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By Mark Anthony, Ph.D., Technical Editor | 07/31/2007
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?
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:
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.”
But the purported role of fructose in obesity goes beyond the charge that it’s more likely than glucose to become body fat. Fructose doesn’t stimulate insulin increase like glucose, and thus does not cause the release of hormones, such as leptin and grehlin, responsible for satiety. And if we’re not satisfied, we eat more. In other words, fructose causes obesity because it has a low glycemic index.
In the July 2003 issue of Metabolism, Wolfgang Kopp argued that modern high-glycemic index nutrition is at the heart of the rapid rise in obesity and diabetes. The mechanism is exactly the opposite of that proposed for fructose: Insulin promotes fat storage and inhibits the conversion of body fat to energy. Thus, if fructose has a unique ability to make us fat, the entire case for a low-glycemic index diet makes no sense whatsoever.
“The concept of glycemic index was developed as a research tool for studying blood glucose control in people with diabetes,” reminds Storey. “The concept should never have been popularized by diet books as a way to lose weight.”
The very concept that fructose, abundant in fruit and honey, is a major player in obesity seems questionable. “Fructose is not a new food ingredient for humans,” says John White, president of White Technical Research, Argenta, Ill. “Early in our history we consumed fructose from dietary sources, such as fruits, vegetables and honey. Some of these sources [notably honey] have the same fructose-to-glucose ratio as HFCS: nearly one-to-one.”
White is science advisor to the Corn Refiners Assn. and has studied HFCS for more than 20 years. “While it is true that fructose is primarily metabolized in the liver, this is not a problem in typical diets containing both glucose and fructose. It is only when specific nutrients are consumed to excess that metabolic upset occurs.
“Those who contend that fructose leads to increased fat deposition and fatty livers do so based on highly prejudicial experiments in which fructose is fed as the only carbohydrate source and at excessive concentrations. There is no one on Earth who eats such a diet. Indeed, any nutrient fed in excess of the body's ability to process it or in excess of the body's caloric need must end up somewhere — fat storage is typically the end result,” says White.
If the argument that fructose causes obesity is questionable, then the theory that HFCS, as a source of fructose, is uniquely linked to obesity must be legless.
First of all, fructose is not the same as high-fructose corn syrup, a point stressed by the scientists at Cargill Inc. (www.cargill.com), Minnetonka, Minn., one of the largest manufacturers of HFCS in North America. “The terms are not interchangeable. HFCS contains fructose, but it also contains glucose. These are the same compounds, in roughly the same proportion, as what you’ll find in sugar,” says Mitch Kanter, nutrition scientist for Cargill Food System Design. “This seemingly simple point is often lost on the public, and the confusion is compounded when nutritionists fail to make careful distinctions.”
However, not all high-fructose corn syrups are alike. HFCS-55, which is used to sweeten beverages, consists of 55 percent fructose and 40 percent glucose, says Storey. HFCS-42, used in bakery products, is 42 percent fructose and 53 percent glucose.
Adds White, “Absorption of sucrose and HFCS are both fairly rapid from the small intestines. Sucrose is readily hydrolyzed from disaccharide [bonded fructose-glucose] to monosaccharides [free fructose + glucose] by a sucrase enzyme in the small intestine. It is thus transported into the blood stream as monosaccharides — just as HFCS and honey and fruit sugars are. And the body cannot tell what source they came from.
“An important but often overlooked point is that the metabolic differences in disposing of the sugars now become moot. No matter what their dietary source, all fructose-containing nutritive sweeteners deliver the same monosaccharide sugars in the same ratios to the same tissue within the same time frame through the same metabolic pathways,” insists White.
There’s no good, scientific reason to flee high-fructose corn syrup. : Focus on the quality of the beverage or product, its nutrient density, phytochemcial richness, freedom from artificial ingredients, and low total sugar content. How long the HFCS scare will last is anyone's guess, but the point that we consume far to many empty calories and artificial ingredients is one that it here to stay.
In fact, we have been consuming HFCS-like sweetener all along. “Sugar-sweetened carbonated beverages were introduced to our diets in the 1880s. Few people realize that sugar is unstable in acidic solutions, such as carbonated beverages (pH around 3.5). The glucose-fructose bond in sugar hydrolyzes to release monosaccharide glucose and fructose in a one-to-one ratio. In essence, we have been consuming HFCS in the form of hydrolyzed sucrose in soft drinks for more than a hundred years,” claims White.
Finally it should be noted that obesity is now a worldwide problem, while HFCS is largely a U.S. sweetener, accounting for less than half of our total caloric sweetener use. “Largely overlooked in this debate is the fact that HFCS accounts for only about 8 percent of sweetener use worldwide,” says White. “The remainder (92 percent) is sucrose. How can HFCS be uniquely responsible for obesity when it is not even available in most areas of the world?”
We’ve managed to export the fast food menu to the rest of the world, and even without the HFCS it’s doing just fine. “Obesity is occurring on a global basis as economies expand, incomes grow, food becomes more plentiful and affordable and lifestyles change so that people are more sedentary in everyday life,” says Storey.
HFCS is a refined sugar, only a source of carbohydrate, nothing more. It’s neither hero, nor villain. That there is a controversy over its specific role in obesity demonstrates how desperately we want a quick answer.
It would be easy to say that we want an answer that absolves us from personal responsibility. But there is just as much reason to believe that we think something simple has been overlooked, and there we may be right. But that doesn’t excuse “over-sciencing” an answer to force a conclusion at the expense of common sense.
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