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their empty, depleting, addictive calories, are bad for you. But the real question is whether HFCS is actually worse for you—more depleting and more damaging— than ordinary sugar. The research indicates that it is. heir empty, depleting, addictive calories, are bad for body weight, this suggests that dietary fructose may you. But the real question is whether HFCS is actually contribute to increased energy intake and weight gain." worse for you—more depleting and more damaging— There is another difference between fructose and han ordinary sugar. The research indicates that it is. glucose metabolism: glucose enters the cells through the action of insulin; fructose enters the cells through the The Obesity Debate action of something called a GLUT5 transporter, which The public became aware of the possible downside of — does not depend on insulin. This transporter is absen HFCS with the publication of a paper in the April 2004 from pancreatic B-cells and the brain, which indicates edition of The American Journal of Clinical Nutrition.’ Authors limited entry of fructose into these tissues. Glucose Bray and others noted the parallel increase in obesity _ provides "satiety" signals to the brain that fructose canno’ and HFCS consumption in the US, and a number of __ provide because it is not transported into the brain. Once columnists publicised his theory that, calorie for calorie, inside the cells, fructose facilitates the formation o HFCS is more likely to cause weight gain than sugar. triglycerides more efficiently than does glucose. The Bray paper provides an explanation for the The Bray paper references a study by Bantle and others mechanism whereby fructose would be more fattening. in which a diet containing 17 per cent fructose (very Sugar is a disaccharide that breaks down into two _ typical of today's consumer) caused a highly significan monosaccharides—glucose and fructose—in the _ increase of 32 per cent triglyceride levels in the blood in intestinal tract. After absorption, fructose must pass __ male subjects, although not in female subjects.’ The hrough the liver. Small paper also discusses the fact tha’ amounts of fructose added to sweetened beverages in general, glucose in the diet increase the as compared to sweeteners production of glycogen {stored Thus, to the extent that added to solid foods, have a d h f Ce a) eee . ter t t i glucose into the bloodstream, | fructose inhibits insulin and foo, citing 2 randomised an outcome that is theoretically leptin levels, one would double-blind European study by elpful to those suffering from Q Q Rabin and others which found ype 2 diabetes. However, large expect an Increase In food that drinking calorically amounts of fructose in the diet intake in a diet that sweetened beverages resulted in rapidly turn into fatty acids—a Q greater weight gain over the 10- process called de novo includes HFCS. week study than did drinking die’ lipogenesis—which are then drinks.’ Since the beverages in stored as fat or released into the this study were sweetened with bloodstream as triglycerides. sucrose, Bray et al. called for a Small amounts of L-fructose—the type of fructose — second randomised controlled study to compare sucrose- hat human beings have traditionally consumed in and HFCS-sweetened beverages. ruit—can actually be beneficial to diabetics because L- tuctose does not stimulate insulin secretion. However, Industry Response research indicates that insulin concentrations in the But instead of providing support for such a study, the central nervous system have a direct inhibitory effect on industry responded with a wallop of damage control in the ood intake: when insulin secretions increase, food form of a report by the University of Maryland's Center for consumption declines. Furthermore, insulin increases Food, Nutrition and Agriculture Policy (CFNAP),’ aided by he release of leptin, a hormone that also inhibits food _ a gift from British sweetener company Tate & Lyle PLC. intake. Individuals who are genetically unable to The magnitude of the deleterious effects of fructose produce leptin are massively obese; low leptin varies depending on such factors as age, sex, baseline concentrations are associated with increased hunger glucose, insulin and triglyceride concentrations, the and gains in body fat. presence of insulin resistance and the amount of dietary Thus, to the extent that fructose inhibits insulin and fructose consumed." Some are more sensitive to eptin levels, one would expect an increase in food fructose than others: people who are hypertensive, intake in a diet that includes HFCS. Bray et al. cite a — hyperinsulinaemic or hypertriglyceridaemic; non-insulin 2002 study by Teff and others, published in Diabetes, in dependent diabetics; people with functional bowel which consumption of high-fructose meals reduced 24- disease; and postmenopausal women.'! The CFNAP our plasma insulin and leptin concentrations and expert panel was able to confuse the issue by citing increased triglyceride levels in women.’ (Although — studies carried out with individuals known to be less published in a major medical journal, this study does _ sensitive to fructose. Conspicuously absent in its review not appear in a MEDLINE search.) According to the are the Teff, Bantle and Rabin studies cited by Bray and Bray paper: “Because insulin and leptin act as key others. The report dismisses both the epidemiological afferent signals in the regulation of food intake and correlation and the large amount of research showing expect an increase in food intake in a diet that Industry Response But instead of providing support for such a study, the industry responded with a wallop of damage control in the form of a report by the University of Maryland's Center for Food, Nutrition and Agriculture Policy (CFNAP),’ aided by a gift from British sweetener company Tate & Lyle PLC. The magnitude of the deleterious effects of fructose varies depending on such factors as age, sex, baseline glucose, insulin and triglyceride concentrations, the presence of insulin resistance and the amount of dietary fructose consumed."” Some are more sensitive to fructose than others: people who are hypertensive, hyperinsulinaemic or hypertriglyceridaemic; non-insulin dependent diabetics; people with functional bowel disease; and postmenopausal women.'' The CFNAP expert panel was able to confuse the issue by citing studies carried out with individuals known to be less sensitive to fructose. Conspicuously absent in its review are the Teff, Bantle and Rabin studies cited by Bray and others. The report dismisses both the epidemiological correlation and the large amount of research showing 12 * NEXUS APRIL - MAY 2010 Thus, to the extent that fructose inhibits insulin and leptin levels, one would includes HFCS. www.nexusmagazine.com