Not to sound like a broken record, but the state of the mitochondria inside your cells is very important. The level of damaged suffered by these mitochondria is a determinant of your future health and longevity because of the further damaging processes set in motion by faulty mitochondria. Furthermore, we can point to some known ways to extend longevity - such as calorie restriction - and show that they cause changes in biochemical processes that act to eliminate damaged mitochondria before they cause significant harm or prevent that damage from occuring in the first place. As this recent abstract points out for one small facet of aging:
The mechanisms by which caloric restriction preserves skeletal muscle health with aging continue to be explored; however, mounting evidence points toward a convergence of effects at the level of the mitochondrion. Specifically, caloric restriction reduces mitochondrial reactive oxygen species production and promotes mitochondrial renewal via enhanced drive on mitochondrial biogenesis and autophagy.
The mitochondrial free radical theory of aging describes in detail how it is proposed that increasing numbers of damaged mitochondria lead to the slow breakdown of systems within the body. A crucial point here is that each of your cells contains thousands of mitochondria, a population constantly in flux with members being broken down when damaged and replaced through binary fission of remaining mitochondria, dividing in two like bacteria. Mitochondria have their own internal DNA, separate from nuclear DNA in your cells, and when that mitochondrial DNA gets damaged then every future generation of mitochondria carry the damage with them.
The core of the mitochondrial free radical theory of aging is an explanation as to how certain forms of mitochondrial DNA damage, such as large deletions, can subvert the normal processes that check for damaged mitochondria to recycle. These damaged mitochondria will be recycled more slowly than their pristine counterparts and will thus soon replicate unchecked to take over the entire mitochondrial population of a cell. Things start to go downhill for that cell and all other nearby cells soon thereafter as the mechanisms of metabolism run awry. Here is a paper providing solid evidence for that concept:
Age-dependent accumulation of partially-deleted mitochondrial DNA (DeltamtDNA) has been suggested to contribute to aging and the development of age-associated diseases including Parkinson's disease. However, the molecular mechanisms underlying the generation and accumulation of DeltamtDNA have not been addressed in vivo.
In this study [we] obtained in vivo evidence that DeltamtDNAs with larger deletions accumulate faster than those with smaller deletions, implying a replicative advantage of smaller mtDNAs. These findings identify DSB, DNA repair systems and replicative advantage as likely mechanisms underlying the generation and age-associated accumulation of DeltamtDNA.
More damage means more replication of damaged mitochondria. This isn't all idle research, of course: having identified damage to mitochondrial DNA as a significant contributer to degenerative aging, there are a wealth of potential ways to reverse or eliminate it through medical science, some already demonstrated in laboratory animals. Look back in the Fight Aging! archives to see some of them: