Scientist at The Fienstein Instute for Medical Research Discovers Quitting Smoking Promotes Anti-Inflammatory Response

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Christine Metz, PhD, is a scientist at The Feinstein Institute for Medical Research who is trying to identify some of the factors that play into a smoker's decision to quit.

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Maybe there are immunological differences in people who can quit and those who can't

If you asked a hundred smokers how they quit - or why they couldn't - you may get an equal number of different answers. Christine Metz, PhD, is a scientist at The Feinstein Institute for Medical Research who is trying to identify some of the factors that play into a smoker's decision to quit.

In collaboration with the Center for Tobacco Control of the North Shore-LIJ Health System, she is examining the effect of smoking cessation on inflammatory responses in female smokers at risk for cardiovascular disease. The grant, funded by the American Heart Association, could lead to improved understanding of the smoking cessation process and the development of more effective smoking cessation programs. Heart disease is the number one killer in women, and behavioral changes can go a long way to prevent many of these deaths. Smoking is a major risk factor. Smoking, Dr. Metz and others have shown, triggers the release of a cascade of inflammatory mediators that can, in turn, increase a person's chances of developing heart disease. Here is how the story unfolds. Smoking is associated with an elevation of inflammatory substances in the body, including tumor necrosis factor, tumor necrosis factor receptors and C-reactive protein (CRP) -- major markers of inflammation. Elevated levels of these mediators suggest that inflammation is brewing somewhere in the body, Dr. Metz said.

In July 2005, she began her collaboration with The Center for Tobacco Control. They wanted to understand why many people can't quit smoking. Dr. Metz thought that the body undergoes an inflammatory response to quitting, which could present an obvious obstacle to their success. (Less than 10 percent of people can quit smoking on their own, while 'assisted' medical and psychological treatments have success rates of about 30 percent.) In addition, they wanted to identify whether inflammatory markers decline after quitting smoking.

For this study, they recruited 45 women between the ages of 35-75 who smoked at least a pack of cigarettes a day and had risk factors for cardiovascular disease such as hypertension, high cholesterol, stroke, and/or abdominal obesity. All participants wanted to quit smoking and participated in a smoking cessation program at the Center for Tobacco Control. This program is the only free smoking cessation program available in Nassau County. Participants pay for the treatment medications, but not for counseling). The program receives referrals from The American Cancer Society, The American Lung Association, The Nassau Department of Health, The Suffolk County Department of Health, The New York State Smoker's Quitline, and the physicians/nurses of the North Shore-Long Island Jewish Health System (NSLIJHS). Study subjects filled out a health history and blood was collected at the initial visit and again within the first 72 hours of quitting. As part of the smoking cessation study, they were given the option to use a nicotine patch and/or Zyban, which is an antidepressant shown to have beneficial effects on blocking nicotine cravings. Counseling was also provided.

The results of the study were published in the July 30 issue of Chest.

At the end of 18 weeks, 30 percent of the women were not smoking. As they anticipated, several inflammatory markers, including tumor necrosis factor, soluble tumor necrosis factor receptors and soluble VCAM-1 (a marker of endothelial cell activation) dropped over time in 'quitters'. Dr. Metz and her colleagues found that those who were successful in quitting had lower C-reactive protein levels during the initial visit than those who continued to smoke despite the treatment. (Counseling was also provided)

"Maybe there are immunological differences in people who can quit and those who can't," said Dr. Metz. If she is right, measuring these inflammatory mediators early on and during the smoking cessation process may prove to be important in designing a treatment that be tailored to a person's biology. What's more, if smokers received their inflammatory mediator 'scores' during the quit process and saw some of these decline, it might be a strong incentive to stop smoking. She also stored genetic material from each smoker and will study the RNA and DNA that helps tell the story of the activity of immune markers.

The Staff at the Center for Tobacco Control and Dr. Metz also conducted another study funded by the New York State Department of Health on smokers with very early signs of chronic obstructive pulmonary disease. This new study included an additional smoking cessation drug, Chantix. They measured immune markers during the smoking cessation process and the results are being analyzed.

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