Effect of Weight Reduction on Respiratory Function and Airway Reactivity in Obese Women

Shawn D. Aaron, MD, MSc; Dean Fergusson, PhD; Robert Dent, MD; Yue Chen, PhD; Katherine L. Vandemheen, BScN; Robert E. Dales, MD, MSc


CHEST. 2004;125(6) 

In This Article


Obesity can have a significant effect on normal lung physiology. In 1960, Naimark and Cherniak[12] demonstrated that obesity is associated with reduced chest wall compliance. The reduction in chest wall compliance that is seen in obesity is reflected by a reduction in functional residual capacity, expiratory reserve volume, and vital capacity, and in patients with severe obesity, by a reduction in the TLC as well.[13] The reduced chest wall compliance represents a substantial elastic load on inspiratory muscles and causes an increased work of breathing.[14] Thus, it is not surprising that obese patients complain of more dyspnea on exertion than patients without obesity. Conceivably, patients who are obese and dyspneic also may be more likely to receive a diagnosis of asthma.

Several large cross-sectional studies[2–5] have clearly demonstrated a positive association between obesity and an increased prevalence of asthma in women. There are several possible theories that can explain the nature of the observed association linking obesity and asthma. One possibility is that diagnostic bias in these epidemiologic studies may have created an artifactual association. The effect of mass-loading the chest by adipose tissue causes dyspnea and may increase the probability of asthma being incorrectly diagnosed. Similarly, response bias may have affected these studies, so that their increased sense of dyspnea might have led obese patients to have incorrectly reported that they had asthma.

Another possibility is that confounding factors associated with both obesity and asthma, such as diet or sedentary lifestyle, could have accounted for the observed relationship. Against this hypothesis is evidence from a previous population-based study[15] that demonstrated that leisure-time energy expenditure was not lower in asthmatic patients compared to nonasthmatic patients. Finally, the potential for a causal relationship exists, such that obesity may cause asthma in women through a yet-to-be-determined mechanism.

Increased airways reactivity is a defining characteristic of active asthma.[16] We sought to find evidence for a causal relationship by objectively measuring changes in asthma severity, which were reflected by changes in airway reactivity, during weight loss. The results of our study suggest that lung function improves in obese women who lose a significant amount of weight and does not improve in those who fail to lose weight. However, our study did not show any significant effect of weight loss on airway reactivity, suggesting that improvements in lung function occur due to a reduction in mass-loading on the respiratory system, rather than improvements in asthma per se.

One cannot exclude a very small effect on airway reactivity that may be detectable in large population-based studies but are not large enough to cause clinically significant differences that are detectable in a patient-based study. However, the results of our study are consistent with those of a population-based study by Schacter et al.[17] These authors studied 1,971 Australian adults in a cross-sectional study, and found that obesity was a significant risk factor for asthma, wheeze, and asthma medication use, but not for airway hyperresponsiveness, atopy, or airflow obstruction. The authors concluded that although subjects with severe obesity reported more symptoms consistent with asthma, their levels of atopy, airway hyperresponsiveness, and airway obstruction did not support the suggestion of a higher prevalence of asthma in this group.

One controlled clinical trial[6] randomized 38 obese asthmatic subjects to a supervised weight reduction program or to a control program. Patients in the weight-reduction group significantly improved their disease-specific health status, as measured by the SGRQ, relative to control subjects who did not go through the weight-reduction program. The results of our study also suggest that patients who go through a weight-loss program experience significant improvements in disease-specific health status, as measured by the SGRQ (Fig 3). Surprisingly, in our study improvements in health status were consistent across the entire cohort of patients, and these improvements did not correlate with the amount of weight lost. This suggests that all patients in our weight reduction program improved their quality of life, regardless of relative weight changes, presumably because the program includes an exercise component (which could improve the activity subscale of the SGRQ) and a counseling/support component (which could improve emotional well-being).

One of the potential limitations of our study is that we did not include a group of obese patients who were not going through the weight-reduction program as control subjects. Rather, we chose to compare those patients in the lower quartile of the cohort who lost the least amount of weight to those in the upper three quartiles who lost more weight. In this fashion, we were able to eliminate referral biases or selection biases that come with selecting a different population for the control arm of the study. Similarly, by ensuring that the control subjects came from the cohort, we were able to ensure that the diet, counseling, and exercise prescriptions were the same for all patients in the study, and, thus, we were able to better control for the possible confounding effects of diet, counseling, and exercise on asthma.

A second potential limitation is that not all patients enrolled in this study had a history of physician-diagnosed asthma. Perhaps only patients with preexisting asthma can be expected to improve their airway responsiveness with weight loss. However, a subgroup analysis of the 24 patients who had asthma did not show any improvement in PC20 with weight loss, and in these patients for every 10% relative loss of weight the log2 change in PC20 improved by only 0.19 (ie, one fifth of a doubling dilution), which is less than the 0.53 improvement seen for the group as a whole. We conclude that weight loss can improve lung function in obese women, however, these improvements appear to be independent of significant changes in airway reactivity.


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