| Description |
1 online resource (249 pages) |
| Contents |
Cover; Title Page; Copyright Page; FOREWORD; PREFACE; THE AUTHOR; Table of Contents; CLINICAL AND PATHOLOGICAL FINDINGS IN ASCORBIC ACID DEFICIENCY; Chapter 1: Vascular Changes; I. Clinical Signs; II. Microvascular Fragility; III. Microvascular Pathology; IV. Histamine Effects; V. Peripheral Vasodilation, Congestion, and Stasis; VI. Loss of Vasoconstrictor Response; VII. Arterial and Venous Pathology; VIII. Aortic Endothelial Pathology; IX. Aortic Wall Chemistry; X. Summary and Conclusion; References; Chapter 2: Diabetes Mellitus; I. Review; II. Conclusions; References; Chapter 3: Anemia |
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I. Human ObservationsII. Animal Studies; III. In Vitro Studies; IV. Megaloblastic Anemia of Infancy; V. Megaloblastic Anemia of Pregnancy; VI. Iron Deficiency Anemia; VII. The Anemia of Hemosiderosis; VIII. The Anemia of Adult Scurvy in Temperate Regions; IX. Conclusions; References; Chapter 4: Defective Wound Healing; References; Chapter 5: Bone Changes; I. Introduction; II. Human Observations; Ill. X-Ray Findings; IV. Guinea Pig Studies; V. Studies of Other Animals; VI. Conclusions; References; Chapter 6: Joint Lesions; I. Introduction; II. Ascorbic Acid Deficiency in Animals |
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III. Experimental Human ScurvyIV. Relevant Laboratory Studies; V. Infantile Scurvy; VI. Adult Scurvy and Arthritis; VII. Conclusions; References; Chapter 7: Dental and Periodontal Changes; I. Introduction; II. Animal Studies; Ill. Human Observations; IV. Conclusions; References; Chapter 8: Atherosclerosis; References; Chapter 9: Mental Depression; I. Observations in Humans; II. Observations in Monkeys; Ill. Observations in Guinea Pigs; IV. In Vitro Findings; V. Conclusions; References; Chapter 10: Amyloid; References; Chapter 11: Venous Thrombosis; References |
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Chapter 12: Decreased Resistance to InfectionI. The Vicious Cycle; II. Increased Susceptibility to Bacterial Toxins; Ill. Decreased Localization of Bacterial Infections; IV. Increased Capillary Permeability to Viruses; V. Increased Susceptibility to Plasmodial Infection; VI. Increased Susceptibility to Fungal Infection; VII. Impaired Leukocyte Metabolism; VIII. Increased Plasma Cortisol Levels; IX. Altered General Metabolism; X. Decreased Leukocyte Migration and Chemotaxis; XI. Studies Relating to Chediak-Higashi Syndrome; XII. Impaired Phagocytic Activity; XIII. Altered Bactericidal Activity |
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XIV. Decreased Humoral Immune ResponseXV. Decreased Production of Interferon; XVI. Decrease in Thymic Humoral Factors; XVII. Decreased Cell-Mediated Immunity; XVIII. Delayed Skin Graft Rejection; XIX. Loss of Primary Immune Response; XX. Peripheral Stasis; XXI. Impaired Leukocytosis; XXII. Decreased Complement Activity; XXIII. Secondary Effects of Disturbed Folic Acid Metabolism; XXIV. Prolonged Upper Respiratory Infections; XXV. Increased Blood Histamine Levels; References; Chapter 13: Liver, Bile, and Gallstones; I. Liver Ascorbate Depletion; II. Histopathology; III. Trypan Blue Studies |
| Summary |
The factors affecting blood vitamin C levels are described in detail in this series. Many factors such as aging, smoking, infection, trauma, surgery, hemolysis, hormone administration, heavy metals, pregnancy, alcohol, ionizing radiation and several medicines have been found to cause a disturbance of ascorbic acid metabolism and to reduce blood vitamin C levels. Indeed, abnormalities of ascorbic acid metabolism, due to factors such as smoking, occur much more frequently than does dietary vitamin C deficiency today.It is now known that low blood vitamin C levels are associated with histaminemia (high blood histamine levels), and also that ascorbate-responsive histaminemia is common in apparently healthy people. High blood histamine levels are believed to cause small hemorrhages within the inner walls of the blood vessels and these may lead to the deposition of cholesterol, as an aberrant form of wound healing. Ascorbic acid not only reduces blood histamine levels, but also aids the conversion of cholesterol to bile acids in the liver. The clinical pathological and chemical changes observed in ascorbic acid deficiency are discussed in detail. Several diseases and disorders associated with low blood vitamin C levels are also 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. An excellent reference for physicians, nutritionists and other scientists |
| Notes |
IV. Electron Microscopy |
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Print version record |
| Subject |
Vitamin C deficiency.
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Vitamin C -- Metabolism.
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Ascorbic Acid Deficiency
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HEALTH & FITNESS -- Diseases -- General.
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MEDICAL -- Clinical Medicine.
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MEDICAL -- Diseases.
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MEDICAL -- Evidence-Based Medicine.
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MEDICAL -- Internal Medicine.
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Vitamin C deficiency
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Vitamin C -- Metabolism
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| Form |
Electronic book
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| ISBN |
9781351077576 |
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1351077570 |
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