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Cochrane Database Syst Rev. 2013 Apr 30;(4):CD004937. doi: 10.1002/14651858.CD004937.pub2.

Effect of longer-term modest salt reduction on blood pressure.

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Wolfson Institute of PreventiveMedicine, Barts and The London School of Medicine & Dentistry, QueenMary University of London, London, UK.



A reduction in salt intake lowers blood pressure (BP) and, thereby, reduces cardiovascular risk. A recent meta-analysis by Graudal implied that salt reduction had adverse effects on hormones and lipids which might mitigate any benefit that occurs with BP reduction. However, Graudal's meta-analysis included a large number of very short-term trials with a large change in salt intake, and such studies are irrelevant to the public health recommendations for a longer-term modest reduction in salt intake. We have updated our Cochrane meta-analysis.


To assess (1) the effect of a longer-term modest reduction in salt intake (i.e. of public health relevance) on BP and whether there was a dose-response relationship; (2) the effect on BP by sex and ethnic group; (3) the effect on plasma renin activity, aldosterone, noradrenaline, adrenaline, cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL) and triglycerides.


We searched MEDLINE, EMBASE, Cochrane Hypertension Group Specialised Register, Cochrane Central Register of Controlled Trials, and reference list of relevant articles.


We included randomised trials with a modest reduction in salt intake and duration of at least 4 weeks.


Data were extracted independently by two reviewers. Random effects meta-analyses, subgroup analyses and meta-regression were performed.


Thirty-four trials (3230 participants) were included. Meta-analysis showed that the mean change in urinary sodium (reduced salt vs usual salt) was -75 mmol/24-h (equivalent to a reduction of 4.4 g/d salt), the mean change in BP was -4.18 mmHg (95% CI: -5.18 to -3.18, I (2)=75%) for systolic and -2.06 mmHg (95% CI: -2.67 to -1.45, I (2)=68%) for diastolic BP. Meta-regression showed that age, ethnic group, BP status (hypertensive or normotensive) and the change in 24-h urinary sodium were all significantly associated with the fall in systolic BP, explaining 68% of the variance between studies. A 100 mmol reduction in 24 hour urinary sodium (6 g/day salt) was associated with a fall in systolic BP of 5.8 mmHg (95%CI: 2.5 to 9.2, P=0.001) after adjusting for age, ethnic group and BP status. For diastolic BP, age, ethnic group, BP status and the change in 24-h urinary sodium explained 41% of the variance between studies. Meta-analysis by subgroup showed that, in hypertensives, the mean effect was -5.39 mmHg (95% CI: -6.62 to -4.15, I (2)=61%) for systolic and -2.82 mmHg (95% CI: -3.54 to -2.11, I (2)=52%) for diastolic BP. In normotensives, the mean effect was -2.42 mmHg (95% CI: -3.56 to -1.29, I (2)=66%) for systolic and -1.00 mmHg (95% CI: -1.85 to -0.15, I (2)=66%) for diastolic BP. Further subgroup analysis showed that the decrease in systolic BP was significant in both whites and blacks, men and women. Meta-analysis of hormone and lipid data showed that the mean effect was 0.26 ng/ml/hr (95% CI: 0.17 to 0.36, I (2)=70%) for plasma renin activity, 73.20 pmol/l (95% CI: 44.92 to 101.48, I (2)=62%) for aldosterone, 31.67 pg/ml (95% CI: 6.57 to 56.77, I (2)=5%) for noradrenaline, 6.70 pg/ml (95% CI: -0.25 to 13.64, I (2)=12%) for adrenaline, 0.05 mmol/l (95% CI: -0.02 to 0.11, I (2)=0%) for cholesterol, 0.05 mmol/l (95% CI: -0.01 to 0.12, I (2)=0%) for LDL, -0.02 mmol/l (95% CI: -0.06 to 0.01, I (2)=16%) for HDL, and 0.04 mmol/l (95% CI: -0.02 to 0.09, I (2)=0%) for triglycerides.


A modest reduction in salt intake for 4 or more weeks causes significant and, from a population viewpoint, important falls in BP in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. With salt reduction, there is a small physiological increase in plasma renin activity, aldosterone and noradrenaline. There is no significant change in lipid levels. These results provide further strong support for a reduction in population salt intake. This will likely lower population BP and, thereby, reduce cardiovascular disease. Additionally, our analysis demonstrates a significant association between the reduction in 24-h urinary sodium and the fall in systolic BP, indicating the greater the reduction in salt intake, the greater the fall in systolic BP. The current recommendations to reduce salt intake from 9-12 to 5-6 g/d will have a major effect on BP, but are not ideal. A further reduction to 3 g/d will have a greater effect and should become the long term target for population salt intake.

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