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High-Quality Parenting Buffers Prenatal Stress Effects on Infant Autonomic Nervous System Function in Low-Income Families

Thu, March 21, 12:30 to 2:00pm, Baltimore Convention Center, Floor: Level 3, Room 328

Integrative Statement

Introduction: Adverse life experiences are associated with a host of later negative health outcomes, yet understanding of the mechanisms responsible for this developmental programming is limited. The autonomic nervous system (ANS) is one mechanism through which adverse experience may “get under the skin”. A growing body of evidence suggests that maternal experiences during the perinatal period may affect ANS responses of infants, via prenatal programming. Given the high occurrence of stressful events during pregnancy and the important role of ANS function in children’s developmental outcomes, it is important to understand these processes and protective factors that might mitigate these effects. Building upon previous research (Bush et al., 2017), this study hypothesized that higher quality parenting behaviors would buffer infants from the potentially adverse effects of maternal prenatal stress on ANS reactivity and recovery.

Methods: Drawn from a larger sample of racially and ethnically diverse, low-income, women and their babies, followed from 2nd trimester through toddlerhood, a subset of 67 dyads with available ANS data at 6 months were examined. Maternal report of stress during pregnancy was assessed via Cohen’s Perceived Stress Scale (PSS). Maternal report of Stressful Life Events (SLE) experienced during pregnancy was assessed using the PRAMS. Maternal behavior and infant ANS activity were assessed during the gold standard challenge, the Still Face Paradigm (SFP). Respiratory sinus arrhythmia (RSA) and pre-ejection period (PEP) were assessed as indices of the parasympathetic and sympathetic nervous systems, respectively. Maternal behavior during the reunion episode (post-stressor) were coded for sensitive behavior (POS) and ability to regulate infant distress (ROD). Regression models testing interactions (stress X parenting) were run separately for each predictor and each ANS outcome.

Results: See Tables 1 and 2. Parental POS modified the association between prenatal stress and infant ANS such that higher prenatal stress (SLE or PSS) was associated with higher RSA reactivity, but only for infants with mothers with low levels of POS; at high levels of maternal POS, associations were insignificant. In a parallel pattern, parental ROD modified the association between prenatal stress and infant ANS such that higher prenatal stress (SLE or PSS) was associated with higher PEP reactivity, but only at low maternal levels of ROD; at high levels of maternal ROD, associations were insignificant. Parenting also modified the association between prenatal stress and PEP during reunion such that higher prenatal stress (SLE or PSS) was associated with shorter PEP, but only at lower levels of ROD or POS; at high levels of ROD or POS, the associations were insignificant. Parenting did not modify the associations between prenatal stress and RSA during reunion, though POS and ROD were positively associated with RSA.

Conclusion: Overall, these results suggest that parenting during the first 6 months of life relates to infant ANS function and moderates the effects of objective and subjective reports of prenatal stress. Importantly, these results suggest that even when mothers are exposed to high levels of prenatal stress, postnatal parental behaviors can act as a buffer against potentially adverse effects on offspring development.

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