November 26, 2018

Cancer

#30 – Thomas Seyfried, Ph.D.: Controversial discussion—cancer as a mitochondrial metabolic disease?

“The standard of care should never have been written in granite. It should be flexible. If you have something else that comes along that might be better, you'd think there would be enthusiasm.” —Tom Seyfried

Read Time 38 minutes

In this episode, Thomas Seyfried, a cancer researcher and professor of biology at Boston College, discusses a controversial view of cancer as a mitochondrial metabolic disease. Many topics related to the causes, treatments, and prevention of cancer are covered in this in-depth conversation.

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We discuss:

  • How Tom got interested in cancer research [9:00];
  • Calorie-restricted ketogenic diets, fasting, and epileptic seizures [18:30];
  • Otto Warburg and the Warburg effect [30:45];
  • Germline mutations, somatic mutations, and no mutations [42:00];
  • Mitochondrial substrate level phosphorylation: Warburg’s missing link [51:30];
  • What is the structural defect in the mitochondria in cancer? [1:02:00];
  • Peter’s near-death experience with the insulin suppression test while in ketosis [1:06:30];
  • Insulin potentiation therapy and glutamine inhibition [1:13:15];
  • The macrophage fusion-hybrid theory of metastasis [1:39:30];
  • How are cancer cells growth dysregulated without a mutation? [1:47:00];
  • What is the dream clinical trial to test the hypothesis that we can reduce the death rates of cancer by 50%? [2:03:15];
  • How can the hypothesis be tested rigorously that structural abnormalities in the mitochondria impair respiration and lead to compensatory fermentation? [2:26:30];
  • Case studies of GBM survivors [2:32:45]; and
  • More.
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Thomas Seyfried, Ph.D.

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, 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). [tomseyfried.com]

Tom’s website: Thomas Seyfried

Tom on Twitter: @tnseyfried

Thomas SeyfriedBiology Departmentscience

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  1. Thomas Seyfried = Ignaz Semmelweis. In 1846, Ignaz Semmelweis discovered that washing your hands before delivering a baby decreased the chances of the mother dying. Doctors disregarded him thinking that “they,” in their high nobility, could not have been the reason why the mother mortality rate was so high. Countless lives could have been saved if doctors were open-minded, but instead, their cognitive dissonance continues today. Those who do not learn history are doomed to repeat it.

    • Bingo John! What’s staggering to me is the near-deaf response to his actual underscore of the underlying biochemistry. He said something prescient in the Podcast regarding the refusal to engage his evidence – a similar thing happened to David Bohm when Oppenheimer basically directed his paper to be ignored because nobody could disprove him. Its very humbling to recognize how dismissive the establishment is when a troubling thesis comes along. Just like the Catholic Church in the Middle-Ages. ‘Sir, please look into the telescope!’ “Away with him, heretic!” Come on guys! If someone I know comes down with cancer I know whose thesis I’m gonna direct them to from now on. Awesome work btw Peter – especially towards the end! Tom has a bit of Semmelweis impatience – pull vs push will certainly advance the discussion.

  2. With the glutamine piece- does this mean supplemental glutamine is contra-indicated if battling cancer? Knowing that glutamine is the primary fuel cell for intestinal lining (and is an important part of healing leaky gut in many protocols), I’m a little confused as to its place in a cancer prevention/treatment plan. Any clarity here would be helpful. Thanks

    • Drew,
      Glutamine is a double-edged sword. It can help the immune system and gut, but can also drive metastatic tumor growth. We plan to evaluate the influence of glutamine supplementation on metastatic tumor growth. We addressed this issue on page 7 of our recent paper (https://doi.org/10.1038/s42003-019-0455-x).

  3. If the essence of cancer is merely “defective” mitochondria with no genome alterations (mitochondrial or otherwise), then how does this defectiveness propagate in a tumor? A tumor is going to be almost entirely made of new cells and their mitochondria are going to be produced via the central dogma. Maybe I am completely misunderstanding what Seyfried is saying, but I don’t see a mechanism for how these tumor mitochondria could all instantaneously become defective.

    • @Quinn The Otto-Warburg paper demystified this for me. Its a longish read but incredible in explanatory power of the biogenesis of cancer.

    • Quinn,
      The defective mitochondria are passed on to the daughter cells in the cytoplasm during mitosis. This can be considered a type of Lamarckian inheritance, i.e., inheritance of an acquired characteristic. The mitochondria become progressively more dysfunctional following each cell division and as the tumor microenvironment becomes more acidic. The dysfunctional produce ROS, which are carcinogenic and mutagenic. Increased ROS will increase somatic mutations in the nucleus. Consequently, the somatic mutations become downstream effects of the mitochondrial dysfunction. I discuss this process in our previous paper published in Carcinogenesis (doi:10.1093/carcin/bgt480).

  4. Stop your posin and stealing research ideas Peter. Seyfried knows his jam! 50% MTh
    PS – standard of’s care – enough bs!

  5. Whatever you think of his thesis – its obvious the current paradigm is flawed. A plummeting airplane cannot insist its motors are operational. Cancer is not a disease, its an attempt at a solution – mitochondrial respiratory disregulation, the evidence is overwhelming. Here’s a man come along to a fire department saying ‘hey – I know the two arsonists, they live here and there’ and the fire brigade says ‘Sir, we are fighting a fire here, please stand back!’ The poor guy – he’ll win of course – truth always does. The system as it operates now is too self-enamored. Instead of a peace treaty we insist on a ‘Space Force’ Kyrie eleison!

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