Inequalities in health outcomes impose substantial human and economic costs on all societies—and the relation between early adversity and lifelong well-being presents a rich scientific framework for fresh thinking about health promotion and disease prevention broadly, augmented by a deeper focus on how racism influences disparities more specifically. This review begins with an overview of advances in the biology of adversity and resilience through an early childhood lens, followed by an overview of the unique effects of racism on health and a selective review of findings from related intervention research. This article presents a framework for addressing multiple dimensions of the public health challenge—including institutional/structural racism, cultural racism, and interpersonal discrimination—and concludes with the compelling need to protect the developing brain and other biological systems from the physiological disruptions of toxic stress that can undermine the building blocks of optimal health and development in the early childhood period.

Objectives: To determine whether early life adversity (ELA) was predictive of inflammatory markers and to determine the consistency of these associations across racial groups. Methods: We analyzed data from 177 African Americans and 822 whites aged 35 to 86 years from two preliminary subsamples of the Midlife in the United States biomarker study. ELA was measured via retrospective self-report. We used multivariate linear regression models to examine the associations between ELA and C-reactive protein, interleukin-6, fibrinogen, endothelial leukocyte adhesion molecule-1, and soluble intercellular adhesion molecule-1, independent of age, gender, and medications. We extended race-stratified models to test three potential mechanisms for the observed associations. Results: Significant interactions between ELA and race were observed for all five biomarkers. Models stratified by race revealed that ELA predicted higher levels of log interleukin-6, fibrinogen, endothelial leukocyte adhesion molecule-1, and soluble intercellular adhesion molecule-1 among African Americans (p < .05), but not among whites. Some, but not all, of these associations were attenuated after adjustment for health behaviors and body mass index, adult stressors, and depressive symptoms. Conclusions: ELA was predictive of high concentrations of inflammatory markers at midlife for African Americans, but not whites. This pattern may be explained by an accelerated course of age-related disease development for African Americans. BMI = body mass index; CRP = C-reactive protein; CVD = cardiovascular diseases; E-selectin = endothelial leukocyte adhesion molecule-1; ELA = early life adversity; GCRC = general clinical research center; IL = interleukin; MIDUS = Midlife in the U.S. survey; SEP = socioeconomic position; sICAM-1 = soluble intercellular adhesion molecule-1.