Maximum life span

Maximum life span

Maximum life span is a measure of the maximum amount of time one or more members of a population has been observed to survive between birth and death.

Most living species have at least one upper limit on the number of times cells can divide. For humans, this is called the Hayflick limit, although number of cell divisions does not strictly control lifespan (non-dividing cells and dividing cells lived 120 years in the oldest known human).



In animal studies, maximum life 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 initial sample size.[1]

Maximum life span is in contrast with mean life span (average life span or life expectancy). Mean life span varies with susceptibility to disease, accident, suicide and homicide, whereas maximum life span is determined by "rate of aging".[2]

In humans

The longest-living person whose dates of birth and death were verified to the modern norms of Guinness World Records and the Gerontology Research Group was Jeanne Calment, a French woman who lived to 122. The maximum (recorded) life span for humans has increased from 103 in 1798 to 110 years in 1898, 115 years in 1990, and 122.45 years since Calment's death in 1997 (See List of the verified oldest people and List of verified supercentenarians who died before 1980.), among steady improvements in overall life expectancy. Reduction of infant mortality has accounted for most of this increased average longevity, but since the 1960s mortality rates among those over 80 years have decreased by about 1.5% per year. "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."[3] Animal studies suggest that further lengthening of human lifespan could be achieved through "calorie restriction mimetic" drugs or by directly reducing food consumption. Although calorie restriction has not been proven to extend the maximum human life span, as of 2006, results in ongoing primate studies are promising.[4]

No fixed theoretical limit to human longevity is apparent today.[5] "A fundamental question in aging research is whether humans and other species possess an immutable life-span limit."[6] "The assumption that the maximum human life span is fixed has been justified [but] is invalid in a number of animal models and ... may become invalid for humans as well."[7] 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.[8] 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.[9]

In other animals

Small animals such as birds and squirrels rarely live to their maximum life span, usually dying of accidents, disease or predation. Grazing animals accumulate wear and tear to their teeth to the point where they can no longer eat, and they die of starvation.[citation needed]

The maximum life span of most species has not been accurately determined, because the data collection has been minimal and the number of species studied in captivity (or by monitoring in the wild) has been small.[citation needed]

Maximum life span is usually longer for species that are larger or have effective defenses against predation, such as bird flight, tortoise shells, porcupine quills, or large primate brains.

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:

The longest-lived vertebrates have been variously described as

  • Macaws (A parrot that can live up to 80-100 years in captivity)
  • koi (A Japanese species of fish, 200+ years, though generally not exceeding 25) Hanako was reportedly 226 years old upon her death.[14][15]
  • Greenland Sharks (A species of shark native to the North Atlantic, believed to be about 200 years)
  • tortoises (Galápagos tortoise) (190 years)[16]
  • tuataras (a New Zealand reptile species, 100-200+ years[17])
  • 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.[18]
  • 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,[19] which, along with analysis of amino acids, has indicated a maximum life span, stated as "the 211 year-old bowhead could have been from 177 to 245 years old".[20][21][22] However, with the possible exception of the Bowhead whale, the claims of lifespans >100 year must be taken with some skepticism as they rely on conjecture (e.g. counting otoliths) rather than empirical, continuous documentation.

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:


  • There may be no natural limit to the Hydra's life span, but it is not yet clear how to estimate the age of a specimen.

In plants

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 4,841 years old (as of 2010) and the Bristlecone Pine called Prometheus was a little older still, at least 4,844 years (and possibly as old as 5,000 years), when it was cut down in 1964. The oldest known plant (possibly oldest living thing) is a creosote bush (Larrea tridentata) in the Mojave Desert called King Clone at about 11,700 years.

Increasing maximum life span

Currently, the only (non-transgenic) method of increasing maximum life span that is recognized by biogerontologists is calorie restriction with adequate nutrition.[26] "Maximum life span" here means the mean life span of the most long-lived 10% of a given cohort, as 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 40–60% of the calories (but all of the required nutrients) 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.[27]). 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[28]).

A few transgenic species of mice have been created that have maximum life spans greater than that of wild-type or laboratory mice. The Ames and Snell mice, which have mutations in pituitary transcription factors and hence are deficient in Gh, LH, TSH, and secondarily IGF1, have extensions in maximal lifespan of up to 65%. To date, both in absolute and relative terms, these Ames and Snell mice have the maximum lifespan of any mouse not on caloric restriction (see below on GhR). Mutations/knockout of other genes affecting the GH/IGF1 axis, such as Lit, Ghr and Irs1 have also shown extension in lifespan, but much more modest both in relative and absolute terms. The longest lived laboratory mouse ever was a Ghr knockout mouse on caloric restriction, which lived to ~1800 days (maximum for normal B6 mice under ideal conditions is 1200 days) in the lab of A. Bartke at Southern Illinois University.

Most biomedical gerontologists (gerontologists who search for ways to extend maximum life span) believe that biomedical molecular engineering will eventually extend maximum lifespan and even bring about rejuvenation.[citation needed]

Aubrey de Grey, a theoretical gerontologist, has proposed that the damage called aging can be reversed by SENS (Strategies for Engineered Negligible Senescence). Dr. de Grey has established The Methuselah Mouse Prize to award money to researchers who can extend the maximum life span of mice. A. Bartker collected the prize for the GhR knockout mouse and Speakman collected the prize for extending the maximum lifespan of an adult mouse, using caloric restriction initiated late in life.

Research data concerning maximum life span

  • A comparison of the heart mitochondria in rats (7-year maximum life span) and pigeons (35-year maximum life span) showed that pigeon mitochondria leak fewer free-radicals than rat mitochondria, despite the fact that both animals have similar metabolic rate and cardiac output[29]
  • For mammals there is a direct relationship between mitochondrial membrane fatty acid saturation and maximum life span[30]
  • Studies of the liver lipids of mammals and a bird (pigeon) show an inverse relationship between maximum life span and number of double bonds[31]
  • Selected species of birds and mammals show an inverse relationship between telomere rate of change (shortening) and maximum life span[32]
  • Maximum life span correlates negatively with antioxidant enzyme levels and free-radicals production and positively with rate of DNA repair[33]
  • Female mammals express more Mn−SOD and glutathione peroxidase antioxidant enzymes than males. This has been hypothesized as the reason they live longer[34] However, mice entirely lacking in glutathione peroxidase 1 do not show a reduction in lifespan.
  • The maximum life span of transgenic mice has been extended about 20% by overexpression of human catalase targeted to mitochondria[35]
  • 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[36]
  • A study of 8 non-primate mammals showed an inverse correlation between maximum life span and oxidative damage to mtDNA (Mitochondrial DNA) in heart & brain[37]
  • A study of several species of mammals and a bird (pigeon) indicated a linear relationship between oxidative damage to protein and maximum life span[38]
  • There is a direct correlation between DNA repair and maximum life span for mammalian species[39]
  • Drosophila (fruit-flies) bred for 15 generations by only using eggs that were laid toward the end of reproductive life achieved maximum life spans 30% greater than that of controls[40]
  • Overexpression of the enzyme which synthesizes glutathione in long-lived transgenic Drosophila (fruit-flies) extended maximum lifespan by nearly 50%[41]
  • A mutation in the age−1 gene of the nematode worm Caenorhabditis elegans increased mean life span 65% and maximum life span 110%.[42] 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 °C and 65% extension at 27 °C.
  • Fat-specific Insulin Receptor KnockOut (FIRKO) mice have reduced fat mass, normal calorie intake and an increased maximum life span of 18%.[43]
  • The capacity of mammalian species to detoxify the carcinogenic chemical benzo(a)pyrene to a water-soluble form also correlates well with maximum life span.[44]
  • Short-term induction of oxidative stress due to 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 mitohormesis.[45]

See also


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