The Cure for Heart Disease: Theory, History and Treatment
Letter to the Editor, Townsend Letter for Doctors and Patients
August/September 2004
Editor:
The theory that Cardiovascular Disease (CVD) is related to a deficiency of
ascorbic acid (vitamin C) was first proposed by the Canadian physician G. C.
Willis in 1953. Willis found that atherosclerotic plaques form over
vitamin-C-starved vascular tissues in both guinea pigs and human beings. In
1989, after the discoveries of the Lp(a) cholesterol molecule (circa 1964) and
its lysine binding sites (circa 1987), Linus Pauling and his associate Matthias
Rath formulated a unified theory of heart disease and invented the cure. Vitamin
C and lysine (and proline) in large amounts become Lp(a)binding inhibitors that
restore vascular health and destroy atherosclerotic plaques.
Theory
"Vitamin C is essential for the building of collagen, the most abundant protein
built into our bodies and the major component of connective tissue. This
connective tissue has structural and supportive functions which are
indispensable to heart tissues, to blood vessels, in fact, to all tissues.
Collagen is not only the most abundant protein in our bodies, it also occurs in
larger amounts than all other proteins put together. It cannot be built without
vitamin C. No heart or blood vessel or other organ could possibly perform its
functions without collagen. No heart or blood vessel can be maintained in
healthy condition without vitamin C."
- Roger J. Williams
Vitamin C is ascorbic acid, (but it is not really a vitamin). The over-whelming
majority of plants and
animals make large amounts of ascorbic acid. Mammals synthesize it in an amount
averaging 5,400 mg (when adjusted for body weight), and they make even more when
under stress. This is about 10-times the amount of CoQIO that is synthesized in
human beings, and roughly 100-times the US. Recommended Daily Allowance (RDA).
Homo Sapiens, like the guinea pig, fruit bat and the high-order primates, cannot
synthesize vitamin C because of a missing enzyme. These species must obtain the
vitamin in the diet or die of scurvy. A mere 10mg of vitamin C prevents acute
scurvy in humans resulting in the long-held hypothesis
that ascorbic acid is a vitamin, required only in minuscule amounts. Those few
species that fail to synthesize ascorbic acid all suffer similar 'heart
disease,' a form of the disease that is not prevalent in other species.
Also, heart disease is a misnomer; the underlying disease process reduces the
supply of blood to the heart and other organs leading to angina ("heart cramp"),
heart attack and stroke. The disease is characterized by scab-like build-ups
that grow on the walls of blood vessels. The correct terminology for this
disease process is chronic scurvy, a slower form of the classic vitamin C
deficiency disease.
The hypothesis that CVD is an ascorbic acid (vitamin C) deficiency disease was
first conceived and tested in the early 1950s. Willis devised a method of
photographing plaques with X-rays and observed a strange phenomenon in his heart
patients. Willis saw that atherosclerotic plaques were not uniformly distributed
throughout the vascular system; rather these "blockages" are concentrated near
the heart, where arteries are constantly bent or squeezed.
Another Canadian, Paterson, had found that the tissue of heart patients was
generally depleted of ascorbate
(vitamin C), and it was well known that vitamin C is required for strong and
healthy arteries. Willis reasoned that only the mechanical stress caused by the
pulse could explain the typical pattern of atherosclerosis that he so often
observed in patients. To Willis, the body was laying down plaque precisely where
it was needed in order to stabilize the vascular system.
By the late 1980s, medical researchers had made several intriguing discoveries.
First came the discovery that heart disease begins with a lesion, a crack or
"stress fracture," in the arterial wall. The question became, and remains, as to
the cause of these lesions in human beings since they do not arise in most other
animals. Then a variant of the so-called "bad" LDL cholesterol called
lipoprotein(a), or Lp(a) for short, was studied and found to be really bad. It
is sticky because of receptors on the surface of the molecule called lysine
binding sites. Work that led to the 1987 Nobel Prize in medicine discovered that
lysine (and proline) binding sites cause the formation of atherosclerotic
plaques. Then, Beisiegel et al. in Germany examined plaques post-mortem and
found only Lp(a), not ordinary LDL cholesterol.
Matthias Rath, a medical student and member of the German team, immediately
understood the importance of the Lp(a) cholesterol molecule (there are scores of
similar lipoprotein molecules) and made the connection with vitamin C. Lp(a) was
the genetic difference between individuals who suffer cardiovascular disease and
those who do not. Lp(a) had evolved only in species that do not make their own
vitamin C - e.g. humans and guinea pigs.
Rath brought Lp(a) to the attention of Linus Pauling and was asked to join
Pauling's Institute of Science and
Medicine. There Pauling and Rath repeated the earlier Willis experiments, but
this time they monitored Lp(a). They discovered that it becomes elevated in
guinea pigs deprived of vitamin C, but not in the controls. These experiments
connecting elevated-Lp(a) with low serum vitamin C and atherosclerosis, provide
the experimental support for their unified theory. They realized that in most
species, sufficient ascorbic acid will prevent stress fractures, but in those
species that suffer chronic scurvy, Lp(a) had evolved to patch cracked blood
vessels. .
Linus Pauling believed that chronic scurvy can be prevented with a daily intake
of between 3,000 to 10,000 mg or more vitamin C. This amount approximates what
the animals synthesize, and matching animal production is the reason Pauling
ingested 18,000 mg daily. Pauling's remedy for destroying existing
atherosclerotic plaques is the large amount of another essential nutrient, the
amino acid lysine. Pauling filmed a video lecture in which he recommended that
heart patients take between 2,000 and 6,000 mg of lysine daily with their
vitamin C (more if serum Lp(a) is elevated). Neither vitamin C nor lysine
have any known lethal dose.
History
In the early1950s the Canadian doctor Willis theorized that plaque build-ups are
the healing response to a repeated insult - the heart beat. Willis observed that
the build-up of atherosclerotic plaques was uniform, and not found throughout
the vascular system. It appeared only in the large arteries near the heart where
the blood pressure is greatest and where the artery is constantly stressed. He
used high-school physics to compute that plaques form precisely where the
mechanical forces were greatest on the arterial wall. Willis reasoned that these
plaques only form over stress fractures when the intake of vitamin C is low.
Was heart disease a mechanical problem exacerbated by a vitamin C deficiency?
Willis decided to find out.
His experiment with guinea pigs is described in his landmark 1957 paper "The
Reversibility of Atherosclerosis."
The animals were divided into several groups; all groups were fed an identical
diet except for the vitamin C.
At first, vitamin C was restricted in all groups. The control group was
sacrificed first and every guinea pig
group was found to have atherosclerosis. The remaining groups were then given
various amounts of vitamin C, having already induced atherosclerosis. Only half
of these pigs were found to have atherosclerosis providing strong evidence that
vitamin C can reverse existing disease. In the other experiments, groups of
guinea pigs that are given almost 10-times the RDA, or roughly 5000 mg of
vitamin C, adjusted for body weight, do not exhibit any sign of atherosclerosis.
Willis noted the similarity of the vitamin C deprived pig's atherosclerotic
lesions to the human lesions, and how unlike these lesions are to the "fatty
streaks" that can be created in experimental animals fed ultra-high
cholesterol diets. From this experiment we know that a single factor, low
vitamin C, can cause the atherosclerosis commonly found in humans.
Willis conducted experiments on his patients. He divided patients into two
groups. One group was given 500 mg of vitamin C, three times daily. Remarkable
for the 1950s, Willis was able to take pictures and "see" the inside of human
arteries for the first time. From these pictures, it was determined that 60% of
those taking vitamin C improved, that is, their plaques were reduced. In 30% the
plaques remained about the same and in 10% he saw their plaques increase
slightly. None of the control's plaques were reduced. These results were
promising, Willis, with this technique, was well ahead of his time. However, the
scientific and medical communities showed little interest in the Willis
experiments.
We now know that 1500 mg of vitamin C is not enough. The Lp(a) molecule and its
binding sites were unknown and the amino acid lysine was not employed. Also,
there was a theoretical problem: All animals have heartbeats, but they rarely
suffer the same type of CVD as humans. How could the beating heart only cause
the disease process in humans'? Willis did not have the answer as to why human
hearts and vascular systems were so different from most animals.
The Key to the Puzzle - Lp(a)
Forty years after the Willis experiments, and after it was discovered that only
one form of cholesterol Lp(a), creates plaques over the arterial lesions, the
American Nobel chemist Linus Pauling, and his associate Matthias Rath, MD,
formulated a new theory that unified vitamin C and Lp(a).
In their view, the strange Lp(a) molecule explained everything. Lp(a), the
friend who may become a foe, has evolved to replace vitamin C only in the very
few species that do not make their own vitamin C. The Lp(a) molecule is
important for human health, in the absence of vitamin C, providing many of the
same functions that the missing vitamin C would have provided.
Now the Willis "problem" had become a cornerstone of their theory: Lp(a) is an
evolutionary adaptation or surrogate for low vitamin C which most animals do not
require. Lp(a) provides an alternate way to strengthen and stabilize
vitamin-starved arteries in species that cannot make the vitamin. Inside the
wall of every blood vessel lies the collagen girder shaped into a triple helix.
Wrapped around the artery, like steel buried in a concrete highway, collagen
provides the artery with its strength and stability. Collagen is a living tissue
and needs to be replenished periodically. If vitamin C is present, collagen will
be strengthened before the artery fractures. When vitamin C is not present,
collagen continues to deteriorate and the arterial wall weakens. Surface
disruptions will emerge, especially where the pulse is great. Strands of lysine
and proline become exposed in these "pot-holes" along our most crowded vascular
highways. The floating Lp(a) comes to the rescue; it is attracted to lysyl or
prolyl strands in the pothole and binds with it, forming a patch, unless -
something happens that makes it unattractive.
Nullifying the Lysine Binding Sites - Reversing Heart Disease
As chronic scurvy progresses, the liver produces more Lp(a) molecules. As the
number of Lp(a) molecules increases, they tend to deposit on top of existing
plaque formations. When the healing process overshoots,
the arteries narrow and the flow of blood is reduced. This problem has a
solution. The Lp(a) molecule has a finite number of lysine binding sites -
points of attachment to lysine. Pauling's invention - the cure for heart disease
- is to increase the serum concentration of the amino acid lysine enough to make
the Lp(a) unattractive. As more lysine enters the bloodstream, the probability
increases that floating Lp(a) molecules will bind with it (rather than with the
patches of plaques growing on the arterial walls.)
After all the Lp(a) molecule's binding receptors are filled with the free lysine
floating in the blood, the Lp(a) molecule becomes as harmless as ordinary LDL
cholesterol.
Pauling and Rath called the substances that treat chronic scurvy and destroy
existing plaques Lp(a) binding inhibitors. Vitamin C, to increase collagen
production and to improve the health and strength of arteries, and lysine, to
prevent and to dissolve Lp(a) plaques, are the primary binding inhibitors. These
substances taken together are clinically effective. Pauling and Rath have been
awarded three US patents for Lp(a) binding inhibitors that destroy
atherosclerotic plaques in vitro and in vivo.
The Lp(a) binding inhibitors become the Pauling Therapy for heart disease only
at high dosages of 3 to 18 g ascorbic acid and 3 to 6 g lysine. In his video,
Pauling recounts the first cases where his high vitamin C and lysine therapy
quickly resolved advanced cardiovascular disease in humans. The effect is so
pronounced, and the inhibitors are so nontoxic, that Pauling doubted a clinical
study was even necessary.
More than 10-years of consistent testimony demonstrate that Pauling's
recommended dosages of the Lp(a)
binding inhibitors are almost always effective - reversing advanced heart
disease within 10-days after achieving the recommended dosage. Unlike the
cancer-cure, which may cause death through toxemia, heart patients only seem to
get better on the Pauling therapy.
Recently, the amino acid proline was found to be an even more effective Lp(a)
binding inhibitor than lysine in vitro. Adding between .5 and 2 g proline may be
of significant additional benefit.
When serum Lp(a) is elevated, Lp(a) binding inhibitors can profoundly interfere
with the disease process.
Binding inhibitor formulas that include proline have been documented to lower
Lp(a) in six to 14 months. In cases where Lp(a) is not reduced, binding
inhibitors become even more important regardless of their effect on serum Lp(a).
The Basic Recommendations for Controlling Heart Disease
Cardiologist have been kept in the dark about the vitamin C connection. Few
cardiovascular drugs benefit heart patients. Several exacerbate heart conditions
and should be eliminated in favor of the following othomolecular protocols:
1. Take Vitamin C as ascorbic acid or sodium ascorbate up to bowel tolerance (3
to 18 g) daily.
2. Take Lysine, 2 to 3g daily for prevention and from 3 to 6 g daily for the
greatest therapeutic benefit.
3. Take Proline from 250 mg to 2000 mg daily. (This added factor may lower
elevated Lp(a) within 6 to 14 months.)
4. Follow Pauling's general heart and cardiovascular recommendations provided in
his book How to Live Longer and Feel Better. Linus Pauling's Basic Vitamin
Program: Vitamin E – 800 to 3200 IU, Vitamin A - 20,000 to 40,000 IU. Super
B-Complex, esp. Vitamins B6 and B3
5. Supplement Coenzyme Q10 (100 - 300 mg) (High vitamin C and several vitamins
will help stimulate your own synthesis of CoQ10 which is vital for proper heart
function.)
6. Supplement the mineral Magnesium (300 to 1500 mg) and avoid Manganese (No
more than 2 mg. USDA researchers report that elevated manganese, more than 20 mg
daily, competes with magnesium uptake in the heart causing irregular heart
beats.)
7. Supplement the amino acids Taurine,Arginine and Carnitine (I to 3 g).
8. Avoid refined carbohydrates, especially sugars which crowd out the similar
vitamin C molecule in cells.
9. Avoid supplemental calcium.
10. Add a good mineral/ multivitamin - to cover all possible nutritional needs.
The following link to the Pauling Therapy and Video provides the scientific
rationale for the Linus Pauling vitamin C/lysine therapy on a I hour video:
http://www.pauling therapy.com/
Summary
The unified theory explains that heart disease, as do many natural healing
processes, begins only after a stress fracture appears on the wall of an artery.
The Lp(a) molecule is attracted to remnants of a broken collagen strand within
the fracture. The most probable cause for lesions forming in a pattern so
familiar to Willis is the mechanical stress caused by the beating heart. Dr.
Willis theorized that heart disease is ultimately a vitamin C deficiency. Most
animals do not have Lp(a) in their blood, Lp(a) acts as a surrogate for vitamin
C, extending life in the few species unable to synthesize ascorbate. Lp(a) binds
to "lysyl" residues and in this way forms plaque. The Lp(a) molecule itself was
discovered circa 1964 and was unknown to Willis. Lp(a) has a similar molecular
weight to LDL cholesterol and most studies grouped it with LDL prior to 1989.
Recently a reevaluation of these studies found that Lp(a) and not ordinary LDL
is highly predictive of CVD and that elevated Lp(a) increases the risk of heart
attack and stroke by 70%.
The on-going lack of scientific curiosity or interest by organized medicine in
the Pauling/Rath theory and Pauling's high-dose therapy, may well be remembered
as the greatest lapse of the 20th century.
Resources:
PaulingTherapy. corn
Hearttechnology.com
VitaminCfoundation.org
BolenReport.com
Other Articles By Owen
Owen Fonorow, Naturopath, PhD
Vitamin C Foundation
P.O. Box 3097
Lisle, Illinois 60532 USA
630-416-1438
www.VitaminCFoundation. org
References and Recent Scientific
Support for the Unified Theory
Harvard Nurses Study: The 15-year Harvard study of 85,000 nurses found that a
single vitamin C pill reduces the incidence of heart disease by almost 30%.
According to the numbers in [this story] a 360 mg vitamin C pill daily would
save more than 300,000 lives per year.
British/Enstrom CVD Mortality Findings:
In 1992 Dr. James E. Enstrom of the UCLA School of Public Health, published his
latest research on how men taking vitamin C, about 300 milligrams or more per
day, on average live six years longer than those who receive less than 50
milligrams of vitamin C daily. See this [article] on the Enstrom work. In late
2003, British researchers confirmed the finding that low vitamin C is related to
higher CVD mortality. (They found no relationship between either vitamin E or
vitamin A and mortality.) See this [article] for a review of
the British mortality findings, CVD Mortality Curves: It is not controversial
that total mortality from all forms of heart disease peaked between the years
1950 and 1970, and that deaths from coronary heart disease peaked around 1970.
It is interesting that in 1970, Nobelist Linus Pauling published his
best-selling book
Vitamin C and the Common Cold. See this [article] on the decline in the death
rate from heart disease since Pauling's first book was published.
Oxford meta analysis of 27 clinical studies: A meta-analysis of 27 large studies
(09/04/2000) at Oxford University found that people with high Lp(a) are 70% more
likely to have a heart attack or stroke than people with normal or low Lp(a).
See this [article] describing the paper published in the American Heart
Association Journal Circulation.
JAMA Jan 23/30 2002: Randomized, Double-Blind Controlled Trial in Humans Found
Statistically Significant 60-second Treadmill Exercise Improvements in 5000 mg
Vitamin C Groups
[Chelation Therapy for Ischemic Heart Disease: A Randomized Controlled Trial,
Knudson, et. al. JAMA, Jan 23/30, 2002 - Vol 287, No 4. Pp 481-486]
Vitamin C transforms stem cells into heart muscle: Stem cells, undifferentiated
cells that can become other cells, have become the subject of intense scientific
research. Patients given their own stem cells have avoided heart transplants,
according to recent news stories, and stroke patients have recovered more
quickly after being given stem-like cells. See this [article] on the Harvard
finding that only I of 880 substances tested vitamin C converted mouse stem
cells into heart muscle.
Genetically-engineered Mice: Mice, like most other mammals, produce their own
endogenous vitamin C, so experiments with these creatures usually have little to
say about chronic scurvy in humans. Scientists recently engineered a strain of
mice that are unable to synthesize ascorbate. See this [article] showing that
mice unable to synthesize vitamin C suffer human-like atherosclerosis.
1700+ studies show Lp(a) is a major CVD risk factor: There are few studies of
Lp(a) in the MEDLINE medical database prior to 1989, the year Pauling began his
lecture tour. Since 1989, the Lp(a) science has exploded, There are now more
than 1700 studies and articles that have investigated Lp(a). See this [link] for
some example abstracts, Cholesterol drugs do not lower Lp(a) and some raise it:
A little known fact is that the top-selling statin cholesterol drugs actually
cause Lp(a) to increase! See this [article] for more information on the dangers
in the popular statin drugs.
CoQ10 connection: There are several reports of the remission of congestive heart
failure in heart patients who have adopted Pauling's therapy. It is known that
CoQ10 is a good treatment for this condition, and it is known that vitamin C is
required for the body to synthesize CoQ10. See this [article] for more
information on the vitamin C and CoQ10 connection.
Dr Linus Pauling's Unified Theory of Cardiovascular Disease (good article)
Buy Video Lecture at PaulingTherapy.com
Purchase Lp(a) Binding Inhibitors at
Hearttechnology.com
Vitamin C Info at VitaminCfoundation.org
Monitor the War Between Health and
Medicine at BolenReport.com
The Cure for Cancer
Other Articles Rv Owen