The author noted here sees aging as programmed, in the sense that it is an epigenetic program selected for by evolution because shorter life spans prevent population-level ecological issues. His writing is usually a good illustration of how this concept of aging as a selected epigenetic program leads to very different conclusions on the nature of aging as a whole, as well as on any specific research result. In the case of this post, the topic is the role of telomere length and telomerase in aging, and their relationship to the established DNA methylation biomarkers of aging.
The mainstream view of epigenetic change with age is that it is a reaction to accumulated cell and tissue damage, one that evolved in the limited selection pressure thought to characterize post-reproductive life span. Both damage and epigenetic changes are components of a decline that is an accidental outcome of the aggressive selection for success in early life. Evolution produces biological systems that do well initially, then corrode and fail in a haphazard fashion, because there was no selection for long-term function. Thus systems that generate damage as a side-effect of normal operation, and