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Mehmet Kanbay, Laura Gabriela Sanchez-Lozada, Magdalena Madero, Richard J. Johnson, Reply, Nephrology Dialysis Transplantation, Volume 26, Issue 10, October 2011, Pages 3420–3421, https://doi.org/10.1093/ndt/gfr415
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Dr White has argued that fructose effects on uric acid are unlikely to have a role in hypertension and metabolic syndrome since only large doses appear to cause elevated blood pressures in humans [ 1 ] and because intake of added sugars has started to decrease over the last few years. First, the study by Perez-Pozo et al. [ 1 ] was purposely a very high dose of fructose so one might be able to see effects rapidly; indeed, healthy male subjects fed fructose showed a significant rise in blood pressure, triglycerides, measures of insulin resistance and a decrease in high-density lipoprotein cholesterol after only 2 weeks; indeed, 25% developed de novo metabolic syndrome. The amount of fructose consumed today is not expected to cause hypertension and obesity in days (unless you are Morgan Spurlock eating at fast food restaurants at each meal) but rather in years. Indeed, the intake of added sugars has been associated with elevated blood pressure in two studies [ 2 , 3 ]; likewise, reducing soft drinks is associated with reduced blood pressure [ 4 ]. In two recent clinical trials, reducing fructose intake from added sugars had significant improvements in blood pressure, especially in those with ‘dipper’ physiology [ 5 , 6 ]. The mechanism for the increase in blood pressure is likely from the intracellular effects of uric acid, given the accruing clinical and experimental data [ 1 , 7–9 ].
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