How to Lie With Science: Seed Oils & Inflammation | Livestream 1

to the audio version of a video live stream that originally appeared on my YouTube channel. A link to this live stream will be provided and that'll take you to that episode on the YouTube channel. We look at various visuals

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First live stream. Thank you for those of you who are joining us. We've got here Tucker Goodrich, my friend, my internet friend. And one of the voices um uh I've I've learned a lot from on you know just uh on the internet, like just seeing seeing the research you've done. And as we talked about on the podcast previously, Tucker.

I pointed out something about you that that drew me to you, which is that you appear to to read the things that you're actually talking about. And as we'll see today. Yeah. As we'll see today in our review of the reviews in the scientific literature. People, illustrious scientists, people with MDs and PhDs at fancy universities, they either aren't reading the literature they cite or uh they are reading it, but they are misrepresenting Oops, my bad, not muted. Are we all good?

I can hear you fine. Okay, great. Um okay, so I'm gonna do a little preamble here um so people have background and then we'll go through this paper and then talk about some of the connected stuff. Um so Do you see that slideshow, Tucker? Not yet. Share screen. What do people see on the screen right now? They don't see this. Hold on. Let me get my settings right. Says I'm sharing. Stop sharing. So I wanna s show this slideshow. Share screen. This one. Boom. I do not

Sharing this tab to my streaming or that's what it says. Ah, I see. I just have to do this. Okay, there we go. Now we can see everything. Okay, thanks, folks. First time doing this. Um, so just as a reminder, right, we're gonna talk about seed oils, we're gonna talk about fats, we're gonna talk about all of that stuff. There's lots of different dietary fatty acids.

Saturated fat, unsaturated fat. And within the unsaturated fat bucket, you've got polyunsaturated fats, omega-3s and omega-6s within the polyunsaturated fats. You've got omega-9s or monounsaturated fatty acids. And it's important to keep all those things in mind for reasons that we'll go over. What I the terminology I use is we've got polyunsaturated fatty acids. That's like the omega-6s and omega uh threes here. They've got multiple double bonds, two or more, hence polyunsaturated.

The omega-6s, the major one that we talk about is linoleic acid. There's other ones we talk about, but with seed oils, when I say seed oils, I'm really talking about omega-6s. And I'm usually particularly talking about linoleic acid. This is the most abundant omega-6 polyunsaturated fatty acid in seed oils, the things that are in most seed oils. There are also the omega-3s, like linolenic acid.

And that's also polyunsaturated. You can see that the double bonds are in different positions. That affects the chemistry of the molecule and therefore what it does in our bodies. The omega sixes and omega-threes are similar at one level, but they're also functionally distinct in many ways. We've talked about that on the podcast and in my content before, but it's important to keep in mind you've got the sixes and the threes because the balance of those things matters.

And then you've got monounsaturated fats, right? One double bond, oleic acid is a major example. Roughly speaking, you can think of these as, you know, oleic acid is what I think of as like olive oil fat because It's a predominant uh fatty acid in olive oil. Linoleic acid is what I often refer to as seed oil fat because it's usually the most abundant fatty acid in a seed oil.

Um the omega threes, like alpha linoletic acid, um like EPA and DHA, those are like your fish oil fats and things like that. But there's different batteries. And that's a important distinction. The the one you have on the screen is a plant omega-3 fatty acid. Yes. From the longer chain ones, which is what our body actually needs, come exclusively from animals. Yeah.

Another important point, oleic acid is a fat that our body can make itself. And the upper two you can only get through consuming them in the dark. Yes, that is a key point as well, right? So our bodies can't make linoleic acid, they can't make the omega polyunsaturated fatty acids, basically. They can make something like oleic acid, they can make saturated fatty acids.

That factors into considerations that we can get into because our body uh regulates those things, it's different mechanisms at its disposal to regulate these things based on whether you can synthesize it in your So

Notice that between if you look at all of the fatty acid profiles across different fatty foods, they all have different profiles, right? And that's important. And I'm going to point out a couple of things here that are going to be key for dissecting the papers we're going to go through.

So let's look at a quintessential seed oil like soybean oil. Notice that the biggest bar here is polyunsaturated six. So that's omega six polyunsaturated fatty acid. And that's linoleic acid predominantly. So soybean oil is predominantly Linoglaic acid, but it's got some, it's got some of the others as well. It's got some monounsaturated, it's got a little bit of omega-3, but notice the relative balance. This seed oil has a lot of omega-3.

Just like other seed oils like sunflower oil. So look at sunflower oil down here, really, really high level of omega 6. A linoleic acid, very, very teeny tiny, almost no omega-3s at all. So the omega-6-3 balance is way high in favor of omega-6s for sunflower oil. It's got some monounsaturated, but but way less than the omega. Compare that to something like a fruit oil, olive oil or avocado oil. Notice that these guys are different. Δεύκα.

Um monounsaturated fatty acids as their predominant fat, right? So they've got linoleic acid, they've got some of these other things. Most of these things have most of them, but the balance is different. The seed oils typically have this characteristic where the predominant or the most abundant oil is the omega-6 polyunsaturated fat linoleic acid. Usually, but not always. Canola oil is down here.

And canola oil is a seed oil because it's made from seeds. But notice that unlike soybean oil or sunflower oil, The omega-6 bar isn't as big. Canola oil actually has a profile that looks a lot more like avocado and olive because it's got the most abundant fatty acid as monounsaturated fatty acid. And it's got some omega-6, but not nearly as much as soybean or sunflower oil. And notice also that it's got more omega-3s than some.

oil, right? So even though canola oil is a seed oil, it is unlike other seed oils, like sunflower or soybean oil, in that it's got a More balanced omega 6 3 ratio, and it's actually got monounsaturated fat, not polyunsaturated fat, as its dominant uh thing. The last distinction I want to point out for people Which makes it the healthiest of the so of the seed oil?

Yes, yes. And we'll and we'll come to that and some of the trickery that's in the literature that has So notice that we've got sunflower oil as well, and we've got this other version of sunflower oil called hyolic sunflower. Remember, oleic acid is monounsaturated. So high oleic sunflower oil is just sunflower oil that's been reconfigured so that it's dominant in monounsaturated food. Okay. rather than linoleic acid, the omega-6.

And that can be a little confusing because sometimes foods have sunflower and sometimes they have hyalic sunflower, but people just call it sunflower. And it's important to keep in mind that there's two versions of sunflower. One of them is what you can think of as like strong seed oil version because it's dominant in omega-6s. And the other one is dominant in monounsaturated fat oleic acid, right? That's more like the the olive or the avocado.

So keep in mind all of this. Canola oil, despite being a seed oil, has a profile that looks a lot more like olive or avocado oil, dominant monounsaturated fat. In contrast, To the typical seed oils like sunflower or soybean, which are predominant in omega.

So what we're gonna review here is this paper that just came out. People have talked about it. It's um What do they call it? They call it it's not just a review paper, they call it, you know, it's got some fancy name like this is an amazing review paper. Um I want to A clinician a clinician's guide for trending cardiovascular nutritional controversies in twenty twenty.

So I've got the copy over here on my other screen that you guys can't see. It's called a state of the art review. Right. So this is being Marketed as not a review, but a review that's for physicians, that's state of the art, that's giving you the newest, the best, the most comprehensive view of all of these dietary topics.

And I saw this posted online by some popular accounts and I looked at it and I immediately noticed something was strange. I don't have deep expertise in every single subject in diet nutrition because nobody But they they discover they they talk about a lot of things in here. Um everything from seed oils to medium-chain triglycerides to beef tallow to all sorts of

Nobody has time to necessarily fact check everyone on everything, but I went to the section that I'm familiar with that has to do with CRLs and inflammation, and they made some claims that I found funny. And so let's go to the claim here. So

First, they start out by talking about seed oils a little bit and they give you a description. And one thing I want you to notice is that they give you the typical profile in this review paper of canola, soybean, sunflower, and corn oil. And something should stick out. So notice that canola oil, as I just showed you from other data, is dominant in mono and saturated fat. And it is. That's just the characteristic of canola.

It's a bit of an outlier compared to the other seed oils in the seed oil care category in this regard. Much lower omega-6 content, but it does have. Um, soybean oil, as we said, dominant in those polyunsaturated fats of the omega-6 variety like linoleic acid. But now look at sunflower. Again, this is in the review paper we're going to be critiquing. They're saying sunflower oil, but they're showing you that it's dominant in monounsaturated fat, not polyunsaturated.

Why is that? Well, because this is actually the Hyolaic sunflower version, even though it's labeled in the review just as sunflower. Okay, so just keep that in mind. So here's the claim. Oop, I'm going back. Here's the claim. Here's the claim that they made. So in the paper in the seed oil section on inflammation, they say the healthy fat In canola oil, especially the omega-6 polyunsaturated fats, improve all.

So they're calling out canola oil as an example of a sea oil. They're saying that some of the fats are healthy, and they're specifically citing the omega-6s as the healthy ones in canola oil. And remember we said canola is dominant and monounsaturated, not poly. unlike other seed oils. So keep that in mind. And then furthermore, they say consistent with these benefits, And contrary to popular belief, canola oil and sun and sunflower oil also reduce inflammation.

Similar to olive oil, right? So they're saying a number of things here. They're saying seed oils in general, including canola and sunflower oil, reduce inflammation, despite contrary uh statements that someone like me or Tucker might

And it's similar to olive oil. So what are they doing here? They're saying canola and sunflower oil and olive oil all reduce inflammation. And they're indirectly saying that people out in the world And a bunch of others are wrong to say that seed oils can be inflammatory. Okay, and I've already sort of hinted at what's what's going on here. Sorry, some of this um

I've already hinted uh a little bit at what's going on. They cited in the review paper that sunflower oil is high in monounsaturated fat, and the hyolic version is, but not the normal sunflower. Um so they make these claims and they cite a study. They cite a randomized controlled trial to say that um canola and sunflower. Reduce inflammation like olive oil. So I thought that was funny because I'm familiar with some of this stuff. And so I went to citation 46 and I looked at it.

And I found it doesn't show that. So here is the randomized control trial they cite. This is an Iranian study in an Iranian population. So they're looking at um women, I believe, in Iran who are unhealthy basically. They have insulin resistance, inflammation, oxidative stress. They're like type two diabetic. So it's an unhealthy population.

The other thing to understand is that this is a population, apparently, that has a high level of seed oil consumption. So Iran, I guess, has more seed oil consumption. capita than other places. So they they sort of already consume a lot of things like sunflower oil at baseline. That's the population we're drawing from. High seed oil consumption and they're unhealthy.

So what they're going to do is split them into three groups. They're going to give some of them sunflower oil. That's your baseline or your uh control group. And then they're going to compare that to two other groups, those that give olive oil and those that give canola.

And the basic question they're going to ask is: in this population of Iranian women, compared to those that just keep eating sunflower oil, what happens to things in their body, like various biomarkers they measure, if we give them olive oil or we give them canola oil? Does inflammation go up or down? What happens to insulin resistance and so on and so forth, right? So three groups sunflower, olive, and canola.

In this paper, so on the left, I'm showing you the fatty acid profiles of the oils in the randomized control trial that were cited by this review project. And this matches what I showed you at the beginning, right? Olive oil is our fruit fat. It's got a very olive oil-like profile because it is olive oil after all, high in monounsaturated fat. And relatively low in PUFAs, right? So it's got a high MUFA to PUFA ratio, more monounsaturated fat than polyunators. Canola oil!

Somewhat different, but as I told you previously, right, it's a dominant in monounsaturated fat like olive oil is. It doesn't have as much MUFA as the olive oil, but it still has about twice as much monounsaturated as it does polyunsaturated. What you're not seeing here is that again, as a reminder, canola oil has omega-threes in addition to omega-6s. So those PUFAs are a combination of

Now the sunflower oil they're using here is plain old regular sunflower oil. It is dominant in omega-6 polyunsaturated fatty acids. It's dominant in linoleic acid with way less MUFA content than the other. Now remember, in the review paper that cites this trial, they're telling you that sunflower oil is dominant and mono unsaturated, and the hyolaic version is. But that is not the version in the randomized control trial that that review paper cites, right? So that's a little bit of a

point of confusion. Um I had to go look at the study to to see the Olive oil group, canola oil group, sunflower oil group, the olive and canola oil groups are going to be consuming. They're all starting out with the baseline diet. Some of them are then going to get olive and canola oil, which is going to amount to a decrease in polyunsaturated fatty. So here's how the three groups start. Start. Starting the stuff.

What's kind of interesting is they're all kind of similar across most of these dimensions. They're all a similar age. They all have a similar um macronutrient um intake, waste circumference, BMI. Most of these things are not statistically significant, but three things were uh almost statistically significant at baseline in terms of differences between the groups, including They're monounsaturated and polyunsaturated fat uh energy.

And notice that the sunflower oil group, the group that's going to continue getting sunflower oil, they start out with slightly higher monounsaturated fatty acid content and slightly lower polyunsatural. We can come back to that as a detail, but the main thing I want to point out to you is look what happens to the MUFA and PUFA ratios when they do this intervention, right? So again, they start out at baseline and they give some of them olive, some of them canola, some of them sunflower.

The MUFA intake during the intervention goes up for the olive oil group, it goes up for the canola oil group, and it doesn't change much for the sunflower oil group. If you go back, right, you can see that these numbers are changing. So the olive oil group goes from 9.6 for MUFA percentage up to 24, right? So it's a big increase. And their poof poof consumption goes down. Same pattern for the canola oil.

Right. So again, just to just to be completely redundant here, the olive oil group and the canola oil group are both seeing an increase in MUFA and a decrease in PUFA. But not the sunflower oil group. They're seeing no change in those things effectively. I laid things out on this table to make it more explicit.

Look at the MUFA levels start out at 9.6 for olive. They go up to 24 and change, right? So a huge difference, a huge increase in MUFA for the olive oil and the canola group, right? Twofold increase basically in MUFAs for the canola oil group. No change for sunflower. Same thing in the opposite direction for PUFA intake. Olive oil group way goes way down for PUFA. Canola oil group also goes down.

Sunflower group doesn't change. It actually goes up slightly, but it's a tiny difference, right? So the Mufa Pufa ratio goes way up for the olive oil group. It goes way up for the canola oil group, and it does not change for the sunflower oil group.

So now let's look at the inflammatory marker of the paper, CRP. And we'll talk about that more. Tucker will teach us um something about it. But basically CRP is uh a typical marker of infl inflammation you see in a lot of trials. It gets measured all the time. Olive oil, CRP goes down. Remember, MUFAs went up, PUFAs went down, CRP went down. Canola oil, similar story. PUFAs went down, MUFAs went up, and CRP again goes down.

Sunflower oil. Again, no drop in PUFAs, no change in MUFA PUFA ratio, and CRP doesn't change in a statistically significant fashion. It's about the same.

In the two groups where you dropped your PUFA intake and increased your MUFA Olive and canola oil. You did not see a significant change in the pufa mufa ratio for the sunflower oil group or a drop in the pufa intake at all. And they saw no change, no decrease.

So this is just showing you that the results are significant. There's a significant drop in CRP for olive and canola oil group, not for sunflower. That's what I just said. But again, go back to the review paper that cites this control trial. The review paper says. Contrary to popular belief, canola and sunflower oil reduce inflammation similar to olive oil. That is not what the trial showed.

Sunflower oil did not reduce inflammation because CRP did not go down. It went down for olive and canola oil. And indeed, canola oil is a seed oil. But remember, canola oil does not have a predominance of omega-6 linoleic acid like sunflower oil. It's got a much higher uh ratio of MUFA to Pufa. It's got more oleic acid and relatively lower omega-6 with a more balanced 6 3 ratio.

So what's effectively happening in this paper is they are saying seed oils reduce inflammation because canola oil reduced CRP in a control trial compared to sunflower oil. Right? Do you see what's happening here? Um it's it's not what it seems in this review page. Again, sunflower oil is what they used in the root control trial. It has high linoleic acid. Canola oil does not. It has much lower linoleic acid. It's got a more olive oil-like profile, dominant oleic acid.

But that result was cited as the evidence to make the false statement that the literature there is showing that seed oils, sunflower, and uh canola are reducing inflammation. But that's not what it showed at all. It showed that olive and canola did. And despite the fact that canola is a seed oil, and we call it that in English, it's got a fatty acid profile that looks way different than the sunflower oil.

And they didn't even cite the correct sunflower oil profile in the review paper, they showed you the Hyolade. So that's that's that's very weird. Um, I just I decided to look up one more RCT from the same group in Iran, just to show you guys one more example. And the point I'm making here is that this is not an isolated incident. If you go look at all of the literature here, you start to see patterns like this over and over again.

So look at this other trial. I believe this is also an Iranian population. And this is another example where they're doing canola versus olive versus sunflower. Look at the omega-6-3 ratio in sunflower compared to canola compared to olive. Canola oil actually has a more balanced, more favorable six three ratio than even olive oil. The sunflower oil ratio is off the charts because it's really high in omega-6 and has almost no omega-three.

And again, they find in this paper that basically like the numbers move in the direction that we would say is good for canola oil, but not for sunflower oil. But because canola oil is called a seed oil. This idea that seed oils can lead to these improvements kind of gets laundered in the literature, but they're comparing something with a very different fatty acid profile from a typical seed oil like sunflower.

Right. If you look at the fatty acid ratios, again, the canola looks a lot more like olive. And in this paper, as I just said a moment ago, it's actually got a more balanced omega-6-3 ratio than even olive. Um, but I also want to talk a little bit about the basic biology here. I think I always like to think about things, I you know, I I sort of think about the truth as being triangulated from multiple angles.

What I just did was almost like a top-down exercise. I went to the review, I looked up the paper it cited, and I like looked at the evidence from that angle. And then I kind of realized that these things weren't adding up in the way that they were telling me in the review paper. Um, but the other thing that you should always think about is like, what are the mechanics of the biology involved here? Um, does what we know from basic research and how like the mechanisms here actually work in cells?

Is that also squaring with what they're telling me in the literature? And I think that takes us to um something Tucker can tell us about, which is what is CRP? What is this inflammatory marker and how does it actually work? And and that's also a very telling thing. Um, so Tucker, I don't know if you want to come in here and just talk a little bit about CRP and and what the mechanics of this inflammatory biomarker actually are.

Oh, do I have to add you to the stage? Yeah, we do. Okay, there you go. Okay, here we go. Can't unmute guests before they choose to mute. Sarah, uh sorry, I muted myself. Um sorry, I kicked myself into backstage by mistake before I clicked the wrong button. Um so CRP is interesting. It's also it's often heard it's often described as an inflammatory mark.

That's not like a lot of these other inflammatory markers, that's not really correct, right? So when you have um And CRP is a reaction to either threat or a dam or damage in the So the threat could be a bacterial infection. the damage could be some kind of a wound. Uh ironically, the now CRP is also often correlated with cardiovascular disease. It's considered to be a primary risk factor for cardiovascular. Can you guess what the easiest way to raise your CRP is?

You go for a long run. I've done it. I ran a half marathon. I went to get blood work from my doctor the next day and the f and a couple days later he called me up in a complete panic because my CRP levels were through the roof. And he wasn't aware that It's a it's a you know. When you Exercise, you do damage to your body, right? Right. Right. And your body gets stronger by reacting to that damage. Yeah.

Got it. So it's like a f it's a physical damage, physical inflammation thing. So like when I go to the gym and I've been I've been lifting a lot the last couple months, I'm elevating my CRP if I go lift a lot. Probably, yeah, exactly. Exactly. So it's not per se a bad thing, right? So what does CRP react to? It reacts to molecular patterns, what are known as danger-associated molecular patterns or pathogen-associated molecular patterns.

So that could be a bacteria or whatever, but it can also be um An oxidized lipid. So Oxidized lipids are very important in the body. They're important signaling models, but in excess they can be quite poisonous, right? That's why we don't eat rancid fats, right? The definition of a rancid fat is basically a fat with oxidized polyunsaturated fatty acids. Got it. So if I go to the beach and I smell like a gross dead fish.

Is rancid omega-3 fat. That is the signature smell of a rancid fat, is it smells like a dead fish. Right. Yes. Okay. And that's why we don't fry our uh potato chips in fish. Because it would smell like that and nobody would ever eat. Um so what CRP does rather than now your body has a couple of reactions to something like this, right? Say a bacteria or a oxidized. Say for instance on an LDL molecu on an LDL molecule.

LDL is a packet of fats and cholesterol wrapped up in a protein molecule so that it can be delivered around the body, right? Um the primary lipids in an LDL particle are Typically in somebody eating the modern diet, uh polyunsaturated fats, linoleic acid, is the number one, right? Those are also the fats that are most susceptible to oxidation in the body. So when your body detects a Mm-hmm. uh bacteria or an oxidized fat, it can react in one of two ways.

It can either send a white blood cell over to eat it, right? Uh a macrophage means large eater. Literally the word macro is large, phage means to eat. Um and it will come over and it will snarfle up the um you know, the bacteria or the oxidized lipid. Um CRP is kind of an alternative pathway. CRP will come along and attach to that pattern on the bacteria or on, say, an oxidized LDA.

And that will activate something called the complement pathway, which is an innate immune system that will dispose of this. You know, suspected pathogen or damage indicator without having to call in the macrophages. Right. So it's some it's basically a less costly way of dealing with this stuff. Yeah. And Tucker, like before like we get into some of some more detail. Like if we just think about this in in basic common sense terms.

We're basically saying that the body is treating oxidized lipids like this the same way that it treats bacteria. It wants to get rid of these things. It doesn't want them there for some reason. That's exactly right. That's exactly right. And there are Uh antibodies in the body that will react to either a single antibody that will react to either a pathogen like staphylococcus. To an oxidized lipid.

in LDL, right? The exact same antibody can't distinguish between the two. Um So CRP in this case is a direct marker. of the presence of oxidized lipids, but only oxidized polyunsaturated. Now it's important to know something about these lipids when you're consuming them, right? Typical seed oil has 400 times the rancid fats, the oxidized lipids. than per unit volume, then say native LDL, right? Normal LDL.

So when you and that's that is a fresh seed oil, say fresh corn oil right out of the factory, the best it's ever gonna be in its life. It's not rancid, it's not even oxidized yet. It is rancid. It's already rancid. It's got 400 times. the number of oxidized lipids that a part of your body has.

Got it. So when we talk about like sometimes people are like, Okay, there's fresh seed oils, but then I could cook with it or deep fry it, uh deep fried my starch at McDonald's in it. You're saying that even when it's Fresh scare quotes right out right out of the factory, there's already ransomed oil. It's already rancid, yes. And in fact, interestingly enough, people also say that you're better off getting something like a cold press. Organic oil.

Well, it turns out that the standard for rancidity in a cold-pressed oil is fifty percent higher than in a refined oil. Right. Fifty percent higher. And why is that? Because the part of the refining process is to remove the rancid molecule. It's actually a way of making it safer. Right, right. So um so yes, any seed oil that you eat is going to have this reaction is going to cause this reaction in your body where it doesn't like these rancid lipids floating around.

Okay, that's not even an exaggeration. Um and You know, but your body, like a lot of things, if you uh if it sees, you know, so Oops. You've got your arm. Next pack. Okay. No, it's a camera thing. Um so like a lot of other things, your body is going if you want to get an accurate understanding of what the CRP in your body

You should be taking your CRP in a can. You shouldn't be taking it right after you go for a run, for instance, like I did. You should be taking it when you're on a low seed oil diet. That would be an appropriate benefit.

Now, when you look at these, there was a review uh paper that came out a number of years ago that people always sight to me to claim that seed oils have no influent influence on inflammation in the body. But what the paper says is that however A rapid increase in linoleic acid will cause a increase in CRP. Which makes perfect sense because CRP is literally a marker for rancid lift.

Right. So we're saying that this is how the biology is set up. CRP is literally sticking to these rancid lipids. That's part of what it does and why it exists. Right. The body wants to get rid of these things just as it wants to get rid of bacteria if you have an infection. And and and I mean one of the other things to add here too that I think is sort of implied is um the population at large is already consuming a high omega-6 diet.

So d does that affect at all like how we think about the literature and like which direction the markers like CRP go, Tucker? Like if you've already got a population that's eating a lot of things that are going to react to TRP, um what like, does that affect the way we interpret these things? Well it ought to, but it often doesn't. So we do have It's one extremely well-studied population.

didn't at the time they were well studied eat uh much in the way of seed oils. They were just getting introduced into their uh population. Now, as I said, CRP is uh correlated with cardiovascular. in an industrial population, eating a lot of seed oils, right? In this uh Amazonian tribe, the uh Chimane, I've heard them pronounced. I'm not quite sure if that's correct, but They don't eat seed oils, but they have extremely high CRP levels, but they don't get cardiovascular.

Right. They've been described in the medical literature as the lowest levels of cardiovascular disease ever seen in a human body. But again, they have high CRP. So why is that? They have a high inflammatory marker, and we're often told that inflammation causes cardiovascular disease, but these people don't get it. Well, the reason that they have high levels of CRP is'cause they have a high infectious birth.

They live in the Amazon, they don't have good hygiene, they're drinking, you know whatever the local water is that's not filtered or Your CRP is going up and it's reacting with bacteria and stuff in in their body. Exactly. But it's not leading to cardiovascular. So CRP itself and inflammation itself are not bad things. They're not correlated with cardiovascular disease, except in populations that eat a lot of Eat a high industrial diet and in my book the definition of that is a lot of seed.

Yeah, yeah. And so Tucker, like uh this diagram from this paper you sent me, which talks about some of this stuff, it's just got like a cartoon of uh uh a typical dying cell. So a cell in your body that's dying for some reason. We were just talking about CRP. So C RP is right here. Talk about that and talk about like what like what are all these other things on this dying cell, MDA, four H and E? What are these things and where do they come from?

Boy, that's that's one of the best softballs ever. Okay. Let's start in the upper. If you could uh I don't think I can point at the screen. I can put it. But if you can start in the upper right hand corner, there's something called EO6. EO six is that antibody I just described that will react to either staph or to oxidized liquid.

Okay. Um, it's commonly used to track uh oxidative stress and cardiovascular disease. It was discovered by these scientists, uh Joseph Steinberg, uh Whitstam, I can't remember the next Whitstam's first name, and um it has been written about extensively by uh Oh goodness, a Greeks a Greek cardio cardiovascular researcher, uh Timikis.

Uh Sam Samikis has written a lot about this, right? This is one of the standard diagnostic tools used for oxidative stress. So EO6 right there is connected to PC, right? PC is phosphodidylcholine. That is a uh phospholipid, like you would find in an LDL particle. It's a standard part of cell membranes. And a phospholipid typically has two fats attached to it, right? So think of it as triglyceride light, right?

It in the body almost always has a saturated fat at the first position, and it always almost always has an unsaturated fat at the second position. That unsaturated fat can be either something like oleic acid or something like lamin. When that unsaturated fat gets oxidized, and it's important to note that one of the nice things about oleic acid and the monounsaturated fats is they are much, they are nearly impervious to oxidative damage. So when that fat in that second position gets oxidized.

All of a sudden, it becomes a trigger for EO6 or CRP to come and attach to it and signal to the body's immune system that this thing needs to be damaged. Okay. Now the next piece, the next to the left of that, that little flowery looking thing, is CRP, as we've discussed, and they show it there attached to another oxidized phospholus. I don't know what LR zero one is, but LR zero one is connected to aux C L. So what is oxyl? OxyL is oxidized cardio.

Cardiolipin is a molecule that's only found inside the mitochondria. It is part of the electron transport chain. It is essential to the function of the electron transport chain. Your mitochondria can't produce energy without cardioliphen. Cardiolipin, again, is a fat that your body prefers to have either a monounsaturated or a polyunsaturated fat. And in certain organs like the heart, it's usually linolic acid.

Now, unfortunately, when you have two linoleic acids next to each other in a cardiolipin, it has cardiolipin has four fats. Um, it's sort of like a double phospholipid. Yeah. Um when you have two linoleic acids next to each other, they become very subject to oxidizing. When they get oxidized, they become one of these danger associated molecular. They cause apoptosis. They directly trigger apoptosis, oxidized linlac acid.

That too much of it will trigger a messy process called necrosis, which is what this is about. Where the cell in apoptosis, your macrophages are gonna come over and eat the cell and it'll go away in a neat, orderly fashion. Um this is sort of like setting a bomb off in a cell. It's going to start it's going to die, it's going to burst, and it's going to spread all these oxidized lipids all over your body.

And you can see that almost now if we go down to that little uh green triangle on the left hand side. You can see four H N E. Four H N E is another oxidized lipid metabolism. four hydroxynonol. This is my favorite thing to track because it can only be made from omega six fat. And you will see there is an another natural uh part of your body's immune system that is coming over to try and get rid of that. Right now, down at the bottom, uh the red Slice of pie.

has a bunch of things called MDA. MDA is malondialdehyde. Now, malondialdehyde can be made from either omega-3 fats or omega-6 fats in the body. It generally There's conflicting literature on this, but from what what I've read, uh it is generally made from omega-6 fats in practice in the body. But it's really interesting because the common text for MDA is something called the T-Bars uh test.

And depending on how that test is done, it may react to MDA or five times as likely it's reacting directly to oxidized linoleic acid. So that big red slice down at the bottom may be either MDA from omega-6 or just a simple peroxidized linoleic acid, which is also highly toxic. So basically every single thing coming out of uh it's also got C E P, just to be fair, that pink slice. I don't know what that is. I can't really make out the uh

Yeah, it's it's binding to a toll like receptor on a phagocyte. Um I don't know what it is specifically either. Okay, so one, two Three, four, five out of the seven. components that are stimulating this uh immune reaction are omega oxidized omega-6 metabolites.

So like literally the body has lots of different things it can recognize That come from oxidized omega-6 fatty acids, and the body recognizes them in order to get rid of them. Not unlike it would recognize an infectious bacteria that you want to clear out. Exactly. And now why why would that be the case? So look at oxidized cardiolipin. Cardiolipin is only found in bacteria, right? Your mitochondria are this bacteria that we're in a symbiotic relationship.

So it is EO6 will bind to either the uh phosphodylcholine or to oxyl because both of them are Pathogen associated molecules. It is cardiolym in particular is a red flag being waved in front of your immune system saying, You've got bacteria. You better do something about it. Right. Now the problem here is. There's a

A phenomenon that they discuss in cardiology called sterile inflammation. What's sterile inflammation? It's inflammation without a pathogen, right? There are no bacteria causing the inflammation and sterile. But it's happening. And now you know why it's happening, because these omega-six fats in our body are oxidizing, becoming rancid, and your body is reacting as if you have a bacterial.

Yeah. Yeah. So it's like if you understand the basic biology here, then you realize like, oh, this thing that the clinical researchers keep measuring, like CRP. Think about what it's doing here, what Tucker just told you. Like it is reacting to oxidized omega-6 polyunsaturated fatty acid. And like all of these things are literally markers of a dying cell. Something's wrong with the cell. It's dying. It's gonna be bad. It's gonna be bad news. And the body wants to get rid of it.

I mean it I mean it should make intuitive sense to people, I think. Like it's it's pretty it makes intuitive sense to me. Like the body wants to get rid of these things. Yeah, that's exact that's exactly right. That's exactly right. And you know, I mean You know, oxidized cardiolipin will directly kill a cell. It'll cause apoptosis because it's a marker of something going dramatically wrong inside. Um I just published a paper on my blog looking at uh

a cancer model where they demonstrated that increasing the consumption of I think they use safflower oil, which is very similar to the sunflower oil you were discussing, and that it's very high in omega six. Yeah. And with uh high consumption of safflower oil or incubating um a type of immune cell called a killer T cell, a C D eight cell. uh will cause an increase in linoleic acid inside the mitochondria, a concentration in the cardiapid

oxidation will result and that will cause in the death of your immune cells. So you could think of it as acquired immune deficiency syndrome, right? AIDS. caused by seed oils, where you're breaking down the immune cells in your body and preventing them from being able to remove tumors, right? One of the CD8 cells' primary jobs is attacking cancer cells. Uh so Tucker, like We went through this paper, you know, just to reiterate for people, right? The claim in the review.

was the omega 6s are healthy. Seed oils like canola oil and sunflower oil reduce inflammation. We went through this paper and we saw, well, wait a minute. No, no, no, no. Sunflower oil did not reduce the inflammatory marker CRP, only olive and oil cola oil. But canola oil has a fatty acid profile that's lower in omega-sixes than sunflower and looks a lot more like olive oil.

And actually the PUFA intake of the olive and the canola oil groups went down. So what do you think is going on here? Like a lot of names were on this review paper. These are high profile people. And like did they Like what one hypothesis would be that they didn't actually read the citation and its sloppy scholarship. They forgot or never knew what the paper actually showed. Another interpretation might be that they know what it shows, but there's

some kind of trickery going on here. Like what do you make of this? Why? I mean, this is a again. They call it a state of the art review. Like this went through some kind of review process, presumably. Why Why does the English printed in the review not match what the trial showed? And and how do you how do you interpret? First thing to always do is read the author read the list of the authors. And One of the authors is one of my

Can't really call him favorite authors. Darius Mozifarian. He's the he's at Tufts. I can't keep quite he keeps changing his title at Tufts. I can't quite what the latest title is. He was Dean of the School of Nutrition at one point. Um, and then he was like Dean of Scientific Policy. I don't know what that means. Um Is this the same Tucker, is this the same tough school of nutrition that like came out with that algorithm that said like fruit loops was better than beef or something like that?

Yes, that was his algorithm. Okay. Got it. Yeah. Yeah. Right. Yeah, the Fruit Loops guy. That's right. Okay. He's also the guy we should note He's the guy, you know, there was that article in I think it was the Atlantic about is ice ice cream actually healthy for you? Yeah, yeah. And they talked about this uh piece of epidemiology where they looked at dairy fat and they said that uh yogurt is

You know, yogurt's really good for you, even though it's high in fat. And then if you you know, that's what the abstract said. If you burrow down into the text of the paper. It actually says yogurt or ice cream. Right. So the headline results, they're marketing the yogurt and then just sort of like papering over the fact that you saw the same result.

For ice cream, right. But they didn't make a big deal out of that'cause you know, they can't be telling people to eat ice cream'cause it's good for you. By the way, I eat ice cream. Um so they asked Mose Farion about it. And he said, well, yeah, that's that's right. It wasn't exactly accurate the way that we put it. Not accurate in my book is You know, you knew you had a result you didn't like, so you buried it in the

Yeah. And your top line was yogurt's good for you. Eat lots of yogurt. And of course, what everybody's gonna do in practice is go out and eat full fat or sorry, zero fat yogurt, right? Right. Uh, which is not as beneficial, folks. Uh full fat dairy is what you oughta be eating, not low fat stuff,'cause they pump the low fat stuff full of starch and sugar to make it taste better. So so Tucker, I so So let's go, let's go. So is is Dr. Mozafarian up to no good on this paper?

Yeah, let's let's be as generous as possible. I don't like the purpose of this isn't to like call someone out, even though that's basically what we're doing. But like let's be we're we're gonna be as generous as possible. Like We're showing you this weirdness in this paper. Tucker's saying there's other weirdness in how they framed and used language in this other paper about ice cream and yogurt. Like, is this is this sloppiness or is something else going on? And how do we know?

So let's one of the one of the interesting things to do in these papers is always to look at who funded it and what conflicts of interest they have. So here's Dr. Mozafarian. He is the member doctor Mo Zuferian is the member of the scientific advisory board of Brightseed, Calibrate, Filtrosine, Instacart Health, January Inc., and Wonder Health. I don't know what any of those are. Has done scientific consulting from for Amazon Health. They have a lot of types of

And Google Health has Equity and Human Co, whatever that is, and has received chapter royalties from up to date. And I don't know what that is either. But oddly enough, what he doesn't mention is a little project he has going over at Tufts called Um What is force, you might add? Tab up. I just added onto the uh screen that I'll show people. Uh this is the conflict of interest section from the review paper that that I went through and and unpacked after looking into its citation.

And you know, you can look through that. Um, but yeah, Tucker, continue with this thread. What is this guy connected to? Yeah, so I just gotta did I send have like 300 tabs open on my screen. Um Uh can I share this? Um I think so. Can I try to share this? Yeah, try try to share it. Let me stop sharing my screen. Do you see um there's a rectangular icon with a plus sign in it? Do you see that? Yep. Yep. Oh here it is. So it's letting me share just one. Yeah, it's like one tab at a time.

Okay. There we go. Oh, this is the what's known as force. You can see from the URL up top. It's at top. Moza Farian is Dean of Nutrition, or was at one point. I don't know what he's doing now. Um Right. So What is force? Yeah, no, I actually don't know. I haven't looked into this yet. What is it?

Our goal is to understand the relationships between fatty acids from our diet and metabolic processes measured using biomarkers on chronic disease outcomes. Okay, that sounds pretty innocuous. Um You will note The our consortium is a collaborative effort with administrative coerce coordination at Tufts University's Friedman School of Nutrition and Science and Policy, Chair D. Mosef Harry.

So this is his group, right? And it's got some of the biggest names in Nutrition. Uh Walter Willett is in here. There's a whole bunch of other people. I won't go through all of them right now. So let's go look at their funding support. Oh. Funding for the Omega-6 fatty acids project. It's funded by an unrestricted grant from Unilever.

Unilever used to be the biggest producer of seed oils in the world, and they sold that business, but they are now one of the biggest producers of ultra processed foods containing large numbers of seed oils. And they have long been a backer of Mozaferian. I mean, going back fifteen, twenty years that I've noticed. Isn't that a bit of a conflict of in interest? See, so wait, are wait, did he not declare that conflict in the review paper we went through that had the weird citation?

That's right. He neglected to mention it. Well, so he maybe he forgot to put it in there just like all those other typos got in there. Maybe they didn't read like so either he's just completely, completely sloppy in his scholarship in all of these ways, or Well, let's there's I did another post years ago on uh that was I think f also funded by Unilever where they were looking at different uh They're not going to be able to do that. Screen. Um

So they were looking at foods that cause obesity. It's one of my favorite papers, right? Different foods that cause obesity. And what they found was that the most obesogenic food was Okay. But they sort of split the result out. They added they had fried potato french fries. They had uh potato chips. And then they had uh I think it was like boiled potatoes or something. And they split.

fried potatoes into two parts and then added in boiled potatoes which were not obesogenic. So what that did was have the effect of making potatoes look much less obesogenic. Now the difference You know. As Dean of the School of Nutrition at Tufts, I'm sure Dr. Mosefarian knows the difference between a boiled potato and a French fry, right? The ingredients of a boiled potato are potatoes and salt. Yeah. Yeah.

Now we're gonna get really complicated here. We're gonna go up fifty percent in the ingredient list. The ingredients in a French fried potato are potatoes. And Cetoid. Right. And one of the things that potatoes do when you fry them is they absorb the seed oils, they absorb the fat. Okay. So What his paper, if you went and looked at the data, without looking at his charts that kind of did their best to hide this relationship similar to this one.

you see that the overwhelmingly most obesogenic food by like a factor of six or seven five or sevenfold. Potatoes fried in seed oils. Nothing else came even clear. Right. And now two different scientists called them out on this. And one said one was uh

His name slipped my mind, but he did the twenty twelve Alfheim paper that showed that linoleic acid, the fat and seed oils, directly causes obesity. He called them out and said, Hey, wait a minute. You know, the other explanation is that the linoleic acid in the potatoes is what's causing

This obesity reaction, which is what we see in our animal model. Right. The paper we're about to publish next year shows that. Right. And then another Yeah, so for those who don't know, we already have independent evidence from animal research that linoleic acid itself, linoleic acid per se, is a besogenic. So it all of that literature fits. French fries being obesogenic because it's potatoes fried in linolic acid, basically.

Right. So then some of the other somebody else wrote a letter in, I forget his name. Um Uh and he pointed out, well, maybe we should be looking at added fats. You know, Dr. Mozifarian replied, Well, added fats aren't a factor in french fries. Back to the ingredient list. Yeah. Right. There are only three ingredients and one of them's an added fat. Yeah.

So we're clearly adding fats into this. Now what's really interesting is if you look at other potatoes with added fats, like mashed potatoes, which is typically dairy fat and butter, they're not obesogenic. Right? No hint of them being ob obesogenic. All the other potatoes, not obesogenic, only fried potatoes, fried and seeds. We went to great lengths in that paper and afterward. Yeah. Oops, we made a mistake. Right. Oops, we made a mistake and it's been pointed out to us twice now. Right.

Obfuscate the facts. Yeah, so so there's no correction of the record or anything like that. You know, people call this out, not people like me and Tucker doing a live stream either, like, you know, other scientists in these fields. And if you've ever put together papers like this, you know how much work it is and you know how much attention needs to be paid to this. Th it looks like they're trying to obfuscate things. It doesn't look like One important distinction between that paper and

in this paper is in the mo the twenty eleven paper, the potato paper, Mozafarian was the first author. Yeah. Which meant that he did most of the work. He wrote he probably basically wrote it himself with some input from other people, but it wasn't like he just signed off on it because he's a co. Exactly. Yeah. Exactly. So now that same group turned around, I think Mozarian made a blessed.

But that same group, some of the same authors, the same senior authors, turned around a couple of years ago and did a paper showing a link between um Diabetes and sea oils. They said that uh Omega-6 intake in the diet is directly associated with uh diabetes. Then we adjusted it. We first adjusted it for other fats, and I can't think of any reason why you would adjust one fat intake for other fat intakes to get rid of a signal.

But then here's the big one. They made the signal go away by adjusting it for obesity. Now think about that for a minute. If they know seed oils cause obesity and they adjust seed oils by obesity to get rid of the link between seed oil consumption and diabetes, which they announce in their paper is their finding. Right. Right. But they can adjust it away. That's basically

fraud. Yeah. It's like it's like if you it's almost like if you did a study on cigarettes and like you were looking at all the things that were correlated with cigarettes um smoking and and you know all the different outcomes and you're like, well we adjusted for you know lung Well, no, because lung cancer is the outcome. The the analogy I already I always use here is imagine that you're doing a study where you're trying to correlate uh gunshots with death and you adjust death by bleeding.

And you find out that oh look, if we adjust death by bleeding, then gunshots that hit people aren't dangerous anymore. Um so so so like this kind of I guess one of the sort of if we step back, a lesson here is Oh, and by the way, the diabetes paper that I just talked about was funded by Unilever and co-written by a couple of Unilever Unilever authors.

Yeah, yeah. So I mean it it's always helpful to follow the money. I don't like to just automatically dismiss things because there's a conflict. I mean, that's you know, it's always good to be aware of these things. But you know, Tucker, we're pointing out for people like all of this trickery that can happen. You can use statistics to manipulate results to make it look one way. You can also use language. You can just say in English.

that the literature shows blank and there's a citation. And most people aren't going to go check the citation. That's what we did earlier. That's what I walked people through. And so there's there's all of these things, these tricks that can happen.

And you know, we're talking about a review paper here. This is at the top of the so-called hierarchy of evidence, right? You've got in vitro studies, you've got animal research, observational, randomized control trials, then you've got the reviews of all. True. The things, you know, this is like w what's considered. They're saying this is a clinician's guide. Yeah. So every doctor should have this on his desk.

Yeah. And the doctors don't doctors in practice treating people in the clinic, they don't have time to go through all the citations and check the statistics and do all of this stuff. And I just Folks, we did this for one citation. This is one paper and we've talked about a few more. Like, think about how much time it would take to go in and fact check all of the claims in a paper like this that has dozens or even a hundred plus citations.

A physician doesn't have time to do that. They have to take these people at their word. That's how this whole thing is set up to operate. Right. That's exactly right. Um Yeah, so Mosefarian, up to his old tricks, as far as I'm concerned. Um, I mean, I could see, you know, in their defense, I could see. How the Uh sunflower results.

You know, that could be an honest mistake. They went to the USDA database and they got Sunflower. Right. And the USDA database, as it happens, has a You mean you mean the table where they show you they show you the hyolitic sunflower profile as opposed to the sunflower? Right, exactly. Right. But then the citation that says it explicitly says canola and sunflower drop inflammation like olive oil. Citation forty six. You check citation forty six, not what it shows. That's not what it should.

Yeah. Right. Which which makes you think they're just They're not up they're they're not on the up and up. Um something's a little messy in there. Um anything else that you wanna talk about? Uh you know, I don't know how much time you have, but sh is there anything else we should go over related to this stuff? Um Any questions out there from people? But I don't know. Like so what are the big takeaways here? Yeah. Um yeah, just comments. I don't see any questions.

Yeah, I mean basically, you know, bottom line, just because something's printed in the literature doesn't mean you can take it to the bank. Not by any means. That's right. Yeah. And you gotta you gotta do your homework. You gotta fact check these guys. And I mean, my background isn't in I don't have a background as a researcher like you do. I don't have a PhD. My background was in fraud detection on Wall Street. So this is exactly what we would do with the office.

We would have somebody come in and we would try and find out if they were up to no good. So, you know, following the footmark, you know, somebody had a portfolio of security. We would go look at the security, download the prospectus, read all the details, find out what the quality of that security was. This saved our company, right? We were uh I was one of the first guys on Wall Street to raise a red flag back in two thousand eight and say, Hey, these mortgages these guys are buying are jumped.

That's so that's so funny, Tucker, because I don't I didn't really know that about you. And when I was like preparing for this, I was thinking to myself of the movie The Big Short. Where like the whole point of the Michael Burry part is he was the only guy that was like autistic enough to go in and look at like the actual mortgages and they're like, You actually went in and looked at all of them? Nobody does that. And it's like

Yeah, well I did. I did. I used to my my b one of my bosses was the chief risk officer of the company, and I used to go harass him about what junk call is. Yeah. Yeah. Um and you know, sure enough. We managed to get out early and didn't go out of business like a lot of people, and we made quite a lot of money by going in the other direction. Yeah.

Big short, it's interesting because the big short all happened after we got out of that trade. Um that was kind of the late game, but we didn't talk to Michael Lewis because he's a journalist. Yeah. Um okay. Uh well Tucker, I mean, thanks for your time. Uh first live stream. I just want to do this um because uh you know I I just I just

stumbled on this review the other day. I you know fact checked the one citation. It was weird. I know that you know about some of this stuff and could contribute to it. Um but yeah, I just want to point out to people like there's so much out there where people are like,

On this topic, there's other topics we could talk about, but on the seed oil topic and on the subtopic of inflammation, they'll be like, no, no, no. The reviews say this is true. So what you're saying can't be true. And it's like you you people are reading the reviews and taking them at their word.

And I understand that not everyone has time to go in and do this level of scrutiny. Um, but you cannot take all these people at their word because this is what you are going to find when you And certainly, you know, there's let's not throw the baby out with the bath water here, not all research. No, no. Crooked. Yeah. Um

There are lots of people who are doing genuinely trying to do good work. Often a lot of these mistakes are potentially innocent. You know, I mean, often you'll read in these the beginning of these papers, you know, it's well known that linoleic acid reduces heart disease. I mean

The paper I was talking about before where they looked at how linoleic acid damages your immune system and causes tumors to go crazy in your body. They said that. I actually think they were doing it rather ironically because then they turned around and showed how bad they are for you. I've seen that before too.

Right. It's it's sort of like it's it's I mean, it's like a setup and then a punchline. You often you'll set up and be like, Look, but then we found the surprising result that you know, that goes against what this lyric. Yeah. Right, exactly. And but then there are, you know, there are other cases. There's one paper that a colleague of mine, uh, Rafael

Sirti is his last name? Rafi. Rafi, I apologize. Um, I'm not ref not being very good with names tonight. He found a paper where they Talked about how saturated fat caused inflammation. Right. And the examples, what they use. to stimulate the inflammatory markers in people was a McDonald's Value meal, right? Right, right, right. Yeah. Yeah. Which which does the French? French fries. Right, right, right. And but Does indeed have saturated fat. Ah but then when you went and looked at the right.

Yeah. When you went and looked at when you did what Nick did here and drilled down and you looked at the table in the I think it was in a supplementary data table showing the fatty acid composition of the McDonald's. Valumeal It was, they said it was 100% saturated fat. Even hamburger is not 100% saturated fat. That's like not a thing. Yeah. And that's just, you know, forgetting about the French fries, which are going to be mostly polyunsaturated fats because of the seed oil.

Actually McDonald's. But that's another one. But I mean that was just flagrant misrepresentation of their find of their evidence to come to a predetermined finding. Yeah. Talk about threatening. Yeah, it's frustrating. Um Nick's doing the big side there.

Yeah, yeah. It's a it's a mess. I mean, that's just why at the end of the day, you can't really know unless unless you check or I mean you have to place your faith in someone, I guess. And uh certainly can't blame a physician for having to read reviews like this and take them at their word.

But the fact that the reviews get put together in this way by these types of people, not all of them are like this, as you pointed out rightly, but like this is a mate, this is a major paper. This is like literally, as you said, Tucker, this is this was made. As a guide for physicians, The J J A C C the Journal of the American College of Cardiology. Yeah. Is what w where it was published. So that's presenting it as, you know, this is what we know, this is what we

This is the settled science. Yeah, this is the best. Right. And it's just it's nonsense. It's misr it's they're misrepresenting the science in this paper, as Nick has demonstrated. Um well Tucker, thank you, my friend. Uh I don't want to take too much more of your time. Um uh This is really fun.

Yeah, this was fun. I tried tried a live stream, decided I would try it. Maybe we'll do another one at some point. Folks can can let us know what you thought and if this was helpful. I love following you, Tucker. You've you're always uh you you've definitely got a background with Front. Yeah, one can tell. And it's great, it's it's great to have an ally in this stuff because you're doing good work. I'm learning a lot of stuff. I just I just listened to your Uh

podcast with uh Doug Wallace uh while I was driving around today. Um and somebody just had a question. This is this is recorded? You're recording this? Yeah, yeah, this will go up on YouTube like a normal YouTube video. Okay, that's great. Um, I would I'd like your permission if you could send me a file to put this up on my channel as well to give it more visibility. Yes.

Yes, I will do that. I believe all that stuff is possible. I will find out in a moment when I end. But um yeah, as far as I know, this will go up on my channel and then I'll send you. Okay, that's great. Thanks, Nick. This is terrific. All right. Lot of fun. Bye everyone.

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