Pre-COVID respiratory sinus arrhythmia moderates associations between COVID-19 stress and child externalizing behaviors: Testing neurobiological stress theories.

Exposure to stress related to the COVID-19 pandemic contributes to psychopathology risk, yet not all children are negatively impacted. The current study examined a parasympathetic biomarker of stress sensitivity, respiratory sinus arrhythmia (RSA), as a moderator of the effects of exposure to pandemic stress on child internalizing and externalizing behaviors in a sample of children experiencing economic marginalization. Three to five years pre-pandemic, when children were preschool-aged, RSA during baseline and a challenging parent-child interaction were collected. Mid-pandemic, between November 2020 and March 2021, children's exposure to pandemic stress and internalizing and externalizing behaviors were collected. Results demonstrated that children who, pre-pandemic, demonstrated blunted parasympathetic reactivity (i.e., no change in RSA relative to baseline) during the dyadic challenge exhibited elevated risk for externalizing behaviors mid-pandemic. Further, this risk was greatest for children exposed to high and moderate levels of pandemic stress. Consistent with diathesis stress and polyvagal frameworks, these conditional effects suggest that blunted parasympathetic reactivity in response to stress in early childhood may escalate the development of externalizing behaviors following stress exposure at school age.

Linking preschoolers' parasympathetic activity to maternal early adversity and child behavior: An intergenerational perspective.

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.