Mainly the Yang Qi substances in TCM such as Ginseng etc.
Because thereās a difference between systemic and localised mTORC1 regulation. When itās gone from the plasma it no longer has systemic effects. I wouldnāt worry about muscle stores of it counteracting rapa.
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We know from studies of mice with IGF-1 genes knocked out, that the less the better with it for longevity. However, stuff that upregulates IGF-1 also have beneficial effects. Stuff like fruit rich in polyphenols and stuff like creatine that aids muscle strength and possibly cognition. If we could get those benefits without upregulating IGF-1 itād be great, but we canāt.
EDIT: Well I guess we can get around it by ingesting polyphenols extracted from fruit. No way around it with amino acids though.
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Great discussion! Aging is an mTOR activator, but stuck in the āonā position:). mTOR has a duality of too much and too little. Balance and modulation seem to be a common theme, but as @Dr.Bart says we donāt know enough other than to make best educated guesses.
If IGF-1 was such a problem the evolution would have taken care of it by now. Just like m-tor, the IGF-1 needs some activation. Laboratory mice studies are not a good model for humans living in the real world, different species and totally different environment.
I disagree on this point. Evolution doesnāt care what happens with us after procreationā¦ if it shortens lifespan but allows you to grow faster when young, thats fine. I think its a classic case of antagonistic pleiotropy. What Is Antagonistic Pleiotropy? - PubMed.
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So you are saying that in a mature individual the IGF-1 serves no positive role?
They have IGF-1 receptor blockers for oncology treatmentā¦ pretty nasty side effects. I would say just like M-tor, some IGF activation is needed even in older individuals.
Well, there may be a positive roll, but the Laron Syndrome people live full lives and their lack of uptake of IGF1 āseems to protect them against cancer and diabetes and maybe even heart disease and Alzheimerāsā.
So it canāt be that large a benefit can it?
Paradoxically, classical studies have shown an association between GH/IGF1 deficiency and a number of age-related features ([50]Some of these traits include thinning of the skin, excess adiposity, reduced muscle mass, reduced physical performance, etc
We can state with a high degree of confidence that lifelong IGF1 deficiency in untreated LS patients does not appear to noticeably prolong their lifespan. On the contrary, if their cardiovascular and metabolic problems are not treated in time, their lifespan might be shortened. In conclusion and despite the absence of definite epidemiological substantiation on longevity in congenital IGF1 deficiencies, the pivotal role of the GH-IGF1 network in the control of lifespan, as described above, has been extensively documented in various animal models.
IGF-1 is clearly needed in child growth, but even in adulthood it seems that some activation is helpful. Usually taking extreme positions on biological processes is not the right answer.
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