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Taurine is a semi-essential amino acid. Dietary taurine supplementation has been shown to modestly slow aging in mice, though as for all such interventions there is always the question of whether it will prove to be less useful in humans, and also whether these results in mice will be disproved by the much more rigorous Interventions Testing Program (ITP), once that group gets around to assessing taurine supplementation. Few of the numerous interventions thought to modestly slow aging in mice on the basis of earlier research actually held up once subjected to the ITP degree of experimental rigor.
Speculatively, taurine may produce its benefits by affecting levels of the antioxidant glutathione. More research is needed on this topic, but if confirmed it would make taurine supplementation more interesting given the benefits produced in a human trial of supplementation with glutathione precursors. The benefits observed in that trial were large for a supplementation approach, and might improve on exercise – though one has to mention that the trial was small, and that benefits to patients tend to diminish in size as trial populations increase.
In today’s open access review, researchers discuss what is known of the effects of taurine supplementation on metabolism. As one might imagine, effects are broad and varied, and little to nothing is known of the relative importance any specific effect when it comes to a potential contribution to slowed of aging. This is par for the course: the research community knows far too little of the fine details of cell metabolism and its adjustment in the context of aging. In the bigger picture this line of research is only interesting because taurine is cheap and readily available. This is generally true for any intervention that produces benefits that are in the same ballpark as those resulting from exercise. As soon as one proposes that years of research must be conducted on top of that, well, people should exercise more than they do, and there are far more useful programs that could be conducted with that funding.
Taurine is not used by the body for protein synthesis and exists in higher concentrations in energy-demanding organs, such as the brain, retina, heart, pancreas, and skeletal muscles, but its abundance almost invariably reduces as animals and humans age. Interestingly, blood taurine levels can also be increased, at least temporarily, after a short period of exercise, with some authors suggested that taurine may play a causal role in explaining why exercise is beneficial to human metabolic health by mediating atheroprotection. At the organ function level, taurine has also been reported to improve bone, retinal, and brain health in animal studies; and furthermore, in small human studies, improvements in glycemic control, exercise endurance and myocardial function after taurine supplementation have been reported.
The mechanisms by which taurine may improve cellular and organ function or health in general are likely multiple, and not necessarily restricted to its direct actions. Specifically, some of the long-term benefits of taurine are believed to be mediated through its interactions with gut microbiome and bile acid conjugation, both of which are currently believed to play a pivotal role in maintaining human health. For instance, at least one of taurine’s conjugated bile acids has been shown to stimulate colonic secretion of glucagon-like-peptide 1 (GLP-1) through activation of the Takeda-G protein-coupled-receptor 5. Taurine is also needed to conjugate fatty acids to form N-acyl taurines in the liver, which have been shown to mediate release of GLP-1. The association between GLP-1 release and taurine supplementation has potential important clinical implications as the use of GLP-1 receptor agonists is now widely accepted as an effective metabolic therapy for patients with diabetes mellitus and people who are overweight. Furthermore, both taurine and taurine-conjugated bile acids (e.g., tauroursodeoxycholic acid – TUDCA) may directly activate insulin receptors (IRs) by binding to docking sites not related to the insulin binding sites on the IRs, thereby improving glucose homeostasis and the other cellular functions related to IRs, including IRs in the brain.
Calorie restriction (CR) has been consistently shown to improve metabolic health and longevity in a wide range of animal species and taurine acts biologically as a CR mimetic. Mechanistically, CR could alter gut microbiome through which it would increase the intestinal levels of taurine and taurine-conjugated bile acids; and transplantation of microbiota from mice with CR to ad libitum fed mice triggered CR-like changes in levels of taurine and taurine conjugates in the mucosa of the ileum. Therefore, there is a strong scientific basis to support the hypothesis that taurine supplementation could improve long-term metabolic health, including optimizing blood glucose control and HbA1c levels, through multiple biologically plausible mechanisms. Because HbA1c has a dose-related positive relationship with long-term all-cause mortality, cardiovascular mortality, and cardiovascular events in both diabetic and non-diabetic individuals, determining whether taurine can improve long-term plasma glucose control, as reflected by HbA1c, has considerable clinical importance.
Specific to the heart, taurine and TUDCA have also been shown to offer some benefits, including improvements in myocardial contractility and exercise capacity of cardiovascular testing, tolerance to ischemia, and a reduction in QT interval, cardiac arrhythmias, blood pressure, trimethylamine N-oxide (TMAO) induced atherosclerosis, and blood lipid levels including the low-density-lipoprotein (LDL) concentration in both individuals with and without diabetes mellitus. Maintaining a long-term normal LDL level is associated with a decreased risk of coronary artery disease and stroke. A large prospective multinational observational study had indeed showed that a high excretion of taurine in the urine (implying a high dietary intake of taurine) had significantly lower body mass index, systolic and diastolic blood pressure, total cholesterol, and atherogenic index (defined as total cholesterol / high-density-lipoprotein [HDL]-cholesterol in this study) than those who had a lower urinary taurine excretion. Similarly, a recent observational study showed that having a low plasma taurine level was associated with an increased risk of developing metabolic syndrome within 5 years. Taken together, epidemiological data suggest that a low taurine intake may increase an individual’s susceptibility to cardiovascular and metabolic diseases; and conversely, a high dietary taurine intake may play a pivotal role in maintaining both long-term cardiovascular and metabolic health.
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