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{{Short description|Longest recorded life span}}
'''Maximum life span''' (or, for [[Humans|humans]], '''maximum reported age at death''') is a measure of the maximum amount of time one or more members of a [[Social:Population|population]] have been observed to survive between [[Biology:Birth|birth]] and [[Biology:Death|death]]. The term can also denote an estimate of the maximum amount of time that a member of a given [[Biology:Species|species]] could survive between birth and death, provided circumstances that are optimal to that member's [[Biology:Longevity|longevity]].

Most living species have an upper limit on the number of times [[Biology:Somatic cell|somatic]] [[Biology:Cell|cells]] not expressing [[Biology:Telomerase|telomerase]] can [[Biology:Mitosis|divide]]. This is called the [[Biology:Hayflick limit|Hayflick limit]], although this number of cell divisions does not strictly control lifespan.

==Definition==
In animal studies, maximum span is often taken to be the mean life span of the most long-lived 10% of a given [[Cohort study|cohort]]. By another definition, however, maximum life span corresponds to the age at which the oldest known member of a [[Biology:Species|species]] or experimental group has died. Calculation of the maximum life span in the latter sense depends upon the initial sample size.<ref>{{cite book |first1=Leonid A. |last1=Gavrilov |first2=Natalia S. |last2=Gavrilova | name-list-style = vanc |year=1991 |title=The Biology of Life Span: A Quantitative Approach |location=New York |publisher=Harwood Academic |isbn=978-3-7186-4983-9}}{{page needed|date=October 2011}}</ref>

''Maximum life span'' contrasts with ''mean life span (average life span'', ''[[Biology:Life expectancy|life expectancy]])'', and ''[[Biology:Longevity|longevity]]''. Mean life span varies with susceptibility to disease, accident, [[Medicine:Suicide|suicide]] and [[Social:Murder|homicide]], whereas maximum life span is determined by "rate of aging".<ref>{{cite news |first=Jane E. |last=Brody | name-list-style = vanc |date=25 August 2008 |title=Living Longer, in Good Health to the End |work=The New York Times |page=D7 |url=https://www.nytimes.com/2008/08/26/health/26brod.html}}</ref><ref>{{cite journal |last1=Levy |first1=G |last2=Levin |first2=B |title=An Evolution-Based Model of Causation for Aging-Related Diseases and Intrinsic Mortality: Explanatory Properties and Implications for Healthy Aging. |journal=Frontiers in Public Health |date=2022 |volume=10 |pages=774668 |doi=10.3389/fpubh.2022.774668 |pmid=35252084 |pmc=8894190 |doi-access=free }}</ref>{{failed verification|this article is about compression of morbidity, and doesn't support these claims without synthesis|date=October 2011}} Longevity refers only to the characteristics of the especially long lived members of a population, such as infirmities as they age or ''[[Biology:Compression of morbidity|compression of morbidity]]'', and not the specific life span of an individual.

==In humans==
{{Main|Biology:Oldest people|Biology:List of the verified oldest people}}

=== Demographic evidence ===
The [[Biology:Oldest people|longest living person]] whose dates of birth and death were verified according to the modern norms of ''Guinness World Records'' and the Gerontology Research Group was Jeanne Calment (1875–1997), a Frenchwoman who is verified to have lived to 122. The oldest male lifespan has only been verified as 116, by Japanese man Jiroemon Kimura. Reduction of infant mortality has accounted for most of the increased average life span [[Biology:Longevity|longevity]], but since the 1960s [[Mortality rate|mortality rate]]s among those over 80 years have decreased by about 1.5% per year. "The progress being made in lengthening lifespans and postponing [[Biology:Senescence|senescence]] is entirely due to medical and public-health efforts, rising standards of living, better education, healthier nutrition and more salubrious lifestyles."<ref>{{cite journal | vauthors = Vaupel JW | title = Biodemography of human ageing | journal = Nature | volume = 464 | issue = 7288 | pages = 536–42 | date = March 2010 | pmid = 20336136 | pmc = 4010874 | doi = 10.1038/nature08984 | bibcode = 2010Natur.464..536V }}</ref> Animal studies suggest that further lengthening of median human lifespan as well as maximum lifespan could be achieved through "calorie restriction mimetic" drugs or by directly reducing food consumption.<ref>{{cite journal | vauthors = Ben-Haim MS, Kanfi Y, Mitchell SJ, Maoz N, Vaughan KL, Amariglio N, Lerrer B, de Cabo R, Rechavi G, Cohen HY | title = Breaking the Ceiling of Human Maximal Life span | journal = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 73 | issue = 11 | pages = 1465–1471 | date = October 2018 | pmid = 29121176 | doi = 10.1093/gerona/glx219 | pmc = 6454488 }}</ref> Although calorie restriction has not been proven to extend the maximum human life span {{asof|2014|lc=y}}, results in ongoing primate studies have demonstrated that the assumptions derived from rodents are valid in primates.<ref>''Nature'', 1 April 2014.</ref><ref>{{cite journal | vauthors = Ingram DK, Roth GS, Lane MA, Ottinger MA, Zou S, de Cabo R, Mattison JA | title = The potential for dietary restriction to increase longevity in humans: extrapolation from monkey studies | journal = Biogerontology | volume = 7 | issue = 3 | pages = 143–8 | date = June 2006 | pmid = 16732404 | doi = 10.1007/s10522-006-9013-2 | s2cid = 2859875 | url = https://zenodo.org/record/1232785 }}</ref>

It has been proposed that no fixed theoretical limit to human longevity is apparent today.<ref>{{Cite book | vauthors = Gavrilov LA, Gavrilova NS | year = 1991 | title = The Biology of Life Span: A Quantitative Approach | location = {{wipe|New York City}} | publisher = Starwood Academic Publishers }}{{Page needed|date=January 2018}}</ref><ref>{{Cite journal | journal = Population Dev Rev | volume = 26 | issue = 2 | pages = 403–04 | title = Book Reviews: ''Validation of Exceptional Longevity'' | last1 = Gavrilov | first1 = Leonid A. | last2 = Gavrilova | first2 = Natalia S. | name-list-style = vanc | date = June 2000 | url = http://longevity-science.org/PDR-00.pdf | access-date = 2009-05-18 }}</ref> Studies in the [[Medicine:Biodemography of human longevity|biodemography of human longevity]] indicate a ''late-life mortality deceleration law'': that death rates level off at advanced ages to a late-life mortality plateau. That is, there is no fixed upper limit to human longevity, or fixed maximal human lifespan.<ref>{{Cite web |url=http://longevity-science.org/Biodemography.html |title=Biodemography of Human Longevity |last=Gavrilov |first=Leonid A. | name-list-style = vanc 
|date=5 March 2004 |publisher=International Conference on Longevity |access-date=2018-01-13}}</ref> This law was first quantified in 1939, when researchers found that the one-year probability of death at advanced age asymptotically approaches a limit of 44% for women and 54% for men.<ref>{{Cite journal | url = http://longevity-science.org/Greenwood-Human-Biology-1939.pdf | vauthors = Greenwood M, Irwin JO | date = 1939 | title = The Biostatics of Senility | journal = Human Biology | volume = 11 | pages = 1–23 | access-date = 2009-05-18 }}</ref>

However, this evidence depends on the existence of a late-life plateaus and deceleration that can be explained, in humans and other species, by the existence of very rare errors.<ref>{{cite journal | vauthors = Gavrilova NS, Gavrilov LA | title = Mortality Trajectories at Extreme Old Ages: A Comparative Study of Different Data Sources on U.S. Old-Age Mortality | journal = Living to 100 Monograph | volume = 2014 | date = 2014 | pmid = 25664347 | pmc = 4318539 }}</ref><ref name=":2">{{cite journal | vauthors = Newman SJ | title = Errors as a primary cause of late-life mortality deceleration and plateaus | journal = PLOS Biology | volume = 16 | issue = 12 | pages = e2006776 | date = December 2018 | pmid = 30571676 | doi = 10.1371/journal.pbio.2006776 | pmc = 6301557 | doi-access = free }}</ref> Age-coding error rates below 1 in 10,000 are sufficient to make artificial late-life plateaus, and errors below 1 in 100,000 can generate late-life mortality deceleration. These error rates cannot be ruled out by examining documents<ref name=":2" /> (the standard) because of successful pension fraud, identity theft, forgeries and errors that leave no documentary evidence. This capacity for errors to explain late-life plateaus solves the "fundamental question in aging research is whether humans and other species possess an immutable life-span limit" and suggests that a limit to human life span exists.<ref>{{cite journal | vauthors = Wilmoth JR, Deegan LJ, Lundström H, Horiuchi S | title = Increase of maximum life-span in Sweden, 1861-1999 | journal = Science | volume = 289 | issue = 5488 | pages = 2366–8 | date = September 2000 | pmid = 11009426 | doi = 10.1126/science.289.5488.2366 | bibcode = 2000Sci...289.2366W }}</ref> 
A theoretical study suggested the maximum human lifespan to be around 125 years using a modified [[Stretched exponential function|stretched exponential function]] for human survival curves.<ref>{{cite journal | vauthors = Weon BM, Je JH | title = Theoretical estimation of maximum human lifespan | journal = Biogerontology | volume = 10 | issue = 1 | pages = 65–71 | date = February 2009 | pmid = 18560989 | doi = 10.1007/s10522-008-9156-4 | s2cid = 8554128 }}</ref>
In another study, researchers claimed that there exists a maximum lifespan for humans, and that the human maximal lifespan has been declining since the 1990s.<ref name=":0">{{cite journal | vauthors = Dong X, Milholland B, Vijg J | title = Evidence for a limit to human lifespan | journal = Nature | volume = 538 | issue = 7624 | pages = 257–259 | date = October 2016 | pmid = 27706136 | doi = 10.1038/nature19793 | bibcode = 2016Natur.538..257D | s2cid = 3623127 }}</ref> A theoretical study also suggested that the maximum human [[Biology:Life expectancy|life expectancy]] at birth is limited by the human life characteristic value δ, which is around 104 years.<ref>{{cite journal | vauthors = Liu X | title = Life equations for the senescence process | journal = Biochemistry and Biophysics Reports | volume = 4 | pages = 228–233 | date = December 2015 | pmid = 29124208 | pmc = 5669524 | doi = 10.1016/j.bbrep.2015.09.020 | arxiv = 1502.00759 }}</ref>

In 2017, the {{wipe|United Nations}} conducted a Bayesian sensitivity analysis of global population burden based on life expectancy projection at birth in future decades. The 95% prediction interval of average life expectancy rises as high as 106 years old by 2090, with ongoing and layered effects on world population and demography should that happen. However, the prediction interval is extremely wide.<ref>Castanheira, H., Pelletier, F. and Ribeiro, I. (2017). A Sensitivity Analysis of the Bayesian Framework for Projecting Life Expectancy at Birth, UN Population Division, Technical Paper No. 7. New York: United Nations.</ref>

=== Non-demographic evidence ===

Evidence for maximum lifespan is also provided by the dynamics of physiological indices with age. For example, scientists have observed that a person's [[Medicine:VO2 max|VO<sub>2</sub>max]] value (a measure of the volume of oxygen flow to the cardiac muscle) decreases as a function of age. Therefore, the maximum lifespan of a person could be determined by calculating when the person's VO<sub>2</sub>max value drops below the basal metabolic rate necessary to sustain life, which is approximately 3&nbsp;ml per [[Kilogram|kg]] per minute.<ref name="Nokes Lore">{{Cite book | vauthors = Noakes T | year = 1985 | title = The Lore of Running | publisher = Oxford University Press }}</ref>{{Page needed|date=January 2018}} On the basis of this hypothesis, athletes with a VO<sub>2</sub>max value between 50 and 60 at age 20 would be expected "to live for 100 to 125 years, provided they maintained their physical activity so that their rate of decline in VO<sub>2</sub>max remained constant".<ref>Nokes (1985) p. 84.</ref>

[[File: Age dynamics of the body mass.svg|thumb|Average and commonly accepted maximum lifespans correspond to the extremums of the body mass (1, 2) and mass normalized to height (3, 4) of men (1, 3) and women (2, 4).<ref name="Age dynamics">{{cite journal| vauthors = Gerasimov IG, Ignatov DY |title=Age Dynamics of Body Mass and Human Lifespan| journal = Journal of Evolutionary Biochemistry and Physiology | volume = 40 | issue = 3| pages = 343–349|year=2004| doi = 10.1023/B:JOEY.0000042639.72529.e1 |s2cid=9070790}}</ref>]]

==In animals==
{{Main|Biology:List of longest-living organisms}}
Small animals such as [[Biology:Bird|bird]]s and squirrels rarely live to their maximum life span, usually dying of accidents, [[Disease|disease]] or [[Earth:Predation|predation]].

The maximum life span of most species is documented in the AnAge repository (The Animal Ageing and Longevity Database).<ref>{{cite web|url=http://genomics.senescence.info/species/|title=The Animal Ageing and Longevity Database|website=Anage}}</ref>

Maximum life span is usually longer for species that are larger or have effective defenses against predation, such as bird flight,<ref>{{cite journal | vauthors = Healy K, Guillerme T, Finlay S, Kane A, Kelly SB, McClean D, Kelly DJ, Donohue I, Jackson AL, Cooper N | title = Ecology and mode-of-life explain lifespan variation in birds and mammals | journal = Proceedings. Biological Sciences | volume = 281 | issue = 1784 | pages = 20140298 | date = June 2014 | pmid = 24741018 | pmc = 4043093 | doi = 10.1098/rspb.2014.0298 }}</ref> chemical defenses<ref>{{cite journal | vauthors = Hossie TJ, Hassall C, Knee W, Sherratt TN | title = Species with a chemical defence, but not chemical offence, live longer | journal = Journal of Evolutionary Biology | volume = 26 | issue = 7 | pages = 1598–602 | date = July 2013 | pmid = 23638626 | doi = 10.1111/jeb.12143 | doi-access = free }}</ref> or living in social groups.<ref>{{Cite book |title=Living in Groups |last1=Krause |first1=Jens |last2=Ruxton |first2=Graeme | name-list-style = vanc |date=19 December 2002 |publisher=Oxford University Press |isbn=9780198508182 |edition=1st }}</ref>

The differences in life span between species demonstrate the role of [[Biology:Genetics|genetics]] in determining maximum life span ("rate of aging"). The records (in years) are these:

*for [[Biology:House mouse|common house mouse]], 4<ref>{{cite web |title=AnAge entry for ''Mus musculus'' | url = http://genomics.senescence.info/species/entry.php?species=Mus_musculus |website=AnAge Database of Animal Ageing and Longevity | access-date = 2009-08-13}}</ref>
* for [[Biology:Brown rat|Brown rat]], 3.8<ref>{{Cite web|url=http://genomics.senescence.info/species/entry.php?species=Rattus_norvegicus|title=Norway rat (Rattus norvegicus) longevity, ageing, and life history|website=genomics.senescence.info|language=en|access-date=2017-03-15}}</ref>
*for [[Biology:Dog|dog]]s, 31 (See List of oldest dogs)<ref name = iberianet>{{cite web|url=http://www.iberianet.com/news/max-misses-world-s-oldest-dog-title/article_a432c462-c251-11e2-96b5-001a4bcf887a.html|title=Max misses 'World's Oldest Dog' title|work=iberianet.com|date=21 May 2013 }}</ref>
*for [[Biology:Cat|cat]]s, 38 (See List of oldest cats)<ref>{{cite book |title=Guinness World Records 2010 |year=2010 |publisher=Bantam |page=[https://archive.org/details/guinnessworldrec00vari/page/320 320] |quote=The oldest cat ever was Creme Puff, who was born on August 3, 1967, and lived until August 6, 2005—38 years and 3 days in total. | url=https://archive.org/details/guinnessworldrec00vari |url-access=registration |isbn=978-0-553-59337-2 }}</ref>
* for common cranes, 43<ref name=Mitchell1911/>
*for [[Biology:Polar bear|polar bear]]s, 42<ref>{{cite web | title = World's oldest polar bear | url = http://www.canada.com/topics/news/national/story.html?id=8a696b53-4d92-420d-99e5-01718168c160 | access-date = 2008-11-19 | url-status = dead | archive-url = https://web.archive.org/web/20090803012005/http://www.canada.com/topics/news/national/story.html?id=8a696b53-4d92-420d-99e5-01718168c160 | archive-date = 3 August 2009 }}</ref> (Debby)
*for [[Biology:Horse#Age|horse]]s, 62<ref>{{cite book |ref=Ensminger|author= Ensminger, M. E.|title= Horses and Horsemanship: Animal Agricultural Series|edition= Sixth|publisher= Interstate Publishers|location= Danville, Indiana |year= 1990|isbn=978-0-8134-2883-3 |oclc= 21977751}}, pp. 46–50</ref>
*for [[Biology:Asian elephant|Asian elephant]]s, 86<ref>{{cite web | title = Lin Wang, an Asian elephant (''Elephas maximus'') at Taipei Zoo | url = http://www.elephant.se/database2.php?elephant_id=1306 | access-date = 2009-08-13}}</ref>
The longest-lived vertebrates have been variously described as

*[[Biology:Companion parrot#Household settings|Large parrots]] (macaws and cockatoos can live up to 80–100 years in captivity)
*Koi (a Japanese species of fish, allegedly living up to 200 years, though generally not exceeding 50 – a specimen named Hanako was reportedly 226 years old upon her death)<ref>{{cite web|url=http://www.japan-nishikigoi.org/ecology.html |title=International Nishikigoi Promotion Center-Genealogy |publisher=Japan-nishikigoi.org |access-date=2009-04-11}}</ref><ref>{{cite news |url=https://www.theguardian.com/uk/2007/apr/12/animalwelfare.world |title=Will you still feed me ... ? |newspaper=The Guardian |date= 12 April 2007|access-date=2009-04-11 | location=London | first=Laura | last=Barton | name-list-style = vanc }}</ref>
*[[Biology:Tortoise|Tortoise]]s ([[Biology:Galápagos tortoise|Galápagos tortoise]]) (190 years)<ref>{{cite web |url=http://www.seedmagazine.com/news/2006/07/week_in_science_623_629.php?page=2 |title=Week In Science: 6/23 - 6/29 |work=Seed |author= |date=31 October 2007 |archive-url=https://web.archive.org/web/20071031231711/http://www.seedmagazine.com/news/2006/07/week_in_science_623_629.php?page=2 |archive-date=2007-10-31 |url-status=unfit}}</ref>
*[[Biology:Tuatara|Tuatara]] (a New Zealand reptile species, 100–200+ years<ref>[[Biology:Tuatara#cite note-43|Tuatara]]</ref>)
*[[Biology:Eel|Eel]]s, the so-called Brantevik Eel (Swedish: Branteviksålen) is thought to have lived in a water well in southern Sweden since 1859, which makes it over 150 years old.<ref>{{cite web|url=https://www.fiskeriverket.se/sidorutanformenyn/reportage/gammelalenhittades.4.323810fc116f29ea95a80003329.html|title=Brantevik Eels may be the world's oldest|date=11 April 2008|url-status=dead|archive-url=https://web.archive.org/web/20100813143538/https://www.fiskeriverket.se/sidorutanformenyn/reportage/gammelalenhittades.4.323810fc116f29ea95a80003329.html|archive-date=13 August 2010}}</ref> It was reported that it had died in August 2014 at an age of 155.<ref>{{cite news |url=http://www.expressen.se/kvallsposten/varldens-aldsta-al-dod--levde-155-ar-i-brunn/ |title=The world's oldest Eek dead - Lived 155 years in a well (Article in Swedish )|date=8 August 2014}}</ref>
*[[Biology:Whale|Whale]]s ([[Biology:Bowhead whale|bowhead whale]]) (''Balaena mysticetus'' about 200 years)—Although this idea was unproven for a time, recent research has indicated that bowhead whales recently killed still had [[Engineering:Harpoon|harpoon]]s in their bodies from about 1890,<ref>{{cite web|url=http://www.whalingmuseum.org/pressroom.html|title=125-Year-old New Bedford Bomb Fragment Found Embedded in Alaskan Bowhead Whale|url-status=dead|archive-url=https://web.archive.org/web/20110728174637/http://www.whalingmuseum.org/pressroom.html|archive-date=28 July 2011}}</ref> which, along with analysis of amino acids, has indicated a maximum life span of "177 to 245 years old".<ref>{{cite web|url=http://www.gi.alaska.edu/ScienceForum/ASF15/1529.html|year=2001|title=Bowhead Whales May Be the World's Oldest Mammals|access-date=2019-01-05|archive-url=https://web.archive.org/web/20091209053409/http://www.gi.alaska.edu/ScienceForum/ASF15/1529.html|archive-date=2009-12-09|url-status=dead}}</ref><ref>
{{cite web|url=http://www.alaskareport.com/science10065.htm|title=Bowhead Whales May Be the World's Oldest Mammals|year=2007 |orig-date=2001}}</ref><ref>{{cite journal | vauthors = George JC, Bada J, Zeh J, Scott L, Brown SE, O'hara T, Suydam R | year = 1999 | title = Age and growth estimates of bowhead whales (''Balaena mysticetus'') via aspartic acid racemization | journal =Canadian Journal of Zoology | volume = 77 | issue = 4 | pages = 571–580 | doi = 10.1139/cjz-77-4-571}}</ref>
* [[Biology:Greenland shark|Greenland shark]]s are currently the vertebrate species with the longest known lifespan.<ref name=Nielsen2016>{{cite journal | vauthors = Nielsen J, Hedeholm RB, Heinemeier J, Bushnell PG, Christiansen JS, Olsen J, Ramsey CB, Brill RW, Simon M, Steffensen KF, Steffensen JF | title = Eye lens radiocarbon reveals centuries of longevity in the Greenland shark (Somniosus microcephalus) | journal = Science | volume = 353 | issue = 6300 | pages = 702–4 | date = August 2016 | pmid = 27516602 | doi = 10.1126/science.aaf1703 | bibcode = 2016Sci...353..702N | s2cid = 206647043 | url = https://ora.ox.ac.uk/objects/uuid:6c040460-9519-4720-9669-9911bdd03b09 | hdl = 2022/26597 | hdl-access = free }}
*{{cite magazine |author=Enrico de Lazaro |date=12 August 2016 |title=Greenland Sharks are Longest-Lived Vertebrates on Earth, Marine Biologists Say |magazine=Science News |url=http://www.sci-news.com/biology/greenland-sharks-longest-lived-vertebrates-04099.html}}</ref> An examination of 28 specimens in one study published in 2016 determined by [[Physics:Radiocarbon dating|radiocarbon dating]] that the oldest of the animals that they sampled had lived for about 392 ± 120 years (a minimum of 272 years and a maximum of 512 years). The authors further concluded that the species reaches sexual maturity at about 150 years of age.<ref name=Nielsen2016/>

Invertebrate species which continue to grow as long as they live (''e.g.,'' certain clams, some coral species) can on occasion live hundreds of years:

*A [[Biology:Bivalvia|bivalve mollusk]] (''[[Biology:Arctica islandica|Arctica islandica]]'') (aka "[[Biology:Ming (clam)|Ming]]", lived 507±2 years.<ref name=Butler_2013>{{cite journal | vauthors = Butler PG, Wanamaker AD, Scourse JD, Richardson CA, Reynolds DJ | title = Variability of marine climate on the North Icelandic Shelf in a 1357-year proxy archive based on growth increments in the bivalve Arctica islandica. | journal = Palaeogeography, Palaeoclimatology, Palaeoecology | date = March 2013 | volume = 373 | pages = 141–51 | doi = 10.1016/j.palaeo.2012.01.016 | bibcode = 2013PPP...373..141B }}</ref><ref name=ScienceNordic>{{cite web|url=http://sciencenordic.com/new-record-world%E2%80%99s-oldest-animal-507-years-old |title=New record: World's oldest animal is 507 years old | first = Lise | last = Brix | name-list-style = vanc |work=Sciencenordic |date=6 November 2013 |access-date=2013-11-14 |archive-url=https://archive.today/20131115121158/http://sciencenordic.com/new-record-world%E2%80%99s-oldest-animal-507-years-old |archive-date=15 November 2013 |url-status=dead }}</ref>)

===Exceptions===
*Some [[Biology:Jellyfish|jellyfish]] species, including ''[[Biology:Turritopsis dohrnii|Turritopsis dohrnii]]'', ''Laodicea undulata'',<ref>{{Cite journal| vauthors = De Vito D, Piraino S, Schmich J, Bouillon J, Boero F |title = Evidence of reverse development in Leptomedusae (Cnidaria, Hydrozoa): the case of ''Laodicea undulata'' (Forbes and Goodsir 1851) o|date = 2006|journal = Marine Biology|doi = 10.1007/s00227-005-0182-3|volume=149|issue = 2|pages=339–346 | bibcode=2006MarBi.149..339D |s2cid = 84325535}}</ref> and ''Aurelia'' sp.1,<ref>{{cite journal | vauthors = He J, Zheng L, Zhang W, Lin Y | title = Life Cycle Reversal in Aurelia sp.1 (Cnidaria, Scyphozoa) | journal = PLOS ONE | volume = 10 | issue = 12 | pages = e0145314 | date = 21 December 2015 | pmid = 26690755 | pmc = 4687044 | doi = 10.1371/journal.pone.0145314 | bibcode = 2015PLoSO..1045314H | doi-access = free }}</ref> are able to revert to the polyp stage even after reproducing (so-called reversible life cycle), rather than dying as in other jellyfish. Consequently, these species are considered [[Biology:Biological immortality|biologically immortal]] and have no maximum lifespan.<ref name="piraino-96">{{cite journal | vauthors = Piraino S, Boero F, Aeschbach B, Schmid V | title = Reversing the Life Cycle: Medusae Transforming into Polyps and Cell Transdifferentiation in Turritopsis nutricula (Cnidaria, Hydrozoa) | journal = The Biological Bulletin | volume = 190 | issue = 3 | pages = 302–312 | date = June 1996 | pmid = 29227703 | doi = 10.2307/1543022 | jstor = 1543022 }}</ref>
*There may be no natural limit to the [[Biology:Hydra (genus)|''Hydra'']]'s life span, but it is not yet clear how to estimate the age of a specimen.
*Flatworms, or Platyhelminthes, are known to be "almost immortal" as they have a great regeneration capacity, continuous growth and [[Binary fission|binary fission]] type cellular division.<ref>{{cite journal | vauthors = Saló E | title = The power of regeneration and the stem-cell kingdom: freshwater planarians (Platyhelminthes) | journal = BioEssays | volume = 28 | issue = 5 | pages = 546–59 | date = May 2006 | pmid = 16615086 | doi = 10.1002/bies.20416 | doi-access = free }}</ref>
*Lobsters are sometimes said to be [[Biology:Biological immortality|biologically immortal]] because they do not seem to slow down, weaken, or lose fertility with age. However, due to the energy needed for moulting, they cannot live indefinitely.<ref>{{cite web |author=Marina Koren |title=Don't Listen to the Buzz: Lobsters Aren't Actually Immortal |date=3 June 2013 |publisher=Smithsonian.com |url=http://www.smithsonianmag.com/science-nature/dont-listen-to-the-buzz-lobsters-arent-actually-immortal-88450872/?no-ist}}</ref>

==In plants==
{{Main|Biology:List of oldest trees}}
[[Biology:Plant|Plant]]s are referred to as [[Biology:Annual plant|annuals]] which live only one year, [[Biology:Biennial plant|biennials]] which live two years, and [[Biology:Perennial plant|perennials]] which live longer than that. The longest-lived perennials, woody-stemmed plants such as trees and bushes, often live for hundreds and even thousands of years (one may question whether or not they may die of old age). A giant sequoia, General Sherman, is alive and well in its third [[Millennium|millennium]]. A Great Basin Bristlecone Pine called Methuselah is {{age|-2832|8|5|format=commas}} years old.<ref>{{Cite web|title=Pinus longaeva (Great Basin bristlecone pine) description - The Gymnosperm Database|url=https://www.conifers.org/pi/Pinus_longaeva.php|access-date=2021-03-01|website=www.conifers.org}}</ref> Another Bristlecone Pine called Prometheus was a little older still, showing 4,862 years of growth rings. The exact age of Prometheus, however, remains unknown as it is likely that growth rings did not form every year due to the harsh environment in which it grew but it was estimated to be ~4,900 years old when it was cut down in 1964.<ref>{{Cite web |last1=Baker |first1=Mailing Address: 100 Great Basin National Park |last2=pm |first2=NV 89311 Phone: 775-234-7331 Available 8:00 am- 4:00 |last3=Thanksgiving |first3=Monday through Friday Closed on |last4=Christmas |last5=Us |first5=New Year's Day Contact |title=The Prometheus Story - Great Basin National Park (U.S. National Park Service) |url=https://www.nps.gov/grba/learn/historyculture/the-prometheus-story.htm |access-date=2022-03-20 |website=www.nps.gov |language=en}}</ref> The oldest known plant (possibly oldest living thing) is a clonal Quaking Aspen (''[[Biology:Populus tremuloides|Populus tremuloides]]'') tree colony in the Fishlake National Forest in Utah called [[Biology:Pando (tree)|Pando]] at about 16,000 years. [[Biology:Lichen|Lichen]], a symbiotic algae and fungal proto-plant, such as ''[[Biology:Rhizocarpon geographicum|Rhizocarpon geographicum]]'' can live upwards of 10,000 years.

==Increasing maximum life span==
{{Main|Philosophy:Life extension}}
"Maximum life span" here means the mean life span of the most long-lived 10% of a given cohort. Caloric restriction has not yet been shown to break mammalian world records for longevity. [[Biology:Rat|Rat]]s, [[Biology:Mouse|mice]], and [[Biology:Hamster|hamster]]s experience maximum life-span extension from a diet that contains all of the nutrients but only 40–60% of the calories that the animals consume when they can eat as much as they want. Mean life span is increased 65% and maximum life span is increased 50%, when caloric restriction is begun just before puberty.<ref>{{cite journal | vauthors = Koubova J, Guarente L | title = How does calorie restriction work? | journal = Genes & Development | volume = 17 | issue = 3 | pages = 313–21 | date = February 2003 | pmid = 12569120 | doi = 10.1101/gad.1052903 | doi-access = free }}</ref> For [[Biology:Drosophila melanogaster|fruit flies]] the life extending benefits of calorie restriction are gained immediately at any age upon beginning calorie restriction and ended immediately at any age upon resuming full feeding.<ref>{{cite journal | vauthors = Mair W, Goymer P, Pletcher SD, Partridge L | title = Demography of dietary restriction and death in Drosophila | journal = Science | volume = 301 | issue = 5640 | pages = 1731–3 | date = September 2003 | pmid = 14500985 | doi = 10.1126/science.1086016 | bibcode = 2003Sci...301.1731M | s2cid = 27653353 }}</ref>

Most biomedical [[Biology:Gerontology|gerontologists]] believe that biomedical molecular [[Engineering:Engineering|engineering]] will eventually extend maximum lifespan and even bring about rejuvenation.<ref>{{cite book |last1=Aging |first1=Institute of Medicine (US) Committee on a National Research Agenda on |last2=Lonergan |first2=Edmund T. |title=Basic Biomedical Research |date=1991 |publisher=National Academies Press (US) |url=https://www.ncbi.nlm.nih.gov/books/NBK234008/ |access-date=20 January 2023 |language=en}}</ref> [[Philosophy:Life extension#Anti-aging drugs|Anti-aging drugs]] are a potential tool for extending life.<ref name=Kaeberlein>{{cite journal | vauthors = Kaeberlein M | title = Resveratrol and rapamycin: are they anti-aging drugs? | journal = BioEssays | volume = 32 | issue = 2 | pages = 96–9 | date = February 2010 | pmid = 20091754 | doi = 10.1002/bies.200900171 | s2cid = 16882387 }}</ref>

Aubrey de Grey, a theoretical gerontologist, has proposed that aging can be reversed by [[Biology:Strategies for engineered negligible senescence|strategies for engineered negligible senescence]]. De Grey has established The Methuselah Mouse Prize to award money to researchers who can extend the maximum life span of mice. So far, three Mouse Prizes have been awarded: one for breaking longevity records to Dr. Andrzej Bartke of [[Organization:Southern Illinois University|Southern Illinois University]] (using GhR knockout mice); one for late-onset rejuvenation strategies to Dr. Stephen Spindler of the [[Organization:University of California|University of California]] (using caloric restriction initiated late in life); and one to Dr. Z. Dave Sharp for his work with the pharmaceutical rapamycin.<ref>{{cite web |url=http://mfoundation.org/work |publisher=Methuselah Foundation |title=Work |access-date=2018-12-10 |archive-url=https://web.archive.org/web/20150214103654/http://mfoundation.org/work |archive-date=2015-02-14 |url-status=dead }}</ref>

==Correlation with DNA repair capacity==
{{Main|Biology:DNA damage theory of aging}}
Accumulated DNA damage appears to be a limiting factor in the determination of maximum life span. The theory that DNA damage is the primary cause of aging, and thus a principal determinant of maximum life span, has attracted increased interest in recent years. This is based, in part, on evidence in humans and mice that inherited deficiencies in DNA repair genes often cause accelerated aging.<ref>{{cite journal | vauthors = Hoeijmakers JH | title = DNA damage, aging, and cancer | journal = The New England Journal of Medicine | volume = 361 | issue = 15 | pages = 1475–85 | date = October 2009 | pmid = 19812404 | doi = 10.1056/NEJMra0804615 }}</ref><ref name=Diderich>{{cite journal | vauthors = Diderich K, Alanazi M, Hoeijmakers JH | title = Premature aging and cancer in nucleotide excision repair-disorders | journal = DNA Repair | volume = 10 | issue = 7 | pages = 772–80 | date = July 2011 | pmid = 21680258 | doi = 10.1016/j.dnarep.2011.04.025 | pmc = 4128095 }}</ref><ref name="Freitas_2011">{{cite journal | vauthors = Freitas AA, de Magalhães JP | title = A review and appraisal of the DNA damage theory of ageing | journal = Mutation Research | volume = 728 | issue = 1–2 | pages = 12–22 | date = 2011 | pmid = 21600302 | doi = 10.1016/j.mrrev.2011.05.001 }}</ref> There is also substantial evidence that DNA damage accumulates with age in mammalian tissues, such as those of the brain, muscle, liver, and kidney (reviewed by Bernstein et al.<ref>{{cite book | vauthors = Bernstein H, Payne CM, Bernstein C, Garewal H, Dvorak K | date = 2008 | chapter = Chapter 1: Cancer and aging as consequences of un-repaired DNA damage.| title = New Research on DNA Damages | veditors = Kimura H, Suzuki A | publisher = Nova Science Publishers, Inc. | location = New York | pages = 1–47 | isbn = 978-1-60456-581-2 }}</ref> and see [[Biology:DNA damage theory of aging|DNA damage theory of aging]] and [[Biology:DNA damage (naturally occurring)|DNA damage (naturally occurring)]]). One expectation of the theory (that DNA damage is the primary cause of aging) is that among species with differing maximum life spans, the capacity to repair DNA damage should correlate with lifespan. The first experimental test of this idea was by Hart and Setlow<ref>{{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 | bibcode = 1974PNAS...71.2169H | doi-access = free }}</ref> who measured the capacity of cells from seven different mammalian species to carry out DNA repair. They found that nucleotide excision repair capability increased systematically with species longevity. This correlation was striking and stimulated a series of 11 additional experiments in different laboratories over succeeding years on the relationship of nucleotide excision repair and life span in mammalian species (reviewed by Bernstein and Bernstein<ref>{{cite book | vauthors = Bernstein C, Bernstein H | date = 1991 | title = Aging, Sex, and DNA Repair | publisher = Academic Press | location = San Diego | isbn = 978-0-12-092860-6 }}</ref>). In general, the findings of these studies indicated a good correlation between nucleotide excision repair capacity and life span. The association between nucleotide excision repair capability and longevity is strengthened by the evidence that defects in nucleotide excision repair proteins in humans and rodents cause features of premature aging, as reviewed by Diderich.<ref name=Diderich />

Further support for the theory that DNA damage is the primary cause of aging comes from study of Poly ADP ribose polymerases (PARPs). PARPs are enzymes that are activated by DNA strand breaks and play a role in DNA base excision repair. Burkle et al. reviewed evidence that PARPs, and especially PARP-1, are involved in maintaining mammalian longevity.<ref name="pmid15743677">{{cite journal | vauthors = Bürkle A, Brabeck C, Diefenbach J, Beneke S | title = The emerging role of poly(ADP-ribose) polymerase-1 in longevity | journal = The International Journal of Biochemistry & Cell Biology | volume = 37 | issue = 5 | pages = 1043–53 | date = May 2005 | pmid = 15743677 | doi = 10.1016/j.biocel.2004.10.006 }}</ref> The life span of 13 mammalian species correlated with poly(ADP ribosyl)ation capability measured in mononuclear cells. Furthermore, lymphoblastoid cell lines from peripheral blood lymphocytes of humans over age 100 had a significantly higher poly(ADP-ribosyl)ation capability than control cell lines from younger individuals.

==Research data==
* A comparison of the heart [[Biology:Mitochondria|mitochondria]] in rats (7-year maximum life span) and pigeons (35-year maximum life span) showed that pigeon mitochondria leak fewer [[Biology:Radical|free-radicals]] than rat mitochondria, despite the fact that both animals have similar [[Metabolic rate|metabolic rate]] and cardiac output<ref>{{cite journal | vauthors = Herrero A, Barja G | title = Sites and mechanisms responsible for the low rate of free radical production of heart mitochondria in the long-lived pigeon | journal = Mechanisms of Ageing and Development | volume = 98 | issue = 2 | pages = 95–111 | date = November 1997 | pmid = 9379714 | doi = 10.1016/S0047-6374(97)00076-6 | s2cid = 20424838 }}</ref>
* For [[Biology:Mammal|mammal]]s there is a direct relationship between mitochondrial membrane fatty acid saturation and maximum life span<ref>{{cite journal |vauthors=Pamplona R, Portero-Otín M, Riba D, Ruiz C, Prat J, Bellmunt MJ, Barja G |date=October 1998 |title=Mitochondrial membrane peroxidizability index is inversely related to maximum life span in mammals |journal=[[Chemistry:Journal of Lipid Research|Journal of Lipid Research]] |volume=39 |issue=10 |pages=1989–94 |doi=10.1016/S0022-2275(20)32497-4 |pmid=9788245 |doi-access=free}}</ref>
* Studies of the [[Biology:Liver|liver]] [[Chemistry:Lipid|lipid]]s of [[Biology:Mammal|mammal]]s and a bird (pigeon) show an inverse relationship between maximum life span and number of [[Chemistry:Double bond|double bond]]s<ref>{{cite journal | vauthors = Pamplona R, Portero-Otín M, Riba D, Requena JR, Thorpe SR, López-Torres M, Barja G | title = Low fatty acid unsaturation: a mechanism for lowered lipoperoxidative modification of tissue proteins in mammalian species with long life spans | journal = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 55 | issue = 6 | pages = B286–91 | date = June 2000 | pmid = 10843345 | doi=10.1093/gerona/55.6.b286| doi-access = free }}</ref>
* Selected species of birds and mammals show an inverse relationship between [[Biology:Telomere|telomere]] rate of change (shortening) and maximum life span<ref>{{cite journal | vauthors = Haussmann MF, Winkler DW, O'Reilly KM, Huntington CE, Nisbet IC, Vleck CM | title = Telomeres shorten more slowly in long-lived birds and mammals than in short-lived ones | journal = Proceedings. Biological Sciences | volume = 270 | issue = 1522 | pages = 1387–92 | date = July 2003 | pmid = 12965030 | pmc = 1691385 | doi = 10.1098/rspb.2003.2385 }}</ref>
* Maximum life span correlates negatively with [[Biology:Antioxidant|antioxidant]] [[Biology:Enzyme|enzyme]] levels and [[Biology:Radical|free-radicals]] production and positively with rate of [[Biology:DNA repair|DNA repair]]<ref>{{cite journal | vauthors = Perez-Campo R, López-Torres M, Cadenas S, Rojas C, Barja G | title = The rate of free radical production as a determinant of the rate of aging: evidence from the comparative approach | journal = Journal of Comparative Physiology B: Biochemical, Systemic, and Environmental Physiology | volume = 168 | issue = 3 | pages = 149–58 | date = April 1998 | pmid = 9591361 | doi = 10.1007/s003600050131 | s2cid = 12080649 }}</ref>
* Female mammals express more Mn−SOD and glutathione peroxidase antioxidant enzymes than males. This has been hypothesized as the reason they live longer<ref>{{cite journal | vauthors = Viña J, Borrás C, Gambini J, Sastre J, Pallardó FV | title = Why females live longer than males? Importance of the upregulation of longevity-associated genes by oestrogenic compounds | journal = FEBS Letters | volume = 579 | issue = 12 | pages = 2541–5 | date = May 2005 | pmid = 15862287 | doi = 10.1016/j.febslet.2005.03.090 | doi-access = free }}</ref> However, mice entirely lacking in glutathione peroxidase&nbsp;1 do not show a reduction in lifespan.
* The maximum life span of [[Biology:Genetically modified organism|transgenic]] mice has been extended about 20% by overexpression of human [[Biology:Catalase|catalase]] targeted to mitochondria<ref>{{cite journal | vauthors = Schriner SE, Linford NJ, Martin GM, Treuting P, Ogburn CE, Emond M, Coskun PE, Ladiges W, Wolf N, Van Remmen H, Wallace DC, Rabinovitch PS | title = Extension of murine life span by overexpression of catalase targeted to mitochondria | journal = Science | volume = 308 | issue = 5730 | pages = 1909–11 | date = June 2005 | pmid = 15879174 | doi = 10.1126/science.1106653 | bibcode = 2005Sci...308.1909S | s2cid = 38568666 }}</ref>
* A comparison of 7 non-primate mammals (mouse, hamster, rat, guinea-pig, rabbit, pig and cow) showed that the rate of mitochondrial superoxide and hydrogen peroxide production in heart and kidney were inversely correlated with maximum life span<ref>{{cite journal | vauthors = Ku HH, Brunk UT, Sohal RS | title = Relationship between mitochondrial superoxide and hydrogen peroxide production and longevity of mammalian species | journal = Free Radical Biology & Medicine | volume = 15 | issue = 6 | pages = 621–7 | date = December 1993 | pmid = 8138188 | doi = 10.1016/0891-5849(93)90165-Q }}</ref>
* A study of 8 non-primate mammals showed an inverse correlation between maximum life span and oxidative damage to mtDNA ([[Biology:Mitochondrial DNA|mitochondrial DNA]]) in heart & brain<ref>{{cite journal | vauthors = Barja G, Herrero A | title = Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heart and brain of mammals | journal = FASEB Journal | volume = 14 | issue = 2 | pages = 312–8 | date = February 2000 | pmid = 10657987 | url = http://www.fasebj.org/cgi/content/full/14/2/312 | doi=10.1096/fasebj.14.2.312| s2cid = 14826037 }}</ref>
* A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span<ref>{{cite journal | vauthors = Agarwal S, Sohal RS | title = Relationship between susceptibility to protein oxidation, aging, and maximum life span potential of different species | journal = Experimental Gerontology | volume = 31 | issue = 3 | pages = 365–72 | year = 1996 | pmid = 9415119 | doi = 10.1016/0531-5565(95)02039-X | s2cid = 21564827 }}</ref>
* There is a direct correlation between DNA repair and maximum life span for [[Biology:Mammal|mammal]]ian species<ref>{{cite journal | vauthors = Cortopassi GA, Wang E | title = There is substantial agreement among interspecies estimates of DNA repair activity | journal = Mechanisms of Ageing and Development | volume = 91 | issue = 3 | pages = 211–8 | date = November 1996 | pmid = 9055244 | doi = 10.1016/S0047-6374(96)01788-5 | s2cid = 24364141 }}</ref>
* [[Biology:Drosophila|Drosophila]] (fruit-flies) bred for 15&nbsp;generations by only using eggs that were laid toward the end of reproductive life achieved maximum life spans 30% greater than that of controls<ref>{{cite journal | vauthors = Kurapati R, Passananti HB, Rose MR, Tower J | title = Increased hsp22 RNA levels in Drosophila lines genetically selected for increased longevity | journal = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 55 | issue = 11 | pages = B552–9 | date = November 2000 | pmid = 11078089 | doi=10.1093/gerona/55.11.b552| doi-access = free }}</ref>
* Overexpression of the enzyme which synthesizes [[Chemistry:Glutathione|glutathione]] in long-lived [[Biology:Genetically modified organism|transgenic]] ''Drosophila'' (fruit-flies) extended maximum lifespan by nearly 50%<ref>{{cite journal | vauthors = Orr WC, Radyuk SN, Prabhudesai L, Toroser D, Benes JJ, Luchak JM, Mockett RJ, Rebrin I, Hubbard JG, Sohal RS | title = Overexpression of glutamate-cysteine ligase extends life span in Drosophila melanogaster | journal = The Journal of Biological Chemistry | volume = 280 | issue = 45 | pages = 37331–8 | date = November 2005 | pmid = 16148000 | doi = 10.1074/jbc.M508272200 | doi-access = free }}</ref>
* A mutation in the '''age−1''' gene of the [[Biology:Nematode|nematode]] worm ''[[Biology:Caenorhabditis elegans|Caenorhabditis elegans]]'' increased mean life span 65% and maximum life span 110%.<ref>{{cite journal | vauthors = Friedman DB, Johnson TE | title = A mutation in the age-1 gene in Caenorhabditis elegans lengthens life and reduces hermaphrodite fertility | journal = Genetics | volume = 118 | issue = 1 | pages = 75–86 | date = January 1988 | doi = 10.1093/genetics/118.1.75 | pmid = 8608934 | pmc = 1203268 | url = http://www.genetics.org/cgi/reprint/118/1/75 }}</ref> However, the degree of lifespan extension in relative terms by both the age-1 and daf-2 mutations is strongly dependent on ambient temperature, with ≈10% extension at 16&nbsp;°C and 65% extension at 27&nbsp;°C.
* Fat-specific Insulin Receptor [[Biology:Knockout mouse|KnockOut]] (FIRKO) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18%.<ref>{{cite journal | vauthors = Blüher M, Kahn BB, Kahn CR | title = Extended longevity in mice lacking the insulin receptor in adipose tissue | journal = Science | volume = 299 | issue = 5606 | pages = 572–4 | date = January 2003 | pmid = 12543978 | doi = 10.1126/science.1078223 | bibcode = 2003Sci...299..572B | s2cid = 24114184 }}</ref>
* The capacity of mammalian species to detoxify the carcinogenic chemical [[Chemistry:Benzopyrene|benzo(a)pyrene]] to a water-soluble form also correlates well with maximum life span.<ref>{{cite journal | vauthors = Moore CJ, Schwartz AG | title = Inverse correlation between species lifespan and capacity of cultured fibroblasts to convert benzo(a)pyrene to water-soluble metabolites | journal = Experimental Cell Research | volume = 116 | issue = 2 | pages = 359–64 | date = October 1978 | pmid = 101383 | doi = 10.1016/0014-4827(78)90459-7 }}</ref>
* Short-term induction of [[Biology:Oxidative stress|oxidative stress]] due to [[Biology:Calorie restriction|calorie restriction]] increases life span in ''Caenorhabditis elegans'' by promoting stress defense, specifically by inducing an enzyme called catalase. As shown by Michael Ristow and co-workers nutritive antioxidants completely abolish this extension of life span by inhibiting a process called [[Biology:Mitohormesis|mitohormesis]].<ref>{{cite journal |vauthors=Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M |date=October 2007 |title=Glucose Restriction Extends ''Caenorhabditis elegans'' Life Span by Inducing Mitochondrial Respiration and Increasing Oxidative Stress |journal=Cell Metabolism |volume=6 |issue=4 |pages=280–293 |doi=10.1016/j.cmet.2007.08.011 |pmid=17908557 |doi-access=free}}</ref>

== See also ==
* Extreme longevity tracking
* [[Biology:Genetics of aging|Genetics of aging]]
* Longevity quotient
* [[Biology:Strategies for engineered negligible senescence|Strategies for engineered negligible senescence]] (SENS)

== References ==
{{Reflist|colwidth=30em|refs=

<ref name=Mitchell1911>{{cite journal |last1=Mitchell |first1=P.C. |year=1911 |title=On longevity and relative viability in mammals and birds; with a note on the theory of longevity |journal=Proceedings of the Zoological Society of London |volume=81 |issue=2 |pages=425–548 |doi=10.1111/j.1096-3642.1911.tb01942.x |url=https://www.biodiversitylibrary.org/part/72357 }}</ref>

}}

== External links ==
* [http://genomics.senescence.info/species/ Anage Database]
* [http://www.senescence.info/ Informational website on the biology of aging]
* [http://www.benbest.com/lifeext/aging.html Mechanisms of Aging]


{{DEFAULTSORT:Maximum Life Span}}
[[Category:Actuarial science]]
[[Category:Senescence]]

{{Sourceattribution|Maximum life span}}