The Cure for Heart Disease Has Been Known For Many Years
- From: "PeterB" <pkm@xxxxxxxxxxxxxxx>
- Date: 3 Mar 2006 12:44:23 -0800
Townsend Letter for Doctors and Patients > August-Sept, 2004 > Article
The cure for heart disease: theory, history and treatment
Linus Pauling
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
overwhelming 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 CoQ10 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 10 mg 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 early 1950s 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.
cause the atherosclerosis commonly found in humans.From this experiment we know that a single factor, low vitamin C, can
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 heart
beats, 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 3 g 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 (1 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 1 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.com
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, Knudtson, 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 1
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 athersclerosis.
[ILLUSTRATION OMITTED]
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 By Owen
COPYRIGHT 2004 The Townsend Letter Group
COPYRIGHT 2004 Gale Group
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