Asthma and psychiatric disorders

Asthma has been associated with psychological factors for centuries: Moses Maimonides in his "Treatise on Asthma" defined asthma as "difficulty of breathing or a pain in the chest" suggesting behavioural changes as one of the measures to cure it. The literature reports a significantly greater risk of depression, anxiety and/or mental disturbances in asthmatics, with important implications including symptom severity, reduced asthma control, lower quality of life, minor therapy adherence, higher incidence of smoking, inactivity and obesity, increase in the use of healthcare services and therefore a rise in financial burden. However, the evidence gathered is not univocal. Population studies suffer from relevant design limitations being frequently limited by a clinically uncontrolled, usually self-reported, diagnosis of asthma; furthermore, many of these studies used instruments of psychiatric self-evaluation, whereas other studies used psychiatric clinical interviews performed by non-specialised interviewers. Studies on clinical populations, which have the strength of a controlled diagnosis of asthma, are also burdened by some limitations, such as the use of self-evaluation instruments for psychiatric diagnosis, almost exclusively concerning anxiety and/or depressive disorders, and the absence of control groups. However, the demonstration of an association between asthma and affective disorders raised the debate on the true nature of this relationship, whether asthmatic disorders are associated with a higher risk of affective disorders, and/or vice versa, whether affective disorders expose to an increased risk of developing asthma. Finally, the mechanisms of the effects of inflammation on the brain have become an area of intensive study, and evidence appears that the high comorbidity between these disorders could be explained by the inflammation due to the mutual pathogenetic mechanisms, linked to the complex psycho-neuro-immunological pathways involving mainly pro-inflammatory cytokines and imbalance towards the Th2 T-cell response.