Obesity and asthma prevalence have been increasing over the past decade. Epidemiological evidence demonstrates that obesity results in an increased risk of developing incident asthma. In fact even modest levels of increased weight produce an increased asthma risk. Recently published data suggest that obese asthmatics may represent a distinct phenotype of asthma. Obese asthma patients demonstrate increased asthma severity as indicated by increased exacerbations and decreased asthma control, though they do not appear to have increased airway cellular inflammation. It seems likely that obesity does not contribute to asthma through conventional TH2 mediated inflammatory pathways, but through separate mechanisms that are specific to the obese state. This may explain why obese asthmatics have variable responses to conventional asthma therapies, specifically relative corticosteroid resistance. Small studies suggest that obese asthmatics experience improvements in disease with weight loss, other interventions to target asthma in the obese need to be investigated. There are several postulated mechanisms for the occurrence of this distinct phenotype. These mechanisms include the presence of co-morbidities such as gastroesophageal reflux disease and sleep disordered breathing; systemic inflammation associated with obesity (with elevated levels of circulating cytokines such as interleukin 6 and TNF-); increased oxidative stress; and hormones of obesity such as adiponectin, leptin and resistin. Although the mechanisms underlying obesity in asthma require further investigation, obesity plays a major role in the current asthma epidemic and likely results in a distinct phenotype of disease.