Micronutrients in Health and Disease, Second Edition

 
 
CRC Press
  • 2. Auflage
  • |
  • erschienen am 15. April 2019
  • |
  • 560 Seiten
 
E-Book | PDF mit Adobe DRM | Systemvoraussetzungen
978-0-429-51318-3 (ISBN)
 

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 Huntington's 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.

2. Auflage
  • Englisch
  • Milton
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  • Großbritannien
Taylor & Francis Ltd
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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 Alzheimer's disease and Parkinson's 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 Parkinson's 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.

  • Cover
  • Half Title
  • Title Page
  • Copyright Page
  • Table of Contents
  • Preface
  • Acknowledgments
  • Author
  • Chapter 1: Basic Facts about Micronutrients
  • Introduction
  • Evolution of the Antioxidant System
  • History of the Discovery of Micronutrients
  • Sources and Forms of Vitamins
  • Solubility of Micronutrients
  • Distribution of Antioxidants in the Body
  • Storage of Antioxidants
  • Can Antioxidants Be Destroyed during Cooking?
  • Absorption of Antioxidants and Its Significance
  • Functions of Individual Antioxidants
  • Antioxidant Defense Systems
  • Antioxidant Enzymes
  • Dietary Antioxidants
  • Endogenous Antioxidants
  • Known Functions of Antioxidants
  • Current Controversies about Antioxidants
  • Misuse of Antioxidants in Clinical Studies
  • Conclusions
  • References
  • Chapter 2: Basic Facts about Oxidative Stress, Inflammation, and the Immune System
  • Introduction
  • Oxidative Stress
  • What Are Free Radicals?
  • Types of Free Radicals
  • Formation of Free Radicals Derived from Oxygen and Nitrogen
  • Oxidation and Reduction Processes
  • What Is Inflammation?
  • Types of Inflammatory Reactions
  • Products of Inflammatory Reactions
  • Cytokines
  • Complement Proteins
  • Arachidonic Acid (AA) Metabolites
  • Endothelial/Leukocyte Adhesion Molecules
  • Immune System
  • What Is the Immune System?
  • Innate Immunity
  • Adaptive Immunity
  • Conclusions
  • References
  • Chapter 3: Scientific Rationale of Current Trends in Clinical Studies of Micronutrients
  • Introduction
  • Levels of Oxidative Stress and Chronic Inflammation in High-Risk Populations
  • High-Risk Populations of Cancer
  • High-Risk Populations of Coronary Artery Disease (CAD)
  • High-Risk Populations of Alzheimer's Disease (AD) and Parkinson's Disease (PD)
  • Distributions and Function of Antioxidants
  • Results of Clinical Trials with a Single Antioxidant in High-Risk Populations
  • Cancer
  • Coronary Artery Disease (CAD)
  • Alzheimer's Disease (AD) and Parkinson's Disease (PD)
  • Why the Use of a Single Antioxidant Produced Inconsistent Results
  • Results of Clinical Studies with Multiple Dietary Antioxidants in Cancer
  • Results of Clinical Studies with Fat and Fiber
  • Rationale for Using a Mixture of Micronutrients for Reducing the Risk and Progression of Chronic Diseases
  • Proposed Mixture of Micronutrients for Reducing the Risk and Progression of Chronic Diseases
  • Proposed Changes in Diet and Lifestyle for Reducing the Risk and Progression of Chronic Diseases
  • Conclusions
  • References
  • Chapter 4: Micronutrients in Healthy Aging and Age-Related Decline in Organ Functions
  • Introduction
  • Trends of Aging Population
  • Evidence for Increased Oxidative Stress During Aging
  • Extracellular Sources for Production of Free Radicals
  • Cellular Sites of Production of Free Radicals
  • Oxidative Stress-Induced Age-Related Decline in Organelle Functions
  • Mitochondrial Dysfunction
  • Impairment of Proteasome and Lysosomal-Mediated Proteolytic Activities
  • Oxidative Stress-Induced Changes in Cell Culture Models
  • Oxidative Stress-Induced Changes in Animal Models
  • Oxidative Stress-Induced Shortening of the Length of Telomere
  • Evidence for Chronic Inflammation During Aging
  • Impaired Immune Function in Aging
  • Changes in the Antioxidant Defense Systems During Aging
  • Antioxidant Enzymes
  • Changes in Antioxidant Enzymes Activities in Animals
  • Changes in Antioxidant Enzymes Activities in Humans
  • Changes in Dietary and Endogenous Antioxidants Levels
  • Vitamin C
  • Glutathione
  • Vitamin E
  • Coenzyme Q10
  • MicroRNAs in Aging
  • MicroRNAs
  • MicroRNAs in Age-Related Diseases
  • MicroRNAs and Their Target Proteins in Aged Animals
  • Oxidative Stress and Pro-inflammatory Cytokine Regulate Expression of MicroRNAs
  • Antioxidants Regulate Expression of MicroRNAs
  • Effects of Individual Antioxidants on Age-Related Functional Deficits
  • Vitamin E
  • Coenzyme Q10
  • Carotenoids and Zinc
  • Melatonin
  • Flavonoids
  • Glutathione and N-Acetylcysteine (NAC)
  • Alpha-Lipoic Acid
  • Multiple Dietary Antioxidants
  • Studies with Individual Antioxidants on Age-Related Neurodegenerative Diseases in Humans
  • Regulation of Activation of Nrf2
  • Reactive Oxygen Species (ROS) Activates Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Existence of ROS-Resistant Nrf2
  • Antioxidants and Phytochemicals Activate ROS-Resistant Nrf2
  • L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
  • Activation of Nrf2 by MicroRNAs
  • Suppression of Chronic Inflammation
  • Proposed Mixture of Micronutrients for Healthy Aging and for Reducing Age-Related Functional Deficits
  • Proposed Changes in Diet and Lifestyle for Healthy Aging and for Reducing Age-Related Functional Deficits
  • Conclusions
  • References
  • Chapter 5: Role of Micronutrients in Prevention of Coronary Artery Disease and Improvement of the Standard Therapy
  • Introduction
  • Prevalence, Incidence, and Cost
  • Evidence for Increased Oxidative Stress in CAD
  • Consequences of Increased Oxidative Stress
  • Evidence for Increased Chronic Inflammation in CAD
  • Evidence for Increased Levels of Homocysteine in CAD
  • MicroRNAs in CAD
  • MicroRNAs
  • Circulating MicroRNAs in CAD
  • Cellular MicroRNAs in CAD
  • Oxidative Stress and Pro-inflammatory Cytokine Regulate Expression of MicroRNAs
  • Antioxidants Regulate Expression of MicroRNAs
  • Role of Antioxidants in CAD
  • Animal Studies after Treatment with Antioxidants
  • Epidemiologic Studies with Antioxidants
  • Intervention Human Studies after Treatment with Antioxidants
  • Vitamin E Alone Producing Beneficial Effects
  • Vitamin C Alone Producing Beneficial Effects
  • Dietary Antioxidants Producing No Effects or Adverse Effects
  • Endogenous Antioxidants Producing No Effects or Beneficial Effects
  • Dietary and Endogenous Antioxidants with Cholesterol-Lowering Drugs
  • Multiple Dietary Antioxidants with Cholesterol-Lowering Drugs
  • Resveratrol and Omega-3 Fatty Acids
  • Resveratrol
  • Omega-3 Fatty Acids
  • Intervention Studies with B-Vitamins to Lower Homocysteine Levels
  • Potential Reasons for the Failure of Individual Micronutrients in Producing Sustained and Consistent Benefits in CAD
  • Regulation of Activation of Nrf2
  • Reactive Oxygen Species (ROS) Activates Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Existence of ROS-Resistant Nrf2 in CAD
  • Antioxidants and Phytochemicals Activate ROS-Resistant Nrf2
  • L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
  • Activation of Nrf2 by MicroRNAs
  • Suppression of Chronic Inflammation
  • Proposed Mixture of Micronutrients for Prevention and Improved Management of CAD
  • Proposed Changes in Diet and Lifestyle for Prevention and Improved Management of CAD
  • Prevention and Improved Management of CAD
  • Primary Prevention
  • Secondary Prevention
  • Improved Management of CAD
  • Conclusions
  • References
  • Chapter 6: Micronutrients in Prevention and Improvement of the Standard Therapy in Diabetes
  • Introduction
  • Incidence, Prevalence, and Cost
  • Incidence
  • Prevalence
  • Cost
  • Types of Diabetes
  • Type 1 Diabetes
  • Type 2 Diabetes
  • Gestational Diabetes
  • Other Types of Diabetes
  • Pre-diabetes and Metabolic Syndrome
  • Complications of Diabetes
  • Evidence for Increased Oxidative Stress in Diabetes
  • Type 1 Diabetes
  • Type 2 Diabetes
  • Metabolic Syndrome
  • Evidence for Increased Chronic Inflammation in Diabetes
  • MicroRNAs in Diabetes
  • MicroRNAs
  • Circulating MicroRNAs in Diabetes
  • Cellular MicroRNAs in Diabetes (Humans)
  • Cellular MicroRNAs in Diabetes (Animal Models)
  • Oxidative Stress and Pro-inflammatory Cytokines Regulate Expression of MicroRNAs
  • Antioxidants Regulate Expression of MicroRNAs
  • Reducing Oxidative Stress and Chronic Inflammation in Diabetes
  • Role of Antioxidants and Phytochemicals in Protecting Against Diabetes
  • Vitamin A (Animal and Human Studies)
  • Vitamin C (Human Studies)
  • Vitamin C (Animal Studies)
  • Vitamin D3 (Animal Studies)
  • Vitamin E (Animal Studies)
  • Vitamin E (Human Studies)
  • Alpha-Lipoic Acid (Human Studies)
  • Alpha-Lipoic Acid (Animal Studies)
  • N-Acetylcysteine (Human Studies)
  • N-Acetylcysteine (Animal Studies)
  • L-Carnitine (Human Studies)
  • L-Carnitine (Animal Studies)
  • Coenzyme Q10 (Human Studies)
  • Coenzyme Q10 (Animal Studies)
  • Omega-3 Fatty Acids (Animal Studies)
  • Omega-3-Fatty Acids (Epidemiologic Studies)
  • Omega-3-Fatty Acids (Intervention Studies)
  • Antioxidant Mixtures (Human Studies)
  • Antioxidant Mixture (Animal Studies)
  • Folic Acid and Thiamine (Human Studies)
  • Folic Acid and Thiamine (Animal Studies)
  • Chromium (Human Studies)
  • Antioxidants with Diabetic/Cardiovascular Drugs and/or Insulin (Human Studies)
  • Antioxidants with Diabetic/Cardiovascular Drugs and/or Insulin (Animal Studies)
  • Treatments of Diabetes
  • Standard Treatments
  • Aspirin (Human Studies)
  • Aspirin Resistance
  • Aspirin (Animal Studies)
  • Potential Reasons for Inconsistent Results with Individual Micronutrients or Aspirin
  • Regulation of Activation of Nrf2
  • Reactive Oxygen Species (ROS) Activates Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Existence of ROS-Resistant Nrf2 in Diabetes
  • Antioxidants and Phytochemicals Activate ROS-Resistant Nrf2
  • L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
  • Activation of Nrf2 by MicroRNAs
  • Suppression of Chronic Inflammation
  • Recommended Mixture of Micronutrients for the Prevention of Diabetes
  • Recommended Changes in Diet and Lifestyle for the Prevention and Improved Management of Diabetes
  • Prevention of Diabetes
  • Primary Prevention
  • Secondary Prevention
  • Improved Management of Diabetes
  • Conclusions
  • References
  • Chapter 7: Micronutrients in Cancer Prevention
  • Introduction
  • Incidence, Prevalence, Mortality, and Cost
  • Proposed Stages of Carcinogenesis
  • Two-Stage Model of Animal Carcinogenesis
  • Some Examples of Tumor Initiators and Tumor Promoters
  • Three-Stage Model of Human Carcinogenesis
  • Diagrammatic Representation of Three-Stage Model of Human Carcinogenesis
  • Some Examples of Environmental-Related Carcinogens
  • Some Examples of Diet-Related Carcinogens
  • Some Examples of Diet-Related Cancer Protective Agents
  • Some Examples of Lifestyle-Related Carcinogens
  • Alcohol
  • Cell Phone
  • Smoking
  • Coffee and Caffeine
  • Evidence for Increased Oxidative Stress
  • Evidence for Increased Chronic Inflammation
  • MicroRNAs in Cancer Prevention
  • MicroRNAs
  • Changes in MicroRNAs after Exposure to Chemical Carcinogens and Oncogenic Virus
  • Functions of Antioxidants Relevant to Cancer Prevention
  • Antioxidants and Phytochemicals Regulate Expression of MicroRNAs
  • Reducing Oxidative Stress and Chronic Inflammation in Cancer Prevention
  • Cell Culture Models
  • Animal Models
  • Epidemiologic Studies
  • Intervention Studies with Single Antioxidants (Lung Cancer)
  • Intervention Studies with a Single Antioxidant (Other Cancers)
  • Intervention Studies with Multiple Dietary Antioxidants
  • Intervention Studies with Vitamin D and Calcium
  • Intervention Studies with Folate and B-Vitamins
  • Intervention Studies with Fat and Fiber
  • Intervention Studies with Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
  • Potential Reasons for Inconsistent Results with Individual Micronutrients or Aspirin in Cancer Prevention Studies
  • Regulation of Activation of Nrf2
  • Reactive Oxygen Species (ROS) Activates Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Existence of ROS-Resistant Nrf2 in Cells Following Exposure to Carcinogens
  • Antioxidants and Phytochemicals Activate ROS-Resistant Nrf2
  • L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
  • Activation of Nrf2 by MicroRNAs
  • Suppression of Chronic Inflammation
  • Recommended Mixture of Micronutrients for the Prevention of Cancer
  • Recommended Changes in Diet and Lifestyle for the Prevention of Cancer
  • Proposed Cancer Prevention Strategies
  • Primary Prevention
  • Secondary Prevention
  • Can Cancer with a Family History Be Prevented?
  • Problems Associated with Implementation of Dietary and Lifestyle Recommendations
  • Toxicity of Micronutrients
  • Conclusions
  • References
  • Chapter 8: Micronutrients in Improvement of the Standard Therapy in Cancer
  • Introduction
  • MicroRNAs in Cancer Cells
  • MicroRNAs
  • MicroRNAs Acting as Tumor Suppressors or Anti-oncogenes
  • Colon Cancer
  • Gastric Cancer Cells
  • Non-Small Cell Lung Cancer (NSCLC)
  • Retinoblastoma
  • Breast Cancer Cells
  • Hepatocellular Carcinoma
  • Bladder Cancer
  • Cervical Cancer
  • MicroRNAs Acting as Oncogenes
  • Bladder Cancer
  • Lung Cancer
  • Non-Small-Cell Lung Cancer
  • Prostate Cancer, Gastric Cancer, and Esophageal Cancer
  • Cervical Cancer, Colorectal Cancer, and Breast Cancer
  • Nrf2 in Cancer Cells
  • Normal Cell Response to Activated Nrf2
  • High Expression of Nrf2 Promotes Cancer Growth and Drug-Resistant
  • Individual Antioxidants Inhibit Cancer Growth in the Presence of Elevated Levels of Nrf2
  • Luteolin
  • Pterostilbene
  • Antioxidants Activate ROS-Resistant Nrf2
  • Synthetic Triterpenoid RTA 405
  • Curcumin
  • Tert-Butylhydroquinone
  • Vitamin E Succinate
  • Vitamin C
  • Vitamin A and Carotenoids
  • Selenium
  • N-Acetylcysteine (NAC) and Alpha-Lipoic Acid
  • Antioxidant-Induced Changes in Gene Expression Profiles in Cancer Cells
  • Effects of Therapeutic Doses of Individual Antioxidants in Combination with Radiation Therapy on Cancer Cells and Normal Cells
  • Cell Culture Studies
  • Animal Studies
  • Human Studies
  • Effects of Therapeutic Doses of Individual Antioxidants in Combination with Chemotherapeutic on Cancer Cells and Normal Cells
  • Cell Culture Studies
  • Animal Studies
  • Human Studies
  • Reasons for Growth-Inhibitory Effects Antioxidants in the Presence of Elevated Levels of Nrf2
  • Preventive Doses of Individual Antioxidants Reduce the Efficacy of Therapeutic Agents
  • Effects of Therapeutic Doses of Individual Antioxidants in Combination with Experimental Therapies on Cancer Cells
  • Hyperthermia
  • Sodium Butyrate and Interferon-Alpha2b
  • Immunotherapy and Gene Therapy
  • Proposed Mixture Therapeutic Doses of Antioxidants During Cancer Therapy
  • Conclusions
  • References
  • Chapter 9: Micronutrients in the Prevention and Improvement of the Standard Therapy for Alzheimer's Disease
  • Introduction
  • Prevalence, Incidence, and Cost of AD
  • Estimated Cost of Treatment of AD
  • Etiology of AD
  • Neuropathology of AD
  • MicroRNAs in the Pathogenesis of AD
  • MicroRNAs
  • Changes in the Expressions of MicroRNAs in Human AD
  • Elevated Expressions of MicroRNAs
  • Decreased Expressions of MicroRNAs
  • Changes in MicroRNAs in Animal and Cell Culture AD Models
  • Elevated Expressions of MicroRNAs
  • Decreased Expression of MicroRNAs
  • ROS and Pro-inflammatory Cytokines Regulate the Expressions of MicroRNAs
  • ROS Upregulates the Expressions of MicroRNAs Causing Neurodegeneration
  • ROS Downregulates the Expressions of MicroRNAs Causing Neurodegeneration
  • Pro-inflammatory Cytokines Upregulate the Expressions of MicroRNAs Causing Neurodegeneration
  • Micronutrients Regulate the Expressions of MicroRNAs
  • Resveratrol Enhances the Expressions of MicroRNAs
  • Resveratrol Decreases the Expressions of MicroRNAs
  • Isoflavone Increases the Expressions of MicroRNAs
  • Genistein Decreases the Expressions of MicroRNAs
  • Quercetin Enhances the Expressions of MicroRNAs
  • Curcumin Decreases the Expressions of MicroRNAs
  • Curcumin Enhances the Expressions of MicroRNAs
  • Coenzyme Q10 Regulates the Expressions of MicroRNAs
  • Vitamin D3 Regulates the Expressions of MicroRNAs
  • Nicotinamide (Vitamin-B3) Regulates the Expressions of MicroRNAs
  • Selenium Regulates the Expressions of MicroRNAs
  • Vitamin E and Delta-Tocotrienol Regulate the Expressions of MicroRNAs
  • Vitamin A (Retinoic Acid) Regulates the Expressions of MicroRNAs
  • Vitamin C Regulates the Expression of a MicroRNA
  • Sources of Free Radicals in the Normal Brain
  • Evidence for Increased Oxidative Stress as an Early Event in the Initiation of AD
  • Studies on Cell Culture Model of AD
  • Studies on Animal Models of AD
  • Studies on Asymptomatic Individuals Carrying Mutated AD Specific Genes
  • Studies on Increased Oxidative Stress in an Early Phase of AD
  • Studies on Increased Oxidative Stress in Established Human AD (Autopsied Brain Tissue)
  • Studies on Increased Oxidative Stress in Established Human AD (Peripheral Tissue)
  • Mitochondrial Dysfunction
  • Processes of Generating Beta-Amyloid Fragments (Aß1-42) and Their Toxicity
  • Oxidative Stress Increases Production of Beta Amyloids (Aß1-42 Peptides)
  • Aß1-42 Peptides Cause Neuronal Degeneration by Inducing Free Radicals
  • Mutations in AD Specific Genes Increases the Production of Beta-Amyloids
  • Oxidative Stress Increases Hyperphosphorylated Tau (P-Tau) Protein in AD
  • Oxidative Stress Inhibits Proteasome Activity in AD
  • Evidence for Increased Levels of Markers of Chronic Inflammation in AD
  • Cholesterol-Induced Generation of Beta-Amyloids
  • Genetic Defects in Idiopathic AD
  • Mutated AD Genes Induce Neurodegeneration by Producing of Beta-Amyloids
  • Neuroglobin in AD
  • Laboratory and Clinical Studies with Individual Micronutrients in AD
  • Alpha-Lipoic Acid
  • Coenzyme Q10
  • Melatonin
  • Nicotinamide (Vitamin B3)
  • Vitamin A, Vitamin E, and Vitamin C
  • Serum Levels of Antioxidants
  • B-Vitamins
  • Curcumin
  • Resveratrol
  • Ginkgo biloba and Omega-3 Fatty Acids
  • Green Tea Epigallocatechin-3-Gallate (EGCG) and Caffeine
  • Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in AD
  • Potential Reasons for Inconsistent Results with Individual Micronutrients or Aspirin in AD
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • ROS Activates Nrf2
  • ROS-Resistant Nrf2
  • Antioxidants Activate ROS-Resistant Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Suppression of Chronic Inflammation
  • Nrf2 in AD
  • Proposed Micronutrient Mixture for Optimally Reducing Oxidative Stress and Chronic Inflammation in AD
  • Proposed Micronutrient Strategies for Prevention of AD
  • Primary Prevention for AD
  • Can AD Symptoms Be Prevented or Delayed in Individuals Carrying Mutated Gene?
  • Secondary Prevention for AD
  • Proposed Micronutrient Mixture for Improving the Management of AD
  • Current Drug Therapy for AD
  • Proposed Micronutrient Mixture in Combination with Drug Therapy for AD
  • Diet and Lifestyle Recommendations for AD
  • Conclusions
  • References
  • Chapter 10: Micronutrients for the Prevention and Improvement of the Standard Therapy for Parkinson's Disease
  • Introduction
  • Incidence, Prevalence, and Cost of PD
  • Etiology of PD
  • Neuropathology and Symptoms of PD
  • Genetic of PD
  • PD Genes and Oxidative Stress
  • DJ-1 Gene
  • Alpha-Synuclein Gene
  • PTEN-Induced Putative Kinase 1 (PINK1)
  • PARKIN Gene
  • MicroRNAs in the Pathogenesis of PD
  • MicroRNAs
  • Changes in the Expressions of MicroRNAs in Neuronal Cell Culture Models of PD
  • 1-Methyl-4-Phenylpyridinium (MPP+) Treatment
  • 6-Hydroxydopamine (6-OHDA) Treatment
  • Rotenone Treatment
  • Changes in the Expressions of MicroRNAs in Animal Models of PD
  • Changes in the Expressions of MicroRNAs in Human PD
  • Changes in the Expressions of MicroRNAs in Impaired Non-motor Symptoms in PD
  • Reactive Oxygen Species (ROS) Regulates the Expressions of MicroRNAs in Neuronal Cells
  • Pro-inflammatory Cytokines Upregulate the Expressions of MicroRNAs
  • Antioxidants Regulate the Expressions of MicroRNAs
  • Evidence for Increased Oxidative Stress in PD
  • Mitochondrial Dysfunction in PD
  • Evidence for Increased Chronic Inflammation in PD
  • Evidence for Increased Glutamate in PD
  • Laboratory and Human Studies in PD after Treatment with Micronutrients
  • In Vitro Studies with Micronutrients
  • Cell Culture Studies with Micronutrients
  • Antioxidant Studies in Animal Models of PD
  • Antioxidant Studies in Human PD
  • Potential Reasons for Inconsistent Results with Individual Micronutrients in AD Prevention Studies
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • ROS Activates Nrf2
  • Nrf2 in PD
  • Reducing Glutamate Release and Toxicity
  • Proposed Micronutrient Mixture for Prevention and Improved Management of PD
  • Primary Prevention
  • Secondary Prevention
  • Current Treatments of PD
  • Proposed Micronutrient Mixture in Combination with Standard Therapy
  • Diet and Lifestyle Recommendations for PD
  • Conclusions
  • References
  • Chapter 11: Micronutrients in Prevention and Improvement of the Standard Therapy in Hearing Disorders
  • Introduction
  • Prevalence and Cost
  • Prevalence
  • Cost
  • Types of Hearing Disorders
  • Conductive Hearing Loss
  • Sensorineural Hearing Loss
  • Tinnitus
  • Meniere's Disease (MD)
  • Agents or Health Conditions Causing Hearing Disorders
  • Measurements of Hearing Loss
  • Evidence for Increased Oxidative Stress in Hearing Disorders
  • Noise-Induced Oxidative Stress (NIHL)
  • Noise and/or Vibration-Induced Oxidative Stress
  • Cisplatin-Induced Oxidative Stress
  • Advanced Age-Induced Oxidative Stress
  • Oxidative Stress in the Meniere's Disease (MD)
  • Evidence for Inflammation in Hearing Disorders
  • Noise-Induced Inflammation
  • Gentamicin- and Cisplatin-Induced Inflammation
  • Bacterial Infection-Induced Inflammation
  • Health Conditions-Induced Inflammation
  • Advanced Age-Induced Inflammation
  • Evidence for Increased Glutamate Level in Hearing Disorders
  • Noise Releases Glutamate
  • Salicylate Activates Glutamate Receptor
  • Aminoglycoside, Cochlea Ischemia, or Trauma-Induced Release of Glutamate
  • MicroRNAs in the Pathogenesis of Hearing Disorders
  • MicroRNAs
  • Expression of MicroRNAs in the Normal Ears
  • Alterations in MicroRNAs Expression in Hearing Disorders
  • Changes in the Expressions of MicroRNAs in Age-Related Hearing Disorders
  • Mutation in MicroRNA Induces Nonsyndromic Hearing Loss (NSHL)
  • Changes in the Expressions of MicroRNAs in Noise-Induced Hearing Loss
  • Changes in the Expressions of MicroRNAs in Kanamycin-Induced Hearing Disorders
  • Changes in the Expressions of MicroRNAs in Damaged Auditory Nervous System
  • Oxidative Stress Regulates the Expression of MicroRNAs in Hearing Disorders
  • Auditory Cells
  • Non-auditory Cells (Neurons and Non-neuronal Cells)
  • Pro-inflammatory Cytokines Could Upregulate the Expressions of MicroRNAs in Hearing Disorders
  • Antioxidants Could Regulate the Expressions of MicroRNAs in Hearing Disorders
  • Studies on Antioxidants in Hearing Disorders
  • Animal Studies
  • Human Studies
  • Potential Reasons for Suboptimal Beneficial Effects with Individual Micronutrients in Hearing Disorders
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • Activation of Nrf2 During Acute Oxidative Stress
  • Failure to Activate Nrf2 During Chronic Oxidative Stress
  • Antioxidants Activate ROS-Resistant Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Importance of Activation of Nrf2 in Auditory Cells
  • Current Prevention and Treatments Strategies
  • Reducing Oxidative Stress Level
  • Reducing Inflammation Level
  • Reducing Glutamate Level
  • Proposed Micronutrients for Simultaneously Reducing Oxidative Stress, Inflammation, and Glutamate Levels in Hearing Disorders
  • Prevention of Hearing Disorders
  • Primary Prevention
  • Secondary Prevention
  • Improved Management
  • Conclusions
  • References
  • Chapter 12: Micronutrients in Improvement of the Standard Therapy in Posttraumatic Stress Disorder (PTSD)
  • Introduction
  • Prevalence and Cost of PTSD
  • Symptoms of PTSD
  • Brain Pathology of PTSD
  • MicroRNAs in PTSD
  • Evidence for Increased Oxidative Stress in PTSD
  • Evidence for Chronic Inflammation in PTSD
  • Evidence for Increased Release of Glutamate and Decreased Levels of GABA in PTSD
  • Glutamate and GABA Levels in PTSD
  • Studies on Antioxidants in PTSD
  • Omega-3-Fatty Acids
  • Curcumin
  • Resveratrol
  • Pentoxifylline and Tempol
  • Flavonoids
  • Valproic Acid
  • Blueberry-Rich Diet
  • Effect of Multiple Micronutrients in Veterans
  • Potential Reasons for the Failure of Individual Micronutrients in Producing Consistent Benefits in Human
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • Activation of Nrf2 During Acute Oxidative Stress
  • Failure to Activate Nrf2 During Chronic Oxidative Stress
  • Antioxidants Activate ROS-Resistant Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Proposed Micronutrient Mixture for Optimally Reducing Oxidative Stress, Chronic Inflammation, and Glutamate Levels
  • Reducing Oxidative Stress
  • Reducing Chronic Inflammation
  • Reducing Glutamate Release and Toxicity
  • Prevention of PTSD
  • Primary Prevention of PTSD
  • Secondary Prevention of PTSD
  • Standard Therapy in PTSD
  • Improved Management of PTSD
  • Diet and Lifestyle Recommendations for PTSD
  • Conclusions
  • References
  • Chapter 13: Micronutrients in Improvement of the Standard Therapy in Traumatic Brain Injury
  • Introduction
  • Incidence, Prevalence, and Cost of TBI
  • Concussion in USA Population
  • National Football League (NFL)
  • High School and College Sports
  • US Veterans
  • US Civilian
  • Penetrating TBI (pTBI)
  • US Troops
  • US Civilian
  • Cost
  • Causes of Concussion
  • Causes of Penetrating TBI (pTBI)
  • Acute Symptoms of Concussion
  • Acute Symptoms of pTBI
  • Long-Term Health Consequences of TBI
  • Concussion
  • pTBI
  • Neuropathology of TBI
  • Concussion
  • pTBI
  • Scoring System of Severity of TBI
  • MicroRNAs in Pathogenesis of TBI
  • MicroRNAs as Potential Biomarkers for TBI
  • Evidence for Increased Oxidative Stress in Concussion
  • Animal Models
  • Humans
  • Evidence for Increased Inflammation in Concussion
  • Animal Models
  • Humans
  • Evidence for Increased Glutamate Level in Concussion
  • Molecular Changes in the Brain after Concussion
  • Evidence for Increased Oxidative Stress after pTBI
  • Animal Models
  • Humans
  • Oxidative Stress and Mitochondrial Dysfunction after pTBI
  • Animal Models
  • Humans
  • Evidence for Increase Levels of Markers of Inflammation after pTBI
  • Animal Models
  • Humans
  • Evidence for Increased Glutamate Level after pTBI
  • Animal Models
  • Humans
  • Role of Matrix Metalloproteinases (MMPS) after Severe TBI
  • Studies on the Effects of Single Antioxidants after TBI
  • Animal Models
  • Humans
  • Potential Reasons for Inconsistent Results with Individual Micronutrients in Other Neurodegenerative Diseases
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • Activation of Nrf2 During Acute Oxidative Stress
  • Failure to Activate Nrf2 During Chronic Oxidative Stress
  • Antioxidants Activate ROS-Resistant Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Nrf2 in TBI
  • Reducing Oxidative Stress Level
  • Reducing Inflammation Level
  • Reducing Glutamate Level
  • Proposed Micronutrients for Reducing Oxidative Stress, Inflammation, and Glutamate Levels in TBI
  • Toxicity of Ingredients in Proposed Micronutrient Preparation
  • Prevention Studies with Proposed Micronutrient Mixture in TBI
  • Primary Prevention
  • Secondary Prevention
  • Standard Therapy of TBI
  • Proposed Micronutrients in Combination with Standard Therapy
  • Diet and Lifestyle Recommendations for TBI
  • Conclusions
  • References
  • Chapter 14: Micronutrients in Prevention and Improvement of the Standard Therapy in HIV/AIDS
  • Introduction
  • History, Prevalence, Incidence, and Cost of HIV/AIDS
  • History of HIV/AIDS
  • Prevalence of HIV Infection
  • Incidence of HIV Infection
  • Cost of Treating HIV Infection
  • Role of Immune Function in HIV Infection
  • Micronutrient Deficiency Impairs Immune Function
  • Illicit Drugs Impair Immune Function
  • Evidence for Increased Oxidative Stress Enhancing the Progression of HIV Infection
  • Evidence for Increased Inflammation Enhancing the Progression of HIV Infection
  • Evidence for Micronutrients Reducing Progression of HIV Infection
  • Potential Reasons for Inconsistent Results with Micronutrients in Patients with HIV/AIDS
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • Activation of Nrf2 During Acute Oxidative Stress
  • Failure of ROS to Activate Nrf2 During Chronic Oxidative Stress
  • Antioxidants Activate ROS-Resistant Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Nrf2 in Patients with HIV Infection
  • Reducing Oxidative Stress Level in HIV-Infected People
  • Reducing Inflammation Level in HIV-Infected People
  • Proposed Micronutrient Mixture for Reducing Oxidative Stress and Inflammation Levels in Patients with HIV Infection
  • Toxicity of Ingredients in Proposed Micronutrient Mixture
  • Primary Prevention Against HIV Infection
  • Secondary Prevention for Reducing the Progression of HIV Infection
  • Treatments of HIV/AIDS
  • Antiviral Therapy in Reducing the Risk of Transmission From Mother to Infants
  • Proposed Micronutrient Mixture in Combination with Antiviral Drugs
  • Conclusions
  • References
  • Chapter 15: Improved Management of Autism Spectrum Disorder (ASD) by Micronutrients
  • Introduction
  • Prevalence and Cost of ASD
  • Prevalence
  • Cost
  • Environmental and Genetic Factors
  • Environmental Factors
  • Health Conditions
  • Genetic Factors
  • Major Symptoms of ASD
  • Brain Changes in ASD
  • MicroRNAs in ASD
  • MicroRNAs
  • MicroRNAs in Serum
  • MicroRNAs in Saliva
  • MicroRNAs in Autopsied Brain Samples
  • MicroRNAs in Cell Culture
  • MicroRNAs in Animals
  • Evidence for Increased Oxidative Stress in ASD
  • Human Studies
  • Cell Culture Models
  • Evidence for Increased Inflammation in ASD
  • Imbalances Between Neuronal Excitation and Inhibition
  • Human Studies
  • Use of Single Antioxidants in the Management of ASD
  • Human Studies
  • Animal Studies
  • Studies with Individual Antioxidants in Human Neurodegenerative Diseases
  • Regulation of Activation of Nrf2
  • Reactive Oxygen Species (ROS) Activates Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Existence of ROS-Resistant Nrf2
  • Antioxidants Activate ROS-Resistant Nrf2
  • L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
  • Activation of Nrf2 by MicroRNAs
  • Suppression of Chronic Inflammation
  • Inhibition of Release and Toxicity of Glutamate
  • Drug Treatment in Human ASD
  • Drug Treatment in Animal ASD Models
  • Proposed Mixture of Micronutrients for Improved Management of ASD
  • Conclusions
  • References
  • Chapter 16: Micronutrients in the Management of Prion Disease
  • Introduction
  • Incidence of Prion Disease
  • Types of Prion Disease
  • Modes of Transmission of Prion Disease to the Brain
  • Pathological Changes in the Brain
  • Symptoms of Prion Disease
  • Factors Facilitating Conversion of PrPc to PrPsc and Mechanisms of Proliferation of PrPsc
  • Effect of Mutations in PRNP Gene
  • Role of Exosomes
  • Effects on Polymorphisms of PNRP Gene
  • Effects of Increased Oxidative Stress
  • Oxidation of Methionine Residues in PrPc
  • Effects of PrPsc-Induced Inflammation in the Brain
  • Mechanisms of Neurotoxicity
  • MicroRNAs in Prion Disease
  • Studies with Individual Antioxidants and Phytochemicals in Models of Prion Diseases
  • Studies with Individual Antioxidants in Other Neurodegenerative Diseases
  • Regulation of Activation of Nrf2
  • Reactive Oxygen Species (ROS) Activates Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Existence of ROS-Resistant Nrf2 in Prion Disease
  • Antioxidants Activate of ROS-Resistant Nrf2
  • L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
  • Activation of Nrf2 by MicroRNAs
  • Suppression of Chronic Inflammation
  • Proposed Mixture of Micronutrients in Prevention and Improved Management of Prion Disease
  • Prevention of Prion Disease
  • Improved Management of Prion Disease
  • Conclusions
  • References
  • Chapter 17: Micronutrients for Improved Management of Huntington's Disease
  • Introduction
  • Incidence, Prevalence, and Cost of HD
  • Incidence and Prevalence
  • Cost
  • Signs and Symptoms
  • Pathology of the Brain in HD
  • Human Studies
  • Animal Studies
  • Receptor Abnormalities in HD
  • Dopamine Receptors
  • Cannabinoid Receptors
  • Adenosine Receptors
  • Transcriptional Deregulation in HD
  • Histone Deacetylation
  • Pre-translational Modification of Proteins in HD
  • MicroRNAs
  • MicroRNAs in Brain Cell Pathology and Protection
  • MicroRNAs in Plasma
  • Post-translational Modification of Proteins in HD
  • Evidence for Increased Oxidative Stress as an Early Event in the Onset of HD Symptoms
  • Studies on Asymptomatic and Symptomatic Individuals
  • Aggregation of HD Protein
  • Studies on Animal Models of HD
  • Studies on Cell Culture Models of HD
  • Mitochondrial Dysfunction in Asymptomatic and Symptomatic Individuals Carrying HD Gene
  • Evidence for Increased Chronic Inflammation in HD
  • Studies on Asymptomatic and Symptomatic Individuals
  • Studies on Animal Models of HD
  • Increased Glutamate Levels and Glutamate Receptor Activation in HD
  • GABA Receptors in Asymptomatic and Symptomatic Individuals
  • Use of Single Antioxidants, Phytochemicals, and B-Vitamins in the Management of HD
  • Alpha-Tocopherol (Vitamin E)
  • Vitamin C
  • N-Acetylcysteine (NAC)
  • Alpha-Lipoic Acid
  • Coenzyme Q10
  • L-Carnitine
  • Lycopene and Epigallocatechin
  • Melatonin
  • Curcumin
  • Resveratrol
  • Ginkgo biloba Extract and Olive Oil
  • Probucol
  • B-Vitamins
  • Studies with Individual Antioxidants in Other Human Neurodegenerative Diseases
  • Regulation of Activation of Nrf2
  • Reactive Oxygen Species (ROS) Activates Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Existence of ROS-Resistant Nrf2
  • Antioxidants Activate ROS-Resistant Nrf2
  • L-Carnitine Activates Nrf2 by a ROS-Dependent Mechanism
  • Activation of Nrf2 by MicroRNAs
  • Nrf2 in HD
  • Suppression of Oxidative Stress by Nrf2 and Antioxidants
  • Suppression of Chronic Inflammation by Nrf2 and Antioxidants
  • Inhibition of Release and Toxicity of Glutamate by Antioxidants and B-Vitamins
  • Proposed Mixture of Micronutrients for Improved Management of HD
  • Prevention or Delaying the Onset of Symptoms by Proposed Micronutrient Mixture?
  • Proposed Micronutrient Mixture in Combination with Standard Treatment
  • Current Treatments of HD
  • Movement Disorder Drugs
  • Antipsychotic Drugs
  • Other Medications
  • Medications for Psychiatric Disorders
  • Antidepressants
  • Mood-Stabilizing Drugs
  • Clinical Studies with Additional Drugs in HD
  • Psychotherapy
  • Speech Therapy
  • Physical Therapy
  • Conclusions
  • References
  • Chapter 18: Micronutrients in Protecting Against Late Adverse Health-Effects of Diagnostic Radiation Doses
  • Introduction
  • Sources of Background Radiation
  • Dose-Estimate of Diagnostic Radiation Procedures and Per Capita Dose
  • Estimated Dose Received by Radiation Workers
  • Estimated Dose Received by Crews of Commercial Flight
  • Health Effects of Low Doses of Radiation
  • Effects of Background Radiation on Human Health
  • Induction of Mutations
  • Induction of Radiation-Induced Cancer
  • Impact of Chemical and Biological Carcinogens, and Tumor Promoters on Radiation-Induced Cancer
  • Models Used for Risk Estimates of Radiation-Induced Cancer
  • Cancer Risks in Populations Exposed to Diagnostic Radiation Procedures
  • Adults and Children
  • Cancer Risk in Children Exposed in Utero During Atomic Bombing of Hiroshima and Nagasaki
  • Risk of Childhood Cancer after Irradiation of Fetuses
  • Women Receiving Gonadal Doses of Radiation Before Conception
  • Cancer Risk Among Radiation Workers
  • Cancer Risk in Military and Civilian Pilots and Flight Attendants
  • Cancer Risk Among Frequent Flyers
  • Risk of Low-Dose Radiation-Induced Nonneoplastic Diseases
  • Reducing Oxidative Stress and Inflammation by Single Antioxidants in Humans
  • Reducing Damage by Multiple Antioxidants in Humans
  • Proposed Strategy to Simultaneously Reduce Oxidative Stress and Inflammation
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • Activation of Nrf2 During Acute Oxidative Stress
  • Failure to Activate Nrf2 During Chronic Oxidative Stress
  • Antioxidants Activate ROS-Resistant Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Proposed Micronutrients for Simultaneously Reducing Oxidative Stress and Inflammation
  • Conclusions
  • References
  • Chapter 19: Micronutrients in Protecting Against Lethal Doses of Ionizing Radiation
  • Introduction
  • Unit of Radiation Doses
  • High-Dose Radiation-Induced Damage
  • Bone Marrow Syndrome
  • Gastrointestinal (GI) Syndrome
  • Central Nervous System (CNS) Syndrome
  • High-Dose Radiation-Induced Damage to Organs
  • Risk of Developing Cancer Among Survivors of High Doses of Radiation
  • Risk of Developing Non-neoplastic Diseases Among Survivors of High Doses of Radiation
  • MicroRNAs in Radiation Damage
  • MicroRNAs
  • Irradiation Alters the Expression of MicroRNAs in Normal Cells
  • MicroRNAs in Radiation-Induced Bystandard Effect
  • MicroRNAs as Biomarkers of Radiation Damage
  • Brief History of Radiation Protection Studies
  • Radiation Protection Studies with Antioxidants in Cell Culture Models
  • Radiation Protection Studies with Antioxidants in Animal Models
  • Radiation Protection Study with a Mixture of Multiple Antioxidants Administered Orally Before and after Irradiation in Sheep
  • Radiation Protection Study with a Mixture of Multiple Antioxidants Administered Orally Before and after Irradiation in Rabbits
  • Radiation Protection Study with a Mixture of Multiple Antioxidants Administered Orally Before Irradiation in Mice
  • Radiation Protection Study with a Mixture of Multiple Antioxidants Administered Through the Diet Before and after Irradiation in Drosophila Melanogaster
  • Radiation Protection Studies with Antioxidants in Humans
  • Rationale for Using Multiple Antioxidants in Radiation Protection
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • Activation of Nrf2 During Acute Oxidative Stress
  • Activation of Nrf2 During Acute Phase of Irradiation
  • Failure to Activate Nrf2 During Radiation-Induced Chronic Phase of Irradiation
  • Antioxidants Activate ROS-Resistant Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Reducing Oxidative Stress Level for Radiation Protection
  • Reducing Inflammation Level for Radiation Protection
  • Proposed Micronutrients for Radiation Protection
  • Guidelines for the Management of Large Number of People Irradiated with Lethal Doses of Radiation
  • Radiation Mitigating Agents
  • Chemical Agents for Mitigating Radiation Injury
  • Antibiotics, Blood, and Electrolytes
  • Erythropoietin
  • Statins
  • Cytokines and Growth Factors
  • Biological Agents for Mitigating Radiation Injury
  • Bone Marrow and Newborn Liver Cells Transplant
  • The Chernobyl Experience in Treating Irradiated Individuals
  • Proposed Micronutrient Mixture for the Treatment of Bone Marrow Syndrome
  • Proposed Micronutrient Mixture for the Treatment of GI Syndrome
  • Conclusions
  • References
  • Chapter 20: Micronutrients in Prevention and Improvement of the Standard Therapy in Arthritis
  • Introduction
  • Prevalence and Cost of Arthritis
  • Types of Arthritis
  • Rheumatoid Arthritis (RA)
  • Osteoarthritis (OA)
  • Juvenile Rheumatoid Arthritis (JRA)
  • Evidence for the Role of Oxidative Stress
  • Evidence for the Role of Inflammation
  • Role of Antioxidants in Arthritis
  • Studies on Animal Models of Arthritis
  • Human Cell Culture Models of Arthritis
  • Studies on Human RA and OA
  • Prevention Strategies
  • Potential Reasons for Inconsistent Results
  • Activation of Nrf2 (Nuclear Factor-Erythroid-2-Related Factor 2)
  • Nrf2
  • Activation of Nrf2 During Acute Oxidative Stress
  • Failure to Activate Nrf2 During Chronic Oxidative Stress
  • Antioxidants Activate ROS-Resistant Nrf2
  • Binding of Nrf2 with ARE in the Nucleus
  • Importance of Activation of Nrf2 in Arthritis
  • Reducing Oxidative Stress Level
  • Reducing Inflammation Level
  • Proposed Micronutrients for Simultaneously Reducing Oxidative Stress and Inflammation in Arthritis
  • Primary Prevention of Arthritis
  • Treatment Strategies of Arthritis
  • Low-Dose Methotrexate (MTX)
  • Anti-cytokines Therapy
  • Toxicity of MTX and Anti-cytokine Therapy
  • Treatment with Glucosamine and Chondroitin
  • Treatment with Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
  • Treatment with Complementary Medicine
  • Proposed Micronutrient Mixture in Combination with Standard Therapy in Patients with Arthritis
  • Diet and Lifestyle Recommendations for High Risk Populations and Patients with Arthritis
  • Conclusions
  • References
  • Chapter 21: Misconceptions about the Functions and Value of Antioxidants in Health and Disease
  • Introduction
  • Misconception 1
  • Misconception 2
  • Misconception 3
  • Misconception 4
  • Misconception 5
  • Misconception 6
  • Misconception 7
  • Misconception 8
  • Misconception 9
  • Misconception 10
  • Misconception 11
  • Misconception 12
  • Misconception 13
  • Misconception 14
  • Misconception 15
  • Misconception 16
  • Misconception 17
  • Conclusions
  • Chapter 22: Dietary Reference Intakes of Selected Micronutrients
  • Introduction
  • RDA (DRI)
  • Adequate Intake (AI)
  • Tolerable Upper Intake Level (UL)
  • Conclusions
  • Index
DNB DDC Sachgruppen

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