Early Life Disadvantage and the Risk of Depressive Symptoms among Young Black Women.

OVERVIEW: We examined the association between early-life socioeconomic disadvantage and depressive symptoms in adulthood and assessed whether social factors in adulthood modify the association. METHODS: The 11-item Center for Epidemiologic Studies-Depression Scale (CES-D) assessed adult depressive symptoms among 1612 Black women and other participants with a uterus (hereafter participants) in the Study of Environment, Lifestyle and Fibroids. Baseline self-reported childhood factors (i.e., parents in the household, mother's educational attainment, food insecurity, neighborhood safety, childhood income, and quiet bedroom for sleep) were included in a latent class analysis to derive an early life disadvantage construct. Multivariable log-binomial models estimated the association between early life disadvantage and adult depressive symptoms. Potential effect modifiers included adult educational attainment, social support, and financial difficulty. RESULTS: Participants classified as having high early life disadvantage had 1.34 times (95% CI: 1.20, 1.49) the risk of high depressive symptoms than those in the low early life disadvantage class after adjusting for age, first born status, and childhood health. Adult educational attainment and social support modified the association. CONCLUSION: Early life disadvantage increased the risk of depressive symptoms in adulthood. Participants with at least some college education and with high social support had greater risk than those with less than college education and low social support, respectively. Thus, the mental health of Black women and other participants with a uterus exposed to early life disadvantage do not necessarily benefit from higher education or from social support.

Residential segregation and prenatal depression in a non-Hispanic Black and Hispanic cohort in North Carolina.

PURPOSE: Investigate residential segregation and prenatal depression in a non-Hispanic (NH) Black and Hispanic North Carolina pregnancy cohort. METHODS: Demographics, prenatal depression (Center for Epidemiological Studies Depression scale ≥16), and residence from the 2006-2009 Newborn Epigenetic Survey were linked to Census-tract levels of racial and economic segregation (Index of Concentration at the Extremes) from the American Community Survey 2005-2009 5-year estimates. Adjusted prevalence ratios (aPR) for prenatal depression compared living in Index of Concentration at the Extremes tertiles 1 and 2 (higher proportion NH Black or Hispanic and/or low income) to 3 (higher proportion NH white and/or high-income), accounting for neighborhood clustering, age, education, employment, parity, and marital status. RESULTS: Among the 773 survey participants (482 NH Black and 291 Hispanic), 35.7% and 27.2% of NH Black and Hispanic participants had prenatal depression, respectively. For NH Black participants, depression prevalence was 17% lower for tertile 1 versus 3 for the NH Black/white (aPR=0.83; 95% CI=0.62-1.10), low/high income (aPR=0.83; 95% CI=0.62-1.11), and low-income NH Black/high-income NH white (aPR=0.82; 95% CI=0.61-1.09) measures. For Hispanic participants, estimates were weaker in the opposite direction for the Hispanic/NH white (aPR=1.02; 95% CI=0.71-1.47), low/high income (aPr=1.14; (95% CI=0.76-1.69), and low-income Hispanic/high-income NH white (aPR=1.12; 95% CI=0.78-1.60) measures. CONCLUSIONS: Residential segregation's impact on prenatal depression may differ by race/ethnicity and level of segregation, but findings are imprecise due to small sample sizes. Longitudinal research spanning greater geographic areas is needed.

Understanding Health Inequalities Through the Lens of Social Epigenetics.

Longstanding racial/ethnic inequalities in morbidity and mortality persist in the United States. Although the determinants of health inequalities are complex, social and structural factors produced by inequitable and racialized systems are recognized as contributing sources. Social epigenetics is an emerging area of research that aims to uncover biological pathways through which social experiences affect health outcomes. A growing body of literature links adverse social exposures to epigenetic mechanisms, namely DNA methylation, offering a plausible pathway through which health inequalities may arise. This review provides an overview of social epigenetics and highlights existing literature linking social exposures-i.e., psychosocial stressors, racism, discrimination, socioeconomic position, and neighborhood social environment-to DNA methylation in humans. We conclude with a discussion of social epigenetics as a mechanistic link to health inequalities and provide suggestions for future social epigenetics research on health inequalities.

Environmental exposures and sleep outcomes: A review of evidence, potential mechanisms, and implications.

Environmental exposures and poor sleep outcomes are known to have consequential effects on human health. This integrative review first seeks to present and synthesize existing literature investigating the relationship between exposure to various environmental factors and sleep health. We then present potential mechanisms of action as well as implications for policy and future research for each environmental exposure. Broadly, although studies are still emerging, empirical evidence has begun to show a positive association between adverse effects of heavy metal, noise pollution, light pollution, second-hand smoke, and air pollution exposures and various sleep problems. Specifically, these negative sleep outcomes range from subjective sleep manifestations, such as general sleep quality, sleep duration, daytime dysfunction, and daytime sleepiness, as well as objective sleep measures, including difficulties with sleep onset and maintenance, sleep stage or circadian rhythm interference, sleep arousal, REM activity, and sleep disordered breathing. However, the association between light exposure and sleep is less clear. Potential toxicological mechanisms are thought to include the direct effect of various environmental toxicants on the nervous, respiratory, and cardiovascular systems, oxidative stress, and inflammation. Nevertheless, future research is required to tease out the exact pathways of action to explain the associations between each environmental factor and sleep, to inform possible therapies to negate the detrimental effects, and to increase efforts in decreasing exposure to these harmful environmental factors to improve health.