Top Natural Treatments for Heart Disease (Cardiovascular Disease)

Form the Book: Healing Factor Vitamin C Against Disease – by Irwin Stone, Linus Pauling, Albert Szent-Gyorgyi 1972,

Source on-line: https://vitamincfoundation.org/stone/

Source download book: https://welib.org/md5/35609ae8abf6e1dcb1cc701374943358

The diseases of the heart and the cardiovascular system are the number one killers of present-day Americans. The reported incidence of these diseases has been rising sharply. A few years ago heart diseases accounted for over 700,000 deaths annually and strokes took another 200,000. The number of cardiovascular deaths among persons under sixty-five (about 240,000) was about as high as deaths from cancer at all ages. Besides death, heart diseases cause widespread illness and disability and impose a multi-billion-dollar burden on the economy each year. In a recent health survey, it was found that of every hundred persons between the ages of eighteen and seventy-nine, thirteen had definite heart disease and twelve more were suspect. Nearly one-quarter of the population, therefore, lives in jeopardy of succumbing to a disease of the heart or circulatory system. The incidence increases with age.

Because our cardiovascular system is so important, let us first look into the equipment with which we are endowed. We have a complicated plumbing arrangement comprising a closed system of interconnected flexible pipes. The system has a dual pumping arrangement combined in one hard-working organ, the heart. The flexible arteries carrying the blood, under pressure, away from the pump are the largest, and subdivide into smaller and smaller vessels until those carrying the blood into the tissues, the capillaries, are microscopic in size. The blood in the tissues is then collected in flexible vessels of increasing diameter, the venules and veins, for its trip back to the pump for another strong push into the arteries. This process goes on twenty-four hours a day for the entire lifetime of the individual.

The pump and the flexible pipes in this system must be rugged to start with and must be in a constant state of self-repair and maintenance to withstand the continual wear and tear of the alternating mechanical stresses of fluid flow. Should any structural weakness in the walls occur or leaks develop anywhere in the closed system, we are in serious trouble with heart disease, strokes, and hemorrhaging.

The main structural element, from which this system is build and which provides the strength, elasticity, and ruggedness is the protein collagen. This protein comprises about one-third of the body's protein content and is the cement substance which holds the tissues and organ together. The synthesis of collagen by the body requires the presence of ascorbic acid. Without ascorbic acid, collagen cannot be produced. If too little ascorbic acid is present during the synthesis of collagen, it will be defective and structurally weak. Ascorbic acid is also required for the maintenance of the integrity of the collagen already synthesized in the continuing process of self-repair and self-maintenance of the tissues and the vascular system.

It is necessary, therefore, to have sufficient ascorbic acid available during fetal life to provide structurally sound collagen for the development of the cardiovascular system and to have sufficient ascorbic acid available during the entire lifetime of the individual to maintain this collagen in the proper state of self-repair. Impaired and structurally weak collagen is the cause of the most distressing symptoms of uncorrected hypoascorbemia (clinical scurvy), the scorbutic bleeding gums, the loose teeth, the capillary bleeding, the reopening of old healed wounds and scars, and the brittle bones. Most of our mammalian relatives, whose livers are continually producing large amounts of ascorbic acid, need never worry about this because they do not develop scurvy.

It is the author's belief that the high incidence of cardio-vascular disease in man is brought on because the greater part of the human population is dependent upon their foodstuffs as a source for their ascorbic acid intake and are thus existing on submarginal levels. These intakes are usually inadequate for the production and maintenance of optimal high-strength collagen over long periods of time. Because the system is subjected to many local ascorbic acid-depleting stresses, an abundant supply of ascorbic acid is demanded, not just "vitamin" levels.

Shortly after the discovery of ascorbic acid in the early 1930s, the intimate association of it with the cardiovascular system was surmised. This resulted in a tremendous amount of research and a considerable body of medical literature.

In 1934, Rinehart nd Mettier (1) found that infected guinea pigs deprived of ascorbic acid developed degenerative lesions of the heart valves and muscles. The changes were strikingly similar to those seen in rheumatic fever. Infected guinea pigs maintained with adequate ascorbic acid did not develop these heart lesions. A year later, Mentenand Kind (2) injected sublethal doses of diphtheria toxin into ascorbic acid-deficient guinea pigs and produced myocardial degeneration and arteriosclerosis of the lungs, liver, spleen, and kidneys. In further tests on guinea pigs with acute or chronic scurvy (3), it was indicated they developed inflammation of their heart valves, myocarditis, and occasional pericarditis.

As early as 1941 (4), it was suspected that inadequate intake of ascorbic acid was a factor in coronary thrombosis due to impaired collagen production, causing capillary rupture and hemorrhage in the arterial walls. Blood plasma ascorbic acid measurements were made in 455 consecutive adult patients admitted to the Ottawa Civic Hospital over a seven-month period and it was found that 56 percent had subnormal levels (below 0.5 mg %) and 81 percent of the coronary patients were in this subnormal range. It was "recommended that patients with coronary artery disease be assured of an adequate vitamin C (ascorbic acid) intake." A 1947 paper (5) showed that inadequate ascorbic acid body levels were not limited to cardiac patients of the lower economic brackets. The scurvy included 556 private patients, of which 123 had organic heart disease. Forty-two percent of all patients, 59 percent of the heart patients, and 70 percent of the coronary thrombotic patients had low plasma levels of ascorbic acid (below 0.5 mg %). Sixty-five percent of the coronary group had dangerously low levels (0.35 mg % or less). Again it was suggested that ascorbic acid be used as an adjunct to the usual methods of treatment, especially in the long-range care in the post-infarctive period.

A provocative series of papers was published by Dr. G. C. Willis and coworkers starting in 1953 that showed the importance of ascorbic acid in the maintenance of the integrity of the arterial walls (the intima). Any factor disturbing ascorbic acid metabolism, either systemically or locally, results in wall injury with subsequent fat-like deposits. In his 1953 paper, Willis (6) concludes that acute or chronic ascorbic acid deficiency in guinea pigs produces atherosclerosis and closely simulates the human form of the disease. Cholesterol feeding interferes with the ascorbic acid metabolism of rabbits, and guinea pigs and intraperitoneal injection of ascorbic acid inhibits the atherosclerosis in cholesterol-fed guinea pigs. Finally he states, "Massive doses of parenteral ascorbic acid may be of therapeutic value in the treatment of arthereosclrosis and the prevention of intimal hemorrhage and thrombosis." In 1954, the Willis group (7) studies the actual progression and regression of atherosclerotic plaques in living patients by a serial X-ray technique. Both progression and regression were observed over relatively short periods of time but did not coexist in the same cases during one period of observation. The rationale for ascorbic acid therapy is again outlined and preliminary results of such therapy were encouraging. In 1955, there appeared another paper (8), in which scientists actually examined the ascorbic acid levels in the fresh arteries from cases of sudden death, hospital autopsy material, and cases treated with ascorbic acid for various lengths of time before death. The conclusions reached in this study are so exciting and important that they are quoted in full:

1. A gross and often complete deficiency of ascorbic acid frequently exists in the arteries of apparently well-nourished hospital autopsy subjects. Old age seems to accentuate the deficiency.

2. The ascorbic acid depletion is probably not nutritional but rather related to the stress of the fatal illness.

3. A localized depletion often exists in segments of arteries susceptible to atherosclerosis for reasons of mechanical stress. Adjacent segments, whose mechanical stress is less, tend to have a higher ascorbic acid content and atherosclerosis here is rare.

4 The significance of this ascorbic acid depletion lies in the fact that scurvy in guinea pigs results in the rapid onset of atherosclerosis. Furthermore it has been reported that the aorta can synthesize cholesterol and the incorporation of radioactive acetate into cholesterol in tissues is said to be several times more rapid in tissues depleted of ascorbic acid.

5.Ascorbic acid deficiency in arteries with resulting ground substance depolymerization may account for the release of glucoprotein noted in the blood of subjects with severe atherosclerosis.

6.Preliminary studies suggest that it is possible to replenish the ascorbic acid in arteries by ascorbic acid therapy.

A similar concept was proposed in 1957, by McCormick (9), noting the importance of ascorbic acid deficiency in coronary thrombosis. He summarized his work as follows:

Thrombosis is not in itself a pernicioud development but rather a protective response of the organism designed normally to effect repair of damaged blood vessels by cicatrization. High blood pressure, excessive stretching of blood vessels and deficiency of (ascorbic acid) vitamin C, resulting in rupture and bleeding of the intima at the site of such stress initiate the development of the thrombosis by means of the clotting of the blood, which is also a protective reaction. This multiple protective mechanism should be sustained and controlled by physiological means (vitamin C therapy) rather than suppressed by anticoagulants with their dangerous side effects.

McCormick believed that an optimal body level of ascorbic acid offered the best natural means of effecting healthy new tissue, and claims that the initial intimal hemorrhage, precipitating thrombosis, would not occur if adequate prophylactic use of ascorbic acid were made to maintain the integrity of the cardiovascular system.

There is an extensive body of published research showing the intimate relationship between ascorbic acid and cholesterol metabolisms. In fact, the published research on the subject of the relationship of ascorbic acid to heart disease is so extensive that it is quite impossible to review it adequately and still keep within the bounds of a reasonable size for this chapter.

Cholesterol was identified as a major constituent of the arterial deposit over a century ago (10). As early a 1913 it was demonstrated that feeding cholesterol to rabbits resulted in atheromatous deposits in the aortas (11). In 1953, an intimate relationship between ascorbic acid and the synthesis of cholesterol in guinea pigs was shown by C.G. King and his group (12). Ascorbic acid depravation greatly increased cholesterolsynthesis. This observation was confirmed on guinea pigs fed an atherogenic diet (13). This group found that the greater the deprivation of ascorbic acid, the more the cholesterol accumulated in the tissues. The feeding of cholesterol to rabbits and guinea pigs lowers ascorbic acid levels (14) in the body, and coronary atherosclerosis appears to be in part a possible result of deficient ingestion of ascorbic acid (15). Increased intakes of ascorbic acid bring down cholesterol levels in rabbits (16), guinea pigs (17), rats (18), and humans (19).

Further confirmation of the ability of ascorbic acid to reduce cholesterol levels was reported in 1971 by R.O. Mumma and coworkers (20) and C.R. Spittle (20). Ascorbic acid sulfate was found to be a significant metabolite of ascorbic acid in human urine by E.M. Baker III and coworkers in 2971 (20). Spittle observed that the blood serum levels of cholesterol could be varied by changing the ascorbic acid intake. She suggested "that atherosclerosis is a long-term deficiency (or negative balance) of vitamin C which permits cholesterol levels to build up in the arterial system and results in changes in other fractions of the fats."

A most exciting paper by G.C. Willis (20) appeared in 1957 entitled "the Reversibility of Atherosclerosis." In this study atherosclerosis was induced in guinea pigs by depriving them of ascorbic acid. Some guinea pigs were then given large doses of ascorbic acid and it was found that in these animals the beginning atherosclerotic lesions were rapidly resorbed while the more advanced atherosclerotic plaques on the artery walls took longer. There was a steady decline in the incidence of the lesions in direct proportion to the duration of ascorbic acid therapy. The significance of these observations for man is tremendous -- they open the way to the megascorbic prophylaxis of atherosclerosis -- but they never were tested further.

Naturally occurring arteriosclerosis is found in many different mammals besides man. A recent study (21) showed there is a pronounced difference between atherosclerotic disease in various mammals as compared to various primates, including man. Fatty deposits play a relatively minor role in the naturally occurring lesions observed in the coronary arteries of the dog, cat, elephant, and other lower animals. In some of these animals there seems to be virtually no lipid involvement in the diseased arteries. In the primates, lipid deposition in the arteriosclerotic lesion is more pronounced, and distinct atherosclerotic plaques develop in man. The most significant physiological difference between the dog, cat, elephant, and other lower animals and the group of primates studies and man is that the former group of mammals are able to produce ascorbic acid in their livers in large daily amounts while the primates used in this investigation and man cannot do this. This is just another pertinent observation on the importance of this synthetic liver-enzyme system for the mammals and the vital involvement of ascorbic acid in the genesis of atherosclerosis A similar observation was made in 1961 (22) regarding the response of rats and guinea pigs to the development of atherosclerosis. Rats are known to be resistant to atherosclerotic changes, while guinea pigs are not. Here again the difference between these two species is that the rat is a good producer of ascorbic acid in its liver while the guinea pig, like man, is genetically unable to do so.

Another property of ascorbic acid that has been neglected in the treatment of edema of heart disease is its diuretic properties at high dosage levels. Abnormal retention of water throughout the body was noted in the post mortem examination by Lind in 1753 of patients dying of scurvy. Soon after the discovery of ascorbic acid in 1936 and 1937 (23), its diuretic properties were recognized in spite of the small doses of ascorbic acid employed. Its use in heart failure was suggested in 1938 by Evans (24), who pointed out the need for "an adequate supply of vitamin C for all patients with heart failure." Other papers in the period from 1944 to 1952 indicated its diuretic usefulness (25). Still, even at the present time it is not being used. In intensive care units for coronaries, ascorbic acid is conspicuous by its absence.

Cerebrovascular Accidents - Strokes

Over 200,000 deaths occur annually from strokes, and another 800,000 persons are totally or partially disabled by them. Major brain hemorrhages or thrombosis account for the sudden demise or total disablement. But of even greater incidence is the slow destruction of neural tissues of the brain by repetitive, small local thrombosis, or capillary rupture, with intimal hemorrhage (little strokes). It has been estimated that there are at least 1,200,000 people in the United States who have suffered one or more of these little strokes. They happen, and most of the time pass unnoticed, with nothing more to indicate their passing than a slight dizziness or nausea. It is only when the summation of these minor brain injuries cause mental or physical deterioration, to a point where it is noticeable by the patient or family, that it becomes evident that something is wrong. By that time, it is too late to do anything about it. What is needed is a prophylactic regime to prevent this situation and forestall little strokes.

In order to maintain the integrity of the vascular system of the brain, ascorbic acid is needed, as it is in any other part of the body except more so. The brain itself requires much ascorbic acid for its own active metabolism and functioning so if one is completely dependent on the submarginal levels of ascorbic acid supplied by foodstuffs, asymptomatic chronic vascular damage results which only becomes evident when a major part gives way and massive hemorrhages or thrombi develop. Suboptimal levels of ascorbic acid not only lead to strokes, but when fresh brain tissue from autopsies on patients dying of cerebral vascular disorders were examined, ascorbic acid was found to be entirely lacking or at extremely low, subnormal levels (26). In a four-year study on the continuous administration of varying amounts of ascorbic acid to thirty-two elderly patients with vascular disease, Gale and Thewlis (27), in 1953, reported six deaths. Four were directly due to heart attacks or cerebral episodes. Of these four, not one had taken more than the low level of 100 milligrams of ascorbic acid daily during the test period. They stated:

Many symptoms of vascular disturbances in the aged suggest that latent scurvy may be a frequent occurrence... Extended studies should be made by public health departments and geriatric clinics to determine the effectiveness of vitamins C and P in controlling cardiac and cerebrovascular illness.

How often do we hear this refrain, and yet nothing is ever done?

In spite of the dire need to do something effective in the prevention and therapy of this terrible plague of cardiovascular disease and cerebrovascular episodes, all this provocative and suggestive research has been glossed over and ignored and none of the crucial large-scale tests have ever been made. One possible excuse for this neglect might be that nearly all of the work was done by researchers whose viewpoint was clouded by the narrow confines of the vitamin C hypothesis and who had used inadequate dosage levels of ascorbic acid for maximal therapeutic effects. This should no longer be the case, for the description of the genetic disease hyposascorbemia in man (28) supplies the needed rationale for the megascorbic prophylactic doses which may be required to reduce the incidence of heart disease and for the megascorbic therapeutic doses which may be required to treat heart disease when it occurs.

The crucial tests would include taking a large population of individuals and administering continued long-term (for the rest of their lifetime) megascorbic prophylactic levels of ascorbic acid (about 70 milligrams per kilogram of body weight per day, or about 3 to 5 grams a day in spaced doses for an adult) and then measure the incidence and morbidity of disease at intervals and the increase in healthy lifespan as compared to a similar population on placebos. For heart disease therapy, we need to try megascorbic therapy in emergency coronary care units using doses of possibly 1,000 milligrams per kilogram of body weight per day, intravenously at first, and then working out a dosage schedule as the patient comes out of danger. Similarly, in cerebrovascular accident treatments, megascorbic therapy may introduce a new era in post-episode survival and recovery, and prevention of future strokes by the mere elimination of the localized cerebral scurvy that exists in stroke victims.

All of this provocative and suggestive research, conducted all over the world for the last four decades, indicates that the simple ingestion of 3 to 5 grams of ascorbic acid a day in several spaced doses may be sufficient as a megascorbic prophylactic regime to prevent the high incidence of heart disease and strokes. The potential victims of these diseases may live a healthier life far beyond the time when these diseases would be cutting them down. In acute cases of massive coronary or cerebral hemorrhage, the prompt application of megascorbic therapy in intensive care units would seem to assure survival to those now destined to die because of their severe, uncorrected hypoascorbemia.

I do not remember why I started mega doses of vitamin C, but it has corrected a couple of problems. A year ago, my spread between systolic and diastolic was typically 75 with a bp 155/80. I just took it a few minutes ago, and it is 143/84, a spread of 59.

I have not taken any meds of any kind for decades. I am 68 yo. male. I started out aiming for 200 grams of vitamin C per day spread out through each day. Now it seems hard to remember, so I end up with about 30 grams a day.

I take 6 grams at a time and try to do it each hour. I try to quit by 4 pm so I can sleep without so much gas.

Another problem that was helped was blood in the semen. It cured it. Makes sense. Vitamin C helps the body to produce collagen, and collagen strengthens the blood vessels. I use ascorbic acid and make my own capsules. At times I will put a spoonful in a glass of water with some honey. The cheapest vitamin C I have found is from Vitacost. Every once in a while, it goes on sale BOGO half off.