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Scientists associate 6 new genetic variants with heart disease risk factor
Date:1/13/2008

Using new techniques for rapidly scanning the human genome, researchers have associated levels of cholesterol and triglycerides, two fats in the blood, to 18 genetic variants, six of which represent new DNA regions never before associated with the traits. The findings, appearing in the January 13 advance online issue of Nature Genetics, help explain some of the variability in cholesterol and triglyceride levels that arises from genes. With the potential to help predict a patients genetic risk of heart disease, the six new loci may point to novel aspects of cholesterol metabolism and could also spur new cholesterol-lowering drugs.

Heart disease is a leading cause of death around the world. Researchers have known for decades that one of the strongest predictors of heart disease risk is the level of cholesterol in the blood. While differences in lifestyle, such as diet and exercise, can influence a persons cholesterol levels, differences in genes can too. Some of these culprit genes are already known, but it is clear that many others remain to be found. By uncovering the genetic determinants of cholesterol levels and, in turn, heart disease risk, we may be able to identify high-risk patients who can benefit from early interventions, in addition to expanding our knowledge of cholesterol biology and opening doors to new treatments, said first author Sekar Kathiresan, director of preventive cardiology at Massachusetts General Hospital and a genetics researcher in the Program in Medical and Population Genetics at the Broad Institute of Harvard and MIT.

Cholesterol and triglycerides are fats known as lipids normal constituents of every cell in the human body. There are two main types of cholesterol in the body, low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol, which are commonly known as the "bad" and "good" cholesterols, respectively." The levels of LDL and HDL cholesterol in the blood have been shown to predi
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Contact: Leah Eisenstadt
leah@broad.mit.edu
617-324-2619
Broad Institute of MIT and Harvard
Source:Eurekalert

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