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LETTER TO THE EDITOR |
Pennington Biomedical Research Center
6400 Perkins Road
Baton Rouge, LA 70808
E-mail: brayga{at}pbrc.edu
Dear Sir:
Two responses to my editorial "How Bad is Fructose" (1) and the accompanying articles in the Journal (2, 3) speak to the interest in this topic. Nearly 2 decades ago, the Federation of American Societies for Experimental Biology (FASEB) consulting group conducted an evaluation of published studies on carbohydrate sweeteners, including fructose, to guide the Food and Drug Administration (FDA) about this class of food products (4). I can remember reading it at the time of its publication and agreeing with the conclusion that sucrose and fructose were probably "benign." As time has passed, however, my views about the potential hazards of fructose, sucrose, and other caloric sweeteners have changed as the adverse data have accumulated. The introduction of high-fructose corn syrup (HFCS) in the United States and of isoglucose in Europe as caloric sweeteners and the increase in its use over the past 40 y have given us more opportunities to examine the effects of fructose. This has played an important part in why my views about fructose have changed.
In his letter, White, a corporate consultant to the food industry, incorrectly suggests that I believe HFCS and fructose are "uniquely" responsible for obesity. Obesity is a multifactorial disease—a disease of energy imbalance appearing in individuals with genetic susceptibility in an environment rich in HFCS and other caloric sweeteners mixed with high-fat foods. As we have argued (5), it is HFCS in beverages that has the strongest relation with the growing epidemic of obesity. A review of calorically sweetened beverages by Vartanian et al (6) showed that beverage intake was significantly related to calorie intake in 10 of 12 cross-sectional studies and in all 5 longitudinal studies. Because beverages are not the sole sources of energy in the diet, it is not surprising that fewer studies showed the relation with weight gain than with energy intake. It is noteworthy that none of the studies showed the reverse effect, ie, a protective effect of soft drinks against weight gain. HFCS and sugar, which is half fructose, particularly when combined with fat, are thus contributors to the epidemic of obesity and the metabolic syndrome and provide a good marker for highly processed foods, the kinds I try to avoid when shopping. These high-HFCS–containing, highly refined-carbohydrate diets are the ones that Taubes (7) calls the "bad calories" in his recent book titled Good Calories, Bad Calories.
White also tries to minimize the importance of the small changes in LDL particle size in Swiss children reported by Aeberli et al (2). In contrast with his perception, small, significant changes in cardiovascular disease risk factors in children of this age related to differences in fructose cannot be lightly brushed aside, because corporate profits cannot be used as a basis for running any risk of decreasing the health of our children. The Bogalusa Heart Study has shown the importance of small changes in body weight at the upper end of the age group in children at risk of developing cardiovascular disease risk factors (8). Thus, we need to do all we can to protect the younger generation from potentially risky foods.
Fructose may also be detrimental to adults (3). A recent paper by Dhingra et al (9) showed that consumption of soft drinks, a major source of fructose, is related to the development of cardiovascular disease risk factors in participants in the Framingham Heart Study. Johnson et al (3) note the relation between the rise in sugar consumption and cardiovascular disease and point out that uric acid, a predictor of cardiometabolic risk, is one of the byproducts of fructose metabolism. The litany of potentially ill effects associated with fructose thus continues to mount and has been a major factor responsible for my change in position from the time of the FASEB review for FDA in 1986.
White also points out that the percentage of calories from added sugars has decreased, but fails to note that total fructose intake has increased because total added sugars have increased (4). The effects of fructose on LDL particle size, the effects of fructose on uric acid production (a predictor of heart disease), and the prediction of weight gain in several prospective clinical trials give me serious concerns about the future of products with high levels of fructose from whatever source, particularly when mixed with fat.
In her letter, Hine notes that the polyol pathway in diabetics is an added source of fructose, and I thank her for this addition to the list of endogenous sources of fructose. She also notes that Glut-5, the fructose transporter, is somewhat more abundantly distributed than I had indicated. It is interesting that these are abundant in many cancers. The biological meaning of this is unclear to me. This being said, the important message is that most fructose is metabolized in the liver with utilization of ATP. The decrease in available ATP during the metabolism of fructose can be graphically seen with magnetic resonance image spectroscopy. The outcome of this metabolism, as noted in the report by Johnson et al (3), is an increase in uric acid. My concerns about the health implications of fructose in our diets—from whatever source—are as strong as when I wrote the editorial.
ACKNOWLEDGMENTS
No conflicts of interest were reported.
REFERENCES
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