Objective Respiratory sinus arrhythmia (RSA) is a parasympathetic-mediated biomarker of self-regulation linked to lifespan mental and physical health outcomes. Intergenerational impacts of mothers’ exposure to prenatal stress have been demonstrated, but evidence for biological embedding of maternal preconception stress, including adverse childhood experiences (ACEs), on infant RSA is lacking. We examine the independent effects of maternal ACEs and prenatal stress on infant RSA, seeking to broaden the understanding of the earliest origins of mental and physical health risk. Method Mothers reported on ACEs and prenatal stress. RSA was recorded in a sample of 167 4-month-old infants (49% female and 51% male) during a dyadic stressor, the Still Face Paradigm. Results Independent contributions of maternal ACEs and prenatal stress to infant RSA were observed. High maternal ACEs were associated with lower RSA, whereas prenatal stress was associated with failure to recover following the stressor. Sex but not race differences were observed. Prenatal stress was associated with higher RSA among boys but lower RSA among girls. Conclusion Infants’ RSA is affected by mothers’ life course experiences of stress, with ACEs predicting a lower set point and prenatal stress dampening recovery from stress. For prenatal stress but not ACEs, patterns vary across sex. Findings underscore that stress-reducing interventions for pregnant women or those considering pregnancy may lead to decreased physical and mental health risk across generations.

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Increasing evidence suggests intergenerational effects of maternal early adversity on offspring self‐regulation. Prior work has demonstrated associations between maternal adverse childhood experiences (ACEs) and infant respiratory sinus arrhythmia (RSA), a parasympathetic biomarker associated with emotional and behavioral self‐regulation. The present study examined these associations and additional potential pathways including children's violence exposure and maternal psychopathology among 123 biological mother‐child dyads. Families were low‐income and oversampled for violence exposure; children were 3–5 years old. RSA was examined during dyadic interaction using latent growth curve modeling (LGCM). On average, females exhibited greater RSA reactivity. Greater RSA withdrawal across the interaction was associated with greater child negative affect during the interaction, linking RSA reactivity to concurrent child behavior. Consistent with previous findings among infants, high maternal ACEs were associated with lower child RSA at task initiation but not with RSA reactivity across the interaction. Findings suggest that the association between high maternal ACEs and a lower set point for offspring RSA persists into the early childhood period, beyond the influence of maternal psychopathology and children's own violence exposure. These data provide further evidence for the biological embedding of maternal early adversity across generations as well as for the relevance of RSA to child behavioral regulation.

Nearly half of preschool-aged children from low-income families in the United States have been exposed to potentially traumatic events (PTEs), yet few are identified or receive trauma-focused mental health care. Given the critical need to accurately and efficiently identify PTE-exposed individuals, the current study examined discordant caregiver self-reporting of PTE exposure and caregiver reporting of child PTE exposure across two assessment methods: checklist and interview. Research has demonstrated significant cross-method discrepancies among adults reporting stressful life experiences, but examinations of caregiver reporting for their young children have not been conducted. Further, given their possible impact on reporting patterns, caregiver and child characteristics were examined in relation to discordant caregiver reporting by trauma type. Participants were 64 low-income, racially and ethnically diverse caregivers and their preschool-aged children from a Northeastern US city. Caregivers reported self and child PTE exposure via checklist and semi-structured interview. Cross-method discordance for caregiver and child exposure by trauma type ranged from 10.9% to 46.9% (Cohen’s kappa =.06-.70). Caregiver race and education were associated with discordant reporting, as were caregiver and child psychopathology. Lower levels of caregiver psychopathology were associated with discordant caregiver reporting of their own exposure, whereas higher levels were associated with discordant caregiver reporting of child exposure. Discordant caregiver reporting of PTE exposure varies by assessment format and trauma type and is differentially related to caregiver demographics and caregiver and child psychopathology. Associations between assessment methods, individual characteristics, and reporting should be considered when assessing PTE exposure to support service engagement and targeted treatment.

This commentary expands on Anderson, Bushman, Donnerstein, Hummer, and Warburton’s agenda for minimizing the impacts of violent media exposure (VME) on youth aggression. We argue that in order to effectively intervene in the development of aggression and other maladaptive traits, researchers and policymakers should take an ecological, developmental psychopathology approach to understanding children’s exposure to VME within developmental, relational, environmental, and cultural contexts. Such a framework holds the most promise for identifying at-risk groups, establishing targets of intervention, and testing mechanisms of change.

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