Commentary

Consumption of high-fructose corn syrup in beverages may play a

role in the epidemic of obesity1,2
George A Bray, Samara Joy Nielsen, and Barry M Popkin

ABSTRACT sucrose. Added sugar is sugar added to a food and includes

Obesity is a major epidemic, but its causes are still unclear. In this sweeteners such as sucrose, HFCS, honey, molasses, and other
article, we investigate the relation between the intake of high-

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syrups. Naturally occurring sugar is sugar occurring in food and
fructose corn syrup (HFCS) and the development of obesity. We not added in processing, preparation, or at the table. Total sugars
analyzed food consumption patterns by using US Department of represents the total amount of sugars present in a food and in-
Agriculture food consumption tables from 1967 to 2000. The con- cludes both naturally occurring and added sugars. Free fructose
sumption of HFCS increased 쏜 1000% between 1970 and 1990, far is fructose that exists in food as the monosaccharide. Fructose
exceeding the changes in intake of any other food or food group. refers to both the free and bound forms of fructose (4).
HFCS now represents 쏜 40% of caloric sweeteners added to foods Added sweeteners are important components of our diet, rep-
and beverages and is the sole caloric sweetener in soft drinks in the resenting 318 kcal of dietary intake for the average American
United States. Our most conservative estimate of the consumption of aged 욷 2 y, or 16% of all caloric intake as measured by a na-
HFCS indicates a daily average of 132 kcal for all Americans aged tionally representative survey in 1994 –1996 (5). Sweet corn-
욷 2 y, and the top 20% of consumers of caloric sweeteners ingest based syrups were developed during the past 3 decades and now
316 kcal from HFCS/d. The increased use of HFCS in the United States represent close to one-half of the caloric sweeteners consumed by
mirrors the rapid increase in obesity. The digestion, absorption, and Americans (6, 7). HFCS made by enzymatic isomerization of
metabolism of fructose differ from those of glucose. Hepatic metabo- glucose to fructose was introduced as HFCS-42 (42% fructose)
lism of fructose favors de novo lipogenesis. In addition, unlike glucose, and HFCS-55 (55% fructose) in 1967 and 1977, respectively, and
fructose does not stimulate insulin secretion or enhance leptin produc- opened a new frontier for the sweetener and soft drink industries.
tion. Because insulin and leptin act as key afferent signals in the regu- Using a glucose isomerase, the starch in corn can be efficiently
lation of food intake and body weight, this suggests that dietary fructose converted to glucose and then to various amounts of fructose. The
may contribute to increased energy intake and weight gain. Further-
hydrolysis of sucrose produces a 50:50 molar mixture of fructose
more, calorically sweetened beverages may enhance caloric overcon-
and glucose. The development of these inexpensive, sweet corn-
sumption. Thus, the increase in consumption of HFCS has a temporal
based syrups made it profitable to replace sucrose (sugar) and
relation to the epidemic of obesity, and the overconsumption of HFCS
simple sugars with HFCS in our diet, and they now represent 40%
in calorically sweetened beverages may play a role in the epidemic of
of all added caloric sweeteners (8). Fructose is sweeter than
obesity. Am J Clin Nutr 2004;79:537– 43.
sucrose. In comparative studies of sweetness, in which the sweet-
ness of sucrose was set at 100, fructose had a sweetness of 173
KEY WORDS Epidemiology, food intake, obesity, artificial
and glucose had a sweetness of 74 (9). If the values noted above
sweeteners, fructose
are applied, HFCS-42 would be 1.16 times as sweet as sucrose,
and HFCS-55 would be 1.28 times as sweet as sucrose. This
INTRODUCTION contrasts with the estimates reported by Hanover and White (10).
As obesity has escalated to epidemic proportions around the In their study, the sweetness of sucrose was set at 100 as in
world, many causes, including dietary components, have been reference 8. Fructose, however, had a sweetness of only 117,
suggested. Excessive caloric intake has been related to high-fat whereas a 50:50 mixture of fructose and sucrose had a sweetness
foods, increased portion sizes, and diets high both in simple of 128. It is difficult to see why fructose and sucrose combined
sugars such as sucrose and in high-fructose corn syrup (HFCS) as would be sweeter than either one alone and as sweet as HFCS-55.
a source of fructose (1–3). In this article, we discuss the evidence On the basis of data in Agriculture Handbook no. 8 from the US
that a marked increase in the use of HFCS, and therefore in total Department of Agriculture (USDA) (11), a cola beverage in 1963
fructose consumption, preceded the obesity epidemic and may be
1
an important contributor to this epidemic in the United States. From the Pennington Biomedical Research Center, Louisiana State Uni-
To provide a common frame of reference for the terms used in versity, Baton Rouge, LA (GAB), and the Department of Nutrition, Univer-
sity of North Carolina, Chapel Hill (SJN and BMP).
this paper, the following definitions should be understood. Sugar 2
Reprints not available. Address correspondence to GA Bray, Pennington
is any free monosaccharide or disaccharide present in a food.
Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808.
Sugars includes at least one sugar; composite sugars refers to the E-mail: [email protected].
aggregate of all forms of sugars in a food and is thus distinguish- Received October 3, 2003.
able from specific types of sugar, such as fructose, glucose, or Accepted for publication December 15, 2003.

Am J Clin Nutr 2004;79:537– 43. Printed in USA. © 2004 American Society for Clinical Nutrition 537
538 BRAY ET AL

had 39 kcal/100 g, whereas a cola beverage in 2003 had 41 kcal/ leptin inhibits food intake, the lower leptin concentrations induced
100 g. Because the number of calories per 100 g has not changed by fructose would tend to enhance food intake. This is most dramat-
substantially over the past 40 y, current beverages are probably ically illustrated in humans who lack leptin (22, 23). Persons lacking
sweeter, depending on the temperature at which they are served. leptin (homozygotes) are massively obese (22), and heterozygotes
HFCS has become a favorite substitute for sucrose in carbon- with low but detectable serum leptin concentrations have increased
ated beverages, baked goods, canned fruits, jams and jellies, and adiposity (23), which indicates that low leptin concentrations are
dairy products (10). The major user of HFCS in the world is the associated with increased hunger and gains in body fat. Adminis-
United States; however, HFCS is now manufactured and used in tration of leptin to persons who lack it produces a dramatic decrease
many countries throughout the world (7). In the United States, in food intake, as expected. Leptin also increases energy expendi-
HFCS is the major source of caloric sweeteners in soft drinks and ture, and during reduced calorie intake, leptin attenuates the de-
many other sweetened beverages and is also included in numer- creases in thyroid hormones and 24-h energy expenditure (24). To
ous other foods; therefore, HFCS constitutes a major source of the extent that fructose increases in the diet, one might expect less
dietary fructose. Few data are available on foods containing insulin secretion and thus less leptin release and a reduction in the
HFCS in countries other than the United States (7). inhibitory effect of leptin on food intake, ie, an increase in food
intake. This was found in the preliminary studies reported by Teff et

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al (25). Consumption of high-fructose meals reduced 24-h plasma
THE BIOLOGY insulin and leptin concentrations and increased postprandial fasting
Absorption of fructose triacylglycerol concentrations in women but did not suppress circu-
lating ghrelin concentrations.
The digestive and absorptive processes for glucose and fruc-
tose are different. When disaccharides such as sucrose or maltose Fructose and metabolism
enter the intestine, they are cleaved by disaccharidases. A sodium- The metabolism of fructose differs from that of glucose in
glucose cotransporter absorbs the glucose that is formed from cleav- several other ways as well (3). Glucose enters cells by a transport
age of sucrose. Fructose, in contrast, is absorbed further down in the mechanism (Glut-4) that is insulin dependent in most tissues.
duodenum and jejunum by a non-sodium-dependent process. After Insulin activates the insulin receptor, which in turn increases the
absorption, glucose and fructose enter the portal circulation and density of glucose transporters on the cell surface and thus facilitates
either are transported to the liver, where the fructose can be taken up the entry of glucose. Once inside the cell, glucose is phosphorylated
and converted to glucose, or pass into the general circulation. The by glucokinase to become glucose-6-phosphate, from which the
addition of small, catalytic amounts of fructose to orally ingested intracellular metabolism of glucose begins. Intracellular enzymes
glucose increases hepatic glycogen synthesis in human subjects and can tightly control conversion of glucose-6-phosphate to the glyc-
reduces glycemic responses in subjects with type 2 diabetes mellitus erol backbone of triacylglycerols through modulation by phospho-
(12), which suggests the importance of fructose in modulating me- fructokinase. In contrast with glucose, fructose enters cells via a
tabolism in the liver. However, when large amounts of fructose are Glut-5 transporter that does not depend on insulin. This transporter
ingested, they provide a relatively unregulated source of carbon is absent from pancreatic ␤ cells and the brain, which indicates
precursors for hepatic lipogenesis. limited entry of fructose into these tissues. Glucose provides “sati-
ety” signals to the brain that fructose cannot provide because it is not
Fructose and insulin release
transported into the brain. Once inside the cell, fructose is phosphor-
Along with 2 peptides, glucose-dependent insulinotropic ylated to form fructose-1-phosphate (26). In this configuration, fruc-
polypeptide and glucagon-like peptide-1 released from the gas- tose is readily cleaved by aldolase to form trioses that are the back-
trointestinal tract, circulating glucose increases insulin release bone for phospholipid and triacyglycerol synthesis. Fructose also
from the pancreas (13, 14). Fructose does not stimulate insulin provides carbon atoms for synthesis of long-chain fatty acids, al-
secretion in vitro, probably because the ␤ cells of the pancreas though in humans, the quantity of these carbon atoms is small. Thus,
lack the fructose transporter Glut-5 (15, 16). Thus, when fructose fructose facilitates the biochemical formation of triacylglycerols
is given in vivo as part of a mixed meal, the increase in glucose more efficiently than does glucose (3). For example, when a diet
and insulin is much smaller than when a similar amount of glu- containing 17% fructose was provided to healthy men and women,
cose is given. However, fructose produces a much larger increase the men, but not the women, showed a highly significant increase of
in lactate and a small (1.7%) increase in diet-induced thermo- 32% in plasma triacylglycerol concentrations (27).
genesis (17), which again suggests that glucose and fructose have
different metabolic effects. Overconsumption of sweetened beverages
One model for producing obesity in rodents is to provide sweet-
Insulin and leptin ened (sucrose, maltose, etc) beverages for them to drink (28). In this
Insulin release can modulate food intake by at least 2 mecha- setting, the desire for the calorically sweetened solution reduces the
nisms. First, Schwartz et al (18) have argued that insulin con- intake of solid food, but not by enough to prevent a positive caloric
centrations in the central nervous system have a direct inhibitory balance and the slow development of obesity. Adding the same
effect on food intake. In addition, insulin may modify food intake amount of sucrose or maltose as of a solid in the diet does not
by its effect on leptin secretion, which is mainly regulated by produce the same response. Thus, in experimental animals, sweet-
insulin-induced changes in glucose metabolism in fat cells (19, ened beverages appear to enhance caloric consumption.
20). Insulin increases leptin release (21) with a time delay of
several hours. Thus, a low insulin concentration after ingestion of Fructose and soft drinks
fructose would be associated with lower average leptin concen- A similar argument about the role of overconsumption of
trations than would be seen after ingestion of glucose. Because calorically sweetened beverages may apply to humans (29 –32).
 HIGH-FRUCTOSE CORN SYRUP AND OBESITY 539
TABLE 1
Availability of high-fructose corn syrup (HFCS) in the US caloric sweetener supply1

HFCS as percentage of total Percentage of HFCS Percentage of HFCS from

Year HFCS Total caloric sweeteners caloric sweeteners from HFCS-42 HFCS-55

g 䡠 person⫺1 䡠 d⫺1 g 䡠 person⫺1 䡠 d⫺1 % % %

1966 0.0 165.9 0.0 — —
1970 0.8 175.1 0.4 100.0 0.0
1975 7.1 168.8 4.2 100.0 0.0
1980 27.3 176.0 15.5 71.2 28.8
1985 64.7 184.4 35.1 34.3 65.7
1990 71.0 195.7 36.3 41.0 59.0
1995 82.3 211.7 38.9 39.9 60.1
2000 91.6 218.0 42.0 38.8 61.2
1
Data from reference 8. HFCS-42 and HFCS-55, HFCS containing 42% and 55% fructose, respectively.

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Mattes (29) reported that when humans ingest energy-containing beverages did not compensate for this consumption by reducing
beverages, energy compensation is less precise than when solid the intake of other beverages and foods and thus gained weight.
foods are ingested. In another study in humans, DiMeglio and The beverages in this study were sweetened with sucrose,
Mattes (30) found that when 15 healthy men and women were whereas in the United States almost all calorically sweetened
given a carbohydrate load of 1880 kJ/d (450 kcal/d) as a calori- beverages are sweetened with HFCS. Thus, we need a second
cally sweetened soda for 4 wk, they gained significantly more randomized controlled study that compares sucrose- and HFCS-
weight than when the same carbohydrate load was given in a solid sweetened beverages. This could establish whether the form of
form as jelly beans. Additional support for our hypothesis that the caloric sweetener played a role in the weight gain observed in
calorically sweetened beverages may contribute to the epidemic the study by Raben et al (32).
of obesity comes from a longitudinal study in adolescents. Lud- The results of the studies by Raben et al (32) and Ludwig et al
wig et al (31) showed that in adolescents participating in the (31) suggest that the rapid increase in the intake of calorically
Planet Health project, the quantity of sugar-sweetened beverages sweetened soft drinks could be a contributing factor to the epi-
ingested predicted initial body mass index (BMI; in kg/m2) and demic of weight gain. Between 1970, when HFCS was intro-
gain in BMI during the follow-up period. Raben et al (32) de- duced into the marketplace, and 2000, the per capita consumption
signed a randomized, double-blind study to compare the effect of of HFCS in the United States increased from 0.292 kg · personҀ1
calorically sweetened beverages with that of diet drinks on · yҀ1 (0.6 lb · personҀ1 · yҀ1) to 33.4 kg · personҀ1 · yҀ1 (73.5 lb
weight gain in moderately overweight men and women. This · personҀ1 · yҀ1), an increase of 쏜 100-fold (8) (Table 1). The
European study found that drinking calorically sweetened bev- total consumption of fructose increased nearly 30%. The con-
erages resulted in greater weight gain over the 10-wk study than sumption of free fructose showed a greater increase, which re-
did drinking diet drinks. Compared with the subjects who con- flected the increasing use of HFCS (Figure 1). During the same
sumed diet drinks, those who consumed calorically sweetened interval, the consumption of sucrose decreased nearly 50%, and

FIGURE 1. Estimated intakes of total fructose (F), free fructose (Œ), and high-fructose corn syrup (HFCS, ⽧) in relation to trends in the prevalence of
overweight (■) and obesity (x) in the United States. Data from references 7 and 35.
540 BRAY ET AL

the intakes of sucrose and HFCS are now nearly identical. Al- and the prevalence of obesity (BMI 쏜 30) were fit with fourth-order
though this shift has clearly led to a major increase in free- polynomial curves so that the limited number of data points could be
fructose consumption, it is unclear how much of the increase in fitted into a curve to capture the US trends. We also included esti-
consumption of calorically sweetened soft drinks is a result of the mates of free-fructose intake and total fructose intake. Total fructose
shift to beverages in which one-half of the fructose is free rather is the sum of free fructose and fructose that is part of the disaccharide
than bound with glucose as in sucrose. A recent review described sucrose. Free fructose is the monosaccharide in HFCS and is also
many facets of this issue (3). obtained in small amounts from other sources. Free-fructose intake
closely follows the intake of HFCS. Total fructose intake increased
nearly 30% between 1970 and 2000.
HFCS USE AND INTAKE

Availability of HFCS in the food supply Estimated HFCS consumption

In 1970 HFCS represented 쏝 1% of all caloric sweeteners The intake of caloric sweeteners in the United States has in-
available for consumption in the United States, but the HFCS creased rapidly, and nationally representative data from 1994 to
portion of the caloric sweetener market jumped rapidly in the 1998 from the USDA allow us to estimate an intake of 318 kcal/d

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1980s and by 2000 represented 42.0% of all caloric sweeteners for the average US resident aged 욷 2 y. This value is one-sixth
(Table 1) (8). HFCS-42 was initially the only HFCS component,
of the intake of all calories and close to one-third of the intake of
but by the early 1980s, HFCS-55 had become the major source
all carbohydrates and represents a significant increase over the past
and constituted 61.2% of all HFCS in 2000. These data are based
2 decades (Table 2). As the intake of caloric sweeteners increased,
on per capita food disappearance data. In the absence of direct
so did the fructose load, which increased from 158.5 to 228 kcal ·
measures of HFCS intake, these data provide the best indirect
personҀ1 · dҀ1 between 1977–1978 (36) and 1994 –1998 (38, 39).
measure of the HFCS available for consumption in the United
Furthermore, as shown in Table 2, the major increase in the
States. The data are useful for studying trends but probably over-
estimate intake patterns. Although it is useful to understand that intake of caloric sweeteners from 1977 to 1998 came from the
HFCS intake represents more than two-fifths of the total intake of intake of soft drinks and fruit drinks, and these intake values were
caloric sweeteners in the United States, it is also important to 105 and 31 kcal · personҀ1 · dҀ1, respectively, of the total added
recognize that the proportion of HFCS in some foods is much sugar intake of 318 kcal · personҀ1 · dҀ1 in 1994 –1998. More-
higher than that in other foods. over, more than one-half of the increased caloric sweetener in-
take during this time period came from the intake of these bev-
Foods containing HFCS erages. The intakes of these 2 types of beverages and of desserts
total about two-thirds of all caloric sweetener intake in the United
In the United States, HFCS is found in almost all foods con-
States today (Table 2).
taining caloric sweeteners. These include most soft drinks and
fruit drinks, candied fruits and canned fruits, dairy desserts and We have no way to directly measure total HFCS use. However,
flavored yogurts, most baked goods, many cereals, and jellies. one Food and Drug Administration study used very conservative
Over 60% of the calories in apple juice, which is used as the base methods to estimate HFCS use for the nationally representative
for many of the fruit drinks, come from fructose, and thus apple dietary intake sample from 1977 to 1978 from the USDA (35).
juice is another source of fructose in the diet. Lists of HFCS- Using measures of the proportion of HFCS in each food, Glins-
containing foods can be obtained from organizations concerned mann et al (40) created food category–wide estimates of the
with HFCS-related allergies (33). It is clear that almost all caloric proportion of caloric sweeteners that is HFCS. We applied those
sweeteners used by manufacturers of soft drinks and fruit drinks same proportions to a set of food groups to estimate the use of
are HFCS (4, 34). In fact, about two-thirds of all HFCS consumed caloric sweeteners not only during 1977–1978 but also during
in the United States are in beverages. Aside from beverages, there later periods. Using our conversion technique applied to the
is no definitive literature on the proportion of caloric sweeteners initial 1977–1978 Nationwide Food Consumption Survey data,
that is HFCS in other processed foods. HFCS is found in most we obtained results that were only 4 kcal higher than the esti-
processed foods; however, the exact compositions are not avail- mates of Glinsmann et al (39). This approach is based on HFCS
able from either the manufacturer or any publicly available food- composition in the early 1980s. With the use of the USDA value
composition table. of 4.2 g HFCS/tsp (0.84 g/mL), the availability of HFCS in the
food supply in the early 1980s was only one-half of the current
Trends in obesity and HFCS availability availability on a gram per capita basis (as shown in Table 1).
There are important similarities between the trend in HFCS Thus, we feel confident that we can use this approach to provide
availability and the trends in the prevalence of obesity in the a conservative lower limit of HFCS intake.
United States (Figure 1). Using age-standardized, nationally rep- In Table 2, the 2 columns at the right contain our estimates of
resentative measures of obesity at 5 time points from 1960 to 1999 HFCS intake and total fructose intake. On the basis of the trend
(35) and data on the availability of HFCS collected annually over in intakes, our estimate of HFCS intake for the most recent period
this same period, we graphed both patterns. The data on obesity are of measurement from 1994 –1998 is 132 kcal · personҀ1 · dҀ1
from the National Center for Health Statistics for the following (37). This represents a shift between 1977–1978 and 1994 –1998
periods: 1960 –1962 (National Health Examination Survey I), from 4.5% of total calories to 6.7% of total calories, or from
1971–1975 [National Health and Nutrition Examination Survey 10.1% of carbohydrates to 13.1% of carbohydrates (41). The
(NHANES)], 1976 –1980 (NHANES II), 1988 –1994 (NHANES estimate of total fructose intake, which was obtained from the
III), and 1999 (NHANES 1999 –2000) (35). The HFCS data are intakes of sucrose and HFCS, would be somewhat higher if
those from Table 1. The prevalence of overweight (BMI of 25–29.9) we knew the fructose content of the fruit drinks.
 HIGH-FRUCTOSE CORN SYRUP AND OBESITY 541
TABLE 2
Trends in intakes of added sugar (sucrose) and high-fructose corn syrup (HFCS) by Americans aged 욷 2 y1

Total added Estimated HFCS Estimated total fructose

Soft drinks Fruit drinks Desserts sugar intake2 intake3

Intake (kcal 䡠 personҀ1 䡠 dҀ1)

1977–1978 52 18 54 235 80 158.5
1989–1991 744 19 474 242 95 170
1994–1998 1054,5 314,5 604,5 3184,5 132 228
Percentage of total energy (%)
1977–1978 2.9 1.0 3.0 13.1 4.5 8.8
1989–1991 4.14 1.1 2.64 13.5 5.3 9.4
1994–1998 5.34,5 1.64,5 3.04,5 16.04,5 6.7 11.5
Percentage of total carbohydrates (%)
1977–1978 6.5 2.3 6.8 29.5 10.1 19.8
1989–1991 8.54 2.2 5.44 27.8 10.9 19.5
10.44,5 3.14,5 5.94,5 31.54,5

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1994–1998 13.1 22.8
1
Data from references 36 –39.
2
Coefficients derived from Glinsmann et al (40) were used to estimate HFCS intake.
3
Estimated as 50% of sucrose ѿ fructose in HFCS.
4
Significantly different from 1977–1978, P 울 0.01 (t test).
5
Significantly different from 1989 –1991, P 울 0.01 (t test).

Distribution of HFCS intake matters! vative estimate. This same group obtains almost one-half of its
We also explored the distribution of HFCS consumption by carbohydrates from caloric sweeteners and one-fifth of its car-
examining quintiles of caloric sweetener intake among Ameri- bohydrates from HFCS.
cans aged 욷 2 y (Table 3). Most of the increase in caloric
sweetener intake from the middle quintile to the upper quintile
came from increases in the intake of calorically sweetened bev- DISCUSSION
erages, particularly soft drinks. Consumers in the top quintile, Genetic factors play an important role in the development of
which represents 20% of all Americans, consume 쏜 11% of their obesity (42). However, the rapidity with which the current epi-
calories from HFCS. Again, remember that this is a very conser- demic of obesity has descended on the United States (35) and

TABLE 3
Distribution of consumption of added caloric sweeteners and high-fructose corn syrup (HFCS) by quintile (Q) of added sugar intake in persons aged 욷 2 y
(1994 –1996, 1998)1

Q1 (n ҃ 3907) Q2 (n ҃ 4259) Q3 (n ҃ 4228) Q4 (n ҃ 3645) Q5 (n ҃ 2988) Total (n ҃ 19 027) P for trend

Added caloric sweeteners

Intake (kcal 䡠 personҀ1 䡠 dҀ1)
Soft drinks 6 31 69 129 290 105 0.022
Fruit drinks 4 14 26 43 69 31 0.003
Total 69 169 263 388 703 318 0.001
Percentage of total energy in kcal (%)
Soft drinks 0.4 1.9 3.7 6.0 10.2 5.3 0.004
Fruit drinks 0.3 0.8 1.4 2.0 2.4 1.6 0.0001
Total 4.9 10.2 14.0 18.1 24.7 16.0 0.0004
Percentage of carbohydrates (%)
Soft drinks 0.9 3.8 7.3 11.6 18.8 10.4 0.003
Fruit drinks 0.6 1.7 2.8 3.9 4.5 3.1 0.0004
Total 10.5 20.8 27.9 35.0 45.6 31.4 0.0002
HFCS
Intake (kcal 䡠 personҀ1 䡠 dҀ1)
Soft drinks 4 22 49 91 205 74 0.022
Fruit drinks 3 10 18 30 49 22 0.004
Total 21 58 103 166 316 132 0.012
Percentage of total energy in kcal (%)
Soft drinks 0.3 1.3 2.6 4.2 7.2 3.7 0.005
Fruit drinks 0.2 0.6 1.0 1.4 1.7 1.1 쏝0.0001
Total 1.5 3.5 5.5 7.7 11.1 6.7 0.0007
Percentage of carbohydrates (%)
Soft drinks 0.6 2.7 5.2 8.2 13.3 7.3 0.003
Fruit drinks 0.4 1.2 1.9 2.7 3.2 2.2 0.0002
Total 3.2 7.2 10.9 14.9 20.5 13.1 0.0002
1
Data from references 38 and 39 (weighted to be nationally representative).
542 BRAY ET AL

many other countries (43) makes environmental factors the more intake decreased by 쏜 50 mg/d (쏜 10%) between 1977 and 1996
likely explanation. From a public health perspective, the key (49). A convincing set of epidemiologic and clinical studies
question is whether there are modifiable environmental agents suggests that dairy products may have a favorable effect on body
that could have triggered this epidemic and that might be altered. weight and insulin resistance in both children and adults (50 –52).
Several environmental agents, including reduced levels of phys- During the interval from 1970 to 1990, the intake of whole milk
ical activity (44), a decrease in smoking, increased portion size decreased 58%. However, the intake of cheese, which is high in
(2), eating outside the home and at fast-food restaurants, and fat, increased and partially offset the decrease in calcium intake
changes in the types of food that are ingested (45), have been from milk (8). Because milk is a major source of dietary calcium
suggested. In this article, we propose that the introduction of for most humans, this decrease in milk intake may play an im-
HFCS and the increased intakes of soft drinks and other sweet- portant role in the decrease in calcium in the diet.
ened beverages have led to increases in total caloric and fructose One possible public health option is to address the sweet taste
consumption that are important contributors to the current epi- preference of humans by reducing HFCS and, if sweetness is
demic of obesity. needed, relying on artificial sweeteners to make up any differ-
In this article, we address an important potential hypothesis by ence in sweetness. It is becoming increasingly clear that soft
which HFCS may have an environmental link with the epidemic drink consumption may be an important contributor to the epi-

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of obesity. When total calorie intake is fixed, ie, if a person eats demic of obesity, in part through the larger portion sizes of these
the same amount of fructose, glucose, or sucrose in a metaboli- beverages and through the increased intake of fructose from
cally controlled setting, the response should be the same, and this HFCS and sucrose (53). If HFCS acts as an agent in the disease,
was shown by McDevitt et al (46). This situation is not one in then reducing exposure to this agent may help to reduce the
which differences in taste and portion size are allowed to operate. epidemic (54).
However, many biological factors that we noted in this article Some will question our measures of HFCS intake and avail-
suggest that calorically sweetened beverages are associated with ability. Our very conservative estimate of HFCS use and the Food
overconsumption when the sweetener is in a liquid form (29 –32). and Drug Administration data showed high HFCS intakes for a
The collective data suggest that overconsumption of beverages large segment of the US population (39).
sweetened with HFCS and containing 쏜 50% free fructose and In conclusion, we believe that an argument can now be made
the increased intake of total fructose may play a role in the that the use of HFCS in beverages should be reduced and that
epidemic of obesity. Whether HFCS used in solid food produces HFCS should be replaced with alternative noncaloric sweeten-
the same overconsumption as it does in beverages is unknown, ers. Sweetness is a preferred taste as well as an acquired one that
but we suspect that if the HFCS was entirely in the solid form, it may be enhanced by exposure to sweet foods. The hypothesis that
would not pose the same problem (30). Total fructose, both free providing sodas and juice drinks in which caloric sweeteners are
fructose and fructose combined in sucrose, in both beverages and partially or completely replaced with noncaloric sweeteners will
solid food may be viewed as a precursor to fat because of the ease help reduce the prevalence of obesity is worth testing. If the
with which the carbon skeleton of fructose can form the back- intake of calorically sweetened beverages is contributing to the
bone for triacylglycerols and be used for the synthesis of long- current epidemic, then reducing the availability of these bever-
chain fatty acids (25). Additional clinical trials are clearly needed ages by removing soda machines from schools would be a strat-
to buttress the conclusions of Raben et al (32) that beverages egy worth considering, as would reducing the portion sizes of
containing sugar caused more weight gain over 10 wk than did sodas that are commercially available (55).
diet beverages.
We thank Dan Blanchette for programming assistance, Tom Swasey for
There is a distinct likelihood that the increased consumption of graphics support, and Frances Dancy for support in administrative matters.
HFCS in beverages may be linked to the increase in obesity. One We also thank Linda Adair for thoughtful comments on an early version of
US study showed that beverages sweetened with HFCS are this article.
linked with increased energy intake and weight gain (31). Fur-
thermore, we showed that the increase in the use of HFCS was
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