While the general consensus in biogerontology circles appears to be that nuclear DNA damage contributes to degenerative aging, this is far from a settled claim. Here is a correlation that should add fuel to the fire: "The identification of the cellular mechanisms responsible for the wide differences in species lifespan remains one of the major unsolved problems of the biology of aging. We measured the capacity of nuclear protein to recognize DNA double strand breaks (DSB) and telomere length of skin fibroblasts derived from mammalian species that exhibit wide differences in longevity. Our results indicate DNA DSB recognition increases exponentially with longevity. Further, an analysis of the level of Ku80 protein [involved in DSB repair] in human, cow, and mouse suggests that Ku levels vary dramatically between species and these levels are strongly correlated with longevity. In contrast mean telomere length appears to decrease with increasing longevity of the species, although not significantly. These findings suggest that an enhanced ability to bind to DNA-ends [such as via the action of Ku80] may be important for longevity." In other words a better ability to repair double strand breaks in DNA correlates with species longevity. If you head over to the Fight Aging! archives for 2004 you'll find discussion of a theory of aging based on double strand breaks.