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El. knyga: Micronutrients in Health and Disease, Second Edition

(Premier Micronutrient Corporation,Novato, California, USA)
  • Formatas: 560 pages
  • Išleidimo metai: 15-Apr-2019
  • Leidėjas: CRC Press
  • Kalba: eng
  • ISBN-13: 9780429513183
  • Formatas: 560 pages
  • Išleidimo metai: 15-Apr-2019
  • Leidėjas: CRC Press
  • Kalba: eng
  • ISBN-13: 9780429513183

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Increased oxidative stress due to the production of excessive amounts of free radicals along with the effects of chronic inflammation plays a major role in the initiation and progression of most chronic diseases. In addition, increased release of glutamate plays a central role in the pathogenesis of various disorders.

This second edition of Micronutrients in Health and Disease proposes a novel concept that in order to simultaneously and optimally reduce oxidative stress, chronic inflammation, and glutamate, it is essential to increase levels of antioxidant enzymes as well as levels of dietary and endogenous antioxidant compounds at the same time. This is accomplished by activating the Nrf2 pathways and by increasing the levels of antioxidant compounds and B-vitamins through supplementation. This book proposes a mixture of micronutrients that achieves this above goal. The mixture of micronutrients together with modification in diet and lifestyle may reduce the risk of chronic diseases and in combination with standard care, may improve the management of these diseases.

KEY FEATURES

Provides evidence in support of the idea that increased oxidative stress, chronic inflammation, and glutamate are involved in the pathogenesis of chronic diseases.

Contains three new chapters on Huntingtons disease, Autism spectra, and Prion disease.

Discusses the role of microRNAs in the pathogenesis of chronic diseases.

Presents information on regulation of the expression of microRNAs by reactive oxygen species and antioxidants.

Micronutrients in Health and Disease, Second Edition serves as a valuable resource for those seeking to promote healthy aging and prevent and improved management of chronic diseases.

Recenzijos

The book is comprehensive. The coverage ranges from the basic fundamentals of micronutrients with explanations regarding the role of the antioxidant system, oxidative stress, inflammatory responses, and adaptive immunity to the scientific rationale underlying the role of micronutrients in promoting/preventing these biological responses and the mechanisms that underlie them. There is a particularly useful description of the healthy aging process versus the common adverse impact of chronic diseases associated with aging, including rheumatoid and osteoarthritis as well as cardiovascular diseases, diabetes, and cancer. Unique features include a chapter on the role of micronutrients in protecting against lethal doses of ionizing radiation and a concluding chapter listing 17 common misconceptions, the underlying rationale, and the proposed explanation for its misinterpretation.

Preface xxvii
Acknowledgments xxix
Author xxxi
Chapter 1 Basic Facts about Micronutrients 1(12)
Introduction
1(1)
Evolution of the Antioxidant System
1(1)
History of the Discovery of Micronutrients
1(1)
Sources and Forms of Vitamins
2(2)
Solubility of Micronutrients
4(1)
Distribution of Antioxidants in the Body
4(2)
Storage of Antioxidants
6(1)
Can Antioxidants Be Destroyed during Cooking?
6(1)
Absorption of Antioxidants and Its Significance
6(1)
Functions of Individual Antioxidants
7(1)
Antioxidant Defense Systems
8(1)
Antioxidant Enzymes
8(1)
Dietary Antioxidants
8(1)
Endogenous Antioxidants
8(1)
Known Functions of Antioxidants
8(1)
Current Controversies about Antioxidants
9(1)
Misuse of Antioxidants in Clinical Studies
9(3)
Conclusions
12(1)
References
12(1)
Chapter 2 Basic Facts about Oxidative Stress, Inflammation, and the Immune System 13(10)
Introduction
13(1)
Oxidative Stress
14(2)
What Are Free Radicals?
14(1)
Types of Free Radicals
14(1)
Formation of Free Radicals Derived from Oxygen and Nitrogen
14(2)
Oxidation and Reduction Processes
16(1)
What Is Inflammation?
16(1)
Types of Inflammatory Reactions
17(1)
Products of Inflammatory Reactions
17(1)
Cytokines
17(1)
Complement Proteins
18(1)
Arachidonic Acid (AA) Metabolites
18(1)
Endothelial/Leukocyte Adhesion Molecules
18(1)
Immune System
18(1)
What Is the Immune System?
19(1)
Innate Immunity
19(1)
Adaptive Immunity
20(1)
Conclusions
20(1)
References
21(2)
Chapter 3 Scientific Rationale of Current Trends in Clinical Studies of Micronutrients 23(12)
Introduction
23(1)
Levels of Oxidative Stress and Chronic Inflammation in High-Risk Populations
24(1)
High-Risk Populations of Cancer
24(1)
High-Risk Populations of Coronary Artery Disease (CAD)
24(1)
High-Risk Populations of Alzheimer's Disease (AD) and Parkinson's Disease (PD)
24(1)
Distributions and Function of Antioxidants
25(1)
Results of Clinical Trials with a Single Antioxidant in High-Risk Populations
26(2)
Cancer
26(1)
Coronary Artery Disease (CAD)
26(1)
Alzheimer's Disease (AD) and Parkinson's Disease (PD)
27(1)
Why the Use of a Single Antioxidant Produced Inconsistent Results
28(1)
Results of Clinical Studies with Multiple Dietary Antioxidants in Cancer
29(1)
Results of Clinical Studies with Fat and Fiber
30(1)
Rationale for Using a Mixture of Micronutrients for Reducing the Risk and Progression of Chronic Diseases
30(1)
Proposed Mixture of Micronutrients for Reducing the Risk and Progression of Chronic Diseases
31(1)
Proposed Changes in Diet and Lifestyle for Reducing the Risk and Progression of Chronic Diseases
31(1)
Conclusions
32(1)
References
32(3)
Chapter 4 Micronutrients in Healthy Aging and Age-Related Decline in Organ Functions 35(28)
Introduction
35(1)
Trends of Aging Population
36(1)
Evidence for Increased Oxidative Stress During Aging
36(1)
Extracellular Sources for Production of Free Radicals
36(1)
Cellular Sites of Production of Free Radicals
37(1)
Oxidative Stress-Induced Age-Related Decline in Organelle Functions
38(2)
Mitochondrial Dysfunction
38(1)
Impairment of Proteasome and Lysosomal-Mediated Proteolytic Activities
39(1)
Oxidative Stress-Induced Changes in Cell Culture Models
39(1)
Oxidative Stress-Induced Changes in Animal Models
39(1)
Oxidative Stress-Induced Shortening of the Length of Telomere
39(1)
Evidence for Chronic Inflammation During Aging
40(1)
Impaired Immune Function in Aging
40(1)
Changes in the Antioxidant Defense Systems During Aging
41(2)
Antioxidant Enzymes
41(1)
Changes in Antioxidant Enzymes Activities in Animals
42(1)
Changes in Antioxidant Enzymes Activities in Humans
42(1)
Changes in Dietary and Endogenous Antioxidants Levels
43(2)
Vitamin C
43(1)
Glutathione
44(1)
Vitamin E
44(1)
Coenzyme Q10
44(1)
MicroRNAs in Aging
45(2)
MicroRNAs
45(1)
MicroRNAs in Age-Related Diseases
45(1)
MicroRNAs and Their Target Proteins in Aged Animals
45(2)
Oxidative Stress and Pro-inflammatory Cytokine Regulate Expression of MicroRNAs
47(1)
Antioxidants Regulate Expression of MicroRNAs
47(1)
Effects of Individual Antioxidants on Age-Related Functional Deficits
47(2)
Vitamin E
47(1)
Coenzyme Q10
48(1)
Carotenoids and Zinc
48(1)
Melatonin
48(1)
Flavonoids
48(1)
Glutathione and N-Acetylcysteine (NAC)
48(1)
Alpha-Lipoic Acid
49(1)
Multiple Dietary Antioxidants
49(1)
Studies with Individual Antioxidants on Age-Related Neurodegenerative Diseases in Humans
49(1)
Regulation of Activation of Nrf2
50(1)
Reactive Oxygen Species (ROS) Activates Nrf2
50(1)
Binding of Nrf2 with ARE in the Nucleus
50(1)
Existence of ROS-Resistant Nrf2
50(1)
Antioxidants and Phytochemicals Activate ROS-Resistant Nrf2
51(1)
L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
51(1)
Activation of Nrf2 by MicroRNAs
51(1)
Suppression of Chronic Inflammation
51(1)
Proposed Mixture of Micronutrients for Healthy Aging and for Reducing Age-Related Functional Deficits
51(1)
Proposed Changes in Diet and Lifestyle for Healthy Aging and for Reducing Age-Related Functional Deficits
52(1)
Conclusions
52(1)
References
53(10)
Chapter 5 Role of Micronutrients in Prevention of Coronary Artery Disease and Improvement of the Standard Therapy 63(32)
Introduction
63(1)
Prevalence, Incidence, and Cost
64(1)
Evidence for Increased Oxidative Stress in CAD
64(1)
Consequences of Increased Oxidative Stress
65(1)
Evidence for Increased Chronic Inflammation in CAD
65(1)
Evidence for Increased Levels of Homocysteine in CAD
66(1)
MicroRNAs in CAD
66(4)
MicroRNAs
67(1)
Circulating MicroRNAs in CAD
67(1)
Cellular MicroRNAs in CAD
68(1)
Oxidative Stress and Pro-inflammatory Cytokine Regulate Expression of MicroRNAs
69(1)
Antioxidants Regulate Expression of MicroRNAs
70(1)
Role of Antioxidants in CAD
70(6)
Animal Studies after Treatment with Antioxidants
70(1)
Epidemiologic Studies with Antioxidants
70(1)
Intervention Human Studies after Treatment with Antioxidants
71(3)
Vitamin E Alone Producing Beneficial Effects
74(1)
Vitamin C Alone Producing Beneficial Effects
74(1)
Dietary Antioxidants Producing No Effects or Adverse Effects
74(2)
Endogenous Antioxidants Producing No Effects or Beneficial Effects
76(1)
Dietary and Endogenous Antioxidants with Cholesterol-Lowering Drugs
76(1)
Multiple Dietary Antioxidants with Cholesterol-Lowering Drugs
77(1)
Resveratrol and Omega-3 Fatty Acids
77(2)
Resveratrol
77(1)
Omega-3 Fatty Acids
78(1)
Intervention Studies with B-Vitamins to Lower Homocysteine Levels
79(1)
Potential Reasons for the Failure of Individual Micronutrients in Producing Sustained and Consistent Benefits in CAD
80(1)
Regulation of Activation of Nrf2
81(1)
Reactive Oxygen Species (ROS) Activates Nrf2
81(1)
Binding of Nrf2 with ARE in the Nucleus
81(1)
Existence of ROS-Resistant Nrf2 in CAD
81(1)
Antioxidants and Phytochemicals Activate ROS-Resistant Nrf2
81(1)
L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
81(1)
Activation of Nrf2 by MicroRNAs
82(1)
Suppression of Chronic Inflammation
82(1)
Proposed Mixture of Micronutrients for Prevention and Improved Management of CAD
82(1)
Proposed Changes in Diet and Lifestyle for Prevention and Improved Management of CAD
82(1)
Prevention and Improved Management of CAD
83(1)
Primary Prevention
83(1)
Secondary Prevention
83(1)
Improved Management of CAD
84(1)
Conclusions
84(1)
References
84(11)
Chapter 6 Micronutrients in Prevention and Improvement of the Standard Therapy in Diabetes 95(36)
Introduction
95(1)
Incidence, Prevalence, and Cost
96(1)
Incidence
96(1)
Prevalence
96(1)
Cost
96(1)
Types of Diabetes
96(1)
Type 1 Diabetes
96(1)
Type 2 Diabetes
96(1)
Gestational Diabetes
97(1)
Other Types of Diabetes
97(1)
Pre-diabetes and Metabolic Syndrome
97(1)
Complications of Diabetes
97(1)
Evidence for Increased Oxidative Stress in Diabetes
97(2)
Type 1 Diabetes
97(1)
Type 2 Diabetes
98(1)
Metabolic Syndrome
99(1)
Evidence for Increased Chronic Inflammation in Diabetes
99(1)
MicroRNAs in Diabetes
100(4)
MicroRNAs
100(1)
Circulating MicroRNAs in Diabetes
100(2)
Cellular MicroRNAs in Diabetes (Humans)
102(1)
Cellular MicroRNAs in Diabetes (Animal Models)
103(1)
Oxidative Stress and Pro-inflammatory Cytokines Regulate Expression of MicroRNAs
103(1)
Antioxidants Regulate Expression of MicroRNAs
103(1)
Reducing Oxidative Stress and Chronic Inflammation in Diabetes
104(1)
Role of Antioxidants and Phytochemicals in Protecting Against Diabetes
104(9)
Vitamin A (Animal and Human Studies)
104(1)
Vitamin C (Human Studies)
104(1)
Vitamin C (Animal Studies)
105(1)
Vitamin D3 (Animal Studies)
105(1)
Vitamin E (Animal Studies)
105(1)
Vitamin E (Human Studies)
106(1)
Alpha-Lipoic Acid (Human Studies)
106(1)
Alpha-Lipoic Acid (Animal Studies)
106(1)
N-Acetylcysteine (Human Studies)
107(1)
N-Acetylcysteine (Animal Studies)
107(1)
L-Carnitine (Human Studies)
107(1)
L-Carnitine (Animal Studies)
108(1)
Coenzyme Q10 (Human Studies)
108(1)
Coenzyme Q10 (Animal Studies)
109(1)
Omega-3 Fatty Acids (Animal Studies)
109(1)
Omega-3-Fatty Acids (Epidemiologic Studies)
110(1)
Omega-3-Fatty Acids (Intervention Studies)
110(1)
Antioxidant Mixtures (Human Studies)
110(1)
Antioxidant Mixture (Animal Studies)
111(1)
Folic Acid and Thiamine (Human Studies)
111(1)
Folic Acid and Thiamine (Animal Studies)
112(1)
Chromium (Human Studies)
112(1)
Antioxidants with Diabetic/Cardiovascular Drugs and/or Insulin (Human Studies)
112(1)
Antioxidants with Diabetic/Cardiovascular Drugs and/or Insulin (Animal Studies)
113(1)
Treatments of Diabetes
113(1)
Standard Treatments
113(1)
Aspirin (Human Studies)
113(1)
Aspirin Resistance
114(1)
Aspirin (Animal Studies)
114(1)
Potential Reasons for Inconsistent Results with Individual Micronutrients or Aspirin
114(1)
Regulation of Activation of Nrf2
115(1)
Reactive Oxygen Species (ROS) Activates Nrf2
115(1)
Binding of Nrf2 with ARE in the Nucleus
115(1)
Existence of ROS-Resistant Nrf2 in Diabetes
116(1)
Antioxidants and Phytochemicals Activate ROS-Resistant Nrf2
116(1)
L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
116(1)
Activation of Nrf2 by MicroRNAs
116(1)
Suppression of Chronic Inflammation
116(1)
Recommended Mixture of Micronutrients for the Prevention of Diabetes
117(1)
Recommended Changes in Diet and Lifestyle for the Prevention and Improved Management of Diabetes
117(1)
Prevention of Diabetes
117(1)
Primary Prevention
117(1)
Secondary Prevention
118(1)
Improved Management of Diabetes
118(1)
Conclusions
118(1)
References
118(13)
Chapter 7 Micronutrients in Cancer Prevention 131(32)
Introduction
131(1)
Incidence, Prevalence, Mortality, and Cost
132(1)
Proposed Stages of Carcinogenesis
132(1)
Two-Stage Model of Animal Carcinogenesis
132(1)
Some Examples of Tumor Initiators and Tumor Promoters
133(1)
Three-Stage Model of Human Carcinogenesis
133(1)
Diagrammatic Representation of Three-Stage Model of Human Carcinogenesis
133(1)
Some Examples of Environmental-Related Carcinogens
134(1)
Some Examples of Diet-Related Carcinogens
134(1)
Some Examples of Diet-Related Cancer Protective Agents
135(1)
Some Examples of Lifestyle-Related Carcinogens
135(2)
Alcohol
135(1)
Cell Phone
135(1)
Smoking
136(1)
Coffee and Caffeine
136(1)
Evidence for Increased Oxidative Stress
137(1)
Evidence for Increased Chronic Inflammation
137(1)
MicroRNAs in Cancer Prevention
138(1)
MicroRNAs
138(1)
Changes in MicroRNAs after Exposure to Chemical Carcinogens and Oncogenic Virus
138(2)
Functions of Antioxidants Relevant to Cancer Prevention
140(1)
Antioxidants and Phytochemicals Regulate Expression of MicroRNAs
141(1)
Reducing Oxidative Stress and Chronic Inflammation in Cancer Prevention
141(5)
Cell Culture Models
141(1)
Animal Models
141(1)
Epidemiologic Studies
142(1)
Intervention Studies with Single Antioxidants (Lung Cancer)
143(1)
Intervention Studies with a Single Antioxidant (Other Cancers)
144(1)
Intervention Studies with Multiple Dietary Antioxidants
144(1)
Intervention Studies with Vitamin D and Calcium
145(1)
Intervention Studies with Folate and B-Vitamins
145(1)
Intervention Studies with Fat and Fiber
146(1)
Intervention Studies with Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
146(1)
Potential Reasons for Inconsistent Results with Individual Micronutrients or Aspirin in Cancer Prevention Studies
146(1)
Regulation of Activation of Nrf2
147(2)
Reactive Oxygen Species (ROS) Activates Nrf2
147(1)
Binding of Nrf2 with ARE in the Nucleus
147(1)
Existence of ROS-Resistant Nrf2 in Cells Following Exposure to Carcinogens
147(1)
Antioxidants and Phytochemicals Activate ROS-Resistant Nrf2
148(1)
L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
148(1)
Activation of Nrf2 by MicroRNAs
148(1)
Suppression of Chronic Inflammation
149(1)
Recommended Mixture of Micronutrients for the Prevention of Cancer
149(1)
Recommended Changes in Diet and Lifestyle for the Prevention of Cancer
149(1)
Proposed Cancer Prevention Strategies
150(1)
Primary Prevention
150(1)
Secondary Prevention
150(1)
Can Cancer with a Family History Be Prevented?
150(1)
Problems Associated with Implementation of Dietary and Lifestyle Recommendations
150(1)
Toxicity of Micronutrients
151(1)
Conclusions
151(1)
References
152(11)
Chapter 8 Micronutrients in Improvement of the Standard Therapy in Cancer 163(28)
Introduction
163(1)
MicroRNAs in Cancer Cells
164(1)
MicroRNAs
164(1)
MicroRNAs Acting as Tumor Suppressors or Anti-oncogenes
165(3)
Colon Cancer
165(1)
Gastric Cancer Cells
165(1)
Non-Small Cell Lung Cancer (NSCLC)
165(1)
Retinoblastoma
166(1)
Breast Cancer Cells
166(1)
Hepatocellular Carcinoma
167(1)
Bladder Cancer
167(1)
Cervical Cancer
167(1)
MicroRNAs Acting as Oncogenes
168(1)
Bladder Cancer
168(1)
Lung Cancer
168(1)
Non-Small-Cell Lung Cancer
168(1)
Prostate Cancer, Gastric Cancer, and Esophageal Cancer
168(1)
Cervical Cancer, Colorectal Cancer, and Breast Cancer
168(1)
Nrf2 in Cancer Cells
169(1)
Normal Cell Response to Activated Nrf2
169(1)
High Expression of Nrf2 Promotes Cancer Growth and Drug-Resistant
169(1)
Individual Antioxidants Inhibit Cancer Growth in the Presence of Elevated Levels of Nrf2
170(3)
Luteolin
170(1)
Pterostilbene
170(1)
Antioxidants Activate ROS-Resistant Nrf2
170(1)
Synthetic Triterpenoid RTA 405
171(1)
Curcumin
171(1)
Tert-Butylhydroqui none
171(1)
Vitamin E Succinate
171(1)
Vitamin C
172(1)
Vitamin A and Carotenoids
173(1)
Selenium
173(1)
N-Acetylcysteine (NAC) and Alpha-Lipoic Acid
173(1)
Antioxidant-Induced Changes in Gene Expression Profiles in Cancer Cells
173(1)
Effects of Therapeutic Doses of Individual Antioxidants in Combination with Radiation Therapy on Cancer Cells and Normal Cells
174(2)
Cell Culture Studies
174(1)
Animal Studies
174(2)
Human Studies
176(1)
Effects of Therapeutic Doses of Individual Antioxidants in Combination with Chemotherapeutic on Cancer Cells and Normal Cells
176(3)
Cell Culture Studies
176(3)
Animal Studies
179(1)
Human Studies
179(1)
Reasons for Growth-Inhibitory Effects Antioxidants in the Presence of Elevated Levels of Nrf2
179(1)
Preventive Doses of Individual Antioxidants Reduce the Efficacy of Therapeutic Agents
180(1)
Effects of Therapeutic Doses of Individual Antioxidants in Combination with Experimental Therapies on Cancer Cells
180(2)
Hyperthermia
180(1)
Sodium Butyrate and Interferon-Alpha2b
181(1)
Immunotherapy and Gene Therapy
182(1)
Proposed Mixture Therapeutic Doses of Antioxidants During Cancer Therapy
182(1)
Conclusions
182(1)
References
183(8)
Chapter 9 Micronutrients in the Prevention and Improvement of the Standard Therapy for Alzheimer's Disease 191(44)
Introduction
191(1)
Prevalence, Incidence, and Cost of AD
192(1)
Estimated Cost of Treatment of AD
193(1)
Etiology of AD
193(1)
Neuropathology of AD
193(1)
MicroRNAs in the Pathogenesis of AD
193(1)
MicroRNAs
193(1)
Changes in the Expressions of MicroRNAs in Human AD
194(2)
Elevated Expressions of MicroRNAs
194(1)
Decreased Expressions of MicroRNAs
195(1)
Changes in MicroRNAs in Animal and Cell Culture AD Models
196(1)
Elevated Expressions of MicroRNAs
196(1)
Decreased Expression of MicroRNAs
196(1)
ROS and Pro-inflammatory Cytokines Regulate the Expressions of MicroRNAs
197(2)
ROS Upregulates the Expressions of MicroRNAs Causing Neurodegeneration
197(1)
ROS Downregulates the Expressions of MicroRNAs Causing Neurodegeneration
198(1)
Pro-inflammatory Cytokines Upregulate the Expressions of MicroRNAs Causing Neurodegeneration
198(1)
Micronutrients Regulate the Expressions of MicroRNAs
199(4)
Resveratrol Enhances the Expressions of MicroRNAs
199(1)
Resveratrol Decreases the Expressions of MicroRNAs
199(1)
Isoflavone Increases the Expressions of MicroRNAs
199(1)
Genistein Decreases the Expressions of MicroRNAs
200(1)
Quercetin Enhances the Expressions of MicroRNAs
200(1)
Curcumin Decreases the Expressions of MicroRNAs
200(1)
Curcumin Enhances the Expressions of MicroRNAs
200(1)
Coenzyme Q10 Regulates the Expressions of MicroRNAs
200(1)
Vitamin D3 Regulates the Expressions of MicroRNAs
200(1)
Nicotinamide (Vitamin-B3) Regulates the Expressions of MicroRNAs
201(1)
Selenium Regulates the Expressions of MicroRNAs
201(1)
Vitamin E and Delta-Tocotrienol Regulate the Expressions of MicroRNAs
201(1)
Vitamin A (Retinoic Acid) Regulates the Expressions of MicroRNAs
201(1)
Vitamin C Regulates the Expression of a MicroRNA
202(1)
Sources of Free Radicals in the Normal Brain
203(1)
Evidence for Increased Oxidative Stress as an Early Event in the Initiation of AD
203(2)
Studies on Cell Culture Model of AD
203(1)
Studies on Animal Models of AD
204(1)
Studies on Asymptomatic Individuals Carrying Mutated AD Specific Genes
204(1)
Studies on Increased Oxidative Stress in an Early Phase of AD
204(1)
Studies on Increased Oxidative Stress in Established Human AD (Autopsied Brain Tissue)
205(1)
Studies on Increased Oxidative Stress in Established Human AD (Peripheral Tissue)
205(1)
Mitochondrial Dysfunction
206(1)
Processes of Generating Beta-Amyloid Fragments (Aβ1-42) and Their Toxicity
206(1)
Oxidative Stress Increases Production of Beta Amyloids (Aβ1-42 Peptides)
206(1)
Aβ1-42 Peptides Cause Neuronal Degeneration by Inducing Free Radicals
207(1)
Mutations in AD Specific Genes Increases the Production of Beta-Amyloids
207(1)
Oxidative Stress Increases Hyperphosphorylated Tau (P-Tau) Protein in AD
207(1)
Oxidative Stress Inhibits Proteasome Activity in AD
207(1)
Evidence for Increased Levels of Markers of Chronic Inflammation in AD
208(1)
Cholesterol-Induced Generation of Beta-Amyloids
209(1)
Genetic Defects in Idiopathic AD
209(1)
Mutated AD Genes Induce Neurodegeneration by Producing of Beta-Amyloids
210(1)
Neuroglobin in AD
211(1)
Laboratory and Clinical Studies with Individual Micronutrients in AD
211(4)
Alpha-Lipoic Acid
211(1)
Coenzyme Q10
212(1)
Melatonin
212(1)
Nicotinamide (Vitamin B3)
212(1)
Vitamin A, Vitamin E, and Vitamin C
212(1)
Serum Levels of Antioxidants
213(1)
B-Vitamins
213(1)
Curcumin
214(1)
Resveratrol
214(1)
Ginkgo biloba and Omega-3 Fatty Acids
214(1)
Green Tea Epigallocatechin-3-Gallate (EGCG) and Caffeine
214(1)
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in AD
215(1)
Potential Reasons for Inconsistent Results with Individual Micronutrients or Aspirin in AD
215(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
216(1)
Nrf2
216(1)
ROS Activates Nrf2
216(1)
ROS-Resistant Nrf2
216(1)
Antioxidants Activate ROS-Resistant Nrf2
216(1)
Binding of Nrf2 with ARE in the Nucleus
216(1)
Suppression of Chronic Inflammation
216(1)
Nrf2 in AD
216(1)
Proposed Micronutrient Mixture for Optimally Reducing Oxidative Stress and Chronic Inflammation in AD
217(1)
Proposed Micronutrient Strategies for Prevention of AD
217(1)
Primary Prevention for AD
217(1)
Can AD Symptoms Be Prevented or Delayed in Individuals Carrying Mutated Gene?
218(1)
Secondary Prevention for AD
218(1)
Proposed Micronutrient Mixture for Improving the Management of AD
218(1)
Current Drug Therapy for AD
218(1)
Proposed Micronutrient Mixture in Combination with Drug Therapy for AD
219(1)
Diet and Lifestyle Recommendations for AD
219(1)
Conclusions
219(1)
References
220(15)
Chapter 10 Micronutrients for the Prevention and Improvement of the Standard Therapy for Parkinson's Disease 235(28)
Introduction
235(1)
Incidence, Prevalence, and Cost of PD
236(1)
Etiology of PD
236(1)
Neuropathology and Symptoms of PD
237(1)
Genetic of PD
237(1)
PD Genes and Oxidative Stress
238(2)
DJ-1 Gene
238(1)
Alpha-Synuclein Gene
238(1)
PTEN-Induced Putative Kinase 1 (PINK1)
239(1)
PARKIN Gene
240(1)
MicroRNAs in the Pathogenesis of PD
240(1)
MicroRNAs
240(1)
Changes in the Expressions of MicroRNAs in Neuronal Cell Culture Models of PD
240(1)
1-Methyl-4-Phenylpyridinium (MPP+) Treatment
240(1)
6-Hydroxydopamine (6-OHDA) Treatment
241(1)
Rotenone Treatment
241(1)
Changes in the Expressions of MicroRNAs in Animal Models of PD
241(1)
Changes in the Expressions of MicroRNAs in Human PD
242(1)
Changes in the Expressions of MicroRNAs in Impaired Non-motor Symptoms in PD
243(1)
Reactive Oxygen Species (ROS) Regulates the Expressions of MicroRNAs in Neuronal Cells
243(1)
Pro-inflammatory Cytokines Upregulate the Expressions of MicroRNAs
243(1)
Antioxidants Regulate the Expressions of MicroRNAs
243(1)
Evidence for Increased Oxidative Stress in PD
243(1)
Mitochondrial Dysfunction in PD
244(1)
Evidence for Increased Chronic Inflammation in PD
245(1)
Evidence for Increased Glutamate in PD
245(1)
Laboratory and Human Studies in PD after Treatment with Micronutrients
246(1)
In Vitro Studies with Micronutrients
246(1)
Cell Culture Studies with Micronutrients
246(1)
Antioxidant Studies in Animal Models of PD
246(1)
Antioxidant Studies in Human PD
247(1)
Potential Reasons for Inconsistent Results with Individual Micronutrients in AD Prevention Studies
248(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
249(1)
Nrf2
249(1)
ROS Activates Nrf2
249(1)
Nrf2 in PD
250(1)
Reducing Glutamate Release and Toxicity
250(1)
Proposed Micronutrient Mixture for Prevention and Improved Management of PD
250(1)
Primary Prevention
251(1)
Secondary Prevention
251(1)
Current Treatments of PD
251(1)
Proposed Micronutrient Mixture in Combination with Standard Therapy
251(1)
Diet and Lifestyle Recommendations for PD
252(1)
Conclusions
252(1)
References
252(11)
Chapter 11 Micronutrients in Prevention and Improvement of the Standard Therapy in Hearing Disorders 263(26)
Introduction
263(1)
Prevalence and Cost
264(1)
Prevalence
264(1)
Cost
264(1)
Types of Hearing Disorders
264(1)
Conductive Hearing Loss
264(1)
Sensorineural Hearing Loss
264(1)
Tinnitus
265(1)
Meniere's Disease (MD)
265(1)
Agents or Health Conditions Causing Hearing Disorders
265(1)
Measurements of Hearing Loss
266(1)
Evidence for Increased Oxidative Stress in Hearing Disorders
266(1)
Noise-Induced Oxidative Stress (NIHL)
266(1)
Noise and/or Vibration-Induced Oxidative Stress
267(1)
Cisplatin-Induced Oxidative Stress
267(1)
Advanced Age-Induced Oxidative Stress
267(1)
Oxidative Stress in the Meniere's Disease (MD)
267(1)
Evidence for Inflammation in Hearing Disorders
267(1)
Noise-Induced Inflammation
267(1)
Gentamicin- and Cisplatin-Induced Inflammation
268(1)
Bacterial Infection-Induced Inflammation
268(1)
Health Conditions-Induced Inflammation
268(1)
Advanced Age-Induced Inflammation
268(1)
Evidence for Increased Glutamate Level in Hearing Disorders
268(1)
Noise Releases Glutamate
268(1)
Salicylate Activates Glutamate Receptor
269(1)
Aminoglycoside, Cochlea Ischemia, or Trauma-Induced Release of Glutamate
269(1)
MicroRNAs in the Pathogenesis of Hearing Disorders
269(1)
MicroRNAs
269(1)
Expression of MicroRNAs in the Normal Ears
269(1)
Alterations in MicroRNAs Expression in Hearing Disorders
270(3)
Changes in the Expressions of MicroRNAs in Age-Related Hearing Disorders
270(1)
Mutation in MicroRNA Induces Nonsyndromic Hearing Loss (NSHL)
271(1)
Changes in the Expressions of MicroRNAs in Noise-Induced Hearing Loss
271(1)
Changes in the Expressions of MicroRNAs in Kanamycin-Induced Hearing Disorders
271(1)
Changes in the Expressions of MicroRNAs in Damaged Auditory Nervous System
272(1)
Oxidative Stress Regulates the Expression of MicroRNAs in Hearing Disorders
273(1)
Auditory Cells
273(1)
Non-auditory Cells (Neurons and Non-neuronal Cells)
273(1)
Pro-inflammatory Cytokines Could Upregulate the Expressions of MicroRNAs in Hearing Disorders
273(1)
Antioxidants Could Regulate the Expressions of MicroRNAs in Hearing Disorders
273(1)
Studies on Antioxidants in Hearing Disorders
274(1)
Animal Studies
274(1)
Human Studies
274(1)
Potential Reasons for Suboptimal Beneficial Effects with Individual Micronutrients in Hearing Disorders
275(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
276(1)
Nrf2
276(1)
Activation of Nrf2 During Acute Oxidative Stress
276(1)
Failure to Activate Nrf2 During Chronic Oxidative Stress
276(1)
Antioxidants Activate ROS-Resistant Nrf2
276(1)
Binding of Nrf2 with ARE in the Nucleus
276(1)
Importance of Activation of Nrf2 in Auditory Cells
277(1)
Current Prevention and Treatments Strategies
277(1)
Reducing Oxidative Stress Level
278(1)
Reducing Inflammation Level
278(1)
Reducing Glutamate Level
278(1)
Proposed Micronutrients for Simultaneously Reducing Oxidative Stress, Inflammation, and Glutamate Levels in Hearing Disorders
278(1)
Prevention of Hearing Disorders
278(1)
Primary Prevention
278(1)
Secondary Prevention
279(1)
Improved Management
279(1)
Conclusions
279(1)
References
280(9)
Chapter 12 Micronutrients in Improvement of the Standard Therapy in Posttraumatic Stress Disorder (PTSD) 289(20)
Introduction
289(1)
Prevalence and Cost of PTSD
289(1)
Symptoms of PTSD
290(1)
Brain Pathology of PTSD
291(1)
MicroRNAs in PTSD
292(1)
Evidence for Increased Oxidative Stress in PTSD
292(1)
Evidence for Chronic Inflammation in PTSD
293(1)
Evidence for Increased Release of Glutamate and Decreased Levels of GABA in PTSD
294(1)
Glutamate and GABA Levels in PTSD
295(1)
Studies on Antioxidants in PTSD
295(2)
Omega-3-Fatty Acids
295(1)
Curcumin
296(1)
Resveratrol
296(1)
Pentoxifylline and Tempol
296(1)
Flavonoids
296(1)
Valproic Acid
296(1)
Blueberry-Rich Diet
296(1)
Effect of Multiple Micronutrients in Veterans
297(1)
Potential Reasons for the Failure of Individual Micronutrients in Producing Consistent Benefits in Human
297(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
298(1)
Nrf2
298(1)
Activation of Nrf2 During Acute Oxidative Stress
298(1)
Failure to Activate Nrf2 During Chronic Oxidative Stress
298(1)
Antioxidants Activate ROS-Resistant Nrf2
298(1)
Binding of Nrf2 with ARE in the Nucleus
299(1)
Proposed Micronutrient Mixture for Optimally Reducing Oxidative Stress, Chronic Inflammation, and Glutamate Levels
299(1)
Reducing Oxidative Stress
299(1)
Reducing Chronic Inflammation
299(1)
Reducing Glutamate Release and Toxicity
299(1)
Prevention of PTSD
299(1)
Primary Prevention of PTSD
299(1)
Secondary Prevention of PTSD
299(1)
Standard Therapy in PTSD
300(1)
Improved Management of PTSD
300(1)
Diet and Lifestyle Recommendations for PTSD
300(1)
Conclusions
300(1)
References
301(8)
Chapter 13 Micronutrients in Improvement of the Standard Therapy in Traumatic Brain Injury 309(32)
Introduction
309(1)
Incidence, Prevalence, and Cost of TBI
310(1)
Concussion in USA Population
310(1)
National Football League (NFL)
310(1)
High School and College Sports
310(1)
US Veterans
310(1)
US Civilian
311(1)
Penetrating TBI (pTBI)
311(1)
US Troops
311(1)
US Civilian
311(1)
Cost
311(1)
Causes of Concussion
311(1)
Causes of Penetrating TBI (pTBI)
311(1)
Acute Symptoms of Concussion
312(1)
Acute Symptoms of pTBI
312(1)
Long-Term Health Consequences of TBI
312(1)
Concussion
312(1)
pTBI
313(1)
Neuropathology of TBI
313(1)
Concussion
313(1)
pTBI
313(1)
Scoring System of Severity of TBI
314(1)
MicroRNAs in Pathogenesis of TBI
314(1)
MicroRNAs as Potential Biomarkers for TBI
315(1)
Evidence for Increased Oxidative Stress in Concussion
316(1)
Animal Models
316(1)
Humans
316(1)
Evidence for Increased Inflammation in Concussion
316(1)
Animal Models
316(1)
Humans
317(1)
Evidence for Increased Glutamate Level in Concussion
317(1)
Molecular Changes in the Brain after Concussion
317(1)
Evidence for Increased Oxidative Stress after pTBI
318(1)
Animal Models
318(1)
Humans
318(1)
Oxidative Stress and Mitochondrial Dysfunction after pTBI
319(1)
Animal Models
319(1)
Humans
320(1)
Evidence for Increase Levels of Markers of Inflammation after pTBI
320(2)
Animal Models
320(1)
Humans
321(1)
Evidence for Increased Glutamate Level after pTBI
322(1)
Animal Models
322(1)
Humans
322(1)
Role of Matrix Metalloproteinases (MMPS) after Severe TBI
323(1)
Studies on the Effects of Single Antioxidants after TBI
323(1)
Animal Models
323(1)
Humans
324(1)
Potential Reasons for Inconsistent Results with Individual Micronutrients in Other Neurodegenerative Diseases
324(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
325(1)
Nrf2
325(1)
Activation of Nrf2 During Acute Oxidative Stress
325(1)
Failure to Activate Nrf2 During Chronic Oxidative Stress
325(1)
Antioxidants Activate ROS-Resistant Nrf2
326(1)
Binding of Nrf2 with ARE in the Nucleus
326(1)
Nrf2 in TBI
326(1)
Reducing Oxidative Stress Level
326(1)
Reducing Inflammation Level
326(1)
Reducing Glutamate Level
326(1)
Proposed Micronutrients for Reducing Oxidative Stress, Inflammation, and Glutamate Levels in TBI
326(1)
Toxicity of Ingredients in Proposed Micronutrient Preparation
327(1)
Prevention Studies with Proposed Micronutrient Mixture in TBI
327(1)
Primary Prevention
327(1)
Secondary Prevention
327(1)
Standard Therapy of TBI
328(1)
Proposed Micronutrients in Combination with Standard Therapy
328(1)
Diet and Lifestyle Recommendations for TBI
329(1)
Conclusions
329(1)
References
329(12)
Chapter 14 Micronutrients in Prevention and Improvement of the Standard Therapy in HIV/AIDS 341(18)
Introduction
341(1)
History, Prevalence, Incidence, and Cost of HIV/AIDS
342(1)
History of HIV/AIDS
342(1)
Prevalence of HIV Infection
342(1)
Incidence of HIV Infection
342(1)
Cost of Treating HIV Infection
343(1)
Role of Immune Function in HIV Infection
343(1)
Micronutrient Deficiency Impairs Immune Function
343(1)
Illicit Drugs Impair Immune Function
344(1)
Evidence for Increased Oxidative Stress Enhancing the Progression of HIV Infection
344(1)
Evidence for Increased Inflammation Enhancing the Progression of HIV Infection
345(1)
Evidence for Micronutrients Reducing Progression of HIV Infection
346(1)
Potential Reasons for Inconsistent Results with Micronutrients in Patients with HIV/AIDS
347(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
348(1)
Nrf2
348(1)
Activation of Nrf2 During Acute Oxidative Stress
348(1)
Failure of ROS to Activate Nrf2 During Chronic Oxidative Stress
348(1)
Antioxidants Activate ROS-Resistant Nrf2
348(1)
Binding of Nrf2 with ARE in the Nucleus
348(1)
Nrf2 in Patients with HIV Infection
348(1)
Reducing Oxidative Stress Level in HIV-Infected People
349(1)
Reducing Inflammation Level in HIV-Infected People
349(1)
Proposed Micronutrient Mixture for Reducing Oxidative Stress and Inflammation Levels in Patients with HIV Infection
349(1)
Toxicity of Ingredients in Proposed Micronutrient Mixture
349(1)
Primary Prevention Against HIV Infection
350(1)
Secondary Prevention for Reducing the Progression of HIV Infection
350(1)
Treatments of HIV/AIDS
350(1)
Antiviral Therapy in Reducing the Risk of Transmission From Mother to Infants
351(1)
Proposed Micronutrient Mixture in Combination with Antiviral Drugs
351(1)
Conclusions
352(1)
References
352(7)
Chapter 15 Improved Management of Autism Spectrum Disorder (ASD) by Micronutrients 359(20)
Introduction
359(1)
Prevalence and Cost of ASD
359(1)
Prevalence
359(1)
Cost
359(1)
Environmental and Genetic Factors
359(2)
Environmental Factors
359(1)
Health Conditions
360(1)
Genetic Factors
360(1)
Major Symptoms of ASD
361(1)
Brain Changes in ASD
361(1)
MicroRNAs in ASD
362(1)
MicroRNAs
362(1)
MicroRNAs in Serum
362(1)
MicroRNAs in Saliva
362(1)
MicroRNAs in Autopsied Brain Samples
363(1)
MicroRNAs in Cell Culture
363(1)
MicroRNAs in Animals
363(1)
Evidence for Increased Oxidative Stress in ASD
363(2)
Human Studies
363(1)
Cell Culture Models
364(1)
Evidence for Increased Inflammation in ASD
365(1)
Imbalances Between Neuronal Excitation and Inhibition
365(1)
Human Studies
365(1)
Use of Single Antioxidants in the Management of ASD
366(1)
Human Studies
366(1)
Animal Studies
366(1)
Studies with Individual Antioxidants in Human Neurodegenerative Diseases
367(1)
Regulation of Activation of Nrf2
368(1)
Reactive Oxygen Species (ROS) Activates Nrf2
368(1)
Binding of Nrf2 with ARE in the Nucleus
368(1)
Existence of ROS-Resistant Nrf2
368(1)
Antioxidants Activate ROS-Resistant Nrf2
368(1)
L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
368(1)
Activation of Nrf2 by MicroRNAs
368(1)
Suppression of Chronic Inflammation
369(1)
Inhibition of Release and Toxicity of Glutamate
369(1)
Drug Treatment in Human ASD
369(1)
Drug Treatment in Animal ASD Models
370(1)
Proposed Mixture of Micronutrients for Improved Management of ASD
370(1)
Conclusions
370(1)
References
371(8)
Chapter 16 Micronutrients in the Management of Prion Disease 379(16)
Introduction
379(1)
Incidence of Prion Disease
379(1)
Types of Prion Disease
379(1)
Modes of Transmission of Prion Disease to the Brain
380(1)
Pathological Changes in the Brain
380(1)
Symptoms of Prion Disease
381(1)
Factors Facilitating Conversion of PrPc to PrPsc and Mechanisms of Proliferation of PrPsc
381(2)
Effect of Mutations in PRNP Gene
381(1)
Role of Exosomes
381(1)
Effects on Polymorphisms of PNRP Gene
382(1)
Effects of Increased Oxidative Stress
383(1)
Oxidation of Methionine Residues in PrPc
383(1)
Effects of PrPsc-Induced Inflammation in the Brain
383(1)
Mechanisms of Neurotoxicity
384(1)
MicroRNAs in Prion Disease
384(2)
Studies with Individual Antioxidants and Phytochemicals in Models of Prion Diseases
386(1)
Studies with Individual Antioxidants in Other Neurodegenerative Diseases
387(1)
Regulation of Activation of Nrf2
388(1)
Reactive Oxygen Species (ROS) Activates Nrf2
388(1)
Binding of Nrf2 with ARE in the Nucleus
388(1)
Existence of ROS-Resistant Nrf2 in Prion Disease
388(1)
Antioxidants Activate of ROS-Resistant Nrf2
388(1)
L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
388(1)
Activation of Nrf2 by MicroRNAs
388(1)
Suppression of Chronic Inflammation
389(1)
Proposed Mixture of Micronutrients in Prevention and Improved Management of Prion Disease
389(1)
Prevention of Prion Disease
389(1)
Improved Management of Prion Disease
389(1)
Conclusions
389(1)
References
390(5)
Chapter 17 Micronutrients for Improved Management of Huntington's Disease 395(28)
Introduction
395(1)
Incidence, Prevalence, and Cost of HD
396(1)
Incidence and Prevalence
396(1)
Cost
396(1)
Signs and Symptoms
396(1)
Pathology of the Brain in HD
397(1)
Human Studies
397(1)
Animal Studies
397(1)
Receptor Abnormalities in HD
398(1)
Dopamine Receptors
398(1)
Cannabinoid Receptors
398(1)
Adenosine Receptors
399(1)
Transcriptional Deregulation in HD
399(1)
Histone Deacetylation
399(1)
Pre-translational Modification of Proteins in HD
400(2)
MicroRNAs
400(1)
MicroRNAs in Brain Cell Pathology and Protection
400(1)
MicroRNAs in Plasma
401(1)
Post-translational Modification of Proteins in HD
402(1)
Evidence for Increased Oxidative Stress as an Early Event in the Onset of HD Symptoms
402(2)
Studies on Asymptomatic and Symptomatic Individuals
402(1)
Aggregation of HD Protein
403(1)
Studies on Animal Models of HD
403(1)
Studies on Cell Culture Models of HD
403(1)
Mitochondrial Dysfunction in Asymptomatic and Symptomatic Individuals Carrying HD Gene
403(1)
Evidence for Increased Chronic Inflammation in HD
404(1)
Studies on Asymptomatic and Symptomatic Individuals
404(1)
Studies on Animal Models of HD
405(1)
Increased Glutamate Levels and Glutamate Receptor Activation in HD
405(1)
GABA Receptors in Asymptomatic and Symptomatic Individuals
406(1)
Use of Single Antioxidants, Phytochemicals, and B-Vitamins in the Management of HD
406(3)
Alpha-Tocopherol (Vitamin E)
406(1)
Vitamin C
406(1)
N-Acetylcysteine (NAC)
406(1)
Alpha-Lipoic Acid
407(1)
Coenzyme Q10
407(1)
L-Carnitine
407(1)
Lycopene and Epigallocatechin
407(1)
Melatonin
407(1)
Curcumin
408(1)
Resveratrol
408(1)
Ginkgo biloba Extract and Olive Oil
408(1)
Probucol
408(1)
B-Vitamins
409(1)
Studies with Individual Antioxidants in Other Human Neurodegenerative Diseases
409(1)
Regulation of Activation of Nrf2
410(1)
Reactive Oxygen Species (ROS) Activates Nrf2
410(1)
Binding of Nrf2 with ARE in the Nucleus
410(1)
Existence of ROS-Resistant Nrf2
410(1)
Antioxidants Activate ROS-Resistant Nrf2
410(1)
L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
410(1)
Activation of Nrf2 by MicroRNAs
411(1)
Nrf2 in HD
411(1)
Suppression of Oxidative Stress by Nrf2 and Antioxidants
411(1)
Suppression of Chronic Inflammation by Nrf2 and Antioxidants
411(1)
Inhibition of Release and Toxicity of Glutamate by Antioxidants and B-Vitamins
411(1)
Proposed Mixture of Micronutrients for Improved Management of HD
412(1)
Prevention or Delaying the Onset of Symptoms by Proposed Micronutrient Mixture?
412(1)
Proposed Micronutrient Mixture in Combination with Standard Treatment
413(1)
Current Treatments of HD
413(1)
Movement Disorder Drugs
413(1)
Antipsychotic Drugs
413(1)
Other Medications
413(1)
Medications for Psychiatric Disorders
413(1)
Antidepressants
413(1)
Mood-Stabilizing Drugs
413(1)
Clinical Studies with Additional Drugs in HD
414(1)
Psychotherapy
414(1)
Speech Therapy
414(1)
Physical Therapy
414(1)
Conclusions
414(1)
References
415(8)
Chapter 18 Micronutrients in Protecting Against Late Adverse Health-Effects of Diagnostic Radiation Doses 423(20)
Introduction
423(1)
Sources of Background Radiation
424(1)
Dose-Estimate of Diagnostic Radiation Procedures and Per Capita Dose
425(2)
Estimated Dose Received by Radiation Workers
427(1)
Estimated Dose Received by Crews of Commercial Flight
427(1)
Health Effects of Low Doses of Radiation
427(2)
Effects of Background Radiation on Human Health
427(1)
Induction of Mutations
428(1)
Induction of Radiation-Induced Cancer
428(1)
Impact of Chemical and Biological Carcinogens, and Tumor Promoters on Radiation-Induced Cancer
428(1)
Models Used for Risk Estimates of Radiation-Induced Cancer
429(1)
Cancer Risks in Populations Exposed to Diagnostic Radiation Procedures
429(2)
Adults and Children
429(1)
Cancer Risk in Children Exposed in Utero During Atomic Bombing of Hiroshima and Nagasaki
430(1)
Risk of Childhood Cancer after Irradiation of Fetuses
430(1)
Women Receiving Gonadal Doses of Radiation Before Conception
431(1)
Cancer Risk Among Radiation Workers
431(1)
Cancer Risk in Military and Civilian Pilots and Flight Attendants
432(1)
Cancer Risk Among Frequent Flyers
433(1)
Risk of Low-Dose Radiation-Induced Nonneoplastic Diseases
433(1)
Reducing Oxidative Stress and Inflammation by Single Antioxidants in Humans
433(1)
Reducing Damage by Multiple Antioxidants in Humans
434(1)
Proposed Strategy to Simultaneously Reduce Oxidative Stress and Inflammation
434(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
434(2)
Nrf2
434(1)
Activation of Nrf2 During Acute Oxidative Stress
435(1)
Failure to Activate Nrf2 During Chronic Oxidative Stress
435(1)
Antioxidants Activate ROS-Resistant Nrf2
435(1)
Binding of Nrf2 with ARE in the Nucleus
436(1)
Proposed Micronutrients for Simultaneously Reducing Oxidative Stress and Inflammation
436(1)
Conclusions
436(1)
References
437(6)
Chapter 19 Micronutrients in Protecting Against Lethal Doses of Ionizing Radiation 443(26)
Introduction
443(1)
Unit of Radiation Doses
444(1)
High-Dose Radiation-Induced Damage
444(2)
Bone Marrow Syndrome
444(1)
Gastrointestinal (GI) Syndrome
445(1)
Central Nervous System (CNS) Syndrome
445(1)
High-Dose Radiation-Induced Damage to Organs
445(1)
Risk of Developing Cancer Among Survivors of High Doses of Radiation
446(1)
Risk of Developing Non-neoplastic Diseases Among Survivors of High Doses of Radiation
446(1)
MicroRNAs in Radiation Damage
447(1)
MicroRNAs
447(1)
Irradiation Alters the Expression of MicroRNAs in Normal Cells
447(2)
MicroRNAs in Radiation-Induced Bystandard Effect
449(1)
MicroRNAs as Biomarkers of Radiation Damage
449(1)
Brief History of Radiation Protection Studies
449(1)
Radiation Protection Studies with Antioxidants in Cell Culture Models
450(1)
Radiation Protection Studies with Antioxidants in Animal Models
450(1)
Radiation Protection Study with a Mixture of Multiple Antioxidants Administered Orally Before and after Irradiation in Sheep
451(1)
Radiation Protection Study with a Mixture of Multiple Antioxidants Administered Orally Before and after Irradiation in Rabbits
452(1)
Radiation Protection Study with a Mixture of Multiple Antioxidants Administered Orally Before Irradiation in Mice
453(1)
Radiation Protection Study with a Mixture of Multiple Antioxidants Administered Through the Diet Before and after Irradiation in Drosophila Melanogaster
454(1)
Radiation Protection Studies with Antioxidants in Humans
454(1)
Rationale for Using Multiple Antioxidants in Radiation Protection
454(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
455(2)
Nrf2
455(1)
Activation of Nrf2 During Acute Oxidative Stress
456(1)
Activation of Nrf2 During Acute Phase of Irradiation
456(1)
Failure to Activate Nrf2 During Radiation-Induced Chronic Phase of Irradiation
456(1)
Antioxidants Activate ROS-Resistant Nrf2
456(1)
Binding of Nrf2 with ARE in the Nucleus
456(1)
Reducing Oxidative Stress Level for Radiation Protection
457(1)
Reducing Inflammation Level for Radiation Protection
457(1)
Proposed Micronutrients for Radiation Protection
457(1)
Guidelines for the Management of Large Number of People Irradiated with Lethal Doses of Radiation
457(1)
Radiation Mitigating Agents
458(1)
Chemical Agents for Mitigating Radiation Injury
458(1)
Antibiotics, Blood, and Electrolytes
458(1)
Erythropoietin
458(1)
Statins
458(1)
Cytokines and Growth Factors
458(1)
Biological Agents for Mitigating Radiation Injury
459(1)
Bone Marrow and Newborn Liver Cells Transplant
459(1)
The Chernobyl Experience in Treating Irradiated Individuals
459(1)
Proposed Micronutrient Mixture for the Treatment of Bone Marrow Syndrome
460(1)
Proposed Micronutrient Mixture for the Treatment of GI Syndrome
460(1)
Conclusions
460(1)
References
461(8)
Chapter 20 Micronutrients in Prevention and Improvement of the Standard Therapy in Arthritis 469(24)
Introduction
469(1)
Prevalence and Cost of Arthritis
470(1)
Types of Arthritis
471(1)
Rheumatoid Arthritis (RA)
471(1)
Osteoarthritis (OA)
471(1)
Juvenile Rheumatoid Arthritis (JRA)
472(1)
Evidence for the Role of Oxidative Stress
472(1)
Evidence for the Role of Inflammation
473(2)
Role of Antioxidants in Arthritis
475(2)
Studies on Animal Models of Arthritis
475(1)
Human Cell Culture Models of Arthritis
476(1)
Studies on Human RA and OA
477(1)
Prevention Strategies
477(1)
Potential Reasons for Inconsistent Results
477(1)
Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
478(1)
Nrf2
478(1)
Activation of Nrf2 During Acute Oxidative Stress
478(1)
Failure to Activate Nrf2 During Chronic Oxidative Stress
478(1)
Antioxidants Activate ROS-Resistant Nrf2
478(1)
Binding of Nrf2 with ARE in the Nucleus
479(1)
Importance of Activation of Nrf2 in Arthritis
479(1)
Reducing Oxidative Stress Level
479(1)
Reducing Inflammation Level
479(1)
Proposed Micronutrients for Simultaneously Reducing Oxidative Stress and Inflammation in Arthritis
479(1)
Primary Prevention of Arthritis
479(1)
Treatment Strategies of Arthritis
480(3)
Low-Dose Methotrexate (MTX)
480(1)
Anti-cytokines Therapy
480(2)
Toxicity of MTX and Anti-cytokine Therapy
482(1)
Treatment with Glucosamine and Chondroitin
482(1)
Treatment with Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
483(1)
Treatment with Complementary Medicine
483(1)
Proposed Micronutrient Mixture in Combination with Standard Therapy in Patients with Arthritis
483(1)
Diet and Lifestyle Recommendations for High Risk Populations and Patients with Arthritis
483(1)
Conclusions
483(1)
References
484(9)
Chapter 21 Misconceptions about the Functions and Value of Antioxidants in Health and Disease 493(6)
Introduction
493(1)
Misconception 1
493(1)
Misconception 2
493(1)
Misconception 3
494(1)
Misconception 4
494(1)
Misconception 5
494(1)
Misconception 6
494(1)
Misconception 7
494(1)
Misconception 8
495(1)
Misconception 9
495(1)
Misconception 10
495(1)
Misconception 11
495(1)
Misconception 12
496(1)
Misconception 13
496(1)
Misconception 14
496(1)
Misconception 15
496(1)
Misconception 16
496(1)
Misconception 17
497(1)
Conclusions
497(2)
Chapter 22 Dietary Reference Intakes of Selected Micronutrients 499(22)
Introduction
499(1)
RDA (DRI)
499(20)
Adequate Intake (AI)
518(1)
Tolerable Upper Intake Level (UL)
518(1)
Conclusions
519(2)
Index 521
Dr. Kedar N. Prasad obtained a Masters degree in Zoology from the University of Bihar, Ranchi, India, and a Ph.D. degree in Radiation Biology from the University of Iowa, Iowa City, in 1963. He received Post-doctoral training at the Brookhaven National Laboratory, Long Island. New York, and joined the Department of Radiology at the University of Colorado Health Sciences Center where he became Professor and Director for the Center for Vitamins and Cancer Research. He has published over 250 articles in peer-reviewed journals, and authored and edited 25 books in the area of radiation biology, nutrition and cancer, and nutrition and neurological diseases particularly Alzheimers disease and Parkinsons disease. These articles were published in highly prestigious journals such as Science, Nature, and Proceedings of the National Academic of Sciences, USA. Dr Prasad has received several honors which include: Invitation by the Nobel Prize Committee to nominate a candidate for the Nobel Prize in Medicine for 1982; The 1999 Harold Harper Lecture at the meeting of the American College of Advancement in Medicine; An award for the best review of 1998-1999 on antioxidant and cancer; and 1999-2000 on antioxidants and Parkinsons disease by the American College of Nutrition. He was a Fellow of the American College of Nutrition, and served as a President of the International Society of Nutrition and Cancer, 1992-2000. In 2017, he was invited to become the member of The Royal Society of Medicine, London. Currently, he is Chief Scientific Officer of the Engage Global.