Alexandra Alvergne

The existence of interindividual differences in personality traits poses a challenge to evolutionary thinking. Although research on the ultimate consequences of personality differences in nonhuman animals has recently undergone a surge of interest, our understanding of whether and how personality influences reproductive decisions in humans has remained limited and informed primarily by modern societies with low mortality–fertility schedules. Taking an evolutionary approach, we use data from a contemporary polygynous high-fertility human population living in rural Senegal to investigate whether personality dimensions are associated with key life-history traits in humans, i.e., quantity and quality of offspring. We show that personality dimensions predict reproductive success differently in men and women in such societies and, in women, are associated with a trade-off between offspring quantity and quality. In women, neuroticism positively predicts the number of children, both between and within polygynous families. Furthermore, within the low social class, offspring quality (i.e., child nutritional status) decreases with a woman's neuroticism, indicating a reproductive trade-off between offspring quantity and quality. Consistent with this, maximal fitness is achieved by women at an intermediate neuroticism level. In men, extraversion was found to be a strong predictor of high social class and polygyny, with extraverted men producing more offspring than their introverted counterparts. These results have implications for the consideration of alternative adaptive hypotheses in the current debate on the maintenance of personality differences and the role of individual factors in fertility patterns in contemporary humans.

Both environmental exposures and genetics are known to play important roles in shaping human aging. Here we aimed to quantify the relative contributions of environment (referred to as the exposome) and genetics to aging and premature mortality. To systematically identify environmental exposures associated with aging in the UK Biobank, we first conducted an exposome-wide analysis of all-cause mortality (n = 492,567) and then assessed the associations of these exposures with a proteomic age clock (n = 45,441), identifying 25 independent exposures associated with mortality and proteomic aging. These exposures were also associated with incident age-related multimorbidity, aging biomarkers and major disease risk factors. Compared with information on age and sex, polygenic risk scores for 22 major diseases explained less than 2 percentage points of additional mortality variation, whereas the exposome explained an additional 17 percentage points. Polygenic risk explained a greater proportion of variation (10.3-26.2%) compared with the exposome for incidence of dementias and breast, prostate and colorectal cancers, whereas the exposome explained a greater proportion of variation (5.5-49.4%) compared with polygenic risk for incidence of diseases of the lung, heart and liver. Our findings provide a comprehensive map of the contributions of environment and genetics to mortality and incidence of common age-related diseases, suggesting that the exposome shapes distinct patterns of disease and mortality risk, irrespective of polygenic disease risk.