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LETTER TO THE EDITOR |
White Technical Research
8895 Hickory Hills Drive
Argenta, IL 62501
E-mail: white.tech.res{at}gmail.com
Dear Sir:
The recent research by Aeberli et al (1), review article by Johnson et al (2), and editorial by Bray (3) continue the current focus on fructose—and by extension on the fructose-containing sweeteners sucrose (common white table sugar), high-fructose corn syrup (HFCS), honey, crystalline fructose, and fruit juice concentrates—but fail to add substantive support for its hypothesized role as a unique cause of obesity and related disease (4).
Aeberli et al attempt to correlate free fructose intake with the development of overweight in Swiss schoolchildren via abnormalities in lipid metabolism. The importance of the correlation must be questioned, however, because they showed no effect of fructose on total and LDL cholesterol, and the effect of fructose on HDL cholesterol, triacylglycerol, and LDL particle size, although reported as significant, is very slight indeed.
The correlation becomes more tenuous yet because normal and overweight children took in similar total energy, fat, and carbohydrates—including total fructose, glucose, and sucrose. The observation that children took in 13% more protein than did normal-weight children might have confounded the purported fructose correlation, because O'Dell (5) reported that protein can actually accentuate certain metabolic effects of fructose.
Furthermore, the Aeberli et al correlation surely fails altogether because the focus of the article—free fructose from sweets and drinks—differs so negligibly between normal and overweight children (0.2 g/d) and represents such an insignificant proportion of the diet (0.04% of daily calories). Free fructose might better be labeled a micronutrient than a macronutrient in the study by Aeberli et al.
Johnson et al fail to build a convincing case for excessive fructose intake as a critical cause of cardiorenal disease, because 1) they present selected macronutrient intake data, suggesting that added sugar intake alone has increased since the introduction of HFCS 35 y ago; and 2) they cite inappropriate experimental comparisons as confirmatory evidence.
According to the US Department of Agriculture–Economic Research Service, per capita daily calories increased by 24% between 1970 and 2005 (6). Significantly, however, added sugars as a percentage of daily calories decreased 1% over this period, whereas flours/cereals and fats actually increased by 3% and 5%, respectively. A more appropriate interpretation of historic calorie intake data than that offered by Johnson et al is that Americans are consuming more of all macronutrients today than they did in 1970.
The typical human diet is neither pure fructose nor pure glucose, yet that is the comparison made in many of the studies cited by Johnson et al (references 50–54 and 56–58 in reference 2) as justification for a role of fructose in cardiorenal disease. Rather, the human diet is typically composed of both fructose and glucose at a ratio of 0.7 to 1 (7). Experiments comparing the metabolic effects induced by pure fructose at excessive levels against pure glucose cannot be used to predict the metabolic effects of common nutritive sweeteners, because 1) human diets of pure fructose or pure glucose are so extreme and so rarely encountered that they surely are of no practical nutritional consequence, and 2) single sugars are poor models for nutritive sweeteners that contain fructose and glucose in equivalent amounts.
HFCS has displaced sucrose in selected food and beverage applications over the past 30 y. The appropriate comparison for judging the metabolic effects of HFCS is, thus, against the sucrose that it displaced in the diet. In the few experiments in which such comparisons have been made, no differences were reported for serum glucose or insulin, the obesity hormones leptin and ghrelin, triacylglycerols, and uric acid (8; J Lowndes, L Zuckley, V Nguyen, TJ Angelopoulos, JM Rippe, unpublished observations, 2007) or for hunger, satiety, or short-term energy intake (9).
Bray's hypothesis that HFCS—and now specifically fructose—is uniquely responsible for obesity has titillated the scientific community for the past several years, but has yet to be substantiated in real world diets. The thesis of Aeberli et al fails because of insignificant fructose intakes and weak correlations, whereas the hypothesis of Johnson et al is founded on effects shown only in extreme and physiologically improbable diets. Neither hypothesis succeeds in proving a unique role of fructose-containing sweeteners in obesity or related diseases.
ACKNOWLEDGMENTS
The author is a consultant to the food and beverage industry in the area of nutritive sweeteners. His clients include individual companies, research institutes, food industry councils, and trade organizations. Those with a particular interest in fructose sweeteners are the Calorie Control Council and the Corn Refiners Association.
REFERENCES
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