Epidemiological data as well as data from mouse models of asthma indicate a relationship between obesity and asthma. The purpose of this review is to evaluate recent data addressing this relationship and its biological basis, and to evaluate the implications of these data for treatment. Obesity increases the prevalence, incidence, and possibly severity of asthma, while weight loss in the obese improves asthma outcomes. Obesity also influences asthma control and the response to standard asthma therapeutics. Moreover, obese mice exhibit innate airway hyperresponsiveness and increased responses to common asthma triggers. The biological basis for the relationship between obesity and asthma may be the result of common etiologies, comorbidities, effects of obesity on lung volume, or adipokines such as tumor necrosis factor alpha, leptin, and adiponectin. Understanding the mechanistic basis for the relationship between obesity and asthma may lead to new therapeutic strategies for treatment of this susceptible population.