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Early adversity is a major risk factor for the emergence of psychopathology across development. Identifying mechanisms that support resilience, or favorable mental health outcomes despite exposure to adversity, is critical for informing clinical intervention and guiding policy to promote youth mental health. Here we propose that caregivers play a central role in fostering resilience among children exposed to adversity via caregiving influences on children’s corticolimbic circuitry and emotional functioning. We first delineate the numerous ways that caregivers support youth emotional learning and regulation and describe how early attachment lays the foundation for optimal caregiver support of youth emotional functioning in a developmental stage-specific manner. Second, we outline neural mechanisms by which caregivers foster resilience—namely, by modulating offspring corticolimbic circuitry to support emotion regulation and buffer stress reactivity. Next, we highlight the importance of developmental timing and sensitive periods in understanding caregiving-related mechanisms of resilience. Finally, we discuss clinical implications of this line of research and how findings can be translated to guide policy that promotes the well-being of youth and families.

Key theoretical frameworks have proposed that examining the impact of exposure to specific dimensions of stress at specific developmental periods is likely to yield important insight into processes of risk and resilience. Utilizing a sample ofN= 549 young adults who provided a detailed retrospective history of their lifetime exposure to numerous dimensions of traumatic stress and ratings of their current trauma-related symptomatology via completion of an online survey, here we test whether an individual’s perception of their lifetime stress as either controllable or predictable buffered the impact of exposure on trauma-related symptomatology assessed in adulthood. Further, we tested whether this moderation effect differed when evaluated in the context of early childhood, middle childhood, adolescence, and young adulthood stress. Consistent with hypotheses, results highlight both stressor controllability and stressor predictability as buffering the impact of traumatic stress exposure on trauma-related symptomatology and suggest that the potency of this buffering effect varies across unique developmental periods. Leveraging dimensional ratings of lifetime stress exposure to probe heterogeneity in outcomes following stress – and, critically, considering interactions between dimensions of exposure and the developmental period when stress occurred – is likely to yield increased understanding of risk and resilience following traumatic stress.

Migrant and refugee children commonly experience traumatic events and stressful conditions along their migration journeys. Migration-related trauma can have persisting effects on children's mental health. Developmental neuroscience suggests neural mechanisms that connect these experiences to mental health conditions such as post-traumatic stress disorder. This research review, focused on migrant families emigrating from Mexico, Central America, and Haiti and bound for the United States, first overviews the nature of trauma exposure faced by migrant families and next delineates potential neurobiological mechanisms underlying the effects of migration-related trauma on youth mental health. Finally, detailed policy recommendations relate to (1) providing mental health care, (2) addressing chronic stressors in the context of daily life, and (3) preventing migration-related trauma.

Decades of research underscore the profound impact of adversity on brain and behavioral development. Recent theoretical models have highlighted the importance of considering specific features of adversity that may have dissociable effects at distinct developmental timepoints. However, existing measures do not query these dimensions in sufficient detail to support the proliferation of this approach. The Dimensional Inventory of Stress and Trauma Across the Lifespan (DISTAL) was developed with the aim to thoroughly and retrospectively assess the timing, severity (of exposure and reaction), type, persons involved, controllability, predictability, threat, deprivation, proximity, betrayal, and discrimination inherent in an individual's exposure to adversity. Here, we introduce this instrument, present descriptive statistics drawn from a sample ofN = 187 adults who completed the DISTAL, and provide initial information about its psychometric properties. This novel measure facilitates the expansion of research focused on assessing the relative impact of exposure to key dimensions of adversity on the brain and behavior across development.

Heightened fear and inefficient safety learning are key features of fear and anxiety disorders. Evidence-based interventions for anxiety disorders, such as cognitive behavioral therapy, primarily rely on mechanisms of fear extinction. However, up to 50% of clinically anxious individuals do not respond to current evidence-based treatment, suggesting a critical need for new interventions based on alternative neurobiological pathways. Using parallel human and rodent conditioned inhibition paradigms alongside brain imaging methodologies, we investigated neural activity patterns in the ventral hippocampus in response to stimuli predictive of threat or safety and compound cues to test inhibition via safety in the presence of threat. Distinct hippocampal responses to threat, safety, and compound cues suggest that the ventral hippocampus is involved in conditioned inhibition in both mice and humans. Moreover, unique response patterns within target-differentiated subpopulations of ventral hippocampal neurons identify a circuit by which fear may be inhibited via safety. Specifically, ventral hippocampal neurons projecting to the prelimbic cortex, but not to the infralimbic cortex or basolateral amygdala, were more active to safety and compound cues than threat cues, and activity correlated with freezing behavior in rodents. A corresponding distinction was observed in humans: hippocampal–dorsal anterior cingulate cortex functional connectivity—but not hippocampal–anterior ventromedial prefrontal cortex or hippocampal–basolateral amygdala connectivity—differentiated between threat, safety, and compound conditions. These findings highlight the potential to enhance treatment for anxiety disorders by targeting an alternative neural mechanism through safety signal learning.

Given the importance of early prevention and intervention strategies for children exposed to trauma, detection of early risk factors for exposure to traumatic events in childhood is critical. The present study examined associations between three known prenatal risk factors that characterize environmental instability in utero—prenatal substance exposure, prenatal violence victimization, and unintended pregnancy—and child exposure to interparental violence and other adverse experiences in a sample of 198 mother–child dyads (Mchild age = 44.48 months) referred to a hospital clinic for treatment following exposure to trauma. Prenatal substance and violence exposure were associated with child trauma exposure, and prenatal violence victimization was also associated with maternal severity ratings of traumatic exposures. Unintended pregnancy was not associated with child trauma exposure or severity. These findings expand our understanding of prenatal risk factors for trauma exposure in childhood and, specifically, highlight prenatal substance exposure and violence victimization as risk factors for subsequent exposure to trauma in early childhood. Results suggest that prenatal prevention and intervention programs should target reducing maternal substance use and in‐utero exposure to violence.