Linus Pauling claimed that specific non-toxic substances called Lp(a) binding inhibitors taken orally will prevent and may even dissolve existing atherosclerotic plaque build-ups.
This work is based on at least 2 Nobel Prizes in Medicine and the efforts of countless medical researchers. The theory and conclusions offered represent the final contribution of an American scientific giant.
The fact that you have not heard about this discovery in the mainstream media is disturbing. It speaks volumes about how powerful interests can somehow suppress vital information that would be detrimental to their financial interests.
In 1989, the eminent American scientist Linus Pauling and his associate Matthias Rath MD, unlocked a medical mystery.
They found the reason human beings suffer heart disease.
Then in 1991, Linus Pauling invented a non-prescription cure. The twice Nobel prize winning genius, chemist, and medical researcher made the strong (and so far unreported) claim that heart disease can be controlled, even cured, by a specific "mega-nutrient" therapy.
Heart patients using the Pauling Therapy routinely avoid angioplasty and open heart surgery. Not by lowering cholesterol, as the media would have us believe, but by attacking the root cause. Rapid recovery has been the rule, not the exception. Strangely, there are no known adverse side effects, yet the medical profession ignores Pauling and Rath.
You Must Unlearn What
You Have Learned
Atherosclerotic plaques deposit in response to injury. This major finding led to the 1985 Brown-Goldstein Nobel prize in medicine. The confusion in the media is cause and effect. The fallacy is that cholesterol causes heart disease, but plaque build-ups are the effect of heart disease.
G. C. Willis, MD, made the crucial observation in the early 1950s. A Canadian doctor, he noticed that atherosclerotic plaques in his patients kept forming in the same places. Usually near the heart where the blood vessels are stretched and bent.
Willis was the first to implicate high blood pressures and the mechanical stress caused by the heart beat.
The Pauling and Rath theory relies on this observation that plaque does not form randomly throughout the blood stream. (Note: In a heart bypass, veins from the leg are used which are without plaque.) Accordingly, it is unlikely that the primary cause of the lesions leading to heart disease are "poisons" circulating in the blood.
What causes the stress fractures in the walls of blood vessels that leads to heart disease?
The Pauling/Rath unified theory blames a lack of a specific protein caused by a specific vitamin deficiency. Visualize a garden hose being continually stepped on 70-80 times per minute. A fate similar to the coronary arteries feeding the heart. Like the garden hose, the arteries lose their strength and stability over time from wear and tear.
According to Pauling, the atherosclerotic plaques of coronary heart disease form only after cracks or stress fractures appear. This healing process begins with one very important "sticky" form of cholesterol.
What is Lp(a) and why is it important?
Lipoprotein(a) "small a" or Lp(a) is a variant of the so called "bad" LDL cholesterol. Lp(a) is "sticky" substance in the blood that Pauling and Rath believe is the lipid that begins the process of forming atherosclerotic plaques in heart disease. The 1985 Nobel prize in medicine was awarded for the discovery of the cholesterol binding sites. The so-called Lysine Binding Sites. We now know that it is Lp(a) and not ordinary cholesterol which binds to form plaque.
Briefly, Lp(a) has lysine (and proline) receptors. You can think of a chemical receptor as a simple lock and key. Only one key (e.g. lysine) will fit into the lock (receptor on the Lp(a) molecule.) There may be multiple receptors on the molecule, but once they are all filled up with keys (lysine or proline) the Lp(a) molecule looses its ability to bind with any more "keys."
When all the Lp(a) locks have keys, Lp(a) will no longer be able to create plaque.
Once Linus Pauling learned that Lp(a) has receptors for lysine, he knew how to counter the atherosclerosis process chemically.
His invention, the Pauling Therapy, is to increase the concentration of this essential and non-toxic amino acid (and proline) in the blood serum.
Lysine and proline supplements increase the concentration of free lysine and proline in the blood. The higher the concentration of the free lysine (and proline) in the blood, the more likely it is that Lp(a) molecules will bind with this lysine, rather than the lysine strands that have been exposed by cracks in blood vessels, or the other lysine that has been attracted to the Lp(a) already attached to the blood vessel wall.
According to Pauling, a high concentration of free lysine can destroy existing plaques.
It is important to keep all this in perspective using the Pauling/Rath Unified theory. If you are not getting enough vitamin C to produce collagen, and your blood vessels are wearing down, then the Lp(a) plaque is of great benefit to you. Simply removing plaque without restoring the vein or artery to health is like tearing a scab off a wound. You do not want to remove the scab until after the tissue underneath has started healing. Your body needs sufficient vitamin C so your veins and arteries can heal.
The Unified Theory blames mechanical stresses (high blood pressures, stretching and bending, etc.) on the blood vessels for exposing lysine that Lp(a) is attracted to. This explains why plaque doesn't always form. Atherosclerosis is a healing process. Like a scab, plaques form after a lesion or injury to the blood vessel wall.
There is an awesome elegance that these binding inhibitors (vitamin C/lysine) are completely non-toxic.
They are also the basic building blocks of collagen. The unified theory blames poor collagen production for the entire problem of heart disease. Therefore, the Pauling Therapy not only melts plaque, but it attacks the root cause by stimulating the bodies' production of collagen.
With enough collagen, arteries remain strong and plaque free.
The Pauling and Rath theory postulates that the root cause of atherosclerotic plaque deposits is a chronic vitamin C deficiency which limits the collagen our bodies can make.
A surprising body of experimental research supports the Pauling/Rath view. Careful studies with animals that do not make their own endogenous vitamin C prove that when the dietary intake of the vitamin is low, collagen production is limited, and blood vessels tend to become thinner and weaker from wear and tear. Plaque deposits then form to compensate for this weakness. Such animals are rare.
Large population studies also support the view that increased vitamin C intake results in lower incidence of cardiovascular disease and lower death rates.
Heart Disease is Chronic Scurvy
If you suffer plaque deposits, it is likely you owe your life to this material that narrows your arteries. Without plaques, your weakened blood vessels would rupture or leak causing a slow death from internal bleeding. A slower version of scurvy, the disease long dreaded by ancient sailors. (James Lind discovered around 1753 that eating fruit prevents this disease.
Acute scurvy can be prevented by a mere 10 mg vitamin C per day.
This process by itself rarely kills people, but plaque lined arteries make heart attack more likely from a blood clot or blockage. (Plaque lined arteries can not easily dilate in response to a clot.) It is currently unknown what amount of vitamin C prevents the atherosclerotic plaques of chronic scurvy, but Linus Pauling often recommended 3000 mg.
Many experts think something circulating in the blood must cause these cracks in our blood "pipes." For many years, ordinary LDL cholesterol has been blamed because elevated levels have been correlated with heart disease. Other scientists correlated elevated homocysteine and oxidized cholesterol.
Again, the confusion is cause and effect. If cholesterol causes cracks or lesions, plaque should be more randomly distributed throughout the blood stream. According to the Pauling/Rath unified theory, both elevated homocysteine and oxidized cholesterol are symptoms of scurvy.
Is the mainstream finally catching up with Pauling?
Before teaming with Pauling, Dr. Rath's German research team examined plaque from human aortas (blood vessels near the heart) post-mortem. They discovered that atherosclerotic plaques are composed primarily of Lp(a), not ordinary LDL cholesterol.
Mainstream medical science has known since 1989 that Lp(a) binds to form plaque, not ordinary LDL.
Dr. Rath, realized that Lp(a) was connected somehow with vitamin C and joined the Linus Pauling Institute of Science and Medicine. Together, Pauling and Rath developed their unified theory which holds that increased Lp(a) acts as a surrogate for low vitamin C and hardens weak blood vessels. Their experiments to test their theory proved that low vitamin C intake will increase blood levels of Lp(a) in test animals compared to controls.
An important finding is that this sticky Lp(a) (an LDL-like cholesterol substance) has only been found in the very few animal species that do not make their own vitamin C, including humans. Today, most animals:
- Make vitamin C in their livers or
kidneys, in large "mega" amounts (9,000 mg to 12,000 mg adjusted
for body weight - which is high by current medical standards),
- Do not have Lp(a) in their blood,
- Rarely suffer cardiovascular disease.
We humans are almost unique among life on Earth in that we must get our vitamin C entirely from the diet.
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 in human beings. The most popular competing theories as to why these lesions occur include:
- Oxidized cholesterol in the blood,
- Elevated levels and oxidized homocysteine
in the blood, and
- Vitamin deficiencies
(It is safe to say that few researchers believe that high levels of fat or cholesterol in the diet are the primary cause of heart disease. An exception may be researchers working for companies that offer high priced cholesterol lowering medications. ) In our view, all competing theories must be able to explain:
- Why occlusive cardiovascular disease
does not occur in animals, and
- Why infarction's in humans usually occur in the arteries at locations where the mechanical stress (blood pressure, arterial bending and stretching, etc.) is a factor, rather than more randomly distributed throughout the body.
These two observations are the cornerstones of the vitamin C theory.
Furthermore, the early findings of Canadian doctors Patterson and Willis should not be forgotten. Their research indicated that arterial tissue levels of ascorbate (vitamin C) are much lower in heart patients when compared with controls, and that ascorbate supplementation could reduce arterial deposits. This pioneering work should have been immediately followed up.
Elevated levels of Lp(a) are frequently overlooked by traditional medicine as a cause of heart disease. It is something that I screen for though on all our patients at high risk for heart disease.
Part of the reason why it is not looked for by traditional medicine is that they really do not have a good way to treat it. They have not discovered any drugs to lower Lp(a). The only thing that appears to work is the specific type of pharmacological nutrient manipulation discussed by Pauling.