The Nick Bare Podcast - Archive - Dr. Paul Saladino: The Dangers Of Seed Oils, Are They Destroying Your Metabolism?

Episode Date: February 14, 2022

What if there was an ingredient in just about every food product being sold in supermarkets today that could potentially have harmful effects to your metabolism and overall health?   Dr. Paul Saladino, the CarnivoreMD, joins host Nick Bare on the podcast for the second time to discuss the potentially harmful effects seed oils may have on your body.  He goes in depth into the science behind how these oils interact with your body and how you can take steps to avoid including them in your diet.   Dr. Paul’s Website: www.carnivoremd.com Dr. Paul’s Social Media: @carnivoremd2.0   More Resources: BPN website: www.bpnsupps.com Nick Bare website: www.nickbare.com Instagram: www.instagram.com/nickbarefitness Youtube: www.youtube.com/user/barelifenutrition  

In this episode of the Bear Performance Podcast, this is really an important thing for me in this work that I want to help people understand from a medical perspective, what are the real problems? Because I think that the majority of people listening to this or people that want to get healthy in general, they feel so overwhelmed by health information.

They think, oh, I should avoid processed sugar and I should avoid wheat and I should avoid gluten. And now I should avoid seed oils, but they're in everything. I love the idea of kind of simplifying it for them and saying these are the things that I think are most problematic for humans. humans. And the top three, when I was at dinner, I was actually with a guy with bear. And he said, what do you think are the top three problems for humans? I've actually a great question. I should do a reel or something on Instagram about this. The first one is seed oils.

And I don't know, the first two are probably interchangeable in terms of the hierarchy. The first one is seed oil. Minimize the amount of linoleic acid in your diet, and you will do better. The second is processed sugar. And I think that that's in contradistinction to sugar that is found in fruit or honey that is raw and organic. I think fructose performs very differently in humans, whether it's in a food matrix or whether it's been processed out of the food matrix. So that's a whole other rabbit hole we can go down. And the third one is probably gluten. So if people eliminate those three things, I think their health will massively improve. Welcome back to another powerful episode of the podcast. I'm your host, Nick Bear, founder and CEO of Bear Performance Nutrition.

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on future episodes that embody the go one more mindset. Ladies and gentlemen, we have our first guest for their second time on the podcast. That's Dr. Paul, Saladino. What's going on? What's up, man?

How are you? I'm great. When did you get back? back into Texas. Yesterday. And I'm realizing that I had these grandiose plans of bringing you raw testicle that we were going to eat on this podcast. And I forgot it because I was rushing a little bit.

I wanted to get a workout before the podcast here at your gym. And I left the raw testicle in the fridge next time. I actually, I would love to do a video or a podcast one time where I try all the things that you eat. I love it. Because I was watching videos you eaten. I mean, the testicle is massive. It's huge.

It's the size of, I don't even know what. It's like it to. It's like two tennis balls put together. It's pretty big. Do you eat the whole thing? If I'm really feeling spicy, I will. And do you have trouble when you're in Costa Rica sourcing testicle or organs? No, there's a great.

There's actually two really good farms in Costa Rica. One of them is called Hacienda del Sur, but the place I get it from is called grass-fed Costa Rica. There's a guy named Diego who's out of San Jose, and they have a farm on the Guantacoste Peninsula, which is where I live at the southern end of the Guantacoste Peninsula. And he gets me whatever I want. Basically, I got intestine the other day. I got spleen, heart, liver, testicle in my fridge. It's all there.

And grass-fed meat. After our last podcast, I tried, I will say, I tried eating the liver. I didn't swallow it. I tried to chew it. I struggled hard. And then did you spit it out or do you swallowed it? I swallowed it. I swallowed it.

And I had two guys in the warehouse also try it. They struggled more than me. But I think what I'm going to do, you recommended it, freeze it, cut it up in a little piece of it. you know, bites and then swallow it whole. Or you can even thaw it and swallow it whole. If you freeze it and you cut it up into small pieces, they're going to be rigid and they can actually abrade the esophagus a little bit.

So you've got to be a little careful with that. Unless you get them really small, like the size of a pill. I think it's better to freeze it, thaw it, have it be thawed and soft. And then you can just take it with a wig of water and it'll go right down. And it's so, I mean, it's, this is a hack, man. Increasing organs in the diet is a huge deal. I need to get back on it. But in today's podcast, in today's episode, I do want to talk about seed oils.

Yeah. I went down a rabbit hole after our last episode where it was more high-level animal-based diet and we touched on seed oils a little bit and linoleic acid. I do want to get to that. But before we do, I do want to talk more about hunting and you getting into hunting. I saw a video on Instagram a few weeks ago. You were at Rome Ranch and you were drinking the warm. fresh blood of a turkey, what is the benefit of the blood?

Blood is amazing. It has, you think about what's in blood, what's carried in blood, hormones, immune cells, immune proteins, immunoglobulins, cofactors, vitamins, vitamin D travels in blood, red blood cells are in blood, which are full of iron, heme iron, and then there's all the serum and all these other things. And blood is kind of the epitome of this concept that fascinates me, which is that we don't really fully understand human nutrition. We think about human nutrition. I think there's, I think there's like two or three levels. People think about this. Macros. The first level, the kindergarten level is, how much protein, how much fat, how many carbohydrates am I getting? And that's, that's the start. That's dipping your toe in nutrition. You can

modify your macros and see changes in your body. But then the next level is micronutrients, and you're getting into things like vitamins and minerals. And so like kindergarten is macros, maybe third or fourth grade is micronutrients that we're aware of, vitamins and minerals, like common minerals, magnesium, zinc, maybe things like iron, and then maybe common vitamins like vitamin A, vitamin D, vitamin C, vitamin E, maybe a couple of B vitamins. Then you go on another level and you graduate maybe sixth grade or middle school or high school, and you're starting to think about like really fine-tuned micronutrients, things like vitamin K2 versus vitamin K1, things like biotin, things like riboflavin or folate, different forms of

the B vitamins that occur in plants versus animals and how oftentimes animal forms of these vitamins are more bio-identical, which means they're more bio-available. And then you can look at more minerals, things like selenium or things like manganese, things like zinc and copper and the balance, and also, again, in the mirrored animal versus plant realms or the sourcing of these minerals, the fact that a lot of these minerals, in fact, I would say the majority of these minerals are much more bio-available in animal foods than plant foods because they're not chelated. So we're thinking along this realm and we're evolving our understanding of nutrition. And then you get into like college level nutrition.

This is obviously all a metaphor. And you're thinking there's even stuff that is beyond vitamins and minerals, things like peptides. People might have heard of BPC 157 or other peptides, which are small protein molecules of less than 50 amino acids that have amazing functions in the human body. Then you get to like graduate school level nutrition. You're thinking there's probably nutritional factors in blood, in liver, in heart, in testicles that we don't even know about. We don't even name them.

They're definitely not in the USDA database, so they don't show up on chronometer or any of these other health trackers. And that's, I think, the limitations of nutrition is people will start and say, I'm going to put my diet into My Fitness Pal or chronometer. And they'll say, look, I'm getting all these things

and I'm deficient in these things. But a lot of these apps don't even have vitamin K2 on them. Like the USDA doesn't even include vitamin K2, which we know as an example, is a critical form of vitamin K. There's K1 and K2. and I'll just illustrate this, K1 is phyloquinone, K2 is a series of compounds called

Manaquinones with MK4 being the most bioactive probably. And there's, I don't think we talked about this in the last podcast, there's a large observational study called the Rotterdam study, and they looked at intakes of vitamin K2 and vitamin K1 in the population. And they divided the population up into three groups depending on how much vitamin K2 they got. We call this tertials. So the lowest group, the middle group, and the top group.

And I think the top group was around 35 micrograms of vitamin K2 a day. And this is observational, so we can't draw causative inference. But it was so clear that the group that had the most vitamin K2 had the lowest rates of heart disease and the lowest rates of aortic calcific, like calcific aortic sclerosis, so calcification of the aortic valve. And vitamin K2 is really only found in animal foods. So what they're saying with this observational study or the hypothesis that you can draw from that is, wait a minute, you know, everybody, not just, you know, colloquially, quote unquote,

everyone thinks, or a lot of people in the media or that can, mainstream media believe that animal foods are bad for us. But here's a nutrient that's essentially only found in animal foods, and I'll qualify that in a moment. That is associated. Again, it's not causative, but it's a real strong association for which the most compelling hypothesis by far is that this vitamin is essential for the movement of calcium in the human body. And if you don't have enough vitamin K2 from animal foods, you're going to develop more heart disease and more calcification of the aerotic valve. Those things fly in the face of our modern sort of paradigm of human nutrition and what's good and what's bad. And so that's

just the beginning of the iceberg, but K2 is not even in the USDA database. And the end of that story is that vitamin K1 from plants, there's no association, meaning that no matter how much vitamin K1 people were getting, there was no decrease in cardiovascular disease and no decrease in calcific aortic sclerosis, suggesting that our body's not that good at converting K1 to K2. Well, that sounds like a really important nutrient to have in the USDA database, but people won't even know about that nutrient if they're just using chronometer. So this is a long-winded answer to your of what's the benefits of drinking blood. So all the things I enumerated, immune cells, cofactors, hormones,

vitamin D, iron, other vitamins, other things that travel in the blood, plus probably a bunch of stuff we don't even know about. And of all the organs, blood is kind of the sleeper. You know, people don't think about, like, how do you drink blood or how do you get blood? People can eat liver and they can eat heart and they can eat spleen or testicle, but it's hard to get blood. So when I was at Rome Ranch, which is this amazing regenerative farm out here in Fredericksburg, Texas, it was at Thanksgiving and we were harvesting turkey.

So I got to like grab the turkey myself and kind of like thank the turkey for its life and then kill the turkey myself and then cut the throat and drink the blood fresh from the turkey and it was delicious. Is it warm? It was warm, bro. I came straight out of turkey. My guy, I remember watching that video. I showed my wife. It's like, you got to see this. This is on another level.

But it's funny because you talk about this graduate level of nutrition. I want to school of nutrition. And I was really let down by the educational. system from which I was learning. So I went the nutrition route, but I was also studying with dietetics and dietetics route as well. And I arrived to college and all my professors were 100 plus pounds overweight. Instantly, I was like, something's not right here. And they never promoted performance nutrition. It was always disease, diabetes, cardiovascular disease. And I remember going with these four years thinking something's not right with what we're learning and what I'm doing.

And I remember being a freshman in college and learning that these oils were, these healthy fats were really good for me. Seed oils. Seed oils. And at night, what I would do before going to bed is I'd pour a tablespoon of canola oil and I would drink it because I was trying to gain weight. I was just trying to buff up. And my professors were telling me these oils are healthy fats.

and I look back now thinking, what the hell was I doing? What was I thinking? But it's this, it's that entry level where I think a lot of people get there. And a lot of times it's macros. It's body composition, manipulating macronutrients to reach a certain level of body fat or body composition. But that's the shallow level of thinking. There's so much depth within it. It's endless.

And that's why I love nutrition. And the connections between nutrition and human health are, astounding. And again, this is the type of thing that doesn't get taught in medical school either. I had a similar experience. When I went to medical school, I would say that like 90% of my professors were obese, sickly, pale, not healthy, not friendly all the time. Physicians I worked with, right, on rotations, residents. I worked with very few individuals who were healthy, even overtly, you know, even by just the way they looked, not to say the way they treated us or they treated other people, which is a whole separate story of like, you know, soap operas in hospitals. So, yeah,

this goes very deep. And in medical school, so I went to the University of Arizona for my MD and then I went to the University of Washington for residency. And, you know, great institutions never was nutrition, nutritional biochemistry talked about with regard to any disease. It's disease management with pharmaceuticals. That's what we do, which is, there's a place for that, but it's completely different than what I got interested in. Yeah, it blows my mind. So yeah, I've been watching you on social media, and I know you're really into bow hunting. Yeah. And open fire cooking.

Yeah. I kind of see my life, like, when I have more free time after some time in business opens up and after I have this baby coming up this summer, I've always wanted to get into hunting. And in the beginning, it was, you know, from central Pennsylvania, a lot of rifle. But for me, like, if I want to hunt, I want a bow hunt. and I want to cook that meat on an open fire. You do a lot of hunting in Costa Rica, a lot of hunting in Texas, or, you know, where are you at on that?

So since moving to Costa Rica about a year ago, I've done a lot less hunting. In fact, I haven't done any. It's been a shift from Texas life to beach surfing life, which is another passion of mine. But so I haven't hunted at all in Costa Rica. I don't even think you can hunt legally in Costa Rica.

I'm thinking about bringing the bow just because I like the endeavor. I'm very moderate bowhunter. I'm not an expert at all, but I enjoy it. And it's just, there's such a focus that comes with it. It's very satisfying. So it's a really interesting way to hunt animals. I've hunted it with a rifle also at Rome Ranch and completely different experience.

The rifle was, we went up into a blind, there was a feeder, the feeder comes on, the deer come in, the rifle is sited in, 120 yards, exhale, calm, boom, the deer's down. And it's the same experience when I walk up to the deer and I think, wow, I'm really good. grateful for this sacrifice, this animal. And this, every time I hunt and kill an animal, I have this immediate sense that I don't get a whole lot else in my life, where it's just this profound sense of respect for this process of life and death and this idea that everything must, in order for something to live, something else must die. So you see that viscerally when you're hunting. I think it's a very good reminder for humans. When I'm going to the store, I went to Whole Foods yesterday. I just got into Texas from Costa Rica, and I went to the meat counter, and I got some rib-eyes, and I got some

surloin flap steaks. And I'm separated from that animal. I don't get to look that animal in the eye like I did with a turkey or like I do with a deer that I've killed. And that's an important thing I think for humans to do. A lot of people don't want to do that. And that's why I think it's so important because it reminds you, hey, in order for me to live and thrive, and I firmly believe that animal foods are the key.

They're at the center. They're not the only piece, but they're a huge centerpiece for humans thriving. We must eat those foods. So every time we eat an animal food, we should be grateful. and I believe we should use that as this reminder to be a good human. And I think the more that we can look at animals that we are killing and know those animals, we'll have so much more of that reminder, that memory that's fresh in our minds. And we'll think, wow, like, I'm so grateful to get to live this life with this successful hunting around me.

It's a spiritual thing. So after our last podcast together, like I said earlier, I went into a kind of a deep dive of some of the things we talked about, specifically seed oils and linoleic acid. And I went home and I looked in our fridge in our pantry. I'm just curious,

like, what's the base for a lot of these foods that we're buying? Which most are promoted healthy or even leading with organic a lot of the times. And it was

canola oil, vegetable oil, soybean oil, sunflower seed oil. And then I remember a few days later, I went to the Whole Foods. I was looking at the hot bar.

Everything in the hot bar led it with canola oil, vegetable oil, soybean oil. I went to the grocery store. Same thing. It's in everything. And I cleared house. Like I pulled all this stuff out of our pantry, our fridge.

And I started finding some brands that don't use seed oils in their ingredients. And there are a few, but not many right now. And it was his eye opener of, holy crap, this is everywhere. So what I'm wondering is where did we transition in time in the last couple decades where seed oils were forward leading from the front? And we've kind of eliminated a lot of beef fat or it's been considered unhealthy. And where do you think that that transition happened

in the last couple years? Oh, it's pretty clear. The history of this is fascinating. There was no such thing as a seed oil before 1870. And then it was first used. as a machine lubricant. So they would grind up seeds and use the oil as a machine lubricant. It wasn't really popularized for human consumption until 1910, 1911 with Crisco. We have a story about Criscoe we could tell later.

But, you know, this is, and this was, I believe, they were using, they had this excess machine lubricant and they were thinking like, oh, let's use this for human consumption. This would be great. It doesn't spoil as well. It's cheaper, it's lighter. And it didn't really catch on until I think the 1950s, and I'll tell that part of the story in a moment, but if you look at human

health, and of course, 1910, 1910, 1910, 1910, not quite the same as we have now with medicine, but we had records, right? We pretty much knew what a heart attack was, and heart attacks were very rare, diabetes, very rare, obesity very rare. There's photos from even 60 years ago, and we look at humans, and they were much less fat than we are today. People post these photos on Instagram all the time, 1950s at the beach, 1960s at the beach. It's all skinny people. But even if you, I'm sure if you wind back even further to the 1900s, early 1900s, we had a lot of skinny people.

We didn't have a lot of massive, obese, overweight humans like we do today. We can get into those numbers. They're staggering what the, like the combination of obesity and overweight today is, is enormous. So there's a clear transition in the last 100 to 110 years. So oil really didn't exist before. Let's just say late 1800s and then introduced into the human supply chain, early 1900s. Now, along with that, again, this is all correlations.

We have to be careful. We can only draw a hypothesis from this, which we must test, and we can go into all of the lines of evidence that make me very concerned about seed oils. But these are all just observational correlations. But with the introduction of seed oils from 1910, we see a steady rise in chronic illness. All of it tracks together, gradually increasing rates of obesity, gradually increasing rates of cancer, gradually increasing rates of heart disease, gradually increasing rates of diabetes. And the most significant data we have is probably in the last 50 years and the trend has continued.

But that trend goes all the way back to the early 1900s. Again, just correlation, but we can talk about why I think there's a really compelling hypothesis to be drawn from that. And then I think it was in the mid to early 1950s that I think it was President Lyndon Johnson had a heart attack. And at that point, people were asking what, it just captured the American imagination. And we thought, why did this hero, you know, this, this, this, this, this, uh, this paragon of our culture have a heart attack.

And I think it almost took him out of office. My history is a little fuzzy there, but that was the beginning of the medical system and the American Heart Association and the American Medical Association beginning to vilify cholesterol, and then in connection with that, animal fats. That's the beginning of the problem.

Then we have the stories of Ansel Keys and the seven country study, which we can go into. But if we back up again for a moment and we look at the health of the population early 1900s, described that a little earlier, pretty darn good. I mean, I don't think everybody had amazing diets, but for the most part, there wasn't any seed oil in 1900 in the American diet. People were eating exclusively tallow, which is rendered beef fat or lard. And the majority of pigs in 1900 were probably fed way better diets than they're fed today.

The majority pigs today get corn and soy. So we had animal fats, which were much probably better for humans. And they were essentially 100% of the human diet of fats was animal fat, maybe a little bit of olive oil, but not. even a whole lot in 1900. And so you're looking at butter, tallow, and lard as the main fats in the human diet. And the rates of chronic illness were very low. Diabetes very low, heart attacks, very low. Cancer, much lower. So you're thinking, wait, how come nobody talks about that, right? So again, it's a correlation. We see the instruction of seed oils in the last 100 years, especially in the last 50 years, we know things have gone down the toilet. So it's a very interesting history.

And it's been marketed to us as originally a cheaper, better alternative. It doesn't spoil looks clean, it's white. Chris goes, you know, is pure white. Margarine is pure white. They have to put, like, pills in it to make it look the same color as butter, which has flavonoids in it from the grass that the cows are eating. And the darker the butter is, the more grass, the cows eating. So it began with that. Again, it's a machine lubricant that got sold to humans as a food. And then in the 1950s, it became around cholesterol. And that was when the cholesterol hypothesis began. And the idea that LDL cholesterol, right? Low density lipoprotein.

At that time, mostly we measured total cholesterol, but low density lipoprotein cholesterol was the blame, was to blame for heart attacks, and that cholesterol was to blame for heart attacks. And what do we know? And this is probably the beginning of all of this, this piece of information. We know that saturated fat from animals

raises LDL in a lot of people, not in everyone, but in a lot of people. So that was the beginning of the end for this. And why seed oils have subsequently been elevated to a place of near sacredness, because, and we'll clarify these statements, because they're very misleading, as I say them, if you eat canola oil, right, if you eat seed oils, which are high in polyunsaturated fatty acids, we can talk about what makes this fat saturated versus polyunsaturated, your LDL generally goes down. An LDL is this thing

we think of as colloquially, quote unquote, bad cholesterol. I'm sort of couching all of this with a lot of air quotes because I don't believe that these paradigms hold true. This is the mainstream perspective over the last 60 years, and I think it's totally wrong, and we've been wildly misled. But it is true that generally, if you consume canola oil, your LDL levels will go down. We can talk about why I think it's a bad thing, why it's misleading, but if you peg LDL as a pure cause of heart disease, as a pure cause of atherosclerosis, this formation of plaque within the arterial wall of the body, and then you can say, look, this saturated fat from animals, this tallow, this lard, which is higher in saturated fat, tallow is about 50% saturated

that will raise LDL in many individuals. Then you can make this connection and people start to fear animal fat. So that is why you were told in nutrition school these vegetable oils are good, presumably, because they lower LDL and wouldn't you know what everyone knows that LDL is the cause of heart disease. Now, within that story, there are so many points that I would contend are incorrect and so many wrong turns that we made that we got way, way, way off track and we can start with any of them, but that's the way I see the history of it. And it continues to this day that people, lipidologists, preeminent people in the medical community, continue to hold steadfast to the notion that low density lipoprotein, or more specifically, now people are

calling it APOB containing lipoproteins, which are APOB-100 containing lipoproteins, which includes low-density lipoprotein, but also includes things like chylomicrons, VL, and LDL, et cetera, that that is a particle that is causative of atherosclerosis. It's hard to separate the discussion of the two. I don't want to get too technical, but I think that there is a ton of evidence to suggest. We probably talked about this on the last podcast, that LDL, this LDL particle and these APOB containing lipoproteins are not causative of atherosclerosis. They may get involved in the process, but I do not believe that a particle that have humans

have evolved with that has an essential role in human physiology is literally circulating in my, I can only see the veins in my arm now, but there are arteries deeper, right? It's circulating my arteries, and right now that LDL particle is crashing into the arteries and causing atherosclerosis in my body. That doesn't make any sense to me.

There's more to that equation, and I think that that is where this whole fabric starts to unravel, and the story that we've been told just starts to really look like a collection of misleading statements that, like I said, lead us way, way, way off path. Before we dive any deeper into that,

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And it also made me realize and correct me if I'm wrong, but I bet you most people that are consuming margarine still think they're consuming butter. I think you're right. And I think it's used in a lot of places as quote unquote butter. And I mean, margarine is, yeah, margarine is potentially the single greatest cause of atherosclerosis. I would argue, and we can talk about why that is, in the human diet. And very few people know what tallow is. I talk about tallow all the time.

and it's almost a historically lost term. It's an anachronism because we don't eat tallow anymore. Nobody knows what Sueet is. Sue is the kidney fat from a cow, and it's very high in this fatty acid called stearic acid, which is an 18-carbon saturated fatty acid. Linolaic acid is an 18-carbon-saturated fatty acid. So these two are sort of two,

there's like a protagonist and it's hard to tell who the bad guy and the good guy is, but I would argue that stearic acid is a good guy. Linolaic acid can be the very bad guy. but this kidney fat is very high in this stearic acid. And again, this is a saturated fatty acid that has very positive effects in the human body. It's very high in tallow. But nobody knows what's who it is. Nobody knows what tallow is.

We don't eat that. Some people might eat butter, which is close. But very few of us are exposed to animal fat. If you go to Whole Foods now, you can find tallow, thanks to the folks at Rome Ranch, who built the company Epic Provisions and General Mills bought Epic and they now make tallow. But I think that when I was growing up in the giant supermarket in Vienna, Virginia, there's no tallow in the store. You could get Crisco, which is partially hydrogenated vegetable oil.

We can talk about what that means. You could get butter. And right next to the butter was the margarine or that I can't believe it's not butter. And I think you're right. I think very few people understand the difference between margarine and butter or the difference between Crisco and Lard or Criscoe and tallow. There's a lot of nuance there. So now we're sort of in a way circling back to the discussion at the beginning of the podcast

because if you just look at macros, you would say fat is fat as fat as fat. It's all just calories, right? Calories in calories out, to which I would say no. It's really important. The nuance is so important. Now we're going to like, quote unquote, metaphorically, college-level nutrition, graduate-level nutrition saying the actual fat molecule is critically important. It's not just that you're eating fat.

It's what type of fat are you eating, and they have very different effects in the human body because of our evolutionary history with these different fatty acid molecules. It's actually, I didn't know that epic beef tallow was from a ranch or originally was Those guys who have Roam Ranch, yeah, they started epic. I didn't know that. Yeah. That's the beef towel I get. Yeah, yeah.

I think before we dive any deeper, we should talk about what makes linoleic acid, which we're talking about in regards to seed oils and stearic acid. What makes him different chemically? Yeah. And saturated fats versus unsaturated fats. And why unsaturated fats are more volatile or susceptible. to oxidation or breakdown. We could dive deeper into just what separates those two.

Yeah, the word saturated fat is almost like a bad word. It is, yeah. It's so funny. And the recent, I think the recent political events, the recent viral events, the pandemic, I think has really made people maybe more aware of the way that the media can really program us, right? And I would say that in the same way,

we've been programmed by the media over the last 70 years to think saturated fat bad, LDL bad. We just have this, you know, this reflexive reaction. So even saying saturated fat, I know people are thinking in their head, like, that's bad. I should avoid saturated fat. But saturated fat is essential. What we know about saturated fat is that a lot of, like if you're eating a saturated fat from an animal, that's associated with increases in things like high-density lipoprotein, which is probably a good molecule in the human body. Not that LDL is a bad molecule, but HDL, even colloquial is considered to be good. Saturated fat seems to raise testosterone, do many, many positive things in the human body for obvious reasons. It's a backbone for the formation of

of the cholesterol molecule, which is a steroid molecule. But, you know, I think a lot of people are listening to this as opposed to watching us on video. So I'll try and illustrate this. So a fatty acid molecule is a long chain of carbons. Every carbon has the ability to bind four four other atoms. So if you just had a carbon with four hydrogens attached to it, that's called methane. That's C-H-4. So if you string a bunch of carbon atoms together, they're all bound to hydrogens. That's the beginning of a fatty acid molecule. The only difference is that there's a carboxylic acid group on the end.

It's a fatty acid. So the carboxylic acid is C double bonded to O and then OH at the end. So it's essentially a chain of carbons and hydrogens with a little bit of oxygen on the very end. That's what a fatty acid looks like. And a saturated fatty acid is every carbon is bound to the maximum number of hydrogens. There are no double bonds in a saturated fatty acid. And the resulting molecule, if you model it out, is a straight like line. It almost looks like a worm, right?

It's essentially a straight worm molecule with carbons and hydrogens and at the end is the carboxylic acid group. And so that's a saturated fat. As soon as you introduce a double bond between those carbons, and so one of the carbons can have a bond to the next carbon, but then it can have two bonds in the next carbon. And that means that each of those carbons with two bonds, they're double bonded, has less hydrogens because they have those sort of positions for bonding on the carbon are occupied by the double bond. And this is where you get into organic chemistry, which a lot of people either

have, you know, visceral reactions to like PTSD or haven't done it because they studied something else. I have straight PTSD from organic chem in college. Yeah, yeah. It's a challenging subject. So based on where the position of the first double bond is in the molecule, we often name the molecule omega-3, omega-6, meaning an omega-3 fatty acid is a polyunsaturated fatty acid, so a chain of carbons with some double bonds in it, with more than one double bond in it, where the first double bond is three positions from the end of the molecule. In omega-6, the first double bond is six positions from the end of the molecule, just how we name the molecules.

So mono-unsaturated versus polyunsaturated means a mono-unsaturated fat is a single double bond in the whole molecule. So saturated fat, no double bonds, mono-unaturated, one. one double bond, polyunsaturated, more than one double bond. Some of these molecules can have three or four double bonds across the whole molecule. As soon as you introduce a double bond, a couple of things happen, the molecule gets kinked. So the worm bends. So you can have molecules that are all bent, and that changes the melting point of the molecule because they don't stack on each other as easily. So we think of saturated fats as solid at room temperature because they're

linear and they essentially stack, which means they have this higher melting point. They can be solid at room temperature, whereas vegetable oil is liquid at room temperature because a lot of the fats and vegetable oil are polyunsaturated or mono-unsaturated, which means they're curved and they don't stack as well, and so the kinetics of the molecules won't let them stack. So there's a lower temperature at which they will actually transition from solid to liquid. That's poly, mono, and saturated fats. And then the last thing to think about is the chain length. There are chains of 12, 8, 10. Most of the fatty acids that we think of in human biochemistry are even length chains. there are even odd chain fatty acids in human biochemistry, specifically 15 carbon chains and 17

carbon chains that as an aside that we probably won't go into in this podcast are very valuable for human health. And they are essentially only found in animal fats, this pentodecinoic acid and heptodecinoic acid. So we're essentially dealing for this purposes of this conversation, we're dealing with even chain fatty acids 14, 12, 16, 18, 20, 22, and whether they're saturated, poly or mono unsaturated. So that double bond, would you say that makes them more susceptible to breaking down?

It does. Through a process, I mean, there is, there's just, that's basic electro, that's basic organic chemistry. It's, they're more susceptible to oxidation. And there's a reaction called lipid peroxidation

where molecules can essentially steal the electrons that are shared between those two carbons. This gets pretty technical. But when you have a double bond between two carbons, those electrons that are shared, a bonding between two molecules like this is a sharing of electrons.

And when those electrons are shared, they're in different orbitals. All this gets into like quantum mechanics and like how we calculate where an electron is. But when they're double bonded, those molecules are much more susceptible to being stripped off and taken by other molecules. Life essentially is the movement of electrons.

People need to understand this. We heard this term reduction, oxidation all the time, or we hear the term redox. Redox is a shortened word that means reduction in oxidation. reduction, gain of electrons is reduction, loss of electrons is oxidation. So life happens because electrons are being moved between molecules. Oxidation is the loss of electrons.

So if we say a molecule, like a fatty acid molecule is oxidized, it's losing electrons. Now, usually in an electron bond, there's two electrons in one of those bonds. And so if you strip one of them away, you have an unpaired electron, which is where you get to a free radical. People probably heard that term free radical. and then other electrons can react with that. So it's essentially a molecule comes in with one unpaired electron, a free radical or some peroxide molecule that has an unpaired electron. It can be, all sorts of molecules can be like that, hydroxyl radicals.

These molecules are very reactive when they have unpaired electrons. It's just the way biochemistry works on this planet in this universe. And they come in and they actually want to pull one of those electrons out of that double bond. Well, that creates an unpaired electron in the fatty acid, and that's what we call a lipid peroxide, and that can create a cascade of reactions where that'll go around and strip electrons of other molecules,

and that's probably, that's at the same time essential for human life, and in excess, it's a very problematic thing for humans. We have a lot of defense mechanisms in our body, molecularly, that try and control the movement of electrons. So sometimes people believe

they should completely abrogate, they should abolish all of this oxidation. Well, it's essential for human life. Like, we need unpaired electrons. We need this to happen. some degree of oxidation happens when you lift weights, and then your body responds to it in a positive way. Your body turns on enzymes and turns on transcription factors

and turns on genes with oxidation. You don't want to completely eliminate all oxidation in your human body. You would die, which is why things like alkaline water and, you know, that doesn't make a whole lot of sense of me. Like, you don't want to totally change the pH of your body. You don't want to completely, you know, you wouldn't want to take the hugest dose of antioxidants

because you would die, right? And if you just completely eliminated all oxidation and human physiology wouldn't work. But when it gets out of control, that's when you run into problems. Because we know that oxidation can happen to things like proteins, right? So now we're moving from a fatty acid molecule to a protein. And if you oxidize part of a protein, that protein can change shape. And then the body might perceive it as something foreign.

Or a lot of things can oxidize. So there's these oxidation-free radical per-oxidation reactions. Does that make sense? Makes sense. So are we actually concerned about the linoleic acid itself or the braced? or is it the breakdown and byproduct of the oxidation? It's both in my belief, and there's a lot of reasons for that. So there's a couple of things going on with linoleic acid.

So certainly we appear to be concerned about the breakdown products of linoleic acid. And we know that the more linoleic acid, and let's just back up, so linoleic acid is an 18-carbon omega-6 polyunsaturated fatty acid that is much higher in seed oils than it is in tallow. So if you look at tallow, it's 2% linoleic acid. Canola oil is like 35%, 30, 35%, I'm just pulling the number out of my mind. Soybean oil, 45, 50%, if you've got some numbers on your sheet. But like seed oils go from 20 to 55% linoleic acids.

You're looking at massively increased levels of linoleic acid in these oils relative to animal fats from ruminants like tallow, which is 2% linoleic acid. You're 10xing, 20xing the amount of linoleic acid in the oil. And when you're making a seed oil, you're also concentrating those oils. I'm not a fan of humans eating corn or soybeans in general. You know, corn is a grain. Soybean is a bean. I think that these foods, these are seeds.

If you plant seeds, if you plant them, they grow into plants. They have defense chemicals. They did a post on Instagram the other day about tofu. And there's phytic acid in tofu, this molecule that keyletes minerals that can steal minerals. There's phytoestrogens, molecules and tofu that can mimic estrogen in the human body, which is harmful for both men and women. So I'm not a fan of eating tofu or soy, but if you take soy and you turn into oil,

then you're concentrating this linoleic acid. You would have to eat a lot of soybeans, a lot of edamame to get the amount of linoleic acid found in a tablespoon of soybean oil, like massive amounts. I don't know off the top of my head, but it would be an insane amount of soybeans to get the amount of soybean oil

and a table spoon of soybean oil. That canola oil you were eating in your studies, That's from rapeseed, which isn't even a food that humans eat. So, like, that's basically from a horrible oil that isn't even a food for humans. And you'd have to eat a ton of these seeds that aren't even really food for humans to get that amount of canola oil, corn oil, peanut oil. I think corn oil, you'd have to eat something, again, I'm just back of the envelope thinking about this.

I don't remember the exact numbers. Like, something like, I don't know, 25 years of corn to get a tablespoon of corn oil or something. What we're doing is we're concentrating this on Aleic acid. I'm not sure that I don't think corn's good for humans, but we're taking these foods that humans would never have had much of, and I believe we're survival foods from the beginning. I don't think humans ate corn unless they were freaking starving. And, you know, in the last 15,000 years, we started domesticating it and growing it, which we know was a real problem with human evolution and our health went downhill. But even before that, like wild corn, like, we didn't eat a lot of wild corn. And we're never going to eat that much seed oil.

And so if you look in nature, like linoleic acid is not that present in nature outside of seeds. nuts, grains, and beans, which are all seeds. And I don't think humans have been eating a lot of those foods unless they were freaking starving. They're just not that available. Maybe in the winter you would when your other reserves go low, but we're just never getting that much linoleic acid from our environment. There's no seed oils in our environment evolutionarily. Like I said, 1910 was the beginning. So we're concentrating this fatty acid, which has a role in the human body, but it's the amount that we're getting now is suddenly massively increased from what we ever would ever encountered in our history as humans. You can look at hunter-gatherer tribes, and this has been

done. I talked to a gentleman on my podcast about this, and you know, you can look at these tribes, and they consistently have maybe 2% of their calories from linoleic acid. There's a recent study that I was going to share with you. Stefan Goyane did a study, and you can look now. Traditionally, I think that the set point for humans is around 2% linoleic acid for calories. We're up to 10, 15. Some people, 17% of our calories are coming. from linoleic acid, and that's been documented in the human diet over the last maybe even 50 to 60 years. We've gone massively up in the linoleic acid. So what we have here is a hypothesis. And there's plenty of interventional experiments which corroborate this and lots of points

of evidence that we can look at that point to why this molecule is so harmful. But we have this molecule that does occur in beef tallow, but it's in much smaller amounts. And so the hypothesis is, and a lot of, I think those of us that are concerned about this would say this seed oil is both easily oxidized, so it's spoiling in the jar, in the plastic bottle, in the grocery store while you're waiting to buy it, or while it's waiting for you to buy it. And the processing of these seed oils is quite harsh and is probably inducing a lot of these linoleic acid products. And we're putting a ton of linoleic acid into our bodies. The other thing to point out, there's so much of the story, is that humans can't get rid of linoleic acid. We can't turn polyunsaturated fatty acids

into mono or saturated fatty acids. Other animals can do this. Cows can take polyunsaturated fatty acids and convert them into saturated fatty acids. Monogastric animals, animals with one stomach, chickens, pork, turkey, duck, and humans,

if we eat polyunsaturated fatty acid, we store polyunsaturated fatty acids. So if you were to take a biopsy from me or you of the fatty tissue, the adipose tissue, whether it's like back of the arm, you don't have a lot of fat on you. But you could find fat,

whether it's like your butt or something, right, you could see in that fat how much linoleic acid you've eaten over the last probably two years because you store in direct proportion to how much you're eating. So what we know is this fatty acid isn't present much in nature. We have massively increased it over the last 50, 60, even 100 years. We store it as humans. We can't get rid of it quickly. We can get rid of it gradually.

But the fatty tissue will be a direct reflection of how much we've been eating. And so then we need to ask, is this potentially the major drug? of chronic illness and humans. And I think it's a very, very strong candidate for this because of both its propensity to oxidize and other things it does in the mitochondria. So your original question was, is it the breakdown products in linoleic acid

or is it linoleic acid itself? It's both. Certainly the breakdown products of linoleic acid look problematic because of this oxidation that happens in linoleic acid because of these double bonds. Did we go too far away from the beginning question? No, that was great.

It makes me think to really pull this together. linoleic acid isn't necessarily the devil because it is essential fatty acid. But what the issue is is that when we've created these seed oils, we've concentrated, and now we have this abundance. We have too much of linoleic acid. That's where the issue is, am I correct? Yes. People say it's an essential fatty acid and they'll use that to defend it.

I don't think anyone, I don't even say think. I know no one would ever become deficient in linoleic acid if they were. were eating any amount of unprocessed animal foods in their diet. You could, I don't, I can't imagine how you become deficient in linoleic acid in the human diet. Maybe if you were eating, like, even if you were eating junk food, you would get linoleic acid. It's hard for me to imagine.

I don't even know why we call this fatty acid essential. I think technically it means that we can't make it, but it's in everything. It's in everything. So, like, it's in, it's in beef in small amounts, correct? It's in beef, yeah. It's in beef fat. It's in eggs. It's in, it's in everything.

So no one needs to worry about getting too little linoleic acid. It's just, it's in everything, which means we, the major problem is getting too much. I don't think anyone, even eating junk food, I don't think anyone's ever gotten a deficiency of linoleic acid. Just because we can't make it as humans, like our physiologists make it, it's abundant in the atmosphere, or excuse me, in the environment, and it's concentrated in these seeds. So what are the most abundant sources of seed oils or linoleic acid in today's? diet. Like, we're a lot of people getting these from.

So I think it's, it's things like you said. It's salad dressings is probably number one because you're actually, that's when you're going to actually get maybe tablespoons of an oil. So a lot of the salad dressings have corn, canola, safflower, sunflower, soybean. A lot of these processed and prepared foods that you don't even know it's in there, the hot bar at Whole Foods. Restaurants will use it a lot. I would advise people, if you have a favorite restaurant, don't ever go back in the kitchen because what you'll see will scare you. It'll probably be a vat of peanut oil

in plastic that is surely full of xenoestrogens like BPA or other bisphenols, just sitting there and they're adding canola oil or they're adding soybean oil to food. I mean, it's abundant in restaurants. They're going to add it to anything that needs an oil because it's cheaper than olive oil and the flavor is more mild than olive oil. And we can talk about olive oil if you want as well. Olive oil is mostly mono-unsaturated fat, but olive oil has between 50s,000. and 20% linoleic acid in it as well. Less than traditional seed oils, but still much more than tallow.

I know you made an olive oil, maybe bullshit post of the day. Yeah. When do you decide to use olive oil or stay away from it? I don't use it at all, nor do I use avocado oil, because I don't see the point. I mean, I try to get the fat in my diet

from the meat that I'm eating. So if I go to Whole Foods and I get ground beef, it's going to be 85, 15, or 8020 ground beef. That has a lot of fat in it, Like I said, I had a sirloin flap steak this morning and a ribby last night. That has fat in the steak. I don't need to add tallow. But I do have a jar of tallow in my house.

If I am stuck with like really, really lean meat, I would add tallow. So I don't use a lot of extra oil. I'm just getting the oil that's in my meat. So I don't see the point of using liquid oils like an avocado oil or an olive oil. I think people are mostly using these for salads, which I don't eat in general. You know this. Most people listening to this, no, I'm not a fan of vegetables or leaves or anything that's going to go in a salad.

So I'm not putting liquid oil on anything that I would eat. So I don't think we should, I'm not a fan of olive oil. I'm not a fan of avocado oil. And I think that if you're using those things, you are increasing the amount of linoleic acid in your body above what you could be eating with tallow, above what you could be eating if you were just focusing on beef fat, the thing that's been vilified. But remember, 1900, everybody eats beef fat,

rates of chronic disease are vanishingly low. So there's plenty of historic precedent and plenty of good evidence to suggest that beef fat is super healthy. It's certainly evolutionarily consistent for humans. Maybe not beef per se, but you go and you kill an inland or an Impala in Africa. It's going to be fairly similar. So there's a lot of things to think about here, but I don't understand why people. I mean, maybe you can ask, maybe you can answer this for me.

Like in your diet, and I'm not going to judge you, I promise. Like, where would you use avocado oil or olive oil? I don't use avocado oil. Olive oil, if I'm cooking potatoes on like a skillet. In a skillet. Or with over like, like, like some veggies that I'm going to bake. I'll use olive oil.

More recently, though, I've been using tallow as much as possible and less olive oil. I personally just, I like the taste of, of tallow better. I've definitely increased my red meat consumption, like fatty red meat consumption. I mean, even for lunch, I'll have 80-20 grass-fed, grass-finished ground beef, and I'll throw a tablespoon of tallow on top of that because I've seen the benefit of feeling better with a higher-fat diet. Exactly. So I've been conscious to, I mean, every time I make something, I'm looking at the back of the bottle to see what's in it. And it's funny you bring up restaurants because I don't want to see the back of a restaurant anymore.

And that's why like if we go out to eat like me and my wife, I want to spend the money on a higher quality restaurant. And I hope, I don't know, but I hope that they are using some better sources of food. But I don't know. That's the thing. You don't know. So, yeah, I mean, I was at a restaurant. I rarely go to restaurants, but I was a restaurant the other day in Costa Rica. I got to hang out with a friend there.

I was actually hanging out with bare grills. I saw that. Yeah, we got a good reel of him eating some testicle. And, you know, when the guy comes to take the order, it's a ribeye. And it's a rare instance that it's not grass fed. I'm like, fine, I'll just eat an angus ribeye. And the waiter comes. And I say, I don't want any oil on the steak.

I want you to cook it on a dry grill. I don't want anything except salt on my. steak for a spice and I want to make it very clear to them. So for me, a steak cooked on a grill is fairly safe because they're not mixing anything, right? There's nothing, but there's nothing fancy about that. And people sometimes when they go, I understand them, they go to restaurants, they want to have flavors and they want to experience food. Anytime there's a sauce or something mixed in, I'm almost certain there's going to be a seed oil in there because, or an olive oil. But let's also say this. So a lot of olive oil and avocado oils also cut with seed oils. So it's just cheaper.

And if you, there's definitely, any, any person listening to this could go to Safeway or a regular grocery store to contrast that with whole foods and find olive oil on the shelf that says olive oil with vegetable oil. And they're trying to sell it as olive oil, but it's at least 50% canola oil. Funny you say that. I was at H.E.B. the other day. And we were looking for, uh, for mayo. My wife was making something. And I saw, I just picked up the jar of security. It said, you know, olive oil.

Big letters. It was green. And I flipped it around, canola, vegetable, and olive oil. And I was like, these suckers, they'll get you. Yeah, they will. They'll absolutely get you. And so I think that's a place where people want to use liquid oils as they're making them mayonnaise.

My diet's really simple. And that's why I think an animal-based diet can help a lot of people. There is a, there's like a, there's a buy-in cost, though, you know, if you want to do this or people want to do this, they have to really give up those things. They have to think about giving up mayonnaise, you know, or sauces and spreads. Because that's all going to have, you can't put tallow in that. is going to be solid at room temperature for the most part. And it's not going to spread as well.

It's not going to be as good. You can't put butter in mayonnaise. I suppose you could, but it'd have to be warm or it would congeal and it wouldn't look good. So, again, if I were going to, like you said, if I were going to, I don't eat potatoes or vegetables. But if somebody wanted to do that, and I've talked on previous podcasts about why I'm not a fan of those things, I would use tallow for that. Or butter would be, those would be much better sources, much lower linoleic acid sources. So, you know, we haven't really fleshed out all the science behind this. I'm sure we'll do that before the podcast is over.

I think that one of the take homes early in the podcast for people is maximize the amount of stearic acid in your diet. We can talk about why I value that and then minimize the amount of linoleic acid. I think that a low linoleic acid diet would be so helpful for so many people. And this is really an important thing for me in this work that I want to help people understand from a medical perspective. What are the real problems? because I think that the majority of people listening to this or people that want to get healthy in general, they feel so overwhelmed by health information.

They think, oh, I should avoid processed sugar and I should avoid weed and I should avoid gluten. And now I should avoid seed oils, but they're in everything. I love the idea of kind of simplifying it for them and saying these are the things that I think are most problematic for humans. And the top three, when I was at dinner, I was actually with a guy with bear. And he said, what do you think are the top three problems for humans?

That's actually a great question. I should do a reel or something on Instagram about this. The first one is seed oils. and I don't know, the first two are probably interchangeable in terms of the hierarchy. The first one is seed oil. Minimize the amount of linoleic acid in your diet and you will do better. The second is processed sugar. And I think that that's in contradistinction to sugar that is found in fruit or honey that is raw and organic.

I think fructose performs very differently in humans, whether it's in a food matrix or whether it's been processed out of the food matrix. So that's a whole other rabbit hole we can go down. And the third one is probably gluten. So if people eliminate those three things, I think their health will massively improve. but that is a big ask for people because it means if you're going to cook potatoes you've got to use tallow. You know, if you're going to cook vegetables,

use tallow, use butter. But I think most people can do that with a little bit of choice. And you have to read the labels like you're doing. You have to avoid things like mayonnaise, which are definitely going to have seed oils. And then we can go wherever you want from here and maybe get into the science of why it's so problematic.

But I think that there's a real, there's action steps for people there. And the lower the linoleic acid is, the better. The flip side, I'll just mention briefly, and then we can go into it more in a second. Issteric acid, again, that's an 18 carbon saturated fatty acid.

all you need to know is that's in tallow. So if you do tallow, you're going to lower your linoleic acid, you're going to increase your stearic acid. Stereic acid's great. In human trials, they've done experiments where they made people vegan for three days. So they starve them of stearic acid. Stereic acid is yet another compound found only or exclusively or predominantly in animal foods that is essential for human physiology and optimal health, in my opinion, my strong belief. And so they made people vegan for three days, no stearic acid.

and they look at their mitochondria, these little cellular powerhouses, where all of this oxidative phosphorylation happens, where we actually take these macronutrients, where we take these carbohydrates and these protein molecules, and we run them through, you know, we run electrons from them through the electron transport chain, and we get energy out of this ATP pump that spins and the inner mitochondrial membrane, et cetera, et cetera.

So you can look at the mitochondria of people who have no stearic acid, and they basically turn off. They stop burning fat. You know, mitochondria can also burn fat in a process. This is called beta oxidation. And so, like, all of that, all that stops when you don't have steoric acid. But then you give them back steoric acid. They give them, I think a big dose of steic acid, like 30 grams of stearic acid and a milkshake.

And you start to see all of this fat burning turn back on for people and the mitochondria fuse. You can see it in the study. The study's in one of the nature journals. It's a very preeminent journal. The mitochondria then fuse and they start working and they turn on in the cell when you give someone back stearic acid until you think, wow, could this be useful for our fat burning, and I think it is. I mean, this is a claim that I think is overly simplified, but if you'd get down in the science, I think that weight loss for people could be distilled down to this simple idea that if you lower

linoleic acid as much as possible and you increase stearic acid, I'm so certain you're going to lose weight. You're just, you're going to lose weight because your mitochondria are going to turn on in your cells. You're going to start burning fat and this linoleic acid and all these problematic things associated with it, which we can go into in more detail will be minimized. That's the formula, lower linoleic acid, more stearic acid. I think why a lot of people get confused. And when I was preparing for this, I was thinking back to my interpretation

of vegetable oil and canola oil growing up. And I remember walking down the aisles of grocery stores and you see all the yellow oils like lined up in the baking aisle. And I vividly remember this red heart on the top of the bottle and says heart healthy. So for years, people were thinking vegetable oils, it's good.

It's in most baked goods. Like, if someone has vegetable oil in their house, they're probably either frying something in it or they're using a cake or something. How did we go so far down the, that spectrum where now we're trying to re-educate people who think that the seed oils are good and now we're telling them bad.

And it's like, people are probably thinking, well, what am I supposed to believe? You know what I mean? It's so hard. I think that we've lost. the evolutionary framework. I mean, that's the biggest problem, I think, is that in the nutrition world, in the medical world, and this may sound hokey to people, but I think it's so helpful for me in the way that I think about things is like what, anthropology is not taught in medical school.

It's not taught in nutrition training, but it should be like, what the heck have humans eaten for 2 million, 4 million years? We didn't eat seed oils. We didn't eat Coca-Cola, how we didn't any of these things. And, you know, philosophically, people may reject that and say, just because we didn't eat it doesn't mean it's bad for us. Yes, that's true. But I think it's a real clue that it might be. An evolutionarily inconsistent food should be taken with a lot of suspicion and really carefully considered in the human diet because it is something that's new. And so if you frame it from the perspective, and this is why I love sort of ancestral perspectives of human nutrition, you think, like, what have we done? We've always eaten meat. We've always eaten organs.

And this gets into so many pieces of the work that I do. We've always eaten meat. We've always eaten organs. When I was with the hodzah in Tanzania, the first thing they think about is meat when they wake up in the morning. They're hunters. That's the only thing they want in a day is to hunt and to get meat. So why would that be bad for us? Well, let's ask questions.

Let's do experiments. Let's generate hypotheses. Something that's been at the center of the human diet, doesn't make sense for it to be bad to us. It's just intuition, right? We have to do the experiments to back that up and they've been done. And it's very clear that including red meat in the human diet is not inflammatory. anyone that says otherwise is quoting studies that don't exist. And I'm very certain of that because I'm very aware of this literature.

But, you know, when you lose that evolutionary framework, you have no anchor. And it doesn't make any sense. And so in 1950s, when Ansel Keys comes around and they do this seven-country study, which is an epidemiology study, and they look at, you know, these seven countries in the world, and they say, oh, look, the amount of saturated fat they correlate inversely with the heart attack, risk, or I should say it actually correlates directly with the heart attack risk. So, Anselkis can cherry pick seven countries where the higher the saturated fat, the more heart disease risk. And that's the seven country studies essentially in a nutshell. And you say, well, wait a minute,

what about other countries? Is it possible there are other countries where that association doesn't exist? And that's totally true when you expand and you go beyond those seven countries. This is what we call cherry picking, saying, oh, you're only going to include the countries in your study that fit your hypothesis, right? Or he'll look at countries and he'll say, oh, this country has low saturated fat and that was because it was during lent or something and they weren't eating animal foods in lent and so they they didn't actually have low saturated fat in general but that time of the year that he surveyed you see what I'm saying here so this is this hypothesis gets propagated because saturated fat gets vilified there's actually an amazing story that's been told here about

potential collusion with the american heart association the american medical association and then the sort of the sugar lobby wanting to point the finger at fat and go that's the problem because I don't know if you remember this from when you were growing up, but I was growing up in the 1980s, everybody was pointing the finger at fat, and nobody was pointing the finger at sugar. There were these cookies called snack wells, which were really low fat, but full of fructose and processed sugar.

And nobody is pointing the finger at sugar because the industry, that sugar industry appears to have very successfully lobbied and said, point the finger at fat and point the finger at animal fat, because we know animal fat raises LDL, and we can do these studies that look at this. So it's crazy.

I remember low fat. I mean, I grew up in the 90s. I was born in 90, but I remember my mom's friends buying everything low fat, low fat this, low fat that, and it was everywhere. I want to take it to,

because you brought this up earlier and talking about fruit and why you consume so much fruit and that's your primary carb source. Yeah. And why you believe that? Because for a lot of people, I mean, over the years,

there's just been this information spread and you find a lot of people who are trying to restrict their fruit intake because of it being a high glycemic carb and they think they're going to get fat from fruit, non-processed carbohydrate source. Can you dive deeper into that? Yeah, yeah. So it's an interesting story. I mean, for me, and we probably talked about my story on the first podcast, but, you know, the carnivore diet, a diet of exclusively meat, organs, animal fat, and salt was my gateway to all of this. So I had eczema, which was pretty severe at times.

asthma as a kid. And I, those things didn't get fixed with a paleo diet. So I was eating this paleolithic diet of meat, vegetables, fruit, nuts, mushrooms, essentially, not really a lot of organs. And the exome would come and go. And at times in my residency at the University of Washington, it was so severe that it was just all over my body. I remember being on a date one time. The girl was looking at my arm, like, what happened to your arm? And I was like, oh, I got in some poison ivy because I was so self-conscious to be like, actually, this is eczema. And I have no, I'm a doctor and I have no idea what's causing this. This is so frustrating. And so that was the point for me where I said, I'm, I'm curious about these plant foods. Could these plant foods and these

fungal foods, these mushrooms, be triggering my immune system? So I cut them all out. And that was really eye-opening for me because the exima completely got better, my actually emotional stability. Like, I didn't really feel like I had issues with anxiety or depression, but I felt better emotionally as well. Fast forward about a year and a half, I'm writing this book, The Carnivore Code. I've seen so many people get better from GI issues and autoimmune issues with this carnivore diet that I think there's something here. But like, you know, like we all learn along the journey, sometimes we get a piece of a truth. We never find that truth, but we find a truth. And so humbly, I had to sort of look at the way I was feeling after a year and a half of a ketogenic diet with no carbohydrates, essentially, other than

what you find in meat and organs, which is very minuscule. It's paltry. And so, you know what, I don't feel as good as I want to feel. I have muscle cramps when I go climbing to the climbing gym. You know, I point my toe to get on a hold and my cramp, my calf cramps up. I get cramps in the morning. I'm having heart palpitations while I'm sleeping. I'm not sleeping really well. And the last time I checked my testosterone at this point in my life, it was lower than I wanted to be.

It was like four or five hundred. And I thought, that's not right. I've seen it, you know, in the 700s before, before I started a carnivore. This is, I'm rewinding the clock back. So I had to kind of look at this and say, you know what? I need to reevaluate this perspective on a ketogenic diet. I've really since come to believe that though ketosis is super helpful for humans and turns on a lot of important genes that are involved in cellular house cleaning, autophagy, and affects genes in a positive way, it's powerful medicine, kind of like fasting, you can overuse it. So I realize, oh, I've overused ketosis and insulin, this peptide hormone that is released when you eat primarily carbohydrates, but some protein induces insulin release.

We think of insulin as a bad hormone, but it's such an important hormone for the human body. If you don't have at least phasic, meaning spikes of insulin throughout the day or throughout the week, you're really not going to be able to hold on to electrolytes at the level of the kidney as much as you want to. And that's why so many people on ketogenic diets do more salt and electrolytes than I've ever seen in my whole life. It's crazy. That's why whole companies have arisen around ketogenic diets trying to fill these electrolyte needs of people who have essentially flatline their insulin signaling and are just wasting electrolytes,

things like sodium, potassium, magnesium, calcium, and their kidneys because there is no or so low signaling of insulin at the level of kidney. Can insulin come back once you reintroduce carbohydrates? Absolutely. As soon as you introduce carbohydrates, your body turns on insulin again.

It takes like a day or two for it to adjust because, you know, your body actually becomes physiologically insulin resistant, which is different than pathological insulin resistance. Well, probably, hopefully we'll get to that in this podcast because I want to talk about the roots of pathological insulin resistance. They do relate to linoleic acid and the breakdown products of linoleic acid very clearly. So that's fascinating. But you do become physiologically insulin resistant when you are ketogenic. So I'm sure you

experience this in the Rangers. You know, you're out, you haven't eaten for a few days. Your body goes into ketosis and your body is then sparing glucose that it's making through gluconeogenesis for the testicles, the red blood cells, the adrenals and the brain. And it doesn't, it says, no, no, muscles don't take up glucose because you can do fine with ketones, right? The brain can run on some ketones, but it needs to have glucose. So the body's very, very wise at partitioning nutrients in states of, quote, semi-starvation, because evolutionarily, it would have been a state of semi-starvation for us if we didn't have any carbohydrates.

It certainly happened to us, but our goal as humans would have been, where can I find honey, where can I find fruit, where can I find carbohydrates all the time? And so if we go for too long in that state, we do suffer physiological consequences. and I did. So I looked at foods, and I thought, where can I get my carbohydrates from? Well, grains are seeds, their plant parts,

their plant babies, they're highly defended. I don't want to eat grains. You know, roots are also defended. That's not my first choice. I'm going to, I think that fruit, the sweet part of a fruit, the sweet part of a plant that's colorful, probably makes the most sense evolutionarily.

And I could find literature to say that if you compare the fruit of a plant to the actual stems or the lean, leaves, the amount of defense chemicals is much lower in the fruit. We know this. This is seen over and over in botanical science. Like in, there's whole literature on this. In fact, I was reading this amazing, like, chapter of a book about plant defense chemicals on the plane over here from Costa Rica. And you can see this over and over that when a plant is making a fruit, it may put defense chemicals in the fruit when it's green, when it's unripe. But as the fruit ripens,

they get lower and lower and lower and lower. And a lot of these defense chemicals are at, much higher levels, five to ten X in the stems and the leaves. So fruit is clearly the least defended part of a plant. I thought, okay, that's going to be the first thing I'm going to try. So I reintroduce things like strawberries. And I started with honey because honey is made by bees. There's no real defense chemicals in honey. You could even argue that honey is an animal food. So I reintroduced honey. I reintroduced fruit in my diet. And because I was so interested in my insulin response in my metabolic health, which we can define my insulin sensitivity. I continue to check my labs. Fasting insulin is perhaps the most important blood test you can check. And we can talk about

why. And I wore a continuous glucose monitor from a company called Nutrisense. You can just put this thing on your arm. It has a stylet. Are you familiar with these? Yeah, I've been wanting to get one, actually. We get you one. Yeah, yeah, for sure. Yeah, I would love to. Yeah, yeah, absolutely. I'll absolutely get you one. I've actually got some. I should have known. I've got some of my house. So you can put this glucose monitor on your arm and has this little plastic stylet that goes into the interstitial space and you can check with your phone

and it'll take a blood sugar measurement every five minutes so you can see your blood sugar in real time throughout the day. So I could see what was happening with my blood sugar when I introduced carbohydrates and it was a fascinating experience. So on my podcast, which is called Fundamental Health, I've gone through all this data and showed my data.

But in summary, my fasting blood sugar, ready for this, went down when I introduced carbohydrates. So my fasting blood sugar sugar goes down when I introduce carbohydrates because as a physiologically insulin resistant human, my blood sugar was kind of flatline, but it was higher. The baseline was higher all day because of gluconeogenesis and the physiology. So for instance, I would say that when I was strict carnivore, my fasting blood sugar was probably 95, sometimes 103 milligrams per deciliter fasting. So

you wake up in the morning, your blood sugar is 103 or 96. You eat food, your blood sugar is 96, 103, right? introduce carbohydrates, fasting blood sugar, 72, 73, 68, these kind of things. And then when you eat food, I'm eating carbohydrates. I would probably, I usually eat like twice a day. My blood sugar might go up to 130, 140. I don't worry about that because then it comes down quickly. This is difficult to illustrate without a visual, but imagine kind of a flat line and then a little spike and the spike comes back down in normal within an hour.

So when you're looking at a continuous glucose monitor, what you want to look at is the area under the curve because it's a reflection of how much insulin load there is needed to move that sugar out of your blood. This is checking glucose. So we're looking at a glucose area under the curve in real time. And you can see that when I was on this honey or this fruit, would go up, come back down and then go right back to baseline, then go up in the afternoon, come back down to baseline. So these are not patterns of metabolic dysfunction. There's really clear visual patterns of metabolic dysfunction on a continuous glucose monitor. It's a much broader peak. It looks like a tombstone or has multiple peaks.

and the area under the curve is much broader, right? So the area from the base, like an integral. I used to love math when I was a kid, but I don't know if everybody understands what an integral is, but you integrate, you sort of like take all the area under that curve. And if you're insulin resistant or you've metabolic dysfunction, all that area under the curve is so much higher when you eat carbohydrates. So you can see on a continuous glucose monitor,

if I put that on someone, I can see immediately how metabolically healthy they are, just by how they respond to sugar, whether it's from fruit or whatever. So you could see, like, I'm just, I'm metabolically, I'm responding, boom. up down, up down, consistently, week after week after week. And then at the end of, I think, two months, I checked my fasting insulin,

and my fasting insulin on a carnivore diet was probably 3.5 micro-IU per ML and a fasting, my fasting insulin, which is the best metric that I think people can easily get of metabolic health on this carbohydrate diet containing at least 100 grams to 150 or even 200 grams of carbohydrates a day is three. So my fasting insulin doesn't change at all

on this diet. So those are the piece of data points that I would advance to say, including carbohydrates in my diet in this whole food form, fruit, honey, did not change my insulin sensitivity at all. In fact, it probably improved it somewhat because you need some phasic release of insulin. My electrolyte issues got better. My heart palpitations went away. My testosterone came back to 800. I'm sleeping better and I'm thinking, oh, okay, humble pie. Like, let's continue to evolve and explore and learn what is, you know, what is the best diet for humans. So, but then the question becomes, well, if fruit is okay for humans and honey is okay for humans, why have we been told that soda is so bad? What's the difference? And in the

ketogenic community, there are many intelligent, well-meaning individuals who will equate honey to a Coca-Cola. They'll say it's the same amount of sugar, like, you're getting the same amount of sugar. And I would say, it doesn't make sense to me. Again, let's go back to the evolutionary framework. Like humans have never been exposed to sucrose, which is a disaccharide of gluten, and glucose and fructose in a sweet beverage. They've been exposed to honey, which is a little, some sucrose, some fructose, some glucose in this gelatinous matrix with about 300 other chemicals and prebiotics, like all these other things in there, some things that affect the gut flora, things that are nitric oxide

precursors. So it's a completely different piece of information for humans. But this is what's been lost in kindergarten, first grade, sixth grade, nutritional science is it's reductionist. And you don't say, oh, what is the information that? that this food is giving your body. This is again back to organs. Organs are this incredibly rich

informational source for your body. You're eating a liver. There are thousands of compounds in there that are pressing all sorts of buttons and doing all sorts of cool things in your body that are really evolutionarily consistent and have been celebrated for millions of years. If you eat sugar, it's just like there's one thing,

just like fructose. You know, it just pulls one lever. It just pushes one button in the human body. So you're thinking like, okay, like the information that you're getting from a table suit of honey is completely different, completely different than the information you're getting from 15 grams of, let's say, equivalent sucrose, which is that disaccharide of glucose and fructose.

So it's so much more complex in honey. It's the same thing with, it's like, say you're eating bananas. Banana is like 20 to 25 grams of carbohydrates in a banana. It's completely different informationally for your body than a tablespoon and a half of table sugar. Orrins juice is a great example because there's been a lot of good studies with red, orange juice, like blood red orange juice, and presumably this is like not pasteurized orange juice. There's like fresh squeezed orange juice. People get worried about fruit juices, but like fresh squeezed orange juice results in a completely different physiology in the human body than the

equivalent amount of fructose or sucrose in a tablespoon. And it does it in mice too. So there's a lot of interesting questions to ask here. And the conclusion that I've arrived at is food matrix, fruit, honey, containing sugar of all sorts of types, fructose, glucose, sucrose, et cetera, in a food matrix is a completely different informational experience for your body than in isolation. So there are people in the nutrition space that go completely the other direction and will say, oh, it's okay, just eat tablespoons of sugar. And I don't think that's true, but I also don't think that fruit is bad for humans. And like I said, there's good studies with red orange juice that show that, hey, endothelial function,

these cells that line the blood vessels gets better when you drink red orange juice. how can fructose be so bad for you? So there's lots of interesting studies. And then in mice, for instance, with honey, this is one of the most striking studies. Humans are not mice, but the physiology is probably pretty well conserved. If you give a mice fructose, they have all sorts of problems. They have oxidative stress.

The liver gets fatty. Their body goes a little haywire. If you give the mouse honey, it's completely different. They don't have oxidative stress. They don't have DNA damage. None of these things occur. When you were with the hodzah, what diseases was prevalent, if any, with them?

when they had very little linoleic acid in their diet, zero or little... Two percent, yeah. Essentially none. So the hunter-gatherer pop... This is why anthropology should be taught in medical school. It's such a fascinating experiment. These hunter-gatherer populations do not suffer

the chronic diseases that we have as humans. There's a whole tribe of these hodder, right? We went to visit one group, maybe 45 members. No one is obese. Not a single person is obese. Actually, that's not true. there was one woman who was obese. And I knew the story behind this because the guy I went with had seen her before.

He's been going to visit the tribe for 12 years. And she's actually the wife of the chief, I think. And he'd asked the chief or he'd asked someone, like, what's going on with this lady? You know, she got a lot more obese since the last time I was here. And their answer was, oh, she's been going to live with the missionaries in the city. What do you think she eats in the city with the missionaries? Seed oils, cornmeal, processed sugar, all these kind of things. So that's the only member of the tribe that's even obese at all.

And she wasn't even, I think if she walked down the street in the United States, you wouldn't even really bat an eye and be like, oh, that person needs to lose weight. You might be like, oh, person's, you know, kind of like big bone or whatever we would say, like a little, you know, a little bit genetically larger. But you wouldn't even bad an eye. But she had gained weight from those interventions being in the city. So they don't have diabetes.

Obviously, they're in the, they're in the bush. Like these people really live in the bush, but they don't, they don't, you know, we don't observe heart attacks in them when they've been studied. I didn't go and do medical work with them. You have to have special permits, but you can look at, my role there was really to live with them, to ask them what they've treasure,

to hunt with them, to understand how they think about food. And then people have done medical studies. They are very cardiovascularly healthy. They don't tend to have autoimmune disease. There's like nobody with vitiligo or XMR or psoriasis in the tribe. And there's 45 people there. Like,

or 50. And you see this across multiple tribes of hunter-gatherers, whether you go visit the other group of the hodz. I mean, you think you get 45 of your best friends together in a party, like somebody's going to have something, you know, like this person's had a stroke or that person, you don't see any of that there. And again, this is just my observation, but there were, there's been studies that are much larger.

Like, the rates of those things are very, very small. So it's essentially, it's pretty darn safe to say that these hunter-gatherer tribes do not suffer chronic disease like we do. They're like chronic disease rates from humans, you know, 20,000 years ago, presumably very, very low, perhaps occasional genetic things, but nothing major in those people. And I want to really emphasize this one point, which always gets misunderstood, is that their health span, so their vitality dwarfs ours, which means that they stay vital long into old age. Hopefully you and I will be lifting weights and surfing and doing awesome shit when we are 60, 65 years old.

But a lot of people don't do that. Like my father's 71. I love the guy. He's hunched. You know, he's like, he's getting shorter. Every time I see him, he has chyphosis of his spine. He's like no butt. He's like no fucking gluteal muscles.

Like, how do you even sit down a chair, dad? You know, like, how do you do this? And you see people in their 60s or 70s now, and they, they're not surfing. They're not paragliding. They're not doing cool. They're not in the gym doing hand over hand ropes or any of the stuff. But with the hodza, there's like guys who are 50, 60 years old in the woods with, in the bush with us, fashioning spikes out of trees with a knife, drilling the spikes into

a Beobab tree, then climbing 35 feet up into a Beob tree to look for honey within the span of three minutes. And you're like, that's a 60 year old. That's incredible. Like, these guys and women have incredible vitality long into life. That's what we call health span. Like, how decrepit are you? How, you know, how vital are you? And within these tribes, the, it's the observation consistently, whether it's the Hadza, the Ikung, other hunter-gatherer tribes, there's only a few left left on the planet. They're vital up until maybe the last few months or weeks of their life. And then it kind of drops off a cliff, right? So when the time has come for them to die, they will decline, but it's all, this is called compression of morbidity or squaring of the morbidity curve. Because

if you look at the morbidity curve of like westernized humans, it just goes down and down and down, right? People have like less function, less function, less function. These hundred gathers are like straight across. It's squared, right? And then they drop off at the end because everybody dies eventually. I remember, I figure where I saw this being shared, but it was, it was, I think the late 1800s, And it was the world's fattest person. Yeah, yeah, yeah. And you go see, I don't know, maybe you shared it. No, I didn't share it, but I saw somebody else share it.

And you could go see the world's fattest person. It was like on display. Yeah. But they only weighed like, I think, maybe 300 pounds. Yeah. The fattest person in the world. And I'm, I'm sure that lifestyle choices and the food available was a reason. But I think a lot of times people will say, oh yeah, that's because lifestyle has changed over time.

and so has the amount of food we can consume. But I think it would also be ignorant to say it's the quality of food that we're consuming as well, like seed oils. It's a huge thing, and we can get into appetite and obesity and connection to seed oils. It's a really fascinating rabbit hole. Before we go there, I want to...

It would be interesting, actually, to talk to that guy and be like, what are the fattest guy in the world in 1800 eat? You know, what was he doing, or 1850? I remember, it would be interesting to see what year was that guy, right? Like, how did he get so fat? Like, there are genetic mutations that can cause massive amounts of adiposity, but it's pretty rare. There's like hyperphasia mutations, Prater Willie syndrome, things like that. But I wonder what that guy was eating and whether there was

after the introduction of seed oils or how somebody gets to be that fat. But the last thing I want to say about hunter gatherers is people say that they have a short lifespan. But if you look at hunter gatherers and you look at their lifespan, excluding infant mortality, they live as long as we do. They just have higher rates of infant mortality. And so it's all averaged together. And that skews the lifespan. That's such an important point. Because whenever I talk about hunter gatherers. And I think they're the crux. A lot of people will say, yeah, but they only live to be 35, which is not true. They live to be 60, 70, 80 years old to the same degree that we do today, even with our life-saving interventions, which are probably not that life-saving. And in the wild,

guess what? Having a baby's dangerous. There's a snake. There's a, there's a hyena that could steal your baby, that baby could fall off a rock and hurt itself. There's infections, like sanitation. Like being a human in the wild is dangerous. when you're a kid. And infant mortality is higher. And that skews the life expectancy. So that will close that chapter. I do want to talk about what you're saying with obesity and appetite because this is a fascinating story. So there's a drug called Ramona Band. Have you heard of this? Recently I have heard about it. I don't know where I heard about it at. So Ramona Band is a fascinating drug. It actually helps people lose weight really, really well. And the way it does this is by

antagonizing, so blocking the endocannabinoid system. So now we're into the realm of like marijuana and cannabinoids. There are endogenous cannabinoids in the human body like anandamide, and there are exogenous cannabinoids like THC or other cannabodial that we can get from marijuana. But one of the receptors for those either endogenous cannabinoids or exogenous cannabinoids is the CB1 receptor. Ramona Bant antagonizes the CB1 receptor. And that leads to massive. of weight loss and improvements in a lot of things in mice and humans. So the first experiments were done in mice and they say, oh, wow, these mice get like really lean and they look really good and we give them Ramonaband.

This could be an amazing weight loss drug. Then they do it in humans and they find that it increases the rates of suicidality and depression because as we find with drugs, and this is a really good lesson to remember, they often have side effects and that's why we do these clinical trials. So, of course, you can antagonize the CB1 receptor and that probably has to do with appetite and obesity. People lose weight. They have less appetite and they don't overeat as much, but that receptor is also important for mood and proper mental health. So, okay, that drug kind of gets thrown out, but it shows you that this mechanism is there. And what's fascinating about this

is that when you eat linoleic acid, whether it's a human or a mouse, and this has been shown in both mouse and human models, a molecule is produced called 2AG, which is a cannabinoid. And that cannabinoid activates that CB1 receptor. So the really compelling formula, the compelling story you can draw here is, is part of the problem with linoleic acid? And you asked me this question earlier. Is the problem with linoleic acid, the linoleic acid itself or the byproducts? So it's both.

And one of the reasons that linoleic acid itself could be problematic is because of this appetite piece. So if you have linoleic acid leading to the production of 2AG, this exogenous cannabinoid, in humans and mice and other animal models, and they get fatter, couldn't that be in the brain? It's telling you, oh, eat, eat, eat. It's like the opposite of Ramonabant. This is another drug that we use. I think it's called droperidol for cancer cichia patients. We can give them drugs that agonize, that turn on that receptor, and they will eat more, right? So you can turn on the receptor, people eat more, they overeat, or you can block

the receptor and people will stop eating and lose weight. And look what linoleic acid does. It makes a product, which will do the same thing. And there's studies in mice, there's studies. There's studies, in C elegance. See elegance is a worm. You can make worms fat by giving them linoleic acid because of these, probably this mechanism

of satiety in the human brain. How crazy is this, right? I do you remember actually I listened to a podcast you did talking about this. That's right. Yeah, yeah. That's right.

That's right. We're Tucker Goodrich. Yep, that's it. Yep. And the end of the story is that one of the reasons that we think gastric bypass works for humans

is that when you do the gastric bypass, you cut away some of the stomach and you take the intestines and you loop them in a special way. sometimes it's called a Rue and Y gastric bypass. But when you cut away part of the stomach, you have to cut away branches of the vagus nerve.

And this is a nerve that runs from the stomach to the brain. And there's also thinking that these cannabinoids that occur from the diet get into that vagus nerve and will trigger in the brain appetite and loss of satiety. So when you cut those vagus nerves in the gastric bypass, people are able to stop eating. They don't feel quite as hungry, or they don't have this disordered satiety,

you know, this appetite when they're eating these foods. So is it possible, and I think there's so many pieces of evidence that point to this, is it possible that this linoleic acid in foods is just in and of itself completely destroying or messing with our satiety? And I mean, I think most people who've eaten processed food will get this. You eat Cheetos. I mean, you know, there's probably a lot of reasons for this, but you eat Cheetos or whatever food you want to eat with seed oils, you want to eat more. You really can't stop eating. So is it possible this is happening with 2AG? and the CB1 receptor, yeah, absolutely. So if humans insist on eating processed food,

you could use a molecule like Ramonabant to block the receptor. Of course, it's going to have these other side effects with these depression and suicidality, which is no good. But we see the mechanism. And again, it just speaks to the same idea that, man, this linoleic acid molecule, if we introduce evolutionarily inconsistent levels of that, it can be problematic for us at a lot of levels,

and one of those is probably satiety. What makes me think, like when I'm on a road trip for example, and don't do this anymore, but back in the day, say you have truck stop snacks in the center console, and you open them up, you grab a few, you start snacking, you close up the bag with the intent of not to open it up again, and then five minutes later, you open it up, you get some more, but before you know, you finish that whole bag off, and there's only certain foods I do that with. and we talked about the insulin resistance.

What other impacts do seed oils, linoleic acid, have on the body like the insulin resistance? Well, let's unpack the insulin resistance. This is a little technical, so I apologize to the listener, but it's really, really important because this actually kind of mirrors the conversation we had about sugars and fruit. I think that there is so much misunderstanding in the popular, just zeitgeist, in the popular thinking, you know, that people believe that carbohydrates cause diabetes. And it's not true. Like, processed sugar probably creates oxidative stress, probably creates a lot of problems,

but fruit doesn't lead people to diabetes. That's false. Honey never caused diabetes in a single freaking human. And there's examples. There's my personal example. There's many examples that, like honey doesn't cause, and I'm talking about it. about raw, real honey, not processed honey that's cut with like high fructose corn syrup, but like honey never caused diabetes in anyone.

Strawberries, oranges, bananas, papaya, pineapple, pineapple, never cause diabetes in anyone. Like, carbohydrates do not cause insulin resistance in and of themselves. If you are insulin resistant, aka metabolically dysfunctional, eating carbohydrates can be hard for you because your body doesn't manage sugars very well. So you see it as a manifestation, but they did not cause that underlying pathology. So let's just break this down a little further. What is insulin resistance? I don't like the term insulin resistance because there is such thing as physiologic insulin

resistance and pathologic insulin resistance. I like the term metabolic dysfunction. Physiologic insulin resistance is physiologic. It's normal. It's quote unquote healthy. There's no disorder there. It's what happens when you're not eating because you're in the field on deployment. When I'm, you know, if I'm fasting for two days, I'm going to get physiologically insulin

resistant. A year and a half of a carnivore diet with no carbohydrates. Physiologic insulin resistance raising my fasting blood sugar, right? That's a normal process in a human. Metabolic dysfunction, not a normal process in a human. That is what happens when you are eating carbohydrates and your muscle is refusing them. Physiologic insulin resistance is you have no carbohydrates, so your body is sparing glucose for other tissues of the body.

Does that make sense? Makes sense. So metabolic dysfunction is you are eating carbohydrates and your body's like, nope, we don't want those because insulin is being released, but all the tissues of your body are saying, we're not listening to you insulin. In physiologic insulin resistance, certain tissues are saying,

we're not listening to you because we're sparing glucose for the other tissues. Metabolic dysfunction, I'm saying this twice, just to make it very clear, is essentially all the tissues of the human body are saying, we're not listening to insulin. We need, and insulin levels have to go higher and higher and higher.

This is the progression to type two diabetes, and the pancreas gets exhausted because the beta cells and the pancreas can't make any more insulin. This is obviously oversimplified. But the insulin goes higher and higher and higher because the cells of the body whether it's muscle or fat or brain or liver are saying,

we're not listening to you insulin. We are insulin resistant. So it's very important that we differentiate pathologic versus physiologic insulin resistance. And that pathologic insulin resistance is a state of metabolic dysfunction. So what is happening there? It's not carbohydrates. There are competing schools of thought. I've had people in my podcast and had friendly debates with them.

But I think it's very, very clear that it is not that insulin-induced insulin resistance is essentially unheard of. the carbohydrate theory of insulin resistance would say that oh people are eating too many carbohydrates therefore it's too much insulin and eventually your body just shuts off i think that's a falsehood like you couldn't do that without a constant IV of sugar into your body like you know even if you're eating you would essentially have to be eating cheetos and corn chips like 20 hours a day and then in the four hours of you're not your body would start to shut off and like recite you know like recycle you got to sleep sometime you know what are you waking up every two hours in the middle of the night and

eating eating junk food i'm sure people some people do that and maybe for those but the majority of people on the planet, they're probably eating 12 hours a day, 14 hours a day, and they might be stretching insulin-producing foods throughout that time, but I don't believe insulin-induced insulin resistance, meaning excess carbohydrates,

even if their process is the main driver of long-term metabolic dysfunction in humans. It's something deeper. It's something hormonal, and that, I think, is driven by seed oil. So that's the statement that I will make for this podcast. I think that long-term chronic insulin resistance, aka metabolic dysfunction,

is driven by excess linoleic acid in seed oils. and that comes from both excess linolayic acid and excess linoleic acid breakdown products. How does that happen? Again, hopefully that's not too technical so far. It happens at the level of the fat cells. The fat cells are where everything, that's the epicenter of metabolic dysfunction for people, your adipose tissues. So everybody has adipose, even a guy like you, super lean.

You have adipose. You have adipose tissue around your organs inside your peritoneum. This is called visceral adipose tissue. You have adipose tissue on the back of your arm, adipose issue in your glutes. a little bit of adipose tissue everywhere. We all have adipose tissue, subcutaneous or visceral inside the peritoneum adipose tissue.

And that adipose tissue is more than just a bag of fat. It's hormonal. It's a cell. If you look at a fat cell, it has a nucleus. It has mitochondria. It sends out adipokines.

Fat cells are a gland. They're essentially like, you know how the thyroid gland sends out thyroid hormones? Fat cells send out hormones to the rest of your body. We call these adipokines. And they send out cytokines,

which are signaling, signaling molecules. So fat is an organ and it's an endocrine organ. It's like your testicles or ovaries in a woman or any other organ in your body, like your adrenals that sends out hormones. The fat cell is an organ and it sends out, it's an endocrine, it sends out these hormones, which we call, like I said, adipokines. So the fat cell gets broken by excess linoleic acid. Well, that kind of makes sense because linoleic acid is a fat. And where do you store it? You store it in the fat cells. So you're not storing excess linoleic acid. linoleic acid in the liver until you get very diseased.

I'm not storing excess linoleic acid in the muscle until you get very diseased. Originally, you're storing excess linoleic acid in the fat. So this is where this fat, linoleic acid, concentrates. It's concentrating in an endocrine organ. And then what happens from there? This is actually the really fascinating part of this. So because I think there's good evidence to suggest that because of the breakdown products of linoleic acid, these are called oxlamps, oxidative products of linoleic acid metabolism.

They have horrible names, but I'll say them just so people have heard these words. Four hydroxinoneanol, 13 H-O-D-E, which we call 13 H-N-H-E, 13 H-N-E, 13 H-N-E are the main oxlams. This is what we talked about earlier. Linoleic acid breaking down into products of oxidation, and those are very problematic. These molecules, specifically 13-H-Ode and 4-H-N-E have linnin implicated in so many problematic things in the human body. increase rates of cancer, basically breaking mitochondria, breaking fat cells. So how does this work? The fat cells, like all the other cells of your body, can do two things when they grow. They can have one cell that gets bigger, we call that hypertrophy, or they can divide. We call that

hyperplasia. Okay. That's really important because what happens to a fat cell, when this fat cell is full of excess linoleic acid and full of excess 4H&E, it breaks the molecular, the genetic mechanism, in the fat cell, and the fat cell as it wants to expand, it won't divide. It just gets bigger and bigger and bigger. You ever seen that guy in Monty Python, the super fat guy who just keeps eating and then finally they put a little thing on his tongue and he explodes? Yeah. It's kind of like that. Like your fat cells probably want to divide. They're like, we're over full. We are getting stuffed right now with fat. We're getting stuffed with calories from even sugar can get in there, you know? So the stats don't want to grow. But because of the 4H&E, and there's really good studies that show this,

when you add 4HNE to fat cells, those fat cells get broken. They can't divide. They hypertrophy, they don't hyperplasia. And what do we know? This is super important. What do we know about fat cells in people with metabolic dysfunction?

They're broken. They're hypertrophied. They're big in fat, and they're not hyperplastic. They haven't divided. So the actual pathophysiology of metabolic dysfunction is fat cells that can't divide.

How do we get that? 4HNE. That's exactly how you get that. That's been shown. humans, it's been shown in animal trials. It's so clear. And so how do you get more 4H&E? Well, you could probably get more 4H&E by stuffing more linoleic acid into your fat cells. So this is super fascinating. I don't know why it's not talked about more. It's fairly technical, but fat cells that are broken, then send out hormones that are broken. They send out adipokines. They send out

cytokines. They get macrophage infiltration of the fat cells. You get inflammation. So as these fat cells get bigger and bigger and bigger and they can't divide because of this 4H&E that is changing the biology of these fat cells, they start spewing out inflammatory mediators, adipokines, hormones, which then go to the rest of your body. And that, I believe, is the most, that is really a super compelling hypothesis for what's going on with metabolic dysfunction. We see all of that happening. So what do we see in people with metabolic dysfunction? We see adipokines that are off. We see free fatty acids in the blood, free fatty acids in the blood, and the adipokines are then going to signal to the liver, to the muscle, to everything, hey, be insulin resistant, be insulin

resistant, but you don't want to be because you're still getting glucose, but the fat cells are broken. And they're broken because of excess linoleic acid. They're broken because of excess 4H&E coming from the linoleic acid, but then they're sending out these signals to the rest of the body saying be insulin resistant. That's pathologic insulin resistance. And then the rest of the body says, hey, I'm getting a signal. I should be insulin resistant, whether it's the liver, whether it's the muscle, and then you have a problem. Because the rest of the body says, we don't want insulin. We're not going to respond, whether it's the kidney, the liver, the muscle. And then what do you have, you have rising levels of glucose as a downstream event, you know. But originally it starts

in the fat cell and it starts with 4H&E and these oxlams that are completely breaking the fat cells. Does that all make sense? Because that's really important. No, it does. I mean, super interesting. Yeah, it's fascinating. You can also like understand though why that's hard for people to comprehend. Yeah. So it's probably hard for, I mean, the world, the government's probably like, how do we pass us along? How we don't? Let's just tell him something else. So if someone that is, is metabolically damaged at this point, say the listener is metabolically damaged from these choices in food, how do they come back?

Yeah, so let's talk about that. Super important. The first thing you need to do is know if you're metabolically damaged. And we hinted at that earlier. Two things to know how metabolically healthy you are. Where a continuous glucose monitor will get you one. Or and, and or get a fasting insulin. I talked about this with Bear.

We actually did a podcast a few months ago. hopefully he's released it, where I believe that if mainstream physicians ordered a fasting insulin on every one of their patients, it would change the face of medicine for the better. It's a $30 test. You can pay for it out of pocket, you know, or if you can't afford that, your insurance should pay for it. Your doctor should order a fasting insulin for you. But I can't tell you how many people have sent me DMs on Instagram other places and they say, my doctor doesn't want to order a fasting insulin, or he doesn't even know what that is, or he thinks that's an academic test. It's only used in people with type 1 diabetes.

It's like, what are you talking about? Like, that is a critical measure of insulin sensitivity and their bioproxy metabolic health. So I believe you want your fasting insulin less than five micro IU per ML, okay? Five micro IU per ML. The reference range on there goes from like three to 24. So if somebody has a fasting insulin of 12, they're massively insulin resistant. The doctor's not going to see a problem. 20?

Holy shit, man. By the time somebody has a fasting insulin of 20, they're probably full-blown diabetic. It's still within the freaking reference range for fasting insulin. The fasting insulin reference range is probably one of the most, like, incredibly wrong things in Western medicine in terms of reference ranges. I think the cholesterol reference ranges are wrong too, right? like LDL doesn't need to, we don't need to worry about it being high if you're metabolically healthy. So that's actually context for the metabolic health discussion with LDL is I believe,

I don't believe LDL is harmful for humans if you're metabolically healthy because, and this is, we'll tie it all together. I think that the reason that atherosclerosis happens is because the blood vessels become insulin resistant. So when those fat cells break and they said that all the bad stuff, that is the beginning of atherosclerosis for humans. And if you are metabolically unhealthy, LDL is a problem. But the answer is fix the root cause, fix the metabolic dysfunction, which you do by detoxing.

I hate that word, by fixing your fat cells. So you have to know you're metabolically unhealthy first, get a fasting blood sugar, wear a continuous glucose monitor, get a fasting insulin. Okay, you're metabolically unhealthy. What do you do? The three things I talked about earlier, really just the first two. Cut out seed oils, low linoleic acid diet, high stearic acid diet, and cut out processed sugars. That will fix it long term.

It's going to take a little time. We don't really know how fast the kinetics are and how fast these fat cells are going to turn over their cell membranes. Because this is actually in this, it's either stored in the fat cell or it's in the cell membrane. And for some people, we believe that it could take six months a year. But I think that if people can stick with this for that amount of time, they will start to see their insulin sensitivity improve.

But that's probably the time frame to think of is six months to a year, a very low linoleic acid and high stearic acid. So if I were working with someone and they are metabolically unwell, I'm going to say, I want your linoleic acid as low as possible. I don't want you eating olive oil or avocado oil. I'm not the worst thing, but no, no, it's all tallow. It's stearic acid. It's the highest stearic acid you can get, the lowest linoleic acid you can get possibly in your diet.

And obviously, you've got to avoid processed sugar, which should be a no brainer for most people, like no sodas, none of that stuff. But fruit is okay. And I'll say this, if someone is full-blown diabetic, you may get some blood. blood sugar reactions to fruit. And in that case, just limit your fruit. You know, it's, if you're getting strong blood sugar reactions to fruit, then limit it. You know, I don't think that fruit and honey are going to work for everyone. If you're full-blown diabetic and your muscles and your liver are refusing the actions of insulin, if you have a tablespoon of honey, your blood sugar is

going to go up. And it's maybe not going to go down the way it should be. So you may need to limit those things in the short term. But in the long term, I think once someone regains metabolic health, they should be able to reintroduce those foods if they want to. So what is this steric acid doing in the body? And what are the best sources other than tallow? Yeah. So we talked about this a little bit earlier with the nature study. It appears to be a signal at the level of the mitochondria to turn on fat burning.

That's right. Yeah. Yeah. And the best sources are tallow. Coco butter is actually a good source as well. But I'm not as much of a fan of cacao or cocoa butter. If you've ever had cocoa butter, it's kind of like chewing gum. Tallow is a little bit easier because you can heat it up.

but you could do cocoa butter. I'm not a huge fan of chocolate for other reasons. People hate to hear that, but chocolate's very high in oxalates. It has lectins. But technically you could get stearic acid from dark chocolate, which is then going to have processed sugar in it and other things that I'm not such a huge fan of.

But technically, dark chocolate will have stearic acid. Not my favorite source. Cacao butter will have stearic acid a little better. It's going to be like chewing gum in your mouth, probably hard to consume. Talos the best source. What about coconut oil? Coconut oil has essentially very little syric acid.

Just a saturated fat. It's a saturated fat. It's different chain lengths. Coconut oil is a lot of meristic and loric acid, which are 12 and 14 carbon fatty acids. Coconut oil doesn't have much stearic. It's mostly in animal foods. So if you're getting a grass-fed, grass-finished rib-eye or beef,

you're getting stearic acid in that. And the odd chain fatty acids we talked about earlier, yeah. I mean, those are the changes I've made in my diet the past couple months since our last episode. The amount of honey I'm consuming, Like I go to HEB and I get this big, raw Honey jar and it's thick and it's, it looks unfiltered, but it's great.

I will tell you, I never, I don't think I ever had papaya before our last episode. I went and bought a papaya. I'm in love. They're good. They're not that great here though. You got to come to Costa Rica, dude. Well, I was in, I was in Mexico.

Oh, perfect. There you go. I was in Mexico. Order papaya. They're good. It was so good. Got one H. H.E.B.

it wasn't the same. It tasted a little rotten. but I've the last couple months had been eliminating, obviously not completely, but minimizing seed oils in my diet and being very conscious with it, but it's tough because it's in everything. But it's such a good, it's a good effort, you know? Yeah. Think about everything else you embody. Go one more, like discipline.

Like this is what it's about, dude. Like that's, it's so simple for people like, you've got to cut them out. You'll be so much healthier. It just improves everything. And for your wife, like those seed oils that she eats are going to get passed to the baby. They're going to get passed in breast milk. This is a crazy story. So you know that infant formula, when we make infant formula in the grocery store, if somebody's not going to breastfeed, how do they know how much linoleic acid to put in that formulaic?

Well, they survey the breast milk of average mothers across the United States and they look at the amount of linoleic acid. Guess what? If those mothers are not eating a standard American diet and they're not eating that much linoleic acid, it goes way down. Breast milk from hunter-gatherers has so much less linoleic acid. acid than breast milk from traditionally surveyed women in the United States. So you're going to have a baby. If your wife's going to breastfeed, think about the linoleic acid that your baby's going to get.

Well, I mean, that's why I had the conversation with her. And she's on board. I was like, that's why we need to start making changes now because I know how long it's in your body. Yeah. And to get that turnover or get that out months. Months. And so, you know, I would say think about the places where it's the hardest, minimize,

minimize, minimize, minimize. Don't use any linoleic acid where you can avoid it. For me, I've been able to, or we've been able to completely eliminate at home. Control the controllables. The things we buy in the grocery store, we bring into our house, no seed oils. It's just when we go on to dinner, that's when you open yourself up to. It's the risk you're sometimes willing to take or have to take. Get a steak.

Yeah. Yeah. Or, I mean, if it's with your wife, hopefully she understands, and it's all kind of this family effort. and you can say, you can say to the waiter or waitress, hey, what do you, what do you cook this in? You know, and you don't get that social pariah status. Like, you know, when I'm with Bear and his friends, it's like I'm with a waiter and I'm, I'm that guy at the restaurant,

but I'm okay being that guy at the restaurant because it's important to me. Do you know any restaurants who actively promote not using seed oils in the kitchen? We could check. Maybe Dai Duay. I've never been there. Their food is like way too complicated for me and has too many ingredients, but they might not use seed oils. I think that guy's really good,

but you'd have to confirm it. You know, Red Ash here in Austin, they're a steakhouse. They're, like, pretty high quality. I would be very surprised if they use seed oils. Interesting stuff, man. It's tough, man, it's tough.

But the restaurants, so okay, so then you go to, like, what did I do? So the reason I'm in Austin right now is George St. Pierre's coming into town. We're doing a collaboration with Hardin Soil, which is the desiccated organ company that I have. If people can't get the fresh organs, you can get these desiccated capsules.

I take a whole package every day. Yeah, like I said, I was going to bring you the fresh one to go with it. But next time. Testicle, blood, and liver. That's amazing. There's, like, the best ones. We got the blood, like the, and the liver, yeah. So he's coming into town and hopefully we'll go to Red Ash with George.

But I was going to say, I totally lost my trade of thought there. Anyway. Just the seed oils and restaurants, but. Yeah, I think it's, that's where we're going to go because we know. Oh, yeah, I remember now that we were, I remember, like. last time he was here, we went to get barbecue, and I think we went to La Barbecue on the other side of town, and the barbecue places shouldn't use seed oils on the barbecue.

They put a rub on, so I don't like pepper because it's a seed spice and it kind of messes with my gut, so I'll scrape off all the pepper. But if it's just a piece of meat from barbecue, they should not be putting seed oils on the barbecues. That was what I was going to say, that other thing, that other, you know, thing you could do if you want to go out to barbecue with your wife or something.

I think a lot of people think we're talking seed oils, that they just assume it's going to be a liquid too. Yeah. So originally it's like, oh, seed oils. Well, what's a liquid? I'm going to check salad dressings and maybe this creamer here. I mean, coffee creamers. So it's coffee cream.

Vegetable oil, number one sometimes. But also, like, any other food item you buy, it doesn't have to be just a liquid. There's going to be possibly seed oils in it. Hummus is another big one. I found one hummus. It doesn't. It's called Grandma's Hummus.

cheapy, no seed oils. But like I was trying to buy, does it have olive oil? No. No oil at all. Nope. I was trying to buy a roasted, like red tomatoes. Sun dried tomatoes.

Right. I was trying to find sun dried tomatoes the other day. And I couldn't find them without any. They're all seed oils. They're all seed oils. Oh man. Bummer. I'm going to like just start creating my own.

There's a market there, obviously. There is a growing, there's a growing market there for seed oil free. I mean, I think the problem, the challenge for food manufacturers is margins, right? You do sun dried tomatoes and olive oil. You're going to have like the price point's going to be higher. They're going to be amazing. They're going to be gourmet though.

So I think there's people willing to, I mean, I'm willing to pay more money for higher quality foods. Yeah. I would love to see a hummus. Well, actually I shouldn't say that because I'm not a fan of chickpeas at all. So I don't think that hummus doesn't matter to me. But if, you know, look, if people want to make gradual changes and this is the change that's going to improve their diet, like hopefully people have listened to the first

podcast and they understand my overall dietary philosophy and the fact that like hummus is a bean of beans in general. I don't think hummus is doing people a lot of favors, whether it's from the seed oils or from the chickpeas, which are going to be problematic for a lot of people in terms of digestive enzyme inhibitors and lectins. But maybe I think there's a market for that. Like I would, I would be happier to see a hummus that was made with no seed oils. I would hope people would realize that hummus and those chickpeas as a garbanzo beans are crowding out other foods that I would prefer them to eat. I'm not a fan of the beans, like I said, but a seed oil free grocery store would be amazing.

And if it contained things that people still wanted to eat, it would improve human health markedly. I love hummus. The hummus I'm referring to might have olive oil in retrospect, but it's like one food I eat every day that I can't hold back on. Oh, bro, you're going to, you'd be better without it. But then you've got to check, like, what kind of olive oil is in it, right? And how good is the olive oil in that hummus?

Because, I mean, there's a couple of people in the nutrition space who are huge fans of olive oil. and a lot of them have their own product. Like, this is this doctor's olive oil. And there was a big recall on his olive oil recently because it was all rancid and oxidized. So anytime you're eating a processed food, say you go to a restaurant, they're like,

we only use olive oil. They're like, no, it's 100% olive oil. It's like, well, how good is it? How long has it olive oil been back there? You know? Like, how long has it olive oil in this hummus? What kind of olive oil? Is it the good olive oil?

Like, is it just like olive? You don't even know what's in it, right? They're going to cut corners. Like, it's just hard to find it. find really good stuff. The best thing to do for you, if you really love hummus and you're going to eat it every day, again, I'm not a fan of Garbonzo Bees. We didn't make your own, right? Which is like, you know, you take tahini. Again, I'm not a fan of sesame seeds, right? All these ingredients. Take tahini, take lemonade beans, and then take a really good olive oil that you know is fresh, right, organic,

and is going to have the least amount of rancidity or oxidation and do that. And then also realize, like, okay, this is a little bit extra linoleic acid. I'm going to be careful with other things. I've just been trying to consume more red meat. I feel great. That's a good thing. Feel freaking great, man. Yeah, I need to eat more organs. I'm going to get back on it, but I cover my bases with the whole package. Yeah. I'm solid there. I'll start cutting up some liver, eat some bowl testicle next time. I love it. You feel like a beast. Yeah, and just people know whole package is, yeah, one of the supplements from hardened soil. It's the testicle one. It's solid. I mean, every time someone comes over to the house, I'm like, y'all, I'm taking testicle daily.

Like, what are you doing? I love it. I'm sure. they're like, give me some of that. Yeah. Well, Dr. Paul, I appreciate you, man. It's always a good one. Super insightful and a lot of takeaways in this one. I hope it's helpful for people. We went a little technical at times,

but it's all really important because I like to kind of go back and forth. And I really want people to understand that there's a lot of good science here. But this is an important one. When you message me and you were like, hey, let's do a podcast on seed oils. I thought, yeah, let's do it because it's such an important topic. Like I said, if you change nothing else, eliminate seed oils, eliminate processed sugar, eliminate gluten. Those are the first three.

Obviously, there's a lot more in the animal-based movement. You know, it's organs, meat, fruit, honey, raw dairy. Those are the foods, I think, are optimal for humans. But if you just want to dip your toe in, do those things, get a fasting insulin, wear a continuous glucose monitor, will get you one. I do want to get one. We'll get you one from Nutrisense and cut out seed oils,

increase stearic acid, don't fear animal fat, and then maybe cut out gluten. I mean, that'll be a massive change in people's health. And I think that if people see that and they feel that spark, then they'll be like, okay, now I'm bought in, and they can go much further if they want. The first step. Yeah, first step.

Cool. All right. Thanks, man. Thank you, brother. Thanks for tuning in to another episode of the Bear Performance Podcast. Please leave a rating and review on the platform you are listening to if you enjoyed it. It helps us to grow and reach more people with the intent of changing lives through the Go One More mindset.

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