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(OR20-06-26) Genetic Predispositions for Taste Preferences Associate With Hyperpalatable Food Intake and Metabolic Disease Risk

Monday, July 27, 2026
3:30 PM - 3:42 PM ET
Location: Maryland Ballroom D

    Presenting Author(s)

  • Julie E. Gervis, PhD

    Postdoctoral Research Fellow
    Massachusetts General Hospital
    Boston, Massachusetts, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • Kenneth E. Westerman, PhD

    Assistant Professor
    Massachusetts General Hospital
    Boston, Massachusetts, United States

  • MM

    Monica Mars

    Wageningen University and Research, Netherlands

  • SC

    Sara J. Cromer

    Massachusetts General Hospital, United States

  • MU

    Miriam S. Udler

    Massachusetts General Hospital, United States

  • JC

    Joanne B. Cole

    University of Colorado Anschutz Medical Campus, United States

Disclosure(s):
Julie E. Gervis, PhD: No relevant financial relationship(s) with ineligible companies to disclose.
Kenneth E. Westerman, PhD: No relevant financial relationship(s) with ineligible companies to disclose.
Objectives: Hyperpalatable foods (HPFs)––high in sugar, salt, and fat and designed to maximize taste and reward––contribute disproportionately to obesity and type 2 diabetes (T2D) risk. Susceptibility to overconsume HPFs is highly variable and may be partially driven by inherited differences in taste preferences. Here, we evaluated whether genetic predispositions for sweet, salty, and fatty taste preferences predict HPF intake and contribute to HPF-associated metabolic disease risk.

Methods: We derived taste preference traits in the UK Biobank (UKB) by applying sensory databases of taste intensity values for foods to food liking questionnaire data. We ran GWAS of taste preferences in a UKB training set (N~160k), then built polygenic scores (PGS) capturing cumulative genetic predispositions to prefer each taste in a held-out UKB testing set (N~330k). We tested for relationships between taste preference PGS (per SD) with intakes of groups of sweet (e.g., desserts/sweets, SSBs) and fatty/salty (e.g., processed meats, fatty condiments) HPFs estimated from 24-hour diet recalls; and with BMI (kg/m2) and T2D, before and after HPF adjustment. All models were adjusted for age, sex, genetic ancestry, and energy intake.

Results: In the held-out testing set, higher taste preference PGS were associated with higher intake of corresponding HPFs. For example, higher sweet preference PGS predicted higher intake of sweet HPFs (β = 7.2 g/day; P = 1.4×10-22) and higher fat and salt preference PGS predicted higher intake of fatty/salty HPFs (both β = 0.9 g/day; P = 6.5×10-9 and 3.4×10-9, respectively). For disease outcomes, positive associations were found for sweet preference PGS with BMI (β = 0.10 kg/m2; P = 8.5×10-28) and T2D risk (OR = 1.02; P = 0.025) and fat preference PGS with T2D risk (OR = 1.02; P = 9.4×10-3), all of which were partially or fully explained by PGS effects on HPF intake (P, after HPF adjustment = 1.0×10-6, 0.088 and 0.103, respectively).

Conclusions: Genetic predispositions for sweet and fat taste preferences associate with HPF intake and downstream obesity and T2D risk, highlighting a previously unrecognized role of taste preference genetics in HPF intake and the potential for taste preference PGS to inform tailored dietary interventions for HPF-associated metabolic diseases.

Funding Sources: Fund for Medical Discovery Clinical Research Fellowship Award