THE RELATIONSHIP BETWEEN SOCIOECONOMIC STATUS AND POLYGENIC RISK SCORES ON BODY MASS INDEX AMONG NON-HISPANIC WHITE AMERICANS

The prevalence of obesity in the United States remains high, especially among individuals
of low socioeconomic status (SES). Studies examining the joint influence of genetics and
social factors, such as early life SES and education, in association with obesity remain
underreported. These social factors might be related to a heightened risk of obesity. Genetic
factors may further exacerbate the high-weight predisposition of those at risk. Genetic and
social factors may act together to shape individuals’ weight. Therefore, this research examined (a) whether the association between polygenic risk for BMI (PGS-BMI) and Body
Mass Index (BMI) is independently modified by early life SES and adult education, (b)
whether the association between PGS and BMI varies by the combination of early life relative SES and adult education, and (c) whether the association between PGS, BMI, early
life SES, and adult education varies by gender. Using data from the U.S. Health and Retirement Study (HRS), I find that the association between PGS-BMI and BMI varied by
level of adult education but was not modified by early life SES in gendered pooled analysis.
However, in gender stratified analysis, education was negatively associated with BMI
among women with average or low genetic risk of high BMI while adult education did not
moderate the relationship between PGS-BMI and BMI. Among men, the association was
modified by early life SES and adult education: for men with high early life SES and high or average genetic risk, education was negatively associated with BMI, however among
low early-life SES men, education associated with obesity only among those with a low
genetic risk. This results in a multiplier effect as those with the least risk gained the largest
benefit from increasing education while those at the highest risk gained little from increasing education. In conclusion, this research indicates the importance of how the social environment and genetic propensity interact to produce outcomes, which may be further differentiated by gender. In line with fundamental cause theory and life course theory, I argue
that adult education and childhood SES are most influential among those with the least
genetic risk for high BMI.