Asthma-obesity study rules out link between systemic and airway inflammation


Asthma-obesity study rules out link between systemic and airway inflammation


Scientists in New Zealand found that while they observed systemic and airway inflammation in people with obesity and asthma, two diseases that are known to be strongly linked in some way, there was no clear evidence of an interaction between the two.

The study appears in the first issue for September of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society, and was the work of lead researcher, Dr D Robin Taylor, from the University of Otago in New Zealand, and colleagues.

Inflammation is one characteristic shared by asthma and obesity, and animal studies have suggested that obesity causes airways to trigger an immune response, but human studies have failed to show clear evidence of either an additive or synergistic link between asthma and obesity via the inflammation route.

For this controlled observational study, the researchers recruited 79 women in four groups. 20 women were obese and had asthma, 19 were of normal weight and had asthma, 20 were obese and did not have asthma, and another 20, the controls, were neither asthmatic nor obese, but of normal weight.

Taylor said he and his colleagues hypothesized that:

"The low-grade systemic inflammation present in obesity would augment the inflammation of asthma (a synergistic effect)."

"Or alternatively, that the inflammation of obesity might affect the airways independently (an additive effect), perhaps resulting in mixed airway inflammation," he added.

The patients wtih asthma stopped using their corticosteroid anti-inflammatory inhalers for a withdrawal period of four weeks and then all patients underwent blood and other tests such as spirometric, lung volume, exhaled nitric acid, induced sputum cell counts and other biomarker tests of systemic and airway inflammation, such as C-reactive protein (CRP) and cytokines.

The researchers analyzed the variables known to be relevant both to obesity and asthma and looked for patterns of interaction between systemic and airway-specific biomarkers of inflammation.

The results showed that:

  • Markers of systemic inflammation were higher in the obese patients.
  • Markers of local inflammation, the Th2 cytokines, were higher in the patients with asthma.
  • But no important interactions were identified.
  • Obesity "adversely affected lung function with increases in functional residual capacity and residual volume in obese but not normal-weight patients with asthma, with a significant obesity by asthma interaction".
Taylor and colleagues concluded that:

"The link between obesity and asthma is unlikely to be explained by enhancement of the "classical" forms of airway inflammation resulting from the systemic inflammatory effects of obesity itself."

"Other mechanisms, possibly related to innate immunity, may explain the relationship between obesity and asthma," they added.

Commenting on their findings, Taylor said:

"We were disappointed not to find a 'smoking gun' that would explain the common association between obesity and asthma."

Although the results did not support the inflammation hypothesis, Taylor explained that they did provide valuable direction for future research.

"This does not change the fact that there is a well-established link between asthma and obesity," said Taylor.

"Sometimes a negative result is important, and the results add to our body of knowledge regarding the obesity-asthma link. Now we need to look in other directions for the answers," he added.

Research on animals has raised the possibility that innate immunity changes in obesity. Taylor said they did not look at this in their study.

"Given that asthma is immunologically driven, this is a potential avenue for further research," he explained.

"Alternatively, it may be that dynamic changes in lung function that occur with episodes of asthma are different with excess body weight," said Taylor.

Obese patients with asthma are harder to treat because they have an exaggerated response to bronchoconstriction that makes it appear that the asthma is worse than it actually is.

"They may well have worse symptoms, but not as a result of underlying airway inflammation," said Taylor.

"Still, the typical response is often to increase their inhaled anti-inflammatory therapy. This is unlikely to provide the answer and may even do harm. The answer lies in dealing with the obesity itself," he added.

"The Association between Obesity and Asthma: Interactions between Systemic and Airway Inflammation."

Tim J. T. Sutherland, Jan O. Cowan, Sarah Young, Ailsa Goulding, Andrea M. Grant, Avis Williamson, Karen Brassett, G. Peter Herbison, and D. Robin Taylor.

Am. J. Respir. Crit. Care Med. 178: 469-475.

First published online as doi:10.1164/rccm.200802-301OC

Click here for Abstract.

Sources: Journal Abstract and the American Thoracic Society.


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