Researchers have found new evidence that soft drinks sweetened with high-fructose corn syrup (HFCS) may contribute to the development of diabetes, particularly in children. In a laboratory study of commonly consumed carbonated beverages, the scientists found that drinks containing the syrup had high levels of reactive compounds that have been shown by others to have the potential to trigger cell and tissue damage that could cause the disease, which is at epidemic levels.
HFCS is a sweetener found in many foods and beverages, including non-diet soda pop, baked goods, and condiments. It is has become the sweetener of choice for many food manufacturers because it is considered more economical, sweeter and more easy to blend into beverages than table sugar. Some researchers have suggested that high-fructose corn syrup may contribute to an increased risk of diabetes as well as obesity, a claim which the food industry disputes. Until now, little laboratory evidence has been available on the topic.
In the current study, Chi-Tang Ho, Ph.D., conducted chemical tests among 11 different carbonated soft drinks containing HFCS. He found 'astonishingly high' levels of reactive carbonyls in those beverages. These undesirable and highly-reactive compounds associated with "unbound" fructose and glucose molecules are believed to cause tissue damage, says Ho, a professor of food science at Rutgers University in New Brunswick, N.J. By contrast, reactive carbonyls are not present in table sugar, whose fructose and glucose components are "bound" and chemically stable, the researcher notes.
Reactive carbonyls also are elevated in the blood of individuals with diabetes and linked to the complications of that disease. Based on the study data, Ho estimates that a single can of soda contains about five times the concentration of reactive carbonyls than the concentration found in the blood of an adult person with diabetes.
Ho and his associates also found that adding tea components to drinks containing HFCS may help lower the levels of reactive carbonyls. The scientists found that adding epigallocatechin gallate (EGCG), a compound in tea, significantly reduced the levels of reactive carbonyl species in a dose-dependent manner when added to the carbonated soft drinks studied. In some cases, the levels of reactive carbonyls were reduced by half, the researchers say.
"People consume too much high-fructose corn syrup in this country," says Ho. "It's in way too many food and drink products and there's growing evidence that it's bad for you." The tea-derived supplement provides a promising way to counter its potentially toxic effects, especially in children who consume a lot of carbonated beverages, he says.
But eliminating or reducing consumption of HFCS is preferable, the researchers note. They are currently exploring the chemical mechanisms by which tea appears to neutralize the reactivity of the syrup.Ho's group is also probing the mechanisms by which carbonation increases the amount of reactive carbonyls formed in sodas containing HFCS. They note that non-carbonated fruit juices containing HFCS have one-third the amount of reactive carbonyl species found in carbonated sodas with HFCS, while non-carbonated tea beverages containing high-fructose corn syrup, which already contain EGCG, have only about one-sixth the levels of carbonyls found in regular soda.
In the future, food and drink manufacturers could reduce concerns about HFCS by adding more EGCG, using less HFCS, or replacing the syrup with alternatives such as regular table sugar, Ho and his associates say. Funding for this study was provided by the Center for Advanced Food Technology of Rutgers University. Other researchers involved in the study include Chih-Yu Lo, Ph.D.; Shiming Li, Ph.D.; Di Tan, Ph.D.; and Yu Wang, a doctoral student.
This research was reported August 23 at the 234th national meeting of the American Chemical Society, during the symposium, "Food Bioactives and Nutraceuticals: Production, Chemistry, Analysis and Health Effects: Health Effects."
What Is High Fructose Corn Syrup, and Why Is It So Bad For My Body?
Ref.- By Bill Sanda, BS, MBA - http://www.westonaprice.org/modernfood/highfructose.html
HFCS was developed in Japan in 1971. It is made from corn, and in the mid 1970’s we had an excess of corn crops in America. At the same time, sugar prices were high, which meant that food prices were higher for the consumer.
Since HFCS is made from corn and is grown right here in the States, it is very cheap to produce, while at the same time being six times sweeter than cane sugar. This meant that all of the excess corn could be used to make HFCS, and food that used to be made with sugar could be produced at a much cheaper cost. Sounds like a good solution because the farmers were winning by selling their surplus crops, and the American consumer could buy sweetened foods at a lower cost.
High fructose corn syrup makes food taste really good, however it serves a few more purposes beyond that. It is a great preservative so it can be used in (almost all) processed foods to extend their shelf life. It protects processed, frozen foods from freezer burn. It is also fabulous for making baked goods look tasty: it was found that by adding HFCS, it would make food appear more “natural looking”.
With all of these wonderful benefits that high fructose corn syrup gives us, why should we care about it, especially since it makes our food taste good? What does it matter that it was banned in Mexico and is rarely found in foods in New Zealand. Is it really that bad? Why should we care about HFCS?
There are several different names and forms of sugar, fructose, sucrose, and dextrose being three. Here we are focusing on fructose, which behaves differently than the latter two in regards to our metabolism.
Both sucrose and dextrose are broken down in our body before they ever make it to our liver, however fructose does not breakdown and reaches the liver “almost completely intact”. This feature of fructose (which in HFCS is of an even higher concentration) has been named “metabolic shunting” since the fructose is “shunted” or sidetracked towards the liver.
Fructose is used to build triglycerides in the liver, which it does by imitating insulin, causing the liver to release fatty acids into the bloodstream. The flood of fatty acids then causes muscle tissue to develop insulin resistance.
Do humans actually consume enough high fructose corn syrup to activate this process in their livers? HFCS is present in fast food, processed food, food found in convenience stores, sodas, cereal, energy bars, and more.
How much of this type of food do many people consume daily in their busy lives? A study was actually done on golden hamsters (their metabolism is very close to ours) in the year 2000 in which they were fed diets with high levels of HFCS. It took only weeks until they had high triglyceride levels as well as insulin resistance.
Studies have also been done on whether or not fructose causes the body to burn sugar as opposed to burning fat. It has been found that our metabolism veers towards fat storage when consuming high levels of fructose. Therefore, HFCS contributes to obesity not only by the fact that our brains don’t know that our stomachs are full, but also by causing the body to burn sugar rather than fat in our cells.
Nancy Appleton, PhD, clinical nutritionist, has compiled a list of the harmful effects of fructose in her books Lick the Sugar Habit, Healthy Bones, Heal Yourself With Natural Foods, The Curse Of Louis Pasteur and Lick the Sugar Habit Sugar Counter. She points out that consumption of fructose causes a significant increase in the concentration of uric acid; after ingestion of glucose, no significant change occurs. An increase in uric acid can be an indicator of heart disease. Furthermore, fructose ingestion in humans results in increases in blood lactic acid, especially in patients with preexisting acidotic conditions such as diabetes, postoperative stress or uremia. Extreme elevations cause metabolic acidosis and can result in death.
Fructose is absorbed primarily in the jejunum before metabolism in the liver. Fructose is converted to fatty acids by the liver at a greater rate than is glucose. When consumed in excess of dietary glucose, the liver cannot convert all of the excess fructose in the system and it may be malabsorbed. The portion that escapes conversion may be thrown out in the urine. Diarrhea can be a consequence. A study of 25 patients with functional bowel disease showed that pronounced gastrointestinal distress may be provoked by malabsorption of small amounts of fructose.
Fructose interacts with oral contraceptives and elevates insulin levels in women on "the pill."
In studies with rats, fructose consistently produces higher kidney calcium concentrations than glucose. Fructose generally induces greater urinary concentrations of phosphorus and magnesium and lowered urinary pH compared with glucose.
In humans, fructose feeding leads to mineral losses, especially higher fecal excretions of iron and magnesium, than did subjects fed sucrose. Iron, magnesium, calcium, and zinc balances tended to be more negative during the fructose-feeding period as compared to balances during the sucrose-feeding period.
There is significant evidence that high sucrose diets may alter intracellular metabolism, which in turn facilitates accelerated aging through oxidative damage. Scientists found that the rats given fructose had more undesirable cross-linking changes in the collagen of their skin than in the other groups. These changes are also thought to be markers for aging. The scientists say that it is the fructose molecule in the sucrose, not the glucose, that plays the larger part.
Because it is metabolized by the liver, fructose does not cause the pancreas to release insulin the way it normally does. Fructose converts to fat more than any other sugar. This may be one of the reasons Americans continue to get fatter. Fructose raises serum triglycerides significantly. As a left-handed sugar, fructose digestion is very low. For complete internal conversion of fructose into glucose and acetates, it must rob ATP energy stores from the liver.
Not only does fructose have more damaging effects in the presence of copper deficiency, fructose also inhibits copper metabolism--another example of the sweeteners double-whammy effect. A deficiency in copper leads to bone fragility, anemia, defects of the connective tissue, arteries, and bone, infertility, heart arrhythmias, high cholesterol levels, heart attacks, and an inability to control blood sugar levels.
Although these studies were not designed to test the effects of fructose on weight gain, the observation of increased body weight associated with fructose ingestion is of interest. One explanation for this observation could be that fructose ingestion did not increase the production of two hormones, insulin and leptin, that have key roles in the long-term regulation of food intake and energy expenditure.
The magnitude of the deleterious effects of fructose varies depending on such factors as age, sex, baseline glucose, insulin, triglyceride concentrations, the presence of insulin resistance, and the amount of dietary fructose consumed. Some people are more sensitive to fructose. They include hypertension, hyperinsulinemic, hypertriglyceridemic, non-insulin dependent diabetic people, people with functional bowel disease and postmenopausal women.
Everyone should avoid over-exposure to fructose, but especially those listed above. One or two pieces of fruit per day is fine, but commercial fruit juices and any products containing high fructose corn syrup are more dangerous than sugar and should be removed from the diet.
REFERENCES
1. Fields, M, Proceedings of the Society of Experimental Biology and Medicine, 1984, 175:530-537.
2. Appleton, Nancy, PhD, Fructose is No Answer For a Sweetener, http://www.mercola.com/2002/jan/5/fructose.htm.
3. Beatrice Trum Hunter, Confusing Consumers About Sugar Intake, Consumer’s Research 78, no 1 (January 1995): 14-17.
4. Fallon, Sally and Mary Enig, Nourishing Traditions, New Trends Publishing, Washington DC, 2001, p. 23.
5. Hallfrisch, Judith, Metabolic Effects of Dietary Fructose, FASEB Journal 4 (June 1990): 2652-2660.
6. American Journal of Clinical Nutrition, November 2002 Vol. 76, No. 5, 911-922.
7. Appleton, Nancy Ph.D., Fructose is No Answer For a Sweetener, http://www.mercola.com/2002/jan/5/fructose.htm.
8. http://www.mcvitamins.com/cornsyrup.htm.