Evolution of aging

Inquiry into the evolution of aging , survival success, and success of aging . Leading hypotheses [1] [2] suggest that a combination of limited resources, and an increasing risk of death by environmental causes determines an “optimal” level of self-maintenance, ie the repair of molecular and cellular level accumulates over time. Darwinian fitness is one of the most important resources of the world. In consequence, traits that improve the individual’s performance in early life are favored by selection, even if they have negative end-of-life effects when the individual has already passed on their genes to the next generation.


August Weismann was responsible for the interpretation and formalization of Darwinian evolution in a modern theoretical framework. In 1889, he theorized that aging is part of life’s program because of the need for the next generation, sustaining the turnover that is necessary for evolution. [3] This theory again has much intuitive appeal, but it suffers from having a teleological or goal-driven explanation. In other words, a purpose for aging, but not a mechanismby which that purpose could be achieved. Aging may have this advantage for the long-term health of the community; But that does not explain how they would acquire the genes that make them get old and die, or that they would be more successful than others lacking such genes. (In fact, there is every reason to believe that the opposite is true: individual fitness decreases .) Weismann later abandoned his theory.

Theories suggesting that deterioration and death are the result of an organism’s evolved design (such as Weismann’s “programmed death” theory) are referred to as theories of programmed aging or adaptive aging. The idea that the age has been selected because of its deleterious effect was largely discounted for much of the 20th century, but a theoretical model suggests that altruistic aging is possible. [4]

Mutation accumulation

The first modern theory of mammal age was formulated by Peter Medawar in 1952. It formed from discussions in the previous decade with JBS Haldane and the selection shadow concept. Their idea was that age was a matter of neglect. Nature is a highly competitive place, and almost all animals in nature before they reach age. Therefore, there is not much reason why the body shoulds REMAIN made for the long haul – not much selection pressure for traits That Would Maintain viability past the time When MOST Would Be Dead animals anyway, killed by predators, disease, accidents gold. [5]

Medawar’s theory is referred to as Mutation Accumulation . The mechanism of action involves random, detrimental germline mutations of a kind that happen to show their effect only late in life. Unlike most detrimental mutations, these would not be easily separated by natural selection. On the grand scale, senescence would be the summation of deleterious genes that only present in older individuals. [6] Hence they would ‘accumulate’ and, perhaps, cause all the decline and damage that we associate with aging. [7] [8]

Modern genetics science HAS Disclosed is feasible problem with the mutation accumulation concept fait que it is Now Known That genes are Typically Expressed in specific tissues at specific times (see regulation of gene Expression). Expression is controlled by some genetic “program” that activates different genes at different times in the normal growth, development, and day-to-day life of the organism. Defects in genes causes problems ( genetic diseaseswhen they are not properly expressed when required. A problem late in life suggests that the genetic program is termed a gene expression in a late life and mutational defect proper proper expression. This implies existence of a program that is called for different expression in that point in life. Why, given Medawar’s concept, would it exist in the future? The maintenance mechanism theory (discussed below) avoids this problem.

Medawar’s concept suggests that the evolution process was affected by the age at which an organism was capable of reproducing. Characteristics that adversely affected the organism’s ability to propagate its characteristics and thus would be highly “selected against” by natural selection . Characteristics that caused the same adverse effects that it would be relatively unlikely to have any effect on the organism’s ability to propagate and then be allowed by natural selection. This concept fits well with the observed multiplicity of mammal life spans (and differing ages of sexual maturity) and is important to all of the following.

Medawar did not suggest that there were fundamental limitations on lifespan. Organisms exhibiting negligible senescence suggest that aging is not a fundamental limitation, at least not in the scale of mammal lifespan.

Antagonistic pleiotropy

Main article: Antagonistic pleiotropy hypothesis

Medawar’s theory was further developed by George C. Williams in 1957, who noted that senescence may be causing many deaths, citation needed ] even if animals are not ‘dying of old age.’ In the earliest stages of senescence, an animal may lose a bit of its speed, and then predators will be sixteen it first, while younger animals will flee successfully. Or its immune system may decline, and it becomes the first to die of a new infection. Such is a competitive place, said Williams, (turning Medawar’s argument back at him), that even a little bit of senescence can be fatal; so natural selection does indeed care; ageing is not cost-free.

Williams’ Objection to Modernization of Demography in Natural Environments. These observations cast doubt on Medawar’s theory. Another problem with Medawar’s theory became apparent in the late 1990s, when genomic analysis became widely available. It turns out that the causes of death are not random mutations; rather, these genes form tight-knit families that have been around as long as eukaryotic life. Baker’s yeast , worms , fruit flies , and mice all share Reviews some of the Sami aging genes. [9]

Williams (1957) proposed his own theory, called antagonistic pleiotropy . Pleiotropy means one gene that has two or more effects on the phenotype . In antagonistic pleiotropy, one of these effects is beneficial and another is detrimental. In essence, this refers to the genes that offer benefits early in life. If evolution is the most successful, then it may be a very important event. [1] Because aging is a necessary effect, Williams considered any alteration of the aging process to be “impossible.”

Antagonistic pleiotropy is a prevailing theory today, but this is largely by default. In fact, experimental biologists have looked for the genes that cause aging, and since 1990 Of the many aging genes that have been reported, some seem to enhance fertility early in life, or to carry other benefits. But there are other age groups for which This is not what Williams predicted. This may be thought of as partial validation of the theory, but logically it cuts to the core premise: that genetic trade-offs are the root cause of aging.

Another difficulty with antagonism and the hypothesis that the aging is an adverse effect of some beneficial function is that the linkage between adverse and beneficial effects would need to be rigid in the sense that the evolution would not be able to evolve a way to accomplish the benefit without incurring the adverse effect even over a very long time span. Such a rigid relationship has not been experimentally demonstrated and, in general, is capable of independently and individually adjusting myriad organism characteristics.

In breeding experiments, Michael R. Pink selected fruit flies for long lifespan. Based on antagonistic pleiotropy, Rose is expected to reduce their fertility. His team found that they were able to survive as long as they lived, but to their surprise, the long-lived, inbred flies. This is another setback for pleiotropy theory, though Rose maintains it may be an experimental artifact. [10]

Disposable soma theory

Main article: Disposable soma theory of aging

A third mainstream theory of aging, the ‘ ‘ Disposable soma theory , proposed in 1977 by Thomas Kirkwood , presumes that the body must budget the amount of energy available to it. The body uses food energy for metabolism, for reproduction, and for repair and maintenance. With a finite supply of food, the body must be compromised, and do not like it. It is the compromised in allocating energy to the repair function that causes the body to gradually deteriorate with age. [11]A caveat to the disposable soma theory suggests that time, rather than energy, is a limiting resource that can be critical to an organism. The concept is that each organism must reproduce in an optimal period in order to ensure the greatest chance of success for the offspring. This optimal period is dictated by the ecological nature of the organization in essence, it limits the time that any given organism can devote to growth and development prior to bearing offspring. Thus, developmental rate and gestational rate are subject to evolutionary pressure. The need to accelerate gestation in the face of increased cellular density, resulting in an accumulation of damage and decreased life expectancy. This concept stems from a comparative analysis of genomic stability in mammalian cells.[12]

There are arguments against the disposable soma theory. The theory clearly predicts that a shortage of food should make the compromise more severe all around; but in many experiments, continued since 1930, it has been demonstrated that animals live much less than controls. This is the caloric restriction (CR) effect, [13] [14] [15] and it can not be easily reconciled with the Disposable Soma theory. Though by decreasing energy expenditure the damage generated (by free radicals, for instance) is expected to be reduced and the total energy budget might well be reduced, but the investment in repair function might still be relatively the same. But dietary restriction has not been shown to increase lifetime reproductive success (fitness), because reproductive status is lower, reproductive output is also lower. So CR does not completely dismiss disposable soma theory.

With respect to Kriete Such limitations [16] Proposed consideration of systems-level properties like robustness to Characterize aging as a robustness tradeoff. Selon cette concept living systems evolve into a state of highly optimized tolerance Promoting beneficial traits for survival and fitness at the cost of fragilities driving the aging phenotype. The view is consistent with aspects of the antagonistic pleiotropy and the disposable soma theory, offers additional goal Mechanisms rooted in complex systems theory.

Other problems with the classical aging theories

The evolution of the theory of evolution is based on the concept of the evolution of metabolism.

One is apoptosis , or programmed cell death. Apoptosis is responsible for killing infected cells, cancer cells, and cells that are simply in the wrong place during development. There are clear benefits to apoptosis, so the existence of apoptosis is not a problem for evolutionary theory. The problem is that apoptosis seems to be rampant in late life and kill healthy cells, causing weakness and degeneration citation needed ] . And, paradoxically, apoptosis has been observed as a kind of ‘altruistic suicide’ in colonies of yeast under stress. [17]It is more likely that the senescence arose because it is more likely to have a positive evolutionary effect, rather than some of the other side effects (pleiotropy).

A second ‘deliberate’ mechanism is called replicative senescence or cellular senescence . Metaphorically, it can be said to ‘count’ (with its telomeres ) the number of times it has divided, and after a set number of replications, it languishes and dies. It has been proposed that this mechanism evolved to suppress cancer. [18] [19] Many invertebrates experience replicative senescence, though they never die of cancer. citation needed ] Even one-celled replication count replies, and they would not have to replenish their telomeres with conjugation (sex). [20]

More strictly, cells can not ‘count’ the number of times they have divided citation needed ] . Telomeres are not a counting mechanism citation needed ] , however they may be used to indicate a particular chromosome has been replicated. Cellular processes for genetic material replication occur in both directions along DNA , 5 ‘to 3’ and on the other strand, 3 ‘to 5’. As the 3 ‘or 5’ end is impossible for DNA polymeraseto get the base of the mark, a handful of basepairs (10-15) are cut off each replication. Over time, it is not possible to replicate that chromosome without cutting into genes.

The dilemma is that classical evolutionary theory says that it is maintained in a way that ensures the viability of an organization and its offspring. Aging can only cut off an individual’s ability to reproduce. So, selon classical theory, aging Could only evolve as a side effect, or epiphenomenon of selection. The disposable soma theory and antagonistic pleiotropy theory are examples in which a compensating individual benefit, compatible with classical evolutiontheory (See neo-Darwinism ) is proposed. Nevertheless, there is accumulated evidence that it is appropriate to adapt to its own right, selected for its own sake. [21] [22]

Semelparous organisms and others that die suddenly following reproduction (eg salmon , octopus , marsupial mouse ( brown antechinus ), etc.) also represent instances of organisms that include a lifespan-limiting feature. Sudden death is more obviously an instance of death or a progressive adaptation than gradual aging. Elements associated with Evolved Clearly Biological Mechanisms Such As hormone signaling-have-been APPROBATION in the death Mechanisms of organisms Such As the octopus . [23]

Impact of new evolution concepts on aging theory

At the time of non-programmed aging theories were developed, there was very little scientific disagreement with classical theories (ie Neo-Darwinism ) regarding the process of evolution. HOWEVER, in addition to suicidal behavior of semelparous species (not handled by the classical aging theories) other Apparently Individually opponent organism characteristics Such As altruism and sexual reproduction Were Observed. In response to these other conflicts, adjustments to classical theory have been proposed:

  • Various group selection theories (beginning in 1962) suggests that this benefit to a group could be offset by the adverse nature of a characteristic such as altruism . The same principle could be applied to the benefits of limited life span.
  • Evolvability theories (beginning in 1995) suggests that a characteristic that has increased organism’s ability to evolve could also offset an individual disadvantage and thus be evolved and retained. Multiple evolvability benefits of a limited lifespan are proposed by Weismann.

Age grouping theories based on group selection

Group selection is often criticized to be too slow to happen in real biology. However, Jiang-Nan Yang [4] has recently been shown to be an individual-based model of the evolution of altruistic aging. Can be based on a population viscosity (limited dispersal offspring, first proposed by Hamilton (1964) for kin selection) that is widely present in natural populations. This population structure builds a continuum between individual selection, kin selection, kin group selection, and group selection. DS Wilson et al. (1992) [24] and Taylor (1992) [25]It may not be possible to co-operate with this population because it is not possible to co-operate with it. cooperation. [4] Mitteldorf and DS Wilson (2000), who later reported that the population was fluctuating, then local populations can not be excluded. [26]By assuming individual differences in adaptations, Yang (2013) provides further evidence that the benefit of local altruism may be stored in the form of The results of this study will be derived from the following table of contents. [4] In Yang (2013) ‘s model, altruistic aging is stabilized by higher-level selection instead of just kin selection. [4]

Mitteldorf [27] proposed a group benefit of a limited lifespan involving regulation of population dynamics . Populations in nature are subject to boom and bust cycles. Often overpopulation can be punished by famine or by epidemic. Either one could wipe out an entire population. Senescence is a means by which a species can take control of its own death rate, and level out the boom-bust cycles. May this story be more plausible than the Weismann hypothesis as a mechanistic explanation, Because It addresses the issue of how group selection can be rapid enough to compete with individual selection.

Libertini [28] also suggests benefits for adaptive aging.

Inversely, a Negative Senescence Theory Lee RD (similarly JW Vaupel). [29] Also postreproductive individuals make intergenerational transfers: bottlenose dolphins and pilot whales guard their grandchildren; 200 species of birds; sex differences in the survival of anthropoid primates or an Efe Infant is often attended by more than 10 people. Developed a formal theory integrating selection with the results of selection.[30]

Ageing theories based on evolvability

Goldsmith [31] Proposed That in addition to Increasing the rate generation, and thereby misses Evolution has limited lifespan Improves the Evolution process by limiting the Ability of older Individuals to dominate the gene pool . Further, the evolution of such characteristics and immunity may be necessary to limit the pathogenicity of the disease. An older and more experienced, but less intelligent animal would have a better, more intelligent animal except for the effects of aging.

Skulachev [32] has suggested that it increases the survival rate by providing a growing barrier to survival and reproduction. In this sense, it would be useful to consider that of mating rituals that take the form of contests or that they should be overcome in order to mate. This suggests an advantage of gradual aging on a sudden death as a way of lifespan regulation.

Weissmann’s 1889 age theory was essentially an evolvability theory. Ageing or otherwise purposely limited lifespan helps, and therefore, presumably better-adapted individuals.

Yang (2013) ‘s model [4] is also based on mechanisms of evolution. Aging accelerates the accumulation of novel adaptive genes in local populations. However, Yang changed the terminology of “evolvability” into “genetic creativity” throughout the paper to facilitate the understanding of how aging can be a short-term benefit than the word “evolvability” would imply.

Lenart and Vašku (2016) [33] also invoked the evolution of aging. However, they are likely to be able to adapt to the aging process. In other words, evolution can change the pace of aging.


If organisms purposely limit their lifespans via ageing or semelparous behavior, they may be very complex, just as mechanisms that provide for mentation, vision, digestion, or other biological function are typically very complex. Such a mechanism could involve hormones, signaling, sensing of external conditions, and other complex functions typical of evolved mechanisms. Such complex mechanisms could explain all the observations of aging and semelparous behavior.

It is typical for a Given biological function to be controlled by a single mechanism That Is able of sensing the terms germane And Then The Necessary executing function citation needed ] . The mechanism signals all the systems and tissues that need to respond to that function by means of organism-wide signals ( hormones ). If aging is indeed a biological function, we would expect a more common mechanism. Various observations (listed below) indeed suggests the existence of a common control mechanism.

It is also suitable for conditions of use. The circadian rhythm and synchronization of mating behavior to planetary cues are examples. In the case of aging as a biological function, the caloric restriction effect may well be an example of the age function being modulated in order to optimize the organism lifespan in response to external conditions. Lifespan prolonged survival, combined with less-frequent reproduction, would be required to maintain a population.

Theories to the effect that aging (or mutation accumulation) is an adverse effect of some other function. The choice of aging theory is therefore more or less determined by one’s position regarding evolutionary processes, and some theorists [34]

Maintenance theories

It is generally accepted that deteriorative processes (wear, other molecular damage) exist and that living organisms have mechanisms to counter deterioration. Wounds heal; dead cells are replaced; claws regrow.

A non-programmed theory of mammal aging [35]that fits with classical evolution theory and is a different concept of different capabilities for maintenance and repair. Longer-lived species possessing many mechanisms for offsetting damage caused by oxidation, telomere shortening, and other deteriorative processes are more effective than those of shorter-lived species. Shorter-lived species, having less need for longevity and thus did not evolve or retain the most-effective repair mechanisms. Damage therefore accumulates more rapidly, resulting in fewer events and shorter lifespan. Since there are many different types of aging, it is likely that there are many different types of maintenance.

A corresponding program based maintenance based on evolvability [36] suggests that the control mechanisms are in a controlled state, which is capable of sensing conditions, such as caloric restriction, and also capable of producing the specific lifespan required by the particular species. In this view, the differences between short- and long-lived species are in the control mechanisms, as opposed to each individual maintenance mechanism.

DNA damage theory

Main article: DNA damage theory of aging

The DNA damage theory of aging is a prominent explanation for aging at the molecular level. This theory postulates that DNA damage is ubiquitous in the biological world and is the primary cause of aging. [37] Consistent with this theory, genetic Elements That Regulate repair of DNA damage in somatic cells Were Proposed to-have pleiotropic effects are beneficial That goal During early development allow deleterious consequences later in life. [37] [38] [39]As an example, studies of mammalian brain and muscle have shown that DNA repair is relatively high during early development when cells are dividing mitotically, but declines substantially as they enter the post-mitotic state. [40] [41] [42]The reduction in DNA repair capability is an important component of neuronal and muscular functions. [37] The effect of reducing the expression of DNA repair capability is to allow increased accumulation of DNA damage. This then impairs gene transcription and causes the progressive loss of cellular and tissue functions that define aging.


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  • Complex program of death mechanisms in semelparous species (eg octopus), including hormone signaling, nervous system involvement, etc. If a limited life is predicted by the age of theories, it would be unusual for an octopus to have a more complex mechanism for accomplishing that function than a mammal.
  • “Ageing genes” with no other apparent function. However, no such date has existed.
  • Caloric restriction effect: reduction of available resources Increases lifespan. This behavior has a plausible group benefit in enhancing the survival of a group under the same conditions.
  • Progeria and Werner syndrome are both single-gene genetic diseases that cause acceleration of many or most symptoms of aging. The fact that a single gene malfunction can cause similar effects on many different manifestations of age. However, both genes have an influence on DNA stability and can be explained by stochastic theories of aging.
  • Although mammal lifespans vary over an approximately 100: 1 range, manifestations of aging (cancer, arthritis, weakness, sensory deficiency, etc.) are similar in different species. This suggests that the deterioration mechanisms and short-lived mammalian functions of a short-lived mammal. All the mammals, therefore all the maintenance mechanisms. This suggests that the difference between mammals is a control mechanism or repair efficiency.
  • Lifespan varies Greatly Among Otherwise very similar species (eg different varieties of salmon 3: 1, 600 different fish: 1) Suggesting That Relatively FEW genes control lifespan and That Relatively minor exchange to genotypeCould causes major differences in lifespan. This method may be used in conjunction with a common control mechanism for the purpose of providing information that is consistent with conventional theories.

Problems with programmed aging theories

Contrary to the theory of death, death, death, death, death, death, death, death, death, death, death, death, death Also, in majority of species, it does not exist anytime after death death rates, but it is expected by the death by age citation needed ] , but the age-dependence of death is very smooth and monotonic. However, as mentioned above, VP Skulachev [43]explained that a process of gradual aging has the advantage of facilitating It is also easy to imagine that animals with a protected environment.

The death rates at the end of the day, which is the opposite of what would be expected if death by age was programmed. From an individual-selection point of view, having genes that would not result in a death death, they would have lost their ability to survive because of death, they would produce more offspring in their lifespan and they could increase the survival of their offspring by providing longer parental support. [44]

Biogerontology considerations

Theories of ageing efforts to understand and find treatments for age-related conditions (see biogerontology ):

  • Those who believe in the idea that they are an unavoidable side effect of some necessary function (antagonistic pleiotropy or disposable soma theories) logically tend to believe that they would be able to do so in the future. Altering ageing is therefore “impossible”, [1] and study of aging mechanisms is of only academic interest.
  • Those believing in theories of multiple maintenance mechanisms tend to believe that ways may be found to enhance the operation of some of those mechanisms. They may be assisted by anti-oxidants or other agents.
  • Those who believe in their age may assume that they may be more likely to interfere with the phenomenon of the phenomenon that appears to be common to multiple symptoms, essentially “slowing down the clock” and delaying multiple manifestations. Such effect may be obtained by fooling a sense function. One such effort is an attempt to find a “mimetic” that would “mimic” the anti-aging effect of calorie restriction . [45]

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