Abstract: 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, I2=75%) for systolic and -2.06 mmHg (95% CI: -2.67 to -1.45, I2=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, I2=61%) for systolic and -2.82 mmHg (95% CI: -3.54 to -2.11, I2=52%) for diastolic BP. In normotensives, the mean effect was -2.42 mmHg (95% CI: -3.56 to -1.29, I2=66%) for systolic and -1.00 mmHg (95% CI: -1.85 to -0.15, I2=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, I2=70%) for plasma renin activity, 73.20 pmol/l (95% CI: 44.92 to 101.48, I2=62%) for aldosterone, 31.67 pg/ml (95% CI: 6.57 to 56.77, I2=5%) for noradrenaline, 6.70 pg/ml (95% CI: -0.25 to 13.64, I2=12%) for adrenaline, 0.05 mmol/l (95% CI: -0.02 to 0.11, I2=0%) for cholesterol, 0.05 mmol/l (95% CI: -0.01 to 0.12, I2=0%) for LDL, -0.02 mmol/l (95% CI: -0.06 to 0.01, I2=16%) for HDL, and 0.04 mmol/l (95% CI: -0.02 to 0.09, I2=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.

Plain-language summary: Our pooled analysis of randomised trials of 4 weeks or more in duration shows that such a reduction in salt intake lowers blood pressure both in individuals with raised blood pressure and in those with normal blood pressure. The fall in blood pressure is shown in both whites and blacks, men and women. Additionally, our results show that a longer-term modest reduction in salt intake has no adverse effect on hormone and lipid levels. These findings provide further strong support for a reduction in population salt intake. This will likely lower population blood pressure and reduce strokes, heart attacks and heart failure. Furthermore, our results are consistent with the fact that the lower the salt intake, the lower the blood pressure. The current recommendations to reduce salt intake to 5-6 grams per day will lower blood pressure, but a further reduction to 3 grams per day will lower blood pressure more. Therefore, 3 grams per day should become the long-term target for population salt intake.