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Mutation accumulation

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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. The development of human civilization has shifted the selective shadow as the conditions that humans now live in include improved quality of victuals, living conditions, and healthcare. This improved healthcare includes modern medicine such as antibiotics and new medical technology.[1] 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. Evolution has not had an opportunity to select against deadly diseases such as cancer and heart disease. Metabolic diseases come along due to the low demand for physical activity in modern civilization compared to times where humans had to forage in the wild for survival.[2] With the selective shadow now shifted, humans must deal with these new selective pressures.

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 mutations, and would explain the overall phenotypic damage we associate with ageing.

  1. ^ Flatt, Thomas; Partridge, Linda (2018-08-20). "Horizons in the evolution of aging". BMC Biology. 16 (1): 93. doi:10.1186/s12915-018-0562-z. ISSN 1741-7007. PMC 6100731. PMID 30124168.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  2. ^ Flatt, Thomas; Partridge, Linda (2018-08-20). "Horizons in the evolution of aging". BMC Biology. 16 (1): 93. doi:10.1186/s12915-018-0562-z. ISSN 1741-7007. PMC 6100731. PMID 30124168.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)