Vitamin C- The Real Story

by Steve Hickey

  Are There Many Types of Cancer?

  Physicians often describe cancer as a large number of different conditions, each involving abnormal cell division and growth. Cancers that arise in specific tissues, or with particular defining characteristics, are considered as individual diseases. The disadvantage of this approach is that it does not provide an overview of the biological mechanisms underlying the illness. However, the “many types” approach also has advantages, specifically in suggesting that some forms of cancer may be more susceptible to particular therapies. For example, hormone-based treatments may be more effective against cancers originating in hormonally responsive tissues, such as the prostate or breast, whereas a cancer originating in the lung might not respond favorably.

  Clinically, cancer is often described in terms of the original site of the tumor. For example, “small cell lung cancer” is a type of cancer arising in the lung, which, as the name suggests, has relatively small cells. As cancer cells proliferate, they form tumors that may be benign or malignant. Many benign tumors are non-invasive and relatively safe, although some, such as uterine fibroids (which can occasionally lead to a hemorrhage or even death), may be life-threatening. Lumps of fatty tissue under the skin (lipomas) are a common form of a relatively harmless benign tumor.

  Malignant tumors are the form of the disease that most people fear, and understandably so. A malignant tumor is an expanding mass of tissue that invades its surroundings, extending fingerlike into the tissues. The name cancer comes from the Greek word for “crab,” as the invading protuberances were thought to resemble a crab’s legs and claws. Malignant cancers do not have well-defined borders or a surrounding capsule. To the touch, a malignant tumor feels more attached to the neighboring tissues, in contrast to the clearly distinct lump that is characteristic of benign tumors.

  Most tumors are classified into two main groups, carcinomas and sarcomas. Carcinomas originate from epithelial and endothelial tissues, which form the coverings of the external and internal surfaces of the body and include the skin and the linings of the mouth and gut. Carcinomas are common, because they arise in tissues that contain continuously dividing cells. Because of their protective function in the body, these tissues can be damaged by mechanical stress, chemical attack, or oxidation. Sarcomas are less common and derive from connective and non-epithelial tissues, such as bone, cartilage, muscle, or fat. Classifying malignant tumors into these different types is somewhat arbitrary, because cancers lose the characteristic features of the cells from which they arise.

  The classification of cancers into particular types can be misleading and it obscures the similarities and the consistent changes in oxidation levels. The multiple disease approach also hides the central role of vitamin C in driving normal tissues into reducing states and sick tissues into oxidative states. Understanding the role of vitamin C and other antioxidants in the generation and growth of cancer brings us closer to the aim of cure.

  A Single Disease

  Viewing cancer as a single disease with many variants enables investigators to determine the core mechanisms. The primary feature of cancer is cell proliferation: a single cancer cell in a favorable environment, with an abundance of nutrients, can produce billions of offspring. A single aberrant cell can theoretically divide to form a large tumor. When growing rapidly, cancer cells may move and invade the surrounding tissues. During the infiltration of neighboring tissues, cancer cells overcome factors that normally limit tissue movement and growth. They often produce enzymes that break down the surrounding tissue matrix, enabling them to spread. This invasive process is both active and aggressive, and invasive tumors can even destroy bone.

  Thinking of cancer as a single disease helps us to understand the process of carcinogenesis in terms of evolution. Cancer is the result of each individual cell’s struggle to survive. We have seen that biology constructs multicellular organisms using a tight system of controls to enforce cellular cooperation and differentiation. However, these delicate controls developed in addition to earlier and tougher mechanisms that promote the survival of individual cells. Damaging a cell can break the continuity of these relatively fragile multicellular control mechanisms, leaving the earlier and more robust individual cell survival mechanisms. These mechanisms instruct the cell to survive by dividing, growing, and spreading—the fundamental characteristics of cancer.

  In other words, cancer cells have the attributes of a biological organism that is struggling for survival in a hostile environment. By the time a cancer achieves malignancy, it is genetically different from the normal host cells. A typical cancer cell will have lost fragments of chromosomes and gained others. However, this idea is misleading, because there are no “typical” cells in malignant tumors. The cells differ widely, as errors in cell division have jumbled the chromosomes. One cancer cell might have only ten chromosomes, while another could have more than a hundred. A malignant cancer is actually an ecosystem containing competing single-celled organisms, each fighting to establish genetic success.

  The simplest way of considering a malignant cancer cell is as a new species. Each cell is growing and trying to leave more offspring than its competitors. Cancer cells that grow rapidly, spread to new areas, and refuse to die will leave more offspring. By the laws of evolution, such “fitter” cells will survive. This is why cancer is so difficult to cure—cancer cells are successful survivors of an evolutionary battleground.

  Multicellular organisms fight a constant battle with cancer. In order to survive, they have to prevent cancer from starting. If cancer does take hold, the healthy cells have a survival advantage if they can destroy it before it reduces their ability to survive. Thus, humans have evolved to resist cancer for long periods of their lives. Host resistance is often assumed to depend on the immune system to remove potentially cancerous cells. Redox substances provide an alternative and more general mechanism for removing aberrant cells, and an explanation for spontaneous remission.

  Spontaneous remission with advanced cancers is rare, but it may involve the changes in the local redox state of the tissue. Over the years, hundreds of cases of spontaneous remission have been described.5 Even by 1966, an estimated 200–300 accepted remissions had been recorded. However, unreported remissions may be much more numerous, as some people may remit before they have any symptoms and others may be on record as having been cured by the treatment they received when actually they recovered spontaneously. Local oxidation or destruction of tumors by the immune system could explain spontaneous remissions. A high intake of vitamin C will assist both the redox and immunological mechanisms behind spontaneous remissions. Indeed, one reason for the abundance of vitamin C and other antioxidants in both animals and plants is resistance to cancer.

  Vitamin C and Cancer

  In 1940, a few years after the vitamin C molecule was identified, researchers studied its effects in leukemia and noticed that cancer patients were often deficient in vitamin C.6 It was thought that correcting this deficit with intravenous sodium ascorbate might be therapeutic. A little later, William J. McCormick, M.D., anticipated a relationship between cancer and shortage of vitamin C.7 In his view, malignant cancer was a disease of inadequate collagen, resulting from a lack of vitamin C.

  In 1969, it was shown that sufficiently high doses of vitamin C were actually toxic to malignant cancer cells. In the decade that followed, exciting research reports on vitamin C and cancer suggested a completely new approach to cancer prevention and treatment. Irwin Stone, Ph.D., also documented a relationship between a shortage of vitamin C and cancer.8 He realized that vitamin C had produced a complete remission from leukemia in at least one report. A researcher had treated a patient suffering from myelogenous leukemia with 24–42 grams of vitamin C each day. The patient twice stopped taking the vitamin C and deteriorated, but when the vitamin C was reinstated, the illness went back into remission.9

  This early research work led Drs. Linus Pauling and Ewan Cameron to perform their influential studies of vitamin C an
d cancer.10 A number of Dr. Cameron’s patients were cured.11 Dr. Pauling reported that “the ascorbate-treated patients have lived, on the average, over five times as long as the matched control patients.”12 More recent research suggests that vitamin C–based redox mechanisms may be of great importance in protecting against carcinogenesis.13 When an abnormal cell starts to divide, it becomes more oxidizing and may be more sensitive to redox and other signals to commit suicide by apoptosis.14 The control mechanisms that multicellular organisms have evolved to combat the problem of cancer may provide new approaches to preventing and treating the disease.

  Boosting Redox Mechanisms

  Vitamin C is a unique antioxidant that keeps the body in a chemically reduced state. However, some scientists suggest that vitamin C can also act as an oxidant, and that oxidants cause damage to cells. They are factually correct, but far from this being a detriment to high doses, it may actually be useful in protecting us from cancer. Changes in the oxidation levels in cells are central to the development of cancer, but high levels of vitamin C can prevent these changes and inhibit carcinogenesis. Furthermore, in cancerous tissues, vitamin C acts as an oxidant, selectively killing the abnormal cells.

  The redox state of a cell is an important biochemical property because the overall level of oxidation regulates genes and their expression. Cells use molecules, such as hydrogen peroxide, as signals both within and between cells. Oxidation and reduction control some of the more important aspects of cellular behavior, including the growth, multiplication, and death of cells. This control is a feature of all multicellular creatures and is one of the foremost mechanisms used to control cancer. The central role of vitamin C in the development and potential treatment of cancer arises from its dual roles as an antioxidant and an oxidant. Reduction and oxidation combine to control the mechanisms for cell division and death.

  The overall redox state of cells is measured in millivolts (mV). Just as electricity involves a flow of electrons, the movement of electrons between molecules in bodily tissues produces a change in electric charge. Electrons carry a tiny negative charge. In a reducing environment with abundant antioxidants, more free electrons are available and the redox state (voltage) of the tissue is more negative. By contrast, a damaged tissue under free radical attack is in an oxidizing state and has fewer antioxidants. Oxidation and tissue damage is associated with a more positive redox state. Changes in the redox state are associated with different cellular behavior.15 At rest, the redox state of the cell is relatively reducing, less than –260 mV, which corresponds to a healthy cell with an active antioxidant defense. Increased oxidation, perhaps signaled by a small increase in hydrogen peroxide or nitric oxide, increases the redox state to between –260 mV and –210 mV, leading to cell proliferation.

  In general, cancer-causing agents induce oxidation or cell proliferation, which can increase any genetic errors that are present or have been caused by free radical damage. Rather than being a side effect of carcinogenesis, cell proliferation increases cell diversity and propels the cells toward malignancy. To prevent cancer developing, cells have inbuilt control mechanisms. As the redox state rises toward the oxidation level needed to produce overly rapid proliferation, cells attempt differentiation, which occurs between –210 mV and –180 mV. Cells that have changed into a more specialized form stop dividing. If a damaged cell cannot divide, it is unable to develop into a cancer—it may be sick or abnormal with little function, but it will not form a tumor.

  A cell that refuses to differentiate faces another defense mechanism. As the redox level increases to between –180 mV and –160 mV, it triggers apoptosis, or programmed cell death. Since the host has been unable to save the cell by turning it into a specialized, non-dividing cell, it uses signals to instruct the cell to die. A dead cell can be cleared away efficiently, so it presents no particular threat to the host.

  If a cell’s apoptosis mechanism has been damaged and the cell refuses to commit suicide, there is a final mechanism available to protect the host. When the redox state becomes very oxidizing, above –150 mV, the cell dies immediately through necrosis. Whereas apoptosis restricts the release of cell contents and increased tissue damage, necrosis is catastrophic: the cell loses its structure and literally falls apart. The oxidation state has increased to the point where the cell is killed without due ceremony. Used as a high-dose treatment, vitamin C has been found to induce cancer necrosis in some patients.

  Vitamin C and other antioxidants inhibit cell proliferation and the risk of cancer by maintaining an antioxidant redox state. The literature on tumor suppressor genes, such as p53, which actively prevent cancer, indicates that they act as antioxidants.16 Conversely, genes that promote cancer (oncogenes) typically increase the oxidation state of the cell. Other cancer-causing and promoting agents, such as x-rays and ultraviolet radiation, also increase the redox state and cause free radical damage. An abundant supply of vitamin C provides free antioxidant electrons and may thus inhibit the development of cancer.17

  A Nontoxic Anti-Cancer Agent

  Vitamin C is a particularly useful anti-cancer agent because of its low toxicity. As we have explained, tumors are populations of cells that can evolve ways of resisting treatment, just as insects become resistant to pesticides or bacteria develop resistance to antibiotics. With treatments other than surgery, doctors hope to change the life/death balance so that more cancer cells die than are produced by cell division. If this is achieved, the tumor will shrink.

  Oncologists use tumor shrinkage as a quantitative measure of the effectiveness of a therapy. Unfortunately, even if a treatment manages to shrink a tumor, it is not certain that the patient will live longer or suffer fewer symptoms. This poor result is because cells that are easy to kill are removed from the population, but the stronger cells that escape are highly resistant to the treatment, otherwise they would not have survived. The duration of conventional chemotherapy or radiation is usually relatively short, because it is poisonous to the patient’s health, resulting in unbearable or even life-threatening side effects. If cancer cells remain following the treatment, the tumor can grow back with a higher proportion of resistant cells. The resistant cancer cells now face less competition for resources from other cancer cells, so they can often grow more rapidly. Subsequent treatments will be less effective, as the cells are less sensitive and selected for toughness. If the patient completes several cycles of treatment, the cancer cells can become completely resistant, and will then be free to grow and invade the body. Thus, the initial shrinking of a tumor is not a reliable indication of treatment success.

  An effective therapy should increase the lifespan of the patients and increase their quality of life. It is important to consider the cost-benefit, pain-gain, relationship of conventional cancer therapies carefully for each patient. Typically, anti-cancer drugs are toxic chemicals that kill cells. In some cases, these toxic drugs kill cancer cells a little more effectively than they do healthy cells. When such drugs are given, the susceptible cells in the tumor may be wiped out quickly, but other susceptible cells, such as those in hair follicles and the lining of the gut, can also be damaged. With a sequence of treatments, cancer cells are selected for resistance, whereas the person’s previously healthy cells become increasingly more damaged and unable to withstand the treatment.

  The solution to this therapeutic impasse is to employ nontoxic anti-cancer agents. There are numerous such compounds available, but the main component of an anti-cancer diet is vitamin C. Vitamin C alone can be effective, but its action can be multiplied several-fold when combined with other redox nutrients and vitamins, such as alpha-lipoic acid or vitamin K3. The nutrients act in redox-synergy to selectively destroy cancer cells. The driving force of this cancer destruction is the availability of massive amounts of vitamin C. A vitamin C–based approach can produce a constant pressure on the population of tumor cells, inhibiting their growth. But vitamin C acts as an antioxidant and protects healthy cells from the toxic effects of chemotherapy.
In general, vitamin C does not appear to interfere with or reduce the effectiveness of chemotherapy.18

  Vitamin C, acting as an oxidant, is selectively toxic to cancer cells, inhibiting their growth or killing them outright. Killing cancer using a redox-based nutritional approach has few side effects and there is evidence that it may increase lifespan, while enhancing the patient’s quality of life. This is the good news about cancer and ascorbate.

  A typical redox-synergy therapy based on vitamin C is given here.19 This would be considered a standard approach for most cancer patients who are not in the final stages of the disease.

  • Vitamin C (as L-ascorbic acid), dynamic flow level, at least 3 grams, five or six times each day, providing a daily total of 20 grams or more (>90 percent bowel tolerance). Liposomal formulations are highly recommended.

  • R-alpha-lipoic acid, 200–500 mg with each dose of vitamin C (up to 5 grams total oral intake).

  • Vitamin D3, 4,000 IU per day.

  • Selenium, 800 μG per day (as methylselenocysteine). This level of selenium intake corresponds to the U.S. government’s “no observed adverse effect level” and is the maximum intake considered safe of any side effects.

  • Absorbable magnesium, 400–2,500 mg per day (as magnesium citrate or magnesium chelate).

  • Very-low-carbohydrate and low-calorie diet.

  • Lots of fresh raw vegetables.

  This is a severe dietary restriction, involving low calories and, in particular, reduced intake of carbohydrates and proteins. Essentially, it corresponds to severe dietary restriction with the highest tolerated intakes of vitamin C and alpha-lipoic acid.

  Case Study

  The following anecdote describes the experience of one of the authors (A.W.S) with a cancer patient taking large doses of vitamin C: