Linus Pauling claimed that specific non-toxic substancescalled Lp(a) binding inhibitors taken orally will preventand may even dissolve existingatherosclerotic plaque build-ups.
This work is based on at least 2 Nobel Prizes in Medicineand the efforts of countless medical researchers. The theory and conclusionsoffered represent the final contribution of an American scientific giant.
The fact that you have not heard about this discoveryin the mainstream media is disturbing. It speaks volumes about how powerfulinterests can somehow suppress vital information that would be detrimentalto their financial interests.
In 1989, the eminent American scientist Linus Paulingand his associate Matthias Rath MD, unlocked a medical mystery.
They found the reasonhuman beings suffer heart disease.
Then in 1991, Linus Paulinginvented a non-prescription cure. The twice Nobel prize winninggenius, 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 routinelyavoid angioplasty and open heart surgery. Not by lowering cholesterol,as the media would have us believe, but by attacking the root cause. Rapidrecovery has been the rule, not the exception. Strangely, there are noknown adverse side effects, yet the medical profession ignores Paulingand Rath.
You Must Unlearn WhatYou 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 cholesterolcauses heart disease, but plaque build-ups are the effect of heart disease.
G. C. Willis, MD, made the crucial observation inthe early 1950s. A Canadian doctor, he noticed that atheroscleroticplaques in his patients kept forming in the same places. Usually nearthe heart where the blood vessels are stretched and bent.
Willis was the first to implicate high blood pressuresand the mechanical stress caused by the heart beat.
The Pauling and Rath theory relies on this observationthat plaque does not form randomly throughoutthe blood stream. (Note: In a heart bypass, veins from theleg are used which are without plaque.) Accordingly, it is unlikely thatthe primary cause of the lesions leading to heart disease are "poisons"circulating in the blood.
What causes the stressfractures in the walls of blood vessels that leads to heart disease?
The Pauling/Rath unified theory blames a lackof 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 gardenhose, the arteries lose their strength and stability over time from wearand tear.
According to Pauling, the atherosclerotic plaquesof 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 whyis it important?
Lipoprotein(a) "small a" or Lp(a) is a variantof the so called "bad" LDL cholesterol. Lp(a) is "sticky"substance in the blood that Pauling and Rath believe is the lipid thatbegins the process of forming atherosclerotic plaques in heart disease.The 1985 Nobel prize in medicine was awarded for the discovery of thecholesterol binding sites. The so-called Lysine Binding Sites. We nowknow that it is Lp(a) and not ordinary cholesterol which binds to formplaque.
Briefly, Lp(a) has lysine (and proline) receptors.You can think of a chemical receptor as a simple lock and key. Only onekey (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 allfilled up with keys (lysine or proline) the Lp(a) molecule looses itsability to bind with any more "keys."
When all the Lp(a) lockshave keys, Lp(a) will no longer be able to create plaque.
Once Linus Pauling learned that Lp(a) has receptorsfor lysine, he knew how to counter the atherosclerosis process chemically.
His invention, the Pauling Therapy, is to increasethe concentration of this essential and non-toxic amino acid (and proline)in the blood serum.
Lysine and proline supplements increase the concentrationof free lysine and proline in the blood. The higher the concentrationof the free lysine (and proline) in the blood, the more likely it is thatLp(a) molecules will bind with this lysine, rather than the lysine strandsthat have been exposed by cracks in blood vessels, or the other lysinethat has been attracted to the Lp(a) already attached to the blood vesselwall.
Accordingto Pauling, a high concentration of free lysine can destroy existing plaques.
It is important to keep all this in perspective usingthe Pauling/Rath Unified theory. If you are not getting enough vitaminC to produce collagen, and your blood vessels are wearing down, then theLp(a) plaque is of great benefit to you. Simply removing plaque withoutrestoring 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 hasstarted healing. Your body needs sufficient vitamin C so your veins andarteries can heal.
The Unified Theory blames mechanical stresses (highblood pressures, stretching and bending, etc.) on the blood vessels forexposing lysine that Lp(a) is attracted to. This explains why plaque doesn'talways form. Atherosclerosis is a healing process. Like a scab, plaquesform after a lesion or injury to the blood vessel wall.
There is an awesome elegancethat 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 problemof heart disease. Therefore, the Pauling Therapy not only melts plaque,but it attacks the root cause by stimulating the bodies' production ofcollagen.
Withenough collagen, arteries remain strong and plaque free.
The Pauling and Rath theory postulates that the rootcause of atherosclerotic plaque deposits is a chronic vitamin C deficiencywhich limits the collagen our bodiescan make.
A surprising body of experimental research supportsthe Pauling/Rath view. Careful studies with animals that do not make theirown endogenous vitamin C prove that when the dietary intake of the vitaminis low, collagen production is limited, and blood vessels tend to becomethinner and weaker from wear and tear. Plaque deposits then form to compensatefor this weakness. Such animals are rare.
Large population studies also support the view thatincreased vitamin C intake results in lower incidence of cardiovasculardisease and lower death rates.
Heart Disease is ChronicScurvy
If you suffer plaque deposits, it is likely you oweyour life to this material that narrows your arteries. Without plaques,your weakened blood vessels would rupture or leak causing a slow deathfrom internal bleeding. A slower version of scurvy, the disease long dreadedby ancient sailors. (James Lind discovered around 1753 that eating fruitprevents this disease.
Acutescurvy can be prevented by a mere 10 mg vitamin C per day.
This process by itself rarely kills people, but plaquelined arteries make heart attack more likely from a blood clot or blockage.(Plaque lined arteries can not easily dilate in response to a clot.) Itis currently unknown what amount of vitamin C prevents the atheroscleroticplaques of chronic scurvy, but Linus Pauling often recommended 3000 mg.
Many experts think something circulating in the bloodmust cause these cracks in our blood "pipes." For many years,ordinary LDL cholesterol has been blamed because elevated levels havebeen correlated with heart disease. Other scientists correlated elevatedhomocysteine and oxidized cholesterol.
Again, the confusion is cause and effect. If cholesterolcauses cracks or lesions, plaque should be more randomly distributed throughoutthe blood stream. According to the Pauling/Rath unified theory, both elevatedhomocysteine and oxidized cholesterol are symptoms of scurvy.
Is the mainstream finallycatching up with Pauling?
Before teaming with Pauling, Dr. Rath's German researchteam examined plaque from human aortas (blood vessels near the heart)post-mortem. They discovered that atherosclerotic plaques are composedprimarily of Lp(a), not ordinary LDL cholesterol.
Mainstream medical sciencehas known since 1989 that Lp(a) binds to form plaque, not ordinary LDL.
Dr. Rath, realized that Lp(a) was connected somehowwith vitamin C and joined the Linus Pauling Institute of Science and Medicine.Together, Pauling and Rath developed their unified theory which holdsthat increased Lp(a) acts as a surrogate for low vitamin C and hardensweak blood vessels. Their experiments to test their theory proved thatlow vitamin C intake will increase blood levels of Lp(a) in test animalscompared to controls.
An important finding is that this sticky Lp(a) (anLDL-like cholesterol substance) has only been found in the very few animalspecies 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, and
- 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 heartdisease. It is something that I screen for though on all our patientsat high risk for heart disease.
Part of the reason why itis not looked for by traditional medicine is that they really do not havea 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 pharmacologicalnutrient manipulation discussed by Pauling.