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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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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.

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