Ageing and immortality (original) (raw)
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Evolutionary theory predicts late-life mortality plateaus
Proceedings of the National …, 1996
Most demographic data indicate a roughly exponential increase in adult mortality with age, a phenomenon that has been explained in terms of a decline in the force of natural selection acting on age-specific mortality. Scattered demographic findings suggest the existence of a late-life mortality plateau in both humans and dipteran insects, seemingly at odds with both prior data and evolutionary theory. Extensions to the evolutionary theory of aging are developed which indicate that such late-life mortality plateaus are to be expected when enough late-life data are collected. This expanded theory predicts late-life mortality plateaus, with both antagonistic pleiotropy and mutation accumulation as driving population genetic mechanisms.
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).
Evolutionary Theories of Aging
Gerontology, 1999
Background: In a Forum article Le Bourg (1998) criticized recent tests of evolutionary theories of aging and suggested alternative explanations for the long lifespan of ant queens and the positive relationship between body size and lifespan in mammals. Moreover, he attempts to criticize evolutionary theories of aging by showing that explanations other than evolutionary theories of aging probably account for the variation in human lifespan across countries. Objective: Here we show that the arguments of Le Bourg suffer several problems. First, many of the arguments reveal a misunderstanding of the process of natural selection. Second, some of the arguments reflect a lack of knowledge of evolutionary theories of aging (e.g. pre-reproductive mortality is not predicted to influence lifespan of organisms contrary to what is claimed). Finally, his final example on lifespan in humans simply is a straw-man because serious evolutionary biologists are well aware of the importance of confounding variables and would certainly not make the type of conclusion suggested by Le Bourg. Conclusion: Although a critical discussion of evolutionary theories of aging is welcome, we believe that the alternative explanations proposed by Le Bourg are implausible and reflect a misunderstanding of the process of natural selection.
My aim, in this essay, is twofold. Firstly, I want to characterise ageing as a normative biological process, rather than a purely physical one. This, in effect, means that “ageing” is not a pure wear-and-tear mechanism. In fact, it isn’t even a mechanism, and I’ll explain why I’m critical of the use of that word in biology. It is therefore not accurate, in my view, to define ageing either as a mere imbalance between exergonic and endergonic reactions in the metabolism, as “the free radical theory of ageing” does, or as an imbalance between the excessive formation of reactive oxygen species and the limited amount of antioxidant defences. As we’ll see, ageing is a process, but it is also a constraint, or a set of biological constraints, values, functions, and norms. More specifically, it is a repulsive constraint (1). This means that ageing is not so much a norm, or function, as a normative property. [I will focus on the example of the mammal, and will give an illustration of this point through the example of vicious molecular circles in connective tissues and in mitochondria.] With the expression “normative property,” I mean that ageing is not simply a regulative property. It is a property through which the structure and constraints of a living being are actually transformed. Ageing is not destruction or degradation, but self-destruction. Ageing indicates that biological systems have a tendency to lose their normative power, that is, their ability to change their norms and generate new ones, and to do so in a way that’s regulated. I suggest we refer to ageing thus understood as a process of alteration. Secondly, I want to analyse the relations between ageing and longevity. Not all organisms age, as everybody knows. In worms, yeast, and other organisms, ageing is opposed to longevity, which counteracts the process of self-destruction. If the dynamic of ageing is also self-regulated, how are we to understand the claim, often found in the found in the literature, that longevity “counteracts” ageing (23)?
Biodemographic Trajectories of Longevity
Science, 1998
Old-age survival has increased substantially since 1950. Death rates decelerate with age for insects, worms, and yeast, as well as humans. This evidence of extended postreproductive survival is puzzling. Three biodemographic insights—concerning the correlation of death rates across age, individual differences in survival chances, and induced alterations in age patterns of fertility and mortality—offer clues and suggest research on the failure of complicated systems, on new demographic equations for evolutionary theory, and on fertility-longevity interactions. Nongenetic changes account for increases in human life-spans to date. Explication of these causes and the genetic license for extended survival, as well as discovery of genes and other survival attributes affecting longevity, will lead to even longer lives.
Extrinsic Mortality Can Shape Life-History Traits, Including Senescence
Evolutionary Biology, 2018
The Williams' hypothesis is one of the most widely known ideas in life history evolution. It states that higher adult mortality should lead to faster and/or earlier senescence. Theoretically derived gradients, however, do not support this prediction. Increased awareness of this fact has caused a crisis of misinformation among theorists and empirical ecologists. We resolve this crisis by outlining key issues in the measurement of fitness, assumptions of density dependence, and their effect on extrinsic mortality. The classic gradients apply only to a narrow range of ecological contexts where density-dependence is either absent or present but with unrealistic stipulations. Re-deriving the classic gradients, using a more appropriate measure of fitness and incorporating density, shows that broad ecological contexts exist where Williams' hypothesis is supported.
Ageing Research Reviews, 2006
Late life is a distinct phase of life characterized by a cessation in the deterioration of survivorship and fecundity characteristic of normal aging. Several theories have been proposed to explain nonaging at late ages, specifically with regards to late-life mortality-rate plateaus. All such theories must be compatible with formal evolutionary theory and experimental findings. Here, we develop a critique of theories of late life based on evolutionary biology.