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As the field of nutritional medicine is developing, there is generally a lack of laboratory technology to help the hard pressed clinician in selecting diets or supplements. This book makes the provocative suggestion that the present disease model is out-moded and old-fashioned. It outlines a new model in which inappropriate oxidative metabolism is responsible for loss of efficiency in tissues. Since the nervous system is the most "oxygen hungry" tissue in the body, nervous symptoms are frequently generated as an early warning of malnutrition, especially that caused by ingestion of “empty calories”. Dr. Lonsdale uses the metabolism of vitamin B-l and the symptoms of Beri-Beri to illustrate the effect of inefficient redox, emphasizing the generic effect that this has on the hypothalamic-autonomic-endocrine axis. The biochemical lesion caused by thiamin pyrophosphate deficiency is easily measured in a clinical laboratory by measuring the activity of erythrocyte transketolase. Using a test of this nature points the way to the methodology of other cofactor deficiencies. More importantly, however, it is one method of assessing hypo-oxidative stress. This book was originally published in 1987 and, before it had a chance to become better known, most of the books were burned in a fire at the publisher’s warehouse. Its title was “A Nutritionst’s Guide to the Clinical Use of Vitamin B-1” but I have changed this title since it is really a monogram, reporting the many facets of clinical and animal research performed during my tenure at Cleveland Clinic Foundation. This centered on the surprisingly versatile activity of thiamin and its derivatives in both clinical and laboratory improvements in many different conditions. Thus, the obvious conclusion was that efficient oxidation is a key factor in many human diseases. It is becoming obvious that the model for drug-based modern medicine is broken. Hospitals are now dangerous places in which to be treated and there must be a shift to accepting the ancient proverb that “prevention is better than cure”. We have to recognize that the human body is an extraordinary “machine” that is designed with breathtaking beauty. Disease is produced by loss of efficiency in the biochemistry and electricity that it uses to create energy for its 70 to 100 trillion cells to function. The most modern research has shown that an important part of this is intracellular communication. It is a good concept to think of the body as being like an orchestra. The organs can be compared with the various instruments, each of which has a program that enables it to participate in the “Symphony o f Health”. It is inconceivable that this complex would function properly if there was not a “conductor”. The limbic system of the brain is visualized as a computer that enables the organs to work together in “playing that symphony”, thus analogized as the “conductor”. Thus, if the genetic program is complete in a given individual, all he/she has to do is to “obey the rules set by Mother Nature”. In the modern world, that is simply not happening and we are moving further and further away from our biologic origins. Through the new science of epigenetics, we have learned that our genes can be manipulated by diet and lifestyle factors and “God made food” is the only fuel that we were designed to ingest. In proof reading the text in preparation for placing this book in the “Soil and Health Library” I have added small sections of updating since more is known about some of the patients described. Readers will encounter some work on amino acid ratios in comparing threatened SIDS infants with patients suffering from Reye’s syndrome, a disease that is now a more or less extinct issue since aspirin as its cause is known. But I would hasten to add that the true underlying cause of both SIDS and Reye’s syndrome is still not defined in biochemical terms. Although not truly showing us this cause in finite terms, it is a hint that biochemistry plays a very important role in both and it may lead to further research. Hans Selye studied the way in which animals adapt to stresses imposed by him in his experiments. He formulated the concept of “diseases of adaptation”. Perhaps a more accurate phraseology would be to call them “diseases of maladaptation” as they apply to humans living in the modern world. The discerning reader will soon note that most of the references are old. In the modern era it has been generally accepted that “if the reference is old it is already out of date”. It is to be noted, however, that the references given here are from an era when much thought was being given to vitamins as therapeutic agents. The simple facts are that the results were “too good to be true” and threatened the pharmaceutical industry. Drugs could be patented and make money whereas naturally occurring substances could not. Vitamin therapy fell into disrepute and was classified as “quackery” by an onslaught of politically driven motives. Healing requires energy and it is a natural process. An orthopedist is a technician who realigns the fractured bones. The healing takes place from within and this applies to all diseases. We have centered on the concept of “kill the enemy”, the bacteria, viruses, cancer cells. Little thought has been given to how we can assist the natural defensive mechanisms by stimulating energy synthesis. The reappearance of the ancient form of therapy known as holistic medicine under the general title of Complementary Alternative Medicine is truly a paradigm shift in concept. The majority of the present medical profession and the pharmaceutical industry will not change. It will be the intelligent consumer that will force the issue eventually Derrick Lonsdale, M.B. B.S. (London) M.R.C.S. L.R.C.P. did his medical training at St. Bartholomew's Hospital Medical College and practiced as a family doctor under the British National Health Service before coming to the United States. He is a Fellow of the American College of Nutrition, a Certified Nutrition Specialist and a Fellow of the American College for Advancement in Medicine He was Clinical Assistant Professor of Genetics and Pediatrics at Case Western Reserve University, Clinical Associate Professor of Chemistry at Cleveland State University and headed the section of Biochemical Genetics in the Department of Pediatrics and Adolescent Medicine at the Cleveland Clinic Foundation (Ohio) until 1982. Currently, Dr. Lonsdale is a private practitioner specializing in nutritional therapy in Westlake, Ohio. (Original Title) A Nutritionist's Guide to the Clinical Use of VITA MIN New title A Monogram of Clinical Research: Presentation of a New Medical Model Derrick Lonsdale, M.D. NOTICE: This internet version has been made by the Soil and Health Library with the authorization of Dr. Lonsdale; further distribution on the internet is not authorized and may constitute a violation of Dr. Lonsdale's copyrights. (18 May, 2006) Life Sciences Press, P.O. Box 1174, Tacoma, WA 98401 © 1987 by Life Sciences Press. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electric, mechanical, photocopying, recording, or otherwise, without the prior written permission of the publisher. Made in the United States of America Library of Congress Cataloging in Publication Data Lonsdale, Derrick, 1924- A Nutritionist's Guide to the Clinical Use of Vitamin B-l Includes index. 1. Dysautonomia—Nutrition aspects. 2. Vitamin Bl—Metabolism. 3. Stress (Physiology). 4. Energy metabolism. 5. Biochemical oxygen demand. 6. Nutrition. 1. Title [DNLM: 1. Stress—metabolism. 2. Thiamin—metabolism. QU189 L862t] RC407.L66 1987 616.8'80654 87-29862 ISBN 0-943685-02-8 (soft) Correspondence address: Derrick Lonsdale, M.D. Preventive Medicine Group 24700 Center Ridge Road Westlake, Ohio 44145 USA TABLE OF CONTENTS INTRODUCTION 1-4 CHAPTER 1 The Autonomic System 5-12 General Arrangement and Functions 5-6 Sympathetic System 6-7 Parasympathetic System 7-8 Cranial Nerves 8-9 Autonomic Balance 9-11 Chemical Transmission 11-12 CHAPTER 2 Familial Dysautonomia and Related Syndromes 13-43 familial Dysautonomia 13-14 Primary Hypoventilation Syndrome (Ondine's Curse) 14-15 Radiologic Signs of Dysautonomia 15 Protean Nature of Dysautonomia 15-16 Incomplete Dysautonomia 16 Dysautonomia in Association with Other Disease 15-18 Autonomic and Endocrine Response to Stress 18-19 The Syndrome of Functional Dysautonomia 19-22 Functional Dysautonomia: Clinical Presentation 22-30 Sudden Death 30-32 Prolonged Q-T Syndrome 32-33 Immaturity of Brain Stem 33-34 Further Evidence of Familial Factors in Expression of Dysautonomic Function 34-43 Case Reports: SIDS Families 35-43 CHAPTER 3 Autonomic Function and Stress 44-77 Transamination 44-45 Transmethylation 45 Thiamine Metabolism 45-48 Physiologically active forms 46-48 Thiamine Pyrophosphate 46 Thiamine Triphosphate 47 Physiologic actions 47-48 Clinical Thiamine Deficiency 48 Clinical Conditions Related to Thiamine Metabolism 48-64 Nutritional Deficiency 49-50 Animal Experiments 50 Pyruvic Dehydrogenase: TPP Dependency 50-56 Other TPP Dependencies 56-58 Miscellaneous Thiamine Dependencies 58-60 Defects in Thiamine Triphosphate 60-63 Naturally Occurring Thiamine Inhibitors 63-64 Allithiamine and Its Synthetic Derivatives 64-70 Thiamine Tetrahydrofurfuryl Disulfide: Effect on Hypertension in Spontaneously Hypertensive Rats 66-70 Biochemistry of Neurotransmission 70-71 Metabolic and Clinical Phenomena of the General Adaptation Syndrome Compared with Effects of Thiamine Deficiency 71-75 Pathologic Anatomy 73-75 Symptoms and Signs of Beriberi 75-77 Autonomic Dysfunction 75 Calories and Thiamine 76 CHAPTER 4 Biochemical Studies in Functional Dysautonomia 78-115 Dynamic State of Biochemistry 78-79 Laboratory Studies 79-115 Urinary Amino Acids 79-83 Urinary Glycine/Alanine and Histidine/Alanine Ratios in Normal Adults, Threatened SIDS, and Reye's Syndrome 83-87 Urinary Keto Acids 87 Red Cell Transketolase 87-89 Serum Folate and B12 89-90 Suggested Relationship Between Oxidation and Transmethylation 90-93 Urinary Creatine, Creatinine and Uric Acid 93-102 Urinary Creatine and Creatinine in Thiamine Deficient Rats 102-108 Serial Studies of Urinary Creatine and Creatinine in 28 Patients 108-115 CHAPTER 5 Illustrative Case Reports 116-170 Nutrition 117-123 Stress 123-131 Genetics 131-170 CHAPTER 6 Energy Metabolism in a New Perspective of Disease in Man 171-194 Introduction 173 Definitions 173-176 Stress 173 Energy expenditure, Energy conservation, Control Stress response, Neurotransmission, Adenosine triphosphate 174 Disease 175 Abnormal Response to Infection 175-176 Health Versus Disease 176-178 Sympathetic Dominance 178-179 Parasympathetic Dominance 179-180 Conclusion 180-182 Testing the Model 182-185 Hypometabolic Versus Hypermetabolic 185-191 Pre Menstrual Tension Syndrome: Example of Autonomic Endocrine Axis Defect 191-193 Summary Conclusion 193-194 DEDICATION To my wife, Adèle. ACKNOWLEDGEMENTS Expert technical assistance in the laboratory was provided by Mrs. Judy Goodman. The animal experiments were performed by Mr. Steven Forgac. Mildred S. Seelig M.D. M.P.H. F.A.C.N for much of the information in Chapter 3 PREFACE By Dr. Myron Brin, M.D. Fellow, Charles A. Dana Research Institute for Scientists Emeriti The metabolic functions of thiamine have been studied extensively in man and experimental animals for over 50 years. Thiamine supports normal metabolism in every tissue of the body. Yet the signs and symptoms of the deficient condition have not been fully explained. Dr. Lonsdale proposes that restricted availability of vitamin coenzymes disrupts cellular energy balance This has an adverse effect upon the function of the autonomic nervous system, thereby resulting in tissue/organ pathology. He draws upon the literature extensively to support his hypothesis. Many of the studies Dr. Lonsdale presents used subjects as their own controls. In some cases he used functional enzyme/coenzyme tests to contribute specificity to the conclusions. These tests were developed some years ago to determine severity of marginal or preclinical deficiency. The latter is a state of vitamin depletion in which non-specific physiological entities such as feeling of well-being, maintenance of body weight, rates of drug metabolism, levels of immunocompetence, modified behavior, etc., are adversely affected before the onset of the classical deficiency syndrome. Accordingly, Dr. Lonsdale has developed a general theme based upon both clinical and experimental data. While acceptance of his hypothesis on the origin of stress may not be universal, at least initially, it is worthy of consideration. In fact, stimulation of additional research on this subject would be an important contribution to nutritional science.