Enquiry into the evolution of ageing aims to explain why survival, reproductive success, and functioning of almost all living organisms decline at old age. Leading hypotheses suggest that a combination of limited resources, and environmental causes determine an "optimal" level of repair regarding molecular and cellular level damage that accumulates over time. This process is known as self-maintenance.
August Weismann was responsible for interpreting and formalizing the mechanisms of Darwinian evolution in a modern theoretical framework. In 1889, he theorized that ageing was part of life's program to make room for the next generation in order to sustain the turnover that is necessary for evolution. The idea that the ageing characteristic was selected (an adaptation) because of its deleterious effect was largely discounted for much of the 20th century, but a theoretical model suggests that altruistic ageing could evolve if there is little migration among populations. Weismann later abandoned his theory and later followed up with his "programmed death" theory.
The first modern theory of mammal ageing was formulated by Peter Medawar in 1952. This theory formed in the previous decade with J. B. S. Haldane and his selection shadow concept. Their idea was that ageing was a matter of neglect, as nature is a highly competitive place. Almost all animals die in the wild from predators, disease, or accidents, which lowers the average age of death. Therefore, there is not much reason why the body should remain fit for the long haul because selection pressure is low for traits that would maintain viability past the time when most animals would have died anyway.
Medawar's theory is referred to as Mutation Accumulation. This theory is based on the idea that random, germline mutations occur that are detrimental to overall health and survival later in life. Overall, senescence would occur through a summation of deleterious genes, and would explain the overall phenotypic damage we associate with ageing.
Medawar's theory was critiqued and later further developed by George C. Williams in 1957. Williams noted that senescence may be causing many deaths even if animals are not 'dying of old age.' He began his hypothesis with the idea that ageing can cause earlier senescence due to the competitive nature of life. Even a small amount of ageing can be fatal; hence natural selection does indeed care and ageing is not cost-free.
Williams eventually proposed his own hypothesis called antagonistic pleiotropy. Pleiotropy, alone, means one mutation that cause multiple effects on phenotype. Antagonistic pleiotropy on the other hand deals with one gene that creates two traits with one being beneficial and the other being detrimental. In essence, this refers to genes that offer benefits early in life, but accumulate a cost later on.
Although antagonistic pleiotropy is a prevailing theory today, this is largely by default, and has not been well verified. Research has shown that this is not true for all genes and may be thought of as partial validation of the theory, but it cuts the core premise: that genetic trade-offs are the root cause of ageing.
In breeding experiments, Michael R. Rose selected fruit flies for long lifespan. Based on antagonistic pleiotropy, Rose expected that this would surely reduce their fertility. His team found that they were able to breed flies that lived more than twice as long as the flies they started with, but to their surprise, the long-lived, inbred flies actually laid more eggs than the short-lived flies. This was another setback for pleiotropy theory, though Rose maintains it may be an experimental artifact.
A third mainstream theory of ageing, the ''Disposable soma theory, proposed in 1977 by Thomas Kirkwood, presumes that the body must budget the resources available to it. The body uses resources derived from the environment for metabolism, for reproduction, and for repair and maintenance, and the body must compromise when there is a finite supply of resources. The theory states that this compromise causes the body to reallocate energy to the repair function that causes the body to gradually deteriorate with age.
A caveat to this theory suggests that this reallocation of energy is based on time instead of limiting resources. This concept focuses on the evolutionary pressure to reproduce in a set, optimal time period that is dictated by age and ecological niche. The way that this is successful is through the allocation of time and energy in damage repair at the cellular level resulting in an accumulation of damage and a decreased lifespan relative to organisms with longer gestation. This concept stems from a comparative analysis of genomic stability in mammalian cells.
One opposing argument is based on caloric restriction (CR) effect, which has demonstrated an increase in life. But dietary restriction has not been shown to increase lifetime reproductive success (fitness), because when food availability is lower, reproductive output is also lower. Moreover, calories are not the only resource of possibly limited supply to an organism that could have an effect on multiple dimensions of fitness.
The DNA damage theory of aging postulates that DNA damage is ubiquitous in the biological world and is the primary cause of ageing. The theory is based off the idea that ageing occurs over time due to the damage of the DNA. As an example, studies of mammalian brain and muscle have shown that DNA repair capability is relatively high during early development when cells are dividing mitotically, but declines substantially as cells enter the post-mitotic state. The effect of reducing expression of DNA repair capability is increased accumulation of DNA damage. This impairs gene transcription and causes the progressive loss of cellular and tissue functions that define aging.
Theories, such as Weismann's "programmed death" theory, suggest that deterioration and death due to ageing are a purposeful result of an organism's evolved design, and are referred to as theories of programmed ageing or adaptive ageing.
The programmed maintenance theory based on evolvability suggests that the repair mechanisms are controlled by a common control mechanism capable of sensing conditions, such as caloric restriction, and may be responsible for lifespan in particular species. In this theory, the survival techniques are based on control mechanisms instead of individual maintenance mechanism, which you see in the non-programmed theory of mammal ageing.
A non-programmed theory of mammal ageing states that different species possess different capabilities for maintenance and repair. Longer-lived species possess many mechanisms for offsetting damage due to causes such as oxidation, telomere shortening, and other deteriorative processes. Shorter-lived species, having earlier ages of sexual maturity, have less need for longevity and thus did not evolve or retain the more-effective repair mechanisms. Damage therefore accumulates more rapidly, resulting in earlier manifestations and shorter lifespan. Since there are a wide variety of ageing manifestations that appear to have very different causes, it is likely that there are many different maintenance and repair functions.
Group selection is based on the idea that all members of a given group will either succeed or fail together depending on the circumstance. With this mechanism, genetic drift occurs collectively to all in the group and sets them apart from other groups of its own species. This is different than individual selection, as it focuses on the group rather than the individual.
Often also postreproductive individuals make intergenerational transfers: bottlenose dolphins and pilot whales guard their grandchildren; there is cooperative breeding in some mammals, many insects and about 200 species of birds; sex differences in the survival of anthropoid primates tend to correlate with the care to offspring; or an Efe infant is often attended by more than 10 people. Lee developed a formal theory integrating selection due to transfers (at all ages) with selection due to fertility.
Evolvability is based on the idea that an organism adapts genetically to its present environment.
Skulachev (1997) has suggested that programmed ageing assists the evolution process by providing a gradually increasing challenge or obstacle to survival and reproduction, and therefore enhancing the selection of beneficial characteristics.
Goldsmith (2008) proposed that though increasing the generation rate and evolution rate is beneficial for a species, it is also important to limit lifespan so older individuals will not dominate the gene pool.
Yang (2013)'s model is also based on the idea that ageing accelerates the accumulation of novel adaptive genes in local populations. However, Yang changed the terminology of "evolvability" into "genetic creativity" throughout his paper to facilitate the understanding of how ageing can have a shorter-term benefit than the word "evolvability" would imply.
Lenart and Vašku (2016)  have also invoked evolvability as the main mechanism driving evolution of ageing. However, they proposed that even though the actual rate of aging can be an adaptation the aging itself is inevitable. In other words, evolution can change the speed of aging but some ageing no matter how slow will always occur.
There are two types of mortality: intrinsic and extrinsic mortality. Intrinsic mortality is thought to be a result of ageing from insider factors, whereas extrinsic is a direct result of environmental factors. An example would be that bats have fewer predators, and therefore have a low extrinsic mortality. Birds are warm-blooded and are similar in size to many small mammals, yet often live 5–10 times as long. They have less predation pressure than ground-dwelling mammals, and have a lower extrinsic mortality.
When examining the body-size vs. lifespan relationship, one also observes that predatory mammals tend to live longer than prey mammals in a controlled environment, such as a zoo or nature reserve. The explanation for the long lifespans of primates (such as humans, monkeys, and apes) relative to body size is that their intelligence, and they would have a lower intrinsic mortality.
Progeria is a single-gene genetic disease that cause acceleration of many or most symptoms of ageing during childhood. Those who have this disease are known for failure to thrive and have a series of symptoms that cause abnormalities in the joints, hair, skin, eyes, and face. Although the term progeria applies strictly speaking to all diseases characterized by premature aging symptoms, and is often used as such, it is often applied specifically in reference to Hutchinson–Gilford progeria syndrome (HGPS).
Werner syndrome, also known as "adult progeria", is another single-gene genetic disease. This syndrome starts to affect individuals during the teenage years, preventing teens from growing at puberty. Once the individual reaches the twenties, there is generally a change in hair color, skin, and voice. This condition can also affect the weight distribution between the arms, legs, and torso.
Theories of ageing affect efforts to understand and find treatments for age-related conditions: