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
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
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
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
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
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
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
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
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.
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,
- 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.