Associations among discrimination, genetic susceptibility to inflammation, and C-reactive protein.

Genetic liability to inflammation may lead to heightened perception of discrimination (gene-environment correlation) or interact with discrimination exposure to amplify inflammation risk (gene-environment interaction). The present study examined the interrelationship between genetic predisposition, self-reported discrimination exposure, and inflammatory phenotypes. Data came from 6344 participants in the 2016 Health and Retirement Study Venous Blood Study. Polygenic risk scores for high-sensitivity C-reactive protein (PRS-hsCRP) were derived from genome-wide association study summary statistics. Daily discrimination was assessed using the Everyday Discrimination Scale and hsCRP was quantified from serum and natural log-transformed for analysis. Linear regression models were fit using multiple imputation, and analyses were stratified by ethnicity. Perceived discrimination exposure was positively associated with ln(hsCRP) levels among European American (b = 0.06, 95% CI: 0.02 to 0.10,  = 0.005) and Hispanic participants (b = 0.11, 95% CI: 0.01 to 0.21,  = 0.033), even after adjusting for genetic liability. No significant association was observed among African American participants. Additionally, no association between PRS-hsCRP and discrimination was found in European American or Hispanic groups. Among African American participants, higher PRS-hsCRP was associated with lower reported discrimination (b = -0.07, 95% CI: -0.13 to -0.01,  = 0.025). No significant gene-environment interactions were found within each ethnic group. We found no evidence to support a gene-environment interaction or gene-environment correlation. Perceived discrimination may influence inflammation independently of genetic liability. Nonetheless, further research is needed to replicate and validate these findings.