Podcasts about acetyl coa

This podcast covers the key catabolic pathways in the mitochondria, including : 1. The 3 catabolic pathways of carbohydrates and fatty acids; 2. The roe of Acetyl CoA as a common metabolite and its dietary sources; 3. The TCA cycle and its energy output; 4. Fatty acid beta oxidation and its energy output; and 5. A comparison of energy (ATP/ CO2) output from glucose, fatty acids, ketone bodies, and amino acids.

Briefing Document: Liver Function During Fasting Subject: Liver's role in energy provision during fasting. Source: Excerpts from "The LIVER During Fasting @Metabolism Made Easy" Main Themes: Ketogenesis: The liver actively synthesizes ketone bodies as an alternative energy source during fasting. Energy Provision: The liver plays a critical role in supplying energy to other tissues when glucose is scarce. Key Ideas and Facts: Ketone Body Synthesis: During fasting, the liver utilizes fatty acids to generate energy. A byproduct of this process is Acetyl-CoA, a portion of which is then used in ketogenesis, the production of ketone bodies. "the liver will be increasing Ketone body synthesis ketogenesis because it's using fatty acids uh as a source of energy producing a lot of acet Co a and some of that aceta is used in ketogenesis" Dual Energy Source: The liver provides two essential forms of energy during fasting: glucose (presumably through gluconeogenesis, though this isn't explicitly stated in this excerpt) and ketone bodies. "note how important the liver is it's providing glucose providing Ketone bodies two different forms of energy to other tissues to use during fasting" Implications: The excerpt highlights the liver's central role in metabolic adaptation during periods of food deprivation. By producing both glucose and ketone bodies, the liver ensures that other tissues, including the brain (which can utilize ketone bodies), have a continuous supply of energy. This demonstrates the liver's importance in maintaining metabolic homeostasis.

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Episode 31: Biochem of Sports Nutrition | Cauliflower Taco Meat Welcome to the Diet NPO Podcast! Your pod for RD Exam and nutrition questions. Come listen this week as we discuss Biochemistry of Sports Nutrition combined with practice questions and some Cauliflower Taco Meat! 1. If an athlete is training and develops a higher VO2 max, they would be relying more on which of the following processes? A. Anaerobic Glycolysis B. Lactic Acid Cycle  C. Creatine-Phosphate Pathway  D. Aerobic Glycolysis 2. Under anaerobic conditions, pyruvate can be converted into ______ through the Cori Cycle and can then be converted to ______ through gluconeogenesis. :  A. Lactate, Acetyl CoA B. Acetyl CoA, Glucose C. Lactate, Glucose D. Acetyl CoA, NADH 3. The pathway of aerobic metabolism that is producing the most amount of ATP through NADH and FADH intermediates, is known as the ________. A. Kreb's Cycle B. Citric Acid Cycle C. Aerobic Glycolysis D. Electron Transport Chain DM for your RD Exam tutoring needs! Instagram: @zak_snacks Threads: @zak_snacks Youtube: Zak Kaesberg MS, RDN

Links mentioned in the episode:www.betterwithcarbo.com/guideEp 14: Is Your Morning Brew the Secret Weapon Against Inflammation?Introduction: Hello and welcome to another episode of Inflamed in the Brain. I'm Krissy, your host, and friendly neighborhood Dietitian. Ever found yourself in a dinner dilemma? Well, I sure did the other day, and it led me to a breakfast-for-dinner solution. Today, I want to dive into a topic that's been a personal favorite of mine to debunk – the whole egg and cholesterol myth.Setting the Scene: Eggs, my go-to protein source, have often been the center of controversy. From fears about fat content to concerns about cholesterol, eggs have faced it all. Today, let's unravel the intricacies surrounding cholesterol, a topic closely tied to the egg debate.The Cholesterol Conundrum: Cholesterol has long been portrayed as the villain linked to heart disease. The American Heart Association advocated for a low-fat diet to curb cholesterol, yet high cholesterol remains prevalent. Approximately 86 million US adults had high cholesterol in 2020, prompting the need for a new approach.The Importance of Cholesterol: Contrary to its bad reputation, cholesterol is essential for health. It plays a vital role in hormone production, bile synthesis for fat digestion, and forms the basic structure of cell membranes. Think of it as the necessary foundation for your body's cells.Cholesterol Production and Transportation: Understanding how cholesterol is made and transported is crucial. Cholesterol is produced through the breakdown of fats or glucose, generating Acetyl CoA, a key player in the cholesterol-making process. LDL and HDL, often labeled as bad and good cholesterol, are lipoproteins carrying cholesterol through the bloodstream.LDL's Role and Concerns: LDL, responsible for transporting cholesterol, can become problematic in an inflammatory state. Frequent damage to blood vessel linings triggers LDL's healing response, leading to potential issues. Smoking, toxins, stress, and poor diets exacerbate LDL-related concerns. Research indicates that LDL particle size matters; small, dense particles pose more significant risks than larger, fluffier ones.Fructose and LDL Particle Size: Recent studies suggest that fructose may influence LDL particle size, making them smaller. However, it's crucial to differentiate naturally occurring fructose in foods like honey, mangoes, and grapes from the concentrated fructose in processed foods, notably high-fructose corn syrup.The Egg Solution: Dispelling myths, there's no reason to avoid whole eggs. In fact, whole eggs can decrease small LDL particles and increase protective HDL particles. Packed with nutrients like vitamin D, E, choline, and folate, eggs contribute to a balanced diet and support overall health.Blood Sugar Management: Managing blood sugar is key, especially for those concerned about cholesterol. Statins, prescribed for high cholesterol, target the HMG-CoA reductase enzyme. Insulin, influenced by a high-glycemic diet, can spike blood sugar, contributing to increased cholesterol production.Conclusion and Takeaways: In conclusion, eggs are not the enemy. They're a versatile, nutrient-packed option that, when enjoyed in balance, can be part of a heart-healthy diet. Remember, the quality of eggs matters, so opt for pasture-raised options with deep orange yolks. If cholesterol concerns you, focus on blood sugar management, and I'm here to guide you.Remember, fat, cholesterol, and eggs aren't the adversaries; itFollow along: https://betterwithcarbo.com/ Instagram

I've selected 2 key metabolic ingredients, Acetyl CoA and Citrate, to explain nutrition metabolism in further detail. I've also selected a different storyline, the mitochondrial amusement park and the Kreb's merry-go-round, to help you visualize some of the most fundamental steps of metabolism. In this episode we cover: Acetyl CoA's role as a key metabolic conductor The metabolic merry-go-round used to explain Kreb's cycle The importance of the Citrate sensor in switching between anabolism and catabolism How these concepts are tied to the root cause for weight gain and insulin resistance A critique of B-vitamin supplements as "energy producers"

This pocast covers the regulation of the Rate-limiting enzyme in fatty acid synthesis, Acetyl CoA Carboxylase allosterically, and by covalent modification. --- Send in a voice message: https://podcasters.spotify.com/pod/show/a-j-ghalayini/message Support this podcast: https://podcasters.spotify.com/pod/show/a-j-ghalayini/support

Malonyl CoA controls the categorical/biochemical logic of hepatic glucose and lipid homeostasis via metabolic inhibition of metabolic antimony. References Dr Dan Guerra Biochemistry Lecture Notes. 2010-2021 Vance and Vance Biochemistry of Lipids, Lipoproteins and Membranes 4th ed. 2002. Elsevier Publisher. --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

This podcast describes the molecules that can produce acetyl CoA as well as the possible metabolic fates of acetyl CoA. This biochemistry content may be useful to premedical and medical students. Similar content is available at: MEDBIOCHEM.ORG --- Send in a voice message: https://anchor.fm/a-j-ghalayini/message

This podcast describes the role of cytosolic citrate in regulating glycolysis, fatty acid synthesis and providing thd vehicle to transport Acetyl CoA to the cytoplasm where it is needed for lipid synthesis. This biochemistry content may be useful to premedical and medical students. Similar content is available at: MEDBIOCHEM.ORG --- Send in a voice message: https://anchor.fm/a-j-ghalayini/message

This podcast describes the unique ability of the liver to synthesize ketone bodies in the mitochondria from Acetyl CoA during fasting. The ketone bodies thus produced can provide an alternative energy source to multiple peripheral tissue including the brain, but excluding the liver. This biochemistry content may be useful to premedical and medical students. Similar content is available at: MEDBIOCHEM.ORG -Check out my YouTube channel : https://youtube.com/playlist?list=PLXy2KYiCd9rlg0JmfA392WrEiOYNu39xn --- Send in a voice message: https://anchor.fm/a-j-ghalayini/message

This podcasts explains why glucose cannot be made from fatty acid beta oxidation products i.e. Acetyl CoA. Exceptions to this concept are also included. This biochemistry content may be useful to premedical and medical students. Similar content is available at: MEDBIOCHEM.ORG --- Send in a voice message: https://anchor.fm/a-j-ghalayini/message

Alessandro Carrer, Principal Investigator, Veneto Institute of Molecular Medicine (VIMM), Associated Fellow, Department of Biology, University of Padova, ITALY speaks on "At the crossroad between metabolism and epigenetics: acetyl- CoA impacts cell plasticity in health and disease".

My AP Biology Thoughts  Unit 3 Cellular EnergeticsWelcome to My AP Biology Thoughts podcast, my name is Nidhi and I am your host for episode #71 called Unit 3 Cellular Energetics: Cellular Respiration:An overview. Today we will be discussing what cellular respiration is,who uses it, and why it's important.  Segment 1: Introduction to Cellular Respiration All organisms perform cellular respiration. The reactants of cellular respiration are glucose, which is oxidized, and oxygen which is reduced and they both produce carbon dioxide, water, and ATP. The purpose of cellular respiration is to make energy for cell work in the form of ATP. This occurs in a series of metabolic reactions. The reactions involved are catabolic reactions, which break down large molecules into smaller ones, releasing energy in the process which is supported by the overall reactions negative delta G. The ATP produced is eventually recycled and used to make more ATP. Most of the energy is released when reduced molecules are fully oxidized to create CO2. The oxidation occurs in a series of small steps allowing the cell to harvest 34% of the energy released. The rest of the energy is lost as heat. Segment 2: More About Cellular Respiration The two types of cellular respiration are anaerobic and aerobic. Anaerobic respiration can occur without oxygen while aerobic respiration requires oxygen to be present. Anaerobic respiration does not release enough energy to power human cells for long. It primarily occurs in muscle cells during hard exercise, after the oxygen has been used up. It also occurs in yeast during fermentation. Many prokaryotes perform anaerobic respiration.Through Anaerobic respiration, glucose is broken down to form 2 pyruvates. The purpose is to regenerate NAD plus for glycolysis, which is a part of aerobic respiration. Anaerobic respiration also keeps the pyruvate produced in the cytoplasm and uses it there. The main reactants are glucose, ADP, and Pi. This then produces ethanol, carbon dioxide and 2 atp. Anaerobic respiration has different products in animals. In animals instead of ethanol being produced, lactic acid is produced.  Aerobic respiration has 4 steps, glycolysis, pyruvate oxidation, the krebs cycle also known as the citric acid cycle, and the electron transport system. Glycolysis occurs in the cytoplasm, pyruvate oxidation and the citric acid cycle occur in the mitochondrial matrix, and the electron transport system occurs in the cristae of the mitochondria. In glycolysis, glucose is converted to pyruvate, ATP is produced, and NADH is produced. The energy transfers include 2 ATP used to produce 4 ATP ,NAD+ being reduced, Glucose being oxidized, and energy lost as heat. Overall, 2 net ATP are produced and no oxygen is used. Next, in pyruvate oxidation, Pyruvate is oxidized which reduces NAD+ to NADH. Coenzyme A reacts with the decarboxylated pyruvate to create acetyl CoA. This process occurs two times per glucose molecule. Again, energy is lost as heat is released. This time, CO2 is produced as a waste product. In the citric acid cycle, Acetyl CoA reacts with oxaloacetic acid to form citric acid . Citrate gets oxidized and loses carbons in the form of CO2. In that process, NAD+ and FAD are reduced into NADH and FADH2. Oxaloacetate is also regenerated since the process is a cycle. ADP+Pi makes ATP and total of 2 ATP is produced. Acetyl COA from the pyruvate oxidation and Pyruvate is needed for the reaction and CO2 is produced and heat is released. Lastly, in the electron transport system, Cells transfer energy from NADH and FADH2 to ATP by oxidative phosphorylation. NADH oxidation is used to actively transport H plus across the inner mitochondrial membrane, resulting in a proton gradient. Electrons from the oxidation of NADH and FADH2 pass from one carrier to the next in the chain. The oxidation reactions are exergonic and the energy released is used to actively transport H+...

My AP Biology Thoughts  Unit 3 Cellular EnergeticsWelcome to My AP Biology Thoughts podcast, my name is Victoria Villagran and I am your host for episode # 70 called Unit 3 Cellular Energetics: Oxidation and Reduction. Today we will be discussing Oxidation and Reduction Segment 1: Introduction to Oxidation and ReductionThey are redox reactions, a type of chemical reaction that involves a transfer of electrons between two species, and are vital to the basic functions of life, including photosynthesis Specifically, an oxidation-reduction reaction is any chemical reaction in which the oxidation number of a molecule, atom, or ion changes by gaining or losing an electron. Energy can also be transferred by the transfer of electrons in reduction-oxidation  Reduction is the gain of one or more electrons; endergonic reactions Oxidation is the loss of one or more electrons; exergonic reactions They always happen together The more reduced a molecules is, the more energy is stored in its bonds OIL RIG (Oxidation Is Loss; Reduction Is Gain) Segment 2: More About Oxidation and Reduction in Cellular RespirationCellular Respiration: glucose is oxidized and oxygen is reduced and  Only looking at where molecules are being either reduced or oxidized Glycolysis Glucose is being slowly oxidized as it is being converted into pyruvate, and then that electron is added to NAD+, reducing NAD+, converting it to NADH.  This produce 4 ATP, 2 Pyruvates, and 2 NADH from 2 ATP, 2 NADH+, and Glucose The energy in oxidizing glucose or lost from it was lost as heat Pyruvate Oxidation Pyruvate is oxidized (removing electrons) which then that electron reduced NAD+ to NADH, connecting glycolysis to the citric acid cycle This produces NADH, Acetyl CoA, CO2 from Pyruvate and Coenzyme A, and energy is released from the oxidation reaction and lost as heat Citric Acid Cycle Acetyl CoA (2C) reacts with oxaloacetic acid (4C) to form citric acid (6C); citrate gets oxidized and loses carbons in the form of CO2. In that process, NAD+ and FAD are reduced into NADH and FADH2. Oxaloacetate is regenerated.  The acetyl group is what is left of the glucose and is broken down (metabolized) in the citric acid cycle  Summary: Gaining electron carriers while oxidizing the carbon molecules or stripping away electrons like glycolysis To sump it up, NAD = to NADH (reduction), FAD is reduced to FADH2 Citrate is oxidized in many steps Electron Transport Chain/ ATP Synthesis Electron transport: electrons from the oxidation of NADH and FADH2 pass from one carrier to the net in the chain. The oxidation reactions are exergonic, energy released is used to actively transport H+ions across the membrane  Cells transfer energy from NADH and FADH2 to ATP by oxidative phosphorylation: NADH oxidation is used to actively transport protons (H+) across the mitochondrial membrane, resulting in a proton gradient Diffusion of protons back across the membrane then drives the synthesis of ATP Segment 3: Connection to the Course of Cell Energetics  Due to oxidation and reduction reactions, cells can use organic and inorganic molecules to create or transfer energy to power the cell, through specific processes such as cellular respiration and photosynthesis, and the synthesis of ATP. Where these molecules are either losing or gaining electrons, and the heat released or absorbed are lost as heat or used to power the step in the process to provide energy for the cell. Which then leads to the bonds in ATP being broken and are strong enough to power different cellular processes or the cell's metabolism.  Thank you for listening to this episode of My AP Biology Thoughts. For more student-ran podcasts and digital content, make sure that you visit http://www.hvspn.com (www.hvspn.com). Have a nice day! Music Credits:"Ice Flow" Kevin MacLeod (incompetech.com) Licensed under Creative Commons: By...

Mitochondrial Dysfunction and Other Causes of Chronic Fatigue - Mold and Candida Contribute | Podcast #287 Podcast Transcription: https://justinhealth.com/mitochondrial-dysfunction-other-causes-of-chronic-fatigue-mold-candida-contribute-podcast-287/ Get Show Updates Here: http://justinhealth.com/beyondwellness-newsletter You-tube Podcast Subscribe: http://www.youtube.com/subscription_center?add_user=justinhealth Recommended glandular support: http://www.justinhealth.com/ancestral Schedule a FREE Consult: http://www.justinhealth.com/free-consultation We are zooming in on the body today looking specifically at how your mitochondria is linked to energy levels, and how its dysfunction can lead to chronic fatigue. Dr. Justin Marchegiani even gives us a little Mitochondria 101 so we can better understand the concept in this podcast. To function properly, your mitochondria needs certain nutrients, the most essential compound being Acetyl-CoA. This means our body needs to be able to properly digest and break down our fats, carbs, and proteins (which make up the acetyl coenzyme A). Dr. J explains that Candida (yeast overgrowth) and micotoxins can also be major stressors to the mitochondria and our immune system. This can further zap energy, contributing to the chronic fatigue. To support this topic, Dr. J and Dr. Evan Brand are using studies and their own medical experience and research. If you experience chronic or accute fatigue, this is a podcast you don't want to miss. Your mitochondria are the powerhouse of your cells that help you generate atp/energy. Your mitochondria require amino acids, b-vitamins, coq10, carnitine, creatine, and other mitochondrial nutrients to name a few. Candida and mold toxins can stress out your mitochondrial, they can decrease nutrients available to your mitochondria. These candida and mitochondrial toxins can also stress our immune system (th1 and natural killer cells), which continue to take more available nutrients and resources from generating energy. References: https://www.ncbi.nlm.nih.gov/pubmed/29535978 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5834427/figure/F1/ http://web.fscj.edu/David.Byres/1005anotes/ch4notes.html https://www.ncbi.nlm.nih.gov/pubmed/7476598 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705282/ ===================================== Subscribe on I-Tunes: http://www.beyondwellnessradio.com/itunes Review us at: http://www.beyondwellnessradio.com/itunes Visit us at: http://www.beyondwellnessradio.com Have a question: http://www.beyondwellnessradio.com/question

In Episode 138 of Keto Talk, Jimmy and Dr. Will Cole answer your questions about Arteriosclerosis Reversal, Acetyl-CoA, Gastro Event Requiring Antibiotics And Pasta, Fasting And Appendicitis, Keto Aggravating Adrenals and more! HOT TOPICS: VEGAN CORY BOOKER SAYS MEAT EATERS’ DAYS ARE NUMBERED  Why is cheating on your keto diet everyone once in a while a bad thing?  What do you think about the new sweetener allulose being used in keto products? Does using collagen, bone broth, and MCT oil break your fast and turn off autophagy?  Could the carrageenan typically found in heavy cream be the cause of my skin issues? Does having chronic pancreatitis requiring prescription pancreatic enzymes preclude someone from eating keto? “Buyer beware when it comes to some of these food substitutes on the market.” – Jimmy Moore “It's not fair that some of us can tolerate certain foods while others can't, but we have to accept where we are on our health journey at this moment.” – Dr. Will Cole HEALTH HEADLINES: We’ll Always Eat Meat. But More of It Will Be ‘Meat' This Mediterranean diet study was hugely impactful. The science has fallen apart. Scientists Accidentally Discover Drug that Prevents Weight Gain Fasting's Health Benefits May Be Broader Than Scientists Previously Realized Are You A Super Pooper? STUDY: Newly isolated human gut bacterium reveals possible connection to depression Jimmy and Will answer your questions: –  Is there any research showing reversal of arteriosclerosis with keto and other lifestyle changes?  Hi Jimmy and Will,  I’m a big fan of the ketogenic diet and you guys consistently provide some of the best information about this way of eating online. I’ve been doing a lot of research lately on how to reverse arteriosclerosis since it seems most people have some varying level of this develop during their lifetime. I've seen people talk about things like taking magnesium and the MK7 variant of Vitamin K2, but these are only theoretical in nature. Is there any scientific evidence that this actually reverses the progression of heart disease? Is there any research that demonstrates keto and other lifestyle approaches help with this reversal of arteriosclerosis? Thanks again for your fantastic podcast.  Tom – Is there any concern with an increased production of Acetyl-CoA when a Type 2 diabetic is eating keto?  Hey guys,  I have someone in my life who has a biochemistry background claiming that going keto is about the worst thing a person with Type 2 diabetes could possibly do because of excessive production of Acetyl-CoA and that it induces a state of ketoacidosis (which I know is flat-out wrong). When I inquired about the mechanism about how the higher Acetyle-CoA issue happens and what the end result would be from this, she responded with something about DNA damage being done on a neurological level. This doesn’t make any sense to me from what I know about healthy nutritional ketosis and I’d love to offer up a counterpoint to her arguments. She seems to be really confused and it would be great to help educate her on this. Thanks for your help!  Sue   – What is the best way to recover my gut health from three rounds of strong antibiotics?  Hello Jimmy and Dr. Cole,  I recently had a gastro event that my gastroenterologist put me on two strong antibiotics (Cipro and Flagyl) for. As a keto dieter, I was shocked when he recommended that I eat lots of pasta before having a colonoscopy. When I told him I eat for ketosis, he chided me by staying that diet is merely political and not actually based on any sound science. I’m almost sure I have leaky gut and declined having the colonoscopy since the antibiotics have surely almost entirely wiped out my gut flora. I’m now eating the Specific Carbohydrate Diet (SCD) and am doing well on it so far. I did have to take another antibiotic (Methylpred) for a pulled tooth recently, so I know my gut health is majorly compromised now. Is there anything else I can do to help further improve my gut health so I don’t have to go through these rounds of antibiotics and recommendations of pasta anytime soon? This has been a very hard winter for me. Thank you for responding to my questions.  Mary  – Does extended fasting lead to appendicitis and gallstone development?  Hey Jimmy and Will,  I was inspired to start doing some longer fasting because of your podcasts and decided to do a 7-day fast. It was surprisingly easy for me to do and I felt great after it was finished. But one week after I finished that 7-day fast, I developed appendicitis. Was this somehow related to the fast or is this merely a coincidence? Checking Dr. Google didn’t help me answer this question at all which is why I’m writing to you today. They did find I had a developed a a gallstone which Dr. Valter Longo has said can happen on fasting. I’d love to go back to my regular 24-36 hour fasts, but now I’m scared because I don’t want to lose my gallbladder. Can you help reassure me about this issue?  Thank you and best regards, Andy in the Philippines   KETO TALK MAILBOX:  – Is keto making my adrenal issues worse?  Hi Jimmy and Will,  Thank you for all you do on Keto Talk to get sound information about healthy eating out to the public. I’ve been keto for just over a year and have lost 32 pounds while improving many of the symptoms of insulin resistance. I’ve felt energetic for my active lifestyle of mountain biking, running, cross country skiing, and snowshoeing. However, lately I’ve been having a few episodes of what I suspect may be symptoms of adrenal insufficiency. I have dealt with low thyroid and my naturopath put me on thyroid hormone replacement to deal with this—but it didn’t help or hinder. The focus of my treatment has been on healing the gut microbiome and I’ve been consuming copious amounts of bone broth and fermented food like yogurt to help with that along with periods of intermittent fasting.   I recently dealt with a virus that wouldn’t let go leaving me pretty sick and worn out for about two weeks. When I started feeling better, I noticed my lymph nodes in my neck were noticeably swollen and tender to the touch. At night, the back of my legs were achy near the back side of my knees. Waking up in the morning felt like I was hungover with my eyes swollen, a low-grade headache, nausea, and incredibly lethargic. When my chiropractor touch my T12 on my back, I felt a hot stinging sensation and immediately because nauseous. She told me that is directly tied to the adrenals. Is keto making these adrenal issues worse? From what I’ve seen, the recommendation for adrenal problems is to eat more carbs, but I don’t want to do that for a lot of reasons.   Thank you for helping me try to figure this out.   Kathy ITUNES REVIEWS: Leave us a review on Apple Podcasts

Insulin and ketone metabolism expert, Ben Bikman, PhD is back on the show for part 2--and it's a epic conversation. (If you missed episode #250, it was a great one, I’ll put a link to it on the show notes page.) ➢ This episode is brought to you by ButcherBox.com   Serving the High Intensity Health community with truly 100% grass-fed, pasture raised beef, chicken and pork. Get $20 off your order and free heritage bred bacon, for life! https://www.butcherbox.com/hih-2 About today’s show: Show Notes: https://highintensityhealth.com/250 Ben and I expand on the first discussion--diving further into why glycogen depletion and glucagon are needed and helpful in helping to kick-start fat loss and ketone production. We also discuss nuances around protein, mTOR and building muscle. Here’ s quick run-down of the time stamps: 05:49 We are applying the low carb ketogenic diet in bizarre ways by dumping oil into their drinks. There is no other nutritional value to the oils. Eggs are loaded with nutrition. Dr. Bikman mixes raw egg into his morning tea. 07:45 Fasted exercise stimulates glucagon. Our red blood cells need glucose. When we need gluconeogenesis, glucagon will be elevated. If you are low carb, exercising in a fasted state, or you are fasted, you need gluconeogenesis. Glucagon will be elevated and insulin, which inhibits gluconeogenesis, will be low. 09:37 People may be confusing gluconeogenesis with an insulinogenic effect. If you are low carb, gluconeogenesis happens only as much as you need it. 10:40 If you have ketogenesis happening, you have gluconeogenesis. Fat is used for fuel, and parallel, we have the need for new essential glucose to be produced. 13:14 Depleting glycogen is a necessary event before ketogenesis kicks in. 14:10 True clinical hypoglycemia is remarkably uncommon. If you are insulin resistant, and your brain has been depending upon high glucose and has had no time to adapt to using ketones for fuel, glucose levels can get low. Your body senses this and panics. There is more than enough glucose. 17:03 There are two phases of hunger. The first phase is hunger from empty guts. It is passing. The second phase of hunger is when your body says that there is a genuine deficiency of energy and you want to eat anything and will do anything to get it. 18:22 As long as you have sufficient salt and water consumption, you are good for exercise. If you have food in your gut, your body is conflicted about sending blood to your muscles or your guts. 19:57 Protein increases insulin and glucagon. Other macros increase one or the other. 21:02 Glucagon is catabolic of fat tissue. There are not many glucagon receptors in muscle. 21:55 If you are low carb or fasted and you need gluconeogenesis, there is no appreciable increase in insulin from the protein, yet a substantial increase in glucagon. 23:00 Glucagon activates lipolysis, increasing free fatty acids. The liver sees more fatty acids, but since insulin is low, the liver will not store the fat. Hormones tell the body what to do with energy. 23:54 Acetyl-CoA is the branch point of all metabolic processes in the liver and most other cells. It can be used for creating new glucose, activating gluconeogenesis, create lipids through lipogenesis and it can to into the citrate cycle and be used for energy, creating ATP, or it can be used for ketogenesis. All of this is dependent upon insulin. Catecholamines and glucagon counter insulin, but insulin reigns supreme. 25:40 Consuming meat or saturated fat does not create lipotoxicity, nor insulin resistance. 27:36 In animal and human studies of saturated fat, fat was administered intravenously. Elsewhere it was tested against muscle tissue in the lab, which does not reflect the complex systems of the body, especially the influence of insulin. Both of these formats helped to form our mechanistic thinking of how saturated fat can cause insulin resistance. 30:17 It is easier to induce insulin mediated lipotoxicity with a vegan diet than a ketogenic diet due to the high carb content. 30:43 Excess palmitate can create an excess of ceramides, as can hyperinsulinemia directly. 32:39 Triglycerides do not effect insulin sensitivity. 33:45 There are more ceramides in sedentary, obese, insulinemic individuals. They also have higher levels of circulating fatty acids. This is because the liver is making more fat or the adipocytes are becoming increasingly insulin resistant. Thus adipocytes are spilling lipid into the blood. The lipids switch from inert triglycerides to ceramides. 34:53 Alpha cells become insulin resistant because of a ceramide accumulation. We have a microenvironment in the pancreas. Butted up against each other, you have an alpha cell that releases glucagon and a beta cell that releases insulin. Insulin from the beta cell tells the alpha cell not to make glucagon. Within this environment is a greater amount of insulin than in our system. This means that the alpha cell is getting hundreds, maybe thousands of times more insulin than other tissues. 35:52 In type 1 diabetes, where you are not making insulin in the microenvironment, too much glucagon is produced, elevating glucose. 36:18 An insulin resistant person, who’s insulin levels have been climbing over the decades, but there is enough to keep glucose in check, remains clinically silent. Viewing diabetes as an insulin disease results in better treatment and earlier detection. 36:43 Eventually, glucose levels rise and you are a type 2 diabetic. This could be when the alpha cells become insulin resistant. Insulin tells the alpha cell to make less glucagon, unless the alpha cell becomes insulin resistant and glucagon climbs. This signals the liver to start pumping out glucose. 37:30 Both insulin and glucagon are high in type 2 diabetics. It should be one or the other. 38:13 Weight gain results from insulin therapy for both type 1 and type 2 diabetics, even if caloric consumption remains the same. 40:15 Exogenous ketones shut down your body’s ability for hepatic ketogenesis. Pulsed exogenous ketones can be helpful with TBI or other neurological issues. 41:55 Glucagon activates processes that are involved in mitochondrial biogenesis. 44:18 Ketones are energy. When you do endurance exercise with high blood glucose, glucose drops. When you do endurance exercise in a fat adapted state, your ketones will drop. 44:47 As you become more fat adapted, your body becomes more efficient and ketone baseline levels drop. 44:57 The definition of ketosis had been arbitrarily set at .5 mml. It is being considered to start at .3 mml due to the body’s efficiency shifts in fat adaptation. Once ketones are detectible from a low carb diet (and not exogenous ketones or MCT), metabolic pathways have been activated and insulin is low. You will be catabolic of your fat tissue. 47:53 You cannot store ketones if insulin is low. If insulin is elevated, even a ketone brought in exogenously, is converted to acetyl CoA and can be stored. 47:57 Hormones drive energy utilization. 51:54 Any cell that you want to maintain and grow requires mTOR. Insulin promotes mTOR activation. 52:55 Leucine is a good mTOR activator in muscle. 53:22 A cancer cell will grow with chronic mTOR activation, but it is not the cause of the cancer. 54:41 Protein consumption does not correlate to cancer incidence. There is evidence that a vegetarian diet, resulting in low levels of LDL. Low LDL is associated with 15 times greater risk of leukemia. 55:41 Animal products are higher in protein and we absorb more. Plants are relatively deficient in protein and we do not absorb it effectively. The longer you live a life with low insulin, the better off you will be. Fasting insulin levels impact Alzheimer’s risk more than age does. 59:17 Carnitine is involved in lipid transport. Longer chain fatty acids need a carnitine shuttle. Low levels of carnitine can be a bottle neck for the mitochondria’s ability to oxidize lipids. 01:00:41 Leucine is the most anabolic amino acid and is a ketogenic amino acid. 01:01:22 Red meat is a great source of carnitine. Carnitine accelerates ketogenesis. We can make our own carnitine. Low carb vegetarians may benefit for supplemental carnitine. Chicken is not a good carnitine source. 01:03:55 Cold induced uncoupling can stimulate mitochondrial uncoupling in muscle. If mitochondria are uncoupled, which means we have mitochondria pulling in glucose and fat and burning it to create heat. Where mitochondria are more tightly coupled, breaking down only enough energy as requested by the cell. 01:05:19 Ketones induce mitochondrial uncoupling in fat tissue, telling it that it is okay to waste energy. In muscle cells, it does not increase mitochondrial uncoupling. It is beneficial for your muscle to only use the energy it needs to use. 01:05:24 Body temperature rises from exercise out of an inherent inefficiency in all chemical reactions. 01:08:56 Cold exposure has an immune benefit and a cognitive benefit, as well as the metabolic benefit. 01:15:39 A main cause of endotoxemia can be LPS (lipopolysaccharide), a membrane component of bacteria. LPS is inhaled or absorbed from the gut. This is accelerated when your body is absorbing lipid. 01:16:47 With lipid absorption, there can be an increase of LPS and endotoxemia. However, dietary lipid consumption also increases LDL. LDL can bind to LPS and result in its removal through the bile duct. Fructose increases LPS, but does not increase LDL. Show Notes: https://highintensityhealth.com/250  

Why You Should Listen: In this episode, you will learn about optimizing Phase 2.5 detoxification, addressing mast cell activation, and balancing mTOR and autophagy. About My Guest: My guest for this episode is Dr. Kelly Halderman. Dr. Kelly Halderman, MD completed a Family Practice Medicine internship with the University of Minnesota and has a Naturopathic Medical Degree from Kingdom College of Natural Health where she is the current Academic Dean of Students. She holds certification in MethylGenetic Nutrition by the Nutrigenetic Research Institute and certification from The American Functional Neurology Institute in Functional Neurology and Neurofeedback. She is the lead researcher for the NutriGenetic Research Institute and also sits on the board. She is currently working on completing her Ph.D in clinical nutrition and has certification in Plant Based Nutrition from Cornell University. Her interests include cancer and Chronic Lyme, of which she has personally experienced and beaten. She does consultations for those interested in optimizing their health. Key Takeaways: - What is Phase 2.5 detox and how is it impacted and optimized? - What are bile salts and bile and how might they be increased? - What is the connection between bile and SIBO? - What is the role of inflammation in detoxification and the importance of reducing inflammation in order to optimize detoxification? - What is the role of the mast cell in inflammation and in detoxification impairment? - How does Acetyl-CoA steal lead to reduced ATP and low energy and fatigue? - What is the role of iron in inflammation? - What are mTOR and autophagy? What stimulates mTOR and shuts down autophagy? - What is Phase 3 detoxification and the role binders in minimizing enterohepatic recirculation? Connect With My Guests: http://drkellybeatlyme.com Interview Date: July 11, 2018 Additional Information: To learn more, visit http://BetterHealthGuy.com. Disclaimer: The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.

Dr Carolyn Lam:                Welcome to Circulation On The Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center and Duke National University of Singapore. Our featured discussion today centers on the challenges of cardiovascular disease risk evaluation in people living with HIV infection, an important discussion coming right up after these summaries.                                                 The first original paper this week provides experimental evidence that nicotinamide riboside could be a useful metabolic therapy for heart failure. First author Dr. Diguet, corresponding author Dr. Mericskay, from University Paris-Sud investigated the nicotinamide adenine dinucleotide or NAD homeostasis pathways in the failing heart. They found that an expression shift occurs in both murine and human failing hearts in which the nicotinamide riboside kinase two enzyme, which uses the nucleoside nicotinamide riboside was strongly up-regulated for NAD synthesis.                                                 Nicotinamide riboside supplemented diet administered to murine models of dilated cardiomyopathy or pressure overloaded induced heart failure restored the myocardial NAD levels and preserved cardiac function. Nicotinamide riboside increased glycolysis as well as citrate and Acetyl-CoA's metabolism in these cardiomyocytes. Thus, nicotinamide riboside supplemented diet may be helpful in patients suffering from heart failure and may help them to cope with the limited myocardial ATP supply by restoring NAD coenzyme levels and its associated signaling.                                                 In the single ventricle reconstruction trial, one year transplant-free survival was better for the Norwood procedure with the right ventricle to pulmonary artery shunt compared with the modified Blalock‒Taussig shunt in patients with hypoplastic left heart and related syndromes. In the paper in this week's journal, authors compare transplant-free survival and other outcomes between these groups at six years. First and corresponding author Dr. Newburger from Children's Hospital Boston and her group showed that the right ventricular pulmonary artery shunt group had similar transplant-free survival at six years, but required more catheter interventions before the Fontan procedure.                                                 Right ventricular ejection fraction, New York Heart Association class and complications did not differ by shunt time. Cumulative incidences of morbidities by six years included 20% with a thrombotic event, 15% with a seizure, and 7.5% with a stroke. These data therefore emphasize the importance of continued follow-up of the cohort, and the need to find new strategies to improve the long-term outlook for those with single ventricle anomalies.                                                 The next paper presents results of the CREATIVE trial, which stands for Clopidogrel Response Evaluation and Anti-Platelet Intervention in High Thrombotic Risk PCI Patients). First and corresponding author Dr. Tang from Fuwai Hospital National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College conducted a head-to-head comparison of the safety and effectiveness of intensified anti-platelet therapies either a double dose clopidogrel or adjunctive cilostazol and conventional strategy in 1078 post-PCI patients at high thrombotic risk as identified thromboelastography, which is a platelet function test.                                                 The primary outcome was the incidence of major adverse cardiac and cerebral vascular events at 18 months post-PCI they find as a composite of all cause death, myocardial infarction, target vessel revascularization, or stroke. The authors found that the primary end point occurred in 14.4% of those in the conventional strategy. 10.6% in those given double dose clopidogrel alone. And 8.5% in those also given adjunctive cilostazol. Now, although both intensified anti-platelet strategies achieved increased platelet inhibition, only the triple strategy with adjunctive use of cilostazol significantly reduced adverse events in the long-term follow-up.                                                 No increased rates of major bleeding was found with the intensified anti-platelet therapy regimes. Thus, in patients with low responsiveness to clopidogrel as measured by thromboelastography, the intensified anti-platelet strategies with adjunctive use of cilostazol significantly improved the clinical outcomes without increasing the risk of major bleeding.                                                 The final original paper sheds light on the prevalence and predictors of cholesterol screening awareness and statin treatment among American adults with familial hypercholesterolemia or other forms of severe dyslipidemia. First and corresponding author Dr. Bucholz from Boston's Children's Hospital and their colleagues used data from the National Health and Nutritional Examination Survey, and showed a high prevalence of screening and awareness above 80%. However, there were relatively low rates of statin use among individuals with familial hypercholesterolemia at 52.3%.                                                 And even lower rates among those with severe dyslipidemia at 37.6%. The discrepancy between the prevalence of cholesterol screening and treatment was most pronounced in younger patients, uninsured patients, and patients without a usual source of healthcare. This study highlights an imperative to improve the frequency of cholesterol screening and statin prescription rates to better identify and treat this high risk population. Additional studies are needed to better understand how to close these gaps in screening and treatment.                                                 And that brings us to the end of our summaries. Now for our feature discussion. The natural history of infection with HIV has completely changed with the use of potent antiretroviral therapies. We now know that people living with HIV actually have morbidity and mortality patterns that really resemble the general population, especially with regards to cardiovascular disease, which is very prominent in this population. And I suppose it's this that has led to the assumption perhaps that risk prediction tools and intervention strategies that we apply in the general population may be used in patients living with HIV.                                                 Is this the case however? Well, this week's feature discussion is going to be so enlightening. And it's so important we are talking across the world here, from South Africa to the United States, and of course with me here in Singapore. I am so pleased to have the authors of this week's feature paper and they are none other than Dr. Virginia Triant from Massachusetts General Hospital, Dr. Ralph D'Agostino from Boston University. And our associate editor, Dr. Bongani Mayosi from University of Cape Town. Thank you so much for joining me for today's exciting discussion. Virginia, could I ask you to first describe your study? Dr Virginia Triant:             As you mentioned in the introduction, we have found that patients infected with HIV have an increased risk of cardiovascular disease. That includes both myocardial infarction and stroke compared to age-matched controls in the general population. And extensive data has suggested that the etiology of this increased risk is related both to traditional cardiovascular risk factors, as well as novel risk factors that are specific to HIV infection. And these include chronic inflammation in the immune activation. So consequently, it remains relatively unknown whether established cardiovascular risk prediction functions are accurate for patients with HIV because they include only risk factors that are traditional factors and they don't reflect the complete mechanism that we know is at play in cardiovascular disease associated with HIV.                                                 So in our study, we assess the performance of three established cardiovascular risk prediction functions, two Framingham functions, and then the ACC/AHA pooled cohort's equations and we applied this to a longitudinal HIV infected cohort that was comprised of men. And we investigated the performance of the risk scores in terms of comparing regression coefficients, discrimination and calibration, which are standard metrics in cardiovascular risk prediction. So I'll briefly summarize our overall results as a start. We found that overall, the risk prediction functions underestimated risk in our group of HIV-infected men.                                                 We found that discrimination was modest to poor, and this was indicated by low c-statistics for all of the equations. And we also found that the calibration or the agreement between observed or predicted risk was also poor across the board for all three risk prediction functions. So our results suggests that simply taking the risk prediction functions and transporting them to an HIV infected group may actually result in mis-classification in terms of patient risk. And in underestimation of cardiovascular risk. Dr Carolyn Lam:                Well, Virginia, beautifully summarized of a beautiful paper. But perhaps at this point, we should take a step back and ask ourselves how exactly were these risk prediction scores originally developed. And I can't imagine asking a better person than Ralph. Ralph, could you take us on a jaunt along history and tell us how were those Framingham risk scores developed in the first place? Who are they supposed to be applied to? And did these results surprise you? Dr Ralph D'Agostino:      After the second World War, what was becoming quite clear is things like cardiovascular disease were becoming very prominent. Things like infections and what have you, we were developing all sorts of ways of handling them with medicines and so forth. But with cardiovascular disease, it's a thing that progresses slowly over the years and it starts wiping out people. And back in those days, one out of three men between the ages of 30 and 60 had some kind of cardiovascular event. Women weren't that bad off, but they were pretty bad off also. And so what happened is the American government and the American Heart Institute set up this study in Framingham, where they took a third of the individuals between the ages of 30 and 60 and actually followed them. They took values of variables like blood pressure, cholesterol, things they thought might be useful.                                                 And took values on them. And they had to come back every two years and after as time went on, they took the data after six years, after 10 years they took the data, and started to look at how each individual's blood pressure related to cardiovascular disease. Does cholesterol, and the answer was yes. And then I started getting involved and we were developing these cardiovascular functions where you could actually take an individual, take their measurements now, and make a prediction that had a lot of validity, good discrimination, high predictability over what was going to happen in ten incidents and then the government, the US Government, started having guidelines and what we did is we ran a study where we took a number of different studies in the US, different cardiac studies, the ARIC studies, number of 'em, and we thought applying our functions how well would they do. And it turned out that for whites in the country, the Framingham functions did very well.                                                 But Japanese-Americans in the country, it over-predicted. Then we found out that you could make a calibration adjustment and what we've gone to, like in China, we have a big study where we had a function and Framingham function it over-predicted but calibration adjustment would make enough corrections and so now with Jeanne and the HIV, our hope was that you could take these functions and see how they work on the HIV population. When we did it we were quite well aware, because people have been looking at different things, there's something beyond the original cardiovascular risk. And what the paper shows, quite nicely, these cardiovascular risks do have some relationship but they don't explain enough. The HIV population have a much bigger burden and a simple calibration adjustment just isn't going to work. We need new variables, we need new insights on what to add to these functions. Dr Carolyn Lam:                Thank you so much for that. That's just such important part of history because I have to thank you for those equations. We apply those definitely in our Asian cohorts with that calibration factor. But I was just reflecting as you were telling that story of how we've come full circle now to actually talk about an infection again. It's the midst of an infection, like HIV infection, that we're now testing these equations once again. What better than to ask than Bongani, you're in the epicenter, if I may, of HIV infection. What do you think of the applicability of these findings to the patients you see? Dr Bongani Mayosi:         Yes. These findings are clearly of great interest to us here in the Sub-Saharan African region because it is really the epicenter HIV pandemic. We found population, in terms of risk factors for arteriosclerosis disease still remains low although there clearly derives, for example, in the incidence of myocardial infarction that's being detected in a number of the leading centers now. And with HIV we have observed cases of myocardial infarction while they tend to be younger men who almost always smoke and who get a lot more of a thrombotic episodes.                                                 When you catch them on a thrombotic load, you do not find arteriosclerosis disease. It's going to be important, I think, as we move forward to make sure that as we develop risk functions that will predict cardiovascular disease in patient HIV that the African epidemiological context is completed teaching that HIV affects younger people, affects large numbers of women, but that, quite clearly, is associated with decreased cardiovascular event and stroke and stroke is well demonstrated. But in terms of actually looking at the risk factor this population was still in the early day and certainly in future studies would have to have a major contribution of the African cohort. Dr Carolyn Lam:                That's true, Bongani, but may I ask how would you, perhaps, advise your African colleagues now to look at these data? Then I'd also like to turn that same question over to you, Virginia. What do we do? What's the clinical take home message of these findings? Dr Bongani Mayosi:         I think the message is true that HIV infection is associated with the increased risk of cardiovascular event, there's no doubt about that. That there are some risk factors that can carry through, such as the smoking population but it's important for all clinicians to be aware of that. The ordinary risk you find in using Framingham and other established risk functions is not going to give us all the information that we need. So that recommendation should come through we need to know that risk factors are unknown, that they're important and we need to learn more about these patients in order to give us a perfect prediction of what will happen in the future. Dr Virginia Triant:             I think the findings have a lot of clinical relevance. This suggests, I think, that there are a lot of clinical implications for any patient who has novel cardiovascular risk factors that may not be accounted for in heart functions. And what our findings suggest is that if functions don't reflect the actual composition of risk factors in the population, that can result in misclassification and thus we underestimate risk, we might miss high-risk individuals, high-risk patients who would benefit from aggressive risk reduction but are not currently receiving it. This is a real clinical challenge as sit in clinic and we pull up the scores and calculate them for our patients, whether that is a trustworthy number or whether we should, perhaps, thinking that it's higher, thinking that it's different than what we're seeing for predicted 10-year risk. I think what this suggests is that the functions may need to be further tailored to different populations and sub-populations to reflect the actual composition of risk factors in that population. Even within HIV patients and populations, the risk factors in South Africa might be different than those in Boston, with different relative contributions.                                                 One of the next stepped planned for our team is to actually look at developing, new risk functions which are tailored to HIV and incorporating both HIV itself as a risk factor, as well as HIV specific variables and to attempt to see if we can improve the performance of these functions for HIV populations. Perhaps HIV or HIV related factors might become sort of a new cardiovascular risk equivalent and we can serve patients in this population as higher cardiovascular risk baseline. I also just wanted to mention, briefly, that I think that there are important clinical implications beyond HIV that extend to other chronic inflammatory conditions. Inflammation is increasingly recognized as important in cardiovascular risk and this way HIV can serve as a prototype population. But these results are likely to extend to a lot of different populations who have chronic inflammation for different reasons. Dr Carolyn Lam:                That's a great point, Virginia. As I'm listening, I'm wondering is there no end to this because now we say HIV and then we put other inflammatory diseases, then we say, "Well, women may be different from men," and then different ethnicities may be different. I think gonna be going closer and closer to precision risk prediction, if I might say. Could I just pick your brain here? What do you think the future is? Where's the room for machine learning approaches for risk prediction, individual almost down to that level? What do you think? Dr Ralph D'Agostino:      I think you're right on target. In some sense, the functions we have there's a sort of massiveness about it, when you come to view this population, back in the 50s and 60s and so forth, cardiovascular disease was such a major ... it still is a major problem ... such a major problem you identify some of the real items like the blood pressure and cholesterol, and you attack and develop functions on that and you'd find that you're affecting positively a huge number of individuals, but now as, like Jeanne was saying, and others have been saying, you start focusing, you've got this massive group of individuals who should have their blood pressure controlled and what have you, but if you go into HIV, you go into a number of other populations and so forth, there are other things that are driving these disease and driving the manifestations of the disease. It isn't that blood pressure isn't important, it's that there's other things that are important. And so it's machine learning and so forth and deep learning that you're gonna have to be dealing with manifestations on very high levels and maybe even get into genetics.                                                 Look in the cancer field ... I do a lot of work with the FDA ... look at the cancer field now; how it's so genetically driven in terms of a lot of the drugs the so-called biomarkers, which are basically driven by uniqueness in populations. I think that's definitely going to be, or is the future of these cardiovascular functions. Dr Carolyn Lam:                Okay audience. You heard it, right here. These are exciting times. In the meantime, thank you so much for this precious, valuable piece of work. Virginia, Bongani, Ralph, it was great having you on the show.                                

Hypoglycemia, the electron transport chain, and beta-oxidation are the subjects we covered on this session of The MCAT Podcast. Don't forget to subscribe. Links:

This lesson covers the regulation of beta-oxidation. The primary regulation of beta-oxidation occurs at the mitochondrial membrane, where fatty acids are transported into the mitochondrion. Acetyl CoA carboxylase governs both the formation of fatty acids from non-carbohydrate precursors and the transport of fatty acids into the mitochondrion. Its product, malonyl CoA, is a substrate for fatty acid synthesis in the cytosol but a regulator of fatty acid transport in the mitochondrion. Thus, there are two isoforms of acetyl CoA carboxylase that are regulated similarly. The cytosolic isoform plays a direct role in fatty acid synthesis and the mitochondrial isoform regulates beta-oxidation. This ensures that the two processes are regulated reciprocally, so that one is shut down to the extent the other is activated, thereby preventing wasteful futile cycling. The primary regulator of acetyl CoA carboxylase activity is, as you might expect by this point, energy status. When a cell needs more energy, it lets fatty acids into the mitochondrion. When it has too much, it shuts down fat-burning. For the full episode, go to chrismasterjohnphd.com/mwm/2/22 Sign up for MWM Pro for early access to content, enhanced keyword searching, self-pacing tools, downloadable audio and transcripts, a rich array of hyperlinked further reading suggestions, and a community with a forum for each lesson.

Short summary: In episode 21 Gabor and I explore how measuring hepatic acetyl-CoA in live rats advances our understanding of metabolism.

Barry Murray is a sports nutritionist and member of the Irish Ultramarathon Team currently working with Pro Tour cyclists. Barry has won several ultra-distance (70-200 km) running races, The Mourne Mountain Way, The Abbots Way, The Giants Causeway, The Wicklow Way, The Kerry Way, all without eating anything for breakfast. How? In a word, fat-adaptation. In this interview, Barry describes his work with the pros and six much overlooked factors for high-performance ultra-endurance training: sunlight, cold thermogenesis, DHA from seafood, grounding, and water quality. Here’s the outline of this interview with Barry Murray: [00:01:56] BMC Racing Team. [00:02:06] Ultramarathon. [00:05:39] Low-carb, high-fat, ketogenic. [00:06:14] Fasted state training. [00:07:16] Sirtuins. [00:12:38] AMP kinase. [00:13:35] Beta-oxidation. [00:13:44] Mitochondrial biogenesis. [00:15:20] Acetyl-CoA. [00:15:38] Peter Attia, MD. [00:16:03] Stepwise adaptation. [00:18:38] What are the pro cyclists doing? [00:19:35] Nutrition is the new doping. [00:23:00] Team Sky. [00:23:55] Steve Cummins. [00:24:29] 2-3 years to adapt. [00:26:00] Can be done in 6-12 months. [00:27:04] Train low, race high. [00:28:26] Rates of brain glucose use. [00:29:30] Pyruvate dehydrogenase. [00:30:34] Ketone MonoEster article. [00:31:21] Are the pros using ketone supplements? [00:32:05] Chris Froome. [00:32:33] Cox, Pete J., et al. "Nutritional ketosis alters fuel preference and thereby endurance performance in athletes." Cell Metabolism 24.2 (2016): 256-268. [00:34:00] Beta-oxidation is the goal, not ketogenesis. [00:35:16] Jack Kruse. [00:37:11] Six things to optimal health and living. [00:37:30] Sunlight. [00:37:53] Cold thermogenesis. [00:38:05] Seafood. [00:38:18] Grounding. [00:38:25] Non-fluoridated water. [00:39:55] UVB tanning booths. [00:40:37] Schumann resonance. [00:41:38] Electron Transport Chain (ETC) [00:43:44] Sven Tuft of Orica Bike Exchange. [00:44:45] Wim Hof. [00:45:30] Kox, Matthijs, et al. "Voluntary activation of the sympathetic nervous system and attenuation of the innate immune response in humans." Proceedings of the National Academy of Sciences 111.20 (2014): 7379-7384. [00:48:28] http://optimumnutrition4sport.co.uk/ [00:48:56] Fasted State Training Adaptations Jack Kruse forum post.