{"product_id":"cancer-as-a-metabolic-disease-isbn-9780470584927","title":"Cancer as a Metabolic Disease","description":"The book addresses controversies related to the origins of cancer and provides solutions to cancer management and prevention. It expands upon Otto Warburg's 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. \u003cp\u003eForword xiii\u003c\/p\u003e \u003cp\u003ePreface xv\u003c\/p\u003e \u003cp\u003e\u003cb\u003e1. Images of Cancer 1\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eHow Cancer is Viewed 2\u003c\/p\u003e \u003cp\u003eReferences 13\u003c\/p\u003e \u003cp\u003e\u003cb\u003e2. Confusion Surrounds the Origin of Cancer 15\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eThe Oncogenic Paradox 18\u003c\/p\u003e \u003cp\u003eHallmarks of Cancer 18\u003c\/p\u003e \u003cp\u003eReassessment 26\u003c\/p\u003e \u003cp\u003eReferences 27\u003c\/p\u003e \u003cp\u003e\u003cb\u003e3. Cancer Models 31\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eProblems with Some Cancer Models 31\u003c\/p\u003e \u003cp\u003eAnimal Charges as a Major Impediment to Cancer Research 38\u003c\/p\u003e \u003cp\u003eProblems with Tumor Histological Classification 39\u003c\/p\u003e \u003cp\u003ePersonal Perspective on Cancer 44\u003c\/p\u003e \u003cp\u003eReferences 45\u003c\/p\u003e \u003cp\u003e\u003cb\u003e4. Energetics of Normal Cells and Cancer Cells 47\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eMetabolic Homeostasis 47\u003c\/p\u003e \u003cp\u003eThe Constancy of the ∆\u003ci\u003eG\u003c\/i\u003e’\u003csub\u003eATP\u003c\/sub\u003e 54\u003c\/p\u003e \u003cp\u003eATP Production in Normal Cells and Tumor Cells 55\u003c\/p\u003e \u003cp\u003eEnergy Production Through Glucose Fermentation 57\u003c\/p\u003e \u003cp\u003eGlutaminolysis with or without Lactate Production 61\u003c\/p\u003e \u003cp\u003eTransamination Reactions 64\u003c\/p\u003e \u003cp\u003eTCA Cycle, Substrate-Level Phosphorylation 66\u003c\/p\u003e \u003cp\u003eCholesterol Synthesis and Hypoxia 67\u003c\/p\u003e \u003cp\u003eSummary 67\u003c\/p\u003e \u003cp\u003eReferences 68\u003c\/p\u003e \u003cp\u003e\u003cb\u003e5. Respiratory Dysfunction in Cancer Cells 73\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eNormal Mitochondria 74\u003c\/p\u003e \u003cp\u003eMorphological Defects in Tumor Cell Mitochondria 77\u003c\/p\u003e \u003cp\u003eProteomic Abnormalities in Tumor Cell Mitochondria 79\u003c\/p\u003e \u003cp\u003eLipidomic Abnormalities in Tumor Cell Mitochondria 81\u003c\/p\u003e \u003cp\u003eCardiolipin: A Mitochondrial-Specific Lipid 83\u003c\/p\u003e \u003cp\u003eCardiolipin and Abnormal Energy Metabolism in Tumor Cells 85\u003c\/p\u003e \u003cp\u003eComplicating Influence of the In Vitro Growth Environment on Cardiolipin Composition and Energy Metabolism 92\u003c\/p\u003e \u003cp\u003eMitochondrial Uncoupling and Cancer 97\u003c\/p\u003e \u003cp\u003eCancer Cell Heat Production and Uncoupled Mitochondria 98\u003c\/p\u003e \u003cp\u003ePersonal Perspective 99\u003c\/p\u003e \u003cp\u003eSummary 100\u003c\/p\u003e \u003cp\u003eReferences 101\u003c\/p\u003e \u003cp\u003e\u003cb\u003e6. The Warburg Dispute 107\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eSidney Weinhouse’s Criticisms of the Warburg Theory 108\u003c\/p\u003e \u003cp\u003eAlan Aisenberg’s Criticisms of the Warburg Theory 110\u003c\/p\u003e \u003cp\u003eSidney Colowick’s Assessment of the Aisenberg Monograph 113\u003c\/p\u003e \u003cp\u003eApples and Oranges 114\u003c\/p\u003e \u003cp\u003eReferences 116\u003c\/p\u003e \u003cp\u003e\u003cb\u003e7. Is Respiration Normal in Cancer Cells? 119\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003ePseudo-Respiration 119\u003c\/p\u003e \u003cp\u003eHow Strong is the Scientific Evidence Showing that Tumor Cells can Produce Energy Through OxPhos? 124\u003c\/p\u003e \u003cp\u003eOxPhos Origin of ATP in Cancer Cells Reevaluated 124\u003c\/p\u003e \u003cp\u003eWhat About OxPhos Expression in Other Tumors? 127\u003c\/p\u003e \u003cp\u003eThe Pedersen Review on Tumor Mitochondria and the Bioenergetics of Cancer Cells 128\u003c\/p\u003e \u003cp\u003eReferences 129\u003c\/p\u003e \u003cp\u003e\u003cb\u003e8. Is Mitochondrial Glutamine Fermentation a Missing Link in the Metabolic Theory of Cancer? 133\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eAmino Acid Fermentation can Maintain Cellular Energy Homeostasis During Anoxia 133\u003c\/p\u003e \u003cp\u003eEvidence Suggesting that Metastatic Mouse Cells Derive Energy from Glutamine Fermentation 134\u003c\/p\u003e \u003cp\u003eFermentation Energy Pathways can Drive Cancer Cell Viability Under Hypoxia 138\u003c\/p\u003e \u003cp\u003eCompeting Explanations for the Metabolic Origin of Cancer 141\u003c\/p\u003e \u003cp\u003eChapter Summary 143\u003c\/p\u003e \u003cp\u003eReferences 143\u003c\/p\u003e \u003cp\u003e\u003cb\u003e9. Genes, Respiration, Viruses, and Cancer 145\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eDoes Cancer have a Genetic Origin? 145\u003c\/p\u003e \u003cp\u003eRespiratory Insufficiency as the Origin of Cancer 150\u003c\/p\u003e \u003cp\u003eGermline Mutations, Damaged Respiration, and Cancer 154\u003c\/p\u003e \u003cp\u003eSomatic Mutations and Cancer 158\u003c\/p\u003e \u003cp\u003eRevisiting the Oncogene Theory 160\u003c\/p\u003e \u003cp\u003eMitochondrial Mutations and the Absence or Presence of Cancer 163\u003c\/p\u003e \u003cp\u003eViral Infection, Damaged Respiration, and the Origin of Cancer 165\u003c\/p\u003e \u003cp\u003eSummary 168\u003c\/p\u003e \u003cp\u003eReferences 168\u003c\/p\u003e \u003cp\u003e\u003cb\u003e10. Respiratory Insufficiency, the Retrograde Response, and the Origin of Cancer 177\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eThe Retrograde (RTG) Response: An Epigenetic System Responsible for Nuclear Genomic Stability 177\u003c\/p\u003e \u003cp\u003eInflammation Injures Cellular Respiration 181\u003c\/p\u003e \u003cp\u003eHypoxia-Inducible Factor (HIF) Stability is Required for the Origin of Cancer 182\u003c\/p\u003e \u003cp\u003eMitochondria and the Mutator Phenotype 183\u003c\/p\u003e \u003cp\u003eCalcium Homeostasis, Aneuploidy, and Mitochondrial Dysfunction 186\u003c\/p\u003e \u003cp\u003eMitochondrial Dysfunction and Loss of Heterozygosity (LOH) 187\u003c\/p\u003e \u003cp\u003eTissue Inflammation, Damaged Respiration, and Cancer 188\u003c\/p\u003e \u003cp\u003eReferences 189\u003c\/p\u003e \u003cp\u003e\u003cb\u003e11. Mitochondria: The Ultimate Tumor Suppressor 195\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eMitochondrial Suppression of Tumorigenicity 195\u003c\/p\u003e \u003cp\u003eNormal Mitochondria Suppress Tumorigenesis in Cybrids 196\u003c\/p\u003e \u003cp\u003eEvidence from rho\u003csup\u003e0\u003c\/sup\u003e Cells 198\u003c\/p\u003e \u003cp\u003eNormal Mitochondria Suppress Tumorigenesis In Vivo 199\u003c\/p\u003e \u003cp\u003eNormal Mouse Cytoplasm Suppresses Tumorigenic Phenotypes 200\u003c\/p\u003e \u003cp\u003eEnhanced Differentiation and Suppressed Tumorigenicity in the Liver Microenvironment 202\u003c\/p\u003e \u003cp\u003eSummary of Nuclear-Cytoplasmic Transfer Experiments 203\u003c\/p\u003e \u003cp\u003eReferences 204\u003c\/p\u003e \u003cp\u003e\u003cb\u003e12. Abnormalities in Growth Control, Telomerase Activity, Apoptosis, and Angiogenesis Linked to Mitochondrial Dysfunction 207\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eGrowth Signaling Abnormalities and Limitless Replicative Potential 208\u003c\/p\u003e \u003cp\u003eLinking Telomerase Activity to Cellular Energy and Cancer 209\u003c\/p\u003e \u003cp\u003eEvasion of Programmed Cell Death (Apoptosis) 209\u003c\/p\u003e \u003cp\u003eSustained Vascularity (Angiogenesis) 210\u003c\/p\u003e \u003cp\u003eReferences 211\u003c\/p\u003e \u003cp\u003e\u003cb\u003e13. Metastasis 215\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eMetastasis Overview 215\u003c\/p\u003e \u003cp\u003eCellular Origin of Metastasis 217\u003c\/p\u003e \u003cp\u003eMacrophages and Metastasis 221\u003c\/p\u003e \u003cp\u003eCarcinoma of Unknown Primary Origin 232\u003c\/p\u003e \u003cp\u003eMany Metastatic Cancers Express Multiple Macrophage Properties 233\u003c\/p\u003e \u003cp\u003eLinking Metastasis to Mitochondrial Dysfunction 233\u003c\/p\u003e \u003cp\u003eRevisiting the “Seed and Soil” Hypothesis of Metastasis 235\u003c\/p\u003e \u003cp\u003eRevisiting the Mesenchymal Epithelial Transition (MET) 236\u003c\/p\u003e \u003cp\u003eGenetic Heterogeneity in Cancer Metastases 237\u003c\/p\u003e \u003cp\u003eTransmissible Metastatic Cancers 240\u003c\/p\u003e \u003cp\u003eThe Absence of Metastases in Crown-Gall Plant Tumors 240\u003c\/p\u003e \u003cp\u003eChapter Summary 241\u003c\/p\u003e \u003cp\u003eReferences 241\u003c\/p\u003e \u003cp\u003e\u003cb\u003e14. Mitochondrial Respiratory Dysfunction and the Extrachromosomal Origin of Cancer 253\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eConnecting the Links 254\u003c\/p\u003e \u003cp\u003eAddressing the Oncogenic Paradox 255\u003c\/p\u003e \u003cp\u003eIs Cancer Many Diseases or a Singular Disease of Energy Metabolism? 258\u003c\/p\u003e \u003cp\u003eReferences 258\u003c\/p\u003e \u003cp\u003e\u003cb\u003e15. Nothing in Cancer Biology Makes Sense Except in the Light of Evolution 261\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eRevisiting Growth Advantage of Tumor Cells, Mutations, and Evolution 262\u003c\/p\u003e \u003cp\u003eTumor Cell Fitness in Light of the Evolutionary Theory of Rick Potts 269\u003c\/p\u003e \u003cp\u003eCancer Development and Lamarckian Inheritance 271\u003c\/p\u003e \u003cp\u003eCan Teleology Explain Cancer? 272\u003c\/p\u003e \u003cp\u003eReferences 272\u003c\/p\u003e \u003cp\u003e\u003cb\u003e16. Cancer Treatment Strategies 277\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eCurrent Status of Cancer Treatment 277\u003c\/p\u003e \u003cp\u003eThe “Standard of Care” for Glioblastoma Management 280\u003c\/p\u003e \u003cp\u003eReferences 285\u003c\/p\u003e \u003cp\u003e\u003cb\u003e17. Metabolic Management of Cancer 291\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eIs it Dietary Content or Dietary Composition that Primarily Reduces Tumor Growth? 292\u003c\/p\u003e \u003cp\u003eDietary Energy Reduction and Therapeutic Fasting in Rodents and Humans 294\u003c\/p\u003e \u003cp\u003eKetogenic Diets 295\u003c\/p\u003e \u003cp\u003eGlucagon and Insulin 297\u003c\/p\u003e \u003cp\u003eBasal Metabolic Rate 298\u003c\/p\u003e \u003cp\u003eKetones and Glucose 298\u003c\/p\u003e \u003cp\u003eMetabolic Management of Brain Cancer Using the KD 299\u003c\/p\u003e \u003cp\u003eGlucose Accelerates Tumor Growth! 301\u003c\/p\u003e \u003cp\u003eGlucose Regulates Blood Levels of Insulin and Insulin-Like Growth Factor 1 302\u003c\/p\u003e \u003cp\u003eDietary Energy Reduction is Antiangiogenic 302\u003c\/p\u003e \u003cp\u003eDietary Energy Reduction Targets Abnormal Tumor Vessels 307\u003c\/p\u003e \u003cp\u003eDietary Energy Reduction is Proapoptotic 309\u003c\/p\u003e \u003cp\u003eDietary Energy Reduction is Anti-Inflammatory 310\u003c\/p\u003e \u003cp\u003eTargeting Energy Metabolism in Advanced Cancer 314\u003c\/p\u003e \u003cp\u003eDifferential Response of Normal Cells and Tumor Cells to Energy Stress 316\u003c\/p\u003e \u003cp\u003eDietary Energy Reduction is Anti-Invasive in Experimental Glioblastoma 318\u003c\/p\u003e \u003cp\u003eInfluence of Growth Site and Host on Tumor Progression 322\u003c\/p\u003e \u003cp\u003eImplications of Dietary Energy Reduction for Anticancer Therapeutics 324\u003c\/p\u003e \u003cp\u003eTargeting Glucose 325\u003c\/p\u003e \u003cp\u003eMetformin 326\u003c\/p\u003e \u003cp\u003eSynergistic Interaction of the Restricted Ketogenic Diet (KD-R) and 2-Deoxyglucose (2-DG) 327\u003c\/p\u003e \u003cp\u003eCan Synergy Occur with the KD-R and Hyperbaric Oxygen Therapy? 331\u003c\/p\u003e \u003cp\u003eTargeting Glutamine 333\u003c\/p\u003e \u003cp\u003eGlutamine Targeting Inhibits Systemic Metastasis 334\u003c\/p\u003e \u003cp\u003eTargeting Phagocytosis 339\u003c\/p\u003e \u003cp\u003eTargeting the Microenvironment 340\u003c\/p\u003e \u003cp\u003eDietary Energy Reduction as a Mitochondrial Enhancement Therapy (MET) 341\u003c\/p\u003e \u003cp\u003eSummary 341\u003c\/p\u003e \u003cp\u003eReferences 341\u003c\/p\u003e \u003cp\u003e\u003cb\u003e18. Patient Implementation of Metabolic Therapies for Cancer Management 355\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eIntroduction 355\u003c\/p\u003e \u003cp\u003eGuidelines for Implementing the Restricted Ketogenic Diet as a Treatment Strategy for Cancer 356\u003c\/p\u003e \u003cp\u003eComplicating Issues for Implementing the KD-R as a Treatment Strategy for Cancer 366\u003c\/p\u003e \u003cp\u003eRadiation and Chemotherapy is a Standard Treatment for Many Malignant Cancers 366\u003c\/p\u003e \u003cp\u003eCompliance 367\u003c\/p\u003e \u003cp\u003eCancer as a Genetic Disease 367\u003c\/p\u003e \u003cp\u003eMechanism of Action? 368\u003c\/p\u003e \u003cp\u003eCachexia 368\u003c\/p\u003e \u003cp\u003eSummary 369\u003c\/p\u003e \u003cp\u003eReferences 370\u003c\/p\u003e \u003cp\u003e\u003cb\u003e19. Cancer Prevention 375\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eCell Phones and Cancer 376\u003c\/p\u003e \u003cp\u003eAlzheimer’s Disease and Cancer Risk 377\u003c\/p\u003e \u003cp\u003eKetone Metabolism Reduces Cancer Risk 378\u003c\/p\u003e \u003cp\u003eMitochondrial Enhancement Therapy 379\u003c\/p\u003e \u003cp\u003eTherapeutic Fasting and Cancer Prevention 379\u003c\/p\u003e \u003cp\u003eAutophagy and Autolytic Cannibalism: A Thermodynamic Approach to Cancer Prevention 381\u003c\/p\u003e \u003cp\u003eCancer Prevention by Following Restricted Ketogenic Diet 382\u003c\/p\u003e \u003cp\u003eReferences 384\u003c\/p\u003e \u003cp\u003e\u003cb\u003e20. Case Studies and Personal Experiences in Using the Ketogenic Diet for Cancer Management 387\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eEffects of a Ketogenic Diet on Tumor Metabolism and Nutritional Status in Pediatric Oncology Patients: Comments from Dr. Linda Nebeling 387\u003c\/p\u003e \u003cp\u003eRaffi’s Story: Comments from Miriam Kalamian 389\u003c\/p\u003e \u003cp\u003eBiological Plausibility that Cancer is a Metabolic Disease Dependent for Growth on Glucose and Glutamine: Comments from Dr. Bomar Herrin 395\u003c\/p\u003e \u003cp\u003eUsing the Restricted Ketogenic Diet for Brain Cancer Management: Comments from Neuro-Oncologist, Dr. Kraig Moore 397\u003c\/p\u003e \u003cp\u003eThe Ketogenic Diet for Brain Cancer Management: Comments from Beth Zupec-Kania 400\u003c\/p\u003e \u003cp\u003eSummary 402\u003c\/p\u003e \u003cp\u003eReferences 403\u003c\/p\u003e \u003cp\u003e\u003cb\u003e21. Conclusions 405\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eMajor Conclusions 407\u003c\/p\u003e \u003cp\u003eReferences 408\u003c\/p\u003e \u003cp\u003eIndex 409\u003c\/p\u003e  \u003cp\u003e“This book offers a refreshing perspective for anyone wanting to get a comprehensive background on the newer emerging interest in targeting cancer metabolism for therapy.”  (\u003ci\u003eDoody’s\u003c\/i\u003e, 11 January 2013)\u003c\/p\u003e \u003cp\u003e“For the first time, an entire issue is being devoted to a review article based on a recent medical book. This is a departure from our usual format, but I think you will agree that this topic warrants the detailed treatment we have given it . . .This book should be required reading for all scientifically literate people who are involved in the cancer problem.”  (\u003ci\u003eAdvances in Cancer Treatment\u003c\/i\u003e, 1 October 2012)\u003c\/p\u003e  \u003cp\u003e\u003cb\u003eTHOMAS N. SEYFRIED, PhD\u003c\/b\u003e, has taught and conducted research in the fields of neurogenetics, neurochemistry, and cancer for more than twenty-five years at Yale University and Boston College. He has published more than 150 scientific articles and book chapters and is on the editorial boards of \u003ci\u003eNutrition \u0026amp; Metabolism, Journal of Lipid Research, Neurochemical Research\u003c\/i\u003e, and \u003ci\u003eASN Neuro\u003c\/i\u003e.\u003c\/p\u003e  \u003cp\u003e\u003cb\u003eA groundbreaking new approach to understanding, preventing, and treating cancer\u003c\/b\u003e\u003c\/p\u003e \u003cp\u003eSupported by evidence from more than 1,000 scientific and clinical studies, this groundbreaking book demonstrates that cancer is a metabolic disease and, more importantly, that it can be more effectively managed and prevented when it is recognized as such. Moreover, the book provides detailed evidence that the traditional view of cancer as a genetic disease has been largely responsible for the failure to develop effective therapies and preventive strategies.\u003c\/p\u003e \u003cp\u003e\u003ci\u003eCancer as a Metabolic Disease\u003c\/i\u003e reevaluates the origins of cancer based on the latest research findings as well as several decades of studies exploring the defects in tumor cell energy metabolism. Author Thomas Seyfried is a biochemical geneticist who has been investigating the lipid biochemistry of cancer for thirty years. In this book, he carefully establishes why approaching cancer as a metabolic disease leads to better understanding and management of all aspects of the disease, including inflammation, vascularization, cell death, drug resistance, and genomic instability. In addition, the book explores:\u003c\/p\u003e \u003cul\u003e \u003cli\u003eOrigin of metastasis\u003c\/li\u003e \u003cli\u003eNew treatment strategies that target tumor cell energy metabolism, including the ketogenic diet\u003c\/li\u003e \u003cli\u003eMore effective prevention strategies in light of the metabolic origin of cancer\u003c\/li\u003e \u003cli\u003eCase studies and perspectives from the point of view of physicians, patients, and caregivers\u003c\/li\u003e \u003c\/ul\u003e \u003cp\u003eThroughout the book, tables, figures, and graphs summarize key information and clarify complex concepts. In addition, the renowned cancer biochemist Peter Pedersen from Johns Hopkins Medical School also provides a historical perspective on the importance of the information presented in his foreward to the book.\u003c\/p\u003e \u003cp\u003e\u003ci\u003eCancer as a Metabolic Disease\u003c\/i\u003e is essential reading for all cancer researchers and clinicians as well as public health professionals. By treating cancer as a metabolic disease, the book sets readers on a new, more promising path to understanding the origins of cancer and developing new, more effective strategies to treat and prevent it.\u003c\/p\u003e","brand":"Wiley","offers":[{"title":"Default Title","offer_id":47988880736485,"sku":"NP9780470584927","price":160.95,"currency_code":"USD","in_stock":false}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/1842\/7735\/files\/9780470584927.jpg?v=1761781897","url":"https:\/\/k12savings.com\/products\/cancer-as-a-metabolic-disease-isbn-9780470584927","provider":"K12savings","version":"1.0","type":"link"}