Dr. Tsimikas and associates reported this study in the New England Journal of Medicine regarding the relationship of oxidation of phospholipids and LDL cholesterol to the development of coronary artery disease. When there are excessive free radicals, for whatever reason, they can easily oxidize or modify LDL cholesterol and phospholipids, primarily Lp(a) lipoprotein. These oxidized lipids have been found to significantly increase inflammation in our arteries and lead to accelerated atherosclerosis or hardening of our arteries. Individuals who had high levels of these oxidized lipids had a significantly greater risk of coronary artery disease. They concluded that the proinflamatory quality of the oxidized LDL cholesterol may be the unifying link between lipid accumulation and inflammation in the vessel wall. Therefore, LDL cholesterol is not the “bad” cholesterol, but instead the oxidized LDL cholesterol.
This study again is pointing out that coronary artery disease is not a disease of cholesterol, but instead, is an inflammatory disease of the arteries. Native or unchanged LDL cholesterol and phospholipids are not the problem. The trouble begins when these highly sensitive lipids are exposed to excessive free radicals, which can easily and quickly oxidize them. These oxidized lipids now create a low-grade inflammatory response in the fine, single layer of our arteries. It is this inflammatory response that causes the damage to our arteries and leads to hardening of our arteries, which can eventual cause a heart attack.
