Is Taurine the Amino Acid of Longevity?
Let’s continue considering whether some level of protein restriction, even occasional, might lead to better metabolism and longer life. Although it may seem obvious that restricting food intake should prolong life, in the previous post this was not the case. The longest lifespan was observed in mice that consumed the most essential amino acids as their protein source (20% cal in the diet). Overall, this was not a deficient diet at all. On the contrary, a very rich diet that excluded unnecessary amino acids—which the body can synthesize as needed—ensured the mice’s health. This could serve as a warning for us: restricting these indispensable nutrients might not be such a good idea, as it may not lead to better health or longer life. Still, in some cases, it might appear that way.
Let’s try a different approach. We know of one amino acid that has a proven effect on cellular aging. It’s called taurine. We’ve already come across it once before when I discussed the effects of restricting sulfur amino acids (SAA). Taurine is one of the many products formed from cysteine and methionine metabolism. I showed that restricting SAA significantly lowered taurine levels and increased hydrogen sulfide production. That tells us what’s happening here. Yes, it’s about enzymatically produced hydrogen sulfide—specifically, sulfhydration of enzymes such as sirtuins. Restricting SAA had a switch-like effect, where sulfur was used for sulfhydration instead of taurine synthesis, with numerous positive effects. That’s quite paradoxical if taurine is supposed to be an elixir of youth, don’t you think? So how could taurine supplementation work?
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| CTH = CSE = cystathionine γ-lyase, CSAO = sulfinoalanine decarboxylase |
It makes sense. There’s no paradox. If we want to stop an enzymatic pathway, we don’t remove the reaction product. Its level would rise sharply and block the reaction. So, if we don’t want cysteine to be lost in taurine production, we supplement taurine externally. Then cysteine can be used for hydrogen sulfide production and sulfhydration. This seems to be the fundamental mechanism by which taurine influences metabolism so effectively. S-sulfhydration of enzymes is indeed a powerful magician, as we’ve already seen.
The first study I’ll show images from examines taurine’s protective effects against carbon tetrachloride (CCl4) poisoning in mice. Taurine demonstrated therapeutic effects. First, the researchers has been poisoning the mice’s livers for 4 weeks. Then, for another 4 weeks, they continued the damage but gave part of the mice taurine in drinking water. Taurine restored antioxidant protection and brought back lipid peroxidation markers (MDA – malondialdehyde from PUFA oils) to baseline values. So here it seems to work excellently.
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| Taurine (+T) suppresses cellular senescence markers p16 and p21 induced by carbon tetrachloride (CCl4). |
There are also human studies, but I’ve set those aside for now. There even seems to be some connection to traditional Chinese medicine. For me, the key issue now is mechanisms and context. Is it better to restrict sulfur amino acids, restrict all amino acids, or supplement taurine? I don’t know. The current level of knowledge is still quite limited, mechanisms are unclear, and few people even know about hydrogen sulfide–induced sulfhydration of enzymes and its effects. Let’s move on.
Another study we’ll look at examines the relationships between insulin secretion, dietary fat, protein restriction, and taurine supplementation—especially regarding insulin secretion. It’s fairly complex. The authors’ interpretation may not be the best, and I couldn’t find much detail on the diet composition, but no matter. Let’s see what they found.
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| 5 mM PAA turns off gluconeogenesis, blocks pyruvate carboxylase |
Again, it’s very interesting. In the end, they had six groups of mice. First, they fed mice a control diet (CD) with 14% protein and compared it to a restricted diet (RD) with 6% protein for 6 weeks. Then they switched them to a high-fat diet (CH, RH) for 8 weeks (35% fat, though I don’t know if by weight or calories). They further divided them so that some groups also received 5% taurine (CHT, RHT). At first glance, taurine supplementation only works when mice consume enough protein (14%). In such cases, taurine protects against the effects of a high-fat diet, lowers insulin secretion—likely due to reduced stimulation of the enzyme PLA2 and thus less release of free fatty acids (FFA) from mitochondrial membranes—improves antioxidant protection, and preserves sensitivity to fat (my note). If you didn’t know, I think the loss of insulin secretion sensitivity to elevated FFA to be a root cause of type 2 diabetes. Insulin secretion should increase with FFA levels, not decrease. This loss of responsiveness occurs with an unhealthy diet and leads to diabetes. Overall, lower insulin secretion combined with preserved sensitivity to fats is a positive effect, indicating greater reserves and reduced risk of diabetes.
But protein deficiency may be problematic for early development. I can’t judge whether protein restriction is good, especially for young organisms. The loss of taurine sensitivity might be explained by already high sulfhydration levels on a baseline restricted diet, making further increase impossible. That would mean low cellular senescence. Perhaps it’s not dangerous—maybe it even prolongs life—but this study doesn’t tell us. A pity.
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| Glucokinase – enzyme activating glucose molecules inside cells, Pyruvate Carboxylase – enzyme enabling new glucose synthesis during shortage, PGC-1α – main regulator of mitochondrial biogenesis and energy metabolism, TFAM – key protein maintaining mitochondrial DNA and enabling its reading and replication |
Taurine likely helps only under conditions of high protein and fat intake, when many amino acids are converted into glucose via pyruvate carboxylase. With reduced protein intake alongside high fat, taurine may not be needed. Does this mean that if we consume protein with fat, we actually need less protein? Could this be the important secret for a healthier, longer life? Conversely, could excess protein combined with taurine deficiency lead to diabetes? I’m speculating, but chronically high insulin levels are definitely harmful—they activate the UCP protein in the pancreas, which you don’t want, as I’ve already discussed here. At this point, we don’t have an answer. The fact that proteins naturally occur together with fats in many food sources could be a clue, although plant proteins often occur with carbohydrates. It almost seems that nature offers certain combinations that shouldn’t be disrupted or mixed, but I won’t speculate further.
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