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Lp(a)—A “New” Risk Factor for Heart Disease

By Stephen Sinatra, M.D.

Yes, blood is thicker than water.

I first met Patrick Kelly in the late ’70s in the emergency room at Manchester Memorial Hospital where I was a staff cardiologist. He was admitted for chest pain. He was 49.

But his troubles didn’t begin then. He had a history of heart disease. At age 42, he had had a heart attack and underwent bypass surgery. At 52, he had a second bypass operation.

Then, Pat’s daughter also had a heart attack. She was 28 at the time, a very young age for anyone to experience such a cardiac event. Shortly afterwards, I was asked to evaluate Pat’s 30-year-old son, Neil, who had an episode of pressure-like pain radiating down his left arm.

I immediately ordered the standard battery of tests, including a nuclear stress test. Because of Neil’s family history, though, I also added a comprehensive metabolic profile of what I call the “newer” risk factors for heart disease: homocysteine, fibrinogen, serum ferritin, and Lp(a). Even now, years later, few cardiologists check for these.

Neil’s stress test was within normal range and his homocysteine and serum fibrinogen were within satisfactory levels. His total cholesterol, meanwhile, was high—248, when it should have been less than 200, and his HDL, “good” cholesterol, was excessively low, at 25.

I was surprised, however, by his level of Lp(a), a combination of protein, lipid, and cholesterol that’s a strong indicator for premature coronary heart disease—particularly in men like Neil with a family history of heart disease. His was 111 (less than 60 is desirable).

Once I had a more complete picture of Neil’s physical risk factors for heart disease, I could help him develop a preventive strategy so that he could avoid what had befallen his father and sister.

I encouraged Neil to be thankful for this information. The heart attacks suffered by his father and sister were a message—a message that he must take a serious look at his own risk profile.

Lp(a) and Your Health

Lp(a) is an LDL particle that is produced by the liver.

We know that levels of Lp(a) increase in unstable diabetics and in menopausal women. In the latter case, we believe the increase is due to falling estrogen levels. This may be why a woman’s risk of heart disease quadruples when she reaches menopause. Conversely, Lp(a) decreases with estrogen replacement therapy.

For this reason, it’s imperative that all menopausal and perimenopausal women with a strong family history of heart disease have their Lp(a) levels checked by their doctor.
Further, post-menopausal women with multiple risk factors for heart disease should consider estrogen replacement therapy, particularly if their Lp(a) is elevated.

What about men? The research shows that elevated Lp(a) levels appear to be even stronger predictors for the development of premature heart disease in men. In fact, The Journal of the American Medical Association recently reported a study of 2,191 men, ages 20 to 54, confirming this.

But let me be clear. Your genetic history, more than any other single factor, is the key driver of Lp(a). That’s not to say, though, that every member of your family will inherit this biological trait for heart disease. Neil’s brother, Kevin, whom I also evaluated, has normal Lp(a) levels, and his other factors are also within normal range.

Drugs Will Not Reduce Your Lp(a)

Standard cholesterol-lowering drugs have no impact on your Lp(a) levels. In fact, a study involving these drugs showed an increase in Lp(a) levels!

Niacin, however, can reduce Lp(a). In controlled studies, niacin has been shown to reduce heart disease, presumably because of its ability to lower total cholesterol and Lp(a).

The best approach to combat high levels of Lp(a) is to take niacin and follow my Mediterranean diet. If you experience side effects like flushing, headache, or diarrhea, simply follow the diet and stop the niacin. You can try a lower dosage at a later date.

Lower Your Lp(a) the Natural Way

If, like Neil, you’re concerned about heart disease because of your family history, I suggest you and your family members have your Lp(a) and other risk factors (homocysteine, fibrinogen, and serum ferritin) evaluated by your doctor. Standard blood panels still do not include a test for Lp(a), but you can get that information from tests such as the VAP test (www.vaptest.com) or Spectracell (www.spectracell.com). Your doctor will need to order one of these tests for you. This is truly the leading edge preventive cardiology.

If you find, as the Kellys did, that high Lp(a) runs in your family, you must attack it with an alternative approach. Here’s what I recommend:

  • Follow my modified Mediterranean diet, making sure to eat fresh fish at least two to three times a week. Fish oils, which contain DHA (docosahexaenoic acid), block Lp(a)’s inflammatory and blood-clotting tendencies. Eat a wide variety of fresh fruits and legumes like chickpeas and lentils regularly, because they indirectly help to lower Lp(a) by lowering insulin levels.
  • Take 100 mg of niacin, twice a day. Niacin is inexpensive. You can increase the dose to 500 mg a day, twice a day for further protection, or reduce it by no less than 100 mg daily if you have side effects.
  • Exercise regularly. Walk or dance, or do something else that you like to do. You do not have to break a sweat. Just get moving!
  • Omit saturated fats. Instead, select monounsaturated fats like olive oil and the good polyunsaturated fats like alpha-linolenic acid, found in organic flax seeds and flax seed oil. This will help raise your good cholesterol and lower your bad cholesterol.
  • Be aware of your other risk factors for heart disease, including smoking, high blood pressure, obesity, glucose intolerance, and repressed emotions.
  • Ask your doctor about current screening techniques to assess your risk factors for heart disease.

Neil, for example, is considering being screened for lipid peroxides, oxidized LDL, and serum antioxidants—all of which also belong to the family of newer risk factors for heart disease.
Thanks to his proactive stance, Neil can take great comfort in knowing that one of his serious risk factors, Lp(a), has been discovered. He is well on his way to overcoming this obstacle and having a healthy heart to show for it!

The Kelly sons should be congratulated for taking these critical preventive steps, knowing what they do about their predisposition to heart disease. For them, there’s no question now about their risk for heart disease. Their call-to-arms shows us that heart disease does not have to be a family affair.

Please remember my oft-spoken words: Genetics are not your destiny, but they can raise your awareness about your risk for heart disease. Prevention is the cure!

References:
· Bostom AG, Cupples LA, Jenner JL, et al. Elevated plasma lipoprotein(a) and coronary heart disease in men aged 55 years and younger. A prospective study. JAMA, 1996; 276:544–548.
· Kostner GM, Gavish D, Leopold B, et al. HMG CoA reductase inhibitors lowers LDL cholesterol without reducing Lp(a) levels. Circulation, 1989; 80(5):1313–1319.
· Lawn, RM. Lipoprotein(a) in heart disease. Scientific American, 1992; 54–60.

 

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