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Surprisingly little formal analysis of this problem exists; the standard explanation that has been put forward is that queens and kings live much longer because they are shielded from extrinsic mortality by the workers [ , ]. Classic theories of aging may also not fully apply to eusocial insects [ ]: their populations exhibit not only age structure but also strong social structure and division of labor.

Since in such a situation survival is not only age- but also state-dependent, the force of selection does not necessarily decline with age [ 83 ]. More theoretical work on aging in eusocial insects is warranted, especially the development of class-structured inclusive fitness kin selection models [ , , , ].

Beyond eusocial insects, work on Volvocalean green algae some of which are unicellular, whereas others form multicellular colonies suggests that division of labor might be a general principle underlying the decoupling of trade-offs [ , ]. Unicellular algae face a trade-off between flagellar locomotion and reproduction. In these small planktonic algae, survival is dependent upon locomotory ability, i. The flagellum in turn depends on the centriole, yet the centriole is also required for cell division reproduction , so that the cell has to forgo locomotion while it divides, thereby leading to a survival-reproduction trade-off.

By contrast, colonial forms of these green algae have apparently managed to uncouple the trade-off by having sterile cells devoted to motility, while other cells are specialized to perform the reproductive function—a situation akin to the differentiation of the germline and soma. A convex trade-off function, i. This principle has been generalized, in a theoretical cost—benefit analysis of accelerating and decelerating performance functions [ ]. A major aim of mechanistic research into aging is to compress morbidity at the end of life, by shortening its duration and lessening its severity.

Importantly, improvement of health during aging should not be associated with adverse side effects. The pleiotropy route to the evolution of aging could be taken to imply that any amelioration of the effects of aging could be achieved only at the cost of problems earlier in adult life, because of the predicted genetic correlation between early and late fitness. However, the finding that increased lifespan can be achieved in the absence of associated costs to reproduction, both in the laboratory and in nature in the case of social insects, indicates that this correlation can be broken.

Generally, across individuals in natural populations, there is a positive phenotypic correlation between fecundity and lifespan.

Inflammation, Nutrition, and Aging in the Evolution of Lifespans

However, the causal connection between the two traits may be the opposite, as experimental manipulations of, for instance, increasing clutch size in birds, often lead to reduced future fecundity or survival [ ]. This difference occurs because the individual variation in condition and circumstances may obscure the underlying cost of reproduction: healthy individuals in a rich environment may have high fecundity and lifespan despite the cost of reproduction, which is only revealed by experimental manipulations.

This underlying cost of reproduction may then constrain the combinations of life history traits that can evolve [ , ]. Organisms that live in an environment that is beneficial for development may indeed not experience costs of reproduction [ , ], as often seems to be the case in laboratory animals [ ].

In addition, positive correlations between fitness-related traits can also be caused by mutational variation in recessive deleterious effects [ ]. This arises because such deleterious mutations can have negative pleiotropic effects on two or more traits but the extent of these negative effects varies genetically among individuals. Prevention of late-life morbidity in humans ideally would involve interventions that could be started at the earliest in middle age.

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Pharmacological prevention of cardiovascular disease, with statins and blood pressure lowerers, is already routine in clinical practice [ ]. Unsurprisingly, many of the proteins that have turned out to be important in aging also play prominent roles in the etiology of age-related diseases, and are already the targets of licensed drugs. Consideration is hence starting to be given to widening the preventative, pharmacological approach, for instance by repurposing drugs such as rapamycin, which inhibits TOR and is used to treat cancer and to prevent rejection of transplanted organs, and metformin, used to treat type 2 diabetes and which may have several modes of action; importantly, both drugs have been found to extend lifespan in model organisms [ , , , ].

Other possible approaches to emerge from experimental work with animals include removal of damaging senescent cells that accumulate during aging [ , ], use of factors from young blood that restore the age-related loss of function of stem cells or synapses between nerve cells in the brain [ , ], and alteration of the composition of the microorganisms in the gut to a younger profile [ , , ], which has already been shown to extend lifespan in the turquoise killifish [ ].

However, despite the considerable promise of these approaches, the extent to which they can yield health benefits free of side effects needs detailed study, since they could pose some new challenges for an aged system. For instance, removal of senescent cells, or restoration of stem cell function, could be beneficial in the short term, but in the longer term could lead to stem cell exhaustion and tissue dysfunction.

Everything we know about the evolution of aging tells us that it is not a programmed process, so it has often been thought of as being intractable to experimental analysis or medical intervention. But evolutionarily conserved high-level regulators of phenotypic plasticity have turned out to be able to produce a major rearrangement of physiology and to ameliorate the effects of aging. Notably also, bats and birds have longer lifespans than mammals with similar body sizes [ ]. Although a major challenge, it will be revealing to understand a lot more about how these slow-aging creatures achieve their long lives, and whether their secrets could help to improve human health late in life.

Some species e. Such organisms clearly deserve much more mechanistic investigation as they might hold key lessons for regeneration and repair and thus for our understanding of how long life can be achieved. Finch CE. Evolution of the human lifespan and diseases of aging: roles of infection, inflammation, and nutrition. Biodemographic trajectories of longevity.


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hrercostare.tk Evolutionary biology of aging. Longevity, senescence, and the genome.

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Senescence in natural populations of animals: widespread evidence and its implications for bio-gerontology. Ageing Res Rev.


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