2 - How Vitamin C Works - Cathcart - with summary

Note: many more good articles about Vitamin C can be found here,
on Dr. Robert Cathcart's website:

http://web.archive.org/web/20130302070632/http://www.orthomed.com/

Here is a summary of how Vitamin C kills viruses and protects against
free-radical damage caused by them (summarized from the article by
Dr. Robert Cathcart below):

White blood cells defeat viral diseases by taking in a chemical fuel
-- NADPH -- from the blood plasma and using it to make oxidizing
substances that kill the viruses. The used NADPH becomes NADP+,
which can no longer function as fuel.

NADPH and the related NADH are also used to restore the body's
free radical scavenger (antioxidant) molecules as they get used up.
Without these antioxidants, the free radicals would destroy our cells.

The body can slowly convert NADP+ back to NADPH, and NAD+
back to NADH by using food energy.

In serious illness, the body can't create enough NADPH and NADH
from food energy to restore the antioxidants and to fuel the white
cells. As a result, the viruses multiply, and various body tissues
are damaged, possibly resulting in death.

Large enough doses of Vitamin C can directly and rapidly convert
NADP+ back to NADPH, and NAD+ back to NADH, restoring the
body's ability to kill viruses and protect against free radical damage
cause by the disease.

Life-threatening viruses can require so much white cell activity to
kill them that hundreds of grams of Vitamin C per day are necessary
to restore the NADPH needed by the white cells, and also to restore
the antioxidants to remove the free radicals created by the disease.

************************************************************
Here is the central part of Cathcart's article describing how Vitamin C
works, in more technical language:

When phagocytes (white blood cells) engulf pathogens into their
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.

The resulting NADP+ is rereduced back to NADPH in the
hexosemonophosphate shunt. Glucose is metabolized for the source
of the high-energy electron. This process is 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.

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.

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 beta-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.

Vitamin C - 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, tocopheryl quinone, etc. back to
their reduced form
s.

************************************************************
Here is Cathcart's entire article:

http://web.archive.org/web/20130302070632/http://www.orthomed.com/unique.htm"

UNIQUE FUNCTION of VITAMIN C

-----------------------------------
--- 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 ----
-----------------------------------
Copyright (C), 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.
_________________________________________________________________________________________

Medical Hypotheses; May 1991: 35:32-37

A UNIQUE FUNCTION FOR ASCORBATE

(C) 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
reduced 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 tocopheryl 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, tocopheryl 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
_________________________________________________________________________________________

Dr. Cathcart Bibliography

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-vitaminbehandling till tarmintolerans 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.
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Content (C) 1995 and prior years, Dr. Robert F. Cathcart.

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