S4:E7 - The Great Cholesterol Myth - Jonny Bowden on the Wolfs Den

Sorry, I said how you going? It's, it's so great to speak to you and have you on and, and all that good stuff. It's— I think the last time we spoke was years, 2012.

Yes, it was. It really that long?

I think it was. I think it was actually that long. Um, so it's— yeah, it's an absolute pleasure to have you on. I've already got some— there's going to be more people joining us as we go along today. Um, oh, I, I, I— we've got— so just so you know, we've got our Enterprise crew on, uh, some of our Enterprise trainers. We're going to have our Wolfpackers on as well. Um, so it'll be, it'll be quite the call. I, um, I introduce you to everyone, and yesterday I was telling my team about, you know, uh, you and your work. I introduce you as the John— as the, as the Michael Jordan of nutrition. Um, and, and I do what?

Michael Jordan of nutrition? Wow, man, thank you. And I feel like I'm not screened in the camera right. I don't know why. Is it a— it seems like a smaller screen.

How's that?

Is that better? Yeah, it's fine.

We can see you, we can see you, we can hear you. Um, can you hear me okay?

I hear you fine.

Yeah, yeah, perfect. Um, for the folks in the chat, if you just want to give us a thumbs up if If you all can hear us, just give us a yes. Awesome. Alrighty. So, welcome, welcome, Jonny. Always great to chat with you. One of my absolute most favorite people to speak to in the world of nutrition. As I said, I refer to you as the Michael Jordan of nutrition. You've been doing this, you've been blogging since 2001. That's, you know, 19 years and counting. You've authored 15 bestselling books. You've spoken around the world. You've no doubt changed countless lives. But, you know, one of the things I just want to share before we get rocking and rolling, you're extremely generous. And I remember it was 2008 where you— I wrote my first ebook, The Truth About Supplements, and I sent it to you. I was quite young and brashly naive and didn't really know how the world worked. And I just thought I was going to send it to Jonny about it. And you got back to me and you wrote, you gave me words of encouragement. And, you know, I'll be forever— that's one of the highlights and really gave me a boost, you know, to continue on the path. So, so I had forgotten about that.

Thank you so much. It's very kind of you to mention and to know, to let me know that that mattered. I appreciate it.

Yeah, it really did. Even our interview. So for me, as I said, I regard you as, as Michael Jordan. You are Michael Jordan. What you are to— what he is to basketball, you are to nutrition in my eyes. So, yeah, I do have to admit one thing. In The Truth About Supplements, I have taken it offline because of the fact that it's just terribly outdated. And obviously you're going to have your stamp of forward. I want it to be at a certain level, but I am working on another book now, so maybe you'll hear from me for another foreword some months. Yeah, so since last time we spoke, it was 2012, a lot has happened in, you know, a lot happened the last year with this crazy, crazy world. And I want to preface this podcast is going to be quite dynamic. We've got— I've got a lot of questions about different topics and these kind of things. We are going to focus on cholesterol following your book, which is being rereleased and updated. We've got folks on the line.

Let me grab it because I don't think it's showing up in the back. So shameless plug, this is the book.

Absolutely. Absolutely. Plug away. And it's been— so it was first released 2012, was it? Am I getting those dates right?

It was first written in 2010 or '11, which is why 10 years later we wanted to do an update. But it came out in 2012, yes.

So the story goes, basically, your publisher came to you, you had the Healthiest Foods on Earth series, and they came to you and they said, hey, Jonny, we've got an idea for you. Can you write a book about the 150 ways to lower your cholesterol? And you were mortified. Yeah, you were saying, I don't want to write a book on how to lower cholesterol, you guys crazy. And then, you know, some convincing, and then they wanted, you know, the cardiologist of cardiologists to give you, you know, the credentials to go put it forward. So 10 years on, what made you feel you need to revise it? And yeah, what was the thing that thought, I need to revise this?

Well, I mean, first of all, the research in this kind of an area, you know, heart disease, cholesterol, anything that's really pressing, there's a lot of research, and a decade's a long time. I mean, a lot of A lot of stuff has come out since then, a lot of not only studies and theories and changes in the way we practice and discovery of different tests and markers and genetics and all the other stuff. But there's also been quite a shift in the response to what we were talking about in the book. We meet doctors at conferences all the time now who said— who say, you have literally changed the way we practice. I've got your books in my waiting room. I had no idea. Now, they're not the majority. The majority of doctors still think we should be the equivalent of disbarred, and they write letters to Dr. Oz like, how could you have these cracks on? That's the majority. But there is such a growing minority of people who have kind of come on board with the notion that cholesterol testing is, as we do it now, as we do HDL, LDL, good and bad cholesterol, is completely obsolete. A lot of people have come on board with the notion that cholesterol doesn't cause heart disease since 2010, which is really when we wrote the book. That's when the research started coming out that saturated fat has no causal relationship to heart disease. First study was in 2010, American Journal of Clinical Nutrition, still quoted to this day, 347,000 patients, no causal relationship. Then they started coming out fast and furious. 2014 was the Annals of Internal Medicine, relationship between saturated fat and heart disease. Just last year, there was a big study in Malaysia where they looked at dietary patterns— low fat, high fat, low carb, high carb. They found that in terms of metrics for heart disease, when you looked at the ones that really mattered, the only thing in the diet that made a difference was carbohydrates. Didn't matter if they were on low-fat diets, high-fat diets, their risk— it correlated with the amount of carbohydrates in their dietary pattern. So this stuff was in the last decade there's been just an awful lot of research and theory on this subject. And it's leaning the way we said it was going to lean in 2012, only more so. And there's a couple other reasons why this was so necessary. And one of them we didn't even know when we started it, and that was COVID. And I'll get to that in a second. When we did a deep dive and said, OK, now let's really go back and see. In 2012, the original edition, we said, testing cholesterol as we know it today. And I want to make sure, Mark, that everybody understands I'm talking about the standard test that you and I and most people listening to get from their doctor that's covered by insurance— HDL, LDL. It's the test that most doctors use to give you a prescription for a statin drug if your LDL is too high. That's the test we're talking about that should be retired. One of the goals of this book, and my greatest goal, I would be so happy if it achieves this, is that they retire that test and never again is a drug prescription ever given on the basis of HDL and LDL. So we knew that back in 2012. What we didn't really know was what people should be testing for. We knew that there were such advanced tests like the particle test but they hadn't been around that long. And we knew there were things like Lp(a) that were more important than there were all these other things, but we didn't have an absolute clear, absolute epiphany vision of like, this is what you need to look at. Now we do.

Right.

So when we went back and we looked at that research, it starts in 1970. And we did a deep dive into what is it. We found that the predictors of heart disease have been hiding in plain sight for what, 70, 50 years, and, and nobody talks about it. So the theory that what we have, what we talk about in the new edition of The Great Cholesterol Myth, is that there is a straight-line continuum in cardiometabolic diseases, by which I mean prediabetes metabolic syndrome, diabetes, pre-heart disease, and heart disease. One line. And the thing that connects them, the thing that shows up 10 years before your doctor says, you know, Mr. Jones, you got some high cholesterol, we might want to look at those statin drugs. 10 years before that happens, something shows up that we could all be looking at right now. And that we can treat, prevent, and reverse with diet. That's the message of this book. And the reason it's so relevant now in COVID that we didn't even know is that every one of those diseases I just mentioned— let's go over them again: metabolic syndrome, prediabetes, diabetes, pre-heart disease, heart disease, obesity— every one of them is a preexisting condition that makes COVID 10 times more dangerous. When you look at who's dying from COVID most of them have these— not all, there's outliers, but we're looking at big actuarial numbers. Most of them have these preconditions. These are the most vulnerable. These are the people with the immune compromise. These are the people who have underlying metabolic conditions that are on that straight line from prediabetes to diabetes to heart disease. And what shows up that predicts that first is something called insulin resistance. And it sounds like a technical term, but basically it's an error in carbohydrate metabolism. Your body cannot handle the sugar load. What happens next is that blood sugar stays high. The body can't bring it down with insulin because insulin's becoming more and more ineffective. Therefore, we call it insulin resistance syndrome. That is a direct line from that to prediabetes, a direct line from— and make no mistake, prediabetes is diabetes. It's just a little— it's not— just hasn't quite gotten the title yet when it's all a continuum. Just like high blood pressure doesn't start at 140 over 80, you know, what happened to 139? It's a continuum, and it's a continuum from diabetes to heart disease. And you can nip diabetes in the bud, or at least keep it from ever getting any worse if you treat the underlying cause, which is insulin resistance, which is just a fancy way of saying carbohydrate metabolism error.

Every time I listen to you speak and have the opportunity to speak to you, I was preparing the podcast questions that I wanted to ask, and I kind of knew that I'm not going to ask any of these questions because it's just going to roll organically, and I love it.

Ask anything. I love your questions. They're smart and they're informed, so please throw them at me.

I'm happy to— One of the things that— an analogy I wanted to start kind of the show with and then kind of give is cholesterol was once said to me that, you know, the analogy that I like to use is if the building is on fire, if the building is on fire, the fire is inflammation. Cholesterol is the fire truck that comes to quench that inflammation. And cholesterol-lowering medication and drugs are essentially terrorists with a rocket launcher shooting the fire trucks and blowing up the cholesterol. So, cholesterol is nothing more than a marker of inflammation. What we need to do is look under the hood. And when we look under the hood, what we, as you pointed to with research, which we usually find is high blood glucose, high insulin, high fasted insulin, metabolic syndrome, diabetes. So what is, and what is the best way to explain— got a lot of trainers on the line who are going to go back and ask, and clients can ask them questions— this term inflammation gets— well, firstly, is one, is the analogy apt? And secondly, how do you explain inflammation as a process?

Well, that's a multi-part question. It's a brilliant question, but has a number of different parts, one of which is the analogy about the fire and the flame. The other of which is inflammation and how does it happen and what does it do. So let's start with inflammation because that really is one of the prime drivers of, I'd have to say, every degenerative disease we know of. I don't know of a degenerative disease from asthma to any of the metabolic diseases we just mentioned, to cancer, to Alzheimer's. I don't know of any major disease like that that does not have as a major component, inflammation. So it may not always cause a disease, but it promotes it. It makes recovery more difficult. It makes it more complicated. It is definitely one of the twin towers of cellular destruction, the other being oxidative damage. So let's clear up what inflammation is for people who might be unclear about it. There are really two forms of inflammation, and everyone listening to this knows form number one. Form number 1 is called acute inflammation. So if you get a toothache and you can feel it like throbbing and it's inflamed, that's acute inflammation. If you bang your knee against a wall and it is throbbing and it gets— that's acute inflammation. If you get an abscess on your skin and it's all swollen, that's acute inflammation. As my friend Barry Sears, the author of The Zone, says, Acute inflammation hurts. Chronic inflammation, which is what you and I are talking about, kills. Chronic inflammation is a kind of relative of acute inflammation, but it flies beneath the pain radar. It's happening at the cellular level. It's happening in the organs and the tissues and the cells and the endothelium and all the other components of the body. But you don't feel it any more than you feel symptoms of diabetes. Or you feel the symptoms of high blood pressure. They're under the hood. They're happening, but they're not something like a toothache or an abscess or a bang on your shins that you feel. And what happens in chronic inflammation is kind of the same thing, only instead of it being a big obvious abscess on your skin or a big knot on your knee, it's little cellular damage that creates little injuries and weaknesses either in the endothelium, which is the lining of the artery wall, or any other place. And that's where the trouble starts. So cholesterol is basically this essential molecule that's just floating around minding its own business, not really harming anything until It gets damaged by either inflammation or oxidation, and then the damaged particles wind up lodging in a parking space they don't belong in. And then the body goes, whoa, we got an invader, and it sends all the artillery. And now you start to have inflammation because that's the first response of the immune system. And then there's more oxidative damage, and then all of a sudden the muscle cells come and let's put a a little cap on all this so you get some calcification, and that's the beginning of the plaque and the small— the narrowing of the artery and all the damage. It's not the cholesterol. Cholesterol just happens to show up and do, you know, be part of the particle mess that's in there. It's the things that damage the cholesterol.

So to perhaps fix the analogy that I said before, it's almost like the fire truck cholesterol gets hijacked on the way and actually becomes part of the flame that is—

becomes part of the problem, comes to burn up itself. That's a good way to put it. The thing that I think which we may have maybe missed in the first edition that is abundantly clear now— I mean, I don't even— I can't even believe anyone argues with this at this point. Cholesterol can't travel in the bloodstream by itself. People need to understand this. It needs to be in a container. So if you think of cholesterol like an oil, it's not, it's a sterol, but it's kind of like an oily structure. If you wanted to get oil across the lake, would you pour it in the lake and assume it's gonna get to the other side and somebody's gonna be able to cook with it? Of course not, it doesn't float, it doesn't go in the water. But if you put it in a bottle and send it on a tube, it'll get there just fine. So cholesterol travels in something called a lipoprotein. Think about HDL. What does it stand for? HDL stands for high-density lipoprotein. LDL stands for low-density lipoprotein. Those are the boats. The lipoproteins are the boats, and cholesterol is the cargo. We've been measuring the cargo. Which is fairly irrelevant. What's very relevant is how many boats are in the water. Because think about it logically, the more boats in the water, the more accidents are gonna happen. The more people who get into a nightclub, the more likelihood there's gonna be a fight. And the more people that crowd into an area, the more likely somebody's gonna bump up against someone else and something bad's gonna happen. It's just the nature of crowds. So when you have a massive amount of lipoproteins, even if they're harmless, there's a greater chance of an accident. There's a greater chance something's gonna go wrong. So what we need to be measuring is not the cholesterol in the boats, but the number of boats. That's called a particle test. And that is the more, that is the 21st century version of a cholesterol test. That's the test we think is worth getting. The old-fashioned HDL, LDL, is nonsense. We now know— they found out in 1963 that cholesterol traveled in these two different kind of boats, and one was low density. If you put it in an aqueous solution, the low density ones would float because they had low density, and the high density ones would go to the bottom. So that— oh, those are kind of different, LDL, HDL. And I don't know, one of the HDL seems to not do such bad, so we'll call that one good and we'll call this one bad. Okay, that's the equivalent of using a flip phone in the age of the iPhone 12 and the Samsung Galaxy. It is the most rudimentary 1963 division of cholesterol. You know how many types of cholesterol there are? Over 13 that have been identified so far. I'll list them, a few of them for you. There's LDL3a, 3b, there's LDL, there's HDL2, 2a, 2b, There's HDL3, there's Lp(a), there's oxidized cholesterol, there's LDL small particle A, big particle— small particle B, pattern A. All of this is data about these particles and their size and their performance in the body. And we are still stuck measuring it like, well, there's this— the good guys and the bad guys. And it's just not true. Look, Mark, we can decode the human genome. We now know there's like 30,000 genes. I'm no geneticist, but I read the papers about 30,000 genes and they've now decoded it. And it's a relatively easy process. Correct? Everybody knows that. Suppose you were still in a world where doctors ignored that and said, well, we can tell a lot about a person's health if we know if they're tall or short. So let's put people in two classes. Tall people and short people, because short people don't get certain diseases like aggro. You know, there are certain diseases that go with tall people and certain diseases that tend to culture. And so we're going to just divide the population into short and tall, and we're going to stop there. And people are going, dude, there's 30,000 genes. What are these metrics? Biometrics, we've got them up, though, textbooks on them. What are you— short and tall? That's like from the Dark Ages. And they're still sticking to their guns, good and bad cholesterol. It's nonsense. So what's really criminal is that people get prescriptions for drugs based on that test, which to me is like getting a prescription for drugs based on a horoscope in People magazine.

One of the things that I've heard you say in an interview before is that your particle number was high, but on a traditional test, the LDL versus HDL, they're just really, as you said, delivery systems to and from the liver. But obviously, you live a very healthy lifestyle. What have you seen? What are some of these attributing factors to making particle numbers higher if it's not the cholesterol? Is it sugar?

Is that— is what?

Is it just sugar? Like, one of the things that you referred to before was prediabetes and diabetes and metabolic syndrome. So are we placing the blame on sugar, or is it excess calories, or is it lifestyle? I mean, it's obviously lots of things, but for you, having a healthy lifestyle? What's the difference that makes a difference?

I'm an interesting case study in this because my regular cholesterol numbers, the 1963 version, are wonderful. And every doctor I've ever had before I became enlightened about this, oh, terrific, 160 cholesterol and 90 LDL, fantastic, no problems. Then when I became enlightened, I started getting tests that actually matter, and I got the particle test. And lo and behold, yeah, my LDL is just fine, except there are millions of particles in there, and they're the nasty little small BB particles of pattern B. This is a level of danger and risk that is completely, completely hidden. In the LDL-HDL test. So it works both ways. Some people have a high LDL, they go on a statin drug, they don't need it because when you look under the hood, they got big fluffy particles and they don't have that many of them, and it's not really any real danger. Other people may have a good LDL like me, but they've got really bad particle number and, and size, and that has to be treated. So it's, it's not just that the LDL-HDL overprescribes statins, which it does, it also may underprescribe treatment for people like me who think, oh, who might have thought everything's just great because my LDL is fine. Your LDL is irrelevant. What's relevant is the number of particles, and there's ways to measure this now. The pattern of those particles is pattern A, pattern B. One's atherogenic, one isn't. What else is happening? What's your Lp(a)? What are your triglycerides and HDL? What's that ratio? So all of these things present a full and complete picture of somebody's risk and somebody's health. LDL and HDL, you might as well throw a dart into a dartboard because we talk about studies in the book where they looked at— they're called meta-analysis. They combine lots and lots of different studies so that they get a huge patient population. In this case, I think it was 375,000 Looked at, and they looked at cardiovascular entries into a hospital, people who are being admitted to hospitals in the United States of America with cardiovascular-related, either CAD, coronary artery disease, or any other kind of cardiovascular, strokes, heart disease, 375,000 people. You know how many of them had normal cholesterol? Between 50% and 60%. Normal LDL cholesterol doesn't predict anything good or bad. It's a crapshoot. It's throwing a dart. And it is simply, to me, disgraceful that we are hanging on to this antiquated measure that tells us nothing and obscures the real causes of heart disease.

So, so for Johnny, for you being healthy, what was like, what were some of the reasons? Because I suppose the reason why I ask is a lot of people on the line who You know, they're like, my cholesterol is good. They get the particle test, whoa, it's high. What are some of the things that when the particle number becomes higher, and otherwise, is it just genetic?

I'm actually working with, with my, my team of functional medicine doctors and advisors to try to try some of those things to see exactly what could make a change. Maybe I wasn't being high fat enough. Maybe my carb, uh, excursions and, and treats once in a while were enough to put it over the edge. So I'm now taking steps to find out what I can do. I'm going to have it retested. I got a glucose— a continuous glucose monitor. I'm really looking at what foods raise and which don't, because we really believe that this stuff starts with insulin resistance, which starts with too much sugar. And yeah, you could be living what looks like a pretty low-carb lifestyle, but if your carbs are more than your body can handle, eventually blood sugar is going to rise, insulin is going to rise, and you're kind of on that pathway. Could that be the— it could be. Could it be genetic? Could it be something that we're not even thinking of yet? Yeah, I don't know. But the point is, by looking at those measures, you get real information that you can use. By looking at HDL and LDL, you are dreaming if you think that that's going to in any way predict something good or bad. It's kind of irrelevant. It's an old-fashioned measure that does not really tell you what's going on with your cholesterol in the body.

So another multifaceted question for you. Cholesterol research, and when we started to demonize cholesterol research, you know, you always point to Ancel Keys as the figurehead. Seven countries study excluding 14 of whatever was the countries, or 22 countries he excluded it. He showed what he wanted to show. Later on, he became, you know, Time Man of the Year, was hailed as a savior of, you know, heart disease, when really probably his work increased heart disease. And that was further spoken about into the Framingham study, which I do want to talk about. As well. But in saying that, almost seems that the first edition of the book, or one of the conclusions that people have pointed out with cholesterol research, and particularly the Seven Countries Study, is that the same— his conclusion was that cholesterol, high cholesterol causes heart disease. But also what can be said was from the statistical analysis is that high cholesterol, low cholesterol is also correlated to high incidence of all-cause mortality and morbidity. And one of those particularly was cancer. So basically, His own research pointed out that if you have high cholesterol, it can be correlated with heart disease. But by the same framework, if you have low cholesterol, it is certainly correlated with cancer just as high as— so it's like, oh, well, you didn't die from cholesterol, you didn't die from heart disease. Well, you died from cancer. So it's like this demonization of cholesterol and cholesterol linking to saturated fat What it seems to me is most of the studies and work that's been done pointing out that the mishaps of cholesterol has been kind of attacking that area, whereas what you're saying, that the revised version of the work that you've done in the book is showing what's actually happening in the last 10 years actually challenges that status even more, which is now saying that cholesterol actually has no causal impact to heart disease whatsoever. Is that the right conclusion that the new research has been—

Not exactly. Not exactly. LDL and HDL are just useless, right? But when you look under the hood, high particle numbers do predict bad events, right? High ApoB numbers, which is kind of the same thing, also predict much better. High triglyceride to HDL ratio, very predictive. LDL and HDL are useless, but it doesn't mean that there's no information to be had by looking under the microscope at the types of cholesterol, the patterns of cholesterol, the number of lipoproteins. That's valuable information. That's 21st century testing. But the— like I said before, it's like the equivalent of a flip phone. It is texting where you have to hit 3 things to get a letter. You remember that in the beginning in the '90s? Yeah, that's what we're doing with HDL.

So, so now we can't— is is correlative, but we have to look under the hood and really know particle sizes. One thing that, you know, yeah, one thing, so normally the saturated fat story goes, you know, ants or keys, but there's something that obviously happened to the rabbits, you know, when they fed saturated fat to rabbits and showed that they, you know, that's where it—

No, they fed cholesterol. They fed cholesterol to rabbits and it was in 1913 and they knew nothing about biochemistry then. And what they didn't realize rabbits are vegetarians. They don't eat cholesterol. They have no mechanism for getting rid of cholesterol. They don't encounter cholesterol. They eat lettuce and celery. They don't eat anything that has cholesterol in it. So yeah, you fed this foreign substance to an animal that has no system able to deal with it on any level. It's never been seen before and they can't get rid of it. What a surprise. So that, that study is just utterly irrelevant.

It doesn't stop vegans from quoting it though.

I think the bigger hit on cholesterol and saturated fat, as you correctly point out, was not from those Russian studies in 1913, but from Ancel Keys' correlation study. So what I think is important that everyone should know, even if you're not interested in the details of cholesterol research, everyone should understand the difference between a clinical study and an observational study. So observational studies, they're called epidemiology. They don't— let me tell you what a clinical study is. I want to find out if this bodybuilding supplement really builds muscle. So I take two groups. Now, I'm not going to just take any random group. Some people might be 80 years old. They're not going to build muscle. I don't care what you give them. And some people might be very gifted athletes. So I have to match those groups. I have to make sure they're pretty identical. I want to make the equivalent of them being almost like genetically equal, like twins. That would be the ideal. But I'm not going to get that. But I'm going to match them on sex. I'm going to match them on age. I'm going to match them on previous athletic experience. I'm going to match them on what supplements they take. I'm going to match them on any previous medical history. I'm going to try to make them as identical as possible. And then I'm going to give one group the bodybuilding supplement and the other group not. And I'm having to exercise the same amount. And at the end of 6 months, I'm going to measure. And if there is a difference, it is a reasonable expectation to say that the only thing different in these two groups was one took the supplement and they gained 2 inches on their arm. I want to say it probably had something to do with the supplement. But if at the end of this controlled study, there's no difference, I'm going to say the supplement probably doesn't work. That is a clinical study. This is an observational study. I go into my neighborhood, I want to find out what people eat. I give them a questionnaire to tell me what they ate in the last 6 months. I make notes, I watch them, I follow this group for a couple of years, and I see how many of them die. And now I want to look at what they ate, and I want to see if there's any correlation between what they eat and how fast they die or how fast they get heart disease. That is an observational study. As you can imagine, it is the most preliminary kind of data because you don't know if these people are matched. You don't know what their history was. You don't even know if they're telling the truth or if they even remember what they ate 6 weeks ago. The food frequency questionnaire is the worst piece of data collection thing I can imagine. And you answer questions about what you ate 6 months ago. So It's basically an absolute—

You're being generous saying that they gave them a questionnaire study, because that research was also done on what food was available in the country. They didn't even give them a— like, it is even worse than that. It was looking at the agricultural— what food is available to that country and saying, well, this country has more meat available and saturated fat, so therefore we can correlate this country with higher rates of that, therefore they're consuming that. In actual fact, they may or may not have been consuming it at all.

That's true. And it's— but it's also true that in current dietary research, they do use the food frequency questionnaire, and it's horrible. And it's true that what they did back then was even worse. But the food— you should— we get— we give an example of it in the book. We actually took something from the food questionnaire and put it in the book. You can't even believe how bad this is. The questions are ridiculous. How many times did you have butter on either beans, string beans, bread, or in the last 4 months? And what— it's just ridiculous. So why I tell you this is because the Seven Countries Study was an observational study. And worse, most nutritional research is observational studies. So we give some examples of observational studies that have been correlated. Every so often, they There's a statistician named Nate Silver who publishes this stuff every so often. Real live correlations, correlations, associations that have been found in studies. There are correlations between the number of movies you watched and what you got in high school, what book you read in high school, between diabetes and Bill Clinton's administration, between, you know, the number of— there are all kinds of spurious correlations that arise that have nothing to do with— the one I teach all the time is that there is an observational study study that has shown for years a correlation, a statistical significant correlation, two things moving together, right, between storks and babies in Denmark.

Ah, you talk about it in this book here.

I do, I do.

Yeah, I remember that. So how kind of you.

So for those who don't know, there is this correlation between storks and babies. The more storks, the more babies. It happens year in and year after. Now, it's a great example because I hope everybody kind of knows that storks don't bring babies, but that would be the corollary, that would be the conclusion. Here's why it happens. It happens because storks like to nest on surfaces that slope, particularly if they're kind of tarry. They love that, that's their nesting. Okay, in Denmark, When young people want to have families, they move out of the city, which is mostly young single people, and they move into the suburbs where they have their babies. Guess what the suburb— the architecture in the Denmark suburbs is? Sloping, tarry rooftops. So yeah, the storks come to the rooftops and they have storks, and the people come to the same areas where they have those rooftops and they have babies. They are correlated, but one doesn't cause the other. And that's the problem with nutritional research like the Seven Countries Study. They see more of something and they assume that caused it. But there's no evidence that saturated fat caused any of the things that they were observing, none whatsoever. And when you go back and you actually look at these diets that they were promoting, the Mediterranean diet, we actually went in the book, and I looked at menus in restaurants in the Mediterranean area. Remember the Mediterranean diet? There's 22 countries in the Mediterranean. There's Israel, there's Syria. There are vastly different countries. They don't all eat the same thing. And I looked at some of the menus in Italy and Greece, and there's pork on the menu. There's beef on the menu. Of course there is. They don't not eat these things. But we have this notion that, like, they ate less saturated fat, they had less heart disease. No one looked at the fact that they lived outdoors a lot, that they actually eat their big meal during the day, that they take naps, that they have social relationships where they share their emotions, that they close down from 2 to 4 in the afternoon. All of this wasn't looked at, but more saturated fat has to be the reason. That they have less heart disease. And, and those studies are inherently flawed. A great example is smoking and lung cancer. It started as observational studies. You know that whenever there's a lot of smokers, there's a lot of lung cancer. No one said it caused it. They found together a lot. Let's make a hypothesis. Now let's test it. 20 years of testing, clinical studies, laboratory studies, They now know, yes, it does. But you don't make health policy based on an observation. That's like saying I go to Gold's Gym in Venice, a lot of guys are wearing red tank tops. I come away and go, oh, red tank tops cause big muscles. You've got to look beyond the observation. And that's what they don't do in those studies. And that's why we wound up with this cockamamie theory that saturated fat causes raised cholesterol, which in turn causes heart and that's kind of been debunked.

Just for the folks who didn't see it and listening on audio, I'm holding up a copy of Living Low Carb, one of Jodie Bowden's great books where he talks about that study, the, what do you call it, I call them pelicans, they're not pelicans, are they, they're babies, whatever they are. Great book, make sure you go pick it up along with everything else. One thing that, you know, we talk about Ancel Keys, but something happens in, what was it, 1911, the formation of Crisco, and we had vegetable oils. And one thing I wanted to get your thoughts on was the thing with vegetable oils, or more particularly hydrogenated and partially hydrogenated oils, which New York City now has completely banned. I know America is on their way. Australia aren't really as forward-thinking. They believe their stance— our equivalent of the FDA— is their stance is that, well, calorie consumption is below 0.1% of someone's diet, so we don't have to do anything about trans fats right now. But the thing with hydrogenated oils is one, They're very high, well most of them except for probably canola oil, is very high in omega-6. The average diet of omega-6 for the Western diet is anywhere from 16:1 omega-6 to 17, 18:1. So highly inflammatory. But the thing, at the same time when we were demonizing saturated fat, what a hydrogenated oil is, is saturating an unsaturated fat with a chemical process. So it seems really ironic to me that Butter, lard, coconut oil, all animal products that contain saturated fat got heavily demonized, but yet hydrogenated oils flew under the radar when they are inherently saturated fat. So, I mean, can you speak to this? Like, kind of, it reminds me a bit of COVID to be honest. Like, there's so many contradictions in it.

Yes, you can't really look for logic in nutritional research. You have to understand, people really don't understand this, and it's It's one of the things I find myself explaining the most. People feel somehow, they look at politics. You're in Australia?

Yeah.

Are you following the American election? All right, so nobody agrees on anything. Politics are like— I'm following quite a bit. There's totally different points of view about COVID ranging from we should lock everything down to we should ignore it. It's all over the map. And people live with these contradictions and this disparate advice in so many areas of their life. I've had two friends who had cancer this year. You don't even want to know about the options and the second opinions and the different— well, you could do this, but there's a problem if you do that. But if you do this, then that's got a 34%— you have to make decisions that are so high level based on contradictory information, different opinions. And we all do it. We have a kid who needs to go to school. You have different opinions about which school system and what things should be emphasized. For some reason, in the field of nutrition, health, and medicine, we, the public, think everybody should be united. We think that somehow these scientists and nutritionists and doctors get together once a year. They have a little club. They go up to the top of the mountain. They figure out what's good. They come back and they tell us. It's not like that. There's wildly disparate points of view about this stuff and very acrimonious debates about it. And the research proceeds very slowly. So it's not surprising to me when people disagree so voraciously about like a high-fat diet or about vegetable fat versus animal fat. So let me tell you a very interesting story that we talk about in the book that was not in the, in the past edition. Ancel Keys, you mentioned Ancel Keys. I'm assuming the audience knows who he is. He was the engineer of the low-fat diet. He designed this the 7-country study we're talking about. But he was involved in other research as well. And there was another study that Ancel Keys was the lead researcher on. It was called the Minnesota Heart Study. And the Minnesota Heart Study was done in 7 different locations, and it was led by Ancel Keys. And you better believe that they expected to and were going to find the same thing they had found everywhere else, that when you take saturated fat out of the diet and you substitute it with all this other stuff and you eat a low-fat diet, people do better. But it was going to be another study that was basically observational, except for one thing, a little-known story that I'm going to tell you now. One of those 7 centers was under the auspices of a doctor named Ivan Franz, and he was a disciple of Ancel Keys. This guy used to measure his family's cholesterol. He would take cholesterol readings in the, you know, once a week. He was fanatic about it. He knew that Ancel Keys was right, that saturated fat caused raised cholesterol, vegetable fat would give an enormous advantage. Everybody would get rid of that saturated fat. So he decides, though, that his arm of the study, he wants to do like a real science study. He knows that the rest of this stuff's epidemiological, it's observational. You don't really know So he wanted to design a rigorous study, double-blinded study, to find out what the advantage of vegetable oil was. So he goes to institutions, like actual residential institutions, hospitals, various places in Minnesota that he had access to. And he designs a study where, first of all, all the patients live there. And they can control all the food they eat because they're in the cafeteria getting plates and they can watch what's there and what they eat and they can decide what to put on it and what to substitute. And he designed such a rigorous study that when they substituted the saturated— for example, butter— back in the day when they had margarine, there were regulations that it couldn't be cut in the same little squares as butter because they didn't want to confuse people. So margarine had to be cut in little triangles. So he gets a special dispensation so that he can actually get the margarine and the butter to look identical on the plate. So nobody knew. That's— and the oil, you can't tell if it's unsaturated, saturated vegetable oil. No one knew what they were eating. The people serving it didn't know. It was truly a double-blinded study, an excellent scientific study. So the results come in, and he looks at the data, and he doesn't know what to make of it because it's weird. It doesn't show a clear advantage for vegetable oil. In fact, the data is just confusing. They expected to go, oh man, the people who got rid of saturated fat, boy, you know, didn't happen. He wasn't sure, and he didn't really publish it. He was confused by it. He was a scientist. He goes, this is not— I mean, it's like I'm testing gravity and there's no gravity. There's got to be a mistake in my data. So he takes the data, shoves it in a drawer, leaves it in his home basement, attic, wherever, where it stays for a decade or more. About 20 years later, a researcher at the NIH named Christopher Ramsden is thinking to himself, you know, for the last couple of decades, we have wholesale told We've given wholesale advice to the entire country to get rid of their saturated fat and replace it with vegetable oil. And I'm putting it in quotes because you and I both know it's seed oil, not vegetable oil. There's nothing from vegetables about soybean or, you know, these are starchy, seedy things that we've been taught somehow are better because they're not saturated. And we've been told to eat that stuff. We are still being told. Harvard University today, if you look at their recommendations, go to unsaturated fat, to go to the corn oil and soybean oil and safflower oil and all of this canola oil, all these crap oils, right? So this is still around today. And we've been telling people this for I don't know how many years since I started 30 years ago. And Christopher Ramdsen was thinking, I wonder if there's any consequence to this. Did anybody ever test this? It would be really interesting to see what is this unsaturated fat. It's called linoleic acid. All of a sudden we're consuming all this linoleic acid that nobody ever consumed before. And it's in all the— wouldn't it be interesting to find out what effect it has? I wish I could do a controlled experiment and feed people linoleic acid or saturated fat and see, but I'll never get funding for that. Nobody will ever agree to it. Nobody will ever fund it because there's no And then he remembers, wait a minute, that study was done. That dude Franz, 20 years ago, he did this study. Where's his data? So he calls up Franz. Franz is long dead, but his son, Robert Franz, is a cardiologist at the Mayo Clinic. And like his father, a serious scientist. Ramson calls him up and says, dude, could you help me find your dad's data? It's got to be somewhere. I got to get to this. It's the only really controlled experiment we have comparing vegetable oil to saturated fat. I got to get my hands on this data because this is what my research interest is. Can you help me? They meet up, they spend 3 days at the family house, which Robert still had access to. You know, they still own that house. They looked in the basement, they find the data. He gives it to Ramson. Ramson takes it back to the National Institute of Health. A month later or so, he calls up the son and he says, I understand why your dad didn't publish this. This is weird. And the son says, how so? And he says, well, not only was there no advantage to the people who substituted saturated fat for vegetable oil, there was a distinct disadvantage, particularly if you were older. These people had higher risk markers for heart disease than the people who ate the saturated fat. And he says to the son, I'm in a bind here. I don't— if I— you gave me this data. If I publish it, it is basically upending everything your father believed and stood for and researched. And God bless him, that son said, publish it. My father cared more about science than about being right. And that study was then published and revealed. It was written about in Nina Teicholz's excellent book, The Big Fat Surprise. Gary Taubes, Good Calories, Bad Calories, Why We Get Fat. It's in there. It was on a Malcolm Gladwell podcast because it's a very interesting father-son story as well as being a research story. But the point is, the only good study we have that compares this crappy vegetable oil to saturated fat found out that it was like 10 times worse than the saturated fat it replaced. So that's the difference between an observational study and a clinical study. And when you control the variables, and we really don't have any evidence that vegetable oil is better for us than saturated fat. In fact, I interviewed— like you do, I interview experts all the time. In this last year, I've interviewed 2 both of whom said to me— we were talking about COVID and both of them said a variation of, you show me one person who has avoided sugar, starch, and vegetable oil for a year or so who's getting a bad case of COVID I'd like to see them. Nobody has come forward. This is the most inflammatory substance. Sugar and vegetable are the two most inflammatory substances in the American diet, and they are at the root of heart disease, not that.

Yeah, yeah, we're in, um, probably not aware, but we're in Melbourne. A lot of the guys on the call at the moment, we're in Melbourne. Melbourne has the, the longest— we've broken the record, folks— the longest lockdown in the world, and also the strictest. So, um, it's been absolutely insane. I haven't been able to trade. My personal training studio has been shut. Since March 23rd, 2020. And we get like 1 to 2 cases a day now. So like, we're, I suppose, now the point that the laughingstock of the world, really, in terms of the way our politicians have handled COVID, it's beyond a joke.

No, no, no, you're not the laughingstock of the world. We're the laughingstock of the world. I mean, let's be honest. No, you don't have a president like we do. So you're not the laughingstock of the world.

Yeah, it's crazy there, hey? I mean, you've got Joe Biden and Trump, and it just seems like a complete mess, Republican Party and Democratic Party.

It's pretty crazy, but I think the connection to COVID is a very important one that I'd love your audience to understand. So if we're right that insulin resistance is the big signal for heart disease and for the entire spectrum of cardiometabolic The whole portfolio of cardiometabolic diseases, starting with prediabetes, metabolic syndrome, diabetes itself, which we think is pre-heart disease, heart disease, obesity, all of them have a common root, which is insulin resistance. And insulin resistance can be treated or prevented or reversed with diet, with diet alone. Here's why it's so important. Every single one of those conditions are the pre-existing conditions for COVID death. When you hear about people who are vulnerable, when you hear about the immunocompromised, or you hear about people with underlying conditions, what are those underlying conditions? High blood pressure, metabolic syndrome, diabetes, obesity, heart disease, and lung and kidney disease also, which have a relationship to insulin resistance. But they're all cardiometabolic diseases. And you can treat that with diet. And the diet we talk about in that book, we talked about it in terms of like, this is a better diet to keep your heart healthy than a high-carb, low-fat diet. We didn't realize at the time it's also a better diet to keep your immune system healthy, because when you have those diseases, you are basically a walking target for COVID.

So the Johnny Madden 4 food groups: hunted, fish, gathered, and plucked. Uh, I have added one more to that because someone caught me out on it, uh, once. So I thought about it— uh, farmed, hunted, fish gathered and plucked, and farmed. And the reason why I had farmed is because people say, uh, well, cows, they're not hunted, you know, from eating beef. It's not— I'm not exactly hunting the beef, it's farmed, I suppose. But you obviously want grass-fed varieties. But they're the main food groups that we want people to, to be eating. Um, you know, no vegetable oils, Reduce and minimize sugar, proper carbohydrates, probably for most folks gluten-free. If you're having dairy in your diet, make sure it's grass-fed, sourcing high-quality real food. And I suppose the big killer is the high fructose corn syrup in America. I know you guys sweeten everything with high fructose corn syrup. That problem isn't quite as bad here in Australia. We use good old Australian cane sugar for a lot of things. I think that's the discrepancy between the non-alcoholic fatty liver disease that is so high and prevalent like, uh, minors in the US compared to— we don't, we don't have that here. And I think it's the— you can see obviously that's observational.

That's a very— that's a good hypothesis. Yeah, but make no mistake, I'm not one of the people who thinks that sugar and high fructose corn syrup are all that far apart when it comes to metabolic damage. High fructose corn syrup, you're absolutely right, is directly related to fatty liver disease and, and definitely has a worse profile. But let's not kid ourselves, I mean, plain old cane sugar ain't much better. It's maybe marginally better, but they're both, you know, one is 50% glucose and 50%, um, uh, fructose, and the other is 55% and 45%. You know, they're not that different. So I agree with you.

Yeah, the evidence-based community would then be urging me to ask and say things like, well, isn't it about calories in versus calories out when it comes to say, for example, sugar?

No, it's not. I mean, that's one of the biggest myths. And yes, you can find some correlations that show calories matter, but it is the composition of those. And I would not— let me back up and say this. When we first discovered the hormonal effect of food and that how different, even if the calories were the same, 1,000 calories of fat does not have the metabolic effect that 1,000 calories of Domino's sugar does, and everything in between. They just don't raise the same hormones. They don't start the same metabolic processes like fat burning versus fat storage. So when we realized how important hormones were, way more important than calories, some of us— and I was among them— took it a little too far and said, Dude, calories don't matter. You gotta look at hormones. And we were just trying to shake people out of this insane dependence on calories while they're ignoring the foods that actually raise fat-storing hormones, for example, like insulin. It's not true that calories don't count at all. And we went a little far by saying that. They do count, but they are not the whole picture. They are not in my opinion, even the most important part of the picture. They are very much eclipsed by the importance of hormones. And let me just give you an example of why. People think you get fat because you eat too many calories. I would say, what are those calories composed of? What makes you fat is your blood sugar goes up, insulin comes along, it takes the sugar out, and when it— there's no need for it in the muscles, it takes it to the fat cells. It is a fat-storing hormone, okay? So we need to look at what the effect of food is on blood sugar and subsequently on insulin, 'cause insulin's gonna follow blood sugar. If your blood sugar goes up, so does your insulin. So look at what causes blood sugar to rise. So we got 3, 4 things that have calories: alcohol, fat, protein, carbohydrate. Let's put alcohol aside. Most people don't get most of their calories from alcohol. It's a combination of fat, carbohydrate, and protein. So what has the most effect on blood sugar and insulin? By far, without— it's no contest— carbohydrates. Protein has an effect on blood sugar. There's some amino acids that can convert to sugar, but it's minor. It's a much smaller effect than carbohydrates. What has zero effect on blood sugar. Zero is fat. So if you're trying to lose weight, wouldn't you want to eat calories that don't raise your fat-storing hormone? And those calories come from fat. You can't assume that it's all just calories, because if I eat maybe 500 calories of sugar, my insulin is going to go through the roof and I'm going to go in fat storage mode. But I've eaten 750 calories of fat, not even going to budge a needle. I never said that calories don't matter. If you ate 10,000 calories a day of fat, it would override whatever hormone thing. It would just be— they would have to be stored at some point. But for an equal number of calories, if it comes mostly from protein and fat, you are not going to start the fat storage process in your body because you're not going to be stimulating that hormone. And to make it all be about calories is just, again, it's 1960s medicine. It just ignores the hormonal effect of food.

You got to look underneath the hood the same as— I mean, the dollar is in the detail, right? I mean, the devil's in the detail. You've got to look underneath the hood. Where are you getting those calories from? Because they paint a story like, why is someone able to eat 5,000 calories? Potentially it's the leptin and the ghrelin response, the elevated blood sugar that enables us. The salt, the sugar, the fat in perfect ratio. It gives us that, that neural drive almost to overconsume and be overrided. You simply don't— you don't get that from broccoli and chicken and steak and, and whatever and butter.

100%. And I would add to that, where calories come in is when you're eating processed food, which is generally nutrient— the opposite of dense. They're not packed with nutrients.

They're void.

What?

Nutrient void. Completely void.

When you're eating that, first of all, you're constantly hungry because your body on some level is saying, where's the magnesium? There's nothing in this food. So you're going to eat more and more in a desperate attempt to get the things that aren't in that food. That's number one. So calories do play a role because you're now eating more and more junk. Most of those junk calories are low-fat, high-sugar, high-starch stuff. So now you're also stimulating insulin even more. So it is related to calories. But guess what happens when you eat a high-fat, moderate protein diet? I'll give you a perfect example. You ever sit and eat cereal while you're watching television? If you— well, for those who do, ask yourself how easy it is to go through 6 bowls of sugar-sweetened cereal while you're watching reruns of Seinfeld versus could you eat 2 steaks and 3 portions of broccoli? Never. Because your body knows what to do with it. It's real food. It's going to go there. It's going to send a message to the gut. Ah, now I've got the nutrients I need. You can relax. You don't have to eat anymore. But that doesn't happen when you eat processed food with a lot of sugar and sweet taste. You're just going, give me more, give me more, give me more. And it's been engineered. To create that response. So there's a very— the calories are not irrelevant. They're kind of the reason that keto people or people who stick to a really high-fat diet most of the time, they're not hungry most of the time. They don't have blood sugar problems. We talk about intermittent fasting a lot. But when I was a trainer in 1990, when I started out for the first 5 or 7 years when I was a personal trainer, we would— if anyone had told us to tell our clients to do intermittent fasting, we would have thought they were mad. Remember, breakfast is the most important meal of the day. You have to eat every 2 hours. You have to graze. You have to do mini meals. That's what we taught because everybody was living on sugar because we could not access the fat on our bodies. We didn't know about a fat-burning metabolism versus a sugar-burning metabolism. So we would— of course we told them to eat every 2 hours or they'd be starving. They could never intermittent fast. How come keto people don't have any trouble with intermittent fasting? Because they can access the fat. They're not running out of energy. They're not hungry all the time. It's way easier to do intermittent fasting when you're on a high-fat diet. You're just not as hungry. And so these things are very related, and they have a lot to do with hormones and not much to do with calories.

So, Jonny, I've got to ask this question. You've been writing— you've published 15 books. You've been writing for some time. I'm working on my first, quote unquote, real book. That I want to get— I've obviously done some ebooks, but one that I intend to get published, I've hit, you know, around the 40,000-word mark. You know, sometimes focus wanes, life gets busy. What do you do? I mean, after publishing so many books, 15 books, what keeps you writing? What keeps you focused?

Well, it's a good question. I like to write. I don't know that I'm going to do any more conventionally published books. I think I may have said everything I need to say about nutrition in those 15 books and, and the weight loss program that I wrote that's available online. I love to write, but I think that the forms are kind of changing. People are looking at videos, they're looking at short forms, they're looking at ebooks and things that really are more concise and more manageable. I think what kept me going then is I was learning at that time all this stuff. And the best way to learn something is to teach it or learn or write about it. And I'm a good teacher and I'm a good writer. And so I need to understand this better. And then I would be so delighted with the information that made it all make sense. I wanted to have other people understand it too. And so I would write about it. So I think part of the drive is to understand it yourself and to make it communicable and usable for other people so that it can help them the way it usually helps you. If you discover it and you want to tell people about it, it's usually because it's had a positive impact on your life. So a lot of things I've done have really turned my life around from being a drug addict and an alcoholic to being a health guru. I've learned some lessons along the way. So I like— I am very driven to share those lessons to the extent that they can help other people, not necessarily avoid the pitfalls I had, but find their way out of some of these things. And one of the pitfalls that people are in is being addicted to crappy food. And it is an addiction as clear and as strong as the addictions I had to drugs and alcohol and all the rest of it. Addiction is— there have been studies at Princeton showing that rats get addicted to sugar, and it's a different, more difficult addiction to break than cocaine. So we know that this stuff's addiction. We know there have been a couple of books written about it. Salt, Sugar, and Fat is a Brilliant one that actually— where they actually did investigative journalism to find out how these processed foods are made.

This one?

Yes, yes, that one. That one. Yeah, I think we are soul brothers across the board. That book basically shows that, you know, we are— poor us, we beat ourselves up for not having willpower. These factories with PhD food scientists who are working in lab coats to make the exact combination of sugar, fat, and salt so that it reaches what's called a bliss point. And that's the point where you go, I got to have more. I got to have more. That's the purpose of that engineering. It's not that we have bad willpower. They're just smarter than us. When you engineer something to be addictive, it's going to override a lot of logical systems in the body. So you've got to know what you're up against. These are addictive foods. You're not some weak person who gave in to— these are addictive foods. They were designed to be addictive. That marketing campaign we had in America about potato It was a very famous campaign that said, "Bet you can't eat just one." Well, they were right. They made it so you can't just eat one. So we got to know what we're up against. It's like when I stopped alcohol and I mean, I didn't say, oh, these are easy things. This is a big enemy. And you got to look at this food as a big enemy because this is not— this is not your friend if you want to live a healthy, vital, engaged life. And I'm passionate about this. Next month, I'm going to be 74. And I look back on the 30-something years since I stopped all that stuff and started doing this, and I go, I look at my audience, which generally is 35 years younger than I am, most of the audiences I speak to, and I want to say, guys, you got to trust me on this. This is like the old guy that put $5 away every week since he was 16, and through the power of compounding interest, he's now 60 and he's a multimillionaire, and he's trying to say to people Put the $5 away. It will pay off. It doesn't seem like now. You can't even imagine it at age 20. But when you get to be 60 or 70, you are going to be so damn happy you did that. And that's what I want to say to people about these foods that are destroying our vitality and our health. I used to travel before COVID I would do lots of morning television shows. I'd go all around the country to do, you know, good morning this, good morning that. And I meet lots of Uber drivers, lots of them. And all of them when they find out I'm a nutritionist, they go, Doc, you got to tell me, I got no energy. You haven't had sex with my girlfriend in weeks. I have to fake it. I'm not interested. I have no libido. I sit here on the— and they are suffering and they're in their 30s. And I just want to say to them, dude, make these changes. It doesn't have to be that way. You know, I'm not that way. And you don't have to be either. And I had a worse beginning than you did. I did heroin for 20 years, you know. So I do really feel this information is not just technical, it's not just theoretical, it is life-changing. We got to get off this crappy sugary diet, this low-fat diet, and eat real foods. And real foods includes real fats.

Amen. Amen. I want to be respectful of time. Just to check in, how much time do we have? We have time to open up to the, to the, to the guys on the line.

I got another 20 minutes. Sure.

Oh, awesome, awesome. All right, so we'll open up to the folks, uh, on the line, Wolfpack and Enterprise crew. Uh, let me bring you all up. Who, who wants to go ahead? Who has a question?

Uh, while you're getting that, let me grab some water.

Awesome. So some, some great information. Francois, Marshall, Tyrone, I'm looking at one of, one of you guys to, to kick off with a question if you want to go ahead, unmute yourself. And switch on your webcam so we can see you. Don't be shy. Raquel, another one who I'm thinking— Carl, you always have a question to ask. They're all scared into silence, or they are not able to unmute themselves. Let me check.

Marshall, I love to answer questions.

It's my favorite. Tyrone. Tyrone. Kick us off.

Hey, Tyrone. Hey, hi, Johnny.

Hey, Mark. Uh, yeah, cool, thanks. That was so much great information. Um, just with a question on, um, you said you were doing the, um, constant, uh, blood glucose monitoring. Is, uh, is that the Freestyle Libre one?

Yes. Okay, cool. Is—

and how have you found, uh, that going as well?

Is there any positive, negative I just got it yesterday, so I'm just starting with it, but I think it's, I think it's very valuable. That's why I got it.

Are you recommending, would you recommend, um, just the first, the initial 14-day cycle that I think it does, or continuously? Are you going for a longer amount of time?

You can go as long— these sensors only last 14 days, but you can keep getting refills. And the good thing about that Freestyle Libre is that you no longer have to buy the reader, which is the expensive part of it. Because the iPhone app replaces it. So you scan it with this thing and the $200 reader is gone, and these things are $30. Cool.

And, um, okay, great, awesome, thanks for that. Okay, was there another one, Tyrone, if you want to follow up on that? I might have another one in a bit.

Sure.

Wasn't there liposomal? You want to tell us something about liposomal before you go? Oh, he's gone. Um, oh yeah, yeah, yeah, yeah. Yes, I thought about that. Yes, so I've obviously listened to a few of your podcasts and I heard you talking about one of the other ones, glutathione. And obviously, and we, so just the way that glutathione, obviously most of us know that glutathione is not very well absorbed when you supplement with it. What is your take? And I, was it, is it glutamine or glycine? I heard you Yeah, I like that stuff.

In fact, hold on a second. So you know that I'm not making it up. It's right here. I actually use it. And it's this stuff I think you're talking about. Continual G, it's called. And it is, it is a proprietary form of the predecessor to glutathione, the two amino acids that are difficult to get, and then they bind with glycine. So the two amino acids they call glytine, and this is a very absorbable form of glutathione. I— there are preliminary studies. I can't tell you there's 10 years worth of research, but the preliminary studies show it gets into the cell way better than any other oral. And as you, you point out, oral glutathione hasn't been very successful. So I, I kind of— I'm banking on this. I think that this one actually works, and I'm hoping you know, that it does.

And how would that compare to like a liposomal glutathione supplement?

Don't know. I don't think they've ever been tested. I mean, this company came to me, they showed me their study, I was pretty impressed. I've been trying it, um, I haven't had blood levels measured. I don't know if you can even do that with glutathione, but it looks like good research to me. It looks very promising, and theoretically it makes sense. I also recently was sent a book on glutathione by somebody who— another doctor who's developed a transdermal version of it. I have no idea if it works yet. I mean, they're looking. I'm sure that one of these will be better than what we've had in the last decade. And I'm kind of betting on— I like this continual G stuff, but I'm open to another form of it.

Yeah, you're the second person I heard in a week um, talk about that, uh, glutathione supplement over anything else. That's what I thought I'd ask as well.

Yeah, I like it. I think it's worth trying. All right, cool.

Thanks.

You're welcome. Awesome.

Um, I know Francois, you were about to unmute yourself, I think, and we've got Raquel as well who's formulating a question in her head. If you have a question, folks— there we go, Francois is on the line. Go ahead, Francois.

Hey, hi Johnny, hi Mark, um, inflammation. Yes, uh, inflammation is a word that gets thrown around a lot by personal trainers. How would you, how would you say that, uh, we could identify chronic inflammation easily? Well, as a personal trainer, you have to— you, without a blood test you can't, you can't, but you have to assume that everybody's got inflammation. There's no way to get rid of inflammation or oxidative damage. What you can do is manage it and try to keep it in a range in which it will not do much damage. That's all you can— you cannot get rid of it. You breathe, and if you're an athlete and you breathe hard, guaranteed you got oxidative damage because that's what all those oxygen radicals are doing. But you can quench the fire with a high antioxidant diet, with antioxidant supplements, with anti-inflammatory foods, with anti-inflammatory supplements like omega-3s. So I always assume everybody has inflammation. Now, if you have a blood test, you look at your high sensitivity CRP is a good marker. Interleukin-6. There are different inflammatory markers that you can, you can look at. Homocysteine. But as a personal trainer, I just think the default diet should be an anti-inflammatory diet. You've got to put out those flames. In America, we consume— one of the markers, dietary markers that might predict a high level of inflammation is the balance between omega-6 and omega-3. As you know, omega-6s are pre— they're essential fats, but they're precursors to inflammatory Eicosanoids and the omega-3s are precursors to anti-inflammatory. And those are— you can think of those as two armies in your immune system, kind of, and you need both of them to be funded. We fund the anti-inflammatory army with omega-3s. We fund the pro-inflammatory army with omega-6s. And don't forget, we need some inflammation. If you get a splinter and the area swells up, that's inflammation. It's white blood cells going, let's go to the rescue. Let's find the microbe. Gets surrounded, that inflammation, getting a temperature when you say that's important, it's part of the healing process. You got to be able to put that fire out once the process is over. And that means funding those armies equally. So the ideal ratio in the diet between 6s and 3s, 1 to 1, maybe you want to— you could get 4 to 1 in favor of omega-6s. Still be okay. I like 1:1. 4:1 is okay. We consume between 16 and 20:1. That's a really bad situation. So you got to assume that between that and the sugar, most people got a lot of inflammation and then exposed to toxicity in the air and pesticides and sprays on foods, or— and stress is inflammatory. So I think the default position for any personal trainer is anti-inflammatory diet, anti-inflammatory diet, anti-inflammatory diet. It never— and as far as you know, it's never going to hurt you. Okay. And as far as omega-3 supplementation for someone who has not taken it before and is eating the average crappy kind of diet, uh, what kind of dosages would you recommend and for how long? Well, then assuming you make changes to the nutrition, of course. Yes. Of course, but in terms of supplementation, this is a real question where reality has to come up against theory. Theoretically, if I had my druthers, for me and my wife, we take 3 to 4 grams a day of combined EPA/DHA. Most people won't do it. So the reality is, what will they take? I have them take as much as they'll take. One capsule of fish oil is better than nothing, but not much better. I mean, you really do need a couple of grams a day of the combined EPA/DHA, in my opinion. For people who get none, of course, eating salmon twice a week is a big upgrade, and taking a capsule of fish oil is a big upgrade.

Our audience is a little bit more obsessed. Sorry, I was just going to say, our audience is a little more obsessed, so 3 grams of fish oil is like before bed kind of stuff for the— oh yeah, yeah, yeah, easy.

Remember, it's not just fish oil, it's, it's the gold nuggets in the fish oil, EPA, DHA. You get some of these really crappy fish oils in the big box drugstores and they go 1,000 grams, milligrams of fish oil. Yeah, then look over on the back, how much of that's EPA and DHA? That's all that matters. That's what you dose on.

Yeah. Okay. It's great, thanks.

And just one last quick one, um, for the inflammation. Would you say that insulin resistance is a big key factor in chronic inflammation? I think they go together like a hand in glove. I mean, you can be inflamed without having insulin resistance. I don't know that you can have insulin resistance without having some collateral inflammation. Got it. The one causes the other, but they are partners in crime, and certainly found a lot together. Okay, I wanted to add, besides omega-3s, which I love and I'm a big fan of, quercetin, which by the way coincidentally is now being investigated as a therapy for COVID. Quercetin, which is found in apples and onions, is a highly anti-inflammatory flavonoid, and you can take it as a supplement like I do, or you can take— you just eat a lot of apples and onions. But that's one of the good things foods.

Cool, awesome, thank you, Johnny.

Of course, we didn't even mention turmeric, curcumin, very anti-inflammatory.

Yeah, have we got time for two more questions?

Gems keep coming.

All right, Raquel, if you want to go ahead, unmute yourself, whack on your webcam. Folks, if you want to join the fun and ask questions at home, this is part of— or either you're going to be an Enterprise Trainer trainer or part of Wolfpack. So that's the way to get onto these calls is to be part of the group. So anyway, Raquel, take it away.

Hey, John, thanks so much for all your info. It's so awesome. I had a couple questions about, so I'm a little confused with high-fat diets and say you have an overweight client. How does that actually work? Like how is a high-fat diet good for an overweight client? It doesn't produce insulin. And insulin is what's making it correct, right? Okay. In my newsletter, which you probably don't get in Australia, but I did a 3-minute video on the rationale for a high-fat diet for people who just don't— can't get their mind around it. Why do we recommend high-fat diets? I did a 3-minute video. It's on YouTube. Just look it up and it kind of lays out the rationale. Just Johnny Bowden.

Boom. Yeah, make sure. And I had a newsletter list. Oh yeah, as well.

And I had another question. Um, I'm not sure, but for some reason I've been thinking about histamine a lot, and I'm not sure how— I don't know my question about it, but I feel like there's a conversation about histamine that I wanted, if you have anything on it in particular. I don't. And I think there is a conversation to be had about it. It isn't at top of mind because it isn't a research interest of mine. It's not something I've really looked into. I've encountered enough to know, yeah, that's something we should pay attention to. But I don't want to talk about something I have no expertise in. And so I would tell you, going back to your clients who are— how can I eat a high-fat diet? We do not— when we talk about a higher-fat diet, we are not talking about adding fat to your cornflakes. We're not talking about— someone said to me, how can French fries be good? That's high fat. No, that's not what we mean by high fat. That's potatoes and fat. So we have to understand that there's a big difference between a diet in which fat is the main macronutrient and one in which you're eating the American high-carb, high-processed diet and you just add more fat to it. That's not what we mean. That will make you fat. Yeah, yeah, 100%, clear as crystal. Thank you, that was my question. Awesome.

And last one, Marshall, if you want to go ahead, put your webcam on, unmute yourself. Go ahead, fire away, Marshall. Hi there, am I on? I'm not, I'm not sure. You're on.

All righty, beautiful. How you going?

So yeah, the question is basically when we actually train and, you know, manipulate the body composition there. You tend to get leaner and, you know, you get a bit more muscle mass and such there. So when that happens, we know that insulin sensitivity or insulin resistance do change there. So would low carbohydrate be relative to, let's say, the body composition of a person? Let's say if someone's very, very lean and has more muscle mass, they could actually handle more carbohydrates in theory. And I'm actually using this question as in relation to, let's say, the extreme of, let's say, competing and bodybuilding itself there. Because we know, you know, in bodybuilding itself you need a surplus. And how do you become healthy whilst pursuing that at the same time?

Well, again, I, I haven't been in the bodybuilding world in a long time. I, I started out and I was really into that and I followed it a lot, but I did work, um, for a long time closely with a man named Charles Poliquin. I don't know if you know him, but he was one of them.

Yeah, I just— he was, he was He was one of my mentors. I'm a level 5. He was one of my mentors. I'm a level 5 PSE, which is the highest level. Yeah, yeah, yeah, we know Charles, of course, by the way.

So, so I, um, Charles was a big high-fat guy to the very end. I mean, he, he trained his athletes on a higher fat diet. He, he was not a high-carb— he was not a carb-loading guy. And, and what I do remember from the bodybuilding years is that, like, for example, contest preparation, you want to be as cut and lean as possible, but you got to train that last week. Where are you going to get the energy? Where are you going to get the calories so that you don't look flat? So what did these guys do back in the '90s when I was doing that? They loaded up on MCT oil. They get the calories from this fat, MCT, medium-chain triglycerides, which gave them enough energy to work out. But MCTs aren't metabolized like regular fat. They tend to be used more like carbohydrates, be used for energy. So they're not stored as readily as the other fat. And they just load up on that for contest week. They'd have enough calories, they'd be able to keep the muscles full and not flat, and they wouldn't be consuming the carbohydrates that makes them look waterlogged. So it is entirely possible to do bodybuilding on a higher fat diet, a higher protein, higher fat, lower carb diet. But I would agree with you that people have Not everybody's insulin resistant. I think a large number of people, a double-digit percentage of the population, has some degree of it. But there are superb athletes who are just genetically— they're able to handle that carbohydrate load. Maybe they even need a little bit more. I was telling somebody in another interview that I worked for a while with the Atkins organization. And at one point, the president of Atkins was a guy named Stuart Trager. Who was an MD, who was an Ironman, and he used to do Ironman all over the country. And he required a slightly— now, his diet was about 125 grams of carbs a day. That's not really considered low carb compared to America. That's low carb. They— yeah, that's less than a third of what Americans— so there's definitely differences in people's metabolism and how well they respond. I know that a lot of my friends who, who do one-on-one counseling and nutrition and personal training find that not all women do that well on ketogenic diets and that make some adaptations for that. Adaptations for that. So I think there's a lot of individual factors. I don't believe in prescriptions that one size fits all for anything except like, yeah, try to eat real food and anti-inflammatory ones and stuff like that. But beyond that, those details, you have to take the individual into account. That's why it's personal training and it's not just giving information to the masses. It's like, what does this person need? Like with injuries, you work around them. I mean, there are individual genetics and, and, and tastes and things that people don't want to give up and things that they love and the ability to process carbohydrates better. Some people have an easier time of it than others. So you got to adjust all those things. And I wouldn't say that there's a right number of grams of carbohydrate for every for everybody. There isn't. I hope that answers it a little bit. I mean, you're definitely hard to individualize it. Your instincts are right, in my opinion.

All right, great. Perfect.

Thank you. You're welcome.

Jonny, thank you so much for your time, your generosity. Everyone go buy Jonny's book. If you just want to hold it up again for the folks, jump on it now. That's the one, The Great Cholesterol Myth. Make sure you get the revised and expanded edition. And also grab this one, Living Low Carb: The 150 Healthiest Foods on Earth. I know this one's been updated, which is Unleash Your Thin. Now it's The Metabolic Factor.

Oh yeah, that's Metabolic Factor. That's—

yeah, thank you so much. Of course, of course.

Um, yeah, thank you. Give me your next book.

I will, I will. I'm chipping away at it. And, um, yeah, I'd love to share it with you and the world. So thank you From the bottom of our heart, and make sure you follow, subscribe. Till we speak to you next time, folks, train hard, eat well, and supplement smart. Bye.

Thank you. Bye-bye.