Where Psyche Meets Soma in Asthma
Where Psyche Meets Soma in Asthma
Nemo Psychologus Nisi Physiologus -- Johannes Mueller
Recognition of the relationship between psyche and soma dates back to antiquity and is captured in written records and historical accounts. Galen, in the first century CE, was reported to have written that the condition of intermittent obstruction of breathing (now called asthma) was secondary to secretions dripping into the lung from the brain. This was arguably among the earliest accounts of the important link between mind and body in medical illness. Indeed, asthma is considered by many to be the prototype of psychosomatic illness. Maimonides, circa 1190 CE, wrote in his Book of Asthma:
When in mental anguish, fear, mourning or distress...his agitation affects the respiratory organs and he can not exercise them at will...The cure of such conditions lies not in food recipes, neither in drugs alone, nor in regular medical advice...psychological methods are a greater help.
Current literature documents negative effects of stress and emotion on asthma. However, there is controversy as to whether emotions and stress adversely influence asthma directly or by exacerbating poor treatment adherence. The purpose of this article is to elaborate pathways of connection between psyche and soma in asthma, placing emphasis on empirical support and rationale for psychophysiologic mechanisms underlying the impact of stress and emotions on asthma.
Definition and Pathogenesis
The National Heart, Lung, and Blood Institute (NHLBI) defines asthma as a chronic inflammatory disorder of the airways, in which bronchial hyper-reactivity causes recurrent episodes of wheezing, breathlessness, chest tightness and cough associated with airflow obstruction that is reversible (NHLBI, 1997). The pathogenesis underlying asthma is best understood as a genetically predetermined vulnerability of the airway to a complex set of interactions involving inflammatory mediators (cytokines and chemokines), effector cells (e.g., eosinophils, T cells) and the (autonomic) nervous system (Middleton et al., 1998). Pharmacologic treatment of asthma is directed both at anti-inflammatory (immune/allergic) and bronchodilator (neural) pathways.
Many diverse stimuli can trigger asthma symptoms including allergens, infections, exercise, cold air and emotions. More than one stimulus may trigger an asthma attack, and it is often difficult to identify with certainty the specific stimuli that triggered symptoms (NHLBI, 1997). An individual's susceptibility to asthma triggers may change in the course of maturation or in response to life circumstances.
Asthma is known to have a strong genetic predisposition. Children with one asthmatic parent have approximately a 20% chance of developing the disease, while those with two asthmatic parents have nearly a 50% risk. Risk factors for the phenotypic expression of asthma in children with genetic loading include early exposure to viral infections, highly allergenic substances and emotional stress in the family (Mrazek et al., 1991).
Morbidity and Mortality
Asthma is one of the most common chronic diseases of childhood, affecting 4.8 million children in the United States (NHLBI, 1997). Among children with chronic medical conditions, asthma is the most common cause for hospitalization and school absence (Newacheck and Halfon, 2000). Asthma is more prevalent in adolescent males than females and in African American children than Caucasians. Asthma prevalence, morbidity and mortality have been increasing over the past two decades, despite new effective medical regimens (Weitzman et al., 1992).