Early Life Adversity and Psychiatric Symptomatology in Late Adolescence: Neural, Cognitive and Inflammatory Processes
Early life adversity is associated with increased risk for a range of psychiatric disorders, including depression and anxiety disorders. A better understanding of the biological and cognitive processes associated with early life adversity may lead to improved prevention and intervention efforts. Nusslock and Miller’s neuroimmune network hypothesis proposes that early life adversity accentuates cortico-amygdala threat sensitivity and attenuates cortico-basal ganglia reward sensitivity both directly and via inflammatory processes, contributing to emotional and physical health problems. To test the neuroimmune network hypothesis, the current studies examined the associations of fear acquisition, reward anticipation and consumption, and working memory with early life adversity, peripheral inflammation and depression and anxiety symptoms in a sample of 18- to 19-year-olds. Rather than taking a cumulative risk approach, the current studies modeled instances of adversity according to the dimensions of threat and deprivation as proposed by McLaughlin and Sheridan’s dimensional model of adversity and psychopathology. Study 1 found that a deprivation adversity composite was significantly associated with neural activation in regions of interest during the acquisition phase of a differential fear conditioning paradigm, but that this neural activation did not predict subsequent anxiety symptoms. Study 2 found that the deprivation adversity composite was significantly associated with neural activation in the ventral striatum during reward consumption, but that neural activation during reward processing did not predict subsequent depressive symptoms. Study 3 found that the threat adversity composite was significantly associated with working memory task performance for both neutral and negative verbal stimuli, and that slower mean reaction time for a block of mixed neutral and negative words predicted lesser subsequent anxiety symptoms. Peripheral inflammation was not significantly associated with early adversity, neural activation during fear conditioning or reward processing, or working memory. The current studies tested recent theoretical models in early life adversity research, providing insight into the neural, cognitive and inflammatory processes thought to underlie the association between early adversity and psychiatric symptomatology.