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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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Protein and Lipid Metabolism
In dealing with muscle and nerve pathology, the metabolism of lipids and protein must also be considered, although in a lesser degree. There is a close relationship between neutral fats and glucose metabolism. The neutral fats, consisting of three fatty acids attached to the three-carbon molecule glycerol, constitutes the majority of the lipid in the body. The breakdown and synthesis of neutral fats is closely associated with the metabolism of glucose because of the formation of intermediates common to both pathways. The breakdown of fatty acids requires coenzyme A and hydrogen carriers such as niacin-adenosine-dinucleotide (NAD). Ascorbic acid can operate as a hydrogen transport in cellular oxidation, thus facilitating these reactions. The starting point for fatty acid synthesis is acetyl coenzyme A. In the diseases in which we are concerned, myelin is very important. Myelin is a fat-like substance forming the principle component of the myelin sheath of nerve fibers. It is composed of cholesterol, certain cerebrosides, phospholipins and fatty acids.

Protein metabolism is far more complicated than lipid or carbohydrate metabolism. Proteins are formed from 20 different amino acids, all of which have different chemical structures and require different pathways for their synthesis and degradation. Synthesis of a protein molecule from amino acids involves more than the formation of chemical bonds between amino acids. The amino acids must be placed in a precise sequential order. Unlike fats and sugars, amino acids contain nitrogen in addition to carbon, hydrogen and oxygen. It is more than of academic interest to know that thiamin hydrochloride is a pyrimidine compound, thus containing nitrogen, like amino acids. Because of this amine factor, Funk originally spelled vitamin with an "e" – vitamine. "Vit" comes from the Greek "vita," meaning life, and E amine for the nitrogen factor. Since only thiamin hydrochloride of all vitamins had this factor, the "e" was dropped, and the name vitamin retained for symbolic reasons. Although all amino acids are important, some more than others, and still others necesary for the continuance of life, the one we are interested in is the amino acid glycine. Glycine is noted for its specific dynamic action. Bodansky states that not only does the body use any preformed glycine that may be present either in the diet or in the tissues, but it is forced, at times, to synthesize this amino acid in large amounts. The conversion of glycine into sugar in the animal body has been well documented. 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 the amino acid glycine stimulates the combustion of other tissue constituents. Glycine with the amidine group from arginine, through a process of trans-amidination and transmethylation, yields creatine.

Comparison Between Multiple Sclerosis and Myasthenia Gravis
Myasthenia Gravis and Multiple Sclerosis differ only in that the former will not require as intensive treatment as will Multiple Sclerosis. The answer for this difference is obvious. One is a peripheral nerve pathology, the other being central nerve pathology. In the diagnosis, one will find the eyelids in Myasthenia Gravis drooping. In Multiple Sclerosis there will be nystagmus – constant involuntary, more or less cyclical movement of the eyeballs. Movement may be in any direction, but usually lateral as the patient follows the examiner's finger. (It is definitely more pronounced than that found in Meniere's disease.) There may be heaviness of the legs in Myasthenia Gravis, but it will always be present in at least one leg in Multiple Sclerosis. Myasthenia Gravis patients will have difficulty in chewing and swallowing, the jaws might sag, and some will present a sad, masked-like expression, but never like Parkinson's disease. Scanning speech will be in evidence in advanced cases in Multiple Sclerosis, and words will come slow and syllabic. General weakness increases as the day goes on in Myasthenia Gravis; some increase in fatigue only with activity in Multiple Sclerosis. Remissions and exacerbations are common in both diseases in the early stages, but more so with Myasthenia Gravis. In Multiple Sclerosis, the patients will experience numbness of the hands and legs as the disease progresses, or a tremor in the hand will develop, making signing of one's name a problem. The tremor is intentional. Well along in the disease of Multiple Sclerosis, the gait will be awkward and stiff. Ataxia is due mainly to the inability to coordinate and control movements. The knee-jerks will be exaggerated, with positive Babinski and ankle clonus. The Babinski can be normal and no clonus, but there are other signs equally as important. Oppenheim's tibia test; Gordon's calf muscle test; Chaddock's external malleolus test, and the Hoffman reflex – a finger reflex. Any one of these, along with temporal whiteness of the optic nerve can be considered early or minimal Multiple Sclerosis. Abdominal reflexes are variable. Pain, bi-lateral, of the sartorius muscles with any positive reflex is always very suspicious of Multiple Sclerosis. In Myasthenia Gravis, the old neostigmine test is conclusive. More detailed symptoms and signs on these two pathological conditions can be found in such common reference as Merck's Manual. The important factor is early diagnosis. Do not hesitate to commence treatment in either disease even though the impression might be guarded. Response to treatment is sufficient evidence that your judgment is sound.

There are three forms of Multiple Sclerosis:
1) Pseudo-Multiple Sclerosis or Cerebral, which is the syndrome characterized by mental symptoms, emotional lability, convulsive seizures, hemiplegia and aphasia. This type is caused by an Adenovirus which gains entry into the brain through damage to the choroid plexus much like the encephalitis that follows pneumonias. Actually, the resulting pathology is an encephalitis. Many who have experienced this syndrome have died; many who have lived might just as well have died, for the return trip is costly, long, and requires a great amount of tender, loving care.
2) Cerebellar-brain-stem-spinal: this is true Multiple Sclerosis and is manifested by nystagmus, scanning speech, intention tremor, ataxia, transient paresthesias, weakness in one or more extremity, and visual disturbances.
3) Spinal or minimal Multiple Sclerosis: These cases are never given a diagnosis. These patients come with other complaints, but singular upper motor neuron pathology will be evident. This might be, as we have seen them, positive Hoffman, positive Gordon, positive Oppenheim, and occasionally, a patient with a footdrop limb.

Importance of Thiamin Hydrochloride in Neurological Diseases
The importance of thiamin in treating Myasthenia Gravis and Multiple Sclerosis cannot be over-emphasized. Two molecules of thiamin hydrochloride in combination with two molecules of phosphoric acid is cocarboxylase. For the reaction to acetyl coenzyme A plus oxaloacetic acid to continue through to citric acid with the release of coenzyme A, cocarboxylase must be present. If this reaction does not take place, due to one of many factors, there will be no coenzyme A present to react with another molecule of pyruvic acid to set in motion the elements necessary for the continuance of the metabolic cycle. In thiamin deficiency, both pyruvates and lactate accumulate in the blood. Pyruvates also accumulate at the neuro-muscular junction causing cloudy swelling of the distal portion of the nerves. Cocarboxylase, also known as diphosphothiamine, is necessary in the synthesis of acetyl-choline and in the control of its hydrolysis. The activity of choline esterase of serum is also strongly inhibited by cocarboxylase.

The chief chemical factor in both diseases is thiamin hydro-chloride. Other fractions of the B-complex are also essential but in lesser amounts. Myasthenia Gravis is due to genetic fault, most likely involving an intermediate lethal gene or group of genes. Multiple Sclerosis is more complex. The initial pathology is sickness caused by the Coxsackie virus. This virus mimics poliomyelitis, and for many years accounted for thousands of so-called polio cases. This virus, like the polio viruses, can cause paralysis but never permanently. The nerve damage is the result of microscopic hemorrhages in the central nervous system. With the contraction of the scar at the site of bleeding, the vessels carrying nutrients to the nerve cells are virtually clamped off. This leaves nerve tissue, in many instances, alive but not capable of work. As time goes on, this wasting of nerve tissue results in loss of its myelin protection. This is similar to electrical wires that have lost their insulation when exposed to the wear of daily use, or exposure to the elements. Myelin is a lamellated structure composed of neurilemma cell membranes. Neurilemma cells have marked affinity for axis cylinders, apply themselves closely and seemingly engulf them. At the same time their cytoplasm flows around the axis cylinder. The myelin sheath is actually part of the neurilemma plasma membrane with its lipid and protein layers. Myelin in the central nervous system is likewise lamellated. It is laid down by neuroglia cells. The sheath of the nerve fiber is known to have a relationship to speed of conduction – the speed of propagation being in direct proportion to the fiber diameter. Impulses are thought to travel along the surface of a nerve fiber and its speed over the large myelinated fibers is approximately 337 miles per hour, 150 meters per second. We can reconstruct the nerve pathways and re-myelinate the damaged nerve channels. There is nothing new about this physiology. Each one of us has demonstrated or experienced positive Babinski reflexes. A child is born without completed laminated sheath. This is the reason for the spastic movements of the child. The nerve channels are minute in comparison to the adult person, thus we can expect a longer interval of time necessary for repair. If the baby can complete the myelination of its nerve channels with only mother's milk, surely we can duplicate this performance – and we can. There will, however, be situations where the pathology has existed for so long a time that recovery seems impossible. This is true because it requires approximately two years of treatment, with massive doses of vitamins and a high protein diet, to repair one year of the disease. Physicians are too afraid to make an early diagnosis, and some patients now under my care experienced as much as ten years in that process.

In Myasthenia Gravis, the chief concern is with the build-up of pyruvic acid at the neuro-muscular junction. We also find decreased amounts of acetyl-choline along with limited amounts of cocarboxylase. As we noted in the discussion of glycolysis, cocarboxylase plays a very important role in various reactions involving principally the decarboxylation of pyruvic acid and other keto acids. In the brain, cocarboxylase participates in the anaerobic dismutation of pyruvate to lactate and acetate, and their subsequent oxidation to carbon dioxide and water. Cocarboxylase is also involved in the synthesis of acetylcholine which is definitely in short supply in Myasthenia Gravis. The activity of choline esterase is strongly inhibited by this same double thiamin unit. The conversion of thiamin hydrochloride to cocarboxylase takes place in the liver, the kidneys and to a small degree, in brain and muscle. One can have nephritis, yet the small amount manufactured in the kidneys continues to be produced. The liver is the main source for this conversion. An individual with liver pathology would have a decreased capacity for phosphorylation of thiamin. The storage capacity of the body for thiamin is limited. It does accumulate rapidly in the liver in its original form and also as the pyrophosphoric ester. Thiamin deficiency inhibits lactic acid metabolism at the stage of pyruvic acid. When we refer to thiamin deficiency, we actually mean a lack of cocarboxylase. Pyruvic acidemia is an index of this type of thiamin deficiency. We might mention here that niacin deficiency can induce hepatic insufficiency. The amount of nicotinic acid required to elevate blood coenzyme, the active physiological form of nicotinic acid, increases dramatically in liver stress. Cocarboxylase (thiamin pyro-phosphate) operates as a coenzyme in the oxidative decarboxylation of ketoglutarate to succinate and of pyrovate to acetoacetate. Succinic acid in turn is acted upon by the enzyme succinic dehydrogenase, yielding fumaric acid by oxidative dehydrogenation. Fumaric acid readily undergoes hydration in the presence of the enzyme fumarase to form malic acid, which on oxidation in the presence of the enzyme malic dehydrogenase, yields oxalacetic acid. At this point of cell metabolism, the entrance of another molecule of pyruvic acid follows the Krebs cycle to be repeated. We are never concerned with the amount of pyruvic acid formed by the various routes, provided we can maintain normal cell metabolism.

Early Use of Thiamin Hydrochloride in Neurological Diseases
In the late thirties, Stern1 from Columbia University, was employing thiamin hydrochloride intraspinally with astonishing results in Multiple Sclerosis. He reported taking patients to the operating room on a stretcher, and following 30 mg. thiamin given intraspinally, they would walk back to their room. The response was relatively transient, but it led Stern to believe that Multiple Sclerosis was nothing more than vitamin B1 avitaminosis, the "modus operandi" being damage to the filter bed of the choroid plexus. Stern also found that the effective dose of vitamin B1, when given in the lumbar subarachnoid space, was too close to the lethal dose as was demonstrated in dogs. Stern's hypothesis was backed by the knowledge that degeneration of the myelin sheaths of peripheral nerves as well as of the ganglion cells of the brain and spinal cord can be produced in experimental polyneuritis. Similar findings are observed in starvation, even when the supply of thiamin appears to be adequate. One school of thought regards the neurological syndrome of polyneuritis as a functional defect concerned with the neurons. From 30 years of observation, I am certain that in Myasthenia Gravis and Multiple Sclerosis, it is not a functional defect, nor is it due to impaired diffusion which would deny to the total metabolism sufficient quantities of the vitamin to satisfy the requirements of the neuro-muscular systems. The problem is supply and demand. In this light, Dr. Leon Rosenberg2 of Yale University Medical School, in working with B vitamins, distinguishes between vitamin-deficiency diseases and vitamin-dependent diseases. He states that the successful treatment of vitamin-dependent diseases requires dosages up to 1,000 times the calculated minimal daily requirement. 1.3 mg. has been established for thiamin hydrochloride which would indicate that in the pathological conditions being considered, the daily requirement would be at least 1300 mg. Moore3, in 1940, published a monograph on the use of high intravenous doses of nicotinic acid for the cure of Multiple Sclerosis. Moore employed a drug combination called "Nicobee." This preparation contained 100 mg. nicotinic acid and 60 mg. of thiamin in each 10cc solution.

Many of the components of the B-complex must also be administered in varying amounts, along with thiamin hydrochloride, since they too exert a dynamic influence in general metabolism. Many believe that the B vitamins are actually metabolic reagents. Hoagland has referred to them as "protective catalysts."

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