One researcher reported that otherwise-healthy soldiers examined after returning from World War II had arteries already occluded 22%, even though they were only 20 years old. Sometimes referred to as the "silent killer," atherosclerosis and cardiovascular disease can progress for years undetected by an individual who may have, or be at great risk from, the disease.
Generally few symptoms arise with the early, and in some cases later, stages of the disease. An elevated or high blood pressure for an individual with normal blood pressure may be an indication of disease presence; however, blood pressure increases generally occur over a long period of time, as the disease slowly advances. A study reported in Circulation (March 4, 1997) confirmed that even borderline blood pressure readings (140/90) represent a risk factor for atherosclerosis and stroke. However, blood-pressure is associated with many other factors such as being overweight, lack of exercise, higher blood sugar, and cholesterol.
Atherosclerosis is a slow, progressive disease that may start in childhood. In some people, this disease progresses rapidly in their 30s and early 40s-in others it doesn't become threatening until later in life.
Exactly how atherosclerosis begins or what causes it isn't known, but some theories have been proposed. Many scientists think atherosclerosis begins because the innermost layer of the artery, called the endothelium, becomes damaged. Possible causes of damage to the arterial wall are free-radical reactions, elevated levels of oxidated serum cholesterol, triglycerides, fibrinogen and , high blood pressure, obesity, lifestyle issues, cigarette smoke, and environmental pollutants.
Specific diseases caused by atherosclerosis include coronary artery disease, angina pectoris, cerebral vascular disease, thrombotic stroke, transient ischemic attacks, and diabetic vascular complications.
Three mechanisms that have been identified as the most probable causative factors in the development of atherosclerosis include the following:
1. LDL cholesterol oxidation. LDL stands for low-density lipoprotein and is often referred to as "bad cholesterol." Oxidation of LDL renders it "sticky" and facilitates its deposition on the internal lining of blood vessel walls. The oxidation of LDL cholesterol, other blood fats, and homocysteine can initiate and significantly contribute to the development of atherosclerosis.
2. Homocysteine overload. There is growing consensus that homocysteine may be a major contributor to degenerative diseases such as atherosclerosis. Detoxification of excess homocysteine requires "methylating factors" such as folic acid, vitamin B12, and trimethylglycine (TMG). factors function to convert (remethylate) homocysteine back into the nontoxic amino acid methionine. Some individuals with elevated serum homocysteine also require higher amounts of vitamin B6, which converts homocysteine to safer substances via a different (trans-sulfuration) metabolic pathway.
Homocysteine often causes the initial lesions on arterial walls that enable LDL cholesterol and fibrinogen to accumulate and eventually to obstruct blood flow. Homocysteine also contributes to the oxidation of LDL cholesterol and the accumulation of arterial plaque and subsequent vascular blockage. Homocysteine damages cells directly by promoting oxidative stress. Homocysteine also can cause abnormal arterial blood clots (thrombosis) that can completely block an artery. Homocysteine alone has been demonstrated to promote atherosclerosis and thrombosis, even if cholesterol and triglyceride levels are not significantly elevated. That is why homocysteine blood testing is strongly recommended (see protocol).
3. Abnormal platelet aggregation (clotting inside an artery). Fibrinogen, platelets, and other clotting factors aggregate with LDL cholesterol, triglycerides, and calcium on the arterial wall to further promote the development of atherosclerotic plaques. Abnormal platelet aggregation can lead to the development of a blood clot (thrombus) on the arterial walls inside the heart, brain, or any other organ, resulting in ischemia (reduced blood flow) and/or infarction (cell death). Abnormal platelet aggregation can cause an acute arterial blood clot that can lead to a suddenly fatal heart attack or stoke.
4. Integrated and Alternative Therapies. There now exists a massive body of evidence that supplementation, combined with appropriate lifestyle, diet, and exercise can prevent and even help reverse cardiovascular disease, evidenced by an April 1998 recommendation by the New England Journal of Medicine titled, "Eat Right and Take a Multivitamin." The conventional medical establishment has long ridiculed vitamin supplementation, but for the first time, a 1998 editorial in the New England Journal of Medicine encouraged the use of homocysteine-lowering vitamin supplements to reduce the risks of cardiovascular disease.
Developmental process of atherosclerosis
The development of arterial atherosclerosis may occur when deposits of cholesterol and plaque accumulate at a tear in the inner lining of an artery. As the deposits harden and occlude the arterial lumen, blood flow to distant tissues decreases and a clot may become lodged, completely blocking the artery.