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Mastering Nutrition — Alternative Health
Mastering Nutrition

Welcome to the Mastering Nutrition podcast.

Mastering Nutrition is hosted by Chris Masterjohn, a nutrition scientist focused on optimizing mitochondrial health, and founder of BioOptHealth, a program that uses whole genome sequencing, a comprehensive suite of biochemical data, cutting-edge research and deep scientific insights to optimize each person’s metabolism by finding their own unique unlocks.

He received his PhD in Nutritional Sciences from University of Connecticut at Storrs in 2012, served as a postdoctoral research associate in the Comparative Biosciences department of the University of Illinois at Urbana-Champaign’s College of Veterinary Medicine from 2012-2014, served as Assistant Professor of Health and Nutrition Sciences at Brooklyn College from 2014-2017, and now works independently in science research and education.

Copyright: © All contents copyright of Chris Masterjohn.

Latest Episodes:

Insulin Shuts Down Fat-Burning | MWM Energy Metabolism Cliff Notes #25 Oct 03, 2017

Show notes

Insulin prevents fat-burning in part by locking fat in adipose tissue and in part by shutting down transport of fatty acids into the mitochondrion inside cells. By downregulating lipoprotein lipase (LPL) at heart and skeletal muscle and upregulating it at adipose tissue, insulin shifts dietary fat away from heart and muscle and toward adipose tissue. By downregulating hormone-sensitive lipase in adipose tissue, it prevents the release of free fatty acids from adipose tissue into the blood. At the cellular level, insulin leads to the phosphorylation and deactivation of AMPK. Since AMPK inhibits acetyl CoA carboxylase, insulin-mediated deactivation of AMPK leads to activation of acetyl CoA carboxylase and the conversion of acetyl CoA to malonyl CoA. Malonyl CoA inhibits carnitine palmitoyl transferase-1 (CPT-1) and thus blocks the transport of fatty acids into the mitochondrion. Nevertheless, all of these steps are also regulated at the most fundamental level by energy status, as covered in lesson 22. Further, insulin stimulates the burning of carbohydrate for energy, as covered in lesson 24. So, is insulin's blockade of fat-burning sufficient to cause net fat storage, or does this critically depend on energy balance? This question will be answered in the next lesson.

For the full episode, go to chrismasterjohnphd.com/mwm/2/25

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Insulin Makes You a Carb Burner | MWM Energy Metabolism Cliff Notes #24 Oct 02, 2017

Show notes

Most people interested in health and nutrition know that insulin clears glucose from the blood into cells, but it is much less widely appreciated that insulin also makes you burn that glucose for energy. Insulin stimulates the translocation of GLUT4 to the membrane of skeletal muscle, heart, and adipose cells, and activates hexokinase 2. GLUT 4 increases the rate of glucose transport across the cell membrane and hexokinase 2 locks the glucose into the cell, making sure that glucose travels inward rather than outward. Insulin stimulates glycogen synthase, causing you to store glucose as glycogen, but it also stimulates pyruvate dehydrogenase, causing you to burn pyruvate for energy. The key determinant of which one of these you do is the energy status of the cell. Glucose 6-phosphate is needed to activate glycogen synthase, and it only accumulates if high energy status is inhibiting phosphofructokinase. If low energy status is stimulating phosphofructokinase, the net effect of insulin is to irreversibly commit glucose to glycolysis, and then to stimulate the conversion of pyruvate to acetyl CoA, which then enters the citric acid cycle to allow the full combustion of the carbons and maximal synthesis of ATP. Thus, if you need the energy, the net effect of insulin is to make you burn glucose to get that energy.

For the full episode, go to chrismasterjohnphd.com/mwm/2/24

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Insulin Isn't Just About Glucose | MWM Energy Metabolism Cliff Notes #23 Oct 01, 2017

Show notes

Insulin secretion. Remarkably, we know from dietary studies that we get the most insulin from eating carbohydrate, yet we know from molecular and cellular studies that insulin secretion is primarily triggered by the ratio of ATP to ADP inside the pancreatic beta-cell. The former implies that insulin is a response to glucose, while the latter implies that insulin is a response to total energy availability. What can explain this discrepancy? In this lesson, we explore the possibility that it is the anatomy and physiology that drive the dietary effect of carbohydrate rather than the biochemistry. Carbs are wired to get soaked up by the pancreas when blood sugar rises above the normal fasting level once the liver has taken its share to replete hepatic glycogen, whereas fats are wired to go primarily to the heart and muscle when those organs need energy and to go primarily to adipose tissue otherwise. The combination of circulatory routes and the relative expression of glucose transporters and lipoprotein lipase by different tissues likely directs fat to the pancreatic beta-cell as a source of ATP only during extreme hyperglycemia or when it exceeds adipose storage capacity due to obesity, insulin resistance, or very high-fat meals. The pancreatic beta-cell does have a diversity of complicated and often controversial secondary biochemical mechanisms that "amplify" the insulin-triggering effect of ATP, and carbs are more versatile at supporting these mechanism than fat. These likely make a contribution to the dietary effect, but they strike me as unlikely to be the primary driver of the dietary effect. Thus, insulin is a response mainly to carbohydrate availability but also to total energy availability, and this driven mainly by the anatomy and physiology but also by the biochemistry. Seeing insulin as a response to cellular energy status will eventually help us broaden our view of insulin as a key governor of what to do with that energy that goes far, far beyond regulating blood glucose levels.

For the full episode, go to chrismasterjohnphd.com/mwm/2/23

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Energy Status Regulates Fat Burning | MWM Energy Metabolism Cliff Notes #22 Sep 30, 2017

Show notes

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Energy Status Regulates Glycolysis |MWM Energy Metabolism Cliff Notes #21 Sep 29, 2017

Show notes

This lesson covers the regulation of glycolysis. The principle regulation occurs at phosphofructokinase, which guards the gate to the first irreversible, committed step to burn glucose for energy. What governs it? Energy. If you need more ATP, you burn more glucose; if you don't, you don't. If the cell has glucose beyond its needs for energy, it uses it for the pentose phosphate pathway, which allows the production of 5-carbon sugars and antioxidant defense if needed, or stores it as glycogen if there is room. If not, glucose-6-phosphate accumulates and shuts down hexokinase. This, together with low AMPK levels, causes glucose to get left in the blood. The other key regulated step of glycolysis is pyruvate kinase, where the primary purpose of regulation is to prevent futile cycling between steps of glycolysis and gluconeogenesis. On the whole, glycolysis and glucose uptake are regulated primarily by energy status and secondarily by glucose-specific decisions about the need for glycogen or for the pentose phosphate pathway. Since we mostly use glucose for energy under most circumstances, the key regulation of the pathway is the regulation of phosphofructokinase by energy status. This means glucose uptake is largely driven by energy status, and our decisions about preventing hyperglycemia should center on total energy balance.

For the full episode, go to chrismasterjohnphd.com/mwm/2/21

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Glycolysis | MWM Energy Metabolism Cliff Notes #19 Sep 27, 2017

Show notes

In this lesson, we examine the entire glycolytic pathway. We use as our theme the transfer of oxygen from phosphate to newly generated water. This explains why the standard stoichiometry of glycolysis found in textbooks show it generating two water molecules, and ties the information together with the analogous principles from substrate-level phosphorylation in the citric acid cycle and the relative differences in water consumption and carbon dioxide generation between fat and carbohydrate. As with our discussion of the citric acid cycle, we also reveal why the standard stoichiometry of glycolysis is misleading and why, when we account for atoms rather than molecules, we find glycolysis to be net water-neutral.

For the full episode, go to chrismasterjohnphd.com/mwm/2/19

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Beta-Oxidation |MWM Energy Metabolism Cliff Notes #20 Sep 27, 2017

Show notes

In this lesson, we examine the beta-oxidation in its simplest form: the breakdown of a long-chain, saturated fatty acid. We see once again the principle that the oxygen content of a molecule determines how much water its metabolism consumes and how much carbon dioxide its metabolism releases. In beta-oxidation, we consume one water per round and release no carbon dioxide. This reflects the fact that fatty acids are not hydrates of carbons like sugars are, which is where the name carbohydrate comes from.

For the full episode, go to chrismasterjohnphd.com/mwm/2/20

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Carbs and Sports Performance: The Evidence | MWM Energy Metabolism Cliff Notes # 18 Sep 26, 2017

Show notes

Can fat fuel intensity in a competitive athlete? This lesson takes a critical look at the commonly cited evidence in favor of a neutral or beneficial effect of low-carbohydrate or ketogenic diets on sports performance, as well as key pieces of conflicting evidence. Bottom line? Fat can fuel duration, but probably can never fuel your peak intensity, just as the physiology would predict.

For the full episode, go to chrismasterjohnphd.com/mwm/2/18

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Carbs and Sports Performance: The Principles | MWM Energy Metabolism Cliff Notes #17 Sep 25, 2017

Show notes

Can athletes fat-adapt their workouts? This lesson lays down the principles of exercise biochemistry and physiology needed to understand the importance of the three energy systems supporting energy metabolism in skeletal muscle: the phosphagen system (ATP and creatine), anaerobic glycolysis (dependent on carbs), and oxidative phosphorylation (dependent on carbs, fat, or protein). We discuss why maximal intensity always depends on carbs if the intensity and duration are sufficient to deplete phosphocreatine concentrations, and clarify the window of time and intensity that can be fat-adapted. This sets the foundation for the next lesson, which looks at the evidence of how carbohydrate restriction and ketogenic diets impact sports performance.

For the full episode, go to chrismasterjohnphd.com/mwm/2/17

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

Carbs Spare Protein In a Way Fat Can't | MWM Energy Metabolism Cliff Notes #16 Sep 18, 2017

Show notes

"Anaplerosis" means "to fill up" and refers to substrates and reactions that fill up a metabolic pathway as its own substrates leak out for other purposes. The citric acid cycle is a central example of this because its intermediates are often used to synthesize other components the cell needs. On a mixed diet where carbohydrate provides much of the energy, pyruvate serves as the main anaplerotic substrate. During carbohydrate restriction, protein takes over. Fat is the least anaplerotic of the macronutrients because the main product of fatty acid metabolism, acetyl CoA, is not directly anaplerotic. There are several very minor pathways that allow some anaplerosis from fat, but they are unlikely to eclipse the need for protein to support this purpose during carbohydrate restriction. Thus, carbs and protein are the two primary sources of anaplerosis. This means carbs can spare the need for protein, and that protein requirements rise on a carb-restricted diet.

For the full lesson, go to chrismasterjohnphd.com/mwm/2/16

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.

Chris Masterjohn, PhD, is the Founder and Scientific Director of the mitochondria test Mitome.

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