ArticleNutrition journal2024
Disproportionately higher cardiovascular disease risk and incidence with high fructose corn syrup sweetened beverage intake among black young adults-the CARDIA study.
Article in Nutrition journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Donor-derived microbial engraftment and gut microbiota shifts associated with weight loss following fecal microbiota transplantation.Applied and environmental microbiology · 2025Trial
- Plasma Lipid Profile Among Perimenopausal Latvian Women in Relation to Dietary Habits.Nutrients · 2025Trial
- Diet, the protective bridge connecting nutrition and cardiovascular health: A review.Food chemistry: X · 2026Review
- Adolescent high fructose consumption induces cardiac dysfunction in adulthood via elevated histone acetylation.Translational pediatrics · 2026Article
- Exploring Glyoxalase Strategies for Managing Sugar-Induced Chronic Diseases.Life (Basel, Switzerland) · 2025Article
- Disproportionately higher asthma risk and incidence with high fructose corn syrup, but not sucrose intake, among Black young adults: the CARDIA Study.Public health nutrition · 2025Article
- The Effect of Boric Acid on Oxidative Stress, Inflammation, and Apoptosis in Embryonic and Fetal Tissues Damage Caused by Consumption of High-Fructose Corn Syrup in Pregnant Rats.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
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2 authors.
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Abstract
backgroundThe black/white heart disease mortality disparity began increasing in the early 1980's, coincident with the switch from sucrose to high-fructose-corn-syrup/(HFCS) in the US food supply. There has been more fructose in HFCS than generally-recognized-as-safe/GRAS, which has contributed to unprecedented excess-free-fructose/(unpaired-fructose) in foods/beverages. Average- per-capita excess-free-fructose, from HFCS, began exceeding dosages/(5-10 g) that trigger fructose-malabsorption in the early 1980's. Fructose malabsorption contributes to gut-dysbiosis and gut-in-situ-fructosylation of dietary peptides/incretins/(GLP-1/GIP) which forms atherosclerotic advanced-glycation-end-products. Both dysregulate gut endocrine function and are risk factors for cardiovascular disease/(CVD). Limited research shows that African Americans have higher fructose malabsorption prevalence than others. CVD risk begins early in life.
methodsCoronary-Artery-Risk-Development-in-Adults/(CARDIA) study data beginning in 1985-86 with 2186 Black and 2277 White participants, aged 18-30 y, were used to test the hypothesis that HFCS sweetened beverage intake increases CVD risk/incidence, more among Black than White young adults, and at lower intakes; while orange juice-a low excess-free-fructose juice with comparable total sugars and total fructose, but a 1:1 fructose-to-glucose-ratio, i.e., low excess-free-fructose, does not. Cox proportional hazards models were used to calculate hazard ratios.
resultsHFCS sweetened beverage intake was associated with higher CVD risk (HR = 1.7) than smoking (HR = 1.6). CVD risk was higher at lower HFCS sweetened beverage intake among Black than White participants. Intake, as low as 3 times/wk, was associated with twice the CVD risk vs. less frequent/never, among Black participants only (HR 2.1, 95% CI 1.2-3.7; P = 0.013). Probability of an ordered relationship approached significance. Among Black participants, CVD incidence jumped 62% from 59.8/1000, among ≤ 2-times/wk, to 96.9/1000 among 3-6 times/wk consumers. Among White participants, CVD incidence increased from 37.6/1000, among ≤ 1.5-times/wk, to 41.1/1000, among 2 times/wk-once/d - a 9% increase. Hypertension was highest among Black daily HFCS sweetened beverage consumers.
conclusionThe ubiquitous presence of HFCS over-the-past-40 years, at higher fructose-to-glucose ratios than generally-recognized-as-safe, may have contributed to CVD racial disparities, due to higher fructose-malabsorption prevalence among Black individuals, unpaired/excess-free-fructose induced gut dysbiosis and gut fructosylation of dietary peptides/incretins (GLP-1/GIP). These disturbances contribute to atherosclerotic plaque; promote incretin insufficiency/dysregulation/altered satiety/dysglycemia; decrease protective microbiota metabolites; and increase hypertension, CVD morbidity and mortality.
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