title: Does obesity produce a distinct asthma phenotype?
abstract: 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. Even modest levels of increased weight increase asthma risk. Recently published data suggest that obese asthma patients may represent a distinct phenotype of asthma. Obese asthma patients demonstrate increased asthma severity, as indicated by increased exacerbations and decreased asthma control; however, they do not appear to have increased airway cellular inflammation. It seems likely that obesity does not contribute to asthma through conventional Th type 2-mediated inflammatory pathways but, rather, through separate mechanisms that are specific to the obese state. This may explain the variable responses of obese asthma patients to conventional asthma therapies, specifically, relative corticosteroid resistance. Small studies suggest improvements in the disease with weight loss in obese asthma patients, and other interventions to target asthma in obese individuals need to be investigated. Several postulated mechanisms for the occurrence of this distinct phenotype have been postulated: 1) the presence of comorbidities, such as gastroesophageal reflux disease and sleep disordered breathing, 2) systemic inflammation associated with obesity (with elevated levels of circulating cytokines, such as IL-6 and TNF-alpha), 3) increased oxidative stress, and 4) 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 asthma epidemic and likely results in a distinct phenotype of the disease.
authors.affiliation: Department of Medicine, Duke University, Durham, North Carolina, USA.
authors.forename: Njira L
authors.initials: NL
authors.lastname: Lugogo
authors.forename: Monica
authors.initials: M
authors.lastname: Kraft
authors.forename: Anne E
authors.initials: AE
authors.lastname: Dixon
mesh_terms: D054392:Adipokines / Q000378:metabolism; D000818:Animals; D001249:Asthma / Q000453:epidemiology / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D015897:Comorbidity; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D009765:Obesity / Q000150:complications* / Q000453:epidemiology / Q000276:immunology / Q000503:physiopathology; D018384:Oxidative Stress; D010641:Phenotype; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D054392:Adipokines; D016207:Cytokines; D018836:Inflammation Mediators