High lipoprotein(a), also known as Lp(a), increases the risk of heart disease and clotting. This is the first in a series of posts where we describe how to determine certain health threatening genetic conditions, and if present, how to combat their effects.

Do you have high Lipoprotein(a), also known as Lp(a)? It would be a good idea to find out. Lp(a) can be measured with a blood test. What is high? For Black people, over 30 mg/dl. For all others, over 15 mg/dl.

Lp(a) circulates in the blood. Elevated levels of Lp(a), can be a risk factor for atherosclerosis and for clotting as well. Lp(a) is a slightly modified form of LDL lipoprotein particles (the so called “bad” cholesterol).

About 10% of the Caucasian and Asian population has high levels of Lp(a). High usually means above 15 mg/dl. Such people have double the risk of heart and clotting problems. The Black population has an even higher rate of elevated Lp(a), around 20%, but are not at increased risk of heart problems for Lp(a) levels as high as 30 mg/dl, as this group usually has an Lp(a) variant that is not as harmful.

There is no cure for high Lp(a), nor is there a known reason for its existence, as people with little or no Lp(a) appear to do fine. Despite the increased heart and clotting risks, there seem to be a couple of benefits. First, the cancer rate is lower in those with high Lp(a), and second, there may be a longevity benefit, as a disproportionately higher percentage of centenarians have elevated Lp(a). (Note, that is not the same thing as saying that people with high Lp(a) are more likely to become centenarians.) Also, some research has reported a lower incidence of adult onset diabetes in those with high levels of Lp(a)

Lp(a) has several properties that cause it to be dangerous.

First, the modification to the LDL interferes with a circulating biochemical that prevents blood clots. With its function partially disabled, clotting risk increases. Heart attacks and strokes are both caused by clots. The risk for heart attacks is close to doubled for those with Lp(a) levels above 30 mg/dl. Stroke risk is also increased.

Second, high Lp(a) levels accelerate atherosclerosis. There could be several reasons for this. Circulating LDL particles are frequently engulfed by cells that need cholesterol. However, these cells will not take the Lp(a) variant, hence these particles stay in circulation longer and have more opportunity to get stuck inside the artery wall. These particles also have a tendency to oxidize and stick to the inner surface of the artery wall, which will promote artery wall cell death and repair, which also leads to atherosclerosis..

Combating Lp(a)

To avoid the cardiac consequences, the Quantitative Medicine exercise and diet recommendations are a must. However, if they are strictly done, not only will heart problems be prevented, but most others as well. Lp(a) has it “vulnerabilities,” which permit a strategy to be developed.

First, consider how Lp(a) is formed. An additional protein is attached to LDL particles outside the liver, in the bloodstream. So one defense is to keep the LDL particle size large. These larger particles will have a harder time getting inside the artery and causing atherosclerosis. Push the LDL size up by pulling triglycerides lower, as explained in posts here, here, and here.

Second, stop the Lp(a) particles from sticking to the artery wall. This mean varying your blood flow with frequent vigorous, but brief, exercise. Barrel up stairs two or three steps at a time. Trot up hills. Keep things stirred up. See this post.

Another benefit of exercise is speculative. The rushing blood may cause the protein strings to unfurl. As such, they may be exposed to various circulating enzymes that can snip it up.

We did not intend to preach in this post, but, readers with high Lp(a): you must combat it. Otherwise cardiac problems are very likely, and often at an early age (forties). Atherosclerosis is much easier to prevent than reverse, so a life-long commitment is called for. However, a person with high Lp(a) that undertakes this will probably avoid all other degenerative disease too. This is no small reward for all that effort.

The Lp(a) Measurement is Problematic

Low means there is no danger regardless of the measurement technique. However, the measurement is not standardized, and there are several techniques that, unfortunately, do not yield comparable results. Further, it is very difficult to figure out how a specific lab did the analysis. At this point, anything over 15 mg/dl should be considered dangerous. It is hoped that a more definitive measurement will be developed in the future.

To actually pin down the risk, we probably need to know how much of the LDL has the protein string stuck to it, and the length of the strings. The measurement situation is in a very bad state. The usual measurement is the amount of Lp(a).

What, Exactly, Is Lp(a)?

Lp(a) constitutes the attachment of an additional protein string called apo(a) to an ordinary LDL particle. The apo(a) string sticks tightly to the LDL particle at one spot, and tends to cling to the LDL particle, covering it. If the particle is flowing rapidly, during exercise, for instance, the apo(a) string unfurls like a streamer. This streamer comes in a large variety of lengths. Some people have mostly short ones, and others mostly long. The increased risk is with the shorter lengths. People of African descent people tend to have the longer ones and are at less risk.

Therapies and Possible Breakthroughs

Aspirin and niacin are frequently proposed, though neither have been properly studied in a way that would determine long term effects. Until such time, these should probably be avoided.

One promising new development is called antisense therapy. This drug is a complement of the messenger RNA that encodes the apo(a) protein string (hence the term “antisense”). The drug attaches to the messenger RNA, thus inactivating apo(a) production. The drug is quite new (2015) and may have numerous problems or side effects. This sort of drug has a generic problem in that it binds to other, similar RNA, and can, therefore, disrupt other important processes. In very early trials, though, this drug did manage to lower Lp(a) up to 80%, so keep an eye on this one.