Key points are not available for this paper at this time.
• Early life stress has been previously connected to long-term health risks through immune system dysregulation and inflammation. • Dietary habits may be one behavioral pathway through which early life stress is related to negative health outcomes. • Adolescents exposed to early life adversity consumed more pro-inflammatory diets than non-adopted adolescents. • More pro-inflammatory diets were associated with elevated levels of inflammatory markers in adolescents. • Dietary inflammation mediated the relationship between early institutional care and increased levels of inflammatory cytokine TNF-α. Early life stress (ELS) is tied to heightened risk of negative health outcomes and mortality across the lifespan. Recent research suggests chronic inflammation may be a key pathway from ELS to adverse health outcomes. ELS, measured as previous institutionalization (PI) in infancy and toddlerhood, is associated with increased inflammation in adolescence. The present study investigates the relationship between ELS and the Dietary Inflammatory Index (DII), and whether DII mediates the association between ELS and inflammation. Using data from the Early Life Stress and Cardiometabolic Health in Adolescence Study (N = 190, ages 12–21 years, N = 95 PI), we utilized multiple regression analyses to test the association between PI and DII from 24-hour dietary recalls in adolescence. We also tested whether DII mediated the previously observed association between ELS and three inflammatory markers: IL-6, CRP, TNF-α. Results revealed PI adolescents had significantly higher DII scores (M = 1.97, SD = 1.78) than non-adopted adolescents (M = 1.19, SD = 1.70), t(185) = -3.04, p = 0.003, indicating more pro-inflammatory diets in PI adolescents. DII significantly predicted levels of IL-6 (ß = 0.17, p = 0.027) and TNF-α (ß = 0.23, p = 0.001), such that higher DII scores were associated with increased levels of these inflammatory cytokines. Further, DII statistically and significantly mediated the indirect effect between PI and TNF-α (ß = 0.05, SE = 0.112, p = 0.027) such that PI youth had higher DII scores and, in turn, higher levels of TNF-α. These findings suggest dietary habits in PI adolescents may play a key role in their heightened levels of inflammation compared to non-adopted adolescents, particularly for TNF-α.
Glaser et al. (Tue,) studied this question.