DLM: Hypertension (2010)
To estimate the effects of low sodium versus high sodium intake on systolic and diastolic blood pressure, plasma or serum levels of renin, aldosterone, catecholamines, cholesterol and triglycerides.
Studies randomizing persons to low sodium and high sodium diets were included if they evaluated sodium intake using 24-hour urinary sodium excretion (either measured on the basis of a 24-hour urine collection, or estimated from a collection over at least eight hours).
Included were studies with subjects that had normal or elevated blood pressure, irrespective of race, who were older than 15 years of age.
Studies in which more than half of the subjects were black were included in a separate meta-analysis. Because there were only a few such studies, subjects with normal and elevated blood pressure were combined in one analysis. One study of 70 Japanese patients was reported separately.
- Studies on pregnant women and children were not included
- Studies systematically investigating unhealthy patients with diseases other than elevated blood pressure, such as diabetes, were excluded. In another meta-analysis by these authors, different races were mixed.
- Studies that were meta-analyses or were not randomized.
Randomized, controlled trials.
Double blind, single blind or open studies with a parallel or a crossover design were accepted. Five studies reported allocation concealment, and two studies used intention to treat.
The intervention was altered sodium intake, randomly dividing the subjects into a low sodium diet group and a high sodium diet group. Studies with subjects who were on a concomitant intervention (such as antihypertensive medication) were not allowed. Potassium supplementation or weight reduction were only included if concomitant intervention was the same during each diet phase.
- Data were analysed using ReviewManager 4.1
- Concerning lipids, cholesterol units of mmol per L were transformed to mg per dL by means of the factor 38.6 and triglyceride units of mmol per L were transformed to mg per dL by means of the factor 88.4. The weighted mean difference was calculated for outcome measures with identical units in the included studies (blood pressure, adrenaline and lipids after transformation). The standardized mean differences were calculated for outcome measures with different units (renin, aldosterone and noradrenaline). This method determined the difference in effect between two treatments by dividing the standard deviation of the measurements. By that transformation, the effect measures become dimensionless and the outcomes from trials that have used different units can consequently be combined. The standardized mean effect was transformed to the most commonly used unit.
- If P was less than 0.05 in the test for heterogeneity, a random effect analysis was carried out (blood pressure in blacks, renin, aldosterone and noradrenaline). In the homogenous meta-analyses, the fixed effect model was used.
- In case of multiple independent comparisons, it is important to avoid coincidental significance.
- Variable 1: Systolic blood pressure
- Variable 2: Diastolic blood pressure
- Variable 3: 24-hour urinary sodium excretion.
Altered sodium intake, both at the low and high ends.
Two authors independently searched MEDLINE and reference lists of relevant articles from 1966 through December 2001. The two authors recorded the following data from each trial:
- Sample size
- Mean age of participants
- Breakdown of females, males; white and black or Asians
- Duration of the intervention
- Sodium reduction measured as the difference between 24-hour urinary sodium excretion during low-sodium and high-sodium diets and standard deviation (SD)
- Systolic blood pressure (SD) and diastolic blood pressure (SD) before and after intervention
- Difference between changes in both blood pressure measurements obtained during both sodium diet phases and the SD of these differences
- Levels of hormones and lipids in the blood and their standard deviations during low sodium and high sodium diets.
In 24 studies, SD of the change was given or was deduced from a given SE of the change. In seven studies, SD of the change was deduced from a given 95% confidence interval. In the other studies, SD of the change was imputed from the formula SD (change) = sq root (SD1sq + SD2sq); SD1 is SD on blood pressure before intervention and SD2 is SD on blood pressure after intervention. Also recorded were the number of urinary sodium excretions analyzed per person per treatment period and data on the completeness of urine collections. For discrepancies between reviewers, the data was reviewed together and an agreement was reached.
- Initial N: 96 trials, including 137 randomized studies, were included in the review. When results were reported by subgroup, the subgroup results were used.
- Age and ethnicity: In 58 studies of whites with elevated blood pressure, the mean age was 49 years (range 23 to 73); the median duration was 28 days (four to 365 days). Concomitant anti-hypertensive treatment was given to both interventions groups for 13 trials. In 57 studies of whites with normal blood pressure, the mean age was 27 years (range 15 to 67 years); the median duration was eight days (four to 1,100).
- In 57 trials with mostly white, normotensive subjects, a low sodium diet reduced systolic blood pressure by -1.27mm Hg (95% CI: -1.76; -0.77 and P<0.0001) and diastolic blood pressure by -0.54mm Hg (95% CI: -0.94; -0.14 and P=0.009) when compared to a high sodium diet
- In 58 trials of mainly white with hypertension, low sodium intake reduced systolic blood pressure by -4.18mm Hg (95% CI: -5.08; - 3.27 and P<0.0001) and diastolic blood pressure by -1.98mm Hg (95% CI: -2.46; -1.32 and P<0.0001) as compared to high sodium intake
- Eight days was the median duration of intervention in the normal blood pressure trials (range four to 1,100) and 28 days in the elevated blood pressure trials (range four to 365). Multiple regression analyses showed no independent effect of duration on the effect size.
- In eight trials of blacks with normal or elevated blood pressure, low sodium intake reduced systolic blood pressure by -6.44mm Hg (95% CI: -9.13; -3.74 and P<0.0001) and diastolic blood pressure by -1.98mm Hg (95% CI: -4.75; 0.78 and P=0.16) as compared to high sodium intake
- Blood pressure reduction was also greater in one trial of Japanese patients
- There was a significant increase in plasma or serum renin, 304% (P<0.0001); aldosterone, 322% (P<0.0001); noradrenaline, 30% (P<0.0001); cholesterol, 5.4% (P<0.0001); and LDL cholesterol, 4.6% (P<0.004); and a borderline increase in adrenaline, 12% (P=0.04); and triglyceride, 5.9% (P=0.03) with a low sodium diet as compared with a high sodium diet.
Due to no significant effect in whites with normal blood pressure, general recommendations to reduce sodium intake are not needed. Lower sodium intake in whites with hypertension reduces blood pressure in the short term. The reviews suggest that the effect of low versus high sodium intake on blood pressure was greater in black and Asian patients than in whites. However, the small number of studies on black and Asian patients was insufficient to make different recommendations.
|University/Hospital:||Copenhagen University Hospital at Herlev, Herlev, Denmark|
Additional long-term trials are needed to study the effect of reduced dietary sodium intake on blood pressure, metabolic components and morbidity and mortality.
Quality Criteria Checklist: Review Articles
|1.||Will the answer if true, have a direct bearing on the health of patients?||Yes|
|2.||Is the outcome or topic something that patients/clients/population groups would care about?||Yes|
|3.||Is the problem addressed in the review one that is relevant to dietetics practice?||Yes|
|4.||Will the information, if true, require a change in practice?||No|
|1.||Was the question for the review clearly focused and appropriate?||Yes|
|2.||Was the search strategy used to locate relevant studies comprehensive? Were the databases searched and the search termsused described?||Yes|
|3.||Were explicit methods used to select studies to include in the review? Were inclusion/exclusion criteria specified andappropriate? Wereselectionmethods unbiased?||Yes|
|4.||Was there an appraisal of the quality and validity of studies included in the review? Were appraisal methodsspecified,appropriate, andreproducible?||Yes|
|5.||Were specific treatments/interventions/exposures described? Were treatments similar enough to be combined?||Yes|
|6.||Was the outcome of interest clearly indicated? Were other potential harms and benefits considered?||Yes|
|7.||Were processes for data abstraction, synthesis, and analysis described? Were they applied consistently acrossstudies and groups? Was thereappropriate use of qualitative and/or quantitative synthesis? Was variation in findings among studies analyzed? Were heterogeneity issued considered? If data from studies were aggregated for meta-analysis, was the procedure described?||Yes|
|8.||Are the results clearly presented in narrative and/or quantitative terms? If summary statistics are used, are levels ofsignificance and/or confidence intervals included?||Yes|
|9.||Are conclusions supported by results with biases and limitations taken into consideration? Are limitations ofthe review identified anddiscussed?||Yes|
|10.||Was bias due to the review's funding or sponsorship unlikely?||Yes|