04/06/2025
Asthma: Psychoneuroimmunologic Implications
The immunosuppressive effects of the HPA can sometimes have beneficial effects when the immune system is overactive. For years it has been known that corticosteroids such as cortisol or its synthetic derivative prednisone can dampen painful inflammation produced by hypersensitive immune cells. Of particular interest here is asthma, a disease in which immunologic hyperreactivity produces mucosal secretions and bronchoconstriction that make it difficult to breathe. In some cases, synthetic corticosteroids can alleviate asthmatic symptoms; in others, the inability of corticosteroids to produce the desired effects has been attributed to faulty steroid receptors in immune cells (Spahn et al., 1995).
Asthma can be mediated by a number of psychological mechanisms in addition to stress and corticosteroids, one being immunoconditiing. Clinicians have long acknowledged the beneficial effects of reverse conditioning through hypnosis to ameliorate asthma. Diamond (1959) reported that conditions were ameliorated through hypnosis in 40 of 55 asthmatic children ages 5 to 13 who had been unresponsive to previous biochemical treatment, with a follow-up time of two years. Diamond used conventional methods with most patients, but he inferred that most of these children had asthma that was mediated largely by psychogenic pathways, which is why they were unresponsive to the chemical treatment but very responsive to psychological (hypnotic) treatment. The first controlled study (although perhaps not ethical by today’s standards) of this phenomenon involved the monitoring of airway resistance during (non-hypnotic) suggestions to asthmatics, healthy controls, and sufferers of bronchitis or other restrictive lung diseases. The subjects were told that they were inhaling a bronchoconstrictor as part of an industrial air pollutant study, when they were really only inhaling an inert substance, saline. Of 40 asthmatics, 12 had extreme asthmatic attacks, and 7 others experienced a significant increase in airway resistance, albeit not enough to induce a full-blown attack. None of the other subjects in the study experienced any significant changes, suggesting that the phenomenon was specific to the asthmatic condition (Luparello et al., 1968). This type of result has been replicated many times with similar experiments, all of which emphasized that the psychological modulation of bronchial functioning was evinced in only a specific portion of the subjects tested, usually 30-40% (see review in Isenberg, Lehrer, and Hochron, 1992). Such results demonstrate that some form of immunoconditioning can occur in certain asthmatic patients, in a manner similar to the rats conditioned to a variety of stimuli. That is, physiological shifts begin to be paired with perceived events to such an extent that the very thought of an allergen or a bronchoconstrictor can produce the phsyiological changes precipitating an asthmatic attack.
Figure 5: Extrinsic and Intrinsic Pathways of Bronchoconstriction (adapted from Mrazek & Klinnert, 1991).
The fact that only some asthmatics respond to suggestions indicates there may be some subjects that respond hypersensitively. There may be more than one pathway involved in asthma, one being primarily psychogenic ("intrinsic") and the other being primarily the result of an "extrinsic" allergen (see figure 5). The vagus nerve is heavily implicated in the intrinsic pathway, as it is the primary parasympathetic innervation of the bronchial tubes and is the major bronchoconstrictor effector. Indeed, vagal blockade by an anticholinergic chemical (the neurons of the vagus are largely cholinergic), atropine sulfate, inhibits the bronchoconstriction to suggestion in tests similar to those described above (Mrazek and Klinnert, 1991). The major contradiction here, however, is that sympathetic arousal (i.e., stress), often triggers psychogenic asthma, but the sympathetic response has a bronchodilating effect, not a constricting one. A possible resolution is that activation of the sympathetic nervous system ("intense affect") may induce a vagal cholinergic reflex response due to a sympathetic/parasympathetic nervous system imbalance. Furthermore, the release of SP is stimulated by sympathetic arousal, and, as discussed earlier, it stimulates the hypersensitive response through mast cell degranulation and inhibition of glucocorticoid production via the HPA (Mrazek and Klinnert, 1991).
