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Maternal cortisol and parenting in infancy: The moderating role of family stress and infant development

Thu, March 23, 4:15 to 5:00pm, Salt Palace Convention Center, Floor: 1, Meeting Room 150 D-E

Abstract

The hypothalamic pituitary adrenal (HPA) axis is a widely researched stress response system (Cicchetti & Walker, 2001). Although effects of salivary cortisol, the end-product of HPA activity, on parenting have gained increasing attention, the direction of effect has not been consistent across studies, with both high (Giardino et al., 2008) and low maternal basal cortisol (Gonzalez et al., 2012) linked with poor parenting. The mixed findings may result from ignoring environmental factors as potential moderators of linkages between parental stress physiology and parenting (Barrett & Fleming, 2011). The current study took a cumulative risk approach to examine whether family stress, represented by socioeconomic risk, household chaos, and negative life events (NLE), might help explain cortisol−parenting associations during the first 6-month postpartum. We hypothesized that dysregulated maternal HPA activity (greater cortisol output and flatter decline) may have greater deleterious effects on parenting in high family stress contexts. Additionally, we explored infant age as a moderator as the emergent developmental competencies of older infants may make parenting more challenging, especially for mothers with HPA dysregulation and high family stress.

Data of 167 mothers with infants (47% male) were drawn from an NICHD-funded study focusing on parenting and infant development. At 1, 3, and 6 months, household chaos was scored by trained observers using the DISCORD (Whitesell et al., 2015). At 1 and 6 months, mothers reported NLE via the Life Experiences Survey (Sarason et al., 1978). Family stress was composited by summing the standardized scores of household chaos (across-time mean), negative life experiences (across-time mean), maternal and paternal educational level (reversed), and family income-to-needs ratio (reversed), with higher scores indicating higher stress. On each occasion, maternal emotional availability (EA) was scored from video recordings during one night of infant bedtime using the Emotional Availability Scales (Biringen et al., 1998) by reliable coders, and maternal afternoon and bedtime cortisol was assessed via saliva samples. Total cortisol output from afternoon to bedtime was calculated using area under the curve with respect to ground (AUCg, log-transformed). Cortisol changes were calculated by subtracting afternoon cortisol (log-transformed) from bedtime cortisol (log-transformed), with higher scores indicating flatter declines.

Multilevel modeling was conducted to examine interactive effects of family stress and maternal cortisol on EA at the between- and within-person level. After controlling for covariates, high family stress was predictive of poorer maternal EA. Consistent with a diathesis-stress model (Monroe & Simons, 1991), family stress interacted with cortisol in predicting parenting (Table 1). At the within-person level, increases in maternal total cortisol output were predictive of decreases in EA under high family stress. At the between-person level, mothers with flatter cortisol decline and higher family stress showed lower EA only at 6 months (Figure 1).

Findings suggested that adverse effects of poor HPA functioning on mothering can be exacerbated by high family stress and become more evident as infant behavioral repertoire expands with development, which creates increased caregiving challenges. Results highlight the importance of considering environmental stress and infant development when studying stress physiology – parenting linkages.

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