CHAPTER 1

SOME BASIC CONCEPTS

"Discovery consists in seeing what everybody else
has seen and thinking what nobody has thought."

Albert Szent-Gyorgyi, M.D., Ph.D.
Awarded the 1937 Nobel Prize in Physiology
or Medicine for the discovery of vitamin C,
in connection with biological combustion

A Theory of Life

Szent-Gyorgyi (1978, 1980) proposed that the essence of the living state is that organic molecules such as the proteins in the tissues of the body must be maintained in a state of electron desaturation. All matter has varying proportions of electrons, protons, and neutrons, but Szent-Gyorgyi held that dead tissue had a full complement of electrons, while live tissue maintained a deficit of electrons. Vitamin C, known chemically as ascorbic acid, interacts with a wide variety of basic chemical substances in the body. Vitamin C literally appears to be one of the primary substances assuring that a vigorous, continuing electron exchange takes place among the body's tissues and molecules. Classically regarded as an antioxidant, vitamin C, depending upon its immediate microenvironment, can also promote oxidation. Phrased another way, vitamin C might not have an antioxidant effect when it gives electrons to oxidation promoters like iron and copper. Although the antioxidant function predominates, vitamin C clearly plays a significant role in the electron mechanics of the body.

Szent-Gyorgyi asserted that energy exchange, arguably life's most important form of cellular communication, can only occur when there is an imbalance of electrons between and among molecules. This imbalance of electrons causes the natural flow of electrons, a biological form of electricity, throughout the body. All of the body's functions are directed, controlled, and regulated by this physiological flow of electricity. Furthermore, this flow of electricity through the body also establishes and maintains the subtle magnetic fields in the body that appear to be involved with good health.

Vitamin C, although possessing other important qualities, appears to be a most important stimulus to this flow of electricity. A greater amount of vitamin C in the body enhances the flow of electricity in the body, thereby optimizing the ability of the cells in the body to maintain their health-sustaining communications. One definition of life, then, is that it is a state in which an optimal degree of electron interchange among cells can take place. Health exists when electrons flow fully and freely, illness exists when this flow is significantly impaired, and death occurs when this flow stops. Furthermore, when this electron flow is impaired, there is a need for more vitamin C to help remedy this impairment. Since poor electron flow throughout the body's tissues appears to cause or be associated with disease, this also means that there is typically a vitamin C deficiency whenever the body is diseased. Because of this interrelationship vitamin C should always be a part of the treatment of virtually any disease state. Just as dehydration requires water, poor electron flow-a primary characteristic of the diseased state-requires vitamin C. This will virtually always apply, even when a deficiency of vitamin C was not necessarily involved in the development of a certain diseased state. There are only a very few situations in which some restraint should be exerted in the administration of vitamin C, and these will be discussed in Chapter 4.

Entrenched Misconceptions

The enormous clinical usefulness of vitamin C remains little appreciated. This lack of appreciation is partially due to its classification as a vitamin, which is a very limiting definition. In the 28th edition of Dorland's Illustrated Medical Dictionary a vitamin is defined as

a general term for a number of unrelated organic substances that occur in many foods in small amounts and that are necessary in trace amounts for the normal metabolic functioning of the body.

While vitamin C is certainly necessary in at least trace amounts for the body to survive and to avoid the deficiency disease known as scurvy, much larger amounts are necessary for the body to achieve and maintain optimal health. The above definition pertains much more to other identified vitamins rather than vitamin C, and only trace amounts of vitamin C will not support the "normal metabolic functioning" of the body mentioned in the definition above. Rather, the chronic underdosing of vitamin C from minimal or no supplementation and from eating depleted food will facilitate the development of nearly all the chronic degenerative diseases that affect man. Furthermore, evidence that will be presented throughout this book will clearly and repeatedly demonstrate that chronic vitamin C depletion is often one of the primary reasons that many common infectious diseases are contracted in the first place. It will become apparent that many people throughout the world, including many in the seemingly well-fed United States, are suffering from the effects of a chronically deficient intake of vitamin C.

It is very possible that much of the success claimed by mainstream medicine in both improving lifespan and decreasing the incidence of infectious diseases has come from the addition of small amounts of vitamin C, along with other antioxidant nutrients, to many of our otherwise depleted packaged foods. The degree of this "success" should improve further as time goes by, as it is becoming increasingly accepted to supplement a greater variety of foods with even larger amounts of vitamin C.

As addressed in some length in the introduction, an established scientific concept, however wrong, is very difficult to correct once accepted and given the credibility of publication in medical textbooks. The information in this book will repeatedly demonstrate that a vitamin-like function is only one of multiple significant properties of vitamin C. Arguably, since it will be shown that much larger than "trace amounts" of vitamin C are needed to be taken on a regular basis to maintain optimal health and "normal metabolic functioning," a strict interpretation of the definition of vitamin C can even support the argument that vitamin C is not a vitamin at all. Ultimately, it should become apparent to the reader that vitamin C is the single most important nutrient substance for the body, regardless of whether it is viewed as a vitamin. However, for purposes of discussing the massive amounts of literature that have been generated on this fascinating substance, I will continue to refer to it as vitamin C throughout this book. The scientific and medical literature contains a few other names for vitamin C based on the nature of its chemical composition, but they will not generally be used to avoid any possible confusion or appearance of inconsistency to the reader.

Another critical misconception regarding vitamin C involves how much of it should be used to achieve the intended therapeutic effect. Real estate agents frequently say that the three most important attributes of a home are "location, location, and location." Similarly, the three most important considerations in effective vitamin C therapy are "dose, dose, and dose." If you don't take enough, you won't get the desired effects. Period! On the other hand, you will rarely ever fail to observe a dramatic response to a wide variety of medical conditions if you take a large enough dose for a long enough time.

On the other hand, even the use of relatively tiny doses of vitamin C will frequently result in some clearly definable benefit in many infectious diseases. Nearly all of the past and present papers in the literature that declare the ineffectiveness of vitamin C for given conditions use incredibly small doses of vitamin C in their experiments and trials, while looking for dramatic and clear-cut benefits. The Recommended Dietary Allowance (RDA) of vitamin C ranges between 30 and 95 mg (milligrams) daily, with 60 mg being recommended for adult men and women. Often, the proper dose of vitamin C in the treatment of an infectious disease may be anywhere from several hundred-fold to several thousand-fold times the amount in this miniscule RDA dose! The RDA serves to prevent only the development of the full-blown clinical picture of scurvy in otherwise clinically healthy people, or to restore vitamin C blood levels in otherwise normal people to the levels deemed to be normal or acceptable. Indeed, in many people who have infectious diseases that metabolize unusually large amounts of vitamin C, keeping body stores of vitamin C depleted, the RDA for vitamin C will not even prevent many of the symptoms of scurvy from developing or restore the blood levels of vitamin C to the normal range. Evidence contained in this book will actually demonstrate that many people with such vitamin C-depleting infectious diseases actually die from complications completely consistent with the symptoms of acute scurvy. For example, many people who eventually die from an infectious disease actually die from a bleeding complication. An acute and severe vitamin C deficiency is often the immediate underlying reason for either subtle bleeding or massive hemorrhage.

Many of the numerous vitamin C research papers are also especially misleading in their conclusions since they persist in labeling the small amounts of vitamin C used in their studies as "megadose." Even the amounts of vitamin C that are termed "megadose" in the literature often need to be increased a thousand-fold or more to reach the necessary dosage actually needed to achieve the desired therapeutic effect. Because of this continued mislabeling in the literature, I will refer to the amounts of vitamin C that really should be used as "optidoses" (optimal doses). Although many of the optidoses recommended in this book will be substantially larger than most of the "megadoses" mentioned in the literature, use of the term optidose may gradually allow doctors and patients alike to realize that the recommended dose is really the optimal dose that the body needs at that time. It is also important to realize that the optidose of vitamin C, even for a single patient, can vary widely depending upon how sick the patient already is when therapy is initiated. Furthermore, one optidose is not necessarily appropriate for two patients with seemingly similar clinical situations, since one patient may have underlying factors consuming vitamin C much more rapidly than the other patient. On the other hand, a megadose only implies that the treating physician feels that a large dose is being recommended, and the dose given may still not necessarily be the physiologically appropriate dose that will support or restore optimal health.

Taking regular optidoses of vitamin C tends to make the patient much more aware of the subtleties of good health. When something occurs that will compromise that good health, such as a new toxic or infectious challenge, it is not uncommon for the experienced vitamin C taker to almost reflexly increase the daily vitamin C optidose to the needed amount. The "chronically healthy" person almost always knows when even small reversals in good health are taking place, and taking enough additional vitamin C at such a time will almost always promptly restore good health, as well as make the contraction of any infectious disease extremely unlikely.

Genetically Lacking

Vitamin C must be directly ingested, usually in the form of supplementation as well as in the diet, to maintain adequate levels inside the cells in the tissues (versus the more commonly measured levels in the blood) throughout the body. Tissue cells contain greater concentrations of vitamin C than are found in the blood (Meiklejohn, 1953). As a result, ingesting only enough vitamin C to maintain a given blood level is no guarantee that many of the vitamin C-rich tissue cells will have enough vitamin C available to them from the blood to reach and maintain their proper concentrations. "Pulsing" of the vitamin C dosage, with intermittent large doses so that temporarily high blood concentrations are reached, may be the only way to assure that the body's various tissues can achieve high enough amounts of vitamin C.

It should also be realized that the human body does not have the ability to synthesize any vitamin C whatsoever. However, this is not the case with most other animals. Generally, nearly all mammals, reptiles, and amphibians have the ability to synthesize at least some of their daily requirement for vitamin C. Most mammals synthesize vitamin C in their livers, first measured experimentally by Grollman and Lehninger (1957), and other animals, primarily reptiles and amphibians, can achieve this synthesis in their kidneys (Chatterjee et al., 1975). This ability is felt to be completely lacking in humans, as well as in primates, fruit bats, and guinea pigs.

Interestingly, the very fact that the guinea pig cannot make any vitamin C for itself is one of the primary reasons that it has served scientific researchers so well. The guinea pig can be made ill or toxic much more easily than a vitamin C-producing research animal, and there is less variability in the guinea pig's response to a given stress compared to other animals that can respond with internally-produced vitamin C. Researchers quickly realized that guinea pigs and primates (including man) seemed uniquely susceptible to a wide variety of clinical syndromes, including life-threatening shock and infectious diseases such as tuberculosis, diphtheria, and polio. Of course, it eventually became apparent that experimentally-induced scurvy required an animal such as the guinea pig that could not produce its own vitamin C, or another animal that could produce only small amounts.

Chatterjee et al. (1975) examined the abilities of different species of animals to produce their own vitamin C. Among the mammals tested, they found that goats were especially capable of producing significant amounts of vitamin C. In fact, goats had a rate of production of vitamin C that was roughly 13 times greater than that of cats or dogs. All wild animals tested had at least a 4-fold greater rate of vitamin C production compared to cats or dogs. This is likely one of the primary reasons that these two most common domestic pets will keep the veterinarian busy with so many of the same diseases that afflict their human owners. Although they do produce some vitamin C, dogs and cats produce it less readily than many other animals, and compared with wild animals, they are much more easily stressed into a state of vitamin C deficiency. For example, the efficient vitamin C-producing adult goat can internally manufacture more than 13,000 mg of vitamin C daily to maintain its optimal health when it is not facing any significant challenges to its health (Stone, 1979). Even more amazingly, goats are also believed by some to produce as much as 100,000 mg of vitamin C daily when faced with life-threatening degrees of infectious or toxic stress! Researchers such as Levine (1986) have argued that it is quite difficult to recommend an optimal daily dose of vitamin C for the human being. However, few investigators familiar with the bulk of research on vitamin C would maintain that the human RDA dosage is nearly enough to meet all of the body's needs.

Conney et al. (1961) demonstrated that animals having the ability to synthesize their own vitamin C could produce about 10 times more than their baseline levels when subjected to enough biochemical stress, such as from drugs. This automatic ability to adequately step up vitamin C production in the face of stress explains why so many wild animals tend to live healthy for their entire life spans until it is time to die. Conversely, generally vitamin C-depleted human beings will typically spend at least half of their lifetimes coping with one or more chronic diseases. Dogs and cats are generally somewhat healthier than people, but their limited vitamin C-synthesizing ability is eventually overwhelmed as they grow older and face greater cumulative toxic stresses, resulting in more disease than seen in wild animals. Even the rabbit, which can produce roughly five times as much vitamin C internally as the dog or cat, can be malnourished to the point of eventually dying from what appears to be a metabolic condition closely akin to scurvy (Findlay, 1921). It should not be hard to understand, then, that an added vitamin C-utilizing condition, such as a significant infection, can push even vitamin C-producing animals to the point of clinical scurvy.

The specific genetic defect that prevents humans from internally synthesizing vitamin C is the lack of a liver enzyme known as L-gulonolactone oxidase (GLO). GLO is the last of a sequence of liver enzymes that ultimately transforms glucose (blood sugar) into vitamin C. Interestingly, the actual GLO genome, or sequence of coding DNA, has been identified to be present in humans (Nishikimi et al., 1988). For unclear reasons, this segment of human DNA remains "untranslated," meaning the recipe for GLO is present in the human but remains unprepared. This raises the possibility of potentially exciting new avenues of research for today's genetic researchers. If a way can eventually be found to get the already present genetic code for GLO to "turn on" and continually produce GLO, the health of the human population will leapfrog to levels that may seem literally unbelievable today. Human beings would then be able to continually synthesize vitamin C from glucose, and there would be far fewer toxic or infectious challenges that could cause illness. As is already seen with the many vitamin C-producing wild animals, such a human could then be expected to remain much healthier until the expected life span had run its course.

A thorough examination of the literature reveals another potentially exciting way to address the human being's inability to synthesize vitamin C that does not appear to have been seriously addressed. While not always practical or clinically effective, genetically-based enzyme defects can sometimes be addressed by the direct administration of the missing enzyme. Sato et al. (1986) administered GLO harvested from either chickens or rats to guinea pigs. Giving this enzyme to guinea pigs enabled them to survive vitamin C-deficient diets. At the very least, this should stimulate further research into the feasibility of giving such direct enzyme replacement therapy to humans. Hadley and Sato (1988) established a protocol involving long-term GLO administration to guinea pigs that was successful in maintaining a high proportion of those animals. These results would certainly seem to warrant further serious research on similar treatment programs for humans. Assisting the liver in performing what should be a natural function is a very desirable clinical goal. Perhaps regular therapy with GLO enzyme replacement, supported by more vitamin C when toxic and other environmental stresses present themselves, might be a very good health-supporting regimen. Certainly, stimulating the liver to release vitamin C directly into the bloodstream would undoubtedly help support the oral and other non-intravenous forms of supplemental vitamin C. The scientific literature specifically addressed in Chapter 2 clearly shows the vast clinical superiority of intravenous vitamin C over any other form of vitamin C administration. Often a significantly smaller dose of intravenous vitamin C, compared to an oral administration, will promptly result in the clinical resolution of an infectious disease.

A human's inability to produce GLO must be considered something of an inborn error of metabolism. This metabolic error was also induced in the vitamin C-producing rat by Mizushima et al. (1984). They were able to establish a mutant rat colony that produced no GLO, the same defect "normally" found in guinea pigs and humans. As with other such inborn errors of metabolism, every attempt should routinely be made by a treating physician to consider this lack of enzyme activity in every medical condition. This translates into a very simple approach: always give vitamin C on a daily basis, and always give enough. To date, there are NO infectious diseases that have ever been found in which vitamin C administration can be considered dangerous or inappropriate. This is the case even though there has already been roughly a century of research on vitamin C, involving the publishing of some 50,000 to 100,000 scientific articles. A handful of case reports, which will be addressed in more detail in Chapter 4, gives good reason to exert a minimal amount of caution when administering vitamin C under a very limited number of clinical circumstances. However, no evidence has ever been produced to demonstrate that a regular optidose of vitamin C should be avoided by anybody. Everybody requires an optidosing of vitamin C on a daily basis to reach and maintain optimal health. No human body can operate effectively and stay healthy without such an optidose. The only real question that remains is what one's individual daily optidose should be. This, too, will be addressed later in more detail.

It is an incredibly rare situation for an inborn error of metabolism to be shared by all humans. There are many other inborn errors of metabolism, but these affect only certain unfortunate individuals. However, there appears to be a primary assumption in the medical community that a 100% GLO deficiency is a genetic trait shared by all human beings. From my review of the scientific literature, however, it does not appear that a serious study was ever undertaken to see if all humans were equally lacking in this critical liver enzyme. Consider the anecdotal reports that one occasionally hears about a certain individual living to 100, while smoking and drinking every day of his adult life. Although one can be blessed with a much better immune system than others, the ability to synthesize GLO, at least to a limited degree, could also be the reason for an otherwise incredibly long and healthy life.

Any inborn error of metabolism is also not "completely expressed" all of the time. Certain enzyme levels may be depressed by 10%, 50%, or 90%, but not necessarily 100%. This must also be considered a possibility for the levels of GLO in different people possessed of great longevity, at least until careful studies can determine otherwise. Cummings (1981) pointed out that some individuals enrolled in vitamin C depletion studies were discontinued from those studies when no symptoms of scurvy developed or when vitamin C levels did not drop significantly over an extended period of time (Kline and Eheart, 1944; Pijoan and Lozner, 1944). It seems that there was never any serious curiosity over whether these individuals could continue to have vitamin C in their bodies over even longer periods of time. If any individuals could be identified with even partial GLO production and internal vitamin C production during periods when dietary vitamin C restriction resulted in scurvy for the remainder of the individuals studied, even more exciting avenues of research could be pursued. It is always easier to research a condition that is not possessed by all.

Further support for the concept that all human beings might not be completely lacking in GLO and the internal production of vitamin C comes from studies with guinea pigs. Williams and Deason (1967) reported that one guinea pig continued to survive after eight weeks on a vitamin C-free diet, which should have produced scurvy. Before long, several other investigators concluded that some guinea pigs could synthesize vitamin C, thereby accounting for the occasional wide variability in the laboratory requirements needed to induce scurvy in these animals (Odumosu and Wilson, 1967; Ginter, 1976). In spite of this research, there still does not appear to be any enthusiasm or significant interest in looking systematically for those occasional humans who can also synthesize some vitamin C.

Cummings (1981) further points out that if the lack of GLO in humans comes from the same recessive genetic trait as is found in other genetic enzyme deficiency states, then occasional mutations should be expected to occur that would again allow GLO to be expressed and vitamin C to be synthesized. However, if any of the above is true, a deliberate search should be made to find such vitamin C-synthesizing individuals. Some findings may fall into a researcher's lap, but many must be specifically sought out or they will not be found.