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(OR04-01-26) Ultra-Processed Food Intake and Long-Term Cognitive Decline: A Weighted Analysis in the ARIC Cohort

Saturday, July 25, 2026
8:30 AM - 8:42 AM ET
Location: Maryland Ballroom C

    Presenting Author(s)

  • Muzi Na, PhD, MHS, FASN

    Associate Professor
    The Pennsylvania State University
    University Park, Pennsylvania, United States

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

    • Co-Author(s)

  • SD

    Shutong Du

    AbbVie, Illinois, United States

  • AF

    Alison Fohner

    University of Washington, Washington, United States

  • HK

    Hyunju Kim, PhD MPH

    Assistant Professor
    University of Washington
    SEATTLE, Washington, United States

  • Casey M. Rebholz, PhD, MPH, MNSP, MS

    Associate Professor
    Johns Hopkins Bloomberg School of Public Health
    Baltimore, Maryland, United States

Disclosure(s):
Muzi Na, PhD, MHS, FASN: No relevant financial relationship(s) with ineligible companies to disclose.
Casey M. Rebholz, PhD, MPH, MNSP, MS: American Diabetes Association: Independent Contractor (including contracted research) (Ongoing)
Objectives: While diet is a modifiable risk factor for dementia, the long-term impact of ultra-processed food (UPF) on cognitive trajectory remains unclear due to selection bias and short follow-up in prior studies. In the U.S., adults consume ~53% of calories from UPFs (~7–10 servings/day). We investigated the association between UPF intake and 30-year cognitive decline using weighting methods to address selection bias.

Methods: This prospective study utilized data from the Atherosclerosis Risk in Communities (ARIC) Study (n = 12,039; mean age 57 ± 6 y; mean follow-up 14 ±10 y). Energy-adjusted UPF intake (servings/day) was derived at baseline via validated questionnaires (NOVA system). Cognitive function was assessed at five visits (DWRT, DSST, WFT) to derive global z-scores. Mixed-effects models with linear splines (knot at 15 years) assessed associations between daily UPF servings and cognitive scores, adjusting for socio-demographics, lifestyle, clinical factors, diet quality (HEI-2015), and APOE genotype. Inverse probability weighting with stabilized weights accounted for non-response due to survival and attendance probabilities.

Results: Higher UPF intake was associated with faster cognitive decline during the initial 15-year period. In weighted, fully adjusted models, each additional daily serving of UPF was associated with a faster decline in global cognitive z-scores (β = -0.001; 95% CI: -0.003, -0.0004; p = 0.04) and DSST z-scores (β = -0.003; 95% CI: -0.004, -0.002; p < 0.001). Associations beyond 15 years were not statistically significant

Conclusions: Higher baseline UPF consumption is associated with faster 15-year cognitive decline, independent of diet quality or APOE, and unlikely due to selection bias from survival and attendance. Given high UPF intake in the U.S., even modest reductions could significantly benefit brain aging.

Funding Sources: NIH