1 Department of Epidemiology and Community Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada.
2 Department of Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada.
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INTRODUCTION |
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Redd and Mokdad (1) raised concerns about the definition of asthma and the potential for misclassification, a concern in most epidemiologic studies. This problem cannot be resolved easily, because a full understanding of the disease and a universally accepted definition of asthma are lacking. In 1999, the Canadian Asthma Consensus Group provided the following definition of asthma:
Asthma is characterized by paroxysmal or persistent symptoms such as dyspnea, chest tightness, wheezing, sputum production and cough associated with variable airflow limitation and a variable degree of airway hyperresponsiveness to endogenous or exogenous stimuli. Inflammation and its resultant effects on airway structure are considered the main mechanisms leading to the development and maintenance of asthma (3, p. 81).
To operationalize such a comprehensive definition is difficult. In epidemiologic research, asthma has usually been represented by one or more of its many characteristics or correlates, which include wheeze, reversible airflow obstruction, physician diagnosis, measured airways reactivity, and eosinophilic airway inflammation. One practical approach to this problem of definitions is to ensure that the operational definition used is stated clearly and does not introduce a systematic bias when asthmatic status among groups is compared. A less strict definition of asthma, such as ours, is likely to provide a more conservative estimate of the strength of the association between obesity and asthma (4).
Both obesity and asthma are multifactorial conditions, leading to legitimate concerns about measured and unmeasured covariates that may confound the relation between the two. Although we used several simple baseline measures of covariates in our report, more quantitative measures of smoking, alcohol drinking, and physical activity did not impact the obesity-asthma association.
It may be instructive to interpret the results of our study (2) in the context of previous work. Shaheen et al. (5
) reported a positive association between asthma and body mass index in women that was not significantly altered by adjusting for maternal smoking during pregnancy, birth weight, paternal social class at birth, number of siblings, education, and smoking. Camargo et al. (4
) found the incidence of asthma to increase with increasing body mass index in women, with the results remaining almost unchanged after controlling for age, race, smoking, physical activity, energy intake, hysterectomy status, birth weight, duration of breastfeeding, and body mass index at age 18 years.
Redd and Mokdad (1) mentioned that our data showed that women who lost or gained weight had a higher risk of asthma (2
). These differences were not pronounced; the 95 percent confidence intervals for the incidence of asthma among weight change categories overlapped substantially. Another reason for the nonsignificant elevated incidence of asthma among women who lost weight is that overweight women tended to lose more weight than those of normal weight. In a randomized controlled trial, Stenius-Aarniala et al. (6
) demonstrated that weight reduction alleviates asthma symptoms, enhances lung function, and reduces the need for emergency medication. However, it is not known whether these changes are explained by a reduction in the mass loading of the thorax and abdomen or due to a reduction in bronchoconstriction and/or inflammation. A clinical study is currently being conducted among obese women at the University of Ottawa (Ontario, Canada) to determine the association of changes in body mass index with airway reactivity and the potential impact of sex hormones on this relation.
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ACKNOWLEDGMENTS |
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NOTES |
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REFERENCES |
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