Effect of Obesity on Asthma Phenotype is Dependent upon Asthma Severity

Abstract

Background. We recently reported that obese and non-obese patients with asthma have similar airflow limitation and bronchodilator responsiveness, but obese patients have more symptoms overall. There is limited information on the effect of obesity on asthmatics of varying severity measured by objective physiological parameters. Understanding how obesity affects asthmatics of differing severity can provide insights into the pathogenesis of asthma in the obese and a rationale for the therapeutic approach to such patients. Methods. Participants with asthma from two American Lung Association—Asthma Clinical Research Center (ALA-ACRC) studies were grouped by tertiles of airflow obstruction (forced expiratory volume in one second (FEV₁%) predicted, FEV₁/forced vital capacity (FVC)) and methacholine reactivity (PC₂₀FEV₁). Within each tertile, we examined the independent effect of body mass index (BMI), divided into normal weight, overweight, and obese categories, on lung function, airway reactivity, and symptoms. Results. Overall, both FEV₁ and FVC decreased and symptoms worsened with increasing BMI; airway reactivity was unchanged. When stratified by the degree of airflow obstruction, higher BMI was not associated with greater airway reactivity to methacholine. Higher BMI was associated with more asthma symptoms only in the least obstructed FEV₁/FVC tertile. When stratified by degree of airway reactivity, BMI was inversely associated with FVC in all PC₂₀FEV₁ tertiles. BMI was directly associated with asthma symptoms only in those with the least airway reactivity. Conclusions. Obesity does not influence airway reactivity in patients with asthma and it is associated with more symptoms only in those with less severe disease.

• asthma
• obesity
• body mass index
• airflow obstruction
• airway reactivity

Acknowledgments

The authors acknowledge all the investigators and coordinators in the American Lung Association's Asthma Clinical Research Centers program who participated in the LOCCS and SARA trials, the Data Coordinating Center at Johns Hopkins University, and patients who contributed the data used in the analyses. Funding sources for this study were American Lung Association, NIH-NHLBI 5U01HL072968 (SARA), GlaxoSmithKline (LOCCS).