Vitamin C, Collagen, and the Pauling Therapy for Heart Disease

by Owen R. Fonorow © Copyright 2000 Revision 1.1 March 20, 2000


The medical profession ignores an extraordinary medical claim that Linus Pauling made almost 10 years ago. This knowledge has been available in research papers and Linus Pauling made a video on the subject. Nature abhors a vacuum and since then, via the internet, almost by default, we have provided people limited advice on the Pauling discoveries that led to the Therapy that he and his associate Matthias Rath, M.D. invented.

Medicine has known since the 1970s that atherosclerotic plaque forms in response to blood vessel injury. Lipoprotein(a) binds to lysine and proline residues in the collagen matrix that are exposed from injury. We now know, if arteries are strong and healthy, then regardless of serum cholesterol levels, there are few lysine binding sites and plaques won't form. The confusion in the media is cause and effect. The fallacy is that cholesterol is the cause of heart disease, but plaque build-ups are the effect of heart disease.

According to the Pauling and Rath unified theory, the root cause of heart disease is a vitamin C deficiency that limits the production of collagen. The Pauling therapy for this condition is to ingest orally large doses of two substances: vitamin C and lysine. The recent USC study that created such a firestorm actually provides important supporting evidence for the Pauling/Rath unified theory. The USC finding is convincing, almost beyond a reasonable doubt, that the elderly can not get the vitamin C they need without supplementing their diet.

The Pauling therapy is so safe, and the medical condition so grave, that there is no logical reason why any physician should resist it, especially in otherwise hopeless cases. Our experience shows that heart patients do benefit from large daily doses of vitamin C and lysine. Hundreds, if not thousands of people have already been helped. And there is new evidence that adding the amino acid proline can increase the benefit. Some of these cases are documented, yet little has been scientifically proven, for reasons that escape me. I am not a doctor. And of course, as is always true in science, Linus Pauling may have been wrong. (Pauling wasn’t often wrong. He used the words "cure" in his last published interview and "miraculous" on the video.)


This is a story of a remedy that has so far been ignored by the medical profession. Dubbed the Pauling therapy (at the high doses Linus Pauling alone recommended), the two primary substances that comprise the therapy; vitamin C and lysine, are not drugs. They are essential foods, extremely safe, and they happen to inhibit the binding of lipoprotein(a), (or Lp(a) for short) to the walls of damaged blood vessels. These perfectly non-toxic substances become the Pauling therapy when taken daily in large therapeutic amounts.

Lp(a) is a sticky cholesterol-like substance similar to LDL that is only found in humans and other beings that do not make their own vitamin C. Pauling and Rath have identified Lp(a) as one of the most important blood factors in heart disease, second to low levels of vitamin C.

In theory, human cardiovascular disease (variously called CVD, atherosclerosis, plaque, narrowing, arteriosclerosis, etc.) is a natural healing process. This process by itself rarely kills people, but plaque lined arteries do make it more likely that people will suffer heart attack from a blood clot or blockage.

Vitamin C keeps vessels strong. Accordingly, strong blood vessels are less prone to injury from mechanical stresses and do not suffer plaque deposits. When the dietary intake of vitamin C is low, collagen production is limited, and arteries become thinner and weaker from wear and tear. Low vitamin C leads to increased levels of Lp(a) in the blood and plaques form that compensate by patching and strengthening the blood vessels. Dr. Rath’s apt analogy for arterial plaque is nature’s "plaster cast."

Pauling believed, and his belief is supported by a United States patent, that large megadoses of vitamin C and lysine taken orally can prevent and even dissolve existing atherosclerotic plaque build-ups. We have monitored the progress of the many people who have contacted our web site and routinely tell people seeking advice to view the Linus Pauling video on heart disease. Many of these people have then reported to us their personal experiences with the Pauling therapy. These reports are universally positive and match the three case studies on the Pauling heart disease video. We have received no complaints, and so far, no deaths have been reported.

Based upon these "miraculous" anecdotal reports, on our understanding of the Pauling/Rath unified theory, and on the Lp(a) medical literature that we have reviewed via MEDLINE, we are now convinced that vitamin C and lysine work. Naturally, no self-respecting medical doctor would take my word for it. But why haven’t the necessary studies been run years ago?

Report after report provides more evidence that the Pauling therapy works in most people in as little as 14 to 30 days (depending on the daily dosage) especially when augmented by proline and antioxidant vitamins. Some have reported that the vitamin C/lysine therapy didn't change their condition, or else required much longer, sometimes over 10 months. But most people (>90%) report relief in weeks rather than months. Not every person who visits the web site and who presumably tries the Pauling therapy communicates with us. To this date more than 100,000 unique visitors have visited the web site since it was first posted in 1995.

Lp(a) levels in the blood provide additional objective evidence. People have shared their lab reports with us that document drops in serum Lp(a) between 70% to 90% down to the accepted safe range (Less than 14 mg/dl). Such drops have been reported in as little as 30 days on the Tower Laboratories Heart Technology product. We have been concerned by the lack of clinical studies, but there is now at least one independent lab thoroughly investigating the effect of the Pauling therapy (e.g., Heart Technology) on serum Lp(a).


Recently, a widely publicized media report associated vitamin C pills and clogged arteries. Surprised by the media coverage, I contacted James Dwyer of the USC Medical School, one of the principal researchers mentioned in the 03/03/2000 news reports. As suspected, this research seems to be good news for elderly vitamin C takers whose carotid arteries have ‘thinned’ with age. Dr. Dwyer informed me that his team only looked at carotid arterial thickness. There is no evidence of occlusion or clogging. The findings show vitamin C supplements induced significant physiological changes, especially for smokers.

The arterial growth was unexpected and alarmed the researchers, whose paper is in peer-review and has not yet been accepted for publication. Thickening has been tied to heart attack, but there is a difference between arteries growing thicker with and without plaque. Plaque lined arteries are less responsive to Nitric Oxide (NO) signals and can’t dilate, leading to a cardiac event. But arteries with sufficient vitamin C can grow "thicker" without plaque, and this collagen-induced thickening is exactly what you want to avoid heart disease. The USC finding is so pronounced that it can only mean one thing: All elderly people should be taking vitamin C pills.

Robert Cathcart III, MD of Palos Altos California learned about the value of vitamin C from Linus Pauling. His medical practice uses high doses and says: "My experience with 25,000 patients since 1969 indicates that this media report is ridiculous. I know that follow-up is not perfect in private practice but I have had no patient who had a good heart when I first saw them and who took massive doses of vitamin C who ever developed heart problems. I have to add that I advise all my patients to avoid sugar, chemicals, and highly processed foods, and put them on a number of other nutrients.

"If it turns out that there is thickening of the carotid, I think it is reversing the thinning that occurs with aging. It is interesting that the effect is so dramatic in the reversing of the effect on smokers. I have to congratulate you at the Vitamin C Foundation on unveiling the other two findings that could have been measured which were not reported . Probably the finding that C helped would not be publishable."


Since we are invoking the name of one of the world’s greatest scientist, it is fair to ask what experimental evidence supports the unified vitamin C theory? Animals, other than guinea pigs (and a few others) manufacture their own vitamin C in the amount adjusted for body weight of several thousand milligrams every day. And according to veterinary texts, animals don’t generally suffer cardiovascular disease. Guinea pigs on the other hand, like humans and other high-order primates, can not manufacture a single molecule of vitamin C in their bodies. If vitamin C deficiency causes heart disease, then experiments with guinea pigs would prove it.

There have been careful experiments with guinea pigs, first attempted by the Canadian medical doctor Willis in the mid 1950s. The result is always the same. When guinea pigs are deprived of vitamin C they die a terrible scurvy death in a matter of weeks. When their vitamin C is limited to the U. S. RDA they live, but develop atherosclerosis. When they are fed the human equivalent of 3 to 5 gm of vitamin C, they thrive with no signs of atherosclerosis. Disease in guinea pigs occurs in weeks, the human form of the disease usually takes decades to develop. While some differences are to be expected in animal experiments, the lesions produced by these experiments in guinea pigs are remarkable for their similarity to the human lesion. Pauling waited until his own experiments were run with guinea pigs at his institute before he made his announcement that heart disease can be "completely controlled" even "cured." Pauling’s results repeated the Willis work, and also showed that Lp(a) rises when vitamin C is limited.

The Pauling/Rath vitamin C theory makes perfect sense, at least to me, I have not been through medical school.


A Nobel prize was awarded for the discovery that damage to the walls of blood vessels are a necessary precondition for the formation of atherosclerotic plaques in human beings. The three most popular competing theories why these lesions occur include:

  1. Oxidized cholesterol in the blood,
  2. Elevated levels and oxidized homocysteine in the blood, and
  3. Vitamin deficiencies.
Note: Elevated LDL (Bad) cholesterol is conspicuous by its absence.

In Pauling and Dr. Rath’s view, any competing theory must account for:

  1. the reason occlusive cardiovascular disease does not generally occur in animals that make their own vitamin C, and
  2. the reason infarction's in humans are not distributed randomly. They usually occur where plaque forms in the arteries where mechanical stress (e.g., blood pressure, arterial bending and stretching, etc.) is a factor.

These two observations are the cornerstones of the unified vitamin C theory. The theory explains the arterial lesions as the effect of weakness in the arterial wall, not from a "poison" circulating in the blood that should affect all blood vessels equally. Thanks to Linus Pauling’s recognition that Lp(a) is acting as a surrogate for low levels of ascorbate, we human beings no longer have to fear heart disease or suffer the chest pain of Angina Pectoris or fear premature death or heart attack caused by progressive cardiovascular disease (CVD). The genius of Pauling was to recognized that blood vessels are made stronger by vitamin C, but when vitamin C is deficient, that they can also be made stronger by Lp(a) plaques. Either way they stay thick, or if they become thin, thicken. And Pauling, the master chemist, has given ordinary people a much safer way to control heart disease than to risk heart by-pass surgery or angioplasty. We don’t even have to run to a doctor for a prescription.

The Pauling invention is to increase both vitamin C and the amino acid lysine. Both substances are safe and are known to improve health well beyond what we normally consume in our diets. These substances attack the root cause of the problem, the lack of proper collagen formation, and they also work to inhibit the binding of Lp(a) to the arterial wall.


A common criticism of Linus Pauling and his recommended vitamin C intake of 3000 mg is based on the faulty assumption that optimal intake is reached when body tissues "saturate" with vitamin C, or when the blood serum reaches the maximum ascorbate (vitamin C) concentration. This focus on saturation misses the point: Vitamin C (ascorbic acid) is transformed or destroyed as the body uses it for a wide variety of metabolic functions. For example, vitamin C is destroyed during collagen production. Ascorbate tissue saturation is just the starting point for many metabolic pathways that are not otherwise activated. Dr. Robert Cathcart's vitamin C bowel tolerance is a better measure of each individual's optimal intake.

It is hard to maintain the fiction that humans require no more than 60 milligrams of vitamin C in the face of what is known about collagen . Collagen is the most abundant protein in animals. Cellulose in plants, collagen in animals, provide the organism with structural integrity. But plants do not require vitamin C to make cellulose. Thus, it is unlikely that plants will have sufficient vitamin C supply to satisfy the needs of the animals eating them. Today’s authoritative pre-med biochemistry textbooks ignore the role of vitamin C in the human body. Completely. Medical students are not taught and don’t know that vitamin C is needed and used up producing collagen. It is little wonder orthodox doctors are ignorant and can not believe a vitamin C deficiency is the cause of heart disease. (The USC scientists are not happy about this lack of information in their text books.)

What is hard to understand is why alternative medical practitioners, who presumably read Pauling, make the same mistake? The following literature presents the concepts that cement the foundation of the unified vitamin C theory. It has been taken verbatim from the books by the nutrition masters Linus Pauling and Dr. Roger J. Williams.

Vitamin C and Collagen: A Tutorial

"We have come upon reasons why we require for good health so much larger amounts of vitamin C than are present in the plants we use as food. It has recently been shown that one molecule of vitamin C is destroyed for each H atom replaced by OH... In the critical reactions that assemble collagen in the tissues, Vitamin C does not serve merely as a catalyst but is destroyed." Linus Pauling


The synthesis of collagen, for which vitamin C is essential, proceeds in the body as one of its major manufacturing enterprises. A person who is dying of scurvy stops making this substance, and his body falls apart – his joints fail, because he can no longer keep the cartilage and tendons strong, his blood vessels break open, his gums ulcerate and his teeth fall out, his immune system deteriorates, and he dies.

Collagen is a protein, one of the thousands of different kinds of proteins in the human body. Most proteins occur in only small amounts: the various enzymes, for example, are so powerful in their ability to cause specific chemical reactions to take place rapidly that only a gram or two or even a few milligrams may be needed in the body. There are a few exceptions. There is a great amount of hemoglobin in red blood cells. There is even more collagen in the skin, bones, teeth, blood vessels, eye, heart, and, in fact, essentially all parts of the body. Collagen as strong white fibers, stronger than steel wire of the same weight, and as yellow elastic networks (called elastin), usually together with macropolysaccharides, constitutes the connective tissue that holds our bodies together.

Like other proteins, collagen consists of polypeptide chains; the long chains of this fibrous molecule contain about one thousand amino-acid residues, about sixteen thousand atoms. It differs from almost all other proteins in being substantially composed of but two amino acids, glycine and hydroxyproline. Collagen is a kind of super- molecule, however, in its three-dimensional architecture. The polypeptide chains of the two amino acids, alternating with one another and punctuated by the presence of certain other amino acids, are coiled in a left-handed helix. Three of these helical strands are twisted around on another, like strands of a rope, in a right handed super-helix, to compose the complete molecule. Understandably, the synthesis of this structure proceeds in steps. While it has been known for half a century [these words written in 1985] that vitamin C is essential to the manufacture of collagen, the process is only now yielding to inquiry. It appears that vitamin C is involved at every step.

First, a three dimensional stranded structure is assembled, with the amino acids glycine and proline as its principal components. This is not yet collagen but its precursor, procollagen. A recent study shows that vitamin C must have an important role in its synthesis. Prolonged exposure of cultures of human connective-tissue cells to ascorbate induced an eight-fold increase in the synthesis of collagen with no increase in the rate of synthesis of other proteins (Murad et al., 1981). Since the production of procollagen must precede the production of collagen, vitamin C must have a role in this step – the formation of the polypeptide chains of procollagen – along with its better understood role in the conversion of procollagen to collagen.

The conversion involves a reaction that substitutes a hydroxyl group, OH, for a hydrogen atom, H, in the proline residues at certain points in the polypeptide chains, converting those residues to hydroxyproline. This hydroxylation reaction secures the chains in the triple helix of collagen. The hydroxylation, next, of the residues of the amino acid lysine, transforming them to hydroxylysine, is then needed to permit the cross-linking of the triple helices into the fibers and networks of the tissues.

These hydroxylation reactions are catalyzed by two different enzymes: prolyl-4- hydroxylase and lysyl-hydroxylase. Vitamin C also serves with them in inducing these reactions. It has recently been shown by Myllyla and his colleagues that, in this service, one molecule of vitamin C is destroyed for each H replaced by OH. [Myllyla et al., "Ascorbate is Consumed Stoichiometrically in the Uncoupled Reactions Catalyzed by Prolyl-4-Hydroxylase and Lysyl Hydroxylase. Journal of Biological Chemistry 259:5403- 5405. 1984]

We have come upon the two big reasons why we require for good health so much larger amounts of vitamin C than are present in the plants we use as food. First, there is the bodies continuing need for the synthesis of large amounts of collagen for growth and for replacement of the collagen degraded by daily wear and tear. Second, vitamin C, in the critical reactions that assemble collagen in the tissues, does not serve merely as a catalyst but is destroyed." Linus Pauling HOW TO LIVE LONGER AND FEEL BETTER (1986) Pages 89-91


Vitamin C is essential for the building of collagen, the most abundant protein built in our bodies and the major component of connective tissue. [Wolbach, S. B.., and Howe, P. R. Ďntercellular substance in experimental scorbutus" Arch. Path., 1:1, 1926] 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 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.

Victims of prison camps who have suffered from vitamin C deficiency have been found to have wide-spread fatty deposits (atherosclerosis) in their arteries. It is quite possible that vitamin C deficiency is directly implicated; it is unlikely that such deposits could have been due to too much fat or cholesterol in diet.

Strong evidence has recently been present that individual needs for vitamin C vary widely, and that some individuals have much higher needs than has hitherto been supposed. While the functioning of vitamin C, except for its role in building collagen, is obscure, it is quite possible that many hearts and blood vessels would be better protected if an abundant environmental supply of this vitamin were available in the circulating fluids that bathe the tissue cells. Roger J. Williams NUTRITION AGAINST DISEASE 1971) Pages 85-86

Owen R. Fonorow
Vitamin C Foundation
PO Box 73172
Houston, TX  77273
Fax:  630/416-1309


1.  Pauling, L; Rath, M (1987). Hypothesis: lipoprotein(a) is a 
surrogate for ascorbate. Proc Natl Acad Sci USA Aug;87(16):6204-7.
2.  Pauling, L, Rath M (1991) Solution to the puzzle of human 
cardiovascular disease: Its primary cause is ascorbate deficiency 
leading to the deposition of lipoprotein(a) and fibrinogen/fibrin in the 
vascular wall. J. Orthomolecular Medicine 6(3&4): 125-133.
3.  Pauling L; Rath M (1990). Immunological evidence for the 
accumulation of lipoprotein(a) in the atherosclerotic lesion of the 
hypoascorbemic guinea pig. Proc Natl Acad Sci USA Dec,87:9388-9390.
4.  Pauling, L; Rath, M (1992). A Unified Theory of Human 
Cardiovascular Disease Leading the Way to the Abolition of this Disease 
as a Cause of Human Mortality. J. Orthomolecular Medicine, 1992.
5.  Bostom AG; Cupples LA; Jenner JL; Ordovas JM; Seman LJ; Wilson 
PW; Schaefer EJ; Castelli WP (1996). Elevated plasma lipoprotein(a) and 
coronary heart disease in men aged 55 years and younger. A prospective 
study. Framingham Study, Epidemiology and Biometry Program, Framingham, 
Mass., USA. JAMA 1996 Aug 21;276(7):544-8.
6.  Fujita T; Takaoka A; Izumi M; Takahashi M  (1997). Association 
of an acute reduction in lipoprotein(a) with coronary artery restenosis 
after percutaneous transluminal coronary angioplasty. Circulation 1997 
Jul 1;96(1):166-73.
7.  Stubbs P; Noble M; Collinson P; O'Connor B Moseley D; Seed M 
(1997). A prospective study of the role of lipoprotein(a) in the 
pathogenesis of unstable angina. Eur Heart J 1997 Apr;18(4):603-7 
8.  Prins J; van Rijn HJ; Bouma BN; Kastelein JJ van der Hoek YY; 
Leus FR (1997), The identification and significance of a Thr-->Pro 
polymorphism in kringle IV type 8 of apolipoprotein(a). Thromb Haemost 
1997 May;77(5):949-54
9.  Frank S; Kostner GM (1997) ,The role of apo-(a) kringle-IVs in 
the assembly of lipoprotein-(a). Protein Eng 1997 Mar;10(3):291-8
10.  Marcoux C; Cohn JS; Davignon J; Lussier-Cacan S  (1997) 
Association of Lp(a) rather than integrally-bound apo(a) with 
triglyceride-rich lipoproteins of human subjects. .Biochim Biophys Acta 
1997 Jun 23;1346(3):261-74
11.  Stein JH; Rosenson RS. (1997) Lipoprotein Lp(a) excess and 
coronary heart disease. Arch Intern Med 1997 Jun 9;157(11):1170-6.
12.  Klezovitch O; Scanu AM; Edelstein C (1996). Evidence that the 
fibrinogen binding domain of Apo(a) is outside the lysine binding site 
of kringle IV-10: a study involving naturally occurring lysine binding 
defective lipoprotein(a) phenotypes. J Clin Invest 1996 Jul 1;98(1):185-
13.  Marcoux C; Cohn JS; Davignon J; Lussier-Cacan S (1997). 
Association of Lp(a) rather than integrally-bound apo(a) with 
triglyceride-rich lipoproteins of human subjects.B iochim Biophys Acta 
1997 Jun 23;1346(3):261-74
14.  Pauling, L (1991). Case report: lysine/ascorbate-related 
amelioration of angina pectoris. J. Orthomolecular Medicine 6(3&4): 144-
15.  McBeath, M; Pauling L (1993). A case history: lysine/ascorbate-
related amelioration of angina pectoris. J. Orthomolecular Medicine 
8(2): 77-78. 
16.  Pauling, L (1993). Third case report on lysine-ascorbate 
amelioration of angina pectoris, Linus Pauling Institute of Science and 
Medicine, 440 Page Mill Road, Palo Alto, CA 94306.
17.  Pauling, L (1993). Heart Disease: Unified Theory of Cause and 
Cure. Video lecture.  Institute of Optimum Nutrition, England. (See 
Appendix I)
18.  Bostom AG; Hume AL; Eaton CB; Laurino JP; Yanek LR; Regan MS; 
McQuade WH; Craig WY; Perrone G; Jacques PF (1996). The effect of high-
dose ascorbate supplementation on plasma lipoprotein(a) levels in 
patients with premature coronary heart disease. Pharmacotherapy 1995 
19.  Rosenburg IH et al. (1996) Homocysteine, Vitamins, and Arterial 
Occlusive Disease: An Overview, J. Nutr. 126, 1235S-1237S
20.  Paterson, J. C.; Some Factors in the Causation of Intimal 
Hemorrhages and in the Precipitation of Coronary Thrombi. Canadian 
Medical Assoc., vol 44: pp 114-120, 1941. 
21.  Willis, G. C, et. al., Serial Arteriography in Atherosclerosis, 
Canadian Medical. Assoc J., vol 69, pp. 17-22, 1953
22.  Willis, G. C., and Fishman, S., Ascorbic Acid Content of Human 
Arterial Tissue. Canadian Medical Association J., vol. 72,Pp. 500-503, 
23.  Willis, G. C.; An Experimental Study of the Intimal Ground 
Substance in Atherosclerosis.  Canadian Medical Association J., vol. 69: 
pp. 17-22, 1953.
24.  Willis, G. C., The Reversibility of Atherosclerosis. Canadian 
Medical Assoc J., vol 77: pp. 106-109, 1957.
25.  Stone, I; The Healing Factor: Vitamin C Against Disease, 
Grosset Dunlap, 1976.
26.  Sokoloff, B; Hori, M.; Saelhof, C.C.; Wrzolek, T; Imai, T. 
1966), Aging, Atherosclerosis, and Ascorbic Acid Metabolism.Journal of 
American Geriatric Society, 14:1239-1260. 
27.  Sokoloff, et. al.; Effect of Ascorbic Acid on Certain Blood Fat 
Metabolism Factors in Animals and Man: Journal of Nutrition, vol 91, 
107-118. 1967.
28.  Shaffer, C.F.; Ascorbic Acid and Atherosclerosis. American 
Journal of Clinical Nutrition, vol 23: pp.27-30. 1970.
29.  Ginter, E.; et. al., The Effect of Chronic Hypovitaminosis C on 
the Metabolism of Cholesterol and Atherogensis in Guinea Pigs, J. of 
Atherosclerosis Research, vol 10: pp 341-352, 1969.
30.  Enstrom, JE et al (1992) Vitamin C intake and mortality among a 
sample of the United States population, Epidemiology 3, 194-202. 
31. O'Leary, Daniel H, et al (1999) Carotid-Artery Intima and 
Media Thickness as a Risk Factor for Myocardial Infarction and Stroke in 
Older Adults, NEJM Vol. 340, No. 1