Affiliations: Overlook Hospital Summit, NJ,
Quality Institute Atlantic Health System Florham Park, NJ,
Johns Hopkins University Baltimore, MD
Correspondence to: Ranjeeta Sinvhal, MD, Chief Resident-Internal Medicine, Overlook Hospital, Summit, NJ 07902; e-mail: firstname.lastname@example.org
We read with extreme interest about the Baltimore Longitudinal Study of Aging (February 2002)1 and have some elementary questions regarding the definition of COPD and the implication of a high body mass index (BMI).
First, the case definition of COPD involved both objective spirometric parameters as well as clinical diagnosis of chronic bronchitis, emphysema, and chronic obstruction. Therefore, an alternate explanation for the study results (low BMI correlating with higher risk for COPD) could be that patients with high BMI are less likely to receive a clinical diagnosis of COPD. It is intuitive that there is a higher chance that the clinical symptoms in volunteers with a high BMI would more likely be attributed by the physicians to the obesity and likewise, in volunteers with a low BMI, be attributed to a pulmonary pathology, ie, bronchitis or emphysema.
Secondly, the study failed to assess the effect of obesity on the FEV1/FVC ratio (the criteria for diagnosing COPD). Obesity, as other extra parenchymal restrictive lung diseases, could have a variable effect on the FEV1/FVC ratio, thereby acting as a confounder. This could conceivably influence the data in patients with a high BMI.
Another parameter in question is the BMI. For instance, could weight-training exercise, which involves an increase in the absolute muscle mass and thereby the BMI, be an explanation of the spirometric outcomes? One would be inclined to think the pulmonary outcomes would be more favorable in the exercisers with a higher muscle mass than the sedentary person with the lower muscle mass. Perhaps controlling for exercise tolerance between the groups would clarify the question. The discussion explaining the relation of low BMI with COPD implied that low BMI correlates with poor nutritional status; however, those in the lower tertile had optimum BMIs of 20 to 25.
Other confounders of the results that deserved discussion are the issues of second-hand smoking and occupational exposures. Like all good studies, this one raises many important questions and was a thought-provoking study of interest in the specialist as well as primary care setting.
We thank Drs. Sinvhal, Tosiello, and Cable for their thoughtful comments on our article.1Although not demonstrated, it is possible that physicians may be biased toward diagnosing COPD in slender individuals in the same manner that men tend to be given this diagnosis more frequently than women.2 In the Baltimore Longitudinal Study of Aging (BLSA), however, physicians had a standardized data set available that included symptoms, physical examination, spirometry, and chest radiography. This would tend to minimize diagnostic bias due to selective testing. Moreover, our conclusions would have been identical if we had only employed spirometric criteria for the diagnosis of COPD.
The relationship between body mass index (BMI) and lung function is complex. In previous analyses of BLSA and Lung Health Study data, we found that BMI had a disproportionately larger negative effect on FVC compared to FEV1 in healthy men as well as those with COPD.3–4 Thus obesity would tend to minimize the spirometric diagnosis of airflow obstruction. Other studies, however, have suggested that overweight might be a risk factor for airflow obstruction or asthma.5–6 We think that there are two opposing effects of BMI on lung function. As Bande et al7 have shown, pulmonary function in young men increases with weight, the “muscularity” effect, but older men show a decrease in FVC with weight gain, the “adiposity” effect. We have tried to reconcile these opposing effects by using abdominal fat deposition, measured as waist-hip ratio, as an index of obesity rather than BMI. We found that waist-hip ratio had comparable negative effects on both FEV1 and FVC in men.,3 The effect of weight training on these relationships is not known, but this practice is quite uncommon among the BLSA participants.
We do not want to leave the impression that protein/calorie malnutrition is a major cause for COPD although, as we cited, it may result in lung lesions similar to emphysema in animal models. We do think it is a plausible hypothesis, however, that nutritional factors associated with increased body weight might be protective against the development of COPD.8
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