Life course disadvantage and systemic inflammation : the role of psychosocial functioning

Thesis (Ph. D.)--University of Rochester. Margaret Warner Graduate School of Education and Human Development, 2015.Experiences of disadvantage over the life course, including childhood adversity and low socioeconomic status (SES), have been linked to low-grade systemic inflammation, a potential risk factor for cardiovascular and other chronic diseases, late-life disability, and earlier mortality. Using data from the Midlife in the United States (MIDUS) survey, this study investigated the extent to which psychosocial functioning mediates or moderates associations of childhood adversity and low SES with systemic inflammation among middle-aged and older adults in the United States. Analytic aims were informed by developmental, reserve capacity, and stress process models, which outline ways in which the preceding exposures might adversely affect psychosocial functioning, thereby increasing susceptibility to the emotional, behavioral, and biological concomitants of stress. Structural equation modeling with latent variables revealed adverse effects of childhood adversity and low SES on both psychosocial resources and psychological distress, although neither psychosocial construct was significantly associated with inflammation. Despite minimal evidence of mediation in full-sample analyses, multiple groups analyses indicated that in women, there were small but statistically significant indirect effects of both exposures on inflammation transmitted through psychological distress and bio-behavioral risk. In Blacks/African-Americans, childhood adversity exerted an indirect effect through the same pathway. Furthermore, resources and distress interacted with SES to predict inflammation in men. Contrary to hypotheses, inflammation was positively associated with resources and negatively associated with distress at higher levels of SES, effects that were not attenuated by bio-behavioral risk. However, in supplemental analyses, effects of resources and distress on IL-6 were in the expected directions at lower levels of SES. Results highlight the psychological cost of disadvantage over the life course, as well as the potential role of associated distress in pathways from social exposures to physiological dysregulation and disease risk. Results also underscore the need for further investigation of how socioeconomic and psychosocial factors interact in giving rise to systemic inflammation