Cocarboxylase

Recommended 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. Niacin (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-gauge 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 Benadryl, IM. 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 times patients will flush with intramuscular niacin when they fail to flush by the oral route. An occasional patient will experience the 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. Eight mg. Decadron given IM 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 of myelin.

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 takes part in enzymic reactions as a dinucleotide prosthetic group, consisting of riboflavin, two phosphoric acids, ribose 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 IM; 25 mg. before meals and bedtime.

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 chronic 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 benefited by liver injections which, of course, contain vitamin B12. Degenerative changes brought on by other factors, therefore, can also be benefited by daily injections of crude liver.

9) Adenosine-5-Monophosphoric acid: One of the purine bases occurring in muscle is adenine. 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 is 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, adenosine-diphosphate (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 hour.

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 plays 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 twice weekly.

14) Calcium pantothenate: 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 acid 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 grams.

17) High protein diet with two to three eggs for 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 be individualized.

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 response.

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 another virus for another disease. In our long practice, we would see, as I am certain many of you have, chickenpox 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. 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, 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 Alter 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, 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 acids 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 Bignami 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 appreciated.

Case Histories

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 associated 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 IV, 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. Seen in our office one month later, we concurred with the impression of Multiple 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. Babinski'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, she 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 factor.

Conclusion

The treatment of Multiple Sclerosis has been empiric since it was first described by Sir Robert Carswell in 1838. Brickner, in 1936, gave a review on treatment which included preparations of Antimony and Arsenic, fever induced by various methods such as diathermy, malaria, typhoid vaccine, 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 Burack on diseases of the nervous system resulting from a deficiency of the vitamin B-Complex, and the paper by Spies and others on the use of nicotinic acid in the treatment of Pellagra associated with mental pathology. Spies and Aring, 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 vasodilation 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, we immediately suspected a virus to be the offending agent.

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 Lewis 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 involving a lethal intermediate gene or group of genes. There is definitely an over-supply of pyruvates, and an under-supply of acetylcholine. The cue in this drama is cocarboxylase. Coenzyme A is also in limited supply. Two molecules of thiamin hydrochloride, and two molecules of phosphoric acid yields cocarboxylase. One way 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 dextrose. 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 life. In treating Myasthenia Gravis with the schedule outlined, the 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 complex than in Multiple 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 2-1/2cm., 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 advisable 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).

Appendix

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. Stern, 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, 1938.

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. Bijou, 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, NC. 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 1936.

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 Nicotinic 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, April 1938.

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, B.L.; 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.

o. 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 laude 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 the answers.

Dr. Klenner's list of honours and professional affiliations is tremendous. He is listed in various "Who's Who" registers, and has published many scientific 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 Advancement 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.

by Frederich R. Klenner, BS, MS, MD

Journal of Applied Nutrition, 1973

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