New genetic evidence strengthens the case that one well-known type of cholesterol is a likely suspect in causing heart disease, but also casts further doubt on the causal role played by another type. The findings may guide the search for improved treatments for heart disease.
Most of us have heard of "good cholesterol" and "bad cholesterol" coursing through our bloodstream. In the conventional health wisdom of the past 30 years, having more of the "good" variety (high-density lipoprotein, or HDL) lowers your risk of heart disease, while more of the bad one (low-density lipoprotein, LDL) increases your risk. Indeed, over the years, clinical trials and other studies have found that drugs that lower LDL also lower your probability of heart disease.
On the other hand, drug trials have not shown heart-health benefits to increasing HDL or to lowering triglycerides, a third type of blood lipid. Now a new study co-led by scientists at The Children's Hospital of Philadelphia and Penn Medicine sheds light on the role of genes and blood lipid levels in cardiovascular health. Newer tools for gene analysis show how variations in DNA are underlying actors affecting heart diseasea major worldwide cause of death and disability.
"Now we are able to pinpoint gene signals that actually cause some of these conditions," says geneticist Brendan J. Keating, D. Phil., of The Center for Applied Genomics at The Children's Hospital of Philadelphia. "Unraveling how genetic variants that influence lipid traits are related to heart disease risk is a step toward designing treatments." Keating and his colleagues, working in large international collaborative groups, are wielding advanced gene-analysis tools to uncover important clues to heart disease.
Keating collaborated with clinical epidemiologist Michael V. Holmes, M.D., Ph.D., of the Perelman School of Medicine at the University of Pennsylvania, in a blood lipid study published online Jan. 27 in the <
|Contact: John Ascenzi|
Children's Hospital of Philadelphia