Socioeconomic status in childhood and C reactive protein in adulthood: a systematic review and meta-analysis

Abstract

Background Inflammation plays a central role in cardio-metabolic disease and may represent a mechanism linking low socioeconomic status (SES) in early life and adverse cardio-metabolic health outcomes in later life. Accumulating evidence suggests an association between childhood SES and adult inflammation, but findings have been inconsistent. Methods We conducted a systematic review and meta-analysis of observational studies to quantify the association between childhood (age <18 years) SES and the inflammatory marker C-reactive protein (CRP) in adulthood. Studies were identified in Medline and Embase databases, and by reviewing the bibliographies of articles published from 1946 through to December 2015. Study-specific estimates were combined into meta-analyses using random-effects models. Results Fifteen of 21 eligible studies (n = 43,629) were ultimately included in two separate meta-analyses. Compared with those from the most advantaged families, participants from the least advantaged families had 25% higher CRP levels (ratio change in geometric mean CRP: 1.25; 95% confidence interval: 1.19, 1.32) in minimally adjusted analyses. This finding was attenuated by the inclusion of adult body mass index (BMI) in adjusted models, suggesting BMI has a strong mediating role on CRP levels. Conclusions We observed an inverse association between childhood SES and adulthood CRP, potentially mediated through BMI. Investigating how childhood SES is associated with childhood BMI and CRP would provide insight into the effective timing of social and clinical interventions to prevent cardio-metabolic disease.

Understanding associations of early-life adversities with mid-life inflammatory profiles: Evidence from the UK and USA

“…the review included general indicators of family environment such as parental divorce, rather than specific adversities. Our 1958 cohort finding of a child socioeconomic disadvantage association with elevated adult CRP agrees with a larger review (for 14 of 21 included studies N>1,000) 13 . Regarding magnitude of associations, our findings concur with previous work suggesting small effects for abuse 12 and moderate associations for childhood socioeconomic disadvantage 13 .…”

“…Regarding the latter, one possible mechanism identified in the literature involves the inflammatory response: some evidence exists to suggest that early-life adversities are associated with later inflammation [8][9][10][11][12][13] and inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) predict subsequent health outcomes including depression, CVD and mortality [14][15][16][17] .…”

“…Such knowledge gaps are important because Mendelian randomisation studies suggest that adiposity causally influences inflammation 20,21 . Alternatively, because socioeconomic disadvantage in adulthood is associated with elevated inflammation 25,26 , associations for early-life adversities could reflect life-course continuities in disadvantage 11,13 . Finally, evidence is limited on the relationship between specific types of early-life adversities and inflammatory markers, in particular for maltreatments, which are typically examined together without an understanding of possible differential effects.…”

C-reactive protein and other biomarkers—the sense and non-sense of using inflammation biomarkers for the diagnosis of severe bacterial infection

“…(Table 3). Moreover, female gender, Afro-American descent, obesity, periodontal disease, alcoholism, diabetes mellitus, uremia, chronic fatigue, and even socioeconomic status (Liu et al 2017) all are associated with elevated CRP levels. Mitigated CRP values can be found in systemic lupus erythematosus (SLE) as type-1 interferons, which are largely increased in SLE, inhibit CRP synthesis (Kushner 2015) (Figure.…”

Gene regulation contributes to explain the impact of early life socioeconomic disadvantage on adult inflammatory levels in two European cohort studies

“…Systemic inflammation is also one of the most studied pathways in the context of the social-to-biological transition 4,5,6,7,8 . Although early life disadvantaged socioeconomic conditions have been consistently shown to lead to elevated levels of inflammation in adulthood 9 , the underlying biological processes through which those socioeconomic exposures are embodied remain unclear.…”