (if any) meat and seafood – and thus less taurine – than most humans despite having elevated circulating levels, we can conclude that endogenous taurine synthesis must be a much more active pathway in these animals than it is in our own species. (Recall that in humans, taurine biosynthesis is a minor pathway that contributes little to total circulating levels.) Again, this indicates that the animal models used in this study differ fundamentally from humans in their taurine biology.
Why does taurine decline with age?
A critical variable largely ignored by the study authors is precisely why taurine levels decrease with age. Given that endogenous taurine synthesis is so low in humans, circulating taurine is determined by a balance of absorption from diet and excretion (primarily in urine). This leaves us with three (non-mutually exclusive) possible reasons for the apparent decline with age: 1) a reduction in dietary intake; 2) a reduction in rates of intestinal absorption of taurine from food; or 3) an increase in the rate of taurine excretion. No nutritional data have ever indicated that people consume less meat and seafood at age 60 than they do as kids, so we can exclude possibility #1. Possibility #2 would suggest that we need to consume more taurine as adults than we do as children in order to absorb the same amount, which in turn might mean that supplementation would boost circulating levels and help mitigate their age-related decline. Possibility #3, on the other hand, would mean that supplementation would have very little effect on circulating taurine.
So which is it? We don’t currently know and have no direct data to address this question, but the pieces of evidence we have make the best case for possibility #3. Taurine reabsorption in the kidneys – a process that returns taurine to circulation and prevents its excretion – requires co-transport with sodium ions moving down their chemical gradient (i.e., from high extracellular concentration to low intracellular concentration), an energetically favorable process which helps to drive taurine transport forward. But with age, renal ability to maintain electrolyte gradients gradually deteriorates, contributing to the well-documented age-related decline in kidney function. Thus, it seems likely that the capacity to reabsorb taurine from urine also falls over time, resulting in increased excretion. This possibility is further supported by the observation that, regardless of age, taurine levels are typically low in the presence of chronic kidney disease.
Why is supplementation unlikely to help most individuals?
In general, amino acids can filter into urine, but most are reabsorbed by the kidneys at rates of ~98-99%, meaning that very little is actually excreted. Taurine is different in that it is only reabsorbed at a high level when circulating levels are low. When dietary intake and circulating levels are high, taurine reabsorption rates can be as low as 20%, resulting in a high level of excretion.
On the other side of the equation, rates of taurine absorption from the gut decrease with increasing circulating taurine levels due to reduced transporter expression. Some have reported that dietary availability thus has relatively little impact on circulating taurine.
Combined, these observations suggest that supplementation would be useless in increasing circulating taurine levels in those already within typical physiological ranges. (Data in humans with unusually low taurine levels, as is often seen with obesity, kidney disease, or strict vegan diets, suggest that supplementation does indeed raise serum levels in these individuals.) Any excess either wouldn’t be absorbed or would be excreted. And if taurine levels decline with age due to an increase in excretion, the threshold that defines “excess” taurine is effectively reduced. For instance, a taurine concentration of 50 µmol/L in a 20-year-old could be raised with supplements, but the same level in a 60-year-old might represent an upper limit.
In this way, we can liken the body’s taurine levels to water collecting in a bucket. As long as the bucket isn’t full, the water level will continue to rise as more is added. But once it reaches the top, any additional water will simply spill over the edge and the amount of water in the bucket can increase no further. Now imagine that over time, the bucket rim slowly erodes, resulting in a shorter and shorter bucket that can hold less and less water. No matter how much water you add, the bucket will never contain as much as it did before.
So why did supplementation “work” in mice? Again, it may relate to a difference in their taurine biology relative to humans. In addition to the three possible explanations described above for the decrease in taurine with age, mice may have another contributing factor that would be largely irrelevant in humans: a decline in endogenous synthesis. Like reduced absorption, this explanation would also suggest that supplementation could have a meaningful impact in elevating circulating levels. To use the bucket analogy again, a loss of taurine due to reduced absorption or synthesis would be comparable to slowing the rate of water flow into the bucket to a point at which the rate of evaporation outpaces the rate of water collection, and the water level gradually drops despite the fact that the bucket remains the same size. In this case, supplementation with another water source would be helpful in refilling the bucket.
The bottom line
All in all, it seems taurine may indeed be an elixir of life – assuming you are a mouse. The relevance of Yadav et al.’s data to humans, meanwhile, is dubious at best. Previous work provides compelling evidence that taurine supplementation is beneficial for those who fall well below typical taurine ranges for their age – particularly those with obesity or kidney disease or on vegan diets. But although findings from this recent study certainly provide some mechanistic insights to complement that earlier body of literature and help justify further investigation and human studies, they ultimately offer no reliable indication that supplementation with this amino acid would result in any improvement in health or longevity in humans or even that supplementation would be effective in raising serum taurine levels in humans falling along the normal physiological curve by age range.
So while it’s reasonable to predict that those who are taurine-deficient for reasons related to diet or certain pathologies may find benefit in these supplements, we can’t conclude that age-related declines in taurine can be treated in the same manner. And until we have more direct insights as to why taurine concentrations fall with age, our best guess is that supplementation is about as useful as adding water to an overflowing bucket.
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