In the past few years, it has been very well scientifically documented that high levels of homocysteine, a by-product of metabolism of the amino acid methionine, is an important risk factor in heart disease and strokes associated with narrowed blood vessels. In fact, high homocysteine levels turn out to be a much more accurate marker of heart disease risk than cholesterol or blood pressure.
Researchers currently believe that excess homocysteine damages blood vessels, so it may turn out to be a primary cause of heart disease and not just an indicator. Homocysteine is an amino acid meant to exist only temporarily in the body. In a healthy body, it’s quickly transformed into harmless substances. If you have a deficiency of certain B vitamins or a genetic predisposition that interferes with the metabolism of homocysteine, your blood levels will rise, and so will your risk of heart disease and stroke.
Excess homocysteine directly harms the cells that line the insides of the arteries, starting (and encouraging) the process that leads to heart attacks and strokes. In fact, when it’s injected into the arteries of experimental animals, homocysteine causes the linings of those arteries to slough off. Eventually, lesions form that look very much like the clogs that form in the arteries of humans with heart disease. High homocysteine also causes the smooth muscle cells that line the artery walls to multiply, thickening them and making them less flexible. It interferes with the activity of blood components that prevent excessive blood clotting, and this sets the stage for clots that can plug up narrowed blood vessels, causing heart attacks, strokes, or thromboembolism (blood clot in the lungs). Excess homocysteine also prevents small arteries from dilating to allow more blood to flow through; it encourages the oxidation of LDL cholesterol, making this “bad” type of cholesterol even more dangerous to blood vessel health; and it generates free radicals. Antioxidants help significantly in reducing the amount of bad cholesterol in the blood, but if homocysteine levels remain high, the damage to arterial walls will continue.
According to a study done at Tufts University School of Medicine in Boston, if your homocysteine levels are just 20 percent above normal, your risk of cardiovascular disease is significantly increased. If your physician wants to measure your homocysteine levels, you should know that a normal homocysteine level is about 12 micro-moles per liter (mmol/L), and cardiovascular risk increases at about 14 to 16 mmol/L.
The case for high homocysteine as a significant risk factor for heart disease has become incontrovertible. In fact, it’s just as significant—if not more so—than cholesterol levels. One researcher states that homocysteine levels are up to 40 times better at indicating cardiovascular disease risk than cholesterol levels. (Of course, the drug companies can’t make nearly as much money selling B vitamin supplements as they can selling statins, so we don’t anticipate any major shift from the focus on cholesterol control anytime soon.)
Here are a few examples of the latest studies on the homocysteine–heart disease link:
• In one study, 131 subjects—each with one blocked coronary artery—were compared with about the same number of control subjects who were free of heart disease. With every 10 percent elevation in homocysteine levels came a 10 percent elevation in risk of developing severe coronary artery disease.
• A study of postmenopausal women found that elevations in homocysteine led to a higher incidence of coronary artery disease.
• In a study of people who developed deep vein blood clots, researchers found that subjects who developed them had much higher homocysteine levels than those who didn’t.
• A study of 21,500 men between the ages of 35 and 64 found that those with the highest homocysteine (more than 15 mmol/L) were about three times more likely to die of heart disease.
• In another study, 587 men with confirmed heart disease had their homocysteine levels measured and were then followed for 4.6 years. Sixty-four of them died. Of those 64, 3.8 percent had homocysteine levels below 9 mmol/L; 8.6 percent had levels between 9 and 14.9; and 25 percent had levels of 15 or greater.
• In a study published in the New England Journal of Medicine, researchers evaluated the effects of homocysteine-lowering folic acid, B12, and B6 on artery narrowing in men who had required angioplasty to open up at least one clogged heart vessel. The men who took the supplements had lower homocysteine levels after six months, and their arteries were only half as likely to renarrow following their angioplasties.
One much-feared disease that is thought to be related to high homocysteine levels is Alzheimer’s disease. This makes sense, because it’s likely that the brain deterioration seen with this disease has something to do with the deterioration of blood vessels that feed brain tissues. In a study from Tufts University, researchers measured homocysteine levels in 1,092 subjects over a span of about a decade. Their average age was 76, and none of them had dementia. Eight years later, 111 of them had developed dementia, 83 of them from Alzheimer’s disease. (In a few cases, dementia was caused by stroke or other vascular diseases that harm brain tissue.) When the researchers looked back at the homocysteine measurements they had taken, they found that those with homocysteine levels above 14 mmol/L were twice as likely to have developed Alzheimer’s several years later than those with average levels. Those who had elevated levels come back from both tests were at the most risk. Milder elevations in homocysteine also caused risk to rise, but not as much. They concluded that if homocysteine were removed from the risk equation for Alzheimer’s, 15 percent of cases would be prevented. As baby boomers age, this percentage would add up to tens of thousands of people.
Some drugs can cause high homocysteine levels, particularly those that interfere with folic acid, such as methotrexate, an immunosuppressive drug given to cancer, rheumatoid arthritis, and psoriasis patients; the anticonvulsant drugs phenytoin (Dilantin) and carbamazepine (Tegretol, Epitol); and the bile acid sequestrants for lowering cholesterol levels, cholestipol (Colestid) and cholestyramine (Questran). It’s ironic that these cholesterol-lowering drugs, given to reduce heart disease, may actually cause it by raising homocysteine levels!
Other research has shown that homocysteine levels rise when daily folic acid intake is 200 mcg (micrograms) per day or less. This is a typical example of how inadequate the Recommended Daily Allowance (RDA) amounts are, because the current RDA for folate is 200 mcg.
Fortunately for nearly everyone, homocysteine can be easily and inexpensively lowered by taking some B vitamins. If you’re taking a daily multivitamin that includes 400 mcg of folic acid, 50 mg of vitamin B6, and 1,000 mcg of vitamin B12, you should be covered. If your homocysteine levels are high, you should be getting an additional 200 mg daily of vitamin B6 (pyridoxine) and 1 to 4 mg of folic acid daily until your homocysteine levels are back to normal.
Since a deficiency of vitamin B12 can also indirectly raise homocysteine levels, and since a high intake of folic acid can mask a vitamin B12 deficiency, make sure your intake of vitamin B12 is at least 1,000 mcg per day. Vitamin B12 is best taken sublingually (under the tongue) or as a nasal gel or spray. Low thyroid levels and excess alcohol can also raise homocysteine levels.
If your doctor asks you to get blood tests for heart disease, be sure to ask him or her to include homocysteine.
Prescription Alternatives: Hundreds of Free, Natural, Prescription-Free Remedies to Restore & Maintain Your Health, by Earl L. Mindell, R.Ph, Ph. D, & Virginia Hopkins, M.A. Published by McGraw-Hill.