At your doctor’s advice, you lowered your LDL (bad) cholesterol and perhaps even raised your HDL (good) cholesterol. Have you completely safeguarded yourself from heart attack—especially heart attacks before 60 years of age?

Unfortunately, no.

Modern medical science has identified a new independent risk factor for a small percentage of heart disease sufferers, especially among younger people. The new threat is lipoprotein(a), an LDL-like particle that has been dubbed “super bad cholesterol.”

I speak from experience as someone who has extremely high lipoprotein(a) yet did not know about it because my doctor never mentioned it or tested me for it. Here is what it is and how you can protect yourself from high lipoprotein(a).

What in the world is lipoprotein(a)?

Lipoprotein(a), often abbreviated as “Lp(a)” and referred to as “Lp little a,” is an LDL-like cholesterol particle with an extra protein called apoprotein(a) connected to it. Curiously, this extra protein is what also makes HDL cholesterol “good.” However, this combination is nothing but trouble. It not only attacks your arteries just like LDL cholesterol, it also causes your blood to clot faster. 

This is the deadly combination that causes most heart attacks.

Recent studies have concluded that persons in the highest third of Lp(a) levels carry a 70 percent increased risk for heart disease. In one such study of 1100 individuals, having an Lp(a) greater than 20 mg/dl and LDL cholesterol greater than 140 mg/dl increased heart attack risk by a factor of 2.75.  Another study showed the combination of Lp(a) greater than 20 mg/dl and having type 2 diabetes increased the risk by a factor of 6.65.

Lp(a) can be easily measured by most blood testing laboratories, but your doctor must first be aware of the potential danger and order the test. Sadly, most doctors are unaware of the danger. Adding to the problem is that the test is not standardized and may vary tremendously from lab to lab. This can cause confusion if you switch the testing laboratory for your blood work. Also, some labs measure Lp(a) in milligrams per deciliter (mg/dL), a measure of weight per volume of blood, while others measure it in nanomoles per liter (nmol/L), a measure of particles in a volume of blood. The typical cut-offs for these two measuring systems is 20 mg/dL and 75 nmol/L. 

Anything higher than these numbers could signal a problem.

How can I reduce lipoprotein(a)?

Unfortunately, Lp(a) is a genetic trait that is extremely difficult, if not impossible, to treat with simple diet and lifestyle changes. Here is what I found out and treatments I have tried.

The nutritional supplement niacin has been tested and found to be the most effective treatment for lowering Lp(a). I have been using it with varying success for years and have reduced my Lp(a) with niacin by up to 50 percent. However, it often requires large doses of two grams or more per day and should be treated as a drug at these doses and only taken at the direction and under the supervision of a doctor. There are both prescription (Niaspan) and over-the-counter (Slo-Niacin) preparations available. These timed-release versions seem to be the best tolerated because of the often unbearable flushing side-effect of immediate-release niacin. Again, both preparations should only be taken under the supervision of your physician. 

Another option that has proven effective for some are the hormones estrogen (for women) and testosterone (for men). Estrogen can reduce Lp(a) as much 25 percent and has been confirmed as effective in several studies. Keep in mind that estrogen is a powerful hormone with many other effects. Only your doctor can determine whether the benefits exceed the risk and prescribe it.

Testosterone for men has been shown to reduce Lp(a) by 25 to 59 percent. Like estrogen for women, testosterone is another powerful hormone and only your doctor can prescribe and properly determine its risks and benefits. I tried this treatment with little effect other than to lower my HDL cholesterol, so I stopped taking it.

Interestingly, aspirin, which many already use, has been shown to reduce Lp(a) levels by 18 to 46 percent at doses of 81 to 150 mg per day. I cannot say whether it has been effective for me as I have always taken aspirin and won’t stop anytime soon.

Omega-3 and other supplements

Another, newer treatment I have tried is high-dose omega-3 fatty acids (fish oil)—and I mean really high doses of over five grams of EPA/DHA per day (that’s five grams of active ingredient, not total capsule weight). I started after reading about a study of 1300 Bantu fishermen in Tanzania, Africa. Bantu fishermen who consumed enough fish to provide 3000 to 5000 mg per day (combined EPA and DHA) had a 48 percent lower Lp(a) than their inland tribesmen who were largely vegetarian. I have seen my Lp(a) fluctuate but have experienced reductions up to 50 percent in a personal experiment I did. The only problem I had was that the results were not consistent over time.

I am currently taking 25 mg of DHEA as it has been shown to reduce Lp(a) by as much as 18 percent in one study. I am not due to test my Lp(a) for another month so I cannot report results just yet. From what I have read, taking DHEA has a reported side effect that it can make men overly aggressive (uh, oh, some claim I may already be too aggressive).

Early on, I tried the amino acid supplement L-carnitine, which several studies showed to be marginally effective (less than 10 percent reduction) but it showed no effect in me so I stopped. 

At one point I had to stop taking niacin because of some stomach problems, so I did some research on other drugs that could help raise my HDL and potentially lower my Lp(a). I discovered that several studies showed that the fibrate drug class provided modest reductions in Lp(a). I tried fenofibrate on two occasions for a six-month period. The first time, it did indeed lower my Lp(a), but not the second occasion. I am now back on niacin.

Dr. Mathias Rath has been a proponent of vitamin C supplementation at high doses to treat Lp(a). I investigated his theories and gave it a try with no success. I would point out that, consistent with my experience, no other researcher has been able to duplicate Dr. Rath’s results. I do still take 1000 mg of time-release vitamin C, but not to treat Lp(a).

Since I was diagnosed with Hashimoto’s Thyroiditis, I have done extensive research on thyroid replacement therapy and was pleasantly surprised that normalizing thyroid hormone levels may reduce Lp(a). I do not have any personal experience to report but did come up with this hope for the future. There is a new “thyroid mimetic” drug that mimics the effect of thyroid hormones on the liver that reported significant reductions in Lp(a) in animal models.

In conclusion, I highly recommend that everyone discuss being tested for Lp(a) with their doctor, particularly if you have a family history of heart attack at early ages. If you do have Lp(a), it is important you address it. While it can be frustrating to treat, it is worth the time and effort if only to reduce other risk factors even further. If you are already fighting high Lp(a), please do report back on things you have tried and what success you have had.