The Rarity of Survival to Old Age Does Not Drive the Evolution of Senescence

Wensink, Maarten Jan; Caswell, Hal; Baudisch, Annette

doi:10.1007/s11692-016-9385-4

Cited by 55 publications

(64 citation statements)

References 37 publications

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“…As stated by Rose (, pp. 13–14) and clearly shown by Wensink and colleagues (), the selection gradient on fecundity measured by the fitness sensitivity function always declines with increasing age in a non‐declining population, on the contrary to the mean number of offspring produced by individuals of a given age, to reproductive values, or to reproductive values weighted by the age‐specific abundance of individuals (Williams and Taylor ). However, although there is thus no theoretical ground for predicting the absence of actuarial senescence in species with increasing fecundity with age when using Hamilton's indicators of selection gradients on mortalities and fecundities, the selective pressure against actuarial senescence will be stronger in these latter species than in species that display reproductive senescence.…”

Section: A Critical Appraisal Of Each Of the Nine Predictions Formulamentioning

confidence: 94%

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The Williams' legacy: A critical reappraisal of his nine predictions about the evolution of senescence

2017

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Williams' evolutionary theory of senescence based on antagonistic pleiotropy has become a landmark in evolutionary biology, and more recently in biogerontology and evolutionary medicine. In his original article, Williams launched a set of nine "testable deductions" from his theory. Although some of these predictions have been repeatedly discussed, most have been overlooked and no systematic evaluation of the whole set of Williams' original predictions has been performed. For the sixtieth anniversary of the publication of the Williams' article, we provide an updated evaluation of all these predictions. We present the pros and cons of each prediction based on recent accumulation of both theoretical and empirical studies performed in the laboratory and in the wild. From our viewpoint, six predictions are mostly supported by our current knowledge at least under some conditions (although Williams' theory cannot thoroughly explain why for some of them). Three predictions, all involving the timing of senescence, are not supported. Our critical review of Williams' predictions highlights the importance of William's contribution and clearly demonstrates that, 60 years after its publication, his article does not show any sign of senescence.

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Section: A Critical Appraisal Of Each Of the Nine Predictions Formulamentioning

confidence: 94%

“…; Furness and Reznick ; Wensik et al. ), although often based on a different reference compared to original Williams' formulation (see Box for an historical perspective of the prediction). When launching his prediction, Williams mostly discussed variation across species.…”

Section: A Critical Appraisal Of Each Of the Nine Predictions Formulamentioning

confidence: 99%

The Williams' legacy: A critical reappraisal of his nine predictions about the evolution of senescence

2017

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“…And yet higher extrinsic mortality does not always lead to accelerated senescence . Instead, selection against aging declines because older individuals have less of their total lifetime reproductive success ahead of them than younger individuals do . As a result of this decline, however it arises, late‐acting variants that cause aging can persist …”

Section: Aging Evolvesmentioning

confidence: 99%

Life history evolution, reproduction, and the origins of sex‐dependent aging and longevity

Brooks

Garratt

2016

Annals of the New York Academy of Sciences

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Males and females in many species differ in how they age and how long they live. These differences have motivated much research, concerning both their evolution and the underlying mechanisms that cause them. We review how differences in male and female life histories have evolved to shape patterns of aging and some of the mechanisms and pathways involved. We pay particular attention to three areas where considerable potential for synergy between mechanistic and evolutionary research exists: (1) the role of estrogens, androgens, the growth hormone/insulin-like growth factor 1 pathway, and the mechanistic target of rapamycin signaling pathway in sex-dependent growth and reproduction; (2) sexual conflict over mating rate and fertility, and how mate presence or mating can become an avenue for males and females to directly affect each other's life span; and (3) the link between dietary restriction and aging, and the emerging understanding that only the restriction of certain nutrients is involved and that this is linked to reproduction. We suggest that ideas about life histories, sex-dependent selection, and sexual conflict can inform and be informed by the ever more refined and complex understanding of the mechanisms that cause aging.

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“…Currently, the aging field is in flux because of rapidly expanding research in longevity and new insights in evolutionary theories of aging. For example, a central prediction of the evolutionary theory that senescence is driven by extrinsic mortality has been shown to be wrong (Wensink et al 2016). Other studies suggest evolution of senescence through mutation accumulation proposed by Hamilton (1966) needs to be revised (Wachter et al 2013) and diverse theories need to be merged to understand evolution of senescence (Wachter et al 2014).…”

Section: Process Point Of View Of Mortalitymentioning

confidence: 99%

Insights into mortality patterns and causes of death through a process point of view model

Anderson

Sharrow

2016

Biogerontology

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Process point of view models of mortality, such as the Strehler-Mildvan and stochastic vitality models, represent death in terms of the loss of survival capacity through challenges and dissipation. Drawing on hallmarks of aging, we link these concepts to candidate biological mechanisms through a framework that defines death as challenges to vitality where distal factors defined the age-evolution of vitality and proximal factors define the probability distribution of challenges. To illustrate the process point of view, we hypothesize that the immune system is a mortality nexus, characterized by two vitality streams: increasing vitality representing immune system development and immunosenescence representing vitality dissipation. Proximal challenges define three mortality partitions: juvenile and adult extrinsic mortalities and intrinsic adult mortality. Model parameters, generated from Swedish mortality data (1751-2010), exhibit biologically meaningful correspondences to economic, health and cause-of-death patterns. The model characterizes the 20th century epidemiological transition mainly as a reduction in extrinsic mortality resulting from a shift from high magnitude disease challenges on individuals at all vitality levels to low magnitude stress challenges on low vitality individuals. Of secondary importance, intrinsic mortality was described by a gradual reduction in the rate of loss of vitality presumably resulting from reduction in the rate of immunosenescence. Extensions and limitations of a distal/proximal framework for characterizing more explicit causes of death, e.g. the young adult mortality hump or cancer in old age are discussed.

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The Rarity of Survival to Old Age Does Not Drive the Evolution of Senescence

Cited by 55 publications

References 37 publications

The Williams' legacy: A critical reappraisal of his nine predictions about the evolution of senescence

The Williams' legacy: A critical reappraisal of his nine predictions about the evolution of senescence

Life history evolution, reproduction, and the origins of sex‐dependent aging and longevity

Insights into mortality patterns and causes of death through a process point of view model

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