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In this interview, Dr. Thomas Seyfried explains why cancer may be a metabolic disease, not just a genetic one. We discuss mitochondrial dysfunction, energy metabolism, and how nutritional ketosis, keto, and carnivore diets may impact cancer risk and treatment outcomes.
Dr. Seyfried breaks down the metabolic theory of cancer, the role of mitochondria in chronic disease, how ketogenic and low-carb diets influence cancer cell metabolism, and why metabolic therapy is gaining attention in the keto and carnivore communities.
summerizer
Core model: cancer as a mitochondrial metabolic disease
- Cancer growth follows chronic mitochondrial injury and disordered energy metabolism, not an initiating nuclear gene mutation.
- Tumor cells shift ATP production away from oxidative phosphorylation and toward substrate-level phosphorylation and fermentation.
- The somatic mutation theory dominates cancer care, and that focus blocks metabolic targeting.
Evidence base
- Nuclear–mitochondrial transfer experiments: normal nucleus placed into tumor cytoplasm yields tumor; tumor nucleus placed into normal cytoplasm yields normal growth control.
- Driver mutations can exist without forming cancer, so mutations do not explain initiation by themselves.
- Environmental exposures and inherited risk interact, so separating “genes” from environment in real people is difficult.
- Hereditary cancer syndromes align with impaired oxidative phosphorylation in a recent Oncology paper with Bob Kaplan.
- Keeping cancer as a gene-only problem leaves about 1,700 people per day dying from cancer in the US.
Fuel logic and therapeutic targets
- The two fuels driving dysregulated tumor growth are glucose and the amino acid glutamine.
- Tumor cells cannot shift to ketone bodies or fatty acids the way healthy cells can.
- Cutting fermentable fuel availability and blocking glutamine use is the direct way to stress tumor metabolism.
Metabolic therapy: baseline approach
- Nutritional ketosis and water-only fasting lower glucose, raise ketones, and reduce inflammatory drive in tumors.
- The glucose–ketone index (GKI) tracks the glucose-to-ketone ratio as a single number to monitor metabolic pressure.
- Achieving ketosis is harder in modern food environments because sugar and ultra-processed foods are engineered for craving and convenience.
Combining metabolic therapy with standard care
- Metabolic therapy is non-toxic in practice; people generally get healthier during it.
- Chemo, radiation, and immunotherapy remain options, but metabolic control first aims to shrink and de-inflame the tumor.
- After the tumor burden and inflammation drop, smaller doses of standard agents can be used with less collateral damage.
- Some immunotherapies help some people, and they also can cause hyperprogressive disease and death; metabolic therapy avoids that risk profile.
Antiparasitic drugs and cancer
- Mebendazole and fenbendazole can hit cancer metabolism because parasites and tumor cells share a survival pathway.
- The shared pathway is mitochondrial substrate-level phosphorylation, fermentation inside mitochondria.
- In pediatric high-grade glioma work, antiparasitic drugs paired with nutritional ketosis are a practical, low-cost direction.
- “Cancer is a parasite” is rejected; parasites are different organisms, even when drug targets overlap.
Obesity, inflammation, and GLP-1 drugs
- Weight alone is less informative than inflammation; some people carry weight without chronic inflammatory drive.
- Ultra-processed carbs and sugar push inflammation; removing them and using fasting or ketosis pulls it down.
- GLP-1 drugs can reduce appetite and body weight, and they do not fix the food environment that drove the problem.
- When lifestyle change fails for years, GLP-1 drugs can be a last-resort tool to break the cycle.
Industry and incentives
- Cancer care is a revenue generator, with multi-billion-dollar drug markets anchored to the genetic model.
- Drug advertising spends heavy time on fatal risks, and metabolic therapy remains underused despite low toxicity.
- A “firewall of ignorance” exists across patients and caregivers who do not read or understand the scientific literature.
Virus, vaccines, and “turbo cancer” talk
- SARS-CoV-2 infection damages mitochondria and can contribute to downstream chronic disease.
- Sorting vaccine damage from virus damage is hard when many people experienced both.
- Regardless of trigger, metabolic behavior is the same: fermentation of glucose and glutamine.
- No clinical trial targets glucose and glutamine together while maintaining nutritional ketosis.
Risk reduction starting now
- Exercise is the top lever for mitochondrial health.
- Reduce ultra-processed foods, especially addictive sugar, and favor more natural foods even when cost is higher.
- Sleep, social connection, and reducing sedentary “doom scrolling” support healthier mitochondria.
- Chronic disease occurs at younger ages, with type 2 diabetes and obesity in children as warning signals.
References
- [00:01] Cancer as a Metabolic Disease: On the Origin, Management and Prevention of Cancer — https://doi.org/10.1002/9781118310311
- [00:03] Hereditary cancer syndromes linked to oxidative phosphorylation insufficiency — https://doi.org/10.1515/oncologie-2025-0301
- [00:12] The glucose ketone index calculator: a simple tool to monitor therapeutic efficacy for metabolic management of brain cancer — https://doi.org/10.1186/s12986-015-0009-2
- [00:19] Ketogenic diet as a metabolic vehicle for enhancing the therapeutic efficacy of mebendazole and devimistat in preclinical pediatric glioma — https://doi.org/10.1101/2023.06.09.544252