The Villain in the Obesity Epidemic: Is High-Fructose Corn Syrup the Culprit?

Lucy Crain, MD

In 2006, the Center for Science in the Public Interest (CSPI) threatened a lawsuit against Cadbury Schweppes for falsely advertising 7 Up as “all natural,” citing that it contains high-fructose corn syrup (HFCS). Although the Federal Drug Administration has no definition of “natural,” CSPI claimed that HFCS was not natural, due to the significant amount of processing and use of one or more genetically modified enzymes required to produce it. Cadbury Schweppes announced in January 2007 that it would cease describing 7 Up as “all natural.”

Since the 2004 publication by Dr. George Bray and associates of an article suggesting a causal association of HFCS in the obesity epidemic, ongoing controversy continues about the role played by this ubiquitous sweetener. Dr. Bray and his coauthors noted that the consumption of HFCS increased more than a thousand percent between 1970 and 1990, exceeding changes in intake of any other food or food group (Bray, Neilson, and Popkin 2004). Others argue that increased food and drink portion sizes and American lifestyle changes, such as more fast foods and eating out, decreased exercise, and more computer and video time versus sports or outdoor activities, also have etiologic roles. Eager to discount any causal role of HFCS, the U.S. Farm and Corn Refiners lobbies have pointed to increasing rates of obesity and diabetes in countries such as Mexico, where HFCS is not a common ingredient in foods and drinks. (It is clear that high U.S. sugar tariffs and import quotas make domestically grown, corn-based sweeteners more economically advantageous.)

So, what is this possibly unnatural, ultra-sweet high-fructose corn syrup, of which the average American consumed 19.2 kg. per in 2004 (versus 20 kg. of sugar), just thirty years after it was developed and promptly included in many processed foods, soda beverages, and other food items in the United States? (The average Australian consumed 56.2 kg of sugar in 2002) HFCS includes a group of corn syrups that have undergone enzymatic processing in order to increase their fructose content, then are mixed with glucose or pure corn syrup in varying amounts. For example, HFCS 90 is approximately 90 percent fructose and 10 percent glucose and is most commonly used in baked goods. HFCS 55 is most commonly used in soft drinks, and HFCS 42 (42 percent fructose and 58 percent glucose) is most often used in sports drinks. The process for enzymatic conversion of d-glucose to d-fructose was originally developed by U.S. scientists Richard Marshall and Earl Kool in 1957 and subsequently refined by Japanese researchers in the 1970s, before widespread introduction into U.S. food production (Marshall and Kool 1957). This provided major economic advantages for the corn market in the U.S., where the price of sugar is artificially higher than its global price. HFCS is rarely used in Europe and other parts of the world, except for Japan, where its use is increasing. 

High-fructose corn syrup is produced by milling corn to corn starch, then further processing the corn starch to yield corn syrup, which is almost pure glucose. Enzymes are then added to change the glucose into fructose. The process is complex and requires numerous enzymatic additions, along with other sugars, in multiple stages to break down the sugar chains and convert them to fructose and glucose. This yields HFCS 90 (90 percent fructose). The other common formulations, noted above, are produced by combining the HFCS with desired proportions of 100 percent glucose corn syrup.

Bray and associates note that the digestion and metabolism of fructose is different from that of glucose, with hepatic metabolism of fructose favoring new lipogenesis. Fructose (unlike glucose) does not enhance leptin production or stimulate insulin secretion, suggesting that dietary fructose may contribute to weight gain.

Cane sugar is essentially pure sucrose, a disaccharide, equally consisting of fructose and glucose. In contrast to fructose, glucose absorption and metabolism is dependent on insulin stimulation to effect the transport mechanism and trigger insulin receptors. Leptin release is stimulated by insulin and is known to inhibit food intake and lessen hunger and gains in body fat.

While there is a provocative temporal association of HFCS with the growing epidemics of obesity and type II diabetes, there are confounding covariables that make it difficult to label this food and drink sweetener as the prime culprit in the epidemics. Possible taxation on its inclusion in foods and beverages may be the only logical means to decrease or eliminate its use but is probably premature until and unless future research convincingly establishes its causal role. Selective elimination of HFCS from anyone’s diet is challenging, as it is contained in almost all U.S.-produced processed or prepared foods and is difficult to avoid if one eats out. Cautious reading of labels of any frozen, baked, or canned goods to prevent consumption of items containing HFCS is encouraged, along with exercise, well-balanced meals, and healthy lifestyles.

Lucy Crain, MD, MPH,FAAP, is a member of the SFMS Board of Directors and a First  Five  San Francisco County Commissioner. Dr. Crain is Past President of the California District of the American Academy of Pediatrics and a former member of the national Board of Directors of the AAP. Since her retirement from full-time pediatric practice and teaching at UCSF, Dr. Crain continues to teach at UCSF as a member of the voluntary clinical faculty and consults at Lucile Packard Children’s Hospital at Stanford in the Child Development Clinic. Mel Heyman, MD, Also contributed to this article. Dr. Heyman is Chief of Pediatric Gastroenterolgy at UCSF.

References:

Bray, George A., Samara J. Neilsen, and Barry M. Popkin (April 2004). “Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity,” American Journal of Clinical Nutrition 79 (4): 537–543.

Marshall, Richard O. and Earl R. Kool, “Enzymatic conversion of d-glucose to d-fructose,” Science, 1957 (125), p. 648.