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Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer

Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer

9780470584927
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Description
The book addresses controversies related to the origins of cancer and provides solutions to cancer management and prevention. It expands upon Otto Warburgs well-known theory that all cancer is a disease of energy metabolism.  However, Warburg did not link his theory to the hallmarks of cancer and thus his theory was discredited.  This book aims to provide evidence, through case studies, that cancer is primarily a metabolic disease requring metabolic solutions for its management and prevention.  Support for this position is derived from critical assessment of current cancer theories.  Brain cancer case studies are presented as a proof of principle for metabolic solutions to disease management, but similarities are drawn to other types of cancer, including breast and colon, due to the same cellular mutations that they demonstrate.
Product Details
75946
9780470584927
9780470584927

Data sheet

Publication date
2012
Issue number
1
Cover
hard cover
Pages count
438
Dimensions (mm)
165.00 x 242.00
Weight (g)
818
  • Forword xiii

    Preface xv

    1. Images of Cancer 1

    How Cancer is Viewed 2

    References 13

    2. Confusion Surrounds the Origin of Cancer 15

    The Oncogenic Paradox 18

    Hallmarks of Cancer 18

    Reassessment 26

    References 27

    3. Cancer Models 31

    Problems with Some Cancer Models 31

    Animal Charges as a Major Impediment to Cancer Research 38

    Problems with Tumor Histological Classification 39

    Personal Perspective on Cancer 44

    References 45

    4. Energetics of Normal Cells and Cancer Cells 47

    Metabolic Homeostasis 47

    The Constancy of the ?GATP 54

    ATP Production in Normal Cells and Tumor Cells 55

    Energy Production Through Glucose Fermentation 57

    Glutaminolysis with or without Lactate Production 61

    Transamination Reactions 64

    TCA Cycle, Substrate-Level Phosphorylation 66

    Cholesterol Synthesis and Hypoxia 67

    Summary 67

    References 68

    5. Respiratory Dysfunction in Cancer Cells 73

    Normal Mitochondria 74

    Morphological Defects in Tumor Cell Mitochondria 77

    Proteomic Abnormalities in Tumor Cell Mitochondria 79

    Lipidomic Abnormalities in Tumor Cell Mitochondria 81

    Cardiolipin: A Mitochondrial-Specific Lipid 83

    Cardiolipin and Abnormal Energy Metabolism in Tumor Cells 85

    Complicating Influence of the In Vitro Growth Environment on Cardiolipin Composition and Energy Metabolism 92

    Mitochondrial Uncoupling and Cancer 97

    Cancer Cell Heat Production and Uncoupled Mitochondria 98

    Personal Perspective 99

    Summary 100

    References 101

    6. The Warburg Dispute 107

    Sidney Weinhouse’s Criticisms of the Warburg Theory 108

    Alan Aisenberg’s Criticisms of the Warburg Theory 110

    Sidney Colowick’s Assessment of the Aisenberg Monograph 113

    Apples and Oranges 114

    References 116

    7. Is Respiration Normal in Cancer Cells? 119

    Pseudo-Respiration 119

    How Strong is the Scientific Evidence Showing that Tumor Cells can Produce Energy Through OxPhos? 124

    OxPhos Origin of ATP in Cancer Cells Reevaluated 124

    What About OxPhos Expression in Other Tumors? 127

    The Pedersen Review on Tumor Mitochondria and the Bioenergetics of Cancer Cells 128

    References 129

    8. Is Mitochondrial Glutamine Fermentation a Missing Link in the Metabolic Theory of Cancer? 133

    Amino Acid Fermentation can Maintain Cellular Energy Homeostasis During Anoxia 133

    Evidence Suggesting that Metastatic Mouse Cells Derive Energy from Glutamine Fermentation 134

    Fermentation Energy Pathways can Drive Cancer Cell Viability Under Hypoxia 138

    Competing Explanations for the Metabolic Origin of Cancer 141

    Chapter Summary 143

    References 143

    9. Genes, Respiration, Viruses, and Cancer 145

    Does Cancer have a Genetic Origin? 145

    Respiratory Insufficiency as the Origin of Cancer 150

    Germline Mutations, Damaged Respiration, and Cancer 154

    Somatic Mutations and Cancer 158

    Revisiting the Oncogene Theory 160

    Mitochondrial Mutations and the Absence or Presence of Cancer 163

    Viral Infection, Damaged Respiration, and the Origin of Cancer 165

    Summary 168

    References 168

    10. Respiratory Insufficiency, the Retrograde Response, and the Origin of Cancer 177

    The Retrograde (RTG) Response: An Epigenetic System Responsible for Nuclear Genomic Stability 177

    Inflammation Injures Cellular Respiration 181

    Hypoxia-Inducible Factor (HIF) Stability is Required for the Origin of Cancer 182

    Mitochondria and the Mutator Phenotype 183

    Calcium Homeostasis, Aneuploidy, and Mitochondrial Dysfunction 186

    Mitochondrial Dysfunction and Loss of Heterozygosity (LOH) 187

    Tissue Inflammation, Damaged Respiration, and Cancer 188

    References 189

    11. Mitochondria: The Ultimate Tumor Suppressor 195

    Mitochondrial Suppression of Tumorigenicity 195

    Normal Mitochondria Suppress Tumorigenesis in Cybrids 196

    Evidence from rho0 Cells 198

    Normal Mitochondria Suppress Tumorigenesis In Vivo 199

    Normal Mouse Cytoplasm Suppresses Tumorigenic Phenotypes 200

    Enhanced Differentiation and Suppressed Tumorigenicity in the Liver Microenvironment 202

    Summary of Nuclear-Cytoplasmic Transfer Experiments 203

    References 204

    12. Abnormalities in Growth Control, Telomerase Activity, Apoptosis, and Angiogenesis Linked to Mitochondrial Dysfunction 207

    Growth Signaling Abnormalities and Limitless Replicative Potential 208

    Linking Telomerase Activity to Cellular Energy and Cancer 209

    Evasion of Programmed Cell Death (Apoptosis) 209

    Sustained Vascularity (Angiogenesis) 210

    References 211

    13. Metastasis 215

    Metastasis Overview 215

    Cellular Origin of Metastasis 217

    Macrophages and Metastasis 221

    Carcinoma of Unknown Primary Origin 232

    Many Metastatic Cancers Express Multiple Macrophage Properties 233

    Linking Metastasis to Mitochondrial Dysfunction 233

    Revisiting the “Seed and Soil” Hypothesis of Metastasis 235

    Revisiting the Mesenchymal Epithelial Transition (MET) 236

    Genetic Heterogeneity in Cancer Metastases 237

    Transmissible Metastatic Cancers 240

    The Absence of Metastases in Crown-Gall Plant Tumors 240

    Chapter Summary 241

    References 241

    14. Mitochondrial Respiratory Dysfunction and the Extrachromosomal Origin of Cancer 253

    Connecting the Links 254

    Addressing the Oncogenic Paradox 255

    Is Cancer Many Diseases or a Singular Disease of Energy Metabolism? 258

    References 258

    15. Nothing in Cancer Biology Makes Sense Except in the Light of Evolution 261

    Revisiting Growth Advantage of Tumor Cells, Mutations, and Evolution 262

    Tumor Cell Fitness in Light of the Evolutionary Theory of Rick Potts 269

    Cancer Development and Lamarckian Inheritance 271

    Can Teleology Explain Cancer? 272

    References 272

    16. Cancer Treatment Strategies 277

    Current Status of Cancer Treatment 277

    The “Standard of Care” for Glioblastoma Management 280

    References 285

    17. Metabolic Management of Cancer 291

    Is it Dietary Content or Dietary Composition that Primarily Reduces Tumor Growth? 292

    Dietary Energy Reduction and Therapeutic Fasting in Rodents and Humans 294

    Ketogenic Diets 295

    Glucagon and Insulin 297

    Basal Metabolic Rate 298

    Ketones and Glucose 298

    Metabolic Management of Brain Cancer Using the KD 299

    Glucose Accelerates Tumor Growth! 301

    Glucose Regulates Blood Levels of Insulin and Insulin-Like Growth Factor 1 302

    Dietary Energy Reduction is Antiangiogenic 302

    Dietary Energy Reduction Targets Abnormal Tumor Vessels 307

    Dietary Energy Reduction is Proapoptotic 309

    Dietary Energy Reduction is Anti-Inflammatory 310

    Targeting Energy Metabolism in Advanced Cancer 314

    Differential Response of Normal Cells and Tumor Cells to Energy Stress 316

    Dietary Energy Reduction is Anti-Invasive in Experimental Glioblastoma 318

    Influence of Growth Site and Host on Tumor Progression 322

    Implications of Dietary Energy Reduction for Anticancer Therapeutics 324

    Targeting Glucose 325

    Metformin 326

    Synergistic Interaction of the Restricted Ketogenic Diet (KD-R) and 2-Deoxyglucose (2-DG) 327

    Can Synergy Occur with the KD-R and Hyperbaric Oxygen Therapy? 331

    Targeting Glutamine 333

    Glutamine Targeting Inhibits Systemic Metastasis 334

    Targeting Phagocytosis 339

    Targeting the Microenvironment 340

    Dietary Energy Reduction as a Mitochondrial Enhancement Therapy (MET) 341

    Summary 341

    References 341

    18. Patient Implementation of Metabolic Therapies for Cancer Management 355

    Introduction 355

    Guidelines for Implementing the Restricted Ketogenic Diet as a Treatment Strategy for Cancer 356

    Complicating Issues for Implementing the KD-R as a Treatment Strategy for Cancer 366

    Radiation and Chemotherapy is a Standard Treatment for Many Malignant Cancers 366

    Compliance 367

    Cancer as a Genetic Disease 367

    Mechanism of Action? 368

    Cachexia 368

    Summary 369

    References 370

    19. Cancer Prevention 375

    Cell Phones and Cancer 376

    Alzheimer’s Disease and Cancer Risk 377

    Ketone Metabolism Reduces Cancer Risk 378

    Mitochondrial Enhancement Therapy 379

    Therapeutic Fasting and Cancer Prevention 379

    Autophagy and Autolytic Cannibalism: A Thermodynamic Approach to Cancer Prevention 381

    Cancer Prevention by Following Restricted Ketogenic Diet 382

    References 384

    20. Case Studies and Personal Experiences in Using the Ketogenic Diet for Cancer Management 387

    Effects of a Ketogenic Diet on Tumor Metabolism and Nutritional Status in Pediatric Oncology Patients: Comments from Dr. Linda Nebeling 387

    Raffi’s Story: Comments from Miriam Kalamian 389

    Biological Plausibility that Cancer is a Metabolic Disease Dependent for Growth on Glucose and Glutamine: Comments from Dr. Bomar Herrin 395

    Using the Restricted Ketogenic Diet for Brain Cancer Management: Comments from Neuro-Oncologist, Dr. Kraig Moore 397

    The Ketogenic Diet for Brain Cancer Management: Comments from Beth Zupec-Kania 400

    Summary 402

    References 403

    21. Conclusions 405

    Major Conclusions 407

    References 408

    Index 409

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