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Key Time Stamps:
02:20 Non-communicable diseases are those induced by diet and lifestyle choices. They develop slowly.
04:50 If you get hangry between meals, you may be metabolically inflexible.
05:30 Metabolic Pushing and Pulling: The post meal window is metabolic pushing. Fasting is metabolic pulling. We pull energy from our fat stores.
06:20 In the post meal window, mitochondria (the energy producing organelles within your cells) are focused on glucose oxidation, ensuring that the macronutrients just ingested favor the oxidation of glucose.
06:35 Glucose is a 6-carbon sugar. It is split into two. Pyruvate goes into the Krebs cycle and begins to make Acetyl CoA. Citrate is made within your mitochondria through the Krebs cycle as a biproduct of glucose oxidation. Citrate leaks out of your mitochondria and it is converted to Malonyl-CoA.
07:25 Malonyl-CoA prevents fat from being oxidized by going through the carnitine palmitoyltransferase protein.
08:14 If you foster glucose oxidation through high carb or constant eating, you are not able to oxidize fats for energy at the cellular level.
08:40 Persistently elevated malonyl-CoA leads to de novo lipogenesis, the creation of new fat.
09:00 You can test for postprandial VLDL or apolipoprotein B (APO B) to see if your VLDL is elevated or your liver enzymes are elevated, indicating that you have excessive metabolic pushing.
10:55 Metabolic pulling during fasting pulls energy from fat tissue and pushes it through the mitochondria to make cellular energy. This increases stress hormones.
11:45 AMPK is a nutrient sensing enzyme which suppresses malonyl-CoA’s ability to block fat from being oxidized. It enables more fat to be oxidized. It affects the ability of glycerol (part of triglyceride) can be made into glucose (gluconeogenesis).
14:30 Chronic metabolic gridlock can lead to exercise intolerance, fatigue, muscle weakness, and muscle catabolism.
15:00 Your mitochondria begin to uncouple with chronic metabolic gridlock. They become inefficient and create heat instead of energy.
16:20 Metabolic gridlock affects mitochondria in the brain which are essential for neuronal transmission, cell to cell communications, memory, mood and affective behavior.
17:00 Adipocyte hyperplasia is caused from the creation of new fat. Enlarged fat cells release large amounts of leptin.
18:00 Leptin negatively impacts your mitochondrial physiology and insulin sensitivity and negatively effects the immune system by suppressing the T-regulatory cell. T-lymphocyte is responsible for preventing awry inflammatory responses.
18:35 Chronic low grade system inflammation is remedied by T-regulatory cells.
19:00 Inflammatory cytokines further induce insulin resistance.
19:53 Enlarged fat cells become hypoxic. When your fat cells enlarge, overfilling with energy, your fat cells outgrow its own blood supply and run out of oxygen.
20:40 The molecule HIF-1 increases when tissues become hypoxic. This drives inflammation and changes genetic expression.
21:50 Adiponectin, which helps with insulin sensitivity, is downregulated during metabolic gridlock.
22:30 Metabolic tempo: feeding and fasting patterns. Fasting helps with metabolic congestion. Feeding window compression is a simple strategy. Find a pattern that works for you. Exercise helps pull energy through your mitochondria.
27:35 Adiponectin can be favorably affected by high quality omega 3.
28:05 Berberine hydrochloride favorably affects AMPK, which facilitates fat oxidation and improves metabolic pulling.
Torsak Tippairote, Geir Bjørklund & Augchara Yaovapak (2021): The continuum of disrupted metabolic tempo, mitochondrial substrate congestion, and metabolic gridlock toward the development of non-communicable diseases, Critical Reviews in Food Science and Nutrition, DOI: 10.1080/10408398.2021.1907299