| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
Springfield, IL
Dr. Elamin is Associate Professor of Medicine, and Director, Critical Care Medicine, Division of Pulmonary and Critical Care Medicine, Southern Illinois University.
Correspondence to: Elamin M. Elamin, MD, MSc, FCCP, Associate Professor of Medicine, Southern Illinois University, Director, Critical Care Medicine, Division of Pulmonary and Critical Care, PO Box 19636, Springfield, IL 62794-9636; e-mail: eelamin{at}siumed.edu
Scientists have long suspected an association between overweight and asthma to be likely.1234 The common assumption is that weight gain occurs because many asthmatic patients avoid exercise since physical activity can trigger their symptoms. The term overweight was defined as a body mass index (BMI) of 25 to 29.9 kg/m2, while obesity was defined as a BMI of 
30 kg/m2.2 Interestingly, during the last 3 decades the incidences of both obesity and asthma have shown a steady raise, with the incidence of asthma more than tripling during that period. Currently, it is estimated that 97 million adults in the United States are overweight or obese and that 5.3% of US adults are affected by asthma.2 In addition to asthma, obesity substantially raises the risk of morbidity from other diseases such as hypertension, type 2 diabetes mellitus, coronary heart disease, stroke, sleep apnea, and respiratory problems.2
Probably one of the most pervasive issues in the relation of obesity and asthma is the relation between airway hyperresponsiveness (AHP) and changes in BMI. While many studies have supported the possible association between obesity and asthma, the scientific literature remains divided regarding the relation between AHP and changes in BMI.
Multiple previous studies56789 have attempted to answer that question through either population-based or cohort studies. A large population-based study9 utilized the data of 11,277 participants in the European Community Respiratory Health Survey (ECRHS). It demonstrated a rise in AHP with the increase in BMI in men (ECRHS slope decrease, 0.027 for each unit increase in BMI; 95% confidence interval, –0.044 to –0.010; p = 0.002),8 but not in women (ECRHS slope decrease, 0.014; 95% confidence interval, –0.033 to 0.005; p = 0.41). However, the study was not designed to allow for the follow-up of a possible variation in AHP with changes in BMI. In a more recent study from Finland, Stenius-Aarniala et al7 evaluated the effect of 14 weeks of controlled dieting on obese asthmatic patients. At the end of the dieting, there was a statistically significant increase in both FEV1 (p = 0.009) and FVC (p = <0.001), but not in the peak expiratory flow (p = 0.06) of the study group compared to the control group. Even after one year, the differences in FEV1 and FVC remained statistically significant (p = 0.02 and 0.001 respectively). However, the study had no account of group airway responsiveness to methacholine challenge either prior to or after the dieting period.
In this issue of CHEST, Aaron and colleagues (see page 2046) investigate the possibility that an intensive weight loss program may improve the severity of adult-onset asthma in obese women. They performed a prospective study for up to 6 months in 58 women with a BMI of > 30 kg/m2. By utilizing Pearson correlation coefficients, they described a possible relation between weight change and unadjusted changes in FEV1, FVC, provocative concentration of a substance causing a 20% fall in FEV1, and St. George Respiratory Questionnaire score. The authors concluded that although weight loss can improve the lung function of obese women, such a change appeared to be independent of changes in airway reactivity.
The study by Aaron et al had a unique approach to the obesity-asthma relationship. Indeed, in order to evaluate such a relationship, the study and control populations underwent a structured dietary program, followed by broncho-provocation challenge (BPC) testing and responding to an asthma symptoms questionnaire. Through that approach, they were able to demonstrate a favorable response to dietary therapy in the form of positive changes in BPC test results. In addition, by electing to include the lower quartile of the cohort who lost weight as their control group, they were able to adjust for possible selection bias by including obese patients who had no access to a weight reduction program.
However, few caveats should be considered when analyzing their conclusion. First, they did not account for other possible unrecognized or unappreciated cofactors that may account for the statistical improvement in BPC test results noted. For example, obesity may increase the risk of gastroesophageal reflux disease, which may then trigger latent asthma. The possible reduction in severity of gastroesophageal reflux disease, with the reported dietary control and weight loss, may result in a decline of the asthma symptoms with subsequent improvement of the BPC test results. In addition, the short follow-up period precluded any firm conclusion about the long-term changes in BPC test results in patients in the study group, who might increase their BMI over time. Finally, since obesity commonly reduces functional residual capacity by 500 mL, weight loss in the study group may account for the reported changes in the BPC testing results rather than having a direct effect on the airways.1011
In summary, while obesity and asthma remains two of the fastest growing and most pervasive public health problems in developing countries, the question remains whether the relation of asthma to obesity is a real connection or just a casual association. Large prospective studies and randomized population-based studies are needed to determine the prevalence of such an association, and the possible relation between AHP and variations in BMI. Indeed, such studies might support the counter opinion that different mechanisms other than AHP are responsible for the development of obesity-associated dyspnea and that asthma might be overdiagnosed in the portion of the population that is overweight.
References
This article has been cited by other articles:
|
|
 |
|
  S. Chinn, S. H. Downs, J. M. Anto, M. W. Gerbase, B. Leynaert, R. de Marco, C. Janson, D. Jarvis, N. Kunzli, J. Sunyer, et al. Incidence of asthma and net change in symptoms in relation to changes in obesity Eur. Respir. J., October 1, 2006; 28(4): 763 - 771. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Chen, D. Rennie, Y. Cormier, and J. Dosman Sex Specificity of Asthma Associated With Objectively Measured Body Mass Index and Waist Circumference: The Humboldt Study Chest, October 1, 2005; 128(4): 3048 - 3054. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
