Abstract

Maternal depression during gestation adversely affects fetal nervous system development and may lead to childhood behavioral problems. Mechanisms of adverse effects are less understood, although cortisol secretion is a potential mediator. Limited research has evaluated links between maternal depression, corticosteroids, and early markers of nervous system development, such as fetal heart rate variability (FHRV), cerebral inhibition, or temperament characteristics. Thus, the objectives were to: 1) evaluate associations between maternal depression, corticosteroids, and FHRV; and 2) test whether FHRV predicts markers of infant inhibition and regulatory capacity. Maternal depression and hair concentrations of cortisol and cortisone were measured during gestation. Heart rate was recorded in 23 fetuses by transabdominal Doppler. The SD of interbeat intervals over 20 minutes was computed to assess FHRV. Higher FHRV values reflect greater physiological regulation. Maternal depression, corticosteroid, and FHRV measurement occurred between 28 and 33 weeks gestation. Subsequent markers of infant nervous system development and temperament were assessed. Newborn development of cerebral inhibition was evaluated at 44 weeks gestation through an auditory sensory gating paradigm. Parents rated their infant’s temperamental regulatory capacity when infants were 3 months of age. Maternal depression was associated with lower FHRV, especially for male fetuses (β = –0.633; p = 0.045). Maternal depression was associated with lower cortisol to total corticosteroids ratios (β = –0.519; p = 0.033). Higher cortisol ratios were associated with increased FHRV (β = 0.485; p = 0.019). Higher FHRV was associated with decreased newborn sensory gating deficits (β = –0.992; p = 0.035), indicating better development of cerebral inhibition. Higher FHRV was also related to increased infant regulatory capacity (r = 0.454; p = 0.029). Maternal depression is associated via corticosteroids with decreased FHRV. Decreased FHRV predicted worse infant inhibition and infant regulatory capacity. Conclusions are limited due to the small sample size. Interventions addressing gestational depression may mitigate biologically mediated adverse effects on infants and thus need further study.

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