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Abstract Enhanced production of dehydroepiandrosterone (DHEA) by the foetal hypothalamic‐pituitary‐adrenal (HPA) axis enables maturational events critical for labour induction and neonatal adaptation. Despite knowledge of the interconnected nature of maternal and foetal physiology and dramatic changes in DHEA production after birth, few studies have examined DHEA levels in newborns and none have examined DHEA’s response to acute stress. Understanding normative patterns of early DHEA activity is needed to accurately assess functioning of the biological stress system with relevance for health and development. The present study analysed DHEA concentrations and change after stress among 93 newborns and associations with pregnancy, delivery and demographic risk factors. Three saliva samples, collected prior to and following a blood draw stressor, were used to determine baseline and stress reactive DHEA levels. Mothers self‐reported on health behaviours during pregnancy. Data on obstetric factors were obtained from medical records. DHEA levels declined from pre‐ to post‐stressor assessments. Results also showed that post‐stressor DHEA change was significantly associated with administration of medications used to treat pain and accelerate labour. However, there was no significant variation in DHEA pre‐stress levels or change after stress as a function of time after birth. By capturing DHEA levels after birth, the present study provides a window into prenatal health of the HPA system. The study also advances knowledge of DHEA in newborns by providing data on reference levels and important covariates. This information on basic adrenal physiology provides a foundation that can be expanded on to enhance understanding of early hypothalamic‐pituitary‐adrenal axis activity. 

Stress is known to affect health throughout life and into future generations, but the underlying molecular mechanisms are unknown. We tested the hypothesis that maternal psychosocial stress influences DNA methylation (DNAm), which in turn impacts newborn health outcomes. Specifically, we analyzed DNAm at individual, regional, and genome-wide levels to test for associations with maternal stress and newborn birth weight. Maternal venous blood and newborn cord blood (n = 24 and 22, respectively) were assayed for methylation at ∼450,000 CpG sites. Methylation was analyzed by examining CpG sites individually in an epigenome-wide association study (EWAS), as regional groups using variably methylated region (VMR) analysis in maternal blood only, and through the epigenome-wide measures using genome-wide mean methylation (GMM), Horvath's epigenetic clock, and mitotic age. These methylation measures were tested for association with three measures of maternal stress (maternal war trauma, chronic stress, and experience of sexual violence) and one health outcome (newborn birth weight). We observed that maternal experiences of war trauma, chronic stress, and sexual assault were each associated with decreased newborn birth weight (p < 1.95 × 10-7 in all cases). Testing individual CpG sites using EWAS, we observed no associations between DNAm and any measure of maternal stress or newborn birth weight in either maternal or cord blood, after Bonferroni multiple testing correction. However, the top-ranked CpG site in maternal blood that associated with maternal chronic stress and sexual violence before multiple testing correction is located near the SPON1 gene. Testing at a regional level, we found increased methylation of a VMR in maternal blood near SPON1 that was associated with chronic stress and sexual violence after Bonferroni multiple testing correction (p = 1.95 × 10-7 and 8.3 × 10-6, respectively). At the epigenomic level, cord blood GMM was associated with significantly higher levels of war trauma (p = 0.025) and was suggestively associated with sexual violence (p = 0.053). The other two epigenome-wide measures were not associated with maternal stress or newborn birth weight in either tissue type. Despite our small sample size, we identified associations even after conservative multiple testing correction. Specifically, we found associations between DNAm and the three measures of maternal stress across both tissues; specifically, a VMR in maternal blood and GMM in cord blood were both associated with different measures of maternal stress. The association of cord blood GMM, but not maternal blood GMM, with maternal stress may suggest different responses to stress in mother and newborn. It is noteworthy that we found associations only when CpG sites were analyzed in aggregate, either as VMRs or as a broad summary measure of GMM. 

The field of social and behavioral epigenetics examines how social and behavioral experiences can cause epigenetically-driven changes in gene expression that in turn influence health and well-being. We work in the eastern Democratic Republic of Congo, where 20 years of conflict and post-conflict violence have subjected women to extreme stress and sexual violence. We collected blood samples from mothers and their offspring at birth, plus follow-up samples from offspring up to five years of age, in three cohorts (2010 cohort, n=25; 2013 cohort , n=103, 2015 cohort, n=77). Using DNA extracted from blood and placental samples, we assayed methylation using Illumina’s 450K and EPIC chips, telomere length, and gene expression using the ClariomS chip. We also collected ethnographic and survey data on maternal stress, newborn health outcomes, and cortisol from offspring saliva and hair samples. Using these data, we tested for associations among maternal stress, DNA methylation, gene expression, and offspring health outcomes. We find that epigenetic aging is accelerated in mothers relative to chronological age, but newborn epigenetic age appears unchanged. In contrast, telomere length is significantly shorter in offspring born to mothers with high levels of war stress, but this effect only emerges after birth. Analyses of epigenome and gene expression data are ongoing. Our study takes a biocultural perspective to understand the molecular, biological, and health effects of stress and violence, particularly from an intergenerational perspective. 

Social and behavioral epigenetics is the study of psychosocial factors that impact biology through an epigenetic mechanism. Epigenetic modifications influence the activity of genes without altering the underlying DNA sequence. DNA methylation is one type of epigenetic modification that has been widely studied and found to associate with a broad range of psychosocial stressors. This paper reviews the landmark studies and current innovations. An evolutionary context for epigenetic changes induced by psychosocial stress, and the possible heritability of such changes, is also presented. The involvement of social and behavioral scientists in this emerging field is essential to ensure that the nuances of the psychosocial environment are well understood and accurately modeled.