Author: J. S. White, White Technical Research
Editor, Experimental and Clinical Endocrinology & Diabetes,
In a recent paper, Gul et al. [1] suggested that increased fructose concentration induces the aging process and myocardial infarction through production of advanced glycation endproducts (AGEs), however, their supporting evidence is unconvincing.
First, it must be recognized that the dietary sources of fructose cited by the authors – honey, fruits, sucrose, and high fructose corn syrup – all contain essentially equal amounts of both fructose and glucose; crystalline fructose does not, but is a relatively minor dietary constituent, accounting for less than 2 % of added sugars [2] . It follows, then, that any increase in dietary fructose must include an equivalent increase in glucose.
Second, increased exposure to added sugars – and fructose – is far lower than the authors believe. While total energy intake increased 515 kcal / d (24 % ) between 1970 and 2008 (USDA-ERS data), energy from added sugars (including honey, sucrose, high fructose corn syrup and fruit juice concentrates) increased only 58 kcal / d; energy from fructose accounted for no more than half this amount. By contrast, energy from fl our / cereal products and added fats increased by 185 and 235 kcal / d, respectively. And loss-adjusted availability of added sugars has been in serious decline since 1999 [3] .
Third, the authors fail to demonstrate that the positive correlation with advanced glycation endproducts (AGEs) is a unique feature of fructose. Indeed, based on the signifi cantly increased fasting blood glucose in senile diabetic subjects with myocardial infarction vs. senile controls reported in Table 1, a similar positive and signifi – cant correlation between serum glucose and AGEs must surely be present.
And fourth, the authors ’ nonspecifi c test for AGEs fails to prove that those reported are due solely or even materially to serum fructose. They could as well be formed from several alternate substrates or endogenous mechanisms continuously at work in the human body: directly from reversible reactions of substantial glucose, other carbohydrates or metabolic intermediates with amines; oxidative stress that converts glucose to dicarbonyls which further bind to proteins; lipid peroxidation; or metabolically, through fragmentation and elimination of phosphate from glycolytic intermediates [4] .
Thus, the suggestion by Gul et al. that increased fructose concentration induces the aging process and myocardial infarction through production of AGEs is unconvincing, as it demonstrates neither a substantial recent increase of fructose in the diet nor a unique role for fructose in the development of AGEs.
Potential Confl ict of Interest: The author is a consultant to the food and beverage industry in the area of nutritive sweeteners. His clients include research institutes, food industry councils, trade organizations and individual companies.