Thread

1. rotbart · 1791018164 · focus · HN ↗

   The strongest evidence we have of the reversibility of epigenetic aging, as well as its limitations -- are embryos which undergo an epigenetic reset.

   After fertilisation, the embryo strips the father's DNA of its age-linked chemical tags and swaps its packaging, destroys his mitochondria, rebuilds telomeres, and clears damaged proteins, though it can't undo the DNA mutations sperm gather as men age.

   (those that result in an non viable embryo result in miscarriage.)

   1. jijijijij · 1791030973 · focus · HN ↗

      Embryogenesis is an early fail-fast process. The vast majority of mutations and instabilities are caught through developmental checkpoints. Every living human passed a ruthless selection process in the womb.

      So part of the magic of that aging reversal is simply abandoning what doesn't stick. You can't do that to a grown human, obviously.

      1. someonebaggy · 1791032000 · focus · HN ↗

         You can at the cellular level. There's a hypothesis that low levels of caloric restriction or oxidative stress are essential, because they weed out underperforming cells, which are replaced.

         1. jijijijij · 1791037243 · focus · HN ↗

            This is not at all comparable to the extent of embryonic rejuvenation. Lol.

            Caloric restriction etc. just aids cellular housekeeping. The processes in maintaining gametic immortality are much more radical and transformative. Somatic and gametic genetics are governed completely differently.

            1. agumonkey · 1791043442 · focus · HN ↗

               Do you have books or articles to read about this ?

               1. rsync · 1791056493 · focus · HN ↗

                  I think the Nick Lane books are quite good - especially:

                  <a href="https:&#x2F;&#x2F;en.wikipedia.org&#x2F;wiki&#x2F;Power,_Sex,_Suicide" rel="nofollow">https:&#x2F;&#x2F;en.wikipedia.org&#x2F;wiki&#x2F;Power,_Sex,_Suicide

                  which, IIRC, discussed the notion of an semi-autonomous population of mitochondria in long lived tissues (like muscle) which could be curated over ones lifetime by high intensity exercise stress. Future mitochondria in these long-lived tissues would then not be descended from the poorer performing members who were weeded out through apoptosis.

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