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      Sugar Sweetened Beverage Consumption among Adults with Gout or Type 2 Diabetes

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          Abstract

          Background

          Current guidelines for the management of type 2 diabetes and gout recommend that people with these conditions limit their sugar sweetened beverage (SSB) intake. We examined self-reported SSB intake among New Zealand adults with gout or type 2 diabetes, including those on hemodialysis.

          Method

          1023 adults with gout and 580 adults (including 206 receiving hemodialysis) with type 2 diabetes, participated in this study of between 2009 and 2012. Participants completed an interviewer-administered SSB intake question “how many sugar sweetened drinks (including fruit juice), but not including diet drinks, do you normally drink per day?” SSB consumption was recorded as a circled number 0, 1, 2, 3, 4, 5, or >5, cans or large glasses (300mL) per day.

          Results

          Consuming one or more SSB per day was reported by 64% (622/1023) of subjects with gout, 49% (176/374) with type 2 diabetes without dialysis, and 47% (96/206) with diabetes on dialysis. Consuming four or more SSBs per day was reported by 18% (179/1023), 9% (31/374) and 9% (18/206), respectively. Such high consumers of SSB were characterized after multivariable analysis to be more likely to be male (adjusted odds ratio (OR) 1.8; 95% confidence interval 1.1–2.9), younger in age (40 vs 65 years: 1.6; 1.1–2.3), current smoker (5.2; 2.7–10.1), obese (BMI 41 vs 26kg/m 2: 1.4; 1–1.9), and report Māori (1.8; 1.2–2.8) or Pacific (1.6; 1.1–2.5) ancestry, compared to Caucasian. People with gout were more likely to report heavy SSB intake compared to people with diabetes (OR 2.4, 95% CI 1.5–3.9). Heavy SSB consumption reported by people with diabetes was similar if they did or did not require dialysis.

          Conclusion

          A high proportion of patients with gout and type 2 diabetes, including those on haemodialysis, are not responding to health messages to abstain from SSB consumption.

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          Most cited references25

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          Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.

          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.
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            Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease.

            Currently, we are experiencing an epidemic of cardiorenal disease characterized by increasing rates of obesity, hypertension, the metabolic syndrome, type 2 diabetes, and kidney disease. Whereas excessive caloric intake and physical inactivity are likely important factors driving the obesity epidemic, it is important to consider additional mechanisms. We revisit an old hypothesis that sugar, particularly excessive fructose intake, has a critical role in the epidemic of cardiorenal disease. We also present evidence that the unique ability of fructose to induce an increase in uric acid may be a major mechanism by which fructose can cause cardiorenal disease. Finally, we suggest that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease, and we provide a list of testable predictions to evaluate this hypothesis.
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              Preliminary criteria for the classification of the acute arthritis of primary gout.

              The American Rheumatism Association sub-committe on classification criteria for gout analyzed data from more than 700 patients with gout, pseudogout, rheumatoid arthritis, or septic arthritis. Criteria for classifying a patient as having gout were a) the presence of characteristic urate crystals in the joint fluid, and/or b) a topus proved to contain urate crystals by chemical or polarized light microscopic means, and/or c) the presence of six of the twelve clinical, laboratory, and X-ray phenomena listed in Table 5.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                15 May 2015
                2015
                : 10
                : 5
                : e0125543
                Affiliations
                [1 ]Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
                [2 ]Maurice Wilkins Centre for Biodiscovery, Auckland, New Zealand
                [3 ]Population Health Directorate, Counties Manukau District Health Board, Auckland, New Zealand
                [4 ]Department of Renal Medicine, Waitemata District Health Board, Auckland, New Zealand
                [5 ]Department of Medicine, University of Otago, Christchurch, New Zealand
                [6 ]Department of Biochemistry, University of Otago, Dunedin, New Zealand
                Uppsala Clinical Research Center, SWEDEN
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: RM ND TM. Performed the experiments: RM JD LS ND TM. Analyzed the data: ST. Wrote the paper: RM ST JD LS ND TM.

                Article
                PONE-D-14-22966
                10.1371/journal.pone.0125543
                4433129
                25978428
                6f8e4a32-b705-4056-8c48-cbde5ba9132c
                Copyright @ 2015

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                History
                : 12 June 2014
                : 25 March 2015
                Page count
                Figures: 0, Tables: 3, Pages: 10
                Funding
                This work was supported by the Health Research Council of New Zealand, Arthritis New Zealand, New Zealand Lottery Health and the University of Otago and Auckland.
                Categories
                Research Article
                Custom metadata
                Data are from the New Zealand study of risk factors for gout and type 2 diabetes and an anonymized data set will be made available to interested researchers upon request to Tony Merriman ( tony.merriman@ 123456otago.ac.nz ). Ethics approval for this study did not include permission to deposit the data in a public repository.

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