Objective To determine the effects of longer term modest salt reduction on blood pressure, hormones, and lipids. Design Systematic review and meta-analysis. Data sources Medline, Embase, Cochrane Hypertension Group Specialised Register, Cochrane Central Register of Controlled Trials, and reference list of relevant articles. Inclusion criteria Randomised trials with a modest reduction in salt intake and duration of at least four weeks. Data extraction and analysis Data were extracted independently by two reviewers. Random effects meta-analyses, subgroup analyses, and meta-regression were performed. Results Thirty four trials (3230 participants) were included. Meta-analysis showed that the mean change in urinary sodium (reduced salt v usual salt) was −75 mmol/24 h (equivalent to a reduction of 4.4 g/day salt), and with this reduction in salt intake, the mean change in blood pressure was −4.18 mm Hg (95% confidence interval −5.18 to −3.18, I²=75%) for systolic blood pressure and −2.06 mm Hg (−2.67 to −1.45, I²=68%) for diastolic blood pressure. Meta-regression showed that age, ethnic group, blood pressure status (hypertensive or normotensive), and the change in 24 hour urinary sodium were all significantly associated with the fall in systolic blood pressure, 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 blood pressure of 5.8 mm Hg (2.5 to 9.2, P=0.001) after adjustment for age, ethnic group, and blood pressure status. For diastolic blood pressure, age, ethnic group, blood pressure status, and the change in 24 hour urinary sodium explained 41% of the variance between studies. Meta-analysis by subgroup showed that in people with hypertension the mean effect was −5.39 mm Hg (−6.62 to −4.15, I²=61%) for systolic blood pressure and −2.82 mm Hg (−3.54 to −2.11, I²=52%) for diastolic blood pressure. In normotensive people, the figures were −2.42 mm Hg (−3.56 to −1.29, I²=66%) and −1.00 mm Hg (−1.85 to −0.15, I²=66%), respectively. Further subgroup analysis showed that the decrease in systolic blood pressure was significant in both white and black people and in men and women. Meta-analysis of data on hormones and lipids showed that the mean change was 0.26 ng/mL/h (0.17 to 0.36, I²=70%) for plasma renin activity, 73.20 pmol/L (44.92 to 101.48, I²=62%) for aldosterone, 187 pmol/L (39 to 336, I²=5%) for noradrenaline (norepinephrine), 37 pmol/L (−1 to 74, I²=12%) for adrenaline (epinephrine), 0.05 mmol/L (−0.02 to 0.11, I²=0%) for total cholesterol, 0.05 mmol/L (−0.01 to 0.12, I²=0%) for low density lipoprotein cholesterol, −0.02 mmol/L (−0.06 to 0.01, I²=16%) for high density lipoprotein cholesterol, and 0.04 mmol/L (−0.02 to 0.09, I²=0%) for triglycerides. Conclusions A modest reduction in salt intake for four or more weeks causes significant and, from a population viewpoint, important falls in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. Salt reduction is associated with a small physiological increase in plasma renin activity, aldosterone, and noradrenaline and no significant change in lipid concentrations. These results support a reduction in population salt intake, which will lower population blood pressure and thereby reduce cardiovascular disease. The observed significant association between the reduction in 24 hour urinary sodium and the fall in systolic blood pressure, indicates that larger reductions in salt intake will lead to larger falls in systolic blood pressure. The current recommendations to reduce salt intake from 9-12 to 5-6 g/day will have a major effect on blood pressure, but a further reduction to 3 g/day will have a greater effect and should become the long term target for population salt intake.

Objectives: To determine the relationship between the reduction in salt intake that occurred in England, and blood pressure (BP), as well as mortality from stroke and ischaemic heart disease (IHD). Design: Analysis of the data from the Health Survey for England. Setting and participants: England, 2003 N=9183, 2006 N=8762, 2008 N=8974 and 2011 N=4753, aged ≥16 years. Outcomes: BP, stroke and IHD mortality. Results: From 2003 to 2011, there was a decrease in mortality from stroke by 42% (p<0.001) and IHD by 40% (p<0.001). In parallel, there was a fall in BP of 3.0±0.33/1.4±0.20 mm Hg (p<0.001/p<0.001), a decrease of 0.4±0.02 mmol/L (p<0.001) in cholesterol, a reduction in smoking prevalence from 19% to 14% (p<0.001), an increase in fruit and vegetable consumption (0.2±0.05 portion/day, p<0.001) and an increase in body mass index (BMI; 0.5±0.09 kg/m ² , p<0.001). Salt intake, as measured by 24 h urinary sodium, decreased by 1.4 g/day (p<0.01). It is likely that all of these factors (with the exception of BMI), along with improvements in the treatments of BP, cholesterol and cardiovascular disease, contributed to the falls in stroke and IHD mortality. In individuals who were not on antihypertensive medication, there was a fall in BP of 2.7±0.34/1.1±0.23 mm Hg (p<0.001/p<0.001) after adjusting for age, sex, ethnic group, education, household income, alcohol consumption, fruit and vegetable intake and BMI. Although salt intake was not measured in these participants, the fact that the average salt intake in a random sample of the population fell by 15% during the same period suggests that the falls in BP would be largely attributable to the reduction in salt intake rather than antihypertensive medications. Conclusions: The reduction in salt intake is likely to be an important contributor to the falls in BP from 2003 to 2011 in England. As a result, it would have contributed substantially to the decreases in stroke and IHD mortality.

Objective: To examine the dose-response relation between reduction in dietary sodium and blood pressure change and to explore the impact of intervention duration.Design: Systematic review and meta-analysis following PRISMA guidelines.Data sources: Ovid MEDLINE(R), EMBASE, and Cochrane Central Register of Controlled Trials (Wiley) and reference lists of relevant articles up to 21 January 2019.Inclusion criteria: Randomised trials comparing different levels of sodium intake undertaken among adult populations with estimates of intake made using 24 hour urinary sodium excretion.Data extraction and analysis: Two of three reviewers screened the records independently for eligibility. One reviewer extracted all data and the other two reviewed the data for accuracy. Reviewers performed random effects meta-analyses, subgroup analyses, and meta-regression.Results: 133 studies with 12 197 participants were included. The mean reductions (reduced sodiumvusual sodium) of 24 hour urinary sodium, systolic blood pressure (SBP), and diastolic blood pressure (DBP) were 130 mmol (95% confidence interval 115 to 145, P<0.001), 4.26 mm Hg (3.62 to 4.89, P<0.001), and 2.07 mm Hg (1.67 to 2.48, P<0.001), respectively. Each 50 mmol reduction in 24 hour sodium excretion was associated with a 1.10 mm Hg (0.66 to 1.54; P<0.001) reduction in SBP and a 0.33 mm Hg (0.04 to 0.63; P=0.03) reduction in DBP. Reductions in blood pressure were observed in diverse population subsets examined, including hypertensive and non-hypertensive individuals. For the same reduction in 24 hour urinary sodium there was greater SBP reduction in older people, non-white populations, and those with higher baseline SBP levels. In trials of less than 15 days’ duration, each 50 mmol reduction in 24 hour urinary sodium excretion was associated with a 1.05 mm Hg (0.40 to 1.70; P=0.002) SBP fall, less than half the effect observed in studies of longer duration (2.13 mm Hg; 0.85 to 3.40; P=0.002). Otherwise, there was no association between trial duration and SBP reduction.Conclusions: The magnitude of blood pressure lowering achieved with sodium reduction showed a dose-response relation and was greater for older populations, non-white populations, and those with higher blood pressure. Short term studies underestimate the effect of sodium reduction on blood pressure.Systematic review registration: PROSPERO CRD42019140812.