Abstract
Select trials of fructose overfeeding have been used to implicate fructose as a driver of cardiometabolic risk. We examined temporal trends of fructose dose in human controlled feeding trials of fructose and cardiometabolic risk. We combined studies from eight meta-analyses on fructose and cardiometabolic risk to assess the average fructose dose used in these trials. Two types of trials were identified: (1) substitution trials, in which energy from fructose was exchanged with equal energy from other carbohydrates and (2) addition trials, in which energy from fructose supplemented a diet compared to the diet alone. We included 64 substitution trials and 16 addition trials. The weighted average fructose dose in substitution trials was 101.7 g/day (95% CI: 98.4-105.1 g/day), and the weighted average fructose dose in addition trials was 187.3 g/day (95% CI: 181.4-192.9 g/day). Average fructose dose in substitution and addition trials greatly exceed national levels of reported fructose intake (49 ± 1.0 g/day) (NHANES 1977-2004). Future trials using fructose doses at real world levels are needed.
Highlights
With the increase in high-fructose corn syrup (HFCS) consumption since 1970s, there has been rising interest in the role of sugars toward the development of cardiometabolic diseases [1]
The present analysis aims to quantify the dose of fructose used in trials assessing the effects of fructose and cardiometabolic risk, and compare it to national levels of fructose consumption in the United States at the average and 95th percentile levels of intake based on the Frontiers in Nutrition | www.frontiersin.org
Two types of trials were identified for the purposes of this analysis-substitution trials, in which fructose was exchanged for equal amounts of energy from other carbohydrates, or addition trials, in which a control diet was supplemented with additional energy from fructose compared to the control diet alone without the excess energy
Summary
With the increase in high-fructose corn syrup (HFCS) consumption since 1970s, there has been rising interest in the role of sugars toward the development of cardiometabolic diseases [1]. Particular attention has focused on the “fructose hypothesis,” which suggests that the metabolic and endocrine responses unique to fructose are the main drivers in the etiology of obesity, diabetes, and cardiometabolic risk [2, 3]. While this perspective is well supported by lower. 617 reports reviewed in full: Glycemic Control: 60 Uric Acid: 35 Blood Pressure: 16 Body Weight (fructose): 81 Body Weight (fructose-containing SSBs): 117 Post Prandial Triglycerides: 48 Fasting Lipids: 167 NAFLD: 93. Select trials of fructose overfeeding have been used to implicate fructose as a driver of cardiometabolic risk
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