Can Evolution Explain Why We Age and Die?

The Mutation Accumulation Hypothesis and The Antagonistic Pleiotropy Hypothesis

Jackie Badilla
Jan 9 · 6 min read
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Photo by Tristan Le on Pexels

verybody ages, and everybody dies. It’s a certainty that we’ve accepted as a fact of life. If something doesn’t take me out earlier in life, I’ll eventually start noticing wrinkles in my skin, my hair will begin to turn grey, my muscles and joints may ache, and my heart may stop working like it used to. No magic elixir or perfect lifestyle can outsmart aging.

But have you ever wondered why our bodies start deteriorating as if automatically programmed? Has aging always been inevitable?

As Peter Godfrey-Smith ponders in Other Minds: The Octopus, the Sea, and the Deep Origins of Consciousness, aging and death don’t naturally make sense. If our cells are continually renewed and replaced, why do our bodies suddenly start breaking down as if on command? If our ‘parts’ are always being updated, are we not machines that could theoretically function indefinitely?

Biologist Peter Medawar had a similar question:

“Natural selection designs organisms for optimal survival and reproductive success, so why does evolution not prevent aging in the first place?”

Fabian & Flatt, 2011

Medawar’s Logic

Fabian and Flatt’s article, “The Evolution of Aging,” provides an insightful description of Medawar’s theory of aging and death. His hypothesis is built around two arguments:

  1. The natural world is dangerous and competitive, so most organisms will die from circumstantial or environmental causes such as predation, accidents, or disease before they have a chance to achieve advanced age. Consequently, most individuals will reproduce at a younger age, with fewer reproductive opportunities later in life for a species overall.
  2. Natural selection cannot effectively influence gene mutations expressed during advanced ages because carriers will most likely have already reproduced earlier in life. Similarly, invisible mutations may never have an opportunity to be expressed as long as mortality rates remain high due to environmental factors.

The Mutation Accumulation Hypothesis

Following this logic, Medawar constructed his Mutation Acculumation Hypothesis.

A human’s life expectancy is now long enough for advanced age mutations to express themselves. Before humans reached this point of longevity, mutations that only expressed adverse effects later in life were able to accumulate. These mutations essentially bypassed natural selection because carriers would reproduce and mutate genes before their effects ever presented themselves.

As Fabian and Flatt state,

The effects of such a mutation accumulation process would only become manifest at the organismal level after the environment changes such that individuals experience less extrinsic mortality (e.g., due to decreased predation) and thus live to an age where they actually express the symptoms of aging.

Their argument affirms that natural selection‘s effectiveness decreases with age. Genes that express in earlier stages in life don’t have the same advantage as those that remain neutral until older age. If the harmful effects of a genetic mutation become visible before or during optimal reproductive stages of an individual, the carrier will be less likely to pass on the gene to future generations.

Williams’s Antagonistic Pleiotropoy Hypothesis

George Williams, an evolutionary biologist, found an interesting implication of Medawar’s theory. He speculates that there may be a trade-off between selecting for early fitness and reproductive success versus longevity.

His argument is based on the assumption that the genetic mutations associated with aging and natural death have pleiotropic effects. According to Fabian and Flatt, pleiotropic genes affect multiple traits. In Williams’s theory, certain genetic mutations would be antagonistically pleiotropic — beneficial early in life and detrimental at old age — making them advantageous during reproductive stages when natural selection is most decisive.

If this were the case, mutations that supported fitness and allowed for reproductive success would accumulate in a population regardless of effects later in life. Consequently, a genetic trade-off would ensue in which early success compromises survival at old age.

Take a look at trees.

Trees demonstrate the existence of genetic and evolutionary-tradeoffs associated with natural selection. A 2008 study on North American trees illustrates how and why stunted, slow-growing trees are among the oldest tree species. In species that dwell in harsh environmental conditions prone to inevitable catastrophic disturbances, evolved traits that promote early success, such as rapid growth rates and early sexual maturity, offset decreased longevity.

On the other hand, species in stable environments can account for more predictable disturbances by investing in defense mechanisms. Long-term defense mechanisms such as high-wood density are costly and ultimately exchange slow-growth rates and limited juvenile success for impressive lifespans.

The trade-off mechanism in pleiotropic genes versus natural selection in trees is notably different. There are several reasons why a species may exhibit extreme growth rates, reproductive success, or lifespans. It is clear that in the case of trees, environmental factors are to blame rather than spatiotemporal gene expression for trade-offs in early success versus above-average lifespans.

Could this mean that truly immortal organisms could exist?

Even with perfect environmental conditions, zero predation, and no disease, probably not.

Bacteria were once believed to not age due to unclear distinctions between germline and soma and a lack of delineated age classes. Not only have studies found that bacteria do age, but deterioration is age-related and theorized to be an evolutionary inevitability.

In “On the Evolutionary Origin of Aging,” Ackermann et al. argue that aging is actually more fundamental than we may think.

The first unicellular organisms needed aging to survive. This is because there was no distinction between an aging parent and the rejuvenated offspring. Any deterioration would be passed down to all individuals within a lineage, causing simultaneous extinction.

To put this into perspective, if there was no distinction between germline and soma cells in us, passing on genes wouldn’t be confined to the DNA in eggs and sperm. Instead, mutations or damage in a somatic cell, such as cancer in a liver cell, would be passed onto offspring. Luckily (or unfortunately, depending on your perspective), somatic mutations die with the cell and only germline mutations, which occur in gametes, can be inherited through sexual reproduction.

Evolving asymmetric damage distribution and rejuvenating reproduction in unicellular organisms was a less costly alternative to repairing the damage. It also meant that cell division would always produce at least one cell with little to no damage.

The outcome? An individual that ages and survives across generations to produce rejuvenated offspring. Lifespans are shortened, but opportunities for reproductive events during one’s lifetime are increased.

You could scour the internet and find a number of different theories regarding why we age and die. The ideas I’ve presented here are just a drop in the bucket of whys, whens, and hows.

The evolution of aging appears inevitable and necessary and would probably re-emerge if somehow eradicated. It exists for a purpose, and immortality likely has consequences that are hard to predict but desirably avoidable. Evolution aside, the possibility of immortality raises ethical and philosophical questions about why we die and what exists after death.

If you could live forever, would you?


Ackermann, M., Chao, L., Bergstrom, C. T., & Doebeli, M. (2007). On the Evolutionary Origin of Aging. Aging Cell, 6(2), 235–244.–9726.2007.00281.x

Black, B. A., Colbert, J. J., & Pederson, N. (2008). Relationships between Radial Growth Rates and Lifespan within North American Tree Species. Ecoscience, 15(3), 349–357.–3–3149

Fabian, D. & Flatt, T. (2011) The Evolution of Aging. Nature Education Knowledge 3(10), 9.

Godfrey-Smith, P. (2016). Other Minds: The Octopus, The Sea, and the Deep Origins of Consciousness. Farrar, Straus, and Giroux.

Mayne, B., Berry, O., Davies, C., Farley, J., & Jarman, S. (2019). A Genomic Predictor of Lifespan in Vertebrates. Scientific Reports, 9.

Ritchie, H., & Roser, M. (2019). Causes of Death. Our World in Data.


We curate outstanding articles from diverse domains and…

Jackie Badilla

Written by

I write about relationships: with ourselves, with others, and with the planet.


We curate and disseminate outstanding articles from diverse domains and disciplines to create fusion and synergy.

Jackie Badilla

Written by

I write about relationships: with ourselves, with others, and with the planet.


We curate and disseminate outstanding articles from diverse domains and disciplines to create fusion and synergy.

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