title: Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials.
abstract: OBJECTIVE
  To determine the effects of longer term modest salt reduction on blood pressure, hormones, and lipids.
  
  
  METHODS
  Systematic review and meta-analysis.
  
  
  METHODS
  Medline, Embase, Cochrane Hypertension Group Specialised Register, Cochrane Central Register of Controlled Trials, and reference list of relevant articles.
  
  
  METHODS
  Randomised trials with a modest reduction in salt intake and duration of at least four weeks.
  
  
  METHODS
  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, I(2)=75%) for systolic blood pressure and -2.06 mm Hg (-2.67 to -1.45, I(2)=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, I(2)=61%) for systolic blood pressure and -2.82 mm Hg (-3.54 to -2.11, I(2)=52%) for diastolic blood pressure. In normotensive people, the figures were -2.42 mm Hg (-3.56 to -1.29, I(2)=66%) and -1.00 mm Hg (-1.85 to -0.15, I(2)=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, I(2)=70%) for plasma renin activity, 73.20 pmol/L (44.92 to 101.48, I(2)=62%) for aldosterone, 187 pmol/L (39 to 336, I(2)=5%) for noradrenaline (norepinephrine), 37 pmol/L (-1 to 74, I(2)=12%) for adrenaline (epinephrine), 0.05 mmol/L (-0.02 to 0.11, I(2)=0%) for total cholesterol, 0.05 mmol/L (-0.01 to 0.12, I(2)=0%) for low density lipoprotein cholesterol, -0.02 mmol/L (-0.06 to 0.01, I(2)=16%) for high density lipoprotein cholesterol, and 0.04 mmol/L (-0.02 to 0.09, I(2)=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.
authors.affiliation: Wolfson Institute of Preventive Medicine, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK. f.he@qmul.ac.uk
authors.forename: Feng J
authors.initials: FJ
authors.lastname: He
authors.forename: Jiafu
authors.initials: J
authors.lastname: Li
authors.forename: Graham A
authors.initials: GA
authors.lastname: Macgregor
mesh_terms: D000450:Aldosterone / Q000378:metabolism / Q000652:urine; D015415:Biomarkers / Q000378:metabolism; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000517:prevention & control* / Q000652:urine; D004039:Diet, Sodium-Restricted; D005260:Female; D006801:Humans; D006973:Hypertension / Q000178:diet therapy* / Q000517:prevention & control* / Q000652:urine; D008055:Lipids / Q000097:blood; D008297:Male; D009638:Norepinephrine / Q000652:urine; D011634:Public Health; D016032:Randomized Controlled Trials as Topic; D012083:Renin / Q000652:urine; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage* / Q000009:adverse effects / Q000652:urine; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D008055:Lipids; D017673:Sodium Chloride, Dietary; D000450:Aldosterone; D012083:Renin; D009638:Norepinephrine