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      Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2 Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA)*

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          Abstract

          OBJECTIVE

          We determined associations between diet soda consumption and risk of incident metabolic syndrome, its components, and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis.

          RESEARCH DESIGN AND METHODS

          Diet soda consumption was assessed by food frequency questionnaire at baseline (2000–2002). Incident type 2 diabetes was identified at three follow-up examinations (2002–2003, 2004–2005, and 2005–2007) as fasting glucose >126 mg/dl, self-reported type 2 diabetes, or use of diabetes medication. Metabolic syndrome (and components) was defined by National Cholesterol Education Program Adult Treatment Panel III criteria. Hazard ratios (HRs) with 95% CI for type 2 diabetes, metabolic syndrome, and metabolic syndrome components were estimated, adjusting for demographic, lifestyle, and dietary confounders.

          RESULTS

          At least daily consumption of diet soda was associated with a 36% greater relative risk of incident metabolic syndrome and a 67% greater relative risk of incident type 2 diabetes compared with nonconsumption (HR 1.36 [95% CI 1.11–1.66] for metabolic syndrome and 1.67 [1.27–2.20] for type 2 diabetes). Of metabolic syndrome components, only high waist circumference (men ≥102 cm and women ≥88 cm) and high fasting glucose (≥100 mg/dl) were prospectively associated with diet soda consumption. Associations between diet soda consumption and type 2 diabetes were independent of baseline measures of adiposity or changes in these measures, whereas associations between diet soda and metabolic syndrome were not independent of these factors.

          CONCLUSIONS

          Although these observational data cannot establish causality, consumption of diet soda at least daily was associated with significantly greater risks of select incident metabolic syndrome components and type 2 diabetes.

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          Most cited references18

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          Dietary patterns are associated with biochemical markers of inflammation and endothelial activation in the Multi-Ethnic Study of Atherosclerosis (MESA).

          Dietary patterns may influence cardiovascular disease risk through effects on inflammation and endothelial activation. We examined relations between dietary patterns and markers of inflammation and endothelial activation. At baseline, diet (food-frequency questionnaire) and concentrations of C-reactive protein (CRP), interleukin 6 (IL-6), homocysteine, soluble intercellular adhesion molecule-1 (sICAM-1), and soluble E selectin were assessed in 5089 nondiabetic participants in the Multi-Ethnic Study of Atherosclerosis. Four dietary patterns were derived by using factor analysis. The fats and processed meats pattern (fats, oils, processed meats, fried potatoes, salty snacks, and desserts) was positively associated with CRP (P for trend < 0.001), IL-6 (P for trend < 0.001), and homocysteine (P for trend = 0.002). The beans, tomatoes, and refined grains pattern (beans, tomatoes, refined grains, and high-fat dairy products) was positively related to sICAM-1 (P for trend = 0.007). In contrast, the whole grains and fruit pattern (whole grains, fruit, nuts, and green leafy vegetables) was inversely associated with CRP, IL-6, homocysteine (P for trend < or = 0.001), and sICAM-1 (P for trend = 0.034), and the vegetables and fish pattern (fish and dark-yellow, cruciferous, and other vegetables) was inversely related to IL-6 (P for trend = 0.009). CRP, IL-6, and homocysteine relations across the fats and processed meats and whole grains and fruit patterns were independent of demographics and lifestyle factors and were not modified by race-ethnicity. CRP and homocysteine relations were independent of waist circumference. These results corroborate previous findings that empirically derived dietary patterns are associated with inflammation and show that these relations in an ethnically diverse population with unique dietary habits are similar to findings in more homogeneous populations.
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            Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight.

            To examine whether artificial sweeteners aid in the control of long-term food intake and body weight, we gave free-living, normal-weight subjects 1150 g soda sweetened with aspartame (APM) or high-fructose corn syrup (HFCS) per day. Relative to when no soda was given, drinking APM-sweetened soda for 3 wk significantly reduced calorie intake of both females (n = 9) and males (n = 21) and decreased the body weight of males but not of females. However, drinking HFCS-sweetened soda for 3 wk significantly increased the calorie intake and body weight of both sexes. Ingesting either type of soda reduced intake of sugar from the diet without affecting intake of other nutrients. Drinking large volumes of APM-sweetened soda, in contrast to drinking HFCS-sweetened soda, reduces sugar intake and thus may facilitate the control of calorie intake and body weight.
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              A role for sweet taste: calorie predictive relations in energy regulation by rats.

              Animals may use sweet taste to predict the caloric contents of food. Eating sweet noncaloric substances may degrade this predictive relationship, leading to positive energy balance through increased food intake and/or diminished energy expenditure. These experiments were designed to test the hypothesis that experiences that reduce the validity of sweet taste as a predictor of the caloric or nutritive consequences of eating may contribute to deficits in the regulation of energy by reducing the ability of sweet-tasting foods that contain calories to evoke physiological responses that underlie tight regulation. Adult male Sprague-Dawley rats were given differential experience with a sweet taste that either predicted increased caloric content (glucose) or did not predict increased calories (saccharin). We found that reducing the correlation between sweet taste and the caloric content of foods using artificial sweeteners in rats resulted in increased caloric intake, increased body weight, and increased adiposity, as well as diminished caloric compensation and blunted thermic responses to sweet-tasting diets. These results suggest that consumption of products containing artificial sweeteners may lead to increased body weight and obesity by interfering with fundamental homeostatic, physiological processes. Copyright (c) 2008 APA, all rights reserved.
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                Author and article information

                Journal
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                April 2009
                16 January 2009
                : 32
                : 4
                : 688-694
                Affiliations
                [1] 1Division of Epidemiology, University of Texas Health Sciences Center, Houston, Texas;
                [2] 2Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, Minnesota;
                [3] 3Center for Human Nutrition, Department of International Health, The Johns Hopkins University, Baltimore, Maryland;
                [4] 4Division of Cardiology, The Johns Hopkins University, Baltimore, Maryland;
                [5] 5Department of Nutrition, University of Oslo, Oslo, Norway.
                Author notes
                Corresponding author: Jennifer A. Nettleton, jennifer.a.nettleton@ 123456uth.tmc.edu .

                *A full list of participating Multi-Ethnic Study of Atherosclerosis (MESA) investigators and institutions can be found at http://www.mesa-nhlbi.org.

                Article
                1799
                10.2337/dc08-1799
                2660468
                19151203
                cb91b6a5-3978-4fd0-bc3d-a28fb18f7b25
                © 2009 by the American Diabetes Association.

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                : 1 October 2008
                : 30 December 2008
                Categories
                Original Research
                Cardiovascular and Metabolic Risk

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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