The Unified Theory
"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 in the Media of theories 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, 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 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.
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:
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)
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.
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)
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.)
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.)
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.)
including Linus Pauling HOW TO LIVE LONGER AND FEEL BETTER 1986 and the
Pauling/Rath Unified Theory)
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,
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.)
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
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.
Reversibility of Atherosclerosis, G. C. Willis, Canad M. A. J, July 15, 1957,
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)
The heart disease process begins with a lesion in the artery.
Brown-Goldstein Scientific American 1982, and Linus Pauling Heart Disease
Veins, in general, do not suffer plaque deposits.
(Source: Common knowledge
from the medical Literature)
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,
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)
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)
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
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.
Circulation Sep 2000)
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)
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:
Primate experiments indicate that a vitamin B6 deficiency in these animals
causes atherosclerosis (Source: Roger J. Williams, Nutrition Against Disease,
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.
The two crucial observations or facts that may help out sort out among the several theories are that a) 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.
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 that 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: 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 our 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.
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.
The author 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
 The exception is that Harvard Rimm epidemiological studies that were flawed and only evaluated 667 with CVD, not the 39,243 as claimed