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Inflammation and Heart Disease

Soothing the Burning Heart

Doctors increasingly consider inflammation as the cause of heart disease.  Here’s why – and what you can do about it…
?2004 By Jack Challem
Over just the past several years, researchers and physicians have been redefining the cause of coronary artery (heart) disease. The old view was that high-fat diets led to cholesterol deposits in arteries, choking off the blood supply and eventually causing a heart attack. The new view is that heart disease begins as an inflammatory disorder of the blood vessels, with cholesterol-laden lesions forming after the initial damage to arteries.
This is a fundamentally different way of explaining the leading cause of death among Americans. Some 60 million people have coronary heart disease, resulting in approximately 725,000 deaths each year. As you might imagine, new thinking on the cause heart disease leads to different strategies for prevention.
LDL Cholesterol and Inflammation
About 15 years ago, researchers began piecing together exactly how the “bad” low-density lipoprotein (LDL) form of cholesterol was related to inflammation and heart disease. In a series of human and cell studies, Ishwarlal “Kenny” Jialal, M.D., then with the University of Texas Southwestern Medical Center, Dallas, discovered that normal LDL did not promote heart disease. LDL caused heart disease only when it became “oxidized,” or damaged by harmful molecules known as free radicals.
Jialal’s studies found that the immune system responded to oxidized LDL much the way it did to bacteria. White blood cells would attack and engulf globules of oxidized LDL, but they would ignore normal LDL. After capturing oxidized LDL, the white blood cells would then become lodged in the walls of arteries, creating the initial lesions that most people call “cholesterol deposits.” Jialal also found that vitamin E, an antioxidant, prevented LDL oxidation and reduced the activity of white blood cells against LDL.
C-Reactive Protein and Inflammation
Still, it was not until 2000 that the role of inflammation in heart disease gained momentum. Paul Ridker, M.D., of the Harvard Medical School, developed a new blood test, known as high-sensitivity C-reactive protein (CRP), to measure inflammation. He reported in the New England Journal of Medicine that people with elevated blood levels of CRP were four times more likely to suffer a heart attack, compared with people who had normal CRP levels.1
CRP is both an indicator and a promoter of inflammation. It is part of a family of molecules called cytokines, which cells use to communicate with each other. CRP, interleukin-6 (IL-6), and many other cytokines tell immune cells to mount an inflammatory response. Other types of cytokines let cells know when it is time to reduce inflammation.
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