Why do we age?
To date, no matter what one's ideologies, wealth, or status, an inescapable scythe has awaited each and every one. This includes those who have taken the best possible care of themselves, those subscribing to one of a myriad of asinine health schemes purporting to bestow immortality or super-long life, and those identified as having the strongest genetic influences for longevity. There is no elixer of life. There is no light at the end of the tunnel. There is, at present, nothing at all that exists to slow or stop the gradual unravelling of the fabric of life that is manifest in senescence and death. To plan a route to change this scenario, it is extremely prudent to first understand the processes that we might undertake to change. This beckons the simple question "why do the processes of aging, senescence, and death happen at all?"
It turns out senescence and aging haven't been around since the origin of life. Our ancient ancestors were immortal; their demise could be claimed only by accident, and not by internal limitations that manifest our mortality. Somewhere upon the tree of evolution, natural selection favored mutations leading to a division of labor in these multicellular ancestors, such that one set of cells functioned to create progeny and another to support these cells. The support cells have been dubbed "somatic cells" or the "soma", and the reproductive cells "germ cells" or the "germline." In this seemingly simple event, aging and senescence first became manifest. The distinction between the soma and germline allowed evolutionary proccesses to favor investing more energy in the germline at the expense of the soma. When the germline continually divided, gave rise to progeny, and enjoyed more efficacious molecular mechanisms for cellular repair, the soma likely divided less, used less energy, and eventually died due to its sacrifice of energy to the germline. The first distinct collection of mortal somatic cells defined part of the first aging organism. And as our ancestor with a competitive edge against those organisms that were immortal, it has left us with its evolutionary baggage of mortality. It might be worth emphasizing that this evolution of mortality was for the most part a pretty positive thing. The allocation of more energy to the germline allows us to reproduce more effectively, copying DNA to our children with more accuracy and with a lower frequency of lethal genetic abberations. It also allows us to reproduce longer, the germline maintaining its integrity for longer periods of time to have healthier children for a longer period of time. From this perspective, having the somatic cells that protect the germline periodically replaced is a small price to pay for the evolutionary advantages that together sum to drastically increased fitness.
How different is the investment in energy between the soma and the germline, and how does this relate to why people age and senesce when they do? To answer this one has to take into account how far the reach of natural selection extends. For the most part, natural selection cannot act past sexual maturity. If someone carries a genome that predisposes them to Alzheimer's disease in their thirties, they will not be at any serious disadvantage in the gene pool; this individual can effectively have just as many children as someone without this predisposition. In the same way, if there is a significant amount of cellular damage that accumulates after sexual maturity, there is no way for natural selection to evolve mechanisms to combat this damage unless this in turn bestows a reproductive advantage. If one assumes that, with age, more and more energy is necessitated to stay alive (eg. to combat accumulated damage or implement costly redundancy in cellular maintainance mechanisms that fail with time), then there comes a point where it is more efficient to spend energy on reproduction rather than maintenance of the soma. The age at which we today age and senesce reflects this equilibrium in our recent ancestors' environments. Natural selection has therefore not favored somatic immortality because mutations that move toward this state have, as a trade-off with a limited amount of energy, compromised energy investment in the germline and resulted in these organisms being less fit. The soma is therefore essentially "disposable," in the sense that it is invested in only to the extent that this investment is returned via giving the germline advantages. This is the basis behind Kirkwood's disposable soma theory.
Thus, we possess insufficient mechanisms to maintain ourselves forever because evolving such mechanisms would compromise our ability to compete in the gene pool (mortal individuals would have more successful children than immortal individuals). The disposable soma serves as a ship that a stronger, more-competetive germline sails on. Aging is therefore an evolutionary side effect of our efficient and successful genes.
Having defined the origins of senescence and aging, many evolutionary biologists and geneticists ask "given genetics influences longevity, which specific genetic mechanisms are responsible for aging and senescence?" No such mechanisms exist! It is rather the lack of mechanisms to maintain our lives and keep at bay these processes that leads to the phenotypes of aging and senescence. If any genes spontaneously evolved to specifically induce aging, they would *never* last in the genepool. They would immediately be outcompeted by organisms that lived longer and could have more progeny. Despite the simplicitly of this concept, the misconception that aging and senescence are genetically pre-programmed is sadly rampant in many high-profile research labs. Such labs attempt to circumvent such non-existent "aging genes" in order to extend the lifespan of organisms. While this research has been intruiging with regard to illuminating a number of interesting genetic pathways, it is no effective way to develop therapeutic interventions for human aging and senescence.
What theoretical mechanisms *would* attenuate and abrogate the processes leading to the manifestation of aging and senescence? Unfortunately, this question cannot at present be properly addressed because the causative processes are unknown. Elucidation of the causative mechanisms will lay the foundation for developing methods to combat them, and this is requisite for an organized approach to acheiving bona-fide life extension.