1082-OR: Associations and Interactions of Genetic Predispositions for Taste Preferences and Socioeconomic Status with Hyperpalatable Food Intake

Introduction and Objective: Hyperpalatable foods (HPFs)-high in sugar, salt, and fat and designed to maximize taste and reward--contribute disproportionately to obesity and type 2 diabetes risk. Susceptibility to overconsume HPFs is highly variable, partially due to genetic and environmental factors. Here, we aimed to quantify the contribution of genetic predisposition for taste preferences to HPF intake and test whether higher educational attainment (a proxy for high socioeconomic status [SES]) may attenuate these genetic effects. Methods: We ran genome-wide association studies of sweet, salty, and fatty food preferences in the UK Biobank (N ~ 180k) and built weighted polygenic scores (PGS) in two cohorts: the Framingham Heart Study and Muti-Ethnic Study of Atherosclerosis. We used generalized linear models to estimate associations of taste preference PGS (per SD) with HPF intake (servings/week, estimated from food frequency questionnaires) and tested for PGS-by-education interactions, adjusting for potential confounders. Cohort-specific estimates were combined and interactions jointly tested via random effects meta-analysis. Results: In adjusted meta-analyses, higher taste preference PGS predicted higher consumption of corresponding HPFs. For example, higher sweet preference PGS predicted higher sugar-sweetened beverage intake (P = 0.017), higher salt preference PGS predicted higher salty snacks intake (P = 0.007), and higher fat preference PGS predicted higher fried food intake (P = 0.041). No PGS-by-education interactions were significant in meta-analyses; however, several cohort-specific interaction tests indicated attenuated PGS-HPF associations among individuals with higher educational attainment. Conclusion: Genetic predispositions for taste preferences associate with HPF intake. Further exploration of our preliminary PGS-by-SES interactions is warranted to inform tailored dietary interventions in these sub-groups to help mitigate HPF-associated metabolic disease risk. Disclosure J.E. Gervis: None. K. Westerman: None. M. Sevilla-Gonzalez: Research Support; Current; Novo Nordisk. P.A. Hanson: None. D. Haslam: None. A. Manning: None. M. Udler: Advisory Panel; Ended; Novo Nordisk. Research Support; Current; Novo Nordisk. J. Merino: None. S. Cromer: Other - Spouse is employee of Depuy Synthes; Current; Johnson & Johnson. Funding American Diabetes Association (7-21-JDFM-005)