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High-Fructose Corn Syrup: Separating Facts from Myths

High-Fructose Corn Syrup: Separating Facts from Myths


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This 13-page paper by the American Council on Science and Health examines the use of high-fructose corn syrup, and whether it is a unique cause of America's obesity epidemic. Sucrose (table sugar) and high-fructose corn syrup have essentially the same composition, and thus is is unlikely for them to have different effects on body weight or metabolism.
This 13-page paper by the American Council on Science and Health examines the use of high-fructose corn syrup, and whether it is a unique cause of America's obesity epidemic. Sucrose (table sugar) and high-fructose corn syrup have essentially the same composition, and thus is is unlikely for them to have different effects on body weight or metabolism.

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Published by: American Council on Science and Health on Jan 08, 2013
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High-Fructose Corn Syrup

Ruth Kava, Ph.D., R.D. January 2013
for the American Council on Science and Health 1995 Broadway, Suite 202 New York, N.Y. 10023 acsh@acsh.org

Separating Facts from Myths

Josh Bloom, Ph.D. American Council on Science and Health Gerald F. Combs Jr., Ph.D. Director, USDA Grand Forks Human Nutrition Research Center Nancy A. Cotugna, Dr.P.H., R.D., C.D.N. University of Delaware Adam Drewnowski, , Ph.D. University of Washington Michael Dubick, Ph.D. U.S. Army Institute of Surgical Research San Antonio, Texas Judith A. Marlett, Ph.D., R.D. Emeritus Professor University of Wisconsin-Madison Alyssa Pelish American Council on Science and Health Gilbert L. Ross, M.D. American Council on Science and Health Svetlana Spivak, M.S. American Council on Science and Health Elizabeth M. Whelan, Sc.D., M.P.H. American Council on Science and Health John S. White, Ph.D. White Technical Research

Since the 1970s, the use of high-fructose corn syrup (HFCS) in the U.S. food supply has increased dramatically — typically as a replacement for sucrose (table sugar) in soft drinks and many food products. The prevalence of obesity has also increased substantially between the 1970s and the early 2000s. Because of this coincidental timing, HFCS has been erroneously demonized as a unique cause of the obesity epidemic in the United States. Sucrose and HFCS have essentially the same composition, and thus it would be highly unlikely for them to have different effects on body weight or metabolism. Experimental evidence, as well as analyses of epidemiologic data, indicate that sucrose and HFCS have equivalent effects on food intake and therefore on body weight. Scientific evidence does not support the notion that HFCS is uniquely responsible for the American obesity epidemic.

Introduction ................... 3 HFCS: What is it? .......... 4 HFCS: Where is it? ........ 7 Health Concerns ........... 8 Conclusions .................... 11


Consumers can access

a great deal of information from the ingredients list on food packages, and many use this information to decide which foods to purchase or avoid. In some cases it makes perfect sense to base food purchase decisions on the ingredient list — for example, to avoid ingredients to which one is allergic. Sometimes, however, shoppers can be influenced by media hype about the supposed health-promoting or health-damaging effects of one or another food ingredient, such as high-fructose corn syrup (HFCS). Over the last eight years, the media have bombarded us with unsubstantiated hypotheses about the deleterious effects of HFCS; it has been blamed for uniquely fueling the obesity epidemic, for causing diabetes and even for causing a condition known as “metabolic syndrome.” How did this happen, and what does the scientific evidence tell us about HFCS? In 2004, Dr. George Bray, a well-respected obesity researcher, presented a talk at a professional meeting in which he noted that the widespread use of HFCS in American foods and beverages in the 1970s coincided with the start of the obesity epidemic. He and his colleagues expanded on this idea in the American Journal of Clinical Nutrition. In general, their hypothesis stated that the consumption of the fructose in HFCS gave rise to metabolic abnormalities that helped fuel the gain of body fat. One implication of this theory was that consuming

HFCS affects health adversely to a greater extent than does consumption of table sugar (sucrose). Further, these authors suggested that consuming HFCS in beverages, particularly soft drinks, was more problematic than consuming it in solid foods, because people are less likely to compensate for consuming extra liquid calories by consuming fewer calories later. Although this reasoning was hypothetical, it was often presented as fact in the lay press, and it has affected the behavior of some consumers. Indeed, as recently as May 2011, a consumer survey found that 44 percent of consumers say they try to limit their consumption of HFCS, and 4 percent of those in a second survey said they actively avoid it. While the scientific literature includes numerous studies that do not support the hypotheses suggested by Bray and colleagues, much of this information is ignored by the media, and thus is unavailable to the public. The purposes of the current report, therefore, are to clarify the composition and utility of HFCS, and to compare these qualities and the health effects of HFCS to those of the most similar caloric sweetener — sucrose.


HFCS and sucrose are the major sweeteners added to the U.S. food supply. All sugars are crystalline carbohydrates — that is, they contain carbon, oxygen and hydrogen in various proportions and configurations. Both sucrose and HFCS consist of glucose and fructose, which are both single molecules called monosaccharides. High-fructose corn syrup is a thick liquid sweetener made from corn syrup. All types of corn syrups are made from cornstarch. The cornstarch is first treated with enzymes to convert the starch into corn syrup. At this point, the corn syrup contains no fructose, only glucose. When this corn syrup is further treated with enzymes under the proper laboratory conditions, some of the glucose is converted to fructose, a similar sugar. Exactly how much of the glucose is changed to fructose in this manner can be easily controlled so that the resulting syrup can consist of 50 percent glucose and 50 percent fructose, or even 10 percent glucose and 90 percent fructose. But the two combinations that are most widely used in food and beverage preparation contain either 42 percent fructose, or 55 percent fructose, and both types are called high-fructose corn syrup. In all cases, however, HFCS consists only of the two monosaccharides—glucose and fructose. HFCS-55 is the type used for most sweetened beverages produced in the United States, but it is not widely used in other countries. Unless otherwise specified, in this document HFCS means HFCS-55. In many cases, HFCS has replaced sucrose, or table sugar, for sweetening — HFCS is easier to handle than sucrose since it is a liquid, and it is also cheaper to use. Sucrose is a disaccharide: it is composed of the two monosaccharides, glucose and fructose. Thus one molecule of sucrose consists of one glucose and one fructose bound together — with a resulting composition of 50 percent of each — quite similar to the composition of HFCS. See FIGURE 1 for diagrams of sucrose, glucose and fructose. Like HFCS, sucrose is a plant-derived product; it is purified from sugar cane or sugar beets and was the traditional caloric sweetener in beverages and foods prior to the 1970s.

FIGURE 1 Sucrose: a disaccharide of glucose (left) and fructose (right)


Although we commonly think of sugars as uniformly sweet, they are not. Indeed, some sugars would hardly seem sweet when tasted in pure form. If we consider sucrose to have a sweetness rating of 100, then fructose would rate anywhere from 117 to 175, and glucose only 74-80, depending on the form (e.g., liquid or solid). Indeed, fructose is the sweetest of the naturally occurring sugars. It is widely distributed in nature — it’s found in honey, tree and vine fruits, flowers, nuts, berries and most root vegetables. Compared to other fruits, apples and pears contain the greatest amount of fructose. In any of these plants, fructose may be present as the monosaccharide and/or as a component of sucrose or other carbohydrates. Even though pure fructose is sweeter than sucrose, HFCS is not. TABLE 1 In fact, HFCS-55 and sucrose are about equally sweet, which is why HFCS-55 can easily be substituted for sucrose in beverages and solid foods. SWEETNESS
(relative to sucrose)

Sucrose and HFCS are both absorbed in the first part of the small intestine — the duodenum. Before absorption can occur, sucrose must be split into its component monosaccharides, glucose and fructose. This is accomplished by the action of the enzyme sucrase in the lining of the small intestine. When present in some preparations, such as somewhat acidic beverages, the sucrose may be partially split before it is consumed. Since the glucose and fructose in HFCS are already single molecules when consumed, they can be absorbed without enzyme action. Importantly, no matter whether the glucose and fructose come from HFCS or from sucrose, each is absorbed in the same way. From the small intestine, the glucose and fructose travel in the bloodstream to the liver where they may be metabolized for energy, used to form other molecules, stored as various products, or they may enter the systemic circulation and travel to other organs.

SWEETENER Sucrose Fructose High-fructose corn syrup (55% fructose) High-fructose corn syrup (42% fructose) Glucose

100 117 99 92 67

TABLE 1. Sweetness compared to sucrose* in aqueous solution
*Adapted from: Hanover LM, White JS. Manufacturing, composition, and applications of fructose. Am J Cin Nutr 1993;58(suppl):724S-732S.


In the liver, glucose and fructose follow somewhat different biochemical pathways. Glucose is the body’s basic energy currency. When it is not needed for this purpose, glucose may be stored in liver and muscle as glycogen, which provides a ready source of energy for later use. When the storage capacity for glycogen is reached, any additional glucose may be converted into fatty acids, which are stored as fat in the adipose tissue (fat), muscle and liver. Fructose cannot be directly converted to glycogen. Fructose can, however, be converted to glucose or fatty acids by the liver, and when present in excess can promote excess storage of fats in the liver (“fatty liver”). When the glucose level in the blood rises, it stimulates the release of insulin from the pancreas. Insulin in turn has two major functions. First, it promotes the uptake of the glucose into muscle and adipose tissue so that they can use it for energy — thereby lowering the level of glucose in the blood. Second, when glucose isn’t needed for energy, insulin stimulates the conversion of glucose to glycogen and fatty acids, A major difference between the metabolism of glucose and fructose is that fructose does not stimulate the release of insulin from the pancreas. Thus, body tissues are not stimulated to take up glucose or, indeed, fructose. HFCS has been blamed for metabolic derangements such as an increase in triglycerides (a form of fat) in the blood, as well as increases in the levels of glucose in the blood. It is important to recognize, however, that studies showing such effects are typically performed with high dietary levels of fructose (sometimes over 25 percent of calories), not with HFCS.



Various forms of HFCS
are used in many beverages and foods. Beverage sweetening is typically accomplished by HFCS-55 (i.e., 55 percent fructose). Major users of HFCS-42 (i.e., 42 percent fructose) include some segments of the beverage industry, cereal and bakery producers, multiple-use food manufacturers, the dairy industry and the confectionery industry.

Much attention has been focused on the fact that use of HFCS has increased greatly since its introduction in the 1970s. Indeed, one might think that sucrose is no longer used at all. In fact, as shown in Table 2, sucrose is still used more than HFCS, and as a percent of total calories from caloric sweeteners HFCS has actually decreased slightly in the last decade.


The most prominent claim about the deleterious effects of HFCS on health is that it is uniquely or largely responsible for the epidemic of obesity. Not only does evidence supporting this hypothesis remain elusive, there are multiple reasons why it cannot be true. For example, the substantial increase in obesity documented in the last several decades is not confined to the United States. World-wide statistics show that overweight and obesity and its co-morbidities, such as type 2 diabetes, are common in other Western countries — Great Britain and Canada — as well as in developing countries such as Egypt and India. These increases have occurred despite the limited or complete absence of HFCS-sweetened beverages in these nations, and thus the increased obesity seen around the world cannot be simply attributed to HFCS. Also, if the increased obesity prevalence in the United States were uniquely due to the change from sucrose to HFCS, there must be some material difference between the two sweeteners to account for this effect. As explained above, however, sucrose and HFCS are essentially the same once they have been digested — both contribute essentially equal proportions of fructose and glucose, and the body absorbs both in the same manner. Another route by which some argue that HFCS leads to weight gain is through increased caloric intake. Theoretically, this occurs because consumption of sweetened beverages is not accompanied by a decrease in the amount of food consumed at a meal (satiety), nor does it decrease the size of subsequent meals (satiation) in the same way that solid foods do. And since in the United States, beverages are typically sweetened with HFCS, it follows (according to this hypothesis) that this sweetener is responsible for the increased energy intake that has been occurring over the past several decades (Table 2). Indeed, this idea has been a focus of nutrition research for some time. This theory fails to take into account the growing consumption of low or non-calorie beverages in the United States. Indeed, USDA data indicate that as a percentage of total calories, consumption of added sugars has been declining. TABLE 2 Thus, the data do not support the conclusion that HFCS-sweetened beverage consumption leads to more calorie consumption than does that of sugarsweetened beverages. Researchers have compared the effects of different sweeteners on food consumption. In one study of young men and women, participants drank cola beverages sweetened with sucrose, HFCS-42, or HFCS-55. The effects of these beverages on consumption of a meal a couple of hours later were compared with the effects of drinking a diet cola, 1 percent milk or no beverage. All beverages except the diet soda contained 215 calories. Participants rated their feelings of hunger, fullness and desire to eat both


YEAR 1970 1980 1990 2000 2009
(Cane/Sugar Beets)





343 282 217 221 214

2 64 167 211 169

402 405 446 502 440

2169 2195 2405 2717 2594

18.5 18.5 18.5 18.5 17.0

TABLE 2. Per capita average daily caloric intake from sucrose and HFCS: average and percent of total calories. *
*From U.S. food availability, adjusted for spoilage and other waste. Source: Buzby J, Wells HF. Loss-adjusted food availability data: calories. USDAEconomic Research Service, 2007. Internet: www.ers.usda.gov/Data/FoodConsumption/ spreadsheets/foodloss/Calories.xls). Updated 2011. (Accessed 15 Oct. 2011)

before drinking the beverages and at intervals thereafter. Whether sweetened with sucrose or either of the HFCS varieties, hunger, fullness and desire to eat were similar in all three study groups. Further, the number of calories consumed at lunch was similar for all the sweetened colas and not significantly different than that consumed in the diet soda or no beverage conditions. Another group of researchers also compared the effects of a preload of sucrose or HFCS-sweetened beverages on energy intake at a subsequent meal compared to an isocaloric (having the same number of calories)∗ drink of milk or of a diet beverage. In addition to energy intake, which did not differ between the sweetened beverages, the study included measurement of

insulin and other hormones that affect food intake. Food consumption approximately one hour after drinking the test beverages was lower after the energy-containing beverages than after the diet beverage. Again, there was no difference in satiety or energy intake effects between drinks sweetened with sucrose or with HFCS. In addition, these drinks did not differ in their effects on appetite-controlling hormones. A review of relevant studies also concluded that beverages sweetened with sucrose or HFCS do not differ in their effects on short-term food intake and hormonal responses. Further, the data did not support a unique contribution by HFCS to weight gain or obesity.


Using data from national surveys, Drs Sun and Empie examined the relationship between obesity risk and sweetened beverage consumption—primarily HFCSsweetened beverages. After controlling for a variety of factors known to be associated with obesity risk, such as smoking, education, physical activity, and TV/ screen-watching hours, they found that populations who frequently consumed sugar/HFCS-sweetened beverages did not have a higher rate of obesity or increased obesity risk than did those who consumed such drinks infrequently. Finally, Drs Drewnowski and Bellisle made two important points about the supposed connection between body weight and sweetened beverages. First, the epidemiologic data on these links come from cross-sectional data or temporal trends, neither of which allow us to conclude that the beverages caused changes in body weight. Second, the evidence that compares the satiating power of various liquids and solids has not been confirmed. They also point out that some liquids, such as those prepared for individuals who can’t eat solid foods (meal replacements) cause, rather than suppress satiety. Indeed, some of these products are effective in helping people lose weight. Given that liquid meal replacements also contain HFCS, these researchers suggested that metabolism and physiology were not the only answer and that more attention must be paid to food-related behavior. For example, HFCS-sweetened meal replacements may have been effective because they were consumed in place of a meal and in the context of weight management. Thus, there are insufficient data to support the hypothesis proposed by Bray and colleagues that HFCS is uniquely, causally related to the epidemic of obesity in the United States.



Concerns about the

purported unique health effects of HFCS are unwarranted. Consumption of HFCS or sucrose in excess, like the excess consumption of any energy-containing nutrient, can lead to weight gain, overweight, and obesity along with its co-morbidities. But the data, experimental as well as epidemiologic, do not support any distinction between beverages or foods sweetened with sucrose and those sweetened with HFCS. It is unfortunate that misunderstanding of a hypothesis about HFCS led to its repetition as though it had been a proven fact. Repetition can lead to belief, whether or not there is any scientific underpinning for that belief. This is what has happened with HFCS.

This is not to say that the increased prevalence of overweight and obesity in the United States is not a serious issue, one that must be addressed with care and based on solid scientific evidence. But no single food or ingredient can be held responsible for what is actually a result, in most cases, of an unhealthy lifestyle — too many calories consumed and too few used.


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