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      Dietary Salt Intake and Mortality in Patients With Type 2 Diabetes

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          Abstract

          OBJECTIVE

          Many guidelines recommend that patients with type 2 diabetes should aim to reduce their intake of salt. However, the precise relationship between dietary salt intake and mortality in patients with type 2 diabetes has not been previously explored.

          RESEARCH DESIGN AND METHODS

          Six hundred and thirty-eight patients attending a single diabetes clinic were followed in a prospective cohort study. Baseline sodium excretion was estimated from 24-h urinary collections (24hU Na). The predictors of all-cause and cardiovascular mortality were determined by Cox regression and competing risk modeling, respectively.

          RESULTS

          The mean baseline 24hU Na was 184 ± 73 mmol/24 h, which remained consistent throughout the follow-up (intraindividual coefficient of variation [CV] 23 ± 11%). Over a median of 9.9 years, there were 175 deaths, 75 (43%) of which were secondary to cardiovascular events. All-cause mortality was inversely associated with 24hU Na, after adjusting for other baseline risk factors ( P < 0.001). For every 100 mmol rise in 24hU Na, all-cause mortality was 28% lower (95% CI 6–45%, P = 0.02). After adjusting for the competing risk of noncardiovascular death and other predictors, 24hU Na was also significantly associated with cardiovascular mortality (sub-hazard ratio 0.65 [95% CI 0.44–0.95]; P = 0.03).

          CONCLUSIONS

          In patients with type 2 diabetes, lower 24-h urinary sodium excretion was paradoxically associated with increased all-cause and cardiovascular mortality. Interventional studies are necessary to determine if dietary salt has a causative role in determining adverse outcomes in patients with type 2 diabetes and the appropriateness of guidelines advocating salt restriction in this setting.

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          Most cited references12

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          Risk of cardiovascular and all-cause mortality in individuals with diabetes mellitus, impaired fasting glucose, and impaired glucose tolerance: the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab).

          Diabetes mellitus increases the risk of cardiovascular disease (CVD) and all-cause mortality. The relationship between milder elevations of blood glucose and mortality is less clear. This study investigated whether impaired fasting glucose and impaired glucose tolerance, as well as diabetes mellitus, increase the risk of all-cause and CVD mortality. In 1999 to 2000, glucose tolerance status was determined in 10,428 participants of the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab). After a median follow-up of 5.2 years, 298 deaths occurred (88 CVD deaths). Compared with those with normal glucose tolerance, the adjusted all-cause mortality hazard ratios (HRs) and 95% confidence intervals (CIs) for known diabetes mellitus and newly diagnosed diabetes mellitus were 2.3 (1.6 to 3.2) and 1.3 (0.9 to 2.0), respectively. The risk of death was also increased in those with impaired fasting glucose (HR 1.6, 95% CI 1.0 to 2.4) and impaired glucose tolerance (HR 1.5, 95% CI 1.1 to 2.0). Sixty-five percent of all those who died of CVD had known diabetes mellitus, newly diagnosed diabetes mellitus, impaired fasting glucose, or impaired glucose tolerance at baseline. Known diabetes mellitus (HR 2.6, 95% CI 1.4 to 4.7) and impaired fasting glucose (HR 2.5, 95% CI 1.2 to 5.1) were independent predictors for CVD mortality after adjustment for age, sex, and other traditional CVD risk factors, but impaired glucose tolerance was not (HR 1.2, 95% CI 0.7 to 2.2). This study emphasizes the strong association between abnormal glucose metabolism and mortality, and it suggests that this condition contributes to a large number of CVD deaths in the general population. CVD prevention may be warranted in people with all categories of abnormal glucose metabolism.
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            A Proportional Hazards Model for the Subdistribution of a Competing Risk

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              Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study.

              The evidence that high salt intake increases the risk of cardiovascular disease has been challenged. We aimed to find out whether salt intake, measured by 24 h urinary sodium excretion, is an independent risk factor for cardiovascular disease frequency and mortality, and all-cause mortality. We prospectively followed 1173 Finnish men and 1263 women aged 25-64 years with complete data on 24 h urinary sodium excretion and cardiovascular risk factors. The endpoints were an incident coronary and stroke event, and death from coronary heart disease, cardiovascular disease, and any cause. Each endpoint was analysed separately with the Cox proportional hazards model. The hazards ratios for coronary heart disease, cardiovascular disease, and all-cause mortality, associated with a 100 mmol increase in 24 h urinary sodium excretion, were 1.51 (95% CI 1.14-2.00), 1.45 (1.14-1.84), and 1.26 (1.06-1.50), respectively, in both men and women. The frequency of acute coronary events, but not acute stroke events, rose significantly with increasing sodium excretion. When analyses were done separately for each sex, the risk ratios were significant in men only. There was a significant interaction between sodium excretion and body mass index for cardiovascular and total mortality; sodium predicted mortality in men who were overweight. Correction for the regression dilution bias increased the hazards ratios markedly. High sodium intake predicted mortality and risk of coronary heart disease, independent of other cardiovascular risk factors, including blood pressure. These results provide direct evidence of the harmful effects of high salt intake in the adult population.
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                Author and article information

                Journal
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                March 2011
                17 February 2011
                : 34
                : 3
                : 703-709
                Affiliations
                [1] 1Endocrine Centre, Austin Health and the University of Melbourne, Victoria, Australia
                [2] 2Mater Hospital, Queensland, Australia
                [3] 3Division of Diabetes Complications, Baker IDI Heart and Diabetes Institute, Victoria, Australia
                [4] 4Department of Intensive Care Medicine, The Queen Elizabeth Hospital & Health Service, Woodville, South Australia, Australia
                Author notes
                Corresponding author: George Jerums, ah-endo@ 123456unimelb.edu.au .
                Article
                1723
                10.2337/dc10-1723
                3041211
                21289228
                496ecb77-88d2-4158-a7bf-0e152ab0c8cd
                © 2011 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
                : 6 September 2010
                : 30 December 2010
                Categories
                Original Research
                Pathophysiology/Complications

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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