D. Jeffrey Newport

Objectives Intergenerational transmission of trauma occurs when the effects of childhood maltreatment (CM) influence the next generation's development and health; prenatal programming via maternal mood symptoms is a potential pathway. CM is a risk factor for bipolar disorder which is present in 1.8% of pregnant women. Mood symptoms are likely to increase during pregnancy, particularly for those with a history of CM. We examined whether there was evidence for intergenerational transmission of trauma in utero in this population, and whether maternal mood was a transmission pathway. Methods CM and maternal mood were self-reported by N = 82 pregnant women in treatment for bipolar disorder. Fetal heart rate variability (FHRV) was measured at 24, 30, and 36 weeks' gestation. Gestational age at birth and birth weight were obtained from medical charts. Results A cluster analysis yielded two groups, Symptom+ (18.29%) and Euthymic (81.71%), who differed on severe mood symptoms (p < 0.001) but not on medication use. The Symptom+ group had more CM exposures (p < 0.001), a trend of lower FHRV (p = 0.077), and greater birth complications (33.3% vs. 6.07% born preterm p < 0.01). Maternal prenatal mood mediated the association between maternal CM and birth weight in both sexes and at trend level for gestational age at birth in females. Conclusions This is the first study to identify intergenerational effects of maternal CM prior to postnatal influences in a sample of pregnant women with bipolar disorder. These findings underscore the potential enduring impact of CM for women with severe psychiatric illness and their children.

Clinical guidelines recommend assessing depression during pregnancy and postpartum but often overlook potential changes in symptoms across this developmental period. Such changes contribute to difficulties in conceptualizing maternal depression. This study aimed to situate depressive symptoms and related concerns (anxiety, stress, sleep) across the perinatal period within a transdiagnostic framework and to use this framework to better understand how depressive symptoms change across the perinatal period. First, items from seven symptom scales were a priori categorized into six transdiagnostic factors: four based on Research Domain Criteria (loss, potential threat, frustrative nonreward, and sleep-wakefulness) and two based on the depression literature (somatic and coping symptoms). Second, using prospective data from women with a history of an affective disorder (n = 657) in an observational study of neuropsychiatric illness, factor analyses were performed in seven periods (three trimesters of pregnancy and four quarters of first year postpartum). For each period, a bifactor model with six transdiagnostic factors and a general factor fit data better than models that combined or dropped a factor (p < .003). Except around delivery, item loadings and intercepts could be fixed between consecutive periods and still adequately fit data from both periods. Means of sleep-wakefulness and somatic factors increased significantly from second to third trimester (p < .01), with trends reversing early postpartum. In conclusion, depressive symptoms and related concerns exhibit factor structures that are only partly congruent across the perinatal period. This conclusion suggests that greater attention to specific life phases is warranted in the conceptualization of depression during this time in women's lives.

Studies examining associations between fetal serotonin reuptake inhibitor (SRI) exposure and child autism spectrum disorder (ASD) diagnoses or delayed language remain mixed and rarely prospectively follow children or employ gold-standard assessments. We prospectively followed a cohort of mother–child dyads from pregnancy through early elementary school (N= 178), and obtained maternal and alternate–caregiver ratings of behaviors related to ASD (N= 137), as well as direct, gold-standard assessments of child ASD symptoms and pragmatic language among dyads who experienced prenatal depression and either took SRIs or were medication free during pregnancy (N= 44). Prenatal SRI exposure was related to maternal ratings of ASD-related behaviors (β = 0.24 95% confidence interval; CI [0.07, 0.48]), and, among boys, alternative caregiver ratings (males-only β = 0.28 95% CI [0.02, 0.55], females-only β = −0.21 95% CI [–0.63, 0.08]). However, results of our direct assessments suggest an association between SRI exposure and reduced pragmatic language scores (β = –0.27, 95% CI [–0.53, –0.01], but not ASD (Autism Diagnostic Observation Schedule β = 0.14 95% CI [–0.15, 0.41]; Social Responsiveness Scale β = 0.08 95% CI [–0.25, 0.40]). These discrepancies point to issues regarding how ASD is assessed, and the possibility that SRIs may be more strongly associated with language or other broader behaviors that coincide with ASD. Larger prospective studies that incorporate thorough, gold-standard assessments of ASD, language, and other ASD-related behaviors are needed.