Autoimmune Diseases

What Are Autoimmune Diseases?

The word "auto" is the Greek word for self. The immune system is a complicated network of cells and cell components (called molecules) that normally work to defend the body and eliminate infections caused by bacteria, viruses, and other invading microbes. If a person has an autoimmune disease, the immune system mistakenly attacks self, targeting the cells, tissues, and organs of a person's own body. A collection of immune system cells and molecules at a target site is broadly referred to as inflammation.

 The autoimmune reaction is directed against the brain in multiple sclerosis and the gut in Crohn's disease. In other autoimmune diseases such as systemic lupus erythematosus (lupus), affected tissues and organs may vary among individuals with the same disease. One person with lupus may have affected skin and joints whereas another may have affected skin, kidney, and lungs. Destruction of insulin-producing cells of the pancreas causes Type 1 diabetes mellitus.

Who Is Affected by Autoimmune Diseases?

 Autoimmune diseases afflict millions of Americans, strike women more often than men; in particular, they affect women of working age and during their childbearing years.

  Lupus is more common in African-American and Hispanic women. Rheumatoid arthritis and scleroderma affect  Native American communities .

alternative treatments of  diseases, "Flame within contents".

Niacin Thiamine use in Multiple Sclerosis

For this reason, the Sister Kenney treatment for Polio had merit, since it helps to maintain muscle and muscle-nerve integrity. Our employment of Niacin 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 Niacin, 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 ACTHnever 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 inovlving a lethal intermediate gene or group of genes. There is definitely an over-supply of pyruvates, and an under-supply of acetyl-choline. The cue in this drama is cocarboyxlase. Coenzyme A is also in limited supply. Two molecules of thiamin hydrochloride, and two molecules of phosphoric acid yields cocarboxylase. One was 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.

Myasthenia Gravis

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 (Vitamin C), 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 A“ any virus. As pointed out by Lipschitz et al., the replenishing of vitamin B1(Thiamine) restores the ability of the nervous system to handle properly pyruvic acid and estrose. 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 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 coplex than in Mulitple 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 2-1/4 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 advisble 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).

Appendix

Since presenting this paper, we have observed that improvement in all categories is enhanced when the intravenous injection contains 800 mg. to 1000 mg. thiamin hydrochloride, 200 mg. pyridoxine, 400 mg. niacinamide, 100 mg. Niacin. The thiamin hydrochloride solution must be clear. The amount of niacin employed must be calculated from the flush factor of a given patient. The injection is made with a 20cc or 30cc syringe, using a 23G x 3/4 inch or 22G x 1 inch needle. Intravenous medication can be given daily; it should be administered at least twice weekly. Due to sensitivity possibilities, we always have the patient take the intramuscular injections for three weeks before starting intravenous therapy. A person getting Niacin for the first time will be deficient and show a greator flush. After a few days the deficiency declines and Flush will dissappear.

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