OBJECTIVES/GOALS: Low birth weight and preterm birth are significant contributors to infant mortality in the United States that disproportionally impact Black pregnant persons and their offspring. Although these outcomes are linked to chronic stress, the contribution of race-related stress remains largely understudied. METHODS/STUDY POPULATION: We investigated the effect of race-related stress on weight and gestational age at birth in a prospective cohort of 115 pregnant Black persons recruited at Grady Memorial Hospital in Atlanta, Georgia. The Index of Race-Related Stress Brief (IRRS-Brief), Perceived Stress Scale (PSS), and Stressful Events Questionnaire (SEQ) were collected at study enrollment during pregnancy. Neonatal birth weights and gestational age were collected via standardized medical record abstraction. We conducted linear regressions to determine whether greater race-related stress was associated with lower weight and gestational age at birth, while controlling for sources of prenatal stress. RESULTS/ANTICIPATED RESULTS: Global racism (total IRRS score) was significantly associated with birth weight when controlling for prenatal perceived stress and stressful life events within the last six months since study enrollment (beta=−16.7, p=.035). Neonatal gestational age was associated with both global racism (beta=-0.03, p=.028) and individual racism (IRRS’Individual’ subscale score) (beta=-0.09, p=.032) when controlling for prenatal perceived stress and stressful life events within the last six months since study enrollment. These results suggest that greater race-related stress contributes to lower weight and gestational age at birth in pregnant Black persons. DISCUSSION/SIGNIFICANCE: Future studies are necessary to determine the mechanisms by which race-related stress contributes to these adverse birth outcomes and to inform the development risk-assessment tools and interventions to mitigate the threat of race-related stress on adverse birth outcomes in high-risk populations.

Although offspring of women exposed to childhood trauma exhibit elevated rates of psychopathology, many children demonstrate resilience to these intergenerational impacts. Among the variety of factors that likely contribute to resilience, epigenetic processes have been suggested to play an important role. The current study used a prospective design to test the novel hypothesis that offspring epigenetic aging – a measure of methylation differences that are associated with infant health outcomes – moderates the relationship between maternal exposure to childhood adversity and offspring symptomatology. Maternal childhood adversity was self-reported during pregnancy via the ACEs survey and the CTQ, which assessed total childhood trauma as well as maltreatment subtypes (i.e., emotional, physical, and sexual abuse). Offspring blood samples were collected at or shortly after birth and assayed on a DNA methylation microarray, and offspring symptomatology was assessed with the CBCL/1.5–5 when offspring were 2–4 years old. Results indicated that maternal childhood trauma, particularly sexual abuse, was predictive of offspring symptoms (ps = 0.003–0.03). However, the associations between maternal sexual abuse and offspring symptomatology were significantly attenuated in offspring with accelerated epigenetic aging. These findings further our understanding of how epigenetic processes may contribute to and attenuate the intergenerational link between stress and psychopathology.

Representation of under-represented minority (URM) faculty in the health sciences disciplines is persistently low relative to both national and student population demographics. Although some progress has been made through nationally funded pipeline development programs, demographic disparities in the various health sciences disciplines remain. As such the development of innovative interventions to help URM faculty and students overcome barriers to advancement remains a national priority. To date, the majority of pipeline development programs have focused on academic readiness, mentorship, and professional development. However, insights from the social sciences literature related to “extra-academic” (e.g., racism) barriers to URM persistence in higher education suggest the limitations of efforts exclusively focused on cognitively mediated endpoints. The purpose of this article is to synthesize findings from the social sciences literature that can inform the enhancement of URM pipeline development programs. Specifically, we highlight research related to the social, emotional, and contextual correlates of URM success in higher education including reducing social isolation, increasing engagement with research, bolstering persistence, enhancing mentoring models, and creating institutional change. Supporting URM’s success in the health sciences has implications for the development of a workforce with the capacity to understand and intervene on the drivers of health inequalities.

For African American emerging adult men, developmental challenges are evident in their escalating substance abuse and depressive symptoms; this is particularly true for men from low-resource communities. The present study tests a developmental model linking childhood adversity and contemporaneous contextual stressors to increases in emerging adults’ substance use and depressive symptoms, indirectly, via increases in defensive/hostile relational schemas and social developmental risk factors (e.g., risky peers and romantic partners, lack of involvement in school or work). We also advance exploratory hypotheses regarding DNA methylation in the oxytocin receptor gene (OXTR) as a moderator of the effects of stress on relational schemas. Hypotheses were tested with three waves of data from 505 rural African American men aged 19–25 years. Adverse childhood experiences predicted exposure to emerging adult contextual stressors. Contextual stressors forecast increases in defensive/hostile relational schemas, which increased social developmental risk factors. Social developmental risk factors proximally predicted increases in substance abuse and depressive symptoms. OXTR DNA methylation moderated the effects of contextual stressors on defensive/hostile relational schemas. Findings suggest that early exposures to stress carry forward to affect the development of social developmental risk factors in emerging adulthood, which place rural African American men at risk for increased substance abuse and depressive symptoms during the emerging adult years.

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.

Oxytocin is a neuropeptide known to influence social and cognitive processing across several mammalian species. There currently exists a mixed and controversial pattern of evidence that oxytocin pathway genes confer individual differences in social cognition and personality in humans. Inconsistencies across studies may in part be explained by the presence of intermediary, epigenetic, variables that exist between genotype and phenotype. This study was designed to investigate the association between epigenetic modification of the Oxytocin Receptor Gene (OXTR), via DNA methylation, and Big-5 personality traits. Genetic data were collected via saliva samples and analyzed to quantify DNA methylation within the promoter region of OXTR. The results indicate that Openness to Experience is associated with OXTR DNA methylation, while controlling for the remaining Big-5 personality dimensions (Neuroticism, Extraversion, Agreeableness, and Conscientiousness) and sex and age. This finding provides additional support for models associating oxytocin with individual differences in personality and identity in humans.