No abstract

The current study examined biomarkers of stress in war-exposed young children and addressed maternal and child factors that may correlate with children's stress response. Participants were 232 Israeli children aged 1.5-5 years, including 148 children exposed to continuous war. Similarly, 56 were diagnosed with posttraumatic stress disorder (PTSD) and 92 were defined as exposed-no-PTSD. Child cortisol (CT) and salivary alpha amylase (sAA), biomarkers of the hypothalamic-pituitary-adrenal and sympathetic-adrenal-medullary arms of the stress response, were measured at baseline, following challenge, and at recovery. Maternal CT and sAA, PTSD symptoms, and reciprocal parenting, and child negative emotionality and regulatory strategies were assessed. Differences between war-exposed children and controls emerged, but these were related to child PTSD status. Children with PTSD exhibited consistently low CT and sAA, exposed-no-PTSD displayed consistently high CT and sAA, and controls showed increase in CT following challenge and decrease at recovery and low sAA. Exposed children showed higher negative emotionality; however, whereas exposed-no-PTSD children employed comfort-seeking strategies, children with PTSD used withdrawal. Predictors of child CT included maternal CT, PTSD symptoms, low reciprocity, and negative emotionality. Findings suggest that high physiological arousal combined with approach strategies may be associated with greater resilience in the context of early trauma.

Research indicates that risk for post-traumatic stress disorder (PTSD) is shaped by the interaction between genetic vulnerability and early caregiving experiences; yet, caregiving has typically been assessed by adult retrospective accounts. Here, we employed a prospective longitudinal design with real-time observations of early caregiving combined with assessment of genetic liability along the axis of vasopressin–oxytocin (OT) gene pathways to test G × E contributions to PTSD. Participants were 232 young Israeli children (1.5–5 years) and their parents, including 148 living in zones of continuous war and 84 controls. A cumulative genetic risk factor was computed for each family member by summing five risk alleles across three genes (OXTR, CD38 and AVPR1a) previously associated with psychopathology, sociality and caregiving. Child PTSD was diagnosed and mother–child interactions were observed in multiple contexts. In middle childhood (7–8 years), child psychopathology was re-evaluated. War exposure increased propensity to develop Axis-I disorder by threefold: 60% of exposed children displayed a psychiatric disorder by middle childhood and 62% of those showed several comorbid disorders. On the other hand, maternal sensitive support reduced risk for psychopathology. G × E effect was found for child genetic risk: in the context of war exposure, greater genetic risk on the vasopressin–OT pathway increased propensity for psychopathology. Among exposed children, chronicity of PTSD from early to middle childhood was related to higher child, maternal and paternal genetic risk, low maternal support and greater initial avoidance symptoms. Child avoidance was predicted by low maternal support and reduced mother–child reciprocity. These findings underscore the saliency of both genetic and behavioral facets of the human affiliation system in shaping vulnerability to PTSD as well as providing an underlying mechanism of post-traumatic resilience.

Early-onset chronic stress does not heal naturally, and its effects appear to exacerbate over time, with trauma-exposed children presenting a more comorbid, chronic, and externalizing profile as they grow older. Our findings demonstrate that responses to trauma are dynamic and variable and pinpoint age-specific effects of maternal and child factors on risk and resilience trajectories. Results highlight the importance of conducting long-term follow-up studies and constructing individually tailored early interventions following trauma exposure.