The Role High Fructose Corn Syrup Plays in Obesity by Hollie Strawn

By at December 23, 2011 | 12:11 pm | Print

The Role High Fructose Corn Syrup Plays in Obesity by Hollie Strawn

High Fructose Corn Syrup, or HFCS, in consumer foods has recently generated controversy concerning its role as a contributor to rising obesity rates in the United States. Two questions stand out. One asks, “Does HFCS actually cause weight gain with obesity indicators such as metabolic changes along with increased adiposity, especially as compared with sucrose?”, and two, “Is HFCS a unique contributor to obesity?” Although varied, two rat studies in particular show increased weight gain among rats fed HFCS as part of their diet, as compared to sucrose (Bocarsly et al. 2010) (Light et al. 2008). The findings from these studies reveal a cause for concern, and the need for additional long-term studies has been expressed.

Understanding how HFCS became so popular with food manufacturers and how it is created gives some helpful background knowledge .Work on HFCS started in the 1950’s and 1960’s, and began being heavily marketed in the States as a sweetener in the 1970’s (White 2008). The reliability, domestic access, lowered expense from governmental corn subsidies combined with the fluctuating price of sugar (due to climate and political instabilities with sugar cane and sugar beet growing areas ) made this sweetener attractive economically for food manufacturers, with the resulting cheaper prices being attractive to consumers. Further, sucrose posed potential problems for food manufacturers, particularly soda, because it tends to hydrolyze, or split, in the acidic solutions used for those products, and affects taste quality. HFCS is also an easily transported liquid that only requires dilution. The rising popularity and demand for packaged foods from consumers during this time combined with the ease of use, access and transport of HFCS made its use surge quickly,. (White, 2008)

How HFCS is produced gives a better understanding of what the sweetener actually contains. White (2008) contends that the name High-Fructose Corn Syrup is misleading as it gives the consumer the impression that the fructose content is unusually high. The name was originally meant to distinguish this product from the glucose-only solutions being produced. The fructose content is not significantly higher that sucrose and was not meant as a comparison with sucrose at all. (White 2009) HFCS is made with harvested corn being soaked at a wet mill to loosen the kernel and is then crushed with the corn starch being separated out. Three different enzymes are added to the liquid for the purpose of converting some of the glucose in the corn syrup to fructose. After being filtered of impurities through activated carbon, the remaining liquid becomes HFCS-42, meaning it contains 42 percent fructose. A portion of this is processed again to further increase the fructose content to 90 percent, (called HFCS-90), which is then blended with the original 42 percent concentration to create HFCS-55 with a 55 percent fructose content. (Sweet Scam 2011) It is final product of HFCS-55 that is used in soda. The makeup consists of 55 percent fructose, 42 percent glucose and the remaining 3 percent are higher saccharides. The higher saccharides include free glucose with smaller amounts of bound glucose in the form of maltose and maltotriose. (White 2009) The type of HFCS used in solid goods like baked items, desserts and canned fruits is HFCS-42, with a 42 percent fructose concentration and a 58 percent glucose concentration. (Hand 2009)

In comparison, sucrose is a disaccharide and is made up of a fructose and a glucose molecule chemically bonded together with a composition of 50 percent glucose and 50 percent fructose. The body must first digest sucrose through hydrolysis using sucrase, which breaks the bond to one glucose and one fructose molecule before it can be absorbed into the bloodstream for use. White (2009) explains that HFCS differs from sucrose in that it is only blended together and presents as a monosaccharide with no bond needing to be broken before absorption, similar to honey and fruit based sweeteners and not unique.

Fructose metabolism differs from sucrose as it is absorbed at a different site in the intestines (Bocarsley et al. 2010), with the majority of the metabolism occurring in the liver. It is then converted into fructose-1-phosphate, which the authors contend is a predeccesor of the structure for the triglyceride molecule. Light et al. (2010) and Bocarsly et al. (2009) write that fructose, being metabolized beforehand, avoids an important step in glycolysis that involves the rate-limiting or regulating control point enzyme phophofructokinase and starts glycolysis as fructose-1-phosphate, and this difference provides an unchecked supply of three-carbon molecules. These three-carbon molecules are then used for the synthesis of glycerol in the form of glycerol-3 phosphate and fatty acids or acetyl-CoA (Stanhope et al. 2008), that lend themselves to the triglyceride development. Light et al. (2008) goes on to explain that circulating triglycerides in the blood are encapsulated in very-low density lipoproteins, or VLDL’s. The VLDL’s carrying these triglycerides are hydrolyzed by LPL’s, or lipoprotein lipase, an enzyme that breaks down the lipoproteins and facilitates tissues taking up the freed fatty acids for storage. These triglycerides being hydrolyzed and taken up by adipose tissues are given as a reason for the larger adipose deposits, or fat accrual, found at the conclusion of their study. (Light, et al. 2008)
White (2009), a noted consultant to the food and beverage industry, also asserts that fructose does avoid a regulatory control point of glycolysis involving phosphofructokinase and is quickly taken up by the liver. He proposes that this is an evolutionary benefit. We are able to absorb nutrients from a diverse assortment of food in resourceful ways. White’s thesis that HFCS is not solely responsible for the rise of obesity in the United States is supported when he writes that negative consequences are a result of overconsumption of any one nutrient, and not the result of any one sweetener.

The rate study published in 2009 titled “The Type of Caloric Sweetener Added to Water Influences Weight Gain, Fat Mass, and Reproduction in Growing Sprague-Dawley Rats” (Light, et al. 2009) stated the objective of the study was to find if different calorie containing sweeteners would influence weight gain, cause metabolic problems or endocrine imbalances.
Previous studies used only fructose in place of HFCS at a concentration of 30 percent. These unusually high doses are not representative of any standard diet, and not likely to be useful in any practical manner in comparison to human physiology. (Light et al. 2009) Also no comparison was made between HFCS and sucrose. This study uses HFC-55, fructose, glucose and sucrose added to ddH2O, deionized distilled water, at a concentration of 13 percent and closely resembling the concentration in most sweetened beverage.

Sprague-Dawley rats are a type of rat commonly utilized in animal studies. The particular rats used in this study were randomly selected into groups of eight or nine and, after acclimation, were assigned a specific sweetener to be added to their water, with the control still receiving unsweetened ddH2O. Rat chow was fed to all groups ad libitum, or free access. The study lasted eight weeks.
The study found that adding the caloric sweetened water caused the rats to ingest more calories, and that higher intake was not compensated for by voluntarily restricting calories in solid food intake. Also, total energy intake was no different for any of the sweeteners. While initial body weights had been the same, after eight weeks the rats drinking the HFCS-55 sweetened water had the most weight gain. HFCS-55 was the only sweetener that caused adiposity compared to the glucose solution. The retroperitoneal and gonadal fat pads were heavier than the controls in the HFCS-55 group, but no statistical difference was found between the sweetener-drinking groups. Liver weight and circulating serum levels were checked after the 8 week period, and no significant differences were found. Liver weight was relatively the same among all groups. Cholesterol, triglyceride, VLDL, LDL and HDL were all checked and found to be within range. Fasting glucose, insulin and C-peptide concentration were tested with no significant differences, although insulin levels were raised for the HFCS-55 group. Also, leptin expression was higher in the HFCS-55 group, but not significantly so. The study asserts that the possible metabolic effects of HFCS-55 may require longer studies to begin emerging. Regardless, no statistically significant metabolic changes were found. And, looking to any effects on the reproductive cycles, the fructose group had a slightly lengthened estrous cycle for cycle six that declined to the regular rate in cycle seven. Reproductive cycles in the HFCS-55 group lengthened, with longer estrous times being reported, on a gradual scale getting longer with each cycle. (Light et al. 2009)

The authors contend that the slightly higher fructose concentration of HFCS than of sucrose may have influenced the higher weight gain in the rats assigned that solution. They assert that further studies into the mechanisms showing the reason for the weight gain should be conducted along with longer study periods to investigate possible reproductive inhibition or problems with the lengthened estrous cycles reported, and if the weight gain develops into obesity. (Light et al. 2009)
The more recent study on HFCS and rats was conducted by Princeton, and is titled “High-Fructose Corn Syrup Causes Characteristics of Obesity in Rats: Increased Body Weight, Body Fat and Triglyceride Levels” and was released in 2010. The original goal of the study was to see if adding HFCS to a standard diet could cause in any way obesity related symptoms in both male and female rats.

The actual experiment is broken up into in two parts. Experiment One is the short term 8 week version using only male rats. All the groups were given chow and water “ad libitum” or free fed (in order to self-regulate), with the control group only receiving chow and water. Group 1 was given 24-hr access to HFCS, Group 2 given 12-hr HFCS, and Group 3 was given 12-hr access to sucrose. The solution concentration for the HFCS was 8 percent from Nature’s Flavors Formula 55 and the sucrose concentration was 10 percent and used Domino Granulated Pure Cane Sugar. Both were dissolved in tap water, and these different concentrations of specific sweeteners were used as they closely mimic the concentrations in sweetened beverages such as soda. (Bocarsly et al. 2010)
The findings of Experiment One are similar to the previous study, and show that again HFCS caused weight gain. The result was the 12-hr HFCS group gained statistically significantly more weight than did either the 24-hr HFCS or the 12-hr sucrose group. No overall caloric intake differences were found between the HFCS or the sucrose groups. Also, no HFCS intake differences were found in either the 24-hr or the 12-hr HFCS groups, but yet the 12-hr group gained much more weight. No significant differences in blood work, such as glucose levels, were found. (Bocarsly et al. 2010)

Longer term studies have been requested based on the results of the previous shorter term studies(Light et al. 2009). Experiment 2 was a long term study that lasted 6 months for male rats, and 7 months for the female rats that were included this time. The male group was formed the same way as Experiment 1, except they did not do a sucrose group. Bocarsly et al. (2010) explains the decision to omit a sucrose group in Experiment 2 as resulting from no observable differenced in body weight using sucrose in the first experiment. The female rats were set up the same way as Experiment 1 (male rats), with differences being the duration was 7 months, included a 12-hr sucrose group, and both 12-hr HFCS and sucrose group only received 12 hour access to chow as opposed to 24 hour access. (Bocarsly et al. 2010)

The results for the long term male rat study were that both the 12-hr and 24-hr HFCS groups gained significant amounts of weight, not just the 12-hr group as seen in Experiment One. Additionally, fat pads were measured and were overall much bigger than the controls, with the most significant differences found in the abdominal region. Triglyceride levels were increased (except for the control) although insulin levels didn’t change. (Bocarsly et al. 2010)
As indicators of obesity, Experiment Two finds for the female rats that the 24-hr HFCS access group gained the most weight with larger fat pad growth than the control, especially the uterine and abdominal fat pads. Triglyceride levels were highest in the 24-hr group compared to the sucrose or the control, however, no triglyceride differences were seen with the 12-hr HFCS and the control. No insulin differences or changes were found. Interesting to note, while the overall weight difference was highest with the 24-hr HFCS group, the 12-hr HFCS group weighed lower than the control group, although not in a statistically significant way. (Bocarsly et al. 2010)

The weight gain when combined with larger and heavier fat areas, particularly in the abdomen in both males and females and uterine fat pads in females, is significant. These findings combined with higher triglyceride levels in the HFCS groups, are used to support the theory that HFCS contributes to obesity. (Bocarsly et al. 2010) The authors cite research (Chang et al. 2007) saying fat intake increases when levels of triglycerides rise. The higher levels of triglycerides in the rats ingesting the HFCS could have effected their resulting larger and heavier fat pad accrual. (Bocarsly et al. 2010)

Interesting specifics to note in this study are the differences in the 12-hr and 24-hr HFCS weight gain between Experiment One and Two, with the 24-HFCS group weighing more at the conclusion of the Experiment Two, while the 12-hr HFCS outweighed the 24-hr HFCS group in Experiment One. Also the surprising finding that the 12-hr HFCS group weighed in even lower than the control in Experiment 2 with the females is confusing. It also is notable that in Experiment Two with the female rats ad libitum chow was not offered to the 12-hr HFCS or the 12-hr sucrose. Differing from the other experiments entirely, only 12 hour access to rat chow was offered.

The two rat studies showed clearly that HFCS at solutions that are similar to commercial sweetened beverages such as soda do increase adiposity, or fat accrual. (Light et al. 2009) (Bocarsly et al. 2010) The more recent study also found higher triglyceride levels in the rats with access to HFCS. The significantly larger and heavier fat pads appeared in the abdominal regions, with uterine fat pads also significantly heavier in female rats. Taken together these are indicators of obesity, as weight gain alone would not signal obesity. (Bocarsly et al. 2010). The differences in the metabolism of HFCS compared to sucrose and how it can lend itself to more fat accrual was investigated in these studies. (White 2009) (Bocarsly et al. 2010) (Light et al. 2008) (Stanhope et al. 2008). More long term research is needed to help us understand the role that High-Fructose Corn Syrup in our food, whether it is determined to be a major or minor player, has on obesity. Longer term studies would also be helpful in determining if HFCS used as an added sweetener has a much greater role to play than that of sucrose alone. The idea that added calories, from any source, without added energy expenditures cause weight gain, regardless of the sweetener used, must be remembered. (White 2009)


Bocarsly, Miriam E., Elyse S., Powell, Avena Nicole M. and Heobel, Bartley G. 2010. High-fructose corn syrup causes characterisitcs of obesity in rats: increased body weight, body fat and triglyceride levels. Pharmacology, Biochemistry and Behavior. 97:1-5
Center for Consumer Freedom 2011. Sweet Scam. How it’s made: high-fructose corn syrup. [Online] Available: . November 17, 2011.

Chang, GQ, Karatayev O., Ashan R., Gaysinskaya, V., Marwil, Z. and Leibowitz, SF. 2007. Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus; role of circulating triglycerides. Am Journal Physiol Endocrinal Metab. 292: E561-70

Hand, Becky. 2009. The truth about high fructose corn syrup: sweet surprise or health demise? SparkPeople [Online] Available Nov. 17, 2011

Light, Heather L., Tsanzi, Embedzayi, Gigliotti, Joseph, Morgan, Keri and Janet C. Tau. 2009. The type of caloric sweetener added to water influences weight gain, fat mass, and reproduction in growing sprague-dawley female rats. Society For Experimental Biology and Medicine 234: 651-652, 654-655, 658-660.

Stanhope, Kimber L. and Havel, Peter. Endocrine and metabolic effects of consuming beverages sweetened with fructose, glucose, sucrose, or high-fructose corn syrup. The American Journal of Clinical Nutrition. 88: 1735S

White, J. 2008. Straight talk about high-fructose corn syrup: what it is and what it ain’t. American Journal of Clinical Nutrition. 88: 1716S-1717S, 1719S

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