I generally avoid the diet and food hyperbole, but my daughter is studying nutrition so I get an earful of terms like trans-fats and the like. Recently, I decided to get a general physical. I learned that my glucose was a little high and my LDL was high. Strangely my HDL levels were good and the triglycerides were excellent. Regardless of my suspicion that the results were skewed by a late meal the night before, I did my homework and adjusted my diet. I have a fairly exhaustive exercise routine which probably accounts for the triglyceride levels so I know that diet was the only variable factor. My weight over the past six years has been 200 lbs plus or minus 3 pounds.

I used to consume Dr. Pepper and Peach Snapple — both quite tasty, as well as various juices. I cut these from my diet as well as any other source of HFCS I could identify. Basically, I restrict myself to boring ice tea and water. My weight for the past two months has been 193 lbs plus or minus 2 lbs — with a loss of 7 lbs. in the initial week. These are my facts.


Sugars in the body are metabolized via the Kegg Pathway. Sugars, specifically sucrose, are disaccharides consisting of a glucose molecule and a fructose molecule coupled by an α1→2-glycosidic bond. In nature, most available sugars occur in this form and it’s not surprising that a pathway evolved to process them. The first process in the metabolism of sucrose is the cleaving of the glucose from the fructose. Glucose can be metabolized anywhere in the body at the cellular level. Fructose is metabolized in the liver.
fructose metabolism

Hepatic fructose metabolism: A highly lipogenic pathway. Fructose is readily absorbed from the diet and rapidly metabolized principally in the liver. Fructose can provide carbon atoms for both the glycerol and the acyl portions of triglyceride. Fructose is thus a highly efficient inducer of de novo lipogenesis. High concentrations of fructose can serve as a relatively unregulated source of acetyl CoA. In contrast to glucose, dietary fructose does NOT stimulate insulin or leptin (which are both important regulators of energy intake and body adiposity). Stimulated triglyceride synthesis is likely to lead to hepatic accumulation of triglyceride, which has been shown to reduce hepatic insulin sensitivity, as well as increased formation of VLDL particles due to higher substrate availability, increased apoB stability, and higher MTP, the critical factor in VLDL assembly.

Since sugars arrive in the body in these paired units, and glucose is the principle energy source, it is understandable that the evolved regulatory mechanisms are associated with the glucose metabolism. The fructose metabolism has essentially no independent regulation and feedback loop, depending upon the glucose component’s parallel metabolism.

This was all well and good when the principle source of free fructose was fruits consumed in sparse quantities. With fructose now saturating food products, via the HFCS component, there is essentially no feedback for the body to say “Whoa there sport, I’m saturated with sugar and really don’t need any more.” So the metabolism process continues. The result is the depletion of enzymes in the liver and the concentration of low density lipids.

Four companies control 85 percent of the $2.6 billion HFCS business–Archer Daniels Midland, Cargill, Staley Manufacturing Co. and CPC International. Recently the Corn Refiners Association has been issuing statements in an attempt to persuade the consuming public that HFCS is not the root of all evil. The association has obtained some support from the Center for Science in the Public Interest:

We respectfully urge that the proposal be revised as soon as possible to reflect the scientific evidence that demonstrates no material differences in the health effects of high-fructose corn syrup and sugar…The real issue is that excessive consumption of any sugars may lead to health problems. ……The Center for Science in the Public Interest

This is an interesting statement. Many are arguing that it is deceptive. True, HFSC is not detrimental per se, although its manufacture has some interesting components, and true obesity does have as a contributory factor the increased intake of sugars. In the interest of accurate science, the CSPI is correct.

What is missing or ignored is mention of the lack of a regulatory feedback loop in the fructose metabolism. Without such a mechanism, self control of fructose intake is difficult to impossible. This asymmetrical regulation of the two sides of the sucrose metabolism is the real danger. Since there is no inherent control mechanism, it is irresponsible to use fructose based sweeteners in literally every food product.

Perhaps in a few thousand years, given a constant diet of HFCS, we will evolve a new regulatory mechanism. Until then, I will continue to attempt to limit my intake of HFCS.