High-fructose corn syrup linked to type 2 diabetes

Countries using high-fructose corn syrup have diabetes rates 20 percent higher than countries that do not, a new international analysis finds.

High-fructose corn syrup (HFCS) in national food supplies around the world might help explain the rising rates of type 2 diabetes around the world, researchers at the University of Southern California and the University of Oxford report in the journal Global Public Health.

After studying 42 countries, researchers found that those that use HFCS in their food supply had a 20 percent higher prevalence of diabetes than those that did not use HFCS, suggesting an association with diabetes independent of total sugar intake and obesity levels.

"HFCS appears to pose a serious public health problem on a global scale," said principal study author Michael I. Goran, MD, professor of preventive medicine , director of the Childhood Obesity Research Center, and co-director of the Diabetes and Obesity Research Institute at the Keck School of Medicine at USC in a release. "The study adds to a growing body of scientific literature that indicates HFCS consumption may result in negative health consequences distinct from and more deleterious than natural sugar."

Not surprisingly, the United States topped the list with the most per-capita consumption of HFCS - 55 pounds per person, per year. The second highest was Hungary, with an annual rate of 46 pounds per person per year. Canada, Slovakia Bulgaria, Belgium, Argentina, Korea, Japan, and Mexico also had high rates while Germany, Poland, Greece, Portugal, Egypt, Finland, and Serbia were found to be among the lowest HFCS consumers.

Countries on the high end of the HFCS scale had an average type 2 diabetes rate of 8 percent, compared to 6.7 percent in countries not using HFCS. Researchers believe this link is driven by higher amounts of fructose in foods made with HFCS than in foods made with regular table sugar or glucose. Some evidence suggests that the body metabolizes fructose differently from glucose , researchers say in the article, though this runs contrary to the positions of the American Medical Association and the Academy of Nutrition and Dietetics, among other groups. The AMA says HFCS is no worse for the body than glucose-containing table sugar - a claim that's hard for some consumers to believe, as HFCS has been vilified for decades because of its suspected role in weight gain and metabolic syndrome .

Regardless, the take-home message is that consumers need to reduce the amount of all forms of sugar and sweeteners in their diets, says Joan Salge Blake, MS, RD, LDN, a spokesperson for the Academy of Nutrition and Dietetics. "Honey, high-fructose corn syrup, corn syrup, sucrose, molasses - these are all sources of added sugars that we need to reduce in our diet," she says. "Sixty-five percent of Americans are overweight, and getting rid of foods like these that are just empty calories can potentially help manage weight."

"While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C(6)H(12)O(6)), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been proposed as mechanisms responsible for these adverse metabolic effects of fructose. Although there is compelling evidence that very high fructose intake can have deleterious metabolic effects in humans as in rodents, the role of fructose in the development of the current epidemic of metabolic disorders remains controversial. Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption."

I can see why you didn't want to print the whole abstract. There's enough indirect evidence.

Thanks for the link which linked the original article. Here's the conclusion:

VI. Perspectives
The potential danger of fructose consumption and its links to various metabolic disorders have been widely documented. Deleterious effects of high fructose intake on body weight, insulin sensitivity/glucose homeostasis, dyslipidemia, and atherosclerotic disease have been identified, and potential mechanisms have been proposed (Fig. 7). These effects, in humans, were often documented at very high levels of fructose intake, however, and some important questions remain to be addressed. Among the numerous deleterious effects of fructose, which ones are directly relevant for human daily nutrition? Most human studies addressing specifically the effects of fructose have administered large doses, often as a supplementation to an isocaloric diet. Nevertheless, there is solid evidence that fructose, even at moderate doses, can cause hypertriglyceridemia. Moreover, although data are scarcer, the fact that fructose may increase intrahepatic lipids and lead to insulin resistance in experimental settings raises some concern. Studies aimed at delineating the dose threshold at which fructose starts to chronically exert such effects remain to be performed. In addition to that, in everyday life, fructose cannot be blamed as the only culprit for all metabolic disorders. Indeed, a high fructose consumption most of the time clusters with additional “risky” behaviors, such as a hypercaloric diet, a diet rich in saturated fat, or low physical activity. Thus which part of metabolic disorders can be attributed to fructose and which results from interactions with other risk factors? Long-term intervention and longitudinal studies may help bring some clues to these issues.
Fig. 7. Potential relationships of high fructose intake with human diseases.

Isocaloric diets mean that the experimental group with more fructose got the same number of calories as the control group.

It's not just an increase in type 2 diabetes over time. This latest study finds about 20 % more in countries that allow HFCS versus no HFCS. Now there are two more diagnoses since HFCS cama on the scene: maturity onset diabetes of the young, MODY, and non-alcoholic fatty liver disease, NAFLD.

Is high-fructose corn syrup worse for our health than common table sugar? I’ve spent a lot of time researching this question.

First, consider how the two differ.

On the one hand, we have table sugar. Table sugar is sucrose. Sucrose is a disaccharide that consists of two larger molecules that are bonded together: a fructose molecule and a glucose molecule. If you look up the chemical diagrams of their common forms, you’ll see the fructose molecule has 5 atoms in a ring, while the glucose has 6.

To make table sugar, the sucrose from beets or cane basically is squeezed out of the plants and then purified.

During digestion inside our bodies, that glycosidic bond between the glucose and fructose molecules is very quickly hydrolyzed by digestive enzymes (like sucrase), converting the sucrose molecule into separate fructose and glucose molecules.

On the other hand, there’s high-fructose corn syrup (HFCS). HFCS is heavily processed using several enzymes to turn cornstarch first into glucose and then partially into fructose. In HFCS, the glucose and fructose molecules are chemically separate, not bonded together.

The molecular mixture of the form of HFCS common in the USA is approximately 55% fructose and 42% glucose. Sucrose, being a disaccaride, is exactly 50% fructose and 50% glucose. (For comparison, the composition of honey lies somewhere between these two ratios.)

So it’s clear that there is not a huge difference between the relative quantities of fructose and glucose in HFCS vis-a-vis sucrose. The proportion of fructose to glucose in HFCS is basically the same as in table sugar. Both sweeteners contain the same number of calories (4 kcal/gram).

Now, consider some differences between fructose and glucose.

Both molecules are natural sugar compounds found commonly in plants, but there are many biological differences resulting from the chemical differences between fructose and glucose. It turns out that fructose is sweeter than glucose. The 5-ring form of fructose fits more easily into the sweetness receptors on your tongue’s taste buds than the 6-ring form of glucose. So your brain thinks fructose tastes sweeter. On the Relative Sweetness Scale (where sucrose scores 100 by fiat), pure fructose scores 140, while pure glucose scores about 80.

Another biological difference is in how the two substances must be digested by the body. The metabolism of fructose is very similar to that of ethyl alcohol (which is just fermented sugar after all) in alcoholic beverages. Both fructose and ethanol must be processed by the liver before the cells of the rest of the body can make use of it. Through a complex chain of metabolic steps, fructose is eventually metabolized in the liver into glucose (glycogen) and fat. Glucose, on the other hand, is the ubiquitous biological fuel readily and directly usable by almost every cell in the body.

On account of the more complex hepatic pathway fructose must take for digestion, high fructose consumption can have a big impact on the liver, causing problems such as fatty liver disease, which is similar to cirrhosis of the liver caused by excessive alcohol consumption. In medical studies fatty liver disease is increasingly being linked with insulin resistance, type-2 diabetes, obesity, dyslipidemia, and high blood pressure.

As with alcohol, fructose increases blood pressure. Fructose reduces the production of nitric oxide within blood vessels, making it difficult for the vessels to relax and dilate. It also raises uric acid in the blood, which shrinks blood vessels. The effect is higher blood pressure on both counts.

Recent studies also show that consuming glucose triggers increases in a ‘satiety hormone’ called leptin that signals to the brain that we’ve eaten enough. It also blunts the effects of ghrelin, a ‘hunger hormone’ that makes us want to eat more. Fructose does not trigger these same ‘fullness’ cues. Fructose actually appears to increase our appetite.

A 2008 study found a substantial risk of gout associated with the consumption of fructose-rich foods.

The differences in metabolism of fructose and glucose have led some leading endocrinologists to call fructose a “dose-dependent toxin,” in the same way ethyl alcohol is. Fructose and alcohol are very similar in regard to disease and the metabolic havoc they wreak when consumed at a rate over 25 grams/day.

Now return to the HFCS/sucrose comparison.

The process of making HFCS is very cheap. It is even cheaper than making refined sucrose, due to government-regulated production quotas on domestic sugar, a 1977 import tariff on foreign sugar, and the subsidization of corn production.

On account of its greater sweetness and lower cost, the use of HFCS as an added sweetener has exploded in the USA: sodas, fruit juices, breads, cereals, breakfast bars, lunch meats, sauces, soups, yogurt, condiments, and many other processed foods are loaded with HFCS. The number of sugar calories Americans get today from food has increased 50% from the 1970s, due to the ubiquity of HFCS sweetening.

The HFCS lobby (Corn Refiners Association) says that HFCS is basically no different than table sugar. Both sucrose (50% fructose, 50% glucose) and HFCS (55% fructose, 42% glucose) contain a similar ratios of fructose to glucose.

They are probably basically right. The amount of fructose in HFCS is only marginally greater in HFCS compared to sucrose. It’s hard to believe the small difference could result in a large effect. But whether unfounded or not, there is a growing backlash against HFCS.

For most of human history refined sugars did not exist apart from the fairly rare consumption of honey. Before the 18th century refined sugar was an expensive luxury item. It became more widely popular in 18th century, and then in the 19th century it became a staple. After George McGovern’s 1977 Senate Select Committee on Nutrition issued a set of nutritional guidelines recommending that Americans consume less dietary fat, HFCS exploded on the scene as a low-fat substitute.

So, again, is high-fructose corn syrup worse for our health than common table sugar? It’s probably no worse. The point is that both are bad in large enough quantities, when fructose consumption exceeds around 25 grams/day, which is far less than the typical daily consumption in the standard American diet.

For more depth I highly recommend this popular video by Dr. Robert Lustig, an endocrinologist who specializes in pediatric obesity:

“Sugar: The Bitter Truth” http://www.youtube.com/watch?v=dBnniua6-oM

I noticed that the specific calorie count of sugar water consumed versus corn sweetened water consumed is not reported.

Do you think scientists write press releases?

High-fructose corn syrup causes characteristics of obesity in rats: increased body weight, body fat and triglyceride levels.

Abstract
High-fructose corn syrup (HFCS) accounts for as much as 40% of caloric sweeteners used in the United States. Some studies have shown that short-term access to HFCS can cause increased body weight, but the findings are mixed. The current study examined both short- and long-term effects of HFCS on body weight, body fat, and circulating triglycerides. In Experiment 1, male Sprague-Dawley rats were maintained for short term (8 weeks) on (1) 12 h/day of 8% HFCS, (2) 12 h/day 10% sucrose, (3) 24 h/day HFCS, all with ad libitum rodent chow, or (4) ad libitum chow alone. Rats with 12-h access to HFCS gained significantly more body weight than animals given equal access to 10% sucrose, even though they consumed the same number of total calories, but fewer calories from HFCS than sucrose. In Experiment 2, the long-term effects of HFCS on body weight and obesogenic parameters, as well as gender differences, were explored. Over the course of 6 or 7 months, both male and female rats with access to HFCS gained significantly more body weight than control groups. This increase in body weight with HFCS was accompanied by an increase in adipose fat, notably in the abdominal region, and elevated circulating triglyceride levels. Translated to humans, these results suggest that excessive consumption of HFCS may contribute to the incidence of obesity.

I’ve spent a lot of time researching this question.

I was a chemist before I became a physician.

Look at the ratio. 55:42 is almost 4:3. 56:42 is 4:3. But that's just the start of this business about numbers.

Sugar content of popular sweetened beverages based on objective laboratory analysis: focus on fructose content.

Abstract
The consumption of fructose, largely in the form of high fructose corn syrup (HFCS), has risen over the past several decades and is thought to contribute negatively to metabolic health. However, the fructose content of foods and beverages produced with HFCS is not disclosed and estimates of fructose content are based on the common assumption that the HFCS used contains 55% fructose. The objective of this study was to conduct an objective laboratory analysis of the sugar content and composition in popular sugar-sweetened beverages with a particular focus on fructose content. Twenty-three sugar-sweetened beverages along with four standard solutions were analyzed for sugar profiles using high-performance liquid chromatography (HPLC) in an independent, certified laboratory. Total sugar content was calculated as well as percent fructose in the beverages that use HFCS as the sole source of fructose. Results showed that the total sugar content of the beverages ranged from 85 to 128% of what was listed on the food label. The mean fructose content in the HFCS used was 59% (range 47-65%) and several major brands appear to be produced with HFCS that is 65% fructose. Finally, the sugar profile analyses detected forms of sugar that were inconsistent with what was listed on the food labels. This analysis revealed significant deviations in sugar amount and composition relative to disclosures from producers. In addition, the tendency for use of HFCS that is higher in fructose could be contributing to higher fructose consumption than would otherwise be assumed.

From the full article as well:

"Altogether, epidemiological studies at this stage provide an incomplete, sometimes discordant appraisal of the relationship between fructose or sugar intake and metabolic/cardiovascular diseases. Part of the discordances may be explained by the fact that intakes of sugar, fructose, fruit juices, or sweetened beverages were often not recorded individually, which precludes an accurate calculation of total fructose intake. In addition, fructose is essentially consumed as either sucrose or HFCS, with the consequence that glucose intakes essentially varies with fructose intake. Confounding factors (i.e., interrelationship between sugar intake and intake of other nutrients, association with physical activity and life-style) are important and difficult to control for. At present, there appears to be strong evidence that consumption of sweetened beverages is associated with obesity, at least in children and adolescents. There is at present not the single hint the HFCS may have more deleterious effect on body weight than other sources of sugar. Regarding the relationship between fructose or sucrose intake and cardiovascular risk factors or type 2 diabetes, the evidence is even sparser. Given the number of confounding variables, there is clearly a need for intervention studies in which the fructose intake of high fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term intervention studies however suggest that a high-fructose intake consisting of soft drinks, sweetened juices, or bakery products can increase the risk of metabolic and cardiovascular diseases. There is, however, no objective ground to support that moderate intake of fructose, or of fructose consumed with fruits or honey, is unsafe."

I can see why you didn't want to print the whole abstract. There's enough indirect evidence.

You dishonor yourself with such snidery. Goodbye, Sir.

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