Fructose: Toxic sugar or tortured logic?

More on arguably one the hottest topics of the moment… The anti-sugar forces turn their attention from HFCS to fructose, even at the expense of fruit consumption.

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, MD, 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 fibre, 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…. Read the full article