Why You Can't Burn Fat (geeky details + practical tips)

Описание: Metabolic Inflexibility is rampant, leading people unable to burn fat and lose weight.

In this podcast we dive into the details and share tips about how to improve the metabolic flexibility for weight loss and health.

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------------------------------------- Key Timestamps---------------------------------

0:00 Intro
02:20 Non-communicable diseases are those induced by diet and lifestyle choices. They develop slowly.
04:50 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 and glucose oxidation
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.
21:50 Adiponectin, which .
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.