In the article, Rose critically evaluates several of the assumptions underlyingSENS(Strategies for Engineered Negligible Senescence) as formulated by anti-aging activistAubrey de Grey, placing them in the context of demographic and population-biological observations. Ultimately, Rose concludes that life-extension therapeutics must address the issue of age-specific adaptation in order to be effective (link; emphasis below is mine):
Making SENSE: Strategies for Engineering Negligible Senescence Evolutionarily
Thirty years ago, in 1977, few biologists thought that it would be possible to increase the maximum life span characteristic of each species over the variety of environmental conditions in which they live, whether in nature or in the laboratory. But the evolutionary theory of aging suggested otherwise. Accordingly, experiments were performed with fruit flies, Drosophila melanogaster, which showed that manipulation of the forces of natural selection over a number of generations could substantially slow the rate of aging, both demographically and physiologically. After this first transgression of the supposedly absolute limits to life extension, it was suggested that mammals too could be experimentally evolved to have greater life spans and slower aging. And further, it was argued that such postponed-aging mammals could be used to reverse-engineer a slowing of human aging.The subsequent discovery and theoretical explanation of mortality-rate plateaus revealed that aging was not due to the progressive physiological accumulation of damage. Instead, aging is now understood by evolutionary biologists to arise from a transient fall in age-specific adaptation, a fall that does not necessarily proceed toward ineluctable death. This implies that SENS must be based on re-tuning adaptation, not repairing damage.As evolutionary manipulation of model organisms shows us how adaptation can be focused on engineering negligible senescence, there are thus both scientific and practical reasons for making SENS evolutionary; that is making SENSE.
In the evolutionary view, increasing risk of mortality is the consequence of a failure to adapt to the selection-pressure landscape specific to a particular age; because post-reproductive lifespan is largely (butnot always) masked from selection, it is easy to see how such age-specific failures of adaptation might occur. The “mortality plateaus” to which the author refers are life-history periods of constant, rather than increasing, mortality risk. Rose argues that the existence of these plateaus in the survival curves of many species imply that accumulation of irreparable damage is — at the very least — not the whole cause of aging. Therefore, the argument goes, reversing this damage cannot be sufficient to prevent or reverse aging as such.
Point of clarification, since I suspect that some confusion will arise: The point of the “E” in Rose’s “SENSE” is not that we must rely on evolutionary timescales in order to extend longevity, or that slow incremental change is our best hope. Rather, Rose’s point is that successful lifespan extension must include countermeasures against the molecular, cellular and systems-level mechanisms that explain and determine age-specific decreases in fitness (or, conversely, exploit the mechanisms that result in mortality plateaus). In the final analysis, the paper does not argue against the importance of accumulated damage so much as its exclusive primacy in the cause (and, therefore, remedy) of aging.