Evo-devo of human adolescence: beyond disease models of early puberty

Abstract

Despite substantial heritability in pubertal development, much variation remains to be explained, leaving room for the influence of environmental factors to adjust its phenotypic trajectory in the service of fitness goals. Utilizing evolutionary development biology (evo-devo), we examine adolescence as an evolutionary life-history stage in its developmental context. We show that the transition from the preceding stage of juvenility entails adaptive plasticity in response to energy resources, other environmental cues, social needs of adolescence and maturation toward youth and adulthood. Using the evolutionary theory of socialization, we show that familial psychosocial stress fosters a fast life history and reproductive strategy rather than early maturation being just a risk factor for aggression and delinquency. Here we explore implications of an evolutionary-developmental-endocrinological-anthropological framework for theory building, while illuminating new directions for research.

Nutritional Status and Menarcheal Age of Rural Adolescent Girls of Salboni Block of Paschim Medinipur, West Bengal, India

“…Much as the secular trend in human size has been an adaptive response to a nutritionally rich environment, the receding age of adolescence and pubertal development has been an adaptive response to positive environmental cues in terms of energy balance [2].…”

The timing of puberty (oocyte quality and management)

“…Longer-term health costs are traded off for increased probability of reproducing before dying via a process of accelerated reproductive maturation. Early adversity, early sexual maturation form the core component linking stress physiology with poor health later in life (Hochberg and Belsky, 2013).…”

Father's death does not affect growth and maturation but hinders reproduction: evidence from adolescent girls in post-war Estonia

“…Relying on anthropometric measures of maturation (rate of development of breasts and axillary hair), growth and reproduction of adolescent girls, we were able to test the predictions of predictive-adaptive hypotheses [1,2,4,12,15,16] that father's death accelerates (i) sexual maturation and (ii) reproduction. Additionally, we tested (iii) whether father's death suppresses growth of daughters in order to elucidate the importance of paternal resource provisioning.…”

“…Additionally, we tested (iii) whether father's death suppresses growth of daughters in order to elucidate the importance of paternal resource provisioning. Growing children may lack sufficient resources to boost maturation under the constraint of extreme nutritional limitation [16] and we expected that such a situation would be revealed by showing impaired growth of girls whose fathers were dead. Ultimately, the negative effect of father's death on somatic growth can also be predicted if the rate of pubertal maturation is traded off against the rate of growth [17].…”

“…Finally, we asked whether father's death affects the number of children eventually born to the girls under study. Fast reproductive strategies are associated with more offspring (reviewed in [4,16]), hence we predicted that (iv) originating from a family where the father was dead would result in a higher total number of children and lower probability of remaining childless. Our dataset is particularly suitable for testing the latter predictions because all women involved in the study had completed fertility by the time their reproductive parameters were recorded.…”