Skip to main content

Thank you for visiting You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

A comprehensive review on salt and health and current experience of worldwide salt reduction programmes


Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. Raised blood pressure (BP), cholesterol and smoking, are the major risk factors. Among these, raised BP is the most important cause, accounting for 62% of strokes and 49% of coronary heart disease. Importantly, the risk is throughout the range of BP, starting at systolic 115 mm Hg. There is strong evidence that our current consumption of salt is the major factor increasing BP and thereby CVD. Furthermore, a high salt diet may have direct harmful effects independent of its effect on BP, for example, increasing the risk of stroke, left ventricular hypertrophy and renal disease. Increasing evidence also suggests that salt intake is related to obesity through soft drink consumption, associated with renal stones and osteoporosis and is probably a major cause of stomach cancer. In most developed countries, a reduction in salt intake can be achieved by a gradual and sustained reduction in the amount of salt added to food by the food industry. In other countries where most of the salt consumed comes from salt added during cooking or from sauces, a public health campaign is needed to encourage consumers to use less salt. Several countries have already reduced salt intake, for example, Japan (1960–1970), Finland (1975 onwards) and now the United Kingdom. The challenge is to spread this out to all other countries. A modest reduction in population salt intake worldwide will result in a major improvement in public health.


For several million years the ancestors of humans, like all other mammals, ate a diet that contained less than 0.25 g of salt per day. About 5000 years ago, the Chinese discovered that salt could be used to preserve food. Salt then became of great economic importance as it was possible to preserve food during the winter and allowed the development of settled communities. Salt was the most taxed and traded commodity in the world, with intake reaching a peak around the 1870s. However, with the invention of the deep freezer and the refrigerator salt was no longer required as a preservative. Salt intake had been declining, but with the recent large increase in consumption of highly salted processed food, salt intake is now increasing towards levels similar to those of the 1870s, and is approximately 9-12 g/day (that is, 50 times more than our evolutionary salt intake) in most countries in the world.1, 2

These changes in salt intake present a major challenge to the kidneys to excrete these large amounts of salt. The consequence is that the high salt intake causes a rise in blood pressure (BP),1, 3, 4 thereby increasing the risk of cardiovascular disease (CVD — strokes, heart attacks and heart failure)5, 6 and renal disease.7, 8, 9 Furthermore, a high salt intake may have direct harmful effects, for example, increasing the risk of stroke,10, 11 left ventricular hypertrophy,12 progression of renal disease and proteinuria,7 independent of but additive to the effect of salt on blood pressure. There is also increasing evidence that salt intake is indirectly related to obesity through soft drink consumption,13, 14 associated with an increased risk of renal stones and osteoporosis,15 and is probably a major cause of stomach cancer.16

In this article, we review the evidence for the harmful effects of a high salt intake and the beneficial effects of reducing salt consumption. Additionally, we provide an update on the current experience of worldwide salt reduction programmes, which have been successfully carried out in several countries and a reduction in salt intake has been achieved in these countries.

Literature search

On the basis of the two search strategies developed earlier for meta-analyses on salt and BP in adults17 and children,18 we updated the search for electronic database—MEDLINE, EMBASE and the Cochrane Library. Furthermore, we reviewed the reference list of original and review articles to search for more studies.

Raised BP: the major cause of death in the world

In the late nineteenth century, life assurance and mortgage companies were the first to realize that the higher the BP, the greater the chances of dying at an earlier age. Extensive epidemiological work and treatment trials have subsequently confirmed this finding. A recent systematic analysis of population health data shows that raised BP is the biggest cause of death and the second biggest cause of disability coming after malnutrition in children worldwide.19

The damage that raised BP does, is mainly through its effect on CVD, which is the major cause of deaths worldwide. It has been shown that raised BP, raised cholesterol and smoking account for over 80% of CVD.20 However, raised BP is the single most important cause, responsible for 62% of strokes and 49% of coronary heart disease (CHD).21 Importantly, there is a continuous graded relationship between BP and CVD, beginning at 115/75 mm Hg.22 Therefore, for most countries in the world, over 80% of all adults are at risk of CVD from their BP. In addition, although the risk of CVD increases progressively with increasing BP, the greatest number of CVD deaths attributable to BP occurs in the upper range of the usual BP (that is, BP around 130/80 mm Hg). This is because there are so many individuals having BP around this level in the population,23 that is, a level which would not currently be treated with drugs. Therefore, a population-based approach through diet and lifestyle, for example, a reduction in salt intake, aimed at achieving a downward shift in the distribution of BP in the whole population, even by a small amount, will have a large impact on reducing the appalling burden of CVD.

Underlying factors that increase BP

Evidence suggests that obesity coupled with a lack of exercise is an important factor involved in the development of high BP. However, there is much stronger evidence that salt intake is related to the development of hypertension, and in particular the rise in BP with age,1 and that fruit and vegetables through an increase in potassium intake have the opposite effect and may, in certain circumstances, partially offset the effects of a high salt intake.24, 25, 26 Excess alcohol intake is related to BP, but the effect appears to be transient and there is debate as to whether excess alcohol consumption causes a more sustained increase in BP. Other dietary factors, for example, calcium, magnesium, fat and protein intake, have also been studied but so far the results are inconsistent.

Evidence that relates salt to BP

A large number of studies have been conducted, all of which support the concept that salt intake is the major factor increasing BP in the population. The diversity and strength of the evidence is much greater than other lifestyle factors, for example, overweight, low consumption of fruit and vegetables and lack of physical exercise.

Animal studies

Numerous studies in rat, dog, chicken, rabbit, baboon and chimpanzee have all shown that salt intake plays an important role in regulating BP.27, 28 Furthermore, in all forms of experimental hypertension, whatever the animal model, a high salt intake is essential for BP to rise. A study in chimpanzees (98.8% genetic homology with man) demonstrates that a gradual increase in salt intake from 0.5 g/day which is close to humans’ evolutionary intake, to 10–15 g/day which is similar to our current salt intake, causes a progressive rise in BP (Figure 1).27

Figure 1

Blood pressure in chimpanzees who either continued on their usual diet (0.5g/day of salt) or were given an increased salt intake (10-15g/day). At the end of the 20-month study, the salt supplements were stopped and blood pressure declined to that of the control group. Adapted from Denton et al.27

Human genetic studies

There are several very rare genetic causes of high BP. All of these result in a reduction in the kidney's ability to excrete salt, and thereby cause high BP.29, 30 The raised BP is considerably aggravated if salt is consumed. Rare genetic causes of low BP have also been described. These result in the kidney being unable to hold on to salt normally, thereby causing low BP. These forms of low BP are ameliorated by a high salt intake. Overall, these studies clearly indicate the importance of salt intake in regulating BP in humans.

Epidemiological studies

There are a number of studies in undeveloped societies that do not or did not have access to salt. These societies have lower BP compared with developed societies and there is no rise in BP with age. Although there may be other factors that also contribute to the lower BP, several studies have clearly demonstrated the profound importance of salt intake. For instance, a study in the Pacific Islands where one undeveloped community used seawater in their food and the other did not, showed that the community using seawater had higher BP.31 Another study of two rural communities in Nigeria, one of which had access to salt from a salt lake and the other did not, showed differences in salt intake and differences in BP, and yet in all other aspects of lifestyle and diet the two communities were similar.32 The Qash’qai, an undeveloped tribe living in Iran who had access to salt deposits on the ground, developed high BP and a rise in BP with age similar to that which occurred in western communities, but in all aspects lived a lifestyle similar to undeveloped communities who did not have access to salt.33

In spite of this evidence, it was felt necessary to set up a large international study on salt and BP (INTERSALT)1 using a standardized method for measuring BP and 24-h urinary sodium. The intention was to study communities with a wide range of salt intake from 0.5 to 25 g/day. However, among the 52 communities recruited into the study, only four had a low salt intake (that is, 3 g/day or less) and the majority lay between 6 and 12 g/day and none had the high salt intake as originally envisaged. Nevertheless, the study demonstrated a significant positive relationship between salt intake (as judged by 24-h urinary sodium) and BP. There was also a highly significant positive relationship between salt intake and the increase in BP with age (Figure 2). It was estimated that an increase of 6 g/day in salt intake over 30 years would lead to an increase in systolic BP by 9 mm Hg.1

Figure 2

Relationship between salt intake and the slope of the rise in systolic blood pressure with age in 52 centres in the INTERSALT study. Adapted from Intersalt Cooperative Research group.1

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 less salt were excluded, there was no overall relationship remaining between salt intake and BP in the 48 communities. Subsequently, the Salt Institute published a paper criticizing the statistics of the study. 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.1, 34, 35

More recent epidemiological studies, for example, the INTERMAP study (International study of macro- and micro-nutrients and BP),36 and the EPIC-Norfolk study (the Norfolk Cohort of the European Prospective Investigation into Cancer),37 have lent further support for the important role of salt in determining the levels of BP in the population.

Migration studies

A number of studies have shown that migration from isolated low-salt societies to an urban environment with an increased salt intake is associated with a rise in BP.38, 39 For example, a well-controlled migration study of a rural tribe in Kenya showed that on migration to an urban environment, there was an increase in salt intake and a reduction in potassium intake, and BP rose compared with those in a similar control group who remained in the rural environment.39

Population-based intervention studies

Several population-based intervention studies have been carried out.40, 41, 42, 43 Some of the studies failed to achieve a reduction in salt intake, it is therefore not surprising that there was no change in BP in such studies.42, 43 However, a number of studies where salt intake was successfully decreased have demonstrated a reduction of BP in the population. The most successful intervention study is the one conducted in two similar villages in Portugal,40 which achieved a difference of approximately 50% in salt intake between the two villages. After 2 years’ intervention, there was a difference of 13/6 mm Hg in BP between the two villages (Figure 3). A recent randomized community-based intervention trial was carried out in 550 individuals in two rural villages in north-eastern Japan. The study demonstrated that dietary counselling for 1 year reduced salt intake by 2.3 g/day as measured by 24-h urinary sodium and this was associated with a decrease of 3.1 mm Hg in systolic BP.44

Figure 3

Blood pressure changes with time in two Portuguese villages, one of which had salt intake reduced, the other had similar measurements of blood pressure but no advice on diet. Note the significant differences in blood pressure at 1 year and continuing differences at 2 years. Adapted from Forte et al.40

Treatment trials

Ambard and Beaujard, in 1904, were the first to show that a large reduction in salt intake lowered blood pressure. These results were confirmed over the next 30 years by several workers, but it was not until Kempner resuscitated the idea of severe salt restriction that it became widely used in the treatment of hypertension.45 More recently, randomized trials have studied the effects of more modest reductions in salt intake, that is, from the current intake of approximately 9–12 g/day to around 5–6 g/day, and have shown that the fall in BP was equivalent to single drug therapy in hypertensive individuals46 and there was also a significant fall in BP in those with normal BP.

Several meta-analyses of salt reduction trials have been performed.47, 48, 49, 50, 51, 52 In two meta-analyses,48, 50 it was claimed that salt reduction had very little effect on BP in individuals with normal BP and a reduction in population salt intake was not warranted. However, these two meta-analyses are flawed. Both included trials of very short duration with many comparing the effects of acute salt loading to abrupt and severe salt restriction for only a few days. It is known that such acute changes in salt intake increases sympathetic activity, plasma renin activity and angiotensin II,53 which would counteract the effects on BP. Furthermore, most BP-lowering drugs do not exert their maximal effect within a few days; this is particularly true with diuretics which are likely to work by a similar mechanism to that of salt reduction. It is, therefore, inappropriate to include the acute salt restriction trials in a meta-analysis that attempts to apply them to public health recommendations for a longer-term modest reduction in salt intake. A recent meta-analysis by Hooper et al.52 is an important attempt to look at whether salt reduction 6 months causes a fall in BP. However, most trials included in this meta-analysis only achieved a very small reduction in salt intake. It is, therefore, not surprising that there was only a small, but still significant fall in BP. A more recent meta-analysis of randomized trials of one month or longer, demonstrated that a modest reduction in salt intake caused significant and, from a population viewpoint, important falls in BP in both hypertensive and normotensive individuals.17 Furthermore, there was a dose–response to salt reduction. A reduction of 6 g/day would lower BP by 7/4 mm Hg in hypertensives and 4/2 mm Hg in normotensives (Figure 4).17

Figure 4

Relationship between the reduction in 24-h urinary sodium and the change in blood pressure in a meta-analysis of modest salt reduction trials.17 The open circles represent normotensives and the solid circles represent hypertensives. The slope is weighted by the inverse of the variance of the net change in blood pressure. The size of the circle is in proportion to the weight of the trial.

Two well-controlled trials have studied three salt intakes (that is, 12, 6 and 3 g/day in one trial and 8, 6 and 4 g/day in the other), each for 4 weeks.54, 55 Both showed a clear dose–response, that is, the lower the salt intake achieved, the lower the BP.

From the dose–response relationship found in randomized trials, it is clear that the current recommendations to reduce salt from 9–12 to 5–6 g/day will have a major effect on BP, but are not ideal. A further reduction to 3 g/day will have a much greater effect.

A reduction in salt intake is additive to antihypertensive drug treatments56 and also additive to other non-pharmacological treatments for BP.55, 57 For instance, the DASH (Dietary Approaches to Stop Hypertension)-Sodium trial,55 a well-controlled feeding trial, studied three levels of salt intake (8, 6 and 4 g/day) on two different diets, that is, the normal American diet and the DASH diet, which is rich in fruits, vegetables and low-fat dairy products. The study demonstrated that a reduction in salt intake lowered BP both on the normal American diet and on the DASH diet. The combination of a low salt and the DASH diet had a greater effect on BP than either intervention alone, though the combined effects were not as great as the simple addition of each separate intervention (Figure 5).

Figure 5

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 (that is, control diet) and on DASH diet. Redrawn from Sacks et al.55

It has been shown that there is a variation in BP response to a reduction in salt intake, that is, for a given reduction in salt intake, the falls in BP are larger in individuals of African origin,55, 58 in older participants,51, 59 and in those with raised BP.17 These larger falls in BP are, at least in part, because of the lower levels of plasma renin activity and, thereby, angiotensin II, as well as the less responsiveness of the renin–angiotensin system in these individuals.53, 58, 60

Evidence that relates salt to cardiovascular disease

A reduction in salt intake lowers BP, and as raised BP throughout the range is a major cause of CVD, this would be predicted to reduce CVD. On the basis of the falls in BP from a meta-analysis of randomized salt reduction trials,17 we estimated that a reduction of 6 g/day in salt intake would reduce strokes by 24% and CHD by 18%. This would prevent approximately 35 000 stroke and CHD deaths a year in the United Kingdom61 and approximately 2.5 million deaths worldwide.

A reduction in salt intake may have other beneficial effects on the cardiovascular system,62 which may be independent of and additive to its effect on BP, for example, a direct effect on stroke10 and left ventricular hypertrophy.12 Therefore, the total effect of salt reduction on cardiovascular outcomes may be larger than those estimated from BP falls alone.

Population studies

In the late 1950s deaths from stroke in Japan were among the highest in the world, and it became apparent that certain regions, particularly the north, had a high salt consumption. It was found that the numbers of strokes in different parts of Japan were directly related to the amount of salt consumed. The Japanese Government initiated a campaign to reduce salt intake. Over the following decade salt intake was reduced from an average of 13.5 to 12.1 g/day. However, in the north of Japan salt intake fell from 18 to 14 g/day. Paralleling this reduction in salt intake, there was a fall in BP both in adults and children, and an 80% reduction in stroke mortality63 despite large increases in population fat intake, cigarette smoking, alcohol consumption and an increase in body mass index. It would appear that the Western influence which was rapidly overtaking Japan had little effect on BP, provided salt intake was reduced, and overall the reduction in salt intake appeared to be associated with large falls in deaths from stroke.

Since the 1970s, Finland has had the aim to reduce salt intake in the whole population.64, 65 This has been conducted through a collaboration with the food industry to develop reduced-salt food products and raise the general awareness among consumers of the harmful effects of salt on health. Over the following 30 years, salt intake has been reduced by one-third. This was accompanied by a fall of over 10 mm Hg in both systolic and diastolic BP, a pronounced decrease of 75–80% in both stroke and CHD mortality, and a remarkable increase of 5–6 years in life expectancy.64 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 have increased during that period. An increase in potassium intake through 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 a part in the fall in CVD.

Prospective cohort studies

Eleven prospective cohort studies have looked at the relationship between salt intake and cardiovascular outcomes.6, 11, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75 Among these studies, seven used dietary assessment methods, one used overnight urinary sodium and three used 24-h urinary sodium to estimate dietary salt intake. The dietary methods, for example, 24-h dietary recall, have been shown to be unreliable in estimating a person's salt consumption, particularly as no account is taken of discretionary salt. Many of these prospective studies had baseline salt intake measured in the 1970s, a time when discretionary salt intake would have contributed substantially to salt intake. These dietary assessment methods have been severely criticized previously. For instance, Karppanen and Mervalaala76 pointed out that, in NHANES-I follow-up study, many women in the lowest quartile of salt intake who had a calorie intake near starvation level, had survived for 20 years and they actually weighed 4 kg more than those in the highest quartile of salt intake who apparently also had a much higher calorie intake. Owing to the methodological flaws, the results from these studies should be interpreted with great caution.

Twenty-four-hour urinary sodium is the most accurate method to measure salt intake. Among the 11 prospective studies, three had 24-h urinary sodium measured. However, in the NY Worksite Study,67 24-h urinary sodium was measured after all hypertensive individuals had their salt intake restricted for 5 days and no measurement was made on the participants’ usual diet. Furthermore, analysis of 24-h urinary data revealed severe methodological problems as individuals in the lowest quartile of salt intake had a much lower 24-h urinary creatinine77 indicating incomplete collection of 24-h urine. The results from this study therefore cannot be used to look at the effects of salt reduction.

The Scottish Heart Health Study,69 which enroled a random sample of 11 629 individuals aged 40–59 years, had 24-h urinary sodium measured while on individuals’ usual diet. The follow-up data showed that a higher salt intake was associated with a higher risk of all coronary events in women, but the association was not significant in men. Another prospective cohort study6 which measured 24-h urinary sodium on usual salt intake in a random sample of 2436 Finnish men and women aged 25–64 years, showed that a higher salt intake was significantly associated with a higher risk of death from CHD, CVD and all causes. An increase of 6 g/day in salt intake was related to an increase of 56% in CHD deaths, 36% in CVD deaths and 22% in all deaths (Figure 6).6

Figure 6

The hazard ratios for coronary heart disease (CHD), cardiovascular disease (CVD) and all-cause mortality associated with a 6 g/day increase in salt intake as judged by 24-h urinary sodium excretion. Adapted from Tuomilehto et al.6

Outcome trials

Cook et al.5 reported the long-term effects of salt reduction on CVD in individuals participating in two large randomized trials, the Trial of Hypertension Prevention (TOHP) I and II. Over 3000 participants with an average baseline blood pressure of 127/85 mm Hg were randomized to a reduced-salt group (for 18 months in TOHP I and 36–48 months in TOHP II) or to a control group. Compared with the control group, individuals in the intervention group reduced their salt intake by 25–30% from an average of approximately 10 g/day in the original TOHP studies. These reductions in salt intake resulted in a fall in BP of 1.7/0.9 mm Hg at 18 months (TOHP I) and 1.2/0.7 mm Hg at 36 months (TOHP II). After the original trials completed, participants were not given further dietary advice. A follow-up study at 10–15 years post trial showed that individuals who were originally allocated to the reduced-salt group had a 25% lower incidence of cardiovascular events after adjusting for confounding factors (Figure 7).5 Another outcome trial of over 2.5 years in elderly Taiwanese veterans (N=1981), demonstrated that switching from the usual salt to potassium-enriched salt (49% sodium chloride, 49% potassium chloride, 2% other additives) with a subsequent reduction of 17% in salt intake and an increase of 76% in potassium intake as measured by urinary sodium/creatinine and potassium/creatinine ratio, resulted in a 40% decrease in CVD mortality.78

Figure 7

Cumulative incidence of cardiovascular disease (CVD) by salt intervention group in the Trial of Hypertension Prevention (TOHP) I and II, adjusted for age, sex and clinic. Adapted from Cook et al.5

Other adverse effects of salt

Much of the focus on salt has been its effect on BP. There is now increasing evidence that salt has other deleterious effects on health, independent of and sometimes additive to its effect on BP.

Salt and water retention

When humans go from a low to a high salt intake, there is retention of salt and thereby water, and this expands the extracellular volume. This increase in extracellular volume is a trigger for various compensatory mechanisms to allow an increase in urinary salt excretion but at the expense of continued retention of salt and water. Approximately 1.5 l of extracellular fluid is retained and this continues as long as a higher salt intake is consumed. This increase in extracellular fluid exacerbates all forms of salt and water retention, for example, heart failure79 and is a major cause of oedema in women, aggravating both cyclical and idiopathic oedema.80

Direct effect on stroke

Experimental studies in animals81 and epidemiological studies in humans10, 11, 82 have shown that a high salt diet may have a direct effect on stroke, independent of and additive to its effect on BP. Perry and Beevers performed an ecological analysis of the relationship between urinary sodium excretion (data from INTERSALT study) and stroke mortality in Western Europe. They found a significant positive correlation between 24-h urinary sodium excretion and stroke mortality (Figure 8),10 and this relationship was much stronger than that found when urinary sodium was plotted against BP.

Figure 8

Relationship between salt intake and deaths from strokes in 12 European countries. Adapted from Perry and Beevers.10

Direct effect on left ventricular mass

Left ventricular hypertrophy is an important independent predictor of cardiovascular morbidity and mortality and is related to raised BP.83, 84 Several cross-sectional studies have shown a positive correlation between 24-h urinary sodium excretion and left ventricular mass in both hypertensives and normotensives, which is independent of BP12, 85, 86 (Figure 9). A reduction in salt intake has been shown to decrease left ventricular mass in patients with essential hypertension.87, 88, 89

Figure 9

Relationship between salt intake and left ventricular mass in individuals with systolic blood pressure >121 mm Hg. Adapted from Kupari et al.12

Cancer of the stomach

An ecological analysis showed a significant direct association between salt intake (as judged by 24-h urinary sodium excretion) and deaths from stomach cancer among 39 populations from 24 countries90 (Figure 10). A recent study from Japan confirms a close relationship between salt intake and stomach cancer within a single country.16 A number of studies have shown that H-pylori infection, which underlies the cause of both duodenal and gastric ulcers and stomach cancer, is also closely associated with salt intake in different countries in both women and men.91, 92, 93 Foods that contain high concentrations of salt are irritating to the delicate lining of the stomach. It is possible that this makes H-pylori infection more likely or more severe and that the H-pylori infection then leads to stomach cancer. A modest reduction in salt intake may reduce H-pylori infection and therefore lead to stomach cancer prevention.

Figure 10

Relationship between salt intake and deaths from stomach cancer. Adapted from Joossens et al.90

Proteinuria and renal disease

Increasing salt intake increases urinary protein excretion and markedly increases the rate of deterioration of renal function in experimental forms of renal disease. Studies in humans have shown that salt intake relates, on a population basis, to the amount of protein or albumin excretion94, 95 which is an important risk factor for the development of kidney disease and CVD.96 A recent randomized double-blind trial in 40 hypertensive blacks demonstrates that a modest reduction in salt intake from approximately 10 to 5 g/day, as currently recommended, reduces urinary protein excretion significantly9 (Figure 11). The effect of salt reduction on urinary protein is more marked when combined with an ACE inhibitor.8 Therefore, individuals with kidney disease should restrict their salt intake because in nearly all forms of kidney disease the kidney retains sodium and water in the body. The increase in sodium retention causes an increase in BP and makes the proteinuria worse and causes a further deterioration in renal function.

Figure 11

Change in urinary sodium and protein excretion with a modest reduction in salt intake from approximately 10 to 5 g/day in 40 hypertensive blacks.

Patients who are on dialysis need to restrict their salt intake as this reduces the amount of fluid that they drink between dialyses. This particularly applies to haemodialysis patients, where BP is a major problem and studies have clearly shown that if they restrict salt intake there is less gain in weight between dialyses, less fluctuation in BP and BP is easier to control.

In patients with diabetes, a reduction in salt intake has been shown to increase the effectiveness of angiotensin receptor blocker (ARB) on reducing proteinuria.97

Renal stones and osteoporosis

Salt intake is one of the major dietary determinants of urinary calcium excretion. Both epidemiological studies and randomized trials show that a reduction in salt intake causes a decrease in urinary calcium excretion.15, 59, 98, 99 As calcium is the main component of most urinary stones, salt intake is therefore an important cause of renal stones. Until recently, it was assumed that when salt intake was increased, the increase in calcium excretion was compensated for by an increase in intestinal calcium absorption. There is now evidence to suggest that, when salt intake is increased, there is a negative calcium balance with stimulation of mechanisms not only to increase intestinal absorption of calcium, but also to mobilize calcium from bone. A study in post-menopausal women showed that the loss of hip bone density over 2 years was related to the 24-h urinary sodium excretion at entry to the study and was as strong as that relating to calcium intake.100 Other studies have shown that reducing salt intake causes a positive calcium balance, and it is likely that reducing salt intake would slow down the loss of calcium from bone that occurs as we grow older.


Although it is not thought that a high salt intake is a cause of asthma, epidemiological evidence suggests that the severity of asthma may relate to salt intake in different countries.101 This is supported by trial data, for example, a double-blind study of modest salt restriction showed a reduction in the severity of asthma attacks and a reduction in the use of medication and an improvement in the measurement of airways resistance.102 The changes seen were only significant in men. Another double-blind study illustrates the mechanism whereby a higher salt intake exacerbates asthma.103

A review of both epidemiological and clinical evidence has concluded that the adoption of a low salt diet for a period of 2–5 weeks may improve lung function and decrease bronchial reactivity in adults with asthma. Similarly, a low salt diet followed for 1–2 weeks also decreased symptoms in people who have exercise-induced asthma.104 However, a recent double-blind trial showed that a lower salt diet as an adjunctive therapy to normal treatment had no additional therapeutic benefit in adults with asthma.105 Nevertheless, a recent population-based study in children aged 6–7 years demonstrated that adding salt to food was strongly and independently associated with an increased risk of respiratory symptoms, that is, wheeze and asthma.106


A high salt intake has been suggested as an indirect cause of obesity, through the effect it has on fluid intake. A carefully controlled metabolic study in adult humans showed that a reduction in salt intake caused a significant decrease in fluid consumption.13 From this experimental study, it was estimated that a decrease in salt from the current intake of approximately 10 g/day to the WHO recommended level of 5 g/day would reduce total fluid consumption by about 350 ml/day. A study in 10 074 free living individuals across the world showed almost an identical relationship between usual salt and fluid intake.13 It is known that a considerable proportion of fluid intake is in the form of soft drinks and that an increase in soft drink consumption is associated with an increase in body mass index (BMI),107 therefore a reduction in salt intake could play a role in helping to reduce obesity.

Karppanen and Mervaala64 analysed the data on the sales of salt and carbonated beverages in the USA between 1985 and 2005, and showed a very close link between the two. They were also in parallel with the trend of prevalence of obesity.

A recent analysis of the dataset of the National Diet and Nutrition Survey for young people in Great Britain showed that, in children aged 4–18 years, there was a significant association between salt intake and total fluid, as well as sugar-sweetened soft drink consumption after adjusting for potential confounding factors.14 A difference of 1 g/day in salt intake was associated with a difference of 100 and 27 g/day (P<0.001) in total fluid and sugar-sweetened soft drink consumption respectively. These results, in conjunction with other evidence, particularly that from experimental studies where only salt intake was changed,13 demonstrate that salt is an important determinant of fluid and sugar-sweetened soft drink consumption during childhood. If salt intake in children in the United Kingdom was reduced by half (mean decrease: 3 g/day), there would be an average reduction of 2.3 sugar-sweetened soft drinks per week per child. This amounts to a total reduction of approximately 1 billion sugar-sweetened soft drinks per year in the UK alone. Sugar-sweetened soft drink consumption has been shown to be related to childhood obesity by epidemiological studies108 and randomized trials have also demonstrated that a reduction in soft drink consumption leads to a decrease in obesity.109 A lower salt intake could therefore help to reduce childhood obesity through its effect on sugar-sweetened soft drink consumption. This would have beneficial effects on preventing CVD later in life, independent of and additive to the effect of salt reduction on BP.

Salt's effects on plasma renin activity, sympathetic nervous activity, lipids and insulin sensitivity

When salt intake is reduced, there is a physiological stimulation of the renin–angiotensin system and the sympathetic nervous system. These compensatory responses are bigger with sudden large changes in salt intake, and much smaller or minimal with a modest reduction in salt intake for a more prolonged period of time, which is the current public health recommendation on population salt intake. Randomized trials have demonstrated that, with a longer-term modest reduction in salt intake, there is only a small increase in plasma renin activity17 and no detectable change in the sympathetic nervous activity.110

Salt reduction lowers BP in a similar mechanism to that of thiazide diuretics. Both stimulate the renin–angiotensin system and, in the short term, the sympathetic nervous system. But outcome trials have demonstrated that long-term treatment with thiazide diuretics significantly reduces cardiovascular morbidity and mortality in hypertensive individuals.111

An acute and large reduction in salt intake causes a reduction in plasma volume, and thereby a small increase in the concentration of plasma lipids. However, a modest reduction in salt intake does not have such effects. Randomized trials have shown that, with a longer-term modest reduction in salt intake, there is no significant change in total cholesterol, triglyceride, low or high-density lipoprotein cholesterol.17

There have been a number of randomized trials looking at the effects of changing salt intake on glucose tolerance and insulin sensitivity.112, 113 However, most of these trials involved a very large change in salt intake for only a few days, which are irrelevant to the current public health recommendations of modest salt reduction for a long period of time. Randomized trials have shown that a longer-term modest reduction in salt intake had no significant effect on glucose tolerance or insulin sensitivity in hypertensive individuals.114 A prospective study in 932 Finnish men and 1003 women with an average follow-up of 18 years demonstrated that a higher salt intake (measured by 24-h urinary sodium) was associated with an increased risk of type 2 diabetes, independent of potential confounding factors including physical activity, obesity and hypertension.115

Long-term treatment with thiazide diuretics may increase the risk of diabetes.116 This is likely to be because of low serum potassium levels induced by the diuretics.116, 117 Concomitant treatment with potassium supplementation or potassium-sparing diuretics could lessen the glucose intolerance and possibly prevent the development of thiazide-induced diabetes.116 The advantage of modest salt reduction over thiazide diuretics is that salt reduction does not have a significant effect on serum potassium, but has a similar BP-lowering effect in hypertensive individuals as demonstrated by randomized trials.118

Salt in children


A well-controlled double-blind study in just under 500 newborn babies showed that when salt intake was reduced by about 30%, as judged by spot urinary sodium concentrations, there was a progressive difference in systolic BP between babies in the reduced salt and those in the usual salt group.119 At the end of 6 months the babies on the lower salt intake had a 2.1 mm Hg lower systolic BP (P<0.01). The study was discontinued at 6 months. Thirty-five percent of these babies were followed up 15 years later.120 There remained a significant difference in BP, when adjusted for potential confounding factors, between those babies who in the first 6 months of life had had a reduced salt intake compared with those who had not. These results suggest a programming effect of salt intake in early life, which fits with several studies in animals (Figure 12).

Figure 12

Difference in systolic blood pressure in newborn babies, randomized to either a usual salt intake or a reduced salt intake over the first 6 months of life. At 6 months, the study was discontinued, with all participants resuming their usual salt intake. Fifteen years later, a subgroup of those in the study had blood pressure re-measured. Adapted from Hofman et al.119 and Geleijnse et al.120

Children and adolescents

There have been over 20 observational epidemiological studies on salt and BP in children and adolescents.121 Many of these studies did not show a significant association. This is not surprising given the large day-to-day intra-individual variations of salt intake. In addition, many studies had methodological problems, for example, the methods used to assess salt intake were unreliable. Among the observational studies that were methodologically stronger (for example, multiple measurements of salt intake were made, urinary sodium was measured and confounding factors were controlled for), the majority showed a significant positive association between salt intake and BP.121, 122 For instance, in a carefully conducted study where seven consecutive 24-h urines were collected by all participants, Cooper et al.123 demonstrated a significant linear relationship between urinary sodium and systolic BP in 73 children aged 11–14 years, that is, the higher the salt intake, the higher the systolic BP. The relationship remained significant after controlling for age, sex, race, pulse rate, height and body weight.

A recent meta-analysis of 10 salt reduction trials with 966 participants, demonstrated that a modest reduction in salt intake had a significant effect on BP in children and adolescents.18 With a 42% reduction in salt intake for an average duration of 4 weeks, systolic BP was reduced by 1.2 mm Hg (P<0.001) and diastolic by 1.3 mm Hg (P<0.001). These findings are important in view of the fact that BP tracks in children, that is, the higher the BP during childhood, the higher the BP in adulthood.124 A lower salt diet, if continued, may well lessen the subsequent rise in BP with age, which would have major public health implications in terms of preventing the development of hypertension and CVD later in life.

Salt intake, because of the increased consumption of processed foods, is very high in many children. Even in 1984, a study in the United Kingdom where two consecutive 24-h urines were collected in 4- to 5-year-old primary school children showed that the average sodium excretion was 4 g of salt per day.125 If this is expressed for adults on a weight basis, it is equivalent to approximately 15–20 g/day. This was at a time when consumption of processed foods by young children was not high. Since then, salt intake in children in developed countries will have increased because of the increasing consumption of processed foods which now account for approximately 80% of total salt intake. Surveys in the United States of America showed that the proportion of foods that children consumed from restaurants and fast food outlets increased by nearly 300% between 1977 and 1996,126 and it is very likely to have increased even further in more recent years. Snack food consumption showed trends similar to those of fast food consumption. The restaurant foods, fast foods and snacks are generally very high in salt, fat and sugar. It is possible that children from the age of three to four onwards now consume a similar amount of salt as adults.

Cost saving of reducing population salt intake

Several cost-effective analyses have been carried out to assess the health effects and financial cost of reducing population salt intake.127, 128, 129, 130 All of these studies have demonstrated that a reduction in salt intake is very cost-effective. For example, Murray et al.130 showed that non-personal health interventions, including government action to stimulate a reduction in the salt content of processed foods, were cost-effective ways to limit CVD and could avert over 21 million DALYs (disability-adjusted life years) per year worldwide. A study in the Norwegian population documented that a reduction of 6 g/day in population salt intake with a very conservative estimate of 2 mm Hg fall in systolic BP could save costs to individuals and society by US$4.7 million per year.127 It is likely that this has considerably underestimated the true cost savings as randomized trials have shown that the fall in systolic BP with a 6 g/day decrease in salt intake is much greater than that projected in this Norwegian study.61 A study in Canada estimated that a reduction of 4.6 g/day in salt intake would decrease hypertension prevalence by 30% and almost double the treatment and control rate of hypertension, and this would save approximately $430 million per year from drugs, physician visits and laboratory testing directly related to hypertension.128

In a more recent study, Asaria et al.129 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 chronic disease burden in the developing world. 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, plus a sustained mass media campaign aimed to encourage dietary change within households and communities. The cost for implementing such salt reduction programmes was estimated to be US$0.09 per person per year. The cost for tobacco control including both price and non-price measures, was US$0.26 per person per year129 (Figure 13). 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.

Figure 13

Number of cardiovascular disease (CVD) deaths averted and the financial costs associated with implementation of salt reduction and tobacco control in 23 low- and middle-income countries. Adapted from Asaria et al.129

Worldwide actions occurring on salt

Currently there is considerable variation in the amount of action being taken to reduce salt intake in populations around the world. Many, but not all countries have produced their own recommendations about how far salt intake should be reduced. The WHO, after an extensive review of the evidence, has set a worldwide target of a maximum intake for adults of 5 g/day.131 Through its regional directorates, the WHO is starting salt reduction strategies.132 The European Union is also following and 11 countries have signed up to make a 16% reduction in salt intake over the next 4 years.133 Several countries, for example, Finland, and the United Kingdom, have already successfully carried out salt reduction programmes. However, many other countries, particularly developing countries where approximately 80% of global BP-related disease burden occurs,134 have not even developed a salt reduction strategy. It is important that each country in the world determines what its salt intake is and where are the major sources of salt in the diet, and then implements a strategic approach to lowering salt intake in the population to the target level.

United Kingdom

The United Kingdom (UK) is one of the countries leading the way and setting an example for other countries in salt reduction strategies. In 1994, an independent advisory panel, COMA (the Committee on Medical Aspects of Food and Nutrition Policy), appointed by the Government reviewed all of the evidence and recommended that salt intake in adults should be reduced to 6 g/day or less.135 However, the recommendations on salt were rejected as some food companies had threatened to withdraw funding from the political party in power. As a result of the rejection of the salt reduction recommendations by the Chief Medical Officer with no reasons given,136 22 scientific experts on salt and BP in the United Kingdom set up an action group, Consensus Action on Salt and Health, known as CASH137, 138 to reverse this policy decision and to persuade food processors and suppliers to gradually reduce the salt content in food and to educate the public in realizing the dangers of eating too much salt and to avoid highly salted foods.

Since CASH was set up in 1996, it has been very successful in raising the awareness of the importance of salt and, within a few years, persuaded the UK Department of Health to change its stance on salt, finally resulting in the new Chief Medical Officer endorsing the original recommendations of the COMA report to reduce salt intake to less than 6 g/day in adults. Before this endorsement, CASH had already persuaded a major supermarket and several food companies to reduce the amount of salt they added to their foods by 10–15%, an amount that cannot be detected by the human salt taste receptors.139 Two years later, CASH ensured that the newly set up UK Food Standards Agency took on the task of reducing salt intake in the UK, and their independent Scientific Advisory Committee on Nutrition (SACN) again confirmed that there was a very strong scientific case to reduce salt intake in the whole population.140

The UK strategy - a model for other countries

The first step for all countries who want to carry out a salt reduction policy is to measure or estimate salt intake, for example, in the UK, a random sample of the adult population collected 24-h urines and this showed that the average 24-h urinary sodium excretion was 9.5 g/day of salt in 2001. From a knowledge of the dietary intake in the UK, it was then possible to roughly calculate what proportion of this salt intake is added by the consumer, that is, in the form of added salt, stock cubes, sauces, pickles, and so on, and how much is contributed by the food industry as a whole, that is, where the consumer has no control over the amount of salt, for example, in supermarkets, fast food, restaurants and takeaways.

In the UK, it was roughly estimated that 15% of the total 9.5 g of salt consumed (that is, 1.4g) was added either at the table or in the cooking. Approximately 5% was naturally present in the food (that is, 0.6g) and the rest, 80% (that is, 7.5g), was not in the hands of the consumer and was added by the food industry either in processed, canteen, restaurant food, and so on. From these figures it can then be worked out (Figure 14) that if the target in a particular country is 6g, which is the target in the UK, and therefore the reduction in salt intake that is needed is from 9.5 to 6g (that is, 3.5g), which is an approximate 40% reduction. This means that the public would have to reduce the amount of salt they add to foods themselves by 40% and the food industry would need to reduce the amount of salt added to all foods by 40%. It was also estimated in the UK that only 15% of food was eaten outside the home, that is restaurant, canteen, and so on, and therefore the main target in the initial phase of salt reduction should be on foods that were bought in supermarkets. These foods, where salt was added, were split into more than 80 different categories. Targets were set for each food category that the food industry needed to achieve within a certain time period. The aim was to reduce the salt added to food by small amounts, that is 10 to 20% which cannot be detected by human salt taste receptors and, furthermore, cause no technical or safety issues to the food in question. After a 1- to 2-year gap, a further 10 to 20% reduction could be made and this could be followed by a further reduction after a further 1–2 years.

Figure 14

UK strategy for reducing salt.

This strategy has worked successfully in the United Kingdom on a voluntary basis with most processed foods bought in supermarkets having now been reduced by 20 to 30% in the last 3 years. The salt targets for the 80 categories have recently been revised so that they will be lower than the previous ones, to ensure that the 6g target for all adults will be reached by 2012. Having successfully shown that the amount of salt can be reduced in foods bought in supermarkets, this message is now being spread out to restaurants, takeaways, caterers, canteens, prisons, hospitals and fast food outlets, and so forth.

At the same time, this has been backed by a major public health campaign, both by the Food Standards Agency and CASH. As a result, the number of people aware they should be eating no more than 6 g of salt/day had risen from 3% to 34% in just 1 year and over 20 million, that is, approximately one-third of the adult population were saying they were trying to cut down on the amount of salt they ate.141

Clear labelling of the salt content of food is essential, so that consumers can see at a glance how much salt is in any food they purchase. A front of pack signpost labelling system142 has been developed which is being implemented by many supermarkets where there is a colour-coding of Green, Amber and Red for low, medium and high amounts of salt, fat, sugar and calories, as well as the amount of salt per portion and per 100 g and the recommended intake for an adult for the whole day. This type of label is much preferred by consumers to others as they can see at a glance whether a product has a little or a lot of salt. It has already been shown to have a dramatic effect on the purchase of foods, particularly when they are in the Red category.

The UK salt reduction strategy started in 2003/2004 and the adult daily salt intake has already fallen, as documented by a random sample of the population where 24-h urines were collected, from an average of 9.5 g/day to 8.6 g/day by May 2008.143 This may seem a small change, but it was on the back of an earlier increasing salt intake and it marks the beginning of a reversal of an increasing trend that is occurring in most other countries with the greater consumption of processed food.

Salt intake will fall further as increasing reductions in salt added to food are made by the food industry, particularly as new targets are currently being set for over 80 categories of food and it is anticipated, with these new targets, that salt intake will reach the target of an average of 6 g/day by 2012. An important aspect of this policy is that it particularly targets the most disadvantaged in the community as the biggest reductions in salt added to food have been made in the cheapest foods as part of the policy. The amount of salt added to children's food is also being reduced. This means that the salt added to food is being reduced across the board and, therefore, the public does not necessarily need to change the foods they eat but, nevertheless, their salt intake will fall without them necessarily being aware of it. At the same time, consumers, who want to, can avoid the most highly salted products and reduce their salt intake even further.


Finland in the late 1970s was one of the first countries to initiate a systematic approach to decrease salt intake in the population through mass media campaigns, co-operation with the food industry and implementing salt labelling legislation.64, 144 Since the 1980s many food companies have reduced the sodium content of their food products by replacing conventional table salt with a sodium-reduced, potassium- and magnesium-enriched mineral salt known as Pansalt. Furthermore, in the early 1990s, the Ministry of Trade and Industry and the Ministry of Social Affairs and Health, set new salt labelling legislation for all the food categories which made a substantial contribution to the salt intake of the Finnish population. Foods that are high in salt are required to carry a ‘high salt content’ warning and if a food product contains a low level of salt the product is allowed to display a low salt label. These different measures have resulted in a significant reduction in salt intake of the Finnish population, from an average of approximately 12 g/day in 1979 to less than 9 g/day in 2002 as measured by 24-h urinary sodium.65

Other countries

Following the success of the UK campaign group—CASH, a World Action group (WASH) was established in 2005 to encourage action on salt reduction worldwide.145 The aim of the group is to improve the health of populations throughout the world by achieving a gradual reduction in salt intake. WASH, like CASH, works to reduce salt in the diet worldwide by exerting pressure on multi-national food companies to make small but repeated reductions in the amount of salt added to their products. WASH is supported by over 300 international members, who are mainly experts in hypertension. WASH members in each country are being encouraged to set up their own country division of WASH, to work together on a localized 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. They have launched a national campaign to lower the salt intake of the Australian population to 6 g/day by 2012. The main objectives of the campaign known as Drop the Salt! are to lower salt in food by 25%, increase consumer awareness about the benefits of a low salt diet and promote clear labelling of foods that makes the salt content immediately apparent to the consumers.

In Ireland a nutrition committee of the Food Safety Authority of Ireland (FSAI) concluded, in 2005, that the scientific evidence supports a link between salt intake and raised blood pressure.146 Subsequently the FSAI set the goal to reduce salt intake in the population from 10 to 6 g/day. The strategic approach includes consumer awareness efforts, as well as action by the food industry to lower the salt content of their food products, where to-date substantial reductions have been made in the salt content of food.

In Canada the first Chair in Hypertension Prevention and Control was appointed in 2006. The Chair is supported by a number of health-related organizations as well as scientists. Together they will lobby the government and public food sector for policies to reduce the addition of salt to food.147 Already the food industry is lowering salt in foods. For example a number of whole grain bread products have had their salt levels reduced by 25%.

Many other countries are stepping up their activity. In the Netherlands the dietary guidelines were revised in 2006 stating that salt intake should be reduced to 6 g/day.148 The Dutch Consumer Organisation (Consumentenbond) has also initiated a number of activities to raise awareness about the harmful effect of too much salt on health. In addition, both the French Food Standards Agency (AFFSA) and the Swedish Food Standards Agency have now considered the evidence and have a programme in place for reducing the salt content of food in both France and Sweden in a similar way as in the UK.

In the USA there has been consistent advice to reduce salt intake to 6 g/day since the 1980s. For example, in January 2000, a large meeting was organized by the National Heart, Lung and Blood Institute in Washington where all of the evidence on salt was reconsidered. There was representation both from the food industry and salt institute. The conclusion of this meeting was that ‘Americans consume more sodium than they need and a population wide strategy of reducing salt in the food supply is an important public health strategy that can lower BP among populations’.149 More recently in 2007, The American Medical Association (AMA) published a report calling for a major reduction in the salt content of processed and restaurant foods.150 The AMA also pressed the FDA (Food and Drug Administration) to cease the rule that allows salt and its component sodium to be treated as ‘generally recognized as safe’. In a petition to the FDA in 2005, the Center for Science in the Public Interest (CSPI) called for tougher regulations on salt.151 However, despite this, little action has been taken.

Food industry's resistance to reducing the salt content of processed foods

The reasons that the food industry adds large amounts of salt to processed foods is mainly because it makes cheap, unpalatable food edible at no cost. If high salt foods are consistently consumed, the salt taste receptors are suppressed and habituation to highly salted foods occurs, with greater demand for profitable highly salted processed foods. Food manufacturers often argue that the reason for the high salt content of their products is because of consumer taste preferences, that is, individuals prefer these saltier products and if the salt content was lowered it would lead to consumer rejection. However, one very important factor to be considered is that as salt intake falls, the specific salt taste receptors in the mouth become much more sensitive to lower concentrations of salt and this adjustment takes only one or two months.152 This means that lower concentrations of salt then taste as salty as the earlier higher concentrations. It is therefore very unlikely that the lowering of salt concentrations in foods will lead to rejection of the foods. Indeed, all of the evidence suggests that once salt intake is reduced, individuals much prefer food with less salt153 and reject the highly salted foods they ate earlier. Consumer experience in the UK has confirmed this, that is, where salt has been reduced in major brand products, there has been no reduction in sales and no complaints about taste.

Salt has two other important properties—one is in meat products where increasing the salt concentration in conjunction with other water binding chemicals increases the amount of water that can be bound as a gel into the meat product and the weight of the product can be increased by up to 20% with water at no cost. The other important property is that salt is a major determinant of thirst and any reduction in salt intake will reduce fluid consumption with a subsequent reduction in soft drink and mineral water sales (Figure 15).13, 14 Some of the largest snack companies in the world are part of companies selling soft drinks. Salt manufacturers and extractors also have a major interest in the salt used in processed foods as approximately 40% by value of their sales of salt go to the processed food industry. However, in those countries where processed foods are a major source of salt intake, reducing the salt content of processed foods to the lowest possible level is essential. Initially Governments should set voluntary salt reduction targets for each category of food in order to achieve the required reduction in salt intake. However, if these are ignored then statutory regulation to lower salt in food products should be considered. In addition, if a multi-national company lowers the salt content of a product in one country, this should be reflected in all countries where that product is sold. At the moment, there is a very large variation in the amount of salt added to the same branded products in different countries or regions of the world. This variation is entirely random.155 This illustrates once again how easy it would be for the food industry to reduce the amount of salt they add to food, particularly as they could do this straightaway to their branded products with the lowest level in the world.

Figure 15

The commercial importance of salt in processed food.


The evidence that relates dietary nutrients, such as salt, saturated fat, fruit and vegetables, to BP and CVD has to rely on weighing all of the findings from various types of research studies—epidemiology, migration, intervention, treatment trials as well as genetic and animal studies. When all of the evidence is considered, the evidence for salt, particularly when judged against other nutrients, is robust and strong. A reduction in salt from the current intake of 9–12 g/day to the recommended level of 5–6 g/day will have a major effect on BP and CVD, and may have other beneficial effects on health as outlined in this article.

It is vital that all countries adopt a coherent and workable strategy to reduce salt intake in the whole population. In most developed countries approximately 80% of salt comes from processed food,154 and the amount of salt added to food by the food industry must be reduced. In these countries, reducing salt intake is one of the easiest changes in the diet to implement, as it does not require consumers to change their dietary practices, but it requires the food industry to make gradual and sustained reductions in the amount of salt they add to food. In other countries where most of the salt consumed comes from salt either added during cooking or from sauces, a public health campaign is needed to encourage consumers to use less salt, perhaps a combination of both, as in developing countries more and more processed food is being consumed. In several countries salt reduction programmes have already been carried out successfully and salt intake has fallen.64, 143 Other countries should follow these examples and start taking action now. A modest reduction in population salt intake worldwide would result in a major improvement in public health—similar to the provision of clean water and drains in the late nineteenth century in Europe.


  1. 1

    Intersalt Cooperative Research Group. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 h urinary sodium and potassium excretion. BMJ 1988; 297: 319–328.

    Google Scholar 

  2. 2

    Henderson L, Irving K, Gregory J, Bates CJ, Prentice A, Perks J et al. Urinary analytes. National diet & nutrition survey: adults aged 19–64. 2003; 3: 127–136.

  3. 3

    Meneton P, Jeunemaitre X, de Wardener HE, MacGregor GA . Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases. Physiol Rev 2005; 85: 679–715.

    CAS  Google Scholar 

  4. 4

    He FJ, MacGregor GA . Salt, blood pressure and cardiovascular disease. Curr Opin Cardiol 2007; 22: 298–305.

    Google Scholar 

  5. 5

    Cook NR, Cutler JA, Obarzanek E, Buring JE, Rexrode KM, Kumanyika SK et al. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ 2007; 334: 885.

    PubMed  PubMed Central  Google Scholar 

  6. 6

    Tuomilehto J, Jousilahti P, Rastenyte D, Moltchanov V, Tanskanen A, Pietinen P et al. Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. Lancet 2001; 357: 848–851.

    CAS  PubMed  PubMed Central  Google Scholar 

  7. 7

    Cianciaruso B, Bellizzi V, Minutolo R, Tavera A, Capuano A, Conte G et al. Salt intake and renal outcome in patients with progressive renal disease. Miner Electrolyte Metab 1998; 24: 296–301.

    CAS  PubMed  PubMed Central  Google Scholar 

  8. 8

    Heeg JE, de Jong PE, van der Hem GK, de Zeeuw D . Efficacy and variability of the antiproteinuric effect of ACE inhibition by lisinopril. Kidney Int 1989; 36: 272–279.

    CAS  PubMed  PubMed Central  Google Scholar 

  9. 9

    Swift PA, Markandu ND, Sagnella GA, He FJ, MacGregor GA . Modest salt reduction reduces blood pressure and urine protein excretion in black hypertensives: a randomized control trial. Hypertension 2005; 46: 308–312.

    CAS  PubMed  PubMed Central  Google Scholar 

  10. 10

    Perry IJ, Beevers DG . Salt intake and stroke: a possible direct effect. J Hum Hypertens 1992; 6: 23–25.

    CAS  PubMed  PubMed Central  Google Scholar 

  11. 11

    Nagata C, Takatsuka N, Shimizu N, Shimizu H . Sodium intake and risk of death from stroke in Japanese men and women. Stroke 2004; 35: 1543–1547.

    PubMed  PubMed Central  Google Scholar 

  12. 12

    Kupari M, Koskinen P, Virolainen J . Correlates of left ventricular mass in a population sample aged 36–37 years. Focus on lifestyle and salt intake. Circulation 1994; 89: 1041–1050.

    CAS  PubMed  PubMed Central  Google Scholar 

  13. 13

    He FJ, Markandu ND, Sagnella GA, MacGregor GA . Effect of salt intake on renal excretion of water in humans. Hypertension 2001; 38: 317–320.

    CAS  Google Scholar 

  14. 14

    He FJ, Marrero NM, MacGregor GA . Salt intake is related to soft drink consumption in children and adolescents: a link to obesity? Hypertension 2008; 51: 629–634.

    CAS  PubMed  PubMed Central  Google Scholar 

  15. 15

    Cappuccio FP, Kalaitzidis R, Duneclift S, Eastwood JB . Unravelling the links between calcium excretion, salt intake, hypertension, kidney stones and bone metabolism. J Nephrol 2000; 13: 169–177.

    CAS  PubMed  PubMed Central  Google Scholar 

  16. 16

    Tsugane S, Sasazuki S, Kobayashi M, Sasaki S . Salt and salted food intake and subsequent risk of gastric cancer among middle-aged Japanese men and women. Br J Cancer 2004; 90: 128–134.

    CAS  PubMed  PubMed Central  Google Scholar 

  17. 17

    He FJ, MacGregor GA . Effect of modest salt reduction on blood pressure: a meta-analysis of randomized trials. Implications for public health. J Hum Hypertens 2002; 16: 761–770.

    CAS  Google Scholar 

  18. 18

    He FJ, MacGregor GA . Importance of salt in determining blood pressure in children: meta-analysis of controlled trials. Hypertension 2006; 48: 861–869.

    CAS  Google Scholar 

  19. 19

    Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ . Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet 2006; 367: 1747–1757.

    PubMed  PubMed Central  Google Scholar 

  20. 20

    Emberson JR, Whincup PH, Morris RW, Walker M . Re-assessing the contribution of serum total cholesterol, blood pressure and cigarette smoking to the aetiology of coronary heart disease: impact of regression dilution bias. Eur Heart J 2003; 24: 1719–1726.

    CAS  PubMed  PubMed Central  Google Scholar 

  21. 21

    World Health Report 2002. Reducing Risks, Promoting Healthy Life. World Health Organisation: Geneva, Switzerland, 2002. Available at (Accessed June 30, 2006).

  22. 22

    Lewington S, Clarke R, Qizilbash N, Peto R, Collins R . Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet 2002; 360: 1903–1913.

    PubMed  PubMed Central  Google Scholar 

  23. 23

    MacMahon S . Blood pressure and the prevention of stroke. J Hypertens 1996; 14 (Suppl): S39–S46.

    CAS  Google Scholar 

  24. 24

    Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med 1997; 336: 1117–1124.

    CAS  Google Scholar 

  25. 25

    He FJ, MacGregor GA . Fortnightly review: beneficial effects of potassium. BMJ 2001; 323: 497–501.

    CAS  PubMed  PubMed Central  Google Scholar 

  26. 26

    He FJ, Nowson CA, MacGregor GA . Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet 2006; 367: 320–326.

    Google Scholar 

  27. 27

    Denton D, Weisinger R, Mundy NI, Wickings EJ, Dixson A, Moisson P et al. The effect of increased salt intake on blood pressure of chimpanzees. Nat Med 1995; 1: 1009–1016.

    CAS  Google Scholar 

  28. 28

    Elliott P, Walker LL, Little MP, Blair-West JR, Shade RE, Lee DR et al. Change in salt intake affects blood pressure of chimpanzees: implications for human populations. Circulation 2007; 116: 1563–1568.

    CAS  PubMed  PubMed Central  Google Scholar 

  29. 29

    Lifton RP . Molecular genetics of human blood pressure variation. Science 1996; 272: 676–680.

    CAS  PubMed  PubMed Central  Google Scholar 

  30. 30

    Lifton RP, Gharavi AG, Geller DS . Molecular mechanisms of human hypertension. Cell 2001; 104: 545–556.

    CAS  PubMed  PubMed Central  Google Scholar 

  31. 31

    Page LB, Damon A, Moellering Jr RC . Antecedents of cardiovascular disease in six Solomon Islands societies. Circulation 1974; 49: 1132–1146.

    CAS  PubMed  PubMed Central  Google Scholar 

  32. 32

    Uzodike VO . Epidemiological studies of arterial blood pressure and hypertension in relation to electrolyte excretion in three Igbo communities in Nigeria. Thesis (MD), University of London, 1993.

  33. 33

    Page LB, Vandevert DE, Nader K, Lubin NK, Page JR . Blood pressure of Qash’qai pastoral nomads in Iran in relation to culture, diet, and body form. Am J Clin Nutr 1981; 34: 527–538.

    CAS  PubMed  Google Scholar 

  34. 34

    Elliott P, Stamler J, Nichols R, Dyer AR, Stamler R, Kesteloot H et al. Intersalt revisited: further analyses of 24 h sodium excretion and blood pressure within and across populations. Intersalt Cooperative Research Group. BMJ 1996; 312: 1249–1253.

    CAS  PubMed  PubMed Central  Google Scholar 

  35. 35

    Elliott P, Stamler J . Evidence on salt and blood pressure is consistent and persuasive. Int J Epidemiol 2002; 31: 316–319.

    PubMed  PubMed Central  Google Scholar 

  36. 36

    Zhou BF, Stamler J, Dennis B, Moag-Stahlberg A, Okuda N, Robertson C et al. Nutrient intakes of middle-aged men and women in China, Japan, United Kingdom, and United States in the late 1990s: the INTERMAP study. J Hum Hypertens 2003; 17: 623–630.

    CAS  PubMed  Google Scholar 

  37. 37

    Khaw KT, Bingham S, Welch A, Luben R, O’Brien E, Wareham N et al. Blood pressure and urinary sodium in men and women: the Norfolk Cohort of the European Prospective Investigation into Cancer (EPIC-Norfolk). Am J Clin Nutr 2004; 80: 1397–1403.

    CAS  PubMed  Google Scholar 

  38. 38

    He J, Klag MJ, Whelton PK, Chen JY, Mo JP, Qian MC et al. Migration, blood pressure pattern, and hypertension: the Yi Migrant Study. Am J Epidemiol 1991; 134: 1085–1101.

    CAS  PubMed  Google Scholar 

  39. 39

    Poulter NR, Khaw KT, Hopwood BE, Mugambi M, Peart WS, Rose G et al. The Kenyan Luo migration study: observations on the initiation of a rise in blood pressure. BMJ 1990; 300: 967–972.

    CAS  PubMed  PubMed Central  Google Scholar 

  40. 40

    Forte JG, Miguel JM, Miguel MJ, de Padua F, Rose G . Salt and blood pressure: a community trial. J Hum Hypertens 1989; 3: 179–184.

    CAS  Google Scholar 

  41. 41

    Tian HG, Guo ZY, Hu G, Yu SJ, Sun W, Pietinen P et al. Changes in sodium intake and blood pressure in a community-based intervention project in China. J Hum Hypertens 1995; 9: 959–968.

    CAS  PubMed  Google Scholar 

  42. 42

    Staessen J, Bulpitt CJ, Fagard R, Joossens JV, Lijnen P, Amery A . Salt intake and blood pressure in the general population: a controlled intervention trial in two towns. J Hypertens 1988; 6: 965–973.

    CAS  PubMed  Google Scholar 

  43. 43

    Tuomilehto J, Puska P, Nissinen A, Salonen J, Tanskanen A, Pietinen P et al. Community-based prevention of hypertension in North Karelia, Finland. Ann Clin Res 1984; 16 (Suppl 43): 18–27.

    PubMed  Google Scholar 

  44. 44

    Takahashi Y, Sasaki S, Okubo S, Hayashi M, Tsugane S . Blood pressure change in a free-living population-based dietary modification study in Japan. J Hypertens 2006; 24: 451–458.

    CAS  PubMed  Google Scholar 

  45. 45

    Kempner W . Treatment of hypertensive vascular disease with rice diet. Am J Med 1948; 26: 545–577.

    Google Scholar 

  46. 46

    MacGregor GA, Markandu ND, Best FE, Elder DM, Cam JM, Sagnella GA et al. Double-blind randomised crossover trial of moderate sodium restriction in essential hypertension. Lancet 1982; 1: 351–355.

    CAS  PubMed  Google Scholar 

  47. 47

    Law MR, Frost CD, Wald NJ . By how much does dietary salt reduction lower blood pressure? III—analysis of data from trials of salt reduction. BMJ 1991; 302: 819–824.

    CAS  PubMed  PubMed Central  Google Scholar 

  48. 48

    Midgley JP, Matthew AG, Greenwood CM, Logan AG . Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials. JAMA 1996; 275: 1590–1597.

    CAS  PubMed  Google Scholar 

  49. 49

    Cutler JA, Follmann D, Allender PS . Randomized trials of sodium reduction: an overview. Am J Clin Nutr 1997; 65: 643S–651S.

    CAS  PubMed  Google Scholar 

  50. 50

    Graudal NA, Galloe AM, Garred P . Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride: a meta-analysis. JAMA 1998; 279: 1383–1391.

    CAS  PubMed  PubMed Central  Google Scholar 

  51. 51

    Alam S, Johnson AG . A meta-analysis of randomised controlled trials (RCT) among healthy normotensive and essential hypertensive elderly patients to determine the effect of high salt (NaCl) diet of blood pressure. J Hum Hypertens 1999; 13: 367–374.

    CAS  PubMed  Google Scholar 

  52. 52

    Hooper L, Bartlett C, Davey Smith G, Ebrahim S . Systematic review of long term effects of advice to reduce dietary salt in adults. BMJ 2002; 325: 628–632.

    PubMed  PubMed Central  Google Scholar 

  53. 53

    He FJ, Markandu ND, MacGregor GA . Importance of the renin system for determining blood pressure fall with acute salt restriction in hypertensive and normotensive whites. Hypertension 2001; 38: 321–325.

    CAS  PubMed  PubMed Central  Google Scholar 

  54. 54

    MacGregor GA, Markandu ND, Sagnella GA, Singer DR, Cappuccio FP . Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension. Lancet 1989; 2: 1244–1247.

    CAS  PubMed  Google Scholar 

  55. 55

    Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med 2001; 344: 3–10.

    CAS  PubMed  Google Scholar 

  56. 56

    MacGregor GA, Markandu ND, Singer DR, Cappuccio FP, Shore AC, Sagnella GA . Moderate sodium restriction with angiotensin converting enzyme inhibitor in essential hypertension: a double blind study. Br Med J (Clin Res Ed) 1987; 294: 531–534.

    CAS  Google Scholar 

  57. 57

    Whelton PK, Appel LJ, Espeland MA, Applegate WB, Ettinger Jr WH, Kostis JB 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. JAMA 1998; 279: 839–846.

    CAS  PubMed  Google Scholar 

  58. 58

    He FJ, Markandu ND, Sagnella GA, MacGregor GA . Importance of the renin system in determining blood pressure fall with salt restriction in black and white hypertensives. Hypertension 1998; 32: 820–824.

    CAS  Google Scholar 

  59. 59

    Cappuccio FP, Markandu ND, Carney C, Sagnella GA, MacGregor GA . Double-blind randomised trial of modest salt restriction in older people. Lancet 1997; 350: 850–854.

    CAS  PubMed  Google Scholar 

  60. 60

    He FJ, MacGregor GA . Salt, blood pressure and the renin-angiotensin system. J Renin Angiotensin Aldosterone Syst 2003; 4: 11–16.

    CAS  PubMed  PubMed Central  Google Scholar 

  61. 61

    He FJ, MacGregor GA . How far should salt intake be reduced? Hypertension 2003; 42: 1093–1099.

    CAS  PubMed  PubMed Central  Google Scholar 

  62. 62

    Antonios TF, MacGregor GA . Salt—more adverse effects. Lancet 1996; 348: 250–251.

    CAS  PubMed  PubMed Central  Google Scholar 

  63. 63

    Sasaki N . The salt factor in apoplexy and hypertension: epidemiological studies in Japan. In: Yamori Y (ed). Prophylactic Approach to Hypertensive Diseases. Raven Press: New York, 1979, pp 467–474.

    Google Scholar 

  64. 64

    Karppanen H, Mervaala E . Sodium intake and hypertension. Prog Cardiovasc Dis 2006; 49: 59–75.

    CAS  PubMed  PubMed Central  Google Scholar 

  65. 65

    Laatikainen T, Pietinen P, Valsta L, Sundvall J, Reinivuo H, Tuomilehto J . Sodium in the Finnish diet: 20-year trends in urinary sodium excretion among the adult population. Eur J Clin Nutr 2006; 60: 965–970.

    CAS  PubMed  PubMed Central  Google Scholar 

  66. 66

    Kagan A, Popper JS, Rhoads GG, Yano K . Dietary and other risk factors for stroke in Hawaiian Japanese men. Stroke 1985; 16: 390–396.

    CAS  PubMed  PubMed Central  Google Scholar 

  67. 67

    Alderman MH, Madhavan S, Cohen H, Sealey JE, Laragh JH . Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men. Hypertension 1995; 25: 1144–1152.

    CAS  PubMed  PubMed Central  Google Scholar 

  68. 68

    Stamler J, Cohen J, Culter JA, Grandits G, Kjeldsberg M, Kuller L et al. Sodium intake and mortality from myocardial infarction: multiple risk factor intervention trial (MRFIT). Can J Cardiol 1997; 13 (Suppl B): 272B.

    Google Scholar 

  69. 69

    Tunstall-Pedoe H, Woodward M, Tavendale R, A’Brook R, McCluskey MK . Comparison of the prediction by 27 different factors of coronary heart disease and death in men and women of the Scottish Heart Health Study: cohort study. BMJ 1997; 315: 722–729.

    CAS  PubMed  PubMed Central  Google Scholar 

  70. 70

    He J, Ogden LG, Vupputuri S, Bazzano LA, Loria C, Whelton PK . Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA 1999; 282: 2027–2034.

    CAS  PubMed  PubMed Central  Google Scholar 

  71. 71

    Alderman MH, Cohen H, Madhavan S . Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet 1998; 351: 781–785.

    CAS  PubMed  PubMed Central  Google Scholar 

  72. 72

    Ascherio A, Rimm EB, Hernan MA, Giovannucci EL, Kawachi I, Stampfer MJ et al. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation 1998; 98: 1198–1204.

    CAS  PubMed  PubMed Central  Google Scholar 

  73. 73

    Cohen HW, Hailpern SM, Fang J, Alderman MH . Sodium intake and mortality in the NHANES II follow-up study. Am J Med 2006; 119: 275 e7–14.

    PubMed  PubMed Central  Google Scholar 

  74. 74

    Cohen HW, Hailpern SM, Alderman MH . Sodium intake and mortality follow-up in the third national health and nutrition examination survey (NHANES III). J Gen Intern Med 2008; 23 (9): 1297–1302.

    PubMed  PubMed Central  Google Scholar 

  75. 75

    Geleijnse JM, Witteman JC, Stijnen T, Kloos MW, Hofman A, Grobbee DE . Sodium and potassium intake and risk of cardiovascular events and all-cause mortality: the Rotterdam Study. Eur J Epidemiol 2007; 22: 763–770.

    CAS  PubMed  PubMed Central  Google Scholar 

  76. 76

    Karppanen H, Mervaala E . Sodium intake and mortality. Lancet 1998; 351: 1509.

    CAS  PubMed  PubMed Central  Google Scholar 

  77. 77

    Meltzer JI . Low urinary sodium and myocardial infacrtion. Hypertension 1996; 27: 156–157.

    Google Scholar 

  78. 78

    Chang HY, Hu YW, Yue CS, Wen YW, Yeh WT, Hsu LS et al. Effect of potassium-enriched salt on cardiovascular mortality and medical expenses of elderly men. Am J Clin Nutr 2006; 83: 1289–1296.

    CAS  PubMed  PubMed Central  Google Scholar 

  79. 79

    He J, Ogden LG, Bazzano LA, Vupputuri S, Loria C, Whelton PK . Dietary sodium intake and incidence of congestive heart failure in overweight US men and women: first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Arch Intern Med 2002; 162: 1619–1624.

    PubMed  PubMed Central  Google Scholar 

  80. 80

    MacGregor GA, de Wardener HE . Idiopathic edema. In: Schrier RW and Gottschalk CW (eds). Diseases of the Kidney. Little Brown and Company: Boston, 1997, pp 2343–2352.

    Google Scholar 

  81. 81

    Tobian L, Hanlon S . High sodium chloride diets injure arteries and raise mortality without changing blood pressure. Hypertension 1990; 15: 900–903.

    CAS  PubMed  PubMed Central  Google Scholar 

  82. 82

    Xie JX, Sasaki S, Joossens JV, Kesteloot H . The relationship between urinary cations obtained from the INTERSALT study and cerebrovascular mortality. J Hum Hypertens 1992; 6: 17–21.

    CAS  PubMed  PubMed Central  Google Scholar 

  83. 83

    Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP . Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990; 322: 1561–1566.

    CAS  Google Scholar 

  84. 84

    Laufer E, Jennings GL, Korner PI, Dewar E . Prevalence of cardiac structural and functional abnormalities in untreated primary hypertension. Hypertension 1989; 13: 151–162.

    CAS  PubMed  PubMed Central  Google Scholar 

  85. 85

    Schmieder RE, Messerli FH, Garavaglia GE, Nunez BD . Dietary salt intake. A determinant of cardiac involvement in essential hypertension. Circulation 1988; 78: 951–956.

    CAS  PubMed  PubMed Central  Google Scholar 

  86. 86

    Du Cailar G, Ribstein J, Daures JP, Mimran A . Sodium and left ventricular mass in untreated hypertensive and normotensive subjects. Am J Physiol 1992; 263: H177–H181.

    CAS  PubMed  PubMed Central  Google Scholar 

  87. 87

    Ferrara LA, de Simone G, Pasanisi F, Mancini M . Left ventricular mass reduction during salt depletion in arterial hypertension. Hypertension 1984; 6: 755–759.

    CAS  PubMed  PubMed Central  Google Scholar 

  88. 88

    Liebson PR, Grandits GA, Dianzumba S, Prineas RJ, Grimm Jr RH, Neaton JD et al. Comparison of five antihypertensive monotherapies and placebo for change in left ventricular mass in patients receiving nutritional-hygienic therapy in the Treatment of Mild Hypertension Study (TOMHS). Circulation 1995; 91: 698–706.

    CAS  PubMed  PubMed Central  Google Scholar 

  89. 89

    Jula AM, Karanko HM . Effects on left ventricular hypertrophy of long-term nonpharmacological treatment with sodium restriction in mild-to-moderate essential hypertension. Circulation 1994; 89: 1023–1031.

    CAS  PubMed  PubMed Central  Google Scholar 

  90. 90

    Joossens JV, Hill MJ, Elliott P, Stamler R, Lesaffre E, Dyer A et al. Dietary salt, nitrate and stomach cancer mortality in 24 countries. European Cancer Prevention (ECP) and the INTERSALT Cooperative Research Group. Int J Epidemiol 1996; 25: 494–504.

    CAS  PubMed  PubMed Central  Google Scholar 

  91. 91

    Beevers DG, Lip GY, Blann AD . Salt intake and Helicobacter pylori infection. J Hypertens 2004; 22: 1475–1477.

    CAS  PubMed  PubMed Central  Google Scholar 

  92. 92

    Forman D, Newell DG, Fullerton F, Yarnell JW, Stacey AR, Wald N et al. Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation. BMJ 1991; 302: 1302–1305.

    CAS  PubMed  PubMed Central  Google Scholar 

  93. 93

    Wong BC, Lam SK, Wong WM, Chen JS, Zheng TT, Feng RE et al. Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial. JAMA 2004; 291: 187–194.

    CAS  PubMed  PubMed Central  Google Scholar 

  94. 94

    du Cailar G, Ribstein J, Mimran A . Dietary sodium and target organ damage in essential hypertension. Am J Hypertens 2002; 15: 222–229.

    CAS  PubMed  PubMed Central  Google Scholar 

  95. 95

    Verhave JC, Hillege HL, Burgerhof JG, Janssen WM, Gansevoort RT, Navis GJ et al. Sodium intake affects urinary albumin excretion especially in overweight subjects. J Intern Med 2004; 256: 324–330.

    CAS  PubMed  PubMed Central  Google Scholar 

  96. 96

    Arnlov J, Evans JC, Meigs JB, Wang TJ, Fox CS, Levy D et al. Low-grade albuminuria and incidence of cardiovascular disease events in nonhypertensive and nondiabetic individuals: the Framingham Heart Study. Circulation 2005; 112: 969–975.

    PubMed  PubMed Central  Google Scholar 

  97. 97

    Houlihan CA, Allen TJ, Baxter AL, Panangiotopoulos S, Casley DJ, Cooper ME et al. A low-sodium diet potentiates the effects of losartan in type 2 diabetes. Diabetes Care 2002; 25: 663–671.

    CAS  PubMed  PubMed Central  Google Scholar 

  98. 98

    Matkovic V, Ilich JZ, Andon MB, Hsieh LC, Tzagournis MA, Lagger BJ et al. Urinary calcium, sodium, and bone mass of young females. Am J Clin Nutr 1995; 62: 417–425.

    CAS  PubMed  PubMed Central  Google Scholar 

  99. 99

    Lin PH, Ginty F, Appel LJ, Aickin M, Bohannon A, Garnero P et al. The DASH diet and sodium reduction improve markers of bone turnover and calcium metabolism in adults. J Nutr 2003; 133: 3130–3136.

    CAS  PubMed  PubMed Central  Google Scholar 

  100. 100

    Devine A, Criddle RA, Dick IM, Kerr DA, Prince RL . A longitudinal study of the effect of sodium and calcium intakes on regional bone density in postmenopausal women. Am J Clin Nutr 1995; 62: 740–745.

    CAS  PubMed  PubMed Central  Google Scholar 

  101. 101

    Burney P . A diet rich in sodium may potentiate asthma. Epidemiologic evidence for a new hypothesis. Chest 1987; 91: 143S–148S.

    CAS  PubMed  PubMed Central  Google Scholar 

  102. 102

    Carey OJ, Locke C, Cookson JB . Effect of alterations of dietary sodium on the severity of asthma in men. Thorax 1993; 48: 714–718.

    CAS  PubMed  PubMed Central  Google Scholar 

  103. 103

    Mickleborough TD, Lindley MR, Ray S . Dietary salt, airway inflammation, and diffusion capacity in exercise-induced asthma. Med Sci Sports Exerc 2005; 37: 904–914.

    CAS  PubMed  PubMed Central  Google Scholar 

  104. 104

    Mickleborough TD, Fogarty A . Dietary sodium intake and asthma: an epidemiological and clinical review. Int J Clin Pract 2006; 60: 1616–1624.

    CAS  PubMed  PubMed Central  Google Scholar 

  105. 105

    Pogson ZE, Antoniak MD, Pacey SJ, Lewis SA, Britton JR, Fogarty AW . Does a low sodium diet improve asthma control? A randomized controlled trial. Am J Respir Crit Care Med 2008; 178: 132–138.

    CAS  PubMed  PubMed Central  Google Scholar 

  106. 106

    Corbo GM, Forastiere F, Sario MD, Brunetti L, Bonci E, Bugiani M et al. Wheeze and asthma in children: associations with body mass index, sports, television viewing, and diet. Epidemiology 2008; 19: 747–755.

    PubMed  PubMed Central  Google Scholar 

  107. 107

    Vartanian LR, Schwartz MB, Brownell KD . Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. Am J Public Health 2007; 97: 667–675.

    PubMed  PubMed Central  Google Scholar 

  108. 108

    Ludwig DS, Peterson KE, Gortmaker SL . Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 2001; 357: 505–508.

    CAS  PubMed  PubMed Central  Google Scholar 

  109. 109

    James J, Thomas P, Cavan D, Kerr D . Preventing childhood obesity by reducing consumption of carbonated drinks: cluster randomised controlled trial. BMJ 2004; 328: 1237.

    PubMed  PubMed Central  Google Scholar 

  110. 110

    Beckmann SL, Os I, Kjeldsen SE, Eide IK, Westheim AS, Hjermann I . Effect of dietary counselling on blood pressure and arterial plasma catecholamines in primary hypertension. Am J Hypertens 1995; 8: 704–711.

    CAS  Google Scholar 

  111. 111

    The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 2002; 288: 2981–2997.

    Google Scholar 

  112. 112

    Grey A, Braatvedt G, Holdaway I . Moderate dietary salt restriction does not alter insulin resistance or serum lipids in normal men. Am J Hypertens 1996; 9: 317–322.

    CAS  PubMed  PubMed Central  Google Scholar 

  113. 113

    Townsend RR, Kapoor S, McFadden CB . Salt intake and insulin sensitivity in healthy human volunteers. Clin Sci (London) 2007; 113: 141–148.

    CAS  Google Scholar 

  114. 114

    Meland E, Laerum E, Aakvaag A, Ulvik RJ, Hostmark AT . Salt restriction: effects on lipids and insulin production in hypertensive patients. Scand J Clin Lab Invest 1997; 57: 501–505.

    CAS  PubMed  PubMed Central  Google Scholar 

  115. 115

    Hu G, Jousilahti P, Peltonen M, Lindstrom J, Tuomilehto J . Urinary sodium and potassium excretion and the risk of type 2 diabetes: a prospective study in Finland. Diabetologia 2005; 48: 1477–1483.

    CAS  PubMed  PubMed Central  Google Scholar 

  116. 116

    Zillich AJ, Garg J, Basu S, Bakris GL, Carter BL . Thiazide diuretics, potassium, and the development of diabetes: a quantitative review. Hypertension 2006; 48: 219–224.

    CAS  PubMed  PubMed Central  Google Scholar 

  117. 117

    He FJ, MacGregor GA . Beneficial effects of potassium on human health. Physiol Plant 2008; 133: 725–735.

    CAS  PubMed  PubMed Central  Google Scholar 

  118. 118

    Singer DR, Markandu ND, Cappuccio FP, Miller MA, Sagnella GA, MacGregor GA . Reduction of salt intake during converting enzyme inhibitor treatment compared with addition of a thiazide. Hypertension 1995; 25: 1042–1044.

    CAS  Google Scholar 

  119. 119

    Hofman A, Hazebroek A, Valkenburg HA . A randomized trial of sodium intake and blood pressure in newborn infants. JAMA 1983; 250: 370–373.

    CAS  PubMed  PubMed Central  Google Scholar 

  120. 120

    Geleijnse JM, Hofman A, Witteman JC, Hazebroek AA, Valkenburg HA, Grobbee DE . Long-term effects of neonatal sodium restriction on blood pressure. Hypertension 1997; 29: 913–917.

    CAS  PubMed  PubMed Central  Google Scholar 

  121. 121

    Simons-Morton DG, Obarzanek E . Diet and blood pressure in children and adolescents. Pediatr Nephrol 1997; 11: 244–249.

    CAS  Google Scholar 

  122. 122

    He FJ, Marrero NM, Macgregor GA . Salt and blood pressure in children and adolescents. J Hum Hypertens 2008; 22: 4–11.

    CAS  PubMed  PubMed Central  Google Scholar 

  123. 123

    Cooper R, Soltero I, Liu K, Berkson D, Levinson S, Stamler J . The association between urinary sodium excretion and blood pressure in children. Circulation 1980; 62: 97–104.

    CAS  Google Scholar 

  124. 124

    Lauer RM, Clarke WR . Childhood risk factors for high adult blood pressure: the Muscatine Study. Pediatrics 1989; 84: 633–641.

    CAS  Google Scholar 

  125. 125

    De Courcy S, Mitchell H, Simmons D, MacGregor GA . Urinary sodium excretion in 4–6 year old children: a cause for concern? Br Med J (Clin Res Ed) 1986; 292: 1428–1429.

    CAS  Google Scholar 

  126. 126

    St-Onge MP, Keller KL, Heymsfield SB . Changes in childhood food consumption patterns: a cause for concern in light of increasing body weights. Am J Clin Nutr 2003; 78: 1068–1073.

    CAS  PubMed  PubMed Central  Google Scholar 

  127. 127

    Selmer RM, Kristiansen IS, Haglerod A, Graff-Iversen S, Larsen HK, Meyer HE et al. Cost and health consequences of reducing the population intake of salt. J Epidemiol Community Health 2000; 54: 697–702.

    CAS  PubMed  PubMed Central  Google Scholar 

  128. 128

    Joffres MR, Campbell NR, Manns B, Tu K . Estimate of the benefits of a population-based reduction in dietary sodium additives on hypertension and its related health care costs in Canada. Can J Cardiol 2007; 23: 437–443.

    PubMed  PubMed Central  Google Scholar 

  129. 129

    Asaria P, Chisholm D, Mathers C, Ezzati M, Beaglehole R . Chronic disease prevention: health effects and financial costs of strategies to reduce salt intake and control tobacco use. Lancet 2007; 370: 2044–2053.

    PubMed  PubMed Central  Google Scholar 

  130. 130

    Murray CJ, Lauer JA, Hutubessy RC, Niessen L, Tomijima N, Rodgers A et al. Effectiveness and costs of interventions to lower systolic blood pressure and cholesterol: a global and regional analysis on reduction of cardiovascular-disease risk. Lancet 2003; 361: 717–725.

    Google Scholar 

  131. 131

    Joint WHO/FAO expert consultation on diet, nutrition and the prevention of chronic diseases. 2002. Geneva. Available at Accessed 30 October 2008.

  132. 132

    Reducing salt intake in populations. WHO Forum and Technical Meeting on Reducing Salt Intake in Populations. (Access verified August 7 2008).

  133. 133

    WHO Regional Office for Europe. Nutrition and food security. Action networks. verified 7 August 2008).

  134. 134

    Lawes CM, Vander Hoorn S, Rodgers A . Global burden of blood-pressure-related disease, 2001. Lancet 2008; 371: 1513–1518.

    PubMed  PubMed Central  Google Scholar 

  135. 135

    Nutritional aspects of cardiovascular disease. Report of the Cardiovascular Review Group, Committee on Medical Aspects of Food Policy. HMSO: London, 1994.

  136. 136

    Godlee F . The food industry fights for salt. BMJ 1996; 312: 1239–1240.

    CAS  PubMed  PubMed Central  Google Scholar 

  137. 137

    Consensus Action on Salt and Health. (Accessed 7 August 2008).

  138. 138

    MacGregor GA, Sever PS . Salt—overwhelming evidence but still no action: can a consensus be reached with the food industry? CASH (Consensus Action on Salt and Hypertension). BMJ 1996; 312: 1287–1289.

    CAS  PubMed  PubMed Central  Google Scholar 

  139. 139

    Girgis S, Neal B, Prescott J, Prendergast J, Dumbrell S, Turner C et al. A one-quarter reduction in the salt content of bread can be made without detection. Eur J Clin Nutr 2003; 57: 616–620.

    CAS  PubMed  Google Scholar 

  140. 140

    Scientific Advisory Committee on Nutrition, Salt and health. 2003. The Stationery Office. Available at (Access verified August 7 2008).

  141. 141

    Food Standards Agency. Parliamentary briefing: Full of it—FSA's salt awareness campaign. March 2007. Available at: ( Accessed 17 April 2008.

  142. 142

    Food Standards Agency. Traffic Light Labelling. Available at – Accessed 22 March 2008.

  143. 143

    Food Standards Agency. Dietary sodium levels surveys. Tuesday 22 July 2008. Available at: Accessed 4 August 2008.

  144. 144

    Pietinen P, Valsta LM, Hirvonen T, Sinkko H . Labelling the salt content in foods: a useful tool in reducing sodium intake in Finland. Public Health Nutr 2008; 11: 335–340.

    PubMed  PubMed Central  Google Scholar 

  145. 145

    World Action on Salt and Health. Press release—Medical experts launch global campaign against salt to prevent over 2.5 million deaths worldwide each year. Available at – (Accessed 29 April 08).

  146. 146

    Salt and Health. Review of the Scientific Evidence and Recommendations for Public Policy in Ireland. 2005. Food Safety Authority of Ireland. Available at (Accessed 27 March 2007).

  147. 147

    Campbell N . Health Check program. CMAJ 2008; 178: 1186–1187.

    PubMed  PubMed Central  Google Scholar 

  148. 148

    Guidelines for a healthy diet 2006. The Health Council of the Netherlands (Gezondheidsraad). Available at (Accessed 27 March 2007).

  149. 149

    Chobanian AV, Hill M . National Heart, lung, and blood institute workshop on sodium and blood pressure: a critical review of current scientific evidence. Hypertension 2000; 35: 858–863.

    CAS  PubMed  PubMed Central  Google Scholar 

  150. 150

    Dickinson BD, Havas S . Reducing the population burden of cardiovascular disease by reducing sodium intake: a report of the Council on Science and Public Health. Arch Intern Med 2007; 167: 1460–1468.

    CAS  PubMed  Google Scholar 

  151. 151

    CSPI Sues FDA to Force End to 20-Year Delay in Regulating Salt. (Accessed 12 June 2008).

  152. 152

    Blais CA, Pangborn RM, Borhani NO, Ferrell MF, Prineas RJ, Laing B . Effect of dietary sodium restriction on taste responses to sodium chloride: a longitudinal study. Am J Clin Nutr 1986; 44: 232–243.

    CAS  PubMed  Google Scholar 

  153. 153

    Teow BH, Nicolantonio RD, Morgan TO . Sodium chloride preference and recognition threshold in normotensive subjects on high and low salt diet. Clin and Exper Hypertens 1985; 7: 1681–1695.

    Google Scholar 

  154. 154

    James WP, Ralph A, Sanchez-Castillo CP . The dominance of salt in manufactured food in the sodium intake of affluent societies. Lancet 1987; 1: 426–429.

    CAS  Google Scholar 

  155. 155

    WASH launch press release. (Accessed November 13, 2008)

Download references


We thank Naomi M Marrero for her valuable contribution to the section on ‘Worldwide actions occurring on salt’.

Author information



Corresponding author

Correspondence to F J He.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

He, F., MacGregor, G. A comprehensive review on salt and health and current experience of worldwide salt reduction programmes. J Hum Hypertens 23, 363–384 (2009).

Download citation


  • salt
  • health
  • salt reduction programmes

Further reading


Quick links