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From the Journal of Applied Nutrition, 1973

Response of Peripheral and Central Nerve Pathology to Mega-Doses of the Vitamin B-Complex and Other Metabolites
by Frederich R. Klenner, BS, MS, MD

The protocol of how to effectively treat Multiple Sclerosis, by Frederich R. Klenner. (In two parts, as originally published in 1973.)


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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.

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 2-1/2 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 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).

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