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"(NaturalNews) A research team from the University of Washington (UW) recently published a study in Physiology & Behavior revealing that moderate consumption of fructose- and high fructose corn syrup-sweetened beverages leads to significant alterations of lipid metabolization in the liver. Conducted on rats, the study also noted marked increases in both cholesterol and triglyceride levels in rats that fed on fructose-sweetened beverages. Fructose is a monosaccharide sugar that is found in various fruits. It is a simple sugar that is often promoted as being a healthy "fruit" sugar, however the reality is that fructose is just one component of the complex sugar composition that occurs naturally in fruit. Most granulated fructose available today, called crystalline fructose, is derived from fructose-enriched corn syrup. Similarly, high fructose corn syrup is a fructose-enriched form of highly-processed corn syrup that is commonly found in soda, ketchup, candy, dressings, and many other processed foods. The biggest concern about fructose is the fact that, unlike sucrose, it passes undigested through the small intestine where it enters the portal vein and heads directly to the liver. "

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. J Clin Invest. 2009 May;119(5):1322-34. Epub 2009 Apr 20. PMID: 19381015 doi: 10.1172/JCI37385. Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

Wednesday, November 19, 2008 The Fructose Index is the New Glycemic Index I stumbled upon an interesting editorial recently in the American Journal of Clinical Nutrition from Dr. Richard Johnson's group, entitled "How Safe is Fructose for Persons With or Without Diabetes?" It was a response to a meta-analysis in the same journal pronouncing fructose safe up to 90 grams per day. That's the amount in eight apples or four cans of soda. Not quite what our hunter-gatherer ancestors were eating! The editorial outlined the case against excessive fructose, which I feel is quite strong. That led me to another, more comprehensive paper from Dr. Johnson's group, which argues that the amount of fructose found in a food, which they call the "fructose index", is more relevant to health than the food's glycemic index.

In the last three decades, fructose corn syrup, also known as high fructose corn syrup, has replaced about half of the sugar added to processed foods such as soft drinks, packaged foods, and many baked goods. The problem here is that fructose corn syrup is a highly refined food product that does not come from fruit.

"Scientists have proved for the first time that fructose, a cheap form of sugar used in thousands of food products and soft drinks, can damage human metabolism and is fueling the obesity crisis. Fructose, a sweetener usually derived from corn, can cause dangerous growths of fat cells around vital organs and is able to trigger the early stages of diabetes and heart disease. Over 10 weeks, 16 volunteers on a controlled diet including high levels of fructose produced new fat cells around their heart, liver and other digestive organs. They also showed signs of food-processing abnormalities linked to diabetes and heart disease. Another group of volunteers on the same diet, but with glucose sugar replacing fructose, did not have these problems."

ScienceDaily (Aug. 27, 2009) - Researchers have established the conditions that foster formation of potentially dangerous levels of a toxic substance in the high-fructose corn syrup (HFCS) that is often fed to honey bees. Their study, which appears in the current issue of ACS' bi-weekly Journal of Agricultural and Food Chemistry, may also have implications for soft drinks and dozens of other human foods that contain HFCS. The substance, hydroxymethylfurfural (HMF), forms mainly from heating fructose.

WASHINGTON (Reuters) - A diet high in a form of sugar found in sweetened soft drinks and junk food raises blood pressure among men, according to research likely to mean more bad news for beverage companies and restaurant chains. One of two studies released on Wednesday provided the first evidence that fructose helps raise blood pressure. It also found that the drug allopurinol, used to treat gout, can alleviate the effect by reducing uric acid levels in the body. The second study, which measured fructose intake in mice, suggested that people who consume junk foods and sweetened soft drinks at night could gain weight faster than those who don't.

"Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology, explores the damage caused by sugary foods. He argues that fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin. Series: UCSF Mini Medical School for the Public [7/2009] [Health and Medicine] [Show ID: 16717] "

"My goal is to gather the basic science and apply it to nutrition - NUTRIGENOMICS. What do I mean? How does what we eat signal our genes in the nucleus. By our food choices, we are sending different signals to our genes. High carbohydrate and high fructose intake signals it is summer time and winter is coming -- grow and store the energy (insulin). High fat, low carbohydrate diet with calorie restriction signals our genes that winter is here -- use the stored energy, repair the genes, and slow down growth (i.e. Sirt1/Foxo pathway). The Sirt1/FoxO1 pathway is important as it aids in repairing DNA. Damaged DNA can lead to uncontrolled cellular replication (i.e. cancers). The immune system (phagocytes) has a mechanism to remove old and unwanted cells called apoptosis (cellular death). "

"Peter at Hyperlipid and Stephan at Whole Health have dispelled yet again myths regarding the indictment of the 16:0 long-chained saturated fatty acid Palmitic Acid as the prime instigator of insulin resistance (IR). Researchers are always wrong -- it's... HIGH CARBS PLUS Palmitic acid. Their brilliant posts discuss below: --Sportzaid (FRUCTOSE) + Palmitate = IR RETARDNESS --High Carb Lab Chow + Palmitate = IR in the brain Yes. Such inferences applied to low carbers (LCers) is pure ridiculousness. Non-applicable. Low/no carb + Palmitic Acid = GOOD THING. All the low-carb/high saturated fat (palmitic acid) and ketosis trials by Hays JH, Volek JS, and Krauss RM have shown reductions in blood insulin, blood glucoses (BG) and peripheral tissue insulin resistance (IR). Directly contrary to the high carb animal or human studies. Palmitic acid has a special evolutionary, adaptive role in mammalian metabolism. Stephan showed that it likely 'fills in' when blood glucose starts to decline. "

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