Obesity and asthma.
Population-based studies have defined a significant, bidirectional, dose-dependent association between obesity and asthma. Obesity does not cause airflow obstruction, but can result in pulmonary restriction and a reduction in airway diameter, and that could contribute to airway hyper-responsiveness. Mouse models of asthma have demonstrated that obesity and adipokines can enhance airway hyper-responsiveness, airway inflammation, and allergic responses, but it is unclear whether obesity-associated inflammatory mechanisms are relevant in human asthma. Shared environmental and genetic factors are incompletely understood, but very likely to be relevant. Obese asthma appears to be a distinct and novel phenotype of asthma, associated with a reduction in lung volumes, lack of eosinophilic inflammation, altered response to asthma controller therapy, glucocorticoid resistance, and poor asthma control.
Beuther
David A
DA
National Jewish Health and Department of Pulmonary and Critical Care Medicine, University of Colorado at Denver Health Sciences Programs, Denver, CO 80206, USA. beutherd@njhealth.org
D001249:Asthma / Q000150:complications* / Q000503:physiopathology* / Q000628:therapy; D015992:Body Mass Index; D006801:Humans; D009765:Obesity / Q000150:complications* / Q000503:physiopathology* / Q000628:therapy; D012123:Pulmonary Ventilation / Q000502:physiology; D012307:Risk Factors