Much evidence confirms this prediction.
For example, bats and mice are mammals of approximately the same size, yet bats can have a maximum life span of up to 30 years, while mice live only 2 or 3 years. The explanation for this is that bats are better protected and have fewer predators. The favorable conditions for survival allowed their late-acting genes to get expressed and selected. Under such favorable conditions, long-lived animals had an advantage over short-lived ones bats generally were able to develop an effective anti-oxidant defense system and the ability to hibernate.
In contrast, in mice, it did not matter whether they had a large or small longevity potential — they just needed enough time to reproduce before getting eaten by predators. This theory, however, has its drawbacks. It seems that evolution is not completely indifferent to events happening late in life, after the reproductive period is over: even a small degree of senescence damage affects survival rates and reproductive success. For example, a prolonged post-reproductive period can improve the success in raising the young. In , the American evolutionary biologist George Williams added an important specification.
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According to him, the very same genes that aid survival and reproduction in an early period of life history, can be damaging and cause senescence in a later period. A large number of observations seem to support it. However, later in life, enhanced calcium deposition can contribute to atherosclerosis.
Thus, high levels of testosterone may give a good edge in sexual competition, yet later in life may contribute to prostate growth. Even at a more fundamental level, oxidative phosphorylation in the respiratory chain is what sustains life, yet the free radicals, formed in the process, cause aging damage. In another instance, the shortening of telomeres plays a part in cell differentiation and prevents cancer, but it also leads to cell replication limit and thus aging and death.
This is indeed a very cogent theory, but also not unproblematic. The concept of temporal antagonism is still largely hypothetical and its epigenetic timing mechanism remains unclear: Why would a gene that helps survival, until say age 40, suddenly become detrimental at the age of 41? Not all discovered genes that affect aging rate, also affect fertility early in life. In fact almost no such genes were found 8 — perhaps with just a few exceptions, such as the decay-accelerating factor DAF genes. The propositions of the above two theories were formalized in by the British evolutionary biologist William Hamilton.
The life histories of semelparous organisms the organisms having a single reproductive episode before death offer perhaps the best demonstration of this principle. Thus, organisms like may-flies or the marsupial antechinus, copulate so vigorously that after several hours of it, they burn out and die of exhaustion. This trade-off mechanism seems to operate also in non-semelparous animals. Thus, several studies of monks and nuns showed that monks have a greater than average longevity according to a recent German study about 5 years above average men, however in earlier Polish and Dutch studies only 1 or 2 years higher.
Still, there exists a wide array of data contradicting this theory. This concept has been challenged by studies professing that sexual activity may actually strengthen the immune system and prolong life, and that survival is not necessarily antagonistic to reproduction. This was suggested for ants by Schrempf et al. On the contrary, greater longevity seems to correlate with greater fecundity.
There seems to be a large number of methodological problems on both sides of the dispute. It is generally difficult to project animal studies e. Human studies also seem to be indeterminate. Regarding, for example, the longevity of monks, the positive effect of their supposed abstinence on longevity may be confounded by many other factors, such as absence of alcoholism or smoking. It appeared in and has been making the headlines since. The Caerphilly study examines men aged , with a 10 year follow up. Thus, it disregards earlier sexual habits and activities that might be determinative for the life span.
It is difficult to disentangle these issues. Since the s, calorie restriction has been consistently shown to increase the life span in almost all animals tried. It is perhaps the only well substantiated experimental method of life prolongation known so far. This, however, does not occur. Moreover, in many calorie restricted models, fertility does not diminish as predicted by the theory. It is interesting to observe how ideological agendas affect areas of scientific interest. The above mainstream theories with the exception of Williams, by British evolutionists figure prominently in almost every review of evolutionary theories of aging.
In contrast, the theories by the American gerontologists Richard Cutler and George Sacher receive there the utmost notice and are cited as the primary authority. According to them, aging has emerged as a result of evolutionary neglect, it is due to an enormous multitude of intractable random mutations, it is inevitable if species are to survive early in life and reproduce. The implied message is that there is not much we can do about it.
The theories by Sacher and Cutler, on the other hand, offer a glimpse of hope. Both authors show a consistent increase in longevity during the evolution of mammalian species, including man. Sacher 29 posited a general formula relating the weight of an animal and the weight of its brain to its maximum life span MLS : Assuming g weight of the human brain, 31 the maximal life span would be somewhere around years. A larger brain, on the other hand, allows for a better internal regulation, and intelligence and social behavior reduce extrinsic mortality.
Thus, an increase in brain size correlates with an increase in longevity. Interestingly, according to it, in any given species, lower body weight is associated with greater longevity, and only the combination of the brain and body weight distinguishes between the life spans of different species.
The optimism implied here is, first of all, that even if conscious human life-extensionist efforts fail, the human race can still rely on evolution for increased longevity of course, if still granted favorable environmental conditions. The limited number of genes associated with aging raises the hopes to pinpoint specific intervention targets. There are obviously huge blank spots in the hominid ancestral descendant sequence.
However, Cutler himself admits that estimations of adaptive gene substitutions differ by orders of magnitude among different authors. And the estimate of 40, genes per human genome is now known to be about twice the actual value. Nevertheless, the suggested tendency of longevity increase is very uplifting. These types of genes could be included in the 0.
These mechanisms seem to be too well orchestrated and directional to be randomly accumulated mutations. The specter of teleology is raised again. Skulachev, Mitteldorf and Goldsmith offer explanations. First of all, according to these authors, an absence of aging would impair variation and thus reduce the species evolvability and adaptability.
The idea here is that the evolution of a higher investment is unlikely to pay off since the return from such an investment may never be realized due to extrinsic mortality. Moreover, investment into reproduction — or early fitness components in general — might withdraw limited resources that could otherwise be used for somatic maintenance and repair. Such resource allocation trade-offs can thus been seen as a physiological extension of Williams' AP model. Whether such trade-offs are physiologically caused by competitive energy or resource allocation — as would be expected under the DS hypothesis — remains somewhat controversial, but the trade-offs themselves are well established see Flatt These elegant experiments represent the first solid empirical tests of the evolutionary theory of aging Rose The classical evolutionary theory of aging has therefore two fundamental cornerstones: MA and AP.
However, it is worth noting that both models are conceptually very similar: under MA, aging evolves through the accumulation of effectively neutral mutations with deleterious late-life effects, whereas, under AP, aging occurs due to mutations with beneficial early- and deleterious late-life effects. In reality, probably both types of mutations occur in populations, yet their relative frequencies remain unknown. Furthermore, the age distribution of mutational effects may be much more complicated than these two scenarios suggest e.
Different species vary dramatically in how long they life. Even older than giant tortoises are certain trees, such as the yew Taxus baccata , with some specimens between 4, and 5, years old c. A few other organisms, such as freshwater polyps of the genus Hydra , are thought to age at a negligible rate or to be even potentially immortal, although this is still somewhat controversial d. Image a courtesy of Matthew Field. Image b courtesy of Fritz Geller-Grimm.
Image c courtesy of Wikipedia. Image d courtesy of Przemyslaw Malkowski. Different organisms vary dramatically in their lifespan Figure 4. Obviously, aging negatively affects the duration of life since it increases the risk of death. These intrinsic, maladaptive effects of aging, unchecked by selection, are, however, not the only factors affecting the length of life. Independent of whether aging occurs or not, reproductive lifespan can evolve adaptively in response to selection for increased reproductive success Stearns A longer lifespan normally implies increased reproductive success, and factors such as low adult mortality permitting more reproductive events per lifetime , high juvenile mortality making it necessary for adults to reproductively compensate for such loss , and high variation in juvenile mortality from one bout of reproduction to the next increasing uncertainty in reproductive success and requiring reproductive compensation as well therefore all tend to lengthen reproductive lifespan Stearns These lifespan promoting effects of selection are balanced by those that tend to increase adult mortality relative to juvenile mortality.
Evolution of Aging
Consequently, if extrinsic, environmentally imposed adult mortality is high, selection becomes weak, thereby allowing the evolution of higher levels of intrinsic mortality i. Moreover, even though selection might favor increased reproductive success, and thus a longer reproductive lifespan, the length of life might be limited by intrinsic trade-offs between reproduction and survival caused by AP. Thus, the evolution of lifespan can be viewed as a balance between selection for increased reproductive success and the factors that increase the intrinsic age-dependent components of mortality Stearns These ideas have been empirically tested and corroborated by several researchers.
For example, using an elegant experimental evolution design, Stearns et al. Clearly, there is a remarkable amount of variation in lifespan among different species, including some extremely short-lived as well long-lived species e. A lot of this diversity in lifespan can be quite readily explained by variation in the levels of extrinsic mortality and the evolution of different optimal lengths of reproductive life, including the existence of semelparous organisms that reproduce only once and then die Stearns For example, species that are well protected from predators — for example, those that have a shell, can fly, or are poisonous — tend to live longer than related, less well-protected species e.
But are there immortal organisms? Although examples of organisms that age very slowly are well known e.
Bacteria are a good case in point. For a long time it was thought that bacteria do not age. Indeed, one of Williams' strongest assertions about the evolution of aging was that only organisms with a separation of germ line and soma should age. Bacteria, by contrast, do not exhibit a clear delineation into germ line and soma, and should therefore be immortal. In symmetrically dividing unicells, for example, individuals should not age because parent and offspring are phenotypically indistinguishable — it is impossible to determine old from young, and age is thus invisible to selection. By the same logic, aging should exist in asymmetrically reproducing organisms where aging parents are phenotypically distinct from offspring.
Indeed, an asymmetrically dividing bacterium has recently been found to show senescence Ackermann et al. Remarkably, however, even the symmetrically dividing E. Moreover, Ackermann et al. However, as soon as such an asymmetry evolves, aging evolves. Thus, aging — despite remarkable variation in the duration of life among different species — might be a fundamental and inevitable property of cellular life. We have introduced what evolutionary biologists think about the evolution of aging. Today, it is clear that aging is not a positively selected, programmed death process, and has not evolved for "the good of the species".
Instead, aging is a feature of life that exists because selection is weak and ineffective at maintaining survival, reproduction, and somatic repair at old age. Based on the observation that the force of selection declines as a function of age, two main hypotheses have been formulated to explain why organisms grow old and die: the mutation accumulation MA and the antagonistic pleiotropy AP hypotheses. Under MA, aging evolves because selection cannot efficiently eliminate deleterious mutations that manifest themselves only late in life.
Under AP, aging evolves as a maladaptive byproduct of selection for increased fitness early in life, with the beneficial early-life effects being genetically coupled to deleterious late-life effects that cause aging.
Aging clearly shortens lifespan, but lifespan is also shaped by selection for an increased number of lifetime reproductive events. The evolution of lifespan is therefore a balance between selective factors that extend the reproductive period and components of intrinsic mortality that shorten it. Whether there exist truly immortal organisms is controversial, and recent evidence suggests in fact that aging might be an inevitable property of all cellular life.
Fecundity - Fecundity is defined as the number of offspring e. Fitness - Fitness sometimes also called Darwinian fitness is a measure of the relative expected contribution of a genotype or phenotype to future generations. The easiest way to think about fitness is in terms of lifetime reproductive success of a genotype or phenotype relative to other such types in a population.
Note that natural selection can be defined as heritable variation among genotypes in fitness. Germ line - The germ line is a specialized lineage of stem cells that gives rise to gametes eggs, sperm. Parsimony, parsimonious - The principle of parsimony sometimes also called Occam's razor states that when choosing among several competing explanations or models, or hypotheses to explain a particular phenomenon it is often best to select the simplest i.
If new evidence becomes available the explanation can be re-evaluated against the facts: if the simplest explanation still explains the facts best, it should be retained. However, if the new evidence suggests that a more complex explanation has better explanatory power, then the simpler alternative should be discarded. Pleiotropy, pleiotropic - Pleiotropy means that a gene or allele or mutation affects two or more traits or processes or functions. Semelparity, semelparous - Semelparous organisms are those that only have one reproductive event per lifetime independent of how many offspring are produced in this single event.
Semelparity is sometimes also called "big bang" reproduction. Senescence - Senescence is essentially synonymous with aging, i. At the demographic level, this physiological deterioration is manifest as a decline in fecundity and an increase in mortality with increasing age. Soma - The non-reproductive parts of the body and its organs, tissues, and cells that carry out all biological functions except reproduction. The soma is typically contrasted with the germ line, i.
The Hardy-Weinberg Principle. Evolution Introduction. Life History Evolution. Mutations Are the Raw Materials of Evolution. Speciation: The Origin of New Species.
Evolutionary theories of aging | Longevity History
Avian Egg Coloration and Visual Ecology. The Ecology of Avian Brood Parasitism. The Maintenance of Species Diversity. Neutral Theory of Species Diversity. Population Genomics. Semelparity and Iteroparity. Geographic Mosaics of Coevolution. Comparative Genomics. Cybertaxonomy and Ecology. Ecological Opportunity: Trigger of Adaptive Radiation. Evidence for Meat-Eating by Early Humans. Resource Partitioning and Why It Matters. The Evolution of Aging. Aa Aa Aa. Aging is an Evolutionary Paradox.
Figure 1. The Force of Selection Declines with Age.
The Mutation Accumulation Hypothesis. The Antagonistic Pleiotropy Hypothesis. Evolution of Lifespan. References and Recommended Reading Ackermann, M. Senescence in a bacterium with asymmetric division. Science , — Ackermann, M. On the evolutionary origin of aging. Aging Cell 6 , — Austad, S. Mammalian aging, metabolism, and ecology: Evidence from the bats and marsupials. Journal of Gerontology 46 , B47—B53 Bailey, C.
Blanco, M. Maximum longevities of chemically protected and non-protected fishes, reptiles, and amphibians support evolutionary hypotheses of aging. Mechanisms of Ageing and Development , — Bronikowski, A. Aging and its demographic measurement. Nature Education Knowledge 1 , 3 Charlesworth, B.
Evolution in Age-Structured Populations. Fisher, Medawar, Hamilton and the evolution of aging. Genetics , — Patterns of age-specific means and genetic variances of mortality rates predicted by the mutation accumulation theory of aging. Journal of Theoretical Biology , 47—65 Finch, C. Longevity, Senescence and the Genome. Fisher, R. The Genetical Theory of Natural Selection. Oxford, UK: Clarendon Press, Flatt, T. Survival costs of reproduction in Drosophila.
Experimental Gerontology , In Press Physiology: Still pondering an age-old question. Integrating evolutionary and molecular genetics of aging. Biochimica et Biophysica Acta , — Haldane, J. New Paths in Genetics. Hamilton, W. The moulding of senescence by natural selection. Journal of Theoretical Biology 12 , 12—45 Hughes, K. Evolutionary and mechanistic theories of aging. Annual Review of Entomology 50 , —