A recent study involving both short- and long-term animal experiments has purportedly linked high-fructose corn syrup (HFCS) to significant weight gain in rats. Miriam Bocarsly, et al., “High-fructose corn syrup causes characteristics of obesity in rats: Increased body weight, body fat and triglyceride levels,” Pharmacology, Biochemistry and Behavior, March 2010. According to a March 23, 2010, Princeton University press release, researchers have “demonstrated that all sweeteners are not equal when it comes to weight gain: Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same.”

In the short-term experiment, the authors reported that “male rats given water sweetened with [HFCS] in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet.” Moreover, the long-term experiment allegedly suggested that when “compared to animals only eating rat chow, rats on a diet rich in [HFCS] showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly.” The accompanying press release hypothesized that, due to molecular differences between HFCS and sucrose, “excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.”

Meanwhile, several health experts have already questioned the study and its interpretation of the results, highlighting several discrepancies and inconclusive data sets. As New York University Professor Marion Nestle responded in a March 24, 2010, Food Politics blog post, “The study is extremely complicated and confusingly described.” In particular, she stated that the results of the first experiment, which involved giving male rats access to either sucrose or HFCS for 12 hours per day, were not borne out when rats were fed HFCS for 24 hours per day. These rats, “which should be expected to be fatter,” in fact “weighed less (470 grams) than the rats fed sucrose for 12 hours per day,” Nestle pointed out. In addition, she noted (i) that the second experiment was not a comparison but “just looked at the effects of HFCS in groups of 8 male rats,” and (ii) that researchers could not replicate the outcome of the first experiment using female rats. “So I’m skeptical,” she concluded. “I don’t think the study produces convincing evidence of a difference between the effects of HFCS and sucrose on the body weight of rats. I’m afraid I have to agree with the Corn Refiners on this one.” See The Los Angeles Times, March 24, 2010.

In a related development, a recent study has reportedly claimed that fructose can worsen the severity of liver scarring in patients with nonalcoholic fatty liver disease (NAFLD). Manal Abdelmalek, et al., “Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease,” Hepatology, March 2010. Duke University researchers apparently surveyed the dietary intake of 427 NAFLD patients, finding that “only 19 percent of adults with NAFLD reported no intake of fructose-containing beverage, while 52 percent consumed between one to six servings a week and 29 percent consumed fructose-containing beverages on a daily basis.” Noting that NAFLD is present in 30 percent of U.S. adults, the lead author claimed to have “identified an environmental risk factor that may contribute to the metabolic syndrome of insulin resistance and the complications of the metabolic syndrome, including liver injury.” See Duke University Press Release, March 18, 2010.

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