Scientific studies on high fructose corn syrup ......

[click image to enlarge] High Fructose Corn Syrup (HFCS) has replaced Sucrose in many food products, which has prompted research comparing these two Sweeteners in rodents. The present study examined the relative palatability of HFCS and Sucrose for rats, offering 11% carbohydrate solutions to match the content of common beverages for human consumption. The animals initially preferred HFCS to Sucrose but after separate experience with each solution they switched to sucrose preference. Approximating the composition of HFCS with a mixture of Fructose and Glucose (55:45) yielded a solution that was less attractive than sucrose or HFCS. However, HFCS contains a small amount of Glucose polymers, which are very attractive to rats. A 55:42:3 mixture of fructose, glucose and glucose polymers (Polycose) was equally preferred to HFCS and was treated similarly to HFCS in comparisons vs. Sucrose. Post-oral effects of sucrose, which is 50% Fructose and 50% glucose, may be responsible for the shift in preference with experience. This shift, and the relatively small magnitude of differences in preference for HFCS and sucrose, suggest that palatability factors probably do not contribute to any possible difference in weight gain responses to these Sweeteners.Misconceptions about high fructose corn syrup: is it uniquely responsible for obesity, reactive dicarbonyl compounds, and advanced glycation endproducts? Misconceptions about high-fructose Corn Syrup (HFCS) abound in the scientific literature, the advice of health professionals to their patients, media reporting, product advertising, and the irrational behavior of consumers. Foremost among these is the misconception that HFCS has a unique and substantive responsibility for the current Obesity crisis. Inaccurate information from ostensibly reliable sources and selective presentation of research data gathered under extreme experimental conditions, representing neither the human diet nor HFCS, have misled the uninformed and created an atmosphere of distrust and avoidance for what, by all rights, should be considered a safe and innocuous sweetener. In the first part of this article, common misconceptions about the composition, functionality, metabolism, and use of HFCS and its purported link to obesity are identified and corrected. In the second part, an emerging misconception, that HFCS in carbonated soft drinks contributes materially to physiological levels of reactive dicarbonyl compounds and advanced glycation endproducts, is addressed in detail, and evidence is presented that HFCS does not pose a unique dietary risk in healthy individuals or diabetics.The effect of high fructose corn syrup consumption on triglycerides and uric acid.
Rates of overweight and obesity have been on a steady rise for decades, and the problems society faces from this and associated metabolic diseases are many. As a result, the need to understand the contributing factors is great. A very compelling case can be made that excess Sugar consumption has played a significant role. In addition, fructose, as a component of the vast majority of caloric sweeteners, is seen to be particularly insidious. Evidence shows that Fructose bypasses many of the body's satiating signals, thus potentially promoting overconsumption of energy, weight gain, and the development on Insulin Resistance. It has also been shown to increase uric acid levels, which in turn promotes many of the abnormalities seen in the metabolic syndrome including hypertriglyceridemia. However, the main source of Fructose in the diet is high-fructose Corn Syrup (HFCS), an artificially manufactured disaccharide that is only 55% Fructose. This review highlights the fact that limited data are available about the metabolic effects of HFCS compared with other caloric Sweeteners. The data suggest that HFCS yields similar metabolic responses to other caloric Sweeteners such as Sucrose. Scientific studies on Fructose;Slc2a5 (Glut5) is essential for the absorption of fructose in the intestine and generation of fructose induced hypertension. The identity of the transporter responsible for Fructose absorption in the intestine in vivo and its potential role in fructose-induced hypertension remain speculative. Here we demonstrate that Glut5 (Slc2a5) deletion reduced Fructose absorption by approximately 75% in the jejunum and decreased the concentration of serum Fructose by approximately 90% relative to wild-type mice on increased dietary Fructose. When fed a control (60% starch) diet, Glut5(-/-) mice had normal blood pressure and displayed normal weight gain. However, whereas Glut5(+/+) mice showed enhanced salt absorption in their jejuna in response to luminal Fructose and developed systemic Hypertension when fed a high fructose (60% fructose) diet for 14 weeks, Glut5(-/-) mice did not display fructose-stimulated Salt absorption in their jejuna, and they experienced a significant impairment of nutrient absorption in their intestine with accompanying hypotension as early as 3-5 days after the start of a high fructose diet. Examination of the intestinal tract of Glut5(-/-) mice fed a high fructose diet revealed massive dilatation of the caecum and colon, consistent with severe malabsorption, along with a unique adaptive up-regulation of ion transporters. In contrast to the malabsorption of fructose, Glut5(-/-) mice did not exhibit an absorption defect when fed a high Glucose (60% glucose) diet. We conclude that Glut5 is essential for the absorption of fructose in the intestine and plays a fundamental role in the generation of fructose-induced hypertension. Deletion of Glut5 results in a serious nutrient-absorptive defect and volume depletion only when the animals are fed a high fructose diet and is associated with compensatory adaptive up-regulation of ion-absorbing transporters in the colon.Direct all cause health care costs associated wit

BACKGROUND : Diabetes and Hypertension are the 2 major causes of endstage renal disease. The rate of Chronic kidney disease (CKD) secondary to Diabetes and/or hypertension is on the rise, and the related health care costs represent a significant economic burden.

OBJECTIVE : To quantify from a health system perspective the incremental direct all-cause health care costs associated with a diagnosis of CKD in patients with diabetes and/or Hypertension.

METHODS : An analysis was conducted of medical claims and laboratory data with dates of service between January 1, 2000, and February 28, 2006, from a managed care database for approximately 30 million members enrolled in 35 health plans. Each patient's observation period began on the date of the first diabetes or hypertension diagnosis (index date) and ended on the earlier of the health plan disenrollment date or February 28, 2006. Inclusion criteria were continuous insurance coverage in the 6 months prior to the index date and during the observation period, age at least 18 years, and at least 2 claims less than 90 days apart with a primary or secondary diagnosis for diabetes or hypertension. Exclusion criteria were cancer, lupus, or organ transplantation or chemotherapy at any time during the observation period. CKD was defined as at least 1 claim with a primary or secondary diagnosis for CKD and at least 2 glomerular filtration rate values of below 60 milliliters per minute per 1.73 square meters of body surface area (60 mL/min/1.73 m(2)) at any time during the observation period. Bivariate and Tobit regression analyses were conducted to compare patients who developed CKD versus those who did not for annualized (per patient per month [PPPM] multiplied by 12) direct, all-cause, health care costs, defined as standardized net provider payments after subtraction of member cost-share. These costs consisted of outpatient services, inpatient services, and pharmacy claims. A subset analysis of the post-versus pre- CKD medical costs was also conducted for cohorts of patients with at least 60 days of observation before and after the development of CKD; that analysis measured both all-cause costs and costs for services directly related to CKD treatment (i.e., claims with a primary or secondary diagnosis of CKD or claims for dialysis services).

RESULTS : 11,531 patients with diabetes, 74,759 patients with hypertension, and 4,779 patients with both conditions were identified, of whom 123 (1.1%), 1,137 (1.5%), and 712 (14.9%), respectively, developed CKD during the observation period. The CKD group was older than the no-CKD group in each cohort (mean ages for CKD vs. no-CKD were, respectively, diabetes only cohort: 60.7 vs. 49.9 years, P < 0.001; hypertension only cohort: 63.6 vs. 53.6 years, P < 0.001; diabetes and hypertension cohort: 63.4 vs. 61.8 years, P < 0.001). CKD was associated with significantly higher total direct all-cause health care costs, with unadjusted annualized per patient mean [median] cost differences of $11,814 [$6,895], $8,412 [$4,115], and $10,625 [$7,203], respectively (diabetes: $18,444 [$11,025] vs. $6,631 [$4,131], P < 0.001; hypertension: $14,638 [$7,817] vs. $6,226 [$3,703], P < 0.001; diabetes and hypertension: $21,452 [$13,840] vs. $10,827 [$6,637], P < 0.001). The largest driver of the all-cause mean cost difference associated with CKD for each cohort was hospitalization cost (diabetes: $6,410, P < 0.001; hypertension: $5,498, P < 0.001; diabetes and hypertension: $6,467, P < 0.001). Among patients developing CKD, all-cause mean [median] annualized costs increased significantly following CKD onset (increases for patients with diabetes: $8,829 [$4,899], P = 0.026; hypertension: $4,175 [$2,741], P = 0.004; diabetes and hypertension: $9,397 [$7,240], P < 0.001). In the post-CKD period, costs directly related to treatment of CKD accounted for 9%--19% of all-cause medical service costs--9.2% for patients with diabetes, 11.6% for patients with hypertension, and 18.8% for patients with both diabetes and hypertension.

CONCLUSION : CKD was associated with significantly higher all-cause health care costs in managed care patients with diabetes and/or hypertension. h chronic kidney disease in patients with diabetes and hypertension: a managed care perspective. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity1,2-besity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged ≥ 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.

Epidemiology food intake obesity artificial sweeteners fructose:

INTRODUCTION:

As obesity has escalated to epidemic proportions around the world, many causes, including dietary components, have been suggested. Excessive caloric intake has been related to high-fat foods, increased portion sizes, and diets high both in simple sugars such as sucrose and in high-fructose corn syrup (HFCS) as a source of fructose (1–3). In this article, we discuss the evidence that a marked increase in the use of HFCS, and therefore in total fructose consumption, preceded the obesity epidemic and may be an important contributor to this epidemic in the United States.

To provide a common frame of reference for the terms used in this paper, the following definitions should be understood. Sugar is any free monosaccharide or disaccharide present in a food. Sugars includes at least one sugar; composite sugars refers to the aggregate of all forms of sugars in a food and is thus distinguishable from specific types of sugar, such as fructose, glucose, or sucrose. Added sugar is sugar added to a food and includes sweeteners such as sucrose, HFCS, honey, molasses, and other syrups. Naturally occurring sugar is sugar occurring in food and not added in processing, preparation, or at the table. Total sugars represents the total amount of sugars present in a food and includes both naturally occurring and added sugars. Free fructose is fructose that exists in food as the monosaccharide. Fructose refers to both the free and bound forms of fructose.

Added sweeteners are important components of our diet, representing 318 kcal of dietary intake for the average American aged ≥ 2 y, or 16% of all caloric intake as measured by a nationally representative survey in 1994–1996 (5). Sweet corn-based syrups were developed during the past 3 decades and now represent close to one-half of the caloric sweeteners consumed by Americans (6, 7). HFCS made by enzymatic isomerization of glucose to fructose was introduced as HFCS-42 (42% fructose) and HFCS-55 (55% fructose) in 1967 and 1977, respectively, and opened a new frontier for the sweetener and soft drink industries. Using a glucose isomerase, the starch in corn can be efficiently converted to glucose and then to various amounts of fructose. The hydrolysis of sucrose produces a 50:50 molar mixture of fructose and glucose. The development of these inexpensive, sweet corn-based syrups made it profitable to replace sucrose (sugar) and simple sugars with HFCS in our diet, and they now represent 40% of all added caloric sweeteners (8). Fructose is sweeter than sucrose. In comparative studies of sweetness, in which the sweetness of sucrose was set at 100, fructose had a sweetness of 173 and glucose had a sweetness of 74 (9). If the values noted above 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 contrasts with the estimates reported by Hanover and White (10). In their study, the sweetness of sucrose was set at 100 as in reference 8. Fructose, however, had a sweetness of only 117, whereas a 50:50 mixture of fructose and sucrose had a sweetness of 128. It is difficult to see why fructose and sucrose combined would be sweeter than either one alone and as sweet as HFCS-55. On the basis of data in Agriculture Handbook no. 8 from the US Department of Agriculture (USDA) (11), a cola beverage in 1963 had 39 kcal/100 g, whereas a cola beverage in 2003 had 41 kcal/100 g. Because the number of calories per 100 g has not changed substantially over the past 40 y, current beverages are probably sweeter, depending on the temperature at which they are served.

HFCS has become a favorite substitute for sucrose in carbonated beverages, baked goods, canned fruits, jams and jellies, and dairy products (10). The major user of HFCS in the world is the United States; however, HFCS is now manufactured and used in many countries throughout the world (7). In the United States, HFCS is the major source of caloric sweeteners in soft drinks and many other sweetened beverages and is also included in numerous other foods; therefore, HFCS constitutes a major source of dietary fructose. Few data are available on foods containing HFCS in countries other than the United States.

THE BIOLOGY:

Absorption of fructose;
The digestive and absorptive processes for glucose and fructose are different. When disaccharides such as sucrose or maltose enter the intestine, they are cleaved by disaccharidases. A sodium-glucose cotransporter absorbs the glucose that is formed from cleavage of sucrose. Fructose, in contrast, is absorbed further down in the duodenum and jejunum by a non-sodium-dependent process. After absorption, glucose and fructose enter the portal circulation and either are transported to the liver, where the fructose can be taken up and converted to glucose, or pass into the general circulation. The addition of small, catalytic amounts of fructose to orally ingested glucose increases hepatic glycogen synthesis in human subjects and reduces glycemic responses in subjects with type 2 diabetes mellitus (12), which suggests the importance of fructose in modulating metabolism in the liver. However, when large amounts of fructose are ingested, they provide a relatively unregulated source of carbon precursors for hepatic lipogenesis.

Fructose and insulin release--
Along with 2 peptides, glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 released from the gastrointestinal tract, circulating glucose increases insulin release from the pancreas (13, 14). Fructose does not stimulate insulin secretion in vitro, probably because the β cells of the pancreas lack the fructose transporter Glut-5 (15, 16). Thus, when fructose is given in vivo as part of a mixed meal, the increase in glucose and insulin is much smaller than when a similar amount of glucose is given. However, fructose produces a much larger increase in lactate and a small (1.7%) increase in diet-induced thermogenesis (17), which again suggests that glucose and fructose have different metabolic effects.

Insulin and leptin:
Insulin release can modulate food intake by at least 2 mechanisms. First, Schwartz et al (18) have argued that insulin concentrations in the central nervous system have a direct inhibitory effect on food intake. In addition, insulin may modify food intake by its effect on leptin secretion, which is mainly regulated by insulin-induced changes in glucose metabolism in fat cells (19, 20). Insulin increases leptin release (21) with a time delay of several hours. Thus, a low insulin concentration after ingestion of fructose would be associated with lower average leptin concentrations than would be seen after ingestion of glucose. Because leptin inhibits food intake, the lower leptin concentrations induced by fructose would tend to enhance food intake. This is most dramatically illustrated in humans who lack leptin (22, 23). Persons lacking leptin (homozygotes) are massively obese (22), and heterozygotes with low but detectable serum leptin concentrations have increased adiposity (23), which indicates that low leptin concentrations are associated with increased hunger and gains in body fat. Administration of leptin to persons who lack it produces a dramatic decrease in food intake, as expected. Leptin also increases energy expenditure, and during reduced calorie intake, leptin attenuates the decreases in thyroid hormones and 24-h energy expenditure (24). To the extent that fructose increases in the diet, one might expect less insulin secretion and thus less leptin release and a reduction in the inhibitory effect of leptin on food intake, ie, an increase in food intake. This was found in the preliminary studies reported by Teff et al (25). Consumption of high-fructose meals reduced 24-h plasma insulin and leptin concentrations and increased postprandial fasting triacylglycerol concentrations in women but did not suppress circulating ghrelin concentrations.

Fructose and metabolism:
The metabolism of fructose differs from that of glucose in several other ways as well (3). Glucose enters cells by a transport mechanism (Glut-4) that is insulin dependent in most tissues. Insulin activates the insulin receptor, which in turn increases the density of glucose transporters on the cell surface and thus facilitates the entry of glucose. Once inside the cell, glucose is phosphorylated by glucokinase to become glucose-6-phosphate, from which the intracellular metabolism of glucose begins. Intracellular enzymes can tightly control conversion of glucose-6-phosphate to the glycerol backbone of triacylglycerols through modulation by phosphofructokinase. In contrast with glucose, fructose enters cells via a Glut-5 transporter that does not depend on insulin. This transporter is absent from pancreatic β cells and the brain, which indicates limited entry of fructose into these tissues. Glucose provides “satiety” signals to the brain that fructose cannot provide because it is not transported into the brain. Once inside the cell, fructose is phosphorylated to form fructose-1-phosphate (26). In this configuration, fructose is readily cleaved by aldolase to form trioses that are the backbone for phospholipid and triacyglycerol synthesis. Fructose also provides carbon atoms for synthesis of long-chain fatty acids, although in humans, the quantity of these carbon atoms is small. Thus, fructose facilitates the biochemical formation of triacylglycerols more efficiently than does glucose (3). For example, when a diet containing 17% fructose was provided to healthy men and women, the men, but not the women, showed a highly significant increase of 32% in plasma triacylglycerol concentrations (27).

Overconsumption of sweetened beverages:
One model for producing obesity in rodents is to provide sweetened (sucrose, maltose, etc) beverages for them to drink (28). In this setting, the desire for the calorically sweetened solution reduces the intake of solid food, but not by enough to prevent a positive caloric balance and the slow development of obesity. Adding the same amount of sucrose or maltose as of a solid in the diet does not produce the same response. Thus, in experimental animals, sweetened beverages appear to enhance caloric consumption.

Fructose and soft drinks:
A similar argument about the role of overconsumption of calorically sweetened beverages may apply to humans (29–32). Mattes (29) reported that when humans ingest energy-containing beverages, energy compensation is less precise than when solid foods are ingested. In another study in humans, DiMeglio and Mattes (30) found that when 15 healthy men and women were given a carbohydrate load of 1880 kJ/d (450 kcal/d) as a calorically sweetened soda for 4 wk, they gained significantly more weight than when the same carbohydrate load was given in a solid form as jelly beans. Additional support for our hypothesis that calorically sweetened beverages may contribute to the epidemic of obesity comes from a longitudinal study in adolescents. Ludwig et al (31) showed that in adolescents participating in the Planet Health project, the quantity of sugar-sweetened beverages ingested predicted initial body mass index (BMI; in kg/m2) and gain in BMI during the follow-up period. Raben et al (32) designed a randomized, double-blind study to compare the effect of calorically sweetened beverages with that of diet drinks on weight gain in moderately overweight men and women. This European study found that drinking calorically sweetened beverages resulted in greater weight gain over the 10-wk study than did drinking diet drinks. Compared with the subjects who consumed diet drinks, those who consumed calorically sweetened beverages did not compensate for this consumption by reducing the intake of other beverages and foods and thus gained weight. The beverages in this study were sweetened with sucrose, whereas in the United States almost all calorically sweetened beverages are sweetened with HFCS. Thus, we need a second randomized controlled study that compares sucrose- and HFCS-sweetened beverages. This could establish whether the form of the caloric sweetener played a role in the weight gain observed in the study by Raben et al (32).

The results of the studies by Raben et al (32) and Ludwig et al (31) suggest that the rapid increase in the intake of calorically sweetened soft drinks could be a contributing factor to the epidemic of weight gain. Between 1970, when HFCS was introduced into the marketplace, and 2000, the per capita consumption of HFCS in the United States increased from 0.292 kg · person−1 · y−1 (0.6 lb · person−1 · y−1) to 33.4 kg · person−1 · y−1 (73.5 lb · person−1 · y−1), an increase of > 100-fold (8) (Table 1⇓). The total consumption of fructose increased nearly 30%. The consumption of free fructose showed a greater increase, which reflected the increasing use of HFCS (Figure 1⇓). During the same interval, the consumption of sucrose decreased nearly 50%, and the intakes of sucrose and HFCS are now nearly identical. Although this shift has clearly led to a major increase in free-fructose consumption, it is unclear how much of the increase in consumption of calorically sweetened soft drinks is a result of the shift to beverages in which one-half of the fructose is free rather than bound with glucose as in sucrose. A recent review described many facets of this issue (
Estimated intakes of total fructose (•), free fructose (▴), and high-fructose corn syrup (HFCS, ♦)

HFCS USE AND INTAKE:

Availability of HFCS in the food supply-
In 1970 HFCS represented < 1% of all caloric sweeteners available for consumption in the United States, but the HFCS portion of the caloric sweetener market jumped rapidly in the 1980s and by 2000 represented 42.0% of all caloric sweeteners (Table 1⇑) (8). HFCS-42 was initially the only HFCS component, but by the early 1980s, HFCS-55 had become the major source and constituted 61.2% of all HFCS in 2000. These data are based on per capita food disappearance data. In the absence of direct measures of HFCS intake, these data provide the best indirect measure of the HFCS available for consumption in the United States. The data are useful for studying trends but probably overestimate intake patterns. Although it is useful to understand that HFCS intake represents more than two-fifths of the total intake of caloric sweeteners in the United States, it is also important to recognize that the proportion of HFCS in some foods is much higher than that in other foods.

Foods containing HFCS:
In the United States, HFCS is found in almost all foods containing caloric sweeteners. These include most soft drinks and fruit drinks, candied fruits and canned fruits, dairy desserts and flavored yogurts, most baked goods, many cereals, and jellies. Over 60% of the calories in apple juice, which is used as the base for many of the fruit drinks, come from fructose, and thus apple juice is another source of fructose in the diet. Lists of HFCS-containing foods can be obtained from organizations concerned with HFCS-related allergies (33). It is clear that almost all caloric sweeteners used by manufacturers of soft drinks and fruit drinks are HFCS (4, 34). In fact, about two-thirds of all HFCS consumed in the United States are in beverages. Aside from beverages, there is no definitive literature on the proportion of caloric sweeteners that is HFCS in other processed foods. HFCS is found in most processed foods; however, the exact compositions are not available from either the manufacturer or any publicly available food-composition table.

Trends in obesity and HFCS availability;
There are important similarities between the trend in HFCS availability and the trends in the prevalence of obesity in the United States (Figure 1⇑). Using age-standardized, nationally representative measures of obesity at 5 time points from 1960 to 1999 (35) and data on the availability of HFCS collected annually over this same period, we graphed both patterns. The data on obesity are from the National Center for Health Statistics for the following periods: 1960–1962 (National Health Examination Survey I), 1971–1975 [National Health and Nutrition Examination Survey (NHANES)], 1976–1980 (NHANES II), 1988–1994 (NHANES III), and 1999 (NHANES 1999–2000) (35). The HFCS data are those from Table 1⇑. The prevalence of overweight (BMI of 25–29.9) and the prevalence of obesity (BMI > 30) were fit with fourth-order polynomial curves so that the limited number of data points could be fitted into a curve to capture the US trends. We also included estimates of free-fructose intake and total fructose intake. Total fructose is the sum of free fructose and fructose that is part of the disaccharide sucrose. Free fructose is the monosaccharide in HFCS and is also 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.

Estimated HFCS consumption:
The intake of caloric sweeteners in the United States has increased rapidly, and nationally representative data from 1994 to 1998 from the USDA allow us to estimate an intake of 318 kcal/d for the average US resident aged ≥ 2 y. This value is one-sixth of the intake of all calories and close to one-third of the intake of all carbohydrates and represents a significant increase over the past 2 decades (Table 2⇓). As the intake of caloric sweeteners increased, so did the fructose load, which increased from 158.5 to 228 kcal · person−1 · d−1 between 1977–1978 (36) and 1994–1998 (38, 39).
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