The evolutionary theory of aging may be considered as part of a more general life history theory, which tries to explain how evolution designs organisms to achieve reproductive success (i.e., avoid extinction). Life history theory is based on mathematical methods of optimization models with specific biological constraints. Among the questions posed and answered by life history theory are:

• Why organisms are small or large?
• Why do they mature early or late?
• Why do they have few or many offspring?
• Why do they have a short or a long life?
• Why they have to grow old and die?

The latter two questions represent the entire scientific agenda of the evolutionary theory of aging. It could be said, therefore, that the evolutionary theory of aging is a subset of the life history theory. On the other hand the evolutionary theory of aging is considered to be the intellectual core of the biodemography of aging and longevity.

Current evolutionary explanations of aging and limited longevity of biological species are based on two major evolutionary theories: the mutation accumulation theory and the antagonistic pleiotropy theory. These two theories can be summarized as follows:

• Mutation accumulation theory: From the evolutionary perspective, aging is an inevitable result of the declining force of natural selection with age. For example, a mutant gene that kills young children will be strongly selected against (will not be passed to the next generation) while a lethal mutation with effects confined to people over the age of 80 will experience no selection because people with this mutation will have already passed it to their offspring by that age. Over successive generations, late-acting deleterious mutations will accumulate, leading to an increase in mortality rates late in life.
• Antagonistic pleiotropy theory: Late-acting deleterious genes may even be favored by selection and be actively accumulated in populations if they have any beneficial effects early in life.

Note that these two theories of aging are not mutually exclusive, and both evolutionary mechanisms may operate at the same time. The main difference between the two theories is that in the mutation accumulation theory, genes with negative effects at old age accumulate passively from one generation to the next while in the antagonistic pleiotropy theory, these genes are actively kept in the gene pool by selection. The actual relative contribution of each evolutionary mechanism to species aging is not yet determined, and this scientific problem is now the main focus of current research in evolutionary biology.

Interestingly, since the 1950s, no fundamentally new evolutionary theories of aging have been proposed. There were, however, attempts to find a better name for the antagonistic pleiotropy theory and to specify in more detail how one and the same gene could have both deleterious and beneficial effects. In particular, the disposable soma theory was proposed, which postulated a special class of gene mutations with the following antagonistic pleiotropic effects: these hypothetical mutations save energy for reproduction (positive effect) by partially disabling molecular proofreading and other accuracy promoting devices in somatic cells (negative effect). The authors of the disposable soma theory argued that "it may be selectively advantageous for higher organisms to adopt an energy saving strategy of reduced accuracy in somatic cells to accelerate development and reproduction, but the consequence will be eventual deterioration and death".

While discussing the disposable soma theory, it is important to keep in mind that it was initially proposed to provide evolutionary justification for another theory of aging called Orgel's error catastrophe theory. The error catastrophe theory, which ultimately failed at least in its original form, considered aging a result of a breakdown in the accuracy of protein synthesis within somatic cells. Most researchers agree that the disposable soma theory is a special, more narrowly defined variant of the antagonistic pleiotropy theory of aging. This was also admitted by the authors of the disposable soma theory themselves: "The disposable soma theory is, in a sense, a special case of Williams's (1957) pleiotropic gene hypothesis [antagonistic pleiotropy theory], the gene in question controlling the switch to reduced accuracy in somatic cells. The good effect of the gene is the reduced investment of resources in the soma, while the bad effect is ultimate somatic disintegration, or ageing".

After the death of the error catastrophe theory, the disposable soma theory became a widowed concept, adjusting to new realities and ideas. Within the same name, the content of the theory has evolved from specific consideration of the accuracy of protein synthesis in somatic cells to general concerns about "the role of somatic maintenance and repair". These concerns reiterate an earlier suggestion made by August Weismann in 1889 about "the perishable and vulnerable nature of the soma".