OVERVIEW

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.

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 the 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 U.S. 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 tissues of heart patients were 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 different 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 beings that suffer cardiovascular disease and those that 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 invention 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.

In the early 1950s the Canadian doctor Willis theorized that 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.

Is 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 [*].

Guinea pigs are one of the few species which, like humans, do not make vitamin C. The pigs 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 in 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.

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.

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 blood stream, 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 U. S. 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, between vitamin 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


AUG 2004: UPDATED PROTOCOL HERE

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. NEW: Eliminate man-made/processed fats, such as trans and hydrogenated fats, and supplement Omega-3 rich oils. "Research has shown that an Omega-3 Index of 8 percent to 10 percent reduces a person's relative risk of death from coronary heart disease by 40 percent, and from sudden cardiac death by 90 percent." This benefit probably results from restored insulin-mediated glucose/vitamin C uptake into cells. [See: Protocol for Reversing Diabetes Type II by Eliminating Hydrogenated and Trans Fats and adding Omega-3 oils... ]

   Note: Following an Atkins-style diet will eliminate most trans fats because these "poisons" appear mostly in processed carbohydrate foods such as cookies, crackers, snacks, etc. Butter is vastly supperior to margarine. Natural saturated fats are vastly superior to any fats or oils processed for longer shelf life.

4. 
   NEW: Eliminate ordinary sugar and refined carbohydrates. New research confirms Dr. John Ely's 30-year theory that sugar (glucose) competes with ascorbic acid (Vitamin C) for insulin-mediated uptake into cells. Taking sugar can effectively crowd out the Ascorbate. The effect of the Pauling Therapy is reportedly much more pronounced and immediate when sugar is eliminated.

5. Take Proline from 250 mg to 2000 mg daily. (This added factor may lower elevated Lp(a) within 6 to 14 months.)

6. Follow Paulings 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

   
   

7. 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.)

8. 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.)

   Manganese alters mitochodrial integrity in the hearts of swine marginally deficient in magnesium ... These results suggest that high Mn, when fed in combination with low Mg, disrupts mitochondrial ultrastructure and is associated with the sudden deaths previously reported.
   

9. Supplement the amino acids Taurine, Arginine and Carnitine (1 to 3 g).

10. Avoid supplemental calcium. [*]

11. 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.paulingtherapy.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 was 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 recognized as the greatest lapse of the 20th century.

Owen Fonorow, Naturopath, Ph.D.
Vitamin C Foundation
PO Box 3097, Lisle IL 60532
www.VitaminCFoundation.org
630-416-1438

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 engodenous 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.

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.