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A theoretical model of the evolution of actuarial senescence under environmental stress.

ABSTRACT: Free-living organisms are exposed to a wide range of stressors, all of which can disrupt components of stress-related and detoxification physiology. The subsequent accumulation of somatic damage is widely believed to play a major role in the evolution of senescence. Organisms have evolved sophisticated physiological regulatory mechanisms to maintain homeostasis in response to environmental perturbations, but these systems are likely to be constrained in their ability to optimise robustness to multiple stressors due to functional correlations among related traits. While evolutionary change can accelerate due to human ecological impacts, it remains to be understood how exposure to multiple environmental stressors could affect senescence rates and subsequently population dynamics and fitness. We used a theoretical evolutionary framework to quantify the potential consequences for the evolution of actuarial senescence in response to exposure to simultaneous physiological stressors--one versus multiple and additive versus synergistic--in a hypothetical population of avian "urban adapters". In a model in which multiple stressors have additive effects on physiology, species may retain greater capacity to recover, or respond adaptively, to environmental challenges. However, in the presence of high synergy, physiological dysregulation suddenly occurs, leading to a rapid increase in age-dependent mortality and subsequent population collapse. Our results suggest that, if the synergistic model is correct, population crashes in environmentally-stressed species could happen quickly and with little warning, as physiological thresholds of stress resistance are overcome.

SUBMITTER: Watson H

PROVIDER: S-EPMC4710637 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature

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A theoretical model of the evolution of actuarial senescence under environmental stress.

Watson H H Cohen A A AA Isaksson C C

Experimental gerontology 20150831

Free-living organisms are exposed to a wide range of stressors, all of which can disrupt components of stress-related and detoxification physiology. The subsequent accumulation of somatic damage is widely believed to play a major role in the evolution of senescence. Organisms have evolved sophisticated physiological regulatory mechanisms to maintain homeostasis in response to environmental perturbations, but these systems are likely to be constrained in their ability to optimise robustness to mu ...[more]

PMID: 26335620

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Project description:The concept of actuarial senescence (defined here as the increase in mortality hazards with age) is often confounded with life span duration, which obscures the relative role of age-dependent and age-independent processes in shaping the variation in life span. We use the opportunity afforded by the Species360 database, a collection of individual life span records in captivity, to analyze age-specific mortality patterns in relation to variation in life span. We report evidence of actuarial senescence across 96 mammal species. We identify the life stage (juvenile, prime-age, or senescent) that contributes the most to the observed variation in life span across species. Actuarial senescence only accounted for 35%-50% of the variance in life span across species, depending on the body mass category. We computed the sensitivity and elasticity of life span to five parameters that represent the three stages of the age-specific mortality curve-namely, the duration of the juvenile stage, the mean juvenile mortality, the prime-age (i.e., minimum) adult mortality, the age at the onset of actuarial senescence, and the rate of actuarial senescence. Next, we computed the between-species variance in these five parameters. Combining the two steps, we computed the relative contribution of each of the five parameters to the variance in life span across species. Variation in life span was increasingly driven by the intensity of actuarial senescence and decreasingly driven by prime-age adult mortality from small to large species because of changes in the elasticity of life span to these parameters, even if all the adult survival parameters consistently exhibited a canalization pattern of weaker variability among long-lived species than among short-lived ones. Our work unambiguously demonstrates that life span cannot be used to measure the strength of actuarial senescence, because a substantial and variable proportion of life span variation across mammals is not related to actuarial senescence metrics.

Dataset Information

A theoretical model of the evolution of actuarial senescence under environmental stress.

Publications

A theoretical model of the evolution of actuarial senescence under environmental stress.

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