Evolutionary theory explains why we don't live forever, and provides a reasonable explanation for the huge variation in lifespan between (often closely related) species.

The geneticist J. B. S. Haldane wondered why the dominant mutation which causes Huntington's disease remained in the population, why natural selection had not eliminated it. The onset of this neurological disease is (on average) at age 35 and is invariably fatal within 10-20 years. Haldane assumed, probably reasonably, that in human prehistory, few survived until age 35. Since few were alive at older ages and their contribution to the next generation was therefore small relative to the large cohorts of younger age groups, the force of selection against such late-acting deleterious mutations was correspondingly small. If a mutation affected younger individuals, selection against it would be strong. Hence, late-acting deleterious mutations could accumulate in populations over evolutionary time through genetic drift. This principle has been proven correct.

Peter Medawar formalized this observation in his Mutation Accumulation theory of aging. “The force of natural selection weakens with increasing age - even in a theoretically immortal population, provided only that it is exposed to real hazards of mortality. If a genetic disaster... happens late enough in individual life, its consequences may be completely unimportant”. The 'real hazards of mortality' are typically predation, disease and accidents. So, even an immortal population, whose fertility does not decline with time, will have fewer individuals alive in older age groups. This is called 'extrinsic mortality'. Young age cohorts, not depleted in numbers yet by extrinsic mortality, contribute far more to the next generation than the few remaining in older age cohorts, so the force of selection against late-acting deleterious mutations, which only affect these few older individuals, is very weak.

The major testable prediction made by this model is that species which have high extrinsic mortality in nature will age more quickly and have shorter lifespans, and it is borne out among mammals, the most well studied in terms of life history. There is a correlation among mammals between body size and lifespan, such that larger species live longer than smaller species in controlled/optimum conditions, but there are notable exceptions. For instance, many bats and rodents are similarly sized, yet bats live much, much longer. For instance, the little brown bat, half the size of a mouse, can live 30 years in the wild. A mouse will live 2-3 years even with optimum conditions. The explanation is that bats have fewer predators, therefore low extrinsic mortality. Thus more individuals survive to later ages so the force of selection against late-acting deleterious mutations is stronger. Fewer late-acting deleterious mutations = slower aging = longer lifespan. Birds are also warm-blooded and similarly sized to many small mammals, yet live often 5-10 times as long. They clearly have fewer predation pressures compared with ground-dwelling mammals. And sea-birds, which generally have the fewest predators of all birds, live longest.

Also, when examining the body-size vs. lifespan relationship, predator mammals tend to have longer lifespans than prey animals in a controlled environment such as a zoo or nature reserve. The explanation for the long lifespans of primates (such as humans and monkeys and apes) relative to body size is that their intelligence and often sociality helps them avoid becoming prey.

Another evolutionary theory of aging was proposed by George C. Williams (Williams 1957) and involves antagonistic pleiotropy. A single gene may effect multiple traits. Some traits that increase fecundity early in life may also have negative effects later in life. Williams suggested the following example: perhaps a gene codes for calcium deposition in bones which promotes juvenile survival and will therefore be favored by natural selection; however this same gene promotes calcium deposition in the arteries, causing negative effects in old age. Therefore negative effects in old age may reflect the result of natural selection on pleiotropic genes early in life.

Ultimately, lifespan differences among species are due to genetics, but this does not explain the "how" question of aging.