Table of Contents
Journal of Allergy
Volume 2013 (2013), Article ID 198068, 11 pages
Review Article

Obesity and Asthma: Physiological Perspective

Chest Research Foundation, Marigold Complex, Kalyani Nagar, Pune, Maharashtra 411014, India

Received 20 February 2013; Revised 27 May 2013; Accepted 3 July 2013

Academic Editor: Anurag Agrawal

Copyright © 2013 Bill Brashier and Sundeep Salvi. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Obesity induces some pertinent physiological changes which are conducive to either development of asthma or cause of poorly controlled asthma state. Obesity related mechanical stress forces induced by abdominal and thoracic fat generate stiffening of the lungs and diaphragmatic movements to result in reduction of resting lung volumes such as functional residual capacity (FRC). Reduced FRC is primarily an outcome of decreased expiratory reserve volume, which pushes the tidal breathing more towards smaller high resistance airways, and consequentially results in expiratory flow limitation during normal breathing in obesity. Reduced FRC also induces plastic alteration in the small collapsible airways, which may generate smooth muscle contraction resulting in increased small airway resistance, which, however, is not picked up by spirometric lung volumes. There is also a possibility that chronically reduced FRC may generate permanent adaptation in the very small airways; therefore, the airway calibres may not change despite weight reduction. Obesity may also induce bronchodilator reversibility and diurnal lung functional variability. Obesity is also associated with airway hyperresponsiveness; however, the mechanism of this is not clear. Thus, obesity has effects on lung function that can generate respiratory distress similar to asthma and may also exaggerate the effects of preexisting asthma.