Stressful events are inherently emotional. As a result, the ability to regulate emotions is critical in responding effectively to stressors. Differential abilities in the management of stress appear very early in life, compelling a need to better understand factors that may shape the capacity for emotion regulation (ER). Variations in both biologic and behavioural characteristics are thought to influence individual differences in ER development. We sought to determine the differential contributions of temperament and heart rate variability (HRV; an indicator of autonomic nervous system function) to infant resting state emotionality and emotional reactivity in response to a stressor at 6 months of age. Participants included 108 mother-infant dyads. Mothers completed a measure of infant temperament at 6 months postnatal. Mother and infant also participated in a standardized stressor (the Repeated Still Face Paradigm) at that time. Electrocardiographic data were acquired from the infant during a baseline resting state and throughout the stressor. Fast Fourier Transformation was used to analyse the high frequency (HF) domain of HRV, a measure of parasympathetic nervous system activity. Infant ER was measured via standardized coding of emotional distress behaviours from video-records at baseline and throughout the stressor. Severity of mothers' depressive symptoms was included as a covariate in analyses. Results of linear regression indicate that neither temperament nor HRV were associated significantly with an infant's emotional resting state, although a small effect size was found for the relationship between infant negative affectivity and greater emotional distress (β = 0.23, p = 0.08) prior to the stressor. Higher HF-HRV (suggesting parasympathetic dominance) was related to greater emotional distress in response to the stressor (β = 0.34, p = 0.009). This greater emotional reactivity may reflect a more robust capacity to mount an emotional response to the stressor when infants encounter it from a bedrock of parasympathetic activation. Findings may inform eventual markers for assessment of ER in infancy and areas for intervention to enhance infant management of emotions, especially during stressful events.

Administration of antenatal corticosteroids (AC) is the standard of care during pregnancy for women who are at risk of early delivery. Evidence indicates that AC improve survival and reduce morbidity for preterm infants. However, research suggests that infants whose mothers receive AC have an altered hypothalamic-pituitary-axis (HPA) response to stressors in early life. Results are mixed regarding the nature of these effects, with studies showing both suppressed and augmented HPA activity. In addition, research is very limited beyond the 4th month of life. The purpose of this study was to determine if AC exposure was associated with infant cortisol levels in a resting state or in response to a stressor at 1, 6 and 12 months postnatal. We also evaluated the moderating role of preterm birth in this association. 181 women and their infants participated in the study. Women were recruited during the 3rd trimester of pregnancy; at this time, they completed the Perceived Stress Scale and provided 8 salivary samples over a 2-day period for cortisol assay. They provided these data again at 6 and 12 months postnatal. At 1, 6, and 12 months postnatal, salivary samples were collected from infants to examine their cortisol levels before and after participation in a 'stressor protocol'. Data were extracted from the medical record on AC exposure, gestational age, maternal obstetric risk, and neonatal morbidity. Mixed effects multilevel regression modeling was used to examine the aims. Infants whose mothers received AC had significantly lower resting state (B = -2.47, CI: -3.691, -0.0484) and post-stressor (B = -2.51, CI: -4.283, -0.4276) cortisol levels across the first year of life than infants whose mothers did not receive AC. There was no moderating effect of preterm birth on the relationship between AC exposure and cortisol. Results indicate a state of dampened HPA activation and cortisol hypo-arousal that persists across the first year of life among infants who were exposed to corticosteroids in utero. Further research is needed to examine mechanisms responsible for any alterations that occur during development of the fetal HPA axis, including epigenetic and biochemical factors that control hormonal secretion, negative feedback, and glucocorticoid receptor function throughout the HPA axis. Findings warrant careful consideration by obstetric clinicians of the benefits and risks of prescribing AC.