Review Article | Published:

Review Article

Harmful effects of dietary salt in addition to hypertension


In addition to raising the blood pressure dietary salt is responsible for several other harmful effects. The most important are a number which, though independent of the arterial pressure, also harm the cardiovascular system. A high salt intake increases the mass of the left ventricle, thickens and stiffens conduit arteries and thickens and narrows resistance arteries, including the coronary and renal arteries. It also increases the number of strokes, the severity of cardiac failure and the tendency for platelets to aggregate. In renal disease, a high salt intake accelerates the rate of renal functional deterioration. Apart from its effect on the cardiovascular system dietary salt has an effect on calcium and bone metabolism, which underlies the finding that in post-menopausal women salt intake controls bone density of the upper femur and pelvis. Dietary salt controls the incidence of carcinoma of the stomach and there is some evidence which suggests that salt is associated with the severity of asthma in male asthmatic subjects.


High blood pressure is the greatest cause of strokes and heart failure and is a major contributor to coronary heart disease. Dietary salt appears to be an important single factor in raising the blood pressure. Throughout evolution the human race only consumed the sodium naturally present in food and the daily intake was about 10 mmol/day.1 It is less than 5000 years ago that salt began to be added to food and the present intake of between 100–400 mmol/day is therefore a considerable, and in evolutionary terms, recent increase.2,3

A dispute which lasted about 100 years over the evidence that suggested that hypertension is in part due to the present high intake of salt is now resolved. There is a consensus that dietary sodium plays a significant role in determining the blood pressure of populations, the number of individuals who have a raised blood pressure, and its severity, and that it is responsible for much of the rise in pressure that occurs with age.4 The previous debate, however, obscured the considerable evidence that in addition to raising the blood pressure dietary salt has other harmful effects, several of which in the cardiovascular system are independent, though additive, to the effect of the hypertension, and some of which appear to be as important as the rise in arterial pressure.

Cardiovascular effects

Left ventricular mass

In humans there is a relation between left ventricular mass and cardiovascular mortality and morbidity independent of the blood pressure.5,6,7 In normotensive subjects left ventricular mass and diastolic filling have been found to be positively correlated with urinary sodium excretion8,9 (Figure 1) and in two other normotensive groups followed up for 3 to 8 years the initial left ventricular mass and wall thickness were significantly related to the subsequent development of hypertension.5 Normotensive rats given 1% saline for several weeks develop an increase in heart weight due to an increase in left ventricular mass without an increase in blood pressure.10,11 In both normotensive humans and the rat therefore, left ventricular mass is positively related to the salt intake which, in normal circumstances is equivalent to the dietary salt intake. Left ventricular mass is independent of the blood pressure, and in normal humans an increase in left ventricular mass predicts the onset of hypertension.

Figure 1

Correlation between salt intake and left ventricular mass in subjects with systolic blood pressure >121 mm Hg. (Adapted from Kupari P, Koskinen P, Virolainor J. Circulation 1994; 89: 1041–1050.)

The relation of left ventricular mass to salt intake in essential hypertension is well documented in that in such patients 24-h sodium excretion is an independent determinant for relative wall thickness, and is a more powerful determinant than the blood pressure.9,12,13,14 These findings have been confirmed using ambulatory blood pressure monitoring.8 In patients with hypertension associated with type I diabetes multiple regression analysis has identified dietary sodium intake as an independent predictor of left ventricular mass, there was no significant association between left ventricular mass and the blood pressure.15 A high intake of salt increases cardiac mass in both the spontaneous hypertensive rat (SHR) and its control, the Wistar-Kyoto (WKY) rat, though the blood pressure in the WKY rat does not rise.16 In rats with experimental reno-vascular hypertension those on a high intake of sodium have an increase in left ventricular mass which is more consistent than the associated change in blood pressure.17 Though the rise in arterial pressure induced by a high salt diet in the Dahl salt-sensitive rat is prevented by the chronic intracerebroventricular administration of Fab fragments to block brain ouabain this does not prevent the increase in the weight of the left ventricle.18

The increase in left ventricular mass, both in the normal rat on an increased salt intake and in the hypertensive rat is associated with an increase in myocardial angiotensin-converting enzyme (ACE) mRNA,19 non-collagenous protein and total collagen content. Angiotensin II increases cardiac protein.20 There is also a marked increase in intramyocardial interstitial fibrosis both in the left ventricle and intramyocardial arteries and arterioles.11,21 In addition there is over-expression of TGF-β, mRNA which parallels the degree of fibrosis.21 In the stroke-prone hypertensive rat a high salt diet has been shown to increase the cardiac expression of the endothelin−1 gene transcript in the absence of a change in blood pressure.22

The increase in left ventricular mass associated with essential hypertension can be reduced by lowering the intake of salt.8,23,24 The Treatment of Mild Hypertension Study Research Group25 showed a significant correlation between the reductions in salt intake and the left ventricular mass. In the whole study group lowering salt intake was the only factor which was significantly correlated with a reduction in left ventricular mass. Similarly in the two-kidney one-clip hypertensive rat a low sodium diet can reverse the myocardial hypertrophy and certain enzyme changes, in the absence of a significant change in blood pressure.26,27 In the stroke-prone spontaneously hypertensive rat a 1% saline intake is associated with severe hypertension and cardiac hypertrophy (heart weight to body weight ratio). This is prevented by the administration of a diuretic which causes a small fall in blood pressure from about 300 to 250 mm Hg but prevents the development of cardiac hypertrophy and practically prevents myocardiac interstitial fibrosis and perivascular fibrosis.28


There is a close link between urinary sodium excretion and left ventricular mass in both man and the rat which is independent of hypertension. In hypertensive patients a reduction in salt intake reduces left ventricular mass independent of a change in blood pressure.


An increase in sodium intake, in both humans and experimental animals, increases the stiffness of conduit arteries and the activity of resistance arteries, and both become hypertrophied.29,30 Stiffness of conduit arteries, measured as an increase in pulse wave velocity31 or pulse pressure,32 is a strong independent predictor of cardiovascular risk. Tobian was the first to show that in various forms of experimental hypertension in the rat a high salt intake induces structural alterations in cerebral and renal vessels independent of the blood pressure.33,34 Levy et al35 found that the administration for 12 weeks of a diuretic to a group of SHR stroke-prone rats on a high sodium intake diminished the increase in carotid artery thickness and collagen content though the blood pressure of the diuretic group was significantly greater than in the control group. Recent studies in humans have shown that a moderate reduction in salt intake causes a reduction in the stiffness and thickness of the arterial wall, independent of the blood pressure.36

In one early study in individuals in a rural community in China, pulse wave velocity in the lower aorta, the arms and the legs was, after adjustment for blood pressure, consistently lower than in a comparable group in an urban community on a higher salt intake.37 Similarly, the pulse wave velocity of a group of normotensive subjects who lowered their salt intake for a mean of about 2 years was significantly lower than that of a control group, independent of the blood pressure.36 The increase in large artery thickness in essential hypertension appears to be due at least in part to angiotensin II in that it is lowered by ACE inhibitors and is independent of any associated change in blood pressure.38 The influence of dietary salt intake and angiotensin II on large artery stiffness in essential hypertension appear to be additive. For instance, neither a 2% NaCl diet or intravenous angiotensin (50 ng/kg/min) for 12 weeks has an effect on the blood pressure or the wall/lumen ratio of small resistance vessels in the Sprague Dawley rat but, when combined, the combination alters both.39

The structural changes in intramyocardial coronary arteries induced by a high salt diet are accompanied by a number of metabolic alterations including an increased generation of reactive oxygen species40 which, among other effects, oxidise nitric oxide thus reducing its dilator effect41,42 and the arteriolar response to acetylcholine.40

As a rise in salt intake is usually accompanied by a small rise in plasma sodium and plasma sodium tends to be raised in essential hypertension43 it is possible that the effect of a small change in sodium concentration on in vitro cultures of endothelial cells may also be relevant to a consideration of the effect of dietary salt on vessels in vivo. For instance increasing the sodium concentration of the culture fluid of cultured myocardial myocytes and vascular smooth muscle by 6 mM/l for 5 days causes hypertrophy.44 Subsequently the investigators responsible for this finding also demonstrated that raising the sodium concentration of the fluid bathing cultured human umbilical vein endothelial cells by 6 mM/l (from 142 to 148 mmol/l) for 5 days raises their content of cellular protein and total RNA. When exposed to a sodium concentration of 152 mmol/l (ie, an increase of 10 mM/l) there is first, after 2 h incubation, a transient increase in c fos proto-oncogenic mRNA expression. After 3 days there is a general increase in mRNA expression of several factors which are related to hypertrophy.45


Dietary salt intake controls the stiffness of the larger conduit arteries, the reactivity of the smaller resistance vessels and the wall thickness of both. A raised intake induces an increase in collagen deposition and an increased generation of reactive oxygen species within the arterial walls. A reduction in salt intake reverses these changes. Small variations in the concentration of plasma sodium which, in vitro, can induce hypertrophying effects on cultured vascular endothelium may contribute to these changes.

Cardiac failure

Cardiac failure in association with essential hypertension is the end product of several harmful consequences of dietary salt.46 Primarily there is systolic contractile dysfunction due to the salt induced hypertension.47 Some older patients may develop diastolic dysfunction due to impaired ventricular filling, this usually precedes systolic dysfunction and is a consequence of the collagen deposition and fibrosis of the ventricle which are closely related to salt intake. Furthermore the salt-induced increase in the size of the muscle mass, due to the hypertrophy and deposition of collagen and fibrous tissue, and the salt-induced thickening of the coronary arteries, impair coronary perfusion, which can be detected as an inadequate reserve of coronary blood flow.48,49 Myocardial function is further impaired by the increase in cardiac output which results in part from the salt-induced rise in right auricular pressure. The gain in weight associated with the salt and water retention that accompanies cardiac failure also increases cardiac work. Reducing salt intake in patients with overt heart failure is commonly used and leads to an improvement of symptoms similar to that which occurs with diuretics. Nevertheless there has, as yet, been no controlled trials of salt restriction in heart failure.


The higher the salt intake, the greater the incidence of strokes.50,51 Multivariate analyses calculated from the urinary electrolyte data obtained from the Intersalt study (from persons aged 20 to 40 years) and from the age and sex-specific stroke mortality data from 25 countries worldwide51 showed no significant relationship between either the systolic or the diastolic pressure and stroke mortality but there was a significant relationship between stroke mortality and sodium excretion in men, and the Na/K ratio in women.51 These findings are similar to those calculated for 12 European countries (Figure 2) in which, whereas sodium excretion was not significantly related to systolic pressure, it was related to stroke mortality.50

Figure 2

Correlation between urinary salt excretion and death from strokes in 12 European countries. (Adapted from Perry IJ and Beevers DG. J Hum Hypertens 1992; 6: 23–25.)

In the rat strokes are related to salt intake independent of blood pressure.33 The separate effect of salt intake, as opposed to blood pressure, in causing strokes in rats has been beautifully delineated by Tobian et al.34 The blood pressure of normal rats on a normal intake of salt was raised by the administration of DOCA. The animals were then divided into two groups, one of which was placed on a high sodium intake and the other on a low intake. The blood pressure remained raised in both groups but the group on the high salt intake had a greater number of strokes and a high death rate. Conversely, in the stroke-prone SHR, the administration of a diuretic can, without changing the arterial pressure, reduce the incidence of cerebrovascular accidents.35

The mechanism responsible for the connection between salt intake and strokes is not clear but may, in part, be related to conduit artery thickness and stiffness, and platelet reactivity.


Stroke mortality has a strong relationship to dietary sodium intake which is independent of the blood pressure.


In one study in normal men platelet aggregation induced by adenosine 5′-diphosphate was significantly greater when they were on a high salt intake.52 Similarly in normal women a change in salt intake from 10 to 200 mmol/day was associated with a significant increase in platelet aggregation.53 In two groups of men with and without a family history of hypertension a high salt intake increased the blood pressure of those with a family history but platelet aggregation increased in both groups, though it rose more in those with a family history.54

The effect of salt intake on adrenaline-induced platelet aggregation and α-2 adrenergic receptors on platelet membrane fraction has been studied in patients with essential hypertension. The response was linked to the associated changes in blood pressure. In those in whom there was a rise in blood pressure, platelet aggregation also rose as did the number of α-2 adrenergic receptors.55


In normal men and women, with and without a family history of hypertension and in patients with essential hypertension, salt intake influences platelet aggregation. These dietary salt-induced changes in platelet reactivity may be a link between salt intake, thrombotic strokes and myocardial infarction.

Renal function

Variable increases in salt intake from 1 to 8% for 7 days to 16 weeks increase the blood pressure and the size and weight of the kidneys in the Dahl salt-sensitive and -resistant rat,56 and the SHR and its control the WKY rat.11 The effect is greatest in the Dahl salt-sensitive and the SHR rats. The kidneys become hypertrophied and develop glomerular and interstitial fibrosis accompanied by a significant increase in collagen in both the SHR and the WKY rat. In the SHR rats there is also an increase in urinary protein excretion.57,58 The increase in glomerular and intertubular interstitial fibrosis, and of TGF-β in the SHR and WKY rat, is greater in the SHR but not the change in collagen deposition, though the rise in blood pressure in the WKY rat is significantly less than in the SHR. In the uninephrectomised SHR salt restriction inhibits compensatory kidney growth.59

In patients with hypertension an increase in salt intake often increases glomerular filtration rate, vascular resistance, calculated intraglomerular capillary pressure and protein excretion.60 In normal humans the effect of a raised salt intake varies from no detectable effect or a decrease in renal vascular resistance, a few have a similar response to that which occurs in those hypertensive patients who have an increase in glomerular filtration.60,61,62,63

Proteinuria and renal function

In human renal disease the reduction in glomerular filtration rate is significantly related to the histological changes observed in the tubules and the intestitium. It is not related to the historical changes that occur in the glomeruli.64,65 It now appears that the interstitial changes are the consequence of increased quantities of filtered proteins overloading the reabsorptive capacity of the proximal tubules.66 The excess filtered protein reabsorbed by the proximal tubules is degraded by lyosomes. The intracellular products of this degradation, and a local intrarenal increase in angiotensin II (see below), up-regulate genes within the proximal tubule cells which are responsible for an excess production of vasoactive and inflammatory substances. When these reach the interstitial space they give rise to focal infiltrates of inflammatory cells with an increased deposition of collagen, matrix and fibrous tissue.67

In renal disease the increase in filtered protein is due in part to an increase in glomerular permeability. There is, in addition, both in renal disease and in hereditary hypertension, an increase in glomerular capillary pressure caused by a relative rise in tone of the renal efferent arteriole.61 This, in turn, appears to be due to a rise in the intrarenal concentration of angiotensin II68 for in the sub- totally nephrectomised rats and the SHR an increase in gene expression of components of the renin- angiotensin system has been detected in the glomeruli.69 Angiotensin II is known to affect the tone of the efferent arteriole more than that of the afferent arteriole.70 In addition the intrarenal increase in angiotensin II increases the expression of heme exogenase71 and NAD(P)H oxidase which increases the production of oxygen radicals. This gives rise to oxidative stress including the consequence of oxidising nitric oxide to nitrite and nitrate72,73 and to other harmful effects which contribute to progressive renal injury.72 These findings are supported, in part, by the observation that the administration of an ACE inhibitor reduces glomerular capillary pressure and proteinuria. The apparent discrepancy between the observation that in renal disease and in hypertension the intrarenal concentration of angiotensin II may be raised, while plasma angiotensin II is usually low, is due to the kidney's intrinsic ability to produce angiotensin II.68,74 Overall the evidence suggests that, in relation to dietary salt, the angiotensin II level is inappropriately high and that this increase is responsible, in part, for many of the damaging effects. This appears to be similar to the changes which occur in the heart.75,76

The effect of dietary salt restriction on proteinuria and renal function

Patients with progressive renal disease on a diet containing 100 mmol of sodium/day have a lower protein excretion and a slower fall in glomerular filtration rate than those who eat a diet containing 200 mmol sodium/day.77 The prevalence of sclerosis, increase in glomerular volume and proteinuria in diabetic rats, or rats subjected to right nephrectomy and partial infarction of the remaining kidney, are either prevented or reduced by a low sodium intake.78,79,80

The antiproteinuric effect of ACE inhibitors or calcium antagonists

In various renal disorders in humans, induced nephropathies in animals and in essential hypertension the administration of ACE inhibitors reduces proteinuria and improves prognosis.66,81 This effect is independent of any associated change in blood pressure or the extent of pre-existing renal impairment. The conclusion that this beneficial effect is indeed due to the induced fall in proteinuria is supported by two studies in experimental nephropathies in animals in which, when ACE inhibitors failed to reduce proteinuria, the kidneys were not protected from injury.66,82

In essential hypertension83,84 and most forms of human renal disease,66 including diabetic nephropathy, proteinuria appears to determine the pro- gnosis. Nevertheless, induced reductions in proteinuria with an ACE inhibitor or a calcium antagonist, which diminish the rate of decline in renal function, are reversed or prevented by a high salt intake.76,85,86 In 12 patients with proteinuria varying from 3.2 to 10.5 g/24 h Heeg et al76 studied the effect of increasing salt intake from 50 to 200 mmol/24 h on the antiproteinuric effect of 10 mg of lisinopril. On a sodium intake of 50 mmol/day, proteinuria fell by 50% whereas on a salt intake of 200 mmol/day the antiproteinuric effect of the ACE inhibitor was abolished (Figure 3). In a group of patients with non-diabetic renal disease the best antiproteinuric effect, accompanying the administration of an ACE inhibitor, was observed on those days when the daily sodium intake was below 100 mmol/day.75 The blunting of the antiproteinuric effect of ACE inhibition is reversed by the administration of a diuretic such as hydrochlorothiazide.87 The blocking effect of a high salt intake on the antiproteinuric effect of an ACE inhibitor has also been demonstrated in diabetic hypertensive rats.

Figure 3

The effect of a rise in urinary sodium excretion on the proteinuria of nine patients who were on lisinopril whose mean proteinuria before the administration of lisinopril was 6.4 g/day; the lisinopril was administered throughout the three consecutive periods of observation. The change in urinary sodium excretion was not accompanied by a significant change in blood pressure.73


In patients and rats with hereditary hypertension or various forms of renal disease dietary salt intake controls intraglomerular capillary pressure and urinary protein excretion, and thus the rate of renal functional deterioration, and it opposes the beneficial antiproteinuric effect of ACE inhibitors and calcium antagonists.

Non-cardiovascular effects

Bone density and renal stones

Urinary sodium excretion and therefore sodium intake controls the urinary output of calcium.88,89 A high dietary salt intake therefore leads to a raised urinary calcium which in the long term may lead to calcium mobilisation from bone.88 In 410 healthy men and 476 healthy women aged 20–79 years Itoh and Suyama found that the higher the sodium intake the greater the loss of urinary calcium and the excretion of hydroxyproline,89 an increase in dietary sodium of 100 mmol/day was associated with an increase in calcium excretion of 0.6–1 mmol. In elderly healthy normal humans an increase in salt intake for 2 to 10 days increases the urinary excretion of calcium, hydroxyproline, cyclic AMP and osteocalcin.90,91,92 An increase in dietary salt and the resultant increase in calcium excretion also stimulate an increase in 1,25(OH)2D3 which appears to be mediated by a rise in parathyroid hormone. The increase in 1,25(OH)2D3 indicates a compensatory response to calcium depletion, while increases in urinary hydroxyproline92 and osteocalcin92,93 are indicators, respectively, of an increase in bone resorption and bone formation. A rise in urinary cyclic aderosine monophosphate (AMP) occurs when there is a rise in plasma parathyroid hormone (PTH).90,92 A rise in salt intake from 70 to 170 mmol/day in elderly women increases their calcium loss.92 Conversely a modest reduction in salt intake reduces urinary calcium excretion.90,94 The finding that in the elderly urinary sodium excretion controls the urinary excretion of calcium and some aspects of bone metabolism suggests that dietary sodium intake may contribute to the reduction in bone density that occurs in the elderly.

The effect of salt intake on the bones, however, is likely to be relevant throughout the life of the individual. A study in 380 girls early in puberty, which confirmed the close association between urinary sodium and calcium excretion, has shown that urinary calcium has a negative effect on total body calcium and total body bone density. It follows, therefore, that the attainment in youth of a reasonable peak bone mass, which has a significant bearing on the incidence of osteoporosis after the menopause, is imperilled by a high sodium intake during puberty.95 In post-menopausal women, Zarkadas et al96 calculated, from the effect of a few days rise in sodium intake, that an increased intake of 50 mmol/day for 10 years would deplete the calcium stores by about 7.5% which is in line with Devine et al’s97 finding in 124 post-menopausal women, studied for 2 years, that urinary sodium excretion is negatively related to bone density at the intertrochanteric and total hip sites. Multiple regressions also showed that both dietary calcium and urinary sodium excretion are significant determinants of the reduction in bone mass which occurred over the 2 years.97 The data suggested that if the daily excretion of sodium were halved it would have an equivalent effect on reducing bone loss to that of increasing calcium intake by 891 mg/day. No bone loss occurred at the hips when calcium intake was above 1768 mg/day or the urinary sodium excretion was below 92 mmol/day.

There is one retrospective study in men and women using 24-h diet recalls, for a 2-year period between 1973 and 1975, and a follow-up mineral density measurement between 1988 and 1991. No effect of sodium intake on bone mineral density was apparent except for a small significant protective effect of a lower sodium intake on the distal radius of men.98 Nordin and Polley,99 however, did find a negative association between forearm mineral density and 24-h sodium excretion in post-menopausal women. A subsequent 9-month period of sodium restriction (by only 30 mmol/day) in a sub-sample failed to reveal any change in bone mineral density. A high sodium intake is also implicated in the pathogenesis and treatment of hypercalciuria in both children and adults100,101,102 and of calcium depletion in corticosteroid treated patients.103 Normal rats given salt supplements also have an increase in urinary calcium excretion, and after a year their bones contain less calcium than their controls.104,105

It is possible that the relation between urinary sodium excretion to bone density in patients with essential hypertension may be more significant than in normotensive controls. For a given salt excretion patients with essential hypertension excrete greater quantities of calcium, hydroxyproline and cyclic AMP than normotensive controls.91 They also have a tendency for a reduced serum ionised calcium, a raised plasma parathyroid hormone and 1,25 dihydroxyvitamin D and an increased calcium absorption. When given a high salt diet the children of hypertensive parents have a greater urinary calcium excretion than children from normotensive parents.106 Over a mean follow-up of 3.5 years in 3676 white women aged 66 to 91 years the rate of bone loss in the femoral neck, adjusted for age, initial bone density, weight, smoking and regular use of hormone replacement therapy, the rate of bone resorption increased with the blood pressure measured at base line.107 The SHR and Milan hypertensive rats are also more likely to develop bone demineralisation than their normotensive controls.108,109 Thiazide diuretics which cause a reduction in calcium excretion when given to men and women with and without hypertension reduce the number of hip fractures.110,111

Inasmuch as kidney stones are known to be associated with a raised urinary excretion of calcium it is probable that the salt-induced increase in urinary calcium excretion in SHR and essential hypertension contributes to their greater incidence of renal stones.112,113,114


In normal humans salt intake influences urinary calcium excretion and bone turnover. In essential hypertension and hypertensive strains of rat urinary calcium excretion is raised, there is an increase in bone turnover and the bones of the SHR and the Milan hypertensive rat tend to be demineralised. In post-menopausal women urinary sodium excretion controls calcium excretion positively and bone density negatively. It is probable that the increase in renal stones in essential hypertension and the SHR is due to the salt induced rise in urinary calcium excretion.

Carcinoma of the stomach

Of all the factors that relate to cancer of the stomach, the second most common cancer in the world, the relationship to salt is the strongest.115 Randomly selected 24-h urine collections from 39 populations sampled from 24 countries were obtained from the Intersalt study. Median sodium excretion levels were standardised for age and sex between the ages of 20 and 49 years and averaged per country. Ecological correlation-regression analyses of the sodium excretion levels in relation to national stomach cancer mortality rates were highly significant in men and women (Figure 4).

Figure 4

The relation of urinary salt excretion to cancer of the stomach. (Adapted from Joossens JB, Hill MJ, Elliott P. Int J Epidemiol 1996; 25: 494–504.)

A high salt diet in both humans and experimental animals is known to cause gastritis and when co-administered with known gastric carcinogens promotes their carcinogenic effect.116,117 One such promoter appears to be Helicobacter pylori, which has been shown to be associated with progression of gastritis to gastric cancer.116 Furthermore a high salt diet increases Helicobacter pylori colonisation.116 Prospective studies have shown a positive association between Helicobacter pylori and gastric cancer amounting to a two-to three-fold increase in risk.118


Carcinoma of the stomach is strongly related to dietary sodium intake.


Regional data from England and Wales have shown that there is a strong correlation between the purchase of table salt and asthma in men and children.119 There are two interventional randomised double-blind, placebo controlled, crossover trials in men with mild to moderate asthma, of the effect of altering the intake of sodium for several weeks. There were 27 patients in the first trial and 36 in the second. The clinical severity of the asthma was assessed in one trial while, in another, the airway's response to histamine was measured.120,121 Both these small trials showed that an increase in dietary sodium, 80 mmol/day in one and 204 mmol/day in the other, increased both the severity of the asthma and bronchial reactivity. There is another randomised, crossover trial in 17 male asthmatics. There were three levels of sodium intake, each for 2 weeks. The largest difference in intake was 118 mmol/day. The only observation recorded was peak expiratory flow which was measured by the patients themselves in their own homes. No effect on peak expiratory flow was detected.122

An observational study on 138 men with initial to moderate asthma showed that bronchial reactivity was strongly related to 24-h urinary sodium excretion, allowing for the effect of age, atopy and cigarettes.123 Three other observational studies on relatively large groups of normal men and boys did not reveal a relation between urinary sodium excretion and bronchial reactivity to methacholine.124,125,126,127


The level of salt intake may be injurious to male patients with asthma. There is no evidence that salt intake effects airway responsiveness in normal subjects.


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Correspondence to H E de Wardener.

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  • dietary salt
  • left ventricular mass
  • conduit and resistance arteries
  • strokes
  • renal function
  • bone mass

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