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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Mar 4, 2017

Do you want beautiful, flawless, radiantly healthy skin? Want to stay healthy during cold season? Want to eat that bagel without your blood sugar spiking through the roof? Then it's time to think about zinc.

Zinc is critical to every aspect of our biology, but the first things to go when we run low are our skin health, our immune system, and our glucose tolerance. Zinc, moreover, is critical to antioxidant defense, so should be considered broadly protective against all of the degenerative diseases that occur with aging.

Wait, are you too young to care about aging? No problem. You at least want healthy skin, great sex, or a lean physique, so listen up.

Zinc-rich foods are harder to come by then you'd think. Nutritional databases can be wildly inaccurate if you don't adjust for inhibitors of zinc absorption in natural foods. And zinc supplements can be valuable, but they're not a panacea. In fact, used wrongly, they can quickly induce a deficiency of copper and other minerals that are just as critical to your health. 

The show notes can be found at They contain recommendations for specific supplements.

This episode is brought to you by Kettle and Fire Bone Broth. Use the link to get $10 off your first order.

This episode is also brought to you by US Wellness Meats. Head to and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice.

In this episode, you'll find all of the following and more: 

0:00:35 Cliff Notes; 11:40 The discovery of zinc deficiency on diets of whole wheat bread with small amounts of milk and potatoes, a quarter pound of clay, and no meat: dry skin, hypogonadism, lack of secondary sex characteristics, short stature, frequent infections; 17:25 The biochemical and physiological roles of zinc; 19:00 structural roles of zinc, with an emphasis on zinc finger motifs; interactions with vitamins A and D, thyroid hormone, adrenal hormones, and sex hormones 24:07 Catalytic roles of zinc, including the RNA polymerases that make it necessary for the production of every single thing in the body; 26:30 Interactions with vitamin A, from transport via retinol-binding protein (RBP) through activation by alcohol dehydrogenases to retinal and retinoic acid through creating vision via rhodopsin and regulating gene transcription via DNA-binding of the retinoic acid receptor; 29:20 Regulatory roles of zinc 32:25 Zinc and oxidative stress (necessity for hydrogen peroxide production in the thyroid gland and immune phagocytes, zinc release from zinc-thiolate clusters; protective effects of metallothionein exchanging zinc for other metals; negative effects of uncoupling of endothelial nitric oxide synthase [eNOS] on blood vessel function and oxidative stress; 42:45 Regulation at the cellular level (metallothionein, MT; ZIP and ZnT transporters) 44:20 Regulation of metallothionein (metal transcription factor-1 [MTF-1] through the metal response element [MRE] controlled primarily by zinc but also heavy metals, antioxidant response element [ARE] via Nrf1 and Nrf2, which provides regulation by oxidative stress and copper, glucocorticoid response element [GRE] which provides regulation by adrenal hormones and inflammation; 53:40 What happens when we eat zinc (effects of phyate, amino acids, calcium, organic acids, and iron) 1:01:00 Plasma zinc and the exchangeable zinc pool 1:06:00 Factors that affect plasma zinc status (variation according to meals, diurnal variation, stress, inflammation, menstruation) 1:10:25 Causes and effects of deficiency 1:14:20 Variations in soil zinc; 1:15:40 Balance of animal protein and phytate in the diet 1:19:00 Causes and effects of toxicity (especially with respect to copper deficiency) 1:27:20 What is the best marker of zinc status? 1:29:45 Plasma zinc as a marker of zinc nutritional status; 1:37:00 Copper deficiency markers as the most sensitive markers of zinc excess 1:38:10 Dietary strategies (animal foods, especially oysters, red meat, and cheese; soaking, sprouting, and fermenting to neutralize phytate) 1:40:35 Zinc supplementation on a plant-based diet (especially relevant to vegan diets but also to vegetarian diets) 1:42:25 Supplementation of zinc (what form? Citrate, acetate, gluconate, picolinate, oxide? What dose? When to take it?) 1:44:35  Recommendations for timing of diet and supplements across the day for best absorption 1:47:00 Wrapping up

Feb 18, 2017

Selenium is critically essential to the defense against oxidative stress and to thyroid hormone metabolism. Soil concentrations cause so much variability in the selenium content of foods that any two of us could be eating the same diet and one of us could have too little selenium and the other too much. That makes it essential to understand how to measure and manage our nutritional status. In episode 35, I continue the series on managing nutritional status by teaching you how to do just that.

The show notes for this episode are found at They contain recommendations about foods and supplements.

This episode is brought to you by Kettle and Fire Bone Broth. Use the link to get $10 off your first order.

This episode is also brought to you by US Wellness Meats. Head to and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice.

In this episode, you will find all of the following and more: 0:00:34  Introducing the new name, Mastering Nutrition; 0:01:00 Cliff Notes; 0:10:55  My story with selenium deficiency: white spots in fingernails and frequent colds; 0:14:14  Soil variation plays a major role in selenium deficiency and toxicity; 0:18:40  Biological roles of selenium (antioxidant protection, immunity, thyroid health, through glutathione peroxidases and thyroid deiodinases, control of protein function through thioredoxin reductase, other poorly understood roles); 0:29:00  Signs of deficiency (vulnerability to viral infection and other infection, hepatic cirrhosis, white fingernails that can fall out, cardiac insufficiency and enlargement of the heart with fibrosis and necrosis as occurs in Keshan disease, increased vulnerability to vitamin E deficiency, iron overload, and toxin exposure) 0:39:45 Signs of toxicity (hepatic cirrhosis, white spots and streaks in brittle fingernails, loss of hair and nails, additional signs in acute toxicity from mistakes in supplement manufacture); 0:43:45  Optimizing between deficiency and toxicity: Hashimoto's thyroiditis and cancer; 0:49:00  Different forms of selenium in plant and animal foods; 0:49:38  How selenomethionine from plants is metabolized to selenocysteine; 0:55:10  How selenocysteine from animal foods enters as selenocysteine; 0:55:30  How selenocysteine is converted to selenide for incorporation into selenoproteins; 0:56:25  How inorganic selenite and selenate are converted to selenide using glutathione; 1:01:46  Markers of nutritional status (selenoprotein P, glutathione peroxidase, selenium concentration of various body tissues with an emphasis on plasma and serum but including other blood fractions, hair, and nails) 1:12:53 Ideal ranges of markers; 1:16:42  Dietary requirements and how to meet them with food (organ meats and offal, seafood, Brazil nuts, bioavailability issues in seafood, mushrooms, and cruciferous vegetables); 1:26:45 Why methyl-selenocysteine is not a substitute for selenocysteine and why selenomethionine is the best currently available option for a supplement; 1:28:13  The proper dose of a supplement; 1:35:07  Things we will learn in the future: implications of needing methylation to both utilize enough selenium and detoxify excess; interactions with glutathione and antioxidant system; selenoprotein P becoming commercially available to health care practitioners and individuals; the rise of novel markers as we learn more about the poorly understood selenoproteins 1:37:10  Wrapping Up

Feb 10, 2017

Stephan Guyenet made a book! The Hungry Brain is available now, and in episode 34, Stephan and I talk all about it.

Stephan is a long-time friend and colleague. He has a PhD in neuroscience, and studies the role of the brain in controlling the food we eat and the other behaviors we engage in that affect our body composition and risk of obesity. His book lays out how the brain makes these decisions and what we can do to outsmart these deeply rooted instincts in today's challenging environment.

We begin by talking about what makes us fat, why we are now fatter than ever, why our environment affects some of us so much more strongly than others, and what we can do about it on both an individual and societal level. Then we move on to the book: what you can get out of reading it, why Stephan decided to write it, and the process he used during the three years of research, writing, and publication. In the last part, I get Stephan's advice for people who want to follow a similar career path, and ask Stephan how he sees his career evolving now that he's left academia but has stayed so intimately involved with science.

You can find the shownotes for this episode at

This episode is brought to you by US Wellness Meats. Head to and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice.

This episode is also brought to you by Kettle and Fire Bone Broth. Use the link to get $10 off your first order.

In this episode you will find all of the following and more:

0:35 Introduction, Stephan’s bio, overview of the interview; 1:00 Why do we get fat and why are we fatter than ever before? 13:00 Teasing apart increased food intake from decreased physical activity; 15:53 If the Hadza (hunter-gatherers in Tanzania) don’t have higher energy expenditure than we do, why are they so lean? 19:03 Food reward hit our society after a long decline in physical activity; what happens when high food reward hits a society where physical activity remains high? 22:25 What is the most fattening diet in the world? 28:15 Are effort costs more powerful than exercise? 33:52 The effect of the “built environment,” the effort costs of exercise and the cultural honor we bestow on convenience; 35:17 If our environment has become so obesogenic, how come so many of us are lean? 39:23 In Nutrition and Physical Degeneration, Weston A. Price took hundreds of photos of people all over the globe who ate themselves into very ill health with diets rich in refined flour and refined sugar, yet none of them are fat. Why not? 43:03 What are the most impactful things we can do as individuals to maintain healthy body composition? 46:50 What are the most impactful things we can do as a society to encourage healthy body composition?
48:56 The risks of food taxes and similar political tools, and the risks of inaction.

51:09 Who should read Stephan’s book, “The Hungry Brain,” and what does he hope they’ll get out of it?

53:26 How did he decide to write “The Hungry Brain,” and why did he find the concept so compelling and book-worthy? 55:20 That the brain regulates body fatness seems obvious in retrospect. What hid its obviousness for so long? 59:56 How receptive are nutrition scientists to the food behavior concepts being studied by neuroscientists?

1:02:35 How researching this topic in such depth caused Stephan to recalibrate the evidence and understanding he needs before he would be willing to challenge the perspectives of experts.

1:05:27 A day in the life of writing The Hungry Brain; 1:06:35 How Stephan got experts to talk to him; 1:09:15 How Stephan made the decision to leave academia from his postdoc to write a book rather than pursuing a tenure-track faculty position, and how he sees his career path evolving; 1:12:53 If someone were to follow in Stephan’s footsteps and write a scientifically rigorous book for a general audience, what do they need to lay the foundations for success? Audience building, funding and frugality, time for writing, pitching a proposal, illustrations, keeping the gears of the publishing gears turning, publicity; 1:16:30 How much time did Stephan spend on this? 1:18:15 Managing a book advance 1:19:38 The surprising hurdles of self-employment: will Stephan keep jumping them, or get a job? 

1:20:00 Wrapping up: where people can find the book, where people can find Stephan’s other work.

Stephan has given us all so much for free over so many years. Let's all buy his book!

Feb 3, 2017

In episode 33, we continue the series on assessing and managing nutritional status. This time we talk about copper. Copper deficiency can cause anemia that is very difficult to tell apart from iron-deficiency anemia, osteoporosis, histamine intolerance, high cholesterol, and a variety of mental effects resulting from neurotransmitter imbalances. Serum copper and ceruloplasmin are excellent tools for assessing nutritional status, but are confounded by inflammation, birth control, menopausal status, and hormone replacement therapy, making it necessary to look at the diet, lifestyle, digestive problems, and other factors that make copper deficiency plausible. 

I discuss how to protect yourself from the small risk of copper in your drinking water, and why I think many claims about excess copper outside the context of frank toxicity are misleading.

Everything converges on the practical questions of what to do in these situations.

You can find the show notes to this episode at

This episode is brought to you by Kettle and Fire Bone Broth. Use the link to get $10 off your first order.

This episode is also brought to you by US Wellness Meats. Head to and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice.

In this episode, you will find all of the following and more:

0.00.35 Cliff Notes; 0.10:25 A case of copper deficiency? 0.14.00 Biochemical and physiological roles of copper (monoamine and diamine oxidases, MAO and DAO, lysyl oxidase, dopamine hydroxylase/beta-monooxygenase, peptidylglycine alpha-amidating monooxygenase, cytochrome C oxidase, superoxide dismutase, ceruloplasmin, hephaestin, metabolism of histamine, tyramine, polyamines, serotonin, norepinephrine, dopamine, conversion of dopamine to adrenaline, production of neuropeptides such as oxytocin, vasopressin, gastrin, neuropeptide Y, cholecystokinin, collagen synthesis, energy production, prevention of osteoporosis and neutropenia, immune support, cholesterol metabolism, antioxidant defense, mental health, and much more); 0:18:55 Copper's intimate relationship with iron; 0:30:10 What is the best marker of copper status (covers copper in serum, plasma, red and white blood cells, and platelets, ceruloplasmin, and other copper-dependent enzymes); 0:33:38 Effect of inflammation on ceruloplasmin; 0:35:10 Effect of estrogen on ceruloplasmin; 0:43:18 Causes of deficiency  0:43:50 How much copper do we need? 0:43:45 Best food sources; 0:48:30 Variation within food sources according to soil; 0:51:00 Zinc supplementation; 0:51:53 Digestive problems (SIBO, Celiac, antacids, proton pump inhibitors, PPIs, gastric bypass); 1:00:52 How to treat deficiency; 1:02:01 Which form of copper to use (oxide, sulfate, glycinate, etc)? 1:04:10 Toxicity: copper-mediated oxidative stress; 1:05:22 Wilson's Disease; 1:08:15 Infants and copper absorption; 1:11:00 Contribution of water to toxicity; 1:16:50 One case of supplement megadosing leading to liver failure; 1:17:30 Toxicity claims based on serum Cu or serum ZN/CU ratio are not reliable; 1:20:50 Summing up


Jan 27, 2017

In episode 32, I tell the story of my personal story with iron overload, and weigh in on the proper use of blood tests and strategies to manage anemia, hemochromatosis, and everything in between. It's important to realize that these are the extremes, and there is a large middle space where we need to not only manage how much iron we accumulate, but how we direct it away from its disease-promoting roles and into its health-promoting roles.

This is a great primer on iron as well as a source of insights you may not have encountered elsewhere, such as the importance of oxidative stress as an independent regulator of ferritin, and the potential dangers of supplements designed to protect against oxidative stress like milk thistle, Protandim, sulforaphane, and green tea extract, for people at risk of anemia.

You can find the show notes to this episode at

This episode is also brought to you by US Wellness Meats. Head to and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice.

This episode is brought to you by Kettle and Fire Bone Broth. Use the link to get $10 off your first order.

In this episode, you will find all of the following and more: 0:33 Cliff Notes; 10:30 Introduction; 13:12 My personal story with iron overload; 30:12 The physiological roles of iron: hemoglobin, myoglobin, nitric oxide synthase, iron-sulfur clusters in the cytochromes of the electron transport chain, guanylyl cyclase, thyroid peroxidase (TPO), myeloperoxidase (MPO), oxygen transport, energy and ATP production, cellular regulation, thyroid hormone production, immunity; 38:20 Iron as a source of oxidative stress: free iron, hydrogen peroxide, and the hydroxyl radical, oxidative stress as an independent regulator of ferritin; 41:10 Regulation of iron status;
Ferritin, long-term storage, protector against pathogens, protector against oxidative stress; Transferrin, short-term iron storage; Hepcidin, master coordinator of iron metabolism; HFE, communicator between transferrin and hepcidin; 49:10 Regulation of dietary absorption of plant and animal iron; 51:00 Measuring and assessing iron status: complete blood count (MCH, MCV, RDW, CHr), full iron panel, sensitivity and specificity of transferrin saturation versus ferritin, differential interpretation of ferritin as a marker of iron overload, inflammation, or oxidative stress; 1:11:43 What to do for anemia: differentiate potential causes, iron in foods (heme, nonheme, vitamin C, polyphenols, phytate, calcium), iron in supplements (iron-saturated lactoferrin, heme iron, liposomal iron), avoid Nrf2-stimulating supplements (like Protandim, sulforaphane, milk thistle, green tea extract), importance of followup measurements of ferritin 01:21:03 What to do for iron overload: blood donation, dietary management, phlebotomy, chelation, importance of followup


Jan 26, 2017

In this special interlude, I lay down the framework of the five core principles that make a good marker of nutritional status. This is to lay down the framework for a series of podcasts in the future about managing nutritional status for specific vitamins and minerals.

Since these core principles will be referred back to as a general reference in so many other episodes, this one has a special place outside of the sequence and you can reach it at any time with the easy-to-remember URL

This episode is brought to you by Kettle and Fire Bone Broth. Use the link to get $10 off your first order.

This episode is also brought to you by US Wellness Meats. Head to and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice.

In this episode, you will find all of the following and more: 37:23 Cliff Notes
09:25 Purpose of this podcast and its place in the upcoming series on managing nutritional status; 11:54 What are the five core principles? 12:05 Principle #1:
We understand its biochemistry and physiology; 15:04 Principle #2: It has been validated against changes in nutritional status; 17:17 Principle #3: Sensitivity; 17:52 Principle #4 Specificity; 19:45 Principle #5: It must be interpreted in the overall context of other markers and the clinical and health history, current signs and symptoms, and diet and lifestyle analysis; 23:20 Example of principle #1: Spectracell vs dp-ucMGP as tests of vitamin K2 status; 27:20 Example of principle #2: 25(OH)D vs. calcitriol; 29:20 Example of principle #3: transferrin saturation vs. ferritin
31:08 Example of principle #4: specificity of 25(OH)D and contexts where its specificity fails; 32:50 Example of principle #5: distinguishing between calcium and vitamin D deficiencies as causes of 25(OH)D by testing PTH, calcitriol, and analyzing the diet and lifestyle; 37:50 Shotgun approaches to nutritional testing; 40:30 Whether to act on leads from shotgun approaches should depend on the risks and other costs of the actions.

Jan 13, 2017

Glutathione is central to recovery from exercise, feeling good, looking good, aging gracefully, and preventing or overcoming both infectious diseases and chronic degenerative diseases. Episode 31 covers everything you need to know about why and how to manage your glutathione status.

This episode is brought to you by Kettle and Fire Bone Broth. Use the link to get $10 off your first order.

This episode is also brought to you by US Wellness Meats. Head to and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice.

In this episode, you will find all of the following and more: 00:35 Cliff Notes; 10:45  Introducing my new health and wellness packages13:25 The health benefits of glutathione: master antioxidant, central to liver detoxification and the defense against glycation, master controller of hundreds of proteins, mucus fluidity, bronchodilation, anti-aging, protection against diabetes and its complications including cataracts and cardiovascular disease, protection against Hashimoto's thyroiditis and other thyroid disorders, protection against infectious diseases by supporting the immune system's respiratory (oxidative) burst, protection against congestion, COPD, asthma, and other lung problems; 25:15 How to measure glutathione status, the importance of measuring it in both is reduced (GSH) and oxidized disulfide (GSSG) forms, and using those to calculate your redox status using my glutathione redox status calculator30:28 The synthesis, recycling, and regulation of glutathione; 37:00      Practical strategies to improve glutathione status: protein, vitamin B6, carbohydrate, whey protein and raw milk, bone broth and collagen, magnesium, metabolic rate (ATP), polyphenols (e.g. EGCG and other green tea catechins) and other phytonutrients (e.g. sulforaphane) as Nrf2 inducers, glutathione in foods, N-acetyl-cysteine and glutathione supplements, insulin and insulin resistance, MTHFR mutations, glucose 6-phosphate dehydrogenase deficiency, niacin, riboflavin, and thiamin, why Jarrow oral glutathione is my current choice of supplement 1:04:24      Tying it all together.

Dec 26, 2016

In episode 30, I talk about the use of zinc lozenges to fight colds. While nutritional zinc does support the immune system and your immunity may benefit from zinc supplements or zinc-rich foods, this has nothing to do with the use of zinc lozenges to kill colds. The science behind their use is strong, but it also suggests that most of the dozens of zinc lozenges on the market are absolutely useless. The only ones I currently use and recommend are Life Extension Enhanced Zinc Lozenges.

This episode is brought to you by Kettle and Fire Bone Broth. Use the link to get $10 off your first order.

This episode is also brought to you by US Wellness Meats. Head to and enter "Chris" at checkout to get 15% off your order as long as the final price is over $75 and you order fewer than 40 pounds of meat. You can use "Chris" to get the same discount twice.

In this episode, you will find all the following and more: 00:37 Cliff notes; 12:55 Zinc status is important to immune function, but that's not what this podcast is about. Nevertheless, I go through basic tips of getting good zinc nutrition; 16:48 My typical use of zinc for colds has missed the point; 18:08 Zinc has to be a lozenge to kill the common cold. In fact, the original discovery of its role in killing the cold was born from a child refusing to swallow a tablet and letting it dissolve in her mouth; 20:15 The main mechanisms by which zinc kills colds; 21:10 Importance of zinc ionization in nasal and adenoid tissue; 23:26      Importance of taking it at the right time (first couple of days of a cold); 27:10 pH of nose and throat tissue, not saliva, is important; 27:55 Gluconate and acetate are effective, but acetate is twice as effective as gluconate; 29:08 Astringency and metallic taste must be present, but are not sufficient; 31:35 Food acids used to cover taste such as citrate or tartrate cannot be present; 34:30 Magnesium cannot be present in a form that ionizes in the nose and throat; 36:30 Time of contact with membranes makes concentration, time to dissolve, and frequency of use important 39:50 Meta-analysis of randomized controlled trials; 42:20 Meta-analysis of individual patient data and lack of effect of age, sex, baseline cold severity, allergy status, race, and ethnicity; 44:00 George Eby's model showing a strong correlation between predicted ionic zinc yield and efficacy in RCTs suggests that the right dose of the right formulation taken at the right time in the right way could constitute a true cure of the common cold; 45:45 Only Life Extension Enhanced Zinc Lozenges fit the criteria; 54:13 My story with Life Extension zinc acetate lozenges.

Nov 23, 2016

Gullermo Ruiz of 3030Strong, a rising soon-to-be ND in the ancestral health community, interviewed me about my decision to leave academia and what I'll be doing to bring you value come January. 

In this episode you can find all the following and more: 17:15 Teaching facts versus teaching skills; 25:55 Good reasons (an inside view of translating research, a career in research), ok reasons (credibility with government, quasi-government, and policy circles) and terrible reasons (credibility in general or with a large audience, interest in the subject) to get a PhD; 34:15 The broken education system 37:45 Elementary school: scant but valuable opportunities to excel; 41:30 The unchallenging, stifling, and oppressive environment of high school; 47:10  the mismatch between ADHD and school; 50:55 Industrialization and the rise of modern schooling 53:55 My experience unschooling (not so much homeschooling) and the influence of John Taylor Gatto and Grace Llewellyn; 1:01:58 Diversity of educational opportunities is key to allowing everyone to thrive; 1:05:18 How I got involved with the Weston A. Price Foundation and nutrition science, and how I wound up with a PhD; 1:16:25 I thrive when solving a new problem, teaching the new solution, and then scaling it; a traditional classroom environment is better suited toward repetitive teaching of what is established, which doesn't feel creative; 1:23:10 The 20th century fragmention of science and the 21st century rise of systems biology and systems thinking; 1:26:40 My business model going forward: consultations, information products, independent research, tech collaborations; 1:36:20 Inspired by Gary Vaynerchuk, why I want to put myself out of business; 1:41:28 Who are my consulting clients 1:45:10 Inspiration and motivation for the path of entrepreneurship 1:48:30 Making the big decision to leave academia

Nov 20, 2016

This is a totally different type of episode. Brady Holmer, a first-year exercise science PhD student, interviews me for career advice. In this episode you can find the following: 11:50 Brady's background in exercise science research; 16:52 Where Brady is now; 18:28 Flow-mediated dilation as a measure of blood vessel function in diabetes and smoking cessation, and the influence of exercise and Vitamin E; 23:00  Brady's expert opinion on whether my CrossFit workout is classified as interval training when I stop to catch my breath; 27:52 Caffeine's effect on exercise physiology and physical performancel; 32:15 How Brady decided to interview one person in his field per month; 33:35 How I discovered Tim Ferris during his work on the 4-Hour Body; 41:10 Brady's selection of interviewees; 42:57 What Brady learned from his first interview; 45:00 Brady's career plan; 45:40 Setting up a research trajectory across doctoral work and postdoctoral work for long-term success in academia; 49:00 Leaving academia for self-employment, autonomy in and out of academia; 53:10 Academia offers massive autonomy within a specific framework, but the framework is more restrictive than it seems:  you can color however you want within the lines, providing you can get funding for the crayons you want, but you don't control the lines; 1:03:35 How to increase productivity during teaching and research; 1:08:48 Automation and leverage in academia; 1:16:48 You have to take time out of productivity now to maximize your productivity in the future; you can't optimize for both at the same time, and you need to be willing to go backwards in maximize your ability to get ahead; 1:23:25 How I decided to get into research; 1: 28:48 How to find ideas for research and project; 1:31:35 How my background in history helps me in science; 1:35:53 Brady's path to choosing his thesis topic; 1:39:10 How to make contact with influential people; 1:45:00 Advice to people thinking about a health career but unsure about graduate school and research; 1:51:15 The face of employment is changing: Uber, Instacart, the rise of the kind-of-employee-kind-of-solopreneur, and the normalization of the side hustle.

Oct 8, 2016

In episode 25, Insulin Resistance Isn't All About Carbs and Insulin, I explained why an individual cell would "decide" to stop taking up energy. Here in episode 26, I explain tissue-level energy overload, focusing on adipose tissue and liver.

At adipose tissue, the problem with fatness isn't the amount of fat. It's that we've reached the point where we can't get any fatter. Well, we can, but we can no longer do so while maintaining a healthy organizational structure within adipose tissue that allows blood, oxygen, and nutrients to get to where they need to go. Surprisingly, some of the things that enable proper expansion, and thus protect our metabolic health, are things that we usually think of as "bad," such as inflammation. In fact, the pro-inflammatory changes in the gut microbiome in response to an obesogenic diet provide information to adipose tissue that it needs to prepare for healthy expansion.  And adipose expansion is most protective at the site of the "bad" body fat: visceral fat in the abdomen.

At liver, the problem is fat gets trapped in the liver, flattening out everything in the cell and hogging the space needed for glycogen storage, and this can happen even in a lean person.

I conclude with some practical recommendations about body composition and nutrient density.

In this episode, you will find all of the following and more:

How adipose tissue expands (triglyceride and lipid droplet formation, extracellular matrix reorganization, capillary bed growth and reorganization); consequences of poor adipose tissue expansion (liver spillover into ectopic deposition in tissues like liver, skeletal muscle, and pancreas, internal oxidative and endoplasmic reticulum stress, hypoxia); providing more glycerol for greater triglyceride formation (via genetic manipulation of PEPCK to allow greater glyceroneogenesis) protects against metabolic dysfunction (which may indicate a protective role of carbohydrate, which provides the glycerol on a mixed diet); deletion of genes involved in lipid droplet formation exacerbates metabolic dysfunction; allowing matrix metallopproteinases (MMPs) to reorganize the collagen-based extracellular matrix known as septa protects against metabolic dysfunction; expression of hypoxia-inducible factor 1-alph (HIF1alpha) contributes to metabolic dysfunction; inflammation (tumor necrosis factor alpha or TNF-alpha, interleukins or ILs, toll-like receptors or TLRs) is necessary to allow proper extracellular matrix (ECM) reorganization and capillary bed reorganization; visceral abdominal fat expansion is most protective because visceral fat drains directly into the liver via the portal vein, and releases more fat into the liver when it cannot expand further; ectopic fat deposition at the liver is central because the liver is the metabolic hub of fat and carbohydrate metabolism; fat accumulation in liver likely directly compromises glycogen storage; sources of liver fat: include adipose and dietary fat; de novo lipogenesis (DNL) from carbohydrate is a minor source of liver fat; oxidative stress and poor choline status are major factors governing triglyceride export; the choline requirement is increased more by fat than other macronutrients and more by long-chain saturated fats than other fats; practical strategies: body composition is king, but it might not be the right time to lose fat; a well rounded, nutrient-dense diet is low-hanging fruit at any time; additional strategies require nutritional analysis with help of health care professional and data generation and interpretation.
Aug 24, 2016

In episode 23, I explained why ketogenesis isn't all about carbs and insulin. Here in episode 25, I explained why insulin resistance isn't all about carbs and insulin. If that doesn't sound crazy, let me put it this way: forget carbs; I'll even say insulin resistance isn't all about insulin.

We start with a riddle: what do obesity, exercise, cigarette smoking, and diets rich in fruits and vegetables all share in common? Hint: it's a centrally important physiological response to each of them that mediates their health effects.

In the course of answering this riddle, I explain the underlying physiology that I consider most important to "insulin resistance" and why I believe insulin resistance is best viewed as subset of something far more important. I conclude by outlining practical strategies to prevent and reverse it.

In this episode, you will find all of the following and more:

Why would an individual cell "decide" to stop responding to insulin?; the limitations of using blood insulin and glucose concentrations as a primary metric of insulin resistance are similar to the limitations of assessing your level of "boss resistance" by the number of phone calls you decline from your boss when you skip work; why your pancreas is sort of like your boss; reactive oxygen species (ROS) are central to the physiology; ROS inhibit aconitase and shunt internal energy toward fat storage; ROS inhibit further intake of energy; ROS inhibit fatty acid uptake into mitochondria; ROS inhibit glucose uptake; ROS increase the expression of the entire antioxidant system and xenobiotic defense system; Subbing players on the field in team sports provides a useful analogy to understand why ROS-mediated inhibition of cellular energy uptake is health-promoting when other cells can fill in; insulin resistance isn't all about insulin; some responses to cellular energy overload antagonize insulin; others mimic insulin; obesity vs. exercise; AMPK activation makes the net effects of ROS in exercise very different from obesity; micronutrient intake determines whether net effects of ROS support antioxidant defense; glutathione synthesis depends on both nutrients and insulin sensitivity and stimulation; insulin resistance isn't all about ROS. It's about the context in which ROS operate; the net hormetic pro-oxidant effects of fruits and vegetable polyphenol; the net toxic pro-oxidant effects of cigarette smoking; again, net effects of ROS aren't about ROS; their about the context in which ROS operate; nutrient density as a practical strategy in insulin resistance; body composition as a practical strategy in insulin resistance; low-carbohydrate diets as a useful practical strategy for body composition, with potential limitations in the long-term because of the importance of carbohydrates for antioxidant defense.

Aug 20, 2016

Whites have higher 25(OH)D than every other racial group, and the conventional explanation is that light skin evolved to allow sufficient vitamin D synthesis far away from the equator. In episode 24, I explain why these differences may relate to genetics of vitamin D metabolism that have nothing to do with skin color and may reflect a lower average need for 25(OH)D rather than a lower average ability to get enough. But "average" is the key word and when it comes to using this information on a practical level we need to look beyond racial categories and treat each person as an individual.

In this episode, you'll find all of the following and more: should I offer online nutrition classes?; this will start of sounding like it's about racial groups, but it's really about individuals; blacks in America have lower 25 (OH)D than whites; the conventional hypothesis explains this as dark skin being poorly adapted to these latitudes; genetic evidence suggests light skin began evolving long after the migration from Africa; aggregate global 25(OH)D data do not support the conventional hypothesis; Caucasians have higher average 25 (OH)D than non-Caucasians at every latitude; Caucasians have higher average 25 (OH)D at temperate latitudes than non-Caucasians have at equatorial latitudes; blacks in America have higher bone mineral content than whites; calcitriol dominance favors getting calcium from our food, while PTH dominance favors getting calcium from our bones; genetic variation in the 1-hydoxylase can account for the difference in 25(OH)D between blacks and whites in America, but this has nothing to do with skin color or racial groups in the way we have socially defined them; calcium intake could influence how the genetic variation translates into 25(OH)D; this does not affect white 25 (OH)D, and it could be related to calcium intake; ancestral calcium intake could have mediated selective pressure on the relevant genes; blacks in the United States have higher average calcitriol and a higher average calcitriol-to-PTH ratio than whites; similar differences between Inuit and Danes: lower 25(OH)D, higher calcitriol, and lower PTH; a traditional diet raises 25(OH)D, raises calcitriol further, and suppresses PTH further; Asians have lower 25 (OH)D than whites in Hawaii; the references ranges may in effect be applying average white requirements to drive recommendations for everyone; the Maasai and Hadza have higher 25 (OH)D, but this may be due to  higher calcium intakes, and/or higher ancestral calcium intakes that influenced their genetics; non-whites are probably adapted to lower 25 (OH)D than whites on average, but it is individual genetics rather than racial groups that are relevant; 25 (OH)D + calcitriol can be summed for a biological activity index; PTH should be in the lower half of the reference range; magnesium deficiency could confound the PTH measurement, but it probably has to be extreme.


Aug 9, 2016

This episode is part personal story, part practical how-to guide, and part insight. The insight I want to emphasize here is one that I think is far too often overlooked: sometimes we shouldn't be trying to lose weight because the time isn't right.

But if the time is wrong, how can we know? And once we know, what can we do to prepare our bodies for weight loss and allow the time to become right? The short answer is that if weight gain is due to stress, I strongly believe we should always destress first. For the detailed answer, listen in.

In this episode, you will find the following and more: why there is a time to lose weight and a time not to; why calories-in calories-out (CICO) is like gravity; the right approach to weight loss is likely to be the one that incorporates 2-3 intuitive principles that allow you to sustain a caloric deficit while feeling satiated and energetic; there are a lot of those principles, so the 2-3 that work best for you probably has less to do with their general efficacy and more to do with your own personal psychological and behavioral traits; my skinny teens, my powerlifting/bodybuilding musclehead body, my grad school-induced dad bod, getting my postdoc fatso on, putting 6-7" on my waist in my first semester as a professor; it all turned around when I read Tim Ferris's 4-Hour Workweek; running on a treadmill while sleeping 10 hours a day, traveling to destress, gaining with CrossFit, leaning out with CrossFit; using the greyhound formula recommended by Alan Aragon and Brad Schoenfeld in The Lean Muscle Diet; using MyFitnessPal to track calories as recommended by CrossFit South Brooklyn; R-Lipoic acid, D-biotin, acetyl-L carnitine, coenzyme Q10 (CoQ10), coenzyme B vitamins to smooth out energy between meals; Headspace app or other mindfulness meditation, yoga, dance, martial arts, could help self-awareness, the key to knowing when the time is right; destressing is the key to make the time right when it's wrong; resisting social pressure and self pressure to lose weight is, ironically, the key to making the time right to lose weight.

This episode is brought to you by US Wellness Meats. I use their livewurst as a convenient way to make a sustainable habit of eating a diversity of organ meats. They also have a milder braunschweiger and an even milder head cheese that gives you similar benefits, as well as a wide array of other meat products, all from animals raised on pasture. Head to and enter promo code "Chris" at checkout to get a 15% discount on any order that is at least 7 pounds but under 40 pounds (it can be 39.99 lbs, but not 40). You can use this discount code not once, but twice!

Jul 28, 2016

Did you know that adding MCT oil to your pasta is more ketogenic than restricting your carbohydrates to ten percent of calories?

Many people think of carbohydrate and insulin as central to ketogenesis, but the direct biochemical event that initiate ketone formation is actually the oversupply of acetyl groups to the TCA cycle during conditions of oxaloacetate depletion.

While largely a biochemistry lesson, in this episode I also teach you the practical implications of this. There is more than one route to ketogenesis, and while they all produce ketones, they are fundamentally different in important ways.

Adding coconut, MCT oil, or exogenous ketones allows you to reap benefits of ketones without necessarily restricting carbohydrates and insulin, and that may be useful if you are also trying to reap some of the benefits of carbohydrate and insulin.

On the other hand, certain conditions that respond to ketogenic diets, for example refractory childhood epilepsy, need stronger degrees of ketogenesis than you can achieve simply by adding MCT oil to pasta.

Understanding the difference allows you to better make practical decisions about your diet that are most consistent with your priorities.

In this episode, you will find all of the following, and more:

An overview of the TCA cycle and burning carbohydrate for energy; the critical importance of oxaloacetate (OAA) to allow acetyl groups to enter the TCA cycle; how we burn fat on a mixed diet; the meaning of the phrase, "fat burns in the flame of carbohydrate" or “fat burns in a carbohydrate flame"; loss of lean muscle mass can occur if dietary carbohydrate and protein are too low to maintain OAA levels, and fat cannot spare this loss; under carbohydrate restriction, OAA is not repleted by carbohydrate and is used for gluconeogenesis, while more fatty acids reach the liver to make acteyl CoA;  the oversupply of acetyl groups in excess of OAA initiates ketogenesis; insulin shifts fat to adipose tissue, but this doesn't cause obesity; MCTs go straight to the liver via the portal vein rather than going to the blood via the lymph in chylomicrons, and they thereby avoid that effect of insulin; insulin suppresses the carnitine shuttle; MCTs do not require the carnitine shuttle and are therefore immune to this effect of insulin; MCTs at breakfast suppress food intake at lunch; MCTs added to pasta increase beta-hydroxybutyrate; two ways of getting ketones: selective deprivation vs. abundance; if you are trying to get ketones but having negative effects of carbohydrate restriction (e.g. declining exercise performance in sports requiring anaerobic glycolysis, declining thyroid hormone and sex hormones, elevated cortisol and LDL-C) you can add MCTs to get the ketones; comparison of beta-hydroxybutyrate concentrations from MCT vs. 10% carb vs. classical ketogenic diet.

Jul 25, 2016

In this episode, I give my take on a recent masters thesis paper by Rachel Gregory from James Madison University, which reports a study where just under 30 members of Rocktown CrossFit and Sports Performance were randomized to do CrossFit for six weeks with a normal diet or a low-carbohydrate ketogenic diet.

The ketogenic diet led to weight loss and loss of bodyfat without hurting the performance on a 6-7-minute for-time workout-of-the-day (WOD)-style test involving a 500-meter row, 40 bodyweight squats, 30 ab mat situps, 20 hand-release pushups, and 10 pullups.

Herein, I explain why I think this study does show that the average person can lose weight and get fit with this method, but why it doesn't really get to the heart of the questions I would be interested in, which are these: how would a ketogenic diet impact maximal performance on weight-lifting sets of 5-12 reps, or in sports involving short bursts of energy such as football, basketball, baseball, soccer, and tennis, and do the hormonal adaptations to the diet ultimately have  the potential for negative impacts on thyroid hormone, cortisol, LDL-cholesterol, and sex hormones?

In this episode you will find all of the following and more:

The protocol of the study; changes in caloric intake, body weight and body composition; why the ketogenic diet's spontaneous decrease in calories can easily be explained by the effect of variety restriction on food reward, as Stephan Guyenet has explained well over at Whole Health Source; the changes in performance that occurred; how carbs, fat, and creatine impact the three energy systems of phosphagen or creatine phosphate, anaerobic glycolysis, and oxidative phosphorylation; why carbohydrate intake would primarily impact maximal performance at tasks requiring 15-90 seconds of intense work rather than a 6-7 minute WOD; why the ability to raise a 5RM to a new PR in trained subjects would have been a better question to address these concerns; why most team sports would also fall into this category; why free T3 (fT3), cortisol, LDL-C, and sex hormones (testosterone, estrogen, progesterone, etc) should be examined; and why how full your "stress bucket" (allostatic load) is will most likely be the ultimate determinant of whether these hormonal systems are negatively affected.

Jul 22, 2016

In this episode, I tell the story of my own battle with eczema. I begin by describing my extraordinary recovery from extreme eczema using the right probiotic. I then describe how a more recent relapse led me to discover the incredible importance of mitigating soap exposure when gut-related approaches don't seem to work.

In this episode, you'll find the following, and more:

Chris Kresser’s interview with Glenn Taylor on fecal microbiota transplants inspired this episode.

My own story with eczema.

Recovery with Garden of Life's Primal Defense (now Primal Defense Ultra).

Mild re-occurrence tied to poor gut, poor sleep, high work stress.

Key feature of an effective probiotic for me is S. boullardii plus bacteria.

Prostaglandin E2, derived from arachidonic acid, plays a central role in preventing eczema by water-proofing the skin.

Humidity can "hide" eczema by preventing water loss through a dysfunctional skin barrier.

Minimizing exposure to soap with kitchen gloves and by avoiding unnecessary hand washing are central to preventing topical aggravation of eczema.

Topical application of a fat -- such as shea butter -- after soap exposure can mitigate the damage caused by the soap.

It's important to pay attention to both the internal, systemic causes of eczema and the external, topical factors that will aggravate eczema once it has started.

Jul 18, 2016

This episode is a recording of the Facebook Live event, "Ask Chris Masterjohn, PhD, Anything About Health, Fitness, and Nutrition" that originally aired on Tuesday, July 12, at 5:00 PM eastern time.

In this episode you will find all of the following and more:

  • For a woman with bruising, spider veins, and cellulite, should we be thinking of collagen, clotting, or calcification? Should we be thinking of vitamin C, copper, glycine, and vitamin K2?
  • Are there nutritional cures for autoimmune diseases?
  • Does eating fruit with protein hurt the digestion and absorption of the protein?
  • Is the Randle cycle a reason to eat a low-fat, high-carbohydrate diet, especially during a caloric deficit?
  • What should we do about elevated Lp(a), and does it make a difference if it's caused by diet, genes, or health status (for example, LDL oxidation)?
  • Why vitamin A and organ meats may be the underappreciated fix for oral allergy syndrome.
  • What do we do for wound healing after surgery?
  • Do we nourish the microbiome by nourishing yeast, bacteria, or both?
  • Why we should be conservative but not paranoid about antibiotics, and why we should be even more conservative about antifungals, even when they're natural.
  • Should we deep fry foods in coconut oil?
  • Is vitamin C an antioxidant or a pro-oxidant? Should this keep us awake at night?
  • Ideas for healthy (and low-PUFA, low-phytate) snack foods to replace granola.
  • General lab tests for vitamin and mineral status without any leads on specific nutrients to investigate.
  • How do we determine the right amount of high-intensity exercise during pregnancy? How do we determine if the "stress bucket" is too full?
Jul 2, 2016

This episode is a recording of the Facebook Live event, "Ask Chris Masterjohn, PhD, Anything About Fat-Soluble Vitamins" that originally aired on Wednesday, June 29, at 5:00 PM eastern time.

In this episode you will find all of the following and more:

Fat-soluble vitamin nutrition during warfarin therapy, and the critical importance of working with the supervising cardiologist or whoever prescribed the warfarin.

Overuse of vitamin D supplements, and the use of parathyroid hormone (PTH), diet, and lifestyle analysis for a more prudent approach.

My opinion on Life Extension's vitamin K supplement.

Too many fat-soluble vitamins versus nutrient imbalances.

Accidental poisoning of pets with warfarin analogues designed to kill rodents, and treating the pet.

Does it matter what time of day you take vitamin D?

Are nutritional databases reliable?

I predict technology that could help nutritional databases become more reliable and usable.

Is Bulletproof coffee sufficient to help fat-soluble vitamins get absorbed?

How I manage my own vitamin D intake and sun exposure to balance the priorities of getting sufficient vitamin D and circadian rhythm stimulation while avoiding sun-induced skin damage.  

Resveratrol: even the hormetic dose requires many nutrients found in foods to have its effect.

Balancing vitamins A and D in pregnancy.

Use of low-dose aspirin in pregnancy.

How to get a day’s intake of calcium.

Fermented cod liver oil: amines and self-experimentation.

Is it ok to take vitamin D in large doses once per week instead of small doses daily?

Do babies need to take vitamin D supplements?

What can be done to help fat-soluble vitamin absorption?

Jun 23, 2016

In this episode, I discuss dietary management of familial hypercholesterolemia (HeFH). This question was asked on the Facebook Live episode from 06/16/2016, "Ask Chris Masterjohn, PhD Anything About Heart Disease," but I was unable to get to the question within Facebook's time limit.

Please note that HeFH is a medical issue and the purpose of this episode is not to diagnose or treat anyone with HeFH. This is educational in nature and the information should only be used to manage HeFH under supervision of a qualified health professional.

Herein, I discuss why I believe the Kitavan diet should serve as an ancestral diet on which to model dietary management of HeFH. It is a low-fat, low-cholesterol, high-carbohydrate diet where most of the fat is highly saturated because it comes from coconut, some of it is is from fish, and where the carbohydrate mostly comes from starchy tubers but some comes from fruit.

The best way to get to the root of the problem in heterozygous FH is to take the one working gene for the LDL receptor and try to bring it up to the expression level that would be found in someone without FH. This can be done by maximizing the biological activity of thyroid hormone (within the range considered euthyroid) and by maximally suppressing PCSK9 activity with the help of strong insulin signaling. These come down to managing good body composition and eating a low-fat, protein-adequate, micronutrient-adequate, high-carbohydrate diet.

Restricting cholesterol may be helpful, but it also comes at the cost of cutting nutrient density, since some of the most nutrient-dense foods -- liver and egg yolks -- are also rich in cholesterol. Therefore, it should be #2 in the line of defense rather than #1.

Replacing saturated fat with polyunsaturated fat and using statins should both be tools in the kit, but they should be tools much further down the line of resort because they are less related to the root of the problem and they may come at costs that compromise health and longevity.

Jun 20, 2016

This episode is a recording of the 06/16/2016 Facebook Live event, "Ask Chris Masterjohn, PhD Anything About Heart Disease."

Among the questions answered in this episode are the following:

Should we be micromanaging specific saturated fatty acids to prevent heart disease?

Should we use our knowledge of our ApoE genotype to help decide what to eat (and specifically, should the E4 allele causes us to avoid saturated fat)?

The persistent importance of the total-to-HDL-cholesterol ratio.

Why the vitamin E content of HDL particles could be determining its protective functions.

Can established heart disease be reversed?

Does moderately high blood pressure directly contribute to heart disease, or is the association between moderately high blood pressure and heart disease reflect some underlying factor that contributes to both?

Do Americans consume too much calcium?

Using essential oils to combat heart disease.

How do we approach the question of using diet and lifestyle versus medication?

Jun 13, 2016

This is a recording of the Facebook Live episode from Saturday, June 11, 2016, where I offered you the chance to ask me anything and did my best to answer your questions. In this episode you can find the following:

2:11 Is it the saturated fat that causes inflammation in animal models of obesity?

9:37 What do I think about Ray Peat’s and Andrew Kim’s views on sugar?

19:01 How essential are antioxidants in the diet? How much is too much?

29:38 What do I think about Brian Peskin’s work on “parent” essential oils?

31:16 What do I recommend as tests for folate status?

35:58 What would I recommend to recover from an accidental exposure to gluten?

44:33 What would I recommend telling a group of doctor’s interested in nutritional therapy about fats and cholesterol? (this includes a bit about choline)

54:49 How much protein should we eat to balance the priorities of muscle mass and longevity?

1:05:36 Is nutritional ketosis desirable for a healthy person, and is 100 grams of carbs per day enough?

1:19:51 What do I think about the potential for gluten withdrawal to help with neuromuscular issues and gross motor delays in children despite negative IgA tests?

1:24:22 Can someone’s triglyceride-to-HDL-cholesterol ratio be too low?

Jun 9, 2016

In this episode, I wrap up glycation week by discussing why glycation may play essential physiological roles in the body. In the early days of methylglyoxal research, Albert Szent-Gyorgyi, who won the 1937 Nobel prize in Physiology or Medicine for his discovery of vitamin C and critical steps in energy metabolism, saw the molecule as part of a regulatory system. In the early research into glycolysis, the system that converts methylglyoxal to pyruvate was seen as part of energy metabolism. Only later did glycation become synonymous with toxicity. Current science can be used to make a compelling case that methylglyoxal is normally produced as part of glycolysis to prevent a dangerous buildup of glyceraldehyde and that it rises during carbohydrate restriction to help preserve much-needed glucose and to enable the conversion of fat to additional glucose. This could be seen as an elegant system of regulation and a key part of energy metabolism. Nevertheless, it is unclear where the dividing line between physiology and pathology lies, and I see the apparent rise of methylglyoxal during carbohydrate restriction as part of a stress response that should not be chronically activated.

Jun 7, 2016

In response to popular demand, this week is glycation week. In this episode, I discuss the strengths and limitations of using Hba1c to measure our cumulative recent exposure to blood glucose and diabetes risk. Many people will be familiar with the fact that variation in red blood cell turnover confounds this measurement. Less well known is that variations in the deglycating enzyme fructosamine 3-kinase (FN3K) also confound the measurement. Counter-intuitively, if you have a higher rate of this deglycating enzyme but a lower rate of downstream metabolism of 3-deoxyglucosone, your lower Hba1c could actually mean MORE glycation. I conclude that Hba1c is a useful test, but only in the context of a bigger picture put together with more information.

May 11, 2016

In this episode, I answer a listener's question about whether I am worried about my phosphorus intake and whether a high phosphorus intake is ok as long as it is balanced by calcium. I describe the biochemistry and physiology of the system that regulates calcium and phosphorus, their distribution in foods, how to determine the right balance in the diet, and how to use parathyroid hormone (PTH) as a blood measurement to assess whether the dietary balance is working for an individual.

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