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Mastering Nutrition

Hi, I'm Chris Masterjohn and I have a PhD in Nutritional Sciences. I am an entrepreneur in all things fitness, health, and nutrition. In this show I combine my scientific expertise with my out-of-the-box thinking to translate complex science into new, practical ideas that you can use to help yourself on your journey to vibrant health. This show will allow you to master the science of nutrition and apply it to your own life like a pro.
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Mastering Nutrition
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Now displaying: September, 2017
Sep 30, 2017

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

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Sep 29, 2017

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

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Sep 27, 2017

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

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Sep 27, 2017

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

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Sep 26, 2017

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

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Sep 25, 2017

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

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Sep 18, 2017

“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

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Sep 12, 2017

One of the advantages of carbohydrate over fat is the ability to support the production of lactate. This is so important that carbohydrate is physiologically essential to red blood cells and certain brain cells known as astrocytes. For the same reason, it plays an important role in supporting the energy requirements of the lens and cornea, kidney medulla, and testes, and supports the quick boosts of peak energy needed during stressful situations that include high-intensity exercise. The biochemical role of lactate is to rescue NAD+ during times when NAD+ becomes limiting for glycolysis and glycolysis becomes a meaningful source of ATP. Through the Cori cycle, lactate can extract energy from the liver’s supply of ATP and deliver it to other tissues such as skeletal muscle in the form of glucose. This lesson fleshes out the physiological and biochemical roles of lactate and serves as a foundation for the next lesson, which explores the role of carbohydrate in supporting sports performance.

Watch the full lesson at chrismasterjohnphd.com/mwm/2/17

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Sep 10, 2017

Did you realize that thiamin deficiency can be caused by your environment? In the old days, beriberi was associated with the consumption of white rice. Nowadays, refined foods are an unlikely cause of thiamin deficiency because they are fortified. We associate deficiency syndromes such as Wernicke’s encephalopathy and Korsakoff’s psychosis primarily with chronic alcoholism. Yet there are regional outbreaks of thiamin deficiency among wildlife attributed to poorly characterized thiamin antagonists in the environment. Thiamin-destroying amoebas can pollute water, thiamin-destroying bacteria have been isolated from human feces, and thiamin-destroying fungi have also been identified. Could toxic indoor molds and systemic infections play a role as well?

Thiamin deficiency is overwhelmingly neurological in nature and hurts the metabolism of carbohydrate much more than fat. Indeed, preliminary evidence suggests thiamin supplementation can help mitigate glucose intolerance. Ketogenic diets are the diets that maximally spare thiamin and are best characterized as treatments for neurological disorders. Anecdotally, ketogenic diet-responsive neurological problems sometimes arise as a result of infection. Could ketogenic diets be treating problems with thiamin or thiamin-dependent enzymes? One must exercise caution here: fat contains little thiamin, and ketogenic diets can actually cause thiamin deficiency if they don’t contain added B vitamins. The relationships between thiamin, glucose metabolism, and neurological health are remarkable and desperately need our attention.

For the full lesson, go to chrismasterjohnphd.com/mwm/2/14

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Sep 9, 2017

The pyruvate dehydrogenase complex catalyzes the one decarboxylation step that carbohydrate undergoes to generate acetyl CoA, which accounts for the one carbon dioxide molecule produced in carbohydrate metabolism that is not produced during the metabolism of fat. It also accounts for why burning carbs requires twice as much thiamin as fat. In fact, the pyruvate dehydrogenase complex is remarkably analogous to the alpha-ketoglutarate dehydrogenase complex, sharing all the same cofactors and catalyzing virtually the same reactions. In this lesson, we look at why this has to be true and how it works. This provides the foundation for our deeply practical look at thiamin in the next lesson.

chrismasterjohnphd.com/mwm/2/13

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Sep 7, 2017

Since carbs are richer in oxygen than fat, they consume less water in their metabolism and release more carbon dioxide. Carbon dioxide puts stress on the lungs and its generation should be restricted in the case of lung injury to allow healing. This calls for a low-carbohydrate, high-fat diet. On the other hand, carbon dioxide is needed to support the action of vitamin K and biotin, and to promote delivery of oxygen to tissues during exercise.

In our first glimpse into glycolysis and beta-oxidation, we find that understanding the basic chemical makeup of these molecules is deeply relevant to how we would manipulate the diet in many contexts of health and disease.

For the full lesson, go to chrismasterjohnphd.com/mwm/2/12

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Sep 6, 2017

Now we take it clinical: how do we use what we’ve learned so far to interpret the section of a urinary organic acids test that reports the citric acid cycle metabolites?

We begin by looking at the underlying chemistry to explain the curious absence of oxaloacetate on these tests. We conclude by mastering the ability to spot three unique patterns: energy overload, oxidative stress, and thiamin deficiency.

For the full lesson go to chrismasterjohnphd.com/mwm/2/11

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Sep 5, 2017

This lesson looks at the fundamental principle that atomic oxygen is the limiting factor for the release of carbon dioxide in metabolism, and when we don’t have enough we take it from water. This will become very relevant when we cover fats versus carbohydrates, because they consume different amounts of water and release different amounts of carbon dioxide for this very reason. That, in turn, relates to a number of health endpoints such as the functions of vitamin K and biotin, delivery of oxygen to tissues, and the stress placed on the lungs during breathing.

Here, we look at the principle in the citric acid cycle. In doing so, we see that, while textbooks only point to two water molecules consumed, a third water molecule is irreversibly consumed to donate oxygen to the cycle via phosphate.

For the full lesson, go to chrismasterjohnphd.com/mwm/2/7

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Sep 4, 2017

This lesson addresses the curious case of why CoA makes a brief cameo in the citric acid cycle during the formation of succinyl CoA only to leave again in the next step. We dig into the chemistry underlying the high-energy thioester bond that CoA forms with acyl groups, which explains more broadly one of the key roles of sulfur in energy metabolism. We conclude by looking at how the appearance of CoA allows us to harness energy released during the decarboxylation of alpha-ketoglutarate to form ATP directly during “substrate-level phosphorylation,” or, alternatively, to use energy from ATP to invest in the synthesis of heme.

chrismasterjohnphd.com/mwm/2/9

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Sep 3, 2017

This complex is so rich in biochemical concepts and relevance to health and disease. Having done the dirty work of looking at its organic chemistry mechanisms in the last lesson, here we explore broadly applicable biochemistry principles like energetic coupling and substrate channeling. We look at how thiamin deficiency, oxidative stress, arsenic, and heavy metal poisoning can affect metabolism, and how to recognize markers of these processes in blood or urine. We make the subtle yet critical distinction between oxidative stress and oxidative damage. We look at the role of this complex in Alzheimer’s disease. We then turn to the product of this complex, succinyl CoA, to examine how it provides an entry into the cycle for odd-chain fatty acids and certain amino acids and an exit out of the cycle for the synthesis of heme. In doing so, we look at the roles of vitamins B12 and B6 in these processes, the use of methylmalonic acid to diagnose B12 deficiency, and the ability of B6 deficiency to cause sideroblastic anemia.

For the full video, go to chrismasterjohnphd.com/mwm/2/8

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Sep 2, 2017

The alpha-ketoglutarate dehydrogenase complex is marvelously complex and incredibly rich in details that are relevant to the big picture of metabolism and to many issues of health and disease. Today, we break down what actually happens so that we can spend all of Wednesday’s lesson discussing the rich array of relevant principles it brings to light.

For the full video, go to chrismasterjohnphd.com/mwm/2/7

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Sep 1, 2017

Are you interested in working with me one-on-one so I can help you better meet your health goals?

Good news! I’m now accepting new clients for both hourly consultations and health and wellness packages.

Here are the core things I’m best at that I would love to do for you:

  • Help you develop actionable priorities and an overall strategy for improving your health.
  • Discuss your experiences with you and suggest useful tests that you could ask your doctor about.
  • Analyze the results of genetic tests, digital food logs, and blood and urine measurements for markers of health and nutritional status. I can then use these analyses to suggest practical strategies that you could implement with proper supervision of a health care professional.

If you want to want to read more about what I have to offer, head over to the main consultations page:

Health and Wellness Consultations With Chris Masterjohn, PhD

Although I have no plans to expire the offer, I suggest you act rather swiftly if you want to book sessions between now and February because the spots available from September through January are limited and will fill up fast. After February, my availability is much more open. 

Once again, here are the links you may need:

Whether sooner or later, I look forward to working with you and helping you fulfill your health goals.

If you have any questions about how this works, please do not hesitate to email me at chris [at] chrismasterjohnphd {dot} com.

Sep 1, 2017

If you develop dry skin on a low-fat diet, especially if you're eating egg whites and throwing out the yolks, it could be a biotin deficiency. Or, it could be an essential fatty acid deficiency. Either way, egg yolks and liver come to the rescue.

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