As someone who has 2 degrees in nutrition with a 3rd on the way, I was highly skeptical when I received an assignment to report on HFCS. As it turns out, HFCS might not be nearly as innocent as we once thought.
I would highly recommend reading this article: http://www.ajcn.org/cgi/content/abstract/79/4/537 written by George Bray, It is extremely informative. But I’ll outline a few highlights below… In short, most of the things they say are indeed true. HFCS was introduced into the US food chain in 1968 which ironically is the same time that Americans really began to increase the rates of overweight and obesity. Seriously, if you look at graphs, it is quite amazing to see the parallel trends. The consumption of HFCS increased more than 1000% in the years between 1970 and 1990. HFCS is the leading sweetener in carbonated beverages but can also be found in cereals, flavored yogurts, most baked goods, dairy desserts, fruit drinks, jams and jellies, candy, canned fruits, and countless others. High fructose corn syrup currently represents more than 40% of caloric sweeteners that are added to foods and beverages and is the only sweetener added to soft drinks in the United States. This research review outlines the biological principles related to fructose including: the absorption of fructose, fructose and insulin release, insulin and leptin, as well as, fructose and metabolism. HFCS has a greater proportion of fructose than other sweeteners. Fructose and glucose are digested and absorbed through different processes. Disaccharides such as sucrose enter the small intestine are cleaved by disaccharidases. A sodium-glucose cotransporter absorbs the glucose that results from such cleavage. Fructose, on the other hand, is absorbed further down in the duodenum and jejunum by a non-sodium dependent process. Once these sugars have been absorbed, both glucose and fructose enter the portal circulation and are either transported to the liver (where fructose can be taken and converted to glucose) or pass into general circulation. Even small amounts of fructose ingested in combination with glucose “increases the hepatic glycogen synthesis in human subjects and reduces glycemic responses” (Bray, Nielsen, and Popkin, 2004). However, when large amounts of fructose are ingested, they “provide an unregulated source of carbon precursors for hepatic lipogenesis” (Bray, Nielsen, and Popkin, 2004). Fructose also affects insulin release. Fructose does not stimulate insulin most likely due to the fact that the ß cells of the pancreas do not have the fructose transporter GLUT-5. Therefore, when fructose is eaten as part of a mixed meal, the increase in glucose and insulin is much smaller than when the same amount of glucose is eaten. However, fructose has been shown to produce a much larger increase in lactate than glucose and a small increase in “diet-induced thermogenesis” (Schwarz, Schutz, and Froidevaux, 1989). This suggests that glucose and fructose have different metabolic effects (Bray, Nielsen, and Popkin, 2004). The small decrease in insulin regulation produced when fructose is consumed can have significant effects. Insulin helps to control food intake by two different mechanisms. In one study, Schwartz and fellow researchers report that insulin concentrations in the central nervous system directly inhibits the intake of food (Schwartz, Woods, Porte, Seeley, and Baskin, 1998). Secondly, insulin may help to control food intake by affecting leptin secretion (Muller, Gregoire, and Stanhope, 1998). Insulin increase leptin release with a time delay. Therefore, a low insulin concentration after eating a meal containing fructose would result in lower concentrations of leptin than if that person were to consume only glucose. Since leptin inhibits food intake, having lower levels would lead one to overeat or at the very lead eat more than their usual (Bray, Nielsen, and Popkin, 2004). Health professionals and dietitians alike have seen that people lacking leptin become morbidly obese. A preliminary study conducted found that “to the extent that fructose increases the diet, one might expect less insulin secretion and thus less leptin release and a reduction in the inhibitory effect of leptin on food intake, i.e., an increase in food intake (Teff, Elliot, Tschoep, Kieffer, Radar, Heiman, et al., 2002). The metabolism of fructose itself might provide some insight into its possible cause of weight gain. Fructose and glucose are metabolized in two different ways. Glucose enters the cell by a transporter, GLUT-4, that is insulin dependent. Fructose, on the other hand, enters cells by a GLUT-5 transporter which does not depend on insulin but is absent from both the pancreas and brain (Bray, Nielsen, and Popkin, 2004). Glucose provides a sort of satiety signal to the brain that fructose cannot due to the fact that it cannot be transported into the brain. Fructose also contributes carbon atoms to synthesize long-chain fatty acids. Therefore, fructose helps to “facilitate the biochemical formation of triacylglycerols more efficiently than does glucose” (Bray, Nielsen, and Popkin, 2004).
Resources:
Bray, G.A., Nielsen, S.J., & Popkin, B.M. (2004). Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. *American Journal *
Schwarz, J.M., Schutz, Y., & Froidevaux, F. (1989). Thermogenesis in men and women induced by fructose vs. glucose added to a meal. American Journal of Clinical
Schwartz, M.W., Woods, S.C., Porte, D.J., Seeley, R.J., & Baskin, D.G. (1998). Central nervous system control of food intake. Nature, 661-671.
Muller, W.M., Gregoire, F.M., & Stanhope, K.L. (1998). Evidence that glucose metabolism regulated leptin secretion from cultured rat adipocytes.
Endocrinology, 551-558.
Teff, K.L., Elliot, S.S., & Tschoep, M.R. (2002). Consuming high fructose meals reduces 24 hour plasma insulin and leptin concentrations, does not suppress circulating ghrelin, and increases postprandial and fasting triglycerides in women. Diabetes, supplement.
Teff, K.L., Elliot, S.S., Tschoep, M.R., Kieffer, T.J., Rader, D., Heiman, M., et al. (2003). Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women. The Journal of Clinical Endocrinology and Metabolism, 2963-2972.
