Pauling has found an answer that can abolish cardiovascular disease (CVD) as a cause for human mortality.

He began using vitamin C in 1966 after being told that this vitamin could extend his life, giving a few more years to continue working to decrease human suffering. In 1973, he started the Linus Pauling Institute of Science and Medicine, Menlo Park, California.

He published books on how vitamin C helps colds and flu (1976); cancer (1979); longer, healthier life (1986); and hundreds of research articles. To Pauling, vitamin C is a panacea that improves health, brings benefits in all forms of illness, extends life and slows aging.

Vitamin C and Cardiovascular Disease

In 1941, the Canadian cardiologist Paterson reported that 80 per cent of his heart disease patients had low vitamin C levels. The study was ignored by medicine. In 1954, Willis showed that vitamin C supplementation reduces atherosclerotic deposits in human arteries. His discovery was also ignored.

In 1970, Pauling published his first book on vitamin C. Over the next decade, heart disease in the US dropped by more than 30 per cent. This decrease, Pauling says, resulted not from better medical treatment but from a 300 per cent increase in vitamin C consumption in the US during that decade.

Medical treatments in all Western countries are the same, but deaths from cardiovascular disease decreased only in the US, because vitamin C intake did not increase in other Western countries during that time.

Pauling, Rath and Lp(a)

How do the protective effects of vitamin C take place? In 1989, Pauling and Rath began to examine a lipoprotein particle called Lp(a), which was discovered in 1963 in human blood. Lp(a) is like low density lipoprotein (the "bad" cholesterol in medical practice). Both contain cholesterol and other fats and a protein called apoB. But Lp(a) differs from LDL in one important respect. It contains an additional protein called apo(a) that is linked to apoB by a sulphur bridge. Apo(a), it turns out, holds a major key to the puzzle of heart disease. Lp(a) is its carrier; vehicle, its way of getting around.

Rath showed in 1989 that Lp(a) strongly increases risk of atherosclerosis, whereas LDL without apo(a) is only a weak risk factor. Lp(a) accumulates in arterial walls of patients with atherosclerosis. For years, LDL and Lp(a) had been lumped together, ignoring the key factor: apo(a). Wrongly blaming LDL, medicines continue targeting the innocent bystander! No wonder treatments fail!

Apo(a): A Sticky Protein

Apo(a) belongs to a group of proteins with adhesive (sticky) properties that includes fibrinogen, a protein that helps stop bleeding, and fibronectin, which plays vital roles in prenatal development, brain differentiation and growth. Apo(a) plays a key role in tissue and disease repair, co-ordinating interactions of cell systems with extracellular matrix.

Apo(a) plays critical roles in heart disease in organisms that have lost the ability to make vitamin C from glucose: humans and a few animals. Animals that synthesize their own vitamin C rarely get heart disease.

Apo(a) and Vitamin C

Both apo(a) and vitamin C keep arteries strong, but they use different methods to achieve this end. Of the two, vitamin C is the preferable way.

Our bodies require vitamin C to produce collagen and elastin, proteins that normally keep arteries strong. Unable to make vitamin C, the body depends on foods to supply this essential nutrient. Without vitamin C, collagen and elastin become defective and arteries deteriorate, degenerate, fall apart. Bleeding into tissue spaces is one result. It is one symptom of the ascorbate deficiency disease, scurvy. When vitamin C supply is less than adequate but more than absent, deterioration simply takes longer.

During Ice Ages, when fresh greens and fruit, the primary sources of vitamin C, were scarce, millions are thought to have died from scurvy. Under such conditions, a genetic coding for other ways to keep arteries strong improved the carrier's chance of surviving long enough to reproduce. Apo(a) is coded on one such gene. Apo(a) sticks to receptors in vitamin C-deficient, deteriorating arteries and helps repair these arteries by thickening them.

A further benefit would accrue if the secondary mechanism kicked in during vitamin C deficiency. That seems to be what happen. When vitamin C levels are up, arteries are strong and Lp(a) levels typically decrease, because less repair protein is needed and therefore less is made.

Apo(a) is made by our liver. Its production is stimulated by low vitamin C levels and inhibited by high vitamin C levels.

Dynamics of Atherosclerosis & Peripheral Arterial Disease

High levels of Lp(a) with tissue-repairing apo(a) and low levels of vitamin C are usually found in atherosclerosis.

Vitamin C deficiency-induced arterial weakness shows up most readily where arteries join, where blood pressure is high, and where blood vessels narrow, ie, where blood flow is most turbulent. This is where atherosclerotic plaque most often occurs. In acute vitamin C deficiency, apo(a) thickens arteries to prevent tissue bleeding or broken blood vessels.

In prolonged deficiency, arteries become thicker and thicker until they become too narrow for blood to flow, resulting in stroke or heart attack. Here, the repair mechanism saves us to kill us later. From nature's point of view of survival of the species, it is better to die from atherosclerosis after reproducing than from scurvy before.

In peripheral arteries, vitamin C's antioxidant activity protects blood vessel walls from the damage by oxygen radicals and toxic substances.

Prevention, Reversal, Cure

We can obtain the needed vitamin C by eating the "gorilla diet": fresh, raw, vitamin C-rich vegetables and fruit; or by taking vitamin C as a supplement.

Pauling and Rath hold vitamin C to be the key to cardiovascular health and consider it the key to prevention, reversal and cure of heart disease. It builds strong arteries. It also prevents damage to arteries by toxic substances.

A Complete Picture

In their report, Pauling and Rath, committed to decrease human suffering, present a unified theory of the cause of CVD which also points the direction to reversal, prevention and cure. It incorporates observations from all cardiovascular conditions: atherosclerosis, high blood pressure, peripheral arterial disease, cardiovascular complications in diabetes, homocysteinuria, tobacco smoke toxicity, and oxidative free radical damage. It explains why deterioration progresses as it does. It provides a scientific rationale for treatment, using natural substances to reverse, prevent and cure. For their findings, Pauling should receive his third Nobel Prize (Medicine), this time shared with Rath.

Other substances help bring Lp(a) to levels conducive to health. They include N-acetyl cysteine, niacin, and lysine. For complete health, all 50 essential nutrients are required in optimum amounts.

Cardiovascular Health and Politics

Pauling and Rath's work upsets the proverbial apple cart of accepted CVD dogma. Pauling submitted the report, titled Solution to the Puzzle of Human Cardiovascular Disease to P.N.A.S., a journal in which he has been published many times before. It was accepted.

"Under questionable circumstances this decision was later revoked by the editor," they write.

"We are aware that this pull-back was not the decision of an individual. It happened in the interest of those who are personally or economically dependent on the present dogma of human cardiovascular disease. We are confident that the scientific historians will make the proper judgment on this interesting development."

Their report is published in the Journal of Orthomolecular Medicine. Rath and Pauling end their prologue to Solution to the Puzzle of Cardiovascular Disease with the following: "...we are convinced that the uncompromised publication of this article lies in the interest of millions of patients and perhaps every human being."


Rath, M. & Pauling, L. 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. Journal of Orthomolecular Medicine, 1991; 6: 125 - 134.


By Udo Erasmus

Share this with your friends