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When fatty substances, such as cholesterol and triglycerides, travel in the bloodstream, they pair with a protein called an apolipoprotein, which enables them to dissolve in the fluid portion of the blood. Examples of these combinations of fat and protein, called lipoproteins, are the low-density lipoproteins (LDLs) and the high-density lipoproteins (HDLs) that are commonly measured in cholesterol screening tests. Lipoprotein(a), or simply lp(a), is a low-density lipoprotein linked to apolipoprotein (a), formed in the liver. Increased levels of lp(a) have been associated with an increased risk for heart disease, stroke, atherosclerosis, and blood clot. Lipoprotein(a) has also been linked to a decreased chance of survival with these conditions.
Scientists have not been able to discover the role for lp(a) in the body. Its structure is similar to a chemical responsible for the breakdown of blood clots called plasminogen. If there is a high level of circulating lp(a), the lp(a) binds to the same receptors as plasminogen. This inhibits the activity of the plasminogen, resulting in the development of more blood clots than normal. Blood clots are contributors to both heart attacks and strokes.
Lp(a) stimulates the deposition of cholesterol into the cells that line the inside bore of arteries. This process narrows the arterial diameter and causes the formation of cholesterol plaques in sites with increased blood flow and turbulence. As the plaques begin to encroach on the column of blood flowing in the artery, the tissue supplied by the artery becomes starved for oxygen. Poor blood flow is another risk factor for heart attack and stroke.
The blood level of lipoprotein(a) is not normally assessed in blood tests. There is no standardized scale for measuring this blood lipid. Furthermore, there are no clinical studies that clearly demonstrate the relationship between Lp(a) and heart disease, and no studies that prove that lowering the lp(a) lessens the overall risk for heart attack or stroke. In addition, high lipoprotein(a) levels are most dangerous when the low-density cholesterol levels are also high, making it difficult to parse out which blood lipid is producing the problem.
Lipoprotein(a) levels are determined primarily by heredity. African populations tend to have higher lp(a) levels than Caucasians. Exercise, diet, and cholesterol-reducing medications make remarkably little difference in modulating high lp(a) levels. Some studies promote the use of low-dose aspirin or niacin to control lipoprotein(a) levels. In a study in Tanzania, fish eaters had lower levels of lp(a) than the other segments of the population, giving rise to the possibility that fish oil supplements may be useful in lowering lipoprotein(a).
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