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Evolution of Aging - Implications For Aging Research

age physiological genetic evolutionary life theory span

Evolutionary biologists have always been very generous with gerontologists in providing advice and guidance on how to do aging research "in directions that are likely to be fruitful" (Williams). Surprisingly, this generous intellectual assistance proved to be extremely injurious for aging studies in the past. This happened because evolutionary theory was interpreted in such a way that the search for single-gene mutations (or life-extending interventions) with very large positive effects on life span was considered a completely futile task, destined for failure for fundamental evolutionary reasons. Researchers were convinced by the forceful evolutionary arguments of George Williams that "natural selection will always be in greatest opposition to the decline of the most senescence-prone system" and, therefore, "senescence should always be a generalized deterioration, and never due largely to changes in a single system. . . . This conclusion banishes the fountain of youth to the limbo of scientific impossibilities where other human aspirations, like the perpetual motion machine and Laplace's 'superman' have already been placed by other theoretical considerations. Such conclusions are always disappointing, but they have the desirable consequence of channeling research in directions that are likely to be fruitful."

As a result of this triumphant evolutionary indoctrination, many exciting research opportunities for life span extension were squandered for a half a century, until the astonishing discovery of single-gene mutants with profoundly extended longevity was ultimately made (see Lin et al., 1997; 1998; Migliaccio et al.), despite all discouraging predictions and warnings based on evolutionary arguments.

Recent discoveries of life-span-extending mutations are spectacular. A single-gene mutation (daf-2) more than doubles the life span of nematodes, keeping them active, fully fertile (contrary to predictions of the disposable soma theory), and having normal metabolic rates. Another single-gene mutation, called methuselah, extends the average life span of fruit flies by about 35 percent, enhancing also their resistance to various forms of stress, including starvation, high temperature, and toxic chemicals. Finally, a single-gene mutation was found in mice, extending their life span by about 30 percent and also increasing their resistance to toxic chemicals. Researchers involved in these studies came to the following conclusion:

The field of ageing research has been completely transformed in the past decade. . . . When single genes are changed, animals that should be old stay young. In humans, these mutants would be analogous to a ninety year old who looks and feels forty-five. On this basis we begin to think of ageing as a disease that can be cured, or at least postponed. . . . The field of ageing is beginning to explode, because so many are so excited about the prospect of searching for—and finding—the causes of ageing, and maybe even the fountain of youth itself. (Guarente and Kenyon).

Now, when single-gene, life-extending mutations are found, evolutionary biologists are presented with the task of reconciling these new discoveries with the evolutionary theory of aging. They are certain to succeed in this task, however, as evolutionary theories of aging are very flexible and can be adjusted to almost any new finding.

However, gerontologists will also have to learn their lessons from the damage caused by decades of misguided research, when the search for major life-extending mutations and other life-extension interventions was equated by evolutionary biologists with the construction of a perpetual motion machine. Perhaps some leads for getting wisdom from this lesson can be found in the title of a recent scientific review on evolution of aging: "Evolutionary Theories of Aging: Handle With Care" (Le Bourg, 1998).



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