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ARTICLES: Katina Nicolacakis, Mary E. Skowronski, Albert J. Coreno, Erin West, Nizar Z. Nader, Robert L. Smith, and E. R. McFadden, Jr. Observations on the physiological interactions between obesity and asthma J Appl Physiol 2008; 105: 1533-1541 [Abstract] [Full text] [PDF]

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Interaction betwen obesity and asthma

D Robin Taylor, Timothy J.T. Sutherland   (14 November 2008)

Response to Dr. Taylor & Dr. Sutherland's Letter

E. R. McFadden, Jr., Katina Nicolacakis, Mary E. Skowronski, Albert J. Coreno, Erin West, & Nizar Nader   (14 November 2008)

Interaction betwen obesity and asthma 14 November 2008
D Robin Taylor, Professor of Respiratory Medicine Dunedin School of Medicine, University of Otago, Timothy J.T. Sutherland Send letter to journal: Re: Interaction betwen obesity and asthma robin.taylor{at}stonebow.otago.ac.nz D Robin Taylor, et al.	Dear Sir We read with interest the paper by Nicolacakis et al. in which the impact of obesity and asthma on lung function singly and together were explored (1). The conclusion of these authors was that asthma and obesity operate independently and additively on pulmonary function, rather than synergistically. Apart from the six minute walk, following which changes in lung function were not measured, the results presented by Nicolacakis et al. focussed on the obesity-asthma interaction in static models. Recently, we have examined the same issues in a dynamic model by measuring changes in lung volumes following methacholine-induced bronchoconstriction. In that study (2), dynamic hyperinflation (as measured by functional residual capacity (FRC) and inspiratory capacity (IC)) associated with increasing bronchoconstriction was significantly greater in obese compared to non- obese asthmatic subjects. Thus, while the data provided by Nicolacakis et al. are important and valid, it is perhaps in the dynamic situation when patients experience bronchospasm in response to an asthma trigger that important interactions between obesity and asthma begin to emerge. Perhaps they are the reason for the perceived increase in severity of asthma associated with obesity (3). We would welcome the comments of Nicolacakis et al. on these further observations. Yours sincerely D. Robin Taylor, Timothy J. T. Sutherland References 1. Nicolacakis K, Skowronski ME, Coreno AJ, West E, Nader NZ, Smith RL, et al. Observations on the Physiological Interactions Between Obesity and Asthma. J Appl Physiol 2008. 2. Sutherland TJ, Cowan JO, Taylor DR. Dynamic hyperinflation with bronchoconstriction: differences between obese and nonobese women with asthma. Am J Respir Crit Care Med 2008;177(9):970-5. 3. Saint-Pierre P, Bourdin A, Chanez P, Daures JP, Godard P. Are overweight asthmatics more difficult to control? Allergy 2006;61(1):79-84.
Response to Dr. Taylor & Dr. Sutherland's Letter 14 November 2008
E. R. McFadden, Jr., Argyl J. Beams Professor of Medicine Case Western Reserve School of Medicine, Katina Nicolacakis, Mary E. Skowronski, Albert J. Coreno, Erin West, & Nizar Nader Send letter to journal: Re: Response to Dr. Taylor & Dr. Sutherland's Letter ermcfadden{at}metrohealth.org E. R. McFadden, Jr., et al.	To the Editor: Dear Dr. Dempsey: We read with interest Drs. Taylor and Sutherland’s letter regarding our paper “Observations on the Physiological Interactions Between Obesity and Asthma” (5) and we appreciate their kind comments. A number of epidemiologic studies have reported an association between obesity and asthma. Our protocol was designed to determine whether these two conditions share overlapping pathogenic features or only represent associations between common conditions that frequently coexist. To this end, we examined the impact of each illness alone and in combination on multiple traditional measures of lung function. Our findings indicate that asthma and obesity appear to influence the respiratory systems through different processes. Asthma impacts airway tone and the tests dependent upon it, while obesity primarily limits lung volume and does not seem to alter tests sensitive to bronchial smooth muscle activity. As pointed out, the endpoints we used focus on static events. We reasoned that such information was an essential first step required to establish a physiologic foundation upon which subsequent studies could be interpreted. It is certainly possible that dynamic interactions between obesity and asthma may occur as suggested by Sutherland, et al (6) and not be reflected in the static evaluations. However, we believe that the available information is not sufficiently developed to conclusively establish this possibility. Sutherland and colleagues (6) demonstrated that functional residual capacity (FRC) was significantly greater and inspiratory capacity (IC) less in obese asthmatics compared to non-obese counterparts following a methacholine challenge and that these changes correlated with the size of the BMI. From these observations, they concluded that obesity conferred a tendency toward dynamic hyperinflation. This might be so, but the types of functional abnormalities presented do not fit with any recognized pattern of obstruction in asthmatics. In the Sutherland study, the changes in FRC and IC were isolated events and there were no differences in residual volume (RV) before and after methacholine in those asthmatics with and without obesity and no association with BMI. This means that the pressure-volume relationship of the thorax shifted to the left without an increase in gas trapping. Further, the changes were most marked in the subjects in whom the thorax was the stiffest initially. For this to occur, RV and FRC would have had to increase concurrently, yet they did not. The failure of RV to change in concert with FRC is in conflict with a variety of studies over the years that have shown that it is not possible to develop airway obstruction in asthma with an increase in air trapping without RV rising (1-4). It is well established that residual volume can increase without an alteration in FRC but not the converse. We are not suggesting that Sutherland and colleague’s (6) observations are incorrect, only that the small number of subjects may be insufficient to validate the conclusions. Clearly more studies are needed in this important area. If the results are confirmed and RV truly does not increase in obese asthmatics post challenge and FRC does, then the current thoughts about the manner in which airway dynamics, gas trapping, and chest wall compliance interact need to be reevaluated in obesity and asthma. Sincerely, Katina Nicolacakis, Mary E. Skowronski, Albert J. Coreno, Erin West, Nizar Nader, & ER McFadden, Jr. Sadly, Robert Smith died after the final acceptance of this manuscript. References: 1. Boulet LP, Turcotte H, Brochu A. Persistence of airway obstruction and hyperresponsiveness in subjects with asthma remission. Chest 1994; 105:1024-1031. 2. McFadden ER Jr. The chronicity of acute attacks of asthma. Mechanical and therapeutic implications. J Allergy Clin Immunol 1975; 56:18-26. 3. McFadden ER Jr, Kiser R, De Groot WJ. Acute bronchial asthma: Relations between clinical and physiologic manifestations. N. Engl. J. Med. 1973; 288:221-5. 4. McFadden ER Jr, Lyons HA. Serial studies of factors influencing airway dynamics during recovery from acute asthma attacks. J Appl Physiol 1969; 27:452-9. 5. Nicolacakis K, Skowronski ME, Coreno AJ, West E, Nader NZ, Smith RL, and McFadden ER Jr. Observations on the Physiological Interactions Between Obesity and Asthma J Appl Physiol 2008 6. Sutherland TJ, Cowan JO, Taylor DR. Dynamic hyperinflation with bronchoconstriction: differences between obese and nonobese women with asthma. Am J Respir Crit Care Med 2008;177:970-5.