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, 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.

https://www.bmj.com/content/bmj/346/bmj.f1325.full.pdf

Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials

Objective To assess the effect of decreased sodium intake on blood pressure, related cardiovascular diseases, and potential adverse effects such as changes in blood lipids, catecholamine levels, and renal function. Design Systematic review and meta-analysis. Data sources Cochrane Central Register of Controlled Trials, Medline, Embase, WHO International Clinical Trials Registry Platform, the Latin American and Caribbean health science literature database, and the reference lists of previous reviews. Study selection Randomised controlled trials and prospective cohort studies in non-acutely ill adults and children assessing the relations between sodium intake and blood pressure, renal function, blood lipids, and catecholamine levels, and in non-acutely ill adults all cause mortality, cardiovascular disease, stroke, and coronary heart disease. Study appraisal and synthesis Potential studies were screened independently and in duplicate and study characteristics and outcomes extracted. When possible we conducted a meta-analysis to estimate the effect of lower sodium intake using the inverse variance method and a random effects model. We present results as mean differences or risk ratios, with 95% confidence intervals. Results We included 14 cohort studies and five randomised controlled trials reporting all cause mortality, cardiovascular disease, stroke, or coronary heart disease; and 37 randomised controlled trials measuring blood pressure, renal function, blood lipids, and catecholamine levels in adults. Nine controlled trials and one cohort study in children reporting on blood pressure were also included. In adults a reduction in sodium intake significantly reduced resting systolic blood pressure by 3.39 mm Hg (95% confidence interval 2.46 to 4.31) and resting diastolic blood pressure by 1.54 mm Hg (0.98 to 2.11). When sodium intake was 0.05). There were insufficient randomised controlled trials to assess the effects of reduced sodium intake on mortality and morbidity. The associations in cohort studies between sodium intake and all cause mortality, incident fatal and non-fatal cardiovascular disease, and coronary heart disease were non-significant (P>0.05). Increased sodium intake was associated with an increased risk of stroke (risk ratio 1.24, 95% confidence interval 1.08 to 1.43), stroke mortality (1.63, 1.27 to 2.10), and coronary heart disease mortality (1.32, 1.13 to 1.53). In children, a reduction in sodium intake significantly reduced systolic blood pressure by 0.84 mm Hg (0.25 to 1.43) and diastolic blood pressure by 0.87 mm Hg (0.14 to 1.60). Conclusions High quality evidence in non-acutely ill adults shows that reduced sodium intake reduces blood pressure and has no adverse effect on blood lipids, catecholamine levels, or renal function, and moderate quality evidence in children shows that a reduction in sodium intake reduces blood pressure. Lower sodium intake is also associated with a reduced risk of stroke and fatal coronary heart disease in adults. The totality of evidence suggests that most people will likely benefit from reducing sodium intake.

https://www.bmj.com/content/bmj/346/bmj.f1326.full.pdf

Effect of lower sodium intake on health: systematic review and meta-analyses

Objective. —To assess the effects of supplementation with oral potassium on blood pressure in humans. Design. —Meta-analysis of randomized controlled trials. Data Sources. —English-language articles published before July 1995. Study Selection. —Thirty-three randomized controlled trials (2609 participants) in which potassium supplementation was the only difference between the intervention and control conditions. Data Extraction. —Using a standardized protocol, 2 of us independently abstracted information on sample size, duration, study design, potassium dose, participant characteristics, and treatment results. Results. —By means of a random-effects model, findings from individual trials were pooled, after results for each trial were weighted by the inverse of its variance. An extreme effect of potassium in lowering blood pressure was noted in 1 trial. After exclusion of this trial, potassium supplementation was associated with a significant reduction in mean (95% confidence interval) systolic and diastolic blood pressure of-3.11 mm Hg (-1.91 to-4.31 mm Hg) and-1.97 mm Hg (-0.52 to-3.42 mm Hg), respectively. Effects of treatment appeared to be enhanced in studies in which participants were concurrently exposed to a high intake of sodium. Conclusions. —Our results support the premise that low potassium intake may play an important role in the genesis of high blood pressure. Increased potassium intake should be considered as a recommendation for prevention and treatment of hypertension, especially in those who are unable to reduce their intake of sodium.

https://jamanetwork.com/journals/JAMA/articlepdf/416446/jama_277_20_033.pdf

Effects of Oral Potassium on Blood Pressure: Meta-analysis of Randomized Controlled Clinical Trials

Objective To conduct a systematic review of the literature and meta-analyses to fill the gaps in knowledge on potassium intake and health. Data sources Cochrane Central Register of Controlled Trials, Medline, Embase, WHO International Clinical Trials Registry Platform, Latin American and Caribbean Health Science Literature Database, and the reference lists of previous reviews. Study selection Randomised controlled trials and cohort studies reporting the effects of potassium intake on blood pressure, renal function, blood lipids, catecholamine concentrations, all cause mortality, cardiovascular disease, stroke, and coronary heart disease were included. Data extraction and synthesis Potential studies were independently screened in duplicate, and their characteristics and outcomes were extracted. When possible, meta-analysis was done to estimate the effects (mean difference or risk ratio with 95% confidence interval) of higher potassium intake by using the inverse variance method and a random effect model. Results 22 randomised controlled trials (including 1606 participants) reporting blood pressure, blood lipids, catecholamine concentrations, and renal function and 11 cohort studies (127 038 participants) reporting all cause mortality, cardiovascular disease, stroke, or coronary heart disease in adults were included in the meta-analyses. Increased potassium intake reduced systolic blood pressure by 3.49 (95% confidence interval 1.82 to 5.15) mm Hg and diastolic blood pressure by 1.96 (0.86 to 3.06) mm Hg in adults, an effect seen in people with hypertension but not in those without hypertension. Systolic blood pressure was reduced by 7.16 (1.91 to 12.41) mm Hg when the higher potassium intake was 90-120 mmol/day, without any dose response. Increased potassium intake had no significant adverse effect on renal function, blood lipids, or catecholamine concentrations in adults. An inverse statistically significant association was seen between potassium intake and risk of incident stroke (risk ratio 0.76, 0.66 to 0.89). Associations between potassium intake and incident cardiovascular disease (risk ratio 0.88, 0.70 to 1.11) or coronary heart disease (0.96, 0.78 to 1.19) were not statistically significant. In children, three controlled trials and one cohort study suggested that increased potassium intake reduced systolic blood pressure by a non-significant 0.28 (−0.49 to 1.05) mm Hg. Conclusions High quality evidence shows that increased potassium intake reduces blood pressure in people with hypertension and has no adverse effect on blood lipid concentrations, catecholamine concentrations, or renal function in adults. Higher potassium intake was associated with a 24% lower risk of stroke (moderate quality evidence). These results suggest that increased potassium intake is potentially beneficial to most people without impaired renal handling of potassium for the prevention and control of elevated blood pressure and stroke.

https://www.bmj.com/content/bmj/346/bmj.f1378.full.pdf

Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses

Two recent meta-analyses of randomised salt reduction trials have concluded that there is little purpose in reducing salt intake in the general population. However, the authors, as with other previous meta-analyses, included trials of very short duration (eg 1 week or less) and trials of acute salt loading followed by abrupt reductions to very low salt intake (eg from 20 to less than 1 g of salt/day). These acute salt loading and salt depletion experiments are known to increase sympathetic tone, and with salt depletion cause a rise in renin release and, thereby, plasma angiotensin II. These trials are not appropriate, therefore, for helping to inform public health policy, which is for a more modest reduction in salt intake, ie, from a usual intake of approximately 10 to approximately 5 g of salt per day over a more prolonged period of time. We carried out a meta-analysis to assess the effect of a modest salt reduction on blood pressure. Our data sources were MEDLINE, EMBASE, Cochrane library, CINAHL, and the reference lists of original and review articles. We included randomised trials with a modest reduction in salt intake and a duration of 4 or more weeks. Meta-analysis, meta-regression, and funnel plots were performed. A total of 17 trials in hypertensives (n=734) and 11 trials in normotensives (n=2220) were included in our study. The median reduction in 24-h urinary sodium excretion was 78 mmol (equivalent to 4.6 g of salt/day) in hypertensives and 74 mmol in normotensives. The pooled estimates of blood pressure fall were 4.96/2.73+/-0.40/0.24 mmHg in hypertensives (P<0.001 for both systolic and diastolic) and 2.03/0.97+/-0.27/0.21 mmHg in normotensives (P<0.001 for both systolic and diastolic). Weighted linear regression analyses showed a dose response between the change in urinary sodium and blood pressure. A reduction of 100 mmol/day (6 g of salt) in salt intake predicted a fall in blood pressure of 7.11/3.88 mmHg (P<0.001 for both systolic and diastolic) in hypertensives and 3.57/1.66 mmHg in normotensive individuals (systolic: P<0.001; diastolic: P<0.05). Our results demonstrate that a modest reduction in salt intake for a duration of 4 or more weeks does have a significant and, from a population viewpoint, important effect on blood pressure in both hypertensive and normotensive individuals. This meta-analysis strongly supports other evidence for a modest and long-term reduction in population salt intake, and would be predicted to reduce stroke deaths immediately by approximately 14% and coronary deaths by approximately 9% in hypertensives, and reduce stroke and coronary deaths by approximately 6 and approximately 4%, in normotensives, respectively.

Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health

A 36 year old man presented with headache, polyuria, thirst and weakness of the lower limbs. Hypertension and a high haematocrit were striking features on initial assessment. Subsequently the full picture of Guillain-Barre syndrome developed. Hormone measurement revealed marked sympathetic nervous system and renin-angiotensin system activation with a return to normal of both blood pressure and hormones with neurological recovery.

https://pmj.bmj.com/content/postgradmedj/61/711/53.full.pdf

Severe hypertension and raised haematocrit: unusual presentation of Guillain-Barré syndrome.

Three cases are described of severe congestive heart failure which failed to respond to digitalis, high doses of loop diuretics, and converting-enzyme inhibitors. The addition of spironolactone produced a substantial diuresis associated with clinical and radiological improvement in each case. Although a reversible deterioration in renal function was observed, this drug combination represents a therapeutic option in end-stage heart failure.

Combined spironolactone and converting-enzyme inhibitor therapy for refractory heart failure.

The hyponatraemic-hypertensive syndrome due to renal ischaemia is presumed to be uncommon. We describe four patients who presented with this syndrome over a period of 21 months. All were women who smoked heavily and had unilateral atherosclerotic renal ischaemia. Hypokalaemia was present in each patient, and in one case resulted in recurrent ventricular tachycardia. All had noted thirst, polyuria, and weight loss. Initiation of treatment with a converting-enzyme inhibitor reduced arterial pressure precipitously in two patients. Removal of the ischaemic kidney, or chronic therapy with a converting-enzyme inhibitor reversed the biochemical abnormalities and the presenting symptoms, and lowered arterial pressure. Detailed studies in two patients before and after treatment confirmed the central role of the renin-angiotensin system in the development of the hyponatraemic-hypertensive syndrome.

Hyponatraemic-hypertensive syndrome due to unilateral renal ischaemia in women who smoke heavily.

Blood-Pressure Response to Moderate Sodium Restriction and to Potassium Supplementation in Mild Essential Hypertension

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Severe hypertension and raised haematocrit: unusual presentation of Guillain-Barré syndrome.

Combined spironolactone and converting-enzyme inhibitor therapy for refractory heart failure.

Hyponatraemic-hypertensive syndrome due to unilateral renal ischaemia in women who smoke heavily.

Blood-Pressure Response to Moderate Sodium Restriction and to Potassium Supplementation in Mild Essential Hypertension