1374-P: Ultra-processed Food Consumption and Cardiometabolic Risk in Individuals With and Without Type 1 Diabetes Mellitus

Abstract

Background: Ultra-processed foods (UPFs) contribute to almost 60% of energy intake in the American diet. The longitudinal association between UPF consumption and cardiometabolic risk is less known, especially in people with type 1 diabetes mellites (T1DM) who are at a higher risk of developing cardiometabolic diseases than people without diabetes (non-DM). Methods: We performed a longitudinal analysis of data from the Coronary Artery Calcification in Type 1 Diabetes study (T1DM: n=652; non-DM: n=764) collected at baseline and years 3, 6, and 14. Baseline age was 37.8±9.3 years. Dietary intake was assessed using a validated semi-quantitative food frequency questionnaire, and cardiometabolic biomarkers (BMI, waist circumference, triglycerides, HDL-C, LDL-C, and systolic and diastolic blood pressure) were measured at all four time points. NOVA food classification was used to compute UPF consumption (servings/d). Linear mixed-effects models were used to estimate longitudinal associations of UPF consumption with cardiometabolic risk, adjusting for potential confounders (race, age, sex, education, physical activity, smoking, energy intake, antihypertensive and lipid-lowering drugs, and diabetes duration for T1DM). Results: People with T1DM consumed more UPFs, including processed meat, soft drinks, salty snacks, and margarine, than non-DM at baseline (8.7±7.8 vs. 7.3±6.7 servings/d, P<0.01). Higher UPF consumption was associated with higher anthropometric measures (BMI: β=0.01±0.01, waist circumference: β=0.03±0.01), worse lipid levels (triglycerides: β=0.21±0.09, HDL-C: β=-0.04±0.02), and higher systolic blood pressure (β=0.05±0.02) when adjusted for diabetes status and other covariates (all P<0.05). Conclusion: UPF consumption significantly worsened the cardiometabolic profile over time in people with and without T1DM. Decreasing UPF intake may reduce the risk of developing cardiometabolic diseases across the lifespan. Disclosure T.Pang: None. A.C.Alman: None. H.L.Gray: None. G.Dagne: None. A.Basu: None. A.W.Buro: None. J.K.Snell-bergeon: None. Funding American Diabetes Association (7-13-CD-10 to J.K.S-B.), (7-13-CE-02 to A.C.A.); National Heart, Lung, and Blood Institute (R01HL079611, R01HL113029); Diabetes Endocrinology Research Center (P30DK57516, P30DK1116073)