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There is an increasing prevalence of obesity worldwide and its impact on respiratory health is of significant concern. Obesity affects the respiratory system by several mechanisms, including by direct mechanical changes due to fat deposition in the chest wall, abdomen and upper airway, as well as via systemic inflammation. The increased mechanical load in obese individuals leads to reduced chest wall and lung compliance and increased work of breathing. While there is generally minimal effect on spirometric values, as body mass index increases, the expiratory reserve volume, and hence functional residual capacity, reduces, often approaching residual volume in more severe obesity. The majority of evidence however suggests that obese individuals free from lung disease have relatively normal gas exchange. The link between asthma and obesity, while initially unclear, is now recognized as being a distinct asthma phenotype. While studies investigating objective markers of asthma have shown that there is no association between obesity and airway hyper-responsiveness, a recent working group identified obesity as a major risk factor for the development of asthma in all demographic groups. Although the temptation may be to attribute obesity as the cause of dyspnoea in symptomatic obese patients, accurate respiratory assessment of these individuals is necessary. Lung function tests can confirm that any altered physiology are the known respiratory consequences of obesity. However, given that obesity causes minimal changes in lung function, significant abnormalities warrant further investigation. An important consideration is the knowledge that many of the respiratory physiology consequences of obesity are reversible by weight loss.
Brazzale et al. (Mon,) studied this question.