Race, cortisol, and subclinical cardiovascular disease in 9- to 11-year-old children.

Abstract

Background: Non-Hispanic Black Americans have a greater risk for certain subtypes of cardiovascular disease (CVD; e.g., stroke and heart failure) relative to non-Hispanic White Americans. Moreover, Black relative to White adults consistently show elevated cortisol, a CVD risk. The impact of race, environmental stress, and cortisol on subclinical CVD has yet to be fully researched in children. Method: We assessed diurnal salivary cortisol slopes and hair cortisol in a sample of 9-to 11-year-old children (N = 271; 54% female) with roughly half self-identifying as either Black (57%) or White (43%). Two subclinical CVD indicators were assessed: carotid-femoral pulse wave velocity (cfPWV) and carotid intima-media thickness (cIMT). We assessed numerous environmental stress indicators. Results: After adjusting for covariates, we found that Black children had significantly flatter diurnal cortisol slopes, higher hair cortisol, and thicker IMT than White children. Significant pathways were found: race → salivary cortisol slope → cfPWV (effect = −0.059, 95% CI [−0.116, −0.002]) and race → hair cortisol → cIMT (effect = −0.008, [−0.016, −0.002]). Black children also experienced significantly more environmental stress than White children; however, only income inequality served as a significant indirect pathway from race to salivary cortisol (effect = 0.029, [0.003, 0.060]). Conclusions: Relative to White children, Black children had significantly greater hair cortisol and flatter diurnal slopes which, in turn, were associated with greater subclinical CVD. As suggested by a significant indirect pathway, income inequality might partially explain the race-cortisol association. Public Significance StatementNumerous health disparities continue to exist among Black Americans relative to White Americans, across the lifespan. Specifically, the present study considers racial differences in subclinical CVD in children, and the potential indirect path through differences in underlying cortisol (the "stress hormone").