Dr. Donald Abrams, chief of the Hematology‐Oncology Division at San Francisco General Hospital, an integrative oncologist at the UCSF Osher Center for Integrative Medicine and Professor of Clinical Medicine at UCSF, explores integrative oncology which provides relationship-centered care, integrates conventional and complementary methods of treatment and prevention, aims to activate the body's innate healing response and uses natural, less invasive interventions when possible.
Emerging evidence indicates that cancer is primarily a metabolic disease involving disturbances in energy production through respiration and fermentation. Cancer is suppressed following transfer of the nucleus from the tumor cell to cytoplasm of normal cells containing normal mitochondria. These findings indicate that nuclear genetic abnormalities cannot be responsible for cancer despite commonly held beliefs in the cancer field. The genomic instability observed in tumor cells and all other recognized hallmarks of cancer are considered downstream epiphenomena of the initial disturbance of cellular energy metabolism. The disturbances in tumor cell energy metabolism can be linked to abnormalities in the structure and function of the mitochondria. Cancer growth and progression can be managed following a whole-body transition from fermentable metabolites, primarily glucose and glutamine, to respiratory metabolites, primarily ketone bodies. This transition will reduce tumor vascularity and inflammation while enhancing tumor cell death. A novel “press-pulse” therapeutic strategy is in development for the non-toxic metabolic management of cancer. Malignant brain cancer in preclinical models and humans will be used to illustrate general concepts. As each individual is a unique metabolic entity, personalization of metabolic therapy as a broadbased cancer treatment strategy will require fine-tuning to match the therapy to an individual’s unique physiology.
Thomas N. Seyfried received his Ph.D. in Genetics and Biochemistry from the University of Illinois, Urbana, in 1976. He did his undergraduate work at the University of New England, where he recently received the distinguished Alumni Achievement Award. He also holds a Master’s degree in Genetics from Illinois State University. Thomas Seyfried served with distinction in the United States Army’s First Cavalry Division during the Vietnam War and received numerous medals and commendations. He was a Postdoctoral Fellow in the Department of Neurology at the Yale University School of Medicine and then served on the faculty as an Assistant Professor in Neurology. Other awards and honors have come from such diverse organizations as the American Oil Chemists Society, the National Institutes of Health, The American Society for Neurochemistry, and the Ketogenic Diet Special Interest Group of the American Epilepsy Society. Dr. Seyfried previously served as Chair, Scientific Advisory Committee for the National Tay-Sachs and Allied Diseases Association and presently serves on several editorial boards, including those for Nutrition & Metabolism, Neurochemical Research, the Journal of Lipid Research, and ASN Neuro, where he is a Senior Editor. Dr. Seyfried has over 150 peer-reviewed publications and is the author of the book “Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer (Wiley Press).”
For half a millennium Western medicine has focused on anatomy and for the past century on nuclear DNA (nDNA), Mendelian, genetics. While these concepts have permitted many biomedical advances, they have proven insufficient for understanding the common "complex" diseases. Life requires energy, 90 percent of which comes from the mitochondrion. The mitochondrial genome consists of thousands of copies of the maternally inherited mitochondrial DNA (mtDNA) plus 1,000--2,000 nDNA genes. The mtDNA has a very high mutation rate, but the most deleterious mutations are removed by an ovarian prefertilization selection system. Hence, functional mtDNA variants are constantly being introduced into the human population, the more deleterious resulting in recent maternally inherited diseases. The milder mtDNA variants have accumulated sequentially as women spread throughout Africa and migrated out to colonize Eurasia and the Americas. Some ancient mtDNA variants alter mitochondrial energy metabolism in ways that were beneficial in different regional environments. In alternative environments and/or with age these same adaptive variants can be maladaptive and increase the risk for disease. For example, one variant increases the penetrance of mutations associated with an inherited form of vision loss, but is adaptive for survival at high altitudes. Mutations in the mtDNAs also accumulate with age in both stem and somatic tissue cells and can be associated with various forms of cancer. The introduction of mtDNA variants into the mouse germline via female embryonic stem cells has confirmed the causal role of mitochondrial deficiency in diseases. Hence, the pathophysiology of some common diseases may be bioenergetic dysfunction and their genetic complexity the result of thousands of nDNA and mtDNA bioenergetic gene variants interacting.
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