Genetics: Longevity Assurance

In the 1970s the prevailing view was that aging was the end point of a developmental program that served to remove older individuals from the population. This prompted a search for so-called death genes that dictated the aging process. However, today most scientists believe that there is no selection for aging and that aging is merely a by-product of natural selection. This new paradigm raises a question: If aging provides no selective advantage, how did longevity genes evolve? The answer lies in the distinction between aging and longevity. Although aging is generally believed to be an essentially random process, longevity is evolutionarily adaptive.

This idea was first formulated in the disposable soma theory (Kirkwood and Holliday, 1979), which is based on the premise that all biological activities come at a price. If an organism devotes resources to one activity, those resources are no longer available for other activities. Due to the competing priorities of reproduction, organisms can not afford to allocate the necessary amount of resources to body (i.e., somatic) maintenance to ensure indefinite survival. It follows that a species with a relatively high probability of being killed by extrinsic forces (e.g., starvation, disease, predation, and accidents) will have evolved to invest heavily in reproduction, so that its members develop rapidly and reproduce at a young age (Kirkwood et al., 2000).

Striking the optimum balance between reproduction and survival is as important for species as it is for individuals. During an individual's lifetime the environment is likely to change and, along with it, the optimal balance between reproduction and somatic maintenance. The majority of longevity genes appear to have evolved to boost somatic maintenance during harsh times and to increase growth and reproduction during good times.

An important corollary of the disposable soma theory is that the causes of aging should be primarily species-specific (i.e., private), whereas longevity assurance mechanisms should be evolutionarily conserved (i.e., public). This prediction has been supported by abundant experimental evidence. For example, a major cause of aging in baker's yeast is the accumulation of circular DNA molecules. In contrast, aging in nematode worms is apparently due to the accumulation of cellular damage caused by reactive oxygen species. Despite their having obviously different aging mechanisms, researchers have recently identified at least two public longevity genes that function in both organisms, SIR2/ sir2-1 and SCH9/akt-1 (Kenyon, 2001). Such findings highlight the potential for experimental organisms to provide clues about human longevity, even if their causes of aging are seemingly unrelated.