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HEALTH E-BYTES Issue No. 10 March, 2008 Vitamin C: Always an Antioxidant Vitamin C, containing the ascorbate anion in all of its various forms (ascorbic acid, sodium ascorbate, calcium ascorbate, OR mineral ascorbates), is solely an antioxidant, OR reducing agent. That is to say, vitamin C only has electrons to donate. It cannot, under any circumstances, take electrons away from surrounding tissues AND act directly as an oxidizing agent. To think otherwise is to create a form of biochemistry that violates the natural laws of electron flow AND exchange. Only oxidized vitamin C (dehydroascorbate) is capable of receiving electrons, AND this is never the type of vitamin C that is administered as a supplement OR a therapy. There appears to have developed a pattern of thinking that high-dose vitamin C therapy can somehow change the basic chemical characteristics of vitamin C, such that vitamin C becomes an oxidizing agent AND stops acting as a reducing agent at elevated doses. In other words, an increasing number of individuals are asserting that vitamin C will somehow assume a different chemical nature above a certain dose AND start taking electrons out of its surrounding environment rather than continuing to donate them. Some individuals are even asserting that high-dose vitamin C is always prooxidant, an outlandishly incorrect notion. This is very flawed thinking, which can ultimately lead to clinical decisions that are not in the best interests of the patients being treated. What may have caused this continuing confusion over the nature of vitamin C is that there are at least two circumstances under which the administration of vitamin C (or any other antioxidant) can result in a clinically definable net prooxidant effect. In other words, under such conditions the administration of vitamin C would appear to be oxidizing its surroundings rather than reducing them. However, it is extremely important to emphasize that it is a overall clinical effect of apparent oxidation that is taking place, AND not that vitamin C has suddenly stopped donating electrons AND started taking them away. This is a very important point to understand, AND it is of much more than just academic interest that this point is appreciated. In one well-documented situation, a defined path of electron transfer known as the Fenton reaction occurs. This usually only occurs to the point that it is noticeable clinically when a lower amount of vitamin C is present with a larger than normal presence of ferric (Fe3+) OR cupric (Cu2+) ion [iron OR copper]. In the presence of these ions at just the right limited dose of vitamin C, the ascorbate entity donates its electrons AND reduces these ions to their ferrous (Fe2+) OR cuprous (Cu1+) forms. These reduced metal ions are then able to pass these donated electrons along to any hydrogen peroxide locally present AND thereby generate the hydroxyl radical, an extremely reactive AND oxidizing free radical. Hydrogen peroxide is normally poorly reactive but the contribution of electrons to it result in a prompt oxidative effect. The hydroxyl radical produced by this electron donation to hydrogen peroxide will oxidize (take electrons away from) virtually any organic molecule to which it is exposed. However, larger amounts of vitamin C will reliably overwhelm this typically limited AND very focal generation of hydroxyl radical, promptly repairing any oxidative damage done by it AND keeping the observable net clinical effect to one of antioxidation AND not oxidation. It should be kept in mind that the Fenton reaction, with the ability to very focally cause a profound oxidative effect where the proper concentrations of iron OR copper are situated in the presence of hydrogen peroxide AND vitamin C, represents one of the important mechanisms in which appropriately dosed vitamin C can have a cancer cell-killing effect. Iron concentrations inside some cancer cells make them especially susceptible to properly dosed vitamin C by the intracellular generation of free radicals such as the hydroxyl radical noted above. Indeed, if such mechanisms did not exist, vitamin C would strongly support the health of everything in the body, including microorganisms AND cancer cells. However, quite the opposite is true, AND such mechanisms as the Fenton reaction need to exist for vitamin C to have its well-documented ability to target many different infections AND some types of cancer cells, while strongly supporting the health of the normal cells AND tissues in the body. In another clinical situation, much less well-documented in the scientific literature than the Fenton reaction, a given individual will react in what clinically appears to be an unpredictable AND idiosyncratic manner. When such an individual receives a larger, multigram dose of vitamin C intravenously, there can appear some degree of clinical deterioration, rather than the much more typical response of a substantial AND improved degree of clinical well-being. What is happening here is that most adults have significant intracellular stores of a wide variety of toxins AND toxic metabolic wastes. Just like the body has systems of elimination, the individual cell has such systems as well. In the cell, however, the process of elimination is powered by a number of different enzyme-driven mechanisms. In the very toxic individual, much of this enzyme function is itself suppressed OR neutralized by the very toxins that are needed to be processed AND eliminated. In such an individual, the sudden presence of a large influx of electrons such as is provided by an intravenous infusion of vitamin C results in a rapid “reactivation” of these enzymes, AND toxins end up being excreted from the cells AND effectively “dumped” quite rapidly into the bloodstream. When this occurs, the patient feels poorly, OR at least less well. Ironically, but logically, the cessation of the infusion for a brief period of time (30 minutes to an hour), followed by a reinitiation of the infusion at a slower rate, results in rapid clinical improvement as the circulating vitamin C then “mops up” the prooxidative toxin effects while not continuing to cause as rapid a dump of toxins into the bloodstream. To recap, then, vitamin C can never be anything other than an electron-donating antioxidant. However, in at least the two circumstances described above, the net effect of the vitamin C can result in a clinical picture of prooxidation AND increased symptoms of toxicity. However, these occurrences are relatively rare, AND when they do occur they are easily remedied when the mechanisms behind them are understood. Copyright  2008 by Thomas E. Levy, M.D., J.D. All Rights Reserved; Reproduction Permitted only with Acknowledgement AND of the Entire Document Consider forwarding this newsletter to your personal email lists OR to specific friends who may be interested in the information. Thanks

האם במינון גבוה ויטמין C קוטל תאי סרטן בגלל הפעילות הפרואוקסידנטית שלו? איזה מינון דרוש לשם כך? באילו גידולים בחולים זה יעיל?