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Does reducing your salt intake make you live longer?

Three Part Question

In [post CABG patients] does a [reduced salt intake] [prove beneficial]

Clinical Scenario

You are seeing a patient at lunch-time 4 days after his coronary artery bypass grafts. He is well and has been walking around the wards. You are aware that he only gave up smoking three weeks ago, when he was admitted with a non-ST myocardial infarction. He thanks you for doing his operation and asks if it is okay to have some salt on his chips for lunch. You tell him that you are sure that it's okay and that he has to have a few pleasures in life. On walking away from the patient, your nurse practitioner tells you off. She had just told him that high salt intake is bad for him and that he should cut down. You sheepishly promise your nurse practitioner that you will look up the evidence.

Search Strategy

Medline was searched using the OVID interface from 1985 to August 2007
[salt.ti OR sodium.ti] AND [diet.ti OR dietary.ti OR reduc$.ti] AND [exp Cardiovascular Diseases/OR exp Cardiovascular Abnormalities/OR Cardiovascular disease$.mp] LIMIT to human studies.

Search Outcome

Four hundred and sixty-two papers were identified from the above-mentioned search from which 14 represented the best evidence on the topic

Relevant Paper(s)

Author, date and country Patient group Study type (level of evidence) Outcomes Key results Study Weaknesses
Stamler et al,
n=10,079 across 32 countries. males and females aged 20-59y.o.Prospective Cohort Study (level 2b)24h urinary sodium excretion,Sodium to Potassium excretion ratio, BMI, Alcohol use, Blood Pressure (BP).Analysis within the populations suggested that a 100mmol/d (5.9g/day) lower sodium intake equated to a BP lower by ~3-6/0-3 mmHg. Analysis between the populations suggested that when median sodium intake 100mmol/d lower, the upward BP slope between 25-55y.o. was lessened by 9/6.3mmHg & the median BP lessened by 7.1/3.8mmHg.Use of single 24h sodium excretion to quantify habitual sodium intake.
Elliot et al,
n=10,079 across 32 countries. males and females aged 20-59y.o.Prospective Cohort Study (level 2b)24h urinary sodium excretion,Sodium to Potassium excretion ratio, BMI, Alcohol use, Blood Pressure (BP).Analysis between the populations associated a 100mmol/24h increase in urinary sodium excretion with a median 5-7/2-4 mmHg increase in BP, and estimated the mean change in BP for a 100mmol/24hr rise in sodium excretion at 55yo vs 25yo to be greater by 10-11/6 mmHg.Use of single 24h sodium excretion to quantify habitual sodium intake.
He & MacGregor,
n=2954, from 28 trials, with those involving children or pregnant women being excluded.Meta-analysis of randomised trials (Level 1a)24h urinary sodium excretion,In hypertensives: a 100mmol/d reduction in sodium intake conferred a 7.11/3.88 mmHg drop in BP.Analysis included Blood-Pressure-Observer-Blinded trials as well as double blind trials, and one non-blinded trial.
BP of subjects allocated to different sodium intakes.In normotensives: an equal sodium intake reduction conferred a 3.57/1.66mmHg drop in BP.
Whelton et al,
n=875, aged 60-80y.o., receiving a single antihypertensive with BP<145/85mmHg.Randomised Controlled Trial (level 1b)24h urinary sodium excretion, Withdrawl of antihypertensive medication, BPBP significantly lower in the group subject to sodium reduction than in the control group.~30% decrease in the need for antihypertensive medication was achieved by reducing the average sodium intake by ~40mmol/d.Population restricted to the elderly. Some effects of the population being motivated to decrease dependence on antihypertensives may manifest in the results.
He et al,
9485 civilians aged 25-74y.o. at commencement. 1971-5. Followed up until 1992 Single 24-hour dietary recall elicited from a trained NHANES person using a standardised form.Prospective Cohort Study (level 2b)Normal weight individualsDietary sodium intake not significantly associated with risk of CV disease in non-overweight individuals.Use of single 24h dietary recall to quantify habitual sodium intake. Data broken down into 4 grades of salt intake . No questioning of addition of salt to food performed which ws estimated to constitute 50% of dietary intake in a later study, questioning the validity of their 2 groups
Overweight individuals with increasing salt intakeStroke: Lowest salt group 95/1658 (5.7%). Highest salt group 109/1668 (6.7%.

Coronary heart disease: Lowest salt group 215/1658 (12.9%). Highest salt group 274/1668 (16%)

All cause mortality: Lowest salt group 363/1658 (22%). Highest salt group 428/1668 (25.6%)
Tuomilehto et al,
n=2436 Finns aged 25-65y.o. 24h urinary sodium excretion. Taken in 1982 and 1987 Follow up for 13 to 18 years:Prospective Cohort Study (level 2b)Cardiovascular mortality, stroke and mortalityOdds control to high salt groups Overweight (n=514) Cardiovascular (n=43) Odds •44 (1•02–2•04) All causes (n=76-14%) Odds 1•56 (1•21–2•00)

Normal weight (n=659) Cardiovascular (n=29) Odds 1•23 (0•76–1•98) All causes (n=60) Odds 0•98 (0•70–1•36)

Odds control to high salt groups (n=2436) Coronary heart disease (n=61- 2.5%) 1•51 (1•14–2•00) Cardiovascular (n=87 – 3.5%) 1•45 (1•14–1•84) All causes (n=180 – 7%) 1•26 (1•06–1•50)

No significant stroke differences
Female population had less than ½ the all-cause mortality of the male population; numbers of end point events were smaller and therefore statistical significance less likely to be reached.
Morimoto et al,
n=350 Japanese patients <70y.o. with essential hypertension whose Mean Arterial Pressure at discharge was <110mmHg. Sodium sensitivity determined by a week of a high salt diet and a week of low salt diet and a BP to sodium excretion ratio calculation.Retrospective Cohort Study (level 2b)Left Ventricular Hypertrophy (LVH) on ECG.LVH, Sodium Sensitive group 38% (of 94pts) Non sodium sensitive group 16% (of 62pts)Japanese population Very small event rate in cardiovascular events.
Cardiovascular events including CVA, MI, Angina, CCF, TIA.Cardiovascular events Non Sodium Sensitive group 2.0 per 100 patient years Sodium sensitive group 4.2 per 100 patient years
Cook et al,
N=3226 prehypertensive participants aged 30-54yo at commencement, followed up over 10-15 years. After randomization to intervention arm or control Intervention arm had dietary sodium reduction with counselling and education. 2415 (77%) successfully followed upRandomised Controlled Trial (level 1b)CV disease, All cause mortalityCV event risk was 25% lower for those given dietary & behavioural counselling in how to reduce and monitor their sodium intake, vs. the control group.Non significant results for cardiovascular complications became significant after controlling for several factors which imbalanced the groups in this RCT.
Cardiovascular disease events over 10-15 yearsSodium intervention group 88/1169 (7.5%)

Control group: 112/1246 (9.0%) P=0.19
Hooper et al,
3 Normotensive studies identified,(n=2326), 5 in untreated Hypertensives (n=387), 3 in treated hypertensives (n=801) Trials involving children, the acutely ill, pregnant, or institutionalised omitted.Systematic Review of Randomised Controlled Trials (level 1a)MortalityThere were only 17 deaths across all studies which were evenly distributed across groups, thus the numbers were too small to make any conclusions about mortalityAs there were not enough events accumulated to provide a definitive answer, this paper was unable to meet its stated aim – to assess the effect of advice to reduce dietary sodium on morbidity & mortality.
Cardiovascular eventsThese were too inconsistently reported to make any conclusions . 46 in controls, and 36 in low sodium groups
Blood pressure reductionSystolic by 1.1 mm Hg, 95% CI 1.8 to 0.4, Diastolic by 0.6 mm hg, 95% CI 1.5 to -0.3),
Alam and Johnson,
n=450 (from 6 trials of participants' mean age close to 60yo, and 5 trials of participants age ≥60yo)Meta Analysis of Randomised Controlled Trials(level 1a)Erect BP, Urinary sodiumPooled mean increase in BP due to increased sodium consumption, weighted for sample size, was 5.58/3.5 mmHg.

Regression analysis showed a significant correlation between Systolic BP and the level of sodium intake.
Pooled mean change in sodium intake not provided
Cutler et al,
N=2635 (22 trials including hypertensive participants and 12 trials involving normotensive participants)Meta Analysis of Randomised Trials (Level 1a)8h or 24h urinary sodium excretion, BP.In hypertensive participants, a 100mmol/d reduction in sodium intake conferred a 5.75/2.54 mmHg drop in BP.

In normotensive participants, a 100mmol/d reduction in sodium intake conferred a 2.28/1.39 mmHg drop in BP.
Multiple trials of ~2 weeks duration could be too short to illicit effects and thus skew data.
Jürgens & Graudal,
Caucasians: Normal diastolic n=5030 Normal systolic n=5096 Raised diastolic n=3391 Raised systolic n=3367 Blacks: Normal & raised diastolic & systolic n=522 Trials involving children or pregnant women omitted.Meta Analysis of Randomised Trials (level 1a)8h or 24h urinary sodium excretion

(the authors declare that "high sodium intake" means normal or above, and "low sodium intake" means below normal),

Mean weighted reduction in BP with low sodium intake (vs. high sodium intake):

Caucasians: Normotensive: 1.27/0.54 mmHg Hypertensive: 4.18/1.89 mmHg

Blacks:Pooled normo and hypertensive: 6.44/1.98 mmHg
Median duration of intervention in normotensive Caucasians was 8 days (versus 28 days in hypertensive trials)
Sacks et al,
n=412, all > 22y.o., BP over 3 visits is 130-159/80-95mmHg.Randomised Controlled Trial (level 1b)24h urinary sodium excretion & BP after 30 days of high (140mmol/day), medium (100mmol/day), or low (65mmol/day) sodium diets.A decrease in blood pressure was found with each decrease in sodium intake.All food including snacks was provided & taste-tested for palatability: concordance with the low sodium diet is likely better here than in real life.
Weinberger et al,
normotensives: n=430 hypertensives: n=278 (as of commencement, 25 years prior to publishing)Retrospective Cohort Study (level 2b)Sodium sensitivity,and after 25 years: CV mortalityNormotensive Sodium Sensitive (SS) subjects >25y.o. at commencement displayed cumulative mortality similar to hypertensive subjects.

Normotensive Sodium Resistant (SR) subjects >25y.o. at commencement were more likely to survive.
No exclusion criteria except for patients taking oral contraception or HRT.


The INTERSALT study (n=10079) ran across 32 countries, and assessed hypotheses of blood pressure reduction. From these data, Stamler and Elliott et al. estimated that a 5.9 g per day (100 mmol/day) rise in salt intake equated to a 3–6/0–3 mmHg rise in blood pressure (systolic/diastolic). Similar changes in BP were seen in a meta-analysis of RCTs which compared salt reduction lasting more than 4 weeks with blood pressure, conducted by He and MacGregor pooling together hypertensive (n=734) and normotensive (n=2220) subjects. In the former group, regression analysis suggested that a 100 mmol/24 h reduction of salt intake conferred a 7.11/3.88 mmHg drop in blood pressure (systolic/diastolic). In the normotensive group salt reduction conferred a 3.57/1.66 mmHg drop in blood pressure. The TONE study found reducing salt intake to 1.8 g/day decreased the need for antihypertensive medication by 30%. Thus, repeated studies confirm that salt restriction reduces blood pressure and need for antihypertensive medication. The NHANES-I study followed-up 9485 patients for 19 years after a single 24-h dietary sodium questionnaire. They found that in non-obese patients, there was no clinical increase in risk of any clinical outcome measures. However, for obese patients there was an increase in stroke risk, heart disease risk and mortality risk. However, between the lowest and highest salt groups, the difference in incidence of any of these risks over the 19 years was no more than 3%. In addition, their questionnaire did not include an estimate of added salt to food, which some authors estimate as contributing to 50% of dietary salt. Tuomilehto et al. reported an increased rate of acute coronary events and an increased mortality in overweight men in a study of 2436 patients having a single measurement of 24-h sodium excretion. However, across all groups the 12–18-year mortality was 7% and an increase in mortality odds in the high salt excretion group was 1.36 and, thus, the incidence in this group will be around 10% giving a 3% increase in absolute risk. Morimoto et al. measured sodium sensitivity in 350 patients by giving them a week of a high and then low sodium diet and seeing if the blood pressure changed. Patients were followed-up for a mean of 7.3 years. There were two events per 100 patient-years in the non-sensitive group and 4.2 events in the sensitive group. The most recent analysis of two randomised trials: Trials of Hypertension Prevention (TOHP I and II) in 2007 reported that cardiovascular events were 25% lower in those given dietary and behavioural counselling in how to reduce their sodium intake as compared to the control patients. This is the most convincing paper to date making the link between sodium restriction and cardiovascular risk. However, on looking further into this study, this difference was 7.0% compared to 9.0% over 10 years for cardiovascular events (of which there were 200 across over 3000 patients). The 2006 Cochrane review that sought to assess the impact of salt restriction on cardiovascular risk found only 11 RCTs of adequate quality for inclusion. In these studies, there were only 17 deaths spread evenly across groups and 46 cardiovascular events in the controls compared to 36 in the low sodium diet groups. They concluded that sodium restriction could be justified to reduce the need for anti-hypertensive medication but not for the reduction of cardiovascular events. Michael Alderman in his Presidential address to the 21st Scientific Meeting of the International Society of Hypertension in Japan in October 2006 stated that there is no question that sodium restriction can reduce blood pressure. However, the link between salt restriction and cardiovascular disease has not been adequately established and is heterogeneous at best from evidence from observational studies rather than randomised trials. There may actually be a J-shaped relationship between salt intake and risk and the contention that salt restriction will reduce cardiovascular risk is an argument of hope over reason. The AHA recommends that the general public consume no more than 6 g of sodium chloride per day in support of the US Dietary Guideline Committee that also gives this recommendation. Slightly higher intakes (6.0–7.5 g/day) have not in their view been demonstrated to increase cardiovascular risk or raise blood pressure in normotensive persons without other cardiovascular risk factors. They state that the guideline is an arbitrary recommendation for avoiding excessive salt intake rather than an attempt to impose low salt intake. In the UK the Scientific Advisory Committee on Nutrition also recommend 6 g/day

Clinical Bottom Line

Restricting sodium intake to levels below 6 g per day reduces blood pressure and in turn may reduce the need for antihypertensives by as much as 30%. However, the ability of dietary sodium restriction to reduce the incidence of cardiovascular events is more controversial. Some of the largest studies such as NHANES and TOHP, which do demonstrate a significant benefit, report a 20–30% relative reduction in adverse events which, due to the low rate of these events equates to an absolute risk reduction over 10–20 years in the region of 2–3% for protection from adverse cardiovascular events from sodium dietary restriction.


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  2. Elliott P, Stamler J, Nichols R et al. Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations. Br Med J 1996; 312:1249–1253.
  3. He FJ, MacGregor GA. Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health. [see comment]. J Hum Hypertens 2002; 16:761–770.
  4. Whelton PK, Appel LJ, Espeland MA et al. Sodium reduction and weight loss in the treatment of hypertension in older persons: a randomized controlled trial of nonpharmacologic interventions in the elderly (TONE). TONE Collaborative Research Group. J Am Med Assoc 1998; 279:839–846.
  5. He J, Ogden LG, Vupputuri S et al, Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. J Am Med Assoc 1999; 282:2027–2034.
  6. Tuomilehto J, Jousilahti P, Rastenyte D et al. Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. [see comment]. Lancet 2001; 357:848–851.
  7. Morimoto A, Uzu T, Fujii T et al. Sodium sensitivity and cardiovascular events in patients with essential hypertension. Lancet 1997; 350:1734–1737.
  8. Cook NR, Cutler JA, Obarzanek E et al. Long-term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). Br Med J 2007; 334:885.
  9. Hooper L, Bartlett C, Davey SG et al. Advice to reduce dietary salt for prevention of cardiovascular disease. 2004; [update of Cochrane Database Syst Rev 2003 (3):CD003656; PMID: 12917977]. . Cochrane Database of Systematic Reviews (1):CD003656
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  13. The Food Standards Agency and the Department of Health Scientific Advisory Committee on Nutrition HMSO UK 2003.
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  15. Cutler JA, Follmann D, Allender PS et al. Randomized trials of sodium reduction: an overview. Am J Clinic Nutr 1997; 65:643S–651S.
  16. Jurgens G, Graudal NA. Effects of low sodium diet vs. high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride. 2003; [update in Cochrane Database Syst Rev 2004 (1): Cochrane Database of Systematic Reviews (1):CD004022
  17. Sacks FM, Svetkey LP, Vollmer WM et al. DASH-Sodium Collaborative Research Group. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. [see comment]. N Engl J Med 2001; 344:3–10.
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