Biofeedback for Asthma Comorbid With Anxiety or Depression

Introduction

Previous published research from our laboratory has demonstrated a clinically significant effect for heart rate variability biofeedback on asthma clinical condition. In an NIH-supported trial just completed, however, the investigators found that, among unmedicated patients with mild or moderate asthma, the effects were no greater than for most placebos found in the literature. Significant effects were found in reducing anxiety and depression, even among a population that was selected neither for clinical anxiety or depression.

There is considerable evidence from the literature that negative affect is common in asthma, and that it may interact with asthma. Anxiety is often accompanied by hyperventilation, as is asthma, and hyperventilation can exacerbate asthma, by increasing exposure to in air that is colder drier than the lung (body temperature at 100% humidity). Indeed some of the asthma symptoms affecting quality of life are associated with hyperventilation, which may partially be stimulated by anxiety, and partially by increased airway resistance, which increases respiratory drive. Thus asthma processes can increase anxiety (through symptoms associated with hyperventilation), just as anxiety can exacerbate asthma (through hyperventilation). Additionally, autonomic hyperreactivity, which is common in anxiety, may produce parasympathetic hyperreactivity that may cause bronchoconstriction. There is considerable evidence that heart rate variability (HRVB) biofeedback ameliorates anxiety, just as it does asthma, so the combined effect may prove particularly beneficial to people with the comorbid condition. The investigators therefore propose a pilot study to test the effect of HRVB on an asthma population that is clinically anxious.

Another consistent effect of HRVB is on ameliorating depression. There is a good physiological rationale for using HRVB to treat negative affect and depression, stemming from anatomical evidence for connections between the site of HRVB effects on the baroreflex (mediated through nucleus tractus solitarius) and brain centers involved in negative emotion, particularly the insula and amygdala. Depression also is highly prevalent among asthma patients, and depressed patients often have poor health care behavior, and this may worsen asthma condition. Depressive symptoms also are associated with bronchoconstriction in asthma. Anxiety and depression are frequently comorbid, with some overlapping symptoms, so many anxiety patients will be expected to also show signs of clinical depression.

Also, it is possible that HRVB may improve by making asthma medication more available to the lungs, through deep breathing. Therefore asthma medication will not be restricted in this study, but medication intake will be monitored as one outcome measure. Similarly medication for anxiety or depression also will not be controlled, but daily intake and changes in medications will be monitored. Additionally patients with all levels of asthma severity will be studied, as long as they continue to be symptomatic. It is possible that, in a previous study, restricting inclusion to patients only with very mild asthma may have contributed to a floor effect that obscured biofeedback effects.