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      Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride

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          Abstract

          In spite of more than 100 years of investigations the question of whether a reduced sodium intake improves health is still unsolved. To estimate the effects of low sodium intake versus high sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol, high‐density lipoprotein (HDL), low‐density lipoprotein (LDL) and triglycerides. The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to March 2016: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (2016, Issue 3), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We also searched the reference lists of relevant articles. Studies randomising persons to low‐sodium and high‐sodium diets were included if they evaluated at least one of the above outcome parameters. Two review authors independently collected data, which were analysed with Review Manager 5.3. A total of 185 studies were included. The average sodium intake was reduced from 201 mmol/day (corresponding to high usual level) to 66 mmol/day (corresponding to the recommended level). The effect of sodium reduction on blood pressure (BP) was as follows: white people with normotension: SBP: mean difference (MD) ‐1.09 mmHg (95% confidence interval (CI): ‐1.63 to ‐0.56; P = 0.0001); 89 studies, 8569 participants; DBP: + 0.03 mmHg (MD 95% CI: ‐0.37 to 0.43; P = 0.89); 90 studies, 8833 participants. High‐quality evidence. Black people with normotension: SBP: MD ‐4.02 mmHg (95% CI:‐7.37 to ‐0.68; P = 0.002); seven studies, 506 participants; DBP: MD ‐2.01 mmHg (95% CI:‐4.37 to 0.35; P = 0.09); seven studies, 506 participants. Moderate‐quality evidence. Asian people with normotension: SBP: MD ‐0.72 mmHg (95% CI: ‐3.86 to 2.41; P = 0.65); DBP: MD ‐1.63 mmHg (95% CI:‐3.35 to 0.08; P =0.06); three studies, 393 participants. Moderate‐quality evidence. White people with hypertension: SBP: MD ‐5.51 mmHg (95% CI: ‐6.45 to ‐4.57; P < 0.00001); 84 studies, 5925 participants; DBP: MD ‐2.88 mmHg (95% CI: ‐3.44 to ‐2.32; P < 0.00001); 85 studies, 6001 participants. High‐quality evidence. Black people with hypertension: SBP MD ‐6.64 mmHg (95% CI:‐9.00 to ‐4.27; P = 0.00001); eight studies, 619 participants; DBP ‐2.91 mmHg (95% CI:‐4.52, ‐1.30; P = 0.0004); eight studies, 619 participants. Moderate‐quality evidence. Asian people with hypertension: SBP: MD ‐7.75 mmHg (95% CI:‐11,44 to ‐4.07; P < 0.0001) nine studies, 501 participants; DBP: MD ‐2.68 mmHg (95% CI: ‐4.21 to ‐1.15; P = 0.0006). Moderate‐quality evidence. In plasma or serum, there was a significant increase in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.03), cholesterol (P < 0.0005) and triglyceride (P < 0.0006) with low sodium intake as compared with high sodium intake. All effects were stable in 125 study populations with a sodium intake below 250 mmol/day and a sodium reduction intervention of at least one week. Sodium reduction from an average high usual sodium intake level (201 mmol/day) to an average level of 66 mmol/day, which is below the recommended upper level of 100 mmol/day (5.8 g salt), resulted in a decrease in SBP/DBP of 1/0 mmHg in white participants with normotension and a decrease in SBP/DBP of 5.5/2.9 mmHg in white participants with hypertension. A few studies showed that these effects in black and Asian populations were greater. The effects on hormones and lipids were similar in people with normotension and hypertension. Renin increased 1.60 ng/mL/hour (55%); aldosterone increased 97.81 pg/mL (127%); adrenalin increased 7.55 pg/mL (14%); noradrenalin increased 63.56 pg/mL: (27%); cholesterol increased 5.59 mg/dL (2.9%); triglyceride increased 7.04 mg/dL (6.3%). The effect of a low salt diet on blood pressure and some hormones and lipids in people with normal and elevated blood pressure Review question Studies in which participants were distributed by chance into groups with high and low salt intake were analysed to investigate the effect of reduced salt intake on blood pressure (BP) and potential side effects of sodium reduction on some hormones and lipids. Background As a reduction in salt intake decreases blood pressure (BP) in individuals with elevated BP, we are commonly advised to cut down on salt. However, the effect of salt reduction on BP in people with a normal BP has been questioned. Furthermore, several studies have shown that salt reduction activates the salt conserving hormonal system (renin and aldosterone), the stress hormones (adrenalin and noradrenalin) and increases fatty substances (cholesterol and triglyceride) in the blood. Search date The present evidence is current to April 2016. Study characteristics One hundred and eighty‐five intervention studies of 12,210 individuals lasting four to 1100 days were included, which evaluated at least one of the effect measures. Participants were healthy or had elevated blood pressure. Longitudinal studies have shown that the effect of reduced salt intake on BP is stable after at maximum seven days and population studies have shown that very few people eat more than 14.5 g salt per day. Therefore, we also perfomed subgroup sub‐analyses of 125 studies with a duration of at least seven days and a salt intake of maximum 14.5 g. Study funding sources Forty‐four studies did not mention support. One hundred and twenty‐two studies were supported by public foundations. Twelve studies were supported by the pharmaceutical industry and one study by an electronic company. Six studies were supported by food industry organisations. Key results The mean dietary sodium intake was reduced from 11.5 g per day to 3.8 g per day. The reduction in SBP/DBP in people with normotension was about 1/0 mmHg, and in people with hypertension about 5.5/2.9 mmHg. In contrast, the effect on hormones and lipids were similar in people with normotension and hypertension. Renin increased 1.60 ng/mL/hour (55%); aldosterone increased 97.81 pg/mL (127%); adrenalin increased 7.55 pg/mL (14%); noradrenalin increased 63.56 pg/mL (27%); cholesterol increased 5.59 mg/dL (2.9%); triglyceride increased 7.04 mg/dL (6.3%). Quality of evidence Only randomised controlled trials were included and the basic grade of evidence was therefore considered to be high, although the grade of evidence was downgraded in some of the smaller analyses. In general, the description of the randomisation procedure was insufficient, introducing a bias which could exaggerate the effects, but many of the studies were published in a period where it was not customary to report such descriptions. The majority of studies were open, but the outcomes of these did not differ from the outcomes of the double‐blind studies. Almost all individual studies of participants with normal blood pressure (BP) show no significant effect of sodium reduction on BP, whereas a large number of studies in people with hypertension did show significant effect of sodium reduction on BP. Thus, there was a high grade of consistency between the outcomes of the individual studies and the outcomes of the meta‐analyses. Sensitivity analyses of studies lasting at least one week (the time of maximal efficacy) confirmed the primary analyses. Finally, the impact of commercial interests on the outcomes was negligible.

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          Most cited references195

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          Sodium and potassium intake and mortality among US adults: prospective data from the Third National Health and Nutrition Examination Survey.

          Several epidemiologic studies suggested that higher sodium and lower potassium intakes were associated with increased risk of cardiovascular diseases (CVD). Few studies have examined joint effects of dietary sodium and potassium intake on risk of mortality. To investigate estimated usual intakes of sodium and potassium as well as their ratio in relation to risk of all-cause and CVD mortality, the Third National Health and Nutrition Examination Survey Linked Mortality File (1988-2006), a prospective cohort study of a nationally representative sample of 12,267 US adults, studied all-cause, cardiovascular, and ischemic heart (IHD) diseases mortality. During a mean follow-up period of 14.8 years, we documented a total of 2270 deaths, including 825 CVD deaths and 443 IHD deaths. After multivariable adjustment, higher sodium intake was associated with increased all-cause mortality (hazard ratio [HR], 1.20; 95% confidence interval [CI], 1.03-1.41 per 1000 mg/d), whereas higher potassium intake was associated with lower mortality risk (HR, 0.80; 95% CI, 0.67-0.94 per 1000 mg/d). For sodium-potassium ratio, the adjusted HRs comparing the highest quartile with the lowest quartile were HR, 1.46 (95% CI, 1.27-1.67) for all-cause mortality; HR, 1.46 (95% CI, 1.11-1.92) for CVD mortality; and HR, 2.15 (95% CI, 1.48-3.12) for IHD mortality. These findings did not differ significantly by sex, race/ethnicity, body mass index, hypertension status, education levels, or physical activity. Our findings suggest that a higher sodium-potassium ratio is associated with significantly increased risk of CVD and all-cause mortality, and higher sodium intake is associated with increased total mortality in the general US population.
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            Is Open Access

            The Association Between Dietary Sodium Intake, ESRD, and All-Cause Mortality in Patients With Type 1 Diabetes

            OBJECTIVE Many guidelines recommend reduced consumption of salt in patients with type 1 diabetes, but it is unclear whether dietary sodium intake is associated with mortality and end-stage renal disease (ESRD). RESEARCH DESIGN AND METHODS In a nationwide multicenter study (the FinnDiane Study) between 1998 and 2002, 2,807 enrolled adults with type 1 diabetes without ESRD were prospectively followed. Baseline urinary sodium excretion was estimated on a 24-h urine collection. The predictors of all-cause mortality and ESRD were determined by Cox regression and competing risk modeling, respectively. RESULTS The median follow-up for survival analyses was 10 years, during which 217 deaths were recorded (7.7%). Urinary sodium excretion was nonlinearly associated with all-cause mortality, such that individuals with the highest daily urinary sodium excretion, as well as the lowest excretion, had reduced survival. This association was independent age, sex, duration of diabetes, the presence and severity of chronic kidney disease (CKD) (estimated glomerular filtration rate [eGFR] and log albumin excretion rate), the presence of established cardiovascular disease, and systolic blood pressure. During follow-up, 126 patients developed ESRD (4.5%). Urinary sodium excretion was inversely associated with the cumulative incidence of ESRD, such that individuals with the lowest sodium excretion had the highest cumulative incidence of ESRD. CONCLUSIONS In patients with type 1 diabetes, sodium was independently associated with all-cause mortality and ESRD. Although we have not demonstrated causality, these findings support the calls for caution before applying salt restriction universally. Clinical trials must be performed in diabetic patients to formally test the utility/risk of sodium restriction in this setting.
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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
                Cochrane Database of Systematic Reviews
                Wiley-Blackwell
                14651858
                April 09 2017
                :
                :
                Affiliations
                [1 ]Cochrane Hypertension Group
                Article
                10.1002/14651858.CD004022.pub4
                6478144
                28391629
                0edf2eb1-db75-4424-8ae2-ea06d33b7abd
                © 2017
                History

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