Life Extension Magazine May 2006
New Blood Test Better Predicts Heart Attack Risk
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), 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
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.