�Scientists in New Zealand found that while they observed systemic and airway inflammation in people with obesity and asthma, iI diseases that
are known to be strongly linked in some way, at that place was no clear evidence of an interaction 'tween the two.
The study appears in the first yield for September of the American Journal of Respiratory and Critical Care Medicine, published by the
American Thoracic Society, and was the work of tether 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 fleshiness causes airways to trigger an
resistant response, only human studies have failed to establish clear evidence of either an additive or interactive link betwixt asthma and obesity via the
inflaming 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 corpulent and did not have asthma, and another 20, the controls, were neither asthmatic nor obese, but of
normal weight.
Taylor aforesaid he and his colleagues hypothesized that:
"The low-grade systemic inflammation present in fleshiness would augment the inflammation of bronchial asthma (a synergistic effect)."
"Or alternatively, that the inflammation of obesity might affect the airways independently (an additive effect), mayhap resulting in mixed air lane
inflammation," he added.
The patients wtih asthma stopped victimization their adrenal cortical steroid anti-inflammatory inhalers for a withdrawal geological period of quartet weeks and then all patients underwent blood
and other tests such as spirometric, lung volume, exhaled nitric acidic, induced phlegm cell counts and other biomarker tests of systemic and flight path
inflammation, such as C-reactive protein (CRP) and cytokines.
The researchers analyzed the variables known to be relevant both to obesity and bronchial asthma and looked for patterns of fundamental interaction between systemic and
airway-specific biomarkers of inflammation.
The results showed that:
Markers of systemic inflammation were higher in the weighty patients.
Markers of local kindling, the Th2 cytokines, were higher in the patients with asthma.
But no crucial interactions were identified.
Obesity "adversely affected lung function with increases in functional residual capacity and residual volume in obese but non normal-weight
patients with asthma attack, with a significant corpulency by bronchial asthma interaction".
Taylor and colleagues complete that:
"The link between fleshiness and bronchial asthma is improbable to be explained by enhancement of the "classical" forms of airway inflammation resulting from the
systemic inflammatory effects of fleshiness itself."
"Other mechanisms, possibly related to inborn immunity, may explain the relationship between obesity and asthma," they added.
Commenting on their findings, Taylor said:
"We were defeated not to find a 'smoking gun' that would explain the common association between fleshiness and asthma."
Although the results did non support the inflammation hypothesis, Taylor explained that they did provide valuable direction for future research.
"This does not change the fact that thither is a well-established link between bronchial asthma and obesity," said Taylor.
"Sometimes a negative result is important, and the results add to our body of noesis 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 non 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 attack are different with excess body weight," said
Taylor.
Obese patients with asthma are harder to treat because they have an enlarged response to bronchoconstriction that makes it appear that the
asthma is worsened than it actually is.
"They may well have worse symptoms, just not as a final result of underlying airway inflammation," said Taylor.
"Still, the typical response is often to increase their inhaled anti-inflammatory therapy. This is unlikely to render the answer and may even do harm.
The answer lies in dealing with the obesity itself," he added.
"The Association betwixt 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 hither for Abstract.
Sources: Journal Abstract and the American Thoracic Society.
Written by: Catharine Paddock, PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today
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Saturday, 6 September 2008
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