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The influence of childhood contexts on adult blood pressure is an important yet understudied topic. Using a developmental perspective, this study examines the association between neighborhood socioeconomic disadvantage in early childhood (0–5 yrs), middle childhood (6–12 yrs) and adolescence (13–18 yrs) on subsequent blood pressure in young adulthood. Data were from 263 college students (52% Black; Mage = 19.21 years) and neighborhood socioeconomic disadvantage was measured using a tract-level Area Deprivation Index. Neighborhood disadvantage in early childhood was significantly associated with diastolic blood pressure and explained 22% of the race difference between Black and White adults. The findings are consistent with the notion that early childhood may be a sensitive period for the effects of neighborhood disadvantage on blood pressure. [ABSTRACT FROM AUTHOR]

Policy PointsPolicies that increase county income levels, particularly for middle‐income households, may reduce low birth weight rates and shrink disparities between Black and White infants.Given the role of aggregate maternal characteristics in predicting low birth weight rates, policies that increase human capital investments (e.g., funding for higher education, job training) could lead to higher income levels while improving population birth outcomes.The association between county income levels and racial disparities in low birth weight is independent of disparities in maternal risks, and thus a broad set of policies aimed at increasing income levels (e.g., income supplements, labor protections) may be warranted. Context: Low birth weight (LBW; <2,500 grams) and infant mortality rates vary among place and racial group in the United States, with economic resources being a likely fundamental contributor to these disparities. The goals of this study were to examine time‐varying county median income as a predictor of LBW rates and Black‐White LBW disparities and to test county prevalence and racial disparities in maternal sociodemographic and health risk factors as mediators. Methods: Using national birth records for 1992–2014 from the National Center for Health Statistics, a total of approximately 27.4 million singleton births to non‐Hispanic Black and White mothers were included. Data were aggregated in three‐year county‐period observations for 868 US counties meeting eligibility requirements (n = 3,723 observations). Sociodemographic factors included rates of low maternal education, nonmarital childbearing, teenage pregnancy, and advanced‐age pregnancy; and health factors included rates of smoking during pregnancy and inadequate prenatal care. Among other covariates, linear models included county and period fixed effects and unemployment, poverty, and income inequality. Findings: An increase of $10,000 in county median income was associated with 0.34 fewer LBW cases per 100 live births and smaller Black‐White LBW disparities of 0.58 per 100 births. Time‐varying county rates of maternal sociodemographic and health risks mediated the association between median income and LBW, accounting for 65% and 25% of this estimate, respectively, but racial disparities in risk factors did not mediate the income association with Black‐White LBW disparities. Similarly, county median income was associated with very low birth weight rates and related Black‐White disparities. Conclusions: Efforts to increase income levels—for example, through investing in human capital, enacting labor union protections, or attracting well‐paying employment—have broad potential to influence population reproductive health. Higher income levels may reduce LBW rates and lead to more equitable outcomes between Black and White mothers. [ABSTRACT FROM AUTHOR]

African American women with systemic lupus erythematosus (SLE) have worse disease outcomes compared to their White counterparts. Stressors associated with race may contribute to poorer health in this population through maladaptive behavioral pathways. This study investigated relationships between stress associated with anticipating racism, smoking, and SLE disease activity. Data were from 432 African American women with SLE in the Black Women's Experiences Living with Lupus (BeWELL) Study. Controlling for sociodemographic and health-related covariates, multivariable regression analyses revealed a significant association between anticipatory racism stress (ARS) and disease activity (p = 0.00, b = 1.13, 95% CI [0.43, 1.82]). A significant interaction between ARS and smoking also indicated that smoking exacerbated the effect of ARS on disease activity (p = 0.04, b = 1.95, CI = 0.04, 3.96). Test for evidence of smoking mediating the effect of ARS on disease activity were not statistically significant (z = 1.77, p = 0.08). Findings have implications for future SLE disparities research among African American women with SLE. [ABSTRACT FROM AUTHOR]

With unprecedented increases, mortality trends in the United States have received significant attention in recent years. To date, research on this topic has emphasized specific causes of death and proximal behavioral or physiological determinants. In this commentary, I consider novel contributions of Zheng and Echave (Am J Epidemiol. 2021;190(11):2242–2255) in examining trends in mental health, health behaviors, and physiological dysregulation. I then discuss broader developments in related research and make a case for: 1) not allowing recent health trends among Whites to overshadow the urgent work that needs to be done to mitigate persistent racial inequities, 2) further investigation of what accounts for increases in income inequality and its life-span health consequences, and 3) broadening the scope of mechanisms considered to include underdiscussed topics such as the role of increases in social media use or environmental toxicant exposures. Underlying several potential explanations for observed trends in health and mortality is the fact that substantial change has occurred on multiple fronts in US society and that policy responses to these changes have been insufficient. An enhanced emphasis on innovative population health research will be essential to provide the evidence base needed for policy makers to rise to these urgent challenges. [ABSTRACT FROM AUTHOR]

Objectives: Black adults in the United States have shorter sleep durations and poorer sleep efficiency relative to White adults, yet reasons for these disparities are not well explicated. The objective of this study was to examine neighborhood safety in childhood as a mediator of subsequent racial disparities in sleep.Methods: Data were from Black and White young adults attending a large, predominantly White university in the Southeastern United States (N = 263; 52% Black, 53% female; Mean age = 19.21 years, SD = 1.01). Sleep parameters were assessed from eight nights of wrist actigraphy (time in bed, sleep duration, and efficiency) and an established self-report measure of daytime sleepiness. Residential histories from birth through age 18 were documented, and retrospective self-reports of neighborhood safety in childhood were assessed.Results: Black participants had less time in bed (p < 0.001), shorter sleep duration (p < 0.001), poorer sleep efficiency (p < 0.001), and more daytime sleepiness (p = 0.009) than White participants. Neighborhood safety mediated race differences in time in bed (p = 0.028), sleep duration (p = 0.033), and daytime sleepiness (p = 0.048), but not sleep efficiency. Findings were substantively unchanged after adjustment for family socioeconomic status, BMI, and substance use.Conclusions: Findings support the hypothesis that neighborhood safety in childhood may partially account for race differences in subsequent sleep duration and daytime sleepiness. Addressing racial inequities in childhood neighborhood safety may be an important step toward reducing racial disparities in sleep health. [ABSTRACT FROM AUTHOR]

• Disparities in insulin resistance between black and white adults are substantial. • Childhood and adult stress measures mediate race differences in insulin resistance. • Adult stress partially mediates effects of childhood adversity on insulin resistance. • Stress effects on insulin resistance are partly meditated by inflammation. • Lower nocturnal cortisol mediates childhood stress effects on insulin resistance. Disparities in insulin resistance between Black and White adults in the United States are well documented, yet relatively little is known about the psychosocial or biological antecedents of these inequities. The current study examined childhood adversity and contemporaneous psychosocial stressors in adulthood as possible mediators of the racial disparity in insulin resistance. Inflammatory and hypothalamic-pituitary adrenal (HPA) axis mechanisms implicated in associations between lifespan stress exposure and insulin resistance were also considered. Data were derived from the biomarker component of the Midlife in the United States Study (N = 1170, 20% Black, 56% female, Mean age = 54.7 years, SD = 11.6). A homeostatic model assessment of insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin concentrations. Twelve risk factors relating to household dysfunction, socioeconomic disadvantage, and maltreatment were sum scored to index childhood adversity. Measures of adult stress included socioeconomic adversity, major stressful events, everyday discrimination, and lifetime discrimination. Levels of insulin resistance were higher among Black than White adults. Childhood adversity was positively associated with HOMA-IR, and attenuated 18% of the race difference. Measures of adult stress mediated 33% of the association between childhood adversity and HOMA-IR, and accounted for an additional 47% of the race difference. Higher inflammation and lower nocturnal cortisol both played an important role in mediating the association between stress exposure and HOMA-IR. Findings are consistent with prior research showing that childhood adversity and adult stress are salient predictors of glucose metabolism, and extend this work by showing that lifespan stress exposures attenuate a significant portion of the Black-White disparity in HOMA-IR. Results also suggest stress effects on insulin resistance through inflammatory and HPA-axis pathways. [ABSTRACT FROM AUTHOR]

Insufficient and disrupted sleep is linked with cardiovascular and metabolic dysregulation and morbidity. The current study examines the degree to which differences in sleep between black/African American (AA) and white/European American (EA) adults explain racial differences in cardiometabolic (CMB) disease risk. Total sleep time and sleep efficiency (percent of time in bed asleep) were assessed via seven nights of wrist actigraphy among 426 participants in the Midlife in the United States Study (31% AA; 69% EA; 61% female; mean age = 56.8 y). CMB risk was indexed as a composite of seven biomarkers [blood pressure, waist circumference, hemoglobin A1c (HbA1c), insulin resistance, triglycerides, HDL cholesterol (HDL-C), and C-reactive protein]. Covariates included sociodemographic characteristics and relevant health behaviors. Results indicated that AAs relative to EAs obtained less sleep (341 vs. 381 min) and had lower sleep efficiency (72.3 vs. 82.2%) (P values < 0.001). Further, 41% and 58% of the racial difference in CMB risk was explained by sleep time and sleep efficiency, respectively. In models stratified by sex, race was indirectly associated with CMB risk via sleep time and efficiency only among females (explaining 33% and 65% of the race difference, respectively). Indirect effects were robust to alternative model specifications that excluded participants with diabetes or heart disease. Consideration of sleep determinants and sleep health is therefore needed in efforts to reduce racial differences in CMB disease. [ABSTRACT FROM AUTHOR]

Objective: Disparities in sleep duration and efficiency between Black/African American (AA) and White/European American (EA) adults are well-documented. The objective of this study was to examine neighborhood disadvantage as an explanation for race differences in objectively measured sleep.Methods: Data were from 133 AA and 293 EA adults who participated in the sleep assessment protocol of the Midlife in the United States (MIDUS) study (57% female; Mean Age = 56.8 years, SD = 11.4). Sleep minutes, onset latency, and waking after sleep onset (WASO) were assessed over seven nights using wrist actigraphy. Neighborhood characteristics were assessed by linking home addresses to tract-level socioeconomic data from the 2000 US Census. Multilevel models estimated associations between neighborhood disadvantage and sleep, and the degree to which neighborhood disadvantage mediated race differences in sleep controlling for family socioeconomic position and demographic variables.Results: AAs had shorter sleep duration, greater onset latency, and higher WASO than EAs (ps < 0.001). Neighborhood disadvantage was significantly associated with WASO (B = 3.54, p = 0.028), but not sleep minutes (B = -2.21, p = 0.60) or latency (B = 1.55, p = 0.38). Furthermore, race was indirectly associated with WASO via neighborhood disadvantage (B = 4.63, p = 0.035), which explained 24% of the race difference. When measures of depression, health behaviors, and obesity were added to the model, the association between neighborhood disadvantage and WASO was attenuated by 11% but remained significant.Conclusion: Findings suggest that neighborhood disadvantage mediates a portion of race differences in WASO, an important indicator of sleep efficiency. [ABSTRACT FROM AUTHOR]