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.)

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

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.

destroys his mitochondria Fine print: only the father’s. Maternal mitochondria from the egg are dormant at first and activated after 10 (?) cell divisions. Those mitochondria are never reset, and return to dormant state as soon as specialization into egg cells allows them, afaik.

Notwithstanding heteroplasmic (paternal) mitochondria making it into the cell in 8% of cases, with unknown effects.

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

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.

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

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