Key Point

While the precise mechanism is not yet known, obesity appears to play a role in airway hyperresponsiveness and asthma severity.

BOSTON—Obesity has been rapidly increasing in prevalence over the past two decades—in children as well as in adults. Although obesity is a recognized risk factor for type 2 diabetes mellitus, hypertension, atherosclerosis, and some forms of cancer, evidence suggests that obesity may also contribute to or even cause asthma. For one, asthma prevalence is increased in obese persons. Furthermore, obese patients with severe asthma account for 75% of emergency department visits for asthma. On the other hand, when morbidly obese asthma patients lose weight, there is a decrease in asthma symptoms and severity.¹

REDUCED PULMONARY FUNCTION

Obesity also may be a risk factor for airway hyperresponsiveness. According to a recent review by Stephanie A. Shore, PhD, and Jeffrey J. Fredberg, PhD, both from the Harvard School of Public Health in Boston, increased abdominal and chest wall mass in obese people causes lower functional residual capacity. And since lung volume is a major determinant of airway diameter, it is possible that these changes in residual capacity allow smooth airway muscles to shorten excessively when activated.

Another possibility is that obese persons breathe at higher frequencies—but substantially smaller tidal volumes—compared with nonobese individuals. As a result, the bronchodilatory effect of tidal strains is compromised and the obese person is predisposed toward increased airway responsiveness. However, in animal studies, even when the mechanical load was removed and tidal volume fixed, obese mice still had greater airway responsiveness than their nonobese counterparts.

Obesity affects the anatomy of both the lungs and airways. In children, for instance, the mechanical load of obesity can affect lung growth, resulting in smaller lungs and reduced pulmonary function. While weight loss improves lung function, it does not affect airway responsiveness. This is consistent with the hypothesis that obesity plays a role in irreversible airway remodeling.

INCREASED INFLAMMATION

Chronic low-level systemic inflammation is present in obese persons—even in the absence of an inflammatory trigger. This inflammation is characterized by the presence of circulating leukocytes, cytokines, cytokine receptors, and chemokines. The inflammation appears to originate within the adipose tissue, and diseases common to obesity (eg, atherosclerosis and type 2 diabetes mellitus) also correlate with systemic inflammation.

Adipose tissue also contains leptin, adiponectin, and plasminogen activator inhibitor-1, all of which contribute to airway hyperresponsiveness. Interestingly, even after controlling for body mass index, leptin levels were increased in obese asthmatic children compared to nonasthmatic children. Studies in animals have suggested that leptin may stimulate mast cells and thus magnify airway hyperresponsiveness to allergens.

In contrast, plasma adiponectin levels are decreased in obese individuals but increase with weight loss. Adiponectin, while mainly having an effect on metabolism, has anti-inflammatory properties as well.

“In summary,” the authors concluded, “the incidence of asthma is increased in the obese. The importance of understanding this relationship is underscored by the extremely high prevalence of obesity in inner-city children, who are at the greatest risk of asthma, and by observations indicating that obesity is a strong predictor of the persistence of childhood asthma into adolescence.”

—Gale Jurasek

Reference
1. Shore SA, Fredberg JJ. Obesity, smooth muscle, and airway hyperresponsiveness. J Allergy Clin Immunol. 2005;115:925-927.

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