Loss of cell identity drives human aging: Two new papers

The two papers:

* https://www.nature.com/articles/s41586-026-10955-0

* https://www.cell.com/cell/abstract/S0092-8674(25)00853-0

These papers simply present the accumulated damage hypothesis with new window dressing. They do not account for the known facts.

The article about these papers does not present a mechanism that would account for the Hayflick Limit.

Nor does it explain why dogs, for example, age and die more quickly than humans. If there is a mechanism of epigenetic drift that would explain this, I do not see it in the article.

The obvious answer to senescence is that we are programmed to do it. Cells die when they are supposed to die; if they don't, we have a problem.

Likewise, mammals die when they are supposed to. It takes less time to train a puppy to survive on its own than it takes to train a human. Hence, dogs are optimized to age and die more quickly. It's better for the species.

If we were not programmed to get old and die, evolution through natural selection would not work. We would never adapt to changing environments and our species would fail.

Aging and death is not an accident or a deterioration from damage or a drift away from a correct instruction set. It is an absolute hard necessity, without which we would all be long gone.

Stop wasting your time on nonsense articles like this and seek the mechanism that provides us as a species with the flexibility to adapt. Until we see aging and death as an core mechanism, we're going to be looking in the wrong place.

No mention of new limit.

In fact there is very little talk about new limit. But what they are doing seems impressive and important.

So chronic stress is one of the main contributors to aging. I hope I make it to my 40s.

Do we currently have the ability to do targeted methylation or de methylation at sites in cells?

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.