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[1] That atherosclerotic plaques deposit in response to injury is accepted. The confusion in the media is cause and effect. The fallacy is that cholesterol causes heart disease, but plaque build-ups are the effect of heart disease. Our understanding of the arterial healing process comes, in part, from research that led to the 1985 Nobel Prize in Medicine. [2]Cholesterol cannot and does not cause heart disease. Human beings are well protected from scurvy by the RDA of vitamin C (now 75-90 mg), but this meager amount virtually guarantees "hardening of the arteries," i.e. the development of occlusive cardiovascular disease as scabs (atherosclerotic plaques) form on the arterial walls weakened by the vitamin deficiency.
[4] The Pauling and Rath theory relies on the Willis observations. (Note: In a heart bypass, veins from the leg are used which are without plaque.) Because plaque does not form randomly throughout the blood stream, it is unlikely that the primary cause of the lesions leading to heart disease are "poisons" circulating in the blood. [5] We now know that plaques form over stress fractures. Visualize stepping on a garden hose 70-80 times per minute, a fate similar to the coronary arteries feeding the heart. Over time, human arteries may wear down and develop small cracks. Mechanical stress then, not cholesterol, causes heart disease. But why are humans more susceptible to this stress than other beings with heart beats? Some factor must cause the lesions in the walls of human blood vessels but not in the coronary arteries of most other animals. Pauling and Rath blame the lack of a specific protein caused by a specific vitamin deficiency. A vitamin deficiency that is impossible in most animals! Roger J. Williams, PhD, in his 1971 book Nutrition Against Disease explained vitamin C's role in collagen:
The Pauling and Rath theory postulates that the root cause of atherosclerotic plaque deposits is a vitamin C deficiency.[6] Pauling called this condition "chronic scurvy." It is normal in humans, but it cannot happen in most other species. Ascorbic acid (vitamin C) is not a vitamin for most animals in the sense that it is not required in their diet. They make it in high amounts in their livers or kidneys. The sad fact is that we humans must obtain all our vitamin C from what we eat. (Unless we supplement, our diets contain less than 1/100th of what animals make, and we lose some in the gut during digestion.) According to the Pauling/Rath theory, suboptimal vitamin C results in less collagen. As collagen supplies dwindle, our blood vessels deteriorate. In an acute shortage, we die of scurvy. In a chronic shortage, humans develop atherosclerotic plaques. Pauling believed that most human beings suffer chronic scurvy.
[7] A vast amount of experimental research supports the Pauling/Rath view. Careful studies with animals that do not make their own endogenous vitamin C (such animals are rare) prove that when the dietary intake of the vitamin is low, collagen production is limited, and blood vessels tend to become thinner and weaker from wear and tear; plaque deposits then form to compensate for this weakness. [Pauling/Rath, 87] Large population studies show that higher C intake results in lower incidence of cardiovascular disease and lower death rates.[Enstrom, 92]
[8] Plaque forms over injured blood vessels. If one suffers plaque deposits, it is likely he/she owes his life to this material that narrows arteries. Without plaque, the weakened blood vessels would rupture or leak causing internal bleeding and death. A slower version of scurvy, the disease long-dreaded by ancient sailors. (James Lind discovered (year 1753) that eating fruit prevents this disease. Acute scurvy can be prevented by a mere 10 mg vitamin C per day. )
[9] The human body's healing response to chronic scurvy is what medicine calls coronary heart disease (CHD), AKA cardiovascular disease (CVD), "heart disease", "atherosclerosis", "arteriosclerosis", "hardening", "plaque", "narrowing", etc. This process by itself rarely kills people, but plaque lined arteries make heart attack more likely from a blood clot or blockage. (Plaque lined arteries cannot easily dilate in response to a clot.) Currently, it is unknown what amount of vitamin C prevents the atherosclerotic plaques of chronic scurvy, but Linus Pauling often recommended 3000 mg.
Lp(a): The Surrogate Healing Factor[10] The chronic scurvy healing process begins with an important "sticky" form of cholesterol. Pauling and Rath were among the first to attach utmost importance to the blood lipid: lipoprotein(a), or Lp(a) for short. From the research that led to the 1985 Nobel prize, medical researchers learned how plaque deposits as Lp(a) binds to lysine strands that appear in the arterial walls. Lysine and proline are building blocks of the collagen super-molecule, but the Cholesterol or Lysine strands the Lp(a) Binding Sites adhered to are not normally exposed. The binding sites can adhere only after blood vessels crack or suffer a small sore or lesion. Scientists have since discovered the Lp(a) Proline Binding Sites too. Note: Mainstream medical science has known since 1989 that Lp(a) binds to form plaque, not ordinary LDL. [2, 4] [11] Many experts believe that something circulating in the blood must cause these cracks in our blood "pipes". For many years, ordinary LDL cholesterol has been blamed because elevated levels have sometimes been correlated with heart disease. Other scientists correlated elevated homocysteine and oxidized cholesterol. Again, the confusion is cause and effect. If cholesterol causes cracks or lesions, plaque should be more randomly distributed throughout the blood stream. According to the Pauling/Rath unified theory, both elevated homocysteine and oxidized cholesterol are symptoms of scurvy.
[12] Before teaming with Pauling, Dr. Rath's German research team examined plaque from human aortas (blood vessels near the heart) post-mortem. They discovered that atherosclerotic plaques are composed primarily of Lp(a), not ordinary LDL cholesterol. [2, 4] Dr. Rath, realized that Lp(a) was connected somehow with vitamin C and joined the Linus Pauling Institute of Science and Medicine. Together, Pauling and Rath developed their unified theory which holds that increased Lp(a) acts as a surrogate for low vitamin C and hardens weak blood vessels. Their experiments, to test their theory, proved that low vitamin C intake will increase blood levels of Lp(a) in test animals compared to controls. [13] An important finding is that this sticky Lp(a) (a form of cholesterol similar to LDL) has only been found in the very few animal species that do not make their own vitamin C, including humans. Today, most animals:
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[3] This realization is not new: G. C. Willis, MD, made the crucial
observation in the early 1950s. A Canadian doctor, he noticed that
atherosclerotic plaques always formed in the same places.
Usually near the heart where the blood vessels are stretched and bent.
Willis suspected a vitamin C deficiency, and his experiments implicated
mechanical stress
caused by the heart beat.
