

Forward:


This is a very detailed description of vitamin C and free radical 
interaction.  It is interesting to note that H2O2 can act as a 
reductant and supply 2 high energy electrons, as ascorbate can, under 
the right conditions.  This makes for some interesting ramifications.  
Under the right redox potential H202 could recycle dehydroascorbate 
back to ascorbate.




Unfortunately, the references were lost from the original source 
during downloading.  We have not attempted to correct the problem due 
to possible errors that could be made.


Medical Hypotheses
May 1991: 35:32-37

A 


UNIQUE FUNCTION FOR ASCORBATE



Robert F. Cathcart, III.  

127 Second Street, 
Los Altos, California 94022, 
USA

Telephone 415-949-2822




ABSTRACT

Vitamin C is a reducing substance, an electron donor.  When 
vitamin C 
donates its two high-energy electrons to scavenge free 
radicals, much 
of the resulting dehydroascorbate is rereduced to 
vitamin C and 
therefore used repeatedly.  Conventional wisdom is 
correct in that 
only small amounts of vitamin C are necessary for 
this function 
because of its repeated use.  The point missed is 
that the limiting 
part in nonenzymatic free radical scavenging is 
the rate at which 
extra high-energy electrons are provided through 
NADH to rereduce the 
vitamin C and other free radical scavengers. 
When ill, free radicals 
are formed at a rate faster than the high-
energy electrons are made 
available.  Doses of vitamin C as large 
as 1 to 10 grams per 24 hours 
do only limited good.  However, when 
ascorbate is used in massive 
amounts, such as 30 to 200+ grams per 
24 hours, these amounts directly 
provide the electrons necessary to 
quench the free radicals of almost 
any inflammation.  Additionally, 
in high concentrations ascorbate 
reduces NAD(P)H and therefore can 
provide the high-energy electrons 
necessary to reduce the molecular 
oxygen used in the respiratory burst 
of phagocytes.  In these 
functions, the ascorbate part is mostly 
wasted but the necessary 
high-energy electrons are provided in large 
amounts.  




DEFINITION AND QUALIFICATION



In this paper, the words, vitamin C, will refer to the 
substance 
C6H8O6 used in tiny doses as a vitamin and an electron 
carrier.  The 
word, ascorbate, will mean the same substance but 
when used in massive 
amounts for its high-energy electrons 
themselves.

This paper is not meant to be an exhaustive review of the 
subjects of 
oxidation-reduction reactions, free radical scavenging,
electron-
transport-chains, or oxidative phosphorylation, etc. 
Readers are 
referred to excellent texts on these subjects (, , 
, , ).

Many of the biochemical processes are deliberately 
simplified.  Some 
intermediate steps are omitted.  Certain 
generalizations are made so 
that the importance of a very simple 
but overlooked idea can be 
described in terms a non-biochemist can 
understand.  The overlooked 
idea is that massive doses of ascorbate 
can actually be the source of 
high-energy electrons used in the 
process of free radical scavenging 
and not just an electron carrier 
used repeatedly in an electron-
transport-chain resulting in free 
radical scavenging.




INTRODUCTION



Clinically, a few physicians have found massive doses of 
ascorbate to 
be effective in the treatment of a wide variety of 
diseases.  It was 
apparent to those using ascorbate in these doses 
that there is some 
physiologic or pharmacologic action much 
different from what might be 
expected of a mere vitamin.

Nevertheless, most physicians remained critical of these 
treatments 
and remained convinced that the usefulness of ascorbate 
is only as 
vitamin C.  Many had recognized that one vitamin C 
function is as a 
free radical scavenger.  In this function, vitamin 
C donates high-
energy electrons to neutralize free radicals and in 
the process 
becomes DHA (dehydroascorbate).  DHA is either further 
metabolized, 
releasing more electrons, or is rereduced back to 
vitamin C to be used 
over and over again.  This regeneration and 
repeated use of the 
vitamin has led to the thought that it does not 
take much to do its 
functions.  Other nonenzymatic free radical 
scavengers such as 
glutathione and vitamin E function in a similar 
manner.  The purpose 
of taking the nutrients making up the free 
radical scavengers is 
ordinarily to replace the small percentage 
inadvertently lost.

Much of the original work with large amounts of ascorbate was 
done by 
Klenner (, , , ) who found that most viral diseases 
could be cured by 
intravenous sodium ascorbate in amounts up to 200 
grams per 24 hours.  
Irwin Stone (, , ) pointed out the 
potential of ascorbate in the 
treatment of many diseases, the 
inability of humans to synthesize 
ascorbate, and the resultant 
condition hypoascorbemia.  Linus Pauling 
(, , )
reviewed the literature on vitamin C, particularly its 
usefulness 
in the prevention and treatment of the common cold and the 
flu. 
Ewan Cameron in association with Pauling (, , )
described the 
usefulness of ascorbate in the treatment of cancer.

In 1970 I noted an increasing bowel tolerance to oral ascorbic 
acid 
with illness.  In 1984 I wrote, ( ) "Based on my experience 
with over 
11,000 patients during the past 14 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.  A person who 
can tolerate orally 
10 to 15 grams of ascorbic acid 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.  The clinical symptoms 
of these diseases and other 
conditions previously described, are 
markedly ameliorated only as 
bowel tolerance dose levels (the amount 
that almost, but not quite,
causes diarrhea) are approached (, , , , 
,
)."

This amelioration of symptoms at a high dosage threshold 
combined with 
the knowledge that ascorbate functions as a reducing 
substance 
suggested that the beneficial effect was achieved only 
when the redox 
couple, ascorbate/dehydroascorbate, became reducing 
in the tissues 
affected by the disease.  It is a characteristic of 
oxidation-
reduction reactions that their redox potential is 
determined by the 
logarithm of the concentrations of the substances
and certain 
constants.  The logarithmic effect would explain the 
threshold; the 
redox potential would suddenly become reducing in 
the diseased tissues 
only when a large amount of ascorbate was 
forced into those tissues 
sufficient to neutralize most of the 
oxidized materials in those 
tissues ( ).




FREE RADICAL SCAVENGING



Radicals are molecules that have lost an electron.  When a 
radical 
escapes its normal location, it becomes a free radical. 
These free 
radicals are very reactive and will seize electrons from 
adjacent 
molecules.  Inflammations whether due to infectious 
diseases, 
autoimmune diseases, allergies, trauma, surgery, burns,
or toxins 
involve free radicals.  Cells injured by free radicals 
will spill free 
radicals onto adjacent cells injuring those cells 
and generating more 
free radicals, etc.  The body must confine 
these free radical cascades 
with free radical scavengers.



Some free radicals spontaneously decay and others are 
destroyed by 
enzymatic free radical scavengers such as superoxide 
dismutase and 
catalase that act on free radicals in such a way that 
they neutralize 
themselves without the addition of extra electrons. 

The remainder must 
be destroyed by the high-energy electrons 
carried by the nonenzymatic 
free radical scavengers.  Free radicals 
that escape all the above 
mechanisms cause symptoms and damage.



It is helpful to remember through all the following 
descriptions that 
technically it is the high-energy electron that 
is neutralizing the 
free radical, not the free radical scavenger. 
The free radical 
scavenger carries the high-energy electron that 
does the neutralizing.




HIGH-ENERGY ELECTRONS THE LIMITING FACTOR

The energy of the electrons which neutralize free radicals 
comes 
ultimately, like all energy used by living things on Earth, 
from the 
Sun.  Plants store this energy by photosynthesis in 
carbohydrates, 
fats, and proteins which are then eaten by animals. 
As animals 
metabolize these substances, this energy is past from 
one molecule to 
another in the form of high-energy electrons which 
often, but not 
always, are in association with hydrogens.  Together 
with a high-
energy electron, one such hydrogen can be called a
hydride anion.

As glucose is metabolized, NAD+ (nicotinamide adenine
dinucleotide) is 
reduced to NADH (the bolded H is to emphasize the 
included high-energy 
electron).  The high-energy electron in the 
hydride anion (H) is added 
to the NAD+.

The most critical but generally unrecognized fact here is that 
NAD+ 
can be reduced to NADH only at a limited rate by the addition 
of the 
hydride anion with its high-energy electron derived from the 

metabolism of carbohydrates, fats, or proteins.  Therefore, this 
NADH 
is not without cost.  Moreover, the energy it carries must be 
shared 
among several other critical functions.  Most must be used 
in the 
process of oxidative phosphorylation to make ATP (adenosine 

triphosphate) which is used as a source of energy by the various 

tissues of the body.

When phagocytes engulf pathogens into its vacuoles, NADPH 

(nicotinamide dinucleotide diphosphate, reduced form) provides the 

high-energy electrons the phagocytes need to make the oxidizing 

substances (radicals) with which they kill various pathogens.  The 

process of making the necessary oxidizing substances is called the 

respiratory burst.  Paradoxically, the first oxidizing substance, 

superoxide, (O2+), in the respiratory burst is made by the 
reduction 

of molecular oxygen (O2) by NADPH.  NADP+ is rereduced back to 
NADPH 

in the hexosemonophosphate shunt.  Glucose is metabolized for the 

source of the high-energy electron.  This process is also rate-
limited 
and the glucose comes from the metabolism of carbohydrates, 
fats, and 
proteins.  Therefore, NADH and NADPH have a common source 
of energy 
and can be made available only at some limited rate.

Remaining NAD(P)H can be used by the body in regenerating free 
radical 
scavengers so that the body may protect itself from free 
radicals.  As 
NAD(P)H is used in these various processes, it gives 
up the hydride 
anion with its extra high-energy electron and 
becomes NAD(P)+ again.  
When the limited rate of availability of 
these hydride anions is 
exceeded by the formation of free radicals, 
then symptoms and damage 
caused by the free radicals occur.




RESPIRATORY BURST LIMITED BY ACCUMULATION OF FREE RADICALS

As these high-energy electrons are used up within the 
phagocytes, the 
phagocytes are unable to produce more oxidizing 
substances within 
their vacuoles to kill pathogens.  Some of the 
previously made 
oxidizing substances leak from within the vacuoles 
into the cytoplasm 
thereby becoming free radicals.  With the 
exhaustion of the high-
energy electrons, the nonenzymatic free 
radical scavengers cannot be 
rereduced.  The free radicals damage 
the phagocytes and interfere with 
phagocytosis.  The phagocytes bog 
down in their own oxidizing 
substances.




REDUCED GLUTATHIONE

To understand the unusual function of massive doses of 
ascorbate, let 
us follow the most important pathway whereby the 
extra electrons are 
passed off to the free radicals thereby 
neutralizing them.  Follow the 
high-energy electron in the hydride
anion through all this process.  
Certain nutrients that could be 
limiting factors in all this will be 
mentioned along the way.

NAD(P)H reduces oxidized flavin adenine dinucleotide (FAD+),
to reduced 
flavin adenine dinucleotide (FADH2), and becomes NAD(P)+
again.  FADH2 
reduces oxidized glutathione (GSSG) to reduce d
glutathione (GSH). 
(Part of NAD(P)H is from vitamin B3, and part of
FADH2 is from vitamin 
B2).

The high-energy electrons of reduced glutathione (GSH) can 
directly 
reduce some free radicals.  But also, some reduces 
dehydroascorbate 
back to ascorbate.  In the process the GSH is 
oxidized back to GSSG.  
Two hydride anions are added to the 
dehydroascorbate reducing it back 
to vitamin C.  (The enzyme 
glutathione peroxidase and its coenzyme 
selenium catalyze these 
reactions).

Ascorbate (C6H8O6 or C6H6O6H2, the bolded and 
separated 
H2 is to 
emphasize the hydrogens containing the high-energy 
electrons) differs 
from dehydroascorbate (C6H6O6) in that it has 
two 
extra hydrogen atoms 
with two high-energy electrons in its 
molecular structure which it can 
donate to reduce free radicals.

The high-energy electrons of ascorbate, C6H6O6H2, can directly 
quench 
free radicals.  But some may reduce to copheryl quinone (an
oxidized 
form of vitamin E) back to -tocopherol (vitamin E).  Some 
high-energy 
electrons are passed to the -tocopherol and then 
quench free 
radicals.

The point I want to emphasize is that these free radical 
scavengers 
cycle from the reduced form carrying the hydride anion 
with the high-
energy electron back to the oxidized form lacking the 
hydride anion.  
Although there is a little loss, most of the free 
radical scavengers 
are rereduced and used over and over again. 
This repeated use with 
only a little loss is why it ordinarily 
takes a small amount of these 
substances to do their electron 
carrying function to the maximum 
allowed by the availability of the 
hydride anion.

The limiting factor in all this, in a well nourished person,
is this 
rate-limited availability of the hydride anion with its 
high-energy 
electron.  The body can make NAD(P)H available for this 
purpose only 
at a limited rate.  When the need to scavenge free 
radicals exceeds 
this rate, then symptoms, damage, and ageing 
occur.  Adding more 
vitamins and other nutrients, even the ones 
noted as being free 
radical scavengers, notably vitamin C, vitamin 
E, vitamin A 
(especially -carotene), cysteine, selenium, etc. do 
not, under 
ordinary circumstances, add much to all this.  All these 
free radical 
scavengers are cycled several times an hour when a 
person is sick.  
The NAD(P)H keeps rereducing these free radical 
scavengers so they are 
used repeatedly.  Taking of the usual 
amounts of nutrient free radical 
scavengers only assures that there 
are no critical deficiencies that 
would limit this free radical 
scavenging electron-transfer chain 
described above.  Still there is 
a normal limit to the free radical 
scavenging ability of this 
system.( ),( ),( ).




ASCORBATE TO THE RESCUE



 . . .except. . .ascorbate, C6H6O6H2, used as the source of 
electrons, 
not just as the electron carrier, can change all this. 
The C6H6O6H2 
used in massive doses substitutes for the limited 
availability of the 
NAD(P)H.  The C6H6O6 part of the C6H6O6H2 used 
this way is thrown 
away; the C6H6O6H2 is only used for the 
electrons
it carries.  Amounts 
of 30 to 200+ grams of C6H6O6H2 provide ample 
high-energy electrons to 
directly scavenge the large amounts of 
free radicals generated in 
disease processes and provide enough 
high-energy electrons to rereduce 
NAD(P)+, FAD+, GSSG, to copheryl 
quinone, etc. back to their reduced 
forms.

Lewin () pointed out that although the C6H6O6H2/C6H6O6 redox 
couple is 
usually reduced by GSH at the concentrations in which 
these substances 
are ordinarily present, when C6H6O6H2 is present 
in 
large 
concentrations, it will reduce GSSG to GSH.  The usual 
direction of 
the redox reaction is reversed and the C6H6O6H2 
supplies 
the high-
energy electrons reducing the GSSG.

If there was some substance that was cheaper, better tolerated 
by the 
body, and had fewer nuisance problems associated with its 

administration than sodium ascorbate, NaC6H6O6H, intravenously and 

intramuscularly, or ascorbic acid, C6H6O6H2, orally, I would use 
it. 

So far, C6H6O6H2 and NaC6H6O6H are the premier sources of 
high-energy 

electrons and therefore the premier free radical scavengers.

The dehydroascorbate, C6H6O6, part of the ascorbate, C6H6O6H2, 
used 
this way is excreted rapidly in the urine or metabolized 
further by 
the body.  Although the complete pathway has not been 
described and 
involves some uncertainty, it is known that certain 
breakdown products 
of dehydroascorbate supply even more high-energy 
electrons.

Bearing in mind that it is the high-energy electron that is 
doing the 
free radical scavenging, one can see that animals which 
can synthesize 
ascorbate within themselves have a higher amount of 
the electron 
carrier available and will not ever suffer from 
scurvy.  However, the 
high-energy electrons ultimately come from 
the same sources as in 
humans.  Ascorbate producing animals still 
must make the ascorbate and 
the high-energy electrons available by 
various metabolic steps using 
glucose.  This process is rate-
limited.  Comparing the ability of a 
human to make C6H6O6H2 to a 
dog 
is like comparing a human's ability to 
fly in a Concorde with a 
humming bird.  The human can make enormous 
amounts of C6H6O6H2 in 
his 
chemical plants.  Humans just have to learn 
to use it properly. 
The usefulness of ascorbate in treating diseases 
involving free 
radicals bears no relationship to how much vitamin C 
animals make 
or consume unless one is satisfied with achieving only 
the level of 
health of that animal.  We are using a natural substance 
in an 
unnatural way to achieve these effects.  It is the high-energy 

electrons, not the ascorbate, that is most important here.



The mechanism I am describing is a pharmacologic effect of the 
high-
energy electrons carried by the C6H6O6H2 that transcends the 
normal 
ability of any species of animal to ameliorate or conquer 
diseases 
involving free radicals.  Any disease process that 
involves free 
radicals can be ameliorated by the high-energy 
electrons carried by 
ascorbate when used properly in massive doses. 

It is true that there 
are certain logistic problems involved in 
delivering the massive doses 
of C6H6O6H2 containing the enormous 
numbers of electrons sufficient to 
quench the excessive free 
radicals of certain severely toxic diseases 
but it is surprising 
what massive doses of ascorbate will accomplish.




RAPID UTILIZATION OF THE HIGH-ENERGY ELECTRONS

Calculations of the total amount of ascorbate in a healthy 
person 
(pool size) with an intake of about 100 milligrams of 
vitamin C per 
day is roughly 2-3 grams and the turnover half time 
is about 20 days 
().  When a person who when well can ingest 
only 15 grams of ascorbic 
acid per 24 hours before it causes 
diarrhea, can take over 200 grams 
in 24 hours when ill with 
mononucleosis, one obtains a suggestion of 
the numbers of extra 
electrons involved.  If 185 grams (200 minus 15) 
extra is used, 
whatever the amount of high-energy electrons carried in 
that 
divided by the amount in 3 grams means that if ascorbate was the 

only carrier of electrons (which it is not), that 3 grams of 
ascorbate 
would be rereduced about every 23 minutes.  There are so 
many facts 
such as the amount of high-energy electrons carried by 
the other free 
radical scavengers that this number is almost 
valueless.  Still, it 
makes one think in terms of minutes to a few 
hours for the rereduction 
of all the free radical scavengers of the 
body when one is seriously 
ill.  This emphasizes the futility of 
using vitamin free radical 
scavengers in the doses described in the 
RDA () to provide the 
necessary high-energy electrons.




A SIMPLE ANALOGY

Suppose you had a house out in the country that had a water 
well about 
300 yards away.  Between the house and the well are two 
high fences.  
Your house catches on fire and your neighbors come 
running with their 
buckets.  One group sets up a bucket brigade 
between the well and the 
first fence and pours the water through a 
hole in the fence into the 
buckets of the second bucket brigade. 
The second bucket brigade runs 
to the second fence to pour the 
water through a hole in the second 
fence into the buckets of the 
third bucket brigade who throw the water 
on the fire.



Unfortunately, the fire goes out of control and it is not 
possible to 
pump the water out of the well at a rate fast enough to 
put out the 
fire.  The arrival of more neighbors does no good 
because there are 
already enough for the three bucket brigades.  A 
couple of neighbors 
run from their homes with their buckets full of 
water but that does 
not help very much.

Then the fire engine roars up and puts out the fire with hoses 
that 
draw water from the fire engine.  The firefighters do not rely 
on the 
water from the well.  We have to stretch the analogy here a 
little but 
imagine microscopic buckets with C painted on their 
sides carrying the 
water out of the fire hose.  The little buckets 
are wasted.  Their 
only function is to carry the water.







CONCLUSION

Free radical scavenging is a very dynamic process.  The 
nutritional 
free radical scavengers in the diet, including vitamin 
C, are not for 
the purpose of providing the large number of high-
energy electrons 
necessary to meet the rate with which free 
radicals are made.  The 
purpose of dietary free radical scavengers 
is to replace those 
scavengers incidentally lost.  The process of 
reducing a free radical 
does not destroy a free radical scavenger 
if it is rereduced before 
being further broken down.  The free 
radical scavengers are 
intermediaries.  It is up to other metabolic 
processes to provide the 
high-energy electrons with which the free 
radical scavengers reduce 
free radicals.



The rate at which free radicals are formed becomes excessive 
and 
causes symptoms when it exceeds the rate of reduction of those 
free 
radicals.  Part of the reduction is spontaneous and part is 
enzymatic.  
The remainder must be reduced by the high-energy 
electrons carried by 
the nonenzymatic free radical scavengers.



Ascorbate in massive doses can perform an unusual function. 
When doses 
of 30 to 200+ grams per 24 hours are used, the high-
energy electrons 
carried in on the administered ascorbate adds 
significantly and 
decisively to the actual electrons doing the 
reducing.  The ascorbate 
is not used as the vitamin C where it is 
rereduced by NAD(P)H and used 
repeatedly; it is used for the high-
energy electrons it carries.

In high concentrations ascorbate reduces NAD(P)H and provides 
the 
high-energy electrons necessary to reduce molecular oxygen used 
in the 
respiratory burst of phagocytes.  In these functions, the 
ascorbate 
part is mostly wasted but the necessary high-energy 
electrons are 
provided in large amounts.

The opportunity to reduce the human suffering from the free 
radicals 
of infectious diseases, autoimmune diseases, allergies, 
trauma, burns, 
surgery, toxins, and to a degree ageing, etc., which 
could be 
neutralized by high-energy electrons carried by high doses 
of C6H6O6H2 
is immense.


REFERENCES



1. Levine SA, Kidd PM.  Antioxidant Biochemical Adaptation.  
   
Biocurrents Research Corporation, San Francisco, (in press),  1984.




2. Pauling L, Pauling P.  Chemistry.  W.H. Freeman and Company, 
S.F., 
   1975. 



3. Stryer L. Biochemistry. 3rd. ed. W.H. Freeman and Company, 
N.Y., 
   1988. 



4. Alberts B, Bray D, Lewis J, Raff M, Roberts K, Watson JD. 
Molecular 
   Biology of the Cell.  2nd. ed. Garland Publishing,  Inc.,
1989. 



5. Newsholme EA, Leech AR.  Biochemistry for the Medical Sciences. 
   
John Wiley & Sons, N.Y., 1983. 



6. Klenner FR.  Virus pneumonia and its treatment with vitamin  C. 
J. 
   South. Med. and Surg., 110:60-63, 1948. 



7. Klenner FR.  The treatment of poliomyelitis and other viral 
   
diseases with vitamin C.  J. South. Med. and Surg., 111:210-214 
   
1949. 



8. Klenner FR.  Observations on the dose and administration of 
   
ascorbic acid when employed beyond the range of a vitamin in  
   human
pathology.  J. App. Nutr., 23:61-88, 1971. 



9. Klenner FR.  Significance of high daily intake of ascorbic  acid 
in 
   preventive medicine.  J. Int. Acad. Prev. Med., 1:45-49,  1974. 



10. Stone I.  Studies of a mammalian enzyme system for producing 
    
evolutionary evidence on man.  Am. J. Phys. Anthro., 23:83-86, 
    
1965. 



11. Stone I.  Hypoascorbemia: The genetic disease causing the 
human 
    requirement for exogenous ascorbic acid.  Perspectives in 
Biology 
    and Medicine, 10:133-134, 1966. 



12. Stone I.  The Healing Factor: Vitamin C Against Disease. 
Grosset 
    and Dunlap, New York, 1972. 



13. Pauling L.  Vitamin C and the Common Cold.  W.H. Freeman and 
    
Company, San Francisco, 1970. 



14. Pauling L.  Vitamin C, the Common Cold, and the Flu.  W.H. 
Freeman 
    and Company, San Francisco, 1976. 



15. Pauling L.  How to Live Longer and Feel Better  W. H. Freeman 
and 
    Company, New York, 1986. 



16. Cameron E. and Pauling L.  Supplemental ascorbate in the 
    
supportive treatment of cancer: Prolongation of survival times in 
    
terminal human cancer.  Proc. Natl. Acad. Sci. USA, 73:3685-3689, 
    
1976. 



17. Cameron E. and Pauling L.  The orthomolecular treatment of 
cancer: 
    Reevaluation of prolongation of survival times in terminal 
human 
    cancer.  Proc. Natl. Acad. Sci. USA, 75:4538-4542,  1978. 



18. Cameron E. and Pauling L.  Cancer and Vitamin C.  The Linus 
    
Pauling Institute for Science and Medicine, Menlo Park, 1979. 



19. Cathcart RF.  Vitamin C: the nontoxic, nonrate-limited, 
    
antioxidant free radical scavenger.  Medical Hypotheses, 18:61- 
    
77, 1985. 



20. Cathcart RF.  Clinical trial of vitamin C.  Letter to the 
Editor, 
    Medical Tribune, June 25, 1975. 



21. Cathcart RF.  The method of determining proper doses of 
vitamin C 
    for the treatment of diseases by titrating to bowel 
tolerance.  
    The Australian Nurses Journal 9(4):9-13, Mar 1980. 



22. Cathcart RF.  The method of determining proper doses of 
vitamin C 
    for the treatment of disease by titrating to bowel 
tolerance.  J 
    Orthomolecular Psychiatry 10:125-132, 1981. 



23. Cathcart RF.  Vitamin C: titrating to bowel tolerance, 
    
anascorbemia, and acute induced scurvy.  Medical Hypotheses, 
    
7:1359-1376, 1981. 



24. Cathcart RF.  C-vitamin behandling till tarmin tolerans vid 
    
infektioner och allergi.  Biologisk Medicin 3:6-8, 1983. 



25. Cathcart RF.  Vitamin C: titrating to bowel tolerance, an- 
    
ascorbemia, and acute induced scurvy.  Let's Live (Japan) 16:9, 
    
Nov 1983. 



26. Cathcart RF.  Vitamin C: the nontoxic, nonrate-limited, 
    
antioxidant free radical scavenger.  Medical Hypotheses, 18:61- 
    
77, 1985. 



27. Lewin S.  Vitamin C: Its Molecular Biology and Medical 
Potential.  
    Academic Press, 1976. 



28. Baker EM, Saari JC, and Tolbert BM.  Ascorbic acid metabolism 
in 
    man.  Am J Clin Nutr, 19,371-8, 1966. 



29. Food and Nutrition Board.  Recommended Dietary Allowances. 
Ninth 
    Revised Edition, 1979. Washington, D.C., National Academy 
    of 
Sciences, 1980. 

