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Childhood socioeconomic status and inflammation: A systematic review and meta-analysis
Author(s) -
Izabela Milaniak,
Sara R. Jaffee
Publication year - 2019
Publication title -
brain, behavior, and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.557
H-Index - 153
eISSN - 1090-2139
pISSN - 0889-1591
DOI - 10.1016/j.bbi.2019.01.018
Subject(s) - meta analysis , medicine , inflammation , socioeconomic status , psycinfo , body mass index , bivariate analysis , systemic inflammation , demography , gerontology , medline , environmental health , population , biology , biochemistry , statistics , mathematics , sociology
Recent research suggests that risk for chronic diseases of aging including cardiovascular disease, diabetes, and even cancer can be programmed early in the lifespan as a result of exposure to chronic stressors like low socioeconomic status (SES) that are hypothesized to promote a pro-inflammatory response in immune cells that results in chronic, systemic inflammation. The present paper conducted a meta-analysis to establish whether exposure to low (versus higher) SES in childhood and adolescence is associated with higher levels of inflammation (as measured by C-reactive protein, IL-6, and fibrinogen) concurrently and in adulthood. We conducted meta-analyses with both unadjusted bivariate associations between SES and inflammation and with adjusted associations that controlled for a range of covariates including demographic factors, body mass index, smoking, physical activity and current SES. A systematic review of Pubmed and PsycINFO identified a total 35 studies (26 with unadjusted and 31 adjusted effect sizes) to be included in the meta-analysis. Random-effects meta-analysis showed that individuals who were exposed to low SES in childhood and adolescence had significantly higher levels of inflammatory markers (r = -0.07, p < .001, 95% CI = -0.09, -0.05). This association remained significant in adjusted analyses (r = -0.06, p < .001, 95% CI = -0.09, -0.03). However, the relationship between childhood SES and inflammation was non-significant in a meta-analysis with longitudinal studies that all controlled for adulthood SES (r = -0.03, p = .356, 95% CI = -0.08, 0.03). Future longitudinal research should utilize measurement of inflammatory markers at multiple time points to further examine the complex relationships between SES and health both in childhood and adulthood.

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