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CARDIA Studies Open Window on Heart, Lung Diseases

Researchers analyze different proteins in progression of risk factors as subjects aged

THURSDAY, May 22 (HealthDay News) -- New insights into lung disease and lung function in young adults are provided in two new studies.

The researchers analyzed data from the U.S. National Heart, Lung, and Blood Institute's CARDIA (Coronary Artery Risk Development in Young Adults) observational cohort, which recently completed 20 years of health assessments in more than 5,000 young adults.

The participants were healthy 18- to 30-year-olds when CARDIA was launched in 1985 and 1986. CARDIA was designed to look for cardiovascular trouble and lung disease risk factors as the participants aged.

One of the studies identified an association between low levels of a protein called adiponectin in fat cells to increased asthma risk in young women. Even though adiponectin is produced by fat cells, obesity may trigger an inflammatory response to the protein. Its production is diminished in obese people, and its levels increase with weight loss.

For this study, researchers divided 2,890 men and women into three groups, according to the amount of adiponectin produced by their fat cells.

Women with the lowest levels of adiponectin, who also tended to be more obese, had almost double the risk of developing asthma compared to women who had the highest levels of adiponectin. This was true regardless of weight, and the association was most evident in premenopausal women.

No similar association between adiponectin levels and asthma was noted in men.

"Our finding that adiponectin may have a protective effect on asthma in women may open up doors to new ways of treating asthma. The findings have particular relevance for obese women, since they are more likely to have low blood adiponectin concentrations," lead researcher Dr. Akshay Sood, an associate professor in the division of pulmonary and critical care medicine at the University of New Mexico Health Sciences Center School of Medicine in Albuquerque, said in a prepared statement.

Research in mice suggest that adiponectin plays a role in airway inflammation and airway hyperactivity (twitchiness), both of which are factors in asthma.

"Because of the increase in asthma prevalence, as well as obesity, there should be a lot of interest in continuing to study the effect of fat cells on asthma," Sood said.

The second study found that high levels of a protein called ICAM-1 are associated with lower lung function. ICAM-1, present in endothelial cells that line the arteries, helps trigger the immune system's inflammatory response to "invaders" such as cholesterol deposits.

"Circulating ICAM-1 is a measure of dysfunction of the endothelial cells, which are the intimal lining of arteries and are in capillaries," study co-author David Jacobs, a professor of public health at the University of Minnesota at Minneapolis, said in a prepared statement.

"We've known that people with lower lung function have more cardiovascular disease and cardiovascular death than those with better lung function, and that these two things are somehow related, but the relationship between the lungs and blood vessels has been puzzling," Jacobs said. "For instance, air pollution, although it is breathed in through the lungs, has been shown to cause more heart disease than lung disease."

Jacobs and colleagues analyzed ICAM-1 levels in 2,455 CARDIA participants in year 15 of the study and compared it to their lung function in year 20.

"We found a fairly substantial decline in lung function in people with the highest levels of ICAM, compared with people with lower levels, regardless of their weight," Jacobs said. "It suggests that lung function and endothelial health are related in some way. I think of endothelial dysfunction, oxidative stress and inflammation as evil triplets, feeding on each other."

The studies were to have been presented May 21 at the American Thoracic Society's International Conference, in Toronto.

More information

The Canadian Lung Association has more about lung diseases.

-- Robert Preidt

SOURCE: American Thoracic Society, news release, May 21, 2008

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