Community Socioeconomic Disadvantage in Midlife Relates to Cortical Morphology via Neuroendocrine and Cardiometabolic Pathways.

Residing in communities of socioeconomic disadvantage confers risk for chronic diseases and cognitive aging, as well as risk for biological factors that negatively affect brain morphology. The present study tested whether community disadvantage negatively associates with brain morphology via 2 biological factors encompassing cardiometabolic disease risk and neuroendocrine function. Participants were 448 midlife adults aged 30-54 years (236 women) who underwent structural neuroimaging to assess cortical and subcortical brain tissue morphology. Community disadvantage was indexed by US Census data geocoded to participants' residential addresses. Cardiometabolic risk was indexed by measurements of adiposity, blood pressure, glucose, insulin, and lipids. Neuroendocrine function was indexed from salivary cortisol measurements taken over 3 days, from which we computed the cortisol awakening response, area-under-the-curve, and diurnal cortisol decline. Community disadvantage was associated with reduced cortical tissue volume, cortical surface area, and cortical thickness, but not subcortical morphology. Moreover, increased cardiometabolic risk and a flatter (dysregulated) diurnal cortisol decline mediated the associations of community disadvantage and cortical gray matter volume. These effects were independent of age, sex, and individual-level socioeconomic position. The adverse risks of residing in a disadvantaged community may extend to the cerebral cortex via cardiometabolic and neuroendocrine pathways.

Personality Correlates of Midlife Cardiometabolic Risk: The Explanatory Role of Higher-Order Factors of the Five-Factor Model.

Varying associations are reported between Five-Factor Model (FFM) personality traits and cardiovascular disease risk. Here, we further examine dispositional correlates of cardiometabolic risk within a hierarchical model of personality that proposes higher-order traits of Stability (shared variance of Agreeableness, Conscientiousness, inverse Neuroticism) and Plasticity (Extraversion, Openness), and we test hypothesized mediation via biological and behavioral factors. In an observational study of 856 community volunteers aged 30-54 years (46% male, 86% Caucasian), latent variable FFM traits (using multiple-informant reports) and aggregated cardiometabolic risk (indicators: insulin resistance, dyslipidemia, blood pressure, adiposity) were estimated using confirmatory factor analysis (CFA). The cardiometabolic factor was regressed on each personality factor or higher-order trait. Cross-sectional indirect effects via systemic inflammation, cardiac autonomic control, and physical activity were tested. CFA models confirmed the Stability "meta-trait," but not Plasticity. Lower Stability was associated with heightened cardiometabolic risk. This association was accounted for by inflammation, autonomic function, and physical activity. Among FFM traits, only Openness was associated with risk over and above Stability, and, unlike Stability, this relationship was unexplained by the intervening variables. A Stability meta-trait covaries with midlife cardiometabolic risk, and this association is accounted for by three candidate biological and behavioral factors.

Cortisol activity partially accounts for a relationship between community socioeconomic position and atherosclerosis.

Compared to others, individuals living in communities of socioeconomic disadvantage experience more atherosclerotic cardiovascular disease (CVD) and a greater extent of preclinical atherosclerosis. Although the mechanisms underlying these associations remain unclear, it is widely hypothesized that alterations in normative cortisol release from the Hypothalamic Pituitary Adrenal (HPA) axis may play a role in linking lower community socioeconomic position (C-SEP) to CVD risk. The current study examined this hypothesis in relation to a marker of preclinical atherosclerosis among 488 healthy midlife adults (30-54 years, Mean age= 43, 52% Female, 81% White). All participants were employed and without clinical CVD. C-SEP was estimated from census tract data, and atherosclerosis was measured as intima-medial thickness of the carotid arteries (cIMT) by duplex ultrasonography. Four indicators of HPA activity [cortisol at awakening and the cortisol awakening response (CAR), rate of diurnal decline in cortisol (diurnal slope), and total output expressed as area under the curve (AUC)] were derived from salivary cortisol measurements obtained from 5 samples on each of 3 working days. Path analyses were used to examine associations of C-SEP with cIMT and HPA activity and to test whether individual differences in HPA activity could account for any association of C-SEP with cIMT using bootstrapping (5000 iterations). All models were adjusted for age, sex, race, and composite measures of both individual-level socioeconomic position (income, education, occupation), and cardiometabolic risk (systolic and diastolic blood pressure, waist circumference, fasting lipids and glucose). Lower C-SEP was related to both greater cIMT (b = -0.004, p = .021) and a flatter diurnal slope of cortisol (b = -0.001, p = .039). An indirect effect showed attenuated diurnal slope to partially mediate the relationship between C-SEP and cIMT (95% CI = -0.0018 to -0.0001), and a residual direct effect of C-SEP on cIMT remained significant (95% CI = -0.0097 to -0.004). These results suggest that low C-SEP associations with preclinical atherosclerosis may be due in part to correlated variation in adrenocortical activity.

Sleep duration partially accounts for race differences in diurnal cortisol dynamics.

OBJECTIVE: Emerging research demonstrates race differences in diurnal cortisol slope, an indicator of hypothalamic-pituitary-adrenocortical (HPA)-axis functioning associated with morbidity and mortality, with African Americans showing flatter diurnal slopes than their White counterparts. Sleep characteristics are associated with both race and with HPA-axis functioning. The present report examines whether sleep duration may account for race differences in cortisol dynamics. METHOD: Participants were 424 employed African American and White adults (mean age = 42.8 years, 84.2% White, 53.6% female) with no cardiovascular disease (Adult Health and Behavior Project-Phase 2 [AHAB-II] cohort, University of Pittsburgh). Cortisol slope was calculated using 4 salivary cortisol readings, averaged over each of 4 days. Demographic (age, sex), psychosocial (socioeconomic status [SES], affect, discrimination), and health behaviors (smoking, alcohol use, physical activity) variables were used as covariates, and sleep (self-report and accelerometry) was also assessed. RESULTS: African Americans had flatter slopes than Whites (F(1, 411) = 10.45, B = .02, p = .001) in models adjusting for demographic, psychosocial, and health behavior covariates. Shorter actigraphy-assessed total sleep time was a second significant predictor of flatter cortisol slopes (F(1, 411) = 25.27, B = -.0002, p < .0001). Total sleep time partially accounted for the relationship between race and diurnal slope [confidence interval = .05 (lower = .014, upper .04)]. CONCLUSIONS: African Americans have flatter diurnal cortisol slopes than their White counterparts, an effect that may be partially attributable to race differences in nightly sleep duration. Sleep parameters should be considered in further research on race and cortisol. (PsycINFO Database Record

Trait positive and negative emotionality differentially associate with diurnal cortisol activity.

Inter-individual variability in metrics of hypothalamic-pituitary-adrenocortical (HPA) activity, such as the slope of the diurnal decline in cortisol, cortisol awakening response (CAR), and total cortisol output, have been found to associate inversely with trait ratings of extraversion and positive affect (E/PA) and positively with neuroticism and negative affect (N/NA) in some, but not all, investigations. These inconsistencies may partly reflect varied intensity of cortisol sampling among studies and reliance on self-rated traits, which are subject to reporting biases and limitations of introspection. Here, we further examined dispositional correlates of HPA activity in 490 healthy, employed midlife volunteers (M age=43 years; 54% Female; 86% white). Trait ratings were requested from participants and 2 participant-elected informants using the Positive and Negative Affect Schedule (PANAS) and Extraversion and Neuroticism dimensions of NEO personality inventories. CAR was assessed as percent increase in cortisol levels from awakening to 30min after awakening; and the diurnal slope and total output of cortisol [Area Under the Curve (AUC)] were determined from cortisol measurements taken at awakening, +4 and +9h later, and bedtime, across 3 workdays. Structural equation modeling was used to estimate multi-informant E/PA and N/NA factors. We used 3days of measurement as indicators to model each of the three latent cortisol factors (slope, CAR, and AUC). With the two latent emotionality and three latent cortisol indices included there was good fit to the data (χ(2)(200)=278.38, p=0.0002; RMSEA=0.028, 90% CI=0.02-0.04; CFI/TLI=0.97/0.96; SRMR=0.04). After controlling for covariates (age, sex, race), results showed higher latent E/PA associated with a steeper diurnal slope (Standardized ß=-0.19, p=0.02) and smaller CAR (Standardized ß=-0.26, p=0.004), whereas N/NA did not associate with any cortisol metric (Standardized ß's=-0.12 to 0.13, p's=0.10 to 0.53). These findings suggest that positive emotionality may be more closely associated with indices of diurnal cortisol release than negative emotionality.