Effect of dietary sodium on the severity of bronchial asthma. Are asthmatics salt-sensitive? A preliminary controlled study. Effect of changing dietary sodium on the airway response to histamine. Dietary chloride as a possible determinant of the severity of exercise-induced asthma. Dietary salt, airway inflammation, and diffusion capacity in exercise-induced asthma. Dietary salt restriction improves pulmonary function in exercise-induced asthma. Effect of alterations of dietary sodium on the severity of asthma in men.
A high sodium intake has been found to increase bronchial reactivity in men with asthma. The effects of change in sodium intake on peak flow rate have not been determined.
                The effect of changing dietary salt intake for two weeks on the severity of asthma as measured by peak expiratory flow (PEF) was studied in 17 patients with mild asthma in an open randomised crossover trial. PEF measurements were made by the patients in their own homes. Patients were placed on three levels of dietary sodium intake: normal, low, and high. Sodium intake was assessed by 24 hour urine collection.
                The mean (SD) urine sodium was 147 (45), 84 (32), and 201 (73) mmol/24 hours in the normal, low, and high sodium intake periods respectively. There were no significant differences in PEF or PEF amplitude (highest--lowest PEF), an index of asthma lability, between the three dietary salt periods. CONCLUSION A low and high dietary salt intake for two weeks has no effect on peak expiratory flow in patients with mild asthma. Epidemiologic evidence suggests that high levels of salt consumption are associated with "spastic" disorders of smooth muscles, ie, essential hypertension and bronchial asthma. Experimentally, it has been shown that high intake of salt leads to increased bronchial hyperreactivity in asthmatics, ie, enhanced contractility of bronchial muscle to spasmogenic stimuli. On the basis of these observations, the following questions were asked: (1) Does salt loading worsen the clinical and functional findings in asthmatics? (2) Is it the sodium or the chloride in salt that is important?
                To answer these questions, the effect of salt restriction (= 5 to 6 g NaCl/d = 86 to 103 mmol Na), salt loading (+ 6.1 +/- 2.8 g NaCl/d = + 105 +/- 48 mmol Na), and loading with sodium citrate in nearly equimolar concentrations (+ 140 +/- 40 ml Shohl's solution, = + 120 +/- 30 mmol Na) was investigated in 14 asthmatics in a controlled crossover study. The total sodium load during the high salt diet was 191 to 209 mmol of sodium per day and during the sodium-citrate phase, 206 to 223 mmol of sodium per day.
                Statistical analysis showed that salt loading worsened symptoms (p = 0.06) and increased the use of inhaled steroids (p < 0.05). The effect on lung function was less equivocal: salt loading worsened the forced expiratory volume in 1 s (p < 0.01) and the peak expiratory flow rate (p < 0.05). This effect was presumably mediated by sodium, not chloride, as is demonstrated by loading with sodium citrate.
                Patients with bronchial asthma seems to be salt-sensitive, the responsible ion being presumably sodium. A low-salt diet appears to have a favorable effect in patients with asthma and to reduce the need for anti-asthma drugs. The airway response to histamine has been shown to be related to the 24 hour urinary excretion of sodium. To assess whether this relation is likely to represent a direct causal association a randomised double blind crossover trial of slow sodium (80 mmol/day) was compared with placebo in 36 subjects having a low sodium diet. The dose of histamine causing a 20% fall in FEV1 (PD20) was 1.51 doubling doses lower when the men were taking sodium than when they were taking placebo (p less than 0.05). On the basis of PD10 values, the difference in men was 1.66 doubling doses of histamine (p less than 0.05). There was no corresponding effect in women. Regressing PD10 against urinary excretion of electrolytes with data from the two occasions during the trial and the measurements made before the trial showed a significant association with sodium excretion after allowance had been made for any effect associated with potassium or creatinine excretion, the latter being a marker of the completeness of the urine collection. Again there was no corresponding effect among women. These findings are compatible with the differences in regional mortality data for England and Wales, which show a relation between asthma mortality and regional per person purchases of table salt for men but not for women. Dietary sodium chloride (NaCl) has been shown to alter the severity of exercise-induced asthma, but it is not known if the sodium and chloride ions have independent effects in this regard. The hypothesis tested in the present study was that both a low sodium, low chloride diet and a high sodium, low chloride diet would improve post-exercise pulmonary function in subjects with exercise-induced asthma (EIA) compared to a normal NaCl diet (NSD); but that neither of these diets would have an effect on post-exercise pulmonary function in control (non-EIA) subjects. Eight subjects who suffered from EIA and eight subjects who did not (control) took part in a double-blind crossover study. Pre- and post-exercise pulmonary function was assessed after 2 weeks on a NSD, a low NaCl diet (LSD, low sodium, low chloride) or a sodium bicarbonate diet (NaHCO3 diet, high sodium, low chloride). A 1 week washout period occurred between diets. Altering dietary sodium or chloride had no effect on pre-exercise (baseline) pulmonary function in either group or on post-exercise pulmonary function in control subjects. However, both the LSD and the NaHCO3 diet lessened the deterioration in post-exercise pulmonary function in EIA subjects. Comparing results from pre- to post-exercise, forced expiratory volume in 1 s (FEV1) at 15 min post-exercise differed significantly (P < 0.05) between diets [mean (SEM) 7 (4)% on the LSD, 14 (4)% on the NaHCO3 diet, and 19 (2)% on the NSD]. Similar patterns were observed for forced vital capacity (FVC), forced expiratory flow rate at 25%-75% FVC and peak expiratory flow rate. The NaHCO3 diet lessened the deterioration of post-exercise pulmonary function, but not to the extent of LSD. These data suggest that both sodium and chloride contribute to the worsening of EIA symptoms seen after consuming a normal or high NaCl diet. Recent studies have supported a role for dietary salt as a modifier of the severity of exercise-induced asthma. The main aim of this study was to demarcate a possible mechanism by which dietary salt modification may alter exercise-induced airway narrowing in asthmatic patients.
                Twenty-four patients participated in a randomized, double-blind crossover study. Subjects entered the study on their normal salt diet (NSD) and were then placed on either a low-salt diet (LSD) or high-salt diet (HSD) for 2 wk with a 1-wk washout period occurring between diets. Pre- and postexercise spirometry, pulmonary diffusion capacity (DLCO) and its subdivisions, and induced sputum were obtained on the NSD and at the end of each 2-wk treatment period (LSD and HSD).
                FEV1 decreased by 7.9 +/- 2.8% on LSD, 18.3 +/- 4.0% on NSD, and 27.4 +/- 3.2% on HSD at 20 min postexercise. The NSD and HSD induced significant reductions (P < 0.05) in DLCO and its subdivisions. However, postexercise pulmonary capillary blood volume significantly increased (P < 0.05) by 6.3 and 9.6 mL on NSD and HSD, respectively, compared with baseline values, with no significant change (P > 0.05) being observed on LSD. Postexercise-induced sputum neutrophil and eosinophil differential cell counts and induced sputum supernatant concentration of eosinophil cationic protein, interleukin (IL)-1beta, IL-8, leukotriene (LT) C(4)-E(4), LTB(4), and prostaglandin D(2) were significantly elevated (P < 0.05) on NSD and HSD compared with LSD.
                Our findings indicate that dietary salt loading enhances airway inflammation following exercise in asthmatic subjects, and that small salt-dependent changes in vascular volume and microvascular pressure might have substantial effects on airway function following exercise in the face of mediator-induced increased vascular permeability. Exercise-induced asthma (EIA) occurs in approximately 90% of persons with asthma. The mechanism has not been delineated. Epidemiological studies have suggested that dietary salt may play a role in airway responsiveness. Therefore, the purpose of this study was to determine the influence of both elevated and restricted salt diets on pulmonary function in subjects with EIA.
                Eight subjects with EIA and eight subjects without EIA (control) participated in a double-blind crossover study. Pulmonary function was determined pre- and post-exercise challenge before and after 2 wk on a normal salt, sodium chloride, diet (NSD), a low salt diet (LSD), and a high salt diet (HSD). A 1-wk washout occurred between diets.
                Diet had no effect on preexercise pulmonary function values in either group and had no effect on postexercise pulmonary function values in control subjects. However, LSD improved and HSD worsened postexercise pulmonary function values in EIA subjects. Forced expiratory volume in 1 s (FEV1) decreased by at least 10% in EIA subjects with exercise. In EIA subjects, FEV1 decreased by 14+/-6% on LSD, 20+/-7% on NSD, and 24+/-6% on HSD at 15 min postexercise. Similar patterns were observed for forced vital capacity and peak expiratory flow rates. Although LSD did not normalize pulmonary function in EIA, it did improve it.
                These data suggest that individuals with EIA might benefit from lower salt diets. There is some evidence of a positive association between increased dietary salt consumption and both increased bronchial reactivity and mortality from asthma in men. This study assesses the effects of alterations in dietary salt consumption on the clinical severity of asthma in adult male asthmatic patients.
                A randomised, double blind, placebo controlled, crossover design was employed. Twenty seven mild to moderate asthmatic patients were established on a low sodium diet (80 mmol/day) at the end of a 4-5 day run in period and then randomised to receive 200 mmol/day slow sodium or matching placebo for five weeks, crossing over to the alternative regime for a further five weeks. Patients used diary cards to record twice daily peak expiratory flow rates, daily symptom scores, and bronchodilator consumption. Spirometry and degree of bronchial responsiveness (methacholine challenge test) were measured at screening and at the end of each treatment period. Twenty four hour urinary sodium excretion was measured at screening and in duplicate for each treatment period.
                Twenty two patients completed the study. For these patients the mean (95% confidence interval (CI)) difference in 24 hour sodium excretion between treatments was 204 (175 to 235) mmol. Compared with placebo, sodium supplementation resulted in deleterious alterations of all measured parameters. Bronchial reactivity rose on slow sodium with a 0.73 (0.2 to 1.3) doubling dose methacholine difference compared with placebo. Estimated median (95% CI) difference in bronchodilator consumption was 1.3 (0.4 to 2.1) puffs per day, the estimated median difference in symptom score was 0.6 (0.2 to 0.9), and mean forced expiratory volume in one second fell by 0.21 (0.05 to 0.37) 1. The peak expiratory flow rate rose on placebo and fell on slow sodium. Median differences between treatments were 5.6% (2.2% to 9.8%) for morning and 7.8% (3.9% to 12.9%) for evening peak expiratory flow rate.
                Our results suggest that large increases in dietary sodium result in physiological deterioration and increased morbidity in male asthmatic patients.