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MS ANTIBIOTICS

 

Virus the cause of MS

 

 MS turning into CIPD

 

Multiple Sclerosis

 

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Multiple Sclerosis treatment

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 Section on MS

 

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MS & Treatment Protocol-3return to page one



 

Our treatment schedule part-3continued from -page-2

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 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 byMedical 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 inThe 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 appreciated.

 

continue to page four for case histories

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