Mastering Nutrition

This is my long-form podcast where I dive deep into a topic.

052: Ask Us Anything About Gut Health

051: Ask Us Anything About Sports Nutrition with Chad Macias, Danny Lennon, and Alex Leaf | May 25, 2019

On May 25, members of the CMJ Masterpass joined me, Chad Macias, Danny Lennon, and Alex Leaf in a live Zoom meeting to ask us anything about sports nutrition, and here’s the full recording!

050: Ask Us Anything About Hormones with Dr. Carrie Jones | May 10, 2019

On May 10, members of the CMJ Masterpass joined me and Dr. Carrie Jones in a live Zoom meeting to ask us anything about hormones, and here’s the full recording!

049: Pantothenic Acid, Part 2 (Foods, Lab Tests, and Supplements)

048: Pantothenic Acid, Part 1 (What It Is and Why We Need It)

047: Niacin, Part 2: Blood Tests, Foods, and Supplements

In part 1 we covered what niacin is and why you need it. Here’s part 2, where Alex Leaf and I cover blood tests, foods, and supplements! 

• How much do we need? The RDA has some flaws, including claiming women need less than men, when all the evidence shows women need *more* than men.

• Why eating enough protein is so essential, yet so unreliable as a way of boosting niacin status.

• How the niacin in your coffee, seeds, and grains is all locked up and unavailable, and how to release it through proper preparation. Do you drink light roast or dark roast? You may either hate or love this episode… or you might just switch coffees.

• Should we take high-dose niacin to lower cholesterol? Alex has a theory on how we can do that without getting diabetes. 😬

• High-dose niacin can cause liver failure and can kill lab mice. But Alex and I know how to steer clear of that problem!

• NAD-boosting supplements are the new darling of the anti-aging industry. But should we take nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), or should we endure all the whole-body burning 🔥 that the folks injecting NAD+ are so hyped up about? We discuss the promises and problems of these approaches.

• Why you should match glycine to one form of niacin and trimethylglycine (TMG) to all of them.

046: Niacin, Part 1: What It Is and Why You Need It

Niacin is vitamin B3. You use it to make NAD, the ultimate anti-aging molecule that repairs your DNA and lengthens your telomeres, and the most foundational molecule in our entire system of energy metabolism. 

It is especially important to protecting your mind, your skin, and your gut.

• You use it to release all your neurotransmitters. This is why depression sets in as the earliest sign of deficiency and why, when it gets bad enough, it leads to suicidality or schizophrenia-like psychosis.

• You use constantly it to repair the microscopic damage done to your skin every time you step out into the sunlight. This is why red, inflamed skin appears on the backs of your hands or on your face when you’re deficient, but only if you get outdoors a lot.

• You use it to fuel the rapid turnover of cells in your intestines (the cells that absorb the nutrients in our food are replaced every 2-3 days!), and to repair those cells from the constant barrage of insults they face (think of everything those cells *don’t* let in our body 💩and the fact that *they* need to stare all that stuff down!) This is why deficiency will give you diarrhea and make you deficient in lots of other nutrients.

• You use it for lots of other things too, like participating with riboflavin to make the methyl group of methylfolate and recycle glutathione, the master antioxidant of the cell. You use it to recycle vitamin K, to support detoxification in the liver, and to synthesize cholesterol, fatty acids, neurotransmitters and nucleotides.

Who needs more? We all do! 

Why? Because just aging alone depletes niacin and getting sick or developing diseases as we age depletes it all the more. Niacin repairs damage, so the more damage we face the more we consume. 

In fact, this is why many people are taking supplements like nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN), to slow the onset of aging, or to age more gracefully. Some people are even injected NAD!

But should we be?

And what about the dark side of niacin? We all know the flush -- the redness and itching that accompanies high-dose niacin that people take to lower cholesterol. At high doses, niacin can even damage the liver. How? By sapping methyl groups. Sapping methyl groups can give you liver failure when it’s *really* bad, but sapping them just a little can leave you feeling weak, emotionally stuck, or tied up in a mental funk.

In this two-part podcast series, Alex Leaf and I tackle all of these questions. This is part 1, where we teach you what niacin is and why you need it. 

In part 2,  we’ll cover how to get niacin in foods, blood tests, and supplements.

045: Why You Should Manage Your Riboflavin Status and How to Do It

Riboflavin is the ultimate fat-burning nutrient. It makes even a bad MTHFR work right, and it keeps you looking young and beautiful forever.

Here’s everything you need to know about why you should manage your riboflavin status and how to do it. 

In this podcast I join with Alex Leaf of Examine.Com. I focus on what riboflavin is and what it does, while Alex focuses on riboflavin supplements.

Going into this podcast I changed my mind about three important things:

• While I had always discussed riboflavin as relevant to methylation and MTHFR, I had kept it in the back seat in my methylation protocol. Half way through recording this podcast I realized that it really deserves a front seat in my MTHFR protocol. In fact, it may be the case that there’s nothing wrong with the common MTHFR polymorphisms at all and that they only appear to hurt MTHFR activity because most of us aren’t getting enough riboflavin. And why aren’t we? Liver. Liver. We just have to eat liver.

• In Testing Nutritional Status: The Ultimate Cheat Sheet, I had included HDRI’s erythrocyte glutathione reductase activity test as test for assessing riboflavin status. After doing the research for this podcast, I am now convinced that this test is only reliable as a marker of riboflavin status when the lab tests the enzyme activity with and without the addition of riboflavin, which HDRI doesn’t do. I will be revising the cheat sheet soon to rely solely on LabCorp’s whole blood riboflavin test for assessing riboflavin status.

• I have, for years, believed that riboflavin 5’-phosphate (aka, flavin mononucleotide or FMN) supplements are better than plain old riboflavin, especially for people who are hypothyroid or have low adrenal status, since these conditions impair the activation of riboflavin to it’s 5’-phosphate form. After doing the research for this podcast I now believe that for healthy people it makes no difference and that for people with small intestinal pathologies, the cheaper, less fancy, plain old “riboflavin” is likely to be more effective.

In this podcast we being by considering the fictional stories of people who seem to have little in common. We then explain their stories by looking at the signs and symptoms of riboflavin deficiency. We consider the science of what riboflavin is, how it is used by the body, what it does for us, how to have great riboflavin status, and how to become deficient. We round this out with an extensive discussion of riboflavin supplementation. 

044: Nutrition in Neuroscience Part 4

043: Nutrition in Neuroscience Part 3

Part 3 of how NUTRITION has a HUGE impact on your BRAIN!

Everything in your brain is something you ate, something you made from something you ate, or, in a few cases, something your mother ate. Nutrition impacts your mental and emotional health, the function of your five senses, and your conscious and unconscious control over your body movements.

Join me as I lead you in a safari through the textbook, “Neuroscience,” pointing out along the way all the interesting connections to nutrition. Listen in for part 2 on the THE FIVE SENSES!

042: Nutrition in Neuroscience Part 2

Part 2 of how NUTRITION has a HUGE impact on your BRAIN!

Everything in your brain is something you ate, something you made from something you ate, or, in a few cases, something your mother ate. Nutrition impacts your mental and emotional health, the function of your five senses, and your conscious and unconscious control over your body movements.

Join me as I lead you in a safari through the textbook, “Neuroscience,” pointing out along the way all the interesting connections to nutrition. Listen in for part 2 on the NEUROTRANSMITTERS!

041: Nutrition in Neuroscience Part 1

Nutrition has a HUGE impact on your brain!

Everything in your brain is something you ate, something you made from something you ate, or, in a few cases, something your mother ate. Nutrition impacts your mental and emotional health, the function of your five senses, and your conscious and unconscious control over your body movements.

Join me as I lead you in a safari through the textbook, “Neuroscience,” pointing out along the way all the interesting connections to nutrition. Listen in for part 1 on the basic cellular functions of neurons!

040: Why You Should Manage Your Thiamin Status and How to Do It

Thiamin, or vitamin B1, is central to both energy metabolism and antioxidant defense. While its deficiency causes many problems, out of all the B vitamins its deficiency is most neurological in nature, because energy metabolism of the brain becomes severely compromised, and because neurotransmitters derived from protein cannot be produced. In its most severe form, beriberi, it can cause loss of muscle control, twitching, muscles freezing into awkward positions, and seizures.

Carbohydrates require twice as much thiamin as fat. This means, on the one hand, that high-carbohydrate diets increase the need for thiamin, and on the other hand, that people who are deficient in thiamin may have neurological symptoms that resolve when they go on a low-carbohydrate, high-fat diet.

Thiamin is widely distributed in foods. Historically, diets high in refined grain produced beriberi, but now refined grains are enriched in thiamin, so its deficiency is rarely caused by diet. However, certain foods such as raw fish and moths that are eaten in some cultures contain thiamin antagonists, gastrointestinal microbes can degrade thiamin, and there are various environmental causes of thiamin deficiency, such the algae that grow in dead zones. As such, environmental exposure to thiamin antagonists may be a more common cause of thiamin deficiency than poor dietary intake.

Still, some foods are much higher in thiamin than most others, with whole grains, legumes, yeast, and red meat being among the best sources.

039: Creatine: Far More Than a Performance Enhancer

Creatine, best known for its ability to build muscle and enhance athletic performance, is also critical for fertility, digestion, mental health, protecting your hearing, and keeping your skin vibrant and youthful.

In this episode, Alex Leaf of Examine.Com and I discuss everything you need to know about creatine. I focus on the basic science of what it does in the body, and Alex takes the lead in discussing the practicalities of supplementation.

038: Are We All Evolved to Eat High Protein?

In August of this year, 25-year-old bodybuilding mom Meegan Hefford was found unconscious in her apartment, brought to the hospital where she was declared brain-dead, and died soon after. The cause? “Too much protein before competition,” according to the New York Post. She had recently doubled her gym routine, started dieting, and begun slamming protein shakes in preparation for an upcoming bodybuilding competition. No one knew she had a rare genetic disorder that would make the breakdown of protein acutely toxic for her until after her death.

Does this tragic case carry lessons for the rest of us without rare genetic disorders? In this episode, I make the answer a definitive YES.

037: Living With MTHFR

MTHFR is an enzyme that allows folate (vitamin B9) to support the cellular process of methylation, which is important for the synthesis of creatine and phosphatidylcholine, the regulation of gene expression, neurotransmitter metabolism, and dozens of other processes. There are two common polymorphisms that decrease its activity, A1298C and C677T, with C677T having the stronger effect. Genetic decreases in MTHFR activity are associated with cardiovascular disease, neurologic and psychiatric disorders, pregnancy complications and birth defects, and cancer.

While discussions of these polymorphism tend to focus on supplementing with methyl-folate, this should only be a small piece of the puzzle, and may be unnecessary in the context of a diet rich in natural food folate. The bigger pieces of the puzzle are restoring choline, creatine, and glycine.

In this episode, I describe how the methylation system works, how it’s regulated, and how it’s altered with MTHFR variations. I then use this to develop a detailed dietary strategy and an evaluative strategy to make sure the dietary strategy is working.

036: Is Insulin Really a Response to Blood Glucose?

Insulin is almost universally considered a hormone whose primary purpose is to regulate blood glucose levels. Indeed, it does this. But is that the whole picture? When we look at what governs pancreatic insulin secretion inside the beta-cell, it’s about total energy and the versatility of the short-term energy supply, not about glucose. When we look at what insulin does to energy metabolism, it does far more than regulate blood glucose: it governs how we use energy and what we do with it.

What is insulin really doing? Find out in this episode. I can’t promise the episode is practical, but I promise it’s incredibly thought-provoking.

035: The Biochemistry of Why Insulin Doesn’t Make You Fat

Do carbs and insulin make you fat? The argument centers on the ability of insulin to promote the conversion of carbohydrate to fat and lock fat in adipose tissue, as well as the necessity of glucose to provide the backbone to fat molecules within adipose tissue. But the argument ignores that all of these pathways are fundamentally regulated at a biochemical level by how much energy you need and how much you have. In episode 44 of Mastering Nutrition, we take a deep dive into the details of the biochemistry and physiology and see how insulin serves as a gauge of whole-body energy and glucose availability but simply can’t be the thing that makes you fat.

034: Methylate Your Way to Mental Health With Dopamine

Our consciousness is like a net. We want the net to be fluid enough to let thoughts that bother us pass through without grabbing our attention, but strong enough to grab on to the ideas and motivations that will drive us to achieve what we value in life. Nutrition has a big impact on this net. In this episode, learn how foods like liver, egg yolks, meat, leafy greens, legumes, collagen, bone broth, spinach, wheat, and beets can help you achieve a fluid yet stable mental disposition resistant to anxiety, depression, and distraction.

033: Can Fat Fuel the Athlete?

In this episode, we look at whether fat can fuel the athlete. We begin with the physiological principles involved, then take a look at the evidence from studies swapping fat for carbs to see how it impacts athletic performance.

032: Is Coconut Oil Killing Us?

In this episode, I weigh in on the American Heart Association’s new Presidential Advisory and Dietary Fats and Cardiovascular Disease, and all the headlines that have been spinning on the supposed risks of coconut oil.

031: Why You Should Eat Glutathione

In episode 31, I explain why glutathione survives digestion and can be absorbed intact, and why supplementing with it or eating it in foods helps support your health.

030: What to Do About High Cholesterol

If you’re concerned about your cholesterol, or confused about what to do, this episode is for you. In this episode, I list the four key factors that control blood cholesterol levels and outline the simplest dietary or lifestyle changes we can make to have the biggest impact.

029: How to Read a Science Paper

In this episode, I explain how to come up with a good question, obtain the background information you need, find research, obtain full texts, organize them, read the different sections of a paper to get the right kind of value out of it, and critically analyze the study design. If you’re a beginner, this is really designed for you. If you’re more advanced, you’ll enjoy the specific examples I give of problems interpreting research studies.

028: Why You Should Manage Your Zinc Status and How to Do It

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.

There’s an easy solution to this mess: let’s master this topic, stat, with the Mastering Nutrition podcast, episode 28.

027: Why You Should Manage Your Selenium Status and How to Do It

Selenium is critically essential to the defense against oxidative stress and to thyroid hormone metabolism. Soil concentrations cause so much variability, however, 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.

026: Why You Should Manage Your Copper Status and How to Do It

In episode 26, 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. Listen in and enjoy!

025: Why You Need to Manage Your Iron Status and How to Do It

In episode 25, I tell the story of my personal struggle 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.

Interlude:What Makes a Good Marker of Nutritional Status?

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 this url: 

The episodes of the series are kept in the show notes section, under Episodes of the Managing Nutritional Status Series.

024: Why You Should Manage Your Glutathione Status and How to Do It

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 24 covers everything you need to know about why and how to manage your glutathione status.

023: Zinc Definitely Fights Colds, But You’re Probably Using the Wrong Kind

 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. Listen in to find out why!

022: What’s New With Vitamin K2?

Yesterday I introduced The Ultimate Vitamin K2 Resource. In episode 22 of the podcast, I’ve extracted from the resource the latest developments and elaborated on them for a more in-depth discussion. I begin by telling the story of my 2007 activator X article. What do I still stand by? What do I see differently? And then I carry us right up through some of the most recent developments as things continue to evolve now.

021: When Fat People Can’t Get Fat Enough and Lean People Get Fat in All the Wrong Places

In episode 20, 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 21, 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.

020: Insulin Resistance Isn’t All About Carbs and Insulin

In episode 17, I explained why ketogenesis isn’t all about carbs and insulin. Here in episode 20, I explain 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.

019: The Evolution of Diverse Vitamin D Requirements

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 19, 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.

018: How I Lost 30 Pounds in Four Months, and How I Knew It Was Time.

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 initiates 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.

017: Ketogenesis Isn’t All About Carbs and Insulin

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 initiates 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.

016: Should You Do CrossFit on a Ketogenic Diet?

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?

015: How I Beat Eczema With the Right Probiotics, but Why Soap May Be Your Worst Enemy

This past Wednesday, we all showed up live on Facebook so you could ask me anything about fat-soluble vitamins. Here’s the video, and the audio recording as a podcast. 

If you love these Facebook Live episodes, make sure to show up at the next one: Saturday, July 9, 2:00 PM Eastern time the theme will be “Ask Chris Masterjohn, PhD, Anything About Health, Fitness, or Nutrition,” which will be a free-for-all in the style of the first Facebook Live event. Just show up to my Facebook page at the right time and you’ll see the video. If you get there just before I start, refresh the screen until the video shows up. When you show up live, you get to contribute to the questions that literally become the show, which is exactly what makes these episodes so great.

014: Dietary Management of Heterozygous Familial Hypercholesterolemia (HeFH)

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.

013: Wait a Second, Is Glycation Actually GOOD For You?

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.

012: What Is Measuring Our Hba1c REALLY Telling Us About Our Blood Glucose and Diabetes Risk?

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.

011: Paleo f(x) Grab Bag: Carbs, Sex Hormones, Type 1 Diabetes, and More

In this episode, I discuss some important insights from my Paleo f(x) talk and audience responses to it, including the potential dangers of treating type 1 diabetes with a low-carb diet, the importance of carbs and body fat for fertility and sex hormones, and why some people might have a great sex hormone profile on a long-term ketogenic diet despite the importance of insulin’s contribution to fertility.

I also discuss Headspace meditation, contrast showers, Snapchat, U.S. Wellness Meats liverwurst, Kettle and Fire’s upcoming chicken broth and chicken mushroom broth, and my interview with Ben Greenfield.

010: How to Know if Your Genetics Contribute to Your Sensitivity to Blue Light and Poor Sleep, and What to Do About it

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.

009: Balancing Calcium and Phosphorus in the Diet, and the Importance of Measuring Parathyroid Hormone (PTH)

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.

008: The Two-Minute Hack Every Computer Junkie Should Be Doing for Their Wrists

In this short episode, I describe how voodoo flossing my computer-damaged wrists has made a tremendous difference in my ability to tolerate weight lifting (especially Olympic lifting) without wrist pain. I don’t think you need to lift weights to benefit from this (though I think you should lift weights). I think this is something that has the potential to provide great benefit to anyone who uses a computer a lot.

007: The Many Uses of Yoga Blocks Around the House, and Why a Standing Desk Isn’t Enough

In this episode I describe why a set of two yoga blocks has been one of my best low-cost investments in the last year, playing a variety of unexpected roles around my apartment, and allowing me to make major strides in increasing the diversity of positions I can work in to get a healthier level of hip mobility.

006: Why “Glycation” Is a Bad Reason to Restrict Carbs

In this episode, I respond to a listener’s question about whether glycation is a good argument against a high-carbohydrate diet. I agree that we should avoid refined carbs and empty calories, but in this episode I describe why “glycation” is really a misnomer and why carbohydrate is actually likely to protect against glycation.

005: My Evening and Morning Routines

In this episode I describe how I have designed my evening and morning routines to maximize my quality sleep and productivity.

004: What I’ve Been Eating, and How I Get It

I’m often asked what I eat, and here I answer the question. In addition, I describe how I have been getting my food and arranging my meals to meet my goals of productivity, fat loss, and good nutrition.

003: The Sugar Conspiracy — Trading One Nutritional Boogeyman for Another

In his April 7, 2016 piece in The Guardian, “The Sugar Conspiracy” Ian Leslie argues that the politics of nutrition has blinded us to the fact that sugar is more deserving than saturated fat of the status of dietary arch-villain and that the politics continue but the status of sugar and saturated fat are starting to switch.

But we need to move beyond nutritional boogeymen, not switch one for another.

Our sense of history and physiology — key concepts about the historical role of Ancel Keys, the rate at which sugar is converted to fat in a process called de novo lipogenesis, and whether insulin’s stimulation of fat storage can offer a plausible explanation of obesity — get distorted when we try to make a public enemy out of sugar, just as they do when we make a public enemy out of saturated fat.

It’s time for a more nuanced view.

002: As the Cholesterol Consensus Crumbles, the Stance Against Saturated Fat Softens

Is it really true that saturated fatty acids (SFAs) are the “bad fats” and polyunsaturated fatty acids (PUFAs) are the “good fats”?

Christopher Ramsden uncovered previously unpublished data undermining the conventional wisdom that we should replace saturated fats with polyunsaturated vegetable oils to lower cholesterol and prevent heart disease.

The public health establishment dismissed the findings. Here’s my take.

001: Coffee

I'm starting the podcast with coffee, because I start my day with coffee.

Why I drink coffee and won't apologize for it, but why I'm skeptical of the large body of literature associating coffee consumption with reduced disease risk.

Do we drink coffee by choice? Sort of. I discuss why our genes may play a role in our
coffee consumption and may be the ultimate influence on the risk of diseases that ultimately cannot be changed by coffee consumption.