Scientists, public health professionals, and policy makers have been looking for the causes of the increased weight gain observed over the past two decades in the American population. Considerable attention has focused on the possible role of foods and beverages containing added sugars. (See the side bar for the meaning of the terms used to describe sugars.) Scientific studies, however, have failed to demonstrate a direct link between body weight and total or added sugars intake, and in many cases studies have actually shown an inverse relationship. Some scientists have recently speculated that increased intake of fructose — particularly as high fructose corn syrup (HFCS) in beverages — is a major factor leading to the rise in obesity. They have based these speculations on simple correlation analyses. (Correlation studies examine the relationship between two simultaneously occurring events, i.e., rise in rates of obesity and introduction of a new food. Such observations provide initial evidence of a possible connection but are useful only for hypothesis formation.) This article provides the basis to help put what we know about fructose, HFCS, and obesity into perspective. It also discusses the issue of the availability of fructose in the food supply, whether from HFCS or other sources, and what is known about how it is metabolized.

Fructose—What is It?

Fructose, as noted in the sidebar, is a single sugar unit, like glucose, and is sometimes referred to as “fruit sugar” since it is the sugar that occurs naturally in fruits, vegetables, and honey. Fructose and glucose are combined in equal amounts (50/50) in table sugar (sucrose). Similarly, fructose and glucose occur in almost equal amounts in HFCS. HFCS is primarily found in two formulations in the United States; “HFCS 55,” which is 55 percent fructose and is used to sweeten beverages, and “HFCS 42,” which is 42 percent fructose and used mostly in baked goods.

The interchangeable use of the words “fructose” and “HFCS” in some media and even scientific documents is potentially misleading to consumers, who may assume that the two are identical. They are, however, quite different in both their structure and uses in the food supply. Although research using fructose alone has led to assumptions about HFCS, as a sweetener, pure fructose is rarely consumed alone. It is generally consumed as a component of table sugar or of HFCS.

Fructose in the Food Supply

The primary factor driving the alleged connection between fructose and obesity is the increased availability of HFCS since its introduction in the 1970s. “Availability” refers to the total amount delivered into the food supply. This amount is greater than actual consumption, since waste and other losses are not accounted for. The proportion of HFCS as a percentage of all caloric sweeteners (added sugars and sweeteners) available in the U.S. food supply has increased from less than 0.5 percent in 1970 to 42 percent in 2001. Although the increased availability of HFCS appears dramatic it must be noted that as the availability of HFCS has increased, the availability of table sugar has decreased at nearly the same rate. Although the increased availability of HFCS parallels the increasing prevalence of obesity, that correlation alone does not prove causality. Further research in this area is warranted.

The combined amount of table sugar and HFCS available in the food supply remained essentially constant from 1970 to 1986 at about 128 grams per person per day, and gradually rose to 161 grams by 2000. Despite the increase in grams available in the food supply, the proportion of available calories in the total diet that comes from table sugar and HFCS combined has remained remarkably constant since 1970 at about 15 to 16 percent. Because sugar and the combination of all varieties of HFCS contain about 50 percent fructose, the relative proportion of fructose in the food supply also has remained constant, at about 8 percent of daily caloric intake. However, total calories available in the food supply increased from 3300 to 3900 per person per day between 1970 and 2000, based on USDA food supply data. (These numbers are based on calorie availability in the food supply, not calories consumed by individuals; hence the numbers here are an over-estimate of intake.) Increased portion sizes may also account for the rise in total calorie availability. Of these 600 additional calories available in the food supply, about 60 to 70 of those calories are from the fructose in sucrose and HFCS.

Fructose and Body Weight

Another hypothesis for correlating HFCS and obesity is the manner in which the body metabolizes fructose, which is commonly obtained from honey, fruit, and vegetables. Compared to glucose, dietary fructose is more easily absorbed and taken up by the liver. It is then further broken down into compounds that can be used as energy, converted to glucose, stored as glycogen, or utilized to synthesize triglycerides. How fructose is used depends on an individual’s health condition, physical activity status, intake levels, consumption pattern (alone or with other foods), and intake of other macro-nutrients such as fiber, total carbohydrates, and fat. An individual’s overall energy balance also plays a key role in determining whether fructose is utilized to synthesize triglycerides and store in adipose tissue or metabolized by the muscle system, central nervous system, or other organs for energy production. In a carefully controlled study with lean and obese women, the study subjects showed no significant differences in levels of body fat regardless whether the excess calories came from the consumption of more fructose, glucose, sucrose, or fat. This was true even when subjects were taking in more calories than they were using in activity. It should be noted that these studies were not performed with HFCS, but were performed only with table sugar, fructose, or glucose. Given this caveat, one can reasonably expect similar results with HFCS because HFCS, like table sugar, is composed of both fructose and glucose. But HFCS remains to be tested in such studies.

Fructose also differs from glucose in that it does not directly stimulate pancreatic insulin production or require insulin for its metabolism. Thus, compared with an equal amount of glucose, dietary fructose does not influence changes in blood glucose or insulin levels as efficiently as dietary glucose does. The relatively lesser effect that fructose has on stimulating blood glucose and insulin levels is proposed as a physiological hypothesis for why fructose ingestion may uniquely contribute to the rise in the rates of obesity. That is, a blunted rise in blood glucose and insulin levels is hypothesized to blunt leptin production, and blunted rises in insulin and leptin levels are hypothesized to interfere with the long-term regulation of food intake and body weight. Scant data from studies with humans exist to evaluate the fructose-insulin-leptin hypothesis, and no data are available to demonstrate whether dietary HFCS has favorable or unfavorable effects on insulin-leptin responses as compared with those of sucrose, glucose, and/or fructose. Relevant data for the hypothesis have come only from animal studies or studies using sucrose, fructose, and/or glucose and not using HFCS. Perhaps arguing against this hypothesis are diet proponents who believe it is precisely a blunted rise in blood glucose and insulin response that can aid in weight control. They recommend not eating foods that stimulate a rise in blood glucose levels.

Some researchers have concluded that calories ingested in liquid form do not contribute to satiety. This theory is cited to support the fructose-obesity connection. However, it is difficult to separate the possible effects because there are different physiological mechanisms for digesting food versus beverages, there are different roles that foods and beverages have in the diet, and there are other potential differences in cognitive cues.

Other studies have shown that the body compensates for calories from beverages depending on the degree of blood glucose rise and time between beverage consumption and test meal. The majority of studies have shown that sucrose solutions suppress food intake if the time between ingesting the solution and consuming the test meal is less than 60 minutes. Stemming from differences in the experimental designs of the various studies that have been performed, the overall data in this area are inconclusive. Because nearly identical amounts of glucose and fructose are found in sucrose and the HFCS used in beverages, similar results would be expected with the types of HFCS commonly used in soft drinks. This remains to be tested.

Earlier in 2004 the American Dietetic Association published a report, Position of the American Dietetic Association: Use of nutritive and nonnutritive sweeteners, that found, on the basis of current scientific evidence, that consumers can safely enjoy a range of caloric and noncaloric sweeteners. They noted that this statement is valid when such sweeteners are consumed as part of a diet that is guided by current nutrition recommendations, such as those in the U.S. Dietary Guidelines for Americans and the Dietary Reference Intakes, as well as individual health goals. This includes fructose from HFCS or from table sugar.

Environmental Changes Since 1970

Obesity is a complex issue with many contributing factors ranging from genetics, social issues, food consumption, and physical activity. As indicated previously in this article, the HFCS in the food supply does not appear to be a major contributor to the increased energy intake of the U.S. population. Many societal as well as dietary changes have occurred since the 1970s that could be contributing to energy imbalance and development of obesity. Changes affecting caloric intake also include: more meals eaten away from home, larger portion sizes, and the relatively inexpensive and abundant food supply. There are also other changes working to reduce energy expenditure: increased reliance on the automobile, cuts in physical education, more “screen time” (television, computers, and video games), more hours working at sedentary jobs, more long distance commuting, and more labor saving devices. Finally, other changes may be contributing to both increased calorie intake and reduced energy expenditure: more sleep deprivation, more night work, certain prescription medicines, and emotional stress.

With so many changes, it may be overly simplistic to advocate a major causal role for any one food, food ingredient, or nutrient in the obesity epidemic. Although it is commonly agreed that overweight and obesity are due to excessive energy intake and lack of physical activity, individually, why and how people become obese is linked to multiple causes. A productive approach might be to evaluate each individual’s total diet and lifestyle. Is energy intake and expenditure balanced? If not, what factors unique to that individual need to be addressed, taking into account job, lifestyle, and other considerations? The key is to help each person control their weight while continuing to conduct research that can lead to greater understanding of the factors contributing to the obesity epidemic.

Coming to Terms with Sugars

The meaning of terms often used when talking about dietary sugars:

Caloric sweeteners…
Sweeteners, typically carbohydrates naturally present in or added to foods, caloric sweeteners have approximately 4 calories per gram

Sugars…
Monosaccharides (single sugar units like fructose and glucose) and disaccharides (two sugar units linked together, like sucrose); sometimes called simple sugars

Sucrose…
A disaccharide containing one fructose unit and one glucose unit bonded together (also known as table sugar); contains 50 percent fructose and 50 percent glucose

Glucose…
A monosaccharide; the main source of energy for the body

Fructose…
A monosaccharide; it has the same chemical formula as glucose but different molecular structure; sometimes called fruit sugar

Added sugars…
Sugars eaten separately, added to foods at the table (such as adding sugar to coffee, tea, or cereal; topping pancakes with syrup, etc.), or used as ingredients in prepared foods; examples include sugar, corn syrup, high fructose corn syrup, honey, and molasses

Table sugar…
Common name for the disaccharide sucrose; obtained from sugar beets and sugar cane

High fructose corn syrup…
A mixture of glucose and fructose produced from corn syrup; the most frequently used types are HFCS 42, common in baking applications, which is 42 percent fructose; and HFCS 55, common in beverage applications, which is 55 percent fructose

Sources of Information

Almiron-Roit E, Flores SY, and Drewnowski A. No difference in satiety profiles between a liquid and a solid food consumed at different times before a test meal. Physiology and Behavior: in press.

American Dietetic Association. Position of the American Dietetic Association: use of nutritive and nonnutritive sweeteners. J Am Diet Assoc. 2004;104(2):255-75.

Anderson GH, Woodend D. Effect of glycemic carbohydrates on short-term satiety and food intake. Nutr Rev 2003;61(5):S17-S25.

DellaValle DM, Roe LS, Rolls B. Does the consumption of different beverages with a meal affect intake? FASEB J 2004;18(4):A1109.

ERS Availability Data taken and/or calculated from databases available at this link:
http://www.ers.usda.gov/data/foodconsumption/

McDevitt RM, Poppitt SD, Murgatroyd PR, Prentice AM. Macronutrient disposal during controlled overfeeding with glucose, fructose, sucrose, or fat in lean and obese women. Am J Clin Nutr 2000;72:369-377.

Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr 1993; 58(suppl):737S-747S.

Saris WHM, Astrup A, Prentice AM, et al. Randomized controlled trial of changes in dietary carbohydrate/fat ratio and simple vs. complex carbohydrates on body weight and blood lipids: the CARMEN study. Int J Obesity 2000;24:1310-1318.

Teff KL, Elliott SS, Tschop M, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab 2004;89:2963-2972.