Salt and Cardiovascular Disease: Insufficient Evidence to Recommend Low Sodium intake

Martin O'Donnell; Andrew Mente; Michael H. Alderman; Adrian J.B. Brady; Rafael Diaz; Rajeev Gupta; Patricio López-Jaramillo; Friedrich C. Luft; Thomas F. Lüscher; Giuseppe Mancia; Johannes F.E. Mann; David McCarron; Martin McKee; Franz H. Messerli; Lynn L. Moore; Jagat Narula; Suzanne Oparil; Milton Packer; Dorairaj Prabhakaran; Alta Schutte; Karen Sliwa; Jan A. Staessen; Clyde Yancy; Salim Yusuf


Eur Heart J. 2020;41(35):3363-3373. 

In This Article

Can we Safely Reduce Salt Consumption to Low Levels?

If we set aside the evidence and assume that low sodium intake does reduce cardiovascular risk (compared to moderate intake), are there available interventions to reduce sodium intake, in individuals or communities, to lower levels? The answer also has implications for calls to conduct large definitive randomized controlled trials.

Population Level

Globally, the mean intake of sodium was estimated at 3.95 g/day by the Global Burden of Disease (GBD) collaboration, in a meta-analysis of surveys from 187 countries, using 24-h urine collections.[21] Based on the INTERMAP study, intakes are highest in East Asia, Central Asia, and Eastern Europe (mean >4.2 g/day) and in Central Europe and Middle East/North Africa (3.9–4.2 g/day). Some counties have adopted WHO-informed approaches to develop, implement, and monitor strategies for lowering sodium intake[106] by targeting food reformulation, consumer education, front of pack labelling, and intervention in public institution settings (e.g. schools, workplaces). Some countries, most of which have a relatively high mean intake of sodium (>4 g/day), have reported reductions in mean sodium intake in sampled populations. For example, in China, where mean intake of sodium is high, there is evidence of a reduction in mean sodium intake over time (from 6.7 to 4.8 g/day; from 1991 to 2009), largely due to reductions in discretionary salt intake.

In countries with mean sodium intakes in the range of 3–4 g/day, there is less impressive evidence of reduction in mean sodium intake with population-level interventions. One study in the UK reported a 0.6 g/day reduction in mean sodium intake from 2000/01 to 2011, during which some targeted strategies to reduce sodium intake, e.g. working with the food industry to reformulate food with less salt and carrying out public awareness campaigns, were implemented.[107] However, a UK report of sodium intake from 2008 (when a salt reduction programme was fully established) reported no significant reduction in mean sodium intake.[108] At an international level, mean sodium intake, both globally and within regions, has not reduced from 1990 to 2010, based on a Global Burden of Disease meta-analysis.[21]

Community Level

As detailed, no community-level intervention has reported a reduction in sodium intake to low intake levels, but reductions in mean sodium intake of about 0.5 g/day appear feasible with multi-component educational interventions.

Individual Level

Feeding trials, such as the DASH-sodium trial, have achieved low sodium intake targets for short periods of time, but none have reported sustaining this level of low sodium intake for longer periods. Intensive dietary counselling does lower sodium intake (~1 g/day), but mean intake achieved in the TOHP-II trial was 3.2 g/day, and the TOHP-II participants were arguably the most representative of the general population among larger trials. A recent meta-analysis of clinical trials concluded that dietary counselling interventions, such as those used in the TOHP-II and TONE trials, were unsuited to routine primary care clinical practice, due to the intensity of the intervention.[109]

Implications for Other Dietary Intake

In setting guidelines for isolated nutrients, it is important to consider the implication for other dietary factors. For example, the recent NAM report included both sodium (<2.3 g/day) and potassium intake (>3.5 g/day) in a single guideline, given their proposed inter-related effect on blood pressure and cardiovascular risk.[5] However, similar to other guidelines that address intakes of isolated nutrients, the feasibility and practical implications of the combined recommendation were not adequately considered. In all studies examining combined sodium and potassium intake in populations, sodium intake was positively correlated with potassium intake,[110] suggesting that increases in potassium intake (>3.5 g/day) are difficult to achieve while maintaining a low sodium intake (1.5–2.3 g/day), and only a very small proportion of the population (<0.01%) had diets that achieved the combined guideline target (Figure 3). In addition, there may be implications for overall dietary quality of targeting a very low sodium intake. A study by Mercado et al.[111] suggests that achieving target diet quality may be more difficult with sodium intake <2.3 g/day than with higher sodium intakes in the NHANES cohort.

Figure 3.

Association of combined sodium and potassium intake with mortality/cardiovascular risk (PURE study) ( O'Donnell et al.80). Heat map of risk for composite of cardiovascular events or death showing lowest risk in region of moderate sodium intake 3–5 g/day and higher potassium intake and highest risk in region of extremes of sodium excretion and low potassium excretion. The reference hazard for these hazard ratios was set at a value of sodium daily excretion/intake of 5.00 g and potassium daily excretion/intake of 2.25 g (median excretion of sodium and potassium), marked as X. The overlaid lines represent joint distribution quartiles; each region contains a quarter of the analysed participants. r = 0.34.

Many dietary factors (e.g. fruit, vegetable, and meat intake) and dietary patterns (e.g. Mediterranean diet) have been associated with differing risk of cardiovascular events.[112–114] Overall diet quality appears to be important in modifying the cardiovascular effects of sodium intake. That conclusion is supported by evidence from the DASH-Sodium trial,[18] which reported a greater blood pressure lowering effect among those with a healthy cardiovascular diet, compared with less healthy one, as well as data from the PURE study reporting that higher potassium intake may favourably modify the association of high sodium intake with blood pressure[71] and cardiovascular risk.[80] Epidemiological studies have also reported that increased potassium intake is associated with reduced cardiovascular risk, particularly for stroke, and also favourably modifies the adverse cardiovascular effects of high sodium intake.[115,116] We have very limited data on the long-term feasibility, tolerability, net health effects, or net effects on other nutrients of low sodium intake (<2.3 g/day) in the general (healthy) population.

The cardiovascular effect of reducing sodium intake may also be influenced by differences in sources of sodium in diet, which may vary by region. In Europe and North America, processed foods and fast foods are important sources of excess sodium intake.[117] Substitution of these food items for healthier food choices (e.g. fresh fruit and vegetables) will reduce sodium intake and will also confer other cardiovascular health benefits through improvements in overall dietary quality. In other regions, diets rich in raw vegetables are also rich in sodium (e.g. traditional Japanese diet), and reduction in such dietary patterns may not have the same cardiovascular benefits.[118]


  1. No intervention (individual, community, or national) has been demonstrated to achieve sustained low sodium intake (<2.3 g/day).

  2. Achieving the concomitant targets for low sodium intake (<2.3 g/day) and high potassium intake (>3.5 g/day) is very uncommon in free-living individuals. Sodium and potassium intake are positively correlated, making the current combined sodium-potassium target difficult to achieve in general populations.

  3. Moderate sodium intake (2.3–4.6 g/day) with higher potassium intake is achievable by a large proportion of the population and associated with low cardiovascular risk in observational studies, but not proven in definitive intervention trials.