Response of Peripheral and Central Nerve Pathology
to Mega-Doses of the Vitamin B-Complex and Other Metabolites – Part
by Frederich R. Klenner, BS, MS, MD
Journal of Applied Nutrition,
Recommended Treatment Schedule
Our treatment schedule:
1) Thiamin hydrochloride: 300mg to 500mg, 30 minutes
before meals and bed hour, and during the night if awake. The higher
amounts in long-standing cases. This requirement is high, since much
is lost through action of gastric juices and loss due to perspiration.
400 mg. daily by needle, given intramuscularly. During summer months
this can be given every 12 hours to good advantage. Two to three times
each week, and where office access is convenient, 20 mg. per kg. body
weight, or at least 1000 mg. is administered intravenously. This is
given with 100 mg to 200 mg. Niacine (nicotinic acid) which is available
100 mg. in 10cc ampules. (The concentrated Niacin, available in 30cc
vials, must be diluted if employed intravenously.) The intravenous dose
is given with the patient in a recumbent position. A 20cc to 30cc syringe,
carrying a one-inch 22-guage needle should be employed. The injection
is given slowly (5 to 7 minutes) holding the syringe with one hand.
The usually-employed three fingers of the other hand must be on the
patient’s pulse. An increased pulse rate indicates too fast a flow of
the medicine. This indicates the rate of phosphorylization. Thiamin
hydrochloride is, indeed, a toxic substance, and anaphylactic reactions
have been reported, but I have never seen a case in treating thousands
of patients, (not necessarily Myasthenia Gravis or Multiple Sclerosis),
in 30 years of clinical observation. I have observed one case of extreme
sensitivity in which itching was present within One minute after an
intramuscular injection of 100mg. This was immediately controlled with
5cc Benedryl, I.M. It must be remembered that once thiamin hydrochloride
is phosphorylated, it is no longer a critical allergic substance, but
is cocarboxylase, a necessary but absolutely harmless agent. (My problem
has been the preservatives now required by FDA regulations, and
they should be removed.) Higher doses of thiamin can be used,
but then the dilution factor must be greater.
2) Niacin (nicotinic acid): We recommend 100mg to 3
grams, thirty minutes before meals and at bed hour, and also during
the night if awake – whichever dose will produce a strong body flush.
Niacin dilates the blood vessels, even those that have been compressed
by scar tissue, allowing a greater amount of nutrient material to reach
the cell laboratory or factor comprising muscles and nerves. This constant,
repeated dilatation of the blood vessels acts in the same manner as
the dilating urethral catheter to correct constriction. One is chemical,
the other is mechanical. Hot fluids taken at the same time as the niacin
will enhance the flush. Pyridoxine has been a suggested stimulant. The
lack of constant flushing in Multiple Sclerosis is disappointing but
not hopeless. It will require a longer time to achieve results. Many
timed patients will flush with intramuscular niacin when they fail to
flush by the oral route. An occasional patient will experience thr sensation
of a chill following nicotinic acid flush. This is transient and of
no consequence. Food, even jelly beans or a glass of milk, will prevent
or minimize the experience. Some patients will flush sometimes and not
at other times, even during a single day. if no flush develops within
45 minutes, the dose should be repeated. A delayed reaction of several
hours can occur, and should this be superimposed upon a previous medication,
the result could be severe. Do not scratch when itching from niacin.
Just press the area with your fingers, or better still, with a cube
of ice. Antihistamines will stop the itching and limit the flush, should
this be necessary. Niacin should be given very slowly by the intravenous
route in the geriatric patient, with or without cardiac pathology, since
it can produce dilatation great enough to effect right-side heart failure.
Myasthenia Gravis patients sometimes attain geriatric status. Vasomotor
collapse of peripheral vessels, although rare, can occur. Light mg.
ecadron given I.M. will reverse this condition.
3) Pyridoxine (Vitamin B6): Lack of this vitamin has
been shown to induce microcytic hypochromic anemia and neurologic lesions
in dogs and pigs. The term B6 includes not only pyridoxine, but also
pyridoxal and pyridoxamine, all three compounds being found in nature.
These derivatives have biological activity equal to that of pyridoxine,
as demonstrated in rats. Pyridoxine plays a part in the metabolism of
unsaturated fatty acids. It is also important in the metabolism of amino
acids. Pyridoxal phosphate functions as a coenzyme, and in transamination
reactions. 100mg to 200mg is given before meals and bed hour. At least
100mg daily is given intramuscularly.
4) Cobalamin (Vitamin B12): It is thought that vitamin
B12 acts as a catalyst in the formation of the purine and pyrimidine
deoxyribosides which are present in deoxyribonucleic acid. Technically,
B12 is cyanocobalamin. vitamin B12 with pterylglutamic reduces the requirement
for choline essential in the treatment of neurological diseases. 1000mcg.
is given three times each week by needle (repository type). The incident
of dermatitis from continued use of vitamin B12 by needle is roughly
15%. I have never seen this develop in a patient with Myasthenia Gravis
or Multiple Sclerosis. B12 is recognized as a factor in the synthesis
5) Ascorbic Acid (Vitamin C): The use of high daily
doses of vitamin C will prevent a superimposed illness and will lend
itself in metabolism. Ten to twenty grams should be taken daily by mouth
in divided doses.
6) Riboflavin (Vitamin B2): A deficiency of vitamin
B2 in young animals results in inhibition of growth terminated by death.
The yellow enzyme can, as demonstrated by Warburg and Christian, participate
in a series of enzyme reactions involved in the metabolism of carbohydrates.
It is capable of transporting hydrogen from reduced coenzyme II, a niacin
coenzyme which attacks hexosemonophosphate, regenerating the riboflavin
phosphate-protein complex. Riboflavin also take part in enzymic reactions
as a dinucleotids prosthetic group, consisting of riboflavin, two phosphoric
acids, riboe and adenine. Riboflavin is very important in the regulatory
function of the hormones involved in carbohydrate metabolism. It is
classified as a low-energy package. 40mg to 80mg given daily by needle
I.M. 25 mg. before meals and bed time.
7) Vitamin E as d-alpha Tocopherol acetate of d-alpha
Tocopherol acid succinate. The latter is more practical since it is
a pure form. Complex biochemical changes in the muscle tissue in chrome
vitamin E deficiency are followed by histalogical lesions characteristic
of muscular dystrophy. Deficiency has also been shown to produce demyelinization
and distortion of the axon pattern in the spinal cord, giving rise to
hypalgesia and progressive paresis. Fatal massive liver necrosis occurs
in animals maintained on diets low in vitamin E and sulfur-containing
amino acids. 800 international units before meals and bedtime must be
adhered to in this treatment.
8) Crude liver: This substance contains factors still
unknown but essential in metabolism. patients with pernicious anemia
often show neurological involvement, and are tremendously benefitted
by liver injections which, of course, contain vitamin B12. Degenerative
changes brought on by other factors, therefore, can also be benefitted
by daily injections of crude liver.
9) Adenosine-5-Monophosphoric acid: One of the purine
bases occurring in muscle is adenne. It, along with other purines, exists
in various forms. Adenosine polyphosphate is of primary interest in
this discussion. The basic structure is adenosine, adenine-9-riboside.
This is esterified with phosphoric acid at the 5-position of the ribofuranose,
to form adenosine-5-phosphoric acid, also known as adenosinemonophosphate
(AMP). Inosinic acid I a commonly-occurring breakdown product of AMP,
formed by deamination in muscle extract. Myosin displays enzymic activity
similar to adenylic deaminase. By attaching further phosphoric acid
residues in pyrophosphate linkage adenosinediphosphate (ADP) and adenosinetriphosphate
(ATP) are obtained. ATP, as previously noted, is the energy package
essential for life. By adding this to our treatment, we enhance all
chemistry dealing with cell metabolism.
10) Choline: Choline is a structural component of fat
and nerve tissue, thus has a strong relationship to the phospholipids
and to its acetyl ester. Acetylcholine plays an important role in the
humoral transmission of parasympathetic and other nerve impulses to
effector organs. It also plays a part in transmethylation. Choline serves
as a methylating agent in the physiological process – guanidoacetic
acid to creatine. We give 700mg to 1400mg after each meal and at bed
11) Lecithin: Lecithin is the glyceryl ester of a pair
of fatty acids and a substituted phosphoric acid group attached to a
choline radical. “Choline” is one of the products of lecithin, representing
about 15% of the molecule. Lecithin placed in water and observed under
the microscope, will diffuse out, forming long, curving strands (myelin
forms). The hydrophilic nature of the lecithin molecule play an important
part in the structure and properties of cell membranes. It is the lipid
used in nerve tissue. We give 1200 mg. Soybean Lecithin after each meal.
12) Magnesium: 100mg. after each meal to supply additional
ions for muscle activity. It is an enzyme activator.
13) Calcium Gluconate (10 grain tablets): We give two
tablets after each meal and at bed hour to supplement dietary intake
for muscle activity. At times, this is given intravenously, one gram
14) Calcium panthotenate: The physiologically active
form of pantothenic acid is coenyzme A. Its acetyl derivative (acetyl
CoA) is synonymous with active acetate. Metabolic transformations are
very complex and involve numerous enzymes and coenzymes. Coenzyme A
participates in the acetylation of amines. The pantothenic cid coenzyme
plays a vital role in carbohydrate metabolism and acetyl transfer also
occurs in the metabolism of fatty acids. We give 200 mg. after each
meal and at bed hour.
15) Aminoacetic acid (glycine): Glycine enters into
a variety of metabolic functions. It is directly concerned in the synthesis
of glutathione, the tripeptide which plays an important part in intracellular
oxidation and reduction. Rapport and Katz have shown that when glycine
is added to perfused muscle, the oxygen absorption is 40% higher than
otherwise, indicating that the presence of this amino acid stimulates
the combustion of other tissue constituents. To the body in general,
glycine is no doubt most important because of its wide adaptability
in the detoxicating process of the body. More than one hundred substances,
when fed, are joined in the body with glycine. In the deamination of
glycine, three products will be formed: ammonia, carbon dioxide and
water. The ammonia from this reaction is then quantitatively converted
to urea. One heaping tablespoon of the powder in a glass of milk four
times each day. Much of the oral medication can be taken with this drink.
16) Make certain that the hemoglobin is at least 13
17) High protein diet with two to three eggs or breakfast.
18) One Theragram-M cap. daily for trace minerals.
19) Dantrium has value for relieving intentional tremor
and Symmetrel for relieving stiffness in Multiple Sclerosis. Dose must
20) Zinc gluconate: 10 mg. three times each day has
some value in Myasthenia Gravis. Take several hours after vitamin B2.
This treatment works so dramatically in Myasthenia Gravis,
that should a given patient’s physician refuse to administer this schedule,
I have this recommendation: One gram thiamin hydrochloride one hour
before meals and at bed hour, and during the night if awake. Niacin
taken at the same time, and in amounts sufficient to produce a good
body flush. Two hundred mg. calcium pantothenate and 100mg pyridoxine
before meals and at bed hour. Ten grams ascorbic acid, taken in divided
doses. Amino acetic acid: one heaping tablespoon in a glass of milk,
four times each day. Naturally, the full schedule will afford more dramatic
For a long time, it has seemed to me that virus bodies
might have the potential to alter their protein coat, and therefore
their dimension, and become annother virus for another disease. In our
long practice, we would see, as I am certain may of you have, chicken
pox just before Thanksgiving, mumps by Christmas, red measles in the
Spring, and polio or a virus mimicking polio in the Summer. German measles,
virus colds, and virus pneumonitis just about any time.
Etiology of Multiple Sclerosis – Historical
As for the etiology of Multiple Sclerosis, a good history
will tell the story. I have one patient who was diagnosed with Polio
in 1950. He experienced total paralysis, but made a complete recovery.
Five years ago, he began to demonstrate the signs and symptoms of Multiple
Sclerosis. He was given a “strong” course of ACTH with relief of symptoms.
Three months later, this had to be repeated, but the results were not
as good. Some three months later, a third series of injections of ACTH
was worthless. (This has been the pattern with the use of ACTH, and
represents nothing more than whipping a tired horse. In my book, it
borders on malpractice.) His myelin sheath has just about been destroyed.
He has so many areas of “no insulation” that his movements are like
that of a newborn baby.4 Had he received our treatment at
the onset of his illness, he would be in good health today without any
physical handicap. This individual never had Poliomyelitis. The virus
that brought him down was the coxsackie virus, and this explains
his initial recovery. Another case seen was a 31 year-old female. This
young lady was diagnosed Poliomyelitis when she was 19 years of age.
Three years ago, she began developing signs and symptoms of Multiple
Sclerosis, and that is her present diagnosis. Her neurologist, who made
the diagnosis of Polio, now tells her that there is no doubt in his
mind that what she has now, actually started when she was 19. He is
absolutely correct, because she had a coxsackie virus infection.
In 80% of the cases that have come under my supervision, an illness
compatible with a Summer virus has been entertained. Unless an illness
is associated with paralysis, it is understandable when a patient or
the family have difficulty in establishing a workable timetable.
Other Hypotheses on Etiology of Multiple Sclerosis
Dr. Henry Kempe,5 from the University of
Colorado School of Medicine, as reported by Medical World News,
believes that Multiple Sclerosis is caused by vaccinia virus. He found
a correlation between severity of the clinical disease and antibody
titer. He also observed that only in demyelinating disease were antibodies
to vaccinia virus in the cerebral spinal fluid. This brings to mind
the work of Horsefall and his co-workers at the Rockefeller Institute.
They were able to culture an organism, which they designated Streptococcus
MG, from a large percentage of their patients with primary atypical
pneumonia. This proved later to have no value, and the viral nature
of the disease was recognized.
The sleeping virus theory of Dr. Milton Alter6
and others, as reported in Medical Tribune, along with the environmental
aspect for Multiple Sclerosis is another “ripe apple” for public consumption
and public press exaggeration. Most of this theory rests with the circumstantial
evidence that filterable transmissible agents having slow virus properties
are present in other diseases.
Another theory, that of Dr. D.K. Schandl,7
a Nova University biochemist, in Fort Lauderdale, Florida, and published
in The Charlotte Observer, relates it to an environmental agent,
specifically carbon monoxide, and the lack of the vitamin pyridoxine
(vitamin B6). Pyridoxine is concerned with the enzymatic decarboxylation
of amino cids and the incidence of Multiple Sclerosis is too low in
terms of the availability of carbon monoxide.
Still another theory has been advanced by Doris Dahl
and Amico Bignami8 of Stanford University, Palo Alto, California.
They report the discovery of a substance that “may” prevent the self-renewing
of myelin. Scar tissue is indeed the problem, but it is the end result
of microscopic hemorrhages following virus invasion.
Concepts Concerning Myasthenia Gravis
In Myasthenia Gravis, the accepted reasoning is initiated
by Thymomas in 20% of patients over forty, and hyperplasia of the thymus
in others. Antibodies to muscle have been reported in roughly 33%. Excessive
pyruvates at the neuro-muscular junction has been recognized but not
Multiple Sclerosis: Male, white, was in a wheelchair
at a Veterans’ Hospital for two years. Patient seen while home on 30-day
vacation. Treatment given every day with marked improvement. Upon returning
to Veterans’ Hospital, the physician in charge recognized the improvement
and advised the young man to return home and continue the treatment.
After three years, he was given a clean bill of health by three neurologists
in three different places and was given a responsible position. This
was in 1950. The individual remains in excellent health, but continues
with modified therapy.
Myasthenia Gravis: Male, white, receiving treatment
from nearby medical centre for one year. He was receiving guanadine
(amount unknown) and 90 mg. prostigmine bromide each day. He was first
seen in a Myasthenia Gravis crisis. The emergency treatment consisted
of two ampules of prostigmine methylsulfate of a strength of 1:2000,
and 5cc of coramine. Within a period of eight or ten minutes, the patient
experienced a generalized convulsive seizure which lasted some five
minutes and required 4 men to hold him on the bed. Prostigmine, by needle,
was continued for three weeks, and then 15mg. tablets every six hours.
Thiamin hydrochloride was given three times each day, intramuscularly,
as well as other fractions of the B complex. In one year’s time, he
had been “weaned off” prostigmine. Although given only two weeks to
live by the physicians at the medical centre the day prior to our first
visit, this individual lived a normal life for 18 years. His death was
due to a cerebral accident.
Female, white, with diagnosis (August 1967), Polyneuritis.
Began with pain and burning of legs associted with jerking. Ran high
fever 10 days. Paralysis started on left side along with weakness of
hands, soon followed with complete paralysis lower extremities. Seen
first time 7/5/69. Paralysis and weakness as described. Started on medication
by mouth and intramuscular injections. Several months later, began intravenous
schedule. In approximately 16 months, was able to move right leg. Upper
extremities returned to normal. On 6/10/72, began to move left foot.
Patient now able to walk approximately 50 yards with knee braces and
walker. Does all the cooking for family of four, as well as sewing clothes
for herself and two daughters. (I can personally vouch for her ability
as a cook.) April 1973, she was able to go without a back brace that
was previously necessary for her to use to even get out of bed. One
marvels at her ability to pedal a stationary bicycle “contraption” made
for her by her husband so that she might exercise her legs. Our diagnosis
in this case is Transverse Myelitis. (200 grams ascorbic acid given
I.V., in divided doses, would have saved this patient from paralysis.)
She has also received 300mg ribonucleic acid four times each week.
Female, white, who developed weakness in extremities
around June 25, 1961. Sensory examination revealed hypalgesia over medial
aspect of right foot and calf. Motor examination revealed a partial
foot drop on the right, with rather marked weakness and inversion, eversion,
and dorsiflexion of right foot. Reflexes upper extremities 3-4 plus.
Abdominal reflexes absent. Knee jerks were 3-4 plus with patellar clonus.
Right ankle jerk was 4 plus and the left, 3 plus. Bilateral, sustained,
ankle clonus. Babinski’s “brisk.”
Later examined and hospitalized at a nearby medical
centre where Medrol was tried. She was sent home with a diagnosis of
Multiple Sclerosis, superimposed by a viral meningoencephalitis. Blurring
of vision was established as due to a left six-nerve paralysis. She
came home to a wheelchair provided she lived. Seen in our office one
month later, we concurred with the impression of Multple Sclerosis.
Our treatment schedule became operative. It has been a long journey
since June 1961, but the results have been phenomenal. This individual
has been returned to full activities, and as a gesture of gratitude,
comes to my office to serve in the capacity of an office assistant several
days each week. She does, however, still maintain her treatment schedule.
Whether this is necessary or not, I follow the advice of another patient
who has been continuing modified treatment for 22 years: “Why stop when
you feel so good?”
Male, white, 28 years. Seen first time 2/26/72. History
of numbness in lower extremities with loss of muscle control from waist
down. This started approximately 2 years before this visit. Difficulty
with bladder control at times. Seen by several neurologists at a nearby
medical centre who failed to make a diagnosis other than to say he had
a central Nervous System Pathology. Babnski’s, Gordon and Oppenheim
signs were all positive, and ankle jerks were 4 plus. Ankle clonus was
bilateral and sustained on right. He demonstrated a right foot drop.
We entertained a diagnosis of Multiple Sclerosis. Treatment was not
started since he had an appointment to be examined at a nearby Veterans’
Hospital clinic. We advised him not to accept ACTH therapy. The following
week we did start treatment. After 5 weeks, we did not see the patient
again for three weeks, at which time he confessed that he thought that
he was well and had stopped treatment. The weakness and other symptoms
were again returning. He has been back to gainful employment for the
past 12 months. Incidentally, he has been a “crack” pistol shooter,
and he still can hold a steady hand on the gun.
Female, white, 57 years. Seen first time 5/19/72. Chief
complaint was fatigue. This started approximately seven years before
coming to our office. The onset of illness was gradual. Generalized
weakness as the day went on, but was always feeling refreshed in the
morning. Drooping of the eyelids became a problem so that she automatically
would tilt her head backward so that the ptosed eyelids would be partially
corrected. Fatigue of the muscles of mastication on chewing became so
embarrassing that for the past several months, she avoided all social
events, even dinner with friends. Swallowing also became a serious problem
forcing her to a bland and sometimes liquid diet. Even a few minutes
talking, while taking the history, would so fatigue her that she found
it necessary to recline on the examining table so as to regain her strength.
She visited many clinics and medical centers in the United States and
Europe, but always was given the same diagnosis – her review of conditions
labeled her as psychosomatic. To us it was obvious that she suffered
from advanced Myasthenia Gravis. 1000mg. Thiamin Hydrochloride and 300mg.
pyridoxine given by needle had her demonstrating jaw and face movements
to her husband in less than 10 minutes. She remarked that she had not
been able to do that in three years. She was given our schedule for
treatment, but had great difficulty getting her local physician or any
physician to give her the needed injections. In desperation, he returned
to one of the medical centres and confronted them with the diagnosis,
which they did not believe. She, however, demanded that they employ
their test for this disease, which they did. From the patient’s description,
given at a later visit, I surmised that Tensilon was used. Her response
was the greatest ever seen in that University. She is also receiving
RNA 300mg. tablets three times each week, which we believe have stimulated
or furthered her progress. She no longer hesitates to eat in public,
and her stamina is approaching normal. During a visit to our office
in April of 1973, she laughed and joked about her experiences in getting
the diagnosis confirmed so that she could receive the vitamin injections
under supervision. She also favored us with a platter of delicious cakes
that she had baked.
Although we could write a book on cases treated and
cured (or established a permanent remission), time is a prohibiting
The treatment of Multiple Sclerosis has been empiric
since it was first described by Sir Robert Carswell in 1838. Brickner,9
in 1936, gave a review on treatment which included preparations of Antimony
and Arsenic, fever induced by various methods such as diathermy, malaria,
typhoid vacine, and fever brought on with the use of drugs. Surgical
procedures such as cervical sympathectomy and root section were also
employed. Serums, hypnotism and intraspinal injections of lecithin had
their day. Moore administered nicotinic acid and thiamin following the
dissertation by Zimmerman and Burack10 on diseases of the
nervous system resulting from a deficiency of the vitamin B-Complex,
and the paper by Spies11 and others on the use of nicotinic
acid in the treatment of Pellagra associated with mental pathology.
Spies and Aring,12 in 1938, published a paper on the effects
of Vitamin B1 on peripheral neuritis as associated with Pellagra. Moore
also had the benefit of the work of Stern, who published an article
on the intraspinal use of Vitamin B1 for the relief of intractable pain,
and for inflammatory and degenerative diseases of the Central Nervous
System. We learned early in our approach to this disease that small
and infrequent doses of thiamin hydrochloride would not accomplish our
purpose, and we also realized that more than one unit of the B-Complex
would be required, even though the physiological chemistry relative
to this phase of metabolism had not been completely established. Although
Moore used nicotinic acid for vaso-dilation purposes, we rationalized
that the degenerative process taking place in nerves, and thus also
in muscle, was of a greater magnitude. Inasmuch as the only sickness
remembered by the patient, family or relatives took place during the
summer months,13 we immediately suspected a virus to be the
This idea gained momentum with the greater incidence
of Multiple Sclerosis following the epidemic of encephalitis lethargia
of 1920 to 1926, and the epidemic of encephalitis B in St. Louis and
Toledo in 1934. However, the incidence of Polio was also up. Mixed,
abortive or unrecognized cases of Poliomyelitis became a tantalizing
factor. After the isolation of the Coxsackie virus with its mimicking
of Polio, and the knowledge that the paralysis with this type virus
infection was never permanent, the real devastating factor, in time
and place, at least to me, became apparent. Flexner and Lewis14
were able to demonstrate that in Polio, vascular and lymphatic lesions
constituted the primary causes of the lesions of the nervous system.
Multiple hemorrhagic accidents take place in Multiple Sclerosis with
ensuing scar tissue. As these microscopic scars contract, they impinge
on the vessels carrying nutrients to the Central Nervous System cells.
In muscle, the “devastation” is brought about through lack of function,
there being no “electrical charge” present to keep muscle active. For
this reason, the Sister Kenney treatment for Polio had merit, since
it helps to maintain muscle and muscle-nerve integrity. Our employment
of nicotinic acid is to effect adequate dilatation of existing vascular
structures, producing over time, chemically, what the Urologist accomplished
with his catheters in a mechanical fashion. Once these channels are
sufficiently operative, the metabolic factors that we supply will go
about revamping the myelin sheaths. Due to lack of full energy components,
cells can temporarily lose the ability of normal physiological activity.
We can restore the normal function of cells which depends upon their
ability to extract and use the chemical potential energy locked within
the structure of organic molecules. We accomplish this by placing massive
amounts of the essential material at the disposal of cells.
We categorically make this statement: Any victim of
Multiple Sclerosis who will dramatically flush with the use of nicotinic
acid, and who has not yet progressed to the stage of myelin degeneration,
as witnessed by sustained ankle clonus elicited in the orthodox manner,
can be cured with the adequate employment of Thiamin Hydrochloride
and other factors of the Vitamin B Complex in conjunction with essential
proteins, lipids, carbohydrates and injectable crude liver. If sustained
ankle clonus is not bilateral, then it is not a deterrent. We have had
patients who did demonstrate bilateral sustained ankle clonus, and who
were in wheelchairs, and who returned to normal activities after 5 to
8 years of treatment. These patients, fortunately, had not received
ACTH. One patient was given a single course of Medrol 4 mg. QID. This
had little effect on her pathology, and apparently no blocking action,
on our treatment. The general use of ACTH in Multiple Sclerosis will
extend the recovery period by a time directly proportional to the amount
of the drug employed. It is hoped that this paper will bring an end
to this senseless practice of medicine, since ACTH never works
the third time.
The theories recognized as playing a part in Myasthenia
Gravis still rest in the main with Thymus enlargement or tumor, Endocrine
dysfunction, Metabolic fault, and the build-up of pyruvic acid in the
vicinity of the motor end-plates. In reality, it is a genetic fault
inovlving a lethal intermediate gene or group of genes. There is definitely
an over-supply of pyruvates, and an under-supply of acetyl-choline.
The cue in this drama is cocarboyxlase. Coenzyme A is also in limited
supply. Two molecules of thiamin hydrochloride, and two molecules of
phosphoric acid yields cocarboxylase. One was of obtaining acetyl coenzyme
A, a by-product of coenzyme A and pyruvic acid, is in the reaction between
pyruvic acid, coenzyme A and diphosphopyridine nucleotide in the presence
of diphosphothiamine (cocarboxylase). Cocarboxylase is also involved
in the synthesis of acetylcholine and in the control of its hydrolysis.
The activity of choline esterase of serum is strongly inhibited by this
same agent. Thiamin occupies a key position in at least the terminal
stages of carbohydrate metabolism. Cocarboxylase plays an active role
in the decarboxylation of pyruvic and other keto acids. In the brain,
cocarboxylase participates in the anaerobic dismutation of pyruvates
to lactate and acetate, and their subsequent oxidation to carbon dioxide
and water. In liver and other tissue cells, cocarboxylase is involved
in the conversion of pyruvates to oxalacetate which combines oxidatively
and irreversibly with another molecule of pyruvate to enter the tricarboxylic
acid cycle. In thiamin deficiency, a form of peripheral neuritis markedly
demonstrated in some cases of chronic alcoholism exists, affecting both
sensory and motor nerves.
The treatment of Myasthenia Gravis is that of any pathology
dealing with the interruption of the normal physiology of nerve cells.
In years past, when we were treating Poliomyelitis successfully with
massive doses of ascorbic acid, we would always follow with an indefinite
timetable, giving the B vitamins for nerve repair. We see the same results
when treating damage to the spinal cord, whether this is due to mechanical
trauma, or to the inflammation caused by a virus – any virus. As pointed
out by Lipschitz et al., the replenishing of vitamin B1 restores the
ability of the nervous system to handle properly pyruvic acid and estrose.
This action of thiamin makes its function in Myasthenia Gravis seem
elementary. A German scientist once speculated that cocarboxylase was
actually the “food” required for nerve intensity with which it is applied
in Multiple Sclerosis will never be necessary. We are not confronted
with the loss of myelin sheaths in extra vital areas. The chemistry,
however, is more coplex than in Mulitple Sclerosis, since it involves
muscle cells to a greater degree. Enzymes and their balance is a necessary
approach. When we realize that over 900 different enzymes have been
identified, it makes more knowledgeable the need for extensive vitamin
therapy. This suggests that normal liver function is necessary for good
results. A simple liver function test can be used to good advantage.
One that I worked out many years ago to demonstrate “liver stress” is
performed as follows. Have patient bring 90cc from first voiding upon
arising. Fill ordinary test tube to within one cm. of top. Allow to
set for 24 hours and read. One will find, in most specimens, a gelatinous
fluid resting at the bottom of the test tube. The amount present, which
can measure 2-1/4 cm., indicates the degree of liver stress present.
Choline by needle or by mouth will remove this finding from the urine.
Some urine specimens will show a heavy, white sediment obstructing proper
reading of liver stress. Glacial Acetic Acid alone, and/or heat will
temporarily remove these phosphates. Should the deposit of phosphate
be exceedingly heavy, then it is advisble to secure a bedtime specimen,
or one 2 hours after breakfast. The night specimen should be placed
in a cool area until delivery. Occasionally, the urine specimen will
look like skim milk.This is due to earthy phosphates and can be cleared
by adding Glacial Acetic Acid to the tube. (After ascertaining liver
stress, one can then add 20 drops Glacial Acetic Acid to the specimen
– if none was previously added – and allow to remain an additional 48
hours to check for Uric Acid Crystals. (A red shower indicating an abnormal
level for uric acid.) This test must be run every week when administering
ribonucleic acid (RNA).
Since presenting this paper, we have observed that improvement
in all categories is enhanced when the intravenous injection contains
800 mg. to 1000 mg. thiamin hydrochloride, 200 mg. pyridoxine, 400 mg.
niacinamide, 100 mg. nicotinic acid. The thiamin hydrochloride solution
must be clear. The amount of niacin employed must be calculated
from the “flush factor” of a given patient. The injection is made with
a 20cc or 30cc syringe, using a 23G x 3/4 inch or 22G x 1 inch needle.
Intravenous medication can be given daily; it should be administered
at least twice weekly. Due to sensitivity possibilities, we always have
the patient take the intramuscular injections for three weeks before
starting intravenous therapy.
Bibliography – Papers
1. Sern, E.L.: The Intraspinal Injection of Vitamin
B1 for the Relief of Intractable Pain, and for Inflammatory and Degenerative
Diseases of the Central Nervous System. Am. J. Surg. 34:495,
2. Rosenberg, L.E.: Vitamin Deficiency Diseases and
the Vitamin Dependent Diseases with Reference to B and D. Natl. Health
Fed’n. Bulletin Vol. XVIII, No. 10, November 1972.
3. Moore, M.T.: Treatment of Multiple Sclerosis with
Nicotinic Acid and Vitamin B1. Archives Int. Med. Vol. 65, pp.
18, Jan. 1940.
4. Eijou, S.W.; Baer, I.M.: Child Development II
Universal Stage of Infancy. Appleton-Century-Crofts, 1965.
5. Kempe, C.H.: Key to the Secret of MS. Medical
World News, July 7, 1972.
6. Alter, M. et al.: Dissertation on Environmental and
Sleeping Virus Theory. Medical Tribune.
7. Schandl, D.K.: Dissertation on Environmental and
Pyridoxine Cause of MS. The Charlotte Observer, Charlotte, ND.
April 23, 1973.
8. Dahl, Doris; Bignami, Amico: Report of Substance
Preventing Renewal Myelin. Reidsville Review, April 23, 1973.
9. Brickner, R.M.: A Critique of Therapy in Multiple
Sclerosis. Bulletin Neur. Inst., New York, Vol. 4:665, April
10. Zimmerman, H.H.; Burack, F: Lesions of the Nervous
System Resulting from a Deficiency of the Vitamin B Complex. Arch.
Pathology, Vol. 13:207, February 1932.
11. Spies, T.D.; Cooper, C.; Blankenhorn, M.A.: The
Use of Nicotninic Acid in the Treatment of Pellagra. JAMA, Vol.
110:622, February, 1936.
12. Spies, T.D.; Aring, C.D.: The Effect of Vitamin
B1 on the Peripheral Neuritis of Pellagra. JAMA, Vol. 110:1081,
13. Klenner, F.R.: Fatigue-Normal and Pathological with
Special Consideration of Myasthenia Gravis and Multiple Sclerosis. Southern
Medicine and Surgery, Vol. III, No. 9; September 1949.
14. Flexner, S.; Lewis, P.A.: Experimental Poliomyelitis
in Monkeys. Journal Experimental Medicine, Vol. 12:227, 1910.
Bibliography – Textbooks
a. Alpers, B.J.: Clinical Neurology, 2nd Ed.,
F.A. Davis Co., 1950.
b. Bodansky, M.: Intro. to Physiological Chemistry,
2nd Ed. John Wiley & Sons, Inc., 1930.
c. Cameron, A.T.; Gilmour, C.R.: The Biochemistry
of Medicine. William Wood & Co., 1933.
d. Evans, A.L.; Hartridge, E.: Starling’s Principles
of Human Physiology 5th Ed., J&A Churchill, London, 1930.
e. Fieser, L.F.; Fieser, Mary: Organic Chemistry.
3rd Ed., D.C. Heath and Company, 1956.
f. Harrow, B.: Casimir Funk: Pioneer in Vitamins
& Hormones. Dodd, Mead & Co., New York, 1955.
g. Hawk, P.B.; Oser, BlL.; Summerson, W.E.: Practical
Physiological Chemistry. 13th Ed., McGraw-Hill Book Co. Inc., 1954.
h. Lichtman, S.S.: Diseases of the Liver, Gallbladder
and Bile Ducts, Vol. I, Lea & Febiger, Philadelphia, 1953.
I. Lowenberg, S.A.: Medical and Physical Diagnosis.
7th Ed. F.A. Davis Co., 1948.
j. Martin, H.N.; Martin, E.G.: The Human Body.
11th Ed. Revised. Henry Holt and Co., 1932.
k. Srb, A.M.; Owen, R.A.; Edgar, R.S.: General Genetics,
2nd Ed., W.H. Freeman and Co., 1965.
l. The Merck Manual, 12th Ed. Merck & Co.,
Inc., Rahway, NJ 1972.
m. The Vitamins: A Symposium, 1939, AMA.
n. Vander, A.J.: Sherman, J.H.; Luciano, D.S.: Human
Physiology McGraw-Hill Inc., 1970.
9. Wells, H.C.: Chemical Pathology, 5th Ed. Revised.
W.B. Saunders Co., 1925.
Frederich R. Klenner, BS, MS, MD
Reidsville, North Carolina
A native of Pennsylvania, Dr. Klenner attended St. Vincent
and St. Francis Colleges, where he received his BS and MS degrees in
Biology. He graduated magna cum lauda and was awarded a teaching fellowship
there. He was also awarded the college medal for scholastic philosophy.
There followed another teaching fellowship in Chemistry at Catholic
University, where he pursued studies for a doctorate in Physiology.
Dr. Klenner then migrated to North Carolina and Duke
University to continue his studies. He arrived in time to use his knowledge
in Physiology and Chemistry to free the nervous system of the frog for
a symposium, by immersing the animal in 10% nitric acid. Taken in tow
by Dr. Pearse, chairman of the department, he was finally persuaded
to enter the school of medicine. He completed his studies at Duke University
and received his medical degree in 1936.
Dr. Klenner served three years in post-graduate hospital
training before embarking on a private practice. Although specializing
in diseases of the chest, he continued to do General Practice because
of the opportunities it afforded for observations in medicine. His patients
were as enthusiastic as he in playing “guinea pigs” to study the action
of ascorbic acid. The first massive doses of ascorbic acid he gave to
himself. Each time something new appeared on the horizon, he took the
same amount of ascorbic acid to study its effects so as to come up with
Dr. Klenner’s list of honours and professional affiliations
is tremendous. He is listed in various “Who’s Who” registers, and has
published many scitnific papers throughout his career. Dr. Klenner is
a: Fellow: The American College of Chest Physicians; Fellow & Diplomate:
The International College of Applied Nutrition; Fellow: The American
Association for the Advancment of Science; Fellow: The American College
of Angiology; Fellow: The American Academy of Family Practice; Fellow:
The Royal Society of Health (London); Fellow (Honorary): The International
Academy of Preventive and Orthomolecular Medicine; Fellow: International
College of Angiology; and Founder-Fellow: American Geriatrics Society.