Effects of early life stress on cognitive and affective function: an integrated review of human literature
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The investigation of putative effects of early life stress (ELS) in humans on later behavior and neurobiology is a fast developing field. While epidemiological and neurobiological studies paint a somber picture of negative outcomes, relatively little attention has been devoted to integrating the breadth of findings concerning possible cognitive and emotional deficits associated with ELS. Emerging findings from longitudinal studies examining developmental trajectories of the brain in healthy samples may provide a new framework to understand mechanisms underlying ELS sequelae.
The goal of this review was twofold. The first was to summarize findings from longitudinal data on normative brain development. The second was to utilize this framework of normative brain development to interpret changes in developmental trajectories associated with deficits in cognitive and affective function following ELS.
Five principles of normative brain development were identified and used to discuss behavioral and neural sequelae of ELS. Early adversity was found to be associated with deficits in a range of cognitive (cognitive performance, memory, and executive functioning) and affective (reward processing, processing of social and affective stimuli, and emotion regulation) functions.
Three general conclusions emerge: (1) higher-order, complex cognitive and affective functions associated with brain regions undergoing protracted postnatal development are particularly vulnerable to the deleterious effects of ELS; (2) the amygdala is particularly sensitive to early ELS; and (3) several deficits, particularly those in the affective domain, appear to persist years after ELS has ceased and may increase risk for later psychopathology.
KeywordsEarly life stress Brain Child abuse Cognitive function Emotion regulation
During the preparation of this paper, Pia Pechtel received research funding from the German Research Foundation [Deutsche Forschungsgemeinschaft (DFG)]. DAP was supported by Award Numbers R01MH068376 and R21MH078979 from the National Institute of Mental Health and by a 2008 National Alliance for Research on Schizophrenia and Depression (NARSAD) Independent Investigator Award. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Mental Health, the National Institutes of Health, or NARSAD.
Dr. Pizzagalli has received research support from ANT North America Inc. (Advanced Neuro Technology (ANT)], consulting fees from ANT North America Inc. and AstraZeneca, and honoraria from AstraZeneca.
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