Cardiovascular disease (CVD) is the leading global cause of death, accounting for approximately 18.6 million
deaths in 2019. Between 2015 and 2018, 126.9 million American adults had CVD, resulting in an annual cost
of $363.4 billion in healthcare, lost productivity and mortality. The CVD burden is not distributed equally among
racial/ethnic (R/E) groups: ~60% of African American (AA) adults have CVD compared to ~48% of Hispanic/
Latinx (HL) and Non-Hispanic Whites (NHW). R/E disparities in CVD are likely due to an interplay of genetic
and sociocultural factors, which are exacerbated by the chronic stress burden that some R/E groups endure.
Chronic stress elicits repeated activation of the stress response systems, increasing allostatic load (AL) and
compromising health. High AL may increase risk for early vascular aging (EVA): arterial stiffness, subclinical
endothelial dysfunction, hypertension and increased left ventricular mass. R/E disparities in EVA emerge by
adolescence, before overt signs of CVD, but no studies simultaneously measured vertically integrated CVD
markers early in development. Links between chronic stress, AL and CVD have been proposed but not studied
comprehensively. Factors that may protect against CVD in some high-risk groups (e.g., HL) have not been
explored across R/E groups. Current CVD prevention and treatment guidelines were developed from data
obtained primarily in men, contributing to missed or delayed diagnoses, non-optimal treatment and poor
outcomes, especially in R/E minority women. Research on the mechanisms of CVD risk in AA was conducted
almost exclusively in men despite high CVD prevalence in both sexes. Importantly, R/E disparities in CVD
are more marked in women. CVDs explain 33% of the mortality variation between AA and NHW men but 45%
for women. Many CVD risk factors have a higher prevalence (e.g., obesity) or a greater impact in women; for
example, chronic stress, which disproportionately affects R/E minorities, is a stronger predictor of CVD-related
mortality in women. Our current study measures multidomain CVD risk factors including cumulative stress,
hypothalamic-pituitary-adrenal activity, inflammatory markers and obesity indices (anthropometry, adiposity,
diet, metabolic markers, and adipokines) in 13 to 17-year-old AA, HL and NHW adolescent girls. We propose
a follow-up study of this well-characterized cohort 4 to 6 years later in emerging adulthood, a critical period
when physical maturity is largely complete but biopsychosocial risk factors that have longterm implications
for CVD emerge. We will determine the magnitude of cumulative stress and AL burden over time, incorporate
vertically integrated markers of EVA with state-of-the-art techniques, and examine the effects of cumulative
stress, AL and adaptive cultural coping practices on EVA. Characterizing R/E differences in modifiable bio-
psychosocial risk and protective factors associated with subclinical CVD during a developmental phase when
humans can exert more control over their lives (with increased autonomy but few adult responsibilities) offers
an opportunity to preempt the transition from health to disease and reduce CVD disparities in at-risk groups.