Vitamin C, Volume II

249 Pages·1989·38.569 MB·English

by  C. Alan B. Clemetson

Vitamin C
Volume II
Author
C. Alan B. Clemetson
Professor
Tulane University School of Medicine
New Orleans, Louisiana
Boca Raton London New York
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Library of Congress Cataloging-in-Publication Data
Clemetson, C. Alan B.
Vitamin C / C. Alan B. Clemetson.
p. cm.
Includes bibliographies and index.
ISBN 0-8493-4841-2 (v. 1)
ISBN 0-8493-4842-0 (v. 2)
ISBN 0-8493-4843-9 (v. 3)
1. Vitamin C deficiency. 2. Vitamin C--Metabolism. I. Title.
RC627.S36C53 1989
616 3’9--dc19 88-14735
A Library of Congress record exists under LC control number: 88014735
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ISBN 13: 978-1-351-07757-6 (ebk)
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FOREWORD
While frank scurvy is rare nowadays, subclinical vitamin C deficiency is common and is
now known to be associated with elevated blood histamine levels, which rapidly return to
normal when ascorbic acid is administered. Epidemiological and experimental evidence
suggests that our common metabolic defect, the inability to synthesize ascorbic acid from
simple sugars, may be largely responsible for the development of subendothelial hemorrhage,
thrombosis, atheroma, and degenerative vascular disease. This book is more concerned with
factors affecting ascorbic acid metabolism, such as aging, smoking, infection, trauma,
surgery, hormone administration, heavy metals, pregnancy, hemolysis, ionizing radiation,
aspirin, alcohol, and other drugs which cause a disturbance of ascorbic acid metabolism and
may thereby lead to vascular disease, than it is with simple dietary deficiency of ascorbic
acid. The clinical, pathological, and chemical changes observed in ascorbic acid deficiency
are discussed in detail; several diseases and disorders associated with abnormalities of
ascorbic acid metabolism are described. Possible toxic effects resulting from the oxidation
of ascorbic acid are noted, and reasons for the use of D-catechin or other chelating fiber to
prevent or minimize the release of ascorbate free radical are detailed.
PREFACE
About 60 years ago, and before the isolation of ascorbic acid, Mme. L. Randoin (1923)*
found the number of research studies on the antiscorbutic vitamin so great as to make it
impossible for her to review them all .
a
• '}a! maintenant parler des recherches de toute Now I must speak of all kinds of studies of the
nature faites sur le facteur ant1scorbut1que. La tache antiscorbutic factor It is a thankless task because
est bien mgrate, car le nombre de ces recherches the number of research studies is so great that it 1s
est si grand qu' il m' est eVldemment impossible de clearly impossible to review them all; moreover, by
les passer toutes en revue et, au surplus, elles pre- failure of agreement, they present such gaps that it
sentent, par defaut de convergence, de telles la- is truly difficult to present a consistent thesis.
cunes, qu' il est vraiment diffie~le d' en donner une
idee d' ensemble."
Today, the profusion of the literature on this subject is even more overwhelming. It is
growing so fast that it is impossible to do justice to all the work that had been done in this
field. Moreover, having written 57 chapters in 36 months, it is inevitable that the chapters
written first will not be as up-to-date as those written last.
Undoubtedly, some important works have been omitted, either because they have
escaped my notice or because they were written in a language that I cannot read. Any workers
whose contributions have been omitted must accept my assurance that it was not by intent.
It is hoped that this book presents a consistent thesis and that its main message is clear.
It does not so much concern the amount of vitamin C in the diet, as it does the factors
affecting ascorbic acid metabolism, the diseases that may result from abnormalities of
ascorbic acid metabolism, and some suggestions as to what we may be able to do to prevent
them.
Although the title of this book is Vitamin C, it could equally well have been entitled
Vitamin C, Heavy Metals, and Chelating Fiber.
C. Alan B. Clemetson, M.D.
Pineville, Louisiana
February, 1987
THE AUTHOR
C. Alan B. Clemetson, M.D., was born in England. He attended the King's School,
Canterbury, Magdalen College, Oxford, and Oxford University School of Medicine, grad-
uating as a physician (B.M., B.Ch.) in 1948. He is an obstetrician and gynecologist, with
fellowships in British, Canadian, and American colleges (F.R.C.O.G., F.R.C.S.C., and
F.A.C.O.G.), but he has devoted most of his life to research and has published papers on
many diverse subjects.
His career has included academic positions at London University, the University of Sas-
katchewan, the University of California at San Francisco, the State University of New York,
and at Tulane University in Louisiana, where he is currently Professor at the School of
Medicine.
He has challenged many conventional ideas and believes that, "certainty of knowledge
is the antithesis of progress." Thus, every statement in this book is backed by reference to
experiments and observations in the literature; contrary findings are cited, weighed, and
given due credence.
VITAMIN C
Volume I
Vitamin C Deficiency
Classical Scurvy: A Historical Review
Chronic Subclinical Ascorbic Acid Deficiency
Factors Affecting the Economy of Ascorbic Acid
Inadequate Ascorbic Acid Intake
Smoking
Aging
Sex
Menstrual Cycle, Estrus Cycle, Ovulation
Infection
Trauma, Surgery, and Bums
Heavy Metals, Water Supplies: Copper, Iron, Manganese,
Mercury, and Cobalt
Bioflavonoids
Dietary Protein
Hormone Administration: Birth Control Pills
Pregnancy
Hemolysis
Stress and the Pituitary-Adrenal System
Lack of Sleep
Time of Day
Season
Achlorhydria
Ionizing Radiation
Aspirin and Salicylates
Alcohol
Other Factors Affecting Ascorbic Acid Needs
Volume II
Clinical and Pathological Findings in Ascorbic Acid Deficiency
Vascular Changes
Diabetes Mellitus
Anemia
Defective Wound Healing
Bone Changes
Joint Lesions
Dental and Periodontal Changes
Atherosclerosis
Mental Depression
Amyloid
Venous Thrombosis
Decreased Resistance to Infection
Liver, Bile, and Gallstones
Volume III
Chemical Changes Associated with Vitamin C Deficiency
Histamine Metabolism
Proline and Lysine Metabolism
Carbohydrate Metabolism
Folic Acid Metabolism
Cholesterol Metabolism
Tyrosine and Phenylalanine Metabolism
Tryptophan Metabolism
Adrenal Corticoid Metabolism
Uric Acid Clearance
Clinical Conditions Associated with Disorders of Ascorbic Acid Metabolism
Rheumatic Fever
Menorrhagia
Wound Dehiscence
Habitual Abortion
Abruptio Placentae
Prematurity and Premature Rupture of the Fetal Membranes
Megaloblastic Anemia of Infancy, Pregnancy, and Steatorrhea
Gastrointestinal Ulcers and Hemorrhage
Ocular Lesions
Cerebral Hemorrhage and Thrombosis
Coronary Thrombosis and Myocardial Infarction
TABLE OF CONTENTS
CLINICAL AND PATHOLOGICAL FINDINGS IN ASCORBIC ACID DEFICIENCY
Chapter I
Vascular Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
I. Clinical Signs ..................................................................... 1
II. Microvascular Fragility ........................................................... 1
III. Microvascular Pathology .......................................................... 5
IV. Histamine Effects ................................................................. 9
V. Peripheral Vasodilation, Congestion, and Stasis ................................. 10
VI. Loss of Vasoconstrictor Response ............................................... 10
VII. Arterial and Venous Pathology ................................................... 12
VIII. Aortic Endothelial Pathology .................................................... 12
IX. Aortic Wall Chemistry ........................................................... 15
X. Summary and Conclusion ........................................................ 16
References ............................................................................... 18
Chapter 2
Diabetes Mellitus ....................................................................... 23
I. Review ........................................................................... 23
II. Conclusions ...................................................................... 37
References ............................................................................... 38
Chapter 3
Anemia ................................................................................. 41
I. Human Observations ............................................................. 41
II. Animal Studies .................................................................. 44
III. In Vitro Studies .................................................................. 45
IV. Megaloblastic Anemia of Infancy ................................................ 45
V. Megaloblastic Anemia of Pregnancy ............................................. 46
VI. Iron Deficiency Anemia ......................................................... 47
VII. The Anemia of Hemosiderosis ................................................... 49
VIII. The Anemia of Adult Scurvy in Temperate Regions ............................. 50
IX. Conclusions ...................................................................... 51
References ............................................................................... 51
Chapter 4
Defective Wound Healing .............................................................. 55
References ............................................................................... 68
Chapter 5
Bone Changes .......................................................................... 71
I. Introduction ...................................................................... 71
II. Human Observations ............................................................. 71
Ill. X-Ray Findings .................................................................. 76
IV. Guinea Pig Studies ............................................................... 79
V. Studies of Other Animals ........................................................ 87
VI. Conclusions ...................................................................... 88
References ............................................................................... 88
Chapter 6
Joint Lesions ........................................................................... 93
I. Introduction ...................................................................... 93
II. Ascorbic Acid Deficiency in Animals ............................................ 93
III. Experimental Human Scurvy .................................................... 103
IV. Relevant Laboratory Studies .................................................... 105
V. Infantile Scurvy ................................................................. 110
VI. Adult Scurvy and Arthritis ...................................................... 111
VII. Conclusions ..................................................................... 115
References .............................................................................. 115
Chapter 7
Dental and Periodontal Changes ..................................................... 119
I. Introduction ..................................................................... 119
II. Animal Studies ................................................................. 119
Ill. Human Observations ............................................................ 129
IV. Conclusions ..................................................................... 141
References .............................................................................. 142
Chapter 8
Atherosclerosis ........................................................................ 147
References .............................................................................. 161
Chapter 9
Mental Depression .................................................................... 165
I. Observations in Humans ........................................................ 165
II. Observations in Monkeys ....................................................... 170
Ill. Observations in Guinea Pigs .................................................... 170
IV. In Vitro Findings ................................................................ 171
V. Conclusions ..................................................................... 171
References .............................................................................. 171
Chapter 10
Amyloid ................................................................................ 173
References .............................................................................. 178
Chapter 11
Venous Thrombosis ................................................................... 179
References .............................................................................. 184
Chapter 12
Decreased Resistance to Infection .................................................... 187
I. The Vicious Cycle .............................................................. 187
II. Increased Susceptibility to Bacterial Toxins ..................................... 188
Ill. Decreased Localization of Bacterial Infections .................................. 188
IV. Increased Capillary Permeability to Viruses ..................................... 189
V. Increased Susceptibility to Plasmodial Infection ................................ 189
VI. Increased Susceptibility to Fungal Infection ..................................... 189
VII. Impaired Leukocyte Metabolism ................................................ 189
VIII. Increased Plasma Cortisol Levels ............................................... 191
IX. Altered General Metabolism .................................................... 191