Podcast Transcription: Mastering Nutrition: How to Think Clearly About Diet in a World of Conflicting Advice with Christopher Masterjohn

Christopher Masterjohn: I think that most people probably shouldn't be adding too much oil to their food. I do think that there's a very individual response to different macronutrients and I, so I know that from the perspective of an intentional modification of body composition. Which is kind of dominates the fitness space, generally added oils to negative. 

I do think that that is a good default, but I personally would say that that people should look at how their diet is impacting their glucose and lactate, and I like waking morning fasted glucose and lactate  

Ted Ryce: before we start. I want to tell you this. If you're waiting for your life to slow down before you take control of your health and your body, it's not happening. 

Life doesn't slow down. There's always gonna be another deal, another deadline, another trip, another fire to put out. Another reason to put it off. So either 2026 is the year you finally lead yourself, the way you lead your business, or it's just another year of excuses. And if you're done negotiating with yourself, go to lean after forty.com and see if you qualify. 

Your business doesn't tolerate inconsistency and your body shouldn't either. If you're over 40, the best time to get in shape was decades ago. There's only now take action now. Let's get back to the show. Welcome to the Legendary Life Podcast, where it's all about taking control of your health, losing fat, transforming your body, and living the life you deserve. 

With celebrity, fitness trainer and longevity enthusiast, Ted Rice, Chris, master John. It's been several years, but really excited to have you back on the show.  

Christopher Masterjohn: Thanks for having me here. Appreciate it. Good to be back.  

Ted Ryce: Yeah. And uh, yeah, I recently saw you on Joe Rogan and I was like, Chris, he's still out there doing his thing and, uh, immediately reached out to you. 

And not only that, Chris, but you have some, I guess, controversial or what some people feel are controversial beliefs about VO O2 max seed oils and more. So that's kind of where I want to take this, this conversation.  

Christopher Masterjohn: I don't know if anyone has an opinion on seed oils. That's not controversial, but,  

Ted Ryce: yeah. 

Well, yeah. Maybe we can, if you're, if you're open to it. Let's just start there, because my reading of the data is that. Well, a lot of the things that, let's say the low carb or keto carnivore community talk about, it's like, well, you know, it kind of morphed from like, carbs are bad, sugar is bad because insulin insulin's a fat storing hormone, blah, blah, blah. 

Right? And then it shifted kind of to start to include seed oil. So all of a sudden fat is. You know, not all fats are bad, but this specific type of fat. So can you talk about what seed oils are for those people who maybe aren't, haven't been following this conversation like you and I have?  

Christopher Masterjohn: So, uh, seed oil is a catchall term for modern oils that did not exist in, for the most part, among our ancestors. 

Primarily because seeds are a lot more, you need more advanced technology to extract oil out of seeds compared to fruits. So olive oil is a fruit oil. You don't take the seeds and crush them to derive olive oil. You take the fruit flesh. Olive is a fruit despite it not tasting sweet. But, um, or you know, coconut is a fruit oil and there's animal fats. 

And so for the most part, through most of human history, we have not been able to extract oils out of seeds very well. There are some kind of exceptions. So sesame seeds, for example, are, you know, traditionally, uh, hummus. Well, hummus has tahini in it, but. Anyway, that that's just generally true right now. If you look at a chemical level, the thing that stands out about the seed oils is that they're very high in polyunsaturated fatty acids, or PUFAs and polyunsaturated Fatty acids are highly vulnerable to oxidation, which plays a role. 

You know, the oxidation of polyunsaturated fatty acids in our cell membranes. And our tissues generally plays a role in chronic disease. Some people would look at that and say, well, yeah, that's because we have too much oxidative stress. We don't have enough antioxidants. That's why they're oxidizing. 

Other people would say, well, yeah, but you're really increasing your risk if you load up on, uh, amounts of polyunsaturated fatty acids that our ancestors never would've gotten. Those two perspectives are kind of where people lie, mechanistically. Then there's a ton of data on them, so there's different types of studies on them. 

There's randomized controlled trials on them. There's ones that last seven to 12 weeks. There's ones that last five to eight years. There's prospective cohort studies, there's cross-sectional studies. There's. There's prospective cohort studies or cross-sectional studies with food frequency questionnaires, with tissue seed, oil fats, and so on, and there's a lot of controversy around interpreting those. 

And a big reason, like one of the major reasons that there is so much controversy as well, is that you could take any disease and you could see conflicting mechanisms. The main reason that seed oils were promoted. In the United States and in the west in general is because it was thought that they lower cholesterol, therefore they will reduce the risk of heart disease. 

But you can look at heart disease, you can say, well, actually oxidation of the cyl oil fats is a major driver of that, independent of the level of cholesterol in the blood. So maybe that makes a difference. And in fact, the guy who was the chair of. The 1984 NIH Consensus Conference that was quoted in the famous 1984 Time magazine cover that showed the frowning face made of, uh, where the frown was made of bacon, the, and the eyes were made of eggs, and it said. 

Cholesterol has been proved deadly and our diets will never be the same, and which was also the basis for the 1985 Nobel Prize given to Brown and Goldstein for their discovery of the LDL receptor, which is the target of all cholesterol lowering drugs, all of that. The guy who was the chair of that conference, Daniel Steinberg, he got quite a bit of anxiety over the promotion of corn oil and other seed oils. 

For the purpose of lowering cholesterol in the blood, because it was his lab that was trying to show the mechanism. There was a lot of evidence that high cholesterol causes heart disease at that time, but the skeptics were saying, well, what's the mechanism? How does the cholesterol get into the artery? 

And his lab showed that it was oxidation of the seed oil fats in the membrane of the LDL particle that drove it. And so he tried to gloss over that by saying. Now I've proven how cholesterol gets into the cell into the arterial wall. So that's the clinching evidence that proves that cholesterol causes heart disease. 

But on the down low, he was kind of like, I don't know if I like promoting corn oil when it's oxidation, these corn oil fats. That's actually mechanistically driving that. So maybe we should promote olive oil instead. 'cause it's kind of neutral and. There was a general and, and also the LA Veterans Administration Hospital study, which was the longest placebo, double-blind, placebo controlled trial of seed oil fats. 

Ever done suggested, maybe, I wouldn't say proved, but suggested that, uh, too much seed oil causes cancer. And so there were a lot of people who were uneasy with the promotion of corn oil that had been going on at that time. And you know, like I, most of us who are alive today don't remember how hard they pushed corn oil. 

And you know, there are other people who, who think corn oil is is bad 'cause it's high in omega six and low in Omega-3 and whatever. So it's like no one promotes corn oil anymore. But my grandparents, you know, they grew up believing that corn oil was gonna save them from heart disease. Um, that's what everyone was told back then. 

They quietly backed away from it because they were like, huh, this might be causing cancer. And it might be kind of a double-edged sword with respect to heart disease. But we already told them that they have to hold the eggs and butter because cholesterol will never be the same, uh, because cholesterol has proved deadly and our diets will never be the same as the Time Magazine cover says, what are we gonna do now? 

And that's kind of where the obsession with olive oil was born. Not to say that olive oil isn't a traditional fat and that it doesn't have a track record in the Mediterranean, it does. But, you know, but the obsession with olive oil as the darling fat exploded after that. And, you know, you don't realize the degree to which the, these what actually caused people to be so obsessed with it. 

But a major part of the history is this unease about whether corn oil was dangerous or not, that led to, to adopting olive oil. But anyway, the, so the point is you can pick your disease. You pick if you pick heart disease, which is the central disease that dominates the entire history of why we transitioned to using seed oil fats in the United States. 

You can look right there and you can see that the people who were in charge of making the big decisions at the NIH Nobel Prize Time Magazine, they were kind of like, huh, I don't know whether these are good or bad. Uh, even the LA Veterans Administration Hospital study. They, you know, they did show a reduction in heart disease, but their conclusion was our study was eight years. 

Most other one were five. Clearly what we need is studies that are well in excessive eight years instead of the five year studies that were the usual goal because our eight year study left the question of whether these oils are toxic, unresolved. That was the major conclusion from the eight year study. 

Um, you know, so the, the community in general was, was quite uneasy with the seed oil fats. Precisely because you could make a case against them and you can make a, and you can make a case for them or a case against them. They do lower cholesterol just like our drugs that we're putting everyone on, but that cancer, I don't know man. 

And so, you know that like they naturally, uh, they naturally are prone to controversy. If you are looking at it from a blank slate perspective, and I think a big problem with this too is the evidence-based community. I think evidence-based medicine is a real thing that's rooted in science, but the on the internet, the evidence-based people who call themselves evidence-based are generally  

Ted Ryce: Yeah, ideological. 

Christopher Masterjohn: Well, I mean the, yeah. Uh, well, uh, let me say this. They use as their, as, I mean, evidence-based medicine does this as well, but it's rooted in statistics, right. And statistics says that. Your default hypothesis, the null hypothesis, and a lot of people confuse null to mean default because of that when they're talking about it, but null means there's no effect. 

So statistics says you assume nothing is anything until you have a reason not to be able to reject the claim, that nothing is anything. You know, to adopt that as your guiding force for statistics is great, but to adopt it as your guiding force for life is kind of stupid because that means that you stand for nothing. 

You think nothing. You believe nothing. It's like it's not it do it do when it, we come from millions of years of history or 7,000 years of history or anything beyond the last. Four weeks of history, you should have something to guide you in during the vast majority of what is a gray area in life other than this, the, other than borrowing from statistics, the concept of the null hypothesis and applying it to your whole life, right? 

And so if you're, what a lot of people are doing who are rejecting seed oils is saying. I don't need a 20 year randomized controlled trial to prove to me that this causes cancer. I'm just gonna look at the fact that my great grandparents never ate it, and I trust the diet that my great grandparents. 

Made more than I trust, whatever the market has put in the grocery store based on the profit motive. You know, because the, the other thing is if you are, if you take the null hypothesis as your guiding central belief until proven otherwise, you don't get the default of randomness. You get the default. You, Nabisco is not using the null hypothesis when they're trying to make you eat more Oreos, right? 

Like the market is, is using value, positive reasons for putting stuff in stores. They don't care about the null hypothesis. They care about a long shelf life. They care about a high profit margin, right? So if you go into the grocery store and you say, I'm gonna use the null hypothesis, my guiding principle. 

Then you are not guided by statistics. You are guided by the profit motives of the corporations that put all the food in there. Right? So I, I think that's the, it's that philosophical divide. That's the, that's the key controversy.  

Ted Ryce: Yeah. And, and thanks for breaking that down. I feel like, uh, the, the people who listen to the show, you know, talking about the null hypothesis, I really wanna stay focused on, uh, at least for the moment, you know, thanks for sharing that history and everything, but. 

I think where, what the issue is, um, is like e even why, like I'm, there's very few people who, who I'd even want to have this conversation with. And, and you're one of them, even though, right? Like, uh, like you said, well, it's very ideological. I am not interested in people's confirmation bias. Right. I'm, I'm interested like, hey, what, what do we know here? 

Right. Just to, just to kinda rewind a little bit and talk about seed oils and, um, getting your perspective right. So if I understand you correctly, what you're saying is, look, there's been a lot of studies done on this stuff. They didn't exist before. And some of the shorter term studies show, right, a drop in cholesterol when at least, at least, you know, my understanding is when it's, when you're replacing saturated fat with seed oils. 

But the, and, and here's the other thing. I think some of the issue is a lot of the people maybe on the carnivore, the, the more extreme ends of the carnivore keto. Groups, if you will. It's like, oh, this will make you fat, independent of calories. And so they make a lot of claims that aren't backed by the evidence at all. 

But, and then people like myself and also the people who follow me, it's like, well. What, what, what do we know? Okay, so it'll lower cholesterol, but it doesn't necessarily raise inflammation or make you fat or do any of the things that it, that, you know, some of the ke uh, keto carnivore extremists say, but there is this issue more long term that it could be causing cancer. 

Is that what you're saying?  

Christopher Masterjohn: I think that I would not say that I am, I would only be concerned about cancer, but I would be con my position, which is not the same as almost anyone else's, but I think the most rational position is to think of enriching your tissues in polyunsaturated fatty acids. Beyond the normal baseline for most of human history, creates an oxidative liability because it makes your tissues more vulnerable to damage and it's hard to see. 

What that does, because if your study does not allow a sufficient amount of time for the damage to occur and is not done in a sufficiently vulnerable population or is not done with an endpoint that is that where that population would be sufficiently vulnerable, then you are not going to see those effects. 

And so. The LA Veterans Administration Hospital Study in Cancer is, one of the interesting things about that is that it's not just the longest study that was ever done, which is very relevant because if you look at the time course of cancer, it, it took years for it to even start happening. But also those people were, uh, the oldest out of anyone. 

Any of the, at a, the mean age in that study was higher than the mean age of any of the other seed oil trials, and you have to be old to get cancer. There are childhood cancers, but in general, at a population level, you get cancer when you're old enough that you didn't die of heart disease like you, you pass heart disease and then you get old enough to die of cancer. 

Right. So it, it's, you know, and then I also think it's complete nonsense that the evidence-based community on the internet, which in totally divorced by the way, from the scientific community in general, rejects reading anything into animal experiments. I, I don't think that we can assume that something works one way in a mouse and therefore works the same way in a human. 

But we can look for things where we have a lot of evidence in humans, and we have some gaps in the data. We know that animal models replicate everything from the human model, and we can fill in some of the gaps that we're not able to investigate in humans or that haven't been investigated yet. So fatty liver disease is very relevant because. 

Massive amounts of people have fatty liver disease. I mean, basically obesity is strongly cor, incredibly strongly correlated to it. So we have a fatty liver epidemic in the same proportion as we have an obesity epidemic. And there are a lot of short, or not a lot of, there are a handful of short-term seven to 12 week trials, which we know from the older trials are useless because the conclusion from the older trials was that none of the older trials were long enough. 

And you know, 1969 we concluded that the major thing we need next with seed oils is for the trial to be a lot longer than eight years. Fast forward to two thousands, and we get seven week trials, 12 week trials. It's like, what is this telling us? But anyway, those trials do show that seed oils decrease the amount of fat in your liver, but human and animal experiments show that that's totally. 

A matter of the ratio of choline to the amount and type of fat in the diet. And that if you increase the, the implication from the human and animal research synthesized together is that if you increase dietary choline by 30%, you would abolish that effect. Why do I say that? Well, what I know in humans is that if you put humans on a choline deficient diet, they get fatty liver in a matter of weeks. 

If you put humans on. Choline deficient, total parenteral nutrition. They get fatty liver. If you add choline to the total parenteral nutrition, the fatty liver goes away in animals in rodents. If you give them fatty liver from alcohol, sugar, or fat, and you give them choline, that fatty liver goes away. 

Right? So someone in the, in the evidence-based. Internet troll community can come to me and say, oh, well there's no study showing that if you switch out the saturated fat for seed oils, that they're going to, that that choline can get rid of that amount of fat in the liver. Well, no kidding, but there are KU and studies showing that choline gets rid of fatty liver and that decrease that. 

Cutting choline causes fatty liver and the fatty liver is coming from whatever the, that is in their diet that they're eating, and you know, together that just shows that choline, abolishes fatty liver from any source in every species tested, right? And so I can quantitatively say that in rats when they switch butter for corn oil, you increase choline by 30% and the fat and the difference in liver fat disappears. 

Ted Ryce: So Chris, what you're saying is,  

Christopher Masterjohn: and evidence-based internet, well, hold on one, one second. So someone can come at me for saying, 30% is taken for an from an animal study, but all the principles are from human evidence. Go ahead.  

Ted Ryce: Yeah. Yeah, sure. And, and I get it, man. You know, you're, you've got a following and there's people constantly, uh, an annoying you with, uh, yeah. 

Look, I'm, I'm with you on that, right? Like, j just to, before I ask you the question, just to clarify what you were saying, look, I totally get it. And, and it is part of the problem, right? The trolling is not helping. And also, I mean, just to keep going with that tangent, a lot of people are there just trying to make a name for themselves and then. 

Uh, trying to use trolling as a way to, you know, cause that to happen. But it's not, to your point, that's not really like, that. You're not being evidence-based if you're doing that, you're, you're being another cultist extremist. Just, you know, a a, a different, a different type. So I'm, I'm with you man. So, but to go back to what you were saying, just just to make it clear for R right. 

Because, uh, evidence-based trolls, I don't think make up the majority of the people that listen Right. Uh, to this particular show. What you're saying is, we know from study, what was that?  

Christopher Masterjohn: I said that's good that that's not the majority of, uh, your audience.  

Ted Ryce: Yeah. Yeah. Yeah, there are people who are more like, uh, trying to figure things out anyway. 

But what you're saying is, well, so my understanding, if, if you look at a lot of,  

Christopher Masterjohn: well, I, I think the reason that I went down that path is because you, you contexted it in the how controversial. The seed oils are, and I guess I the controversy is, is really is between those crowds like the, it's between the people who are coming down on a philosophical divide of I'm gonna do what my ancestors did, and the people who are, who are misleadingly over concluding from. 

The trial evidence is, is kind of the two camps.  

Ted Ryce: Yeah. And I think that's important for people to know because probably the biggest, like I I, I don't know if you still work with, with, uh, clients directly, but I do. And one of the biggest issues is like, I don't know who to believe, what to believe and, you know, and I think it's extremely hard to trust people. 

Right now because of the biases involved, people can't check their confirmation. And certainly I have that too. I'm not immune or like, you know, but, but I've really worked over the years, uh, to, to be open to everything and, you know, have conversations when it, when, when the people make sense to, to speak with at least, right? 

There's a lot of people saying things, you can just totally throw them out, uh, because of. Right. Uh, just not an expert on the subject a anyway, but, uh, yeah, no, I, I appreciate you putting some context around it. But going back to your point about choline and, um, fatty liver and it developing, so for the person who doesn't understand the physiology as well as you, can you explain the fatty liver saturated fat seed oils and the the choline. 

Like what the practical takeaway there,  

Christopher Masterjohn: where I was going with that, the, the, the one thing that I didn't mention is that we know also from the animal experiments that behave just like humans do. That although a, uh, more saturated fat without enough choline will increase the amount of liver fat, the major metabolic problem that you should really be worried about with fatty liver is less about the amount of fat in the liver, although that is a problem. 

The big problem is when you have oxidative damage and inflammation leading from. Simple s steatosis, which is a fancy word, meaning liver fat to non-alcoholic steatohepatitis or nash, which now, uh, other, some people are calling metabolic disorder associated Sato, hepatitis or whatever. So NASH or mash or whatever. 

But that means that you actually have damage to the liver. And I, I personally. I do believe that having more fat, I think that there is a negative consequence to liver fat in general, and I think that it's very simply because you can either store fat in your liver cell or you can store glycogen, and if you displace the glycogen storage capacity with fat, you're gonna get a proportional reduction in your ability to handle glucose. 

Because you know, when you, when you eat carbs, basically the liver takes up first dibs on the glucose before the pancreas even sees it, and so you're. Need to use insulin to handle glucose, to dispose of it in muscle. And adipose is, uh, contingent upon, or it's proportional to the degree to which your liver glycogen has been saturated. 

So I do think that more liver fat is bad 'cause of that, but if you transition from simple fat accumulation to NASH or mash. Now you are at risk for cirrhosis. You are at risk for liver failure. You're at risk for liver cancer. The, so, the real bad stuff happens under those conditions. And what the animal experiments show you is that seed oils are the one necessity in the diet to give an animal nash or mash. 

Ted Ryce: What do you mean by that? Okay, I,  

Christopher Masterjohn: I told you that, uh, the polyunsaturated fats are vulnerable to damage before, right?  

Ted Ryce: Right.  

Christopher Masterjohn: When you load up the liver with polyunsaturated fat, it's a lot more easily damaged than if you load up the liver with saturated fat. You can think of the polyunsaturated fat as like the kindling would for the fire of Nash or mash, you know, so it's, yeah, it's a problem to have fat in the liver beyond the normal amount. 

That's a problem. But the type of fat you have in, in the in the liver is the main determinant of whether it's even possible for it to transition from the kind of bad thing that everyone who's fat has. Which is simple fat accumulation in the liver to the terrible thing that drives major liver problems, right? 

So the idea that like, oh, I'm going to load up on seed oils and raise my polyunsaturated fat intake from 5% of my calories to 30% of my calories because that'll give me 20% liver fat. When in fact that is the prerequisite for the, for the, um, inflammatory and oxidative damage that allows the liver to be destroyed as the endpoint, that's the risk reward is kind of insane. 

Then also, you know, you look at these, at these studies that showed that saturated fats cause more fat in the liver than than polyunsaturated fats. None of them caused fatty liver in anyone. And you can, I mean, because the liver fat was all, was all within the healthy range, right? Like if, if, you know, if you have a cutoff of like 5% liver fat is considered fatty liver and it, it depends how you're measuring it, which threshold you use. 

But just throwing that number out to make the math easy, right? Let's say 5% is the threshold to be diagnosed with fatty liver. We're talking about, uh, you know, saturated, they fed saturated fat for 10 weeks versus seed oils. And seed oils led to 0.7% fat and saturated fat led to 1.3% fat. So you can look that relative difference and be like, oh, it's a lot more liver fat. 

Um, but the problem is. On what basis do you think that can be extrapolated forever? You know, at a minimum to say that you can extrapolate something over time, you at least need two time points to show that it's going up and hasn't stopped. I mean, even. I mean, ideally you would want a lot more than that, but you know, for all we know, this is a, this is a short term change that then stops at 12 weeks, in which case it's totally meaningless. 

But you know, as a thought exercise, I took the time dependent change. From one of these studies, and I drew a line that went up to, you know, from the baseline of the study in the saturated fat group to the endpoint in the study. And I drew a horizontal line at the point where you diagnose someone with liver failure. 

And I just drew that line up to that point. And then I said, okay, I'm gonna do the same thing with the line from the Cedar Oil Group, which goes down. And then it crosses zero into negative liver fat before the saturated fat crosses the threshold of the fatty liver diagnosis. So like maybe this extrapolates linearly over 40 weeks to cause fatty liver in the saturated fat group, but what the hell is negative liver fat? 

You know what I'm saying? Why can't I, if I can extrapolate one, one line to the distance that causes fatty liver. Why can't I extrapolate the other line the exact same way, but then I get negative. There's no such thing as negative liver fat. It's not a thing. Right? So I'm So, I'm saying I, so I'm saying that little thought experiment. 

Proves beyond a shadow of, of a doubt that you cannot just extrapolate the line and draw it up to the point where it causes fatty liver in the future. That's, that's pure stupidity. And it's your imagination. It's not evidence-based. Extrapolating something from a 12 week study to a five year outcome isn't evidence-based. 

That's imagination based.  

Ted Ryce: Right. I get it. It could happen, but it could not happen. Right? We don't know. We need longer studies.  

Christopher Masterjohn: Well, it might happen, but no one studied it.  

Ted Ryce: Right. Right. Well, obviously it doesn't increase to the point where you're having 101% more Right. Or, or, or, uh, fat in your liver because then Right. 

Anyway, so, right. I, I get what you're saying.  

Christopher Masterjohn: Oh, practically, I, you know, I think the practical take home is that you wanna diet that's high in choline from liver, egg, yolks, vegetables, and so on, and that, you know, that, that you should probably err on the side of. Traditional fats instead of seed oils. 

That's, that's what I would do. And I've spent a lot of time looking at fatty liver and I, I mean, the, the overall synthesis of the evidence to me means that you could abolish fatty liver with enough choline. You just have to eat a good diet to, most people don't get enough choline, so you should focus more on getting more choline, more than you should. 

Focus on what type of fat you have in your diet. But the risk that seed oils are going to make your liver more vulnerable to oxidative damage, massively outweighs the small difference in liver fat that these studies are showing. So I just, I think it's, I just think it's crazy to promote seed oils on the basis of those studies. 

Ted Ryce: Yeah. And, and Chris, just so you know where I'm coming from, 'cause we didn't really have a lot of preliminary conversation. I'm with you. I don't, I don't eat like, I'm not like buy that corn oil that that's what we're gonna cook everything in because, right.  

Christopher Masterjohn: Well, I mean, corn oil is, corn oil is kind of like, no one promotes corn oil anymore, but Canola oil. 

Soybean oil. Yeah.  

Ted Ryce: Canola oil. Right, right. Right. It was just, uh, going on, uh, the, the right, the example you gave earlier, but Right. Canola oil. I cook almost exclusively. Well, I try to not add oils honestly, but, uh, so. So it's really about all mostly olive oil for some of the reasons you mentioned, but also because, you know, it's one of the oils that has at least, uh, you know, my reading of the literature has some positive health benefits versus neutral with the polyphenol content and all that. 

But, um. I, you know, I even sometimes feel like this conversation is a bit right. I, I'm glad, uh, we're having it, but it's just like, yeah, you shouldn't be having added oils in your diet. Generally speaking, if you have a belly, if you are not ideal body fat percentage, right? As a man under 20%, under 25% if you're a woman, right? 

And it's like shouldn't be adding oils and shouldn't be frying things. And so your point is like there's not enough. There is some long-term, longer term studies, eight years, if I remember what you said correctly, and there's some questions about the. Stability of these fats because when you eat them, they get incorporated into cell membranes and Right. 

They, they become part of you and they make you less. They're, or let's say the, they're weaker to oxidative stress and other things. It's like you really should ignore, uh, avoid them. But at the same time, I guess for me having this conversation, it's like. I don't wanna freak out about this stuff. If I have it, if I go out to eat, I'm not gonna stress out about it. 

Right. Uh, Chinese food has a lot of seed oil, uh, uh, sesame oil rather in, in some of the dishes, so I just kind of don't stress out about it. Is that what you, uh, what do you, what are your thoughts about that as an approach?  

Christopher Masterjohn: I think that. Most people probably shouldn't be adding too much oil to their food. 

I do think that there's a very individual response to different macronutrients and I, so I know that from a body composition, from a, from the perspective of an intentional modification of body composition, which is kind of dominates the fitness space, generally added oils to negative, I do. Think that that is a good default, but I personally would say that that people should look at how their diet is impacting their glucose and lactate, and I like waking morning fasted glucose and lactate. 

I find that most of my health, whether from self-rated health metrics. Or glucose and lactate looks best when I eat about 150 grams of carbs a day, and I have some wiggle room for about 40 to 50 grams of that, but I don't have that much wiggle room with protein. I can eat maybe 140 to 170 grams of protein per day. 

But if I hit that. Higher than that, it's definitely gonna interfere with my sleep, and the higher my carbs are, the more protein I can get away with without it hurting my sleep. But I still can't eat more than 170 grams of protein a day under any context and not have it interfere with my sleep. You know, if I'm gonna eat that, I can sleep if I take a bunch of melatonin and gaba and theanine, but I don't think it's good that I, if I have to take those things to be able to fall asleep, right? 

So for me, if my calorie demand is not that high, then I can get away with no added fats. But if my calorie demand goes higher. I kind of have to fill the gap with fat because if I'm, I'm generally eating right around my max for protein, you know, like I, I can get away with eating a hundred sixty five, a hundred seventy grams of protein without it hurting my sleep. 

So I'm eating like 165 grams of protein every day, right? So my calorie meat goes up, I can, I can, it can go up with carbs or it can go with fat, and I generally find that. I'm best off adding fat. Uh, like I, like I told you, I have a wiggle room with the carbs. So if I'm at 150 grams of carbs and I want another 120 calories, I can add that with carbs, no problem. 

It's not a big deal. But if I have to add three, 400 calories. I'm gonna wind up adding more fat to my diet and it doesn't have to be with fats and oils. I do think the average person would be better off if, if they need to add fat to their diet would be better off adding something like fresh coconut or macadamia nuts because your mineral balance will be better. 

Like added fats have no micronutrients for the most part, so you know your magnesium and potassium will be, will be better off if you add whole fat foods that are high in fat. Avocado, flesh.  

Ted Ryce: Or eating the olives instead of the oil,  

Christopher Masterjohn: but yeah, but you know, like I, I, so I don't do well with oxalate and olives are actually pretty high in oxalate, so I'm fine with adding five to eight olives on top, on top of a salad for taste and for polyphenols and for whatever else. 

But I'm not, but I, for me, it's kind of a bad idea to, to just like add 400 calories from olives. And I also am genetically vulnerable to manganese overload, and I find that macadamia nuts and fresh coconut are just, if I'm doing them in volume to get calories. It's just too much manganese for me. So, um, you know, right now I just put extra cream in my coffee, which is an added fat. 

I mean, it's the same as adding butter and as if I added butter to another meal. So I would say that's an example. I, I do think it should be. You should be a little bit more strategic about it. It's, it's certainly like the average person's gonna get fatter more easily if they have more added oils in their diet and they're gonna, it's gonna be, you know, if you're trying to cut your calories, I, those are the first things I would cut, but I'm not a fan of cutting calories to lose weight anyway. 

I, um,  

Ted Ryce: uh, what do you mean you're not a fan of cutting calories to lose body fat?  

Christopher Masterjohn: Well, I think if you're, if you're, um. If you have to qualify for a weight class as a, uh, martial artist or if you have to, or if you're a bodybuilder and you're doing contest prep, makes sense. If you're fat, then I think by fat I mean objectively over, uh, objectively obese and objective, at least objectively overweight and not like, oh, I don't like the way I look in my bikini. 

Then I, it might be the best thing to do if you can't find some other way to lose weight, but it is always better. I mean, so first of all, if you're gonna intentionally create a caloric deficit, the literature is very clear that you wanna lose weight slowly. You wanna high protein intake, and you wanna create your caloric deficit with exercise. 

If you look at the studies where they've shown. People that gain muscle while they lose fat. Those people are doing the most mind blowing amounts of exercise, and like most people would, the average person would be going to over training with the amount of exercise that they're doing. But what it shows you is that, is that, you know, you sh like if you are not able to create your caloric deficit with exercise. 

Then you should be trying to lose weight as slowly as possible. Like, you know, like a quarter pound a week. 'cause otherwise you're gonna lose a lot of lean mass and people debate about whether it's worth it. And you know, half that's not muscle. It's really other lean mass or it's water. Like it's, I think that's kind of dumb. 

Why would you lose muscle if you could avoid losing muscle? Like the, uh, I mean, gi, to give you another example, if you just wanna decrease your body fat percent, why wouldn't you just gain muscle? I, I, um, over the course of two years for 2000, uh, 23 to earlier this year, I, my body fat percentage went down like. 

Several percentage points, but I gained, I think, two pounds of fat, but I gained something like 11 pounds of, of muscle or something like that. So I'm leaner now. I didn't even lose any fat and I'm leaner. Right? Like, so I, I just think it's, it's so much harder.  

Ted Ryce: Yeah. I, I'm with you body fat percentage wise. 

Christopher Masterjohn: Well, yeah, but I mean, by any metric be, I mean by any metric except a dexa measured adipose mass. You know, like if you, but no one would look at me and say, I don't look leaner, because the, because the more fat is distributed over more muscle. It looks leaner. It looks leaner. It behaves leaner. It, it doesn't look leaner inside the, the DEXA report. 

That's the only, yeah. But anyway, so I, my, I guess my point is like, it's so much easier to lose fat than it is to gain muscle. So I, and sarcopenia is a major problem with aging, so I think it's, I think it's. Crazy for someone who's not like, it's like an emergency, how fat they are. Um, I, I think it's, I don't wanna use the word crazy, but I think it's the wrong risk reward ratio to focus on quickly losing fat instead of preserving muscle at all costs and trying to build it. 

And so I think, and then another thing is. What time horizon is it necessary for you to lean out? Right? If, if it's a competitive thing or it's, you know, you've got a photo shoot coming up or whatever, or wedding night or like if there's there, yes, there could be time sensitive issues that you have to deal with, but in general, if it's longevity, man, you got decades, right? 

So I think that. You know, if, if I'm like, well, I think I would live longer, if I were five percentage points lower in my body fat percentage, I would take 10 years to do that because, you know, because I could be building muscle and gymnastics skill or like whatever. While I'm leaning out and I could drop 5%, like I, I'm nowhere near my genetic potential for muscle mass. 

So I could, I could do that by adding muscle over the next 10 years and I, but the thing is, I can lose that amount of fat in a few weeks if I don't mind losing my muscle mass. And having to drug myself to sleep, you know? You see what I'm saying? Like losing fat is easy,  

Ted Ryce: right? 100%.  

Christopher Masterjohn: Losing fat is easy. 

Gaining muscle is hard. So prioritize the muscle mass is my perspective. Oh, but let me say one more thing. So everyone, if they try, can find low hanging fruit that can. Create an almost accidental caloric deficit from raising their metabolic rate because they're healthier, where if they don't match it with amount, the amount of food will lead to weight loss over time. 

And when you do that, it's always healthier than intentionally cutting your calories. I'll give you one example. When I started creatine supplementation, I've been off and on, but I've been on long-term creatine for the last year and a half. So when I started the creatine. I was losing body fat so imperceptibly that I didn't notice it until months later when I looked back at my logs and I realized that I was very, very slightly losing fat. 

During that time, I got stronger. Then I said to myself, you know what? I wanna finish this off. I'm gonna lean out to an intentional point. I'm gonna go at what from the literature says is a reasonable pace where I'm not gonna lose muscle mass, but I'm gonna step it up by a factor of two or three so that I can achieve this goal once and final in two months. 

So I did that. It worked out okay, but I'll tell you what, I lost strength on every lift, whereas I gained it when, when I was doing it by accident. So I'm not saying no one should cut their calories. I'm just saying that like think about your goals, prioritize your muscle mass, and your strength and your health first. 

Then think can, given my goals, can I, can I find something that is gonna improve my health a little bit where I'm not gonna spend what I've gotten in metabolic rate on eating more food? And I'm just gonna let that just like ease off as butter. Like if you're doing, if all you care about is your health and longevity or way better off doing that, that's what I think. 

Ted Ryce: Yeah. And, and thanks for sharing that, Chris. It, it's a bit of a different, like I have a different view 'cause I, that's kind of like my bread and butter, what I, what people come to me for. But it's more, I think I, and I don't even want to debate that with you or get into the nuance unless you really, really want to have that conversation. 

Because I think what we're missing here is like the psychological side of things, right? Where, um. And then nuance. I mean, I've had clients lose fat slowly and then we dexa scan them and they lost a little bit of muscle. And then, and then I've had clients lose a lot of fat fast, and, uh, their muscles stayed the same or they even gained some, uh, I had a client who gained six pounds of muscle in two months. 

Uh, again, lean mass according to Dexa ray, but it lost 11 pounds of fat. So I, I think there was some. I think there's some variance here, but, but I don't disagree with you and I think ultimately every, or I don't disagree with you, like in an ultimate way. 'cause eventually what happens is you hit the, your peak leanness where you don't really need or necessarily want to get any leaner. 

It's like, well, where do you, where do you get your reward from when the scale doesn't go down anymore? Well, you need some sort of. You need to get it from exercise and pursuing something and long term, that's what's gonna keep the weight off as well when you get into it. So, so thanks for sharing that perspective. 

Um, I think it's good for people to hear, although a lot of the guys I work with, they're like, Hey, I, I didn't lose a pound. Uh, I'm freaking out here, you know? Anyway. How about, uh, if, if you've got a follow up to that, I'm happy to, to go there with you.  

Christopher Masterjohn: Well, no, I, I, I mean, I'll just say that I, I think your perspective makes complete sense and mine, my pers, I mean, I did give, the example is applied to me and it might apply very differently to someone else, but I think you and I would probably agree on the big picture where for the average person whose main interest is health and longevity. 

You do want to tell, you wanna structure the fat loss system around whatever would be maximally, preserving strength, athleticism, muscle mass, and other markers of health. We would probably agree on that much. And so I think it's just, uh, yeah,  

Ted Ryce: 100%. But human beings are tricky. Otherwise they wouldn't be trolling you on on x. 

They'd be doing, they'd be posting content, but, uh, let's change directions. I feel, oh, oh my gosh, it's already like almost an hour here, but, but it's been like, like I wanted to talk about VO two max and, and I don't think we'll be able to do that justice, so maybe, maybe we can. Get you back on the show to discuss it because you and Brady Homer on X kind of went back and forth on some things and I thought it was, I thought what you were saying is interesting and like the C oil discussion. 

I really want to, I really want to just kind of. Organize information and, you know, take what's practical for people. And, uh, there's another guy who on, on X who's also been on my show, Steve Magnus, if I'm getting his last name right, who also is very critical of VO two max. But let's say that for another day. 

How about we keep going with nutrition here? And um, Chris, you mentioned about. Testing glucose in the morning and testing lactate. Now, most people have had a fasting glucose done when they go see their doctor and probably a hemoglobin A1C and maybe a C-peptide and fasting insulin, and then Homa ir and all those things if they worked with someone, uh, you, you know, a little bit more educated in that stuff. 

But lactate, why? Uh. Like, uh, can you talk about why you measure lactate and why that, why you feel that's important and how you do it?  

Christopher Masterjohn: Well, I do it with a finger prick. I use a Nova Biomedical, lactate plus, but, um, it adds context to the glucose and I usually, I measure glucose ketones and lactate at the same time in the morning, and. 

You know, ketones give you a, a contextual factor about what you're using for energy, whether it's more glucose, more fat. Lactate gives you a contextual indicator of. What you're doing with your glucose and whether it's stressing out your mitochondria. So generally if glucose is rising and lactate is going down, you, you could, you could imply that you have a problem with glycolysis that might respond well to supplementation with niacin or potassium since those are a, uh, co-factors of glycolysis. 

If the lactate's going up. Then you might respond to thiamine, which helps with pyruvate metabolism, which is the end product of glycolysis. And if you don't have enough, the lactate can go up or you got a mitochondrial problem. And there's a lot of nutrients that are important to mitochondrial energy production. 

But I, and that's its own. Can of worms, but I think the short answer is that if your lactate's going up, that's an indicator that your mitochondria are being stressed by the amount of glucose going into the system. Doesn't mean that glucose is a problem, but it means that. That you've got a problem to fix. 

And I think that can be very valuable just looking at just the response to different strategies that you try. So for example, if you're supplementing with something and your lactate starts going up a lot, I think that's usually a leading indicator that it's hurting your metabolism. And you might see that with glucose, but often you wouldn't. 

And I just find that lactate is usually a better leading indicator of problems with the strategy that you're doing at any given time.  

Ted Ryce: And strategy, meaning the combination of both exercise and diet,  

Christopher Masterjohn: um, could be usually the response. I mean, it is funny that lactate is usually mostly measured in the context of exercise. 

I, I think that the lactate response to your exercise is probably gonna be behave pretty independently of your waking lactate for the most part. And I do, you know, exercise probably on more of a week's to months scale could have a pretty strong influence on lactate. Resting lactate by improving baseline mitochondrial efficiency. 

But I, you know, I think waking lactate is largely a reflection of your liver's mitochondrial health. And I think that is relevant to exercise, but is probably gonna be a lot more relevant to. The type of exercise that would be exceeding, uh, in intense, uh, probably, you know, high intensity interval training, for example, where you've got a lot of on and off and you've got a lot of high, like where the on can be very intense. 

That's a case where your lactate is going up during the exercise and. That's because your muscles aren't oxidizing it and they're relying on your liver to turn it back into glucose and send it back. So that type of exercise trains the liver's mitochondria to improve their lactate oxidation. I think if you're doing high intensity interval exercise or something equivalent, it doesn't have to be a hit routine. 

It could be a team sport with an a lot of off and on. So for example, basketball players in the middle of a basketball game, their lactate's gone up like 15 fold. Then it does that because basketball players are generally doing sets lasting seconds. Of a why. You know, they're doing hundreds of things that last several seconds at a time of varying intensities. 

But halfway through the game, they've done a lot of things. That are real high intensity for a few seconds, and they have not recovered from them in between. And so that's why their, the lactate goes up so high, and I mean, anything that makes the lactate go way high in the blood during the exercise is gonna train the liver mitochondria to ramp up their oxidation p uh, capacity. 

So I do think that if you're doing that type of exercise. You are gonna see an improvement in your waking fasting lactate, because when you wake up in the morning, the lactate in your blood is really lactate. That's coming from your red blood cells, but it's, you know, the lower it is, that means that your liver has done a great job oxidizing it. 

And so, yeah, exercise will train that indirectly, but I think you're gonna see way more short term time horizon changes if you're playing around with supplements. You start playing around with your macros or you start, you know, eating a certain food you don't tolerate and things like that, you know, that, that might be like, I added a, I added a B complex and you know, lactate. 

Lactate went up, um, from like 0.8 to point to 1.0. Then it went to 1.2, then it went to 1.4, then it went to 1.6. You're probably not gonna feel great at, uh, at the end of a few weeks.  

Ted Ryce: Got it. Yeah. I feel like we're going down a whole nother road here where probably, uh, 'cause I don't have the, the JRE three hour, uh, podcast. 

Maybe in the future we'll see. But I would love to have you back get, you know, get into some of what you're talking about with VO two max, with lactate and you have something called mione, an at home mitochondrial mitochondrial function test and getting into that as well. But, uh. Uh, yeah. Um, just so much to talk to you about and if you enjoyed the conversation with Chris Master John today, you really gotta check him out at Chris master John uh, phd.com. 

And Mione, you gotta check out Mione, M-I-T-O-M-E. And certainly, you know, there's that interview that you had on Joe Rogan, where, where you ended up going into, uh, quite a bit of this stuff. But, uh, Chris, uh, really had a great time today. Really appreciate you taking the time to, to share what you've been up to, your, you know, I really appreciate your approach that you take. 

Uh, it's very different, you know, uh, meaning like, I know you're coming from the place where you just want to figure this stuff out for people and you don't wanna fall into any. Of the camps that are kind of thinking short term. So really appreciate your time and sharing your wisdom today, man.  

Christopher Masterjohn: Thank you Ted. 

Great to be here.  

Ted Ryce: Yeah. And for, where would you, are you hanging out mostly on X these days or where would you like people to connect with you?  

Christopher Masterjohn: Um, my newsletter at chris master john phd.substack.com and, and mitos@mito.me. And, uh, I'm generally on. Most social, but you can easily find me from there.  

Ted Ryce: Sounds great. 

Well, again, thanks so much and uh, let's do it again soon.  

Christopher Masterjohn: Cool. Thanks Ted.