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Low Salt Diet No Help for Asthma Control 7-15-08
For patients with asthma, a low sodium diet did not improve lung function,
bronchial reactivity, or other measures of disease control, researchers here
found.
These findings from a six-week randomized controlled trial counter those from
most small interventional trials, reported Zara Pogson, M.R.C.P., of the
University of Nottingham and Nottingham City Hospital, and colleagues in the
July 15 issue of the American Journal of Respiratory and Critical Care Medicine.
"Despite the clear benefit of a low sodium diet on cardiovascular risk factors,"
they wrote, "there is no therapeutic benefit in the use of a low sodium diet
based on a dietary information sheet on asthma control in our study population."
Sodium, perhaps through its role in membrane transport, was thought to have an
impact on asthma by changing the ability of airway smooth muscle to contract,
the researchers said.
The trial included 199 men and women with physician-diagnosed asthma and
bronchial reactivity on challenge with inhaled methacholine. All patients
followed a low sodium diet with a daily intake target of 80 mmol.
They were randomized to six weeks of double-blind treatment with sugar-coated
sodium replacement tablets to achieve a normal sodium intake or placebo tablets
to maintain a low sodium diet.
Participants in the low sodium group were unable to reduce their sodium intake
as planned.
The 98 participants in the low sodium group had a median baseline 24-hour
urinary sodium excretion of 117 mmol (one gram of sodium = 44 mmol) with a mean
change from baseline in 24-hour urinary sodium excretion of -19.6 mmol (SD
63.6), and the 98 participants in the normal sodium intake group had a median
baseline 24-hour urinary sodium excretion of 119.5 mmol with a mean change of
+27.9 mmol (SD 74.2).
The final difference in daily sodium excretion was 50 mmol between groups.
"This is probably due to the fact that the participants already had a relatively
low baseline sodium intake," Dr. Pogson and colleagues suggested. The median
daily sodium urinary excretion averaged 117 to 119.5 mmol in the study compared
with the mean of about 168 mmol in the local population.
In the intent-to-treat analysis, there was no difference in bronchial reactivity
with the low sodium diet as measured by change in the inhaled dose of
methacholine that provoked a 20% fall in forced expiratory volume in one second
(FEV1) from baseline (doubling dose 0.42 versus 0.46, P=0.90).
Nor were there differences in any of the secondary outcomes. Comparing the low
sodium diet to normal sodium intake, the change from baseline findings included:
* No improvement in lung function (FEV1 -37.3 versus -62.0 ml, P=0.34).
* No benefit in forced vital capacity (FVC -16.8 versus -37.7 ml, P=0.55).
* No significant benefit for mean morning and evening peak flow (difference 1.5
L/min, P=0.73, and 1.2 L/min, P=0.82, respectively).
* No change in daytime and nighttime symptom scores in either group (P=0.12 and
P=0.49, respectively).
* No change in morning and evening bronchodilator use (P=0.92 and P=0.62,
respectively).
* No difference in scores on the Juniper Standardized Asthma Quality of Life
Questionnaire (+0.1 for both, P=0.49).
Adjusting for gender didn't appreciably change the findings (P=0.17 for
interaction), suggesting a lack of a large, sex-specific effect of the low
sodium diet on asthma control, the researchers said. Nor did a per-protocol
approach yield a difference between diet groups.
The study was powered to rule out an increase of more than 76 ml in FEV1, "and
we consider that this is not likely to be clinically important at the level of
the individual patient relative to the benefits that can be derived from other
interventions," they said.
However, the researchers noted that they were unable to exclude the possibility
that a longer intervention period or different patient subgroups may have shown
benefits to a low sodium diet.
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