I noted a review paper a few months back that considered the proximal cause of aging in terms of the evolution of cellular damage versus damage repair mechanisms. That aging is caused by an accumulation of certain forms of molecular and cellular damage is the dominant paradigm at present, though there is always debate over which forms of damage are primary, which secondary, and which important over a human life span. Of those researchers who aim to intervene in aging, most look to merely slow down the pace of damage by manipulating metabolism, while a minority follow the Strategies for Engineered Negligible Senescence (SENS) plan and aim to repair and reverse the damage without changing our metabolism.
Meanwhile, off in left field there are those who theorize that aging is an evolved program, and therefore could be halted or reversed by suitable changes to metabolism or the genes governing it. To their eyes damage doesn't cause aging, it is a result of the program. This is something of a dangerous viewpoint, should it gather steam, even worse than the "slow aging by metabolic manipulation" camp for steering researchers away from the most effective course for treating aging - which is the SENS approach of repairing damage. But it is a sign of just how complex aging is as a phenomenon that we can still see such widely divergent interpretations of the existing data.
Here is an open access consideration of the proximal cause of aging from one of the more prolific researchers in the programmed aging camp, by way of illustrating the points made above. You should probably read the whole thing, as the argument made is somewhat hard to excerpt and condense:
As discussed in detail previously, aging is of course not a program, but it is a quasi-program, a useless and unintentional continuation (or run on) of developmental programs. Similarly, cellular senescence is a continuation of cellular growth. In brief, over-stimulation leads to increased functions - [harmful hyperfunctions].
But what about the molecular damage? It was assumed that molecular damage contributes to aging because it accumulates with time. Well, over time you may accumulate money in your bank account. However, neither accumulation of molecular damage nor accumulation of money is a cause of your aging. Yes, molecular damage must accumulate. But although molecular damage accumulates, it does not necessarily limit lifespan, particularly if other causes limit life span. By analogy, if everyone died from accidents, starvation and infection early in life, then aging and age-related diseases (such as obesity and atherosclerosis) would not even be known. By the same token, "aging" due to molecular damage will not manifest itself, if aging due to hyperfunction invariably limits life span.
For complex organisms like mammals the relationships between hyperfunctions (aging), diseases and damage (decline) are:
1. Hyperfunctions (increased cellular functions) including hypertrophy are primary. This is the essence of aging, which silently causes malfunctions and age-related diseases.
2. Decline of functions, malfunctions and atrophy are secondary. For example, hyper-stimulation of beta-cells by nutrients and mitogens can cause its apoptosis. Here is important to emphasize however that apoptosis can be also a form of hyperfunction, unneeded continuation primary function such as apoptosis during development of the immune system.
3. Damage is caused by aging, not the reverse.
4. Damage is not molecular. It is macro-damage (tissue, system and organ damage), like stroke, infarction, metastases, broken hip fracture and renal failure. Damage may take a form of sudden "catastrophe", even though hyperfunctional aging slowly generates diseases for decades. If a patient survives infarction (due to medical intervention), she can live for many years, reflecting the fact that catastrophe was not due to the burden of molecular damage.