Fructose: Toxic Sugar or Tortured Logic?

The anti-sugar forces turn their attention from HFCS to fructose, even at the expense of fruit consumption.

By Mark Anthony, Ph.D., Technical Editor

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Americans haven't been told that, after all the fuss, the case against high-fructose corn syrup (HFCS) lacked a smoking gun. There was simply no evidence to show that HFCS — a glucose-fructose disaccharide generally between 42 and 55 percent fructose — is metabolically different from table sugar (sucrose), a nearly identical combo of 50-50 glucose-fructose.

Nevertheless, the name high-fructose corn syrup became toxic on a label. Meanwhile, some researchers, determined to demonstrate once and for all that sugar is directly responsible for obesity and type 2 diabetes, turned their attention toward fructose itself, expanding the guilty parties to include all foods that contain fructose, including HFCS and sucrose, along with all fruit juices.

Leading the charge against fructose is Robert Lustig, M.D., an endocrinologist at the University of California at San Francisco, whose popular video on YouTube brought the case to the masses that fructose is poison -- responsible for obesity, diabetes, heart disease and nonalcoholic fatty liver disease, among others.

This is an uncomfortable message for many to hear because fructose is found in abundance in fruits. And while Lustig absolves fruit of responsibility for obesity because it contains fiber, the fructose-is-poison charge can still work in the mind of anyone biting into an apple. Central to his thesis is the idea that fructose is more easily converted to fat by the liver than is glucose. The process is called de novo lipogenesis (DNL), which simply means making fat from scratch. (In this case, "scratch" means sugar, since the liver can also make fat from excess protein.)

Some scientists point to serious problems with the case against fructose. In response to Lustig’s 2010 Journal of the American Dietetic Association article, "Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanol," John Sievenpiper, Ph.D., at McMaster University, Hamilton, Ontario, points out that DNL from fructose is relatively small in humans. (It was dramatic in the rodents fed unnaturally high levels of this one sugar -- 60 percent of calories — a diet impossible for humans to follow.) And since the average American takes in and only about 49g of fructose per day, fructose-stimulated DNL is insignificant.

Lustig counters this by stating that DNL from fructose must be taken in the proper context, in the light of the factors that increase it — that the body is more likely to make fat from fructose in conditions of overeating, obesity, insulin resistance and taking in glucose at the same time as fructose.

But this line of reasoning raises a problem: Fructose has a very low glycemic index. Central to the indictment of any carbohydrate as the cause of obesity is that insulin drives glucose into fat cells, yet fructose doesn't stimulate an insulin response. It takes plain overeating to get fat on carbohydrates, because the first store of metabolized glucose is as glycogen in muscle cells, not fat in fat cells.

Another obstacle in mounting a case against fructose is that its calorie contribution is dwarfed by other sources of calories in our diet. According to USDA food availability data, adjusted for spoilage and other waste, we’ve increased our per capita food intake by 458 calories since 1970. About 242 of these calories come from added fats and oils. Another 167 calories come from flour and cereal products, which contain no fructose. Only 34 of those increased calories come from added sugar. (This data also points to a serious flaw in a basic assumption underlying the usual attack on carbohydrates, that Americans decreased their fat intake in favor of sugar.)

Sugar intake has been on the decline since 1999, but obesity and type 2 diabetes continue to rise. This is not just an American phenomenon. In response to Lustig’s 2012 article in the journal Nature, "The Toxic Truth About Sugar," the Dietitians Assn. of Australia points out that sugar consumption there decreased by 23 percent since 1980, yet obesity doubled and type 2 diabetes tripled.

There is no question the global pandemic of obesity is heavily dependent upon the consumption of foods that are energy-dense and nutrient-poor, coupled with increasingly sedentary lifestyles. But to place the blame on processed foods and beverages containing a component abundant in fruits and vegetables, labeling it "toxic" and "addictive," fails simple common sense.

This article originally appeared in our April 2013 issue of Food Processing magazine.

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