December 3, 2018

Nutritional Biochemistry

#31 – Navdeep Chandel, Ph.D.: metabolism, mitochondria, and metformin in health and disease

"I pay more attention today to stress than anything else." —Nav Chandel

Read Time 11 minutes

In this episode, Nav Chandel, a professor of medicine and cell and molecular biology at Northwestern University, discusses the role of mitochondria and metabolism in health and disease. Nav also provides insights into the mitochondria as signaling organelles, antioxidants, and metformin’s multifaceted effects on human health, among many topics related to well-being.


We discuss:

  • What got Nav interested in mitochondria [5:00];
  • Reactive oxygen species (ROS) [16:00];
  • Antioxidants: helpful or harmful? [20:00];
  • Mitochondria as signaling organelles [22:00];
  • Hydrogen peroxide (H2O2) [25:00];
  • Mitochondrial DNA [28:00];
  • Mitochondria and aging [45:00];
  • Metformin [52:45];
  • Metformin and the gut microbiome [54:00];
  • Metformin as complex I inhibitor and the importance of the NADH/NAD ratio [1:01:00];
  • Anticancer benefits of metformin [1:07:45];
  • Mitochondrial function is necessary for tumorigenesis [1:15:00];
  • Are somatic mutations the result of mitochondrial dysfunction? [1:31:30];
  • Vitamins and antioxidants [1:37:00];
  • Targeting inflammation in disease [1:43:00];
  • NAD precursors [1:45:45];
  • MitoQ [1:52:00];
  • Metabolite toxicity [1:56:30];
  • Cortisol and healthy aging [2:02:00];
  • Nav turns the tables and asks Peter how he deals with the “So what should I eat?” question during social encounters [2:09:00]; and
  • More.

Featured image credit: Richard Wheeler via visually



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Navdeep Chandel, Ph.D.

Navdeep S. Chandel is a Professor in the Department of Medicine and Cell Biology at Northwestern University. He received a BA in Mathematics and a PhD in Cell Physiology at the University of Chicago. Dr. Chandel is well recognized for his work on the role of mitochondria as signaling organelles.

Focus of work: Historically, reactive oxygen species (ROS) have been thought to be cellular damaging agents, lacking a physiological function. Accumulation of ROS and oxidative damage have been linked to multiple pathologies, including neurodegenerative diseases, diabetes, cancer, and premature aging. This guilt by association relationship left a picture of ROS as a necessary evil of oxidative metabolism, a product of an imperfect system. Yet few biological systems possess such flagrant imperfections, thanks to the persistent optimization of evolution, and it appears that oxidative metabolism is no different. More and more evidence suggests that low levels of ROS are critical for healthy cellular function. We are testing whether mitochondrial release of H2O2 has evolved as a method of communication between mitochondrial function and other cellular processes to maintain homeostasis (e.g. stem cell function and immune responses) and promote adaptation to stress (e.g. hypoxia). []

Nav’s Lab: Chandel Lab

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  1. I’m a 62 year old man with metastased prostate cancer. After surgery my cancer was back in less than a year. Since then I went vegan to theropetic ketosis on the diet front with positive results with keto and HBOT. Keto is hard to maintain for a number of reasons but especially because of weight loss. I am now on a whole food diet with some grass fed meat, free range chicken and wild caught fish. I take some supplements and fast regularly. The last 7 months my cancer is stable which I think is huge given my diet changes. Now to get the numbers down. I’m presently on day 3 of a 10 day fast.

    Related to the above your work and podcasts provide so much useful information and hope. Me and many others, I’m sure, are thankful for your work.

    Gary 🙂

  2. It’s actually a bit of a relief to know that the leading minds in the field still have to refer to diagrams when it comes to energy generation (ie glycolysis, kreb’s cycle, beta oxidation, oxphos). It gives me hope as a mere mortal that I don’t actually have to know all of this by heart going forward.

  3. I loved how you challenged Navdeep’s hypothesis on the benefit of metformin being more based on the inhibition of complex 1 other than the drop in glucose production in the liver and subsequent decline in insulin and IGF. Another experiment that could be used to test this would be to study the effects of metformin on cancer cells in vivo lacking the transporter to get the metformin across the membrane. There’s so much conflicting research in the mitochondrial function of cancer cells. I gotta agree that the best approach is to hit it from as many angles as possible (well, I personally wouldn’t undergo chemotherapy, but that’s my personal choice and everyone needs to decide for themselves what therapies are right for them).

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