Mark Bell's Power Project - EP 575 - Are PUFAs Killing You? Debate Between Alan Flanagan & Tucker Goodrich

Episode Date: August 17, 2021

We brought together Alan Flanagan and Tucker Goodrich to debate a few topics, mainly the dangers of Poly Unsaturated Fats. Alan Flanagan has an MSc in Nutritional Medicine, is currently pursuing his PhD. He is also a former practicing Lawyer (Barrister) from Dublin, Ireland. Alinea Nutrition is his online education hub, dedicated to empowering others with clear, impartial evidence-based knowledge and understanding about the science of nutrition. Tucker Goodrich is a technology executive in the financial industry who designs, runs, and debugs complex systems in high-risk environments. Areas of expertise include risk management, systems management, and cyber-security. He is also an Expert Advisor for the nutrition start-up Nutrita, and has been a guest on numerous podcasts. Links and info Tucker Referenced in the discussion: http://yelling-stop.blogspot.com/2021/08/show-notes-for-flanagan-and-goodrich-on.html Subscribe to the Podcast on on Platforms! ➢ https://lnk.to/PowerProjectPodcast Special perks for our listeners below! ➢Marek Health: https://marekhealth.com Use code POWERPROJECT15 for 15% off ALL LABS! Also check out the Power Project Panel: https://marekhealth.com/powerproject Use code POWERPROJECT for $101 off! ➢Eat Rite Foods: http://eatritefoods.com/ Use code "POWERPROJECT25" for 25% off your first order, then code "POWERPROJECT" for 10% off every order after! ➢LMNT Electrolytes: http://drinklmnt.com/powerproject ➢Piedmontese Beef: https://www.piedmontese.com/ Use Code "POWERPROJECT" at checkout for 25% off your order plus FREE 2-Day Shipping on orders of $150 Subscribe to the Power Project Newsletter! ➢ https://bit.ly/2JvmXMb Follow Mark Bell's Power Project Podcast ➢ Insta: https://www.instagram.com/markbellspowerproject ➢ https://www.facebook.com/markbellspowerproject ➢ Twitter: https://twitter.com/mbpowerproject ➢ LinkedIn:https://www.linkedin.com/in/powerproject/ ➢ YouTube: https://www.youtube.com/markbellspowerproject ➢TikTok: http://bit.ly/pptiktok FOLLOW Mark Bell ➢ Instagram: https://www.instagram.com/marksmellybell ➢ Facebook: https://www.facebook.com/MarkBellSuperTraining ➢ Twitter: https://twitter.com/marksmellybell ➢ Snapchat: marksmellybell ➢Mark Bell's Daily Workouts, Nutrition and More: https://www.markbell.com/ Follow Nsima Inyang ➢ https://www.breakthebar.com/learn-more ➢YouTube: https://www.youtube.com/c/NsimaInyang ➢Instagram: https://www.instagram.com/nsimainyang/?hl=en ➢TikTok: https://www.tiktok.com/@nsimayinyang?lang=en Follow Andrew Zaragoza on all platforms ➢ https://direct.me/iamandrewz #PowerProject #Podcast #MarkBell

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We did. People talk shit, man. They never thought we would make it, but look at us. We got our own show. If we could only get somebody to watch or listen. We have a few. I think my mom listens. Yeah.

God bless her. We'd be in big trouble if she listens she's still hanging in there listening listening to this garbage i got a bunch of family members that listen to this and i'm like man you need to do something better with your time i still remember my uh stephanie's cousin so my my cousin, we were at Jasmine's like dance recital and he comes up to me like, man, you guys made me laugh so hard the other day. I'm like, oh, what do you mean? And he brought up some definitely super embarrassing thing that we spoke about. And I was like, ah, shit, you really listen. Like, yeah. So like I'm flattered.

And at the same time, like, you really listen. Like, so like I'm flattered and at the same time, like just totally horrified. I'm excited for today's show. I'm excited with some of the diverse conversation we get into on this show. You know, yesterday talking, talking with somebody that, you know, really went through it and had a lot of life experiences with particular things that happened, uh, Michaela Peterson with her diet. And, uh, she had went through many different battles and diseases and so forth. Um, and that was very non-scientific, even though Michaela has researched some things and she did pull out some stats here and there, uh, what didn't get like real thick with that. It was more of just like a life story. But for today, you know, having this debate between Alan Flanagan and Tucker Goodrich,

I'm really excited to hear these guys talk in depth about what they feel is, you know, really hurting us, especially as Americans with processed foods. And Alan Flanagan has been on the podcast before, and he spoke quite a bit about circadian rhythm. He talked about a lot of other healthy practices. But these guys have a little bit of a debate going on. Tucker Goodrich is really well versed in polyunsaturated fats for people that are unfamiliar. They're also called PUFAs. And some of these polyunsaturated fats will get cooked. They'll get heated to a degree that is harmful to us. And they end up in

a lot of our processed foods. And so Alan Flanagan is on the side of like thinking like these things are probably not that huge of a deal. Um, probably in consideration if we're not overeating and if we're moving around and exercising and expending some energy and Tucker, uh, he thinks he thinks these things are pure hell and pure poison. So I'm excited to kind of hear these guys go back and forth. Some people are starting to recognize these polyunsaturated fats as being worse than sugar. So I'm interested to hear what both these guys have to say today about this topic. Yeah, I'm really interested in just the practical implications of this, just because it's interesting what happens when you start eating a lot of meat and you start cooking it like we do or like I do.

I use my air fryer a lot. So what's happened is without even realizing it, I have cut down my oil consumption drastically. I can't remember the last time I literally poured oil into a pan to cook something literally um maybe like you know bacon grease or something seriously no like even even when i like cook fattier cuts if i do it's like i just use its own fat to cook it it's right i just haven't needed it so uh it's going to be interesting to see if you do like maybe if you use a little bit maybe there's not that big of a deal but that's what I'm interested in. I think where it might have some real application for our listeners is when they go to restaurants, you know, and listeners that may follow a diet where it's like they're doing if it fits your macros or something like that.

They might be might want to be more cautious about some of the things that they choose to fit their macros. You also might be, you know, want to be careful of going out to eat because they could be putting all kinds of weird different oils on your food. And then anyone having salads and stuff, you might want to reconsider the type of dressings that you use. Maybe you switch over to using some primal kitchen stuff from our boy, Mark Sisson, or you just, you know, make your own concoction at home with olive oil or something like that. Cause there are oils that are, that seem to be a lot less harmful. But I think one thing to consider when it comes to any oil, and I think that's great. And Seema, that you eliminated a lot of them is just to know that any of our foods that we have in a liquid form is just going to be quite different than

the way that it was meant to be. So an olive, eating an olive is great. Turning into olive oil, while I would say it's not horrible, it's not bad probably, it's just a really dense version of the olive oil or of the olive. And when you have that, you could end up having excess calories and maybe getting excess of a bunch of other stuff that you're maybe not even aware of. And switching over to being primarily meat-based maybe not even aware of and switching over to being primarily meat-based, um, it seems to do just a lot of wonders for me as well. And it helped me cut back on things that I wasn't even aware of that I ate. Like, I don't really feel like I have this urge or need to dump a bunch of oil on, on my food anyway. But when you're eating, um, you know, ribeyes and stuff like that,

they certainly could just use a little bit of salt and you're usually good to go. Yeah. As far as oils, Mark, like what, when you do use some, just before, uh, these two guests come in, what is the stuff that you use when you do cook with oils? So just in case people are like, well, if I do get something, maybe I could try grabbing this. Just in case people are like, well, if I do get something, maybe I could try grabbing this. I'm a little bit like you, so I won't normally use anything. But occasionally I might use some like ghee butter or I might use a lot of times like if I'm cooking eggs, I just use spray. And I know that people are like, oh, my God, spray's got crazy stuff in it or whatever. But sometimes I might use a little bit like coconut oil.

The issue with the oils versus the spray is I feel like I have to use kind of a lot of oil. And I'd just rather not have those calories. Sometimes I'll just cook. If it's eggs, I'll just cook them in regular butter which I really like a lot so it'd be great to know from these guys like do they see any harm in any of those things or even cooking in bacon grease which is pretty common an interesting thing is you know years and years ago like maybe like almost 100 years ago there was the invention of Crisco. And there was a lot of switch to people frying stuff and stuff other than animal fat. And that actually caused a lot of problems.

And it gave us trans fatty acids and a bunch of other fats that are extremely harmful to the body. And there's been a lot of data and research to show some of that. So we were on the right track years ago when we just used the animal fats. And if I am to use any oil on anything, it might be some olive oil because I'll eat a salad here and there and I'll have a salad with some olive oil and some balsamic vinaigrette. Avocado oil is great. It can be cooked, and when I say it's great, it can be cooked at a high temperature. Coconut oil can work really well also.

Yeah, I was just thinking, like, so it looks like both guys are ready to go. So back when I used to, like, no, you got to have kale shakes. You got to juice things. I'm going to avoid soy. I'm going to avoid all the, you got to have kale shakes. You got to juice things. I'm going to avoid soy. I'm going to avoid all the canola oil. I still don't really eat corn, but I'm going to get rid of all of that. So no tortilla chips, none of that shit. And I feel so much better today when I don't even really think about it.

I don't know if that's just because I'm moving more or just my overall diet is better. So I wish I'm trying to like remember everything that we did. But I mean, like literally everything like I wouldn't drink anything other than water and like coconut water. Like it was I was like super like just bad. And now I'm like very chill and feel way better look better everything's better right now but like i don't know it's just interesting no artificial sweeteners i was another one too i never touched any of them because i'm like oh they're supposed to be bad but you know it's just interesting you know like thinking about it right now but yeah let's get these guys in here

oops there's one there we go getting them hooked in yeah oh wow look at not depth of field it's a zoom feature that i'm told is a pro zoom move which is to use their uh blur the background feature i dig it i'm gonna have to mess with that next time i'm in zoom like for on my own like house setup yeah Yeah, well, it's, you know, that looks good. I've got my computer sitting here on a plastic crate with a couple of textbooks on top of it to get it to the right height. All the way pro setup.

Can we hear Alan as well? Good morning, gentlemen. Can you? Yeah. There we go. Good evening. Good evening, Alan. Nice you? Yeah. There we go. Good evening. Good evening, Alan. Nice to virtually make your acquaintance. You too, Tucker. I think we're all in different time zones, are we?

I'm in Idaho. Yeah. Okay. Right. London to Idaho. Awesome. I'm really excited to have you guys on the show today. Let's just try to do our best to not over talk one another.

I think probably the most appropriate way to kick off the show is to maybe just get a little bit of background. And then if one of you guys doesn't mind kind of sharing how we kind of got to this point, because I know that I believe Alan, I believe you wrote an article and I believe Tucker wrote a rebuttal to it. And I know Stan Efferding is the one that kind of paired us up. He said, you guys should you guys should have a fight to the death, a duel on Mark Bell's power project. So, well, hopefully we won't be doing that. Alan, you mind kicking things off and sharing, you know, who you are, kind of what your background is, and then we'll go on over to Tucker. Yeah, so I'm currently writing up my PhD thesis. I'm based at the University of Surrey, which is where I did my MSc. Prior to that, I spent a decade working as a barrister, which is the type of lawyer that we have in jurisdictions like Ireland and the UK. Was always interested in nutrition. Initially did my MSc with a view to just doing it for personal interest.

I got bitten by the research bug and got offered a full time PhD and made the transition. I'd offered a full-time PhD and made the transition. I guess to short circuit here, the article in question I wrote, I'm active enough on social media. I'm not actually on Twitter. So all of my social media activity is on Instagram. And a particular conversation would keep coming up, posting about a lot of interest in lipids cardiovascular disease generally speaking i'm at the heart uk advisory panel in the uk um and so i would post about this

regularly enough and i would get into conversations broadly speaking about polyunsaturated fats now sometimes that may be specific to omega-6 linole acid, but not always. It was just kind of this umbrella. So I wrote the article broadly in relation to polyunsaturated fat. It wasn't necessarily specific to seed oils. So there was a mix of studies that would have included either a specific focus on omega-6 or a specific focus on omega-3 or indeed some analyses would have included both um and the article was kind of laid out in a certain form i i went i i started it by talking about certain narratives that were common that i hear a lot in the conversations that i have with people they would be focused a lot on kind of

ideas about ancestral diets or the Paleolithic diet in particular. And then some of this kind of mixed in, I would say, you know, narrative about how we got dietary guidelines, very much focused on Ancel Keys, demonizing saturated fat and all this stuff. So that wasn't necessarily an evidential part of the article. It was was just like these were the common things when i would question someone who would question me these were the common things i would hear back and then i focused on uh human studies for lipid peroxidation in particular and then human studies that are often cited in support of specifically in relation to omega-6 and negative effect. And they tend to be older studies and we've got missing data with them.

And there are some parts that are hard to tease out. But the real meat of it was the, for me anyway, was the final part. And this seems to have not got as much kind of attention as some of the narrative parts. You know, with science we try and base conclusions off converging lines of evidence and not necessarily one specific line. And when it came to this question in particular,

you know, I find that for human outcome data, we've got prospective cohort studies where diets measured initially and followed up over time. We've got biomarker studies. We've got human intervention studies. We've got the substitution analyses, we've got meta-analyses of both control trials and of prospective and observational research. And for me, that body of evidence all seems to point to an overall conclusion that we're probably barking up the wrong tree when it comes to vilifying polyunsaturated fats generally, omega-6 in particular, at levels of current consumption and otherwise, I find it hard to see how they're having

the deleterious effect that some people would claim that they do. Habitual levels are not particularly. I think in the US, maybe 7% on average energy intake, but Tucker might correct me on that. I'm more familiar with the UK data. You're right. So I find it hard to, and then when we look at globally, the range tends to be between about 2% and 11%. And when we look in that range with the prospective data, it seems to suggest a fairly, but the higher end of that range is better than the lower end. I think there are other component parts in terms of explaining cardiovascular disease,

which has come down by over 50% since the 60s, although still the leading global cause of mortality, diabetes and other conditions. I think there are other culprits that we can look at that warrant more of our focus in this respect. And so just to kind of wrap up my, I guess, my little intro, I think that I find it very difficult to support by reference to human outcome data. I know that there are these potential mechanisms that might explain an effect, but they seem to not translate to actual effects and outcomes in humans. And so for all those reasons, I find it difficult to sustain a case that omega-6 linoleic acid is particularly detrimental for human metabolic health or even cardiovascular health.

All right, Tucker, you want to take it away? Okay. Screen just froze. I missed your last sentence there. I just said, Tucker, you want to take it away? Okay. So my background, I was a technology executive on Wall Street, had absolutely no interest in diet stuff.

I grew up with a mother who was always going through Weight Watchers, and I knew that that approach didn't work. a number of times for different conditions, including what at first appeared to be a stroke when I was 38, and then acute diverticulitis, which is a perforated colon when I was in my 40s. I unfortunately acquired an interest in health, trying to figure out what was going on and why I was getting so sick at such a young age, because I came from a long long lived family. So I was expecting the same outcome. Through basically dumb luck, I got into this diet topic and specifically the effect of seed oils on health. Unlike most people who fix their diet, removing seed oils from my diet was the first thing that I tried. And I had an immediate and dramatic shift in my health for the better.

The chronic bowel condition that I had suffered from for 16 years resolved in two days. My weight fell off immediately. My propensity for sunburn. immediately my propensity for sunburn. I mean, if you're listening to a podcast version of this, I am blonde, blue eyed and fair skinned, and I would roast in about 45 minutes. So very quickly, I became somewhat intolerant to sunburn. You know, that was a surprising change. So I got very interested in why this was happening and understanding why what I had thought the dietary better. I worked with my doctor who said to me, I'm very concerned about what you're doing. And I said, well, doc, that's why I'm here with you. You can run the test and you can tell me if you're killing yourself, if I'm killing myself or not.

And the conclusion of that experiment was him telling me I was going to live to 100 and my firing him because I no longer needed the regular physician visits that I had needed up until that point. So since then, I'm largely a self-taught problem solver. And I delved into the literature, educated myself on what was going on and tried to understand what was happening to me. And then as I started understanding that it could be of value to other people, I started talking about the research I was doing and the findings I had had. As far as Alan's article, I have a number of objections to it. From the top line, he's conflating omega six and omega three PUFAs, polyunsaturated fats.

That's a bit of a straw man argument. There's really nobody who argues with the health benefits of omega-3 fats. There's a small group of people who follow the teachings of Ray Peet, who cautions against excess omega-6 fat intake. As far as I'm aware, he has almost no influence outside of the nutrition community that we all live in. So I don't think it's, you know, and Alan never mentions him. So to his credit, but conflating those two together is a bit of an unfair tactic in this debate because really nobody takes that position. He's largely not fairly representing some of the studies that he critiques, in particular by complaining that some of these studies are old. Old is irrelevant in science. As I point out in my rebuttal, omega-6 fats are considered to be essential fats.

And essential in nutrition science has a very specific meaning that they are required for life. There is nobody who disputes that they are required for life, A. And B, the studies that show that come from the 1930s. So if we can use studies from the 1930s to demonstrate the essential quality of these fats, then I think it's a little unfair to paint well-performed studies from decades after that as being too old to be worthy of consideration, especially when they're done by the leading researchers and scientists of the period in which they were done. I also think, I mean, there are huge problems with the epidemiological evidence in general and specifically in polyunsaturated fats. Ansel Keys is the fellow who largely created the science of nutritional epidemiology to his credit. And he was not the first epidemiologist, but he really built the science that, you know, we all look to now to try and help us figure out what's going on in our nutrition.

But there are two problems with that. First, a lot of the data used in nutritional epidemiology is very poor. The results don't tend to replicate. A. B. The populations examined are typically populations in industrial societies who have universities and are capable of carrying out these sorts of research projects. I mean, Ancel Keys' seven countries study was conducted in the countries it was conducted in because he could find people in those countries to do the research. Right. So developing countries weren't included. Only first world countries were included. And you're thus looking at a subset of humans. Now, omega six fats and industrial quantities entered entered the human diet in the late 1800s, almost 100 years before he started doing his research.

So by only looking at populations that have been consuming these fats for 100 years, well, Gary Taubes put it really well in one of these books. It's an old joke about a cop walking down the street, finds a drunk looking, calling around on the ground under a streetlight. And he asked him what he's looking for. And the guy says, I'm looking for my car keys. And he says, did you lose them here? He said, no, I lost them over there. I lost them over there. Well, why are you looking here? Well, because this is where the light is.

Right. Well, because this is where the light is, right? There's clear and overwhelming evidence that the transition, the nutritional transition from a pre-industrial diet to an industrial diet was accompanied by a mass increase in the incidence of chronic diseases. And that transition was accompanied by the introduction of seed oils into the diet. Not looking at that transition in an epidemiological survey of these diseases and the possible causes of them is a huge mistake to make. Wouldn't these metabolic diseases be more spawned from just simply overeating, maybe rather than just a specific type of fat or blaming it on sugar or salt or whatever we end up blaming it on?

What are your guys' thoughts on just the simplification of if we're not overconsuming and we're moving around, maybe we can still avoid some of these diseases. Alan, you want to go ahead with that? Yeah. You know, again, there's another saying in medicine of when you hear hoofbeats, think of horses, not zebras. I'm inclined to put my chips in that basket for a number of reasons. One is, so Tucker's correct in terms of the nutrition transition for industrialized countries started earlier, but really we see this acceleration of it in the post-Second World War period. And that is a period where we can measure diet,

and there are epidemiological studies that go from not just the seven country studies, there are a couple of others that are also interesting that go from not just the seven country studies, there are a couple of others that are also interesting that go from that period. And you see this accelerated change in the food supply from the late 60s, early 70s onwards, it's happening even before the introduction of dietary guidelines. But in the modern context, we can actually look at the nutrition transition that has been occurring in low middle income countries in Asia as a kind of almost proxy for how that's changed. And I'll come back to that in one second. But as it relates to, for example, the USA, there was a 2009 analysis by Boyd Swinburne and colleagues, which looked at one of

the challenges with measuring energy intake is it can be difficult to account for the difference between in-home intake and out-of-home intake. And out-of-home intake has increased significantly. People eat a lot out. They eat on the road. They eat out and about. So what they did was they used an energy availability in the food supply, food supply energy availability, which is a nice metric for how much availability per capita you can use. And what they found was that on average, per capita daily energy availability, food supply energy availability in the US had increased by between five and 700 calories a day.

If you were to model that based on the weight change that has occurred in the population, that's practically sufficient to explain the change in average population weight between the 70s and now. And so when you then start to look at isolated nutrient components of that diet, although you can see percentage changes, because of the overall increase in total energy, you tend to see that everything has increased. So you could say that, well, fat as a percentage

of energy has come down. We're eating a low fat diet because of the guidelines. Well, total absolute fat intake has increased because we're just eating more. When you look at the nutrition transition in Asia, we've seen this occur. So in the early 90s, the average macronutrient composition of the Chinese diet still reflected what we might call the traditional Chinese diet. Total fat was only about 20%, give or take, of energy intake. Carbohydrate, 66%, reliance on a dietary staple like white rice, and protein, the remainder. If you look at the nutrition composition now, it reflects more of what we

might call a Western macronutrient composition. Dietary fats now about 33% of total energy intake. Carbohydrate lower than before, but still what would be typical in Western countries at about 55%. We've seen food industry tactics to how they penetrate these markets. It usually starts with sugar-sweetened beverages. They change the food supply in terms of access points. And we see the significant increase in calorie intake across the board. And yes, there are dramatic increases in nutrients of interest, for example, free sugars. So all in all, although it's interesting, look, we can plot the rise of Starbucks against the rise of chronic disease. And we can I'm very cautious against kind of comparisons in terms of timeline, because we can end up with post hoc fallacy where because, you know, B followed A, we assume that A caused B.

We could do that with any component of the diet. could do that with any component of the diet. What I find difficult, even though, so Tucker's correct when he says that our large prospective investigations in observational nutritional epidemiology are in industrialized countries. But given that that's the population in which we want interventions to be applied, I don't think that's a limitation because it's generalizable to the populations. We're studying the populations that are relevant to what we are ultimately going to ask people to do. And even before major guidelines come in, we see this association with things like the polyunsaturated to saturated ratio. We saw it in the Israeli civil servant study, which started in 1963, you know, 13 years before guidelines came in. We do see this replicated across populations, which is why, you know, we can see these syntheses,

pooled analyses of prospective data encompassing Europe, North America, and even Middle Eastern countries, and again, see the same trends emerge. So in terms of metabolic disease and the continued higher levels of cardiovascular mortality, although that has halved since the 1960s, I'm inclined to think that the lowest hanging fruit for us to go at is the dramatic increase, not just in total energy intake, but also in the kind of composition of diets itself, and therefore the absence of other nutrients. So the absence of dietary fiber, the absence of polyphenols, the absence of other, you know, monounsaturated fats,

the absence of foods that we would generally associate with benefit in the context of a hyper palatable, hyper energetic diet over time. And for me, that's a much more plausible explanation for the disease states that we have, whether that's fatty liver, diabetes or cardiovascular disease. Okay. To your point, Mark, yes, too much food is not good for you, regardless, it seems, of what kind of food you're eating. Your body doesn't like to be stuffed. And it's a common problem one sees in the nutritional literature. with Kevin Hall, the NIH researcher, where I told him he was putting his finger on the scale by having isocaloric feeding experiments, because if the effect of the dietary intervention is a

reduction in calories, which would be really interesting, then by overfeeding those people, you are causing them to eat more than they ought to be, more than they want, and potentially putting your finger on the scale of the result. So, yeah, that's a definite factor in, you know, any diet that you're looking at. As far as Alan's conversation goes, I was just reading a paper over the weekend on the nutrition transition, new trends in the global diet from 1997. And they go through the various different changes in the human diet over that period. And they noted that in the current era, the big difference from the previous nutrition transitions has been the large availability of vegetable fats and vegetable oils.

They specifically look at the change in China and note that the biggest difference in China is the importation and then domestic production of vegetable oils. So what they note is that this nutrition transition has a couple of common qualities across all societies that they looked at at any rate is that carbohydrate consumption goes down, which is kind of a ding for the carbs cause disease argument, because in every one of these countries that you look at, you see that as it gets more wealthy, it goes, carb consumption goes down, meat consumption goes up,

fat consumption goes up, right? Fruit and vegetable consumption tends to go up for a little while. And as we saw in Japan, it tends to plateau. But the biggest difference, again, as they note in the modern transition, has been an economic driven increase in the consumption of vegetable oils. And unlike all the previous transitions, this also happened in poor countries because these are cheaper fats. This also happened in poor countries because these are cheaper fats. So, yeah, I agree. What Alan said so far as he went was correct, but he didn't go far enough. Now, let's get into a little bit of a mechanistic study.

Alan's correct that there was an increase in overall calorie intake. You know, we'll narrow it to the United States because that's the place where we have the best data as people became obese. We also had the introduction of an anti-obesity drug called Ramonivant. Ramonivant came out, I think, in the middle 2000s, maybe 2006, I think in the middle 2000s, maybe 2006, and was fairly quickly pulled from the market because it turns out rats in cages don't really have the opportunity to commit suicide. So they weren't able to detect that people's reaction to taking this drug was in fact to want to kill themselves. So it was yanked from the market. But it's really illustrative, the mechanism behind that drug, because we know it worked in the animal models. We know it worked in the humans because we have RCTs, numerous RCTs showing that it worked in various different human populations. And the mechanism of that was to block the endocannabinoid systems uptake of a chemical called 2-AG. 2-AG induces hyperphagia.

Hyperphagia is overeating. Specifically, it induces overeating of carbohydrates, which is the part of the diet that went up the most over the 70s, or sorry, over the last few decades as the obesity epidemic occurred, right? Specifically sugar and starch. 2-AG is really interesting because after the drug was pulled, people continued to research it in animal models, which is how one does these things to try and determine what a mechanism is. And it turns out that dietary seed oils convert to a chemical in your brain that induces overeating. Now, the fact that that

chemical, as this nutrition transition and many other papers notes, is the biggest change that's occurred in the human diet over the last hundred years, the increase in omega-6 fats, and that we can block it with a pharmaceutical that works the same way in humans and in animals is a pretty notable fact to explain, gee, why do we all start eating more? Well, it's pretty interesting. 2-AG is a mimetic to THC, the active drug in pot. THC is actually used as a prescription drug in humans to induce eating in cancer cachexia, wasting in cancer, and also in anorexia. So you see where I'm going here. We have a very clear mechanistic pathway to explain our overeating epidemic that Alan described so well.

Do omega-6s give us the munchies? Bingo. That's exactly right. And some of the papers actually say exactly that. But do they say that in relation to... So here's the thing that I... This is a general comment that is, for me, applicable to almost all aspects of the conversation we can come at. We can look at mechanisms, and we have to look at mechanisms in science,

and we have to understand them. But mechanism does not equal effect. And this is, I think, a fairly common line of kind of reasoning within the omega-6 having a particularly negative effect is we'll take a mechanism. We can propose and we can look at and say that this A will follow and B will follow C, whatever the mechanism is. And yet there can't be an upholding of that mechanism until we have a translational effect in human outcome data. in human outcome data. And what I find, and so what you've just described is a putative mechanism involving a drug, which has nothing to do with linoleic acid.

So it's framing a circumstantial argument that this mechanism happens in this way. Not a correct statement, Alan. What did I miss? It has nothing to do with linoleic acid. The pathway from linoleic acid to 2-AG has been repeatedly demonstrated in animal experiments. So what I'm saying is the evidence that you're citing for this hyperphagic effect comes from the drug, not linoleic acid. No, the drug blocks the effect of linoleic acid conversion to 2-AG in the body. The drug prevents obesity. And it is a human-approved drug,

or it was at one point before it was pill to the market. So here we have a clear translation from a mechanistic model into a human demonstration that this effect takes place and it's not the only place that this has happened right but we've all heard let me let me just come back to that because because i want to i want to kind of work and thanks for you know coming in on that because so this is the line so we have the the drug is the anti-hyperphagic drug, right? It acts by inhibiting a pathway through which linoleic acid can act. Correct.

So is there human evidence that linoleic acid fed in high doses to humans has this effect? Yes, there is. this effect uh yes my my answer to that would be no um based on human evidence that we have well then we can we can go through that okay okay um and and and again even adding so mechanistic evidence while important must also be married to biological plausibility. And so even because this point will be relevant to the difference between percentage changes in diet as a result of increased calorie intake and absolute changes. And so we said that linoleic acid specifically constitutes around 7% of the diet in the US. And so if this putative mechanism is going to have evidence of actual effects in humans of increasing energy intake as a result of feeding linoleic acid well then it it has to be within

the bounds of the biological plausibility of where we're at in terms of linoleic acid intake and i i mean i've i've seen a number of studies looking at fat specific satiety that have compared different um fat subtypes um but i have to say unless you can point me in the direction of it i can't see any human evidence that would suggest that linoleic acid specifically increases subsequent calorie intake? Well, since I like these primitive society models, let's discuss the Tsimane. The Tsimane are a Bolivian hunter-gatherer tribe living in the Amazon desert.

They are very popular research subjects because they're another one of these populations that doesn't have heart disease. They don't have diabetes. And up until recently, they didn't have obesity. Well, they discovered something very interesting in that CMA that people were starting to get fat. And the first pass association they came up with was motorboats. Turned out, team and I with motorboats were more likely to get overweight. And it wasn't because they weren't exercising. It was because we all know that exercise is a really lousy way to keep weight off, although it's great for our health. What they discovered was the people with the motorboats were the ones who could go to the market and buy industrial foods on a regular basis. So they did an analysis of the change in their diet to see

what factor was driving their little obesity epidemic, and it was their consumption of vegetable oil, right? There are lots of papers looking at 2-AG specifically. And again, there's only one path for this to be metabolized in the body. It's made exclusively from arachidonic acid. And the and again, in the animal models, the variation in 2-AG in the body is driven by the linoleic acid content of the diet. In humans, 2-AG associates with obesity, as do various other omega-6 fats, specifically DGLA, which is an intermediate in the production of arachidonic from linoleic acid. Now, you correctly note in your article that arachidonic acid intake or arachidonic acid

levels in the body tend to be pretty stable when linoleic acid consumption is varied. Arachidonic acid is a very important fat. It's a long chain omega-6 fat. And the amount of it in serum, where they look, tends to be very tightly controlled. In animal models, it's quite clear that you can vary it and change it in other tissues and it's also quite clear that the metabolites like 2ag are varied by the dietary consumption even though arachidonic acid stays at a steady state so there's you know there's a lot of research going on into the endocannabinoid system and obesity because, we had a human approved drug tested in human RCTs

that showed that that pathway was relevant to human obesity. We also have another pathway. We've all heard of gastric bypass surgery. So the animal models show that what drives the change. Yeah. How do I? Okay. Let me back up just a half second here.

So the animal models show that the effect of linoleic acid on obesity is driven through the human brain, through the brain, right? There's a circuit going through the vagal nerve that detects the conversion of linoleic acid into arachidonic acid and 2-AG in the gut as you're digesting your food. And if you cut the vagal nerve, you eliminate the ability of linoleic acid to drive obesity in an animal model, right? So now they've looked at what happens in gastric bypass surgery, and it turns out you're cutting that circuit in animals or in humans, right? You are basically, it's almost like a lobotomy.

You're disconnecting the part of the brain that senses this hyperphagic signal in the gut, and it causes an immediate reduction in hyperphagia, which is why we use this surgery in humans to treat obesity. Now, because the gut is a very robust organ, I had to have a colon surgery. And I was astonished by the fact that they could cut eight inches out of my colon. And three days later, I was able to eat a normal diet and go for a walk. The gut has an amazing ability to repair. And what seems to happen after gastric bypass surgery is that the gut rebuilds its ability to sense this hyperphagic signal, which is why in the long run, people who undergo gastric bypass surgery, unless they fix their diet, tend to regain all of their weight or a lot

of their weight so clear human model clear described pathway in the medical literature describing what i'm talking about here i think it's really important that we address all of the the evidence absolutely but again the i and and not to kind of labor this but yes we have the clear potential mechanism i mean the factors that influence post-ingestive satiety or both within meal satiety and then subsequent meal satiety as it relates to the endocannabinoid system are highly complex we've seen that with the we've seen that we've seen that with the for example like just a slight detour but we've seen that with the sugar research right where you know in an animal model you can infer uh some of the dsm-5 criteria for addiction you can see the effect on the endocannabinoid system and the dopaminergic system and the wanting and

the liking sides of the brain. And then you start looking in humans and there's some key pieces that are absent that. And what I'm coming back to, although the Simine observation is interesting, you know, is that they're going in and eating industrialized foods. There are other factors that are component parts of that food and isolating the effect of vegetable oils. The point of their analysis was to focus on what was actually changing. I was really surprised to see that study because from my point of view, it was a gift.

I didn't do it. But again, we're talking about one study that is observational. Now, because I'm particularly sensitive to this being in nutrition, I think there are sometimes oversimplistic dismissals of nutrition epidemiology. Observational research is hugely valuable in interventions with with feeding, looking at fat. Because there's been a lot of hypotheses about the effects of dietary fat on satiety. studies that have looked at factors like the degree of saturation of fatty acids and how that might influence um you know satiety uh the fat composition of the diet broadly speaking as it relates to unsaturated and saturated fats and and some studies that have looked at you know feeding high high intakes of linoleic acid gamma linoinoleic acid, or oleic acid, which we kind of find in olive oil,

and looking at energy intake and parameters of appetite and otherwise. And, you know, I find it difficult to see, you don't really see any relationship between fat-specific aspects of satiety or even indeed overconsumption as a result of a specific fatty acid. So interesting mechanistic potential plausibility, but lack of outcome data in humans that suggests that all of this mechanism adds up to an effect that would actually explain the observations that we're seeing. And I think that disconnect is where it becomes difficult to reconcile this in favor of an adverse effect, because in favor of a potential benefit, or at least a lack of adverse effect, we can make the link in that chain with human outcome data. And so...

Well, human outcome data is quite, you know, obvious in my view. If so, let's say you're trying to figure out what causes lung cancer. Right. We all agree what we'll get into one of the other causes of lung cancer maybe today. But say you're trying to figure out what causes lung cancer and you look at a population of smokers and you try and vary the rate of smoking. So they all smoke two packs a day. And we'll all agree that that's too many cigarettes, right? The appropriate amount of cigarettes in a human diet is probably zero. So let's say you vary their cigarette intake. You take one group down to a pack a day and you put the other group up to three packs a day. Well, we happen and we've, you know, let's just posit that the amount

of cigarettes that causes lung cancer is a half a pack a day. You're not going to see any effect of that intervention on lung cancer because they're all above the minimum amount that's required to induce it, right? So if all you're doing are these intervention studies and everything you've described so far is a study that's done on an industrial population that has been consuming excess amounts of seed oils from an evolutionarily perspective. And that's according to an NIH study for 100, 150 years in most cases. Now, if you go, say, to Asia and you start comparing, this is outside of obesity. If you start comparing these diseases, the chronic diseases to America,

the older studies, you see a huge difference in incidence and prevalence between Asia and America. I mean, one of my favorite studies, which I've just been going over again, looked at the geographic incidence of heart disease. And they did it by using an unassailable model. They did autopsies. They looked at the hearts. If you have a heart attack, it does permanent damage to your heart that never heals, right? So even if you die of a car accident 40 years later, they can still do an autopsy and see that you had a heart attack 40 years prior. So they looked at. Caucasians in America, they saw there was a 24 percent incidence of heart attack over the course of their life. heart attack over the course of their life, right? I mean, they died of it. Then they looked at Japanese Americans and they saw a, I think it was about an 18% heart attack prevalence. Then they looked at African Americans. They saw a 13% heart attack prevalence. Now this was done back in the

fifties and sixties. I mean, you know, as far as I understand, African-Americans have much higher rate of heart disease now than they did back then. Then they went to Japan and they looked at autopsies in Japan and the rate of heart attack in Japan was three percent. OK, and that's really interesting because most of that came from Tokyo. The rate of heart attack outside of Tokyo was around 1%. Okay. Then they went, they looked at African Americans in the various cities in the United States.1%. In Nigeria, they did 4,500 autopsies and they found one heart attack, right? If you go back and look at the consumption data that we have for seed oils, what you will see between Asia and here is a massive differential back then and a huge increase. Japan's a great place to look at because we know why the Japanese

started eating seed oils after World War II. We have Japanese papers. It's a first world country. They have top universities and they were doing the epidemiological research. It's why Ancel Keys included them in the seven countries study. Their seed oil consumption went up after World War II because the American government pushed it on them, right? And they went from a minute heart attack rate, a fraction of what we have over here, to something that's now about half the American rate. And, you know, as you pointed out in your article, omega-3 PUFAs are protective. That's a big confounder. Japan's the best example that we have of that confounder because they still eat a lot of fish, a lot of omega-3 fatty acids.

But we have papers from the 90s coming out of Japan. The excess linoleic acid term came from Japan and came from them trying to understand why their incidence of these chronic diseases skyrocketed after the end of World War II. Yeah. Okay. So I think the cross-country comparisons are always useful and i think in in many respects that's why although it gets bashed around a bit i think some of the criticism of the seven countries study is a little unfair because there were aspects to that study design the contrast between diets being one of them that nutritional epidemiology faces the challenge like your analogy of the cigarette packets we're often comparing

half a pack to one pack how do you see a differential in effect compare you know a quarter of a pack to four packs you might see a more meaningful contrast if what we're saying is we have this correlation between between increased uh vegetable consumption generally and we have this then difference in rates of incidence well that should be if what we're declaring there what's being declared there is a kind of empirical fact, then it should be evident when it is studied in the population. And on the whole, I guess this from the perspective data, on the whole, it isn't. And I think that's where, again, we could have all of the correlations with change in human diet. with change in human diet. But unless we link it to actual outcomes,

then we're into various kind of illusory correlation potential fallacies. So just as an example, like the 2019, the Jacobson paper, 11 cohorts, 400,000 odd participants, 400,000 odd participants, a range of intake of about 1.7% to 10.6%. I'm sorry, the Farvey meta-analysis of linoleic acid intake up to about 11%, give or take, which seems to be the upper threshold globally although countries differ you don't tend to see any nation with a higher than maybe around 11 percent linoleic acid intake some some people in the united states get up to like 15 but yeah you're making a valid point so so within this range of intake from, you know, two up to maybe like 11%, this linear reduction in risk for coronary heart disease events. And this is just looking at the dose response analysis.

This isn't factoring in if we substitute saturated fat, for example. So just looking at the dose response analysis, and that's cohorts across, that's the US, Europe, and Israel. There was another analysis published last year, again, range of 1.1 to 11.6%, each 5% increase. And this is linoleic acid specifically associated with lower risk. And so while cross-country comparisons are particularly important, ultimately, you know, my concern, for example, would be, well, how do we further reduce cardiovascular mortality in the UK? Your concern would be how do we further reduce it in the US?

And if we were being guided by outcome evidence prospectively in relation to that, then the outcome evidence in relation to linoleic acid would suggest that increasing from very low 1% to 2% increases, and not very far, up about 5% or even up to about 10% would benefit in lower risk of heart disease. So the correlation analyses can only go so far when the actual outcome data shows a linear reduction in risk across these thresholds. I find any study claiming that they found an industrial population with a 1.1% consumption of linoleic acid to be incredible, to put it politely. I mean, the NIH just finished an intervention study and failed to get linoleic acid. This was a targeted intervention by the NIH trying to get linoleic acid consumption down to above that level. And they weren't able to do it because it's so prevalent in the population. So when you have when you have.

Wait a minute. So I just don't believe this gets us into the wonderful land of epidemiology and perspective studies and the absolutely abysmal quality of the data that they use in these papers. I mean, I just came across a paper where Frank Hu, who is now co-author with Walter Willett on this paper, said that they threw the data out where people didn't have a plausible caloric consumption, right? The plausible level they used was 800 calories a day over decades. That's a joke. There's nobody who can eat 800 calories a day for decades and not die. So according to the nutritional epidemiologists, 801 calories a day is an acceptable human calorie consumption.

I think we can all agree that that's absurd. So just wait, wait, wait, wait, wait. I'm not finished with my point yet. So we can look at human interventions, which we both agree are a better standard of evidence. We've all heard of the Mediterranean diet, right? We've all heard of the benefits diet, right? We've all heard of the benefits that it has for heart disease consumption. The most successful heart disease prevention trial ever, the one that made the Mediterranean diet, you know, after giving credit

where it's due, years of promotion of that diet by Ancel Keys, was the Lyon Diet Heart Study, which was the first paper was released in 1994. That was specifically and explicitly a linoleic acid reduction study. They made a point of getting it down and they talked in depth in the paper about the mechanisms behind excess linoleic acid consumption and cardiovascular disease. And I will note, and we probably have to get into this, that the only explanation in the literature for causation in heart disease and the different incidence of heart disease between more ancestral societies, as I've described, and industrial societies,

is the pathway that starts with dietary seed oils. This goes back to Brown and Goldstein in the 70s when they were trying to induce the first steps of heart disease and failed doing it with LDL. And only a later group of researchers, Steinberg and Whitstam, were able to demonstrate that varying seed oil consumption in the diet versus olive oil. Just the same thing that the Lyon diet heart study did, although they used a low omega-6 seed oil, canola oil, or I think it was actually rapeseed oil in their study. I think it was actually rapeseed oil in their study. That's the only pathway that's described in the literature to heart disease is one that depends on oxidized linoleic acid. This is overwhelming data. There isn't even another explanation offered.

I just want to back up just a bit. And where are these fats prevalent? I know we touch upon polyunsaturated fats, and sometimes it sounds confusing because I believe there's polyunsaturated fats that are omega-3s that most people would recognize as being fairly healthy. They come from fish, and you know, people supplement with lots of fish oil. But we're talking more specifically about omega-6 fatty acids, linoleic acid. And are these like manufactured fats? Like why are these fats bad for us? If, you know, some of these things are just in nature, wouldn't they, you know they normally be pretty good for us? Are these cooked and manufactured? Sure. Okay.

So great point, Mark. These are natural fats. They are present in all foods, both omega-3 and omega-6 to some amount. There is no point to try and avoid them because unless you're in a lab, there is no way to eat a diet that is void of omega-6 and omega or omega-3 fats. Right. The issue seems to be that we have had a big shift in the diet where our omega-3 consumption has gone way down and our omega-6 consumption has gone way up. So my argument would be a healthy human diet looks like something prior to that transition being made, where you are going to be eating, I mean, beef has linoleic acid, right? And omega-6 fat. And

I think beef is a perfectly healthy food. That's a whole nother topic. Maybe we'll do another show on that one. But fish has omega has omega six fats in it, along with the omega three fats. So the large amounts of omega six fats in the modern diet primarily come from refining oils from seeds like, you know, corn, cotton seeds, soybean oils, etc. And their concentration, I mean, somebody did a really great job of showing how many years of corn you have to take to get a gallon jug of Wesson corn oil. And it's a lot. You couldn't conceivably eat that much corn in that short of a period of time. So this is not an argument that these fats are inherently bad. It's just that we are,

you know, I mean, anything water in excess is toxic, right? That's what hyponatremia is. It's water poisoning. So source is also important because, so if we are talking,

cause Mark, you're like, so Tucker's described, obviously these these fats are natural and occur. And yes, there's this industrial processing. But in terms of where we to kind of look at dietary sources, and I think the UK and the US are pretty much on a par on this. The biggest contribution from diet is not that someone in their home is using some rapeseed oil like they did in Leon Diet Heart for a salad dressing or to cook on a pan. The primary vehicle of these is processed foods, is packaged foods or ultra processed foods if we talk about the NOVA categorization so these are foods that you couldn't make in your home kitchen if you tried because they rely on a mix of fats starch refined grain sometimes added sugar other additives sodium etc so they are like everything from like ice cream to cereal to potato chips to french fries i mean it's in a ton a ton of stuff right so so yeah and? There's one important thing, though.

Chicken is the number one source of omega-6 fats in the American diet. And that is because these fats concentrate up the food chain. And what we feed industrially raised animals like chicken or pork or farm-fed fish in some part is concentrated sources of these oils. So their consumption of it raises the amount in their adipose tissue. And then when we eat it, we are eating those fats as well. So that's been demonstrated in eggs, for instance. But so there's two points, Tucker, and I'm interested to get, because this is something that has always struck me as somewhat of a disconnect between, and I know to be fair in your article, I know that you mentioned this in relation to Lauren Cordain's research or Lauren Cordain's research. And I try and kind of, because a lot of, I'm not

saying, by the way, I'm not implying you think this, but you will probably be aware that a lot of people, or I would say maybe almost prevailing thought within the ancestral health community, whatever you want to call it, paleo, ancestral, whichever, seems very focused on saturated fat, whichever, seems very focused on saturated fat, for example. And concomitantly by saying, look, it's this omega-6 is the problem. Saturated fats are demyelinated. Eat more saturated fats to reduce. And then you go to the actual literature from these seminal paleolithic diet researchers,

and it's imperfect, right? We're using things like carbon-stable isotope analysis to try and piece together the diet but i've never seen an estimate of the saturated fat content of the paleolithic diet above six to eight percent of of estimated energy which is significantly lower than is almost akin to a modern mediterranean diet but certainly is much lower than a lot of modern people who profess to follow a Paleolithic diet. And what I found interesting is some of... I'm getting off topic, but... No, no, no, it's not. I'm bringing it back to just to round this out. So my point is that when you look at some of the research on... Cordain posited this, the fatty acid composition, and he based it off game meat, as you would find in kind of modern day Africa.

That fatty acid composition, yes, it does have more omega-3s. But in terms of overall fatty acid composition, more polyunsaturated fats generally, and a fatty acid composition that isn't too dissimilar to, if we just look at the fatty acid composition from something like a, you know, a rapeseed oil, for example,

if we look at some of the contents of that. And so, so if the argument is some degree of ancestral consistency, why is it, or is it simply that the dose is different? Why is it that the fatty acid composition of this ancestral diet may have been quite low in saturated fat and had more of a proportion of polyunsaturated fats? And is it just the omega-6 that's different in your opinion it's yeah so for starters everything that you said with about their

that you said about their research is correct um there is a wide variety within that research though of fat consumption i mean you're going from you know populations in i mean most tropical populations eat a lot more you know hunter gatherers eat a lot more carbohydrates and then you look at people like the Inuit who are eating an enormous amount of saturated fats. And also, I mean, there are Inuit populations who live inland and eat caribou exclusively. They don't get whatever benefits we have from eating fish. And, you know, historically, they didn't get these chronic diseases.

You can go through, I mean, we could, you know, the interplay between saturated fat and polyunsaturated fats is a broad one. And there is interplay where, you know, one of the benefits, for instance, of the Mediterranean diet appears to be that oleic acid, the primary fat in olive oil, is more diet appears to be that oleic acid, the primary fat in olive oil, is more successful at replacing linoleic acid in LDL than saturated fats are. So you wind up with a lot of confounded studies where they don't recognize that that is a factor in the different composition of their diets, which is why you see low-fat diets producing worse outcomes

in cardiovascular disease markers. At the same time, we have the Virta Corporation, which is currently doing a study amongst humans. It's not an RCT, but they are treating actual people and tracking their changes. Sarah Hallberg is the doctor who is leading that. And she's working with Steve Finney and Jeff Folek. Finney's an MD and a PhD and Jeff Folek is a registered dietitian. I mean,

great team. And they've really changed thinking on how to treat diabetes in the last few years. that Steve Finney did back in the 1990s, where he saw acute toxicity in a study population from trying to feed them too much, one presumes, soybean oil mayonnaise, since that's generally what soybean mayonnaise is made with nowadays. So they explicitly advise you against doing that. It's not a strict prohibition, but nevertheless, they are able to, you know, I mean, we'll argue about terminology, but they are significantly improving people's diabetes disease and simultaneously lowering all of their cardiovascular disease risk factors, or at least the markers for those risk factors. So yeah, I would argue that, you know, you can look at lots of different populations

with lots of different saturated fat intakes and find wildly divergent outcomes that to me seems to be because of the background PUFA intake with the observation that there are confounders. But omega-3 is the most obvious confounder. I mean, the Japanese and the Chinese genetically are very similar. They both share high frequencies and one of the most of the ALDH2 star 2 mutation, which is the most common human genetic mutation. And it's pretty much exclusively in Chinese-derived populations.

So we know they're genetically very similar, and yet they have wildly divergent rates of obesity. China is becoming one of the fattest countries on earth, and the Japanese are one of the least fat countries on earth, even though they are both industrial countries, they're both in the same neighborhood. And traditionally, they ate very similar diets. So, you know, there are confounders that can have huge effects on outcomes. And one of the most to your previous comment about how complex this is, that's an understatement. going on and there are a lot of different interplays between these fats and different parts of the diet that need to be taken into account to explain some of these discrepancies and yeah we won't be able to go through them all today but i wanted to point out a few of them just to make that clear i and i mean so one of the things that i you know you've raised there the the metabolic health specifically and and again this is is where we don't even have to go into observational research because what I'm thinking specifically of is the research in the last really six years, probably 2014 was the first study.

Control studies, randomized control trials, looking specifically at the effects of dietary fat modification and composition for effects on hepatic fat and liver fat. You know, liver fat, actual diagnosis of NAFLD is likely to be underestimated in the population. So there's estimates the prevalence of people with fatty liver is probably as high as 25%. And the diagnosis, the threshold is over 5% of your liver cells have fat in the cell. And their cells are, you know, liver cells are full of fat. 5% of liver cells are full of fat. And just a little backstory for the audience here. That process is thought to be the primary cause of liver failure and the need for liver transplants so it's not just an academic interest it's a serious disease

and it correlates with cancer and diabetes and everything else that we don't like it's like this initial spectrum of naffled and then you get this down nash and this progression fibrosis liver all sorts of liver diseases and and as it relates to metabolic health, particularly the overlap with diabetes, the liver becomes fatty, it becomes insulin resistant, elevated free fatty acids. We get into this vicious cycle of fat spillover to the pancreas, impaired beta cell, insulin secretion, all of this stuff. We have studies controlling for energy balance. So they're energy maintenance and we have

overfeeding studies where saturated fat has been head to head with omega-6 the muffin saturated fats and and the lipogaine and the hep fat study and a couple of others and there was a really nice review by hanalei yuki arvin and bernadette moore and a couple of others and there was a really nice review by hannah leigh giarvin and bernadette moore and a couple of others in nature recently on just dietary modifications for hepatic fat generally and we see not just that omega-6 overfeeding if we're talking about overfeeding context now you see a protective effect saturated fat makes the human liver into human foie gras, you see enormous increases in intrahepatic triglycerides from overfeeding saturated fat. And you either see a minimal increase or no increase at all from overfeeding omega-6. If you take that into energy balance context, so we're not even overfeeding calories, you see saturated fat increase intrahepatic triglyceride to a magnitude

of up to 50 to 60%. And you see no effect or reduction from overfeeding or from omega-6. So when it comes to these deleterious metabolic effects in humans, and some of these studies have added stable isotope tracers to look at the metabolic fate. We know that polyunsaturated fat has tended to be thought of to result in lower chylomicron secretion. So the vehicles that transport fat from the diet into the circulation, and you tend to get lower chylomicron triglycerides with polyunsaturated fat versus saturated fat. And it may be because it's simply broken down quicker. So again, human outcomes, factors that relate to metabolic health, fatty liver in particular, where is this evidence of a deleterious effect of omega-6 versus saturated fat? To me, the negative effect, particularly as it relates to liver fat and metabolic health

would clearly be from saturated fat intake even at energy balance levels so i just looked at a study van name uh 2020 out of yale looking at human children overweight and varying the omega 6 omega 3 content of their diet in the context of a high-carbohydrate diet. And they were able to improve their markers of fatty liver disease by explicitly lowering the omega-6 content. The overfeeding study you mentioned, I can't remember the authors, but I always refer to it as the muffin study. It may be, with respect, one of the worst um nutritional studies i've ever seen in my entire life so they took a bunch of people they have no idea what they ate they didn't make any attempt to measure their base diet and they gave them two kinds of muffins one

of which was mostly saturated fatty acid the other one was mostly saturated fatty acid. The other one was mostly saturated fatty acid. And indeed, as you say, they got the worst outcome on saturated fatty acid muffins. But as we've already discussed, overfeeding anybody is bad for them. Right. So really. And of course, in that study, they had no idea what they were eating because they made no attempt to track their background consumption right so if you know back to our cigarette analogy they have no idea how many cigarettes those people were smoking they gave them all they gave some you know some of them some filtered cigarettes and some of them some unfiltered cigarettes but they literally don't know what was behind the diet so i don't think that's a particularly useful study except don't know what was behind the diet. So I don't think that's a particularly useful study, except don't eat too many muffins. I mean, that's

too much. So wait, wait, wait, wait, wait. Bear with me here. So let's talk about an AFL day and AFL day is I will deposit the single best example of the causation of omega-6 fat and chronic disease in the human diet. For starters, it's a new disease, right? When non-alcoholic fatty liver disease was first described, it was in like some granny who the doctors were convinced was chugging alcohol when she was home because nobody who wasn't an alcoholic got fatty liver disease. And this was, if I remember correctly, back in the 1960s,

right? There was no such thing as non-alcoholic fatty liver disease. They thought the old lady was lying. Prevalence of NAFLD, as you observe, is now up at, I think, the 20-30% level in the United States. This is an entirely new disease. Now, luckily, we have a model that we can use in humans and have been using since 1961 to induce non-alcoholic fatty liver disease in humans, and it's called soybean oil. So soybean oil is made into a product called intralipid. Intralipid is fed intravenously or through the mouth to people who are unable to eat food orally. There are lots of cases where that's the case. It could be trauma. It could be a kid who's born without a gut. And there are many problems with feeding people

intralipid. One of them is fatty liver disease in adults. In children, it is cholestasis, where basically their cholesterol flow through stops working and it kills their liver. It ultimately gives them liver cancer and they are then candidates for a liver transplant. So over the last couple of decades, a pharmacist up at Boston Children's Hospital has been looking into what causes this liver failure in these people who are given soybean oil. And she has demonstrated that it's the omega-6 content of the fats that they are fed, and that if you switch them out from soybean oil to fish oil, a product called omega-Ven, they don't get the liver failure. And if they already have the liver failure, it goes away. And if they already have the liver failure, it goes away.

Her evidence of this was so convincing. Intralipid carries an FDA black box warning, which is the highest warning that the FDA will put on an approved medical product, basically telling you that this product will kill you. Right. Her evidence was so convincing that she never needed to do an RCT. And she got the FDA to remove the black box warning from OmegaVen because it doesn't cause liver failure because it doesn't contain any omega-6 fats. Furthermore, in the animal models, she went through and showed that every single infusion that contained any level of omega-6 fats causes liver disease. And even blending omega-Ven, the fish oil substitute, with a little bit of soybean oil

prevents omega-Ven from healing liver failure in humans. So yes, open-shut case in humans, decades of evidence, FDA-approved product. That's not even a close one in my view. product, that's not even a close one in my view. And again, I will note the biggest single change in the worldwide diet over the last century has been 70% of the fats in the United States now, according to that paper I cited before, are from soybean oil. Soybean oil is obesogenic in animal models. I mean, there's literally a paper in the scientific literature where the title is soybean oil is obesogenic in animal models. I mean, there's literally a paper in the scientific literature

where the title is soybean oil is obesogenic. GMO soybean oil with less linoleic acid is less obesogenic, right? It is the human model for inducing insulin resistance, another disease that we have an epidemic of. So scientists who want to make humans insulin resistant, that we have an epidemic of. So scientists who want to make humans insulin resistant, they inject them with soybean oil because we've known since 1964 that soybean oil causes insulin resistance and hyperglycemia in humans. Thank you, Alan. That is the best argument I have for this position. What are current levels of soybean oil in the US?s oh boy i don't know they're up i don't know what the absolute level is but they're up according to the nih a thousand fold since the 1900s when it wasn't really used as a food but in terms of in terms of now because because so the evidence

that you've cited there in relation to the effect of soybean oil is like largely either the in vitro cell culture or or animal model effects no no austin children's hospital they've been treating children this way for decades it took them 14 years to prove that soybean oil was the cause of the diseases they were seeing in human children. And they had a lot of deaths. But this is specific to, because I'm just trying to marry this up. I don't see soybean oil, for example, in the UK. So this is the evidence that you cited there is very specific to soybean oil as the exposure of interest, yes? Omega-6 fat there was another uh there was another um parenteral

nutrition product that was made out of cottonseed oil which has more omega-6 than soybean oil and that had to be pulled out of the market decades ago tucker is the feed that's used when people are put on ventilators is that in any way related to that's exactly it it's total parenteral nutrition and the most commonly used product is this intralipid which is a soybean infusion so they used intralipid in this study with children sorry i'm unfamiliar with this boston children's study so um just kind of asking some questions so they used the intralipid which is usually used in total parenteral nutrition and they used they used that as the exposure in that so they had they had kids consuming uh the intralipid versus a control no these were not this was not a study

this was treatment they've been using intralipid as a treatment in humans since 1961. That's when this product was introduced. Sure. And there's an enormous literature on, you know, TPN related liver failure. And Kathleen Gura, this pharmacist at Boston Children's was able to prove that it was related to the omega-6 content in these infusions. But I'm just, so how was she able to prove it if there was no, like surely they even did a control group in the hospital setting? Pair-controlled feeding. That was the data they gave to the FDA to get it approved. Pair-controlled feeding. By the time they finally got around to doing an RCT in Hong Kong, it was so well known

in the parent community how bad soybean oil was for children that they weren't able to complete the RCT because the parents refused to have their children put on soybean oil because of the toxicity. It's unethical to do a soybean oil infusion RCT at this point. And that was the evidence that the FDA used in approving this product and removing the black box warning. Right. But again,

you know, so soybean oil is obviously a vehicle for Omega six fats. It's not entirely omega-6 fats. And so the idea that that holds invariantly for any other potential oil, you know, we can't make that extrapolation that that would apply. They've used other oils. There are a variety of different products on the market. I mean, one of them is called Clinilic, which is made from olive oil, which has a lot less omega-6 fat than soybean oil,

and it's preferred to soybean oil because it doesn't induce liver dysfunction that soybean oil does. It produces much less hyperglycemia. Sure, but again, we're talking about this specific product, right? No, no, no. We're talking about a treatment approach and the evidence showing that fatty liver disease is caused by omega-6 fats in humans. But that's not what

the body of evidence shows in this specific case. You just said you weren't familiar with this body of evidence, Alan. No, I said you weren't familiar with this study, with this body of evidence, Alan. No, I said I'm not familiar with that study. I'm familiar with the evidence for NAFLD and interventions in humans. It's not a study. It's decades of treatment.

I mean, if you go read the guidelines on how to do TPN in humans, they say that intralipid is harmful and they say the only reason we use it is because there's nothing else on the market this is standard medical practice here it's not a study okay okay um real quick i i am curious about both of your suggestions just to the practical individual who's listening to this information it's like maybe if i'm using certain oils can i just cut down a bit like from the most practical perspective i i would assume maybe tucker you'd say get rid of all of it but like how can people take this information and just put it into practice even if they're being cautious let's say that they

hear what you're saying and they're like, I just want to be maybe a little bit cautious with this and be careful until more research comes out. How can people apply it in the best way? Can I get both of your opinions on that? Well, okay. But before I say that, I'd like to address one point that Alan's made a couple of times by saying consumption of this is only 7%. That sort of begs the question because that assumes that 7% is a healthy amount. And that hasn't been shown. 7% is

several times as high as an evolutionarily appropriate level based on what we know from populations who don't consume seed oils and industrial chicken and pork. We don't know oils and industrial chicken and pork. We don't know what the safe amount is. Okay. And another point that I think Alan and I would agree on, since he's obviously looked at the paleo diet, people eat lots of different diets and they can be quite healthy, right? I mean, everywhere from the Inuit who eat nothing but meat and fish to the Tuka Senta who eat 94% yams, for heaven's sake, or no sweet potatoes,

and are apparently just fine. A diet I think we'd all agree that we'd rather not go on, even if it's good for you. So basically, what I would propose is that you're trying to get back to some sort of evolutionarily appropriate, which is not zero level of these fats with the understanding that you cannot get them out and you do need some amount of them in your diet. like seed oils, obviously, but also animals fed concentrated sources like farm-raised salmon, chicken, pork. There's a really neat study from Norway looking at what happens when you feed salmon soybean meal. They get fat, they get sick. If you then feed those salmon to mice, the mice also get fat and sick. So you're turning, you know, healthy food, salmon into something that seems to have negative effects on the salmon and on the things that are eating the salmon. Yeah. So, oh, I think these, these, these parts are complications because I i one thing i'm going to that one one thing one thing i'm quite conscious of is when we have these conversations where i'm going to assume typically i'm fortunate enough to have some means and to have the means to be able to have some degree of control over our diet and i'm

conscious that that is not necessarily the norm for huge sections of the population, particularly, I'm not sure about the US, but in the UK, huge issues with access to healthy food and poverty and the impact on diet. So I'll maybe take two kind of angles with this. One is assuming someone... If I could kindly interject to say I agree with that 100%, it's a huge issue. Yeah. And so maybe two angles. One assuming a lot of your listeners are fortunate enough like us to be able to kind of maybe cook and make these decisions

I find that a lot of people are not necessarily going to if they are doing a lot of their own in-home cooking are likely not their fat composition, unless they're, you know, bulletproof coffeeing or something like that. Their polyunsaturated fat composition is not going to be enormous. Most people likely use something like an olive oil as their primary added fat in terms of kind of addressing or something like that. For me, I don't see a difficulty personally with adding like a cold

press rapeseed oil, which would be really common here and in Europe. Rapeseed oil is what was used in the Lyon diet heart study. Sure. So I think that as a kind of a healthy polyunsaturated oil that could be added for some variety, you know, and consumption of oily fish, I think, but that's not been something we've been talking about today. So people that can have that control, yeah, consumption of regular oily fish, I think two meals a day,

two meals a week seems to be the kind of minimum effective dose for oily fish. And then the addition of oils like olive oil or rapeseed oil. And I think that's pretty much a lot of those bases covered. For people that don't have that level of control over their diet and are having to rely a lot on either eating out of the home or a more processed food diet, that becomes really tricky. And one thing that I think if you look at population diets on average, I think in that context, it might be a case of adding more than trying to substitute. So in the UK, for example, average fruit greater than worrying about getting the 7% of omega-6 linoleic acid down to nothing. Because potentially of the displacement, it might occur in other areas of their nutrition. So if they eat more fruits and vegetables, maybe potentially they'll eat a little bit less of some other stuff.

They eat more fruits and vegetables. Maybe potentially they'll eat a little bit less of some other stuff. Yeah. And adding, you know, there was a nice study here called the Cressida trial, which looked at, you know, because people complain about dietary guidelines. I would argue no one has ever followed the dietary guidelines. The guidelines are here. The food industry is over here putting out whatever it wants. So there was a study here that looked at getting people to actually comply with what over here is called the Eat Well Guide, right?

Meaning substituting refined grains for whole grains, increasing their fiber, increasing their fruit and vegetables, lowering their saturated fat. From it here, it's still about 13% and other dietary modifications. And it compared it to just your average British diet. And you saw significant reductions in cardiovascular risk factors, lipids, and blood pressure that would be expected to translate into a meaningful reduction in event risk. And I think about that, and I think about those changes. For me, they're more accessible. I don't know if I was talking to someone in the general population who has to purchase a lot of their food or is on a tight budget. I'd be trying to get them more to focus on those factors like replacing

a refined grain product with a whole grain product, trying to increase fruit consumption for example. And I don't know that I would be having them sweat that much over any you know percentage of intake of of linoleic acid given the levels that it's currently at here and i'm i'm personally not convinced in human data that that seven percent is too much um particularly when saturated fat here still sits at about 14 percent of energy i mean if people got that down to 10 or 9 and replaced it with monounsaturated fats,

then you might see. So they're the kind of things that I'd be looking for people to do, you know, cooking less with butter and more with olive oil, for example. Okay, well, we... I mean, in general, I think, you know, Alan's focus on home cooking and the problems of eating out, I agree with 100%. Obviously, I would put reducing your intake of these concentrated omega-6 sources, seed oils, and whatever else, very high on the to-do list.

But I think we seem to agree a lot. I mean, it is hard eating out. But I think we seem to agree a lot. I mean, it is hard eating out. I'm, you know, super gluten intolerant. That's why I was hospitalized multiple times. And doing stuff like that when you're trying to eat out is a real challenge. Yeah. things like coconut oil, which appears to be a very healthy fat in the obesogenic soybean oil

paper. They used coconut oil as the control and it didn't have any negative effect on the animals they were using. And there are human populations like the Catawans who eat huge amounts of saturated fat from coconut oil and they're perfectly healthy. As long as you don't mind the taste and it's not always appropriate with every dish. You know, I wouldn't want, you know, my muffin to taste like coconut oil, frankly. But there are other, you know, palm oil, olive oil, as Alan mentioned, avocado oil, all have lower linoleic acid takes. And, you know, until we have some better fat options, that's about the best you can do. And I mean, I've talked to people in India and they, you know,

they're vegetarian by their religion and they don't have a lot of options. And I've told them, look, canola oil is one of the best seed oils because it's got one of the lowest linoleic acid. Canola oil is what we Americans call, what you folks's got one of the lowest linoleic acid. Canola oil is what we Americans call, what you folks over in the UK call rapeseed oil. Same plan. It's just better branding by the Canadians here in the United States. Tucker, you talked a little bit early on about sunlight. And I know a lot of what Alan has talked about on my podcast previously, uh, was about circadian rhythm and stuff, but I find it really fascinating what you said about

sunburn. And I think sometimes when we start to talk about some of these things, I think people think, uh, that we're crazy or, um, and same with Alan, you know, coming on and talking about circadian rhythm, how it, you know, it, it about circadian rhythm how it you know it it appears that it matters kind of when we eat and some of these things um i think a lot of us sometimes are just like this sounds like crazy talk but then we find out years later that maybe we're on the right track uh what have you found uh with the sunlight you kind of mentioned uh maybe being able to handle more sunlight. What do you think happened there? Well, the literature is really clear on that one.

They can control susceptibility in these animal models by how much seed oils they feed them, how much polyunsaturated fats they feed them. They break down from UV light into toxins. The toxins are inflammatory and cause a lot of the inflammatory response that you see in sunburn and skin cancer. There's a gene, the TP53 gene, which they call the anti-tumor gene, which is broken. The term they use in the papers is preferentially mutated by these linoleic acid breakdown products. And alarmingly, we didn't really get into cancer in this talk, but alarmingly, that particular mutation is the most common mutation in human cancers. And we know that the breakdown products that are specific to linoleic acid induce that mutation.

And it specifically happens in skin cancer. There's a Dr. Black out of Australia, I think, who did a lot of research on this years ago. Unfortunately, he was also saturated fat phobic. So he advised you to eat a no fat diet, which I don't think it's really optimal. So there's a clear literature showing that's the case. To the old epidemiological evidence, which I'm really partial to, there's a neat paper looking at some high Andes indigenous population. I think the American military did this paper and they noted that they lived in a treeless area in a high desert and never got skin cancer their entire lives.

I mean, that's what we evolved for. We evolved in Africa, for heaven's sake. Right. And skin cancer, if you look at skin cancer incident rates, it's a steadily climbing rise over the 20th century. That is also not a natural condition. Something has to be causing it. also not a natural condition. Something has to be causing it. And I've talked to lots of other people who've noticed the same thing that I have. A lot of people who go carnivore are like, I don't sunburn anymore. I don't understand what's happening. For me, I went from like 45 minutes in the sun to six or seven hours before I'll get a sunburn. I mean, I'm not invincible. I'm not going to claim that it will make you invincible, but that's like the difference between I live in Idaho in the high desert now, and I can be out all day in the sun without having to use sunscreen. And I just get

tanned the next day. I think that's, and you know, I mean, again, as I said, blonde, blue eyes, fair skin, I'm never going to be the equivalent to somebody with a more shall we say yeah exactly um i'm you know i don't have dark skin i'm much more susceptible to sun damage regardless of what i eat but the difference to me has been just life-altering i haven't used sun screen in since in eight years i think and i mountain bike and I hike and I backpack and I'm out in the sun all the time. And, you know, I just don't even, unless I'm going on an all day backpack or something,

I don't really worry about it. So that's been fun. That's interesting. I'm completely unfamiliar with any skin related literature although i have a good friend of mine here who is a dermatologist um so yeah it'll be it'll be an interesting conversation for me in the future but it's certainly something i have never looked into fair enough we can't all know everything i you know, I've got my little area of focus here. There are lots of things that I'm clueless on and try to pretend. you know, some of the advantages of eating, you know, certain,

certain times of day. Has anything changed since you weren't on the show that long ago, but did anything pop up more recently? You find a fascinating study that you can maybe share with us today. So in terms of recent studies and not yet, so there's, you know, the, the kind of, there are more human interventions now that have looked at distribution of energy and tend to find a kind of a negative impact of later evening energy distribution on glycemic control in particular. Glucose levels, insulin, you get this really high level of glucose you get this impaired insulin response it's elevated through the night while people are are asleep

so i think you know there's just an accumulating body of evidence um in relation to this from from from human studies now which is good because previously a lot of the associations were observational. I think for me, the interesting part, I have a study running right now. I've got about 100 people who are, it is observational, but it's the relationship. I think we talked a little bit about this between your chronotype, your individual time of day preference. Some people are morning larks, night elves, and this kind of thing so how do people who have that natural time of day preference self-select for when they eat so that's the study that i have running now and there's some associations with you know your preference

your time of day preference corresponding to certain dietary patterns um and that people who are morning types tend to have a more regulated meal pattern where people who are evening types tend to have a much more dysregulated meal pattern so i'm kind of interesting to see what data i guess as a night owl that really strikes true really okay yeah so yeah not one here well not now it seems to be that you know owls, particularly if they have to get up early, so they're not hungry, their appetites aren't, you know, it takes a while to get going. And they kind of only come into the day a little bit later, and then they kind of start eating later in the afternoon. But then they're kind of, you know, in their peak, you know, mental zone in the evening. And that's kind of when they're starting to raid the fridge a bit more. You just described me to a team, my friend.

On a lot of this today, really fascinating. I appreciate the time from, from both of you guys. I think one of the things that is a constant and consistent battle that we all face is, you know, it sounds like a maybe more simplified version of just about what everybody's talking about. Alan, I loved your idea of adding, you know, I think addition by subtraction could really help some folks, especially people that have kind of just fallen into just really struggling with figuring out how to manage their diet on a daily basis.

But I think ultimately... Yeah, right? No, he'd mentioned the paleo diet before. And I think the important thing to know about how that relates to what we eat now is we don't know. They ate all sorts of things. We don't know what any one person ate back then. But we do know what they weren't eating. And it was the ultra-processed foods that so many people rely on. And I think we could both agree that getting that, you know, without getting into

all the components, getting that out of your diet is probably the single biggest thing you can do to improve your dietary quality. And the hard part is the people that really enjoy those foods probably won't listen to this podcast. And so we got to figure out, you know, as many ways we can to keep getting that, getting that message out there. Tucker, how are you getting your message out there? You have social media. Have you written any books or do you have your own podcast or anything like that? I am, I have a website, yelling-stop.blogspot.com my blog which has been up there for ages um I'm very active on Twitter um not I post lots of nice pictures on Instagram but I don't really participate there or I think they're nice pictures anyway um and I am in the process of writing a book and I've

also been doing a bit of podcasting of late mainly interviewing science scientists which has been a really amazingly educational process because the one thing you can't ever stop doing in this field and i'm sure alan will agree is learning it's a constantly changing field and we're constantly refining things and it's, you know, you're always going to learn something new. Constantly changing to go back to the beginning to tell us to eat. Exactly. Andrew and Seema, you guys have anything else to add before we wrap her up? This was exciting. It was, it was, it was, it was a lot of fun to listen to.

And the big thing that, again, the big thing that I was trying to kind of understand was how can anyone just apply this into their daily life and then see how they can benefit. So I'm happy that we both were able, or we were all able to get to that for the people. But I hope we do this again at some point, because it was great.

It was great fun. Thank you, gentlemen. Thanks for having me again, lads. Really appreciate it. Tucker, it was good to trash out some stuff in good faith good faith so thanks for being likewise very nice to talk to you alan i hope to do so again absolutely awesome guys thank you so much for your time have a great rest of your day alan alan where can people find you too there you go we did the first one um so yeah so uh only on instagram i've done the reversal of Tucker Twitter. Twitter goes too fast for me.

Uh, the nutritional underscore advocate. Um, I also produce content with Sigma nutrition. So myself and Danny, um, have a weekly or sorry, bi-monthly podcast.

And we do some written statements and my own website, Alinea nutrition, which is really a healthcare professional research review-focused platform for nutrition science. So thanks again, guys. Appreciate it. Thank you. Cheers, lads.

See you guys. Cool stuff, man. Nice diving in there. That was nice and deep. That was real thick. Way, way deep. Yeah. That was like,

Ooh, what it reminded me of. This is probably like the, like the first week of like college. Um, this is like a, a weird analogy, but like when all my friends were like still in the 13th grade trying to get

into like a legit like English class. Um, I went from high school and i just walked right into like and i am bragging a little bit because like i don't do well in school but like for writing in english and shit like i was like leaps and bounds better than everybody else yeah so i walked into this like legit college class when everyone around me is like way older and i'm like oh shit this is a community college so a lot of like parents are like trying to get their degree and shit and so yeah here i am like whatever 17 18 years old and then we start

to like kind of get down into what's like we have to start doing and i'm just like oh i fucked up like this is too much so with today's conversation like man, man, I was that I was that was a lot. There's actually some really interesting stuff that we didn't get into when it comes to meat consumption. But some of the things that that Tucker believes happen from eating some of these omega-6 fats, they get kind of blunted by eating meat because meat has carnosine in it. And carnosine is a scavenger of these damaging fats, at least according to some of the information that he had. But I just, you know, the more that we do this podcast, the more I know that sometimes things get really, uh, deep and complicated and complex, but the more complex they get, the more simple they end up

because we just end up going, oh yeah, that was the right way to eat the whole time is to just stick with whole foods. And, um, we even heard, um, Michaela Peterson talk about this. I've heard many others talk about this. Sean Baker is an advocate of this. He doesn't really, and Paul Saladino. I think Paul does some different stuff with his diet. But a lot of these people, they're not even really trying to intermittent fast. They just chose to have a diet that is comprised of a low variety of food. I know some people are like, you need food variety.

Well, that may be true for some, but other people might find this to be really effective to have a small variety of food. And most of the people that we know, their variety of food is tiny. Like the people that are getting on stage, that are competing in fitness, even the power lifters that we know that are really efficient usually their variety of food is not uh not massive either i think at some point it just gets to be easier when you're uh don't have so many different decisions to make on what the hell to eat and you're concerned and worry over does this have polyunsaturated fats in it does this

have high fructose corn syrup in it? The answer is no. Every time, if you're eating some beef, eating some Piedmontese beef, you know that it's grass-fed, grass-finished. You know a lot about it. You know that it's high in protein and that it's more modest in fat, and you know exactly what you're getting. But you go out to eat or you start to kind of roll the dice on some processed foods. You don't really know what you're ending up with. Straight up, man. Like they're doing this podcast through the years. Like my diet has just continued to get distilled down. So now if somebody comes to my house and they go into my pantry or my fridge, they're like, they see a lot of meat. Um, maybe

they see some kimchi, maybe some yogurt, like. Like my diet has just distilled down. And as we were talking today, that's why like practically, I mean, I'm actually very interested that he mentioned palm oil. Palm oil is used in a lot, like a lot in West Africa and a lot of Nigerian foods. They use heavy amounts of palm oil. Nigerians, they got no heart attacks. What's up with that? But palm oil is the main oil that's used because also

from palm trees they get something called palm wine i'm not going to get into that that's a nigerian meme if you're nigerian what's up you get it um but i'm gonna start bringing back some palm oil because that stuff is good but yeah like i don't you know with the way that we cook you know all of us here um i don't use vegetable oils. I almost ever have olive oil in my house, but they're all at open. And it's not because I choose not to use it. I'm not avoiding it. Just the nature of the way I cook. Yeah. I just haven't used it in a very long time. So you'll, you'll notice. And like, I used to think like I used to eat more variety. Don't need to now. And I don't, I don't feel like I'm restricted either just because of the way we eat.

I think that fasting plays into that a bit too. It does. As wild as that sounds, it doesn't seem restricted to be fasting and to have a low variety of food. have a low variety of food in some weird way. Like once you cook, like it's, I've, I've never cooked up a steak after I've been fasting for 16 hours or 20 hours and been like,

this is going to suck. I've been so excited, so pumped, you know, I'm like literally like drooling. I'm not super fired up. And a lot of times I'm even trying to cook something else first so I can get to something else first. I'm throwing in the eat right into the microwave way when I get

home and I'm cooking up some shrimp or something like that. But it can really be useful to have a low variety of foods and you can help yourself to avoid a lot of the uh a lot of the potential dangers in eating some of the foods that we talked about today and running into some of those weird fats yeah it takes time though right i'm again thinking back i remember i used to like you know again getting into all of this stuff remembering when i was trying to eat everything healthy it was like you know like oh you got to eat you know chicken broccoli and rice and then like i would even have like boiled chicken because i'm supposed to have like the healthiest like non-artificial anything and i'd be like after like a day and a half like i would i would have it for lunch one day and then the next day

i would heat it up and i just like would pick at it i couldn't eat i just couldn't do it it was i was done so then i believe that i'm like oh i'm somebody that needs variety i'm somebody that needs something different every meal every single day and then now it's like dude yeah i can i can handle chicken every day if i had to um now i'm eating a lot more steak and i'm eating a lot more fatty cuts. So I am having salmon from eat right. But yeah, it's, it's tough because I would get super frustrated because I would look around and be like, oh, well fuck, like they're, they're able to do it. Like what's wrong with me? But it just, it just takes a little bit of time and, you know, taking some of the other

bullshit out of your diet definitely helped me, you know, like I was again, thinking back about all the stuff that I was doing. I remember I would like go to In-N-Out and be like, oh, no i was again thinking back about all the stuff that i was doing i remember i would like go to in and out and be like oh no salt like get rid of all the salt like i don't want any salt because i'm trying to be healthier but it's like dude i'm still eating the fries and you know that's cooked with uh sunflower seed oil have no idea if that's good or bad or not it doesn't matter it's definitely not something if i'm trying to like cut all the bad shit out of my diet i'm'm going to have that and then wonder, man, why can't I eat chicken and be happy? You know, it's like there's I'm just putting all the odds against myself and then now taking all that shit out and just trying to eat more steak from Piedmontese.

And, you know, it's just yeah, it just takes a little bit of time and some focus. Yeah, it just takes a little bit of time and some focus. I think it's good for people to recognize that you may want variety, but you don't need variety. You know, there's huge. We would just humans just we wouldn't be around. You know, there's points in time where we didn't have a we didn't have as many choices. we didn't have as many choices. We didn't have hardly any choices at all on what we ate, ate whatever animal was around or whatever berries or whatever was,

was growing at the time. So I think it's just important just to understand that, that the psychology of your nutrition, a lot of it is we, a lot of it, we make it up, you know, we make, we make it up that we,

Oh, I need snacks. I hear people say all the time, I need something crunchy. And those kinds of things are interesting because crunchy foods could be, could still be healthy foods. I mean, you could eat it. You could eat some cucumbers. You could eat an apple. You could eat, I mean, there's plenty of things that have celery. There's plenty of things that have some snap and pop to them that have some crunch to them. But usually when people say they want something crunchy, they're almost always talking about something that's processed.

And it's like there's not really a lot of room in really anyone's diet for those types of foods. I mean, you can have them here and there. Maybe they represent 5% of your diet or something like that. That sounds plenty reasonable, but not something you probably want to be munching on all the time. Andrew, want to take us on out of here, buddy? I will. Huge shout out and thank you to Element Electrolytes for sponsoring today's episode. Make sure you guys check out.

Ow. You hit me with that thing. I know that right? Links to them down in the description as well as the podcast show notes. DrinkLMNT.com slash PowerProject. Make sure you pick up a value bundle because you're going to get four boxes for the price of three. Follow the podcast at MarkBell's PowerProject on Instagram, at MBPowerProject on TikTok and Twitter.

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Just might. I think it might just work. It's not going too bad. My TikTok is blowing up really well. Thanks to Jessica Smith, who's always plugging away, working at it. And my TikTok life coach in SEMA just basically just tells me to take my shirt off and play with my nipples a lot. That's all you got to do. For some reason, that works really well.

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