Why do living things age?

No gene is thought to exist for the purpose of causing decline and death. The Max Planck Institute for Biology of Ageing describes ageing as having evolved not because it is beneficial but as a side effect of something else. Damage accumulates in cells and tissues, and evolution has not fully prevented it. Why evolution has not done so is where the theories differ. [1]

Ageing is the progressive loss of physiological functions that increases the probability of death, according to [bio.libretexts.org](https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Biology_(Kimball)/13%3A_Aging/13.01%3A_Aging). Evolutionary biologists define it as a decline in a component of fitness at increasing age. Senescence is a nearly universal feature of multicellular organisms, as noted by [annualreviews.org](https://www.annualreviews.org/content/journals/10.1146/annurev.ento.50.071803.130409). [2] [3] [4]

Lifespans range from hours in mayflies to around five hundred years in Icelandic mussels. Sea anemones and Hydra do not appear to age, and the Greenland shark may live up to 400 years. Some animals, such as the Pacific giant octopus, die soon after reproducing. As [age.mpg.de](https://www.age.mpg.de/why-do-we-age) puts it, what determines these differences is much less understood. [1]

Peter Medawar's mutation accumulation theory of 1952 holds that natural selection is strong until first reproduction and then declines. Harmful mutations that act late in life escape selection, an effect called the selection shadow. In a related argument, individuals die from causes unrelated to age, so fewer reach old age for selection to act on. [1] [3]

George Williams's antagonistic pleiotropy theory of 1957 adds that selection can favour gene variants that help early in life even if they harm later, because the harm falls after reproduction. Both theories predict that animals facing high external hazards evolve shorter lives, while those that avoid danger, such as flying birds and bats, tend to live longer. [1]

A 2025 review sorts explanations into three groups. Mechanistic theories, such as oxidative damage from free radicals (Harman, 1956) and the older rate-of-living idea, focus on how damage occurs and leave evolution out. Weakening-force-of-selection theories, such as Medawar's, say selection cannot prevent ageing. The NCBI Bookshelf also describes a metabolic view in which about 2 to 3 percent of oxygen taken up by mitochondria forms reactive oxygen species. [3] [5]

The third group, optimisation theories, holds that selection actively favours ageing. Because energy and resources are finite, the fitness-maximising balance may invest too little in survival to prevent ageing. Kirkwood's disposable soma theory is the main example. The review's authors argue that only this group fits all the observed data, including caloric restriction results, mortality plateaus and long-lived eusocial insect queens. They also predict that lifespan-extending mutations usually reduce fitness in natural conditions. This is a position argued in one review. The Max Planck account presents the side-effect view as the conclusion drawn from the Medawar and Williams theories, so the sources do not agree on a single framing. [3] [1]