Asthma and obesity genetic link is established

Researchers from the University of Buffalo say two related studies they have conducted demonstrate that chronic inflammation in asthma is more prominent in people who are overweight or obese.

“Our findings point the way to the management of asthma in the obese through simple weight reduction,” said first author Paresh Dandona, MD, PhD, SUNY Distinguished Professor and Chief of Endocrinology, Diabetes and Metabolism at the University at Buffalo.

The findings were published online in the 26 June edition of journal Obesity and involved a study contrasting people in a normal weight range against people classified as obese; in addition to analysis of if/how biological indicators – such as the behaviour of asthma-linked genes – were altered following obese patients receiving weight loss surgery (a gastric bypass).

Assessed were 22 patients of normal weights, 23 obese patients (11 with Type 2 diabetes, 12 without) and 15 morbidly obese patients with Type 2 diabetes.

The Scientists involved with the research discovered in the comparative study that the four genes linked to chronic inflammation in asthma were more active in obese and morbidly obese people, as much as 100% in some cases.

This increased gene expression matters as it can result in mononuclear cells (white blood cells) to generate significantly more inflammatory factors such as interleukin 4, LIGHT and lymphotoxinβ receptor. These help to induce allergic inflammation and other abnormalities in the bronchial passages in asthma.

MMP-9, a contributor to inflammation, and nitric oxide metabolites (NOM), an indicator of oxidative stress, are both asthma-related compounds which were found in higher concentrations within the plasma of both obese and morbidly obese patients.

Interestingly, concentrations of MMP-9 and NOM decreased in morbidly obese diabetics after they had received gastric bypass surgery, together with the expression of six asthma-related genes including the key factors, interleukin 4, LIGHT, lymphotoxinβ and interleukin 33.

The study could hold some weight behind it as none of the participants actually suffered from asthma, meaning any findings or correlations were not a direct result of the lung condition.

“Ours is the first study to provide a mechanistic link between obesity and asthma through biological/immunological mechanisms,” Dandona said. “There has been, until now, no biological, mechanistic explanation other than the fact that obesity may raise the diaphragm and thus reduce lung volumes.”

According to Dandona, the next stage of research into asthma and obesity will involve clinical studies to find information about if or how weight loss can be beneficial for obese asthma patients. “We are embarking on this project now,” he said.