A recent study by M. Brumpton et al., published in the International Journal of Epidemiology has shed light on the complex interactions and joint effects of anxiety, depression and obesity on the onset and asthma development.
Approximately 300 million people suffer from asthma, amounting to nearly 1% of the total global disease burden, worldwide. Historically, asthma was often been viewed as a ‘psychosomatic’ condition.
This dates back to Hippocrates, who stated that the “asthmatic should guard himself against his own anger”, and Maimonides, in the 11th Century suggesting that “mental anguish and fear” may cause asthma, while, more recently, Sir William Osler (1892) referring to asthma as ‘‘a neurotic affection” (cf. J. Douwes et al., 2011).
A limited number of prospective studies have investigated this association. Jonas and Wagener found a moderate association of anxiety or depression symptoms with incident asthma in non-smoking adults. Scott et al. found that early-onset worry and depression (at <21 years of age) had a moderate association with adult-onset asthma.
Much of past research has found an association of anxietyor depression with the prevalence of asthma, whereas obesity has also been related to an increased risk of asthma.
Previous studies have also discussed that the obesity-asthma correlation or the impact of worry and depression may be due to inflammation. This indicates that a common underlying pathway may link these conditions with asthma. However, the combined effects of anxiety, depression and obesity on asthma development has not been previously investigated.
Brumpton et al. (2013) in their prospective cohort study conducted over the period of 11 years included 23 599 adults, 19–55 years old and that were free from asthma at baseline. Their findings show that individuals that had reported incidents of worry or depression at baseline had an increased risk of incident asthma during the follow-up, and this effect was increased even more when obesity was involved.
This large prospective study indicates that obesity may interact with worry or depression to further increase the risk of asthma in adults. The study provides further insights into the pathogenesis of asthma, and also supports previous research indicating that psychological factors influence the onset of atopic disorders.
Lifestyle-related behaviours such as smoking, and less physical exercise due to distress, may be mediators leading to the development of asthma. On the other hand, these health behaviour variables may also be confounding factors that cause both psychological distress and asthma.
The authors do acknowledge the difficulty in determining causality, but they put forward a strong argument suggesting the involvement of a common pathway, such as inflammation, that may bring together all three conditions – anxiety, depression and obesity.
This is substantiated by a previous research showing that anxiety is related to increased production of pro-inflammatory cytokines, whereas both depression and obesity are characterized as conditions of low-grade chronic inflammation.