There are papers showing senescent cells in humans with signs of shortened telomeres and replicative stress (e.g. [1,2]), so I wouldn’t say the Hayflick limit is nonsense or irrelevant in humans. But there is perhaps a broader point that the Hayflick limit / telomere erosion has been over-hyped as the fundamental driver of ageing. Case in point, I once talked to a guy who told me “Immortality is impossible, because: telomeres”.
The problem is that telomere erosion tells a simple and compelling story about what ageing is, like every cell has a built-in clock that prevents us living too long. From skimming the article, the point Ray Peat seems to be making, in a rather snarky and conspiratorial way, is that it’s much more complicated than that, which is true. The point I’m making in this post is that there is no primary mechanism or process which is or causes ageing. Ageing is driven by a multitude of unavoidable cellular and molecular changes, but the list is finite, and fixing it is a tractable engineering problem.
Ray Peat claims the Hayflick limit is nonsense, but… It’s Ray Peat, so apply salt. http://raypeat.com/articles/articles/stemcells.shtml
There are papers showing senescent cells in humans with signs of shortened telomeres and replicative stress (e.g. [1,2]), so I wouldn’t say the Hayflick limit is nonsense or irrelevant in humans. But there is perhaps a broader point that the Hayflick limit / telomere erosion has been over-hyped as the fundamental driver of ageing. Case in point, I once talked to a guy who told me “Immortality is impossible, because: telomeres”.
The problem is that telomere erosion tells a simple and compelling story about what ageing is, like every cell has a built-in clock that prevents us living too long. From skimming the article, the point Ray Peat seems to be making, in a rather snarky and conspiratorial way, is that it’s much more complicated than that, which is true. The point I’m making in this post is that there is no primary mechanism or process which is or causes ageing. Ageing is driven by a multitude of unavoidable cellular and molecular changes, but the list is finite, and fixing it is a tractable engineering problem.