Conclusions on Buteyko trial have no scientific basis.

Peter Kolb

A surprising aspect of the Bowler study was the conclusion that was reached. The failure by Bowler to recognize the theory on which Buteyko breathing therapy (BBT) is based, led one of the authors to dissent and withdraw her name from the paper.

Bowler came to the conclusion that Buteyko patients were probably persuaded, by more frequent telephone contact, to reduce their medication, and that this reduction in medication made them feel better. He rejected the Buteyko theory on the basis that BBT failed to show any statistically significant improvement in lung function. However, we question the science behind the lung function tests, particularly in the context of the Buteyko theory.

Let's take another look at the results. Apart from ETCO2, all of the results of the study support Buteyko’s hyperventilation theory. The problem lies with their scientific interpretation. Here again, are the significant findings:

On the question of ETCO2, it should be noted that since this result contradicts the reduced minute volume found in the Buteyko group, and since ETCO2 was used only as a surrogate for PaCO2 (they are not necessarily the same in obstructive airway disease), no conclusion can be drawn from this finding.

Failure in lung function improvement is being interpreted as a failure by BBT to change the "objective measures of asthma". This implies that there is only a perception by the patient that his asthma is reduced.

This thinking is fundamentally flawed on three levels:

  1. At the lowest level, Bowler recognised that, although there was a substantial reduction in medication, PEF and FEV1 did not get any worse. And that's where the matter should have ended. But what they were looking for was a reduction in medication and an improvement in lung function.

    Basic science tells us that when comparing two processes you alter only one variable at a time to determine its effect on another. While keeping all other variables constant, you can either

    Since asthmatics medicate to maintain patency of their airways, the latter is more realistic. This was met by the trial results. Looking for a reduction in medication and an improvement in lung function is like comparing the performance of two cars. You can say one travels further than the other on the same fuel, or you can say it uses less fuel to travel the same distance. It makes no sense to expect it to travel further and use less fuel.

  2. At the second level, much of the confusion results from the fact that the lung function tests were originally developed without any clear understanding of the disease they were intended to measure. The hyperventilation theory, which is the subject of this study, clearly precludes the use of these tests, since it predicts that the hyperventilation manoeuvres inherent in the tests produce an increase in airway resistance, which is the quantity being measured. This was confirmed by Gayrard (see reference below) who found that a single deep breath as is taken during a PEF test, increases the specific airway resistance by 70% in asthmatics. It is a fundamental principle in scientific measurement, apart from it being common sense, that you cannot use a measurement technique which changes the variable being measured.
  3. And finally, at the highest level, according to the theory the bronchospasm produced by hyperventilation is not part of any disease process, but a natural response to low CO2. It just happens that the genetic predisposition of asthmatics provides for a stronger bronchoconstrictive response to hypocapnia than in non-asthmatics.

Although PEF and FEV1 have become accepted as the gold standard for measuring asthma, new insights into asthma provided by the hyperventilation theory should make us question the value of these tests. They tell us something about airway resistance during alveolar hyperventilation manoeuvres. They tell us nothing about airway resistance during normal breathing.

Peter Kolb BSC(Eng),MSc(Med),CPEng(Biomed)

Ref: Gayrard P et al, “Bronchoconstrictor effects of deep respiration in patients with asthma” Am. Rev. Respir. Dis. 1975;111:433-439

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