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Published ahead of print on April 20, 2006, doi:10.1164/rccm.200602-231PP

Am. J. Respir. Crit. Care Med., Volume 174, Number 2, July 2006, 112-119

A more recent version of this article appeared on July 15, 2006
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Submitted on February 16, 2006
Accepted on April 20, 2006

Pulmonary Perspectives: Obesity and Asthma

David A Beuther1, Scott T Weiss2, and E. Rand Sutherland1*

1 National Jewish Medical and Research Center, Denver, CO, USA; University of Colorado Health Sciences Center, Denver, CO, USA, 2 Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: sutherlande{at}njc.org.

Asthma and obesity are prevalent disorders, each with a significant public health impact, and a large and growing body of literature suggests an association between the two. The systemic inflammatory milieu in obesity leads to metabolic and cardiovascular complications, but whether this environment alters asthma risk or phenotype is not yet known. Animal experiments have evaluated the effects of leptin and obesity on airway inflammation in response to both allergic and nonallergic exposures and suggest that airway inflammatory response is enhanced by both endogenous and exogenous leptin. Cross-sectional and prospective cohort studies of humans have shown a modest overall increase in asthma incidence and prevalence in the obese, although body mass index does not appear be a significant modifier of asthma severity. Studying the obesity-asthma relationship in large cohorts, in which self-reports are frequently used to ascertain the diagnosis of asthma, has been complicated by alterations in pulmonary physiology caused by obesity which may lead to dyspnea or other respiratory symptoms but do not fulfill accepted physiologic criteria for asthma. Recent investigations toward elucidating a shared genetic basis for these two disorders have identified polymorphisms in specific regions of chromosomes 5q, 6p, 11q13 and 12q, each of which contains one or more genes encoding receptors relevant to asthma, inflammation and metabolic disorders, including the {beta}2-adrenergic receptor gene ADRB2 and the glucocorticoid receptor gene NR3C1. Further research is warranted to synthesize these disparate observations into a cohesive understanding of the relationship between obesity and asthma.
Key words: Obesity, asthma, pathogenesis, inflammation, epidemiology




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