Associations of Maternal Trait Anger Expression and Lifetime Traumatic and Non-traumatic Experiences with Preterm Birth.

OBJECTIVES: Most studies examining psychosocial factors contributing to preterm birth (PTB) have focused on negative life events. Studies examining the influence of negative emotion, in particular maternal anger, remain sparse. We examined associations of maternal trait anger expression and lifetime traumatic and non-traumatic experiences with the risk of PTB. METHODS: Mother-newborn pairs were enrolled in the PRogramming of Intergenerational Stress Mechanisms pregnancy cohort based in Boston and New York City. Women completed the State-Trait Anger Expression Inventory-2 (STAXI-2), Life Stressor Checklist-Revised (LSC-R), and Childhood Trauma Questionnaire (CTQ) in pregnancy. We used modified Poisson regression to estimate the relative risk (RR) of PTB (1) in relation to continuous STAXI-2 Anger Expression-In (AX-I) and Anger Expression-Out (AX-O) subscales, (2) in relation to continuous LSC-R scores, and (3) between women who did versus did not experience childhood sexual, emotional, and/or physical abuse in six separate models. We also examined interactions between maternal anger expression and lifetime stress/childhood trauma. RESULTS: Younger, single, minority women had higher outward anger expression and inward anger suppression. AX-I and AX-O scores were higher among women who experienced abuse in childhood and who had higher lifetime stress. Maternal lifetime stress, outward anger expression, and inward anger suppression were associated with an increased risk of PTB in separate models; however, stress, trauma and anger did not interact to further increase the risk of PTB. CONCLUSIONS FOR PRACTICE: Higher anger expression and higher lifetime stress experiences were associated with an increased risk of PTB among a racially and ethnically diverse sample of pregnant women.

Prenatal cortisol modifies the association between maternal trauma history and child cognitive development in a sex-specific manner in an urban pregnancy cohort.

Women's experience of trauma may cause lifelong alterations in physiological stress regulation, which can be transmitted to offspring in utero. We investigated, in a prospective pregnancy cohort, associations among maternal lifetime interpersonal trauma (IPT) history, prenatal cortisol dysregulation, and children's memory domains. Sex-specific effects were also explored. Pregnant women were enrolled from Brigham & Women's Hospital and affiliated clinics near Boston, MA, in 2002-2007. IPT was assessed with the Revised Conflict Tactics Scale, short form. Salivary cortisol was measured at five time points on each of three days in one week at 29.0 ± 5.1 weeks gestation, and morning rise and diurnal slope were calculated. The Wide Range Assessment of Memory & Learning, 2nd Edition was administered at 6.5 ± 1.0 years and scores were generated for general memory and three sub-domains: verbal, visual, and attention/concentration. In total, 258 maternal-child dyads provided memory and IPT and/or cortisol data. IPT was positively associated with verbal memory in boys (ß ± SE: 4.6 ± 2.6) and inversely associated with visual memory score in girls (-6.5 ± 3.2). IPT did not predict prenatal cortisol, but prenatal cortisol modified the association between IPT history and child memory in varying coefficient models allowing for non-linear effect modification. The strongest evidence of interaction was for visual memory in boys: IPT history was associated with poorer visual memory only in those with flatter prenatal diurnal slope (interaction p = .005). Maternal lifetime IPT that leads to prenatal HPA dysregulation may have consequences for child memory, more so than either trauma or elevated cortisol alone. Boys may be more vulnerable to effects. Sex- and timing-specific effects require further investigation.

Fetal sex and maternal postpartum depressive symptoms: findings from two prospective pregnancy cohorts.

BACKGROUND: Fetal sex is known to modify the course and complications of pregnancy, with recent evidence of sex-differential fetal influences on the maternal immune and endocrine systems. In turn, heightened inflammation and surges in reproductive hormone levels associated with pregnancy and parturition have been linked with the development of perinatal depression. Here, we examined whether there is an association between fetal sex and maternal depression assessed during the prenatal and postnatal periods. METHODS: The study included two multi-ethnic, prospective pregnancy cohorts that enrolled women from prenatal clinics in the Northeastern United States between 2001 and 2018. Maternal depressive symptoms were measured during the prenatal and postnatal periods using the Edinburgh Postpartum Depression Scale (EPDS), and newborn sex was reported by the mother following delivery. We used logistic regression to examine associations between fetal sex and maternal depressive symptoms (EPDS > 10) during the prenatal period only, postnatal period only, or both periods versus no depressive symptoms during either period. We considered both unadjusted models and models adjusted for a core set of sociodemographic and lifestyle variables. RESULTS: In adjusted models using PRISM data (N = 528), women pregnant with a male versus female fetus had significantly greater odds of depressive symptoms during the postnatal period compared to women without depressive symptoms during either period (odds ratio [OR] = 5.24, 95% confidence interval [CI] = 1.93, 14.21). The direction of results was consistent in the ACCESS cohort, although the findings did not reach statistical significance (OR = 2.05, 95% CI = 0.86, 4.93). Significant associations were not observed in either cohort among women with prenatal symptoms only or women with prenatal and postnatal symptoms. CONCLUSIONS: Male fetal sex was associated with the onset of depressive symptoms during the postnatal period.