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1 From the Department of Nutritional Sciences, University of Toronto, Toronto, Canada
2 Reprints not available. Address correspondence to GH Anderson, Department of Nutritional Sciences, University of Toronto, Toronto, Ontario M5S 3E2, Canada. E-mail: harvey.anderson{at}utoronto.ca.
See corresponding article on page 1586.
Claudio: I pray you leave me.Benedick: Ho, now you strike like the blind man—’twas the boy that stole your meat, and you'll beat the post (1).
Over the past 35 y the prevalence of obesity has risen concurrently with an increased availability of added sugars in the food supply. Food disappearance data, used as an indicator of trends in food consumption, have shown a 20% increase in the availability of caloric sweeteners (sugars) in the United States from 1970–1974 to 2000 (2). Obesity has been blamed on sugars and sugar-sweetened beverages, but the debate has raged for many years with little resolution (3). More recently, the intensity of the debate was fueled by the hypothesis that introduction in the 1970s of high-fructose corn syrup (HFCS) as a caloric sweetener in beverages was specifically at fault (4). HFCS was proposed to lead to obesity because fructose bypasses food intake regulatory systems and favors lipogenesis.
However, although the availability of sugars has increased in the US food supply over the past 4 decades, it has not increased disproportionately as a contributor to the increase in total energy availability. From 1970–74 to 2000 the increase in per capita availability of total energy, sugars, carbohydrates, and fats was 25%, 22%, 26%, and 48%, respectively (2).
Furthermore, in the United States, HFCS has primarily been used to substitute for sucrose as a caloric sweetener rather than to be used in addition to sucrose. Sucrose use has declined from 80% of total caloric sweetener availability in 1970 to 40% of caloric sweetener availability in 1997. This reduction in sucrose consumption was simply made up for by HFCS, which has increased from nearly 0% in 1970 to 40% of total caloric sweeteners in 1997. The availability of HFCS in the US food supply did not change from 1997 [60.4 pounds (27.4 kg) per capita annually] to 2004 [59.2 pounds (26.9 kg) per capita annually] (2), during a time of continued weight gain.
There is no evidence that the ratio of fructose and glucose consumed from sugars has changed over the past 4 decades as a result of HFCS replacing sucrose in many applications. The term "high fructose corn syrup " is not a good descriptor of its composition, but the term was mandated to distinguish the newly developed fructose-containing corn syrup from the traditional all-glucose corn syrup. HFCS is predominantly sold as HFCS-55 (55% fructose, 41% glucose, and 4% glucose polymers) or HFCS-42 (42% fructose, 53% glucose, and 5% glucose polymers) (5). In North America, the former is used in beverages and the latter in solid foods.
The significance of replacing sucrose with HFCS in soft drinks and other beverages is addressed in this issue of the Journal by Soenen and Westerterp-Plantenga (6) and merits emphasis because it challenges the argument of biologic plausibility that was proposed to support the hypothesis. When compared with a diet drink, subjective appetite and food intake were decreased by the consumption of solutions of sugars (86 g/800 mL water). The drink mixtures contained primarily HFCS or sucrose and were prepared by using syrups added to beverages consumed in Europe. They contained either sucrose or HFCS to which was added glucose syrup (90% glucose and 9% fructose). The final composition of the sucrose beverage was 64% glucose and 36% fructose, whereas the HFCS beverage contained 41% glucose and 59% fructose. Thus, the difference in fructose content of the test beverages was exaggerated relative to the differences in beverages containing only sucrose or HFCS. Yet, no difference in food intake was found at a meal consumed 50 min later or in postprandial blood concentrations of glucose, insulin, glucagon-like peptide 1, or ghrelin—all components of food intake regulatory mechanisms.
Implicit in the argument that HFCS in soft drinks is different from sucrose is the notion that sucrose, as the disaccharide, may in some way stimulate metabolic satiety signals or increase fatty acid synthesis more than the monosaccharide mixtures. However, these possibilities were recently explored also (7). HFCS and sucrose, compared with solutions containing equal proportions of glucose and fructose, resulted in no differences in food intake 80 min after consumption. Sucrose and solutions of its monosaccharide equivalents resulted in no differences in postprandial blood glucose, insulin, and ghrelin concentrations. Thus, there is no evidence that sucrose—when consumed in its intact form—would confer any benefits over HFCS, which contains the 2 unbound monosaccharides. Furthermore, when added to the acidic environment of soft drinks, sucrose is most likely consumed as the monosaccharide because of hydrolysis.
The article by Soenen and Westerterp-Platenga (6) also suggests that all beverages may be created equal. The results support the view that compensation for calories in beverages is incomplete. Neither food intake nor caloric compensation was different after subjects consumed HFCS, sucrose, or milk drinks (1.5 mol). However, caloric compensation, the reduction of intake at the test meal as a percentage of calories in the preload, averaged <40% for women and 60% for men. Whether compensation would be higher for a solid food of similar composition remains to be determined (8).
There are multidimensional determinants of obesity. It was previously noted that neither sugar nor carbohydrate consumption has been clearly delineated as a direct cause of obesity (9). However, it is clear that energy imbalance for most individuals is accounted for by energy intake exceeding expenditure. The lifestyle factors that lead to this problem are too little exercise and too much food, but the determinants of such vary greatly between individuals. A food solution to obesity remains elusive, but a reductionist approach that focuses on one food or one component of the food supply, in the presence of too much (9), is unlikely to succeed.
Unfortunately the recent focus on HFCS has done little to resolve the role of sugars in contributing to energy imbalance. The hypothesis that the replacement of sucrose with HFCS in beverages plays a causative role in obesity is not supported on the basis of its composition, biologic actions, or short-term effects on food intake. Had the hypothesis been phrased in the converse, namely that replacing HFCS with sucrose in beverages would be a solution for the obesity epidemic, its merit would have been seen more clearly. Put simply, a proposal that a return to sucrose-containing beverages would be a credible solution to the obesity epidemic would have been met with outright dismissal. In many countries where trade barriers have prevented the replacement of sucrose with HFCS, the prevalence of obesity is high. Therefore, what role HFCS in beverages plays in the etiology of obesity, as in Much Ado about Nothing (1), may simply be a play on words.
Claudio: Now you talk of a sheet of paper, I remember a pretty jest your daughter told us of.Leonato: O, when she had writ it and was reading it over, she found Benedick and Beatrice between the sheet (1).
ACKNOWLEDGMENTS
I thank David Jenkins for his comments during the preparation of this editorial.
GHA serves as a science advisor to the Canadian Sugar Institute and to Archer Daniels Midland, a producer of HFCS, but has no equity or other financial interests in either industry. GHA has received unrestricted grant funding from the US Sugar Association and from the Canadian Sugar Institute.
REFERENCES
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