Maternal depression and cortisol in pregnancy predict offspring emotional reactivity in the preschool period.

Prenatal exposures to higher levels of maternal cortisol and depression have been linked to a variety of adverse physiological, neurological, and behavioral outcomes, such as dysregulated cortisol production, structural and functional differences in limbic areas of the brain, and greater negative emotionality. This study investigated prospective associations between maternal prepartum depression/cortisol levels and offspring emotional reactivity in 163 mother-child pairs. Women were assessed repeatedly during pregnancy, and later participated in a laboratory visit with their preschool-aged children. Mothers self-reported on depressive symptomatology during pregnancy and provided saliva samples for cortisol assay. Offspring emotional reactivity was assessed through multiple measures, including caregiver reports, cortisol response following a stressor, and laboratory observations of behavior. The findings suggest potential prenatal timing effects, with depression and maternal cortisol measured in the first and second trimesters being more strongly associated with child emotional reactivity. Sex was found to moderate associations between maternal prepartum depression/cortisol and child emotional reactivity, with the general pattern reflecting positive associations in girls, and negative associations in boys.

Maternal early-life trauma and affective parenting style: the mediating role of HPA-axis function.

A history of childhood trauma is associated with increased risk for psychopathology and interpersonal difficulties in adulthood and, for those who have children, impairments in parenting and increased risk of negative outcomes in offspring. Physiological and behavioral mechanisms are poorly understood. In the current study, maternal history of childhood trauma was hypothesized to predict differences in maternal affect and HPA axis functioning. Mother-infant dyads (N = 255) were assessed at 6 months postpartum. Mothers were videotaped during a 3-min naturalistic interaction, and their behavior was coded for positive, neutral, and negative affect. Maternal salivary cortisol was measured six times across the study visit, which also included an infant stressor paradigm. Results showed that childhood trauma history predicted increased neutral affect and decreased mean cortisol in the mothers and that cortisol mediated the association between trauma history and maternal affect. Maternal depression was not associated with affective measures or cortisol. Results suggest that early childhood trauma may disrupt the development of the HPA axis, which in turn impairs affective expression during mother-infant interactions in postpartum women. Interventions aimed at treating psychiatric illness in postpartum women may benefit from specific components to assess and treat trauma-related symptoms and prevent secondary effects on parenting.

Maternal depression and infant cortisol: influences of timing, comorbidity and treatment.

BACKGROUND: The current study examines the relationship between maternal depression and infant cortisol concentrations. The potential roles of comorbid maternal anxiety disorders, timing of maternal depression, and maternal treatment with psychotropic medications during pregnancy are addressed. METHODS: Women with 6-month-old infants (105 boys and 84 girls) participated in a laboratory paradigm that included infant saliva collection at six points, noise burst and arm restraint stressor tasks, and a diagnostic interview of the mother. RESULTS: Lifetime history of maternal depression was associated with increased baseline and mean (average) infant cortisol levels. Comorbidity with anxiety disorder was related to infant cortisol reactivity. Peripartum (prepartum and/or postpartum) maternal depression, rather than a pre-pregnancy history of disorder, was associated with higher infant cortisol reactivity. Prenatal and postnatal exposure to maternal disorder had similar effects, but prenatal maternal psychotropic medication treatment appeared to attenuate infant cortisol increases associated with prenatal maternal disorder exposure. CONCLUSIONS: These data suggest that exposure to maternal depression and anxiety during pregnancy and the postpartum period may increase infant salivary cortisol. This maternal depression-infant cortisol association is independent of the effects of delivery complications, and appears to be modulated by prenatal maternal psychotropic treatment.

The impact of maternal childhood abuse on maternal and infant HPA axis function in the postpartum period.

BACKGROUND: Early life trauma, particularly child abuse, has been associated with aberrations in hypothalamic-pituitary-adrenal (HPA) axis functioning in adulthood. However, the relationship of early abuse and later adult neuroendocrine changes may be moderated by additional factors such as comorbid psychopathology and recent life stress. Parental exposure to child abuse may have transgenerational effects, with offspring of abuse victims showing similar neuroendocrine profiles as their mothers. The majority of previous studies in this area focus on adult offspring, and the degree to which the effects of parental child abuse can be detected earlier in the development of the offspring remains obscure. METHODS: The current study utilized a clinical sample of women with a history of MDD (N=126), to examine the effects of maternal early life sexual and physical abuse (Childhood Trauma Questionnaire (CTQ)) on both maternal and infant salivary cortisol levels during a laboratory stress paradigm at 6 months postpartum. RESULTS: Maternal child abuse was associated with steeper declines in cortisol in the mothers and lower baseline cortisol in their infants. Comorbid maternal PTSD, current maternal depressive symptoms, and recent life stressors were significant moderators of maternal cortisol change. Maternal abuse history was associated with increases in cortisol levels in those mothers who experienced these additional stressors. Similarly, a history of early maternal abuse and comorbid PTSD was associated with greater increases in infant cortisol levels. CONCLUSIONS: Maternal childhood abuse was associated with HPA axis function in both the mother and the infant during the postpartum period.