All ETDs from UAB

Advisor(s)

Elizabeth Baker
David Warner

Committee Member(s)

Gabe Miller
Myles Moody
Noha Sharafeldin

School

College of Arts and Sciences

Document Type

Thesis

Department (new version)

Medical Sociology

Date of Award

9-9-2024

Abstract

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 ex-amined (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 rel-ative 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 Re-tirement 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 increas-ing education. In conclusion, this research indicates the importance of how the social en-vironment and genetic propensity interact to produce outcomes, which may be further dif-ferentiated 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.

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