Evolution of Aging
The hallmark of biological aging is the loss of molecular fidelity and hence loss of physiological capacity. The classical evolutionary theory of aging states that given high hazard ecologies, one would expect strong selection pressures for rapid development, comparatively large numbers of progeny and comparatively short life spans. Given a relaxation of these selection pressures it becomes advantageous for overall reproductive fitness and longer lifespan can be expected to emerge because higher reproductive fitness is associated with enhanced mechanisms for the maintenance of the soma. According to this theory all senescent phenotypes are considered to be non-adaptive and stochastic. Evolution has not selected genes to minimize or maximize longevity. Indirectly, longevity determinants are present in the genome in order to ensure the reproductive fitness of the organism.
Gerontogenes
Most of the genes that have influence on longevity have well-defined roles in normal metabolism, in intra- and intercellular signaling, and in maintenance and repair functions including stress response. It is the damage-induced changes in the regulation, structure, and/or activity of their gene products that result in their altered biological role with age. The inefficiency and failure of maintenance, repair, and turnover pathways are the main causes of age-related accumulation of damage. This failure results in an increased vulnerability to age-related diseases, including cancer. It has been proposed that replicative senescence is a last-ditch protective mechanism against cancer. But this hypothesis fails because replicative senescence is far older than cancer. Many invertebrates experience replicative senescence, though they never die of cancer. Even one-celled organisms count replications, and will die if they do not replenish their telomeres with conjugation (sex).
Inspired by Suresh I. S. Rattan and George M. Martin