Testing Life Course Models Whereby Juvenile and Adult Adversity Combine to Influence Speed of Biological Aging.

The present study extends prior research on the links between social adversity and aging by employing more comprehensive measures of adversity and a new gene expression index of aging. Hierarchical regression and 20 years of data from a sample of 381 black Americans were used to test models regarding the impact of social adversity on speed of aging. Consistent with the early life sensitivity model, early adversity continued to predict accelerated aging after controlling for adult adversity. Contrary to the pathway model, adult adversity was not related to aging following controls for early adversity. The cumulative stress model received partial support as high adversity during adulthood amplified the effect of early adversity on aging. Finally, consonant with the social change model, low adversity during adulthood buffered the effect of early adversity on aging. These findings held after controlling for health behaviors such as smoking, diet, and exercise.

Discrimination, segregation, and chronic inflammation: Testing the weathering explanation for the poor health of Black Americans.

Several studies have reported a relation between race-related stressors and the poor health of Black Americans. Such findings raise questions regarding the mediating biological mechanisms that might account for this link. The present study investigated elevated systemic inflammation, a factor shown to be a strong predictor of chronic illness and mortality in all ethnic populations, as a possible factor. Using 7 waves of data from the Family and Community Health Study, collected over a 20-year period from over 400 Black Americans, we investigated the extent to which exposure to discrimination and segregation at various points in the life course predicted adult inflammation at age 28. Our analyses examined whether cumulative stress, stress generation, or predictive adaptive response (PAR) models best accounted for any associations that existed between these race-related stressors and adult inflammation. At every wave of data collection, assessments of discrimination and segregation were related to adult inflammation. However, multivariate analyses using structure equation modeling indicated that the PAR model best explained the effect of these race-related stressors on inflammation. Exposure to discrimination and segregation during the juvenile years predicted adult inflammation and amplified the inflammatory effect of adult exposure to these race-related stressors. These effects were considerably more robust than that of traditional health risk factors such as diet, exercise, smoking, and low SES. Implications of these findings are discussed, including the limitations of the widely accepted risk factor approach to increasing the health of Black Americans. (PsycINFO Database Record