So why do we age?

Aging – the deterioration of the body (soma) and diminished reproductive output over time – is a phenomenon that has puzzled evolutionary biologists for decades. Mechanistic causes show the how, through the soma wearing out from oxidative stress, cellular signalling breakdown etc., but assessing the why brings us to question the ultimate evolutionary causes for aging.

Taking a reductionist view, aging is just another evolvable trait, as lifespan is variable within a population, is genetically heritable from parent to offspring (heritability of 0.17~0.35 for humans) and is intimately linked to fitness; living longer gives you more time to reproduce.

But if aging reduces an individual’s fitness, why hasn’t natural selection eliminated the process?

An extremely valid question is that if evolution enables a climb to optimised fitness in a given environment, why haven’t species evolved towards immortality? A few carefully crafted evolutionary models have been proposed to explain this apparent biological paradox.

Mutation Accumulation (MA) Model:

This model states that early-onset mutations – diseases that affect children and young adults – are rapidly diminished from the population as they severely affect fitness and reproductive capacity. However, natural selection is blind to late-onset mutations (ie. dementia and Parkinson’s disease) in that their fitness decrease in later life doesn’t affect earlier reproductive success, and is unable to decrease their frequency in the population. MA model experiments tested the hypothesis that late-onset mutations were more frequent than early-onset, through creating inbred (homozygous) Drosophila lines – artificially accumulating mutations in the offspring – to determine their inbreeding depression (‘sickness’ or fitness of offspring as a proxy for deleterious mutation load) across a range of ages. The results confirmed that older flies had higher inbreeding depression.

Later, an extrapolation of the MA model was developed to take into account the idea that late-onset mutations may actually positively affect fitness early in life.

Antagonistic Pleiotropy (AP) Model:

This model dictates that deleterious late-onset mutations are more likely to accumulate in the population if they are beneficial in early life. Think of an allele that increases reproductive rate at the cost of somatic maintenance later in life. The difference from the MA model is instead of being passively maintained, mutations are actively selected for in the population by natural selection. A clinical example of this phenomenon arises in males that produce high levels of testosterone throughout life – this hormone increases sex drive and reproductive success in young men, but has been associated with an increased risk of prostate cancer in later life [1].

A subset of the AP model is the disposable soma (DS) model, which specifies that there is a finite resource allocation challenge between somatic maintenance vs. reproduction, which must be resolved in order to optimise fitness. Reproduction is energetically costly, as seen in the Tater experiment where seed beetles that were forcibly kept as virgins lived significantly longer lives than those that were given reproductive freedom.


[1] Gann P.H.; Hennekens C.H.; Ma J.; Longcope C.; Stampfer M.J. (1996). “Prospective Study of Sex Hormone Levels and Risk of Prostate Cancer”. Journal of the National Cancer Institute. 88 (16): 1118–1126. doi:10.1093/jnci/88.16.1118. PMID 8757191.

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