| The
Long Neglected Theory Of
Cardiovascular And Heart Disease
By: Owen Richard Fonorrow
"Vitamin
C has been under investigation, reported in thousands of scientific
papers, ever since it was discovered (circa) fifty years ago. Even
though some physicians had observed forty or fifty years ago that
amounts a hundred to a thousand times larger (than the RDA) have
value in controlling various diseases, the medical profession and
most scientists ignored this evidence.
" Linus Pauling HOW TO LIVE LONGER AND FEEL BETTER, 1986, pg
106 paperback.
We often hear of theories in the Media that attempt to explain what
causes cardiovascular disease (CVD) leading to heart attack and
stroke. There is a cholesterol theory, a fat (saturated and polyunsaturated)
theory, the long neglected Dr. Kilmer McCully homocysteine theory,
an oxidized cholesterol theory, a free-radical/heavy metal theory,
and even a microbe theory. Each of these theories attempts to explain
what causes the lesion in the artery that is the precursor to CVD.
At least one major theory is never mentioned in the medical journals
or lay media: The vitamin C Theory. Linus Pauling and Matthias
Rath, MD, jointly identified the great problem of cardiovascular
disease as a vitamin C deficiency disease; chronic rather than acute.
This idea has yet to be seriously investigated by modern medicine.
Cardiologists routinely tell their patients that there is no "proven"
value in taking vitamin C for heart disease. Technically, this statement
may be accurate, but it is misleading. The implication is that experiments
have been run that prove vitamin C has no value. No such experiments
have ever been run. On the contrary, all research and experiments
we know of provide evidence that vitamin C does, in fact, have great
value . It is incredible that after more than a decade since Pauling
and Rath first published their Unified Theory, modern medicine and
its schools, the pharmaceutical companies and the United States
government have failed to make the slightest effort to investigate
the effects of large amounts of vitamin C and the amino acid lysine
in relation to CVD and heart disease. This is even more surprising
when one considers that there are no proven treatments for heart
disease. According to Dr. Julian Whitaker, heart by-pass operations
and angioplasty were never clinically "proven" before
being adopted by the medical profession.
The neglected vitamin C theory, proposed by Nobel Laureate Linus
Pauling and his associate Matthias Rath, MD, is a unifying theory
that encompasses homocysteine, lipid imbalances including Lp(a)
excesses, infections and stresses, diet, free-radicals, lesions,
lack of CVD in most animals, and raises the important issue of mechanical
stresses in the blood stream. The arguments are straight-forwarded
and most people can understand them. If more cardiovascular patients
could learn about the Vitamin C Theory much suffering would end.
Pauling's recommended high-dosage treatment is having spectacular
success among the lay public who have discovered it.
Jeff Fenlason - The Two Day "Miracle"
Recovery
Jeff Fenlason, 52, of North Carolina is but one of
thousands of people who have experienced the Pauling Therapy miracle.
His case provides clear and convincing evidence in favor of the
Vitamin C Theory. Jeff has allowed his real name to be used and
his entire testimony is posted at
http://www.paulingtherapy.com/. Fenlason is somewhat unique
in that he did not have Chelation or any other alternative therapy
before adopting the high-dosage Pauling therapy. His "two day"
reversal was after ten years under the care of modern cardiology.
Alternative doctors, who routinely offer their patients nutritional
support, are not likely to witness a Fenlason-style miracle. But
we have witnessed this "
miracle" almost every time a patient under the care of a modern
cardiologist begins the therapy, probably because these people are
routinely told there is no value in taking extra vitamin C. A rapid
"cure" requires 5-6 g of the amino acid l-lysine with
at least the same amount of vitamin C daily. (Note: Fenlason reports
that he immediately adopted a 14 g daily amount of vitamin C, along
with 5-6 g lysine.) The wisdom of Linus Pauling bear repeating:
"Although physicians, as part of their training, are taught
that the dosage of a drug that is prescribed for the patient must
be very carefully determined and controlled, they seem to have difficulty
in remembering that the same principle applies to the vitamins."
HOW TO LIVE LONGER AND FEEL BETTER, pg 142 paperback.
What are the Facts?
So how do scientists or the lay public choose among
competing theories? The first step is to analyze the mass of data
and try to identify facts. For the purposes of this discussion,
we focus on cardiovascular disease, and not necessarily myocardial
infarction - heart attack. The Pauling/Rath Vitamin C Theory is
for occlusive cardiovascular disease. The How and Why plaque forms.
(Of course arteries lined with plaque are not able to dilate in
response to a clot, like healthy arteries can, making heart attack
more likely.)
Lets begin by reviewing what we think we know about cardiovascular
disease:
1. CVD leading to Heart Attack is the leading cause of mortality
in the USA (Source: American Heart Association http://www.amhrt.org/catalog/Scientific_catpage70.html)
2. In the USA, the mortality rate from CVD increased from a very
low rate at the beginning of the 20th century to its peak in the
1960s/1970s. (Source: MMWR, February 16, 2001 / 50(06);90-3, Mortality
From Coronary Heart Disease and Acute Myocardial Infarction ---
United States, 1998 http://cisat.isciii.es/mmwr/preview/mmwrhtml/mm5006a2.htm
3. The CVD mortality rate has declined 40% from its peak (circa
1970) in the USA. (Source: From Pauling's 1986 Book HOW TO LIVE
LONGER AND FEEL BETTER, the number of heart related death in 1970
was around 740,000. The American Heart Association places the number
of deaths in the year 2000 between 400,000 and 500,000. Note: the
larger population in 2000.)
4. After Pauling's first book on Vitamin C was published in 1970,
vitamin C consumption increased 300% in the USA, and the USA has
been the only industrialized country to experience the 40% reduction
in heart disease mortality. (Source: Linus Pauling Institute of
Science and Medicine.)
5. Most high order mammals a) make their own vitamin C in high amounts
(3-11 g daily) in their livers (or kidneys) and b) do not suffer
the same type of cardiovascular disease as humans. (Guinea pigs
do not make vitamin C and do suffer the same CVD if vitamin C is
restricted in their diet.) (Various sources including Linus Pauling
HOW TO LIVE LONGER AND FEEL BETTER 1986 and the Pauling/Rath Unified
Theory)
6. The Enstrom analysis (1992) of NIH data showed that vitamin C
supplements of only 500 mg increased longevity in men by 40% (or
almost 6 years) and a somewhat lesser improvement in woman. (Source:
Enstrom, Epidemiology 1992, The Harvard/Rimm study obviously designed
to "debunk" Enstrom only evaluated some 667 who developed
CVD and ignored the dietary intakes of nearly 40,000 thousand who
did not get CVD.)
7. Homocysteine levels rise when vitamin C levels are low. Dr. McCully
is cited in the Pauling/Rath Unified Theory paper because of his
experiment that showed homocysteine levels rise in scorbutic guinea
pigs and not controls. (Source: McCully KS, Homocysteine metabolism
in scurvy, growth and arteriosclerosis. Nature 1971;231:391-392
from Pauling/Rath Unified Theory. See http://www.orthomed.org/
8. Repeatable experiments with guinea pigs show that depriving the
animal of vitamin C causes atherosclerosis which is quite similar
to the human lesion. No plaque forms in the control group getting
"adequate" vitamin C. (Source: The Reversibility of Atherosclerosis,
G. C. Willis, Canad M. A. J, July 15, 1957, Vol 77)
9. Pauling and Rath showed the apo(a)/Lp(a) increased in the animals
deprived of vitamin C, but not in the controls. (Source: Immunological
evidence for the accumulation of Lp(a) in the atherosclerotic lesion
of the hypoascorbemic guinea pig, Pauling/Rath, Pro. Nat. Acad.
Sci USA, Vol 87, pp 9388-9390, Dec 1990, Biochem)
10. The heart disease process begins with a lesion in the artery.
(Source: Brown-Goldstein Scientific American 1982, and Linus Pauling
Heart Disease Video)
11. Veins, in general, do not suffer plaque deposits. (Source: Common
knowledge from the medical Literature)
12. Plaques are often localized to areas around the heart (coronary
arteries or carotid arteries). (Source: An Experimental Study of
the Intimal Ground Substance in Atherosclerosis, G. C. Willis, Canad
M. A. J., July 1953, Vol 69, pg 17)
13. Vitamin C is required (and used up) making collagen - the most
abundant protein in the human body. (Source: Roger J. Williams,
Nutrition Against Disease, 1971, Linus Pauling HOW TO LIVE LONGER
AND FEEL BETTER, 1986)
14. Scurvy is caused by a deficiency in making collagen which is
in turn caused by a lack of vitamin C. (Source: James Lind, 1753,
Linus Pauling HOW TO LIVE LONGER AND FEEL BETTER 1986)
15. The Beisiegel studies in Germany of post-mortem human aortas
in 1989 determined that plaque consists of Lp(a) and only Lp(a)
- no ordinary LDL. (Source: Morphological detection and quantification
of lipoprotein(a) deposition in atheromatous lesions of human aorta
and coronary arteries in Virchows Arch A Pathol Anat Histopathol
1990;417(2):105-11, Niendorf A; Dietel M; Beisiegel U; Arps H; Peters
S , Wolf K; Rath M and Lipoprotein(a) in the arterial wall. Beisiegel
U; Rath M; Reblin T; Wolf K; Niendorf A, Eur Heart J 1990 Aug;11
Suppl E:174-83)
16. Elevated cholesterol has been correlated with CVD, but many
studies were conducted before Lp(a) was known, Lp(a) was lumped
in with LDL. In September, 2000, an Oxford meta-analysis of 27 large
studies showed that people with elevated Lp(a) are 70% more like
to suffer a heart attack or stroke. (Source: Circulation Sep 2000)
17. According to the Life Extension Foundation, 50% of all individuals
50 years or younger who die from heart disease, succumb without
any established risk factors. (Source: Life Extension Foundation
Treatment Protocols, Fibrinogen and Cardiovascular Disease, See:
www.lef.org/protocols/prtcls-txt/t-prtc149a.html)
18. Elevated Homocysteine is considered a leading risk factor for
(has been correlated with) Heart Disease. (Source: Life Extension
Foundation Treatment Protocols, Fibrinogen and Cardiovascular Disease,
See: www.lef.org/protocols/prtcls-txt/t-prtc149a.html)
19. Primate experiments indicate that a vitamin B6 deficiency in
these animals causes atherosclerosis (Source: Roger J. Williams,
Nutrition Against Disease, 1971.)
We are not aware of any contradictions to the above list and we
welcome suggestions for additional assertions of fact for purposes
of debate. There are also common observations that may be relevant.
The cardiovascular disease process seems to be accelerated in older
people, in people who consume polyunsaturated fats without adequate
vitamin E, and in people who undergo common heart by-pass surgery
or angioplasty. Popular writers (e.g. Adell Davis) in the 1950s,
1960s and 1970s and forward have helped disseminate the scientific
knowledge of the health value of supplemental nutrition, especially
vitamin C. As the knowledge became more widespread, the CVD mortality
rate stopped increasing and began to decrease. Young people are
known to have CVD and people in their 30s die from Myocardial Infarction
(heart attack.) Older people do suffer peripheral arterial disease,
but CVD is generally localized to the coronary and carotid arteries
near the heart. A frank copper deficiency has been implicated in
atherosclerosis. The author is not aware of any individual who regularly
and consistently consumes more that 10,000 mg of vitamin C daily
who suffers any form of cardiovascular disease.
Which Theory Best Fits the Facts?
The two crucial observations or facts that may help
sort out among the several theories are a) that animals do not generally
suffer the same type of CVD as humans and b) plaques formations
are uniform (not random) and usually in arteries near the heart.
The first observation, that animals do not generally suffer CVD,
indicates that there is a difference in the genetic makeup between
humans and most other animals. We fail to see how any popular theory,
save perhaps diet, can explain this phenomenon. One of the largest
differences between most animals and humans is that we humans are
virtually alone (with the guinea pig) in that we do not make any
vitamin C in our bodies. Other mammals make 3000 to 11000 mg of
vitamin C in their livers (adjusted for body weight) which goes
directly into the blood stream. Humans can not make a single molecule
of vitamin C.
The second observation, that plaque deposits are uniform close to
the heart, tends to rule out poisons circulating in the blood (e.g.
oxidized cholesterol, fats or homocysteine) as being the primary
cause of CVD (although these substances probably aggravate or accelerate
the disease). The cholesterol, homocysteine, oxidized cholesterol,
microbe, fat, and even heavy metal/free radical theorists have yet
to explain why plaque deposits are not randomly distributed throughout
the blood stream. We must ask why infarctions do not occur in the
ears, nose and fingers if something in the blood, i.e. fat or homosysteine,
causes the lesions leading to CVD. The Vitamin C Theory explains
these observations as the effects of mechanical stress on arteries
without sufficient collagen to remain strong and resilient. Lesions
or cracks develop that attract Lp(a).
The vitamin C/collagen Theory of atherosclerosis explains the vitamin
B6 connection (also required to produce collagen) and copper (also
required to produce collagen). Usually the deficiency of vitamin
C is the primary factor. For example, vitamin B6 and copper are
not usually implicated in scurvy. Vitamin C's antioxidant properties
and ability to support the immune system are well known, which may
also explain away the oxidized cholesterol findings as well as the
microbe theory. Irwin Stone has suggested that vitamin C is really
not a vitamin, and is better classified as the Missing Stress Hormone
in humans. Finally, McCully has shown the homocysteine levels are
elevated in the scorbutic guinea pig, perhaps even initiating atherosclerosis
in the absence of vitamin C.
Conclusion
The common theories for heart disease fail when faced
with two simple observations: Plaques do not generally form in
animals that make their own vitamin C and plaques do not form randomly
in humans throughout the blood stream. These two observations
are the cornerstone of the Pauling/Rath unified Vitamin C theory.
The vitamin C theory, which holds the Lp(a), an LDL variant, acts
as a surrogate for vitamin C, also fits all other known facts and
most observations. It makes sense. It is almost too simple. It is
hard to believe that medical science could have overlooked it, but
this is precisely the reason Pauling himself gave for writing his
first book on Vitamin C: Pauling wrote his book to counter the medical
profession's bias against the vitamins, especially ascorbic acid.
(Source: Linus Pauling in his Own Words, Edited by Barbara Marinachi)
Others may offer additional facts and observations, but we have
become convinced that the Pauling/Rath theory is essentially correct,
and that the Pauling high vitamin C/lysine therapy is the cure for
CVD. We back up this belief with a challenge to ANY competing therapy
in a clinical setting - wager negotiable. (See http://www.internetwks.com/pauling/short.html
for terms and conditions.) Winner takes all. Antagonist group therapy
can not include supplemental vitamin C above 200 mg or any supplemental
lysine/proline. So far, no takers. We directly challenged the Life
Extension Foundation, and their Folic acid, Vitamins B6 and B12
homocysteine therapy. William Faloon declined citing the CVD patient's
need for vitamin C.
We do not understand why humans evolved so differently from most
animals. How did we survive as a species without the ability to
manufacture our own vitamin C? One is reminded of the fictional
"Lysine Contigency" in Jurasic Park. (Perhaps those who
made us in their image decided to incorporate a similar built-in
control mechanism for humankind?) Theological questions aside, there
is little doubt this great deficiency in our genetic makeup, the
lost ability to produce the enzyme L-gulonolactone oxidase in our
livers, an enzyme that would otherwise allow us to convert ordinary
glucose (sugar) into ascorbic acid, is what ultimately causes CVD.
Owen R. Fonorow
The Vitamin C Foundation
http://www.vitamincfoundation.org/
http://www.paulingtherapy.com/
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