A viewpoint from Vladimir Skulachev, whose research group works on mitochondrially targeted antioxidant compounds: "'It is recognized that in exceptional circumstances the possibility exists for selection to favor limiting survival. In acknowledging that at least in theory, aging might occasionally be adaptive, however, the high barriers to validating actual instances of adaptive ageing are made clear' ... A few years ago it was hardly possible to find the latter statement in an article written by the most famous proponents of non-programmed aging. Certainly, this conclusion is accompanied by some reservations. Nevertheless, the balance between concepts of programmed and non-programmed aging seems to be really shifted to the programmed one. ... The idea that programmed death was invented by biological evolution was introduced in the end of nineteenth century by August Weismann, who suggested that such a death is useful for evolution as a mechanism which (i) purifies the population from weak individuals and (ii) promotes succession of generations. For sure, both these roles may be inherent in aging. However, they failed to explain why aging represents slow and concerted decline of many physiological functions (slow phenoptosis) rather than simple fast switching off of a single function of vital importance (acute phenoptosis). ... There is, it must be acknowledged, an instinctive attraction to the idea that aging is programmed. Aging is widespread across species and applies universally to all individuals within a species in which it is observed. There is also reproducibility about changes that occur with aging .... I may only add that, if aging is programmed, it can be retarded, prevented, and perhaps even reversed by treatments interrupting execution of this program, just as we already can interrupt programs of cell death. In other words, programmed aging can be cured like a disease. As for the concept of non-programmed aging, assuming occasional accumulation of stochastic injuries as its reason, it is quite pessimistic for finding any way of successful treatment. Here we simply observe and describe such a process without the possibility of improving the situation." This last viewpoint is exactly the wrong way around - repair of damage is likely to be far easier through SENS and similar programs than safely altering the exceedingly complex systems of metabolism to change the way in which aging happens. We should hope that genetic programs are of limited and narrow influence as a driver of aging - that they are merely reactions to underlying accumulations of damage where they exist at all. Because otherwise we're in for a long, slow road when it comes to extending healthy life.

Link: http://impactaging.com/papers/v3/n11/full/100403.html