CVD - Weak Walls due to chronic scurvy

Atherosclerotic plaques are not the cause of CVD.   Instead they are a means by which the body repairs damaged arterial walls, weakened by a lack of collagen resulting from a long-term, low-level Vitamin C deficiency

The answer to what is really going on in CVD was discovered over a decade ago by two men:

 -   The brilliant, biochemist, physicist, molecular biologist Dr. Linus Pauling.   Tthe world's only recipient of two unshared Nobel prizes,awarded nearly 40 honorary degrees, PHDs and DScs;

-   The renowned Dr. Matthias Rath, a research physician from Germany.

Dr. Pauling, who died in 1994 at the age of 93, devoted his last years working with Rath to discover the root causes of cardiovascular disease.

In 1985, Brown and Goldstein were awarded a Nobel Prize in medicine for their major finding that atherosclerotic plaque deposits formed in the coronary and brain arterial walls as a response to injury (lesions) to the arterial walls, by attaching to lysine and proline binding sites exposed in the walls by the injury.

Rath and his colleagues at Hamburg University found that the main constituent of plaques was not in fact LDL cholesterol (as formally believed), but a similar cholesterol-based protein called lipoprotein(a) or Lp(a)

Rath and Pauling met, and then decided to work together to answer the following questions:

(1) Why did the lesions form in the first place?

(2) Why did the Lp(a) plaques form on the lesions?

(3) Why do heart patients and others at risk of cardiovascular disease and stroke have more LDL and Lp(a) cholesterol in their bloodstream?

Rath and Pauling discovered that CVD is primarily a consequence of Vitamin C deficiency

To properly REPAIR and RENEW constantly decaying arterial walls (and also every other tissue in the body), your body must produce a binding protein called COLLAGEN, which requires ample quantities of Vitamin C (aka ascorbate or ascorbic acid) - if you don't have enough Vitamin C to make collagen, then artery wall lesions will not repair properly; if you took no Vitamin C at all, you would experience scurvy, the lesions would rupture and you would die of internal bleeding. This is how British sailors died in the 1500-1800's on long voyages without access to Vitamin C.

If you don't have enough Vitamin C, then LDL and Lp(a) cholesterol will accumulate in your bloodstream.   The liver intentionally manufactures Lp(a) and LDL cholesterol ascomponents of repair material for a C-deficient damaged artery (lesions are usually formed in the highest-stress areas, such as at the entrance to the coronary arteries); additionally ascorbate is used to convert cholesterol to bile for excretion through the intestines.

Your body compensates with a temporary “fix” to at least try to keep you alive long enough to reproduce and so keep the human race going.    In a healing response to a breakdown of collagen, Lp(a) - “The Repair Man” is attracted to the lesions, forming repair patches, called arterial plaques.

Combining with other repair substances (E.g. fibrin), the plaques grow in size until the blood flow is partially / completely cut off (usually due to blockage by a blood clot that forms when the plaque ruptures) or an artery bursts.   Eventually, possible consequences include:

•   Angina;

•   Arrhythmia;

•   Heart attack.   Usually arterial plaque ruptures and forms a blood clot (thrombus) which travels (embolus) until it blocks the coronary artery providing blood to the heart; other consequences related to ischemia (low blood supply) include, high blood pressure, angina, arrhythmia or death;

•   Stroke.    By blocking / bursting (hemorrhage) the small arteries in the brain; this can lead to limb paralysis on one side of the body, and/or an inability to understand or formulate speech, or to see one side of the visual field in both eyes;

•   Death.

Most mammals produce their own Vitamin C and do not have CVD (exceptions include humans, non-human primates (apes, monkeys, lemurs), guinea pigs, the European hedgehog and the fruit bat)- most animals convert glucose to Vitamin C in their kidneys or liver. Animals that produce their own ascorbate generally do not have CVD and do not have significant Lp(a) in their bloodstream.    Humans are no longer able to produce Vitamin C, because some time long ago there was a mutation of the gene which encodes for the enzyme L-Gulono-g-Lactone, necessary to convert glucose to Vitamin C.  As such, cardiovascular disease is not really a disease, but rather the consequence of a missing enzyme!

How much Vitamin C do we need ?

In his previous research on Vitamin C, Pauling discovered that the 60mg amount of daily Vitamin C recommended by the FDA is 30 to 300 times smaller than the concentration found in other mammals.    i.e. Humans, whose entire C intake must come from their diet, need to eat about 3-12 grams of Vitamin C /day to have as much ascorbate as other animals(adjusting for body weight).

In 1991 Rath and Pauling published their groundbreaking paper explaining the cause of CVD:

"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."

Later, in 1994, Rath and Pauling obtained a patent on a cure for atherosclerosis that comprises Vitamin C and Lysine. Later, proline was added to improve the cure:

CVD -A Simple Cure