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Video Presentations on Cancer and the Ketogenic Diet

025: SURVIVE CANCER, LIVE LONGER with the KETO DIET! (Prof. Dr. THOMAS SEYFRIED Full Interview)

Prof. Dr. Thomas N. Seyfried is a distinguished American professor of biology, genetics, and biochemistry at Boston College. He holds a master's degree in Genetics from llinois State University and a PhD in Genetics and Biochemistry from the University of Illinois Urbana-Champaign. He further honed his expertise with postdoctoral studies in Neurochemistry and Genetics at Yale University School of Medicine’s Department of Neurology where he served as Assistant Professor.

Prof. Seyfried’s illustrious career spans over 200 peer-reviewed publications, focusing on the mechanisms underlying chronic diseases such as cancer, epilepsy, and neurodegenerative disorders. He currently serves on the editorial boards of several journals, including Nutrition and Metabolism, the Journal of Lipid Research, Neurochemical Research, and ASN Neuro. His groundbreaking work with his preeminent book on “Cancer as a Metabolic Disease - On the Origin, Prevention and Management of Cancer” has positioned him at the forefront of cancer research worldwide.

*PROF. SEYFRIED'S BOSTON COLLEGE PAGE 👉 https://www.bc.edu/bc-web/schools/morrissey/departments/biology/people/faculty-directory/thomas-seyfried.html

*PROF. SEYFRIED in the WEB 👉 https://tomseyfried.com

*LCHD DR. SEYFRIED PAGE: https://www.lowcarbhealthmd.com/resources/experts/seyfried

"Cancer as a Metabolic Disease" - Prof. Dr. Thomas Seyfried, PhD

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 honours have come from such diverse organisations as the American Oil Chemists Society, the National Institutes of Health, The American Society for Neurochemistry, the Ketogenic Diet Special Interest Group of the American Epilepsy Society, the Academy of Comprehensive and Complementary Medicine, and the American College of Nutrition.

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, 1st ed., 2012). 

"Cancer as a Metabolic Disease" - Interview with Prof. Dr. Thomas Seyfried, PhD

Current cancer research focuses on genetic origins of cancer, and standard treatments generally involve combinations of surgery, chemotherapy and radiation. In Cancer as Metabolic Disease, Dr. Thomas Seyfried presents an alternative origin of cancer based on the theories of Otto Warburg, wherein cancer is viewed as a disease of cellular metabolic dysfunction due to damaged mitochondria. In addition to pointing to new directions of research, Dr. Seyfried elaborates on a non toxic mode of treatment, the ketogenic diet, which capitalizes on the inability of the damaged cancer cell mitochondria to metabolize ketones, thus starving them while maintaining healthy cells.

Thomas Seyfried is Professor of Biology at Boston College. He is a senior editor of the American Society of Neurochemistry’s journal ASN Neuro and is on the editorial boards of Journal of Lipid Research, Neurochemical Research and Nutrition & Metabolism.

"Cancer: A Metabolic Disease with Metabolic Solutions" - Prof. Dr. Thomas Seyfried, PhD

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).” 

Can a Keto Diet Eliminate Cancer Growth? Prof. Dr. Thomas Seyfried Says Yes

Can a keto diet eliminate cancer growth? Dr. Thomas Seyfried says yes | TARGET: Cancer Podcast | Ep. 42

In this episode, Dr. Thomas Seyfried discusses metabolic approaches to cancer. Learn how depriving cancer cells of fermentable fuels like glucose and glutamine can starve and kill them. Challenge the genetic disease model and discover the impact of ketosis on mitochondrial health. Uncover the truth about cancer as a metabolic, not genetic, disease. Empower yourself with the knowledge to combat cancer through metabolic strategies and learn about the dangers surrounding us: processed foods.

Cancer as a Mitochondrial Metabolic Disease - Dr. Thomas Seyfried

Thomas Seyfried, Ph.D., is a biochemical geneticist, professor of biology at Boston College, and author of the groundbreaking book Cancer as a Metabolic Disease. As part of a lecture delivered on July 31, 2018, at the annual CrossFit Health Conference, Seyfried presented a report card on our current approaches to treating cancer in the United States. Looking at data from the American Cancer Society on cancer incidence and deaths per day between 2013 and 2017, he noted death rates are actually on the rise. “The more money we raise for cancer, the more cancer we get,” he observed. “So you have to ask, ‘What is going on here?’ ... This is a failure of monumental proportions.”

The reason for the failure “has to do with a fundamental misunderstanding of what the nature of this disease is,” he explained. “We’ve been led to believe that this is a genetic disease, and I’ll present evidence to say that it’s not.”

The belief that cancer is a genetic disease associated with somatic mutation has become dogma, Seyfried explained, and this dogma shaped much of the cancer research and treatment protocols of the twentieth century. So-called cutting-edge treatments, such as personalized therapy and precision medicine, are based on this viewpoint.

Unfortunately, the viewpoint is wrong, as Seyfried explained in “Cancer as a Mitochondrial Metabolic Disease,” an article published in Frontiers in 2015. There, he aggregated existing research on cancer and reevaluated the information in light of the two competing theories on the origin of the disease (i.e., cancer as a genetic or metabolic disease).

The research he surveyed supported Otto Warburg’s theory that cancer develops as a result of disturbed energy metabolism. Seyfried and his colleagues compared nuclear-cytoplasmic transfer and mitochondrial transfer experiments and found that the mitochondria are “calling the shots, not the nucleus,” which is “the opposite of what we would expect if this were a genetic disease,” he explained.

Seyfried then described what he and his colleagues believe is the missing link in Warburg’s theory. Normal healthy cells derive energy from oxidative phosphorylation. Cancer cells, on the other hand, get energy through fermentation. What Seyfried and his colleagues discovered — and what Warburg did not know — is that cancer cells can ferment not only lactic acid but amino acids as well. That is to say, cancer cells can derive energy for proliferation from glucose and glutamine. Thus, to remove a cancer cell’s energy source, one has to remove its access to fermentable fuels, and an effective way to do this, Seyfried found, is through calorie restriction and ketosis.

Calorie restriction and ketosis, he explained, are anti-angiogenic, anti-inflammatory, and pro-apoptotic. “No cancer drug is known that can do this without toxicity,” he said. He then added that those who claim they don’t understand the mechanism by which calorie restriction and ketosis work are full of “bullshit.” “They don’t read the literature. Nor do they contribute to it,” he said.

Seyfried’s cancer research, particularly on aggressive forms of cancer such as glioblastoma multiforme (GBM) and other stage 4 cancers, led to his development of a glucose-ketone index calculator and the press-pulse therapeutic strategy. The calculator helps patients monitor their progress toward therapeutic ketosis. The press-pulse method pairs press therapies, such as following a keto diet while taking ketone supplements and practicing stress management, with pulse therapies, such as taking glucose and glutamine inhibitors while undergoing hyperbaric oxygen treatments. During his presentation, Seyfried explained how and why these methods are more effective for cancer patients than traditional standard of care.

“GBM and other stage 4 cancers — I don’t consider them as terminal cancers,” he said. 

Can We STARVE CANCER? What You NEED TO KNOW! | Dr. Thomas Seyfried

Over the years, it has become a widely held belief that cancer is predominately a genetic disease or simply the consequence of bad luck. An empowering evolution in cancer research, however, suggests we have far more control over our risk than previously thought. 

I’m excited to talk to Dr. Thomas Seyfried about the underlying causes of cancer and why addressing metabolic dysfunction is a very important and often overlooked area of its prevention and treatment. 

Dr. Thomas Seyfried is an American professor of biology, genetics, and biochemistry at Boston College. He received his Ph.D. from the University of Illinois Urbana-Champaign in 1976 and did his postdoctoral fellowship at the Yale University School of Medicine. Dr. Seyfried has over 150 peer-reviewed publications, and his research focuses primarily on the mechanisms driving cancer, epilepsy, and neurodegenerative diseases and calorie-restricted ketogenic diets in their prevention and treatment. He is the author of Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer and presently serves on the Nutrition & Metabolism, Neurochemical Research, Journal of Lipid Research, and ASN Neuro editorial boards.

Cancer as a Mitochondrial Metabolic Disease - Dr. Thomas Seyfried, PhD

Thomas N. Seyfried is Professor of Biology at Boston College. He 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, Normal, IL. 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. Dr. Seyfried has over 170 peer-reviewed publications and is author of the book, Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer (Wiley Press).

Shocking Truth About Cancer: Fix Your Diet & Lifestyle To Starve It For Longevity | Thomas Seyfried

When I started medical school in 1995, we were taught that one in four people were likely to develop cancer in their lifetime. Today, that statistic has changed to one in two – a rapid rise that can’t be explained by genetics. But if our modern diet and lifestyles are the cause, we have more control than we might think. 

That’s the message my guest, Professor Thomas Seyfried, has worked tirelessly to prove and communicate over his four decades as a cancer researcher. Professor Seyfried is a professor of biology, genetics and biochemistry at Boston College, Massachusetts, and author of more than 150 peer-reviewed publications, as well as the 2012 book Cancer As A Metabolic Disease. 

Through his research, and in this conversation, he sets out to explain how it’s a malfunction in our mitochondria – the energy powerhouses in each of our cells – that’s at the root of every cancer he’s studied. Normal-functioning mitochondria, he explains, use oxygen to make energy. In cancer, this process is disrupted. Cancer cells cannot use oxygen, so they fall back on a primitive form of energy creation known as fermentation. 

It follows then, explains Professor Seyfried, that if we can somehow stop this fermentation process, then cancer cells will die. Cancer uses glucose and glutamine to fuel fermentation. While we don’t want to block glutamine, as it has other uses in the body, we can drastically lower our glucose levels to stop driving cancer growth. 

We discuss some of the ways in which we can start doing this – for example, using specific low-carb diets and nutritional ketosis. Professor Seyfried also talks us through his ground-breaking ‘metabolic therapy’ protocols for treating cancer – sometimes, alongside conventional treatments like chemotherapy and radiotherapy.

Professor Seyfried has spent decades researching and proving a metabolic cause for this devastating disease. This a compelling and optimistic conversation, packed with actions we can all take to reduce our risk not just of cancer, but all the chronic conditions driven by metabolic disruption.

Dietary Recommendations for Cancer/Warburg Metabolism - Dr. Colin Champ

Filmed at the Emerging Science of Carbohydrate Restriction and Nutritional Ketosis, Scientific Sessions at The Ohio State University

An impressive body of scientific evidence over the last 15 years documents long term benefits of carbohydrate-restricted, especially ketogenic, diets. We now understand molecular mechanisms and why they work. Popular books and articles now challenge the advice ‘carbohydrates are good and fats are bad.’ Circa mid-19th century urinary ketones were identified in diabetics sealing their toxic label for the next 150 years. Despite work four decades ago showing ketones were highly functional metabolites, they are still misidentified as toxic byproducts of fat metabolism. The vilification of fat by regulatory and popular dogma perpetuates this myth. But the nutrition-metabolic landscape is improving dramatically.

A growing number of researchers have contributed to what is now a critical mass of science that provides compelling clinical evidence that ketogenic diets uniquely benefit weight loss, pre-diabetes, and type-2 diabetes. In the last five years, basic scientists have discovered that b-hydroxybutyrate (BHB), the primary circulating ketone, is a potent signaling molecule that decreases inflammation and oxidative stress. BHB has been suggested to be a longevity metabolite, with strong support from recently published mouse studies showing decreased midlife mortality and extended longevity and healthspan. Although type-2 diabetes is often described as a chronic progressive disease, emerging evidence indicates that sustained nutritional ketosis can reverses the disease. There is growing interest in studying potential therapeutic effects of ketosis on cardiovascular diseases, cancer, and neurodegenerative diseases including Alzheimer’s and Parkinson’s. There are even reasons certain athletes may benefit from nutritional ketosis and ketone supplements ─ debunking the long-standing dogma that high carbohydrate intake is required to perform optimally.

With the support of the well-established Ohio State Food Innovation Center, this conference will bring together the top experts in these fields to share what has been achieved and what remains to be done to advance this exciting field of scientific discovery.

Cancer Prevention Through Diet - Dr. Colin Champ

In this presentation, Dr. Champ discusses the evidence of the role diet plays in helping us reduce our risk of cancer - from over a hundred years ago to present day. He synthesizes this data to leave the listener with tangible dietary recommendations that are able to be both followed and enjoyed to help lower the risk of cancer. 

Colin Champ M.D. is an oncologist and assistant professor at the University of Pittsburgh Medical Center where he practices radiation oncology and integrative medicine, while researching the impact of diet and exercise on cancer incidence and treatment. His work has been published in many peer-reviewed journals, including the New England Journal of Medicine and Journal of Clinical Oncology. Recently, he founded the Cancer Prevention Project, to provide the public with recommendations to help prevent cancer with tangible lifestyle changes.

He began viewing medicine and health with a critical eye during his studies at the Massachusetts Institute of Technology and he continues to question current medical studies and recommendations for scientific backing. He has an uncanny ability to synthesize complex health topics to make them understandable and entertaining to the common reader and blogs for several online sources including his own website, colinchamp.com. He Is author of Misguided Medicine and Misguided Medicine: Second Edition. He has been invited to present his research around the world and has been featured in many media outlets including the Boston Globe, the National Cancer Institute, the Gupta Guide with Sanjay Gupta, and the American Society for Clinical Oncology.

Fighting Cancer with Food and Fitness - Dr. Colin Champ

As educated members of society, we are consistently inundated with conflicting reports when it comes to which foods and activities are healthy or unhealthy – one day wine will help us to live forever like Southern Italians, the next day it will give us cancer. Regardless of the conflicting reports, we have a century of studies indicating which lifestyle activities can prime our body and its cells to fight cancer, and the results are surprisingly inconsistent with much of what we have been told for the past four decades. Interest in the science on the influence of our food and activities to help prevent cancer is undergoing a renaissance, with many of the older unknown studies revisited and confirmed by modern research. Several dietary and lifestyle activities have been shown to enhance our ability to fight cancer: fasting, carbohydrate restriction, high baseline activity levels, resistance training, vegetables teeming with defensive chemicals, and a low-carbohydrate/ketogenic diet have been shown to help prevent cancer in animal and human studies. In this presentation, Dr. Champ discusses the research revealing the impact these lifestyle habits can have in the fight against cancer.

Biography

Colin Champ M.D. is an oncologist and Clinical Assistant Professor at the University of Pittsburgh, where he practices radiation oncology and integrative medicine. He researches the impact of diet and exercise on cancer incidence and treatment and has presented his research around the world. He is a Diplomate of the American Board of Integrative and Holistic Medicine and has published 45 articles in peer-reviewed journals, including the New England Journal of Medicine. He founded the Cancer Prevention Project to provide the public with recommendations to help prevent cancer through tangible lifestyle changes.

Dr. Champ began viewing medicine and health with a critical eye during his studies at the Massachusetts Institute of Technology and he continues to question current medical studies and recommendations for scientific backing. He has an uncanny ability to synthesize complex health topics to make them understandable and entertaining and blogs on his website, colinchamp.com. He is author of the Amazon Bestseller Misguided Medicine: Second Edition and has been featured in many media outlets including the Boston Globe, the National Cancer Institute, the Gupta Guide with Sanjay Gupta, and the American Society for Clinical Oncology.

Augmenting Cancer Therapy with Diet - Dr. Colin Champ

Unknown to many scientists and practicing physicians, there is nearly a century of data revealing the effect of diet on cancer diagnosis and treatment. More recently, preclinical and clinical data have been confirming this effect. Most notably, the potentiation of radiation therapy and chemotherapy via carbohydrate restriction and intermittent fasting is currently being assessed in clinical trials. Some data has even shown that it may reduce side effects of current cancer treatment. The potential metabolic treatment and management of cancer is an exciting new area in the field of oncology. This presentation will discuss the connection between cancer treatment and diet by highlighting both the historical data and Dr. Champ’s research in the field.

Dr. Champ is a board-certified radiation oncologist and assistant professor at the University of Pittsburgh Cancer Institute and University of Pittsburgh Medical Center. He researches cancer treatment as well as diet and nutrition and has been invited to lecture on the topic around the country and world. He is one of the few physicians invited to present academic Oncology Grand Rounds as a resident, an honor usually reserved for experts after years or decades in the field. While only a resident, he published over 20 peer-reviewed articles, started a health and fitness website and company, and co-hosted a podcast that was top-ranked in the U.S., England, and Australia. He has been featured in the Boston Globe, The Gupta Guide with Sanjay Gupta, the National Cancer Institute at the National Institute of Health, and the American Society of Clinical Oncology newsletter, to name only a few. During his medical training, he created Cavemandoctor.com in an effort to simplify the complex aspects of evidence-based medicine for the common reader. The website quickly gained nearly three million readers. He is considered an energetic voice in the field of medicine as he adamantly emphasizes the benefits of a healthy lifestyle. Most importantly, he practices what he preaches by stressing a healthy diet and lifestyle for both his patients and himself.

The Ketogenic Diet and Cancer: Teaching an Old Dog New Tricks - Dr. Colin Champ

Colin Champ, MD, is an oncologist and assistant professor at the University of Pittsburgh Medical Center where he heads the diet and nutrition division of the Integrative Oncology Department. His research focuses on diet, exercise, and lifestyle optimization for cancer treatment and prevention. His work has been published in many peer-reviewed journals and he has been featured by multiple media sources, including the National Institute of Health, Sanjay Gupta’s Gupta Guide on Medpage, and the Boston Globe. He is the author of Misguided Medicine and is an avid online blogger of a range of health-related topics.

The Ketogenic Diet and Cancer Research - Dr. Dominic D'Agostino

Nutritional interventions in conjunction with the standard of care may augment the treatment for some cancers. Researchers have observed synergism between the ketogenic diet and hyperbaric oxygen against tumor cells. Moreover, Dr. D'Agostino suggests that ketosis stimulates the immune system, increasing its ability to detect cancer cells. However, he cautions that some cancer cells can use ketones as fuel, and this domain needs more research. In addition, a ketogenic diet may be designed to incorporate anti-carcinogenic phytonutrients and fiber. In this clip, Dr. Dominic D'Agostino discusses the implications of adding a ketogenic diet to cancer treatment protocols.

Ketogenic Diet to Treat Cancer: What the Science Says - with Dr. Angela Poff, PhD

Cancer. The word no one wants to hear. A terrifying diagnosis with treatments aptly named "toxic" therapies.

Dr. Angela Poff is a leading researcher investigating revolutionary, non-toxic metabolic therapies for cancer. Ketones are a leading candidate for that role.

How do different types of cancer respond to ketones? How do different types of ketones affect cancer cells? The answers to these questions could revolutionize the way we treat one of the most feared and deadly diseases.

Both ketogenic diets and exogenous ketone therapy show tremendous promise, but the science is still mostly in the pre-clinical stage, meaning non-human studies. Dr. Poff is on the front lines of this important research, helping us make progress toward evidence-based answers.

Ketogenic Diets to Prevent and Treat Cancer? - Dr. David Harper, PhD

Dr. David G. Harper is a science educator, researcher, and technology CEO. He holds a BSc. and Ph.D. from the University of British Columbia in mathematical biofluiddynamics and completed a post-doctoral fellowship in comparative physiology at the University of Cambridge. 

Dr. Harper is currently an associate professor of kinesiology at the University of the Fraser Valley and a visiting scientist at the BC Cancer Research Center, Terry Fox Laboratory. He is on the scientific advisory board of the Canadian Clinicians for Therapeutic Nutrition and is a member of the Institute for Personalized Therapeutic Nutrition.

As a Visiting Scientist at the BC Cancer Research Centre, Terry Fox Lab, his current research focuses on the therapeutic benefits of ketogenic diets for women with metastatic breast cancer. He has just completed a book called BioDiet: The Ketogenic Way to Lose Weight and Improve Health.

Keto Prevents and Treats Cancer - Dr. David Harper, PhD

What is the best diet for cancer? Published & ongoing research is showing that a ketogenic diet is power for preventing & treating many types of cancer.  

David G. Harper, PhD is a science educator, researcher, and technology CEO. He holds a BSc. and Ph.D. from the University of British Columbia in mathematical bio-fluid dynamics and completed a post-doctoral fellowship in comparative physiology at the University of Cambridge. He is currently an associate professor of kinesiology at the University of the Fraser Valley and a visiting scientist at the BC Cancer Research Center, Terry Fox Laboratory. He is on the scientific advisory board of the Canadian Clinicians for Therapeutic Nutrition and is a member of the Institute for Personalized Therapeutic Nutrition. As a Visiting Scientist at the BC Cancer Research Centre, Terry Fox Lab, his current research focuses on the therapeutic benefits of ketogenic diets for women with metastatic breast cancer.

     Dr Harper's site:  www.biodiet.org

Consequences of Ketogenic Diets in Cancer: from RECHARGE to Biomarkers - Dr. Eugene Fine

An impressive body of scientific evidence over the last 15 years documents long term benefits of carbohydrate-restricted, especially ketogenic, diets. We now understand molecular mechanisms and why they work. Popular books and articles now challenge the advice ‘carbohydrates are good and fats are bad.’ Circa mid-19th century urinary ketones were identified in diabetics sealing their toxic label for the next 150 years. Despite work four decades ago showing ketones were highly functional metabolites, they are still misidentified as toxic byproducts of fat metabolism. The vilification of fat by regulatory and popular dogma perpetuates this myth. But the nutrition-metabolic landscape is improving dramatically.

A growing number of researchers have contributed to what is now a critical mass of science that provides compelling clinical evidence that ketogenic diets uniquely benefit weight loss, pre-diabetes, and type-2 diabetes. In the last five years, basic scientists have discovered that b-hydroxybutyrate (BHB), the primary circulating ketone, is a potent signaling molecule that decreases inflammation and oxidative stress. BHB has been suggested to be a longevity metabolite, with strong support from recently published mouse studies showing decreased midlife mortality and extended longevity and healthspan. Although type-2 diabetes is often described as a chronic progressive disease, emerging evidence indicates that sustained nutritional ketosis can reverses the disease. There is growing interest in studying potential therapeutic effects of ketosis on cardiovascular diseases, cancer, and neurodegenerative diseases including Alzheimer’s and Parkinson’s. There are even reasons certain athletes may benefit from nutritional ketosis and ketone supplements ─ debunking the long-standing dogma that high carbohydrate intake is required to perform optimally.

With the support of the well-established Ohio State Food Innovation Center, this conference will bring together the top experts in these fields to share what has been achieved and what remains to be done to advance this exciting field of scientific discovery.

"Ketogenic Cancer Therapy: In vitro mechanisms -- pilot in vivo results" - Dr. Eugene Fine

Dr. Eugene Fine's research interests include inhibition of aggressive cancers by an insulin inhibiting ketogenic diet-human trials as well as pre-clinical study.  Additionally, he is also interested in coupling dietary interventions with selected cancer drugs.

Dr. Fine's professional interests have centered on: 

Non-invasive measurement of physiologic and molecular function, especially with radiotracer technology. This was applied to the heart and especially to measurement of kidney function and its role and contribution to hypertension; and more recently has focused on radiotracers for diagnosis, monitoring, prognosis, and identification of cancers for appropriate therapy. 

The effects of dietary and nutritional manipulation, and especially of reducing carbohydrate content, on altering our metabolic environment. Carbohydrate restriction in humans mimics many of the metabolic effects of fasting, and may be systematically studied using appropriate in vitro, cell culture, animal models and in vivo biochemical and radiotracer techniques. Of particular interest is the potential for differential systemic metabolic effects on normal compared to malignant/transformed cells.

"Ketosis and Cancer in Cells, Animals, and People" - Dr. Eugene Fine

2nd Annual Conference on Nutritional Ketosis and Metabolic Therapeutics 

February 2017, Tampa, FL

Tumor Metabolism and the Ketogenic Diet - Dr. Adrienne Scheck

An impressive body of scientific evidence over the last 15 years documents long term benefits of carbohydrate-restricted, especially ketogenic, diets. We now understand molecular mechanisms and why they work. Popular books and articles now challenge the advice ‘carbohydrates are good and fats are bad.’ Circa mid-19th century urinary ketones were identified in diabetics sealing their toxic label for the next 150 years. Despite work four decades ago showing ketones were highly functional metabolites, they are still misidentified as toxic byproducts of fat metabolism. The vilification of fat by regulatory and popular dogma perpetuates this myth. But the nutrition-metabolic landscape is improving dramatically.

A growing number of researchers have contributed to what is now a critical mass of science that provides compelling clinical evidence that ketogenic diets uniquely benefit weight loss, pre-diabetes, and type-2 diabetes. In the last five years, basic scientists have discovered that b-hydroxybutyrate (BHB), the primary circulating ketone, is a potent signaling molecule that decreases inflammation and oxidative stress. BHB has been suggested to be a longevity metabolite, with strong support from recently published mouse studies showing decreased midlife mortality and extended longevity and healthspan. Although type-2 diabetes is often described as a chronic progressive disease, emerging evidence indicates that sustained nutritional ketosis can reverses the disease. There is growing interest in studying potential therapeutic effects of ketosis on cardiovascular diseases, cancer, and neurodegenerative diseases including Alzheimer’s and Parkinson’s. There are even reasons certain athletes may benefit from nutritional ketosis and ketone supplements ─ debunking the long-standing dogma that high carbohydrate intake is required to perform optimally.

With the support of the well-established Ohio State Food Innovation Center, this conference will bring together the top experts in these fields to share what has been achieved and what remains to be done to advance this exciting field of scientific discovery.

The Ketogenic Diet: A Targeted Metabolic Approach to Cancer Treatment - with Miriam Kalamian, EdM, MS, CNS (American Nutrition Association)

The Ketogenic Diet: Living Well Webinar Series for Brain Tumor Survivors - UCSF Neurosurgery

The UCSF Sheri Sobrato Brisson Brain Cancer Survivorship Program presents 'The Ketogenic Diet' as part of an ongoing Living Well Webinar series for brain tumor survivors. 

This recorded webinar features UCSF veteran dietician Natalie Ledesma, and Chad Findlay who speaks from his personal perspective using the ketogenic diet in his brain tumor recovery as an empowering adjunct to his standard treatment.

To learn more about UCSF's support programs for brain tumor patients and their families, visit https://braintumorcenter.ucsf.edu

Andrew Scarborough - My Brain Tumour Journey #PHC2023

Filmed on the 19th & 20th May 2023 at the Public Health Collaboration Annual Conference in Sheffield. World-renowned speakers convened to share their expertise about how we can harness the power of lifestyle to help fix healthcare together.

Scholarly Articles on Cancer - a Mitochondrial Metabolic Disease

Press-pulse: a novel therapeutic strategy for the metabolic management of cancer - Nutrition & MetabolismBackground A shift from respiration to fermentation is a common metabolic hallmark of cancer cells. As a result, glucose and glutamine become the prime fuels for driving the dysregulated growth of tumors. The simultaneous occurrence of “Press-Pulse” disturbances was considered the mechanism responsible for reduction of organic populations during prior evolutionary epochs. Press disturbances produce chronic stress, while pulse disturbances produce acute stress on populations. It was only when both disturbances coincide that population reduction occurred. Methods This general concept can be applied to the management of cancer by creating chronic metabolic stresses on tumor cell energy metabolism (press disturbance) that are coupled to a series of acute metabolic stressors that restrict glucose and glutamine availability while also stimulating cancer-specific oxidative stress (pulse disturbances). The elevation of non-fermentable ketone bodies protect normal cells from energy stress while further enhancing energy stress in tumor cells that lack the metabolic flexibility to use ketones as an efficient energy source. Mitochondrial abnormalities and genetic mutations make tumor cells vulnerable metabolic stress. Results The press-pulse therapeutic strategy for cancer management is illustrated with calorie restricted ketogenic diets (KD-R) used together with drugs and procedures that create both chronic and intermittent acute stress on tumor cell energy metabolism, while protecting and enhancing the energy metabolism of normal cells. Conclusions Optimization of dosing, timing, and scheduling of the press-pulse therapeutic strategy will facilitate the eradication of tumor cells with minimal patient toxicity. This therapeutic strategy can be used as a framework for the design of clinical trials for the non-toxic management of most cancers.

Scholarly Articles on Cancer and the Ketogenic Diet

Metabolic reprogramming induced by ketone bodies diminishes pancreatic cancer cachexia - Cancer & MetabolismBackground Aberrant energy metabolism is a hallmark of cancer. To fulfill the increased energy requirements, tumor cells secrete cytokines/factors inducing muscle and fat degradation in cancer patients, a condition known as cancer cachexia. It accounts for nearly 20% of all cancer-related deaths. However, the mechanistic basis of cancer cachexia and therapies targeting cancer cachexia thus far remain elusive. A ketogenic diet, a high-fat and low-carbohydrate diet that elevates circulating levels of ketone bodies (i.e., acetoacetate, β-hydroxybutyrate, and acetone), serves as an alternative energy source. It has also been proposed that a ketogenic diet leads to systemic metabolic changes. Keeping in view the significant role of metabolic alterations in cancer, we hypothesized that a ketogenic diet may diminish glycolytic flux in tumor cells to alleviate cachexia syndrome and, hence, may provide an efficient therapeutic strategy. Results We observed reduced glycolytic flux in tumor cells upon treatment with ketone bodies. Ketone bodies also diminished glutamine uptake, overall ATP content, and survival in multiple pancreatic cancer cell lines, while inducing apoptosis. A decrease in levels of c-Myc, a metabolic master regulator, and its recruitment on glycolytic gene promoters, was in part responsible for the metabolic phenotype in tumor cells. Ketone body-induced intracellular metabolomic reprogramming in pancreatic cancer cells also leads to a significantly diminished cachexia in cell line models. Our mouse orthotopic xenograft models further confirmed the effect of a ketogenic diet in diminishing tumor growth and cachexia. Conclusions Thus, our studies demonstrate that the cachectic phenotype is in part due to metabolic alterations in tumor cells, which can be reverted by a ketogenic diet, causing reduced tumor growth and inhibition of muscle and body weight loss.
Modified Atkins diet in advanced malignancies - final results of a safety and feasibility trial within the Veterans Affairs Pittsburgh Healthcare System - Nutrition & MetabolismBackground Dysfunctional mitochondrial processes limit malignant cells ability to use energy from fatty acids and ketones. Animal studies using ketogenic diets for cancer show encouraging results. We tested the diet’s safety and feasibility in cancer patients across a broad variety of solid tumors. Methods We recruited 17 advanced cancer patients who were not on chemotherapy. They consumed 20 to 40 g of carbohydrates daily with evaluations performed weekly until week 4, then every 4 weeks until 16 weeks. Quality of life questionnaires monitored for tolerability and compliance. Positron emission/computerized tomography was ordered at baseline, 4,8 and 16 weeks. Student t-testing evaluated differences between baseline and last visit scores for quality of life, weight, body mass index, and serum parameters. Correlations between weight loss and serum ketones, glucose, lipids and creatinine were done. Two-tailed unpaired t-testing of the mean weight loss compared responders against non-responders. Results Eleven out of seventeen enrolled patients were evaluable. Mean age was 65+/- 11.7 years, weight 203 +/- 4.98 lbs. (92 ± 2.3 kgs.) and previous treatment failures was 1.7, +/- 0.97. All lost significant weight with hematologic, biochemical and lipid tests remaining stable. Quality of life scores slightly improved. At 4,8 and 16 weeks, six (54.5 %), five (45.4 %) and four (36 %) patients were stable or improved. We observed no correlations between serum glucose, ketones or lipids. Clinical response did not correlate with ketosis or glycemia. Responders (stable disease or partial responders) lost statistically more weight than non-responders. Dietary compliance was difficult. Only three patients continued dieting past 16 weeks. Out of these, two patients developed brain metastases and were on steroids. They survived 80 and 116 weeks respectively. The third patient underwent residual tumor resection and has no disease at 131 weeks. Conclusions Modified Atkins diets are safe and feasible in advanced cancer. Quality of life was preserved. Patients who lost at least 10 % of their body weight responded the best. Steroid intake affected optimal ketone and glucose levels. Despite this, survival improved in some melanoma and lung cancer patients. Further studies are recommended. Trial registration Clinicaltrials.gov NCT01716468 . Registered on September 18, 2012

Scholarly Articles on Brain Tumors and Ketogenic Diet

Nontoxic Targeting of Energy Metabolism in Preclinical VM-M3 Experimental GlioblastomaIntroduction: Temozolomide (TMZ) is part of the standard of care for treating glioblastoma multiforme (GBM), an aggressive primary brain tumor. New approaches are needed to enhance therapeutic efficacy and reduce toxicity. GBM tumor cells are dependent on glucose and glutamine while relying heavily on aerobic fermentation for energy metabolism. Restricted availability of glucose and glutamine may therefore reduce disease progression. Calorically restricted ketogenic diets (KD-R), which reduce glucose and elevate ketone bodies, offer a promising alternative in targeting energy metabolism because cancer cells cannot effectively burn ketones due to defects in the number, structure, and function of mitochondria. Similarly, oxaloacetate, which participates in the deamination of glutamate, has the potential to reduce the negative effects of excess glutamate found in many brain tumors, while hyperbaric oxygen therapy can reverse the hypoxic phenotype of tumors and reduce growth. We hypothesize that the combinatorial therapy of KD-R, hyperbaric oxygen, and oxaloacetate, could reduce or eliminate the need for TMZ in GBM patients.Methods: Our proposed approach for inhibiting tumor metabolism involved various combinations of the KD-R, oxaloacetate (2 mg/g), hyperbaric oxygen, and TMZ (20 mg/kg). This combinatorial therapy was tested on adult VM/Dk mice bearing the VM-M3/Fluc preclinical GBM model grown orthotopically. After 14 days, tumor growth was quantified via bioluminescence. A ...
The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for metabolic management of brain cancer - Nutrition & MetabolismBackground Metabolic therapy using ketogenic diets (KD) is emerging as an alternative or complementary approach to the current standard of care for brain cancer management. This therapeutic strategy targets the aerobic fermentation of glucose (Warburg effect), which is the common metabolic malady of most cancers including brain tumors. The KD targets tumor energy metabolism by lowering blood glucose and elevating blood ketones (β-hydroxybutyrate). Brain tumor cells, unlike normal brain cells, cannot use ketone bodies effectively for energy when glucose becomes limiting. Although plasma levels of glucose and ketone bodies have been used separately to predict the therapeutic success of metabolic therapy, daily glucose levels can fluctuate widely in brain cancer patients. This can create difficulty in linking changes in blood glucose and ketones to efficacy of metabolic therapy. Methods A program was developed (Glucose Ketone Index Calculator, GKIC) that tracks the ratio of blood glucose to ketones as a single value. We have termed this ratio the Glucose Ketone Index (GKI). Results The GKIC was used to compute the GKI for data published on blood glucose and ketone levels in humans and mice with brain tumors. The results showed a clear relationship between the GKI and therapeutic efficacy using ketogenic diets and calorie restriction. Conclusions The GKIC is a simple tool that can help monitor the efficacy of metabolic therapy in preclinical animal models and in clinical trials for malignant brain cancer and possibly other cancers that express aerobic fermentation.
The Ketogenic Diet Is an Effective Adjuvant to Radiation Therapy for the Treatment of Malignant GliomaIntroduction The ketogenic diet (KD) is a high-fat, low-carbohydrate diet that alters metabolism by increasing the level of ketone bodies in the blood. KetoCal® (KC) is a nutritionally complete, commercially available 4∶1 (fat∶ carbohydrate+protein) ketogenic formula that is an effective non-pharmacologic treatment for the management of refractory pediatric epilepsy. Diet-induced ketosis causes changes to brain homeostasis that have potential for the treatment of other neurological diseases such as malignant gliomas. Methods We used an intracranial bioluminescent mouse model of malignant glioma. Following implantation animals were maintained on standard diet (SD) or KC. The mice received 2×4 Gy of whole brain radiation and tumor growth was followed by in vivo imaging. Results Animals fed KC had elevated levels of β-hydroxybutyrate (p = 0.0173) and an increased median survival of approximately 5 days relative to animals maintained on SD. KC plus radiation treatment were more than additive, and in 9 of 11 irradiated animals maintained on KC the bioluminescent signal from the tumor cells diminished below the level of detection (p<0.0001). Animals were switched to SD 101 days after implantation and no signs of tumor recurrence were seen for over 200 days. Conclusions KC significantly enhances the anti-tumor effect of radiation. This suggests that cellular metabolic alterations induced through KC may be useful as an adjuvant to the current standard of care for the treatment of human malignant gliomas.

Scholarly Articles on Ketogenic Diet and Other Tumors

The Ketogenic Diet and Hyperbaric Oxygen Therapy Prolong Survival in Mice with Systemic Metastatic CancerIntroduction Abnormal cancer metabolism creates a glycolytic-dependency which can be exploited by lowering glucose availability to the tumor. The ketogenic diet (KD) is a low carbohydrate, high fat diet which decreases blood glucose and elevates blood ketones and has been shown to slow cancer progression in animals and humans. Abnormal tumor vasculature creates hypoxic pockets which promote cancer progression and further increase the glycolytic-dependency of cancers. Hyperbaric oxygen therapy (HBO2T) saturates tumors with oxygen, reversing the cancer promoting effects of tumor hypoxia. Since these non-toxic therapies exploit overlapping metabolic deficiencies of cancer, we tested their combined effects on cancer progression in a natural model of metastatic disease. Methods We used the firefly luciferase-tagged VM-M3 mouse model of metastatic cancer to compare tumor progression and survival in mice fed standard or KD ad libitum with or without HBO2T (2.5 ATM absolute, 90 min, 3x/week). Tumor growth was monitored by in vivo bioluminescent imaging. Results KD alone significantly decreased blood glucose, slowed tumor growth, and increased mean survival time by 56.7% in mice with systemic metastatic cancer. While HBO2T alone did not influence cancer progression, combining the KD with HBO2T elicited a significant decrease in blood glucose, tumor growth rate, and 77.9% increase in mean survival time compared to controls. Conclusions KD and HBO2T produce significant anti-cancer effects when combined in a natural model of systemic metastatic cancer. Our evidence suggests that these therapies should be further investigated as potential non-toxic treatments or adjuvant therapies to standard care for patients with systemic metastatic disease.
The Ketogenic Diet in Colorectal Cancer: A Means to an EndSome diets, such as high lipid and high glucose diets, are known to increase the risk of colorectal cancer. On the other hand, little is known about diets that prevent colonic carcinogenesis. The ketogenic diet, which is characterized by high fat and very low carbohydrate content, is one such diet. The ketogenic diet decreases the amount of available glucose for tumors and shifts to the production of ketone bodies as an alternative energy source for healthy cells. Cancer cells are unable to use the ketone bodies for energy thus depriving them of the energy needed for progression and survival. Many studies reported the beneficial effects of the ketogenic diet in several types of cancers. Recently, the ketone body &beta;-hydroxybutyrate has been found to possess anti-tumor potential in colorectal cancer. Despite its beneficial effects, the ketogenic diet also has some drawbacks, some of which are related to gastrointestinal disorders and weight loss. Thus, studies are being directed at this time towards finding alternatives to following a strict ketogenic diet and supplementing patients with the ketone bodies responsible for its beneficial effects in the hope of overcoming some potential setbacks. This article discusses the mechanism by which a ketogenic diet influences growth and proliferation of tumor cells, it sheds the light on the most recent trials regarding its use as an adjunctive measure to chemotherapy in patients with metastatic colorectal cancer, and it explains the limitations of its usage in metastatic patients and the promising role of exogenous ketone supplementation in this setting.
The Ketogenic Diet and Hyperbaric Oxygen Therapy Prolong Survival in Mice with Systemic Metastatic CancerIntroduction Abnormal cancer metabolism creates a glycolytic-dependency which can be exploited by lowering glucose availability to the tumor. The ketogenic diet (KD) is a low carbohydrate, high fat diet which decreases blood glucose and elevates blood ketones and has been shown to slow cancer progression in animals and humans. Abnormal tumor vasculature creates hypoxic pockets which promote cancer progression and further increase the glycolytic-dependency of cancers. Hyperbaric oxygen therapy (HBO2T) saturates tumors with oxygen, reversing the cancer promoting effects of tumor hypoxia. Since these non-toxic therapies exploit overlapping metabolic deficiencies of cancer, we tested their combined effects on cancer progression in a natural model of metastatic disease. Methods We used the firefly luciferase-tagged VM-M3 mouse model of metastatic cancer to compare tumor progression and survival in mice fed standard or KD ad libitum with or without HBO2T (2.5 ATM absolute, 90 min, 3x/week). Tumor growth was monitored by in vivo bioluminescent imaging. Results KD alone significantly decreased blood glucose, slowed tumor growth, and increased mean survival time by 56.7% in mice with systemic metastatic cancer. While HBO2T alone did not influence cancer progression, combining the KD with HBO2T elicited a significant decrease in blood glucose, tumor growth rate, and 77.9% increase in mean survival time compared to controls. Conclusions KD and HBO2T produce significant anti-cancer effects when combined in a natural model of systemic metastatic cancer. Our evidence suggests that these therapies should be further investigated as potential non-toxic treatments or adjuvant therapies to standard care for patients with systemic metastatic disease.