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Ep. 110: The True Cause of Insulin Resistance and Diabetes from the Bioenergetic View — Key Takeaways

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Ep. 110: The True Cause of Insulin Resistance and Diabetes from the Bioenergetic View

Jay Feldman Wellness1h 21mMar 6, 2024

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Insulin resistance is caused by impaired mitochondrial glucose oxidation and excess fatty acid burning (the Randle cycle), not carbohydrate intake — and increasing carbohydrate consumption, even in diabetics, improves insulin sensitivity by lowering stress hormones and reducing free fatty acid oxidation.

Key takeaways

Excess fatty acid oxidation causes IR by blocking glucose uptake via three distinct mechanisms

Excess fatty acid oxidation causes IR by blocking glucose uptake via three distinct mechanisms

  • Beta-oxidation raises NADH:NAD+ ratio → shuts down PDH; excess acetyl-CoA also inhibits PDH; excess citrate blocks phosphofructokinase (rate-limiting step of glycolysis).
  • This is the Randle cycle — well-established biochemistry, not a fringe claim.

Rising fasting blood glucose on low-carb signals stress-driven gluconeogenesis, not carb intake

Rising fasting blood glucose on low-carb signals stress-driven gluconeogenesis, not carb intake

  • Cortisol/glucagon/adrenaline upregulated by carb restriction stimulate hepatic glucose output — fasting BG rises even with zero carb consumption.
  • This is a stress marker, not evidence that carbs should be further restricted.

Insulin resistance is a glucose oxidation failure, not an insulin signaling defect

Insulin resistance is a glucose oxidation failure, not an insulin signaling defect

  • Cells in IR have excess intracellular glucose — they're full, not starved; the engine is broken, not the fuel supply.
  • The Randle cycle shows fat oxidation directly blocks pyruvate dehydrogenase (PDH), preventing glucose from entering the Krebs cycle.

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In this video

  1. 1mIntro
  2. 1mmetabolic flexibility, earning your carbs, the carb-insulin model of obesity, and dispelling other common insulin resistance myths
  3. 8mlow-carb, keto, and carnivore diets may improve symptoms but are not the solution for insulin resistance
  4. 13mwhat the mainstream view of insulin resistance gets wrong when it comes to what causes insulin resistance
  5. 16mwhy you might not want to use a continuous glucose monitor and the unnecessary fear of blood glucose spikes
  6. 18mwhether insulin is harmful and whether we want to keep insulin levels as low as possible
  7. 22mwhether we can restore optimal insulin sensitivity without low-carb diets
  8. 25mthe bioenergetic view of insulin resistance
  9. 27minsulin resistance as an adaptive evolutionary process that is crucial for survival
  10. 31mthe difference between physiological and pathological insulin resistance
  11. 35mhow inhibited glucose oxidation causes insulin resistance
  12. 41mhow fatty acid oxidation causes increased production of ROS, slows cellular respiration, and blocks glucose oxidation (The Randle Cycle)
  13. 51mthe harms of ROS production from fatty acid oxidation and other forms of stress
  14. 53minsulin resistance as an energy deficient state
  15. 54minsulin resistance is not an insulin signaling problem, it’s an energy production problem
  16. 59mthe role of stress hormones (like cortisol) in insulin resistance
  17. 1h 2mhow insulin and carbohydrates decrease stress
  18. 1h 6mhow to fix insulin resistance and restore insulin sensitivity by fixing our capacity to produce energy
  19. 1h 11mspecific diet, movement, and supplementation recommendations for insulin resistance and diabetes
  20. 1h 18mwhy you don’t need to tailor your carb intake to your carb tolerance

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