Unraveling the Evolutionary Paradox of Ageing
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One of the least-addressed questions of ageing is the apparent paradox between the optimising drive of evolution, and the inevitable deterioration of the body...Why hasn’t life countered the inefficiency of ageing? How has ageing persisted within the Darwinian framework of evolution? For evolution to occur, there must first be genetic variation, a difference between individuals within a population for a measurable characteristic (phenotype) arising from genetic and environmental factors, inheritance of these genetic factors from parents to their offspring, and differential reproductive success, such that certain genetic factors manifest themselves in an individual’s capability to survive and reproduce…
There is an obvious variation in lifespan across different individuals throughout the world, impacted by genetic factors, but also influenced strongly by external factors such as the country’s gross domestic product. Lifespan is also an inherited trait, with approximately 23 to 26 per cent of the variation in lifespan between individuals caused by genetic factors, otherwise known as heritability. Moreover, it makes sense that an increased lifespan, or improved health over your life leading to an increased lifespan, would render you more attractive to the other gender, and increase your likelihood of reproductive success. So, if these three evolutionary criteria have been met for the trait of longevity, why don’t we live for an unheralded number of years?
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The British biologist Peter Medawar formalised the first evolutionary theory of ageing, the mutation-accumulation model…[which] relies upon the fact that mutations acquired by an individual can be early acting or late-onset. Early acting mutations manifest themselves during the period where individuals are reproductively active, so that whatever effect the mutation has will be acted upon by natural selection. However, natural selection is ‘blind’ to late-onset mutations. Mutations that reveal themselves later in life cannot be retroactively selected against, if reproduction has already occurred, and passed on to the next generation. Therefore, the force of selection diminishes with age and reproductive decline. This phenomenon is known as the selection shadow…
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The American evolutionary biologist, George C Williams, elaborated further on the relationship between early acting and late-onset mutations. A mutation can have multiple effects that present themselves differently in different tissue types, or different stages of life, a genetic phenomenon known as pleiotropy. When the mutation has opposing effects on fitness at different life stages, for example during early and late life, it is known as antagonistic pleiotropy. Williams postulated that if a mutation has a beneficial effect on survival and reproduction in early life, but a negative ageing-related impact in later life, selection will act upon the early benefit and enrich this mutation in the population. This antagonistic-pleiotropy model presents ageing as a maladaptive by-product of selection for survival and reproduction during youth. Some early life traits that improved survival and reproduction had an evolutionary trade-off against age-related disorders…
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Ultimately, reproduction is the focal point by which evolution acts. Human evolution permits late-onset effects on health that arise after this reproduction window, especially if it benefits individuals in their early life exploits. In the context of environmental constraints, the individual must effectively allocate resources, creating trade-offs between reproduction, safety and long-term health. In the drive towards the cure for ageing, evolutionary medicine has the potential to further our understanding of why human diseases arise, and elucidate the unanticipated costs of subverting this intrinsic biological process.
