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Maximum life span

Article Discussion

Template:Short description Maximum life span (or, for humans, maximum reported age at death) is a measure of the maximum amount of time one or more members of a population have been observed to survive between birth and death. The term can also denote an estimate of the maximum amount of time that a member of a given species could survive between birth and death, provided circumstances that are optimal to that member's longevity.

Most living species have an upper limit on the number of times somatic cells not expressing telomerase can divide. This is called the Hayflick limit, although this number of cell divisions does not strictly control lifespan.

DefinitionEdit

In animal studies, maximum span is often taken to be the mean life span of the most long-lived 10% of a given cohort. By another definition, however, maximum life span corresponds to the age at which the oldest known member of a species or experimental group has died. Calculation of the maximum life span in the latter sense depends upon the initial sample size.<ref>Template:Cite bookTemplate:Page needed</ref>

Maximum life span contrasts with mean life span (average life span, life expectancy), and longevity. Mean life span varies with susceptibility to disease, accident, suicide and homicide, whereas maximum life span is determined by "rate of aging".<ref>Template:Cite news</ref><ref>Template:Cite journal</ref>Template:Failed verification Longevity refers only to the characteristics of the especially long lived members of a population, such as infirmities as they age or compression of morbidity, and not the specific life span of an individual.Template:Cn

In humansEdit

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Demographic evidenceEdit

The 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 longevity, but since the 1960s mortality rates among those over 80 years have decreased by about 1.5% per year. According to James Vaupel, "The progress being made in lengthening lifespans and postponing senescence is entirely due to medical and public-health efforts, rising standards of living, better education, healthier nutrition and more salubrious lifestyles."<ref>Template:Cite journal</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>Template:Cite journal</ref> Although calorie restriction has not been proven to extend the maximum human life span Template:Asof, results in ongoing primate studies have demonstrated that the assumptions derived from rodents are valid in primates.<ref>Nature, 1 April 2014.</ref><ref>Template:Cite journal</ref>

It has been proposed that no fixed theoretical limit to human longevity is apparent today.<ref>Template:Cite bookTemplate:Page needed</ref><ref>Template:Cite journal</ref> Studies in the 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>{{#invoke:citation/CS1|citation |CitationClass=web }}</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>Template:Cite journal</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>Template:Cite journal</ref><ref name=":2">Template:Cite journal</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>Template:Cite journal</ref> A theoretical study suggested the maximum human lifespan to be around 125 years using a modified stretched exponential function for human survival curves.<ref>Template:Cite journal</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">Template:Cite journal</ref> A theoretical study also suggested that the maximum human life expectancy at birth is limited by the human life characteristic value δ, which is around 104 years.<ref>Template:Cite journal</ref>

In 2017, the 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 evidenceEdit

Evidence for maximum lifespan is also provided by the dynamics of physiological indices with age. For example, scientists have observed that a person's VO2max 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 VO2max value drops below the basal metabolic rate necessary to sustain life, which is approximately 3 ml per kg per minute.<ref name="Nokes Lore">Template:Cite book</ref>Template:Page needed On the basis of this hypothesis, athletes with a VO2max 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 VO2max remained constant".<ref>Nokes (1985) p. 84.</ref>

File:Age dynamics of the body mass.svg
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">Template:Cite journal</ref>

In animalsEdit

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} Small animals such as birds and squirrels rarely live to their maximum life span, usually dying of accidents, disease or predation.Template:Cn

The maximum life span of most species is documented in the AnAge repository (The Animal Ageing and Longevity Database).<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

Maximum life span is usually longer for species that are larger, at least among endotherms,<ref name="Shiner & Uehlinger 2001">Template:Cite journal</ref> or have effective defenses against predation, such as bat or bird flight,<ref>Template:Cite journal</ref> arboreality,<ref name="Shattuck & Williams 20210">Template:Cite journal</ref> chemical defenses<ref>Template:Cite journal</ref> or living in social groups.<ref>Template:Cite book</ref> Among mammals, the presence of a caecal appendix is also correlated with greater maximal longevity.<ref name="Collard et al. 2021">Template:Cite journal</ref>

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

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  • for Brown rat, 3.8<ref>{{#invoke:citation/CS1|citation

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|CitationClass=web }}</ref> The longest-lived vertebrates have been variously described as

  • 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>{{#invoke:citation/CS1|citation

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  • Tuatara (a New Zealand reptile species, 100–200+ years<ref>Tuatara#cite note-43</ref>)
  • Eels, 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>{{#invoke:citation/CS1|citation

|CitationClass=web }}</ref> It was reported that it had died in August 2014 at an age of 155.<ref>Template:Cite news</ref>

  • Whales (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 harpoons in their bodies from about 1890,<ref>{{#invoke:citation/CS1|citation

|CitationClass=web }}</ref> which, along with analysis of amino acids, has indicated a maximum life span of "177 to 245 years old".<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref> {{#invoke:citation/CS1|citation |CitationClass=web }}</ref><ref>Template:Cite journal</ref>

  • Greenland sharks are currently the vertebrate species with the longest known lifespan.<ref name=Nielsen2016>Template:Cite journal
  • Template:Cite magazine</ref> An examination of 28 specimens in one study published in 2016 determined by 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:

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ExceptionsEdit

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In plantsEdit

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} Plants are referred to as annuals which live only one year, biennials which live two years, and 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. A Great Basin Bristlecone Pine called Methuselah is Template:Age years old.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</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>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> The oldest known plant (possibly oldest living thing) is a clonal Quaking Aspen (Populus tremuloides) tree colony in the Fishlake National Forest in Utah called Pando at about 16,000 years. Lichen, a symbiotic algae and fungal proto-plant, such as Rhizocarpon geographicum can live upwards of 10,000 years.Template:Cn

Increasing maximum life spanEdit

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} "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. Rats, mice, and hamsters 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>Template:Cite journal</ref> For 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>Template:Cite journal</ref>

Most biomedical gerontologists believe that biomedical molecular engineering will eventually extend maximum lifespan and even bring about rejuvenation.<ref>Template:Cite book</ref> Anti-aging drugs are a potential tool for extending life.<ref name=Kaeberlein>Template:Cite journal</ref>

Aubrey de Grey, a theoretical gerontologist, has proposed that aging can be reversed by 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 Southern Illinois University (using GhR knockout mice); one for late-onset rejuvenation strategies to Dr. Stephen Spindler of the 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>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>Template:Better source needed

Correlation with DNA repair capacityEdit

{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} 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>Template:Cite journal</ref><ref name=Diderich>Template:Cite journal</ref><ref name="Freitas_2011">Template:Cite journal</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>Template:Cite book</ref> and see DNA damage theory of aging and 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>Template:Cite journal</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>Template:Cite book</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">Template:Cite journal</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.Template:Cn

Research dataEdit

See alsoEdit

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ReferencesEdit

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External linksEdit

Template:Longevity

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