Dr.CATHCART, Titrate, dose, Antibdy, Non-Rate, 3 Face, Func, AIDS, L.AIDS, IV Prep, Bib, Xref

Unpublished letter on AIDS, 1992

                                                                March 10, 1992

Critical Path Project, Inc.
2062 Lombard Street
Philadelphia, PA 19146

Dear Sir:

The article, The Nontoxic Path: Vitamins, Dietary Supplements, Adjunctive Therapies, part 1, shows that there is again some interest in the nutritional treatment of AIDS. Unfortunately, the vitamin C doses described in the article are too small and will not be of help treating an AIDS patient.

Enclosed are miscellaneous articles and references I have written on ascorbate. I began utilizing ascorbate and other nutritional substances in a number of diseases in 1969 and against AIDS in 1983. As you can see I made some effort toward making the value of ascorbate in AIDS known but, being only interested in clinical medicine and not at all in politics, burned out on the subject. Nevertheless, two or three physicians call me each week about the use of ascorbate, especially about its intravenous use. Hundreds of physicians (more from foreign countries than the U.S.) have written for reprints of these articles. Some of the articles have either partially or completely been translated into different languages. Please note that I have been referenced in Jariwalla's paper and Pauling's latest book. The only physician I know who has significantly embellished the program is Joan Priestly, M.D. of Los Angeles. Also enclosed is an outline of a combined (Cathcart and Priestly) program for an uncomplicated HIV positive person. This nutritional program works much better than AZT.

There are several problems convincing the medical community to use ascorbate in the manner I describe. It is impossible to double blind the oral doses of ascorbic acid taken to bowel tolerance because there is no possible placebo. The method of increasing doses of ascorbate until a noticeable clinical amelioration is obtained precludes a double blind study. A study of the effect of intravenous ascorbate on a disease such as acute infectious hepatitis A, B, or C would be easy but the effect is so dramatic that it would be immoral for any physician who has seen this effect to do a double blind study. How can you go to a patient with hepatitis saying that you want to test on them ascorbate that will flat out .... (a physician cannot ever say cure because that means a legal guarantee but I have never seen it fail) acute hepatitis and that there will be a 50% chance they will get ascorbate and a 50% chance they will get something of no value or relatively worthless and perhaps harmful. Maybe someone could do such a study at a university or charity hospital but they could not do it in a private practice.

Ascorbate does not cures AIDS but it will prolong the life of AIDS patients and make their life much more comfortable. I have had patients tell me that they have never felt better in their life as after starting the nutritional program. There is no reason the ascorbate and other nutrients should not be used in conjunction with standard treatments where necessary.

One of the great problems is that ascorbate (used in massive doses) is too important. It sounds like a panacea. However, It has importance in the treatment of any disease that involve free radicals. This means that ascorbate should be used in conjunction with other treatments in not only infectious diseases but injuries, burns, radiation injury, surgery, cancer, allergies, cardiovascular disease, allergies, autoimmune diseases, aging, etc. The financial implications are enormous.

The following is the major point about the use of ascorbate that hardly anyone fully appreciates:

In the sense that when you throw a bucket of water on a fire, it is the water that extinguishes the fire, not the bucket; when free radical scavengers meet free radicals, it is the reducing equivalents that neutralize the free radicals, not the free radical scavengers.

Technically, enzymatic free radical scavengers such as catalase neutralize specific free radicals such as, in this case, peroxide without additional energy. However, many free radicals have to be neutralized by reducing equivalents carried by non enzymatic free radical scavengers. The energy required for these reducing equivalents originally comes from the sun, is incorporated into plants by photosynthesis, eaten by animals, and then by metabolic pathways involving glycolysis, the citric acid cycle, NADPH, glutathione, etc., processes too long to describe here, becomes reducing equivalents. This same energy has to be doled out for making ATP, keeping us warm, growing and repairing tissues, fueling the respiratory burst of phagocytosis, etc. When you are very sick and do not have the energy to move around much, you have little energy remaining for reducing equivalents to scavenge free radicals. Massive doses of ascorbate can supply those needed reducing equivalents.

Certain nutrients that are also free radical scavengers may be necessary for special metabolic processes. An example is the necessity of vitamin C in the hydroxylation of proline in the synthesis of collagen. In most, if not all, of its vitamin functions, vitamin C functions as an electron donor (by donating reducing equivalents.) By reading the medical, nutritional, and biochemistry literature, one can easily overlook the fact that most of the total of the reducing equivalents carried by vitamin C, vitamin E, -carotene, selenium, and yes, glutathione, cysteine, NAC, etc., which neutralize free radicals, come not from the ingested nutrient but from the energy distributing pathways mentioned above. One molecule of ascorbate carries two reducing equivalents (maybe one or two more if you count further breakdown products of dehydroascorbate) and that is it. When it gives up those reducing equivalents, it becomes DHA and has to be rereduced by reducing equivalents from the metabolic pathways or else be destroyed. The vitamin C cycles and is used over and over again. Very few of the total reducing equivalents used to scavenge free radicals come from the dietary free radical scavengers.

The AIDS patient cannot possibly take enough NAC to provide the amount of reducing equivalents necessary to quench most of the free radicals generated in the AIDS process. It is true that NAC provides cysteine in a readily available form so the body can make glutathione. Glutathione has been shown to be low in HIV (+) people; I have no quarrel with that; but the amount of reducing equivalents necessary to neutralize the free radicals generated in AIDS far exceed that which can be brought in on the NAC and other nutrients. Except ascorbate can supply the necessary reducing equivalents when huge amounts are used. The body simply cannot tolerate enough of any other antioxidant nutrients to supply the amount of reducing equivalents being discussed here.

I dwell on this point to emphasize that I am using ascorbate to supply reducing equivalents (the vitamin C supplied becomes incidental), If you miss this point, you will not appreciate the unique role of the massive doses of ascorbate.

The majority of people with AIDS are probably taking vitamin C but only a small number appreciate what is being described here. They do not take enough ascorbate to supply the necessary reducing equivalents.

To reduce some oxidized substance, there is a threshold in the concentration of reducing substance that has to be exceeded before the reaction will proceed. This required threshold is the reason that the usual doses of ascorbate seldom accomplish the desired reducing redox potential necessary to eliminate the free radicals in the affected tissues.

In many cases the amount of ascorbic acid requisite for this function can be taken orally. Diarrhea (really just a softening of the stools) is the usual limiting factor. This is because as ascorbate destroys free radicals, the free radicals destroy ascorbate. And, of the ascorbate, what does not reach the rectum, does not cause diarrhea. This process is why the sicker you are, the more ascorbic acid will be tolerated orally without it producing this diarrhea. I have named this process of determining the effective dose of oral ascorbic acid titrating to bowel tolerance.

It is only when large amounts of ascorbate are forced into affected tissues sufficient to restore a healthy reducing redox potential in those tissues that one experiences a marked amelioration of all symptoms resulting from free radicals. I have named this sudden effect the ascorbate effect.

If oral doses are inadequate or not tolerated in adequate doses, intravenous sodium ascorbate may be necessary. Unfortunately, intravenous ascorbate is not generally covered by insurance and frequently cannot be afforded by the patients. This refusal of insurance companies to cover intravenous ascorbate is shortsighted even from their selfish financial point of view because hospitalizations, far more expensive than the intravenous ascorbate, can usually be avoided.

Intravenous ascorbate in combination with the appropriate antibiotic will usually abort an impending PCP attack. It does this so reliably that usually prophylactic treatment for PCP can be avoided. The ascorbate in these massive doses drastically reduces the incidence of allergic reactions to antibiotics. It seems that the reason patients have so high a rate of allergic reactions to drugs, especially antibiotics, is that they take them when they are sick. The free radicals activate the immune system. Clinically, massive doses of ascorbate usually prevent allergic reactions. Allergic reactions underway can be terminated abruptly with adequate doses of ascorbate.

Free radicals are an almost universal sign of damage to the body. It would not do for the immune system to be taking off after every foreign macromolecule that enters into the body. Actually this is what frequently happens when one is chronically ill for long periods of time. The immune system is activated by the resulting free radicals. All this is a theory of mine to explain the observed facts but there is experimental evidence that the affinity of antibodies for their antigen is greater in an oxidizing redox potential. No one else seems to make anything of that fact.

Fortunately, while ascorbate in massive quantities suppresses this humeral immunity of antibodies, it augments the cellular immunity of phagocytic cells. I think it does this both by providing reducing power that initiates the respiratory burst (by the reduction of molecular oxygen); and by protecting the white cell from those very radicals the white cell makes in its vacuoles to kill the pathogens. White cells are unable to continue to produce these "good" radicals when the radicals leak significantly into the cytoplasm (then becoming "bad" free radicals) and exceed the ability of their free radical scavengers to neutralize.

All this is useful in the treatment of autoimmune diseases and allergies but this is another story. However, I have been maintaining for several years that we should be trying to keep HIV (+) patients from becoming sick with anything. We should not be trying to "stimulate" the immune system because this eventually results in the autoimmune destruction of the T4 cells. I am pleased that the autoimmune theory of AIDS is being seriously considered now. One could inject feces under the skin and stimulate the immune system if the immune system is relatively intact. DNCB, other noxious substances (AZT?), and immunizations will increase the T4 cells in the early stages of the disease; this should be expected. However, this type of treatment hastens the final autoimmune destruction of the T4 cells. DNCB was sometimes seen to be beneficial in increasing the number of T4 cells while they were still above 200. This stimulation would sometimes have some beneficial effect on secondary infections such as KS for a period of time. I think, however, that these approaches that are productive of free radicals hasten the final autoimmune attack on the T4 cells. We should not be so obsessed with increasing the numbers of T4 cells, certainly not with noxious substances; especially while the T4s are in the range of normal. We should concentrate on feeding and protecting the T4 cells.

When free radicals dominate in a tissue for long, the small amount of vitamin C ordinarily present is converted to dehydroascorbate (DHA) which has a very short half-life. This results in a condition I have named acute induced scurvy in the tissues involved in the disease. When one observes a patient dying of AIDS, many of the classic signs of scurvy can be observed. One of the most important problems in acute induce scurvy is that the white cells become nonfunctional. Another point of titrating to bowel tolerance with ascorbic acid and taking intravenous sodium ascorbate is to restore the vitamin C in all tissues affected by disease. The vitamin C levels can be conserved only if a reducing redox potential is maintained in those tissues.

If I can be of any additional help in assisting your readers to properly utilize ascorbate, please let me know.


Robert F. Cathcart, III, M.D. 
127 Second Street, #4
Los Altos, CA 94022