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Why do the two sexes have different lifespans and rates of aging? Two hypotheses based on asymmetric inheritance of sex chromosomes ("unguarded X") or mitochondrial genomes ("mother's curse") explain sex differences in lifespan as sex-specific maladaptation leading to increased mortality in the shorter-lived sex. While asymmetric inheritance hypotheses equate long life with high fitness, considerable empirical evidence suggests that sexes resolve the fundamental tradeoff between reproduction and survival differently resulting in sex-specific optima for lifespan. However, selection for sex-specific values in life-history traits is constrained by intersexual genetic correlations resulting in intra-locus sexual conflict over optimal lifespan. The available data suggest that the evolution of sexual dimorphism only partially resolves these conflicts. Sexual conflict over optimal trait values, which has been demonstrated in model organisms and in humans, is likely to play a key role in shaping the evolution of lifespan, as well as in maintaining genetic variation for sex-specific diseases.

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We examined associations between Five Factor Model personality traits and various outcomes of reproductive behavior in a sample of 15 729 women and men from the Wisconsin Longitudinal Study (WLS) and Midlife Development in the United States (MIDUS) survey. Personality and reproductive history was self-reported in adulthood (mean age: 53 years). High extraversion, high openness to experience, and low neuroticism were associated with larger number of children in both sexes, while high agreeableness and low conscientiousness correlated with larger offspring number in women only. These associations were independent of marital status. There were also more specific associations between personality and timing of childbearing. The findings demonstrate that personality traits of the Five Factor Model are systematically associated with multiple reproductive outcomes.

The environment that an offspring experiences during its development can have lifelong consequences for its morphology, anatomy, physiology and behaviour that are strong enough to span generations. One aspect of an offspring's environment that can have particularly pronounced and long-lasting effects is that provided by its parent(s) (maternal effects). Some disciplines in biology have been quicker to appreciate maternal effects than others, and some organisms provide better model systems for understanding the causes and consequences of the maternal environment for ecology and evolution than others. One field in which maternal effects has been poorly represented, and yet is likely to represent a particularly fruitful area for research, is the field of cooperative breeding (i.e. systems where offspring are reared by carers in addition to parent(s)). Here, we attempt to illustrate the scope of cooperative breeding systems for maternal effects research and, conversely, highlight the importance of maternal effects research for understanding cooperative breeding systems. To this end, we first outline why mothers will commonly benefit from affecting the phenotype of their offspring in cooperative breeding systems, present potential strategies that mothers could employ in order to do so and offer predictions regarding the circumstances under which different types of maternal effects might be expected. Second, we highlight why a neglect of maternal strategies and the effects that they have on their offspring could lead to miscalculations of helper/worker fitness gains and a misunderstanding of the factors selecting for the evolution and maintenance of cooperative breeding. Finally, we introduce the possibility that maternal effects could have significant consequences for our understanding of both the evolutionary origins of cooperative breeding and the rise of social complexity in cooperative systems.

An increasing number of studies have documented phenotypic selection on life-history traits in human populations, but less is known of the heritability and genetic constraints that mediate the response to selection on life-history traits in humans. We collected pedigree data for four generations of preindustrial (1745-1900) Finns who lived in premodern fertility and mortality conditions, and by using a restricted maximum-likelihood animal-model framework, we estimated the heritability of and genetic correlations between a suite of life-history traits and two alternative measures of fitness. First, we demonstrate high heritability of key life-history traits (fecundity, interbirth interval, age at last reproduction, and adult longevity) and measures of fitness (individual and lifetime reproductive success) for females but not for males. This sex difference may have arisen because most of the measured traits are under physiological control of the female, such that a male's fitness in monogamous societies may depend mainly on the reproductive quality of his spouse. We found strong positive genetic correlations between female age at first reproduction and longevity, and between interbirth intervals and longevity, suggesting reduced life spans in females who either started to breed relatively early or who then bred frequently. Our results suggest that key female life-history traits in this premodern human population had high heritability and may have responded to natural selection. However genetic constraints between longevity and reproductive life-history traits may have constrained the evolution of life history and facilitated the maintenance of additive genetic variance in key life-history traits.genetic correlation ͉ Homo sapiens ͉ animal model ͉ natural selection ͉ tradeoff T he cultural and biological factors that determine human life-history evolution are of interest to scientists from several different fields of science. Evolutionary biologists and anthropologists are interested in revealing the importance of different life-history traits in affecting fitness and longevity and whether these traits are under natural selection. Many studies have reported phenotypic correlations between different life-history traits, longevity, and measures of fitness in humans, but the nature of such associations is often contradictory. For example, although some studies have shown negative effects of high total reproductive effort on postreproductive longevity (1-3), most studies have found no association, or even positive correlations, between total reproductive effort and longevity (4-10). Likewise, some studies have shown a negative relationship between age at first reproduction (AFR) and postreproductive mortality (1, 11), whereas others found no evidence for such an association (6,12,13). In a historical northern Finnish population, the most important component of female fitness (i.e., the phenotypic trait with the highest selection differential) was the number of delivered offspring, but women also gained higher fitness (...

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Individuals with insufficient nutrition during development often experience poorer later-life health and evolutionary fitness. The Predictive Adaptive Response (PAR) hypothesis proposes that poor early-life nutrition induces physiological changes that maximize fitness in similar environments in adulthood and that metabolic diseases result when individuals experiencing poor nutrition during development subsequently encounter good nutrition in adulthood. However, although cohort studies have shown that famine exposure in utero reduces health in favorable later-life conditions, no study on humans has demonstrated the predicted fitness benefit under low later-life nutrition, leaving the evolutionary origins of such plasticity unexplored. Taking advantage of a well-documented famine and unique datasets of individual life histories and crop yields from two preindustrial Finnish populations, we provide a test of key predictions of the PAR hypothesis. Known individuals from fifty cohorts were followed from birth until the famine, where we analyzed their survival and reproductive success in relation to the crop yields around birth. We were also able to test whether the long-term effects of early-life nutrition differed between individuals of varying socioeconomic status. We found that, contrary to predictions of the PAR hypothesis, individuals experiencing low early-life crop yields showed lower survival and fertility during the famine than individuals experiencing high early-life crop yields. These effects were more pronounced among young individuals and those of low socioeconomic status. Our results do not support the hypothesis that PARs should have been favored by natural selection and suggest that alternative models may need to be invoked to explain the epidemiology of metabolic diseases.developmental plasticity | silver spoon | human life-history | DoHAD