“High-Fructose Corn Syrup”? Never Heard of It.


If you can’t beat ‘em…confuse them. That seems to be the new motto of our good friends at the Corn Refiners Association, the lobbying group and manufacturing association that represents makers of high-fructose corn syrup. The AP is reporting that the group has petitioned the FDA for permission to identify high-fructose corn syrup on food packaging as–wait for it–”corn sugar.”

After all, HFCS sales are at a 20-year low. More and more, science is indicating that the body metabolizes HFCS differently from table sugar in a way that increases the risk of diabetes, liver disease, and obesity. (Yes, we consume too many sweeteners of all kinds, but as I wrote in this recent post, there is evidence that this industrially extracted combination of fructose and glucose has more health consequences than the ones that humans have been consuming for far longer.) As the Corn Refiners president observed sadly, HFCS of late “has been highly disparaged and highly misunderstood.” Well, I’ll certainly agree with the first part of that statement. All the recent marketing muscle put behind HFCS seems to have been a sweetly surprising waste of money.

So, when the facts and consumer sentiment are against you, what is a poor, misunderstood oligopoly to do?

The answer: obfuscate!

Surely, in wonderfully Orwellian style, a name change will take care of matters. I don’t even know what to call this latest bit of corporate idiocy. Cornwashing?

This latest move proves the old adage that, when it comes to industrial food, the customer is always wrong, wrong, WRONG!!

It also demonstrates the fundamental bad faith under which these groups operate. As long as government policy and industrial agricultural practices ensure a vast overproduction of cheap corn, food processors will continue finding creative ways (animal feed, vehicle fuel, wallboard) to use it all. The only option that remains is the last refuge of marketing scoundrels everywhere: deception.

And though the name change could take up to two years, the marketing push will begin immediately. Forewarned is forearmed.

One Comment

The news from this week’s NYTimes: Since HFCS is getting a bad name, let’s re-name it (and ignore the science behind the concerns). Even noted nutrition scholar Marion Nestle says in the article that “there is no meaningful biochemical difference between table sugar and high-fructose corn syrup.”

Let’s first accept the premise that sugar is NOT a nutritionally rich food, and then ask what about table sugar versus HFCS. Table sugar is a disaccharide, a double sugar, one half of the molecule is glucose, the other fructose. HFCS is synthetic mixture of fructose and glucose; it does not exist in nature, and as a manufactured product it may include contaminants. Another question is whether there a difference between glucose and fructose? Science says yes, that fructose significantly increases the production of body fat and, specifically, intra-abdominal fat! Eat HFCS and see your waist grow!
However, a better investigation would be to compare HFCS directly to table sugar. In the meantime, how about good old tap water as a fine drink?!

Here’s the recent persuasive scientific study published in the Journal of Clinical Investigation, along with comments by the journal’s editors below.

This is the link to the article describing the experiments that were done on HFCS in humans.


This is the citation, author list, and the abstract [summary] of the findings of the article.

Journal of Clinical Investigations Volume 119, Issue 5 (May 1, 2009)

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.

By Kimber L. Stanhope,1,2 Jean Marc Schwarz,3,4 Nancy L. Keim,5 Steven C. Griffen,6
Andrew A. Bremer,7 James L. Graham,1,2 Bonnie Hatcher,2 Chad L. Cox,2 Artem Dyachenko,3
Wei Zhang,6 John P. McGahan,8 Anthony Seibert,8 Ronald M. Krauss,9 Sally Chiu,9
Ernst J. Schaefer,10 Masumi Ai,10 Seiko Otokozawa,10 Katsuyuki Nakajima,10,11 Takamitsu Nakano,11 Carine Beysen,12 Marc K. Hellerstein,12,13 Lars Berglund,6,14 and Peter J. Havel1,2
1Department of Molecular Biosciences, School of Veterinary Medicine, and 2Department of Nutrition, UCD, Davis, California, USA. 3College of Osteopathic Medicine, Touro University, Vallejo, California, USA. 4UCSF, San Francisco, California, USA. 5United States Department of Agriculture, Western Human Nutrition Research Center, Davis, California, USA. 6Department of Internal Medicine and 7Department of Pediatrics, School of Medicine, UCD, Sacramento, California, USA. 8Department of Radiology, UCD Medical Center, Sacramento, California, USA. 9Children’s Hospital Oakland Research Institute, Oakland, California, USA. 10Lipid Metabolism Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, and Tufts University School of Medicine, Boston, Massachusetts, USA. 11Diagnostic Division, Otsuka Pharmaceutical Co., Tokyo, Japan. 12KineMed, Emeryville, California, USA. 13Nutritional Sciences and Toxicology, University of California, Berkeley, California, USA. 14Veterans Affairs Northern California Health Care System, Sacramento, California, USA.

Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not
after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle–triglyceride and –cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

The below is from the editorial comment in the same issue of the journal.

Observations indicated that consumption of dietary fructose had unfavorable effects on lipid metabolism: consumption of fructose-sweetened but not glucose-sweetened beverages for 10 weeks increased the synthesis of lipids in the liver (de novo lipogenesis) as well as the total volume of intraabdominal fat depots (known to be have more adverse health effects than subcutaneous fat depots) in the overweight adult participants. In subjects consuming glucose-sweetened beverages, only the volume of the subcutaneous fat depots (believed to be less detrimental to metabolic health) increased. Consumption of fructose-sweetened but not glucose-sweetened beverages also led to larger increases of postprandial and 24-hour plasma triglyceride levels. Fructose-induced alterations of several processes, including hepatic lipid synthesis and reduced lipid clearance, appear to have contributed to that outcome, as Stanhope and colleagues
show, using tracer studies and measurements of lipoprotein lipase (LPL) activity. The apparently largely fructose-specific nutrient-induced changes in lipid metabolism were not limited to postprandial triglyceride concentrations, storage efficiency, and regional distribution of triglycerides; levels of apoB, LDL cholesterol, small, dense LDL (sdLDL), oxidized LDL-cholesterol, remnant lipoprotein triglyceride, and the apoB/apoA1 ratio (all biomarkers of increased risk for cardiovascular disease [CVD]) were also increased during consumption of fructose and unchanged during consumption of glucose. One intriguing facet in these findings was a pattern throughout the chronic dietary treatment study in which postprandial fat metabolism showed greater differences between the two sugar-consuming groups of volunteers than under fasting conditions.