Salt intake, plasma sodium, and worldwide salt reduction

Abstract

There is overwhelming evidence that a reduction in salt intake from the current level of approximately 9–12 g/d in most countries of the world to the recommended level of 5–6 g/d lowers blood pressure (BP) in both hypertensive and normotensive individuals. A further reduction to 3–4 g/d has a greater effect. Prospective studies and outcome trials have demonstrated that a lower salt intake is related to a reduced risk of cardiovascular disease. Cost-effectiveness analyses have documented that salt reduction is more or at the very least just as cost-effective as tobacco control in reducing cardiovascular disease, the leading cause of death and disability worldwide. The mechanisms whereby salt raises blood pressure and increases cardiovascular risk are not fully understood. The existing concepts focus on the tendency for an increase in extracellular fluid volume. Increasing evidence suggests that small increases in plasma sodium may have a direct effect on BP and the cardiovascular system, independent of extracellular volume. All countries should adopt a coherent and workable strategy to reduce salt intake in the whole population. Even a modest reduction in population salt intake will have major beneficial effects on health, along with major cost savings.

Key words::

• Blood pressure
• cardiovascular risk
• plasma sodium
• salt intake
• salt reduction programme

Key messages

• There is strong evidence that a reduction in salt intake lowers blood pressure and reduces cardiovascular risk. Salt reduction is one of the most cost-effective interventions to reduce cardiovascular disease.

• Small changes in plasma sodium could be one of the mechanisms whereby salt intake raises blood pressure and increases cardiovascular risk.

• All countries should adopt a coherent and workable strategy to reduce salt intake in the whole population.

During several million years of evolution, the ancestors of humans ate a diet which contained a very small amount of salt that existed in natural foods, i.e. less than 0.5 gram of salt (0.2 g sodium) per day (1). Only about 5000 years ago, the Chinese discovered that salt could be used to preserve foods. Salt then became of great economic importance and the most taxed, traded commodity in the world, with intake reaching a peak around the 1870s (1). Salt intake had been declining with the invention of the deep freezer and the refrigerator as salt was no longer required as a preservative. However, with the recent large increase in the consumption of highly salted processed foods, salt intake is now increasing again. The current salt intake in many countries is between 9 and 12 g/d (2). This large increase in salt intake is relatively recent in evolutionary terms. It presents a major challenge to the physiological systems to excrete these large amounts of salt through the kidneys. The consequence is a gradual rise in blood pressure (BP) (3,4), thereby increasing the risk of cardiovascular disease (i.e. stroke, heart attack, heart failure) and renal disease. Furthermore, a high salt intake may have direct effects on stroke (5,6), left ventricular hypertrophy (LVH) (7), progression of renal disease and proteinuria (8), independent of but additive to the effect of salt on BP. There is also evidence that a high salt intake is indirectly related to obesity through increased soft drink consumption (9,10), associated with a higher risk of renal stones and osteoporosis (11), and probably a major cause of stomach cancer (12,13). The evidence on these harmful effects of salt has been comprehensively reviewed in several recent articles (3,14). In this paper, we provide a brief update on the evidence relating salt to BP and cardiovascular disease, as well as the potential mechanisms, in particular the role of plasma sodium. Additionally, we provide a brief update on the current salt reduction programmes which have been successfully carried out in several countries.

Evidence on salt and BP

Various types of studies, including animal experiments, human genetics, epidemiology, migration, population-based intervention studies, and treatment trials, have consistently shown that dietary salt intake is a major cause of raised BP (3). The most relevant animal studies are those in chimpanzees (98.8% genetic homology with man), which demonstrated progressive and large increases in BP when salt intake was increased from 0.5 g/d, which is close to humans’ evolutionary intake, to 10–15 g/d which is similar to our current salt intake (15). In chimpanzees who had been on a high salt intake, a modest reduction in salt intake lowered BP, and the fall in BP was as large as or larger for salt intakes at or below the recommended levels of 5–6 g/d (16).

In humans, epidemiological studies have shown that salt intake is directly related to BP (4,17,18). The large international study on salt and BP (Intersalt) (4), which enrolled 10,079 individuals from 52 centres around the world, also demonstrated a highly significant positive relationship between salt intake and the increase in BP with age. It was estimated that an increase of 6 g/d in salt intake over 30 years would lead to an increase in systolic BP by 9 mmHg (4). One criticism of the Intersalt study made by the Salt Institute (a public relations company defending the interests of salt extractors and manufacturers worldwide) was that when the four communities consuming lower salt were excluded, there was no overall relationship remaining between salt intake and BP. The Intersalt's investigators re-analysed their data and showed that the highly significant within-population association between salt intake and BP across all 52 centres was virtually unchanged when the four low-salt populations were excluded, and the association between salt intake and the rise in BP with age persisted across 48 centres (4,19,20).

Population-based intervention studies have shown that when salt intake is decreased, there is a reduction in population BP (21,22). One of the most successful intervention studies was conducted in two similar villages in Portugal (21) where salt intake was very high (21 g/d) and the prevalence of hypertension and stroke was also very high. During 2 years of intervention through vigorous, widespread health education to reduce the consumption of salt especially from foods that had previously been identified as the major sources of salt, there was a difference of ≈50% in salt intake between the two villages (i.e. intervention versus control). This was associated with a difference of 13/6 mmHg in BP. Another community-based intervention trial in two rural villages in north-eastern Japan reduced salt intake by 2.3 g/d through dietary counselling. This reduction in salt intake was associated with a decrease of 3.1 mmHg in systolic BP (23). Several other studies (24,25) showed no significant change in BP; however, these studies failed to achieve a reduction in salt intake, and such results are therefore not surprising.

There have been a large number of randomized trials looking at the effect of salt reduction on BP. Meta-analyses of these trials have demonstrated that a modest reduction in salt intake lowers BP in both hypertensive and normotensive individuals, and there is a dose-response to salt reduction (26). The most persuasive evidence on the dose-response relationship comes from rigorously controlled trials with three levels of salt intake (27,28). One of such trials was the randomized double-blind cross-over study in 20 individuals with untreated essential hypertension, where salt intake was reduced from 11.2 to 6.4 and to 2.9 g/d, each for one month (27). BP was 163/100 mmHg with a salt intake of 11.2 g/d, and reduced to 155/95 mmHg when salt intake was decreased to 6.4 g/d (i.e. a decrease of 8/5 mmHg). BP fell further to 147/91 mmHg when salt intake was reduced to 2.9 g/d (i.e. a further fall of 8/4 mmHg). After the trial was completed, individuals continued the lowest salt intake. Among the 20 participants, 19 were followed up for 1 year. In 16 individuals, BP remained controlled without any antihypertensive medication, and the average BP was 142/87 mmHg with a salt intake of 3.2 g/d (27). The DASH (Dietary Approaches to Stop Hypertension)-Sodium trial (28) which studied 412 individuals with normal or mildly raised BP also demonstrated a clear dose-response relationship when salt intake was reduced from 8 to 6 and to 4 g/d. The fall in BP was greater at a lower level of salt intake, i.e. from 6 to 4 g/d compared with that from 8 to 6 g/d. The dose-response relationship was observed both on the normal American diet and the DASH diet which is rich in fruits, vegetables, and low-fat dairy products (Figure 1) (28).

Figure 1. Changes in blood pressure and 24-h urinary sodium excretion with the reduction in salt intake in all participants (hypertensives: n = 169; normotensives: n = 243) on the normal American diet (i.e. control diet) and on DASH diet. Redrawn from Sacks et al. (28).

From the well-controlled trials, it is clear that the current recommendations to reduce salt from 9–12 g/d in most countries of the world to the WHO (World Health Organization) recommended level of ≤ 5 g/d will have a major effect on BP, and the target of ≤ 5 g/d should now be implemented worldwide. It is important to note that this recommendation is based on the feasibility of reducing population salt intake to 5 g/d, but not on the potential maximum beneficial effects of salt reduction. Randomized trials have demonstrated a clear dose-response to salt reduction, and a further reduction to 3 g/d will have a much greater effect on BP. Therefore, a target of 3 g/d should become the long-term target for population salt intake. Recently the UK government's health advisory agency, the National Institute for Health and Clinical Excellence (NICE) has recommended a reduction in the population's salt consumption to 3 g/d by 2025 (29).

It has been shown that, for a given reduction in salt intake, the fall in BP was larger in individuals of African origin, in older people, and in those with raised BP compared to whites, young people, and individuals with normal BP, respectively (30). These differences in the fall in BP were, at least in part, due to the differences in the responsiveness of the renin-angiotensin system (31,32). The term ‘salt sensitivity’ has been commonly used to describe the variations of BP response to salt reduction. However, almost all of the studies on ‘salt sensitivity’ have used a protocol of very large and sudden changes in salt intake. As described previously, these studies are irrelevant to the public health recommendations of more modest reduction in salt intake for a prolonged period of time. There is strong evidence that a modest reduction in salt intake should be carried out universally in the entire population. A reduction in population salt intake lowers population BP. Even a small reduction of BP across the whole population would have a large impact on reducing the appalling burden of cardiovascular disease (33).

Evidence on salt and cardiovascular disease

There is much evidence that raised BP throughout its range starting at 115/75 mmHg is a major cause of cardiovascular disease (34). A modest reduction in salt intake lowers BP and, therefore, would reduce cardiovascular risk. Based on the fall in BP from a meta-analysis of randomized salt reduction trials (26), it was estimated that a reduction of 6 g/d in salt intake would reduce stroke by 24% and coronary heart disease by 18%. This would prevent ≈35,000 stroke and coronary heart disease deaths a year in the UK (35) and ≈2.5 million deaths worldwide.

Both prospective cohort studies and outcome trials have shown that a lower salt intake is related to a reduced risk of cardiovascular disease (36,37). A recent paper by Stolarz-Skrzypek et al. in the Journal of the American Medical Association (38), however, claimed that a lower salt intake was associated with higher cardiovascular mortality in spite of lower blood pressure. Detailed examination of this study reveals many methodological flaws (39), particularly serious problems with the 24-hour urine collection, therefore the results from this study should be interpreted with great caution. A meta-analysis of 12 cohort studies showed that an increase of 5 g/d in salt intake was associated with a 23% increase in the risk of stroke and a 17% increase in the risk of cardiovascular disease (Figure 2) (36). Even when the study by Stolarz-Skrzypek et al. (38) was included in an updated meta-analysis, the association of salt intake with stroke remained significant, and the association with cardiovascular disease was borderline significant (39).

Figure 2. Relative risk of stroke and total cardiovascular disease (CVD) associated with a 5 g/d increase in salt intake in a meta-analysis of cohort studies. Adapted from Strazzullo et al. (36).

Evidence from outcome trials of long-term salt reduction is very limited due to the innate difficulty in conducting such trials. A recent meta-analysis of seven randomized trials by Taylor et al., published simultaneously in The Cochrane Library (40) and the American Journal of Hypertension (41), claimed that ‘Cutting down on the amount of salt has no clear benefits in terms of likelihood of dying or experiencing cardiovascular disease’ (40) and The Cochrane Library's press release headline stated ‘Cutting down on salt does not reduce your chance of dying’ (42). Both of these statements are incorrect. Despite this, these headline-grabbing statements received very misleading worldwide media publicity.

Among the seven trials included in the meta-analysis by Taylor et al., one in heart failure (43) should not have been included as the subjects were severely salt- and water-depleted due to aggressive diuretic therapy (43). Additionally, the findings in patients with severe heart failure on multiple drug treatments are not generalizable to the general population. In the remaining six trials, there is a reduction in all clinical outcomes (all-cause mortality, cardiovascular mortality, and events), although none of these are statistically significant (Table I). The non-significant findings are most likely due to a lack of statistical power, particularly as Taylor et al. analysed the trials for hypertensives and normotensives separately. A re-analysis of the data by combining hypertensives and normotensives shows that there is a significant reduction in cardiovascular events by 20% (P < 0.05) (Figure 3) and a non-significant reduction in all-cause mortality (5%–7%), in spite of the small reduction in salt intake of 2.0–2.3 g/d. These results add strongly to the evidence that salt reduction has a major impact on reducing strokes, heart attacks, and heart failure (44).

Table I. Reduction in salt intake, blood pressure and clinical outcomes using the results from the meta-analysis by Taylor et al. (41), excluding the trial in heart failure.

	Trials in normotensives (n = 3)^a	Trials in hypertensives (n = 3)^a
Reduction in salt intake at end of trial, g/d (95% CI) (duration: 6 to 36 months)	2.0 (1.1 to 2.9)	2.3 (1.8 to 2.8)
Fall in blood pressure at end of trial, mmHg (95% CI) (duration: 18 to 36 months)
Systolic	1.11 (−0.11 to 2.34)	4.14 (2.43 to 5.84)
Diastolic	0.80 (0.23 to 1.37)	3.74 (−0.93 to 8.41)
Difference in all-cause mortality at longest follow-up (95% CI) (duration: 7 months to 12.7 years)	10% reduction (RR 0.90, 0.58 to 1.40)	4% reduction (RR 0.96, 0.83 to 1.11)
Difference in CVD events at longest follow-up (95% CI) (duration: 7 months to 11.5 y)	29% reduction (RR 0.71, 0.42 to 1.20)	16% reduction (RR 0.84, 0.57 to 1.23)
Difference in CVD mortality at longest follow-up (95% CI) (duration: 7 months to 6 years)	–	31% reduction (RR 0.69, 0.45 to 1.05)

RR = relative risk; CVD = cardiovascular disease.

^aNot all measurements were made in all trials.

Figure 3. Cardiovascular disease (CVD) events at longest follow-up (duration varied between 7 months and 11.5 years) in a meta-analysis of randomized salt reduction trials using fixed effect model with normotensives and hypertensives combined. TOHP I = Trial of Hypertension Prevention, phase 1; TOHP II = Trial of Hypertension Prevention, phase 2; TONE = Trial of Nonpharmacologic Interventions in Elderly.

Potential mechanisms whereby salt raises BP and increases cardiovascular risk

Role of extracellular volume

The mechanisms whereby salt raises BP and increases cardiovascular risk are not fully understood. There is much evidence, particularly from the kidney cross-transplantation experiments, demonstrating that the kidney plays an important role in the rise in BP associated with a high salt intake (45,46). In individuals who develop high BP there is an underlying defect in the kidneys’ ability to excrete sodium. This causes sodium and water retention, particularly on a high salt intake, leading to volume expansion and the stimulation of various compensatory mechanisms. The persistent presence of some of the compensatory mechanisms eventually causes BP to rise which in turn helps overcome the kidneys’ difficulties in excreting sodium. Based on experiments in 70% nephrectomized dogs given large amounts of saline intravenously daily for two weeks, Guyton suggested that volume expansion raises BP by the autoregulatory effect on resistance vessels (47).

Role of plasma sodium

There is now increasing evidence that small changes in plasma sodium may be an important mechanism for the changes in BP with changing salt intake. A number of studies have shown that an increase or a decrease in salt intake causes parallel changes in plasma sodium in both hypertensive and normotensive individuals (48,49), e.g. a decrease of ≈3 mmol/L (P < 0.001) in plasma sodium when salt intake was reduced from 20 to 1 g/d for 5 days. In a well-controlled double-blind trial of one month, plasma sodium was reduced by 0.4 mmol/L (P < 0.05) when salt intake was decreased from ≈10 to 5 g/d in 118 hypertensive individuals. The decrease in plasma sodium was weakly but significantly correlated with the fall in systolic BP (48).

Several epidemiological studies have shown a significant positive association between plasma sodium and blood pressure (50–52). In a study of 3578 London civil servants, a 1 mmol/L increase in plasma sodium was associated with a 1 mmHg increase in systolic BP after adjusting for confounding factors (50). In another study of a Japanese population (3222 normotensives and 741 patients with essential hypertension), serum sodium distribution was shifted by ≈2 mmol/L towards higher values in the hypertensives (51). However, the Framingham Heart Study showed that serum sodium was not associated with BP cross-sectionally or with the development of hypertension during 4 years of follow-up (53).

Plasma sodium is a major determinant of extracellular volume, thereby influencing BP. At the same time, small changes in plasma sodium may have a direct effect on BP, independent of extracellular volume (54). Using peritoneal dialysis in rats, Friedman et al. were able to change plasma sodium in an opposite direction to extracellular volume by altering sodium concentration of the dialysis fluid (55). When plasma sodium was increased by 10–15 mmol/L, there was a rapid increase in BP despite a reduction in extracellular volume. When plasma sodium was decreased, there was a fall in BP despite an increase in extracellular volume. The changes in BP were directly related to the changes of intracellular sodium. Friedman et al. suggested that increases in intracellular sodium may affect vascular smooth muscle tension, thereby increasing BP (55,56). In humans, it is difficult to study the effects of changes in plasma sodium without there being an associated change in extracellular volume. A recent study in patients on haemodialysis indicated that changes in plasma sodium could have an immediate and direct effect on BP (57). Ten individuals were studied, in random order, on two separate haemodialysis sessions, one with dialysate sodium set at 145 mmol/L and the other at 135 mmol/L, each for 2 hours with no ultrafiltration (57). This reduction in dialysate sodium concentration resulted in a significant decrease in plasma sodium of 3.4 ± 0.3 mmol/L at 1 hour (P < 0.01) and 4.8 ± 0.3 mmol/L at 2 hours (P < 0.001). This was associated with a fall in systolic BP of 8 ±  3 mmHg (P < 0.05) at 1 hour and 12 ± 5 mmHg (P = 0.05) at 2 hours. During the study, there was no fluid removed and there was no significant change in haematocrit which is a crude index of extracellular volume. These results suggest that changes in plasma sodium could have a direct effect on BP, although small changes in extracellular volume due to the movements of fluid between intracellular and extracellular compartments could not be ruled out.

Tissue culture experiments demonstrated that increasing bath sodium concentration within the physiological range caused marked cellular hypertrophy in both arterial smooth muscle and cardiac myocytes (58). In cultured bovine endothelial cells, when bath sodium concentration was increased from 137 to 142 mmol/L, endothelial nitric oxide synthase (eNOS) activity was reduced by 25%. The decrease in eNOS activity was in a sodium concentration-dependent manner within the range studied (137–157 mmol/L) (59). Using cultured human endothelial cells, Oberleithner et al. demonstrated that an increase in the sodium concentration of the culture medium from 135 to 145 mmol/L stiffened endothelium and reduced nitric oxide release (60).

Recent studies in humans have shown that salt intake does affect endothelial function (61,62). A randomized trial in 29 overweight and obese normotensive individuals showed that, when salt intake was reduced from 9.2 to 3.8 g/d for 2 weeks, there was a significant improvement in endothelial function as measured by brachial artery flow-mediated dilatation (61). Another study showed that a high-salt meal has an immediate adverse effect on endothelial function in normotensive individuals (63).

Salt reduction is a cost-effective public health measure to reduce cardiovascular disease

Several studies have shown that a reduction in salt intake is one of the most cost-effective interventions to reduce cardiovascular disease in both developed and developing countries (64–70). For instance, a recent study in the US showed that even a very modest reduction in salt intake of only 10% which could be easily achieved, as demonstrated in the UK (71), would prevent hundreds of thousands of strokes and heart attacks over the lifetimes of adults aged 40–85 years who are alive today, and could save more than $32 billion in medical expenses in the US alone (70). A larger decrease in salt intake would result in a larger health improvement and greater cost savings (68). The UK salt reduction campaigns which started in 2003/2004 have been successful, and the average salt intake, as measured by 24-hour urinary sodium, has fallen from 9.5 to 8.6 g/d by May 2008 (71). The campaigns, which cost just £15 million, led to 6000 fewer cardiovascular deaths per year, saving the UK economy ≈£1.5 billion per annum according to a recent report by NICE (29,72).

Asaria et al. estimated the effects and cost of strategies to reduce salt intake and control tobacco use for 23 low- and middle-income countries that account for 80% of the chronic disease burden in the developing world (66). They demonstrated that, over 10 years (from 2006 to 2015), a 15% reduction in mean population salt intake could avert 8.5 million cardiovascular deaths and a 20% reduction in smoking prevalence could avert 3.1 million cardiovascular deaths. The modest reduction in salt intake could be achieved by a voluntary reduction in the salt content of processed foods and condiments by manufacturers combined with a sustained mass-media campaign aimed at encouraging dietary change within households and communities. The main costs of the strategy to reduce salt consumption would be awareness campaigns through mass-media outlets and regulation of food products by public health officers, with an average cost estimated to be US$0.09 per person per year (66). The cost for tobacco control, including both price and non-price measures, was US$0.26 per person per year (66). These figures clearly suggest that a reduction in salt intake is more or at the very least just as cost-effective as tobacco control in terms of reducing cardiovascular disease on its own, the leading cause of death and disability worldwide.

Worldwide action on salt

In most developed countries, 80% of salt consumed is added to foods at the stage of manufacturing (73), and the consumers have no say over how much salt is added. Therefore, to achieve a reduction in population salt intake, it is imperative that the food industry make a gradual and sustained reduction in the amount of salt they add to all foods. Several countries, e.g. Finland and the UK, have successfully carried out salt reduction programmes, and salt intake has fallen.

Finland was one of the first countries to initiate a systematic approach to reduce salt intake, in the late 1970s, through mass media-campaigns, co-operation with the food industry, and implementing salt labelling legislation (74–76). This has led to a significant reduction in the average salt intake of the Finnish population (74,76) from ≈14 g/d in 1972 to less than 9 g/d in 2002 (74). The reduction in salt intake was accompanied by a fall of over 10 mmHg in both systolic and diastolic BP, a pronounced decrease of 75%–80% in both stroke and coronary heart disease mortality, and a remarkable increase of 5–6 years in life expectancy (74). The reduction in salt intake was a major contributory factor for these results, particularly the fall in BP as both body mass index and alcohol consumption had increased during that period. An increase in potassium intake via the use of reduced-sodium, potassium- and magnesium-enriched salt, an increased consumption of fruit and vegetables, a reduction in fat intake, and a decrease in smoking rate in men also played an important part in the fall in cardiovascular disease.

The UK has successfully developed a programme of voluntary salt reduction in collaboration with the food industry. In 1996, 22 experts on salt and BP set up an action group—CASH (Consensus Action on Salt and Health)—following the government's rejection of the 1994 COMA (the Committee on Medical Aspects of Food and Nutrition Policy) panel's recommendation to reduce salt intake (77,78). CASH has waged a high-profile campaign to persuade food manufacturers and suppliers to reduce, universally and gradually, the salt content of processed foods, educate the public in becoming more salt-aware in terms of understanding the impact of salt on their health, and translate the evidence into public health policy. CASH persuaded the UK Department of Health to change its stance on salt, finally resulting in the Chief Medical Officer endorsing the original recommendations of the COMA report to reduce salt intake to less than 6 g/d in adults, and also ensured that the UK Food Standards Agency (FSA) took on the task of reducing salt intake.

A nationwide strategy to reduce salt intake has been developed based on the UK's average salt intake of 9.5 g/d (79) as measured by 24-h urinary sodium (Table II). In order to reach the target of 6 g, a total reduction of 3.5 g (i.e. 40%) is needed. Therefore, the food industry, who contribute approximately 80% of the salt in the UK diet, need to reduce the amount of salt added to foods from 7.6 to 4.6 g (40% reduction) and the public need to reduce the amount of salt they add to foods themselves from 1.4 to 0.9 g (40% reduction). The aim is to implement a step-wise reduction in salt added to foods, i.e. 10% to 20% reduction and repeated at 1–2 year intervals. Such reductions are not detectable by human salt taste receptors (80).

Table II. UK strategy for reducing salt.

Salt intake
Source	g/d	Reduction needed	Target intake (g/d)
Table/cooking (15%)	1.4 g	40% reduction	0.9 g
Natural (5%)	0.5 g	No reduction	0.5 g
Food industry (80%)	7.6 g	40% reduction	4.6 g
	Total: 9.5 g		Target: 6.0 g

In 2006, the FSA set target levels of salt for 80 food categories that the food industry needed to achieve within a certain time period, and these targets were revised down in 2009 to ensure that salt intake will reach the target of 6 g/d by 2014 (81).

Following the success of the UK campaign group (CASH), a world action group—WASH (World Action on Salt and Health)—was established in 2005 (82). The aim of WASH is to set up similar groups modelled on CASH, suited to each individual country to reduce salt intake with an appropriate strategy relevant to the needs of that particular country, and to stimulate actions from the government and/or department of health, the food industry, media, and public. WASH is supported by more than 430 members from 81 countries.

WASH works to reduce salt in the diet worldwide by exerting pressure on multinational food companies to reduce the salt content of their products. In 2009, WASH and the international WASH members conducted a survey of over 260 branded products from KFC, McDonalds, Kellogg's, Nestle, Burger King, and Subway in different countries and revealed huge variations in salt content in global brands unrelated to local traditional taste preferences. Not one product surveyed had the same salt content around the world, and some displayed huge differences from one country to another. For instance, Kellogg's All Bran contained 2.15 g of salt per 100 g in Canada, but only 0.65 g of salt per 100 g just over the border in the US, less than a third of the Canadian level (82). This illustrates once again how easy it would be for the food industry to reduce the amount of salt they add to foods, particularly as they could do this straightaway to their branded products. Pressure from campaigns such as this has resulted in several large multinational manufacturers pledging to reduce the amount of salt added to foods across the world.

WASH members in each country are encouraged to set up their own country division of WASH to work together on a local level to lower salt intake specifically in their own population. For example, in 2007 an Australian Division of World Action on Salt and Health (AWASH) was established (83). AWASH has launched a national campaign to lower the salt intake of the Australian population to 6 g/d by 2012.

Many developed countries, e.g. Canada, the US, Portugal, Ireland, New Zealand, France, Italy, Holland, Belgium, Switzerland, Sweden, Denmark, Slovenia, Bulgaria, Croatia, Serbia, and Barbados, are stepping up their activities to reduce salt intake (84,85). The WHO is starting salt reduction strategies through its regional directorates (86). The European Union is also following suit, and 11 countries have signed up to make a 16% reduction in salt intake over 4 years. In February 2010, the Pan American Health Organization (PAHO)/WHO Regional Expert Group on Cardiovascular Disease Prevention through Dietary Salt Reduction (87) produced a policy statement outlining the recommendations for a population-based approach to reduce dietary salt intake in the Americas. The Policy Statement provides countries with a road map for concerted actions by governments, non-governmental organizations, and the food industry.

South Africa has recently set a target to reduce salt intake to less than 5 g/d by 2020. This reduction will be achieved by regulation of the food industry. Several other developing countries, e.g. China, Pakistan, Bangladesh, Nepal, Cuba, Kenya, and Ghana, have set up action groups and launched national salt reduction initiatives. However, many developing countries have not developed dietary guidelines or strategies to reduce salt intake. It is important that each country determines what its salt intake is and where the major sources of salt are in the diet, and then implements a strategic approach to lowering salt intake in the population to the target level (88). In developing countries the major sources of salt consumption are additions during cooking and in sauces (e.g. soy sauce), spice mixes, seasonings, pickles, etc., rather than pre-packaged prepared foods. Public health campaigns are needed to encourage people to use less salt in their own food preparations.

In many developing countries, more and more processed foods are being consumed as their diets are becoming Westernized. The food industry in these countries is poorly regulated with very little or no food content labelling, making informed eating almost impossible. Therefore, these countries need a combined policy of getting the public to use less salt at home and getting the food industry to reduce the amount of salt added to foods and to adopt a clear labelling system such as the sign-post labelling system (89). At the same time, developing countries need to ensure that all imported food products are low in salt.

Conclusions

The totality of evidence, including epidemiological studies, animal studies, randomized trials, and outcome studies, shows the substantial benefits in reducing the average intake of salt (3,35,36,44,90). The WHO has recommended salt reduction as one of the top three priority actions to tackle the global non-communicable disease crisis (91,92). Many developed countries are now adopting a policy of reducing salt intake, firstly by persuading the food industry to reformulate food with less salt, as is occurring successfully in the UK (71) and Finland (74), and also encouraging people to use less salt in their own cooking and at the table. The major challenge now is to spread this to all other countries, particularly developing countries where often salt intake is high and ≈80% of the global BP-related disease burden occurs (93). All countries should adopt a coherent and workable strategy to reduce salt intake. A recently published paper has provided a simple and very useful guide on how to establish and implement national salt reduction programmes (88). A reduction in population salt intake will have major beneficial effects on health along with major cost savings in all countries around the world.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.