In the 65 years since Clive M. McKay of Cornell University first noticed that the regimen doubled the life span of his lab rats, and in the decade or so since calorie restriction moved from the fringes of longevity research to the mainstream, much of the laboratory work has been aimed at discerning the fundamental biology underlying the beneficial effects. What researchers generally agree on is that the response to calorie restriction in organisms seems to be an evolutionary adaptation to periods of scarcity. That would keep the organisms alive long enough to find food, and at that point they could go back to reproducing and to a normal aging process, which is exactly what happens in the laboratory. The question of how this might work is still open. The leading hypothesis is that calorie restriction reduces the amount of oxidative damage to the body.
Oxidative damage is the foremost theory as to what causes the deterioration that comes with age.
The electrons are then captured by oxygen atoms, which join with hydrogen to form water. But the process is inefficient, and the electrons often go astray, resulting in the formation of highly reactive molecules known as free radicals. The oxidation that occurs in the human body is identical to the way in which rust is formed in metals, so it is not unreasonable to say that we will all eventually rust to death if given the opportunity. The free radicals damage the tissues but also seem to damage the genetic material, the DNA, that codes for the proteins required for the body's physiological functions. The primary candidate for most of this damage is the mitochondria themselves, which are not spared by the free radicals they produce.