Background

One in seven women experience postpartum depression, posing a serious public health concern. One of the most robust predictors of elevated postpartum depressive symptoms is major stressful life events that occur during pregnancy. Having greater resilience resources that promote successful adaptation to stressful demands may be protective in the face of stress during pregnancy. The current study tested whether three resilience resources- mastery, dispositional optimism, and spirituality- each predicted early symptoms of postpartum depression and moderated the hypothesized association between experiencing stressful life events during pregnancy and symptoms of postpartum depression.

Methods

The sample included 233 women who participated in a prospective longitudinal study from pregnancy through postpartum. Depressive symptoms were assessed at approximately 4 to 8 weeks after birth, whereas resilience resources and stressful life events were measured in pregnancy. Multiple linear regressions were used to test hypotheses.

Results

Stressful life events predicted greater symptoms of depression postpartum. Mastery and optimism predicted fewer symptoms of depression postpartum. Mastery moderated the association between stressful life events and symptoms of depression when controlling for previous psychiatric history, t(231) = -1.97, p=.0497.

Limitations

There was some attrition among study participants across timepoints, which was accounted for in analyses with multiple imputation.

Conclusions

These findings point to the protective nature of a mother's sense of mastery in the face of major life stressors during pregnancy and suggest this is an important construct to target in interventions addressing postpartum depression.

A longitudinal study of a sample of women and their offspring from two urban areas (N = 233) was conducted to test whether maternal prenatal anxiety trajectories from early to late pregnancy are associated with 12-month infant developmental outcomes, independent of maternal postpartum anxiety symptoms, prenatal and postpartum depressive symptoms, parity, birth outcomes and maternal education. Three types of maternal anxiety trajectories over the course of pregnancy were identified and labeled increasing, decreasing, and stable-low. Only increasing maternal prenatal anxiety was associated with 12-month infant outcomes, specifically lower Bayley-III scores on receptive language and gross motor skills. Maternal anxiety measured at each individual timepoint in pregnancy was not associated with infant Bayley-III outcomes, highlighting the importance of examining trajectories of maternal affect.

Purpose

To determine whether a diagnosis of a perinatal mood and anxiety disorder (PMAD) is associated with adverse perinatal outcomes.

Methods

Mental health symptom screening and diagnostic data from 82 women with single gestation in the Healthy Babies Before Birth study conducted from 2013 to 2018 were obtained by clinic interview. If a woman scored over 10 on the Patient Health Questionnaire (PHQ-9) or endorsed the suicidality item; or scored over 7 on the Overall Anxiety Severity and Impairment Scale (OASIS), a Structured Clinical Interview for DSM-IV (SCID) Axis I Disorders was administered. An adverse perinatal outcome was operationalized as a diagnosis of gestational diabetes mellitus, intrauterine growth restriction, preeclampsia, chorioamnionitis, hemorrhage, fetal death, preterm birth, or a low birthweight baby, and abstracted from the medical records.

Results

Women were between 22.0 and 45.0 years old (Mean age = 33.1 ± 4.3). Mean BMI was 24.7 ± 5.6 (Range 16.8 to 47.1). Nineteen percent (16) of the 82 women had a SCID diagnosis of a PMAD. Thirty-seven percent (30) had a diagnosed adverse perinatal outcome. Multiple logistic regression was conducted with these predictors: SCID diagnosis of a PMAD, maternal age, BMI. All predictors were significant with respective odds ratios as follows: OR = 3.58, 95% CI 1.03-12.44, p = .045; OR = 2.30, 95% CI 1.21-4.38, p = .011; OR = 1.69, 95% CI 1.06-2.69, p = .027.

Conclusions

A PMAD diagnosis was associated with 3.5 times higher odds of having an adverse perinatal outcome. For every 5 years a woman aged or every five units her BMI increased her odds of having an adverse perinatal outcome increased. Older age and increased BMI are well established adverse perinatal outcome risk factors. These results suggest that mental illness risk should also be consistently assessed in obstetric settings.

Objectives

Anxiety is prevalent in pregnancy and predicts risk of adverse birth outcomes. Many instruments measure anxiety in pregnancy, some of which assess pregnancy anxiety defined as maternal concerns about a current pregnancy (e.g., baby, childbirth). The present study examined covariance among four anxiety or distress measures at two times in pregnancy and tested joint and individual effects on gestational length. We hypothesized that the common variance of the measures in each trimester would predict earlier delivery.

Method

Research staff interviewed 196 women in first and third trimester utilizing a clinical screener of anxiety severity/impairment, two instruments measuring pregnancy anxiety, and one on prenatal distress. Birth outcomes and medical risk factors were obtained from medical records after birth. Structural equation modeling fit latent factors for each trimester from the four measures. Subsequent models tested whether the latent factors predicted gestational length, and unique effects of each measure.

Results

The third-trimester pregnancy anxiety latent factor predicted shorter gestational length adjusting for mother's age, education, parity, and obstetric risk. Scores on a four-item pregnancy-specific anxiety measure (PSAS) in third trimester added uniquely to prediction of gestational length. In first trimester, scores on the clinical screener (OASIS) uniquely predicted shorter gestational length whereas the latent factor did not.

Conclusion

These results support existing evidence indicating that pregnancy anxiety is a reliable risk factor for earlier birth. Findings point to possible screening for clinically significant anxiety symptoms in the first trimester, and pregnancy-specific anxiety thereafter to advance efforts to prevent earlier delivery. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Background

Advanced biological aging, as measured by epigenetic aging indices, is associated with early mortality and morbidity. Associations between maternal epigenetic aging indices in pregnancy and pregnancy outcomes, namely gestational length and birthweight, have not been assessed. The purpose of this study was to examine whether epigenetic age during pregnancy was associated with gestational length and birthweight.

Results

The sample consisted of 77 women from the Los Angeles, CA, area enrolled in the Healthy Babies Before Birth study. Whole blood samples for DNA methylation assay were obtained during the second trimester (15.6 ± 2.15 weeks gestation). Epigenetic age indices GrimAge acceleration (GrimAgeAccel), DNAm PAI-1, DNAm ADM, and DNAm cystatin C were calculated. Gestational length and birthweight were obtained from medical chart review. Covariates were maternal sociodemographic variables, gestational age at blood sample collection, and pre-pregnancy body mass index. In separate covariate-adjusted linear regression models, higher early second trimester GrimAgeAccel, b(SE) = - .171 (.056), p = .004; DNAm PAI-1, b(SE) = - 1.95 × 10^-4 (8.5 × 10^-5), p = .004; DNAm ADM, b(SE) = - .033 (.011), p = .003; and DNAm cystatin C, b(SE) = 2.10 × 10^-5 (8.0 × 10^-5), p = .012, were each associated with shorter gestational length. Higher GrimAgeAccel, b(SE) = - 75.2 (19.7), p < .001; DNAm PAI-1, b(SE) = - .079(.031), p = .013; DNAm ADM, b(SE) = - 13.8 (3.87), p = .001; and DNAm cystatin C, b(SE) = - .010 (.003), p = .001, were also associated with lower birthweight, independent of gestational length.

Discussion

Higher maternal prenatal GrimAgeAccel, DNAm PAI-1, DNAm ADM, and DNAm cystatin C were associated with shorter gestational length and lower birthweight. These findings suggest that biological age, as measured by these epigenetic indices, could indicate risk for adverse pregnancy outcomes.

Background

Maternal depressive symptoms in pregnancy may affect offspring health through prenatal programming of the hypothalamic-pituitary-adrenal (HPA) axis. The biological mechanisms that explain the associations between maternal prenatal depressive symptoms and offspring HPA axis regulation are not yet clear. This pre-registered investigation examines whether patterns of maternal depressive symptoms in pregnancy are associated with infant cortisol reactivity and whether this association is mediated by changes in placental corticotropin-releasing hormone (pCRH).

Method

A sample of 174 pregnant women completed assessments in early, mid, and late pregnancy that included standardized measures of depressive symptoms and blood samples for pCRH. Infant cortisol reactivity was assessed at 1 and 6 months of age.

Results

Greater increases in maternal depressive symptoms in pregnancy were associated with higher cortisol infant cortisol reactivity at 1 and 6 months. Greater increases in maternal depressive symptoms in pregnancy were associated with greater increases in pCRH from early to late pregnancy which in turn were associated with higher infant cortisol reactivity.

Conclusions

Increases in maternal depressive symptoms and pCRH over pregnancy may contribute to higher infant cortisol reactivity. These findings help to elucidate the prenatal biopsychosocial processes contributing to offspring HPA axis regulation early in development.

Early life adversity is a potent risk factor for poor mental health outcomes across the lifespan, including offspring vulnerability to psychopathology. Developmentally, the prenatal period is a sensitive window in which maternal early life experiences may influence offspring outcomes and demarcates a time when expectant mothers and offspring are more susceptible to stressful and salutary influences. This prenatal plasticity constituted the focus of the current study where we tested the association of maternal early life adversity with infant stress regulation through maternal prenatal internalizing symptoms and moderation by prenatal social support. Mother-infant dyads (n = 162) were followed prospectively and mothers completed assessments of social support and depressive and anxiety symptoms across pregnancy. Infants completed standardized stress paradigms at one month and six months. There were several key findings. First, maternal prenatal depressive symptoms significantly mediated predictions of infant cortisol reactivity to the heel stick at one month from maternal early life adversity: specifically, maternal early life adversity positively predicted depressive symptoms in pregnancy, which in turn predicted dampened infant cortisol reactivity. Second, prenatal social support did not significantly moderate predictions of depressive or anxiety symptoms in pregnancy from maternal early life adversity nor did it alter the associations of maternal depressive or anxiety symptoms with infant stress regulation. These results suggest that maternal prenatal mental health is a key mechanism by which maternal early life adverse experiences affect offspring risk for psychopathology. We discuss potential clinical and health implications of dysregulated infant cortisol reactivity with respect to lifespan development.

Problem

Epigenetic age indices are markers of biological aging determined from DNA methylation patterns. Accelerated epigenetic age predicts morbidity and mortality. Women tend to demonstrate slower blood epigenetic aging compared to men, possibly due to female-specific hormones and reproductive milestones. Pregnancy and the post-partum period are critical reproductive periods that have not been studied yet with respect to epigenetic aging. The purpose of this paper was to examine whether pregnancy itself and an important pregnancy-related variable, changes in body mass index (BMI) between pregnancy and the post-partum period, are associated with epigenetic aging.

Method of study

A pilot sample of 35 women was recruited as part of the Healthy Babies Before Birth (HB3) project. Whole blood samples were collected at mid-pregnancy and 1 year post-partum. DNA methylation at both time points was assayed using Infinium 450K and EPIC chips. Epigenetic age indices were calculated using an online calculator.

Results

Paired-sample t-tests were used to test differences in epigenetic age indices from pregnancy to 1 year after birth. Over this critical time span, women became younger with respect to phenotypic epigenetic age, GrimAge, DNAm PAI-1, and epigenetic age indices linked to aging-related shifts in immune cell populations, known as extrinsic epigenetic age. Post-partum BMI retention, but not prenatal BMI increases, predicted accelerated epigenetic aging.

Conclusion

Women appear to become younger from pregnancy to the post-partum period based on specific epigenetic age indices. Further, BMI at 1 year after birth that reflects weight retention predicted greater epigenetic aging during this period.

Background

Preterm birth or shorter gestation is a common adverse pregnancy outcome. Pregnancy-specific anxiety is robustly associated with risk for shorter gestation. Hypothalamic-pituitary-adrenal (HPA) dysregulation, indicated by diurnal cortisol index variability [slope, area-under-the-curve (AUC) or cortisol awakening response (CAR)], could mediate associations between pregnancy-specific anxiety and shorter gestation. The purpose of this study was to explore whether diurnal cortisol index variability mediates associations between pregnancy-specific anxiety and gestational length.

Methods

A sample of 149 women from the Healthy Babies Before Birth study reported pregnancy-specific anxiety in early pregnancy. Saliva samples were taken at three times during pregnancy, for two days each, at wake, 30 min post wake, noon, and evening. Diurnal cortisol indices were calculated using standard approaches. Pregnancy cortisol index variability was calculated across pregnancy timepoints. Gestational length was derived from medical charts. Covariates were sociodemographics, parity and obstetric risk. Mediation models were tested using SPSS PROCESS.

Results

There was a significant indirect effect of pregnancy-specific anxiety on gestational length via CAR variability, b(SE)= -0.102(0.057), .95CI [- 0.227,- 0.008]. Higher pregnancy-specific anxiety was associated with lower CAR variability, b(SE)= -0.019(0.008), p = .022, and lower CAR variability was associated with shorter gestation, b(SE)= 5.29(2.64), p = .047. Neither AUC or slope variability mediated associations between pregnancy-specific anxiety and gestational length.

Conclusion

Lower CAR variability during pregnancy mediated the association between higher pregnancy-specific anxiety and shorter gestational length. Pregnancy-specific anxiety could dysregulate HPA axis activity, as indicated by lower CAR variability, demonstrating the importance of the HPA axis system in regulating pregnancy outcomes.

Objective

High pregnancy anxiety is a consistent predictor of earlier labor and delivery. Placental corticotropin-releasing hormone (pCRH) predicts earlier delivery consistently and it has been identified as a biological mediator of the association between pregnancy anxiety and gestational length. However, studies have not examined whether changes in pregnancy anxiety are associated with earlier birth as mediated by changes in pCRH during pregnancy. Accordingly, this study tests whether linear changes in pregnancy anxiety are associated with length of gestation indirectly through nonlinear increases in pCRH over pregnancy.

Methods

A sample of pregnant women (n=233) completed prenatal assessments in early pregnancy, second trimester, and third trimester that included a 4-item assessment of pregnancy anxiety and collection of blood samples assayed for pCRH using radioimmunoassay. Length of gestation was abstracted from medical records after birth.

Results

Increases in pregnancy anxiety from early pregnancy to third trimester predicted shorted length of gestation, as did nonlinear increases in pCRH over pregnancy. However, there was no evidence of an indirect effect of changes in pregnancy anxiety on length of gestation via changes in pCRH.

Conclusions

These results indicate that linear changes in pregnancy anxiety and nonlinear changes in pCRH during pregnancy are independent risk factors for shortened gestational length. This study adds to a small but growing body of work on biopsychological processes in pregnancy and length of gestation. Modeling changes in psychological and biological processes during pregnancy could provide more insight into understanding risk for adverse pregnancy outcomes.