Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease.
By Richard J. Johnson, M. Segal, Y. Sautin, T. Nakagawa, D. Feig, D. Kang, Michael S. Gersch, S. Benner, L. Sánchez-Lozada. American Journal of Clinical Nutrition, 2007
1,066 citations recorded by the source corpus.
Currently, we are experiencing an epidemic of cardiorenal disease characterized by increasing rates of obesity, hypertension, the metabolic syndrome, type 2 diabetes, and kidney disease. Whereas excessive caloric intake and physical inactivity are likely important factors driving the obesity epidemic, it is important to consider additional mechanisms. We revisit an old hypothesis that sugar, particularly excessive fructose intake, has a critical role in the epidemic of cardiorenal disease. We also present evidence that the unique ability of fructose to induce an increase in uric acid may be a major mechanism by which fructose can cause cardiorenal disease. Finally, we suggest that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease, and we provide a list of testable predictions to evaluate this hypothesis.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/dcaf78b12db79b39d2b1bfc8f2abc392e023eff6
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Citations in the corpus
- Pro v Con Debate: Role of sugar sweetened beverages in obesity Resolved: there is sufficient scientific evidence that decreasing sugar-sweetened beverage consumption will reduce the prevalence of obesity and obesity-related diseases (2013, positive): “Fructose is the only sugar known to increase serum uric acid levels by increasing adenosine triphosphate degradation to adenosine monophosphate, a uric acid precursor (53).”
- Sugar-sweetened beverages and risk of obesity and type 2 diabetes: Epidemiologic evidence (2010, background): “ATP fromADP,which in turn serves as a substrate for uric acid formation [96].”
- Fructose consumption as a risk factor for non-alcoholic fatty liver disease. (2008, background): “Many studies suggest that the mechanism by which sugar or HFCS may induce metabolic syndrome is due to the fructose content [13,14,15,16].”