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High Fructose Corn Syrup – not so sweet?
(Is HFCS making us fat?)
Introduced in the 1970s, high-fructose corn syrup (HFCS) has become an increasingly popular substitute for sugar as a sweetener in processed foods—particularly soft-drinks—since HFCS is relatively inexpensive, enhances sweetness, and allows for an extended shelf-life (Vos, 2008). HFCS is manufactured by passing corn starch (a complex carbohydrate) through a series of enzymes that break down the starch into monomers of glucose; glucose is then isomerized into fructose, becoming a mixture of 55% fructose and 45% glucose ("The Murky World of HFCS"). Even with the rising corn prices (due to increases in ethanol production for automobiles), HFCS is still cheaper than sugar in the United States, primarily because so much of the sugar crop is grown in Cuba, and is therefore under embargo.
Fructose is a six-carbon sugar that is slightly different from glucose—the main source of energy in the human body. Sucrose, a twelve-carbon dimer sugar that is better known as simply “sugar” (though all substances ending in –ose are technically sugars) is composed of one fructose molecule and one glucose molecule; the digestive system breaks sucrose down to 50% glucose and 50% fructose. Fructose is also found naturally in fruits and vegetables. Fructose, glucose, and sucrose have the same number of calories per gram, so from a purely chemical standpoint, they are energetically the same.
Since approximately the same time period as HFCS appeared in carbonated beverages (the 1980s), the US has seen a rising obesity epidemic. In addition, food resources have become much more readily available, and processing foods for increased shelf-life and taste has become more feasible and cost-effective than ever before. It makes sense, then, that the estimated consumption of fructose per capita increased 26% between 1970 and 1997—from 64 g/day to 81 g/day (Elliott, 2002); an average of those 24 g/day come from sweetened beverages (i.e. not fruit or 100% fruit juices) (Vos, 2008). Because of the correlation between the rise in obesity and the increased use of HFCS, many critics began to cite HFCS, particularly as a component of soft-drinks, as a probable cause of weight-gain. This paper seeks to examine the available information to determine whether HFCS, rather than other sources of energy or population-based factors, is the primary culprit in the obesity epidemic.
Previous claims – HFCS is BAD!
The general public today seems to view HFCS as a “must-avoid” component of unhealthy foods. If one searches the Internet for “high-fructose corn syrup,” dozens of articles and blog posts appear about the dangers of HFCS. According to TIME magazine, many conscientious consumers put HFCS in the same category as trans-fats ("Is High Fructose Corn Syrup Really Good for You?"). In response to this belief, Juicy Juice has been touting for years that their products do not contain HFCS (JuicyJuice.com) and many other products have followed suit—even leading a northwest health-foods grocery chain to ban all HFCS-containing products from its shelves (Seattlepi.nwsource.com). This fear of HFCS may stem initially from the long, unnatural sounding name, or even from knowing that HFCS is processed, but many health-nuts are certain that HFCS is the “newest health villain,” and many do not have the facts to back it up (Datamonitor.com).
New claim – HFCS is no different than sugar!
Recently, the Corn Refiners Association launched a marketing campaign to assure the public that eating products containing HFCS is no different than eating products with sugar. Sweetsurprise.com has quotes from the American Medical Association, Food and Drug Administration, Center for Food Safety and Applied Nutrition, and Harvard School of Public Health scrolling on the homepage, stating that there is no clear and convincing evidence that HFCS plays any more a role in obesity than sucrose does. The group has also aired a slew of commercials depicting situations where, for example, a girl offers a popsicle containing HFCS to her boyfriend; he then refuses it, but when asked why, cannot offer a response. The girl then reassures him that “it’s no different than sugar, and it’s fine in moderation” (http://www.sweetsurprise.com/press.php). These commercials address consumers’ factually unsupported fears, by stating their position directly. However, since the group producing these ads has a clear financial stake in the production and consumption of HFCS, their data stems from a conflict-of-interest, and therefore must be treated with extreme caution.
What does the peer-reviewed research say?
To get an accurate, unbiased picture of the effects of HFCS and its relation to the obesity epidemic, one must examine the peer-reviewed research studies. The issue can be approached in a few different ways; the characterization of HFCS on a molecular/cellular level, the effects of HFCS on an organismal level, and the impact of HFCS consumption on a population. By examining each of these levels individually and in concert, the scientific community can gain a better picture of the relationship between HFCS and obesity.
Biochemical research has fairly well characterized the mechanisms behind sugar intake and metabolism, and science has established many properties of how fructose is expected to behave when ingested. Once digested to its monomeric form, fructose is transported to the liver; unlike glucose, fructose catabolism is not regulated by the primary rate-limiting enzyme in glycolysis, and so fructose consumption results in larger amounts of metabolic by products in circulation (Elliott, 2002). Also, in comparison to studies of glucose consumption, several studies have found that fructose consumption in humans causes increased rates of de-novo lipogenesis, whereby sugar is converted into lipid and stored in adipose tissue (Elliott, 2002). Finally, fructose does not stimulate the same hormonal cues as glucose does; insulin and leptin—which are both involved in energy regulation and satiety cues—are produced in response to glucose ingestion, where as fructose has seemingly no effect on these hormones (Bray, 2004). Without these satiety cues, it is thought that fructose-containing foods would not leave one as satisfied as would the same amount of glucose, and would thus leads to overeating. This evidence, widely accepted by health professionals, lends itself to a hypothesis that consumption of fructose, in the form of HFCS, would lead to weight gain, more than would an equal amount of sucrose or glucose.
In-Vivo Studies of HFCS
Though we know how the body should process fructose in theory, the best way to test the hypothesis that fructose is processed differently than sucrose, and therefore contributes to the obesity epidemic more substantially, is to isolate this variable by the use of controls (as much as possible) in human subjects. By having research volunteers consume HFCS under controlled circumstances, investigators can compare those outcomes to the results of experiments when patients consume other similar substances.
Three very recent studies have looked at the differences in metabolic data, hormone concentration, and qualitative satiety assessments to examine the effects of sweetener consumption on hunger. In the first study, Monsivais, Perrigue and Drewnowski recruited thirty-seven adults to consume sucrose-sweetened soft drinks, HFCS beverages, or a type of HFCS made of 42% fructose, along with diet soda and 1% milk as controls (2007). The HFCS and sucrose drinks each contained 215 kcal. Participants had a standard breakfast two hours before consuming the beverages, and were asked to rate hunger, thirst, and satiety every twenty minutes following the consumption of the drinks. Two hours later, an identical large lunch was given to each participant, and investigators recorded how much each participant consumed. The results showed that there were no differences in reported hunger between those consuming both HFCS drinks and the sucrose beverage. Also, the amount that the subjects ate for lunch was essentially the same for those who had consumed the HFCS, sucrose, and milk drinks; only those who had had diet soda ate more lunch than the others. The investigators suggest that their results show that, in an isolated situation, the substitution of HFCS for sucrose did not promote overeating as previously suggested (Monsivais, Perrigue and Drewnowski, 2007).
In a similar study, investigators gave 800 mL drinks containing HFCS, sucrose, milk, (each containing 1.5 MJ/358 kcal) or diet soda to adult participants, and then later tested satiety using a self-reported scale, levels of satiety hormones in the blood (insulin and ghrelin), and amounts of overconsumption using a test meal (Soenen and Westerterp-Plantenga, 2007). This study also found no significant differences in these measures of satiety between the HFCS and sucrose groups.
Finally, Stanhope and colleagues conducted a study in which subjects ate three standardized meals (as in-patients, content calculated based on calculated energy requirements), along with either a sucrose-sweetened or HFCS-sweetened beverage (2008). Throughout the study days, investigators collected blood samples to examine circulating glucose, insulin, leptin, and ghrelin concentrations in response to each meal. This study found that while insulin levels were higher following consumption of sucrose (as expected), leptin and ghrelin levels were no different between the two samples, indicating that there are no significant satiety differences following consumption of HFCS or sucrose.
These three studies, both individually and in concert, suggest that in a controlled environment, there is no significant metabolic difference between consuming isocaloric amounts of sucrose and HFCS, even though the concentrations of fructose in each substance are different. Translated to a practical matter, if one had to choose between a drink sweetened with HFCS and one with sucrose, there is no evidence to suggest that one would be hungrier or less sated if the HFCS drink is chosen. Therefore, it seems that the metabolic properties of HFCS alone are not a contributing factor to obesity.
So even though the functional characteristics of HFCS do not seem to be the cause of obesity any more than does sucrose, it is possible that circumstances surrounding the use of HFCS is contributing to the obesity epidemic. According to several population based epidemiological studies, HFCS and the beverages it sweetens are positively correlated with weight gain in both adults and children.
As an example, Ludwig, Peterson, and Gortmaker conducted a prospective, observational study of 548 school children over two years to determine whether consumption of sugar-sweetened drinks (including, soda, Hawaiian punch, lemonade, Koolaid, sweet tea, and sweetened fruit drinks—most of which contain HFCS) predicted a change in BMI (2001). After accounting for variables of physical activity, time watching television and playing video/computer games, and total dietary intake, the investigators found that the odds ratio of becoming obese increased 1.6 times for each additional sugar sweetened drink consumed per day in children. These results led the researchers to conclude that sugar-sweetened drinks can be implicated in the rise of obesity.
Since obesity in children is often cited as the top pediatric problem currently, Ludwig’s study is just one of many looking at factors implicated in obesity in children; one of the more common factors studied is that of sweetened beverages, many of which contain HFCS. In a systematic review, Malik, Schulze, and Hu examined fifteen cross-sectional studies and 10 prospective studies, each of them looking at the relationship between sugar-sweetened beverages and weight gain (2006). Fourteen out of fifteen of the cross-sectional studies found a positive correlation between the consumption of sugar-sweetened beverages and being overweight or obese, and nine out of the ten prospective studies saw an association (six of them, a significant association) between sugar-sweetened beverage intake and becoming more overweight. The authors concluded that there is significant evidence that the intake of sugar-sweetened beverages is linked to the rise in obesity.
However, Sun and Empie examined data from the National Health and Nutrition Examination Surveys from 1988-1994, 1999-2000, and 2001-2002 (all of which were one component of Malik’s study), and came to a slightly different conclusion (2007). These authors found that based on the fourteen years of data, “gender, age, education level, smoking habit, TV/screen watching hours, physical activity, and dietary calories from total fat” were risk factors more highly associated with obesity than was consumption of sugar sweetened beverages.
It seems on first glance that the in-vivo experimental studies conflict with the population based studies in some of their conclusions, and thus “Is HFCS really causing obesity?” is still a hot topic. But can the health food nuts, who believe HFCS is responsible for obesity, and Sweet Surprise, who says that HFCS is no different than sucrose, both be right? Possibly. Sweet Surprise claims that metabolically, sucrose, glucose, and fructose are not meaningfully different, and the in-vivo studies seem to resoundingly support that conclusion. But the population-based studies agree with the concerned general public by showing strong correlations between a rise in obesity and an increase in use of HFCS. However, as suggested by the epidemiological studies, the increased consumption of beverages with empty calories (most of which happen to be sweetened with HFCS) is also associated with obesity. This is a reasonable finding, based on a, for example, a 2004 study, in which DiMeglio and Mattes found that calorie-filled beverages were much more likely to lead to a positive energy balance (and therefore to weight gain) than were the same amounts of solid carbohydrates. To expand upon this hypothesis, it is important to remember that the availability of HFCS has made sweetening drinks cheaper and easier since its introduction over thirty years ago; therefore it is also possible that sweetened beverages, and therefore empty calories, have become more plentiful and popular for consumption. Examination of these hypotheses would require further research. Even so, the available data suggests that HFCS itself is not the “health food villain” – the real culprit is the ready availability of HFCS as a calorie source and the unsatisfying liquid form in which it is most often consumed.
Bray, G.A., S.J. Nielsen, and B.M. Popkin. (2004). Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr. 79(4): 537-43.
DiMeglio, D.P. and R.D. Mattes. (2000). Liquid versus solid carbohydrate: effects on food intake and body weight. In J Obes Relat Metab Disord. 24(6): 794-800.
Eliott, S.S., N.L. Keim, J.S. Stern, K Teff, and P.J. Havel. (2002). Fructose, weight gain, and the insulin resistance syndrome. Am J Clin Nutr, 76(5): 911-22.
Ludwig, D.S., K.E. Peterson, and S.L. Gortmaker. (2001). Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet, 357(9255): 505-8.
Malik, V.S., M.B. Schulze, and F.B. Hu. (2006). Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr, 84(2): 274-88.
Monsivais, P., M.M. Perrigue, and A. Drewnowski. (2007). Sugars and satiety: does the type of sweetener make a difference?. Am J Clin Nutr, 86(1): 116-23.
Soenen, S. and M.S. Westerterp-Plantenga. (2007). No Differences in satiety or energy intake after high-fructose corn syrup, sucrose or milk preloads. Am J Clin Nutr, 86(6): 1586-94.
Stanhope, K.L., S.C. Giffen, B.R. Bair, M.M. Swarbrick, N.L. Keim, and P.J. Havel. (2008). Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. Am J Clin Nutr. 87(5): 1194-203.
Sun, S.Z., and M.W. Empie. (2007). Lack of findings for the association between obesity risk and usual sugar-sweetened beverage consumption in adults – A primary analysis of databases of CSFII-1989-1991, CSF-1994-1998, NHANES III, and combined NHANES 1999-2002. Food Chem Toxicol, 45(8): 1523-36.
Vos, M. B., J. E. Kimmons, C. Gillespie, J. Welsh, and H. M. Blanck. (2008). Dietary Fructose Consumption Among US Children and Adults: The Third National Health and Nutrition Examination Survey. Medscape J Med, 10(7): 160.
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