(cross-posted from
Ouroboros: Research in the biology of aging) 
Prominent biogerontologist and evolutionary biologist Michael Rose
(recently named the
chief scientific officer of the Biogerontology Research Foundation)
has reviewed the decades-old interplay between evolutionary
theories of aging and efforts to extend animal lifespans.
In the article, Rose critically evaluates several of the
assumptions underlying
SENS (Strategies for Engineered Negligible Senescence)
as formulated by anti-aging activist Aubrey 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.
(cont.)
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 (but not 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.
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