Vitamin C and Vascular Disease
Our Distant Ancestors Lost The Ability to Produce Vitamin C
Ice Ages, Scurvy and Natural Selection
Risk Factors: Lipoprotein(a), LDL, Lipids and Oxidized Cholesterol
All The Known Actions of Ascorbate
Lipoprotein(a) Is The Real Risk Factor for Vascular Disease
You May Have to Educate Your Doctor
The Startling Facts about Lipoprotein(a)
Animals in The Wild Do Not Get Heart Attacks
The Cost in Lives
The Cost in Dollars
Program for The Reversal of Heart Disease
An individual by the name of Matthias Rath, M.D. has come up with a comprehensive explanation of the cause, prevention, and treatment of vascular disease which I find rational and compelling. Dr. Rath has done seminal research at the University of Hamburg and has published twelve papers in respected research journals on the subject of vascular disease. He now lives in the U.S. and was a friend and colleague of the only double Noble prize winner, the late Dr. Linus Pauling. Dr. Rath has established a company called Health Now to educate the public about the prevention and treatment of vascular disease. In his public presentations and in his book Eradicating Heart Disease, Dr. Rath explains the known facts from his research on vascular disease and provides proof at each critical turn in his reasoning. I have reviewed his work and concluded that what he has to say is critically important. Therefore, I choose to throw what weight I have behind the effort to bring Dr. Rath’s information to your attention.
The best part of Dr. Rath’s discoveries is that they provide effective action anyone can take to both prevent and treat vascular disease in a powerful way by natural means without relying on Draconian changes in diet and lifestyle or dangerous drugs which lower cholesterol but do nothing to decrease overall mortality. Let us go to the beginning of this story.
It long has been known that human beings do not produce ascorbic acid (vitamin C). Because vitamin C — which I shall refer to as "ascorbate" from here on out — is essential to life and because we cannot produce it, it is known as a vitamin in human metabolism. We are rare among species, because almost all mammals can make abundant supplies of ascorbate. There are only four species of mammals which do not make their own ascorbate. These are (1) humans, (2) gorillas, (3) guinea pigs and (4) fruit bats.
All these species, except humans, are vegetarian by nature. Humans probably were vegetarians with rare exception, until the invention of animal husbandry. Gorillas are constantly foraging for plant food rich in vitamin C. Guinea pigs do the same, and fruit bats, well, why do you suppose we them call them fruit bats? These three animals know, by instinct, they must ingest large quantities of ascorbate to stay healthy.
In the body of an ascorbate-making mammal, the ascorbate molecule is made from a few small modifications of the glucose molecule. Glucose is in abundant supply in humans and animals at all times. There are four enzymes required to convert glucose into vitamin C. Humans have the first three enzymes, having lost the fourth enzyme somewhere in our development.
In mammals which retained the ability to make ascorbic acid, it is made in response to all sorts of stress, especially the stress of infection. The normal everyday non-stress production of ascorbate, when proportioned up to represent the amount made on a weight basis corrected to the size of the average man (seventy kilograms), is from five to ten grams (5,000-10,000 mg.) per day. Under stress, that amount can be quadrupled.
Compare this to the official federal government recommendation (RDA or recommended deficiency allowance) of 60 mg. (six one-hundredths of one gram or 12 one-thousands of five grams). The increased production of ascorbate under stress in animals goes a long way toward explaining why we do not see anything like the rate of infection among animals which we see in human beings. When was the last time you saw an animal with a cold?
Why did these four mammals — humans, gorillas, guinea pigs and fruit bats — lose the ability to make ascorbate? Probably, because they could. I suspect that these four animals had abundant sources of ascorbate in their diets, and loss of ability to produce their own ascorbate did not put them at excess risk of being weeded out by natural selection. Only the human being has changed his dietary preferences since then. Humans are the only species to both eat meat and be unable to produce ascorbate. There are no other carnivores which cannot make ascorbate.
This explanation dovetails nicely with research in genetics which suggests that we all had a common mother and a common father who lived sometime between 100,000 to 200,000 years ago, all other branches of the human family since having died out. This would explain why all, and not just some, humans are deficient in this fourth enzyme. These common ancestors are thought to have lived in tropical regions of Africa where ascorbate-containing food was abundant.
However, our common ancestors did not stay in Africa. They migrated to cover the entire earth. Then came the Ices Ages, one after another, each lasting around 10,000 years. We know from the archeological evidence that human beings lived through these ice ages in northern climates. They somehow toughed it out. Ascorbate, because it is made by plant food, is not easy to come by in an ice age. The old vegetable garden does not do so well under a thick layer of ice. These ancestors suffered from ascorbate deficiency, a disease called scurvy, a fact borne out by examination of their remains.
Scurvy is marked by the breakdown of collagen tissue throughout the body and frequent infections. Collagen is the protein with which strong connective tissue is made throughout the body. Sailors were known to have had scurvy on long voyages, until someone discovered that a little citrus fruit intake avoided the disease. The way those "scorbutic" (the term we apply to a person with scurvy) sailors died was by leakage of blood out of their blood vessels. Their blood vessels literally cracked open and they bled to death.
The same sort of thing happened to many of our ancestors who lived through the ice ages. Many of them bled to death because they had little or no ascorbate, and without ascorbate there is no collagen production or repair throughout the body. The wall of a blood vessel is made of collagen. Therefore, when you run out of ascorbate, it is only a matter of time until that wall of collagen breaks down, is not repaired, cracks open and you bleed to death.
However, not all our Ice Ages ancestors died of cracked open blood vessels. Many did, but some had the ability to repair leaky blood vessel walls without the assistance of ascorbate. These people, as a group, lived long enough to have children, and we are the descendants of those children. Therefore, we have inherited this ability to repair our blood vessel walls without much ascorbate.
When a crack develops in a blood vessel wall due to a shortage of ascorbate, certain fat packages in the blood have the ability to plug the leak by forming a kind of plaster cast. These packages of fat are known as cholesterol, lipids, low density lipoproteins (LDL), and one especially effective leak plugger, lipoprotein(a), a special type of LDL.
LDL is a bag of several thousand cholesterol and other fat molecules with the bag itself made of protein. In itself, despite all the hype in the media, ordinary LDL is no problem. However, there is one type of LDL, namely lipoprotein(a) which has an extra protein cover on the outside of the usual protein cover. Lipoprotein(a) is a double bag of fat. This outer bag is called apoprotein(a) or apo(a). The "a" could well stand for adhesive, because it is a very sticky substance. When a crack develops in the wall of a blood vessel, this sticky double-bagged fat sack finds its way through the crack. Once there, the apo(a) adhesive outer bag glues it down and begins the process of plugging the leak. This both avoids death by scurvy and sets the stage for blood vessel disease.
Once having plugged the leak the apo(a) outer bag sticks to whatever other bags of cholesterol (i.e. LDL) float by and glues them down as well. The process looks like the following:
- The scorbutic (ascorbate deficient) crack in the blood vessel wall is the first step in atherosclerosis.
- The plugging of the leak with lipoprotein(a) is the second step.
- The gluing down of other LDL (single layer bags of cholesterol and lipids which are not sticky in themselves) is the third step.
- The fourth step is the stimulation, by lipoprotein(a), of the muscle cells in the artery wall to multiply, thus forming a tumor (swelling).
- Then the cleanup crew arrives, also known as macrophages, and they try to eat the whole mess and carry it away. However, many of them overeat, get fat, and become part of the problem by dying and being glued down into the plaque. Because they contain so much fat, they appear under the microscope to be full of foam, and they are therefore known as "foam cells."
The tumor, i.e., the proliferation of excess smooth muscle cells is not cancerous. Nevertheless, it can cause death by pushing this mass of plaque into the lumen (passage way) of the blood vessel in which this process is happening. This narrows the passage way through which blood passes and can eventually lead to heart attack, stroke and other problems, depending on where in the body it develops.
- Increases HDL (high density lipoprotein) production. (HDL is able to help resorb fat located in plaque. In the process it changes from a disc shape to a globular form of HDL, and takes this fat to the liver to be burned.)
- Decreases the production of lipoprotein(a). (Somehow the liver knows when there is plenty of ascorbate on board, and therefore no need for high levels of lipoprotein(a) which is, after all, a repair factor for the cracks in blood vessel walls which come up in the absence of sufficient ascorbate.)
- Down-regulates cholesterol and triglyceride production in the liver. [These are secondary repair factors in that they are glued into the plaque by lipoprotein(a).]
- Lowers blood sugar and insulin requirements.
- By relaxing the blood vessel walls, lowers blood pressure when hypertension is present. (This is not the total answer to a case of hypertension, but it can help.)
- Inhibits inappropriate intravascular clot formation (the final and sometimes deadly event in cases of heart attacks and strokes).
The bottom line is that lipoprotein(a) is the real risk factor in cardiovascular disease and that ascorbate and niacin are the only major lines of defense against high levels of lipoprotein(a). Cholesterol, even LDL cholesterol, can serve as a statistical risk factor only to the degree that it is correlated with the level of the real problem: the special type of LDL called lipoprotein(a).
The best test, by far, for risk of cardiovascular disease is the direct measurement of this special type of LDL, namely a lipoprotein(a) level. A lipoprotein(a) level is ten times more accurate and specific for prediction of vascular disease.
By the way, this is new information, right out of the research journals. It will be many years before the average doctor knows about it and many more years before it is generally accepted and then a few more years before this test is routinely ordered in the evaluation for vascular disease. Medicine is dominated by a conservative inertia in which, for what they conceive of as medical-legal safety, 95% of the entire pack moves forward slowly, and together, to incorporate advances in science.
If you want this test now, you will probably have to educate your doctor about it and then insist on it. Also, you can be sure the anti-cholesterol industry is not going give up their position easily and adopt lipoprotein(a) as the new standard, regardless of the scientific truth behind the matter. If they do, they lose big money!
The presently accepted levels of lipoprotein(a) are the following.
|0||–||20 mg./dl||low risk|
|20||–||40 mg./dl.||moderate risk|
|>40 mg./dl.||high risk|
- Lipoprotein(a) levels are largely determined by inheritance.
- Special diet does not influence lipoprotein(a) levels.
- None of the available cholesterol lowering drugs lower lipoprotein(a) blood levels.
- Ascorbate and niacin both lower lipoprotein(a) blood levels.
- L-lysine and L-proline, two natural amino acids, can prevent the apo(a) adhesive from sticking, serving as a kind of Teflon coating. Of these, L-proline is several times more powerful than L-lysine. These aminos also assist to shrink the plaque which is already present.
- Lipoprotein(a) blood level is the single greatest risk factor predicting the restenosis of vessels used in bypass surgery.
The process of atherosclerosis is limited to humans. Animals in the wild do not develop atherosclerosis, therefore no heart attacks and no strokes occur among these citizens of nature. To induce an animal to have atherosclerosis you have to put it in captivity and feed it the kind of diet which humans use to cause the problem. The guinea pig and fruit bat make good models, if this is what you want to do. The gorilla would make a good model, but who wants fifty gorillas lined up in a laboratory?
Animals in the wild do not get heart attacks because they make their own ascorbate, and therefore the process of atherosclerosis does not begin. We humans could take the hint, load up on vitamin C and a few other vitamins twice each day for life and eradicate heart disease. This is already happening in the U.S. where ascorbate consumption has skyrocketed over the past 25 years, and heart disease has dropped by one third. The war against smoking may also have something to do with this, yet in countries where smoking has declined in the absence of increased ascorbate consumption, there has been no equivalent change in heart disease rates.
Nevertheless, there is still a long way to go. In the U.S., every other person will die of vascular heart disease. Many more will die of stroke, another complication of vascular disease. Every year 1.5 million Americans die of heart attack, one fifth of them suddenly, before reaching the hospital or medical attention. Death is the first symptom of heart disease for forty percent of those who learn they have it. More than seven million Americans are living with vascular heart disease right now, and 2.5 million have cerebrovascular disease. Eight million Americans have arrhythmia: irregular heartbeat related to vascular disease.
One hundred billion dollars are spent on vascular heart disease every year, $200,000 every minute of every day. Coronary bypass, an extremely inappropriate procedure for the great majority of heart patients — considering the alternatives — sucks ten billion dollars out of American pockets every year.
The only people gaining from this situation are the drug companies, the hospital industry, vascular surgeons and cardiologists. Do you think any of these folks are going to tell you what I am telling you about ascorbate and heart disease? Would you cut off your income, given the opportunity. No you would not. If you were even sufficiently up-to-date with the current scientific literature to know these things, you would develop doubts and rationalizations about the research demonstrating the relationship between heart disease and anything which the public could control on its own. You would then believe your own doubts and rationalizations. In your own private life, you would load up on ascorbate everyday, just in case.
If you have vascular disease, and if you want not to have it, there is a plan for you.
- Get yourself into chelation therapy and stay the course. This is the fastest, most proven method of dealing with this life-threatening condition. The literature proving this is extensive, despite what uninformed doctors may tell you. Then, in consultation with a doctor who practices nutritional medicine, take the following steps: (All the following dosages may be adjusted by your doctor, based on his or her experience and medical opinion.)
- Vitamin C to bowel tolerance — as much as you can take without diarrhea. For most people this will be in the range of five to ten grams (5,000-10,000 mg.) each day. Spread this amount into two equal doses 12 hours apart. (Vitamin C prevents further cracking of the blood vessel wall — the beginning of the disease.)
- Co-enzyme Q10 90-180 mg. twice each day (strengthens the heart muscle).
- L-carnitine 3 grams twice each day (also strengthens the heart muscle).
- L-lysine 3 grams twice each day (acts to release lipoprotein(a) from plaque formation and prevent further deposition of same).
- L-proline 3 grams twice each day (acts to release lipoprotein(a) from plaque formation and prevent further deposition of same).
- Niacin decreases the production of lipoprotein(a) in the liver. Inositol hexaniacinate is a form of niacin which gives less of a problem with flushing and therefore allows for larger therapeutic doses. Begin with 250 mg. at lunch, 500 mg. at dinner and 500 mg. at bedtime the first day; then increase gradually over a few days until you reach four grams per day, or the highest dose under four grams you can tolerate. Be sure to aks your doctor for liver enzyme level tests every two months or less to be sure your liver is able to handle the dose you are taking.
- Vitamin E (as Unique E) 800-2400 IU per day. (This inhibits the proliferation of smooth muscle cells in the walls of arteries undergoing the atherosclerotic changes.)
- Stop smoking. (This decreases the free radical load on your body.)
- Adopt a sensible diet with plenty of veggies and not so much fat. (The metabolism of fat decreases your body vitamin pool dramatically.)
- Ask your doctor for a comprehensive stool analysis (Great Smokies Lab) to see if you are digesting well all that good food. Your diet does not matter much if it is not getting into your body.
- Lower stress in your life however you can.
- Adopt a sensible exercise program in collaboration with your doctor.
- Rath M, Niendorf A, Reblin T, Dietel M, Krebber H-J, and Beisiegel U Detection and quantification of lipoprotein(a) of the atertial wall of 107 coronary bypass patients. Arteriosclerosis 9:579-92 (1989)
- Rath M and Pauling L Hypothesis: Lipoprotein(a) is a surrogate for ascorbate Proceedings of the National Acad of Sciences USA 87:6204-07 (1990a), ,Rath M and Pauling L Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig Proceeding of the National Academy of Sciences USA 87:9388-90 (1990b)
- Rath M and 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. J of Orthomolecular Med 6:125-34(1991a)
- Rath M and Pauling L Apoprotein(a) is an adhesive protein J of Orthomolecular Med 6:139-43(1991b)
- Rath M and Pauling L A unified theory of human cardiovascular disease leading the way to abolition of this disease as a cause for human mortality J of Orthomolecular Med 7:5-15(1992a)
- Rath M and Pauling L Plasma induced proteolysis and the role of lipoprotein(a), lysine and synthetic lysine analogs J of Orthomolecular Med 7:17-23(1992b)
- Rath M Lipoprotein(a) reduction by ascorbate J of Orthomolecular Med 7:81-2(1992c)
- Rath M Solution to the puzzle of human evolution J of Orthomolecular Med 7:73-80(1992d)
- Rath M Reducing the risk for cardiovascular disease with nutritional supplements J of Orthomolecular Med 7:153-62(1992e)
- Rath M Cationic-anionic and anionic-cationic oligopeptides in apoprotein(a) and other proteins as modulators of protein action and of biological communication J of Applied Nutrition 44:62-9(1992f)
- Rath M Discovery of new elements of biological communication leading the way to the abolition of infectious diseases, cancer and other diseases as causes of human mortality J of Orthomolecular Med 8:11-20(1993)