Neighborhood Socioeconomic Deprivation in Early Childhood Mediates Racial Disparities in Blood Pressure in a College Student Sample.

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.

Experiences of Discrimination and Urinary Catecholamine Concentrations: Longitudinal Associations in a College Student Sample.

BACKGROUND: Experiences of discrimination are a risk factor for subsequent cardiovascular disease. However, there is a lack of longitudinal research examining associations between discrimination and urinary catecholamines. This is surprising given the likely mediating role of sympathetic nervous system dysregulation in the association between psychosocial stress and cardiovascular morbidity. PURPOSE: The current study examined the 3 year longitudinal association between experiences of discrimination and urinary catecholamines. METHODS: The sample included 149 college students (mean age at baseline = 18.8, standard deviation = 0.96; 45% Black/African American; 55% White/European American). Concentrations of epinephrine and norepinephrine-urinary catecholamines with established links to psychosocial stress exposure and subsequent morbidity-were determined from 12 hr overnight samples. RESULTS: Results indicated that experiences of discrimination were associated with increases in both epinephrine (ß = .284, standard error [SE] = .117, p = .015) and norepinephrine (ß = .306, SE = .114, p = .001). These longitudinal associations persisted after adjusting for negative affect, depression, and rejection sensitivity and did not vary as a function of race/ethnicity. CONCLUSIONS: Results suggest that examination of overnight urinary catecholamines as a biological mediator of associations between experiences of discrimination and cardiovascular morbidity is warranted.

Disparities in insulin resistance between black and white adults in the United States: The role of lifespan stress exposure.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.