Ep. 48: A Critique of The SCD1 Theory of Obesity (The Croissant Diet Part 2)

22 Feb 2021 Ep. 48: A Critique of The SCD1 Theory of Obesity (The Croissant Diet Part 2)

Posted at 05:49h in Podcast by Jay Feldman 0 Comments

3:00 – an introduction to SCD-1 in the context of obesity and lipogenesis

15:46 – SCD-1 in relation to ROS, fat oxidation, and fructose

23:51 – the relationship between PUFA, AMPK, and SCD-1

29:13 – whether the oxidation of saturated fats would decrease SCD-1 by increasing ROS and why this wouldn’t be ideal

44:03 – why the potential for fructose to increase SCD-1 is not a concern

56:29 – why PUFA are harmful even if they decrease SCD-1

1:04:45 – whether SCD-1 is the culprit behind obesity

PUFA decrease hepatic lipid production by increasing oxidative stress (1, 2)
Metformin inhibits efficient mitochondrial respiration (1, 2)
Metformin causes lactic acidosis (1, 2)
Metformin decreases intestinal permeability and has antimicrobial effects (1, 2, 3)
The effects of various stressors and oxidative stress on SCD-1 levels and the resulting lipotoxic cardiomyopathy (1)
Ep. 5: Blood Sugar Part 2: Cravings, Anti-Fructose Misconceptions, and the Best Starch Sources (podcast episode)
Sugar Does NOT Cause Inflammation (Part 1) (article)
Sugar Does NOT Cause Inflammation (Part 2) (article)
Sugar Does NOT Cause Insulin Resistance or Diabetes (article)
The True Cause of Type 2 Diabetes and Insulin Resistance (video)
Glycogen storage capacity during carbohydrate overfeeding (1)
Leptin resistance is caused by low ATP (1, 2)
The protective effects of SCD1 (1, 2, 3, 4, 5)