Chronic disease prevalence among children and adolescents is rising, which is thought to result in part from elevations in allostatic load (AL). AL is the cumulative physiological dysregulation that results from exposure to biological, social and environmental stressors over time. Socioeconomic disparities in chronic disease and AL have been well-documented in adult populations, including links between childhood socioeconomic disadvantage (CSD) and AL, yet little is known as to whether CSD may begin to impact AL earlier in life. Differential exposure and vulnerability to stress among racial/ethnic minorities may increase risk for elevated AL among those experiencing CSD. Framed by the Life Course Perspective and the Allostatic Load Framework, the purpose of this dissertation was to determine the best measurement approach for AL, examine direct and indirect pathways between CSD and AL through several environmental and behavioral mediators, and determine whether these relationships varied across race/ethnicity. This was a cross-sectional, correlational study of 1900 adolescents (aged 12 to 18) from four waves (2003 to 2010) of the National Health and Nutrition Examination Survey (NHANES). We constructed latent variables for AL and CSD, based upon biologic and self-reported indicators. Smoking and lead exposure were measured with biomarkers, while nutrition, physical activity, and race/ethnicity were self-reported. Structural equation modeling (SEM) was used to examine relationships between latent construct variables and measured mediating variables across three race/ethnicity groups. The data best supported a unidimensional AL factor structure, with the highest factor loadings found for metabolic indicators. The only significant total effects pathway for CSD on AL was for Whites, indicating the model best explained AL variance for this group. There were small, positive direct effects pathways significant for African Americans (AAs) and Whites, indicating higher CSD predicted higher AL for those groups. A single indirect pathway between CSD and AL mediated by lead was significant for AA adolescents, though the reversed directionality suggests a need for a different measurement approach for cumulative lead exposure. These findings highlight the importance of exposure to CSD as a predictor for development of AL for adolescents, while also elucidating different mechanisms at play across different racial/ethnic populations
