Abstract
Childhood adversity is associated with altered or dysregulated stress reactivity; these altered patterns of physiological functioning persist into adulthood. Evidence from both preclinical animal models and human neuroimaging studies indicates that early life experience differentially influences stressor-evoked activity within central visceral neural circuits proximally involved in the control of stress responses, including the subgenual anterior cingulate cortex (sgACC), paraventricular nucleus of the hypothalamus (PVN), bed nucleus of the stria terminalis (BNST) and amygdala. However, the relationship between childhood adversity and the resting-state connectivity of this central visceral network remains unclear. To this end, we examined relationships between childhood threat and childhood socioeconomic deprivation, the resting-state connectivity between our regions of interest (ROIs), and affective symptom severity and diagnoses. We recruited a transdiagnostic sample of young adult males and females (n = 100; mean age = 27.28, SD = 3.99; 59 females) with a full distribution of maltreatment history and symptom severity across multiple affective disorders. Resting-state data were acquired using a 7.2-min functional magnetic resonance imaging (fMRI) sequence; noted ROIs were applied as masks to determine ROI-to-ROI connectivity. Threat was determined by measures of childhood traumatic events and abuse. Socioeconomic deprivation (SED) was determined by a measure of childhood socioeconomic status (parental education level). Covarying for age, race and sex, greater childhood threat was significantly associated with lower BNST-PVN, amygdala-sgACC and PVN-sgACC connectivity. No significant relationships were found between SED and resting-state connectivity. BNST-PVN connectivity was associated with the number of lifetime affective diagnoses. Exposure to threat during early development may entrain altered patterns of resting-state connectivity between these stress-related ROIs in ways that contribute to dysregulated neural and physiological responses to stress and subsequent affective psychopathology.
Highlights
Due to its high prevalence (Hillis et al, 2016; Merrick et al, 2018; Cuartas et al, 2019) and importance as a predictor of affective risk, childhood adversity is at the forefront of psychiatry’s public health burden (Sara and Lappin, 2017)
Childhood Adversity and Resting-State Connectivity We examined whether childhood threat and socioeconomic deprivation (SED) variables were associated with resting-state connectivity between our regions of interest (ROIs); six resting-state ROI-to-ROI connections were examined (Amygdala-bed nucleus of the stria terminalis (BNST), Amygdala-paraventricular nucleus of the hypothalamus (PVN), Amygdala-subgenual anterior cingulate cortex (sgACC), BNSTPVN, BNST-sgACC and PVN-sgACC)
We found that childhood threat was associated with lower restingstate-connectivity among our central visceral, limbic forebrainhypothalamic ROIs (BNST-PVN, Amygdala-sgACC and PVNsgACC)
Summary
Due to its high prevalence (Hillis et al, 2016; Merrick et al, 2018; Cuartas et al, 2019) and importance as a predictor of affective risk, childhood adversity is at the forefront of psychiatry’s public health burden (Sara and Lappin, 2017). Childhood adversity is associated with dysregulated (heightened or diminished) stress reactivity in childhood and later in life (Al’Absi et al, 2021), with alterations in both neuroendocrine and autonomic physiology and stress reactivity (Heim et al, 2000, 2001; Chen et al, 2004; Koopman et al, 2004; Carpenter et al, 2007, 2011; Gunnar et al, 2009; Lovallo et al, 2011; Hackman et al, 2012). There is evidence to suggest that there may be differential influences of childhood adversity dimensions, threat (e.g., abuse, traumatic events) and deprivation (e.g., neglect, socioeconomic deprivation, institutional rearing) (McLaughlin et al, 2014; Sheridan and McLaughlin, 2014) on stress reactivity, with threat blunting (Carpenter et al, 2007, 2011; Doom et al, 2014; Peckins et al, 2015; Bernard et al, 2017) and deprivation (i.e., low socioeconomic status, SES) heightening reactivity (Lupien et al, 2001; Cohen et al, 2006; Chen et al, 2009; Lê-Scherban et al, 2018). Despite evidence linking childhood threat and deprivation to altered physiological stress systems, how childhood adversity shapes specific, proximally stress-responsive neural circuits remains unclear
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