Summary of Dr. McCully's research studies:
Dr. McCully found that homocysteine levels could explain many known high risk factors in heart attacks and strokes.

• Smoking raises homocysteine levels.
• Obesity raises homocysteine levels.
• When heart disease runs in a family, the victims often share a minor flaw in one of their genes that governs homocysteine metabolism.
• During a woman's reproductive years, homocysteine levels are on average 20% lower than man's. During these same years a woman's risk of a heart attack is 20% lower than man's risk.
• After menopause women's homocysteine levels, and their risk of heart disease, rise to equal a man's level.
• Both men and women experience homocysteine levels that increase with old age. At the same time their body becomes less efficient at absorbing B vitamins. NADH and a series of B vitamin are used in treating high homocysteine blood levels.
• Both sexes have increasing levels of cardiovascular disease and heart disease risk that correlates closely with increasing homocysteine levels.

In the medical world, this is all circumstantial evidence.

Summary of additional homocysteine research studies:
There are some good reasons to suspect the relationship between high homocysteines levels and heart disease and cardiovascular disease. This is more than just coincidence.

• In test tube studies, homocysteine not only injured blood vessel lining but accelerated the build up of scar tissue which formed blot clots. To learn more about the advancing stages of cardiovascular disease and heart disease, visit the the events leading to a heart attack.
• Researchers have proven that homocysteine injections produce arterial plaque in animals.
• A famous 1992 Harvard University study of 14,000 male physicians found the top 5% of males with highest homocysteine levels were 300% more likely to have a heart attack than the bottom 95%.
• A 1995 Framingham, Massachusetts Heart Disease Study found that people with high homocysteine levels are most likely to suffer from a dangerous narrowing of the carotid artery (the main blood vessel feeding the brain.)
• The AHA says, a homocysteine level of less than 14 micromoles per liter of blood is considered normal. The Framingham Heart Disease Study found any reading above 11.4 micromoles brought an sharp increase in the risk of heart attacks and strokes.
• In July 1997, University of Washington study reported that high homocysteine levels doubles the risk of heart attacks in young women.
• A clinical study done in Norway found that heart patients with high homocysteine levels can predict their survival rate.
• Recent medical research found that in the U.S. 1 person in 8 inherits the gene that that slows or inhibits the liver's disposal of homocysteines.

Current research efforts:
To date, no one has taken the final steps in performing a double blind, controlled clinical study that identifies the specific amounts of nutritional supplement NADH, and vitamins B6, B12 and folic acid that should be used in the treatment high homocysteine levels. In July 1997, Harvard University started a research study to see whether a daily nutritional supplements of folic acid can help prevent strokes. (The results won't be available for years.)

Until clinical evidence is definitive, an annual physical isn't likely to include a blood test for homocysteine levels. Heart and cardiovascular disease industry experts take this stand:

• They will continue to ignore homocysteine levels in the blood in favor of cholesterol tests until the evidence is definitive.

The clinical research work will take time. Our question to you is why wait? With what we know today, you have nothing to lose, and so much to gain. NADH is available here and vitamins B6, B12 and folic acid can be purchased where you buy vitamins.

If you want more information about homocysteine levels, read Dr. McCully's new book, "The Homocysteine Revolution" (242 pages, Keats. $14.95) The damages of homocysteine levels are also discussed in an article "The Heart Attackers", by Geoffrey Cowley, Newsweek, August 11, 1997. page 54:60.

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