I walked into a health food store the other day and was offered a sample of chocolate sweetened with agave syrup. The young lady who handed out the sample explained this was a healthy snack with a low glycemic index and no high-fructose corn syrup (HFCS). I enjoyed the sample, but it was the juxtaposition of low glycemic index, healthy and no HFCS that I found interesting.
HFCS is the new devil sweetener, the one called on the carpet for making us fat. In fact, its reputation has been so besmirched that some companies now boast of sweetening products with pure cane sugar -- you know, white sugar, table sugar, one of the "deadly whites," as one best-selling diet book once labeled it.
How did HFCS gain such a sordid reputation, and more importantly, is that reputation justified? Is any one sweetener to blame for making us fat? Still more importantly, what does this controversy say about the science behind carbohydrates and obesity?
A new sugar in town
HFCS is, quite simply, sugar made from corn. Field corn is rich in starch -- chains of glucose molecules linked together like a complex string of pearls. Break the strings apart and you release individual glucose sugars to form glucose syrup.
In 1970, Japanese scientists added a new twist: an isomerization step that converted some of the glucose into fructose, between 42 and 55 percent, depending on the final method of processing. The resulting product was named high-fructose corn syrup, a seemingly reasonable name at the time, though accurate only in the relative sense.
HFCS is high in fructose only when compared to regular corn syrup, which is 100 percent glucose. In reality, the glucose/fructose ratio of HFCS is similar to that of sucrose, a disaccharide consisting of a glucose molecule linked to a fructose molecule, and thus 50 percent fructose. In fact, HFCS could have easily been named low-glucose corn syrup.
When HFCS was introduced, fructose was considered beneficial; after all, it's naturally abundant in fruit. Sucrose was fast becoming the icon of empty calorie foods, along with white flour, as fast food joints replaced both home-cooked meals and mom-and-pop restaurants. Rich in fat, loaded with sugar and ready to eat, fast food took the nation, and indeed the world, by storm. Soon, a super-sized nation struggled with obesity on a scale never before seen.
By the time obesity was epidemic, HFCS was caught red-handed, sweetening nearly every beverage we used to wash down a giganto burger and bucket-o-fries, while driving to work or playing video games.
The stats are unmistakable: Since 1966, the use of HFCS increased from zero (since it didn't exist) to nearly 64 lbs. per person per year by 1999, declining slightly since then to about 59 lbs. This coincides with the rise in obesity, which skyrocketed since 1970. At the same time consumption of other sugars flattened.
That should be a slam-dunk -- case closed! Of course no one noticed that cheese consumption went from about 9 lbs. per capita to over 31 lbs., and that frozen potatoes (mostly used as french fries) went 19 lbs. to nearly 55 lbs. Instead, we needed to know exactly how HFCS was able to pull this trick off.
The so-called smoking gun was fired in the April 2004 issue of the American Journal of Clinical Nutrition. George Bray, Samara Neilson and Barry Popkin presented the mechanism by which HFCS may be causally linked to the epidemic of obesity. It consisted of the following pieces of evidence:
- The increase in HFCS consumption paralleled the rise in obesity.
- Fructose is metabolized differently from glucose, and can be more easily made into fat.
- Rats overfed fructose got fatty livers and high blood tryglycerides.
- Fructose has a low glycemic index and therefore does not stimulate insulin, and thus does not provide satiety.
Upon closer scrutiny, this line of reasoning makes little sense. It didn't implicate HFCS directly, only circumstantially via fructose. Bray, Neilson and Popkin point out that fructose is absorbed further down in the small intestines than glucose (though both end up in the same portal vein on the way to the same liver). And though a little fructose helps the liver store glycogen, when large amounts of fructose are ingested, they do "provide a relatively unregulated source of carbon precursors for hepatic lipogensis." In other words, if you eat too much fructose, the liver can make the excess into fat.
But that's true of any sugar eaten to excess. In June 2000 issue of the same journal, R. M. McDevitt reports that subjects overfed glucose, fructose and sucrose in a metabolically controlled setting displayed no difference in the distribution of excess calories as fat, regardless of the source.
Dr. Moreen Storey, director of the Center for Food, Nutrition and Agricultural Policy at the University of Maryland, and her colleagues have studied the HFCS/obesity question at length, and have authored an article to appear soon in the journal Food Chemistry and Toxicology. In direct response to our inquiry, Dr. Storey says: "When fructose is consumed in excess, animals and humans typically experience abdominal cramping and diarrhea, sometimes severe diarrhea. There is no evidence that reasonable consumption of fructose in a typical diet has any adverse effect on the liver or that it produces more body fat than sucrose or glucose."