Aging (senescence) is hard to reconcile as an evolutionary outcome of natural selection. Senescence (defined as a persistent decline in the survival probability or reproductive output of an individual because of internal physiological deterioration) was a longstanding evolutionary enigma. Why would natural selection have permitted a state of affairs in which genetic predispositions for aging and death appear to be almost universal to multicellular life?
senescence; selection; antagonistic pleiotropy
Aging (senescence) is hard to reconcile as an evolutionary outcome of natural selection. Senescence (defined as a persistent decline in the survival probability or reproductive output of an individual because of internal physiological deterioration) was a longstanding evolutionary enigma. Why would natural selection have permitted a state of affairs in which genetic predispositions for aging and death appear to be almost universal to multicellular life?
In 1952, the Nobel Prize-winning immunologist Peter Medawar wrote an essay that laid the conceptual foundation for solving this puzzle. Medawar noted that natural selection inevitably declines in force through successive age cohorts in any age-structured population of self-reproducing entities. For example, the strength of natural selection on genes in 80-year-old humans is inevitably less than the strength of selection on the same genes in teenagers because teenagers’ genes under any multi-generation scenario are destined on average to be survived by many more descendants than will those of 80-year-olds. Thus, senescence in any species is a feature that evolved as a logical consequence of the declining force of natural selection through successive age classes in a population. In effect, even a small advantage conferred early in life may outweigh a catastrophic disadvantage withheld until later, such that natural selection can be said to be biased in favor of youth whenever a conflict of interest arises.
Medawar’s insight provided the ultimate evolutionary explanation for aging. It led in turn to several penultimate or more proximate evolutionary hypotheses regarding how diminishing selective pressures with age might translate into genetically hard-wired propensities for aging. For example, under the “mutation accumulation” hypothesis, later-age classes in effect become garbage bins where alleles with age-delayed deleterious somatic effects accumulate in evolution because of weak selection pressure there against their loss. By contrast, under the hypothesis of “antagonistic pleiotropy”, alleles for aging are favored by natural selection because their beneficial effects at early stages of life outweigh any antagonistic deleterious effects later in life. An example might be a gene that promotes strong bones in youth but, as an ancillary byproduct, hardens arteries (promotes atherosclerosis) later in life.
Although Medawar’s concepts paved the path to solving an evolutionary genetic mystery to nearly everyone’s general satisfaction, I have given it only a modest PS-score because its direct implications and applications are confined mostly to the field of gerontology. Nevertheless, Medawar’s reasoning also exemplifies evolutionary thought in the broader fields of life-history biology and demographic theory.
1. Medawar P. An Unsolved Problem of Biology London, UK: H.K. Lewis; 1952.
2. Williams GC. Pleiotropy, natural selection, and the evolution of senescence. Evolution. 1957;11:398–411.
3. Bernstein C, Bernstein H. Aging, Sex, and DNA Repair San Diego, CA: Academic Press; 1991.
4. Rose MR. Evolutionary Biology of Aging New York, NY: Oxford University Press; 1991.
5. Roff D. The Evolution of Life Histories: Theory and Analysis New York, NY: Chapman & Hall; 1992.
6. Stearns S. The Evolution of Life Histories Oxford, UK: Oxford University Press; 1992.
7. Austad SN. Why We Age: What Science is Discovering about the Body’s Journey Through Life New York, NY: Wiley & Sons; 1997.