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Life Extension Magazine

LE Magazine July 1997

HOMOCYSTEINE AND HEART ATTACKS

How SuperNutrients Can Protect You

By Paul Frankel, Ph.D. and Terri Mitchell

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Heart disease is the No. 1 killer in the U.S., killing more people than cancer, infectious diseases, and homocides combined.

Nearly a third of all victims will not survive their first symptom.

Half of all victims won't reach the hospital alive.

For the past few decades, cholesterol has been the demon of heart disease. Fat consciousness has become America's favorite dietary preoccupation, with entire industries growing up around the idea of reducing dietary fat and cholesterol. While cholesterol is associated with heart disease in some studies, and Americans do eat too much fat, it appears that cholesterol may have less to do with heart disease than most people think.

A much stronger case has emerged for a toxic amino acid called homocysteine. Homocysteine is a naturally synthesized by-product of methionine metabolism. If the right cofactors are present, it will eventually convert to cysteine and other beneficial compounds. If the cofactors are lacking, it will build up to toxic levels.

Data from a study on healthy U.S. physicians with no prior history of heart disease shows that highly elevated homocysteine levels are associated with a more than three-fold increase in the risk of heart attack over a five-year period. This finding was published in 1992 in JAMA as part of the Physicians' Health Study. The study included 14,916 male physicians; it is the same one that showed the benefits of aspirin. The Framingham Heart Study and other studies have confirmed that elevated homocysteine is an independent risk factor for heart disease.

It is especially imperative for people with a family history of cardiovascular disease to control their homocysteine levels. In one study, 37 men and women with early familial heart disease had 29% higher levels of homocysteine than controls. Dr. Rene Malinow of the Oregon Health Sciences Center concluded that some cases of elevated homocysteine could be the result of an inherited abnormality. This would be one explanation for premature coronary artery disease that runs in families. Mostly, however, elevated homocysteine levels can be traced to inadequate or improper nutrition.

The Different Forms Of Heart Disease

Cardiovascular disease manifests as peripheral artery disease, coronary artery disease, myocardial infarction (heart attack), stroke, aneurysm, thromboembolism, extracranial carotid artery and stenosis.

As an artery (or vein) becomes diseased, the inner arterial wall becomes thick - a condition known as arteriosclerosis. Cells lining the artery proliferate and combine with protein and lipids in a mass called an atherosclerotic plaque. Plaques are commonly the first indication of cardiovascular disease. Plaques change with time, gathering cholesterol and fat, finally becoming atheromas. Atheromas distort the artery wall, allowing calcification. Eventually, the inside of arteries become so rough that if you run your fingers over them, they feel like bits of broken glass.

When an atheroma blocks blood to the heart, it is referred to as a heart attack. When it blocks blood to the brain, it is a stroke. If the penile artery is damaged or occluded, impotence results. Partial blockage in the chest (which causes pain) is referred to as angina, and weaknesses or rupturing of the arteries or veins are referred to as aneurysms.

Homocysteine is thought to initiate these events by irritating the inner lining of arteries and veins. In addition, it was recently reported in the journal Circulation that hyperhomocysteinemia (high homocysteine) impairs blood vessels' ability to dilate, or expand. Millions of dollars are spent annually on drugs designed to lower blood pressure by dilating blood vessels. It is likely that in some people, this life-threatening problem could be reversed by the supernutrients that lower homocysteine.

Stroke and Homocysteine

According to a study in the European Journal of Clinical Investigation, 40% of stroke victims have elevated homocysteine compared to only 6% of controls. The study found increased homocysteine in lacunar, hemorrhagic and embolic strokes. A study published in Lancet in 1996 showed that even after adjustment for other risk factors, homocysteine was an independent risk factor for stroke and arterial thrombosis in patients with the autoimmune disease lupus.

Another study published in Lancet came to the same conclusion after studying 107 middle-aged British men who participated in a 2-year investigation. The authors concluded that "these findings suggest that homocysteine is a strong and independent risk factor for stroke." It has even been reported that the level of homocysteine in blood correlates with the thickness of arteries. And it was reported in the Journal of Nutrition that men with levels of homocysteine above 14 µmol/L had a greater than 50% chance of stenosis in an extracranial carotid artery, whereas men with levels below 9.1 µmol/L only had a 27% incidence of stenosis. (The data for women were slightly different. Women with levels of homocysteine greater than 14.3 µmol/L had a 39% chance of having carotid artery stenosis: below 9.1 µmol/L, their chances were about even with men).

A New Demon EmergesA New Demon Emerges

In 1982, Edward Gruber and Stephen Raymond of MIT wrote in their book, Beyond Cholesterol: B6, Arteriosclerosis and Your Heart:

"Homocysteine rapidly induces the initial states of arteriosclerosis and cholesterol's effects are not apparent."

A comparison of the data on homocysteine with the data on cholesterol illustrates the strength of the homocysteine theory. There are many problems with the theory that dietary cholesterol causes heart disease. For one thing, non-oxidized cholesterol is not atherogenic in animals. Further, dietary cholesterol doesn't cause vascular disease in animals except under extreme conditions. Heart and vascular disease can be observed in the complete absence of added dietary cholesterol in animals.

The cholesterol hypothesis preaches that a multitude of things increase the risk of heart attack. The list includes triglycerides, lipoprotein(a), fibrinogen, smoking, blood pressure, inactivity and poor genetics. Such a multiple risk factor approach should raise a red flag. Dr. Lewis Thomas (former president of Memorial Sloan-Kettering Cancer Center) has stated that every disease turns out to have one central mechanism of action. Cholesterol has too many ifs, ands and buts to be the cause of heart disease. Levels of cholesterol in blood do correlate with heart disease. However, cholesterol is no longer thought to be the cause of heart disease.

Also, a recent study by Dr. Franziska Loehrer and co-workers at University Hospital in Switzerland showed that cholesterol and triglycerides failed to demonstrate a statistically significant correlation with coronary artery disease. Elevated homocysteine, low S-adenosylmethionine (SAM), age, and body mass index did. According to Dr. Loehrer:

"...high levels of homocysteine occur before the disease. The finding of similar homocysteine values in patients after an interval (of approximately) one year supports the idea that this parameter [homocysteine] plays a role in the disease process and is not just altered by the disease itself."

Homocysteine is a clearly-established risk factor for heart disease. Based on large and small-scale studies, it is a better predictor of heart attacks than cholesterol.