ABSTRACT
Childhood adversity can have life-long consequences for the response to stressful events later in life (1). Repeated exposure to trauma alters neurodevelopment (2), enhances the activity of endocrine mechanisms involved in the stress response (3, 4) and increases the risk of multiple forms of psychopathology (5, 6). For example, the risk of suicide is strongly linked to childhood sexual and physical abuse or severe neglect (7-9). Sexual and physical abuse or severe neglect in childhood are also well-known risk factors for adult forms of post-traumatic stress disorder (PTSD), at least in part via changes in neural systems mediating the endocrine response to stress (10). The hypothalamic-pituitary-adrenal (HPA) axis shapes the endocrine response to stress in addition to its role in many other physiological
processes, including immune and metabolic function. As such, the HPA axis plays an adaptive role by maintaining allostasis (i.e., stability amid change) in the face of challenging environmental conditions. Part of the explanation for the enhanced impact of adversity in early life is thought to lie in the relatively high degree of plasticity during this period, when environmental factors exert pervasive effects on a number of health trajectories (11, 12). Accumulating evidence indicates that this phenomenon, sometimes called “biological embedding,” involves persistent changes in gene regulation via epigenetic mechanisms (13). The goal of this review is to highlight research on epigenetic mechanisms of early life adversity and parental care – prime mediators of offspring neurodevelopment (11) – that addresses several critical issues for research in this rapidly evolving area. We conclude by providing examples of the ways in which research in this area may provide insights for PTSD researchers on the epigenetic impacts of early adversity and highlight challenges for the field going forward.
