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Coronary Heart Disease

Please see related story: A Personal Awakening
Read information about Linus Pauling
Information about Vitamin C
A Lipoprotein Risk Assessment Test for Informed Cholesterol Management
The Benefits of the VAP Test Comprehensive lipoprotein analysis
Who is a candidate for a VAP Test? Risk Factors

The Cause of Heart Disease

Science has known for almost two decades that damage to the walls of blood vessels (or lesions) are a necessary precondition for the formation of atherosclerotic plaques. Competing theories for the reason this damage occurs include a) oxidized cholesterol in the blood b) oxidized homocysteine in the blood and c) vitamin deficiencies. The oxidized choleterol and homocysteine theorists, while pointing to their own experiments, have yet to explain why infarctions are usually close to the heart, i.e., where mechanical stress is great, rather than randomly disributed throughout the body. Nor do these theories satisfactorily explain why animals, that produce their own vitamin C, do not suffer the same disease.

During the last decade, 2-time Nobel Prize winner Pauling and his associate and heart researcher Dr. Matthias Rath, M.D., independently formulated their own assessment regarding the cause and nature of occlusive heart disease. They agree that heart disease is essentially a repair process that is started by a lesion; their theory explains the primary reason these lesions occur. Accordingly, CVD is a natural body healing process for the walls of arteries and veins weak from insufficient collagen, a condition caused by inadequate vitamin C in the diet.

(Since vitamin C is a powerful anti-oxidant, it would be a prudent remedy even if either the oxidized cholesterol or oxidized homocysteine theories have merit. Experiments are needed to determine whether either oxidized substance is dangerous when the body pool of vitamin C is high, such as the case with most animals.)

Vitamin C Deficiency and Heart Attacks

The Life Extension Foundation reported on page 19 of the September 1997 issue:

"A study of 1,605 randomly selected man in Finland, aged 42 to 60 years, was conducted between 1984 and 1989. None of the men had evidence of pre-existing heart disease. After adjusting for other confounding factors, men who were deficient in vitamin C had 3.5 times more heart attacks than men who were not deficient in vitamin C. The scientists's conclusion was, "Vitamin C deficiency, as assessed by low plasma ascorbate concentration, is a risk factor for coronary heart disease." British Medical Journal (Vol 314, Iss 708, 1997)

Furthermore, recent German reports, as mentioned by the American Heart Association, credit vitamin C in the blood stream with "almost completely" reversing "endothelial dysfunction" in smokers. In other words, ascorbic acid prevents damage to the walls of blood vessels that may lead to heart disease.

LDL Look-Alike

Dr. Rath was part of a research team in Germany that studied post-mortem human aortas. They identified a "sticky" variant of LDL cholesterol in human atherosclerotic plaques -- the only component, according to Dr. Rath. This substance is not found in most animals, i.e., those that manufacture vitamin C in their bodies. Animals, generally, do not suffer the same kinds of occlusive cardiovascular disease. Although similar in composition to LDL, the significance of this mysterious substance escaped most other researchers, until recently.

According to Pauling/Rath,

"The concept that Lp(a) is a surrogate for ascorbate (vitamin C) is suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals. Properties of Lp(a) that are shared with ascorbate, in accordance with this hypothesis, are the acceleration of wound healing and other cell-repair mechanisms, the strengthening of the extra cellular matrix (e.g. blood vessels), and the prevention of lipid peroxidation. High plasma Lp(a) is associated with coronary heart disease and other forms of atherosclerosis in humans, and the incidence of cardiovascular disease is decreased by elevated ascorbate. Similar observations have been made in cancer and diabetes. We have formulated the hypothesis that Lp(a) is a surrogate for ascorbate in humans and other species and have marshaled the evidence bearing on this hypothesis."

These two scientists performed careful laboratory experiments on animals in order to test their theory. They were able repeat earlier experiments and induced atherosclerosis in guinea pigs by restricting the intake of vitamin C to the U. S. RDA (adjusting for body weight).This time, Pauling and Rath measured Lp(a) levels in the animals.

Over time, roughly five weeks in these animals, vitamin C restriction leads to poor production of the protein collagen; ultimately, blood vessels lose strength, causing the lesions that result in the arterial healing process we call atherosclerosis. Microscope pictures show the animal lesions mimic the human form of the disease. Lp(a) levels in animals deprived of vitamin C were shown to rise as decribed in their 1994 U. S. Patent.

Animals in the control group that were fed the same except for the addition of a human equivalent of 3 to 5 gm of vitamin C per day showed no signs of atherosclerosis. Lp(a) remained low in these animals.

The subject of intense scientific scrutiny, these scientist's insight about the "missing link" in heart disease -- the coagulating healing factor lipoprotein(a) -- has been confirmed during a reevaluation of The Framingham Heart Study.

Dr. Pauling stated that, "if you have more than 20mg/dl of lipoprotein-(a) in your blood it begins depositing plaques, causing atherosclerosis."

According to Dr. Rath, studies show that special diet does not influence lipoprotein(a) blood levels. Vitamin C and vitamin B3 (niacin) can lower blood levels of lipoprotein(a).

Furthermore, according to Dr. Rath, significant documentation attests that:

"Vitamins belong to the most powerful agents in the fight against heart disease. This fact has been established by studies of thousands of people over many years. Here are some important results of recent clinical studies:

Vitamin C cuts heart disease rate almost in half (documented in 11,000 Americans over ten years) Vitamin E cuts heart disease rate by more than one third (documented in 36,000 Americans over six years.) Beta Carotene (provitamin A) cuts heart disease rate almost in half (documented in 36,000 Americans). No prescription drug has ever been shown to help prevent heart disease similar [vitamins A, C and E]. These results and those of countless other studies are so clear that anybody questioning the value of vitamins in the prevention of heart disease may safely be considered as uninformed."

A Surprisingly Safe, Effective, and Simple Cure?

You will hear and read in the media that Lp(a) is a "genetic" factor and that there is no known treatment. Believe these pundits and risk your life!

The Lp(a) Threat Can Be Neutralized -- 100% Success Rate Reported

Armed with knowledge as to how and why plaque forms in human arteries, Pauling devised what has turned out to be empirically a viable cure. Based on their Lipoprotein(a) experiments, and the Nobel discoveries of the "cholesterol-binding region," Pauling theorized that large amounts of an essential amino acid (in combination with vitamin C) would be therapeutically effective.

Quoting Pauling:

"Many investigators contributed to demonstrating that it is lipoprotein(a) that is deposited in plaques, not merely LDL, but Lp(a). If you have more than 20 mg/dl in the blood it begins to deposit plaques and atherosclerosis. The question then is: What causes Lp(a) to stick to the wall of the artery and form these plaques?

"Well countless biochemists and chemists discovered what in the wall of the artery causes Lp(a) to adhere and form atherosclerotic plaques and ultimately lead to heart disease, strokes, and peripheral arterial disease. The answer is that there is a particular amino acid in a protein in the wall of the artery - lysine - which is one of the twenty amino acids that binds the Lp(a) and causes atherosclerotic plaques to develop.


Furthermore, Pauling said, "knowing that lysyl residues are what causes lipoprotein-(a) to get stuck to the wall of the artery and form atherosclerotic plaques, any physical chemist would say at once that the thing to do is prevent that by putting the amino acid lysine in the blood to a greater extent than it is normally. You need lysine to be alive, it is essential, you have to get about 1 gram a day to keep in protein balance, but you can take lysine, pure lysine, a perfectly non toxic substance in food [as supplements], which puts extra lysine molecules in the blood. They enter into competition with the lysyl residues on the wall of arteries and accordingly count to prevent Lp(a) from being deposited, or even will work to pull it loose and destroy atherosclerotic plaques."

Dr. Pauling became convinced that this new understanding of cardiovascular disease would aid in the prevention of the disease and help doctors treat the condition, thereby, saving countless lives. In response to a question as to whether or not the new therapy of vitamin C and large amounts of the amino acid L-Lysine could really reverse the atherosclerotic process?", Dr. Pauling replied:

"I think so. Yes. Now I've got to the point where I think we can get almost complete control of cardiovascular disease, heart attacks and strokes by the proper use of vitamin C and Lysine. It can prevent cardiovascular disease and even cure it. If you are at risk of heart disease, or if there is a history of heart disease in your family, if your father or other members of the family died of a heart attack or stroke or whatever, or if you have a mild heart attack yourself then you had better be taking vitamin C and Lysine."

Please see related story: A Personal Awakening
Read information about Linus Pauling
Information about Vitamin C
A Lipoprotein Risk Assessment Test for Informed Cholesterol Management
The Benefits of the VAP Test Comprehensive lipoprotein analysis
Who is a candidate for a VAP Test? Risk Factors

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Last Updated: 08-17-02 by SJM