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Pearson et al1 have failed to tease out any additional benefit of vitamin E supplementation in patients with mild to moderate asthma. Before concluding that this is the case, it is relevant to highlight several points in their study.
It is notable that the authors failed to measure any surrogate marker of inflammation such as exhaled nitric oxide, sputum eosinophils, or airway hyperresponsiveness (AHR) to an indirect bronchoconstrictor stimulus. Indeed, non-specific AHR to methacholine is only very tenuously linked to underlying endobronchial inflammation and tends to be related to changes in airway calibre.2,3 In this respect, the use of adenosine monophosphate or mannitol to assess AHR may have provided information regarding the underlying inflammatory status as these agents, which act similarly,4 cause the release of inflammatory mediators rather than directly causing contraction of airway smooth muscle. Use of these bronchoconstrictor stimuli are also more akin to real life situations as cold air and exercise also act in a similar physiological fashion. Moreover, the use of adenosine monophosphate has been shown to be more sensitive in detecting shifts in AHR than methacholine by approximately one doubling dilution.5
It is important to point out in the present study1 that patients in both groups at baseline had neither demonstrable symptoms nor short acting bronchodilator use. This in turn highlights the fact that these patients were clinically stable and there was no actual signal from which a discernable improvement in symptoms could be observed.
Before dietary manipulation with vitamin E is neglected, further studies are required in symptomatic asthmatics evaluating other important outcome parameters such as exacerbations and surrogate inflammatory biomarkers.
The aim of our study was to investigate “the effect of 6 weeks regular supplementation with vitamin E on the clinical control of asthma”.1 We thus used a combination of objective and subjective measures of asthma as our outcomes. The entry criteria were designed to be as inclusive as possible and to cover a population with mild to moderate asthma.
However, as Currie et al highlight, our study population had few symptoms, with a median daytime and night time symptoms score of 0. A similar intervention study of vitamin C and magnesium from our group covering a comparable population also recruited a population with few asthma symptoms,2 which was why we used bronchial responsiveness to methacholine as one of our entry criteria in the current study. We considered this the best measure of bronchial responsiveness when we designed the study, but agree that an alternative technique may have produced a different result.
We also agree with Currie et al that further studies of vitamin E are required in patients with asthma, including symptomatic asthmatics, particularly with regard to clinically relevant outcomes such as exacerbations.
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