High-fructose corn syrup (HFCS) is back in the news. A research team from Princeton has concluded that high-fructose corn syrup outdoes sugar when it comes to increasing body fat.
Just to be clear, sugar causes a lot of trouble–raising inflammation and contributing to insulin resistance, diabetes and obesity.
But according to some research, high-fructose corn syrup is even worse.
It might seem that this much maligned sweeter would have seen its day. Instead, high-fructose corn syrup continues to be a powerhouse, sweetening soft drinks like Coke and Pepsi and sports drinks like Gatorade. HFSC is the frosting on Frosted Flakes, and the syrup in Hershey’s Chocolate Flavor Syrup. It adds a touch of sweetness to Heinz ketchup, and provides stickiness to barbeque sauce.
The connection between high-fructose corn syrup and obesity has been explored in studies conducted at research centers in locations such as Louisiana State University (LSU) and the University of California. Writing in the American Journal of Clinical Nutrition, the LSU researchers note: “The consumption of HFCS increased more than 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group.” (Bray et al.)
Researchers in Germany have also studied the HFCS and weight gain connection. Publishing their findings in the journal Obesity Research, researchers from the German Institute of Human Nutrition gave mice drinks containing either fructose, sucrose or artificial sweetener to see the impact on weight gain and metabolism. They found that mice drinking the fructose containing beverage increased body fat, while the others did not.
Here’s what the Princeton team had to say about its research:
Researchers from Princeton’s Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup (HFCS) and obesity. The research was supported by the U.S. Public Health Service and published in the journal Pharmacology, Biochemistry and Behavior.
They found that when it comes to weight gain, all sweeteners are not equal. In laboratory tests on rats, those 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 addition to the weight gain, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides in the lab animals.
The leader of the Princeton team, Professor Bart Hoebel, a specialist in the neuroscience of appetite, weight and sugar addiction explained: "Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn’t true, at least under the conditions of our tests,” He continues: "When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they’re becoming obese — every single one, across the board. Even when rats are fed a high-fat diet, you don’t see this; they don’t all gain extra weight."
The first study showed that male rats given water sweetened with high-fructose corn syrup 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. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.
The second experiment — the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals — monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup 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. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet.
High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there are at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars — it is 50 percent fructose and 50 percent glucose — but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.
The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that 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.
High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.
Princeton University Press Room
Pharmacol Biochem Behav. 2010 Feb 26.
High-fructose corn syrup causes characteristics of obesity in rats: Increased body weight, body fat and triglyceride levels.
Bocarsly ME, Powell ES, Avena NM, Hoebel BG. Department of Psychology, Princeton University, Princeton, NJ 08540, USA; Princeton Neuroscience Institute, Princeton University, Princeton, NJ 08540, USA.
Am J Clin Nutr. 2004 Apr;79(4):537-43.Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.
Bray GA, Nielsen SJ, Popkin BM. Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA.
Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.
J Clin Invest. 2009 May;119(5):1322-34. Epub 2009 Apr 20.
Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.
Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. Department of Molecular Biosciences, UCD, Davis, California 95616, USA.
Comment in: J Clin Invest. 2009 May;119(5):1089-92.
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.
Obes Res. 2005 Jul;13(7):1146-56.
Consuming fructose-sweetened beverages increases body adiposity in mice.
Jürgens H, Haass W, Castañeda TR, Schürmann A, Koebnick C, Dombrowski F, Otto B, Nawrocki AR, Scherer PE, Spranger J, Ristow M, Joost HG, Havel PJ, Tschöp MH.
Department of Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany.
OBJECTIVE: The marked increase in the prevalence of obesity in the United States has recently been attributed to the increased fructose consumption. To determine if and how fructose might promote obesity in an animal model, we measured body composition, energy intake, energy expenditure, substrate oxidation, and several endocrine parameters related to energy homeostasis in mice consuming fructose.
RESEARCH METHODS AND PROCEDURES: We compared the effects of ad libitum access to fructose (15% solution in water), sucrose (10%, popular soft drink), and artificial sweetener (0% calories, popular diet soft drink) on adipogenesis and energy metabolism in mice. RESULTS: Exposure to fructose water increased adiposity, whereas increased fat mass after consumption of soft drinks or diet soft drinks did not reach statistical significance (n = 9 each group). Total intake of energy was unaltered, because mice proportionally reduced their caloric intake from chow. There was a trend toward reduced energy expenditure and increased respiratory quotient, albeit not significant, in the fructose group. Furthermore, fructose produced a hepatic lipid accumulation with a characteristic pericentral pattern.
DISCUSSION: These data are compatible with the conclusion that a high intake of fructose selectively enhances adipogenesis, possibly through a shift of substrate use to lipogenesis.