Lipoprotein (a) or Lp(a) is a small LDL-like particle that strongly increases your risk for heart attacks, strokes, and other cardiovascular problems. Studies show a very direct, linear correlation between high lipoprotein (a) in your blood and risk: the higher your Lp(a) cholesterol numbers, the more plaque builds up in your arteries and the higher your risk of cardiovascular disease.
Lipoproteins are molecules made of fat (lipo) and proteins. They carry cholesterol and similar substances through the blood. Lp(a) consists of a certain subtype of LDL cholesterol bound to a protein called apolipoprotein(a).
How does Lp(a) cause heart disease?
Scientists are still working out the exact mechanisms by which Lp(a) is involved in the formation of plaque within arteries. Lp(a) has many properties in common with low density lipoprotein (LDL), but the fact that it is attached to the unique apolipoprotein (a) is thought to make it exceptionally more dangerous. Lp(a) is known to accumulate in plaques and to promote atherosclerosis in the walls of arteries. It’s also known to promote blood coagulation and to impair the breaking up of blood clots, leading to blot clot formation within blood vessels. This is linked to another type of cardiovascular disease known as venous thrombosis, which increases the risk for pulmonary embolism.
A high level of Lp(a) is considered a very strong risk factor for heart disease, coronary artery calcification, heart attacks, strokes, peripheral arterial disease, and venous thrombosis. These risks occur regardless of other lipid values, such as total cholesterol or LDL cholesterol numbers. That means that just because your total cholesterol and your LDL levels are fine, you still could be at risk for blood vessel disease if you have high Lp(a) levels.
What causes high lipoprotein (a) levels?
Lp(a) is entirely genetically determined. Some people are genetically predisposed to have a lot of lipoprotein(a) and others very little. Because of this, Lp(a) levels can vary greatly from person to person. Unlike other total cholesterol, LDL, HDL, and triglycerides, Lp(a) levels are not influenced by diet, exercise, fat loss, weight loss, stress, or other environmental or lifestyle factors. The one exception to this may be inflammation. Inflammation seems to make Lp(a) an even more potent cause of plaque build-up, so living a more “anti-inflammatory” lifestyle may decrease the risk of Lp(a).
Conventional cholesterol tests (lipid panels) don’t measure Lp(a) cholesterol numbers. To take a lipoprotein a test there are many of the newer, more sophisticated, advanced lipid panels, such as the VAP and the Lipoprotein Particle Profile. Like most lab tests, these tests can now be purchased online without a doctor’s order. Different labs have different ways of measuring Lp(a) and they report the results in different ways. In general, though, a normal Lp(a) level is less than 30 mg/dL. Anyone with a Lp(a) level 30 mg/dL or greater has high Lp(a) and is at increased risk.
Treatment for high lipoprotein a
Although heredity plays a large role in the levels of Lp(a), treatment with supplemental niacin (Vitamin B3) can lower levels of Lp(a) cholesterol numbers. Statin drugs generally have no effect, and there is no current FDA approved drug for directly lowering Lp(a). Niacin in very high (pharmaceutical-like) doses is the most commonly recommended treatment, even by conventional cardiologists.
Most cardiologists recommend either regular or extended release niacin, rather than the no-flush form of niacin (inositol hexaniacinate), because some studies have shown that the no-flush form of niacin does not work as well. The typical recommendation is to gradually work up to a dose of 1000 to 3000 mg regular or extended release niacin per day, in divided doses. This much regular or extended release niacin is hard on the liver and can cause serious liver problems in susceptible individuals. You should therefore be working with a doctor if taking high-dose niacin. It is sometimes recommended that you start with no-flush niacin first, at 1000–3000 mg per day in divided doses, since this form is not toxic to the liver and may still lower Lp(a) in some people.
A recent study on how to lower lipoprotein found that supplementation with coenzyme Q10 can inhibit expression of lipoprotein(a) receptor and result in lowering lp(a). In a recent study, 100 mg per day of oral CoQ10 for three months significantly reduced Lp(a) levels. Both niacin and CoQ10 are available without prescription from your health food store or favorite online supplement provider.
If you have a family history of high cholesterol or early heart disease, or if you’re at high risk for cardiovascular disease already because of your cholesterol, your weight, or other risk factors, it is recommended you determine your Lp(a) levels and take advantage of niacin or CoQ10 to reduce your cardiovascular risk. To learn more about CoQ10 and/or niacin supplementation, read our articles: CoQ10 Benefits Patients Taking Statin Drugs, Top 3 Nutrients to Reduce Triglycerides Naturally or Lowering Cholesterol Naturally with B Vitamins.
 Greif M, Arnoldt T, von Ziegler F, Ruemmler J, Becker C, Wakili R, D’Anastasi M, Schenzle J, Leber AW, Becker A. Lipoprotein (a) is independently correlated with coronary artery calcification. Eur J Intern Med. 2012 Sep 26.
 Momiyama Y, Ohmori R, Fayad ZA, Tanaka N, Kato R, Taniguchi H, Nagata M, Ohsuzu F. Associations between serum lipoprotein(a) levels and the severity of coronary and aortic atherosclerosis. Atherosclerosis. 2012 May;222(1):241-4.
 Zamboni M, Facchinetti R, Armellini F, Turcato E, Bergamo Andreis IA, Bosello O. Effects of visceral fat and weight loss on lipoprotein(a) concentration in subjects with obesity. Obes Res. 1997 Jul;5(4):332-7.
This article was originally published in 2012 and has been updated.