C and ALLERGY TREATMENT

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C and ALLERGY TREATMENT

--

--- Dr. Robert F. Cathcart, M.D. --- --- Allergy, Environmental, and ---

----- Orthomolecular Medicine ----- ------- Orthopedic Medicine -------

--- 127 Second Street, Suite 4 --- --- Los Altos, California, USA --- ----

Telephone: 650-949-2822 ---- ---- Fax: 650-949-5083 ----

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Copyright ©, 1994 and prior years, Dr. Robert F. Cathcart. Permission

granted to distribute via the internet as long as material is distributed in

its entirity and not modified.

 

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Submitted to Medical Hypotheses February 13, 1986.

 

 

THE VITAMIN C TREATMENT OF ALLERGY AND THE NORMALLY UNPRIMED STATE OF

ANTIBODIES

_http://www.mall-net.com/cathcart/unprimed.html#C%20and%20ALLERGY_

(http://www.mall-net.com/cathcart/unprimed.html#C%20and%20ALLERGY)

 

ABSTRACT

 

 

I previously described that bowel tolerance (the amount that almost causes

diarrhea) to oral ascorbic acid, increases in a person somewhat proportionally

to the " toxicity " of his disease. Ascorbic acid ameliorates symptoms and

sometimes cures certain diseases at high threshold levels near bowel tolerance.

High concentrations of ascorbate cause the redox potential of the redox

couple (ascorbate/dehydroascorbate, AA/DHA) to become reducing in diseased

tissues. Allergic and sensitivity reactions are frequently ameliorated and

sometimes completely blocked by massive doses of ascorbate. I now hypothesize

that

one mechanism in blocking of allergic symptoms is the reducing of the

disulfide bonds between the chains in antibody molecules making their bonding

antigen impossible. I further hypothesize that antibodies seek to match

antigens

only in areas where stray free radicals or a relatively oxidizing redox

potential exists. The redox state of normal, healthy tissue does not allow for

the bonding of antibodies to antigen. When antioxidant, free radical

scavenging systems are overwhelmed, inflammatory, hypersensitivity, and

" autoimmune "

conditions may result.

 

 

INTRODUCTION

 

 

Based on my experience with over 12,000 patients during the past 15 years,

it has been my consistent observation that the amount of ascorbic acid

dissolved in water which a patient, tolerant to ascorbic acid, can ingest

orally

without producing diarrhea, increases considerably somewhat proportionately

with

the " toxicity " of his illness (1,2). A person who can tolerate orally 10 to

15 grams of ascorbic acid in divided doses per 24 hours when well, might be

able to tolerate 30 to 60 grams per 24 hours if he has a mild cold, 100 grams

with a severe cold, 150 grams with influenza, and 200 grams per 24 hours

with mononucleosis or viral pneumonia. Patients with hay fever, asthma, or

environmental, drug, and food allergies and sensitivities usually tolerate from

between 15 to 50 grams per 24 hours divided in 4 to 12 doses. Occasionally,

tolerance is elevated even to higher amounts. There is frequently a dramatic

decrease in symptoms just before diarrhea is produced. The individual

patient has to be tolerant to oral ascorbic acid to achieve this effect but

fully

80% of patients are tolerant enough. I call the process whereby the patient

determines an appropriate dose of ascorbic acid, titrating_to_bowel_tolerance.

Intravenous sodium ascorbate is even more effective.

 

I had previously hypothesized (3,4) that this ameliorating effect is largely

due to the antioxidant, free radical scavenging effect of massive doses of

ascorbate. Additionally, I had hypothesized that oxidants and free radicals

formed in pathologic processes, oxidize ascorbate in the diseased tissues,

exhausting the ascorbate first in the involved tissues, and then in the body

more

generally. There is then no vitamin C left over for known vitamin C

functions first in the involved tissues, and then in the body more generally. I

call

this phenomenon acute_induced_scurvy. To the extent that free radicals are

formed in allergic and sensitivity reactions, I think that these mechanisms

apply. I have much clinical evidence that massive doses of ascorbate will

ameliorate the secondary inflammatory cascades of injury and surgery.

 

I had hypothesized that the threshold where high doses of ascorbate suddenly

became effective was where the ascor- bate/dehydroascorbate (AA/DHA) redox

couple became reducing in the affected tissues (5). The dehydroascorbate

formed, as ascorbate reduces free radicals and oxidizing substances, is not as

toxic as the substances it reduced because the oxidizing redox potential of the

dehydroascorbate is not as great as the oxidizing redox potential of the

free radicals and oxidizing substances reduced. But additionally, if the

amount

of ascorbate ingested is enough to cause the AA/DHA redox couple to become

reducing in the affected tissues, the dehydroascorbate formed will not be at

all toxic. We should not just think of the ascorbate being a reducing

substance and the dehydroascorbate being an oxidizing substance but should

think of

the redox potential of the redox couple, ascorbate/dehydroascorbate. I am

able to negate any oxidizing effect of dehydroascorbate formed by making sure

that the patient always ingests or is administered enough ascorbate to drive

ascorbate into the depths of the diseased tissues in concentrations that

exceed the dehydroascorbate formed. The redox potential of the redox couple is

made reducing in the depths of the diseased tissues.

 

ASCORBATE_BLOCKAGE_OF_ALLERGIC_REACTIONS

 

 

I have found that ascorbic acid in bowel tolerance doses is able to block

many allergic reactions. I was alerted to this possibility when my own

seasonal hay fever symptoms were blocked with 16 grams of ascorbic acid orally

per

24 hours under conditions of moderate exposure to pollen. However, with

exposure to higher doses of pollen, it required increased doses to maintain

reasonable blockage of symptoms. Acute exposure to antigens could increased

tolerance to 50 grams or more per 24 hours. When the exposure to allergens was

very

great, the blockage of symptoms was frequently incomplete. Experience with

at least 1000 allergic patients has verified this finding in most cases. The

limiting factor frequently seems to be the ability of the individual patient

to consistently take that amount which almost causes diarrhea. The

combination of ascorbate treatments with other treatments may result in even

more

optimum results.

 

Asthma attacks are frequently ameliorated similarly. When asthma is induced

by exercise, massive doses taken before, during, and after the exercise will

usually prevent otherwise expected attacks. Asthmatic attacks provoked by

infections, especially upper respiratory infections, are most frequently

prevented. The efficacy in these cases is mostly dependent upon the ability of

the

patient to tolerate sufficient doses of ascorbate. In severe acute

situations, intravenous ascorbate may be especially effective in patients

unable to

take adequate amounts orally.

 

Urticaria, bee stings, poison oak, eczema, etc. can be ameliorated to

varying degrees depending upon the tolerance of the patient to ascorbate and

upon

other as yet undefined variables. Ascorbate frequently works synergistically

with other treatments for these allergic conditions.

 

 

SCARLET_FEVER

 

 

Three patients with scarlet fever were treated who had the typical sandpaper

like rash. The rash in these cases, the fever, and all other manifestations

of the disease vanished in a few hours when the patients ingested bowel

tolerance doses of ascorbic acid. The effect of ascorbate on scarlet fever and

some food poisonings is so dramatic as to suggest a destruction of a finite

amount of toxin which is not being replenished by the disease process.

 

DRUG_REACTIONS

 

 

About 2,000 patients were treated with penicillin, ampicillin, and

cephalosporins in conjunction with bowel tolerance doses of ascorbate without

any

immediate allergic reactions to those medications. There was one delayed serum

sickness-like reaction to penicillin in a young child. Her symptoms were

temporarily lessened with large doses of ascorbate. It was most likely that

she

had not taken amounts of ascorbate sufficient to obtain the blocking effects

being described here.

 

Several mononucleosis patients were inadvertently given penicillin along

with ascorbic acid and had no allergic reactions. This experience is of note

because of the very high incidence of allergic reactions to penicillin in

patients with mononucleosis. One patient (having been given penicillin without

ascorbate elsewhere) who presented with a typical allergic rash, had the rash

disappear in minutes when given ascorbate intravenously.

 

As the protection of ascorbic acid against allergic reactions to certain

antibiotics became increasingly more apparent, I expanded my indications for

antibiotics somewhat. While the treatment of established Candida infections

with ascorbate is complicated and of value only in conjunction with other

treatments, women who have a tendency to vaginal yeast infections whenever

given

antibiotics, have a marked reduction of this complication when taking bowel

tolerance doses of ascorbic acid along with the antibiotics. Additionally,

ascorbate seems to act synergistically with antibiotics and significantly

broaden

the spectrum of activity of the antibiotics.

 

I have not as yet had a patient have an anaphylactic reaction to anything

while taking large doses of ascorbate. The number of possibilities of

anaphylactic reactions may have been so few as to make this observation of

limited

value. However, the spectrum of conditions which ascorbate ameliorates

suggests

that ascorbate should be taken along with any other indicated treatments

whenever there is any danger of anaphylactic reaction.

 

 

The observation of Kalokerinos (6) that ascorbate prevents sudden infant

death syndrome (SIDS) may or may not be relevant here but bears repeating

whenever possible.

 

<>H3>ASCORBATE NOT STRICTLY AN ANTIHISTAMINE

 

 

While vitamin C has been described as having an anti-histamine like effect

(7,8), it is not strictly an antihistamine. Most antihistamines have an

ethylamine moiety as is present in histamine but not ascorbate. Antihistamines

appear to act by occupying " receptor sites " on effector cells and exclude the

histamine; they are pharmacological antagonists. Vitamin C has no real

stimulating effect on the central nervous system, as do most antihistamines at

certain doses. The relief by ascorbate of malaise and some toxic effects on

the

brain and body in general, may be interpreted by a patient as somewhat

stimulating however. Certainly ascorbate has no depressant effect on the CNS

as do

antihistamines. Vitamin C has no local anesthetic effect nor an

atropine-like effect found with antihistamines. Ascorbate has no acute

poisoning effect

on the CNS no matter what dose is taken orally as do antihistamines.

 

Lewin described mechanisms whereby ascorbate assists in the formation of

cyclic AMP (9) and cyclic AMP inhibits the release of histamine (10,11) from

mast cells or basophils, but this is not an effect of antihistamines.

 

Therefore, ascorbate may be found to have some of the beneficial clinical

effects which in a few instances might be similar to antihistamines, but

ascorbate would often ameliorate a condition where an antihistamine had not

helped.

Additionally, ascorbate seems at times to work synergistically with

antihistamines. Ascorbate is certainly not to be considered an antihistamine

and

has no similar pharmacological mechanism of action.

 

 

FOOD ALLERGIES, SENSITIVITIES, AND POISONINGS

 

 

Food allergies, as those which produce classical IgE mediated symptoms such

as urticarial rashes often respond rapidly. Bowel tolerance doses to the

extent that they produce softened stools, even diarrhea, and decreased bowel

transit time, reduce the duration of the reactions in addition to the blockage

of the reactions.

 

Food sensitivities, or reactions not mediated by IgE frequently present more

difficulties but bowel tolerance doses should be tried. Depending upon the

underlying cause, one can expect in a significant percentage of patients that

the intensity of reactions will be reduced and the duration of the reactions

lessened.

 

Food poisoning and gastroenteritis may be dramatically relieved by massive

doses of ascorbate. Experience is helpful in treating these conditions

because the patients fear that ascorbic acid will intensify the diarrhea and

other

bowel discomfort. In an otherwise healthy bowel there is little difficulty.

Doses of ascorbic acid far in excess of what would ordinarily be tolerated

are administered. These doses do not usually add to the diarrhea but subtract

from it. If one inadvertently overdoses greatly on the ascorbic acid,

diarrhea will be produced, but there is relief of all of the other toxic

symptoms

and the diarrhea is benign, not usually associated with any pain.

 

While it is not always successful, I always test the effect of ascorbic acid

on the food or chemical allergic patient. Bowel tolerance doses of ascorbic

acid frequently have an ameliorating effect. However, the taking of the

necessary doses of ascorbate is frequently difficult because of common nuisance

problems in these patients. The production of much intestinal gas is

frequent. Many patients with these allergies have a bowel flora that contains

Candida albicans (12,13) and other gas producing organisms. Clinically, the

sometimes enormous production of gas is suggestive that Candida and other

organisms actually ferment ascorbate, or that ascorbate somehow accelerates

their

fermentation of other foods. However, some patients seem to break through a

barrier where even larger doses of ascorbate reduce the amount of gas produced.

Perhaps the decreased transit time associated with these large doses of

ascorbic acid physically wash out much of the gas producing flora, or perhaps

high enough levels of ascorbate finally inhibit fermentation. Interestingly,

large amounts of intravenous sodium ascorbate in the range of 60 grams a day

for a day or two, administered while the patient takes as much ascorbic acid as

possible orally, may " prime " the patient in such a way that large doses of

ascorbic acid are well tolerated by mouth. Measures to starve and kill

intestinal Candida should be taken and when effective will reduce the

intestinal

gas.

 

Some of these patients will be allergic to certain vitamin C preparations.

I find that by using the synthetic ascorbic acid fine crystals derived from

corn syrup, the incidence of these reactions is reduced. Nevertheless,

allergic symptoms will sometimes occur. Experience has shown that it is not

the

ascorbate itself which causes the allergic reaction but that some trace

contaminant introduced in the manufacturing processes is responsible. When

difficulties are encountered, other forms of ascorbate should be tried.

Ascorbic

acid made from sego palm, certain preparations labelled " natural " , sometimes

tablets or even timed-release forms may be better tolerated by individual

patients. But these forms are more expensive and if used initially, may even

more

likely cause reactions. The most serious problem with certain alternative

forms of ascorbic acid is that they may not have as beneficial an effect

because blood levels of ascorbate reached are frequently not as high.

 

If mineral ascorbates are used, be mindful of the fact that it is the

ascorbate part which is being discussed here and that the amount of mineral

taken

should be considered. Mineral ascorbates alter bowel tolerance in ways which

have nothing to do with the mechanisms being discussed here. Calcium,

magnesium, and potassium salts are sometimes used by allergic patients to block

certain reactions and, when effective in an individual patient, may as well be

used in the ascorbate form. This introduces a subject beyond the scope of this

paper.

 

While it is not always successful, it is worth the effort to have every food

allergic patient try to take bowel tolerance doses of ascorbic acid. If the

bowel can tolerate it, tolerance doses may ameliorate symptoms of food and

chemical allergy to varying degrees.

 

 

The definite effect of ascorbate on IgE mediated and other immunoglobulin

mediated allergies has suggested to me a possible mode of action which can be

understood in specific biochemical terms.

 

 

<>H3>STRUCTURE OF ANTIBODIES

 

 

Although there are five distinct classes of human immunoglobulins, IgG, IgA,

IgM, IgD, and IgE antibodies, the basic unit of immunoglobulin structure

consists of two identical light polypeptide chains and two identical heavy

polypeptide chains linked together by disulfide (SS) bonds. The classic model

of

this basic unit has these chains arranged in a " Y " shape. The two heavy

chains have an angle (called the hinge) toward their middle and are linked

together by SS bonds in such a way as to form together the base of the " Y " .

This

base, or Fc fragment, mediates the binding of the antibody to host tissues,

including various cells of the immune system, some phagocytic cells, and

compliment. The SS bond linking in the base of the " Y " differs in different

classes and even different subclasses of immunoglobulins. In the case of IgM,

five

of the basic units are joined together at their bases.

 

Each of the two light chains link to either side of the " V " of the " Y "

shaped arrangement of the heavy chains, each by way of a single SS bond. Each

of

the two sides of the " V " , made up of about half of a heavy chain and the

whole of a light chain and bound together by the SS bond, are named Fab

fragments. The upper ends of these Fab fragments are the specific antigen

binding

sites and are where antigens are bound.

 

Although the following analogy involves some inaccuracies, think of each Fab

fragment of the " V " as being like a clothespin, the two wooden parts (part

of one heavy chain and all of one light chain) being held together by a

spring. The spring represents the SS bond. The far end of the wooden parts

are

called variable domains and are variously shaped so that they fit different

antigens. When the pair of " clothespins " of an antibody find a match with an

antigen, they hold onto that antigen.

 

In the IgE molecule there are 20 SS bonds. Sixteen are intrachain bonds.

Two interchain SS bonds link the two heavy chains in the hinge region of the

upper end of the Fc portion. One interchain SS bond links each of the two

light chains to the adjacent heavy chains near the hinge. In vitro, by

consecutive increases in the concentration of such reducing agents as

dithiothreitol

(DTT) and alkylation, one can sequentially disrupt the SS bonds (14). With a

DTT concentration of 1 mM, the interchain SS bonds between the heavy and

light chains are disrupted. These bonds are in the variable regions that bind

antigen. Like taking the spring out of the clothespin, the antibody becomes

unable to bind antigen. At a concentration of 2 mM of DTT, the SS bond within

the heavy chains near the hinge are reduced and there is a marked decrease

in the ability to attach to target cells (basophils and mast cells in the case

of IgE). Higher concentrations of DTT cause more reduction and disruption of

the IgE antibody.

 

Lewin (9), has analyzed biochemically the complex conditions favoring the r

eduction of disulfides by ascorbate in the human body. He concludes that

under the conditions which exist in the human body, the ascorbate/dehydro-

ascorbate system can reduce the thiol/disulfide system (i.e., ascorbate is

capable

of reducing SS bonds) when ascorbate is well supplied. Although Lewin did

not specifically mention the SS bonds of antibodies, he did mention the

dithiothreitol (DTT) (utilized in the experiment above), cystine, glutathione,

and

adrenochrome among others.

 

 

Symbolically, the reactions may be represented:

 

AA = DHA + 2e + 2H+

 

-S-S- + 2H+ + 2e = 2-SH

 

 

 

One gains the impression from Lewin's analyses of several metabolic systems

in the human body, that it is very possible that certain systems are in an

equilibrium such that if the concentration of ascorbate to dehydroascorbate is

high, the system will be reduced and usually favorably influenced. My

clinical experiences have verified these impressions. I would differ with

Lewin

only in that I have found the magnitude of the doses necessary clinically to

accomplish these feats are 10 to 15 times what he anticipated in serious

disease states.

 

 

 

UNLINKING OF ANTIBODIES

 

 

Clinically, allergic reactions are blocked by ascorbate somewhat to the

degree that a threshold concentration of ascorbate might be being pushed into

the

affected tissues. The amount of ascorbate required seems somewhat

proportional to the inflammation in the affected tissues. The threshold amount

could be

the amount of ascorbate necessary to reduce the free radicals and other

oxidants present in the inflamed tissues, establish a relatively reducing redox

potential in those tissues, and reduce the SS bonds of the antigen binding

ends of the antibodies.

 

I hypothesize that an important effect of normal levels of vitamin C and

other antioxidants is to reduce each of the interchain SS bonds of the two

antigen binding ends of the antibody. The antigen binding ends are altered in

such a way as they cannot bind anything. The pieces do not fly off in every

direction but are held together, probably by Van der Waals forces, but still

cannot bind anything.

 

Additionally, I hypothesize that this " unprimed " state is the usual state of

antibodies in normal, healthy tissues. Antibodies are not " primed " to match

antigens unless the antibodies wander into areas that have many free radicals

or a relatively oxidized redox state. The problem in humans is that with

surgery, injury, infection, allergic reaction, etc., the redox potential of

affected tissues, because of free radicals and oxidants and the inability to

make ascorbate, becomes less reducing too easily and antibodies become primed

over an unnecessarily wide area and for too long a duration of time.

 

At first this unpriming effect might seem very undesirable under certain

conditions but I think that ascorbate assists the body in modulating the

antibody response toward an optimum. Certainly, the antibody response in hay

fever,

asthma, urticarial rashes, etc. does no good and that ascorbate should block

these is desirable. An ideal situation would be that pollen, lying

harmlessly on mucous membranes, would not be bound by antibodies because the

antibodies would be unprimed, but that a bacteria or virus, etc. putting out

toxins to

ward off the immune system, would prime antibodies and cause antibodies to

start seeking a match.

 

In my limited experience with ascorbate producing animals, I have noticed

that in the cases of their surgery, injury, and infection, there is seemingly a

shorter period of pain and disability than with humans. It is as if there

were not the degree of secondary inflammatory cascade which is experienced by

humans. This impression was verified by veterinarians. It was my impression

dealing with many human injuries in a ski resort area that while acute pain

immediately following an injury or surgery is not reduced, the pain the next

day is reduced considerably when the patient is saturated with ascorbate.

When an injury is totally immobilized or is not disturbed, it is common for

there to be almost no pain at all in 24 hours. The lack of secondary

inflammation is striking.

 

My experience with avulsed pieces of skin has been that when the piece was

properly reapplied surgically, that if at the time of reimplantation the piece

was viable, it would almost invariably survive. The dying of autogenous

grafts caused by circulation being impaired due to secondary inflammation was

virtually eliminated when large doses of ascorbate were taken.

 

In the case of infections, inflammation seems less in amount and duration in

patients taking bowel tolerance doses of ascorbic acid. The inflammation

seems more confined to the limited area directly involved in the infection.

Nevertheless, most infections are shortened or aborted by ascorbate, seemingly

by mechanisms mostly unrelated to inflammation. The theoretical value of

reducing inflammation in treating many infections is attested to by the fact

that

physicians sometimes use steroids when treating infections, despite the fact

that steroids seem to inhibit certain infection fighting mechanisms. In

contrast, adequate doses of ascorbate seem to block inflammation to a more

optimum degree while augmenting various infection fighting mechanisms.

 

I think that ascorbate, at the dose levels being discussed, manages to

reduce the interchain SS bonds of antibodies except directly down on the

tissues

directly infected where the free radicals and oxidants are intensely

concentrated. In the depths of infection, ascorbate assists the phagocytes

maintain

the respiratory burst killing of pathogens while protecting adjacent tissues

from stray free radical damage (5).

 

Secondary inflammatory cascades are shut down by high doses of ascorbate

scavenging free radicals, thereby preventing an unnecessarily wide area of

relatively oxidized redox potential. Antibodies therefore remain unprimed,

except

in the small area most intensely directly affected by the injury or

infection. The antibodies are prevented from unnecessarily matching antigens

in what

would have otherwise been large areas of secondary inflammation. Therefore

the tendency toward autoimmune reactions is cut down considerably.

 

My hypothesis does not in anyway negate any of the elegant mechanisms of

immunoregulation which have been worked out to explain necessary controls of

the

immune response but it adds a very effective control mechanism which

markedly limits the area in which the more complex mechanisms must act.

 

 

 

AUTOIMMUNE REACTIONS

 

 

Clinically, it is not uncommon to have a patient complain that an area of an

old injury or old infection becomes symptomatic when he becomes ill

subsequently with some other condition. Antibodies, formed by matching

slightly

altered self-molecules, slightly altered by the previous injury or infection,

were at the time of the original insult suppressed as the original inflammation

resolved. There have been described multiple mechanisms of immunoregulation

in immunology texts whereby antibody reactions are brought under control

(15). I hypothesize that an additional mechanism of suppression is that as the

normal relatively reduced redox potential of the tissues is restored, the

antibodies become reduced and unprimed. Subsequently, when the patient's free

radical scavenging mechanisms are overwhelmed by some different condition, the

redox potential in the body systemically becomes more oxidizing and old

antibodies begin to seek matches. Some antibodies generated during the

previous

insult may then match those previously affected areas and result in pain and

inflammation. Additionally, those antibodies may cross react with tissues

similar to the previously affected tissues and more generalized conditions such

as arthritis, myositis, tendonitis, neuritis, etc. may result. Foreign body

molecules, especially from foods and chemicals, similarly may multiply

antibodies which cross react with self-molecules. Ascorbate is frequently

extremely

effective in averting this situation because the systemic redox potential is

kept relatively reducing despite local pathological processes generating

considerable quantities of free radicals.

 

Sometimes fully developed autoimmune reactions can be markedly ameliorated

by massive doses of ascorbate by driving reducing redox potentials directly

into the depths of the autoimmune reactions. Quite frequently, if high levels

of ascorbate are maintained such that the autoimmune response is mostly but

not completely blocked, the reaction may become intermittent and reveal itself

to be related to some previously unsuspected antigen and not be a true

autoimmune reaction after all. In patients suspected of having food and

chemical

sensitivities, it may be difficult to determine by history which foods and

chemicals are causing reactions because the reactions last for days.

Frequently, the duration of these reactions are shortened by large doses of

ascorbate

sufficiently that the cause of the reactions become more obvious.

 

 

VARIABLE ALLERGIES

 

 

It is not uncommon to have a patient confused as to whether he is allergic

to a certain substance or not because sometimes he seems to react to it and

sometimes not. If, for instance, the patient has antibodies to certain milk

proteins but he is otherwise under no stress, there are no inflammations going

on, and the free radical scavengers of the body have a relatively reducing

redox potential established in all tissues, then the patient will be able to

drink some milk because all the antibodies will be in an unprimed state. But,

if the free radical scavenging mechanisms have been overwhelmed systemically

or locally in the gut exposed to the milk, the antibodies will be primed and

will react if exposed to the milk antigen.

 

Free radical scavengers can be exhausted systemically by free radicals

resulting from exposure to chemicals such as formaldehyde, chronic infections

such

as Epstein-Barr viral infections, other allergic reactions, injury,

emotional stress, etc. resulting in priming of antibodies systemically. The

more

antibodies primed systemically, the more likely cross reactions will occur with

self-molecules and autoimmune reactions occur.

 

Local reactions may exhaust free radical scavengers locally and prime

antibodies. Particularly bothersome in this manner is Candida which is able to

prime antibodies in the gut and lead to sensitivity reactions to the Candida

itself and to many of the foods currently being eaten. Amoeba, Giardia and

other

intestinal pathogens may act similarly. As the inflammatory reactions

become more intense and more free radicals are released, establishing more

oxidizing redox potentials over wider areas, more antibodies are primed and

sensitivities become more severe and more numerous. Inflamed mucous membranes

are

not as able to make appropriate digestive enzymes and therefore more

macromolecules (e,g. undigested whole food proteins) would gain entrance into

the body

and be more likely to cause the production of matching antibodies.

 

 

RELATED VARIABLES

 

Diseased mucous membranes and skin are more likely to admit antigens of all

sorts including improperly digested macromolecules. Poor diet or

overutilization of certain nutrients caused by stress, can result in digestive

enzyme

deficiencies from lack of nutrients necessary to make those enzymes. Poor diet

and stress can also result in insufficient free radical scavengers to keep

the redox potential sufficiently reduced to unprime antibodies. Junk foods

can cause a patient to become allergic to good foods. Clinically. I have seen

sugar ingestion cause hay fever attacks to pollen.

 

On the other hand, relief of exposure to antigen may allow the body to quiet

inflammatory reactions, temporarily catch up with free radical scavenging,

and allow for a temporary tolerance to an antigen because the antibodies are

unprimed. For instance, a person with hay fever may, if put into an

environment completely free of pollen for a period of time, subsequently be

able to

tolerate a moderate amount of pollen without immediately reacting because the

antibodies in the nose had become unprimed. As a topical mild irritation

starts in the nasal mucosa, a more oxidative redox potential is set up, the

antibodies prime over a wider area and a more severe allergic reaction ensues.

High doses of ascorbate can keep the area reduced to a greater degree and allow

tolerance to higher exposure to pollen depending upon the concentration of

ascorbate achieved in the mucous membranes. Sometimes when moderate doses of

ascorbate are taken, there will be superficial irritations in the mucous

membranes from pollen but the usual deep edema is averted.

 

 

Vigorous treatment of infections of the gut, such as Candida, Giardia, and

other unfavorable intestinal pathogens, may reverse the relatively oxidizing

redox potential and unprime the antibodies in the gut wall. Many times food

and chemical sensitivities will be relieved if treatment is early enough.

However, food sensitivities present for long periods may be more fixed.

Nevertheless, massive doses of ascorbate, if taken in sufficient amounts,

frequently

add enough relief to make the result more satisfactory.

 

 

 

ASCORBATE AND PNEUMOCYSTIS CARINII PNEUMONIA

 

 

Pneumocystis carinii pneumonia (PCP), the most common immediate cause of

death in AIDS patients, is particularly effectively treated with a combination

of ascorbate and sulfa drugs. Of the complications of AIDS, PCP is the most

easily treated with ascorbate. The responsiveness of PCP is because of the

principles being discussed here.

 

The profound debility, fatigue, malaise, weight loss, etc., typical of PCP

must be from acute induced scurvy because of the rapidity with which the

condition responds specifically to ascorbate taken in high doses. Additional-

ly,

a major problem in PCP patients is that the incidence of allergic reactions

to the indicated sulfa drugs is so high as to ultimately prevent their use in

a high percentage of patients. The experimental drug, pentamidine, which

causes many unfavorable reactions itself, is used partly as a result of this

high incidence of allergic reaction to sulfa drugs and partly because some PCP

cases seem not to respond favorably to the sulfa drugs.

 

Clinically, ascorbate blocks the allergic reactions to the sulfa drugs

probably because of the mechanisms being discussed here. Additionally,

ascorbate

seems to works synergistically with sulfa drugs in the treatment of PCP.

Usually it is possible to treat the patient who has a tendency toward PCP with

ascorbate alone. Ascorbate, in combination with the rest of the AIDS protocol

(3,4), will prevent the majority of attacks of acute PCP. The common cold

and other respiratory diseases which predispose to the development of PCP can

usually be prevented or treated with ascorbate. Occasionally, treatment with

intravenous ascorbate is indicated if a respiratory viral disease is very

severe. A patient with an actual attack of PCP can usually be treated as an

outpatient, if caught early, with bowel tolerance doses of ascorbate plus the

appropriate sulfa drug without difficulty and with very little probability of

allergic reaction to the sulfa drug.

 

I think that the reason this combination is so successful is that the

ascorbate prevents the acute induced scurvy, part of which is the creation of a

relatively oxidative redox potential systemically which primes the antibodies.

When ascorbate is used in adequate doses the priming of the antibodies is

confined to an optimum small area directly about the primary site of the

disease. The widespread priming of antibodies which increases enormously the

probability of allergic reactions is mostly averted. If antibodies are formed

to

the sulfa drug in the primary site of the disease, those antibodies are in a

unprimed state when circulating through the skin and cannot cross react with

the skin and cause a skin rash.

 

 

B CELLS AND THE FORMATION OF ANTIBODIES

 

 

Antibodies are secreted by the B cells (15). Each B cell produces

antibodies which match a single antigen. There are elaborate methods whereby

antigen

is presented to the B-cell receptors by antigen-presenting cells with the help

of T-helper cells. The B cells are stimulated to differentiate and divide

into antibody forming cells which secrete the antibodies.

 

I think that if all the digestive enzymes are functioning properly and if

the skin and mucous membranes are intact not allowing pathogens and other

foreign macromolecules inside the body, not much antigen will be presented to

the

B cells. With inflammation damaging those membranes, more antigens will leak

into the body and more antibodies will be produced. Ascorbate would lessen

the area of secondary inflammation and thereby reduce the amount of antigen

presented to the B cells and therefore reduce the amount of antibodies formed.

 

Additionally, it may be that the B-cell receptors

(being identical to the antibodies) on the surface of the B cells are also

reduced in tissues with relatively reduced redox potential and the formation

of antibodies lessened for that reason.

 

 

 

THE T CELL AND ITS RECEPTOR

 

 

T cell receptors have a structure similar to antibodies. The T cell

receptor is made up of two polypetide chains, an alpha chain and a beta chain,

which

are, similarly to the antibodies, joined by a single disulfide bond (16). I

hypothesize that this SS bond will be reduced and the T cell receptor site

will be in an unprimed state when existing in normal tissues where there is a

relatively reduced redox state. The receptor site would become primed when

encountering free radicals or an area of relatively oxidized redox state.

This mechanism would provide a similar restraint on cellular immunity cross

reactions as with those of humoral immunity. To the extent this mechanisms

unprimed cytotoxic T cells, it would restrict cellular immunity. To the extent

it

unprimed helper T cells, it would also (along with unpriming antibodies and

B cells) limit humoral immunity.

 

 

 

ASCORBATE AND EVOLUTION

 

 

The late Dr. Irwin Stone pointed out that most animals have the ability to

make ascorbate. The higher primates lost the ability to make ascorbate about

65 million years ago. This inability to make ascorbate came about because of

the loss of the liver enzyme l-gulonolactone oxidase which is necessary for

the last step in making ascorbate from glucose (17).

 

Levine speculated that in emergency stress such as fighting for its life, an

ascorbate making animal might utilize over 50 grams of glucose per hour in

order to make

50 grams of ascorbate. This drain on blood glucose levels and resulting

fluctuating levels of blood sugar, might impair its ability to fight (18).

Additionally, I would add that there is an advantage to an animal in not

utilizing glucose for the production of large amounts of ascorbate in that it

could

go longer without food without starvation.

 

But, perhaps more importantly, animals living on the ground who nose around

in their own and other animals' wastes and eat dead and partially rotting

foods, need the extra protection of detoxification afforded by the ascorbate

free radical scavenging system. This ascorbate system is probably the reason a

dog can bury a bone and let it rot for a few days and then dig it up and eat

it without any difficulties. Up in the trees, wastes and dead things drop to

the ground. The higher primates probably became relatively picky about what

they ate, and living in sparse populations in the trees, had less to worry

about from infectious diseases. The history of mankind indicates that as

humans came out of the trees and lived together in large groups that infectious

disease became more of a problem. Smallpox, cholera, plague, typhoid fever,

typhus, etc. would regularly kill large percentages of the population of

humans in large areas. Only with the advent of modern sanitation and medical

science has there been a decrease in the deaths. AIDS is perhaps a disease

which

results from laxity of certain sanitation principles necessary in humans

because of their lack of ability to make ascorbate.

 

Whatever the reason, higher primates lost their ability to make ascorbate.

They probably could not have survived unless there had been some compensatory

mechanisms available to make up for the lack of the ascorbate mechanism such

as the enzymatic free radical scavengers, superoxide dismutase, catalase,

glutathione, etc. A very complex immune system had been evolved in mammals who

lived on the ground which was more than adequate for survival in the trees.

 

The evolutionary process fine tuned the immune system for hundreds of

millions of years in animals who were able to make ascorbate. The mere 65

million

years of evolution of the nonascorbate making primates has not completely

solved a moderate hypersensitivity tendency in those primates. Perhaps one of

the results of the big brain of homo sapiens will be that he will be able to

acquire some of the advantages of the ascorbate making mechanisms without

losing the advantage of not utilizing glucose for making ascorbate in a crisis

and also not losing the advantages of the compensatory enzymatic free radical

scavenging mechanisms.

 

It should be noted that when an organism which is not able to produce free

radicals enters a host, the host's cellular immune systems can directly

phagocytize that organism. If the organism has the ability to make enough free

radicals to suppress cellular immune mechanisms, then antibodies of humoral

immunity come to the rescue. Where cellular immunity is suppressed by free

radicals, the antibodies are primed by those same free radicals. Where

cellular

immunity can accomplish its assigned task, antibodies need not become overly

involved. Ascorbate assists cellular immune mechanisms and makes less likely

the overproduction of antibodies and the risk of autoimmune reactions.

 

 

CONCLUSION

 

 

I suspect that these hypotheses will be difficult to prove because of the

Heisenberg Uncertainty Principle. Even with the slightest disturbance, tissues

are no longer normal and healthy. Nevertheless, such hypotheses as

presented here would explain some clinical observations about the immune

system.

Particularly, these hypotheses would explain some of my observations of the

actions of large doses of ascorbate in allergic conditions.

 

I hypothesize that a relatively reduced redox state normally exists in

healthy tissues and that the disulfide bonds between the long and short chains

of

antibodies are reduced to thiols under these circumstances. The antibodies

in this state are unprimed and unable to match antigens. This situation would

apply whether the immunoglobulin existed in intra or extravascular pools,

mucous secretions, on the surface membranes of B lymphocytes, basophils or mast

cells. I hypothesize that a similar situation exists with T cell receptor

sites. When the antibodies come into areas of the body where free radicals or

an oxidizing redox potential exist, the antibody becomes primed and seeks

antigen matches. This mechanism limits the area and time where antibodies may

cross react with self-molecules and therefore reduces the probability of

autoimmune disease. It is hypothesized that where this mechanism fails, a

state

of hypersensitization comes to exist despite other immunoregu- latory

mechanisms. It is hypothesized that in fact, certain pathological conditions

overwhelm free radical scavenging mechanisms in the human body and cause this

state

of hypersensitization to come to exist. Large doses of ascorbate can restore

the relatively reduced redox state and disarm the antibodies systemically

limiting the antigen seeking of antibodies to the primary areas of disease.

Ascorbate producing animals do this naturally.

 

This mechanism provides an effective means where widespread secondary

inflammatory cascades can be prevented. The morbidity from injury, surgery,

allergy, tumors, and infection is reduced.

 

Rinse ascorbic acid and carbonated ascorbates off the teeth as prolonged

exposure may cause damage to the enamel. Do not stop large doses of ascorbate

suddenly when large doses have been taken for some time; especially do not stop

it in a crisis situation.

 

 

REFERENCES

 

--

 

Dr. Cathcart Bibliography

 

1. Cathcart RF. Clinical trial of vitamin C. Letter to the Editor,

Medical Tribune, June 25, 1975.

 

 

2. Cathcart RF. Vitamin C: titrating to bowel tolerance, anascorbemia, and

acute induced scurvy. Medical Hypotheses, 7:1359-1376, 1981.

 

3. Cathcart RF. Vitamin C function in AIDS. Current Opinion, Medical

Tribune, July 13, 1983.

 

 

4. Cathcart RF. Vitamin C in the treatment of acquired immune deficiency

syndrome (AIDS). Medical Hypotheses, 14(4):423-433, Aug 1984.

 

 

5. Cathcart RF. Vitamin C: the nontoxic, nonrate-limited, antioxidant free

radical scavenger. Medical Hypotheses, 18:61-77, 1985.

 

6. Kalokerinos A. Every Second Child. Keats Publishing, Inc., New Canaan,

1981.

 

7. Zuskin E, Lewis AJ, Bouhuys A. Inhibition of histamine- induced airway

constriction by ascorbic acid. J. Allergy Clin. Immunol. 51:218-226, 1973.

 

8. Dawson W, West GB. The influence of ascorbic acid on histamine

metabolism in guinea pigs. Brit. J. Pharmacol.

24:725-734, 1965.

 

9. Lewin S. Vitamin C: Its Molecular Biology and Medical Potential.

Academic Press, London, 1976.

 

10. Kakiuchi S, Rall TW. The influence of chemical agents on the

accumulation of adenosine 3',5'-phosphate in slices of rabbit cerebellum. Mol.

Pharmacol. 4:367-378,

1968.

 

11. Shimizu H, Daly JW, Creveling CR. A radioisotopic method for measuring

the formation of adenosine

3',5'-cyclic monophosphate in incubated slices of brain. J. Neurochem.

16:1609-1619, 1969.

 

12. Truss CO. The Missing Diagnosis. C. Orian Truss, P.O. Box 26508,

Birmingham, Alabama 35226, 1983.

 

13. Crook WG. The Yeast Connection. Professional Books, P.O. Box 3494,

Jackson, Tenn, 1983.

 

14. Ishizaka K. Structure and Biologic Activity of Immuno- globulin E. p

13-23 in The Biology of Immunologic Disease. (Dixon FJ, Fisher DW, eds)

Sinauer Associates, Sunderland, Massachusetts, 1983.

 

15. Roitt IM, Brostoff J, Male DK. Immunology. The C. V. Mosby Company,

St. Louis, 1985.

 

16. Marrack P, Kappler J. The T Cell and Its Receptor. Scientific American,

254(2):36-45, February 1986.

 

17. Stone I. The Healing Factor. " Vitamin C " Against Disease. Grosset and

Dunlap, New York, 1972.

 

18. Levine SA, Kidd PM. Antioxidant Adaptation. Its Role in Free Radical

Pathology. Allergy Research Group, 400 Preda Street, San Leandro, Calif, 1985.

 

 

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