Curry DL. Effects of mannose and fructose on the synthesis and secretion of insulin. Central nervous system control of food intake. Regulation of hepatic de novo lipogenesis in humans. Annu Rev Nutr ;— Fructose, weight gain, and the insulin resistance syndrome. Clinical Nutrition, Nov ; — Fructose, insulin resistance, and metabolic dyslipidemia.
Nutr Metab Lond. Bray, G. American Journal of Clinical Nutrition, April ; vol pp Journal of Food Science, ; 49 1 , — A critical examination of the evidence relating high fructose corn syrup and weight gain. Crit Rev Food Sci Nutr. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr. Help the OAC to raise awareness, advocate for improved access, provide evidence-based education, fight to eliminate weight bias and discrimination and elevate the conversation of weight and its impact on health.
This way…. Donate Today. Sort By:. Related Articles. What Is Fructose Intolerance? Is Sugar Bad for Your Heart? How to Lower Your Triglycerides Naturally. Trending Topics. What Parents Need to Know. Share this article via email with one or more people using the form below. Thus, eating HFCS will decrease the total nutrient content of your diet, as the more HFCS you consume, the less room you have for nutrient-dense foods.
Over the past few decades, high-fructose corn syrup HFCS has become affordable and widely available. Experts now attribute its excessive intake to many serious health issues, including obesity, insulin resistance, and metabolic syndrome, among others. Avoiding high-fructose corn syrup — and added sugar in general — may be one of the most effective ways to improve your health and lower your risk of disease.
This is a detailed article about high fructose corn syrup HFCS. What it is, how it is made and how its health effects compare to regular sugar.
High-fructose corn syrup is seriously bad for your health, but it's being added to all sorts of foods. Here are 20 foods that are often loaded with it. Some foods can drive inflammation and raise your risk of chronic disease. Here are 6 foods that increase inflammation in the body. Consumption of the natural sugar fructose and the man-made sweetener high fructose corn syrup appear to increase the risk of gout.
A gout-friendly…. Not all sugars are created equal, which matters when it comes to your health. Here's the difference between sucrose, glucose and fructose. 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. 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. 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 , 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. 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 , 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 , 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 h energy expenditure 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 Consumption of high-fructose meals reduced h plasma insulin and leptin concentrations and increased postprandial fasting triacylglycerol concentrations in women but did not suppress circulating ghrelin concentrations.
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 glucosephosphate, from which the intracellular metabolism of glucose begins.
Intracellular enzymes can tightly control conversion of glucosephosphate 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. Once inside the cell, fructose is phosphorylated to form fructosephosphate 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. One model for producing obesity in rodents is to provide sweetened sucrose, maltose, etc beverages for them to drink 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.
A similar argument about the role of overconsumption of calorically sweetened beverages may apply to humans 29 — Mattes 29 reported that when humans ingest energy-containing beverages, energy compensation is less precise than when solid foods are ingested.
Additional support for our hypothesis that calorically sweetened beverages may contribute to the epidemic of obesity comes from a longitudinal study in adolescents. 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 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 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. The consumption of free fructose showed a greater increase, which reflected the increasing use of HFCS Figure 1.
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 3. Data from reference 8. Data from references 7 and These data are based on per capita food disappearance data.
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.
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. It is clear that almost all caloric sweeteners used by manufacturers of soft drinks and fruit drinks are HFCS 4 , 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. 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 to 35 and data on the availability of HFCS collected annually over this same period, we graphed both patterns.
The prevalence of overweight BMI of 25— 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. 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 Data from references 36 — Moreover, more than one-half of the increased caloric sweetener intake during this time period came from the intake of these beverages.
The intakes of these 2 types of beverages and of desserts total about two-thirds of all caloric sweetener intake in the United States today Table 2. We have no way to directly measure total HFCS use.
We applied those same proportions to a set of food groups to estimate the use of caloric sweeteners not only during — but also during later periods. Using our conversion technique applied to the initial — Nationwide Food Consumption Survey data, we obtained results that were only 4 kcal higher than the estimates of Glinsmann et al This approach is based on HFCS composition in the early s.
With the use of the USDA value of 4.
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