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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.)
Online publication only. . .


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In this two-part series Klenner defines an orthomolecular treatment of MS that has been effectively employed by Dale Humpherys and other patients. (For Humpherys' report, see his article in the December 2005 issue of the Townsend Letter.)

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Part I

Two devastating pathological syndromes affecting nerves are Multiple Sclerosis and Myasthenia Gravis. To adequately understand the significance of these diseases, one must have a working knowledge of fatigue, normal and abnormal. The phenomena of fatigue according to Starling's Principles of Human Physiology has been recognized for years to depend on two factors:
1) the consumption of the substances available for the supply of potential energy to the contractile material;
2) The accumulation of products of the contractile process. We must consider a third: The inability to use available energy-producing substances because of distribution roadblocks.

Two general locations for normal fatigue are:
1) At the synapses, the delicate junction between neuron and neuron, recognized as highly susceptible to fatigue;
2) The junction between motor nerves and the fibers of skeletal muscle, made possible by motor end plates.
Synaptic fatigue and end plate fatigue occur in such minute structures that quick recovery seems always possible. We must recognize, however, that although the feeling of fatigue may apparently be quickly dissipated, actual restoration of the fatigued structure will require much time.

When a plant is fatigued it wilts; unless relieved of the fatigue, it dies. Proper atmospheric conditions, proper soil, or these equivalents conferred by man will restore, to some degree, the faltering plant. Even prayer has been advanced as an active agent to not only relieve the failing plant of its fatigue, but also to encourage its growth. Plants do indeed have a soul – the soul of growth. This predicates a potential capable of responding to "kindness" of various types. In this light, then, people with "green thumbs" are nothing more than accepted plant missionaries. When an animal is fatigued, it usually follows an innate faculty supplied by nature and rests. When sick, like the dog, it will eat grass to relieve the gastric complaint. The dog's master can go further and supply various drugs or vaccines to either cure the malady or to prevent several types of illnesses from ever coming into existence. Animals have not only a soul for growth like the plant, but also a soul of sensation. Proper rest, proper drugs and proper food, along with understanding, will secure for the dog mental and physical relaxation, thus assuring the animal a more serene and longer life as compared to a dog running loose on the streets or in the wild, and required by circumstances to scavenge for itself.

It is a common experience to obtain marked relief from physiological fatigue by taking a short nap, the often called "Edison cat nap." An ordinary night's rest is none too long for recovery from fatigue created by a day's labor. The almost universal habit of abstaining from ordinary duties one day out of seven has real significance It acknowledges the necessity of allowing, at intervals, a longer period for restoration than the usual nightly ones in order that accumulative fatigue will not be experienced. Work is labor, and so is play. There is a real and significant difference between being pleasantly tired and being fatigued. The share-cropper working in the field, where fresh air abounds, can easily expend far more energy than one who works in a poorly-ventilated factory, yet the farm worker will register only relative fatigue, as compared to the factory worker who often will be physiologically exhausted. This suggests that oxygen plays an important role in the production of fatigue.

Muscle Fatigue
In the laboratory one can demonstrate that repeated stimulation of striated muscle diminishes the force of the contraction, and that indefinite repetition of such stimulation will so exhaust the muscle that eventually it will fail to respond. The fatigue which is here observed can be due either to the exhaustion of the glycogen and the hexose phosphates or to the accumulation of lactic acid within the muscle. Muscle contraction is essentially an anaerobic process. Lactic acid production, the fundamental chemical reaction producing energy for muscle contraction, does not require oxygen. Such energy-yielding reactions of partial decomposition, not requiring oxygen, are called fermentations. Muscle, then, obtains energy independently of its immediate oxygen supply by the rapid fermentation of glycogen to lactic acid, in the same way as brewer's yeast derives energy by the fermentation of sugars to alcohol. This anaerobic explosion of energy is akin to jet propulsion, and similarly, its potential is limited. Ultimately, muscle requires oxygen for the maintenance of normal irritability, for oxidative energy production, and for the restoration of its anaerobic energy-yielding system. Muscle action and muscle fatigue is indeed a very complex chemical system. Such units as phosphocreatine, adenosine triphosphate and calcium and magnesium ions deserve limited explanation. Eagleston and others, independently, discovered that most of the creatine in muscle is in labile combination with phosphoric acid. The free creatine which occurs in muscle fatigue is proportional to the amount of phosphocreatine which is decomposed. Creatine is derived in the body from the amino acids Arginine and Glycine, plus a labile methyl group. According to Cameron and Gilmour, creatine, in acid solution, readily loses water to give a ring compound, an internal anhydride, creatinine. Creatinine is a constant constituent of urine, and its amount is sometimes increased in the later stages of nephritis and always in Myasthenia Gravis. The simplest conception of creatine-creatinine metabolism is that creatinine is formed from creatine during periods of muscular activity when creatine is transiently free in muscle, and then passes by way of the blood, without change, into the urine. Creatine phosphate breaks down in the presence of adenosine diphosphate (ADP) to form adenosine triphosphate (ATP). Creatine phosphate acts as the immediate energy source for the synthesis of adenosine triphosphate for relatively short periods during bursts of contractile activity. The usable life of creatine phosphate is limited. Once it is used up by muscle action, the muscle must then rely on the adenosine triphosphate (ATP) which is synthesized during the chemical activity of the Kreb cycle in glycolysis. Adenosine triphosphate is the essential high-energy package, and it is responsible for delivery of necessary power for the activation of all cells; it is the basic energy unit for life. During muscle relaxation phase, some of the adenosine triphosphate reacts with creatine to form creatine phosphate at the expense of adenosine triphosphate which is reduced to adenosine diphosphate (ADP), a low-energy package. This change of reactions continues until such a situation exists when muscle cells can no longer synthesize ATP due to lack of oxygen and essential substrates. When this happens, a state of muscle rigor mortis exists. Frequently, Myasthenia Gravis patients experience minimal rigor mortis; sometimes no adenosine triphosphate is available and so actual death.

We must briefly discuss still other phases of muscle activity. The filaments in skeletal muscle are composed primarily of the proteins actin and myosin. Small amounts of other proteins play important roles in the contractile cycle. Part of the energy for movement comes from the splitting of adenosine triphosphate by the myosin molecule. Actin increases the ability of myosin to split adenosine triphosphate. Magnesium ions and calcium ions are also necessary in muscle action. Besides actin, tropomyosin and troponin are responsible for the effects of calcium on the contractile apparatus. One must also consider the part played by acetylcholine and its esterase in muscle activity. Too much or too little of these substances prevents or slows down muscle action even when all other factors are within normal limits. The neuromuscular junction potential can be modified by drugs and disease. One such drug is curare. Curare merely occupies a reactive site so that acetylcholine is prevented from interaction with motor end plates. Myasthenia Gravis is a disease whereby too much pyruvic acid (pyruvates), due to faulty metabolism, affects the interaction of acetylcholine at the site of the motor end plates at the neuro-muscular junction. In Multiple Sclerosis, the sluggish and sometimes bizarre muscle activity is due to absence or inability to utilize essential factors because of mechanical and chemical road blocks.

Like nerve action potential, muscle action potential is an all-or-none event. The overall effects of motor unit recruitment depends upon the anatomical relationship between the contracting units. Specifically whether the fibers are in series or parallel. When linked in parallel by connective tissue, the force generated by each fiber is additive, producing a total force proportional to the number of fibers contracting. When the fibers are in series, the total force is equal to that generated by a single fiber no matter how many fibers fire simultaneously. These relationships exert quite a different effect on the degree and velocity of shortening. No matter how many fibers in parallel contract together, the amount of shortening and velocity are the same as when a single fiber contracts, but both the degree and the velocity of shortening are proportional to the number of contracting fibers in series. Long muscles shorten more and faster than short muscles; thick muscles exert more tension than thin muscles. These differences, however, disappear when the values are expressed per unit length and cross-section area. The total range of length changes a muscle can undergo while attached to the bone is much less than the changes that would cause the active tension to fall to zero. Muscle exerts a force on the bones to which they are attached through tendons. As muscle shortens, it exerts only a pulling force called flexion. Opposing muscles straighten the unit flexed which is known as extension. This review on muscle action and fatigue is, apologetically, very elementary, but sufficient to establish a basic understanding of what is happening in the pathological conditions entertained in this treatise.

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