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Study Shows Gene May Boost Smoking-Related Heart Disease

Date:
April 13, 2000
Source:
University Of North Carolina At Chapel Hill
Summary:
A common gene appears to boost the risk of coronary heart disease among smokers, according to a new study of heart disease and heart attack patients in four U.S. communities.

CHAPEL HILL -- A common gene appears to boost the risk of coronary heart disease among smokers, according to a new study of heart disease and heart attack patients in four U.S. communities.

The study, conducted by University of North Carolina at Chapel Hill School of Public Health faculty and colleagues at other institutions, found that smokers faced almost twice the risk of heart problems if they carried the gene GSTT1 than if they did not.

A report on the research appears in the April issue of Atherosclerosis, a scientific journal. Authors include Drs. Rongling Li, former postdoctoral fellow; Andrew F. Olshan, associate professor; James S. Pankow, assistant professor; Herman A. Tyroler, professor; Gerardo Heiss, professor; and Lloyd E. Chambless, research associate professor, all of public health at UNC-CH.

Using data collected between 1987 and 1993, scientists studied 14,239 people enrolled in the continuing Atherosclerosis Risk in Communities study, a federally supported effort to improve understanding of risk factors for heart attacks and strokes. Subjects lived in Forsyth Co., N.C., the northwest suburbs of Minneapolis, Washington County, Md. and Jackson, Miss.

During the period studied, 458 people suffered heart attacks or were newly diagnosed with heart disease, Pankow said. The final sample consisted of 400 cases and 890 others who served as controls.

"Subjects already had been asked about their smoking habits and had provided a blood sample for genetic analysis, and so we looked more closely at those people who had had heart problems," he said. "We found that those who had heart attacks and heart disease were more likely to be smokers, which was nothing new because it agreed with many other studies conducted around the world.

"What was new was that individuals without the gene had about a 60 percent greater risk of heart problems if they smoked and that those with the gene had about a 180 percent greater risk," Pankow said. "Among people who don’t smoke, the gene seems to make no difference in heart disease."

Roughly four of five study subjects carried the GSTT1 gene, which is thought to be important in the body’s ability to process chemicals found in tobacco smoke, he said. The gene already has been linked to some other smoking-related illnesses such as bladder cancer.

"We’ve known for a long time that smoking is bad for the heart, but we don’t fully understand why," Pankow said. "We hope this research will provide some clues."

Others participating in the research were Drs. Eric Boerwinkle and Molly Bray of the University of Texas Health Science Center’s Human Genetics Center, and Gary S. Pittman and Douglas A. Bell of the National Institute of Environmental Health Sciences in Research Triangle Park, N.C. Other collaborating institutions were Johns Hopkins and Wake Forest universities and the universities of Minnesota and Mississippi.

The National Heart, Lung and Blood Institute supported the study.


Story Source:

The above story is based on materials provided by University Of North Carolina At Chapel Hill. Note: Materials may be edited for content and length.


Cite This Page:

University Of North Carolina At Chapel Hill. "Study Shows Gene May Boost Smoking-Related Heart Disease." ScienceDaily. ScienceDaily, 13 April 2000. <www.sciencedaily.com/releases/2000/04/000410091620.htm>.
University Of North Carolina At Chapel Hill. (2000, April 13). Study Shows Gene May Boost Smoking-Related Heart Disease. ScienceDaily. Retrieved September 23, 2014 from www.sciencedaily.com/releases/2000/04/000410091620.htm
University Of North Carolina At Chapel Hill. "Study Shows Gene May Boost Smoking-Related Heart Disease." ScienceDaily. www.sciencedaily.com/releases/2000/04/000410091620.htm (accessed September 23, 2014).

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