Linus Pauling's Unified Theory and Therapy
for Heart Disease
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
In 1989, the eminent American scientist Linus Pauling
and his associate Matthias Rath MD, unlocked a medical
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
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
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
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
With enough collagen, arteries remain strong and plaque
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 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
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
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
- 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
- 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.