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Commentary| Volume 40, ISSUE 4, P287-295, August 2016

Sickeningly Sweet: Does Sugar Cause Chronic Disease? No

  • John L. Sievenpiper
    Correspondence
    Address for correspondence: John L Sievenpiper, MD, PhD, FRCPC, Toronto 3D Knowledge Synthesis and Clinical Trials Unit, St. Michael's Hospital, 6137-61 Queen Street East, Toronto, Ontario M5C 2T2, Canada.
    Affiliations
    Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada

    Division of Endocrinology and Metabolism, Department of Medicine, St. Michael's Hospital, Toronto, Ontario, Canada

    Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, St. Michael's Hospital, Toronto, Ontario, Canada

    Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada
    Search for articles by this author
      Sugars have emerged as 1 of the most important public health concerns. Special attention has focused on the fructose moiety of sugars owing to its unique metabolic and endocrinologic responses. Low-quality ecologic studies (
      • Bray G.A.
      • Nielsen S.J.
      • Popkin B.M.
      Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.
      ,
      • Basu S.
      • Yoffe P.
      • Hills N.
      • Lustig R.H.
      The relationship of sugar to population-level diabetes prevalence: An econometric analysis of repeated cross-sectional data.
      ,
      • Goran M.I.
      • Ulijaszek S.J.
      • Ventura E.E.
      High fructose corn syrup and diabetes prevalence: A global perspective.
      ), animal models of overfeeding at levels of exposure far beyond mean population levels of intake (
      • Sievenpiper J.L.
      • de Souza R.J.
      • Kendall C.W.
      • Jenkins D.J.
      Is fructose a story of mice but not men?.
      ) and select human interventions lacking control for energy (
      • Lustig R.H.
      • Mulligan K.
      • Noworolski S.M.
      • et al.
      Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome.
      ) have been used to implicate fructose-containing sugars in the epidemics of obesity and diabetes. Although experimental models have been invoked to offer plausible biochemical mechanisms to support these positions, whereby fructose acts as an unregulated substrate for de novo lipogenesis, depletes intracellular adenosine triphosphate and impairs satiety signalling through insulin, leptin and ghrelin (
      • Lustig R.H.
      • Schmidt L.A.
      • Brindis C.D.
      Public health: The toxic truth about sugar.
      ,
      • Lustig R.H.
      Fructose: It's “alcohol without the buzz.”.
      ,
      • Johnson R.J.
      • Perez-Pozo S.E.
      • Sautin Y.Y.
      • et al.
      Hypothesis: Could excessive fructose intake and uric acid cause type 2 diabetes?.
      ,
      • Johnson R.J.
      • Nakagawa T.
      • Sanchez-Lozada L.G.
      • et al.
      Sugar, uric acid, and the etiology of diabetes and obesity.
      ), the clinical translation of these mechanisms remains in question.
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