Selection for Optimal Life Histories: The Effects of Age Structure

Ecology ◽  
1974 ◽  
Vol 55 (2) ◽  
pp. 291-303 ◽  
Author(s):  
William M. Schaffer
2008 ◽  
Vol 2 (2) ◽  
pp. 172-186 ◽  
Author(s):  
Lesley G. Campbell ◽  
Allison A. Snow ◽  
Patricia M. Sweeney ◽  
Julie M. Ketner

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Beatriz Diaz Pauli ◽  
Sarah Garric ◽  
Charlotte Evangelista ◽  
L. Asbjørn Vøllestad ◽  
Eric Edeline

2019 ◽  
Vol 286 (1916) ◽  
pp. 20192070 ◽  
Author(s):  
Thomas R. Haaland ◽  
Jonathan Wright ◽  
Irja I. Ratikainen

In order to understand how organisms cope with ongoing changes in environmental variability, it is necessary to consider multiple adaptations to environmental uncertainty on different time scales. Conservative bet-hedging (CBH) represents a long-term genotype-level strategy maximizing lineage geometric mean fitness in stochastic environments by decreasing individual fitness variance, despite also lowering arithmetic mean fitness. Meanwhile, variance-prone (aka risk-prone) strategies produce greater variance in short-term payoffs, because this increases expected arithmetic mean fitness if the relationship between payoffs and fitness is accelerating. Using evolutionary simulation models, we investigate whether selection for such variance-prone strategies is counteracted by selection for bet-hedging that works to adaptively reduce fitness variance. In our model, variance proneness evolves in fine-grained environments (lower correlations among individuals in energetic state and/or payoffs), and with larger numbers of independent decision events over which resources accumulate prior to selection. Conversely, multiplicative fitness accumulation, caused by coarser environmental grain and fewer decision events selection, favours CBH via greater variance aversion. We discuss examples of variance-sensitive strategies in optimal foraging, migration, life histories and cooperative breeding using this bet-hedging perspective. By linking disparate fields of research studying adaptations to variable environments, we should be better able to understand effects of human-induced rapid environmental change.


2020 ◽  
Vol 375 (1803) ◽  
pp. 20190492 ◽  
Author(s):  
Dominik Deffner ◽  
Richard McElreath

Social learning and life history interact in human adaptation, but nearly all models of the evolution of social learning omit age structure and population regulation. Further progress is hindered by a poor appreciation of how life history affects selection on learning. We discuss why life history and age structure are important for social learning and present an exemplary model of the evolution of social learning in which demographic properties of the population arise endogenously from assumptions about per capita vital rates and different forms of population regulation. We find that, counterintuitively, a stronger reliance on social learning is favoured in organisms characterized by ‘fast’ life histories with high mortality and fertility rates compared to ‘slower’ life histories typical of primates. Long lifespans make early investment in learning more profitable and increase the probability that the environment switches within generations. Both effects favour more individual learning. Additionally, under fertility regulation (as opposed to mortality regulation), more juveniles are born shortly after switches in the environment when many adults are not adapted, creating selection for more individual learning. To explain the empirical association between social learning and long life spans and to appreciate the implications for human evolution, we need further modelling frameworks allowing strategic learning and cumulative culture. This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’.


mBio ◽  
2014 ◽  
Vol 5 (6) ◽  
Author(s):  
Martin J. Blaser ◽  
Glenn F. Webb

ABSTRACT The age structure of human populations is exceptional among animal species. Unlike with most species, human juvenility is extremely extended, and death is not coincident with the end of the reproductive period. We examine the age structure of early humans with models that reveal an extraordinary balance of human fertility and mortality. We hypothesize that the age structure of early humans was maintained by mechanisms incorporating the programmed death of senescent individuals, including by means of interactions with their indigenous microorganisms. First, before and during reproductive life, there was selection for microbes that preserve host function through regulation of energy homeostasis, promotion of fecundity, and defense against competing high-grade pathogens. Second, we hypothesize that after reproductive life, there was selection for organisms that contribute to host demise. While deleterious to the individual, the presence of such interplay may be salutary for the overall host population in terms of resource utilization, resistance to periodic diminutions in the food supply, and epidemics due to high-grade pathogens. We provide deterministic mathematical models based on age-structured populations that illustrate the dynamics of such relationships and explore the relevant parameter values within which population viability is maintained. We argue that the age structure of early humans was robust in its balance of the juvenile, reproductive-age, and senescent classes. These concepts are relevant to issues in modern human longevity, including inflammation-induced neoplasia and degenerative diseases of the elderly, which are a legacy of human evolution. IMPORTANCE The extended longevity of modern humans is a very recent societal artifact, although it is inherent in human evolution. The age structure of early humans was balanced by fertility and mortality, with an exceptionally prolonged juvenility. We examined the role of indigenous microbes in early humans as fundamental contributors to this age structure. We hypothesize that the human microbiome evolved mechanisms specific to the mortality of senescent individuals among early humans because their mortality contributed to the stability of the general population. The hypothesis that we present provides new bases for modern medical problems, such as inflammation-induced neoplasia and degenerative diseases of the elderly. We postulate that these mechanisms evolved because they contributed to the stability of early human populations, but their legacy is now a burden on human longevity in the changed modern world.


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