The Trouble with Fructose

It's different from glucose. That sugar goes directly into our bloodstream so that our tissues and organs can use it as energy, with only 30 to 40 percent passing through the liver.

“The more fructose in the diet, the higher the subsequent triglyceride levels in the blood,” Taubes writes on page 200. While our health authorities have focused largely on the health risks of high LDL cholesterol levels, Taubes demonstrates that our triglyceride – fat – levels are even more important in terms of our risks for heart attacks.

And especially troublesome for people with diabetes is that high-fructose diets lead us to secrete more insulin, which in turn leads to more insulin resistance. That’s because fructose seems to block both the metabolism of glucose in the liver as well as the synthesis of glucose into glycogen, the way that the liver stores glucose.

It’s even worse, Taubes writes. Fructose is perhaps 10 times worse than glucose in the way our bodies form AGEs.

It happened that just as I was reading Taubes, my favorite Certified Diabetes Educator brought to my attention a thought-provoking interview with Dr. Lustig. This interview, broadcast originally on Australia’s ABC Ratio National, confirms the outlines of Taubes’s brief against fructose.

“The only organ in your body that can take up fructose is your liver,” Dr. Lustig told interviewer Norman Swan. The first thing that eating fructose does is causing an increase in uric acid, Dr. Lustig said. Fructose inhibits nitric oxide, which would otherwise reduce our blood pressure. “So fructose is famous for causing hypertension (high blood pressure).”

“The second is that fructose initiates what’s known as de novo lipogenesis, excess fat production….And then the last thing that fructose does in the liver is it initiates an enzyme….What happens is that your insulin receptors in your liver stop working….That means your insulin levels all over your body have to rise.”

When I wrote Dr. Lustig today to ask him the name of the enzyme that fructose initiates in the liver, he told me that they call it “c-jun N-terminal kinase-1” or just JNK-1 or Junk-1. "It serine phosphorylates a protein in the liver called IRS-1 (insulin receptor substrate-1), thereby rendering it inactive. This induces hepatic insulin resistance."

Dr. Lustig also sent me a PDF of a slides for a talk he recently gave that he called "The trouble with fructose." I swear that this just happens to be the same title I had already decided to use for this article. I have uploaded his article to my site.

Damning stuff, this. In fact, “we’re being poisoned to death,” Dr. Ludwig concludes.

The trigger for the recent trouble with fructose began in 1978, when high-fructose corn syrup entered the market. The most common form, HFCS-55, is 55 percent fructose and 45 percent glucose.

HFCS is now the most common sweetener in the U.S. It has replaced sucrose (table sugar) especially in soft drinks, but it is in many other foods too.