While researching thousands of articles over the last few years in the preparation of my latest book on vitamin C (Levy, 2002), interesting patterns began to emerge. Even though the effects of vitamin C on over 25 different infectious diseases and over 100 different toxins were examined, common mechanisms of action became apparent. This was especially significant to me since I had long wondered how a single chemical entity (ascorbate, or vitamin C) could have such dramatically positive clinical effects on such a wide array of completely unrelated chemical compounds and infectious agents. Quite literally, there seemed to be no exceptions to this vitamin C effect. Even if vitamin C did not cure a given infection or toxic state, it always helped resolve such a condition to some degree.
Dr. Albert Szent-Gyorgyi, the brilliant scientist who won the Nobel Prize in 1937 for his discovery of vitamin C, also advanced what I would call a true theory of life in two of his last publications. Szent-Gyorgyi (1978, 1980) asserted that energy exchange in the body can only occur when there is an imbalance of electrons among different molecules, assuring that electron flow must take place. Natural electron donators give up electrons to natural electron acceptors. Szent-Gyorgyi maintained that dead tissue had a full complement of electrons; a state in which no further exchange or flow of electrons could take place. Another way of viewing this is that brisk electron flow and interchange equals health, impaired or poor electron flow and interchange equals disease, and cessation of flow and interchange equals death. Vitamin C, as the premier antioxidant in the body, is perhaps the most important ongoing electron donor to keep this electron flow at optimal levels.
Oxidation involves the loss of electrons, and an antioxidant counters this process by supplying electrons. Although vitamin C is the most important antioxidant in the body, there are many different antioxidants present in the body, and many of them work to keep the more important antioxidant substances in the body in the reduced state, which allows the donation of electrons. For example, vitamin E is an antioxidant that is fat soluble, which is important in allowing it to be the primary antioxidant present in the lipid-rich cell membranes of the body. Vitamin C, which is water soluble, helps to recharge oxidized vitamin E in those cell membranes back to the electron-rich reduced form. Even though vitamin C is not the primary antioxidant in the cell wall, it plays a vital role in maintaining the optimal levels of the metabolically active antioxidant, vitamin E, at that site.
It appears, then, that the local loss of electrons (oxidation) represents the primary degeneration, or metabolic breakdown, of the tissue or chemical substance losing the electrons. An antioxidant can serve to immediately restore this loss of electrons, resulting in a prompt "repair" of that acutely oxidized tissue. Also, an antioxidant can often neutralize the oxidizing agent before it gets a chance to oxidize, or damage, the tissue initially.
All of the vitamin C/toxin exposure studies reviewed showed one or more of the following findings or consequences in the test tube, tissue, intact animal, or human studied:
1. Decreased levels of vitamin C and other antioxidants (blood and/or the tissues most specifically affected.
2. Increased levels of oxidative stress in the test setting, indicating ongoing oxidation.
3. Increased liver production of vitamin C (in those species capable of this), as an adaptive response.
4. Increased rates of consumption of vitamin C and other antioxidant.
5. A direct correlation between toxin activity and antioxidant levels (lower antioxidant levels, greater clinical toxicity).
6. The acute induction of scurvy or other clinical findings consistent with the acute depletion of vitamin C.”