Research now suggest that a more fundamental physiological factor contributes to the onset of heart disease. Atherosclerosis begins when something injures the lining of an artery. For many years, cholesterol was assumed to do the initial damage, though no conclusive research ever confirmed these suspicions. Then, these macrophages eat oxidized fatty acids that travel through the bloodstream before eventually dying. Ultimately, this process results in the buildup of scar tissue, which compromises blood flow and contributes to the formation of clots.
Clots inhibit blood flow and thus cause heart attacks or strokes.
Scientists have sought to discover what is really responsible for the initial damage done to the arteries in hopes of unraveling the mechanisms of atherosclerosis. While the scientific community was caught up on cholesterol, Dr. Kilmer McCully, a pathologist at the VA Medical Center in Providence, Rhode Island, was investigating the role homocysteine played in cardiovascular disease. Normally, excess homocysteine is converted into other molecules or broken down and excreted with the aid of vitamins B6, B12, and folic acid. McCully was studying a genetic disorder, homocystinuria, when he discovered that the arteries of young victims resembled those of elderly cardiovascular patients. These children lacked normal levels of liver enzymes which process homocysteine because of their genetic defect.