Plasticity in developmental programming has evolved in order to provide the best chances of survival and reproductive success to the organism under changing environments. Environmental conditions that are experienced in early life can profoundly influence human biology and long-term health. Developmental origins of health and disease and life-history transitions are purported to use placental, nutritional, and endocrine cues for setting long-term biological, mental, and behavioral strategies in response to local ecological and/or social conditions. The window of developmental plasticity extends from preconception to early childhood and involves epigenetic responses to environmental changes, which exert their effects during life-history phase transitions. These epigenetic responses influence development, cell- and tissue-specific gene expression, and sexual dimorphism, and, in exceptional cases, could be transmitted transgenerationally. Translational epigenetic research in child health is a reiterative process that ranges from research in the basic sciences, preclinical research, and pediatric clinical research. Identifying the epigenetic consequences of fetal programming creates potential applications in clinical practice: the development of epigenetic biomarkers for early diagnosis of disease, the ability to identify susceptible individuals at risk for adult diseases, and the development of novel preventive and curative measures that are based on diet and/or novel epigenetic drugs.

With child growth being multifactorial and the glucocorticoids (GC) having many target physiological and biochemical mechanisms, growth and the GC collide in several meeting points. Indirectly, GC have a general anti-anabolic and catabolic influences that include bone, cartilage and muscle proteins. The GC interfere with the GH–IGF-1 axis at the hypothalamic, pituitary and target organ levels, affecting hormone release, receptor abundance, signal transduction, gene transcription, pre-mRNA splicing and mRNA translation. GC disturb normal calcium balance at the intestine and kidney. Direct effects at the growth plate include the suppression of multiple gene expression, chondrocyte proliferation and matrix proteoglycan synthesis, sulfation, release and mineralization as well as the augmentation of hypertrophic cell apoptosis. At the tissues adjacent to the growth plate, GC enhance osteoclast and suppress osteoblast recruitment and function, they reduce muscle strength and disrupt the normal control of vascular invasion at the cartilage–bone interface. Growth damage from GC is maximal during the initial months of treatment and prevention is more effective than post-factual therapy. To reduce these growth-retarding effects, the following measures, which are partly experimental, may be effective in a decreasing order: minimize GC dose and use an alternate-day treatment; utilize the oxazoline analog of prednisolone deflazacort, normalize calcium balance; employ hGH or IGF-1.

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.

This review attempts to use evolutionary life-history theory in understanding child growth in a broad evolutionary perspective. It uses the data and theory of evolutionary predictive adaptive strategies for transition from one life-history phase to the next, and the inherent adaptive plasticity in the timing of such transitions. Humans evolved to withstand energy crises by decreasing their body size, and evolutionary short-term adaptations to energy crises utilize a plasticity that modifies the timing of transition from infancy into childhood, culminating in short stature at the time of an energy crisis. Transition to juvenility is part of a strategy of conversion from a period of total dependence on the family and tribe for provision and security to self-supply, and a degree of adaptive plasticity is provided and determines body composition. Transition to adolescence entails plasticity in adapting to energy resources, other environmental cues, and the social needs of the maturing adolescent to determine lifespan and the period of fecundity and fertility. Conclusion Life-history transitions are the times when the child adaptively responds to environmental cues in order to enhance growth–body composition–lifespan–fecundity schedules and behavioral strategies that yield the highest fitness in a given environment.