A reassessment of sexual dimorphism in human senescence: Theory, evidence, and causation (original) (raw)

Why Men Matter: Mating Patterns Drive Evolution of Human Lifespan

PLoS ONE, 2007

Evolutionary theory predicts that senescence, a decline in survival rates with age, is the consequence of stronger selection on alleles that affect fertility or mortality earlier rather than later in life. Hamilton quantified this argument by showing that a rare mutation reducing survival is opposed by a selective force that declines with age over reproductive life. He used a female-only demographic model, predicting that female menopause at age ca. 50 yrs should be followed by a sharp increase in mortality, a ''wall of death.'' Human lives obviously do not display such a wall. Explanations of the evolution of lifespan beyond the age of female menopause have proven difficult to describe as explicit genetic models. Here we argue that the inclusion of males and mating patterns extends Hamilton's theory and predicts the pattern of human senescence. We analyze a general two-sex model to show that selection favors survival for as long as men reproduce. Male fertility can only result from matings with fertile females, and we present a range of data showing that males much older than 50 yrs have substantial realized fertility through matings with younger females, a pattern that was likely typical among early humans. Thus old-age male fertility provides a selective force against autosomal deleterious mutations at ages far past female menopause with no sharp upper age limit, eliminating the wall of death. Our findings illustrate the evolutionary importance of males and mating preferences, and show that one-sex demographic models are insufficient to describe the forces that shape human senescence.

The evolution of premature reproductive senescence and menopause in human females

Human Nature, 1991

Reproductive senescence in human females takes place long before other body functions senesce. This fact presents an evolutionary dilemma since continued reproduction should generally be favored by natural selection. Two commonly proposed hypotheses to account for human menopause are (a) a recent increase in the human lifespan and (b) a switch to investment in close kin rather than direct reproduction. No support is found for the proposition that human lifespans have only recently increased ed. Data from Ache hunter-gatherers are used to test the kin selection hypothesis. Ache data do not support the proposition that females can gain greater fitness benefits in old age by helping kin rather than continuing to reproduce. Nevertheless, one crucial parameter in the model, when adjusted to the highest value within the measured 95% cbnfidence interval, would lead to the evolution of reproductive senescence at about 53 years of age. Further investigation is necessary to determine whether the kin selection hypothesis of menopause can account for its current maintenance in most populations.

Senescence: Evolution, Genetics and Some Factors Affecting It

One of the greatest mysteries in the life of almost every living organism is the fact that most organisms, as they age, experience deterioration in their functional status. (Lemaître et.al. 2014; It is due to this then that these organisms can be said to have a continually decreasing fitness as their survival and reproductive performance decline as they age. This effect on their fitness is why selection should act against senescence persisting in organisms. This then has led scientists to ask the reason behind senescence evolving and actually becoming prevalent. Several theories have been raised to address this question. Three of which, namely the mutation accumulation theory, the antagonistic pleiotropy theory, and the disposable soma theory, will be discussed below.

Senescence Viewed through the Lens of Comparative Biology

Although mortality and longevity are inherently biological phenomena, their study has historically been the purview of demography and the actuarial sciences. An infusion of biological thinking into these disciplines transforms demography into biodemography and provides expectations and coherency to observations on age-determined mortality that would not be explainable otherwise. Comparative biology teaches us that reproduction is life's solution to the inevitability of death in the hostile environments of Earth. That solution, however, places a higher priority on investing physiological resources into reproduction that could otherwise have been used to maintain the soma (body) longer. As such, aging is an inescapable but inadvertent byproduct of imperfect maintenance and its attendant surveillance and repair. Biology also reveals that while bodies are not designed to fail, neither are they designed for extended operation. In other words, bodies are subject to biological warranty periods for normal operation. For sexually reproducing species, that warranty period includes the time from conception to sexual maturity, the production and nurturing of offspring, and a period of grand-parenting in some species. Humans are the only species capable of exploiting the loophole in the biological contract of life (bodies that are not designed to fail). Human ingenuity (science, medicine, public health) has produced interventions that manufacture survival time by delaying death, and in so doing, has created a phenomenon never before seen in the history of life-population aging (and all the societal and health consequences that go with it).

Evolution of human longevity and the genetic complexity governing aging rate

Proceedings of the National Academy of Sciences, 1975

Genetic complexity of processes governing the aging rate of man was estimated by determining the maximum rate lifespan has evolved along the hominid ancestral-descendant sequence. Maximum lifespan potential was found to have increased approximately 2-fold over the past 3 million years, reaching a maximum rate of increase of 14 years per 100,000 years about 100,000 years ago. It is estimated that about 0.6% of the total functional genes have received substitutions leading to one or more adaptive aminoacid changes during this 100,000-year time-period. This suggests that aging is not the result of an expression of a large number of independently acting processes. Instead, primary aging processes appear to exist where only a few genetic changes are necessary to decrease uniformly the aging rate of many different physiological functions.

Sex and aging: A comparison between two phenoptotic phenomena

Biochemistry (Moscow), 2017

Phenoptotic is a phenomenon that is genetically programmed and favoured by natural selection, and that determines death or increased risk of death (fitness reduction) for the individual that manifests it. Aging, here defined as age-related progressive mortality increase in the wild, if programmed and favoured by natural selection, falls within the definition of phenoptosis. Sexual reproduction (sex), as for the involved individuals determines fitness reduction and, in some particular species, even certain death, also falls within the definition of phenoptosis. In this paper, sex and aging are analysed as phenoptotic phenomena, and the similarities between them are investigated. In particular, from a theoretical standpoint, the genes that cause and regulate these phenomena: - require analyses that consider both individual and supra-individual selection because they are harmful in terms of individual selection, but advantageous (that is, favoured by natural selection) in particular conditions of supra-individual selection; - determine a higher velocity of and greater opportunities for evolution and, therefore, a greater evolutionary potential (evolvability); - are advantageous under ecological conditions of K-selection and with finite populations; - are disadvantageous (that is, not favoured by natural selection) under ecological conditions of r-selection and with unlimited populations; - are not advantageous in all ecological conditions and, so, species that reproduce asexually or species that do not age are predicted and exist.

Evolution of human lifespan: Past, future, and present

American Journal of Human Biology, 1998

The only satisfactory general theory for understanding the biology of aging is that provided by evolutionary genetics. The central theoretical result of the evolutionary theory of aging is that aging is caused by a fall in the force of natural selection, beginning at the time of the onset of reproduction and continuing until the cessation of reproduction. This formal result has been tested using breeding experiments in which the force of natural selection is altered in replicated laboratory populations. As predicted by the evolutionary theory of aging, such experiments can readily postpone aging. A recent advance has been the discovery of late-life mortality plateaus in human and other populations. These can be predicted theoretically from the late-life plateau in the force of natural selection, when it remains at or near zero. It is virtually certain that human lifespan has substantially increased over its last few million years of evolution. Evolutionary theory can explain this increase in terms of decreased ecological vulnerability resulting from increased brain size. The immediate future of human evolution is unlikely to see extensive genetic increases in lifespan, given the experimental data on rates of change in lifespan with experimental populations. But, evolutionary research suggests that there are few fundamental biological barriers to the extension of human lifespan, only practical barriers. Am.

Reproductive senescence: new perspectives in the wild

Biological reviews of the Cambridge Philosophical Society, 2017

According to recent empirical studies, reproductive senescence, the decline in reproductive success with increasing age, seems to be nearly ubiquitous in the wild. However, a clear understanding of the evolutionary causes and consequences of reproductive senescence is still lacking and requires new and integrative approaches. After identifying the sequential and complex nature of female reproductive senescence, we show that the relative contributions of physiological decline and alterations in the efficiency of parental care to reproductive senescence remain unknown and need to be assessed in the light of current evolutionary theories of ageing. We demonstrate that, although reproductive senescence is generally studied only from the female viewpoint, age-specific female reproductive success strongly depends on male-female interactions. Thus, a reduction in male fertilization efficiency with increasing age has detrimental consequences for female fitness. Lastly, we call for investiga...