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2 August 2011
A Cochrane Review found that, compared with control groups, reducing dietary salt intake decreased blood pressure (BP) by 1 to 4 mmHg in people with or without hypertension. Although results were consistent with a beneficial effect on mortality and cardiovascular (CV) disease, there was insufficient data to demonstrate a statistically significant effect.
Level of evidence:
Level 2 (limited quality patient-oriented evidence) according to the SORT criteria.
Action
Healthcare professionals should continue to advise people to follow NICE public health guidance for prevention of CV disease with regard to dietary salt intake. This Cochrane Review should not deter people from restricting their salt intake to current guideline levels. Advice to help people reduce their salt intake can be found on the NHS choices website. Although not sufficient to demonstrate statistical significance for reductions in mortality or CV morbidity, the currently available data from randomised controlled trials (RCTs) are consistent with the wider body of evidence suggesting that salt reduction is beneficial in people with or without hypertension.
What is the background to this?
The relationship of salt intake to BP is the basis for the belief that restricting dietary sodium intake will prevent BP-related CV events, such as stroke. However, the effects of reduced dietary salt on CV events and mortality, as demonstrated in RCTs, are unclear. The present systematic review identified RCTs with follow up of at least 6 months that compared dietary salt reduction (restricted dietary intervention or advice to reduce salt intake) with control/no intervention in adults. Meta-analyses were carried out to assess the effects on the patient-oriented outcomes of all-cause mortality and CV morbidity.
What does this study claim?
Although claimed as collating more event data (665 deaths in around 6250 participants) than previous systematic reviews of RCTs, the Cochrane Review was unable to identify a statistically significant effect of reduced dietary salt on all-cause mortality in people without hypertension (relative risk [RR] 0.67, 95% confidence interval [CI]: 0.40 to 1.12, 60 deaths) and people with hypertension (RR 0.97, 95%CI 0.83 to 1.13, 513 deaths). Also, no statistically significant effect was found for CV morbidity in people with normal BP (RR 0.71, 95%CI 0.42 to 1.20, 200 events) or raised BP at baseline (RR 0.84, 95%CI 0.57 to 1.23, 93 events) Salt restriction increased the risk of all-cause death in those with congestive heart failure (one study, n=232, RR 2.59, 95%1.04 to 6.44, 21 deaths). The estimates of benefit from dietary salt restriction, though not statistically significant, were consistent with the predicted effects on clinical events attributable to the small BP achieved (on average 1 mmHg in people without hypertension and 2 to 4 mmHg in people with hypertension and those with heart failure).
How does this relate to other studies?
The causal relation between dietary salt intake and BP has been established through experimental, epidemiological, migration, and intervention studies. As reported in a WHO Forum and Technical meeting in 2006, although our understanding of long-term effects of reducing dietary salt intake on CV morbidity and mortality can be improved by further studies, the currently available scientific evidence is strong enough to justify reducing sodium intake in the whole population through cost-effective public health approaches.
In 2009, A systematic review and meta-analysis in 2009 (Strazzullo, et al ) of 13 prospective studies (19 cohorts) published between 1966 and 2008, supported this stance. It included 177,025 participants (follow-up 3.5 to 19 years) and over 11,000 vascular events, and concluded that higher salt intake was associated with a significantly increased risk of stroke and total CV events — stroke: pooled RR 1.23, 95%CI 1.06 to 1.43, p = 0.007; CV events: pooled RR 1.14, 95%CI 0.99 to 1.32, p = 0.07 — with a dose dependent association.
So what?
High dietary intake of salt has been identified as an important risk factor for CV disease and is considered an important public health issue. Since 2003 the Food Standard Agency has had in place a programme of work to help UK consumers reduce their salt intakes. NICE public health guidance for prevention of CV disease at population level recognises that high levels of salt in the diet are linked with high BP which, in turn, can lead to stroke and coronary heart disease. Salt intake is considered a major determinant of CV events in the UK, mainly due to its effect on BP. NICE recommends a number of initiatives to reduce dietary salt intake at the population level, calling for an acceleration of the reduction of salt intake in the general population to a maximum intake of 6 g/day per adult by 2015 and to 3 g/day by 2025.
In its clinical guideline for the management of hypertension, NICE recommends that patients are encouraged to keep their dietary sodium intake low, either by reducing or substituting sodium salt, as this can reduce BP.
The Cochrane review identified insufficient evidence from RCTs that dietary restriction in salt produces a reduction in long-term patient-oriented outcomes in people with or without hypertension. Estimates of relative risk for mortality and CV disease in the Cochrane review were not statistically significantly different from controls, however confidence intervals were wide and the point estimates suggested a possible benefit, not inconsistent with the findings of the Strazzullo review. Because of the small number of studies and outcome events included in the Cochrane review, the study was underpowered to detect a significant difference.
More rigorous long-term RCTs of sufficient statistical power are required to definitively demonstrate whether there is a benefit for restricting dietary salt intake on long-term patient-oriented outcomes. Although, not unequivocally demonstrating a clinical benefit for reducing dietary salt, the findings of the Cochrane review should not be interpreted as ruling out a clinically significant benefit on long term outcome, and it should not deter people from following public health dietary advice regarding salt intake.
Further studies are also needed to confirm the findings of the one study included in the review that identified an increased risk of mortality for low-sodium in people with heart failure. The current full NICE guideline for chronic heart failure recognises that salt reduction is commonly recommended by physicians to help control fluid status, although, as with other aspects of dietary advice, the evidence for this is limited and further research in this area is required.
Also published in Am J Hypertens 2011;24:843–53
Design
Systematic review and meta-analysis of seven RCTs with at least 6 month’s follow-up.
Patients
Adults (normotensives, three trials, n=3518; hypertensives, two trials, n=758; mixed population, one trial, n=1981; heart failure, one trial, n=232)
Intervention and comparison
Reduced dietary salt (restricted salt dietary intervention or advice to reduce salt intake) compared with control (usual, control or placebo diet, or no intervention).
Outcomes and results
- RRs for all cause mortality in normotensives (end of trial RR 0.67, 95%CI 0.40 to 1.12, 60 deaths; longest follow up RR 0.90, 95%CI 0.58 to 1.40, 79 deaths) and hypertensives (end of trial RR 0.97, 95%CI 0.83 to 1.13, 513 deaths; longest follow up RR 0.96, 95%CI 0.83 to 1.11, 565 deaths).
- CV morbidity (including fatal and non-fatal myocardial infarction, stroke, angina, heart failure, peripheral vascular events, sudden death, revascularisation [coronary artery bypass surgery or angioplasty with or without stenting] and CV related hospital admissions) in people with normal BP (longest follow-up RR 0.71, 95%CI 0.42 to 1.20, 200 events) or raised BP at baseline (end of trial RR 0.84, 95%CI 0.57 to 1.23, 93 events).
- Salt restriction increased the risk of all-cause death in those with congestive heart failure (end of trial RR: 2.59, 95%CI 1.04 to 6.44, 21 deaths).
- Systolic BP was reduced in all intervention arms, compared with control — normotensives (1.1 mmHg, 95%CI –0.1 to 2.3), hypertensives (4.1 mmHg, 95% CI 2.4 to 5.8) and those with heart failure (by 4.0 mmHg, 95%CI 0.7 to 7.3).
- Urinary sodium was reduced by a similar amount across the three study subgroups compared with controls — normotensives (34.2 mmol/24 hrs, 95%CI 18.8 to 49.6, hypertensives (39.1 mmol/24 hrs, 95%CI 31.1 to 47.1) and heart failure (27.0 mmol/24hrs, 95%CI 24.5 to 29.5).
- No information on participants’ health-related quality of life.
Sponsorship
Supported by an NIHR programme grant
Further information can be found on NHS Evidence and in the hypertension and lifestyle e-learning sections of NPC.
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