Abstract

BackgroundEarly life adversities including harsh parenting, maternal depression, neighborhood deprivation, and low family economic resources are more prevalent in low-income urban environments and are potent predictors of psychopathology, including, for boys, antisocial behavior. However, little research has examined how these stressful experiences alter later neural function. Moreover, identifying genetic markers of greater susceptibility to adversity is critical to understanding biopsychosocial pathways from early adversity to later psychopathology. MethodsWithin a sample of 310 low-income boys followed from 1.5 to 20 years of age, multimethod assessments of adversities were examined at 2 and 12 years of age. At 20 years of age, amygdala reactivity to emotional facial expressions was assessed using functional magnetic resonance imaging, and symptoms of antisocial personality disorder were assessed via the Structured Clinical Interview for DSM. Genetic variability in cortisol signaling (CRHR1) was examined as a moderator of pathways to amygdala reactivity. ResultsObserved parenting and neighborhood deprivation at 2 years of age each uniquely predicted amygdala reactivity to emotional faces at 20 years of age over and above other adversities measured at multiple developmental periods. Harsher parenting and greater neighborhood deprivation in toddlerhood predicted clinically significant symptoms of antisocial behavior via less amygdala reactivity to fearful facial expressions, and this pathway was moderated by genetic variation in CRHR1. ConclusionsThese results elucidate a pathway linking early adversity to less amygdala reactivity to social signals of interpersonal distress 18 years later, which in turn increased risk for serious antisocial behavior. Moreover, these findings suggest a genetic marker of youth more susceptible to adversity.

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