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What to make of this paper on BCAAs=>longevity?


Alex K Chen

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First, as I've posted many times before, one should ignore studies on interventions in aging in C. elegans, Drosophila, and all other non-mammalian species: they age and anti-age too differently to be given any credence until at least translated into mice.

 

In this particular case, it happens that they find that the key effect of BCAAs on lifespan in C. elegans is mediated via their activation of neuronal mTOR, such that it is reduced when combined with rapamycin administration (even tho' they confirm, for the upteenth time, that rapa increases lifespan when administered alone), and is in fact abolished when combined with selective neuronal RNA interference of the C. elegans mTOR homolog let-363.

 

The thing is, the most important Bad Thing that mTOR does in the mammalian periphery is contribute to cancer — but C. elegans' mature bodies are composed entirely of cells that don't divide, so they don't develop cancer.

 

Unless and until you have a foolproof way to prevent cancer, IOW, this finding is of zero relevance to aging and lifespan in mammals (including avoidance of BCAAs, particularly leucine (see this and this for more recent studies on health effects of high intake of leucine; we were discussing this study and this one)). And, of course, even then you'd want to first see a mammalian confirmation of the benefit of selective central mTOR activation in these roundworms.

 

It's risky to bet the course of your aging on rodent research; letting studies in flies and worms sway your praxis is beyond foolhardy.

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