Fueling the Obesity Epidemic? Artificially Sweetened Beverage Use and Long-term Weight Gain

Sharon P. Fowler, Ken Williams, Roy G. Resendez1, Kelly J. Hunt, Helen P. Hazudaand Michael P. Stern; From the Department of Medicine, Division of ClinicalEpidemiology, The University of Texas Health Science Center at San Antonio. FROM ABSTRACT: We have examined the relationship between artificially sweetened beverage (ASB)consumption and long-term weight gain in the San Antonio Heart Study. From 1979 to 1988, height, weight, and ASB consumption were measured among5,158 adult residents of San Antonio, Texas. Seven to eight years later, 3,682participants were re-examined. Outcome measures were incidence of overweight/obesity (OW/OB). A significant positive dose – response relationship emerged between baseline ASBconsumption and all outcome measures. Consuming >21 ASBs/week (vs. none) was associated with almost-doubled risk ofOW/OB (93% increase incidence). Among the baseline normal-weight individuals, a doubled risk of OW/OB was notedat follow-up (103% increased incidence). These findings raise the question whether AS use might be fueling rather thanfighting our escalating obesity epidemic. KEY POINTS FROM ARTICLE: 1) Over 6,000 products including foods, beverages, cosmetics, andpharmaceuticals contain aspartame alone. 2) These authors assessed long-term weight change among participants in theSan Antonio Heart Study who use AS products compared with those who did not. 3) During the past 30 years, people have increasingly turned to artificiallysweetened (AS) foods and beverages in an attempt to lose weight or control it. 4) Manufacturers messages and conventional wisdom suggests that use of ASproducts would enhance weight loss or prevent further gain. 5) Sugar-sweetened beverage consumption was 75% less in ASB userscompared to nonusers. 6) Percent of calories from protein, total fat, and saturated fat were significantlyhigher in AS users. [Suggesting appetite control damage] 7) Dieting rates about the same in both groups. 8) The researchers adjusted the ORs for baseline BMI, age, ethnicity, gender,education, socioeconomic index, baseline and interim change in exercise frequency,baseline smoking status, and interim smoking cessation. 9) Overall, obesity showed significant dose – response relationships with ASBconsumption. 10) For each AS beverage consumed, users experienced significantly higherincrease in BMI. 11) Several studies have described increased appetite, hunger, and foodconsumption following AS exposure. 12) Other studies show that the incidence of metabolic syndrome increases withincreased diet soda consumption (by 34% to 53%). Increased incidence ofmetabolic syndrome has been observed among AS users in two major observationalstudies. 13) The authors suggest that because AS are 180 – 13,000 times sweeter thansugar, their consumption leads to taste distortion, increasing appetite forintensely sweet, highly caloric foods. AS use or sweet taste itself may increasehunger, cravings, or food intake. 14) Studies have shown that AS cause elevated insulin levels. [Important: GaryTaubes (Good Calories Bad Calories {2008}, Why We Get Fat {2011},Newsweek May 14 2012 The New Obesity Campaigns Have It All Wrong)notes that elevated insulin levels upregulates the enzyme lipoproteinlipase which opens the door to the fat cell, increasing fat storage] 15) Aspartame is 40% aspartate. Aspartate is toxic to neurons in the arcuatenucleus of the hypothalamus. The arcuate nucleus of the hypothalamus is a keysite for leptin signaling. Leptin signaling in the arcuate nucleus of thehypothalamus instructs us to reduce food intake. The earlier the exposure to excessaspartate, the more profound the damage to the arcuate nucleus. [ByronRichards (The Leptin Diet {2006}) notes that the hormone leptin is key forturning off our hunger so that we stop eating] 16) Animal experiments show that in utero exposure to aspartate producesoffspring obesity and causes severe loss of neurons in the arcuate nucleus. 3 17) The authors suggest that aspartame exposure may cause neurotoxicity withincreased leptin resistance and obesity. 18) We observed a classic, positive dose – response relationship between ASbeverage consumption and long-term weight gain. 19) Are ASs fueling rather than fighting the very epidemic they were designedto block? These authors suggest the answer is yes. 20) These results, together with findings of increased lymphoma and leukemia inyoung rodents exposed to aspartame, should be carefully considered when policyrecommendations to deter the development of obesity in children and adolescentsare being formulated particularly those recommending increased AS consumption.