Croissant Diet, Theory of Obesity and Raising Low PUFA Pigs, Episode 16

Thanks everyone for joining us today. I have Brad Marshall, who is, as you heard in his bio, is a very much a Renaissance man. So welcome, Brad. How are you doing?

Thank you. Thanks for having me.

Yeah, so, um, you have been kind of making the rounds lately because you have this diet that you sort of created that is somewhat controversial, but I love the name of it because I've always been a big fan of French food, and that is the Croissant Diet. So maybe you could tell us a little bit about your background, how you came to start experimenting with this stuff, and how you got interested in the croissant diet part.

Sure. And so, um, my— well, my background dietarily is I've been keto a lot of my life, um, but I also went to the French Culinary Institute back in the late '90s, I guess, in, in New York City. Um, and so You know, as I've been a keto adult, and knowing that that works and seeing that it helps people, I've had this struggle knowing that at the same time, you know, they're like the traditional French diet where they're combining starch with butter seems to be keeping people thin as well. And I'm kind of a food historian and I love like looking at dietary history of like people in New York State who were mostly dairy farmers back in the day. Looking at people in New York City even into the '50s and '60s, when you look at those old photos, you can see that everybody is— almost everyone is universally slim. Not even that they're not fat, but they're like really skinny. You can look at menus of the day and food trends and USDA data and everyone was combining starch and butter and meat and potatoes and they stayed lean. Then something changed and people started to get fat. My thought is that what changed— I started reading the blog Hyperlipid. I gained weight. I was working. I was working a lot, running a farm and a butcher shop. Paying very close attention to my diet because I was overwhelmed and I was eating restaurant food and whatever, so I gained weight. I wanted to turn it around, so I went back and started reading Hyperlipid again. I also have a molecular biology degree really from Cornell, so I understand a lot of the science of it. I was reading his blog, and his blog is really dense, and there's a lot of vocabulary that you have to learn to really get into it. And so anyway, I kind of— he talks a lot about the effects of saturated fats in the mitochondria, how they generate reactive oxygen species, and reactive oxygen species have a number of effects, including limiting insulin signaling. So the idea is that insulin causes you to store energy, to store fat. And, and so if you're eating a diet that's very high in saturated fat specifically, your fat cells actually become a little bit insulin resistant. And this is a reversible short-term insulin resistance that he calls physiological insulin resistance, and that, that actually will limit the amount of fat that the fat cells will take up.. And in the same time, I found there's some interesting papers in both rodents and in humans showing that stearic acid specifically has this metabolic effect. The paper that everybody loves, I call it the banana milkshake paper, but they took people, they put them on a low-fat vegan diet for 2 days and Then they took a blood sample and stained their white blood cells and showed that the, their mitochondria were actually, um, uh, fragmented. They were very small. And then they gave them this milkshake, which has somewhere around 25 grams of stearic acid in it. And within like 6 hours, um, again, they drew blood and showed with staining that their mitochondria grow into this like fused network of mitochondria. They actually all the mitochondria themselves fuse and grow into these chains. And in that state, they're doing a lot more fat oxidation. And so anyway, there's a study that was done by a grad student, and she was feeding starch and stearic acid to mice, and those mice got really thin. And so, you know, given my background in French culinary, I said, well, you know, saturated fat and starch together, that, that's like a French recipe. That's like a croissant or something. Right. And so that's when, that was sort of the eureka moment that I had thinking about the French diet and these mice eating flour and stearic acid and the difference between that diet and what Americans eat, which is, you know, flour or starch with vegetable oil and thinking about mitochondrial dynamics and, insulin and all these things, I was like, this— it all kind of just like came together, right? And that's when I decided to try making these very high stearic acid croissants, which led me to—

Which is absolutely brilliant, by the way. I don't know if you know that, but it is. And just to backtrack one second for people that, just in case this is the first time they're hearing from you or hearing more about kind of the science back stuff. I, I love all this stuff, but basically the, the basic way for a layperson to understand mitochondria is, is the cellular powerhouse. It's what generates energy. Would that be fair?

Absolutely, absolutely. And so what happens in the mitochondria is, um, you know, that's where we're literally oxidizing the fuels that we eat, right? Which might be starch or might be fat. And, and there's a, um, there's a system within the mitochondria that they can switch back and forth from burning either carbohydrates or fats, and they can do that pretty quickly. And so, you know, one of the things I say about the stearic acid is it turns on fat burning mode. And that's like why, you know, in response to the stearic acid, that's why the mitochondria fuse and they actually switch over to the part of the cycle where they're burning fat. As opposed to carbohydrate. So even though I'm combining some starch into the croissants, they're actually, you know, they're probably only— by the time I was actually eating like croissant sandwiches, so I was adding like ham and cheese to the croissant, which was already very high in fat. So it's probably only 20% carbohydrate in the meal, even though it's a croissant sandwich, which— so it's, it's really a low-carb meal. Which probably is counterintuitive to lots of people when they think about croissants.

But well, if you actually ever seen how they're made, you might understand that more, because if they're made really well, they have— they do have a very high fat content and a lot of air. So a croissant that looks rather large is actually— I don't know, it's probably what, 50% air or something like that if you do it really well. So, um, anyway, so that's a side note. But so you had been working really hard, and luckily you have this background in both food and science. And you're— so you were working really hard, were stressed, you noticed you were putting on a little weight, and then you have this eureka moment with the croissant diet. So before we got on this more formal conversation, you were saying that you had done, um, sort of some experiments on your— additional experiments maybe on yourself from when you first discovered this. So I'd love to hear more about what you discovered and, and what you're thinking with this, uh, iteration of your diet?

Sure. So I published in the fall, the fall of 2020, a series of articles called the SCD1 theory of obesity. And one of the things that I discovered while researching stearic acid, etc., was that there's a gene called SCD1, which stands for stearoyl-CoA coenzyme A desaturase, doesn't matter. But it, um, the only, its only job is to take stearic acid, which is a saturated fat, and it removes a couple hydrogens from it and it introduces a double bond. And, and when that happens, it becomes oleic acid, which is the, the dominant component of olive oil. So the only thing this enzyme does is it takes stearic acid, which is found naturally in sources like chocolate or cocoa butter. It's found in beef suet, which is beef kidney. It's found in, in all foods to some extent, but the things that are really high in it are beef suet and chocolate and, or cocoa butter and a couple other things. Um, and so The only function of this enzyme is literally to just convert stearic acid to oleic acid, which is in olive oil, avocados, and foods like that. And so it doesn't sound like a very dramatic effect, but in fact, it turns out there was a lab that did a really interesting set of experiments in the— really between around 2002 and 2012. Showing that this enzyme is really this kind of master metabolic regulator. And by introducing that double bond, uh, it, it has all of these metabolic effects. It basically causes anything that you produce a lot of this enzyme in— and when I say anything, it could be like a heart, a human heart cell, or it could be like a C. elegans worm, this tiny worm, or anything. If you make too much of this SCD1, they will store a bunch of fat. And if you, if you prevent them from making SCD1, they will lose fat. So SCD1 is this kind of like master. And they, they had these mice that were— they didn't have leptin receptors. So these mice become very obese, leptin is a hormone made by our fat cells and it, it controls a couple of different things. It controls satiety in our hypothalamus, but it also turns out that it regulates the expression of SCD1. And so if you have mice that don't have leptin in them, they get very fat. But if they also don't have the SCD1 gene, they become lean again. So you can actually override the effects of leptin. So leptin turns off SCD1, um, in natural systems. And so, you know, a lot of people now are leptin deficient— or no, they're not. We have lots of leptin. Sorry, we're, we're leptin resistant, so we're not responding to leptin in the ways that we should. And so, but if you get rid of the SCD1 you start, you know, you start behaving as if you are— you have leptin and it's working effectively, and your metabolic rate goes up. And so, um, so I start— so I did a blood test to see. You can, you can actually test in a, in an indirect way how much SCD-1 you're making by, by a blood test that compares the ratio of your stearic acid to your oleic acid in your blood cell membranes because if you're making a lot of the enzyme, then your stearic acid is getting converted to oleic acid, right? And so if you have a lot of oleic acid and very little stearic acid, you probably make a lot of this SCP-1. So I did the blood test and sure enough, even though I have been avoiding, vegetable oils and I've been avoiding polyunsaturated fats and those levels were low and I'd been eating a lot of stearic acid, my body wasn't holding on to the stearic acid. It was converting it all to oleic acid. And you know, I've struggled with obesity my whole life, which is why I've been doing keto on and off, you know, since for 20 years now. And so that's when I realized this is, I have this metabolic problem that my body is overproducing this SCD-1. What leptin is supposed to do is it's supposed to— it is supposed to lead to a process called thermogenesis, which just means making heat. The way that your body controls— is supposed to control the level of obesity is when you get fat, your fat cells make leptin, so your leptin levels go up. The leptin, um, increases the amount of fat being shuttled into your mitochondria, and it downregulates SCD1, which is to say that the fat going into the mitochondria is more saturated and more of it is entering quicker. And when that happens, the effect is you make a whole bunch of these reactive oxygen species. Which are free radicals, which is like a scary word, but it's okay. This is— we have systems to deal with it. This is normal human physiology. In response to that happening, the mitochondria make something called uncoupling protein. And I don't want to get too far in the weeds on this, but the ultimate action of uncoupling protein is that your calories are are simply burned off as heat rather than being stored. And that's what's supposed to happen, right? If you have a lot of leptin, that's the signal to your body that you're getting very fat. And so the leptin says, okay, we'll saturate the fat, send it into the mitochondria. That's gonna allow us to uncouple and do thermogenesis and safely burn off the calories, right? That's how it's supposed to work. So my argument is that, okay, so what happened between 1960 and now? Well, it turns out that if you have too many of the polyunsaturated fats, um, they don't generate the same amount of reactive oxygen species. They limit you from doing thermogenesis. Um, your body temperature drops and you're unable to burn off the calories in response to leptin. I actually think—

I'm so glad you gave the real explanation there because the way I've been explaining it, 'cause I've been talking about this quite a bit on social media after hearing you and Paul talk about it and Peter and a couple of other people. And I kind of describe it as, you know, if you, the polyunsaturates, they muck up your system and don't allow you to easily reduce or release fat. Is that accurate in a layperson's kind of wording?

Yes, I would say, you know, in my situ— you know, my understanding has evolved even since I went and talked with Paul Saladino. But so what I'm seeing— so I just wrote an article which I think is really interesting. It's called "This is Your Body Temperature on Vegetable Oil." And there was an article that came out just last year. So there's a well-documented tribe in the Amazon— I'm pretty sure it was Bolivia. And they were basically eating— they were eating a lot of starch. Starch is interesting because if your metabolism is in good shape and you're not producing a lot of SCD1 and you're eating almost all starch, your stored body fat is very saturated. And so, uh, this tribe in Bolivia was eating plantain and, um, uh, there's another root vegetable that's eaten a lot in the tropics. Its name isn't coming to me, but yeah, something like that. Yeah. And so anyway, they were living on that. They had a normal body temperature of 98.6 in 2002 to 2004, you know, as documented by a, you know, a new medical station that was built there, right? So they took everybody's body temperature, it was 90.6, great. Well, by, you know, recently, within the last 5 years, everyone's body temperature in that tribe dropped to like 97.7. So they lost an entire degree of body temperature in the last 20 years, and nobody really knows why. And the only thing that changed on the island was— or not on the island, um, was they built a store so that they could buy food from— they could buy industrial food, basically, which is to say food that contains vegetable oil. And so I think that, um, I put another study on there in mice showing that mice eating starch, uh, have a high body temperature even when challenged with, with cold, you know, external temperature. But mice eating starch and margarine, uh, vegetable oil, they cannot keep their body temperature high when it gets cold. Uh, they get cold very quickly. They're unable to do this thermogenesis, um, and this mitochondrial uncoupling. And so, you know, basically what I'm arguing if we distill it down, is that to make— in most Americans, industrial body temperatures have also dropped by about the same amount. The tribe in Bolivia now has the same body temperature as the average citizen of Great Britain according to another article that came out in the last year. So body temperatures have dropped around the world. We know that. I think it's because of the polyunsaturated fats don't allow us to drive the ROS, which doesn't allow us to do thermogenesis, which is to say just simply burning off our calories. Interesting.

Um, how long— just as an— to use myself as an example, and I wonder how long this would take. So I've been low carb for 5 years, keto for 4, and I'm— I do pretty clean. I don't do any intentional PUFAs. I do go out to eat on occasion though, so I know almost with unidentifiable fact that I've gotten some at some point. But for the most part, I'm— and I've certainly added beef tallow into my diet for the stearic acid most recently. Um, but I have observed that my body temperature, especially since now everybody takes your temperature everywhere you go, right? But my body temperature is always quite low, like maybe even 96 point something. Um, yeah. And you know, part of that might be my age getting a little older and all that, but I'm just curious because of your new revelation.

I think the forehead reading is probably a little bit lower than if you did it with a, yeah, you know, an actual under the tongue thermometer.

Well, even under the tongue though, mine does tend to be low. So I'm just curious, like, as—

no, my own was my whole, my whole adult life, my blood temperature was low. And so, so here's, I'll, I'll finish my story and my experiment. And so I became super rabid about avoiding all polyunsaturated fat in the, uh, January of 2019, I guess it would have been. And so, you know, I've now been really avoiding them for about 2 years, um, and I've done— I have this blood test that I suggest on my blog. There's a link to it from my article, The SCD Theory of Obesity Part 2, I believe. Um, there's other people's results on there, but it's a met— an OmegaQuant test. And so I've showed that my— at least in my red blood cells membranes, uh, the level of polyunsaturated that I have now is like well below the range of 99% of Americans. Um, So that was, that was a cool affirmation of that. But yet, you know, my body temperature was still low and I could see on that same test, like I say, I was not storing a lot of stearic acid. My body was converting it all to oleic acid. And so I got ahold of some of this, um, sterculic oil, which inhibits the SCD1 enzyme, the thing that is like unsaturating all of your fat and preventing you from doing the thermogenesis. Mm-hmm.. And so I took that over 2 months and there was a remarkable change in my body fat composition. Like it went from being, you know, the amount of stearic acid that I had almost doubled and the amount of oleic acid went down by, I don't know, 30% or something.

Wow.

And so you can see on the blood test like, okay, well that enzyme definitely worked. Um, I also over last summer invested in this metabolic tester because I've just become really curious about this issue of like Can we change our underlying metabolic rate?

It's not—

and I think we can. And I think that, that our— everyone's collective drop in body temperature over the last 100 years or so, or 150 years, shows that most of us are not good at, at doing this adaptive thermogenesis, as they call it. And so anyway, so I took that oil for 2 months and I did notice, um, a couple of things. Within about a week of taking it, I started getting body temperature reading backs that were like 98.6 or 98.4 or at least 98.1, which I'd never even— I was usually like 97.2 in the weeks before I started taking it. So I quickly, you know, my, my body temperature just became normal. In like a week. So I was like, well, that's cool. Um, and over about 2 weeks, my metabolic rate increased. So I had been— before I started taking it, I was, I was intentionally not supplementing any stearic acid. I was just kind of doing like what I call a— I was trying to be very regular, and I was eating like, like, um, toast and eggs with butter in the morning, and for dinner I was eating like steak and a potato, and I was eating like 2 or 3 meals a day. I wasn't doing any fasting. I wasn't doing any stearic acid supplementation. I was just like trying to get a baseline of where my metabolic rate was if I wasn't like going out of my way to, you know, to change anything, right? And so at that point, my metabolic rate was like 2,200 calories a day. And that's— I always did it about the same time of day, sitting on my couch, same spot., and it measures your heart rate. So same heart rate, like trying to control all the variables. So I was getting consistently around 2,200 calories a day. And then after I started taking the oil, within a few weeks, uh, my metabolic rate actually went up to around 2,500 to 2,600 calories a day. And it stayed there. Um, that was pretty consistent. And I was like, that's cool. Like the, you know, By inhibiting this enzyme and saturating my body fat, I definitely changed my basic metabolic rate, right? And, and I'm like, that's awesome. But, you know, then the holidays came. Despite the higher metabolic rate, I managed to pack on a few pounds during the holidays while eating with my family. My whole family loves eating, so we ate a lot. And so then anyways, Holidays go by. Okay, so it's January 2nd or 3rd or whatever. I went back to my, what I call my stearic acid macrodosing diet, which is like, basically I'm trying to get all my calories in, in one single big meal. And it's a very high stearic acid-based meal to try to, you know, because I knew that I had kind of fixed my body fats and now it was like, okay, now let's see what happens if I add to this. The, the dietary stearic acid, which I think has its own separate effects from your stored body fats. And I think they're probably synergistic, right? And so I do this big feast meal, um, and on my blog, if you look for the article "Stearic Acid Macrodosing," you can see the kind of meal that I'm talking about. Um, I do this big feast meal, and then the next morning my metabolic rate was at like 2,800 degrees. And I was like, cool, that's the highest I've ever measured, right? And then between the feast days, I do a fast day. That's the whole gambit of this. It's like a weight loss diet. And it's like you're feasting every other day to keep your metabolic rate high, and then you fast to like lose weight, right? In between. And so on the fasting day, my metabolic rate went up to like 2,900 degrees. And then on the third— and then that evening I might have the day slightly wrong. I had the big feast meal again, um, and the morning after the second big feast meal, my metabolic rate hit, uh, 3,100 calories a day. Wow. Just sitting on my couch. So that was a 900-calorie difference. It, it, since then it kind of like leveled back out around 2,800 or 2,900.

Um, but still higher than your baseline.

So that's like 700 or 800 calories higher than my baseline, which is 5,000 to 6,000 calories a week. You know, that's like 2 whole days of food.

Yeah, that's amazing.

And I'm not— it's— I didn't exer— I'm not exercising. I'm not— you know what I mean? I'm not doing anything other than fixing the fats that I'm eating, or fixing my stored fat and my dietary fat, right? Those are the 2 things. That led to that change.

I think that you mentioned that you now, that oil that you mentioned that inhibits this specific enzyme, you actually sell that now, is that right?

I am, yes. It's been quite a process to actually have it imported and labeled and bottled, and I'm sort of way behind schedule, but it's coming very, very soon.

Oh, shoot. I was going to say I'm ordering it immediately, but it's not available yet.

It should be in the next week or two.

Okay, awesome. I'm going to be one of your first customers.

I'll put this caveat out there. I want to tell people this. Along with taking that oil, I did see increased inflammatory markers. Oh, interesting. Because you are literally playing with fire. Our basic body signaling works off of these reactive oxygen species. And, um, most of us, if you're healthy, our body has really good ways of— well, it's not that we have good ways of dealing with them. They're actually how those reactive oxygen species are how cell signaling works in your cells. So if the mitochondria is making a bunch of reactive oxygen species, that's a signal to the nucleus like Okay, something's happening. We're burning fat now. And, and the, the nucleus makes proteins that, you know, deals with that reality. And if the nucleus doesn't see a lot of reaction reactive oxygen species being produced, it thinks, okay, we're burning blood glucose now. And it produces proteins to deal with that situation, right? So either— so it's, it's not bad to make reactive oxygen species, but in my case in particular, since I've already eliminated all of the— well, not all, but a substantial amount of the polyunsaturated fat that I did have, so my fat is already pretty unsaturated. And, um, since I'm overweight, since I have extra fat, that means my body's making a lot of leptin. And leptin is also something that's shuttling fat into the mitochondria, right? It's adding fuel to the fire. And then also I block the enzyme. So now all of the fat that's being rapidly shuttle— shuttled into the mitochondria because I have all this leptin and because I'm eating these big stearic acid feast meals, it's like the maximum.

I'm—

my whole goal is maximum generation of these reactive oxygen species. Because that ultimately is what causes your mitochondria to uncouple. And, um, that uncoupling is what increases your metabolic rate. So once that happens, once the mitochondria uncouple, then you have— you're going to generate a lot less reactive oxygen species after that. So the whole reason that your mitochondria are uncoupling in the first place is to get rid of the reactive oxygen species. Because what happens is once they uncouple the— it's like, it's kind of like depressurizing a balloon. It's like you're trying to pump up a balloon. You're trying to like blow air into a balloon and the balloon's really tight and it's hard to blow air into it. And it's uncoupling the mitochondria is like putting a couple little prick holes in the balloon and all of a sudden you can keep blowing air into it cuz you know, air is just blowing out the other side. It's fine. It's like eliminating the pressure when your mitochondria uncouple. So, so the end result— so you have to build up the reactive oxygen species in the first place so that this uncoupling event happens, which is the thing that increases your metabolic rate. But then the reactive oxygen species go back down, if that makes sense. That's a lot of technical stuff.

No, so that's where the inflammation is coming from, is when you're in that process of building the reactive oxygen species before the uncoupling happens.

Exactly.

So you're thinking though that that's just a temporary rise due to this metabolic process.

Exactly. So my thinking is that you have to kind of make this flip, and in the early stages of building up this flip, you're going to have some inflammation, but then Hopefully, once you get over the hump, you basically solve the first problem, and the way that you've solved it is actually by increasing your metabolic rate. It's like the increase in the metabolic rate is the thing that cures the inflammation in the first place, if that makes sense.

No, that's pretty awesome. Actually, I wonder if— and this might not really be related, but Dr. Fung has this idea that he talks about how, you know, every once in a while you'll be in a long fast and you'll take your blood glucose and it's like high. And he's kind of explained it before that your body has over the years stored some of these toxins and, you know, sugar within the fat cells. And so once you start this process of releasing things from the fat cells, which sounds very similar to what you're talking about, that you sometimes get these, you know, just like weird things being released from your fat cells. So I'm wondering if based on what you just said, if some of this process of uncoupling within the cells releases, you know, maybe the polyunsaturates, even though you're mostly unsaturated now, but maybe it's releasing some of those, like the body's going around finding those and trying to get rid of a few more, and maybe that creates some more inflammation or something.

Yeah, I mean, it could be. Um, there's another really interesting paper that I I just posted about on my blog, which I love because I think it's hilarious, but it probably makes some people a little uneasy.

So your blog or the research?

The article, uh, this, this, this specific piece of research, um, was about a strain of mice and they— so there's a, there's something called NRF2 and I'm not gonna get that deep into it, but it's, it's a primary regulator that prevents oxidative stress. And so in the mice, they removed their NRF2 gene so that they were no longer able to deal with oxidative stress. Um, so these mice absolutely are in an extended stage of oxidative stress. And so what do they do? They uncouple their mitochondria their metabolic rate goes up, and they are protected from obesity because they have oxidative stress.

Hmm.

So, you know, I, I actually think that in a lot of ways, many of us are in a state of reductive stress, which is the opposite of oxidative stress. And I think reductive stress is the inability to create the biologically appropriate level of reactive oxygen species for the purposes of biological signaling and responding to, you know, the fact that we're burning fat versus glucose. And so I, and I think there's, you know, oxidative stress is a wide-ranging concept and I'm talking specifically about within certain intercellular components. You know, just right around the mitochondria and signaling back and forth in the nucleus, that's where you want it. If you have it in your, like, other parts of the body, it, it can be a less good thing. And I think that if you reduce your— when you have oxidative stress, the first thing that gets oxidized, it leads to, like, real bad things happening downstream, is polyunsaturated fats. Polyunsaturated fats are very highly prone to oxidation. And so if you have a lot of them,, and then you have oxidative stress, they make these, like, peroxides, these lipid peroxides, and those, those definitely lead to a lot of damage. And so, you know, I think about this altogether. I'm like, well, I don't want the bad kind of oxidative stress. I want to eliminate vegetable oils, but I do want to generate free radicals, which is to say reactive oxygen species. In order to do what I consider to be appropriate biological signaling. So it's, it's, it's like a, it's a balancing act, you know. You, you need to generate some, um, for your metabolism to function efficiently, but you also want to, uh, protect from real oxidative damage by avoiding polyunsaturated fats. That's kind of, that's kind of where I fall down on it. So, so I'm okay with generating the free radicals because I've been very careful about not filling myself up with vegetable oil, right?

No, that makes sense. So before we go in, and I would say the biggest takeaway from that, if people don't get into the geeky science like we do, is don't eat it. Polyunsaturated fats, the end. Yes, polyunsaturated bad, stearic acid good. So, um, exactly. Yeah, we're in it. It is interesting though to try to— I mean, you've had to go through all these iterations and experiments before you kind of brought this all together in a way that, you know, people that are in just nutrition science or just oxidative stress science or whatever, they're not thinking of it from sort of a whole body perspective and how it affects your weight, your energy, the ability of your mitochondria to couple or uncouple. I think that, you know, this is kind of a unique area of interest that you've developed here and probably the only one with the background to really, uh, I understand it. But before we— I have two more things I want to cover, and I want to be respectful of your time, of course. The first one has to do with your farm. We haven't even talked about your farm yet, and you're doing some really cool things with your, um, particularly your pork, with their diet, based on this research that you learned. And I think it was basically that you were just finding that because of what they were eating, when they were eating a lot of corn or polyunsaturated fats, their fat was ending up having that in it. And then we in turn, we think we're eating something healthy, we're having some pork instead of our nightly steak on our keto diet, and meanwhile we're getting polyunsaturated fats by eating pork, which is kind of crazy to me. So can you talk a little bit about how you've changed things in your farm to kind of address that problem?

Right. And so I want to clarify, I'm not the— I have a company called Firebrand Meats and we are selling, uh, low PUFA pork. I've actually, at this point, I'm I've outsourced that to a farmer friend of mine. They're not actually grown on my farm, but this guy is a great pig. He's actually honestly a much better pig farmer than I am. He's like a 5th generation pig farmer. He's great. And he's, he's, he's, um, he thinks a lot like I do in a lot of ways. So he's really clever about helping me design the right kind of feeds that I want because he has his own feed mill and it's a great operator. And so But for a long time, I did run a farm and I ran a butcher shop. And so that gave me the advantage that I was seeing— I was seeing the both ends. I was seeing what the animals were being fed, and then I was seeing how the meat came out in the butcher shop. And I knew that traditionally in, in Europe and in like northern Canada, they had— they were known as having the best, firmest pork. And like in the 1800s, American pork sold at a discount in European markets. People didn't want the American pork because the fat was soft. And the reason the fat was soft is that the American pigs were being fed corn, and corn is about 5-ish percent, um, corn oil. And the European and the Canadian pigs are being fed barley and peas, and barley and peas are only about 2% oil. And so That doesn't sound like a huge difference. It's only 3%. But what happens is the pigs sort of bioaccumulate because they're eating, you know, because they're eating corn all day, every day. That little difference in the amount of dietary fat, you know, builds up in their fat. And so, you know, American pork traditionally was maybe 10% polyunsaturated fat and the The European pork might have been half that. Um, in recent decades, what we've done is we've switched to leaner breeds of hogs, um, the other white meat, if anyone remembers that from the '90s. And, and we also have started doing, um, we make a lot of our corn crop into ethanol now. 30 or 40% of the American corn crop gets made into ethanol. And so the— when they make corn into ethanol, all the starch is removed to make the ethanol, and that leaves behind the fat and the fiber and the protein. And so they take those things called dried distillers grains and they feed those to the pigs, and that actually concentrates the fat even more. So, you know, I've seen pigs— I've seen studies with pigs having 25% of their fat as polyunsaturated fat, and that's that's way more linoleic acid, which is the primary poly— that's the omega-6 polyunsaturated fat that people hear about. I've seen that as high as, yeah, 23-25%, which is more than canola oil. Canola oil is around 14-15%, and I think most American pork now has around 15%. I think from the, the numbers I've seen that people have tested it and sent to me, I think American pork is around 15% polyunsaturated fat, which is to say the same as canola oil. And so I'm— and anyways, what I noticed on the farm was, you know, the less oil that I fed the pigs and the better the genetics that I used, the firmer the fat was. And so then once I finally did get a sample tested one time These were finished on basically on whole wheat, honestly, and pasture. Wheat is low in fat like barley is. Those pigs only had about 6% linoleic acid. That's my goal is to make fat in that 6% or less. I know we can do it. It takes a minute. We've got a new program off the ground. The first batch I'm pretty happy with, but I know we can do better. So we're tinkering with the genetics and we're trying some different things to really get that. We're actually using one of our main feeds that we're using is pea flour, which is, which is actually made in the Midwest. This is where my friend comes in. He's, he knows how to get contracts on things like this. So pea flour is, is kind of like the traditional Canadian barley and pea-fed pigs, except that they The reason that there's pea flour is they're, um, they're removing the pea protein to make things like the Impossible Burger, right? And then so they're separating out the protein and the fat and basically the starchy part of it. And so we're now able to buy just the pure starchy part of the peas, um, that's left over from making the Impossible Burger, and that's what we're feeding back to the, um, to the Firebrand Meats pigs, and that basically doesn't have any fat in it. So we're able to make pigs that are, that are given a diet that's very, very low in fat, even lower than I was able to do on my farm here. So, um, so that's the whole backstory on all of that crazy stuff.

Yeah. And, uh, you actually— I visited your website the other day and I was getting ready to go out of town, so I didn't want to order yet, but I think you have two, like, you can do a March and a May or something like that right now.

Yeah, there's— so there's probably the next The first 100 boxes are going to ship probably late March. And then the next batch after that is a little bit to be determined. I'm hoping for May. It may slip into June. And then once— by the end of summer, I want to have it so that we have stock regularly and you can just sign up and it'll ship at a— like, people can subscribe and get one a month or just buy one and it'll ship to them. But for now, it's still this— It's very batch. They're just batches.

Yeah, I got it. And I can't wait to try that, by the way, because I've been avoiding pork for the most part after learning about most of this stuff, which, by the way, I mean, obviously we want people to be more into, you know, supporting local farmers and, you know, doing practices that are more like regenerative— that word is always hard to say— regenerative farming and that sort of thing. But if they can't find that in their area, or they just, you know, can't afford it, can you— I mean, a lot of pork, say like a pork chop, is generally pretty lean. Is the fat still held within the muscle as well? Or if they go for a very lean piece of pork, is that a little bit better?

Right, yeah. So you can, if you get a, you know, like a, like a, like a boneless pork loin and trim the fat off of it, that's a really low-fat cut of meat. You're not getting a lot of fat from the pork, and that's fine. The other thing, chickens on average have more polyunsaturated fat than pork does. If you eat a whole roasted chicken with the skin and everything, you're getting a lot of polyunsaturated fat. If you eat a boneless, skinless chicken breast, you're, you're not. Um, so yeah, uh, so I think eating really lean cuts, you can kind of skirt the issue. But if you— what you really want is bacon or a nice roasted chicken, then, you know, you've got to think a little harder.

No, that makes sense. And but so at least people in like— maybe part of the thing with their diet, they could do the lean chicken breast and then just, you know, cook it in stearic acid, right?

Well, that's, that's what I do sometimes is I'll, I'll I'll do like a breaded chicken breast and I'll fry it in my like my stearic acid butter oil.

Nice, I like that idea. So the last thing that I have to ask you about before you go is that you were— you went to the French Culinary Institute and you make these croissants that you've been using for your diet, right?

Yes.

I had a very, uh, ill-fated attempt at croissants before, so I am just curious if you have any plans, or maybe you've already done this and I just didn't see it like on your blog or anywhere, to number one, share share your hyaluronic acid croissant recipe, or do you have like a tutorial that walks us through it?

Yeah, so it's funny, uh, so right now, um, I don't know, uh, so Dave Feldman, um, if you know Dave Feldman, and just for people that don't know, he has a lot of work with cholesterol, right? And so Dave is a really interesting guy because he does He does all of these experiments on himself and he's an engineer and he is very rigorous about the experiments and he collects tons and tons and tons of data. And so he has all this baseline data on his, like, everything, all of his blood numbers. He knows it going back years now. Right. And so he's actually going to do, um, a test of The Croissant Diet. So I just sent him some croissants and he tried them. And so we're gonna— so, and the other good news is that I'm not— I went to Culinary Institute, I'm not a baker. So my croissants that I made in the experiment kind of sucked. I mean, they weren't terrible, but they weren't great.

So it sounds like we both might need to work on that a little bit, right?

So, but, um, so I've enlisted a good friend of mine who is a baker on this mission, and so she's actually baking the croissants for Dave. And so I worked with her, we did test batches, we picked the one we liked, and so I'm gonna try to get a video tutorial of her making croissants when we make the actual batch for Dave and hopefully post that. So that's, that's my, that's my hope.

Awesome. Well, that addresses the— that addresses the question then, because I, I would love to try it again, especially based on what I know now. Because the other thing, um, that I did actually buy this in anticipation, not for croissants but maybe just a loaf of French bread. I know I just said bread on the keto podcast here, but I know, um, but I similarly to you, um, have thought about that issue with, you know, Italians and French eating in the way they eat, and yet they are, for the most part, still a lot of them are much leaner than we are as Americans. And the other thing I think it has to do with is the flour. I just think our flour is so, you know, genetically modified, highly processed. It's, it's a really a different product than a lot of the things they get in Europe, because I have been fortunate to travel Europe quite a bit, and I've eaten things over there where I just feel fantastic. Yeah, you know, carby things even. And, um, and then, you know, you can't really eat the same here. So I thought about doing this experiment with, uh, just making a loaf of a baguette of regular American flour bread, test my blood sugar with that, and then test it with— I bought some French flour that's made from, you know, locally French wheat or whatever. And I haven't done that yet, but I'll let you know how that turns out.

That'd be really interesting. I know there's also some like— I know there's regions of Italy where they have like special flours that are the ones that were grown there from time immemorial.

Yeah, like semolina, right?

Especially the semolina, although that's not so good for baking French bread probably.

No, I don't think so either. Just for pasta probably. But yeah, well, I just want to thank you again, Brad, for taking the time to do this today and to share this with people, because I think the stuff that you guys have been talking about, especially in relation to stearic acid, is just super interesting. And I'm just like on the edge of my seat waiting to see, hear what the next experiment is and what you guys are figuring out next. And then I try to just distill it down to like a more normal person version and try to pass that along to people. Now, I'm not saying you're not normal. You're just—

it's fine. I'm not— I don't take offense.

But anyway, again, thank you so much for taking the time. And just where can people— what's the easiest way to keep track of you? I know you're a big Twitter person. I am not. But where else can they find you?

So yeah, so I'm on Twitter. I'm the— just the user is @fire_bottle. My blog, of course, is fireinabottle.net. And the Firebrand Meats blog or the Firebrand Meats website is firebrandmeats.com. There's also a couple— there's a Reddit subgroup that a lot of people use that talks about all of these same topics called— it's r/SaturatedFat. So that's been pretty popular, and I'm on Reddit as fire_inabottle, all one word, and I'm on Instagram as fire_inabottle, all one word, and on Facebook, it's Again, it's Fire in a Bottle and there is a Croissant Diet Results discussion group that I should check more often but I've got a lot going on so they're kind of— but that's also busy. People are posting over there and talking about it and so that's happening too.

Awesome. Well, again, thank you so much and I'll be interested to reading your blog over the next year and see what else you figure out.

Excellent. Yeah, we'll keep in touch.

All right, sounds good.

We'll do it again.

Great, thank you.

All right, thanks. Bye-bye.