Ancient origins of human developmental plasticity

Abstract

Animals have the ability to alter development, physiology, growth, and behavior in response to different environmental conditions. These responses represent critical assessments of both external and internal factors. For example, the timing of metamorphosis, hatching, or birth depends on the trade-offs between growth opportunity and mortality risk in the developmental habitat. Physiological sensors compute these trade-offs as a function of energy balance and environmental stress, and effectors initiate physiological, developmental, and behavioral responses to these determinations. The neuroendocrine stress axis provides a means for animals to integrate information from multiple sources and to respond accordingly. Considerable evidence now supports the view that the secretion of hormones critical to development (corticosteroid and thyroid hormones) is controlled by a common neuroendocrine stress pathway involving corticotropin-releasing factor (CRF) and related peptides. CRF produced in the hypothalamus stimulates the biosynthesis and secretion of both thyroid and corticosteroid hormones, leading to accelerated tadpole metamorphosis. Similarly, in mammals CRF of fetal and placental origin has been shown to influence the timing of birth. Studies in several experimental animal models and in humans show that early life experience can have long-term phenotypic consequences. Furthermore, there is evidence that phenotypic expression is strongly influenced by the actions of stress hormones produced during development. The integrated neuroendocrine response to stress, and its role in timing critical life history transitions and establishing long-term phenotypic expression, arose early in the evolution of vertebrates.

Corticosterone stimulates hatching of late-term tree lizard embryos

“…This group of adrenal steroid hormones coordinates behavioral and physiological responses to environmental conditions, allowing the animal to respond accordingly . Thus, one might predict them to have an important role in regulating the timing of hatching, as well as other life history transitions such as metamorphosis and birth (Crespi and Denver, 2005). Indeed, an increase in endogenous glucocorticoids is found among embryonic birds and crocodiles near hatching (Marie, 1981;Scott et al, 1981;Shepherdley et al, 2002), larval amphibians near metamorphosis (Glennemeier and Denver, 2002), and fetal mammals near parturition (Mulay et al, 1973;Fencl et al, 1980;Whittle et al, 2001).…”

Evo–devo of child growth II: human life history and transition between its phases

“…Predictive adaptive responses require trade-offs, such as reduced fetal growth in favor of survival, or early puberty with lower quality offspring against slow maturation and later first pregnancy with higher quality offspring. A given genotype can generate multiple phenotypes depending on the environmental conditions experienced by the organism during development (15).…”

The Barker hypothesis and obesity: Connections for transdisciplinarity and social justice

“…Social and temporal factors can impact the development of the foetus because of its 'developmental plasticity' (Crespi and Denver, 2005) during the critical and largely irreversible period of growth occurring in utero. A plastic organism can develop in response to stimuli that indicate conditions outside the womb, adapting a 'best fit' for those conditions (Bateson et al, 2004) such that 'one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development' (Barker, 2004, p. 589S).…”