Youㅤ
seriousmaxxing , only talk serious
- Joined
- Oct 16, 2023
- Posts
- 3,722
- Reputation
- 4,454
@autistic_tendencies thoughts ?i concede on saying ur perspective is the same as SENS
yes , they do believe damage can be slowed modestly but they discourage this approach without their damage repair technology .
the fundamental program for ageing IMO is the telomeres . single celled eukaryotes called paramecium can reproduce sexually and asexually . but asexually their telomeres shorten , and thus they have limited divisions they can make without finding a mate to sex and restore the offspring's telomeres . therefore paramecium that only reproduce asexually will die out .
i am speculateing that telomeric ageing evolved when single cells were given the option to reproduce sexually . u can think of the human body of a very large clump of human cells in symbiosis divideing (akin to asexual reproduction) with the goal of sexual reproduction , because the telomeres shorten with divisions .
telomeric ageing is IMO the most primitive aspect of programmed ageing , but in animals the program is much more complex . gene expression changes with age , part of this is programmed (self destructive) and part of this is adaptive ; the body is at war with itself until it dies . i dont believe this is an accident but it was beneficial for evolution .
ur say that ageing is programmed in shorter lived species . this is definitely true , a mouse clearly is programmed to not live long , its not some accident , there no real benefit for antagonistic pleiotropy alone to cause this .
u brought up greenland shark as a neglible senescence animal . well , first of all , ill mention their body temperature is around 1 degree celsius (extreeeemly cold) , which could be important mechanistically . but my main point is that their ancestors have probably had extreme longevity since ancient times (i did not check this yet) . well what were *our* ancestors ? the answer is monkeys , a short lived species . so if ageing is programmed for short lived species due to evolutionary pressure , then i would say that we have been evolveing to resist and undo this program since our livespan has been increaseing , but human lifespan is very recent in evolution unlike (presumeably) greenland sharks . so maybe we arent benefited much by the program of ageing , but our ancestors were . and the selection shadow and antagonistic pleiotropic genes would make the trend toward longevity a slow one (although it seems to have been gradually lengthening) .
so we still do have a program for ageing . the telomere shortening limits our lifespan at a predicted age of 125 years . well , certain damages can also shorten telomeres , and we can mitigate this to prevent accelerated ageing , but replicative senesensce can only be slowed by slowing cell division . i think we have a program for ageing because , as u yourself said , shorter lived species do , and i think at best this ancient program has a lingering effect in us today , and at worse there is still pressure to age in modern humans . but if u look at what happens during ageing , it is hard not to conclude that the body seems to *destroy itself* with age , people think of these destructive processes as dysfunctions but these "dysfunctions" seem to be deliberately hostile IMO . damage accumulation is accelerated in many lethal ways and endogenous antioxidants dangerously fall . also , take DNA methylation , DNA methylation is said to function as a way of gene expression control for organisms to "adapt" during their lifespan . if this is so , then reverseing DNAm age would *hasten* death . and now some aspects do seem to be adaptive to age but others not . it could still be reasoned that these harmful DNAm changes are dysfunctions , but i disagree . i find it interesting that OSKM expression can de-age cells , but too much OSKM expression and the cell is an induced pluripotent stem cell . this shows that DNAm ageing and developmental DNAm are connected . and development is a program . FSH and LH increase in specific times in development to modulate development . they also increase multi-fold in midlife during the time of female menopause (in both men and women) . this suspiciously seems like part of the ageing/death program . in salmon , the fish die shortly after reproduction and coincidently get a massive surge of of FSH increased by 4500% .
well i do think u may be onto something . there are things that can induce telomerase in somatic cells to lengthen telomeres (currently nothing proven to lengthen telomeres even close to enough to counter shortening) . telomere shortening IMO is the most ancient program for ageing , and we have the genes to lengthen them (obv all animals lengthen the germline cells , suspicious how they shut off telomerase in somatic cells . the cancer trade off perspective is weak IMO , and actually short telomeres are damageing to DNA and can induce cancer . also , i dont believe in trade offs as biological limits , but they are just lazy evolution when there is insuffienct evolutionary pressure )
sounds like ur describeing hormesis . well , i assure u that the majority of the damage that accumulates with age comes from metabolic processes essential to basic normal human functioning . it is perplexing , the phenomenon how increased damage can lead to overcompensation in stress resistance .
