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In prior work, we identified a novel gene-by-stress association of  EBF1 ’s common variation (SNP rs4704963) with obesity (i.e., hip, waist) in Whites, which was further strengthened through multiple replications using our synthetic stress measure. We now extend this prior work in a precision medicine framework to find the risk group using harmonized data from 28,026 participants by evaluating the following: (a)  EBF1  SNPxSTRESS interaction in Blacks; (b) 3-way interaction of  EBF1  SNPxSTRESS with sex, race, and age; and (c) a race and sex-specific path linking  EBF1  and stress to obesity to fasting glucose to the development of cardiometabolic disease risk. Our findings provided additional confirmation that genetic variation in  EBF1  may contribute to stress-induced human obesity, including in Blacks ( P  = 0.022) that mainly resulted from race-specific stress due to “racism/discrimination” ( P  = 0.036) and “not meeting basic needs” ( P  = 0.053). The  EBF1  gene-by-stress interaction differed significantly ( P  = 1.01e−03) depending on the sex of participants in Whites. Race and age also showed tentative associations ( P s = 0.103, 0.093, respectively) with this interaction. There was a significant and substantially larger path linking  EBF1  and stress to obesity to fasting glucose to type 2 diabetes for the  EBF1  minor allele group (coefficient = 0.28, P = 0.009, 95% CI = 0.07-0.49) compared with the same path for the  EBF1  major allele homozygotes in White females and also a similar pattern of the path in Black females. Underscoring the race-specific key life-stress indicators (e.g., racism/discrimination) and also the utility of our synthetic stress, we identified the potential risk group of  EBF1  and stress-induced human obesity and cardiometabolic disease.

translational psychiatry

Evaluating the precision of EBF1 SNP x stress interaction association: sex, race, and age differences in a big harmonized data set of 28,026 participants