The United States is characterized by persistent and growing socioeconomic and race-based disparities in a wide range of health outcomes, including chronic inflammation. Measuring inflammation in early adulthood is important because it predicts risk for major public health burdens, including cardiovascular disease, metabolic syndrome, disability, and adverse birth outcomes. As such, there is an urgent need to understand the pathways through which social and economic environments contribute to chronic inflammation, and recent research provides compelling evidence that infancy and childhood are sensitive time periods during which exposure to socioeconomic disadvantage can have lasting effects on health, including the regulation of inflammation. The proposed research applies a biosocial life course approach to investigate the early-life origins of disparities in chronic inflammation, with the following specific aims: 1) Document socioeconomic disparities in chronic inflammation, and investigate body fat, health behaviors, and psychosocial stress as pathways mediating associations between socioeconomic status and inflammation; 2) Investigate early-life socioeconomic status?and correlated exposures?as predictors of chronic inflammation in young adulthood; and 3) Evaluate chronic inflammation as a risk factor for adverse birth outcomes, including pregnancy complications, pre-term delivery, and lower birth weight.
These aims will be implemented using existing data from five waves of the National Longitudinal Study of Adolescent to Adult Health (Add Health), a large, nationally-representative cohort with rich contextual and behavioral data, as well as physiological and health data, collected at multiple time points over the life course. C-reactive protein (CRP)?a key biomarker of inflammation?will be the primary dependent variable in a series of structural equation models (SEM) that test the hypothesis that lower socioeconomic status contributes to higher inflammation through its associations with increased body fat, health-damaging behaviors, and increased exposure to psychosocial stressors. Models representing sensitive time period effects (stronger and independent associations between early SES and adult CRP), cumulative adversity (additive effects of early and later SES), and environmental continuity (early SES predicts adult SES) will also be compared to reveal the life course processes through which early-life SES contributes to disparities in chronic inflammation in adulthood. In addition, since dysregulated inflammation is associated with adverse birth outcomes, pregnancy represents an important life stage for evaluating the public health significance of chronic inflammation. Among the female participants who have transitioned to motherhood, we will test the hypothesis that elevated CRP?during pregnancy, as well as preconception? predicts pregnancy/birth complications, pre-term delivery, and offspring birth weight. Knowledge gained from these analyses may provide evidence that inequalities in chronic inflammation trace their origins to experiences early in the life course, and thereby inform future efforts at prevention.
Chronic inflammation contributes to adverse birth outcomes and cardiovascular and metabolic diseases?all of which represent costly public health problems in the United States. It is therefore important to understand the factors that lead to chronic inflammation in order to guide efforts aimed at prevention. The proposed research will contribute by advancing knowledge of how social and economic environments experienced during development increase risk for chronic inflammation in adulthood.
