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We explored the associations among perceived stress, depressive symptoms, loneliness, and social support during the COVID-19 pandemic; and differences in perceived stress, depressive symptoms, and social support prior to the pandemic and during the pandemic among pregnant Black women. A sample of 33 pregnant Black women who participated in the Biosocial Impact on Black Births (BIBB) and were still pregnant in May–June 2020 were invited to complete an online survey about their experiences during the pandemic. Fifteen women responded very much or somewhat to experiencing stress and anxiety because of the COVID-19 pandemic. Eight women had CES-D scores ≥23, which have been correlated with depression diagnosis. Women who reported higher levels of loneliness during the COVID-19 pandemic also reported higher levels of perceived stress and depressive symptoms and lower levels of social support during the pandemic. Women who reported lower levels of social support during the pandemic also reported higher levels of perceived stress and depressive symptoms during the pandemic. There were no changes in perceived stress, depressive symptoms, or social support prior to the pandemic and during the pandemic. Clinicians should assess for signs of loneliness and depressive symptoms for pregnant women and offer recommendations for therapy and support groups. [ABSTRACT FROM AUTHOR]

Epigenetic modifications are chemical changes that can modify gene expression without changing the sequence of the gene. These modifications are potentially identifiable and reversible, making the epigenome an important area of research for discovering biomarkers to identify those who may be at risk and providing therapeutic interventions to prevent adverse health outcomes. African Americans bear a disproportionate risk of adverse health outcomes (e.g., hypertension, cancer). Indeed, African American women experience preterm birth (PTB; <37 completed weeks gestation) at more than twice the rate of non-Hispanic White women. Research suggests that environmental influences may play a significant role in PTB outcomes for this population. However, the biological pathways by which these influences contribute to PTB are poorly understood. This paper describes research methods and ethical considerations for the collection and analysis of biological samples based on our study examining the epigenetic regulation of stress pathways in PTB in pregnant African American women. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study was to see if timing of prenatal care initiation was related to psychological wellbeing of Black women. Study Design and Methods: Using a cross-sectional design, a sample of 197 pregnant Black women completed a self-reported survey between 8 weeks and less than 30 weeks gestation as part of the Biosocial Impact on Black Births study. The questions asked about the initiation of prenatal care, perceived stress, depressive symptoms, and psychological wellbeing. Multiple linear regression was used to examine if timing of prenatal care initiation was related to psychological variables. Results: Sixty-three women (32%) reported they were not able to initiate their first prenatal care visit as early as they wanted due to various barriers. After adjusting for cofounders, not initiating prenatal care as early as women wanted predicted lower levels of psychological wellbeing. Clinical Implications: Perinatal nurses should assess psychological wellbeing in Black women throughout pregnancy; advocate for Black women who report high levels of stress, psychological distress, or depressive symptoms for further mental health evaluation by their health care provider; and provide resources and education (e.g., support groups, counseling) for these women. [ABSTRACT FROM AUTHOR]

Objective: We compared blood-based DNA methylation levels of endoglin (ENG) and transforming growth factor beta receptor 2 (TGFβR2) gene promoter regions between women with clinically-overt preeclampsia and women with uncomplicated, normotensive pregnancies. Methods: We used EpiTect Methyl II PCR Assays to evaluate DNA methylation of CpG islands located in promoter regions of ENG (CpG Island 114642) and TGFβR2 (CpG Island 110111). Preeclampsia was diagnosed based on blood pressure, protein, and uric acid criteria. N = 21 nulliparous preeclampsia case participants were 1:1 frequency matched to N = 21 nulliparous normotensive control participants on gestational age at sample collection (±2 weeks), smoking status, and labor status at sample collection. Methylation values were compared between case and control participant groups [(ENG subset: n = 20 (9 cases, 11 controls); TGFβR2 subset: n = 28 (15 cases, 13 controls)]. Results: The majority of the preeclampsia cases delivered at ⩾34 weeks' gestation (83%). Average methylation levels for ENG ([M ± (SD)]; Case Participant Group = 6.54% ± 4.57 versus Control Participant group = 4.81% ± 5.08; P =.102) and TGFβR2 (Case Participant Group = 1.50% ± 1.37 vs Control Participant Group = 1.70% ± 1.40; P =.695) promoter CpG islands did not differ significantly between the participant groups. Removal of 2 extreme outliers in the ENG analytic subset revealed a trend between levels of ENG methylation and pregnancy outcome (Case Participant Group = 5.17% ± 2.16 vs Control Participant Group = 3.36% ± 1.73; P =.062). Conclusion: Additional epigenetic studies that include larger sample sizes, investigate preeclampsia subtypes, and capture methylation status of CpG island shores and shelves are needed to further inform us of the potential role that ENG and TGFβR2 DNA methylation plays in preeclampsia pathophysiology. [ABSTRACT FROM AUTHOR]

Objective: This study examined whether cigarette smoking mediated the association of racial discrimination with depressive symptoms among pregnant Black women. Design: Cross‐sectional. Sample: Two hundred Black women at 8–29 weeks gestation. Measurements: Women completed questionnaires including the Experiences of Discrimination and the Center for Epidemiologic Studies‐Depression (CES‐D) scales, as well as questions about sociodemographic characteristics and cigarette smoking. Results: The mean age of the sample was 26.9 ± 5.7 years and the mean gestational age at data collection was 15.6 ± 5.7 weeks. Approximately 17% of women reported prenatal cigarette smoking; 27% had prenatal CES‐D scores ≥23, which have been correlated with depression diagnoses; and 59% reported ever (lifetime) experiencing discrimination in at least one situation (e.g., at work). Path analysis results indicated that the standardized indirect effect of experiences of racial discrimination on CES‐D scores through prenatal smoking was statistically significant (standardized indirect effect = 0.03; 95% CI: 0.001, 0.094; p =.042). Conclusion: Cigarette smoking during pregnancy partially mediated the association between lifetime experiences of racial discrimination and prenatal depressive symptoms among pregnant Black women. Smoking cessation programs should focus on identifying and treating depressive symptoms among pregnant Black women. [ABSTRACT FROM AUTHOR]

Offspring born preterm (ie, before 37 weeks of gestation) are more likely to die or experience long-standing illness than full-term offspring. Maternal genetic variants (ie, heritable, stable variations in the genetic code) and epigenetic modifications (ie, chemical modifications to the genetic code that can affect which genes are turned on or off) in response to stress have been implicated in preterm birth. Fetal genetic variants have been linked to preterm birth though the role of offspring epigenetics in preterm birth remains understudied. This systematic review synthesizes the literature examining associations among stress during pregnancy and epigenetic modifications to offspring DNA, with 25 reports identified. Ten reports examined DNA methylation (ie, addition/removal of methyl groups to/from DNA) across the epigenome. The remainder examined DNA methylation near genes of interest, primarily genes linked to hypothalamic-pituitary-adrenal axis function (NR3C1, FKBP51), growth/immune function (IGF2), and socioemotional regulation (SLC6A4, OXTR). The majority of reports noted associations among stress and offspring DNA methylation, primarily when perceived stress, anxiety, or depression served as the predictor. Findings suggest that differences in offspring epigenetic patterns may play a role in stress-associated preterm birth and serve as targets for novel interventions. [ABSTRACT FROM AUTHOR]

Abstract Rationale Psychological stress-induced cortisol elevations appear to contribute to preterm birth. Yet, some studies suggest that the biological ramifications of racial discrimination-associated stress are unique and may involve development of decreased glucocorticoid sensitivity despite normalized cortisol levels. Objective In this study, we examined the effects of racial discrimination on maternal cortisol output, leukocyte glucocorticoid sensitivity, and the degree of correspondence between cortisol levels and birth timing in an African American cohort. Method A generally healthy prospective cohort was enrolled at 28–32 weeks gestation (n = 91). The Experiences of Discrimination scale was administered, whole blood collected, and plasma cortisol levels, cytokine levels, and leukocyte counts quantified for examination of patterns of endogenous feedback. Results Racial discrimination in the mid-tertile was associated with greater maternal cortisol levels than the bottom tertile among women reporting internalizing responses (b* = 0.68, p = 0.001). Decreased leukocyte glucocorticoid sensitivity was witnessed at greater frequencies of experiences of racial discrimination, as evidenced by decreased correspondence between maternal cortisol levels and plasma IL-8 levels, monocyte counts, and lymphocyte counts (p values ≤ 0.043). The association between maternal cortisol levels and birth timing differed by discrimination tertile (p values ≤ 0.005), with greater cortisol levels predictive of earlier birth among women without (b* = −0.59, p < 0.001) but not with racial discrimination (p s ≥ 0.497). Conclusion We provide novel evidence of decreased glucocorticoid sensitivity at increasing frequency of exposure to racial discrimination. Our findings suggest that the biology of preterm birth may depend upon racial discriminatory exposures, favoring pathways dependent upon glucocorticoid-induced increases in leukocyte tissue surveillance versus glucocorticoid resistance-associated inflammatory aberrations at increasing levels of exposure. Precision approaches to prenatal care are sorely needed to combat preterm birth, particularly among African American women, with efforts dependent upon further research examining the pathways contributing to the syndrome dependent upon the totality of an individual's exposures. Highlights • Racial discrimination predicts lower maternal leukocyte glucocorticoid sensitivity. • Elevated cortisol levels predict earlier birth in women without past discrimination. • Findings suggest biology of preterm birth may be unique based on prior exposures. [ABSTRACT FROM AUTHOR]

Background: The etiology of pre-eclampsia (PE) is unknown; but it is accepted that normal pregnancy represents a distinctive challenge to the maternal immune system. C-reactive protein is a prominent component of the innate immune system; and we previously reported an association between PE and the CRP polymorphism, rs1205. Our aim was to explore the effects of additional CRP variants. The IBC (Cardiochip) genotyping microarray focuses on candidate genes and pathways related to the pathophysiology of cardiovascular disease. Methods: This study recruited 140 cases of PE and 270 matched controls, of which 95 cases met criteria as severe PE, from an American Indian community. IBC array genotypes from 10 suitable CRP SNPs were analyzed. A replication sample of 178 cases and 427 controls of European ancestry was also genotyped. Results: A nominally significant difference (p value <0.05) was seen in the distribution of discordant matched pairs for rs3093068; and Bonferroni corrected differences (P<0.005) were seen for rs876538, rs2794521, and rs3091244. Univariate conditional logistic regression odds ratios (OR) were nominally significant for rs3093068 and rs876538 models only. Multivariate logistic models with adjustment for mother's age, nulliparity and BMI attenuated the effect (OR 1.58, P = 0.066, 95% CI 0.97–2.58) for rs876538 and (OR 2.59, P = 0.050, 95% CI 1.00–6.68) for rs3093068. An additive risk score of the above two risk genotypes shows a multivariate adjusted OR of 2.04 (P = 0.013, 95% CI 1.16–3.56). The replication sample also demonstrated significant association between PE and the rs876538 allele (OR = 1.55, P = 0.01, 95% CI 2.16–1.10). We also show putative functionality for the rs876538 and rs3093068 CRP variants. Conclusion: The CRP variants, rs876538 and rs3093068, previously associated with other cardiovascular disease phenotypes, show suggestive association with PE in this American Indian population, further supporting a possible role for CRP in PE. [ABSTRACT FROM AUTHOR]

Preceding studies have shown that cardiac cytochrome c oxidase (CCO) deficiency occurs in the offspring of Cu-deficient rats on postnatal days (PND) 15 and 21. In order to determine if the CCO deficiency resulted from low prenatal Cu intake rather than from low postnatal Cu intake, pups from dams fed AIN93G diet containing 1 mg Cu/kg (CuD dams) were cross fostered to dams fed diet containing 6 mg Cu/kg (CuA dams) and vice versa on PND 1. Pups that remained with their birth dams served as controls. All dams began dietary treatment with either CuD or CuA diets 3 weeks before conception and remained on their respective diets until PND 21. On PND 21, CCO activities (U/mg protein, mean±SEM) in isolated cardiac mitochondria were 3.25±0.06 in pups of CuA dams (N=26), 3.30±0.11 in pups of CuA dams cross fostered to CuD dams (N=8), 2.52±0.10 in pups of CuD dams cross fostered to CuA dams (N=10), and 1.81±0.07 in pups of CuD dams (N=18). CCO activity was lower (P<0.05, Tukey's test) in pups of CuDdams cross fostered to CuA dams compared to pups of CuA dams or pups of CuA dams cross fostered to CuD dams, but higher (P<0.05) compared to pups of CuD dams. Differences in heart Cu concentrations corresponded to the differences in CCO activity. These findings indicate that Cu intake during pregnancy has a greater influence than postnatal Cu intake on cardiac CCO in the first generation. [ABSTRACT FROM AUTHOR]