Abstract

BackgroundChronic and/or extreme stress in early life, often referred to as early adversity, childhood trauma, or early life stress, has been associated with a wide range of adverse effects on development. However, while early life stress has been linked to negative effects on a number of neural systems, the specific mechanisms through which early life stress influences development and individual differences in children’s outcomes are still not well understood.Main textThe current paper reviews the existing literature on the neurobiological effects of early life stress and their ties to children’s psychological and behavioral development.ConclusionsEarly life stress has persistent and pervasive effects on prefrontal–hypothalamic–amygdala and dopaminergic circuits that are at least partially mediated by alterations in hypothalamic–pituitary–adrenal axis function. However, to date, this research has primarily utilized methods of assessment that focus solely on children’s event exposures. Incorporating assessment of factors that influence children’s interpretation of stressors, along with stressful events, has the potential to provide further insight into the mechanisms contributing to individual differences in neurodevelopmental effects of early life stress. This can aid in further elucidating specific mechanisms through which these neurobiological changes influence development and contribute to risk for psychopathology and health disorders.

Highlights

  • ConclusionsLife stress has persistent and pervasive effects on prefrontal–hypothalamic–amygdala and dopaminergic circuits that are at least partially mediated by alterations in hypothalamic–pituitary–adrenal axis function

  • The current paper reviews the existing literature on the neurobiological effects of early life stress and their ties to children’s psychological and behavioral development

  • While the question of how to best conceptualize early childhood adversity and stress has shifted over time [14, 15], the two predominant models of early life stress fall into the categories of (1) General or “lumping” models, in which various types of stressors are treated as a heterogeneous, broad category, often labeled “adversity,” “early life stress,” or “negative life events” [16,17,18,19]; and 2) Specific or “splitting” models, which are based on the premise that different types of adversity each confer specific effects, and links to neurobiological or cognitive systems may be masked by heterogeneous samples [20,21,22]

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Summary

Conclusions

We have highlighted recent research speaking to the neural mechanisms underlying the effects of early life stress on development. The existing literature supports effects of early life on the development of the prefrontal cortex, hippocampus, hypothalamus, and amygdala, along with communication across those areas, in ways that produces increased vulnerability to mental and physical health disorders later in life. These changes appear to be at least partially mediated through hormonal and neuropeptide alterations in the HPA axis along with interactions with genetic and epigenetic factors. To date, we still lack a good understanding about how these changes come about, what aspects of the child’s environment produces these changes, and, given not all children who experience early life stress develop later psychopathology, what their role is in individual differences in children’s outcomes after early life stress

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