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.