Evolution of ageing

Enquiry into the evolution of ageing aims to explain why survival, reproductive success, and functioning of almost all living organisms decline at old age. Leading hypotheses suggest that a combination of limited resources, and environmental causes determine an 'optimal' level of repair regarding molecular and cellular level damage that accumulates over time. This process is known as self-maintenance. Enquiry into the evolution of ageing aims to explain why survival, reproductive success, and functioning of almost all living organisms decline at old age. Leading hypotheses suggest that a combination of limited resources, and environmental causes determine an 'optimal' level of repair regarding molecular and cellular level damage that accumulates over time. This process is known as self-maintenance. August Weismann was responsible for interpreting and formalizing the mechanisms of Darwinian evolution in a modern theoretical framework. In 1889, he theorized that ageing was part of life's program to make room for the next generation in order to sustain the turnover that is necessary for evolution. The idea that the ageing characteristic was selected (an adaptation) because of its deleterious effect was largely discounted for much of the 20th century, but a theoretical model suggests that altruistic ageing could evolve if there is little migration among populations. Weismann later abandoned his theory and later followed up with his 'programmed death' theory. The first modern theory of mammal ageing was formulated by Peter Medawar in 1952. This theory formed in the previous decade with J. B. S. Haldane and his selection shadow concept. Their idea was that ageing was a matter of neglect, as nature is a highly competitive place. Almost all animals die in the wild from predators, disease, or accidents, which lowers the average age of death. Therefore, there is not much reason why the body should remain fit for the long haul because selection pressure is low for traits that would maintain viability past the time when most animals would have died anyway. Medawar's theory is referred to as Mutation Accumulation. This theory is based on the idea that random, germline mutations occur that are detrimental to overall health and survival later in life. Overall, senescence would occur through a summation of deleterious genes, and would explain the overall phenotypic damage we associate with ageing. Modern genetics science has disclosed a possible problem with the mutation accumulation concept with the knowledge of a mechanism that regulates genes (see regulation of gene expression). Medawar's theory was critiqued and later further developed by George C. Williams in 1957. Williams noted that senescence may be causing many deaths even if animals are not 'dying of old age.' He began his hypothesis with the idea that ageing can cause earlier senescence due to the competitive nature of life. Even a small amount of ageing can be fatal; hence natural selection does indeed care and ageing is not cost-free. Williams eventually proposed his own hypothesis called antagonistic pleiotropy. Pleiotropy, alone, means one mutation that cause multiple effects on phenotype. Antagonistic pleiotropy on the other hand deals with one gene that creates two traits with one being beneficial and the other being detrimental. In essence, this refers to genes that offer benefits early in life, but accumulate a cost later on.