Editing Life expectancy (section)

==Evolution and aging rate==
{{Main|Life history theory}}

Various species of plants and animals, including humans, have different lifespans. Evolutionary theory states that organisms which—by virtue of their defenses or lifestyle—live for long periods and avoid accidents, disease, predation, etc. are likely to have genes that code for slow aging, which often translates to good cellular repair. One theory is that if predation or accidental deaths prevent most individuals from living to an old age, there will be less natural selection to increase the intrinsic life span.<ref>{{cite journal|vauthors=Williams G|title=Pleiotropy, natural selection, and the evolution of senescence|journal=Evolution|volume=11|pages=398–411|year=1957|doi=10.2307/2406060|issue=4|publisher=Society for the Study of Evolution|jstor=2406060}}</ref> That finding was supported in a classic study of opossums by Austad;<ref>{{cite journal|vauthors=Austad SN|title=Retarded senescence in an insular population of Virginia opossums|journal=J. Zool. Lond.|volume=229|issue=4|pages=695–708|year=1993|doi=10.1111/j.1469-7998.1993.tb02665.x}}</ref> however, the opposite relationship was found in an equally prominent study of guppies by Reznick.<ref>{{cite journal|vauthors=Reznick DN, Bryant MJ, Roff D, Ghalambor CK, Ghalambor DE|title=Effect of extrinsic mortality on the evolution of senescence in guppies|journal=Nature|volume=431|issue=7012|pages=1095–1099|date=October 2004|pmid=15510147|doi=10.1038/nature02936|s2cid=205210169|bibcode=2004Natur.431.1095R}}</ref><ref>{{cite journal|vauthors=Mitteldorf J, Pepper JW|title=How can evolutionary theory accommodate recent empirical results on organismal senescence?|journal=Theory in Biosciences = Theorie in den Biowissenschaften|volume=126|issue=1|pages=3–8|date=August 2007|pmid=18087751|doi=10.1007/s12064-007-0001-0|s2cid=7305206}}</ref>

One prominent and very popular theory states that lifespan can be lengthened by a tight budget for food energy called [[caloric restriction]].<ref>{{cite journal|vauthors=Kirkwood TB|title=Evolution of ageing|journal=Nature|volume=270|issue=5635|pages=301–304|date=November 1977|pmid=593350|doi=10.1038/270301a0|s2cid=492012|bibcode=1977Natur.270..301K}}</ref> Caloric restriction observed in many animals (most notably mice and rats) shows a near doubling of life span from a very limited calorific intake. Support for the theory has been bolstered by several new studies linking lower [[basal metabolic rate]] to increased life expectancy.<ref>{{cite journal|vauthors=Hulbert AJ, Pamplona R, Buffenstein R, Buttemer WA|title=Life and death: metabolic rate, membrane composition, and life span of animals|journal=Physiological Reviews|volume=87|issue=4|pages=1175–1213|date=October 2007|pmid=17928583|doi=10.1152/physrev.00047.2006|url=http://pdfs.semanticscholar.org/0c1b/ece43845df356bc2dda22dd27a82a8ef95e8.pdf|url-status=dead|s2cid=11903260|archive-url=https://web.archive.org/web/20190218133041/http://pdfs.semanticscholar.org/0c1b/ece43845df356bc2dda22dd27a82a8ef95e8.pdf|archive-date=18 February 2019}}</ref><ref>{{cite journal|vauthors=Olshansky SJ, Rattan SI|title=What determines longevity: Metabolic rate or stability?|journal=Discovery Medicine|volume=5|issue=28|pages=359–362|date=August 2005|pmid=20704872|url=http://www.discoverymedicine.com/S-J-Olshansky/2009/07/25/what-determines-longevity-metabolic-rate-or-stability}}</ref><ref>{{cite journal|vauthors=Aguilaniu H, Durieux J, Dillin A|title=Metabolism, ubiquinone synthesis, and longevity|journal=Genes & Development|volume=19|issue=20|pages=2399–2406|date=October 2005|pmid=16230529|doi=10.1101/gad.1366505|doi-access=free}}</ref> That is the key to why animals like giant [[tortoise]]s can live so long.<ref>{{cite web|url=http://www.immortalhumans.com/the-longevity-secret-for-tortoises-is-held-in-their-low-metabolism-rate/|title=The Longevity Secret for Tortoises Is Held in Their Low Metabolism Rate|archive-url=https://web.archive.org/web/20131112164840/http://www.immortalhumans.com/the-longevity-secret-for-tortoises-is-held-in-their-low-metabolism-rate/|archive-date=12 November 2013|url-status=dead}}</ref> Studies of humans with life spans of at least 100 have shown a link to decreased thyroid activity, resulting in their lowered metabolic rate.{{No source|date=January 2023}}

The ability of [[dermal fibroblast|skin fibroblasts]] to perform [[DNA repair]] after [[UV]] irradiation was measured in [[shrew]], [[mouse]], [[rat]], [[hamster]], [[cow]], [[elephant]] and [[human]].<ref name="pmid4526202">{{cite journal|vauthors=Hart RW, Setlow RB|title=Correlation between deoxyribonucleic acid excision-repair and life-span in a number of mammalian species|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=71|issue=6|pages=2169–73|date=June 1974|pmid=4526202|pmc=388412|doi=10.1073/pnas.71.6.2169|doi-access=free|bibcode=1974PNAS...71.2169H}}</ref> It was found that DNA repair capability increased systematically with species [[maximum life span|life span]].  Since this original study in 1974, at least 14 additional studies were performed on [[mammal]]s to test this correlation.<ref name = Bernstein1991>{{cite book|vauthors=Bernstein C, Bernstein H|date=1991|title=Aging, Sex, and DNA Repair|publisher=Academic Press|location=San Diego, CA|pages=109–113}}</ref> In all, but two of these studies, lifespan correlated with DNA repair levels, suggesting that DNA repair capability contributes to life expectancy.<ref name = Bernstein1991/> See [[DNA damage theory of aging]].

In a broad survey of zoo animals, no relationship was found between investment of the animal in reproduction and its life span.<ref>{{cite journal|vauthors=Ricklefs RE, Cadena CD|title=Lifespan is unrelated to investment in reproduction in populations of mammals and birds in captivity|journal=Ecology Letters|volume=10|issue=10|pages=867–872|date=October 2007|pmid=17845285|doi=10.1111/j.1461-0248.2007.01085.x|bibcode=2007EcolL..10..867R}}</ref>