Essay: Nutritional Approach
Essay: Nutritional Approach
Note 1: This essay is a condensation of my “book in progress” entitled A Nutritional Approach to the Prevention and Cure of Cardiovascular Disease. It details the creation of the Pauling Therapy, an innovative approach to the treatment of coronary artery disease. It is my hope that this will provide you with further information, such as the cause of plaque in arteries, and why my method for cholesterol reduction works.
Note 2: I have embedded the references within the text, rather than use the standard footnote format, because the conclusions drawn from some of the cited studies are so astounding that I want it to be as obvious as possible that (as Dave Barry would say), “I am not making this up.”
--Ray Ellis
Acute scurvy is a nasty disease. Your body literally falls apart. Your joints wear out and your tendons shrivel. Your blood vessels grow thin and start to leak, causing severe bruising. Your teeth first loosen, then fall out as your gums and the connective tissues holding your teeth in place erode. Your organs loose their structural strength and begin to dissolve. Eventually, when enough blood leaks from your vascular system into your body cavities, your heart – with nothing left to pump – simply stops, and you (mercifully) die. And this takes only 3 – 4 months!
The earliest written reference to scurvy is in the Ebers Papyrus, an ancient Egyptian medical scroll dated to about 1500 BC. The hieroglyph is a figure of a kneeling man pointing to his mouth with bleeding gums.
Hippocrates (about 400 BC) described a disease that sounds much like scurvy.
Pliny the Elder (AD 23-79), in his Natural History , describes a disease of Roman soldiers in Germany that seems like scurvy. The plant herba Britannica was said to be the cure.
But our history lesson really starts when the first sailing ships left port on voyages of months at a time. Sailors everywhere considered acute scurvy to be nothing less than a plague. Case in point: in 1519, Magellan set sail with a fleet of 5 ships to circumnavigate the globe. Three years later, he returned to Spain with one ship that had only 18 crew members. At the beginning of the 1700′s acute scurvy was killing tens of thousands of sailors annually in the British Royal Navy (the largest navy at the time).
As early as 1593, Admiral Sir Richard Hawkins, during a voyage to the South Pacific, protected the crew of the Dainty from scurvy. How? He noted in his journal, “That which I have seen most fruitful for this sicknesse, is sower oranges and lemmons.” He made this observation known to the Admiralty but they did not act upon it.
In 1601, Commodore James Lancaster unintentionally conducted a controlled study that demonstrated that lemon juice can prevent scurvy. His fleet of four ships left port on April 21, 1601. Lancaster’s ship was the only one to have been provisioned with bottles of lemon juice. He gave 3 spoonfuls of lemon juice to each seaman on his ship every morning.
By August 1 (4 months after sailing) scurvy had set in on the three ships without lemon juice. The men on Lancaster’s ship saw no signs of scurvy. By the time of arrival, September 9, the three ships were so devastated by scurvy that the men of Lancaster’s ship had to assist the rest of the fleet into the harbor. The Admiralty received Lancaster’s report but did not act upon it.
In 1636 John Woodall, a famous medical doctor, published a book entitled, The Surgeon’s Mate. In this book he wrote, “The juyce of lemmons is a precious medicine and well tried; being sound and good . . . It is to be taken each morning two or three teaspoonfuls . . .” Every British ship’s surgeon had a copy of this book. It would seem, however, that they paid little attention to its nutritional advise.
Then, in 1747, James Lind a young surgeon’s mate set sail on the H.M.S. Salisbury. Lind had seen the ravages of scurvy on his previous voyages and was determined to do something about it. Lind did something extraordinary. He took twelve seamen suffering from scurvy and divided them up into six groups of two men each. In addition to their regular diet, he gave each group a different common treatment for scurvy. Only one group got better: the one which received lemons and oranges. Lind had successfully conducted the very first, properly controlled, clinical therapeutic trial on record. He announced the results of his research to the Admiralty but they did not act upon it.
In 1748 Lind left the Royal Navy to pursue a career in medicine. He continued his work on scurvy and in, 1753 he published what is now a classic of medical literature, A Treatise of the Scurvy. In this book he wrote, “Experience indeed sufficiently shows, that as greens or fresh vegetables with ripe fruits, are the best remedies for it, so they prove the most effective preservative against it.” The Admiralty was aware of this book and Dr. Lind’s conclusions, but they did not act upon them.
One sea captain did take his advice, however. Captain James Cook stocked all his ships with supplies of fresh fruits, vegetables and sauerkraut and replenished these supplies whenever he made landfall. On his famous round-the-world voyage, Captain Cook lost only one man of his crew of 118 (not from scurvy). He was so successful that The Royal Society honored him in 1776 by awarding him the Copley Medal.
But it was not until 1794, that one navy squadron was supplied with lemon juice before a voyage. On that voyage, which lasted twenty-three weeks, not one sailor came down with scurvy. Still, it took the British Admiralty till 1804 before regulations were enacted requiring sailors to drink a daily ration of lemon juice. With this enactment, scurvy became a thing of the past for the British sailor.
At the time, the word “Lime” was used for both lemons and limes. This is why English sailors, even to this day, are called “Limeys.”
It is interesting to note that it took 211 years between the time that Admiral Hawkins informed the admiralty that citrus fruits prevented scurvy and the implementation of a daily ration of lemon juice. It is estimated that a total of 2 million sailors died of scurvy during this period of time.
Roddis, Louis H. (1941), A Short History of Nautical Medicine. New York, London, P. B. Hoeber, Inc.
Mark R. Anderson, M.D. (2000), A Short History of Scurvy, www.riparia.org/scurvy_hx.htm.
Stone, Irwin (1972) The Healing Factor: Vitamin C Against Disease, Grosset & Dunlap , New York.
In 1926, S. B. Wolbach and P. K. Howe, discovered that guinea pigs with scurvy were unable to produce collagen within their intercellular matrix. They also discovered that this inability to produce collagen could be reversed by adding citrus fruits to the guinea pig’s diet.
Wolbach, S. H., and Howe, P. K., (1926), Intercellular Substances In Experimental Scorbutis, Arch. Pathol. Lab. Med. 1:1-24.
Because collagen is a very important substance in your body. Collagen is the most abundant protein in your body. More than a third of your body’s protein is collagen. Collagen is a structural protein that provides the scaffolding for your body. Collagen controls the shape of every cell in your body. Your bones and teeth are made by trapping calcium crystals within a matrix make of collagen. Collagen forms itself into long, white fibers that strengthen tendons and cartilage. Collagen forms itself into sheets to protect and support softer tissues such as the lining of your organs. When you get cut, it’s collagen that glues the tissues back together again (scare tissue is 100% collagen). Your skin is 75% collagen. Collagen is the major connective tissue in your body; it – in essence – holds your body together.
As important as collagen is, it actually has a fairly simple chemical structure. It is composed of only three amino acids: glycine, proline and lysine. The glycine and proline form polypeptide chains that twist around each other like the strands of a rope. These strands are “glued” together with cross-linkages of the amino acid lysine. This ropelike structure makes collagen a very strong molecule with a tensile strength greater than steel wire!
Because collagen is so pervasive in your body and so necessary for life, your body devotes a lot of time, energy and resources to manufacturing it in sufficient quantities. In his book,How To Live Longer And Feel Better, Dr. Linus Pauling called the body’s production of collagen a “major manufacturing enterprise.”
Collagen gives your blood vessels their form, strength and flexibility. Your blood vessels are made up of 3 different layers. The inner layer is a membrane of endothelium cells (similar to skin cells) which is held in place by a sheet of collagen. The middle layer is made of smooth muscle held in place by a network of collagen fibers that run lengthwise. The outer layer is made up of collagen fibers that encircle the blood vessel. Even the smallest capillaries have a thin layer of collagen. If they didn’t, the endothelium cells would have nothing to adhere to and they would simply float away.
Collagen makes your blood vessels both strong and flexible. Because arteries are closer to the heart than veins they need to be able to expand and contract in rhythm with your beating heart. This expanding and contracting is what you feel when you “take your pulse” by putting your fingers on your wrist or on the side of your neck. What you feel is the expanding and contracting of your radial artery (wrist) or carotid artery (neck).
I remember, many years ago, cutting up a section of old garden hose in order to use it to help brace a newly planted tree. I was surprised to notice that the hose was made up of 3 layers. The outer layer was pretty tough, the inner layer was made of a softer rubber, and between these two layers were strands of fiberglass running in counter-directional spirals throughout the length of the hose. It was those strands of fiberglass that gave the hose both its strength and flexibility.
So, it was S. H. Wolbach and P. K. Howe, way back in 1926, who discovered that guinea pigs got scurvy BECAUSE their cute, little, furry bodies stopped producing collagen. And when they stopped producing collagen, their blood vessels lost their structural integrity and started to leak. When citrus was put back into the diet, their cute, little, furry bodies went back to producing collagen, healed their blood vessels, and made them healthy little critters again.
It was not until 1932, however, that W. A. Waugh and C. G. King at the University of Pittsburgh and Alvert Szent-Gyorgyi, a Hungarian scientist, isolated and synthesized the chemical in citrus fruits that enables them to cure and prevent scurvy. They called it Ascorbic Acid. It is more commonly know as Vitamin C. For their discovery, these gentlemen were awarded a Nobel Prize in Chemistry.
It was common knowledge in the 1930′s that Vitamin C was essential to a healthy cardiovascular system, as the following quote from The Food and Life Yearbook (U.S. Department or Agriculture, 1939, pg 236) attests:
“Even when there is not a single outward symptom of trouble, a person may be in a state of vitamin C deficiency more dangerous than scurvy itself. When such a condition is not detected, and continues uncorrected, the teeth and bones will be damaged, and what may be even more serious, the blood stream is weakened to the point where it can no longer resist or fight infections not so easily cured as scurvy.”
Shortly after Vitamin C was discovered many more guinea pigs were subjected to the indignities of experimentation (brave little critters!) in order to prove that scurvy was a disease brought on by a deficiency of Vitamin C.
Between 1937 and 1944, the studies conducted by T. H. Lanman & T. H. Ingalls, H. A. Hunt, M. Bartlett et al., and G. H. Bourne all proved beyond a shadow of a doubt, that when you subject guinea pigs to a diet that is lacking in Vitamin C, they get scurvy, usually within a few short weeks. And when Vitamin C is reintroduced into the diet, the scurvy goes away, usually within a few short weeks.
Lanman, T. H., Ingalls, T. H. (1937) Tensile Strength Of Healing Wounds Is Lowered In The Presence Of Scurvy Plasma Levels, American Surgery, Vol. 105, 616.
Hunt, H. A. (1940) The Role Of Vitamin C In Wound Healing, British Journal of Surgery 28:111, 436-461.
Bartlett , M., Jones, C. M., and Ryan, A. E. (1942). Vitamin C and Wound Healing. II. Ascorbic Acid Content and Tensile Strength of Healing Wounds in Human Beings. New England Journal of Medicine 226:12, 474-481, March.
Bourne, G. H. (1944) Effect Of Vitamin C Deficiency On Experimental Wounds. Tensile Strength And Histology, Lancet 1:688-692.
You may be wondering why all these researchers were using guinea pigs. It wasn’t just because they were handy. You see, guinea pigs and humans are alike in one very special way. Neither guinea pigs nor humans can manufacture Vitamin C within their livers. Most other animals produce Vitamin C (in large amounts) in their livers, but you (and guinea pigs) can’t. This means that you have to get all of your Vitamin C from your diet. This makes guinea pigs good test subjects when investigating diseases caused by a lack of Vitamin C in the diet. (Besides, they are awfully cute!)
In the 1930′s a number of researchers began to wonder if a lack of Vitamin C could be involved in the development of atherosclerotic plaque deposits on the inside of the coronary arteries. J. F. Rineheart & S. R. Mettier, M. L. Menten & C. G. King, and S. Taylor all conducted research that correlated low levels of Vitamin C in the diet with atherosclerosis.
Rineheart, J. F. & Mettier, S. R. (1934) The Heart Valves and Muscle in Experimental Scurvy with Superimposed Infection, American Journal of Pathology, vol. 10, 61-79.
Menten, M. L. & King, C. G. (1935) The Influence of Vitamin C Level upon Resistance to Diptheria Toxin, Journal of Nutrition, vol. 10, 141-153.
Taylor, S. (1937) Scurvy and Carditis, Lancet, Vol. 1, 973-979.
Because of this research Dr. W. Evans pointed out the need for, “an adequate supply of vitamin C for all patients with heart failure.”
Evans, W. (1938) Vitamin C in Heart Failure, Lancet, Vol. 1, 308-309.
Then in 1941, Dr. Paterson measured the level of Vitamin C in the blood of 455 consecutive adult patients admitted to the Ottawa Civic hospital. He found that 56% had subnormal levels of Vitamin C (below 0.5 mg/dl) and that 81% of the coronary patients were in the subnormal range. In his paper, Dr. Paterson recommended that “patients with coronary artery disease be assured of an adequate vitamin C intake.”
Paterson, J. C. (1941) Some Factors In The Causation Of Intimal Hemorrhages And In The Precipitation Of Coronary Thrombi, Canadian Medical Association Journal, Feb, 114-120.
And in 1948, R. W. Trimmer and C. J. Lundy duplicated Paterson’s results in a private hospital in America with wealthy patients. They found that 42% of all patients, 59% of heart patients, and 70% of the coronary thrombotic patients had low blood levels of Vitamin C. In fact, 65% of the coronary group had dangerously low levels of Vitamin C. Again, Trimmer & Lundy urged their fellow doctors to use Vitamin C therapy as an adjunct to the usual methods of treating heart patients.
Trimmer, R. W. & Lundy, C. J. (1948) A Nutrition Survey in Heart Disease, American Practitioner, Vol. 2, 448-450.
In 1948 Sir Hans Adolf Krebs, an English medical doctor, conducted an amazing experiment with healthy volunteers between the ages of 20 and 30 years. Dr. Krebs decided to see what would happen if he placed healthy, young people on a diet that was lacking in Vitamin C. The result: half of his volunteers had heart attacks! Fortunately, none of them died. Also, fortunately, the experiment was discontinued. Dr. Krebs reported that, after going back to eating a normal diet, all of his volunteers seemed to have suffered no more ill effects. (Lest you think Dr. Krebs was a wacko: he won the Nobel Prize in Chemistry in 1953 for his work on the Citric Acid Cycle; AKA – the Krebs Cycle!)
Krebs, H. A. (1948) The Sheffield Experiment on the Vitamin C Requirement of Human Adults, Lancet, Vol. 1, 835.
In 1946 Dr. J. B. Duguid, apparently unwilling to experiment on his students, went back to using (yes, you guessed it) guinea pigs. This time Dr. Duguid did something different. Instead of just eliminating Vitamin C from the guinea pigs’ diet, he gradually reduced it over an extended period of time. After a few months his guinea pigs developed atherosclerotic plaque deposits within their coronary arteries. Upon close examination, it was discovered that these plaque deposits were identical to the deposits that form in human coronary arteries.
Duguid, J. B. (1946) Thrombosis As A Factor In The Pathogenesis Of Coronary Atherosclerosis, J Pathol Bacteriol, 58:207-212.
So, it would seem that atherosclerosis is just another form of Vitamin C deficiency. It’s similar to scurvy in that it effects the cardiovascular system, but it’s slower and more progressive. So, perhaps, instead of calling it atherosclerosis, we should call it Chronic Scurvy!
But why, you might ask, does plaque accumulate in the coronary arteries? Canadian Doctor G. C. Willis was asking this same question back in 1953. Dr. Willis conducted an animal study to determine the effect of mechanical stress on the lining of the coronary arteries in two groups of animals: one eating a diet rich in Vitamin C, and the other eating a diet with sub-optimal levels of Vitamin C. In the group with sub-optimal levels of Vitamin C, lesions appeared in the lining of the coronary arteries at the point of greatest mechanical stress (repeated stretching). He noticed that it was only AFTER these lesions appeared that plaque began to accumulate. Willis concluded that, “Massive doses of ascorbic acid [Vitamin C] may be of therapeutic value in the treatment of atherosclerosis.”
Willis, G. C. (1953) An Experimental Study Of The Intimal Ground Substance In Atherosclerosis, Canadian Medical Association Journal, 69:17-22.
In 1940, a brave researcher named J. H. Crandon decided to experiment, not on guinea pigs or volunteers, but on himself. After eating a diet that was reduced in Vitamin C content for six months, he underwent a skin incision on his forearm. The wound failed to heal properly.
Crandon, J. H.; Lund, C. C.; Dill, D. B. (1940) Experimental Human Scurvy, New England Journal of Medicine, 223:353.
Similar results were later confirmed by Wolfer and coworkers in 1947. Between 1947 and 1953 many such investigations were conducted. In a review article written by Robertson and Schwartz the conclusion was clear. The reason the wounds did not heal properly in people experiencing sub-optimal intake of Vitamin C, was an impaired ability to synthesize and lay down enough collagen. Proper healing can not occur unless your body can make enough collagen to “glue” the tissues back together again.
Wolfer, J. A., Farmer, C. J., Carroll, W. W., and Manshardt, D. O. (1947) An Experimental Study in Wound Healing in Vitamin C Depleted Human Subjects, Surgery, Gynecology and Obstetrics 84:1, 1-15, January.
Robertson, W. B., and Schwartz, B. (1953) Ascorbic Acid And The Formation Of Collagen, Journal of Biological Chemistry, 201:689-696.
Remember our discussion of the structure of collagen? Collagen is made from procollagen. There are actually 14 different types of collagen in the human body. All of them are manufactured from procollagen. Procollagen is made by combining the two amino acids glycine and proline along with cross linkages of the amino acid lysine. In order to get these amino acids to link up correctly your body has to catalyze a chemical reaction that substitutes a hydroxyl group (OH), for a hydrogen atom (H). This chemical reaction is called hydroxylation.
The Vitamin C molecule is what contributes the hydroxyl group (OH) to the whole equation. Giving up the hydroxyl group destroys the Vitamin C molecule. In other words, your body has to use up (consume) Vitamin C in order to manufacturer collagen. So, If you don’t consume enough Vitamin C to manufacture enough collagen, eventually the structural integrity of your blood vessels will become compromised.
Myllyla R., Kuutti-Savolilanin, E. R., and Kivirikko, K. I. (1978) The Role Of Ascorbate In The Prolyl-Hydroxylase Reaction, Biochem. Biophys. Res. Commun. 83:441-448.
Myllyla R., Majamaa K., Gunzler V., Hanuska-Abel H. M. and Kivirikko K. I. (1984) Ascorbate Is Consumed Stoichiometrically In The Uncoupled Reactions Catalyzed By Prolyl-4-Hydroxylase And Lysyl Hydroxylase, Journal of Biological Chemistry, 259:5403-5405.
Dr. Anthony Verlangieri at the University of Mississippi ‘s Atherosclerosis Research Laboratory discovered another way that Vitamin C deficiency contributes to atherosclerosis. Dr. Verlangieri demonstrated that both Vitamin C and Vitamin E are required for the synthesis of a substance called glycosaminoglycan (GAG). GAG is a crucial ingredient in the “cement” that holds the arterial endothelium cells in place. A dietary deficiency of Vitamin C & E leads to the deterioration of the artery’s lining, eventually resulting in arterial lesions.
Verlangieri, A. J. & Stevens, J. W. (1979) L-Ascorbic Acid: Effects on Aortic Glycosaminoglycan S Incorporated in Rabbit Induced Atherogenesis Blood Vessels. 16(4): 177-85.
Verlangieri, A. J. & Sestito, J (1981) Effect of Insulin on Ascorbic Acid Uptake by Heart Endothelial Cells: Possible Relationship to Retinal Atherogenesis, Life Sciences, 29, 5-9.
Verlangieri, A. J., Bush, M. J. & Kapeghian (1984) Duplex Ultrasound Analysis of the Carotid Arteries in Macaca Fascicularis [monkeys], J. Card. Ultrason. Vol. 2 (4): 293-302.
Verlangieri, A. J. (1985) The Role of Vitamin C in Diabetic and Nondiabetic Atherosclerosis, Bulletin, Bureau of Pharm. Services. Univ. Miss. Vol 21.
Your body recognizes these lesions as a bad thing and tries to repair the damage. If your body can not manufacture enough collagen or GAG due to a vitamin deficiency, it does the next best thing. It repairs the damage using selective raw materials that are readily available (free-floating in the bloodstream): LDL cholesterol, calcium, and a sticky, fibrous substance called fibrinogen (the scab that forms on you skin when you are cut is mostly fibrinogen). Your body, in essence, places a patch over the damaged portion of the artery in much the same way as a homeowner would fix a crack in a bathtub with a patch of fiberglass and resin.
If you have plaque deposits in your coronary arteries, you should be thankful for your body’s ingenuity. Why? Because these plaque deposits have been keeping your cardiovascular system from springing a leak! Which is better: To suffer from atherosclerosis or to be dead?
But, as we all know, this life-saving plaque can cause problems of its own. If your Vitamin C deficiency continues, your blood vessels will continue to deteriorate, and your body will have no choice but to place thicker and thicker patches on your damaged arteries. When the plaque deposits grow thick enough, they can significantly restrict the blood flow to your heart and cause Angina pain, or can block the flow of blood entirely and cause a heart attack.
Remember Dr. Duguid and his guinea pigs back in 1949? He gradually reduced the level of Vitamin C in their diet and they developed atherosclerosis. But he didn’t stop there. He then slowly raised the level of Vitamin C back to normal. When he did this, a very interesting thing happened: the atherosclerotic plaque deposits went away. They simply disappeared!
And remember Dr. Willis? He conducted a study at Queen Mary Veterans’ and St. Anne’s Hospitals. He took patients suffering from atherosclerosis and divided them into two groups. One group got no treatment and the other was given 1500 mg of Vitamin C per day. After a year, the atherosclerotic plaque deposits in the control group either stayed the same (50%) or grew larger (50%). In contrast, the plaque deposits in the patients who were getting the Vitamin C actually decreased in 30% of the cases. This was the first time in history that any treatment had demonstrated a REVERSAL in the growth of atherosclerotic plaque deposits in human beings!
Willis, G. C. (1957) The Reversibility of Atherosclerosis, Canad. Med. Ass. J., 77:106-109.
And Willis was not the only researcher to obtain these results. K. R. Sebrov in Russia, W. J. McCormick, R. O. Mumma at Rutgers University, G. C. Ginter, Raiforth (Shute 1969) and C. R. Spittle all demonstrated that, in both animals and humans, when Vitamin C levels are elevated, atherosclerotic plaque deposits begin to disappear.
And in 1974, Drs. C. Krumdieck and C. E. Butterworth obtained a 60% reduction of plaque deposits using nothing but Vitamin C.
Sebrov, K. R. (1956) Prophylaxis and Treatment of Arteriosclerosis with Ascorbic Acid, Terapevticheskii Arkhiv (Moskva), vol. 28, 55-65.
McCormick, W. J. (1957) Coronary Thrombosis: A New Concept of Mechanism and Etiology, Clinical Medicine, 839-845.
Mumma, R. O. (1968) Ascorbic Acid as a Sulfating Agent, Biochimica et Biophysica Acta, Vol. 165, 571-573.
Mumma, R. O. & Verlangieri, A. J. (1971) In Vivo Sulfation of Cholesterol by Ascorbic Acid 3-Sulfate as a Possible Explanation for the Hypocholestemic Effects of Ascorbic Acid, Federation Proceedings, Vol. 30, No. 2.
Ginter, E. et al (1969) The Effect of Chronic Hypovitaminosis C on the Metabolism of Cholesterol and Atherogenesis, Journal of Atherosclerosis Research, Vol. 10, 341-352.
Shute, Evan (1969) Your Heart & Vitamin E, London , Canada : The Shute Foundation for Medical Research.
Shute, Wilfrid E. (1969) Vitamin E for Ailing and Healthy Hearts, New York : Pyramid House.
Spittle, C. (1971) Atherosclerosis and Vitamin C, Lancet, 11:1280-1281.
Krumdieck, C., and Butterworth, C. E., Jr. (1974) Ascorbate-Cholesterol-Lecithin Interactions: Factors of Potential Importance in the Pathogenesis of Atherosclerosis, American Journal of Clinical Nutrition, 27: 866-876, August.
Then in 1963, Kare Berg in Oslo, Norway discovered a very sticky form of Low Density Lipoprotein (LDL) in human blood plasma and called it Lipoprotein (a) – Lp(a) for short. The “a” stands for adhesive.
Berg, K. & Mohr, J. (1963) Genetics of the Lp System, Acta Genet. 13(4): 349-360.
In the early Eighties, two studies demonstrated that the calcium component of the plaque deposit could be dissolved with high doses of Vitamin C. It appears that Vitamin C is involved in the chelation of the calcium ions in the plaque deposit and the transportation of the calcium ions to the kidneys where they can be excreted.
Horsey, J., Livesley, B and Dickerston, J. W. T. (1981) Ischaemic Heart Disease and Aged Patients: Effects of Ascorbic Acid on Lipoproteins, Journal of Human Nutrition, 35:53-58.
Geoly, K. and Diamond, L. H. (1980) Ascorbic Acid and Hypertriglyceridemia, Ann. Int. Med. 93:551.
And Vitamin C isn’t the only nutrient that can help with Angina and Heart Disease. In 1985, T. Kamikawa published the results of a double-blind, placebo-controlled, crossover study on the effect of coenzyme Q10 on Angina Pectoris pain. After 4 weeks of oral supplementation with CoQ10 there was a reduction in anginal frequency and nitroglycerin use and an increase in exercise time and time to ST-segment depression.
Kamikawa, T. et al (1985) Am J Cardiol, August 1, 56 :247-251.
Another nutrient that is proven to help with Angina pain is L-carnitine, another amino acid necessary for life. In 1985, A. Cherchi et al conducted a double-blind, placebo-controlled trial of 44 patients with stable chronic angina, where subjects received either L- carnitine at 1 g, twice daily, or a placebo. The L-carnitine group showed an increase in exercise workload and an increase in the watts to onset of angina. 22.7% became free of angina compared with 9.1% in the placebo group.
Cherchi, A. et al (1985) Int J Clin Pharmacol Ther Toxicol, 23 (10), 569-572.
The 1985 Nobel Prize in Medicine was awarded to Michael S. Brown and Joseph L. Goldstein, of the University of Texas Southwestern Medical Center at Dallas, for their discovery that – when a lesion occurs in the endothelium of a blood vessel – certain “Lysine Binding Sites” are exposed to the blood. They also discovered that it is Lp(a) (and not ordinary LDL cholesterol) that initially binds to the damaged blood vessel.
This discovery caused quite a commotion and prompted more research to be conducted on the relationship between Lp(a) and atherosclerosis.
In the latter half of the 1980′s V. W. Armstrong et al., G. H. Dahlen et al., G. Zenker et al., L. A. Miles et al., and H. Hoff et al. – to name just a few – documented that high levels of Lp(a) in the bloodstream are associated with a high incidence of cardiovascular disease.
Armstrong, V. W., Creamer, P., Eberle, E., Manke, A., Schulze, F., Wieland, H., Kreuzer, H. & Seidel, D. (1986) The Association Between Serum Lp(a) Concentrations and Angiographically Assessed Coronary Atherosclerosis, Atherosclerosis, 62:249-257.
Dahlen, G. H. et al. (1986) Association of Levels of Lipoprotein Lp(a), Plasma Lipids, and Other Lipoproteins with Coronary Artery Disease Documented By Angiography, Circulation, 74(4): 758-765.
Zenker, G., Koltringer, P., Bone, G., Niederkorn, K., Pfeiffer, K & Jurgens, G. (1986) Lipoprotein(a) as a Strong Indicator for Cerebrovascular Disease, Stroke, Vol 17, 942-945.
Miles, L. A. et al. (1989) A Potential Basis for the Thrombotic Risks Associated with Lipoprotein(a), Nature, 339:301-302.
Hoff, H. et al. (1988) Serum Lp(a) Level As A Predictor Of Vein Graft Stenosis After Coronary Artery Bypass Surgery In Patients, Circulation, 77(6):1238-1244.]
In 1987, P. F. Jacques et al. tested the relationship between Vitamin C (plasma and dietary) and plasma HDL cholesterol in a population of 235 males and 445 females, age 60-98 years. The results show that both dietary and plasma Vitamin C levels are significantly correlated with HDL. The higher the Vitamin C level in the diet, the higher the HDL level in the blood. This is important because HDL transports fat molecules from the artery walls and carries them to the liver for removal.
Jacques, P. F., Hartz, S. C., McGandy, R. B., Jacob, R. A., Russell, R. M. (1987) Ascorbic Acid, HDL, And Total Plasma Cholesterol In The Elderly, J Am Coll Nutr. Apr;6(2):169-74.
Then, in 1989 & 1990, studies by Dr. Matthias Rath et al., G. L. Cushing et al., and A. Niendorf et al, determined that it was indeed Lp(a), and not ordinary LDL cholesterol, that was clogging the coronary arteries.
Rath, M., Niendorf, A., Reblin, T., Dietel, M., Krebber, H-J, and Beisiegel, U. et al. (1989) Detection And Quantification Of Lipoprotein(A) In The Arterial Wall Of 107 Coronary Bypass Patients, Arteriosclerosis, 9(5):579-592.
Cushing, G. L. et al. (1989) Quantitation And Localization Of Apolipoproteins [A] And B In Coronary Artery Bypass Vein Grafts Resected At Re-Operation, Arteriosclerosis, 9(5):593-603.
Niendorf, A., Rath, M., Wolf, K., Peters, S., Arps, H., Beisiegel, U. and Dietel, M. (1990) Morphological Detection and Quantification of Lipoprotein(a) Deposition in Atheromatous Lesions of Human Aorta and Coronary Arteries, Virchow’s Archive Pathol Anat 417: 105-111.
Beisiegel, U., Niendorf, A., Wolf, K., Reblin, T. and Rath, M. (1990) Lipoprotein(a) in the Arterial Wall, European Heart Journal 11 (Supp. E): 174-83.
And in the same year, studies by K. A. Hajjar et al. and E. M. Salonen et al. showed that Lp(a) can, not only attach itself to the Lysine Binding Sites of damaged coronary arteries, but is also involved in the deposition of fibrinogen (the beginning of plaque formation).
Hajjar, K. A. et al. (1989) Lipoprotein(A) Modulation Of Endothelial Cell Surface Fibrinolysis And Its Potential Role In Atherosclerosis, Nature, 339: 303-305.
Salonen, E-M, et al. (1989) Lipoprotein(A) Binds To Fibronectin And Has Serine Proteinase Activity Capable Of Cleaving It, EMBO J. 8(13):4035-4040.
And again in 1989 (a very productive year), P. Harpel et al. discovered that lysine binds to the free-floating Lp(a) in the blood and thereby prevents it from attaching itself to the lysine binding sites of the damaged artery.
Harpel, P. C., Gordon, B. R. & Parker, T. S. (1989) Plasminogen Catalyzes Binding Of Lipoprotein(A) To Immobilized Fibrinogen And Fibrin, Proc. Natl. Acad. Sci. USA 86:3847-3851.
Gonzalez-Gronow et al. also found that lysine binds to the lysine binding sites exposed by the damaged artery, thereby preventing Lp(a) from doing so.
Gonzalez-Gronow, M., Edelberg, J. M. and Pizzo, S. V. (1989) Further Characterization Of The Cellular Plasminogen Binding Site: Evidence That Plasminogen 2 And Lipoprotein(A) Compete For The Same Site, Biochemistry, 28:2374-2377.
These two studies strongly suggested that lysine, taken as a supplement, could PREVENT THE DEPOSITION OF PLAQUE – AND MAY EVEN HELP TO DISSOLVE IT!
A study by Greenberg and Frishman found that 150 mg of CoQ-10 reduced the frequency of angina attacks by up to 46%, while improving the capacity for physical activity in those patients.
Greenberg, S, & Frishman, W. H. (1990) Co-Enzyme Q10: A New Drug For Cardiovascular Disease, Journal of Clinical Pharmacology, 30[July] (7).
Dr. Linus Pauling was so impressed with Dr. Rath’s work at the University of Hamberg, Germany and at the German Heart Center in Berlin that he invited him to come to America and continue his work at the Linus Pauling Institute of Science and Medicine. And in 1990, Dr. Rath became Director of Cardiovascular Research at the Institute. It didn’t take very long for them to get down to work!
At the 1990 Proceedings of the National Academy of Sciences USA (87:6204-6207), Drs. Pauling and Rath presented a paper entitled, Hypothesis: Lipoprotein(A) Is A Surrogate For Ascorbate [Vitamin C] wherein they suggested that, since a body deficient in Vitamin C can not produce enough collagen to repair damaged coronary arteries, it does the next best thing: it sends a very sticky form of LDL – Lp(a) – and fibrinogen to put a patch over the lesions.
The same year, Pauling and Rath published their research with guinea pigs that demonstrated that Vitamin C deficient guinea pigs develop atherosclerotic plaque deposits and that these deposits consist of Lp(a) and fibrinogen.
Rath, M. & Pauling, L. (1990) Immunological Evidence For The Accumulation Of Lipoprotein(A) In The Atherosclerotic Lesion Of The Hypoascorbemic Guinea Pig, Proceedings of the National Academy of Sciences USA, 87: 9388-9390.
Also in 1990, Rath and Pauling were granted a U. S. Patent (No. 5278189) on their Lp(a) binding inhibitors. Here’s a quote from the patent:
“We have also discovered substances that inhibit the binding of Lp(a) to components of the arterial wall, particularly to fibrinogen, fibrin and fibrin degradation products herein identified as binding inhibitors, such as lysine or .epsilon.-aminocaproic acid used alone or in combination with ascorbate, cause release of Lp(a) from the arterial wall. Thus, ascorbate and such binding inhibitors are not only useful for the prevention of occlusive cardiovascular disease, but also for the treatment of such disease. The present invention, then, provides methods and pharmaceutical agents for both the treatment and the prevention of occlusive cardiovascular disease.”
These binding inhibitors included Vitamins C & E, Beta-Carotene, Lysine, and Benzoic Acid.
In the June 1991 issue of the Journal of Orthomolecular Medicine, Pauling and Rath published 3 papers. The first was a remarkable case report, written by Pauling, detailing the elimination of Angina Pectoris pain in a man with severe coronary artery disease (CAD). Here are some quotes from the report:
“In late April 1991, a biochemist National Science Medalist with a familial trait of CAD told me that he experiences effort angina, in spite of medication and three coronary bypass operations. His father and a brother both died of CAD at age 62 and he had his first angina attack at age 38. Now aged 71 . . . His first operation in 1978 (two vein grafts and one LIMA graft) precipitated a second operation (a parallel vein graft) five months later. . . A third operation in April 1990 followed attacks of unstable angina, a small MI, and angiography that revealed total occlusion of his right coronary artery and all bypass grafts except for a patent LIMA graft. . .
“Medication with beta-receptor and calcium-channel blockers and lovastatin was reinstated . . . To this medication, he added 6 g of ascorbate [Vitamin C] (acid form), 60 mg CoQ-10; a multivitamin tablet with minerals; additional vitamins A, E and a B-complex; lecithin; and niacin . . . Nevertheless, he still had to take nitroglycerin sublingually to suppress angina during a daily two mile walk and when working in his yard. This effort angina continued to worsen, imparting a feeling of impending doom that was reinforced by his cardiologist’s admonition during a check-up in March 1991 that a fifth angiographic test and a fourth bypass operation were no longer options. Also, the saphenous veins from his groin regions and legs had all been used for previous grafts . . .
” . . . I suggested that he continue ascorbate and add 5 g of L-lysine daily . . . to try to mitigate the atherosclerotic activity of Lp(a). . . he began taking 1 g[ram] of lysine in early May 1991 and reached 5 g (in divided doses eight hours apart) by mid-June . . . He could now walk the same two miles and do yard work without angina pain and wrote, ‘the effect of the lysine borders on the miraculous.’ By late August, he cut up a tree with a chain saw, and in early September started painting his house. . . He also cut the amount of his heart medications in half . . . He attributes his newfound wellbeing to the addition of lysine to his other medications and vitamins. His wife and friends comment on his renewed vigor. . .
“. . . it was known that Lp(a) binds to lysine-Sepharose, immobilized fibrin and fibrinogen (Harpel et al., 1989); and the epithelial-cell receptor for plasminogen [similar to fibrinogen] ( Gonzalez-Gronow et al., 1989). . . In this scenario, high-dosage lysine could inhibit or reverse plaque accretion by binding to Lp(a). . . the addition of lysine to medications and vitamins, including ascorbate, markedly suppressed angina pectoris in this intractable case of CAD.”
Pauling, L. (1991) Case Report: Lysine/Ascorbate-Related Amelioration Of Angina Pectoris, Journal of Orthomolecular Medicine, 6: 144-146.
The second article written by both Pauling and Rath was entitled, 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. Again, let me quote from the paper:
“The primary cause of human CVD is a deficiency in ascorbate [Vitamin C] leading to the deposition of Lp(a) and fibrinogen/fibrin in the vascular wall . . . Ascorbate, a potent reducing and hydroxylating agent has been shown to be effective in achieving critical prophylactic aims: lowering the plasma Lp(a) level, preventing Lp(a) deposition in the vascular wall (Rath & Pauling 1990), decreasing elevated LDL levels (Ginter 1979), increasing HDL levels (Bates et al 1977), preventing oxidative modification of lipoproteins, protecting against oxidative damage by scavenging oxygen free radicals and by regenerating tocopherol, preventing the oxidative modification of lipoproteins (Jialal et al 1990), and, above all, preserving the integrity of the vascular wall and preventing the formation of atherosclerotic plaques (Rath & Pauling 1990) . . .
“Ascorbate is able not only to prevent the formation of atherosclerotic lesions but also to reduce existing plaques. It is well-established that ascorbate increases HDL plasma levels, thereby promoting reverse cholesterol transport by uptake of intra- and extracellular lipid from the vascular wall . . .
“On the basis of our finding that plaque development is paralleled by the extracellular deposition of Lp(a) it is evident that a major focus of therapeutic development is the release of Lp(a) or its lipid component from the arterial wall. Ascorbate may be involved in two ways: by dissociating apo (a) from the LDL-like component of Lp(a), thus enhancing the lipoprotein efflux from the vascular wall and by converting lysyl residues in this wall into hydroxylysyl residues, thereby decreasing the binding affinity to components of the vascular wall by way of the lysyl haptenic group. . .
“For patients with advanced cardiovascular disease therapeutic amounts of these inhibitors, together with ascorbate and as adjuncts to appropriate conventional therapy, might be prescribed . . . These substances have been used in long-term studies for different indications without compromising side effects . . . The combination of these substances with ascorbate may be considered ideal since ascorbate reduces the need for further Lp(a) deposition in the vascular wall and the inhibitors would enhance the release of already deposited Lp(a). Moreover, ascorbate is known to have anti-coagulative properties (Bordia & Verma 1985).”
Rath, M. & Pauling, L. (1991) 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, 6: 125-134.
The third article documented that the protein segment of Lp(a) is just as sticky as the lipo segment.
Rath, M. and Pauling, L. (1991) Apoprotein(a) is an Adhesive Protein, Journal of Orthomolecular Medicine 6: 139-143.
In 1991 R. A. Riemersma et al., at the University of Edinburgh ‘s Department of Cardiology, investigated the relationship between angina pectoris pain and plasma concentrations of vitamins A, C, and E and carotene in a population case-control study of 6000 men. They found that angina pain got worse when the amount of Vitamins A, C and E and carotene in the blood went down. Angina pain lessened when the levels of Vitamin A, C and E and carotene in the blood went up.
Riemersma, R. A., Wood, D. A., Macintyre, C. C., Elton, R. A., Gey, K. F., Oliver, M. F. (1991) Risk Of Angina Pectoris And Plasma Concentrations Of Vitamins A, C, And E And Carotene, Lancet, Jan 5; 337(8732):1-5.
In January 1991, the results of a large study was published by the World Health Organization in Geneva, Switzerland. The study reported that a low blood level of vitamin E was a more important risk factor than either high cholesterol or high blood pressure. The authors stated that, “increasing the consumption of important vitamins seems to be more than twice as important in protecting a person from heart attack than any other factor.”
Gey et al. (1991) Inverse Correlation Between Plasma Vitamin E and Mortality from Ischemic Heart Disease in Cross Cultural Epidemiology, American Journal of Clinical Nutrition, 53 (January): 326-334.
In 1992, Drs. Pauling and Rath again monopolized an issue of the Journal of Orthomolecular Medicine publishing 5 separate papers. The first was entitled, A Unified Theory Of Human Cardiovascular Disease Leading The Way To The Abolition Of This Disease As A Cause For Human Mortality (7: 5-15) and explained in evolutionary terms how human’s inability to manufacture Vitamin C leads to our susceptibility towards athersclerosis.
The second paper detailed how apoprotein(a) contributes to the degradation of the collagen in the artery wall and describes how the amino acid lysine can prevent this from happening.
Rath, M. & Pauling, L. (1992) Plasmin-induced Proteolysis and the Role of Apoprotein(a), Lysine, and Synthetic Lysine Analogs, Journal of Orthomolecular Medicine 7: 17-23.
The third paper documented that Vitamin C lowered the Lp(a) levels by 27% in outpatients with coronary heart disease.
Rath, M. (1992) Lipoprotein(a) Reduction by Ascorbate, Journal of Orthomolecular Medicine, 7: 81-82.
The fourth paper was a more fleshed-out version of their evolutionary theory.
Rath, M. (1992) Solution to the Puzzle of Human Evolution, Journal of Orthomolecular Medicine, 7: 73-80.
In the fifth paper, Dr. Rath states that, “The amino acids L-lysine and L-proline competitively interfere with the binding of lipoprotein(a) to constituents of the vascular wall and atherosclerotic lesions. The therapeutic use of these amino acids could prevent further accumulation of lipoprotein(a) in the vascular wall. More importantly, optimum concentrations of L-lysine and L-proline could release deposited lipoprotein(a) and other atherogenic lipoproteins from the vascular wall. This paper defines a new therapeutic goal: The pharmaceutical, non-invasive reversal of existing CVD with nutritional supplements.”
Rath, M. (1992) Reducing the Risk for Cardiovascular Disease with Nutritional Supplements, Journal of Orthomolecular Medicine, 7: 153-162.
In 1992, A. J. Verlangieri and M. J. Bush at the University of Mississippi Department of Pharmacology, induced atherosclerosis in monkeys by feeding them a diet deficient in Vitamins, then divided them into a control group (no change in diet) and a group that was fed the same diet but with Vitamin E supplementation. After 8 months, the plaque deposits in the arteries of the Vitamin E monkeys were reduced from 33% blockage down to 8% blockage. The researchers concluded that, “These results indicate that d-alpha-tocopherol [Vitamin E] may be prophylactically and therapeutically effective in atherosclerosis.”
Verlangieri, A. J. and Bush, M. J. (1992) Prevention And Regression Of Primate Induced Atherosclerosis By D-Alpha-Tocopherol, Journal of the American College of Nutrition, Vol 11, Issue 2, 131-138.
In 1993, Dr. Pauling and M. McBeath published another case history of the Pauling Therapy relieving angina pain. A 67 year old, former professor of chemistry at the University of New Bruswick, Canada, was experiencing stress angina daily for several years and was taking 6-7 nitroglycerine tablets per day. She read Dr. Pauling’s first case history and put herself on Dr. Pauling’s Vitamin C & Lysine Therapy. Within 3 weeks she was able to go all day, despite stressful occurrences, without taking any nitroglycerin. She telephoned Dr. Pauling with these results and described them as “miraculous.” She also told him that she and her husband were setting off on a 3-month trip around the world; something they had planned to do earlier, but couldn’t because of her ill health.
McBeath, M. & Pauling, L. (1993) A Case History: Lysine/Ascorbate-Related Amelioration Of Angina Pectoris, Journal of Orthomolecular Medicine, 8: 77-78.
Also in 1993, Dr. Pauling related another case history in a video tape produced by the Institute for Optimum Nutrition. Dr. Pauling described a patient who had had 2 extensive bypass operations, yet his coronary arteries had become clogged again, and was not a candidate for another bypass or angioplasty. He was living in the same town as the person described in Dr. Pauling’s first case history, was introduced by friends, and started taking the Pauling Therapy. Within a month, he was riding his bicycle into town from his house out in the country several times a week (a 9 mile round trip). He described the Pauling Therapy as being “almost miraculous.”
Cardiovascular Disease: A Unified Theory of the Cause and Treatment, Institute for Optimum Nutrition, Video Tape, 1993.
In a paper entitled, A New Era In Medicine, Dr. Rath wrote:
“The eradication of heart disease is a realistic goal. Based on the discoveries above and on growing scientific evidence accumulated over the years [Dr. Pauling and I have] developed nutritional recommendations for optimum cardiovascular health. Hundreds of patients are already following these recommendations. [These patients are experiencing]:
“These effects are achieved by nutritional supplements reversing impaired blood flow to the heart muscle as well as improving metabolism of millions of heart cells. The most important among these nutrients are vitamin C, vitamin E, niacin, lysine, proline, coenzyme Q10, carnitine as well as certain minerals. Moreover, a new therapeutic mechanism is described by which lysine and proline, together with other essential nutrients, decrease the “atherosclerotic tumor” in the vascular wall caused by smooth muscle cells . . .
“The[se] recommendations . . . take nutritional medicine one step further towards a comprehensive nutritional resupplementation for optimum cardiovascular health. The immediate and profound health improvements even in patients with a variety of severe heart conditions prove these recommendations most effective for the treatment of different heart diseases and related conditions. These recommendations stand any comparison with prescription drugs in the therapy of angina pectoris, arrhythmia, hypertension, heart failure as well as for the prevention of diabetic vascular disease and other forms of cardiovascular disease.”
Rath M. (1993). A New Era in Medicine, Journal of Orthomolecular Med, 8: 134-135.
On July 27, 1993 Drs. Pauling and Rath were granted their second U. S. Patent (No. 5230996) entitled, Use of Ascorbate and Tranexamic Acid Solution for Organ and Blood Vessel Treatment Prior to Transplantation. The patent described 3 uses of this invention:
1) The treatment of occlusive cardiovascular disease with the use of Vitamin C covalently linked with binding inhibitors which inhibit the binding of Lp(a) to blood vessel walls,
2) The prevention of atherosclerosis by the same method, and
3) Reducing the plaque on (or in) organs or blood vessels prior to transplantation.
The third use involves an aqueous solution of Vitamin C, binding inhibitors, and antioxidants. The organ or blood vessel is dipped into this solution and the atherosclerotic plaque deposits simply melt away leaving a clean and healthy organ or vessel for transplantation. The use of this solution is standard procedure in bypass operations because it ensures that the grafted blood vessel is free of plaque.
In 1994, Dr. Linus Pauling was interviewed by Tony Edwards and Patrick Holford of BBC Television at the Power of Prevention conference in England . The interview was later published in the August 1994 issue of the British Journal of Optimum Nutrition. The following is a segment from this interview:
Many investigators contributed to showing that lipoprotein A is what is deposited in plaques, not just LDL, but lipoprotein A. If you have more than 20 mg/dl in your blood it begins depositing plaques and atherosclerosis. So the question then is what causes lipoprotein A to stick to the wall of the artery and cause these plaques? Well countless biochemists and other chemists are pretty smart people and they discovered what it is in the wall of the artery that causes lipoprotein A to get stuck to the wall of the artery and form atherosclerotic plaques and ultimately lead to heart disease, strokes and peripheral arterial disease. The answer is there is a particular amino acid in a protein in the wall of the artery – lysine, which is one of the twenty amino acids that binds the lipoprotein A and causes atherosclerotic plaques to develop. I think it is a very important discovery.
Well, now, if you know that there are residues of lysine, lysyl residues, that hold the lipoprotein A to the wall of the artery and cause hardening of the arteries, then any chemist, any physical chemist would say at once that the thing to do is to prevent that by putting the amino acid lysine in the blood to greater extent than is normally. Of course, you get lysine normally in your food. Meat in particular contains a good bit of lysine. And you need lysine to be alive, it is an essential amino acid, you have to get about a gram a day to keep in protein balance, but you can take lysine, pure lysine, a perfectly nontoxic substance in food, as 500 mg tablets and that puts extra lysine molecules in the blood. They enter into competition with the lysyl residues on the wall of the artery and accordingly count to prevent the lipoprotein A from being deposited or even will work to pull it loose and destroy the atherosclerotic plaques.
I think so. Yes. Now I’ve got to the point where I think we can get almost complete control of cardiovascular disease, heart attacks and strokes by the proper use of vitamin C and lysine. It can prevent cardiovascular disease and even cure it. If you are at risk of heart disease, or if there is a history of heart disease in your family, if your father or other members of the family died of a heart attack or stroke or whatever, or if you have a mild heart attack yourself then you had better be taking Vitamin C and lysine.
In my opinion adults should be taking at least 2 grams a day. There is much evidence about increased health with 2 grams a day, and of course even more with 4 or 6 grams a day. Even an extra 60 mg has been shown to add value in cutting down the death rate from heart disease, cancer and other diseases. Now my feeling is as people grow older they ought to be increasing their Vitamin C and perhaps they should follow the policy that I have followed of increasing the intake. It can be either one chunk, one dose in the morning, or even better three doses throughout the day, increasing the intake until a laxative effect is observed, speeding up the rate of elimination of waste material from the bowel. So my suggestion is every person who wants to have the best of health should increase the intake of Vitamin C to somewhat less than the amount that causes significant looseness of the bowel.
Linus Pauling died of prostate cancer at the age of 93 only a few months after giving this interview. Dr. Pauling followed his own nutritional advice. For many years he consumed 18 grams (18,000 mg) of Vitamin C per day with no adverse effects. In fact, as you can tell from this interview and that he was traveling abroad only months before his death, he was active both physically and mentally right up to the very end.
Dr. Rath left the Linus Pauling Institute in 1992 but continued his research and advocacy of the nutritional approach to the prevention and cure of heart disease.
In 1996, Dr. Rath and Dr. Niedzwiecki reported the results of a yearlong study to determine the effect of a nutritional supplementation program on the natural progression of coronary artery disease. 55 patients with various stages of coronary artery disease, aged 44-67, were put on a daily nutritional supplementation program of 2,700 mg of vitamin C, vitamin B complex, 600 IU of vitamin E (d-alpha-tocopherol), 450 mg of L-proline, 450 mg of L-lysine, 390 mcg of folic acid, 30 mg of coenzyme Q-10, and 450 mg of citrus bioflavinoids.
Changes in the progression of coronary artery calcification before and during the program were determined by Ultrafast Computerized Tomography. Before the intervention, the natural progression rate of the coronary artery calcification averaged 44% per year. During the year of treatment, however, the progression of coronary artery calcification decreased by an average of 15%. In a subgroup of patients with early stages of coronary artery disease, treatment resulted in a statistically significant decrease, with no further progression of coronary calcification. In individual cases, reversal and complete disappearance of previously existing coronary calcification were documented.
Dr. Rath later explained the results by saying, “The natural amino acids lysine and proline form a protective “Teflon” layer around the Lp(a) molecules. This prevents the deposition of more fat molecules in the artery wall and also releases lipoprotein molecules that had already been deposited there. Releasing fat molecules from the atherosclerotic deposits leads to a natural reversal of cardiovascular disease. These fat molecules are transported to the liver where they are converted to bile acids and excreted or used to make hormones . . .
“These same nutrients are used in the reconstitution of the vascular wall. Ascorbate is essential for the synthesis and hydroxylation of collagen. L-lysine and L-proline are important substrates for the biosynthesis of matrix protein. Maintaining the integrity and physiological function of the vascular wall is the key therapeutic target in controlling cardiovascular disease . . .
“Briefly, Lp(a) has lysine and proline receptors. You can think of a chemical receptor as a simple lock and key. Only one key (e.g. lysine) will fit into the lock (receptor on the Lp(a) molecule.) There may be multiple receptors on the molecule, but once they are all filled up with keys (lysine or proline) the Lp(a) molecule looses its ability to bind with any more “keys.” When all the Lp(a) locks have keys, Lp(a) will no longer be able to create plaque . . .
“It needs to be emphasized that the reversal of fatty deposits in the artery wall is a process common in nature. Bears and other hibernating animals use it regularly. During several months of winter sleep these animals do not eat, and therefore, get no vitamins in their diet. Moreover, during hibernation Vitamin C production decreases to a minimum. As a consequence, fat molecules are deposited on the artery walls. In the spring, when the animal wakes up, its vitamin supply increases dramatically from both its diet and from its body’s production. With this increase in vitamin supply, the fatty deposits on the artery walls gradually dissolve and the arteries regain their natural fat-free state. If atherosclerosis could not be reversed by an increase in Vitamin C, then all hibernating animals would eventually die from heart disease. Clearly, this is not the case.”
Rath, M. & Niedzwiecki, A. (1996) Nutritional Supplement Program Halts Progression of Early Coronary Atherosclerosis Documented by Ultrafast Computed Tomography, Journal of Applied Nutrition, 48: 68-78.
Rath, M. (1999) Why Animals Don’t Get Heart Attacks – But People Do: The Discovery That Will Eradicate Heart Disease, Matthias Rath Inc., El Dorado Hills , CA .
The Cambridge Heart Antioxidant Study conducted by the Department of Medicine at Cambridge University was also published in 1996. This randomized, controlled study involved 2000 patients with heart disease. Half of the patients received a placebo, the other half received either 400 or 800 IUs of Vitamin E per day. After 18 months, the Vitamin E group had 75% fewer new heart attacks, compared to the placebo group. The researchers concluded that Vitamin E supplementation significantly decreases the risk of cardiovascular disease and nonfatal myocardial infarction. The researchers made a point of explaining that these benefits came from the vitamin E SUPPLEMENTS, and not from food sources.
Stephens, N. G., Parsons, A., Schofield, P. M., Kelly, F., Cheeseman, K., Mitchinson, M. J. (1996) Randomized Controlled Trial Of Vitamin E In Patients With Coronary Disease: Cambridge Heart Antioxidant Study (CHAOS), Lancet, (Mar), 23;347(9004):781-6.
In 1997, the Research Institute of Public Health, University of Kuopio, Finland released the findings of a study of 1,605 randomly selected men in Finland, aged 42 to 60 years, conducted between 1984 and 1989. Finland has a population with low average Vitamin C concentrations and high mortality from coronary heart disease. None of the men in the study had evidence of pre-existing heart disease. After adjusting for other confounding factors, men who were deficient in Vitamin C had 3.5 times more heart attacks than men who were not deficient in Vitamin C. The scientist’s conclusion, “Vitamin C deficiency, as assessed by low plasma ascorbate concentration, is a risk factor for coronary heart disease.”
Salonen, Jukka T. (1997) Vitamin C Deficiency: A Risk Factor For Heart Disease, British Medical Journal, Vol 314, No 7081.
A study funded by the National Institutes of Health and conducted by collaborating scientists from the Linus Pauling Institute at Oregon State University and Dr. John F. Keaney, Jr., and Dr. Joseph A. Vita at the Boston University School of Medicine, concluded that “moderate, daily supplements of Vitamin C taken by people with coronary artery disease may be effective in improving the function of blood vessels, preventing the chest pains of unstable angina pectoris, and reducing the risk of heart attack and stroke.” The researchers discovered that 500 mg of Vitamin C per day provided blood vessels with significantly improved vasodilation (the ability to relax and avoid dangerous constriction).
Journal of the American College of Cardiology, April 1998.
German researchers examined cardiovascular risk factors in 788 middle-aged men and then tracked their rate of major coronary events (such as heart attack and stroke) over the next ten years. The risk factors included blood levels of traditional markers such as LDL and HDL cholesterol, as well as Lp(a). The researchers found that Lp(a) levels were higher in the men who eventually suffered a major coronary event. In fact, the risk of a major coronary event nearly tripled in the men whose levels fell within the highest 20% of the group’s range, compared to those with lower levels.
von Eckardstein, A., Schulte, H., Cullen, P., Assmann, G. (2001) Lipoprotein(a) Further Increases The Risk Of Coronary Events In Men With High Global Cardiovascular Risk, J Am Coll Cardiol, (Feb) 37(2):434-9.
Inspired by a report appearing in the Archives of Internal Medicine, Kathie M. Dalessandri, M.S., M.D., a general surgeon in Point Reyes Station, California, wrote the journal about her own experiences with the Pauling Therapy. Dr. Dalessandri is a 53-year-old woman with higher than optimal levels of Lp(a) and a family history of heart disease. She had been combining HRT and niacin to lower Lp(a) before the side effects of niacin became too much for her. (Niacin can cause flushing, headache, and liver dysfunction.) She wrote in her report that, “after a thorough review of the literature, I began to follow the advice of Linus Pauling.” Dr. Dalessandri began taking 3 grams per day of both ascorbic acid and L-lysine monohydrochloride. After six months of this treatment – with no side effects – her Lp(a) level had dropped to 14 mg/dl, a reduction of 48%.
Dalessandri, K. M. (2001) Reduction Of Lipoprotein(A) In Postmenopausal Women [letter], Arch Intern Med, 161:772-3.]
In 2002, Ulrich-Merzenich and co-workers at the University of Bonn, Germany, discovered that the vitamins C and E modulate human vascular endothelial and smooth muscle cell proliferation. Cells in culture were incubated with ‘preventive’ concentrations of vitamins C and E or both together. Cell proliferation and DNA synthesis were then measured. Vitamin C alone or in combination with vitamin E increased significantly cell proliferation and DNA synthesis in endothelial cells but decreased both in smooth muscle cells. It was found that the oxidized form of LDL promotes the proliferation of smooth muscle cells but decreases the growth of endothelial cells. Its effects could be reversed by high concentrations of antioxidant vitamins. They concluded that the Vitamins C and E may act to prevent atherosclerosis in two steps: first by stimulating regrowth of the endothelium, and second, by inhibiting smooth muscle cell growth.
Ulrich-Merzenich, G., Metzner, C., Schiermeyer, B., Vetter, H., et al. (2002) Vitamin C and E Antagonistically Modulate Human Vascular Endothelial And Smooth Muscle Cell DNA Synthesis And Proliferation, European Journal of Nutrition, 41 (1): 27-34, Feb.
The most recent work is a soon to be published study concluded in March 2003. The principle investigator, Dr. K. Kenton, conducted a 3 year clinical trial on 200+ males using a nutritional protocol very similar to the Pauling Therapy. Dr. Kenton was kind enough to send us the following e-mail:
“From 1997 to year 2000 we conducted a trial using 6 g/day magnesium-ascorbate, 6 g Lysine and 800 IU Vitamin E and in addition flavonoids. We now have a lot of data on 200+ male individuals including Lp(a), but also on atherosclerotic plaque size progression, plod pressure, lipid profiles (cholesterol, triglycerides).
“One main important observation was that the plaque growth progression was nearly halted to about 2-3% per year in comparison with natural progression of 15-30%. [Plaque growth 800-1500 % less in supplement group] We did not find a significant reduction in Lp(a) as such, but a clear reduction in Apo (b). There were also other benefits such as the hair started to re-grow in several individuals. The frequency of common colds were also reduced. Best regards, Dr. K. Kenton, London , United Kingdom . Date: Wed, 5 Mar 2003 17:53:32 .”
Taking the right nutritional supplements in the right dosages can greatly assist your body’s ability to prevent and cure cardiovascular disease.
Why this is not common knowledge and why most medical doctors involved in the “heart disease industry” do not use (and often actively oppose) the use of nutritional supplements in their treatment protocols is the subject for another essay.
