Table Of ContentAs 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.
