Intersecting Social Disadvantages and Chronic Inflammation: Exploring Heterogeneity and Proximate Risk Factors

Open Access
- Author:
- Richman, Aliza Dresner
- Graduate Program:
- Sociology
- Degree:
- Doctor of Philosophy
- Document Type:
- Dissertation
- Date of Defense:
- June 18, 2014
- Committee Members:
- Stephen Matthews, Dissertation Advisor/Co-Advisor
Melissa Hardy, Committee Member
Jason Ramone Thomas, Committee Member
Marianne Messersmith Hillemeier, Special Member - Keywords:
- Social Disadvantage
Chronic Inflammation
C-reactive protein
Health - Abstract:
- Disadvantaged social statuses, such as being female, poor, or a minority, are associated with increased psychosocial stress (Chida and Hamer 2008; Hänsel et al. 2010; Johnson, Abbasi, and Master 2013). Chronic psychosocial stress has the capacity to cause physiological dysregulation by marking immune cells with proinflammatory phenotypes, increasing circulating C-reactive protein concentrations within the body (T. V. Johnson et al. 2013; Segerstrom and Miller 2004). As an indicator of chronic low-grade inflammation, C-reactive protein is associated with premature chronic disease onset and mortality (Danesh et al. 2004; Kaptoge et al. 2010; Ridker et al. 2000). This dissertation expands on prior work by examining chronic inflammation at the intersection of race and ethnicity, gender, and socioeconomic status to understand which individuals in society are most vulnerable to the cumulative effects of social disadvantage. Further, I explore body composition, physical activity, smoking, and alcohol consumption as proximate risk factors potentially mediating the effect of social disadvantage on C-reactive protein. Using data from the National Health and Nutrition Examination Survey 2007-2010, findings reveal that all race and ethnicity by socioeconomic status demographic subgroups experience higher inflammation concentrations compared to non-poor white males and females, with the exception of non-poor Hispanic women who exhibit C-reactive protein levels on par with that of non-poor white women. Disparities in inflammation on account of social disadvantage are most evident among those aged 45-64 years and diminish for those 65 and older in both men and women. Among women, proximate risk factors account for variation in inflammation levels among poor white women, poor black women, and non-poor black women. Poor Hispanic women’s elevated inflammation levels persist after adjustment for proximate risk factors individually and as composite lifestyles. Similarly, among all male demographic subgroups, proximate risk factors, whether analyzed individually or as composite lifestyles, attenuate the strength of the focal association, but inflammation disparities persist. Thus, proximate risk factors explain higher C-reactive protein concentrations among most socially disadvantaged women, but only partially account for elevated inflammation levels among socially disadvantaged men. This study emphasizes that mechanisms explaining chronic low-grade inflammation vary across gender, race and ethnicity, socioeconomic status, and age group and interventions aimed to reduce health disparities in inflammation should reflect these heterogeneous pathways.