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New Blood Test Better Predicts Heart Attack Risk

May 2006

By William Davis, MD, FACC

Triglycerides and VLDL

For several decades, researchers have debated the question of whether triglycerides contribute to heart disease risk. The issue has been conclusively settled: while triglycerides by themselves do not cause heart attacks, they are the driving force behind lipoprotein particles that are potent causes of heart disease, such as small LDL and very low-density lipoprotein (VLDL).33 This phenomenon occurs when triglyceride levels are in the 100–400 mg/dL range. Levels over 400 mg/dL may also contribute to heart disease, but your doctor will need to consider a number of other issues, such as thyroid and kidney disease.

VLDL particles are the most densely triglyceride-packed lipoprotein. Triglycerides and VLDL particles commonly go hand in hand, but excessive VLDL can be present even when triglycerides are low. This is when specific measurement of VLDL is most helpful. When plentiful, VLDL particles circulate in the blood and interact with other lipoprotein particles such as LDL and HDL. This interaction forces triglycerides into LDL and HDL particles, and is the initial step in the formation of undesirable small LDL and deficient large HDL.34

VLDL and triglycerides respond to the same treatments. In general, aim for a triglyceride level below 100 mg/dL, as all triglyceride-rich particles (including small LDL) are minimized at this level. Fish oil in higher doses (4000–10,000 mg/day) is an effective way to lower triglycerides and VLDL by 30–50%.29 This is likely at least part of the reason fish oil has such a powerful impact on reducing death from cardiovascular events. Increasing the fiber content of your diet to 50 grams/day, adding raw nuts, maintaining healthy body weight, and avoiding foods with a high glycemic index are healthy strategies that may contribute to lowering triglycerides to the desired level of less than 100 mg/dL, thereby reducing or eliminating VLDL.35

Lipoprotein (a)

Lipoprotein (a), or Lp(a), is a powerful, much underappreciated cause of heart disease. Up to 20% of people with heart disease will have increased Lp(a), which can lead to heart attacks early in life, often in a person’s forties or fifties. Lp(a) not only is a direct cause of plaque growth and the plaque rupture that can cause a heart attack, but it also magnifies the dangers of all other risk factors, especially LDL particle size and number.36

Treatment for elevated Lp(a) is controversial. Most experts agree that, at the very least, Lp(a) should be lowered to a level no higher than 30 mg/dL, and that this significantly reduces heart attack risk.37 Niacin is the most effective direct treatment for lowering Lp(a), though higher doses are required than for other abnormalities (1000–4000 mg per day, which should be prescribed and monitored by a physician).

In females, the use of estrogen preparations may lower Lp(a), generally around 25%, though estrogen presents other issues that should be fully discussed with your doctor. Testosterone can be very helpful for men, and may lower Lp(a) by 25%. The supplement L-carnitine can be a useful adjunct; 2000 mg per day (1000 mg twice a day) can reduce Lp(a) by 7-8% and occasionally by up to 20%.38 Other nutritional strategies that help lower Lp(a) include ground flaxseed (2 tablespoons daily), raw almonds (1/4 cup daily), and vitamin C (more than 1000 mg daily), with reported reductions of approximately 7%.39-41


Shortly after the release of his autobiography, former President Bill Clinton developed unstable symptoms that warned of impending heart attack. Extensive blockages of all three coronary arteries (greater than 90%) were diagnosed through heart catheterization, and Mr. Clinton underwent a quadruple coronary bypass operation.

According to a USA Today report, “Dr. Allan Schwartz, chief of cardiology at the hospital, said that given the extent of Clinton’s blockage, there was a ‘substantial likelihood that he would have suffered a substantial heart attack in the near future.’ Doctors stopped Clinton’s heart for 73 minutes and put him on a heart/lung machine, a common practice in bypass surgery. [Surgeon Craig] Smith said that it was ‘obvious relatively quickly that what he needed was an operation.’”

After the procedure, the doctors addressing the media corps at New York-Presbyterian Hospital/Columbia boasted of their success, calling the procedure lifesaving. Media reports glowed with descriptions of the high-tech hospital care Mr. Clinton received. Senator Hillary Rodham Clinton publicly expressed her and daughter Chelsea’s gratitude for the high-quality care the former President received in the hospital.


Before congratulating our medical system, several important questions need to be answered. Mr. Clinton had passed an annual thallium stress test for the preceding five years. His cholesterol was reported in the press as excellent at 179 mg/dL, and doctors monitored his cholesterol values frequently. Mr. Clinton jogged and complained of no symptoms with vigorous exercise.

If coronary disease takes years to develop, why was it not it recognized earlier, before it became life threatening? How could stress test after stress test be normal when extensive coronary disease was present? How could doctors be satisfied with cholesterol values that permit life-threatening disease to develop? The answers to these questions are already available to us.

Had Mr. Clinton and his doctors been better informed, it is highly likely that his procedure would not have been necessary.


Mr. Clinton’s doctors might have suggested that he undergo lipoprotein testing. Through no more effort than administering a conventional cholesterol test, they would have obtained insight into several previously unrecognized and potent causes of heart disease. These hidden causes could have been easily corrected, potentially reducing Mr. Clinton’s coronary plaque.

Alternatively, had Mr. Clinton’s doctors simply advised him in, say, 1996 (on assuming the presidency for his second term) to take a 30-second heart scan, they would have been shocked to learn that his “score” was very high—probably over 400 (desirable is 0), signifying extensive hidden coronary plaque. Once Mr. Clinton’s high heart scan score was identified, a search for the causes should have ensued, followed by corrective measures.

Had his doctors been really smart, they would have had Mr. Clinton undergo a heart scan and lipoprotein testing. With five minutes of Mr. Clinton’s time, a powerful prevention program could have been devised. This kind of information would likely have eliminated Mr. Clinton’s need for bypass surgery.


Learn from the mismanagement of Mr. Clinton’s health and do not wait for the appearance of symptoms before you take action to prevent heart disease. If you have no symptoms, a stress test, even with blood-flow images, like the thallium stress test, is virtually useless and does not accurately predict the potential for heart attack in the vast majority of cases. Do not rely on cholesterol to predict your potential for heart attack. Look at the complete picture: do you have high blood pressure, a history of heart disease or stroke in your family, diabetes, or smoking now or in the past? Consider monitoring your lipoproteins to better assess your sources of risk.

Other Measures of Heart Disease Risk

Several other measures are important components of a comprehensive assessment of heart disease risk. Although not lipoproteins, these measures are often included in cardiovascular health panels.


Homocysteine was first suspected to be a cause of heart disease when children with a rare metabolic disorder called “homocystinuria” were observed to develop coronary disease. High levels of homocysteine—often greater than 200 micromoles per liter (µmol/L)—were recorded in the blood of these children.

Since these preliminary observations, it has become clear that elevated homocysteine levels are associated with coronary disease risk in adults, and that this risk occurs at levels far below 200 µmol/L. In adults, homocysteine levels in the 15-50 µmol/L range are associated with a significantly increased risk of heart disease, while some evidence suggests that levels as low as 8-10 µmol/L may elevate risk.

Homocysteine causes arterial injury, increases oxidization of LDL particles (thereby making them more damaging), constricts arteries, and provokes blood clot formation. The net result is a threefold increase in heart attack risk. Many people with heart disease have elevated homocysteine levels.42-43

Once you have recognized that your homocysteine is elevated, management is relatively easy and consists of B vitamin supplementation. Common starting regimens are vitamin B6 (25-50 mg), vitamin B12 (1000 mcg or more), and folic acid (1000-5000 mcg). Folic acid can be obtained over the counter in doses up to 800 mcg. Higher doses are available by prescription. Very rarely, taking folic acid by itself will “mask” hidden vitamin B12 deficiency, causing red tongue, anemia, and neurological effects. Therefore, folic acid is best taken in combination with vitamins B12 and B6. For modestly elevated homocysteine levels, a combination B vitamin complex is a good way to begin.