Comment by Chance-Device
4 hours ago
I suspect that epigenetic aging is adaptive; a deliberately programmed sequence wherein genes more likely to contribute to age-related mortality are shut down progressively. This being in response to random genetic damage accumulating at a predictable rate.
What we think of as aging then becomes primarily the epigenetic response to the problem of DNA damage, much like the symptoms of a virus are mostly the result of the immune response rather than the virus’s direct effects.
There's a lot of indirect evidence for this from the fact that some naive attempts at stopping aging give you cancer, like turning telomerase on indiscriminately.
Almost everything in nature has multiple functions or causes, but one cause of aging is probably an evolutionary compromise between longevity and not getting cancer.
One option, I guess, would be turning the guard rails off and just getting incredibly good at treating cancer or inventing some extraneous cancer detection and killing mechanism.
It’s rarely such a simple tradeoff that only two things are being optimized. Modern humans live way longer than wolves for example despite being of similar body mass. However that’s fairly new in our evolutionary history as wild chimps for example cap our at ~63.
Cancer is extremely rare as a cause of death in wild animals. Again is more common but late enough that reproduction has produced multiple offspring.
Energy expenditure isn’t something we’re concerned with but drives a great deal of evolutionary optimization.
> one cause of aging is probably an evolutionary compromise between longevity and not getting cancer
Yes, and proteinopathies, and likely lots else besides. We probably don’t even understand the failure modes that aging protects against.
This assumes there are genes that:
a) contribute to age-related mortality, and
b) shutting down helps combat aging.
Can you state which genes these are that do that? Because I don't know of any.
Plus, many genes have pleiotropic effects. There is no specific aging gene.
On top of that, aging is a word that combines to many different factors. For instance, progeria was called accelerated aging. Well, turns out you have a mutation in lamin A. So, it is about cytoskeletal structure that is defect, rather than aging in itself. Of course the effects that this has, looks like an older person then, so it is related to aging. But one can not say it is "accelerated aging" as such. People having a normal lamin A allele still age nonetheless. So the whole term is problematic. And you can find many more such descriptions where xyz is about aging. Well, most of that it is about damage rather than aging. The Hayflick limit, though, is not about damage; that's just that cells fatigue for some reason when their telomeres shorten, but I have not yet read a sound explanations about why that is the case - after all there must be a mechanism in place.