December 3, 2018

Podcast

#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

by Peter Attia

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.

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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). [northwestern.edu]

Nav’s Lab: Chandel Lab

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