The Joe Rogan Experience - #1175 - Chris Kresser & Dr. Joel Kahn

Episode Date: September 27, 2018

Chris Kresser, M.S., L.Ac is a globally recognized leader in the fields of ancestral health, Paleo nutrition, and functional and integrative medicine. Dr. Joel Kahn is one of the world’s top cardiologists and believes that plant-based nutrition is the most powerful source of preventative medicine on the planet. https://chriskresser.com/rogan https://drjoelkahn.com/joe-rogan-experience-reference-guide/

Five, four, three, two, one. Gentlemen, thank you very much for being here. Really appreciate it. Dr. Kahn, before we get started, why don't you just tell everybody what your background is. You will be representing the vegan portion of this discussion. Tell people about yourself a little bit. Thank you.

I feel like the head broccoli in the United States today. But I am from Motown, Motor City. Badass. Born and raised University of Michigan School of Medicine, summa cum laude. Internal medicine training, cardiology training in Dallas, Texas. Very hard to be vegan in Dallas, but I did it in the 80s because I've been doing this. 42-year vegan. 42 years. 42-year vegan. Thank you. That's impressive. Age 18. And then Kansas City, Missouri. Another tough town to eat plants in only, the Steakhouse KC Masterpiece, did training in stenting. I was blasting open heart attacks from 1990 on.

Came back to Michigan, very active cath lab heart attack. You're dead. I bring you back. Practiced 24 hours a day with great partners. And about three to four years ago, I used all these decades of plant-based medicine I've been basically bringing my family up with and teaching patients, but opened a completely preventive cardiology practice. And along the way with my wife and son, we now own three plant-based restaurants, two

in Detroit, one in Austin, Texas. Write books, do TV, write blogs, teach, teach, teach. Not going to stop them 150. Because there's a lot of erectile dysfunction to stamp out. That's my passion. That? Oh, my God. What else?

What better purpose in life? Well, we can get to that later. Heart disease is somewhere in that mix, too. Okay. And if people want to read more about you, website is? Yeah. D-R-J-O-E-L-K-A-H-N, Dr. Joel Kahn. And you've written a ton of books, right?

Five books and a bunch of medical papers and a whole lot of blogs. Awesome. And Chris? Yeah, Chris Kresser. I did my undergrad at UC Berkeley and then got a master's of science and co-director of the California Center for Functional Medicine, which is a functional medicine clinic here in California up in Berkeley. And I came to this from my own experience with chronic illness. As you know, Joe got really sick back in my early 20s when I was traveling around the world.

And, you know, conventional medicine didn't have much to offer for me. And so that led me on a path of trying to figure out the best approach from a diet and behavior and lifestyle perspective to heal from my own chronic illness. And then that evolved into me starting to write, you know, I started a blog and a website and then wrote a couple of books and now have an organization that trains practitioners in functional medicine and also trains health coaches. And you at one point in time were vegan? I was a macrobiotic vegan. I was apprenticing with a macrobiotic chef. So what's the difference between a macrobiotic vegan for folks and a regular vegan? Macrobiotic is a particular philosophy. It's a particular approach that came from Japan. And

it's vegan, but it's, you know, it's heavily influenced by Japanese tradition and cuisine, and it has some kind of different beliefs than a typical vegan approach. So when I was originally studying Chinese medicine, I was working and apprenticing with a macrobiotic vegan chef, and we were going around cooking for people who were really ill, often people with cancer who were following a macrobiotic diet. And before that, I had been a vegetarian for quite a while as well. When I was traveling around the world and got sick, actually, I was a vegetarian at

that point too. And you discovered through your own personal... What are you doing over there, buddy? And you discovered over there through your own personal practice that you your body worked better and your illnesses went away when you changed your diet away from macrobiotic yeah for me personally vegetarian diet and particularly vegan diet was a disaster but I'm just one person I don't put a lot of stock into you know a single person's experience one way or the other. But certainly that did lead me down the path of questioning some of my earlier beliefs

that I had about vegetarianism and veganism. And it led me to make some different choices. And that is important to discuss here, that everybody's body really is different. And different people's bodies and lifestyles, they're going to have different requirements. Absolutely. I mean, I would say just to start off this whole discussion, if we're trying to answer the question, what's the optimal diet for everyone? I think that's a terrible question and it's an unanswerable question. We share a lot in common as human beings, but we have a lot of important differences too. And from the beginning, I've always argued that there's no one-size-fits-all approach

when it comes to diet. But I think there are some common themes, and I'm sure we'll get to those later. I think that's really important, right? It's really important to discuss that people really do have different requirements. Yeah, and I mean, we'll get in the mud a little bit as we need to, but also Chris and I share a lot in common. I mean, one, if we ate together, it would probably be 90% the same. We both are really respectful of what we call functional medicine, root cause medicine. I don't write scripts without thinking about the patient. He certainly doesn't do that

without thinking about the entire patient. It's pretty unusual. And we're going to represent a very small section. I honor what he's doing with his new book, Unconventional Medicine and the Rest. That is what is happening throughout medicine, and it's necessary because we're just running out of dollars and health when we're just pushing pills and not even asking a person what they eat, how they sleep, the whole thing. We're real people. Yeah, we know that. We all agree on this. Yeah. But it's still rare, Joe.

I mean, this is pretty rare segment. I don't know that 2% of the people in America will have a patient leave the office and actually ask what they ate today. You know? Yeah. It's true. It doesn't happen. Let me say one more thing about this, though, because I think you hit on a really important point. And I'm glad you did it right off the bat.

The biggest problem with nutritional research epidemiology is that it starts with the assumption that there is one diet for everybody. That's something that's rarely discussed, but it's this idea that, you know, should everyone be on a low carb diet? Should everyone be on a high carb, you know, low fat or low fat diet? You know, should everyone do this? Should everyone do that? And the whole, you know, there's a guy in Australia, a professor who calls this approach nutritionism, this idea that we can reduce foods down into these individual components, just like macronutrients, you know, protein, fat, carbohydrates, and we can figure out what works best for everyone just by looking at these isolated components without considering the whole context

of the diet. So I think, you know, Joel would agree that if you talk about a diet that's 50% calories and fat, and one diet is they're getting all of those fat calories from pizza and chips and candy bars and things like that. And then another diet, they're getting 50% of fat from avocados and olive oil and even eggs and animal foods. Those are two totally different diets. And yet in the scientific literature, those are equated as the same because all they're looking at is the calories from fat.

They're not considering the quality of the diet. And I'll just add in, and again, we go anywhere with this conversation, but a lot of the problem has been imprecision of language. So even the word low carb diet, I eat a low carb diet if we talk low refined carbs. I don't eat white flour. I don't eat sugar. I'm very careful about all those components. I eat a very high complex carbohydrate diet. So a giant study that's been released this year, it's a pure study, talks about carbs in the diet. They didn't differentiate complex and refined. Very hard to know what to do with data that doesn't spread that apart in your own life. I mean, low fat, high fat. I mean, we need to talk about, is it soybean oil that's processed and rancid?

Are we talking about avocados and healthy whole foods? So the precision of language, even protein. Protein, the big divide, is animal versus plant. So anytime that word comes up, we need to differentiate. Be precise, and then we'll help more people if we're precise. Yeah, and if you can, just to illuminate this for people, what is the problem with epidemiology studies? Oh, boy. You know, i'll go there real quick i mean i don't think there's a problem but they're a part of the solution they're

not the whole solution a lot of scientists i'll give a shout out to los angeles brightest nutrition mind somebody that i know chris honors to walter longo no label not vegan not paleo not nothing he's a usc been honored by the Royal Academy of Swedish Medicine, which is a Nobel Prize committee and this and that. He says, you know, you do basic science, and then you do an epidemiology study to test the hypothesis. You see something in a petri dish. You see something in a mouse.

You see something in a cell. You ask the question, is animal protein pro-longevity, pro-early aging? Do you mind explaining epidemiology studies to people? So you would take that concept. I'll just remember that. You look at an amino acid found in animal protein, throw it out, methionine, leucine, in a petri dish looks like it might cause accelerated aging in a single cell. That's biochemistry.

That is something you honor, but it's a long jump from there to human. Then you look at a database. Sometimes it's a crappy old database. Sometimes it's Harvard has these gigantic ongoing database. Loma Linda, an hour from here, has a gigantic database. And there's others, an epic study, this pure study I mentioned. You can test a hypothesis of what happens if our data may be crappy, but it's still data, and it allows you to go further with 100,000 people, 50,000 people, 500,000 people.

Do we have the data to ask the question, does protein correlate with survival? Protein correlate with early death? Animal protein, plant protein? These studies have been coming out a lot lately and they let you parse it out. Now it's what Chris talks about. Do you know everything about the person in the database? Do you know smoke or do you know diabetes? Do they go to the gym?

Do they lift weights? Do they smoke dope? Do they smoke crack? You don't know everything. Nowadays, most of these things you're going to ask are your blood pressure, cholesterol, all the basics to try and take those factors away and isolate the question you're asking. It will be imperfect. And then you go to the best study, but it won't happen often, the randomized clinical trial.

I mean, there's never been a randomized clinical trial of smoking because that would be unethical. You're never going to do it. It was epidemiology that proved an association strong enough to recommend to the public, don't smoke. There'll never be a randomized trial. And not everything, parachutes don't need a randomized trial. You know, taking folic acid in a pregnant woman to not have spina bifida doesn't need a randomized trial. You know, taking folic acid in a pregnant woman to not have spina bifida doesn't need a randomized trial. I mean, there's some things that are so pressing, the public health can't allow that.

And there's even more than that. The last little section is you can study old people. Chris enjoys studying ancient societies. I enjoy studying the elderly in current, you know, modern environment, which is called the blue zones, and there's others. But, you know, what do old people do, the old healthy people, what we would like to be? Would you like to be 90 and have your brains and have your joints and everything working? Well, we have that database. So that little four-pod pedestal to sit on, basic epidemiology, randomized studies, and centenarian studies allows you

to make reasonable conclusions. You know, we'll be wrong sometimes. We're not going to be very wrong. Chris? I think there's huge problems with epidemiology. So epidemiology, observational studies are studies that look at a certain group of people and then try to draw inferences from their behavior about associations with disease. So let's say we take a group and we look and see, you know, how much saturated fat are they eating?

And we separate them into, you know, low consumption, medium consumption, high consumption. And in a prospective study where we're watching them over time, we might then look 20 years later and see how many people had heart attacks and died. Okay. And then we try to, you know, correlate that with their amount of saturated fat intake. Now, I actually just published two articles with going in detail on the problems with observational nutritional research. And you can find them at kresser.co slash Rogan. There's a whole bunch of information that we're going to be talking about today there. So people can go and get the details themselves. But I'll just give

you three of the, I think, the worst problems with nutritional epidemiology. The first is data collection. So there's a saying in science, which is that data are only as good as the tool used to collect them, all right? And in nutritional observational studies, the tool used to collect them. And in nutritional observational studies, the tool used to collect data is a questionnaire. And so that relies completely on memory. And we know that memory is not a precise, accurate, or literal representation of events. It's more like a highly edited anecdote of what happened in the past.

It's a little bit like the Kavanaugh thing going on right now. Back in the 13th century, you had Francis Bacon who said, for something to be scientific, it has to be independently observable, measurable, and falsifiable, and then accurate and valid. And so let's use an analogy. If you're sitting there eating an apple, and I'm watching you do that, I can observe that you're eating the apple, I can measure how much of the apple you eat, and I can confirm or refute that you're eating the apple. If you tell me that you were eating an apple 15 years ago or 10 years ago, I obviously can't observe that, I obviously can't measure it, and I obviously can't confirm or refute it. And yet our entire foundation of nutritional epidemiology is based on that. Basically,

people reporting on what they ate at some time in the past. So, you know, how much of a problem is this? There's a guy named Edward Archer, who's done some really interesting studies. And he looked at the NHANES data, the Nurses' Health Data, which is one of the longest-running nutrition studies, 39 years, and he found that the self-reported calorie intake in those studies was either physiologically implausible or incompatible with life. So the average person in those studies reported a calorie intake that would not support

an elderly, bedridden, frail woman. So it's just inaccurate. It's completely inaccurate. And the people who are most likely to under-report are people who are overweight and obese. So if calories are that much under-reported, all nutrition comes through calories. Everything we get, fat, protein, carbohydrates, micronutrients, they all come through calories. So if calories are that underreported, that completely invalidates the data set. So this is an obesity study. So they're underreported because of shame? It's not an obesity study.

It's just Americans are overweight and obese. The majority of Americans are overweight and obese. The majority of Americans are overweight and obese. So in any data set of Americans, you're going to have the majority of them overweight or obese. So that's the first problem. The second problem is a healthy user bias, which I know we talked about before, but it's basically the idea that because, you know, when someone engages in an unhealthy and a behavior that's perceived as unhealthy, they are more likely to engage in other behaviors that are perceived as unhealthy and vice versa. So let's say you do a study of people who eat more red meat. Well, red meat has been perceived as unhealthy for a long time.

And so what we know is that in those observational studies, the people who eat more red meat are also smoking more, they have higher body mass index, they're eating less fewer fruits and vegetables, they have a lower level of education, they're less physically active. So how do you know that it's the red meat that's causing the problem and not those other things? You don't, because they cannot control for all of those potential confounding factors. The third problem with observational research, and maybe the biggest, is that the relative risks in nutrition are so low that they're indistinguishable from chance. So in fields outside of nutrition and epidemiology, nobody would consider a relative risk, an increase in risk less than 100%, a doubling, to be really worth paying attention to. So to put this in perspective, the observational studies that Joel was referring to that confirmed that cigarette smoking led to lung cancer, that showed between a 1,000 and 3,000% increase in lung cancer in smokers. Okay. And the studies that have shown that eating aflatoxin, which is a mycotoxin increased liver cancer risk,

that's 600 percent increase. Okay. The IARC, the WHO report that suggested that processed red meat was a carcinogen, that was 18% increase. Most epidemiologists you talk to will say that is so low that it's really indistinguishable from chance, especially given the healthy user bias and the problems with the data collection that I mentioned before. So the studies that are cited, so when people are talking about red meat causes cancer, they're literally talking about something that showed an 18% increase. Yeah. And this is over people that are also consuming sugar. So that translates into four and a half, there were four and a half cases of cancer out of a hundred in people with no lowest intake of processed meat. And that went up to 5.3 cases out of a hundred in people with the highest intake of processed meat, and that went up to 5.3 cases out of 100 in people with the highest intake of processed meat.

So, you know, there are quotes, like, if you look even 20 years ago, like, there's an article in Science, the journal Science, and Marcia Angel, who was the former editor of New England Journal of Medicine, was quoted as saying, we wouldn't even accept a paper for publication if it didn't have at least a 200% increase, especially if it was a new association or the biological mechanism wasn't known. And here we are today saying that, you know, this increased that by 7% or by 10%. And when you consider that the data is usually questionnaires of what people ate and all of these confounding factors like exercise and fruit and vegetable consumption and things like that are not accounted for, then we're really just playing games with numbers. the problem as well that there's this clickbait culture now in terms of journalism where they just want to publish something that says a study shows you know 18 of people eat red may get cancer that's a huge problem and there is a study that was done that showed that 43 percent of findings

came from observational studies were portrayed in the media as being causal, which any epidemiologist would tell you that that's a faux pas. You can't do that. But nobody is going to click on a headline that says, you know, small association between these two variables seen. We don't know what it means, but please read the story. It's really interesting. Let me just grab a couple. And again, a lot of respect and agreement, but if we throw epidemiology away, we've thrown away about 80% of nutrition knowledge, because that is the most common kind of study. And that still leaves us with basic science, which is rocking. It leaves us with randomized clinical trials, which are very hard in nutrition, and they're very expensive, and there's less than we need. And it finally leaves us with studying old, healthy people, centenarian studies.

We'll just go to Loma Linda. Ten times more people in Loma Linda are over 100 than there are in Los Angeles. Ten times more. That's by definition. Yeah, it's called the Blue Zone, and we'll talk about Blue Zone. Well, it was discovered in the 1950s. If you lived in Loma Linda, you were living 12. Where's Loma Linda?

Loma Linda is an hour east of here. What's going on over there? Well, it's the center of the Seventh-day Adventist Church, which teaches people, eat your veggies, don't drink, don't smoke, and exercise. So it's an amazing lifestyle-oriented aspect of the Christian church. And they, in 1958, got huge funding from the government to explore

why the heck are they living 12 years, 8 years, 10 years longer, and they've parsed that out in probably 1,000 publications. It's not a randomized study. It wasn't L.A. versus Loma Linda, we'll feed you different diets and fat. It won't ever happen. But it is a reliable, long-term peer review. This stuff's published in the finest of journals, and it at least lets you ask questions.

I mean, why is there a 104-year-old cardiac surgeon, Elliot Worsham, walking around doing his gardening, and he just finished operating on heart patients? I mean, it's insane. 104, Elliot Worsham. Love you, buddy. But let me go back for a minute. If we throw epidemiology out, we are left with basic biochemistry. I'm not suggesting that, by the way. No, I know, I know, I know. But so food, this is all technical stuff, but you've got a sophisticated audience. Food frequency questionnaires, what Chris said, is the source of a lot of these epidemiology studies. You fill out a four-page, a 40-page in Loma Linda. It's a 58-page survey.

But you do it once. That's called the pure study. The headlines, you've seen them. Cheese, eggs, meat are good for your heart. It's been in the news the last two weeks. That comes from a giant international study. They did one food frequency questionnaire at the beginning. Twelve years later, they're reporting the data.

It's all clickbait headlines. It's like you say, people love to see this stuff. So if we throw out some studies, we have to throw out the largest nutritional study that's been reported and the most recent one that's getting all the headlines. It's got to be played fair. Now, you go to Loma Linda, it's every four years they're asking. You go to Harvard School of Public Health, every four years, they update the data. So if you change your diet, that's the weakness. You fill out the survey and then you get healthy or you

get sick and you make changes and then they're counting if you're dead or alive. Well, it might be what you did year six, not what you filled out year one. So there are better and worse forms. The second, I'd say healthy user bias is the idea that people pick a certain diet, might have other lifestyles. It might be as or more important. It's going to be true of the paleo group. I mean, these guys are, look at Chris. He looks wonderful.

He's healthy. He's thin. He's not the obese American, the 75% that are overweight and obese. I mean, that's true in the plant community to some extent. We have chubby vegans. Oh, my God. But there's no observational studies with significant numbers of paleo dieters, Joel. Oh, I know. I know that.

So the healthy user bias is not an issue for paleo people. But if you don't have data, it doesn't mean – I mean, you don't have data because it's a new movement that hasn't had the data. But it's not to cast stones that plant-based eaters go to the gym more. It's probably true. We don't know. And that's the third thing. But to stop you for a second, meat eaters do get lumped in with the paleo group they consider paleo group part of the meat eater group like when people talk about these epidemiology studies where they show that people that consume red meat that's right more likely to get sick more likely to get cancer they're not referring to paleo dieters that are eating avocado and grass-fed beef. Well, you got to remember, I mean, most of the paleo movement is the last dozen, 15 years.

You know, we can talk about that. 1985, 2002. Lauren Cordain published her book in 2002. The book didn't sell. Republished 2010. It took off. This is a relatively new movement. So if you've filled out the study in Loma Linda in 1958, you don't have to worry. There weren't too many people following a classic paleo diet. That's also true at Harvard. The last is just the relative risk. That's what we call it. These are pure statistics.

I'm a heart doc, not a statistician. But there are some exceptions. I mean, anybody, and I'll just say, I've got a red button on my website that says Rogan references, because I thought it would be good to have people, a place to go, just like Chris mentioned. And I'm not massaging the data. It's scientific peer-reviewed data. There was a study October 2016, October 1, 2016, Song is from Harvard, 6,000 people, observational data, animal protein, plant protein.

Actually, let me go to 2014, Morgan Levine. This is an amazing Harvard researcher, beautiful woman, Morgan Levine. She looked at 6,000 people prospectively. Observation, fill out all these data. If you were an animal protein eater, that's called meat, you had a 3% to 400% increase in cancer risk. 3% to 400%, that's three to four times, isn't 1.1%, 1.08%, 18%. The data's there. This is peer-reviewed data.

If you ate plant-based proteins, the risk of cancer goes down. This is in the highest level. Pause for a second. Let's pause on that. Pause on that. I just want to say there are nutritional data that are powerful risks. But this is also an epidemiology study? That's where 80 – nobody's going to do a randomized study of 6,000 people.

You eat beans and you eat – Listen, I think I have a good example that can clear some of this up. So you mentioned the Loma Linda and the Seventh-day Adventist studies. So first of all, let me just make a comment about observational nutritional research. There are good observational studies and there are bad ones. You can design an observational study in a way that controls for some of these potentially confounding factors like the healthy user bias, et cetera. So, but this is a story that will, I think, clear some of this up. So there are about eight studies, major studies that have compared lifespan in vegetarians and vegans and omnivores. So the earlier studies,

there are three studies that were Seventh-day Adventist studies. So they were done in the Seventh-day Adventist community, which Joel mentioned is a religious group that has as part of its credo, you know, a healthy lifestyle, diet and lifestyle. Yeah, about 20 million, 20 million people. Let's not talk over each other. Let's just make sure we give each other a chance to breathe. You know, vegetarian diet, but also, you know, live healthy, eat fruits and vegetables, don't smoke, don't drink excessively, et cetera. So, you know, health conscious group of people. And the first one, the Seventh-day Adventist study in the Netherlands compared them

with the general population, which is just garbage because of the healthy user bias. So we can just cross that one off the list. The two Seventh-day Adventist studies that were done in Loma Linda in the U.S., they did a better job because they compared people who do eat meat amongst the Seventh-day Adventist population with people who don't. And there was a slight advantage in lifespan in the vegetarians versus the meat eaters. But one of those studies didn't control for smoking and body mass index. So that data is highly suspect. And the other study did, and there was a slight advantage. Since then, there have been four studies that I think did a much better job. So this is kind of an interesting design. So they said, let's try to find a group of more health-conscious omnivores to compare these vegetarians against.

So the first one was called the Health Food Shopper Study. So they looked at people who shop at health food stores, when the idea is people who shop at health food stores are going to be generally more health-conscious. And they found- By health food store, you mean like a Whole Foods or Air One? I mean, there was no Whole Foods at this point, but that was the idea, right? And so that study found that both groups, vegetarians and omnivores who shop at health food stores, had a hugely reduced risk of death compared to the general population, but there was no difference between vegetarians and omnivores. Second study, Oxford Vegetarian Study in the UK, they recruited people by, first they recruited vegetarians,

and then they asked the vegetarians to ask their friends who also ate meat. So the idea was the people that the vegetarians were hanging out with might be more health conscious than the general population. Same result. Big difference in lifespan between those two groups in the general population, but no difference between vegetarians and omnivores. Epic Oxford cohort, same thing, same way of recruiting people, same result, big difference between the two groups in the omnivores, but no difference between vegetarians and omnivores. And then the Heidelberg study was in Germany, and similar way.

I think they recruited people who read vegetarian magazines, and then they asked them to bring their friends or family members who ate meat. and a similar way, I think they recruited people who read vegetarian magazines, and then they asked them to bring their friends or family members who ate meat. Big difference in lifespan between the two groups and general population. No difference between vegetarians and omnivores. And then you had the 45 and up study that was recently done in Australia. This was a little different because they didn't set out to find more health-conscious people. Instead, they looked at 250,000 people, big sample size, and they did a much better job of controlling for all of the various factors that might affect, you know, the results. So

exercise, physical activity, fruit and vegetable consumption, cigarette smoking, alcohol, education level, because we know that has a big impact on lifespan. And they found that there was no difference in lifespan between omnivores and vegetarians in that study as well. And then there have been two meta-analyses of all of the studies that have looked at this. Both meta-analyses found no difference between vegetarians and omnivores in lifespan. So I think this is a really good example of what we're talking about here.

That's all observational data. So we're not throwing it out or saying we should throw it out. But all of those studies did a better job at dealing with the potential pitfalls of observational studies. And when they did that, they found no difference. And I want to point out that those ways of picking more health-conscious omnivores, they still weren't comparing like someone on a paleo type of diet with a vegetarian. They were just guessing that someone who shopped at a health food store was at least a little more conscious about health than the general population. Can I quickly clean up? Quick, quick, quick,

I just want to go back for a minute to meat and cancer. World Health Organization is not a vegan group. It's not a nothing group. You know, it's a fairly well-respected international organization that puts out health claims. So although I absolutely, Chris had the data right, 18% increase in cancer risk with processed red meat. I want to make that clear. I hope you don't eat too many hot dogs, salami, bologna, pepperoni. That's the... Nitrates. Yeah. Well, it may be more than nitrates, but it's just the whole wayologna, pepperoni. That's the— Nitrates.

Yeah. Well, it may be more than nitrates, but it's just the whole way. It's the salt. It's the preservatives. It's junky pieces of the animal that they're putting into a hot dog. That was a group. That's an 18% increase. You can go 4.5% to 5.5%.

That's still 50,000 to 60,000 people a year that get colon cancer if that data's right. They wouldn't get colon cancer if they just would stop eating hot dogs. At a minimum, and I know Chris will agree, frigging hospitals are serving hot dogs, and the data's out there that it promotes cancer to people getting chemotherapy with the IV pole. It's insanity. So 50,000 people avoid colorectal cancer with small differences that the World Health Organization suggests. It was 800 papers and 22 world experts. There's no perfect study, but when they announced that October 25, 2015, the world was shocked. You just said that processed red meat causes cancer.

They didn't say related. They were strong enough to say cause. They've been beat up. They published more data. They haven't backed down. I just want to put that out. The healthy user bias will exist in the paleo community when the study is done. Look at Paleo FX.

It's everything, And I honor that. I mean, we should promote healthy lifestyle. Food's only one part of this. I mean, we will all at this table live longer than the average American. We're not smoking two-pack a day. We don't have 38-inch waistlines. The whole deal. We're doing the whole thing.

Hopefully you guys are enjoying a little Cabernet now and then. That's always on the list. Just don't overdo it. But the healthy user bias, that particular, that health food study paper, it's 1996, it's a pretty old paper, in the paper, in the limitations, they beat themselves up. We were missing this or that. Anybody just read the paper.

It's not that it doesn't bring up an interesting point, but to say that we, again, throw away all these papers because they are biased. Lastly, and I'm done, multivariate analysis. Chris was just talking about better studies that factor all this stuff. Let's not bore your audience with statistics, statistics. But there's certainly the ability now to say, does animal protein associate with an increased risk of cancer and put in smoking and weight and diabetes and blood pressure

and vegetable intake and alcohol intake and family history? And then you just isolate the one thing. Is there foibles? Are there downsides? Of course. But all modern epidemiology does multivariate analysis to try and isolate it. You know, you can cast stones everywhere. But, you know, there are, you know, the World Health Organization, I mean, there's 21 organizations

say limit your saturated fat in your diet and none that are in international society say increase it. So you put nutrition science needs incorporate as much as you can with as much reliability and at the end of the day you can see we'll still have questions but i can't throw us used to say don't eat much cholesterol now they don't they used to say limit your total fat and now they don't that's wrong because they've gone out it's not wrong actually the us says in the guideline, eat as little cholesterol as possible. It says cholesterol is not a nutrient of concern.

Because they couldn't identify the exact milligram to recommend. It used to be 300. Because the science doesn't support limiting dietary cholesterol anymore. Let me go back to this question. They say limit cholesterol. They say limit cholesterol to as little as possible. What's this they? Who is they?

USDA. USDA. The guidelines come out every five years, and they are used for school menus and hospital menus. It was a big buzz in 2016 when it was announced. They no longer were giving so many milligrams of cholesterol a day, you'd never exceed. They said we can't pick the number. Isn't USDA behind the and in terms of science total mortality is the most important endpoint we should be talking about here that means deaths

from any cause okay so if because that's what we care about most right if you if i die of uh you know if i if an intervention reduces the risk of a heart attack but increases the risk of cancer, I'm not happy with that. In fact, I'd rather go out and have a heart attack in my sleep. One shot, bam. So you need to consider total mortality. And if meat increases the risk of cancer and cancer mortality, then why aren't we seeing that in the studies that compared lifespan with vegetarians and omnivores? mortality, then why aren't we seeing that in the studies that compared lifespan with vegetarians and omnivores? We have, as I said, we have five studies that did a better job of controlling for that healthy user bias, and there was no difference in any of those studies. There's not a single

study that compared relatively equivalent groups of people that shows that vegetarians or vegans have a lifespan advantage, period. There is not. And so if we're saying processed meat increases the risk of cancer by 18%, maybe, maybe not, but that's not showing up in any of the total mortality data. The second thing, and this is a really good example of what we talked about at the very beginning of the show, context is everything. Quality is more important than quantity. So let's think about processed meat. So there's several proposed mechanisms for how processed meat causes cancer. One is that it increases N-nitroso compounds or NOCs, which damage the gut lining. Another is that when you cook meat at a high temperature, it forms

heterocyclic amines or HCAs, which damage the gut. Another is that the heme iron content in meat causes oxidative stress and increases the risk of cancer that way. And then there's TMAO and NU5GC. But let me just give you a few examples of why context is important. So there's evidence that chlorophyll-rich green vegetables prevent myoglobin from being turned into N-nitroso compounds. So if you're eating processed meat, but you're also eating kale and broccoli, then it's not going to have the same effect on the body as if you're just eating a hot dog. Cruciferous vegetables and spices and marinades

have been shown to reduce the formation of heterocyclic amines or HCAs. So same thing. If you're, you know, if you're marinating meat or if you're eating broccoli and cruciferous vegetables with meat, it's not going to have the same impact. There are several studies that have shown that eating fruits and vegetables attenuates the oxidative capacity of heme iron and even reduces the absorption of heme iron in the gut. And, you know, dietary antioxidants have been shown to reduce the risk of gastric cancer. So heme iron intake, really, you can think of it as a proxy for a crappy diet in these observational studies. There's a quote from a study that did find a relationship with heme iron and cardiovascular disease. But the study author himself said, with respect to heme iron intake, we found a significant association only in the studies that were based on American cohorts.

They didn't find an association in the Netherlands, Canada, France, Italy, Japan, and Sweden, which suggests that it's because of the standard crappy american diet you know most people who are eating processed meat in in the u.s are eating it in the form of hot dogs and all kinds of other unhealthy food and it's another example of healthy user bite i'm not saying i'm open to the possibility that too much processed meat can be problematic but you have to consider the context it's not going to have the same effect if someone's eating a ton of fruits and vegetables versus someone who's on a standard American diet. And we have no studies that separate that out.

I think we have a gong moment because I really want your listeners to come away with a few tips from Chris and I that make a difference. Because I know your listeners aren't going to stop eating meat at the end of the show. They might. Chris just said meat with vegetables is safer than meat without vegetables. Meat with chlorophyll is safer than meat without. I can give you a cardiac study. He said, agree. I teach.

He said processed meat. Well, it's all meat. I teach that if you... Is it all meat? Is it the same? No, listen, we agree here. I want people to hear this. But do we? When you grill, how many people in the audience grill barbecue? Everybody. If you grill meat, another chemical group that's formed are called advanced glycation end products, AGEs that go along with the list. But if you grill meat that's marinated, and this is the tip in dark beer.

This is science. Randomized science. You put a piece of beef in dark beer and you grill it. You don't create as many of these toxic chemicals as a dry piece of beef. So let's like right now, everybody listening, next time you eat meat, get a salad. Next time you eat meat, order broccoli. Next time you have bacon, get a, you know, sliced tomatoes. You will actually improve your health.

There's this classic, and now I'm shifting to cardiology, that they took healthy volunteers and they took them down to the hospital cafeteria and they fed them a hospital burger, and they were measuring on their arm how their arteries function. Cardiology topic. Artery function goes down in three hours when you eat a hospital burger. It acts like you just had a toxin in your body. You did. They took the same group a week later.

They had them eat the same burger with a big salad. They didn't see that finding. I mean, I want this to be an important point. You know, Everybody should be jamming fruits and vegetables, or at least vegetables with some fruits. You can go low glycemic berries. I'm fine with papayas, cantaloupe, and apples, but

up your veggies, listeners, and you'll counteract a lot of the crap that's out there in the world. It's an important message. I don't disagree with that. No, you know you wouldn't. You have to. We glossed over this very quickly in the beginning of this, but there was a dispute about cholesterol and a dispute about saturated fat. Nah. Serious? You were saying that saturated fat, that there's recommendations to reduce saturated fat and reduce cholesterol. So let me get a real quick overview, and I'm

going to talk fast. Just talk normal it was felt plenty of time it was felt so until the 40s it was not common to have a heart attack heart attacks were described in 1916 not to say they didn't happen but the first medical article that used the word myocardial infarction 1916 1940 there were not many heart attacks seen in a modern american city after world war ii where our economy went up. In the city of Minneapolis, executives started suffering heart attacks. It was also Franklin Delano Roosevelt died of high blood pressure. A few years later, Eisenhower had a massive heart attack. That's when our government, National Institutes of Health, started funneling major money into studies like the Framingham

study. You're from Newton. Framingham's a city outside of Boston, and they basically invaded this town in 1958 to today. So we're spending money. We're going to figure this crap out. The idea had come up. Heart disease wasn't just aging. Heart disease could be explained by what's called risk factors. Smoking might not. You can smoke and live to 100, but it's going to increase your risk. And then they got into blood pressure and cholesterol and family history. They identified what we call risk factors. So until that point, diet was not considered a factor in the development of the number

one killer of men and women. I want to point out, and Chris puts this on his website, I do too, during this interview, every 39 seconds, an American dies of heart disease. Every 39 seconds, the most frequent cause of death. So there will be about 200 people, perhaps, that will die during this podcast as the number one killer. And 80% of it's preventable. Chris is going to prevent some. I'm going to prevent some.

Because the biggest enemy out there is smoking and crap diet. Calorie-rich and processed foods, crap, sad diet, standard American diet. It became apparent in the early 1950s diet might play a role. And a notorious scientist and many others, his name, Dr. Ansel Keys, PhD, PhD, two of them, suggested dietary fat might be a factor. It was a hypothesis. It's his early stage epidemiology. It doesn't prove anything. He went out and did studies.

Other people went out and did studies. And the idea transitioned. Actually, he was criticized for saying dietary fat. The conversation transitioned. Actually, he was criticized for saying dietary fat. The conversation transitioned. There's some good fats, like omega-3 fatty acids are essential. You have to have them. And then maybe polyunsaturated fats from plants are more helpful. But the focus went on saturated fat in food, which is basically chicken, red meat, pizza.

Those are the highest sources. And subsequently enough data accumulated that guidelines started to suggest we've got this huge problem with heart disease. We should limit saturated fat in the diet. It was never limit all fat, 35% of calories. That's not in anybody's word a low-fat diet. And that has now promulgated in 21 international statements. There is no opposite.

Whether it's the World Health Organization, the American Heart Association, American College of Cardiology, whether it's the Institute of Medicine says eat as little saturated fat as possible. They couldn't be more clear. And these are highbrow. These are not associated with vegan movements or paleo movements or whatever. These are medical authorities. If there was half and half, you'd say controversy. 21 to 21 say the same thing.

They might pick a different cutoff point, but we will enhance the health and cut down on the number one killer, whether it's in Asia, whether it's Europe, whether it's Australia, whether it's in the United States. There's unanimity. Okay, but why did they come to the conclusion of saturated fats? Well, basic science, because there is basic science. Let me tell you, when you eat foods rich in saturated fat, which is called meat, cheese, eggs, and such, receptors on your liver for cholesterol.

I've got cholesterol in my blood. I'd like to get some of it out into the liver to be metabolized. I need a receptor. You eat saturated fats, receptors go down. Cholesterol has no place to go. Cholesterol stays in the blood, bumps into your artery while I'm putting a stent in your artery. That's the basic biochemistry. Then they had epidemiology studies, flawed, perfect. It doesn't matter. It does matter. Whoa, whoa, whoa, Chris, Chris, thank you very much. Then they did controlled

trials. Everybody just go read Clark 1997, 395, it's called metabolic studies, change the diet, see what happens. You add saturated fat, cholesterol skyrockets on average, not in a single person. If I gave you a steak, Chris a steak, and me a steak, our cholesterol would rise differently. It would rise. It would rise differently. It's our microbiome. It's our genetics. It would rise.

So that's a problem in the studies when you average everything together. So they had that. And then finally, finally, they looked at populations that live over 100. These are called the pillars of longevity. They don't eat foods rich in saturated fat. They have a little. They don't have a lot. They eat a lot of olive oil in Italy and Greece.

They eat almost no dietary fat in Okinawa, Japan, and they have the greatest longevity in the world in 1970. They eat almost no dietary fat, about 6%, 7%. Okay. So you put all that together. about 6%, 7%. Okay. So you put all that together. Well, no, it's actually, that is the basis for a major push to say

cut back on animal products because that's largely with the exception of coconut and palm, you know, where saturated fat comes from. So to negate that is to throw out every major health agency in the world. I don't believe Chris Kresser can do that. No disrespect. I don't think Chris can throw can do that. No disrespect. I don't think Chris can throw out

a hundred years of cholesterol research. Okay, let's back up a little bit here. Yeah, so first of all, every food that we consume has all of the fats in it. Polyunsaturated, monounsaturated, and saturated fat. And in fact, two tablespoons of olive oil

has more saturated fat than a seven ounce pork chop. That's a little known fact. The oily fish, mackerel, you know, which all of these health agencies that Joel is talking about advises us to eat, has twice the total fat and one and a half times the saturated fat of the meat that we're told to avoid. Does it make sense that nature, you know, would include that you could include that you could eat mackerel and the polyunsaturated fats in it are good for you, but the saturated fat in it is bad for you? That's kind of nonsensical. But, you know, let's talk a little bit more about the research.

So there never really was good evidence to suggest that dietary cholesterol and saturated fat are connected to heart disease. And Zoe Harcombe, who has a PhD in nutritional researcher, she wrote her thesis, her PhD thesis on the evidence back in the 70s that led to the restrictions on saturated fat and cholesterol. And then she also reviewed the evidence all the way up until 2016. And I have this information on my website. If you go kresser.co slash rogan, you can find it. And what you'll find is there never was really good evidence to support the limitations on saturated fat and cholesterol. And people have started to look at this more recently. And for example, you have a meta-analysis of observational studies, including about 350,000

participants recently that found no relationship between saturated fat intake and cardiovascular disease. You have an exhaustive review of studies, something like 25 randomized controlled trials, gold standard of clinical evidence, and almost 40 observational studies involving 650,000 participants. And I'll read you a quote from the conclusion. Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of saturated fatty acids. Now look, one of my favorite quotes is the philosopher Anatoly France, even if 50 million people say a foolish thing, it's still a foolish thing. And the other thing to consider is that the history of science is really the

history of most scientists being wrong about most things most of the time. And, you know, in science, we have to continually challenge our hypotheses and try to falsify them. And that's how the scientific process moves forward. And that's why in 2010, the US federal government removed restrictions on total fat, whereas before there was a restriction on total fat, because they acknowledged that the research was showing that not all fat is the same and that, you know, we don't need to be restricting fat from avocados and things like that. And then in 2015, they removed the restriction on dietary cholesterol. Now, they did that fairly quietly because how do you think it looks when people have been told to, you know, limit their fat and limit their cholesterol?

And then the federal agency goes back on that recommendation after so many years of telling people to do that. People lose faith in the agencies that are issuing these guidelines. And don't take it from me. You know, I'm not expecting anyone to believe me. And don't take it from me. You know, I'm not expecting anyone to believe me. And that's why I've put all of the studies and the research supporting this at Cressor.co slash Rogan. But how about Johnny Onidis, who's one of the most renowned epidemiologists in the world?

He's a professor of medicine at Stanford. And he has written some scathing critiques of nutritional research recently that have been published in JAMA and British Medical Journal. So here's a quote from one of them. Some nutrition scientists and much of the public often consider epidemiological associations of nutritional factors to represent causal effects that can inform public health policy and guidelines. However, the emerging picture of nutritional epidemiology is difficult to reconcile with good scientific principles. The field needs radical reform. And he goes on to point out that meta-analyses of observational studies have found that almost all foods are associated with a higher risk of death if you crunch the data in certain ways. So it's not enough to say that governments are recommending this or that.

We have to look at the science and what the science is saying. And as I said, two recent meta-analyses covering over a million people are not showing a relationship between saturated fat and heart disease, and they're not showing any benefit from replacing saturated fat with polyunsaturated fats. So these organizations, Joel, that you were describing, why do you think that they recommend, based on what Chris has just said, why do you think that they recommend reducing your saturated fat, reducing your cholesterol? Okay. And thank you. And you know, the importance here, we are, you know, technical in the weeds, but I want to bring it back. This discussion is, do you have a stroke, heart attack, erectile dysfunction, lose a leg,

This discussion is do you have a stroke, heart attack, erectile dysfunction, lose a leg, or do you not? Because at least one factor in development of these horrible medical problems that are 80% preventable, at least one of it is your nutrition and the content of your nutrition. I mean, there's no doubt. It's a single most important factor. It's never been the only factor. Okay, but why do you think these organizations are saying this if he's saying that the studies don't support that? Well, I disagree that the science, and I want to be very specific. Let's talk about cholesterol. Let's talk about saturated

fat. So let's stay with saturated fat because there is differences there. They're both, you know, contents of food, fatty contents of food, but they're chemically different and the volume weight is very, very different. Cholesterol only comes from animals. Saturated fat is in animals and plants, depending on the food source. So when this rise in heart attacks developed, research began, 1948, 1950, 1958. There were observations made that carefully done dietary logs suggested these were hypotheses. There might be a connection between what you eat and heart attacks, and then it's centered on, you know, is it foods

high in protein, foods high in sugar, foods high in fatty sources. Ultimately, they got sophisticated foods high in plant fat sources, foods high in animal fat sources. So by the late 1950s, there was a very strong consensus already that foods high in animal products with saturated fat, they go together. We're talking meat, egg, and cheese may be a rule. Let me give you a great example. In 1959, you grew up in Japan. You have a cholesterol of 120. You almost never see a heart attack. You move to Hawaii because there's migration. Your cholesterol rises to 180. Welcome to America. Your heart attack risk triples. You move to this great city, Los Angeles. This was published in 1959. Your cholesterol is now 210.

You have 10 times the heart attack risk that you had when you lived in Japan. Genetics don't change that quick. This was within one generation. They're called Nisei. People that leave Japan to move to California, the Nisei. And there's the Nisei-Hann study that tracked these people. Now, is it the air? Is it that they adopted other bad habits? Sure, it could be. But within a very short time, they had 10 times the risk of heart

attack. So public research and dollars, this stuff matters. Why is this correlated with animal fats and proteins? And why isn't it correlated with sugar and refined carbohydrates? So carefully done studies say, and I think we all agree, more so now because we're overweight and now we're more insulin resistant and added sugars in the diet are more important in 2018 than they were when the country was thin in 1960. They weren't good then. They aren't good now.

But when you parse it out, multivariate analysis, there's a stronger relationship between the number one food in studies like this is usually butter. More than red meat, it's actually butter. That's just at our value. It's called statistics. I don't want to go so deep into statistics. It is. Somewhere there is sugar. I'll give you a classic study. If you could hold sugar the same and increase dietary saturated fat, heart disease rockets. If you could hold saturated fat the same and increase sugar in these manipulations, coronary heart disease doesn't increase. Let's point something out. I've been inside a heart 15,000 times. I've never scooped sugar out of a blocked artery.

I scooped cholesterol out of blocked arteries. 20% of every blockage in a heart is cholesterol. It's a fact that was discovered in 1910. It's never varied. Then we fed animal. Let's pause for a second. Chris, do you have something to say about that? Yeah.

So that doesn't mean that the cholesterol is there because people were eating it, Joel. You know that. It could be, though. Hold on. Let's look at what the research says again here. So they've done controlled feeding studies where they fed people two to four eggs a day, and those show that in 75% of cases that has zero impact on blood cholesterol levels. For the other 25% of people, they're termed hyperresponders,

and in that group dietary cholesterol or does modestly increase ldl cholesterol but it also increases hdl cholesterol and it does not increase the risk of heart disease this is why the the guidelines were changed on dietary cholesterol is there is no evidence that the consuming dietary cholesterol increases the risk of blood cholesterol in most people and even when it does there's no evidence that it increases the risk of blood cholesterol in most people. And even when it does, there's no evidence that it increases the risk of a heart attack, which is, again, why the dietary guidelines change. For saturated fat, again, most of the studies that showed harm were short-term studies. These longer-term studies have shown that, on average, eating saturated fat does not increase

saturated fat levels in the blood. And of all of the long-term studies that looked at this, only one showed any association between saturated fat intake and cholesterol levels in the blood. Then we have a meta-analysis, lots of meta-analyses actually, but one of the best-known meta-analyses was of 17 randomized controlled trials of low-carb diets that were high in saturated fats and published in the journal Obesity Reviews, and they found that low-carb diets neither increased nor decreased LDL cholesterol. But what they did find was that low-carb diets were associated with decrease in body weight, improvements in several cardiovascular risk factors, including triglycerides, fasting glucose, blood pressure, body mass index,

abdominal circumference, plasma insulin, C-reactive protein, as well as an increase in HDL cholesterol. Now, there have now been 10 meta-analyses of randomized controlled trials looking at low-carb diets for weight loss. All 10 showed that the low-carb diet either outperformed in most cases or was at the same level as low-fat diets. There have been several meta-analyses now, you can see them all at kresser.co slash rogan, that have looked at low-carb diets for diabetes and even cardiovascular risk markers. And all of these meta-analyses have found that low-carb diets are superior for glycemic control, for reducing insulin, for reducing triglycerides, and have beneficial effects across the board without increasing cardiovascular risk markers.

So we're now talking about randomized controlled trials, which is the best form of evidence that we have, and we're not seeing any harm from increased consumption of saturated fat. So is the problem that you're citing epidemiology studies from the 1940s and the 1950s? I would definitely, I think we need to prefer randomized controlled trials over that kind of evidence for sure. Why do you continue to go back to these studies from the 1940s and 1950s? Why do you think they're relevant?

Well, they're just the beginning. Well, they're the beginning. But Chris just took 14 topics and put them into one, from meta-analysis to randomized controls to low-carb to low-fat. I mean, they're all different topics, and I don't know how you put that all together. You need clarity and laser focus. So we were talking saturated fat. I mean, so hypothesis is generated. Saturated fat in the diet, butter, eggs, and cheese may be bad for heart disease.

Something killing Americans left and right in the 1940s and 1950s. Let's go into countries with wildly different diets. Let's see what they're eating. Let's actually take their frigging diet back to Minneapolis. Let's analyze it so it's not guessing, not food frequency questionnaires. We're taking their meals back to the United States to analyze them. But boom, there's a relationship between dietary saturated fat and your risk 50-year follow-up. There's no short-term follow-up. The study I'm referring to has 50-year follow-up, 1958 to now. And that

strongly suggested that dietary saturated fat and heart disease, that's not what's called the ultimate randomized clinical study, but it's one high quality. Second study done in China at the same time with years of follow-up. So these are right up to date. There's publications right now from studies starting at then, but the publications are now. But then you get the best kind of study. Okay, I'm still on saturated fat. I'm not talking any other topic. You put people in a metabolic ward at the National Institute of study. Okay, I'm still on saturated fat. I'm not talking any other topic. You put people in a metabolic ward at the National Institute of Health. 395 of these studies published

in 1979. You change their diet. This is the ultimate careful experiment. It might be for four weeks or six weeks. You up their saturated fat, their cholesterol rises as sure as can be. We're all different. The change in cholesterol is consistent. You're going to go up 20%, 20%, 20%. We start at different points. You have to track the change in cholesterol. Chris referred to, actually, can I go off on a tangent? It's really interesting. This will fascinate your listeners, but it's right on the topic. 2008, this is published data. I don't bullshit on this. 2008, Mexico City, the International Dairy Council meet, and they published their notes, which is why we know this. And they said, we are losing the battle. People are eating less dairy around the world, and we are losing sales. What we can do is influence

researchers, influence academicians, influence speakers. This is in Mexico, though. Well, it's every dairy council in the world just happens to meet in Mexico City that year. Then they go meet in Portugal. Then they go meet in New York, whatever. 2008, we're going to put dollars into changing research and influencing people. Doesn't mean it's all bad. They published those notes that are global initiative for the next year. They looked for sympathetic researchers that would change public opinion. That was right before the Milk Mustache campaign.

They find a guy I actually respect now, but I'm going to beat him up a little. Dr. Ronald Krauss, MD in Berkeley, California, right by him, runs a lipid center. He's had beef funding for 10 years. He's had dairy funding. All of a sudden, he's speaking to dairy industries all over. In 2010, two years later, he publishes, we call it a meta-analysis that's not new research that's statistical playing with previous studies that can be fair can be unfair whatever whatever it is their conclusion is they could not find and verify that saturated fat in the diet butter eggs and cheese raises the risk of heart disease they never said eat butter eggs and cheese they just couldn't

verify it what's amazing it's of Clinical Nutrition, that same journal is a editorial that destroys the study. This is 15 reasons this is horrible epidemiology by a guy named Jeremiah Stamler. I've never seen a medical journal destroy a piece that they accepted for publication. Okay, so everything's like stirred up. And 2014, a guy named Chowdhury publishes a similar analysis that is the reason that time magazine put on the cover butter is back because it was not new research it's a meta-analysis it's all following this mexico city uh effort to uh fund dairy positive publications a study so bad that both the journal required them to adjust and republish the data because of mistakes the harvard school of public health said take this thing away statistically

this is nonsense since those two times and that's just the bottom line we have had confusion in the public we've got experts like chris experts like me experts like dr mark hyman experts like dr walter willett on and on there is a quote from the tobacco industry that our product is confusion. They didn't care about winning the battle when the public's confused. They're just going to keep on doing habits they have. I've got to stop you because now we're in the weeds with conspiracy theories. I'd like to go back to saturated fat. Well, but that's when the pendulum of 1950, 1960, 1997, 395 of the best done studies in the world say you eat more saturated

fat, your cholesterol goes up. You eat more saturated fat, coronary heart disease goes up. It was crystal clear and the guidelines said it. The guidelines still say it. The guidelines still say limit saturated fat. Are you suggesting that the same science from the 1950s and the 1940s is applicable today? If it's in retrospect valid, let's point out one. But is it? Yeah, absolutely.

Do you think it is? Absolutely. Why do you think it's not? Because we keep bringing this up. We're going back to observational studies done 50, 60 years ago that suffer from all the problems that I mentioned to begin with, and several more that we didn't have time to go into. We have randomized controlled trials now. And, you know, observational studies were never meant to prove a hypothesis. They're meant to generate a hypothesis. And it's true that in some cases, it's not possible to do a randomized controlled trial, like with cigarette smoking, you'd have to, you know, have the trial

last for so long, and you'd have to isolate people in a ward so they weren't exposed to air pollution and other factors that could affect the result. You can't do that. But in that case, the risk was 1,000 to 3,000 percent higher. So there are criteria called the Bradford Hill criteria, which you can use and apply to observational studies to assess the chance that there's a causal relationship. studies to assess the chance that there's a causal relationship. And in the case of smoking, which actually was when the Bradford Hill criteria were created, that meets many of those criteria. In the case of nutrition research, very seldom do they meet more than a couple of the Bradford Hill criteria. Now, observational research, in order to be valuable, needs to be confirmed. You know, the results need to be replicated in a randomized controlled trial.

That's how science is supposed to work. But there was one analysis that found that zero of 52 claims that were made in observational nutrition studies were replicated when they were tested later. And, in fact, five were replicated in the opposite direction. In other words, when they did an experiment, they found the opposite result to what the observational studies suggested. So good examples of this are observational studies originally suggested that beta carotene, an antioxidant, that people with the highest intake of beta carotene had something like a 30% reduced risk of death, which is not really plausible anyways. a 30% reduced risk of death, which is not really plausible anyways.

But then when they started doing trials where they were giving people beta-carotene supplements, not only did it not improve their lifespan, they got more cancer. It increased the risk of cancer. So this is why it's so important not to rely just on observational data and to do these experiments. Now, going back to saturated fat, as I said, we've got a 2013 meta-analysis of 20 randomized controlled trials that found that low-carb, high-protein diets led to greater improvements in glycemic control compared to low-fat American Heart Association, American Diabetic Association diets. We've got a 2014 meta-analysis of 10 randomized controlled trials that showed that low-carb diets are more effective than high-carb diets for patients with type 2 diabetes. And we've got another meta-analysis of 25 randomized controlled trials just published in 2018 that found the same thing.

So, you know, science marches on. We learn more, we change, and now we've got randomized controlled trials that are replacing some of the observational evidence from the 50s and 60s and 70s, which, by the way, in Dr. Harcone's paper, you'll see that that evidence was never strong to begin with. And this is what we should be looking at. So why are you consistently bringing up these studies from the 50s? Because Chris is mixing everything up. He's talking low-carb data.

Let's talk low-carb diet. That's keto diet. That's low-carb diet. Before we go to that. Yeah, I know. Before we go to that. He's talking low-carb data. Let's talk low-carb diet. That's keto diet. That's low-carb diet. Before we go to that. Yeah, I know. Before we go to that. That's what he— But you consistently bring up these studies from the 1950s and the 1960s.

Low-carb diets are high in saturated fat. Okay. But 1950s, 1960s was the initiation. 1997, Clark, 395 randomized clinical trials, what Chris is looking for. In metabolic ward, say, you jack up the saturated fat in your diet, you jack up your cholesterol. We can talk about cholesterol in a minute, but cholesterol matters, Eldale. Cholesterol matters. Can I just ask you a question?

Yeah. Did you say 395 randomized controlled trials? Clark, 1997. Clark, 1997. 395 metabolic- I'd love to see that reference. Yeah, metabolic ward study. I can show you here.

I mean, it's right here. I'll give you the reference. There's 395- Are you saying he reviewed 395 randomized controlled trials in a meta-analysis? In metabolic ward. The tightest dietary exchange studies, the best science. I understand what a metabolic ward is, but I don't understand the 395. That's how many were there. 395 people. No, 395 individual studies that played with fat content of diet and looked at markers of cardiovascular risk.

There's 395 metabolic ward studies that were randomized controlled trials. In metabolic wards. Yeah, they're going to be short-term. That's true. You've got to read the literature. It's there. It's there for you. Oh, I've read the literature.

Well, you missed that one. That's a pretty important one. Okay, but let's go back. But hold on a second. This is a dispute here, right? So what is your issue with this? I mean, I'll just give you – it's no big a second. This is a dispute here, right? So what is your issue with this? I mean, I'll just give you – it's no big deal. I'll give you the reference.

But Chris, what is your issue with this? I'm not aware of 395 randomized controlled trials that have been done in a metabolic ward on this question. So I'd love to learn more about that if that's true. I'll give it to you in one second. It's for Clark. So, I mean, I'm not stuck in the 1950s, but if you don't – But you would agree that science has moved far past that, and our understanding of nutrition and our understanding of the mechanisms

of the effect of the food on the body, all that has changed radically. We have not changed. Our food source has changed. But that's not what I asked you. Has our understanding of food changed? Yes, the science has advanced pretty radically. But that's not what I asked you. Has our understanding of food changed? I actually think, well, actually, I would say that the observations made in the 50s and 60s have held up, which is why 21 international societies still say you will lower your... What observations have held up?

That saturated fat in the diet, chicken, eggs, cheese, beef, is related to raising your cholesterol, is related to your increased risk of heart attacks and stroke. Based on these 1950s epidemiology studies. Initial. Initial. Then we got randomized clinical trials. Those are called metabolic ward studies and such. The first chink in the armor was a 2010.

I gave you the background to it, the Siri-Torino study, the Chowdhury study. But we've decided to throw out 50 years of science I just mentioned several other meta analyses of I know probably 50 randomized controlled trials collectively here we these are modern studies so Joel what is the difference like what why why do you think that these old studies are applicable and why are you dismissing this new evidence? Okay. So just so Chris and I can resolve this issue, British Medical Journal, 1997, dietary lipids and blood cholesterol, 395 individual dietary experience put together in a meta-analysis. It's a classic study that people know.

They actually estimated if we could lower the saturated fat content of the British population by 60%, we would save X number of heart attacks every year. This is in what year? 1997. Yeah, 1997. So to answer your question, why do I think old studies are relevant? You have to keep probing and questioning and probing and questioning. But until this date, every major medical society, not one, if there was one, you'd question it.

21 international societies say you will further the populace health if you lower saturated fat in the diet. And we can't pinpoint the amount of cholesterol you should lower, which is only from animal sources, but you should lower it to as low as possible, according to the USDA. But again, these are epidemiology studies, correct? Well, this is randomized data. It's randomized data based on – And the guidelines have changed, as we said. In 2010, they changed the relationship. But wouldn't you agree that the new evidence is the new science?

Like whatever they've studied today. Right. Like they have better methods of detection, more understanding, more data to go from. Wouldn't you agree that we should look at new studies? Well, we should. Let me tell you one. So what did he just say? So wait, let me tell you one.

I published a study in 2012 that's been quoted 100,000 times from a major medical journal. It uses something called Mendelian randomization. We don't need to do randomized clinical trials all the time. There are these gigantic databases now about genetic abnormalities and certain other parameters. So there is a database with 300,000 people. We know what's called their SNPs. You've probably heard of SNPs. You know, Chris's biology and genes aren't the same as mine, and there's variability. If you're born with one of nine SNPs that keeps your cholesterol low your entire life, this is a genetic gift to you. The observation

in this major study quarter all over the world, the first author is Brian Ferentz, but I'm there number five, LDL randomization is new data that it is an advantage to your survival and advantage your risk of heart attack stroke to have a low LDL your whole life. New data. Is it consistent with 60 years of science? But boom, it sure was. We actually have learned stuff that has changed our mind. When you do that same cutting-edge science on HDL, the happy one, the high one, you cannot show the same association anymore. We're totally confused by the HDL particle. LDL is the focus of atherosclerosis, low LDL. And I'll just finish. Dr. Lauren Cordain, I'd love to talk about the history of the paleo movement.

Dr. Lauren Cordain, who had the first popular book, a PhD in Colorado, has written an article in 2004. It says the ideal LDL cholesterol is 50 to 70. Well, man, he should be a cardiologist because I'm going to hug him for that because he thought that saturated fat raises your blood cholesterol, increases your risk of heart attack and stroke. This is the founding father of the Paleo. This is what year was this? 2004.

This is in a medical journal. I mean, this is peer-reviewed. It was an editorial, but it's peer-reviewed. 50 to 70 LDL. I'm really cool there with Lauren Cordain and 50 to 70. But our understanding of nutrition has advanced pretty radically since 2004. Would you agree? Yeah, and I'm not here to represent paleo. I mean, I have never been ideological about paleo.

Even if you read my first book, it's like I'm recommending dairy products. But I don't want to get lost in this because you, pause for a second. So what is your response though to all these studies that he was citing? You're citing these old studies that seem to contradict what he's saying, but these new studies that he was citing. You're citing these old studies that seem to contradict what he's saying,

but these new studies that he's showing, and we can go over them again, but you didn't address why you did. Well, he didn't say them by name. I'm saying them by name. The big one. I'll tell you the exact one. Why are the results so different in the new studies? Well, people better at statistics than me would say manipulation of what's called meta-analyses.

These aren't new studies. I mean, these are old studies lumped together with different analyses that led to a conclusion that was surprising. Is that accurate? No, these are randomized controlled trials. Name one. Name one. Name one. Hold on.

Here we go. That's long-term. That's 20 years, 30 years, 40 years. There's no such piece. Joel, of course they're not doing 20 or 30 or 40-year randomized controlled trials. We have 50-year data on seven-country studies. You have observational study of 50 years, and that suffers from all the same problems. We agree that there's a big difference.

Again, we've already outlined there's a big difference between epidemiology studies and randomized trials. Absolutely. 100%. These randomized controlled trials are not short-term. Many of them go up to two years in length. If we're going to see changes in lipids, we're going to see them within a few weeks and certainly within a few months. So if we're not seeing them in a few months, we're not going to see them later.

And, you know, if you look at Dr. Harcombe's paper, she reviews all of the meta-analyses and looking at saturated fat and the connection with heart disease there are 39 meta-analyses of rcts or prospective cohort studies that looked at saturated fat and health outcomes 35 of 39 did not show significant correlations between saturated fat and any outcome. Okay, 35 of 39. Of the four that did, one was more related to trans fats, not saturated fats. One showed a benefit of replacing saturated fat with polyunsaturated fat, but it excluded two studies that would have totally changed the result. And as I mentioned, there's the meta-analysis of 25 RCTs and 40 observational studies that showed no benefit

of replacing saturated fat with polyunsaturated fat. And then the last two were Cochrane reviews, and in those two, saturated fat and cardiovascular disease were correlated, but saturated fat was not correlated with total mortality, cardiovascular disease mortality, fatal heart attack, non-fatal heart attack, stroke, or death from heart disease or death from any diagnoses of diabetes. Now, Joel, I'm going to let you get to this in a second. Out of those 39 trials, virtually none showed that eating saturated fat will increase your risk of heart disease, and none showed that it will increase your risk of death from any

cause. So that is pretty damning evidence. Now, if I could summarize for you or get you to summarize, your position is that his reciting of these older studies, that they are not relevant, that they are epidemiology study, that they are not as rigorous, and that this new evidence is based on new understanding and new science and that this new evidence is based on new understanding and new science and that he's ignoring this. Yeah.

That early studies showed some relationship, but they were short, very short term between eating saturated fat and then, and then cholesterol. The other problem is they were using cholesterol as a proxy marker. They weren't looking at, did people eat saturated fat and die more? They looked at did saturated fat increase cholesterol?

So when they did longer-term studies, there's no increase in cholesterol on average. That doesn't mean no one will experience an increase. That's not true. Some people will. But on average, there was no increase. And then when they looked at, they just took cholesterol out of the equation. Let's just look at, is there an increase in heart attacks or death from eating saturated fat? When they did that, there's no increase.

And those are observational studies, and we have all these randomized controlled trials that are showing no increase in cholesterol, no increase in insulin levels, and actually a decrease in all of those markers. Joel? insulin levels, and actually a decrease in all of those markers. Joel? Important stuff, and a lot of stuff was said. And I doubt, unless you're really high level, you understood. I just want to pick out one thing Chris said. Does anybody know what the Cochrane database, a word that flew out of his mouth,

Cochrane, C-O-C-H-R-A-N-E, is a group of scientists that try and be very objective, very independent, don't have any emotional, any books, any supplements, any food, and nothing. And we all love supplements around this table, but let's get out of that. Cochrane Database, every five years, comes out with a statement, does saturated fat relate to the risk of heart disease? In 2015, the most recent, Hooper, look up Hooper, look up Cochrane Database. Yes, it does. Chris said it, but he flew by it. No, it wasn't powerful enough that your choice of butter, eggs, meat, and cheese necessarily predicted your total lifespan. But it absolutely predicted your risk of developing a heart attack and stroke according to this independent database.

How so? How did it do that? That's 2015. Well, how does it do it? Saturated fat in the diet lowers the LDL receptors in the liver. Let's talk some real science. Your liver, my liver, Chris's liver, when you don't have LDL receptors or less than you should on the surface of your liver cells, your LDL stays in your blood. It gets into your arterial wall. That's my field.

Don't jack with me on arterial walls. It gets picked up by monocytes. It becomes macrophages. It becomes foamy cells. And you're fucking dead. And that's how it starts. When you eat saturated fat, there's a chain of events that biologists and chemists and scientists know. There's no question.

1985 Nobel Prize in Medicine. Okay, let's not go to the 80s again. We keep going to these old studies. So I just want you to refute what he's saying about these recent studies. Okay, 2012, I published a study. Which one of us is a scientist around the table? I've got it open. It's a journal, American Chirology.

May I please read the conclusion? The lower your LDL level beginning in life, the greater is your reduction in your risk of developing a heart attack and stroke. And I'll give you an interesting statistic. If you take Lipitor and you drop your LDL cholesterol 30%, you will typically drop your risk of a heart attack if you're in the coronary range by 30%. If you drop your LDL by 30% because you're born with a genetic gift that it's just lower than the average American, you drop your risk of heart attack by 90%. When you keep your cholesterol down your whole life, I'm talking your blood cholesterol level your whole life, you are golden in the heart attack and stroke risk. The problem is they do,

we pick up people at age 50, 60, and we start jacking with their diet and jacking with their drugs, and that's wonderful. They've had 50, 60 years of deteriorating their arteries, and we help them. We can't help them like teaching children, eat fruits and vegetables and stay away from hot dogs. That's where we got to go. That's the second gong here. Get kids healthy because they got their whole life.

Please, what is wrong with what he said? Well, there's allusions to rant. So number one, two things wrong. And I'm really not trying to nitpick. He doesn't like epidemiology, but he totally uses epidemiology to support his case. You can't have it both ways. I love basic biochemistry. I love epidemiology. I love randomized studies. I love centenarian studies. My foundation is broad broad and it's what's called the scientific method that's used by scientists in Los Angeles and that's who taught me it. Number two, besides that there's there's allusions to significant randomized clinical trials and meta-analyses. We've got to keep the science clean as can be. The breakthrough

has been the meta-analyses, Siri Torino, Chowdhury 2010, 2014, D'Souza 2015. They have severe flaws. They're not new research. They're rehashing old data. There has not been a randomized clinical trial that really challenges the coronary heart disease risk of meaning an increased saturated fat diet. You have three right now. How long are they? Hold on. There's American Journal of Clinical Nutrition, 2013,

Ajala or Hala. I'm not sure how to pronounce the name. These are all on my website. If you go to Cressor.co slash research, you can see them or Cressor.co slash Rogan and you scroll down to the saturated fat section, you can see them. This is a total of 20 randomized controlled trials, and the results, low-carb, low-GI, Mediterranean, and high-protein diets are effective in improving various markers of cardiovascular risk in people with diabetes and should be considered the overall strategy of diabetes management. Then we've got one from SnoreGuard, Systematic Review and Meta-Analysis of Dietary Carbohydrate Restriction in Patients with Type 2 Diabetes. And this was a review of 10 RCTs, and they found not only was the low-carb

diet more effective for diabetes than the low-fat diet, the greater the carbohydrate restriction, the greater the effect. And then we have one from 2018. This is Sainsbury et al., and this is effect of dietary carbohydrate restriction on glycemic control in adults with diabetes. And they found that the low-carb, the conclusion, this review suggests that low-carb restricted, or carbohydrate restricted diets could be offered to people living with diabetes as part of an individualized management plan. So these are finding that these are reviews of several randomized controlled trials that are finding that there's no increase in cardiovascular risk markers. There's actually an improvement in cardiovascular risk markers, and there's an improvement in diabetes markers like blood sugar, insulin, weight, visceral fat, et cetera.

So, I mean, this is the gold standard of evidence that we have is randomized controlled trials. And meta-analyses, of course, they do. There are problems. They can be done poorly. They can be done well. That's true of any kind of scientific research. But we can't throw out really the highest standard of evidence is a meta-analysis of randomized controlled trials. Because you can just – anyone can pick one randomized controlled trial to support their view.

What a meta-analysis does is it looks at all of the evidence and it looks at the quality of evidence and then it comes up with a result from looking at all of these trials. And that's where science is today. And these low-carb diets are high in saturated fat. They're high in saturated fat. Yeah, unless they're explicitly doing a trial where they're doing a low-carb diet that's higher in monounsaturated fat. But those are rare. Generally, people who are eating low-carb diets are eating a lot more saturated fat. Joel?

Just three quick bullet points. Number one, it is low-carb literature. We're talking saturated fat and coronary heart disease. That's a mixture. It's not the topic we're talking about. Number two, these are by— It's not the topic we're talking about? Low-carb's a whole different nutritional topic.

But he's talking about high-saturated fat. Well, that's that we haven't seen it. That's just what he said. You can do low-carb and jack up protein, but most of the experts say don't do that. That's called meat. You can do low-carb and jack up fat. That most of the experts say don't do that. That's called meat. You can do low-carb and jack up fat. That doesn't necessarily mean you're jacking up your saturated fat. I do low-carb plant-based.

That's a whole different topic. But it is not, number one, these are, okay, so one is low-carb. It's not the main topic that's dominated cardiovascular research for 60 years, which is consistent to this day in every guideline. Limit saturated fat so you don't die of a heart attack stroke. Number two, these are words your listeners may not know. These, he said, are biomarker studies. I'm talking about dying of heart attacks, having heart attacks, having stroke. I care if your blood sugar marker called hemoglobin A1C goes down. I care if your LDL and your high sensitivity C-reactive protein goes down. But that's not life and death. Those are

biomarkers. They're usually correlated with better health. If you're not tracking an artery, you're not in my scientific field because I track arteries in clinic. We track arteries in our research studies. I think that's the second thing I wanted to say. But, you know, I'm not here to actually negate the data that compared to the crappy calorie rich and processed diet that most Americans are eating. What Chris is presenting is alternative diet won't improve numbers in the lab.

Absolutely. It's a better choice. I like your diet. I do, Joe. I like your diet, Chris, because I'm looking at people walking in Wendy's and Hardee's and McDonald's and hospital cafeterias and gas stations. That's what we need to shut down and we'll make a main difference. And all we're left with is Chris's diet, Joe's diet, and Joel's diet. We're going to have an amazing country.

Then you can decide what you want. Okay, we all agree with that. But I still need to bring you back to this. What he's talking about in terms of saturated fat and not being a risk and not increasing your cholesterol. You seem to disagree with that. Sure, because the science says it does. I mean, he just cited a bunch of science.

It does not say that it does. And let me clarify something, too. I wasn't I'm not just talking about biomarkers. Biomarkers are important. But I was the one who argued for looking at total mortality is the most important endpoint and mortality from any of these other diseases. And the conclusion from Dr. Harcomb's paper where she reviewed all of the evidence on saturated fat that I talked about before, I just mentioned 35 of 39 studies didn't

show any relationship. Here's the conclusion. No meta-analysis of randomized controlled trials and or prospective cohort studies, those are observational studies, has found any significant difference for dietary fat interventions in all-cause mortality, that's deaths from any cause, or deaths from heart disease, or associated with dietary fat and heart disease mortality. In other words, there's no meta-analysis of randomized controlled trials that shows that eating more saturated fat will increase your risk of death. And your take on this is that this is the latest science and that what he's citing in terms of these studies from the 1950s and 1960s aren't really relevant. Yes. Even if we look at epidemiology, like I said earlier, that there's a meta-analysis of studies including 350,000 participants that found no relationship between saturated fat intake and cardiovascular disease. And then a more recent review that included both randomized controlled trials, 25 of them,

and 40 observational studies with 650,000 participants that concluded current evidence doesn't clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fat and low consumption of saturated fat. So whether you look at the epidemiology or whether you look at the randomized controlled trials or the meta-analyses of randomized controlled trials, you end up in the same place. Joel? Most modern data, we already talked this. Everybody, please Google Cochrane Database Saturated Fat 2015. Hooper is the author. The introduction is, reducing saturated fat reduces serum cholesterol, but we're not sure of the importance. So we took 15 randomized studies with 59,000 participants. The conclusion,

there is a potentially important reduction in heart disease risk by reducing saturated fat in your diet, 2015, which is why 21 international societies are solid, that we will help the public, we will help the listeners. Have your piece of meat. Make it four ounces, not 14 ounces. Have your bacon. Make it one strip, not four strips. Have your cheese. Just don't eat it every day and don't eat large amounts. The amount of cheese the United States has got, insane, because the USDA funds cheese manufacturers. Okay, so 2015, I can't get you a better one. They'll update Cochrane database in 2020. It'll be the same. What's your take on what he said, though? So here's John.

I don't care, honestly, what he said. I've got to go with the best science in the world because I deal with patients who have serious disease. I can tell my patients the most up-to-date analysis of randomized clinical studies say saturated fat in your diet raises your cholesterol, lowering saturated fat like eating less animal products. That's not the most up-to-date, Joe. 2015, Cochrane-Dandis? I just mentioned several meta-analyses from 2018. This is not meta-analysis. This is randomized clinical studies, 59,000 participants. No, they're reviewing studies. We have to look at the weight of evidence. There are lots of studies published all the time.

And that's, again, why looking at meta-analyses of randomized controlled trials, looking at very large reviews of observational studies with over a million participants, and you end up in the same place. Of course, we can go and find one study here, one study there that is different, has a different result, but that's not the scientific method. The scientific method is to look at the weight of the evidence and to continue to evaluate that over time as the evidence changes. And, you know, this is a great quote from John Ioannidis, the Stanford epidemiologist that I mentioned, that reminds us that we can't just rely on the past to inform the present. He said, claimed research findings may often be simply accurate measures of the prevailing bias.

findings may often be simply accurate measures of the prevailing bias. And that what that means is that, let's say, you know, you have a paper that, you know, 30, 40, 50 years ago, that says saturated fat increases the risk of cholesterol, then later, somebody makes that claim in a paper, just like that initial sentence, saturated fat raises cholesterol, you see a little number, they're referencing that one paper, then a couple years later, somebody else makes that initial sentence, saturated fat raises cholesterol. You see a little number. They're referencing that one paper. Then a couple years later, somebody else makes that same claim. They reference the second paper, which was referencing the first paper, and on and on it goes. And the whole thing is a house of cards.

That's what most people don't realize. That's bad science. That is bad science. This is good science. That's bad science. What is bad science? Hold on a second. You're saying what he's saying is because people are listening and not looking at your gestures.

Again, he's making comments that have no reference. Certainly, if there's misquotes. I just provided the references here and they're on my website. How does he have no references? A scientific peer-reviewed paper that quoted a reference and everybody simply passively keeps re-quoting their reference. It was wrong in the beginning. I can give you a real-life Internet example, which goes to Gary Taubes, my new friend, but sometimes my adversary. But I can't give you a literature reference.

It might be one, but these are very general statements. I think we should move on. No, we definitely shouldn't because we're not really clearing this up. What is he saying that's wrong? Okay. The best scientific analysis of the global topic, the saturated fat-rich containing foods, which are animal-sourced foods at high amount in your diet,

increase your risk of dying of heart attack and stroke or having a heart attack and stroke, goes to the biochemistry. The saturated fat in your diet will lower the number of LDL receptors on your liver and your blood cholesterol goes up. That's backed by 395 metabolic ward studies, but that is biochemistry. Then you get to epidemiology. Countries that eat more saturated fat, Finland, great story, and I got to tell it.

1970, the highest heart attack rate in the world was Finland. Guys were dying your age and my age at the highest rate. The lowest heart attack rate in the world was Finland. Guys were dying your age and my age at the highest rate. The lowest heart attack rate in the Mediterranean was Crete. 40% of calories were from fat in Finland. 40% of calories were from fat in Crete. You say, how can that happen? Because I'm not an advocate for a low-fat diet, except for very selective clinical cases. It was olive oil in Crete. That's very low, not zero, low in saturated fat. It was cheese. It was meat. It was beef. It was butter in Finland. They instituted a national program to lower the content of saturated fat in the diet in Finland.

Five years later, heart attack dropped 80%. Okay, but do you understand that he's saying something totally different? You're citing epidemiology studies about what people eat? I started with biochemistry, then I went to epidemiology. I want to know what's wrong with what he said. Because he's not being broad with the science. He's getting mired in the woods. I'm telling you, the broadest view from 50,000 feet up, biochemistry supports it, epidemiology supports it, 395 metabolic ward studies, my randomized Mendelian randomization study.

What's wrong with what he said, though? Because he's not looking at the entirety of the data. And I'm telling you the entire data. Then you go to Loma Linda, Okinawa, you go to Icarus, you go to Costa Rica, and you go to Sardinia. If you live to 100 and you're still operating on somebody's heart, is your diet likely high in animal saturated fat or not? The answer is it isn't.

It's as low as 3% of the diet in Okinawa. But couldn't it possibly be other factors? That's not the user bias. There's a great new study recently that came out that showed that just following the top five health behaviors, which are basic. So we're talking about not smoking, not drinking, maintaining a healthy body weight, getting some physical activity, and eating a, quote, relatively healthy diet, like not junk all the time, increases your lifespan by 13 years. And that's Walter Willett. You can't look at these populations and make inferences about animal products being the driving factor one way or the other because there's just too many other factors.

There's no way to control for all of those factors in a study. And that's why we have to come back to the scientific method. We use observational studies to come up with hypotheses. Then we do randomized controlled trials to either confirm or refute those hypotheses. As I said before, in many cases, what is apparent in observational studies or what seems apparent is not later confirmed in randomized controlled trials. And that's where we're at now with saturated fat and dietary cholesterol. I just mentioned three very large meta-analyses of randomized controlled trials that failed to confirm any association of saturated fat and heart disease and, or saturated fat and increase in these risk markers. And I mentioned two reviews of very large observational study data, including 350,000 in one study

and 650 in another showing no relationship. So the mechanistic arguments about liver, you know, like saturated fat does this or that, that's not convincing if it's not showing up in the data. If it did that, then we would see it in the observational studies and the randomized studies. Now, specifically, Joel, what is your take on what he just said? Well, we just had another gong moment. So Chris just quoted, and it's actually a little bit comical, a Harvard School of Public Health study on how do you live 14 years longer. It's epidemiology, but he's using it. The senior author is Dr. Walter Willett, a guy he calls a

vegan pro-advocate who's not at all all vegan he's written a book about the mediterranean diet with all kinds of animal recipes in it which is fine with me he's a brilliant he's a brilliant brilliant senior harvard researcher but he's using data that he says is weak and such yet the teaching point is there how do you live 14 years longer you don't smoke exercise 30 minutes a day you eat better than average that's a day, you eat better than average. That's very broad, but you eat better than average. You keep your waist under 25, BMI under 25, and you have a few alcoholic beverages a week. I want your listeners to write that down because that is solid epidemiologic data that's very consistent across the spectrum. So let's all use something to teach your listeners.

But that's my point. So you can't look at cultures that have a completely different lifestyle than the standard American lifestyle and draw any inferences about animal products. So a really good example of this is, you know, the Seventh-day Adventists, the claim is that it's the vegetarian diet that makes them live longer than the general population. But as I mentioned before, as part of their belief system, they don't smoke, they don't drink, they have a healthy lifestyle in general. What if there was another population that also had those kind of belief systems about not smoking, not drinking, and healthy lifestyle, but they also ate meat? Well, it turns out there is, the Mormons. And there have been three studies on Mormons,

and each of the studies that have been done on Mormons found that their mortality, I'll give you the exact numbers here in just a second. For whatever reason, that's not coming up here. But their risk of death compared to the general population was something like 50% lower than the general population on average. And yet they're eating animal foods. They're not vegetarian like the Seventh-day Adventists. So your point of bringing that epidemiology study in the first place, bringing up healthy lifestyle, increasing your lifespan by 14 years, is to show that any positive move is going to show, whether it's just exercise and not eating sugar or whatever, is going to show an increase in your lifespan. isolate single variables and the influence of those single variables in an observational study on those effects. And, you know, this is something that John Ioannidis has said over and over again, is that it's almost impossible, if not impossible, to disentangle the influences of all of these

single variables in observational research. And again, I'm not saying we shouldn't use observational research. I'm saying we should be circumspect about how we use it. And we should be aware of the limitations and the flaws and keep those in mind when we're designing observational studies and when we're interpreting their results. So, Joel, what is your opinion on what he's saying about saturated fat and cholesterol and mortality risk. Okay. Well, I think I've said it, but I'll repeat it. I just want to point out, we just shared another common moment. We're both lifestyle medicine doctors, of which nutrition is just one part. We just went through a list of lifestyle factors. We now add sleep. We add social support.

We add stress management skills. It's not all smoking, diet, exercise, and the size of your body. But we are aligned, and we will go at patients side by side and do a lot of exactly the same thing. In fact, I think the only thing there's squabble about in lifestyle medicine is optimal nutrition to prevent chronic disease. And there's probably more than one path, but God knows the plant-based medicine group has a tremendous body of science. I'll conclude one more time, and I don't know how many times I can say it. The highest level of science is to integrate all that's available. Biochemistry is on the side. Saturated fat raises your risk of coronary heart disease. It doesn't mean nobody eats a no-saturated fat diet, but you can lower it. Observational studies were there. Epidemiology studies were to test that hypothesis.

They confirmed Finland and Crete. I've talked about it. I won't go there again. Randomized clinical trials have confirmed it. Hooper, Cochrane database, 2015. My study, 2012, widely cited worldwide, has confirmed it. Get your LDL cholesterol down genetically or by diet as long as you can, as early as you can. And finally, and the last is is what do old healthy people do?

Actually, Chris, I just think there's a good concept to let your listeners know. It isn't all about lifespan. In fact, lifespan in the United States is dropping, which is very scary for all the frigging money we spend on health. There's something called healthspan, which is to avoid chronic disease and die dancing or die swimming or die skydiving, but don't die in a frigging hospital with a peg tube and a trach and a Foley up your hoo-hoo. And many of these studies that show you can reduce your risk of heart disease,

stroke, and diabetes are talking about better quality of life. So when you put all that together, these centenarian studies that have low saturated fat diets are just one more piece. I just mentioned four incredibly solid pieces of evidence. Not one. It's four. It's all that's out there. It's what Nobel Prize winners use when they describe the cholesterol hypothesis.

Is this correct? Well, he may not know it. In this city of Los Angeles, our shared friend, Dr. Walter Longo, often considered, and you should have him on the show, perhaps the world's leading expert in nutrition, longevity, and such, will say you incorporate all the bases for nutritional evaluation. You keep it big picture. He calls it pixel mentality. You don't get hung up on one study.

You get the whole picture, biochemistry, epidemiology, randomness, clinical trials, finally centenarian studies. I think it's very consistent. You will enhance your health by lowering animal-based products. Now, we can argue, is that 70%, 80%, 90% plant-based? Lauren Cordain and the founder of the paleo movement, Boyd Eaton, we were talking about 70% plants on your plate. I love that.

You know, I'm not telling people quit eating meat today or you'll die. I'm not a reactionary. But to say that plant-based medicine doesn't have a strong basis, that I can't reverse plaque with just plant-based medicine, we haven't even talked about the ability to do that, but is absolute heresy because it, in fact, is one of the most powerful pieces of nutrition we have. Okay, but what's wrong with these studies that he's talking about? They're pixel mentalities. Picking one. mentalities, picking one. I don't know how observational data of over a million people and three different meta-analyses of 20 to 25 randomized controlled trials each is pixel mentality. This is the gold standard for assessing a question like this in medicine. It's not

mechanistic data or mechanistic arguments are not persuasive if they don't translate into real outcomes that you can measure in randomized controlled trials or observational studies. I'm trying to boil this down. So what is your take on that? Without any references to the past and people who lived in Mongolia that lived longer? These are the three disruptive randomized trials from 2010 on. They question the relationship between diet and... No, those are different trials, Joel. Well, then... These are three different trials. I'm not referring to Krause's research or Chowdhury's.

You need to throw them out there and let us know the reference. I did before. You want me to do it again? No, because we'll get mired. What is wrong with what he's saying? Look, I'm obviously the non-expert here and i'm baffled so i'm trying to boil this down with as little rhetoric as possible okay it takes a heretical conspiracy attitude to say everybody's got it wrong for 60 years 21 international

societies have it wrong they could but it's a controversy theory to say that Hooper-Cochran Database 2015, they've got it wrong, that metabolic ward studies got it wrong. This is one or two or three pieces of data, and they're observational. You don't throw out the baby with the pathway. Randomized controlled trials. Why are you saying they're observational if they're not? Well, meta-analysis by nature is implying it's not a new study. It's taking previous studies and doing it. So let me give you one quick example. In the Chowdhury meta-analysis, created butter is back on the cover of Time magazine,

created a whole fervor out there that we can go back to eating all these great foods that Atkins wants us to eat. They correlated your blood cholesterol with your risk of having heart disease. They couldn't confirm it. Well, they allowed people in their meta-analysis who were on Lipitor. Well, of course, you're on a medicine lowers your cholesterol. They didn't exclude those people. That has been resoundingly criticized as, yes, it looks good. It's in a journal. It's a meta-analysis. That is fraudulent or at least relatively inappropriate statistics. It's a meta-analysis. That is fraudulent or at least relatively inappropriate statistics.

It's so technical. It's beyond, I think, the importance of this discussion. But I just say 50,000 feet elevation view of the best nutrition is, again, four pillars that I keep talking about indicate you'd be very wise to limit the amount of saturated fat. And that's endorsed by every major medical society in the world. It's not controversial. It's not controversial. I don't think it's conspiracy. I think it's just a natural progression of science. We used to think the world was flat.

We used to think ulcers were caused by stress. There are a lot of things that have changed over time as the evidence evolves and as we become more educated and aware. So why are you implying that it's some sort of a belief in a conspiracy? Well, Chris is suggesting we got it wrong, which means the American Heart, the American College, the World Health, the Institute of Medicine, the European Society of Atherosclerosis, the Australian Society of Health,

all these people that tell you 10% or less saturated fat, some say as little as you can possibly get in your diet, have got it wrong. And that suggests there's been a total misrepresentation of all the science. Can I pause you for a second there? What are their recommendations based on? Is it based on old science? No, I mean these are— How long have they been saying this, and what is it based on, and have they adjusted to this new science that he's discussing?

They republish, republish, republish. So the USDA republishes every five years. 2016, not long ago. Every five years. 2016 was the last USDA publication. They'll do it again in 2020. But doesn't this science change pretty rapidly? Not that fast.

Not that fast. Not that fast. There's nothing new since 2016 that rocks the idea that 21 international societies got it wrong. There's nothing. There isn't. The 2015 report did not use, there was, the USDA set up the Nutrition Evidence Library to help conduct systemic reviews to answer some of these questions. And in the 2015 report, the committee stated that it didn't use that database for 70% of the topics. And a lot of the guidelines hadn't used any newer science since 2010. And there had been large reviews. newer science since 2010. And there had been large reviews, as I just mentioned,

these three reviews that I mentioned, one was in 2013, one was in 2017, and one was in 2018. These are the reviews of the randomized controlled trials that didn't show increase in cardiovascular risk markers from saturated fat consumption. And then we had those reviews of observational studies of 300,000 and 650,000 people. I think the same thing will happen with saturated fat. As I said, in 2010, they changed their recommendations on total fat. They used to limit total fat, and then they changed those in 2010. 2015, they changed their recommendation on dietary cholesterol. And I think probably the next time, you know, maybe it's the next time, or maybe it's the time after that,

you'll see a change in the saturated fat guidelines. And it's not a big conspiracy. I'm not saying, you know. It's not a conspiracy. It's the advancement of science. So your take is that these organizations are behind the curve? Yes. And if we want to talk about conflicts of interest, there are huge conflicts of interest in these organizations, something like 40% of the funding of the, well, I don't want to get this number wrong, but a lot, the American Heart Association, American Diabetic Association, a lot of these organizations have funding from big food. You know, Coca-Cola, you talk to a nutritionist who goes to these conferences and they, you know, Coca-Cola. You talk to a nutritionist who goes to these conferences and they, you know, there's like Nestle bars and Coca-Cola at the nutrition conferences. That's hilarious. Yeah,

it's hilarious, isn't it? It's just hilarious if it wasn't. Yeah. I mean, it's, it's actually funny and sad at the same time. And so I'm not saying there's a big conspiracy, but I am saying there's a problem in terms of scientific integrity when you have these organizations that are tasked with creating the guidelines that have these financial conflicts of interest. That's not really how it should be. But I don't even want to go too far down that road because we don't need to go there in order to show what the science is showing in peer-reviewed journals. So, Joel, what is wrong with what he just said? showing in peer-reviewed journals.

So, Joel, what is wrong with what he just said? Well, I'll say this. Until 2020 USDA guidelines come in, I actually think he's factually wrong because the USDA guidelines say keep the percentage of calories from saturated fat to 35% or less. I could be wrong on that. I'm not an encyclopedia. I know they say keep – Oh, I agree with that. Well, right.

Well, you said they eliminated it. I said they changed their limitation on total fat in 2010. And I'm speculating that they will eventually change their guidelines on saturated fat because the science has evolved. And I will buy you guys an all-paid trip to Bali if you see in the 2020 guidelines that saturated fat is still not to be limited to that right so what's wrong with what he said um i i don't know we just well it's about i agree there are conflicts of funding but they're not unique to any particular sector um we just had one of the most famous food psychologists in connecticut brian wancic who was a hero of mine said eat on small plates because when you're on small plates, you're mindful and you don't get obese.

Had to have six papers retracted and had to resign. It's pervasive. It's a problem. Doesn't mean there's not a majority of good scientists. And I think most of the people we've been talking about are largely good scientists that their reputation hasn't been tainted. I don't want to get too mired in this, but if you look at the egg industry prior to 1990, get too mired in this, but if you look at the egg industry, prior to 1990, about 30% of egg studies on nutrition were funded by the Egg Board.

Since 1990, it's 92%. It's a conflict. Who's got the money to study nutrition? It's not the broccoli growers. I'm going to stop you because we're getting in the weeds again. What is wrong with what he said? Well, he's predicting that there'll be a change in the recommendation. Forget about that.

Forget about that. What about what he said about Well, he's predicting that there'll be a change in the recommendation. Forget about that. Forget about that. What about what he said about saturated fat? I think there's no substantial new data on saturated fat since 2015 Hooper and 2016 USDA that changes anybody to question that they should not recognize and follow the leadership of 21 international societies

that are out there to try and improve the public health. Okay, let me stop you there, because those 21 international societies and all these different organizations, they rely on current science to make the recommendations, correct? Sure, sure. Okay, and are they often behind the curve? I don't believe so. The USDA goes through this whole process.

Now, they haven't published anything new since 2016. It's an expensive process. Right, but they did change, like he said, their total fat requirements. They did change what they believe to be healthy and not healthy. You said they changed it in 2010, correct? They changed the limitation on total fat in 2010, and then they changed the limitation on dietary cholesterol in 2015. So they admit that the science has advanced and changed their perceptions of what is and is not healthy. So what's wrong with what he's saying about saturated fat?

They didn't change saturated fat. So if we stick just on topic. But not them. They rely on the current science. Right. So he's saying that the current science is showing that there is no negative consequence of saturated fat. That's BS. That's BS.

So what is wrong with these studies that he's citing? Well, I don't know. I have not read every article in the world, nor has Chris. I don't know specifically. There are three famous studies that I've read, Siri Torino, Chowdhury, and D'Souza. Those have been dissected. Those are generally felt to be weird. So you believe those, but you don't believe the ones that he's citing? Well, I don't know. Actually, he would probably cite those to support his case, but they've been so resoundingly criticized. And they created fervor and all. I don't know the three studies.

Have they been resoundingly criticized? I'm aware that there has been criticism, but you could say the same thing about the vegetarian lifespan studies, the IARC report on processed meat. But have they been scientifically criticized? They have not been debunked by any stretch of the imagination. The papers stand. The authors have defended against those criticisms. And it's nothing like what Joel was just talking about with Brian Wansink, who had to, you know, all the papers were proven to be fraudulent, and he had to retract them.

There's nothing like that that has happened with those papers. And those were not the ones that I cited anyways. I just want to say the USDA in 2015 said total fat intake should be 20% to 35% of all your calories. They didn't eliminate anything in 2010. That's 2015. I think that's a factual error, Chris. They clearly changed the cholesterol recommendation to say as little as possible. They just didn't put a number on it. We all know that. My cardiology group went bananas

and got them to add that sentence as keep cholesterol as low as possible. Chris? It says cholesterol is no longer a nutrient of concern. But you were talking that they removed the total fat intake. That's actually inaccurate. It's right here. I mean, I haven't got the guideline open. You know, it is. I mean, we're allowed to make mistakes. We're trying to incorporate the whole world literature, and we're just two guys. Is that a mistake, Chris? It's right here. I mean, it's a mistake.

So what was his mistake? What did he say that was wrong? He said that in 2010, the USDA guidelines, which are supposed to be followed by schools and colleges and the rest, removed a total fat percentage recommendation. It remains at 20 to 35 percent. That's fairly modest fat intake. I have to look at the specific language to see. My recollection is that in the same way that there's some contradiction with the cholesterol, there's a sentence that says cholesterol is no longer a nutrient of concern.

And then Joel mentioned that he and his cardiologist friends got them to add something back that was, you know, kind of seemed to step back from that. Um, and I think this, uh, the same thing happened with total fat. I don't know. And I can't, I don't have it to look at right now. Can we find it? So, because it seems like a pretty major point of dispute. And Joel says it isn't it isn't because the still the question at hand is, what do the meta analyses of randomized controlled trials and what do the reviews, large reviews of observational studies, including over a million participants suggest about the influence of saturated fat on important markers like heart disease and total mortality. I'm still waiting to hear about a study that shows that eating more

saturated, a convincing review of meta-analyses, a meta-analysis of randomized controlled trials, or even large observational data that lasted for more than a short period of time that shows that eating saturated fat. And I'm not even talking about in the context of a healthy diet, which is a whole other discussion. Right. But just in any diet increases the risk of heart disease. Can I stop you, please? Because we were discussing this on the assumption that the USDA had changed the requirements for fat. Joel's saying that's a mistake.

I really think we should clarify that. We should find out if he's right. You can go choosemyplate.gov. It's right here, 2015-2020, questions about the USDA guidelines. It said healthy diets can include up to 35% of calories from fat. They put a clear-cut limit on it. It's right here. I'm reading it.

I'm not making it up. It on it. It's right here. I'm reading it. I'm not making it up. It's USDA. It's a government. So what was it that you remembered from 2010, and did you remember it erroneously? Let's see here. This is so fucking complicated. It's so bad.

Yeah, eat your vegetables. Everything else follows. Have some fun. love your fellow man i have an anecdote can i this came from a paper it was talking about the um the shift in the guidelines and i need to um you know if if why don't you tell us your anecdote, Joel, and we'll get into this. I can tell you anecdotes. I love Chris Kresser. I want everybody to know that.

There's a very famous food doc in Santa Rosa named John McDougall. He's been treating people with crazy plant-based, high-complex carb diets. He reverses diabetes, this and that. His newsletter came out just as I'm pulling up here and bumped into Chris. We actually walked in exactly the same time. He quotes the New Testament, and I'm going to read this because as a Jewish boy, I just got to read it. One man's faith allows him to eat everything. There's some people around the table who would do that.

Another man's faith allows him to eat only vegetables. The man who eats everything must not look down on him who eats only vegetables. The man who does not eat everything must not condemn the man who does. There should be peace. I think that is such a freaking beautiful concept because we do need to leave here as promoters of healthy lifestyles, whether we call it the Harvard School of Public Health, how to live 14 years longer, the Blue Zones, how to live like Loma Linda, whether you want to eat game that you hunt that is probably eight times less in saturated fat than what you're buying at the damn grocery store. You know, people eat your vegetables.

People be really quality over quantity. And I'm going to tell you, at some point, let's talk about eating less and taking some breaks from eating so you can activate anti-aging pathways. Because, you know, it isn't all food. It's sometimes too much food is probably one of the biggest problems. For sure. For sure. For sure. We all agree about that. I think the real question isn't for someone like me who really doesn't know.

Yeah. I'm baffled by the saturated fat dispute because it seems to be there's like one of you has got to be wrong here. The evidence has got to point one way or the other. Chris is saying the evidence points to it being not an issue at all. And you're saying it points to being the major issue. Worldwide consensus. Worldwide consensus by these groups that rely on current science that may or may not be behind the times. Yeah, and I want to step back and just clarify my position here.

Because I'm not saying, you know, we started by saying there's no one-size-fits-all approach, right? So these studies just tell us about averages. They tell us what happens on average when a group of people do something. They don't tell us actually what happens for person A, person B, person C, and that can be different. So if you get like some people may experience a slight increase in their cholesterol from eating saturated fat, some people might actually experience a slight decrease. And on a net basis, that averages out, right? I think the next generation of science is going to be more of an understanding of how various dietary components and various foods affect people on an individual level. Because let's say there's someone who's got genetic polymorphisms

that mean that for that person, if they eat a diet that's very high in saturated fat, their LDL particle number, which is a risk factor for heart disease, is going to go up. I've seen that in my clinic. Absolutely. I'm not saying that saturated fat will never increase cholesterol or LDL particle number in people. That's just not true. It will in some cases. It will happen in some cases. But I'm just, I'm reporting on the science as in terms of the general question of is saturated fat going to

increase the risk of heart disease? And is it going to increase the risk of death on average, according to the available research? And the answer to that is no. Now, then the next question is like, should you, Joe, eat a diet high in saturated fat? Or should I? Or should Jamie? That's a different question. And unfortunately, science is not, we've been so focused on these population level recommendations and the idea that there's one diet that works for everyone. And we don't have a lot of research that answers that question. That's a big gap in current science. I have two questions. One, did you find out if you made an error on this 2010 requirement from the USDA. So this came from a

study that's that reference said, despite a lack of evidence supporting low fat diets, only in 2010 did the Dietary Guidelines Committee stop recommending limits on total fat. But I don't have the full guidelines in front of me. And and I'm sure what the the language says so i could have made an error it's possible so you made it based on that what you just said that was what in another study now in terms of saturated fat isn't there an increased risk when you consume saturated fat with refined sugars there absolutely is this is another example of where context matters. Well, let me just even step back a second and say that the primary sources of saturated fat, and this is important to understand when you're looking at epidemiological data.

So the sources of saturated fat in the American diet, 33% comes from pizza, desserts, candy, potato chips, pasta, tortillas, burritos, and tacos. 24.5% is unaccounted for but most likely processed foods, according to the authors. And then 10% is, or almost 10%, sausages, hot dogs, bacon, ribs, and burgers. So the vast majority of saturated, oh, 13% is chicken and mixed chicken dishes. Think KFC or chicken nuggets. And eggs and mixed egg dishes. So the vast majority of saturated fat that Americans are eating is coming from junk. saturated fat that Americans are eating is coming from junk. So even in an observational, even if we did see an increase in harm from saturated fat and observational studies, we still couldn't say

that that would be true for someone who's eating what I would call like a nutrivor diet, which is, you know, whole foods, fruits and vegetables, nuts and seeds, some starchy plants like sweet potatoes and animal products, including saturated fat. We have no research that suggests that saturated fat in that context is harmful. What is the mechanism that makes saturated fat more harmful when it's consumed with sugar? Well, there is an interesting study that was done that showed that in the context of a ketogenic diet where there's no sugar, essentially, or very low amounts of sugar, that dietary saturated fat will actually decrease blood levels of saturated fatty acids, and that if you're eating refined carbohydrates, then you see an increase in saturated fatty acids that comes from the effects of insulin, essentially. Let me find you the specific. So if you're eating a high-carbohydrate diet, it will increase insulin, which inhibits the oxidation of saturated fat. And so then when insulin levels are high, saturated fat tends to be stored rather than being burned as fuel. And then high-carb diet can – and I mean refined carbs here, not fruits and vegetables – can promote the synthesis of saturated fat in the liver.

So it actually causes the liver to make more saturated fatty acids in the serum. But this study here is, this showed that controlled feeding studies have shown that refined carbohydrates will actually increase levels of saturated fat in the blood, whereas eating saturated fat in the diet does not if the diet is not high in those carbohydrates. Joel, what's your take on that? You know, the only key point I make to answer your question, follow up to Chris, is why does high sugar diets combine with high saturated fat diets? Because again, and go back to biochemistry, this is serious science. Where's saturated fat? It's usually found in meat and other animal-based products.

It does exist in plants like some in avocado, some in olives and olive oil. But anyways, there's a pathway. Get in science, but it's real stuff. The amino acids found in red meat combined with their saturated fat that's content triggers a pathway that accelerates aging. You don't want to age fast. That's called the mTOR pathway, the IGF-1 pathway. Then you eat a diet rich in sugar.

Well, we know the biochemistry right here in Los Angeles, University of Southern California, BioGerontology Institute. You eat a lot of sugar, you activate another aging pathway called PK-RAS. And these two pathways, mTOR, IGF-1, PK Ras, will make you an old man or an old woman quicker. So when you're eating pastries, which is high saturated fat and high sugar, or you're eating meat with a Coke, how common is that? I mean, my God, a hamburger and Coke, you're activating everything we know about science that will make you age faster. That sucks. So is that true that eating meat and the amino acids accelerate the aging process?

There's no studies that show that eating meat in the context of a healthy diet shortens your lifespan. And so if that were true, then we would see that in the data. But Joel, you're talking about an actual physical mechanism that accelerates the aging process. Yeah, this is well-known. What is it called again? Well, it's mTOR, IGF-1 is one pathway, and PK-RAS. The biochemistry is not – I mean, this is like high-level science. It's not – I'm not stretching on the limb here.

But, you know, protein is really amino acids. You know, I get this question. You're a vegan. Where do you get your protein? My answer is where do you get your amino acids. You know, I get this question, you're a vegan, where do you get your protein? My answer is, where do you get your amino acids? Because my body breaks protein down into the building blocks, and then I build it back up to wherever the hell I need it for. It's amino acids in meat, there's amino acids in my edamame, wherever I want to get them. The split of those 20 amino acids is different in meat than it is in edamame. There's more methionine and more leucine,

very technical stuff, leucine. And there are some mixes of branched chain amino acids of leucine. I don't know what the hell that does your aging, but we do know that meat rich in methionine will activate mTOR and IGF-1, and it is a very strong factor in aging. You want a low methionine diet. It's another reason plant-based eaters need to take B12 to keep their homocysteine and methionine down. That's a separate topic. But, yes, the amino acid mix found in animal protein is different than the amino acid mix found in vegetable protein, which is why when Morgan Levine looks at the question, what's your survival, what's your cancer risk, what's your heart risk on animal protein and plant protein, plant protein beats the crap out of animal protein.

This is high-level cell metabolism. Try and publish a paper in cell metabolism. Why does it beat the crap out of animal protein? Because there's a 300% to 400% increase in cancer of those that diet concentrate on protein of animal source. And there's a 25% reduction in cardiovascular disease. Cell metastasis in 2014. Morgan Levine of Harvard. Nobody's questioning her work.

October 1, 2016, Song at Harvard. Animal protein, plant protein lead to very different outcomes in large database observational studies at the highest level. Because you can't take 6,000 people and randomize them in that way. So if you're waiting for that to resolve the question, you know, good luck. That's actually not the case. And, you know, good luck. That's actually not the case. The IARC panel that concluded that processed meat led to an 18% increase in cancer risk,

which, again, is, like, indistinguishable from chance using that low of a relative risk. Their conclusion was that fresh red meat was 0.02, 1.02. That's a 2% increase. And many other studies have shown that unprocessed red meat is not associated with increasing cancer risk and is not associated with increase in heart disease risk. So again, you can talk about these proposed mechanisms all day long, but if it's not showing up in actual events that are meaningful to people then you might be missing something maybe red meat does you know act in certain way that would you might think would increase the risk of death but maybe it does other things that reduce the risk of death and that's why we can't just focus on mechanistic studies we have to look at actual endpoints that

matter to people in terms of the quality of animal- I think death and cancer matter, Chris, and I know you know- That's what I just said. The studies don't show that fresh red meat increase the risk of death and cancer and heart disease. And Joel, what was the number that you were saying? 300%? It's right here. Anybody look. March 4th, 2014, Selma Tassel and Morgan Levine. Right here, animal protein, 75% increase in death, 400% increase in cancer, over 18-year follow-up. These findings were not found with plant-based protein. So let's talk about reviews. It's not reviews.

This is science. This is science. No, reviews are science, Joel. You're saying that reviews of observational studies and reviews of meta-analyses are not science, Joel. You're saying that reviews of observational studies and reviews of meta-analyses are not science, and you would prefer to draw conclusions based on a single study? No, I wouldn't want to base them on a single study, but this is very consistent with the overall high level of mTOR, IGF-1, PKRs. I was just referring to research that several large reviews that have not found a relationship between red fresh red meat

and cancer and fresh red meat and heart disease so look at reviews that include lots of studies and just a single study that supports a particular viewpoint maybe maybe maybe well we need more than a minute well okay the 300% let me let me let it's it's human study these are real lives these are real deaths and Well, we need more than a maybe. Well, okay. The 300%. What is that number based on? It's human study. These are real lives. These are real deaths, and these are real cancer cases. This is original science in one of the highest levels.

But is it epidemiology where they don't take into account all the other risk factors, including the rest of their diet, smoking, sedentary lifestyle, obesity, all the various factors? I'll answer in a second. I'll download the whole paper. But, you know, they do that. They do multivariate analysis. Well, he's downloading that. There's a 2011 meta-analysis of 34 prospective studies on red meat and colorectal cancer, which said that's 34 studies.

The available epidemiologic data are not sufficient to support an independent and unequivocal positive association between red meat intake and colorectal cancer. A 2015 meta-analysis did find a relationship with processed meat, but did not find a relationship with fresh red meat. There's also an issue of dose response. If red meat did cause cancer, then you'd expect to see a continuous increase in cancer rates as the intake of red meat increased. But in many cases, you actually see the opposite. You can see a decrease in cancer rates in the people who ate the most red meat, which casts some doubt on that association. And again, we come back to the relative risks.

And again, we come back to the relative risks. Even with processed meat, it's only 18%. And you have to consider the healthy user bias that we talked about before. And with fresh red meat, it's either nothing, zero, or maybe like 2%. And that level in observational research is not distinguishable from chance. You cannot draw any conclusions on that. Observational research is not distinguishable from chance. You cannot draw any conclusions on that. And you cannot assume that someone who's eating a Nutrivor diet with fresh whole foods and is including some red meat in that diet is going to have the same response as someone who's eating pizza, candy, hot dogs, and all kinds of other junk food.

That's just, you know, common sense will tell you that. Hence the problem with these kind of studies. food. That's just, you know, common sense will tell you that. Hence the problem with these kind of studies. Exactly. Joel? Chris, you want a low IGF-1 or a high IGF-1? You want a low IGF-1, you know it. Just say it. I want to live a long, healthy life. I don't want to be obsessing over individual markers.

I want to live a long, healthy life. You like a lot of markers when it comes to low-carb studies. You want a low IGF-1 for survival. The science is strong. This is L.A. science, so we're not making this stuff up. Anyways, methionine and leucine in meat raises IGF-1, and at least periodically take a break. Raises insulin growth factor.

One, which will take your prostate and your breast tissue, makes you start growing at age 50. Breast tissue? Yeah. For males or for women? For women. Well, just because of the frequency of breast cancer in women. It's women.

So, you know, there is a relationship between animal products and breast cancer. There's an opposite relation. These are relationships. There is Petri dish. Let me just say, go back to biochemistry. You take breast cancer cells in a Petri dish, you put plant proteins, they stop growing. You put animal proteins, they start growing. That's pretty good science. Now, you say that's a petri dish. They happen to be human breast cancer cells. But until you do a

randomized controlled study of animal versus vegetable, it won't be done. Should a breast cancer patient eat more broccoli? Yeah, let's dong the bell there again for sure. And I can tell you how to cook the broccoli so they get the best benefit. Eat broccoli sprouts, you get 50 times more of the benefit than broccoli. You were going to respond to that? Yeah. I come back to important end points. Total mortality or death from any causes and diseases.

I'm not persuaded by mechanisms unless they're tied to real outcomes that we care about. I think mechanisms are interesting, but as I said, you have to be aware that if foods have multiple effects, they might have one impact that you might think would lead to harm, but then they could have several other impacts that would be beneficial. And that's why you need to look at the real outcomes because there have been so many examples in the past of ideas where the mechanism that was originally proposed for the harm doesn't turn out to be what we thought it was. And so total mortality is the most important endpoint, deaths from all causes, but then also deaths from specific conditions are important too. And I would put that higher in the hierarchy of evidence than mechanisms. Absolutely.

Joel? I don't know how you abandon the unbelievable dedication and explosion of scientists around the country and around the world to come up with mechanisms of disease, because we're on the verge of this unbelievable breakthrough to change your genetics and alter your mechanism if you don't understand them you can't do it i think chris has it backwards more commonly basic science drives questioning a human population an epidemiologic study and then maybe a randomized clinical trial that's a usual progression um for example we have not even talked cholesterol this literally has been all saturated fat. 1975, my mentors in Dallas, Texas, but this is relevant in 2018, Brown and Goldstein in basic science identify your liver

cell has a receptor called the LDL receptor. Nobody knew it. It completely controls the metabolism of cholesterol in the body. They then find that there's a disease where you don't have that receptor and your cholesterol is a thousand and you die before you're 15. And I took care of those children in Dallas, Texas in 1986, 1989. From that came the development of a drug called Mevacor and Lipitor and Lovastat and all the rest. And we were able to test in humans. Does that basic science make a difference? Kaboom, the 4S study says you live longer if you have heart disease and you take a stat. Yeah, there's side effects. Yeah, there's this and that. Go down to the bottom line.

You want your LDL cholesterol like Loren Cordain, the founder of the Modern Paleo Movement, said, 50 to 70. And it's all consistent across epidemiology, basic biochemistry, randomized clinical studies. And what's the average LDL cholesterol in a hunter-gatherer in Okinawa, in Loma Linda? LDLs are 70 or 80. In fact, humans are the only free-living animal on the planet with an LDL cholesterol over 80 because we eat and we gorge and we have jacked up saturated fat that drives our cholesterol up. We're the only animal on the planet and we're suffering terribly from it. Let me pause you there.

Does saturated fat raise your cholesterol? That's the whole point. We need to keep coming back to dietary cholesterol and dietary saturated fat. The evidence is showing that on average, they do not raise cholesterol in the blood. And even when they do, that doesn't translate into an increased risk of heart disease. That's what the data show. We've talked about, I mean, I don't know what more I can say. Well, actually, we haven't just said i call bullshit on that it's called the hegastetic equation and the keys equation i shared the data on controlled feeding you you mentioned metabolic word studies as a high standard of evidence controlled egg feeding studies where 75 of people experience no change

in their blood cholesterol from eating two to four eggs a day. I don't know how more clear it can be than not. Eggs is an isolated topic because that's a cholesterol topic. We have not talked cholesterol. We've been talking saturated fat. But we're talking about cholesterol right now. Okay, well, but you just asked saturated fat, and I'm trying to be very specific. Well, does saturated fat raise blood cholesterol? To deny that is whack, and I'm sorry that's called the hegestead

equation google it look it up on wikipedia it's called the keys equation the change in the class the change in the blood saturated fat raises cholesterol in the blood yeah it's what you're saying it does it's known it's a but he's saying chris is saying that it doesn't know i'd say i say it does sometimes for some people but on average the studies is saying that it does. No, I'd say it does sometimes for some people. But on average, the studies are saying that it doesn't have a significant effect. On average. Disagree. So meaning if you get a large enough group of people, you'll have some aberrations. And some people will find a significant rise of their cholesterol.

Yeah. And again, more importantly, the presumption here is that serum cholesterol, we care about it because it will increase your risk of a heart attack. As I said before, large studies that have forgotten about cholesterol just analyzed the relationship between saturated fat intake and heart attacks, which is what everyone cares about, right? If they're thinking about cholesterol, it is like the middle is a mediator in that situation. So they remove that and they just say, does eating saturated fat increase your risk of heart disease? And that large review of 350,000 participants did not show a relationship on average. So is the concept that cholesterol is just one factor and that perhaps we've isolated it as more significant than it really is?

In our typical reductionist paradigm, absolutely. There are many factors that contribute to heart disease, and that's one of them. And so that's why, again, it's important to look at the studies that directly examine the relationship between saturated fat intake and heart disease rather than doing this dance where we go, does it increase cholesterol? And then assuming that high cholesterol will lead to heart attack. Joel, I'm sure you can understand why this is so confusing for me. I actually feel really badly for your viewers and listeners.

No, no, no. They're going to be able to go over this with a fine tooth. This is so important. I thank you both for doing this because this is the kind of conversation that you just don't get to have, where you get two experts with opposing views, and you have a decent conversation where you go over all the actual details of it, and you get to see how each one of you thinks about these things and how you've drawn these conclusions. I agree with that, actually. I think it's great and all, but we've had a couple moments of clarity and advice, and I just want people to have as many as possible because it does matter.

A friend of mine says heart disease is not theoretical. I mean, we've had many 39-second deaths while we've been doing this. So just to respond, I mean, does saturated fat-rich diets raise cholesterol? Absolutely. It's such a tight relationship. There's a line with a correlation that's just straight up now. Can I pause you for a second? What is wrong with these studies that he's showing that show that it doesn't in most people? No, I believe, and again, there are studies that are being referenced, but we're not looking at, and that's a limitation. We can live with that.

Since 2010, the question has come up, does an increased saturated fat cause coronary heart disease? And that has been questioned in some studies. The idea that it doesn't raise blood cholesterol is, you know, it's the reason all the guidelines up through 2015, 2016 still say limit saturated fat because that science hasn't changed. There's such a tight correlation. The line is straight up. Percentage of dietary fats, percentage of dietary saturated fat, blood cholesterol, blood cholesterol. The challenge is how much yours is going to raise and how much mine is going to raise

is going to depend on your genetics and your microbiome and where you're starting. If I ate a steak, my cholesterol goes up. If I ate an egg, this has been shown because I don't eat any dietary cholesterol as a plant eater, my cholesterol skyrockets. You become habituated to eating two, three eggs a day, and the curve flattens out after two, three eggs a day, which is 400 or 500 milligrams of cholesterol a day. It's like if you smoke 20 cigarettes and you go to 24,

it's going to be pretty hard to show much of a difference. Two, three eggs a day for a chronic eater is tough to challenge. So your body just creates tolerance for it? There's a level of absorption that starts to level off. But an interesting statistic, a toothpick is 100 milligrams. Most of us eat 300 to 400 milligrams of cholesterol a day, three to four toothpicks. We're talking fat.

We're talking 150 grams. So that's why the saturated fat, it's like overwhelmingly more of a topic than three to four toothpicks of cholesterol a day. Okay, hold on a second because he disputes this. I just come back to the studies. Two to four eggs a day, controlled metabolic ward, feeding studies do not have any impact on blood cholesterol in 75% of people. That's about as conclusive as the evidence can get. Quote, reference, reference, reference.

Okay. I'll give one to you. You got to give it. I always have it. And they're always there at Kresser.co slash Rogan. Yeah, I know. And here it is. If you Google Kresser saturated fat, that's the first article that comes up.

So this is Dius from 2009, Dietary Cholesterol and Coronary Artery Disease, a Systemic Review. I'll just show you. I know your viewers. Maybe your viewers can see it. I don't know. That's called saturated fat in the diet. That's called changing your LDL. that's called changing your ldl that's called the line going up like a straight rocket and that's it tell me where someone can

see this and we'll have jamie pull it up on the big screen yeah anybody that googles it's called hegstead equation h-e-g-s-t-e-d okay hegstead he's from the late 1970s. This was a 1993 reference. I know, but the Hegstead equation comes from Hegstead, who was one of the doctors who was involved with the McGovern report in 1977, which was the original report that led to the limitation on dietary cholesterol and saturated fat. So I think that's a little bit outdated, perhaps. If humans have changed. Like I said, you know, a while ago. But what's wrong with the studies? Like what Joel just said, though, if humans have changed. As I said, one study doesn't, you know, the exception doesn't make the rule.

We have a meta-analysis of observational studies, including 350,000 participants that found no relationship between saturated fat intake and cardiovascular disease. The review of 25 RCTs and 40 observational studies, 650,000 people that concluded that replacing saturated fat with polyunsaturated fat doesn't lower the risk of cardiovascular disease. We have to look at the weight of the evidence. We can't just choose one study or a mechanistic argument to support our view. So it's your take that this study is flawed and outdated? That's not a study. That's an equation that was meant to represent the relationship between saturated fat intake and blood cholesterol that was created by a doctor in the late 70s that was originally involved in this diet hypothesis and the McGovern report, which

led to the restrictions on cholesterol and saturated fat in the first place. So yes, I am saying that we should be looking at more recent evidence, large reviews of meta, of observational studies, and then meta-analyses of randomized controlled trials. That's a much more persuasive source of evidence for me. Joel? It was based on metabolic or carefully done studies at Harvard. The equation derived from human data where you put people in, change their diet, dietary change studies drives up LDL cholesterol, and you just plot it out.

The plot's very clear. It's changing cholesterol to dietary saturated fat. It's well accepted in the medical community and it's incorporated in the guidelines. It'll never change. Human physiology is not going to change. LDL receptors don't change. It all goes back to basic biochemistry. When we understand it, we can manipulate it to better health. We can do it through pharmacology. We can do it through diet. We'll be doing it through gene therapy, stem cell therapy. But if we don't understand the biochemistry, we're cutting out a pillar we have to have for better health. Chris? I don't know how many more times. I mean, I feel like I'm just saying the same thing over and over

again. We have to look at the research, the weight of the evidence. We have to look at randomized controlled trials that actually look at what happens when people consume saturated fat and dietary cholesterol. And you're saying that these studies that he cited, this graph does not. Mechanistic arguments are not persuasive if it's not happening in real people. You're measuring in a randomized controlled trial, you're controlling, you know, you're measuring what happens when people eat saturated fat and cholesterol. And then you do a meta-analysis of these controlled trials and you're finding what I just said. That's way more persuasive to me.

What is your take on that, Joel? The Royal Academy of Science. But what is your take on that? I'm going to tell you, I'm going to tell you, the Royal Academy of Science in Sweden gave the Nobel Prize in Medicine for what we're talking about, and nobody's changed that. I mean, I totally disagree with Chris that human physiology didn't change from 1985 Nobel Prize to 2018, that the relationship between eating saturated fat, lowering your LDL receptor, raising your blood LDL, developing atheroma, I go in at three in the morning and bust open

your plaques, you live, has not changed. But how are these studies made and what's wrong with them then? Nothing's changed but I understand the biochemistry of our lipid metabolism and cells. Of course, there's always advancements, but the LDL receptor has led to the statin field, a new class of drugs called PCSK9 inhibitors. It's all because of the biochemistry that people are living longer, living better. Their plaques are being reduced through lifestyle medicine. But thank God we also have pharmacology that's advancing.

Right, but what is wrong with these studies? These studies that are showing these results that he's describing that you're disputing. What is wrong with these studies and what is wrong with the results? Again, I would urge everybody to take the broad, high-level view of science and not pixels. What's the basic biochemistry? I know we're circling around. What's the epidemiology? What's the clinical randomized trials?

And what's the centenarian studies? There is no new data that you live to 100 by adding saturated fat to your diet. Yeah, but we're not talking about that. We're talking about the actual physical results on human bodies when you consume saturated fat, what he's just describing. I mean, it would take a new metabolic ward study that negated the Keyes equation, the Hegstead equation, that there's a linear relationship, 395 metabolic studies. It doesn't exist. What are you saying to that, Chris? A metabolic ward study that says eating saturated fat. It would not take that, Joel. We have randomized controlled trials, which is a very high standard of evidence,

and observational data, large amounts of observational data that have been reviewed that answer this question. And we have many RCTs of low-carb diets and even ketogenic diets that are not showing significant impacts. Joel, is it possible that this is correct? Here's a 2018 review of all the previous science on dietary cholesterol and eggs, and the conclusion says overall recent intervention studies with eggs, recent, demonstrate that the additional dietary cholesterol does not negatively affect serum lipids and in some cases appears to improve lipoprotein particle profiles, like have a beneficial effect, and HDL functionality, which is the so-called good cholesterol. And he talks about here in the conclusion that eggs shift LDL particles to the less detrimental large buoyant LDL, which is less atherogenic.

He says eggs also typically increase HDL. He says that eggs probably have other beneficial impacts in terms of their phospholipid contacts and that there's no relationship between the consumption of eggs and heart disease. So this is a 2018 review. It's by Christopher Blesso, Dietary Cholesterol, Serum Lipids, and Heart Disease. Are Eggs Working For and Against You? Published in Nutrients. Joel, is it possible that that's correct and there's just some misunderstanding about the previous data? It's a different topic.

It's eggs. It's eggs. It's cholesterol. We were talking saturated fat. Does it raise your cholesterol? So they're different topics. And then we've introduced a very hot topic about LDL particle size, which we should break down and talk about. So I'm not sure quite how to respond because we got off track by shifting to consistently low-carb and eggs and other things. Actually, we were talking about cholesterol.

Well, we were talking about does saturated fat raise blood cholesterol? So I stand by the fact human physiology will not change. We have receptors. But doesn't our understanding of human physiology advance? I don't. Well, I'll give you an example.

Until 20 years ago, nobody ever heard a word PCSK9. God or somebody gave us a protein in our blood, PCSK9, that goes to your liver, sits in a receptor, causes the LDL receptor to go internal, and your frigging blood cholesterol goes up. Now there's a class of drugs that's an antibody to PCSK9, lowers your cholesterol dramatically, and we're finding it reduces plaque and lowers your risk of heart attack. Sure, new science, amazing, totally consistent with what Brown and Goldstein showed that led to statins. Now we have a new treatment.

That's a wonderful thing. It didn't rock the boat. We still don't know to this day why we have that protein in our blood. And if you're lucky enough to be born with a low level of PCSK9, your cholesterol is lower, you have less disease, you live longer. That was part of the data I published in 2012 with Brian Ferentz at Wayne State University. So yes, we've learned more about human physiology, totally consistent, didn't disrupt anything, and led to better treatments. That's great. Has human physiology been challenged? I'll give you another. We've learned, and Chris mentioned this, so I think it's fair to go there. It's like a court of law. He opened it up. I'm cross-examining. Nobody in the world ever

heard the word of four letters, TMAO, 2011. Cardiologists sitting at the Cleveland Clinic said, there's got to be more in the blood that hurts arteries. Let's go find him. They found this chemical. They learned how to measure it. They patented how to measure it, TMAO. They took 4,000 people on the cath lab table. They said, I wonder if the level of TMAO in the blood correlates with how clogged up your arteries are. But doom, it worked perfect. Then they figured out if you eat red meat that has rich in L-carnitine amino acid, you eat eggs that's rich in choline, a nutrient, I think amino acid. I'm blanking for a minute. Those directly led your liver to create TMAO. They took studies where they reduced carnitine, reduced choline in the diet, TMAO goes down.

What does TMAO do? It stuns your HDL so it doesn't reverse cholesterol transport. It causes LDL to enter the cell wall and create foam cells, macrophages, plaque, and you get a heart attack. It actually screws up your kidney and causes it to be fibrose. If you have heart failure, diabetes, or heart disease, or hypertension, your TMAO is up. I've actually drawn more TMAO levels than I think any physician in the United States. This is my baby. New human physiology that has not led us to back off the idea that limiting the animal product consumption, in this case specifically egg yolk and red meat, may have benefit to your health. We just learned a new pathway. Actually, Joel, what in the diet increases TMAO orders of magnitude more than red meat? Fish, because fish has it right in

their fish flesh, along with that mercury in their PCBs and their DDT. What is the association of seafood intake with heart disease and mortality? Can we use epidemiology studies? I thought they're off the table. As I said before, we can use epidemiology when we use it wisely. Oh, that's so selective, Chris. Use it or don't use it. I always use epidemiology when we use it wisely. Oh, that's so selective, Chris. Use it or don't use it. I always use epidemiology, 100% of the time. What do you mean, Joel? We've been talking about large reviews of epidemiology that suggest that saturated fat and cholesterol don't increase the risk of heart disease. So if you could answer the question, I'd appreciate it. Quality over quantity. What is the association of fish with cardiovascular?

What would most doctors and researchers say about fish consumption and cardiovascular disease and mortality? Well, since it has saturated fat, most high-level 2018 advisors are two meals a week of fish, balancing out with 19 meals a week of plant-based. Is the USDA guidelines honest? I'll answer the question. Dr. Valter Longo. If you look at the data, there are a few things that are associated with a greater decrease in cardiovascular disease risk than fish consumption.

Fruits and vegetables. T-M-A-O is, if you look at a graph, and you can, if you Google, let's see, maybe Jamie, you can pull if you Google, let's see, maybe, Jamie, you can pull this up. Cressor TMAO. And you click on that first link, red meat and TMAO. And you scroll down and there's a picture. Oh, cool, Jamie. Where you been?

There's a picture. Scroll down. There you go. So that picture shows the increase in TMAO from eggs, beef, cheese, milk, clams, and then look at cod and halibut. Wow. Let me just see the reference. What's the reference here, buddy? Egg and beef. The reference is in the article, Joel, as always.

I would see it. I would see it. You can see it. It can't be Chris Masterjohn reference. That's not fair. It's not Chris Masterjohn. And that's so cod and halibut are increasing TMAO, as I said, orders of magnitude more than beef or eggs. You can't even see eggs and beef there. And the data show that fish consumption, I think almost every public health authority would recommend, you know, would agree with this, is reducing the risk of heart disease and

mortality. So TMAO is another mechanism. It's another interesting mechanism, but it's not fully understood. And again, we have to look at the data on red meat consumption and heart disease and mortality to really figure this out. We can't, you know, it's a speculative mechanism. I don't disagree that it's important to look at mechanisms, but you can't draw conclusions based on them.

And this single fact about TMAO just kind of blows the thing apart. The other thing about TMAO to know is that certain types of gut bacteria metabolize choline and carnitine into TMAO, whereas others don't. And so a lot of scientists have speculated that high TMAO levels are essentially a result of a disrupted gut microbiome. And that makes sense. If you have 60% of the calories that Americans are consuming are from ultra processed food, and we know that that totally screws up the gut microbiome, then if you get a person eating a standard American diet, then their TMAO levels may go up with red meat. Whereas if you take someone who's got a healthy microbiome, because they're eating,

you know, lots of plant foods that support healthy gut, then you may not see the same association. And part of what supports that is there's studies showing that rifaximin, which is an antibiotic that treats bacterial overgrowth in the small intestine, reduces serum TMAO levels, which suggests that it's mediated by the gut microbiome. So consumption of fish has been universally shown to decrease heart disease. The mechanism is interesting, but overall, it may be very complicated with many factors, and we might not know all of them. Yeah, and then that's what takes us back to let's look at the data on whether red meat increases the risk of death or heart disease.

Joel? Chris's reference was giving credit to another blogger's article. That's not science. You have to go to the blogger's article and look at it. It was number 16. Joel, there's— I know, but we have to find the article. The reference is number 15.

It's okay. It's sloppy referencing. Hold on. Hold on. Let him explain what the reference is because he challenged it. It said there that that graph came from now. But let him explain it. Number 15 is the reference.

Dietary precursors of trimethylamine and man, a pilot study. TMAO is, you know. Okay, so it's not a blog. It's actually a study. Okay. TMAO is a hot topic right now that is largely being researched in terms of egg yolk and meat consumption. It doesn't really matter. It's not preliminary science.

No, no. It's not preliminary science. They're coming up with pharmacologic agents right now to block it. And we'll see a new class of drugs. Wait a minute. But is that what's significant? Or is it more important to concentrate on gut biome and healthy diet? Why are we instantly giving the ball to pharmaceuticals?

You asked the question, is there any new human physiology that's relevant? We started with PCSK9. I'm introducing TMAO as new human physiology that's relevant that could lead to improvements in clinical outcomes as suggested by observational studies. Right, but we're talking about what he just showed in the graph. You dismissed the graph, then he gave you a study for the graph, and you just sort of glossed over it. Right. The one that contributed, fish is a flesh source of TMO.

We can talk about whether fish in 2018 is uniformly a healthy food product. But that's not what he's saying. And he's also talking about gut biome and gut bacteria and the consumption of red meat being significantly less than the consumption of fish which is universally said to be a good thing for your heart so a bunch of layers there real quick everybody who studies tmao knows that the microbiome is a critical component two people can eat a steak it's classic study cleveland clinic study feed a vegan a steak this is a classic cleveland clinic research study in the New England Journal of Medicine. I don't make TMAO.

Why? Because my microbiome is different than yours. Feed an omnivore a steak, they make TMAO within 12 hours. An omnivore eating a standard American diet. Sure. But nonetheless, it pointed to the fact that it was the microbiome. You give a mouse meat and give it an antibiotic that wipes out a microbiome, it won't make TMAO. The microbiome dependency of TMAO is well-known science.

So that does not denigrate the topic. I mean, it's a side topic. Is fish always healthy in a world of DDT, PCB, mercury? I don't know about Chris's practice, but every patient I see gets blood mercury levels, and those that eat routinely heavy are very often very high. Okay, but that's another subject. That's another subject, because you were talking about- No, you want to look at old data on fish, and now I'm bringing up 2018 clinical experience.

No, no, no, that's not what he's doing. We're not bringing up old data on fish. I was being beat up for old data, and I'm bringing relevant clinical material of 2018. You were talking about the absolute mechanism that's caused by the consumption of meat. He brought up fish consumption, which vastly elevates this. And yet fish consumption is not correlated with heart disease. In fact, it's correlated with people having healthier hearts. So if you're suggesting to me is the recommendation today in this discussion eat fish but limit egg

yolk and meat i'd agree with that that's not what it says because the fish consumption vastly elevates what you were saying was a significant issue he's saying it's not a significant issue that it's a mechanism and it's an interesting mechanism but it's part of a much larger and probably very poorly understood situation. I don't think that's completely true. What we do know— Is that true? Well, yeah, I would say that's true, and I would say it's another proxy marker for a crappy diet.

What we know is that eating red meat in the context of a standard American diet may slightly raise your TMAOo but not nearly as much as eating fish will so you brought up this tmao and he's basically just squashed that argument yeah but i think he's scientifically wrong because again the wealth of the body and i mean is that about tmao about gmao because what about the fish because a few specific fish number one the way that egg yolk and red meat cleveland clinic new england journal medicine is is this a step of ingesting the precursor going through your microbiome going through an enzyme called lyase in your small intestine going to your liver is tma and metabolize the tmao that process is correlated with atherosclerosis that process is correlated with with increased activity of LDL within your cell wall.

Correlated by epidemiology studies? No, no, no, by biochemistry, biochemistry. We know how it works in the Petri dish. That was the brilliance of this rapid development from 2011 to 2013 to now. So it's specifically meat and fish or meat and eggs? What hasn't been studied is if fish flesh already has preformed TMAO. We don't know if it activates LDL activation. We don't know if it stuns HDL.

Nobody's looked at the correlation of fish flesh preformed TMAO and a 4,000 patient study in the cath lab table. We don't know. They're wonderful questions to ask. But until they're done, there is reason to be concerned that there's a new pathway that might be involved in atherosclerosis. Okay, well, now we're talking about a totally different thing. Yeah, exactly. If consuming food that raises your TMAO increased the risk of heart disease, then you'd see

people who are eating the most fish having the most heart attacks, and that's the opposite of what you see. Well, I think that's reductionist, because what does fish have? But isn't it reductionist to bring up TMAO in the first place because you brought up a significant factor? No, even more reductionist than what I just said because I zoomed out a little bit to look at the actual relationship with mortality. Well, that was a blood level. That's not atherosclerosis. That's not outcome.

That's not kidney function. That's not stroke risk and heart risk, which have been studied. But you're talking about TMAO. I am talking about TMAO. That's what that graph showed was TMAO. So back it up. You eat red meat're talking about TMAO. I am talking about TMAO. That's what that graph showed was TMAO. So back it up. You eat red meat, you make TMAO if your microbiome is of a certain constitution. You eat egg yolk, you make TMAO if that's a certain constitution.

Is it good to have high levels of TMAO in the blood, whether they're from fish, egg yolk, or red meat? The science suggests it's not good. What can you do to lower your TMAO? Let me pause you. Let me pause you. How does the science suggest it's no good if there's large do to lower your TMAO? Let me pause you. How does a science suggest it's no good if there's large levels of TMAO that come from fish, and when you eat that fish, it's directly correlated with less heart disease? Well, it would take an evaluation,

what's the calorie content in the United States that's from cod, halibut, red meat, and egg yolk? I would think the calorie content of egg yolk and red meat is higher than cotton halibut. I don't have that data, and that's a global perspective. But if you are up to date in the science and say, I'd like to lead a low TMAO life, which again, I'm going to say with all boldness, I've drawn more blood levels on than anybody in the United States, I believe, according to the Cleveland Heart Labs, you will want to do all steps to lower it. And maybe you want to leave fish in because the complementary benefit that fish has shown may be from omega-3. This is purely speculative, though, right? We don't understand.

But you're talking about TMAO as a mechanism. Right. It's purely speculative to say that the TMAO from fish is healthy, but the TMAO from beef and eggs is not. No, I don't think it's speculative. I don't think we know the answer because it's seven-year-old science. But you're stating it, though. No, I'm not stating it. But you I don't think we know the answer because it's seven-year-old science. But you're stating it, though. No, I'm not stating it. But you're stating that TMAO is a massive concern.

That is scientifically true. But how is it scientifically true if there's so much TMAO in fish and there's no concern? There's two species of fish that have the highest levels. You saw the other levels. What are the other ones? Fish in general is higher in TMAO. Those are very popular fish. This isn't rare fish. It's cod.

We're not talking about higher. We're talking about like beef and eggs barely even register on that graph. Sensationally higher. So orders of magnitude higher. Like what percentage? I don't know. It was higher. Yeah, probably 20-fold higher. 20-fold. 20 times higher.

I might have even mentioned that in my original article. Joel, the problem is you brought up TMAO in the first place like it was this magic bullet. Well, but let me just tell you. Okay, let's everybody look at molecular nutrition food research 2016. Does fish protein, when it elevates TMAO, accelerate atherosclerosis? According to a research study, when fish raise TMAO, they accelerate atherosclerosis. Anybody can check the reference.

Lead author, I cannot say the name, Yazdikashki. How is this conclusion reached? A Petri dish data is a Petri dish. I'm looking for a minute. It's basic biochemistry. What happens to atherosclerosis in arteries when you feed? This is mouse data. That's how you generate hypotheses.

Well, it hasn't been done in humans yet. Not such a unique thing to do. But why are you bringing it up as pure fact then? Well, the assumption is that fish is a superfood. I've already knocked it down for several reasons. One, the fish intake is associated with increased risk of diabetes. I'm sorry, that's epidemiology. Wait a minute.

Fish is associated with increased risk of diabetes? Risk of diabetes, that's epidemiology. Wait a minute, fish is associated with increased risk of diabetes? Risk of diabetes, yes. It's got protein and saturated fat. This is also epidemiology studies? So the question is, is there a randomized study? Basic biochemistry, you'd understand it from the saturated fat content of fish. It would be largely epidemiologic studies. But when you're saying epidemiology studies, you're asking people,

what do you eat on a regular basis? And they say fish and French fries and hot dogs. You say, oh, the fish is associated with an increase. But it's connected to all these other things, and it's not isolated. It's connected to all these other things, but it's not isolated. Well, you try and isolate out things by multivariate analysis. I mean, it's not one study. It's many studies.

But diabetes and fish? Really? Yeah. Is that real? It's real. It's in the science. There was one review that said that. Why is there a review?

Because there's many papers. Here's a 2012 review that does not find any association between fish consumption and diabetes. find any association between fish consumption and diabetes. So you're thinking that this was 440,000 people with an average of 11 year follow up published in the American Diabetes Association Diabetes Care Journal. So, yeah, I don't think, you know, it's hard, I think, to make a claim that fish consumption is harmful for health, given the enormous weight of evidence. And yes, there are concerns now about toxins, and it might change over time. And there are also issues with overfishing and all of that. Different story.

Yeah, different story. We're talking about just the association of fish consumption and health and longevity. And I think if you got 100 scientists in the room, maybe 99 of them would agree that that's, that, you know, there are a few things in nutritional research that are less controversial than that. Well, maybe. I mean, I'm just, I'm not making this shit up. Journal of American College of Nutrition,

intake of fish was correlated positively with the increased risk of diabetes. I mean, the science is out there. Is it crystal clear? Is this as well-defined as the Hegastead equation, dietary saturated fat, change in cholesterol? No. Is it an association that could be of concern? And basic biochemistry said fish have saturated fat. That could possibly cause something called lipotoxicity. Fish have animal protein. We've already talked where animal protein is very different than plant protein.

The concept is plausible. Sure. Is it resolved? It's not resolved. Is fish a better choice than eating fried chicken or a piece of Philly hoagie steak? Absolutely, it's a better choice. Jamie just pulled something up here. It says the findings do not support a beneficial effect of total fish, type of fish, or EPA and DHA intake on the risk of type 2 diabetes. Alternatively, other dietary components such as selenium and unmeasured contaminants present in fish might explain our results.

Jamie, dude, read the sentence. Total fish intake was associated positively with the risk of type 2 diabetes. That says there's epidemiology that should be further studied, but maybe somebody wants to cut back their fish. But we're looking at a single study here. I agree. We need to look at the weight of evidence. Jamie, you're bad, man.

But wait a minute. It says findings do not support a beneficial effect of total fish, type of fish, or EPA, DPA on the intake on the risk of type 2 diabetes. Even lean fish was associated with developing type 2 diabetes. Fatty fish was not, because you probably want that omega-3. But I'm not telling anybody, it's a resolved issue.

But you were saying TMAO from animal protein is what causes this problem. It's actually more specific. It's choline and carnitine. Egg yolk, it's not really animal protein. But you said TMAO. Yeah, TMAO. TMAO is, okay, so what's in meat that's not good for you? Although if you're hungry on an island and you're dying, eat meat.

We all recognize it. But if you're looking for optimal health, you should be concerned about the saturated fat content. You should be concerned that animal protein accelerates aging through mTOR and IGF-1. Has it been proven that animal protein accelerates aging? If he says no, we should just stop because that's – Well, because it's world-class science. I mean – Just because you say it doesn't mean it's true.

We need to go over this. We need to open to the possibility that high intakes of methionine, which is one of the amino acids in animal protein, in the absence of sufficient intakes of glycine, which is another amino acid that's in animal proteins, and then intake of nutrients like B12 and B6 and B9, which is folate, could some of the animal studies suggest that that has an effect on longevity. But this is why I've always been an advocate of eating nose to tail. So not just eating lean meats that

are very high in methionine, making sure you're getting enough of the glycine-rich foods, the bone broth, et cetera. And then you're also eating plenty of a mixed diet that contains B12 and folate and B6 and the other nutrients that balance out the effects of excess methionine. As well as fiber for a healthy gut bile. Absolutely. And when you pulled up that conclusion, Jamie- No fiber in meat. No fiber in meat. Yeah. Well, you eat other things with it. I've never argued for an all-meat diet.

I've never argued for an all-meat diet. Except Sean Baker. Well, there's a whole other ball of wax with that whole carnivore diet. Conclusions. An accumulated evidence generated from this meta-analysis does not support the overall inverse association of fish or fish oil intake with incidence of diabetes. So that's saying that increased fish intake doesn't lower the risk of diabetes. It's not saying that it increases the risk.

So it says there's no relationship there that they can analyze. So no one's saying that it causes diabetes. So whatever it does – where does it say that it causes diabetes and what is this study? Nobody said it causes. This is classic association. Okay. Because you don't know if it's the protein, the fat, the mercury, the PCBs, the DDT. Or the other factors in your diet.

Yeah, they're eating fish and chips, watching TV. Absolutely. Right. This is clearly not to the level of saying processed red meat caused cancer. This is saying fish consumption in some studies is associated with type 2 diabetes. But these are heavily flawed studies. Would you agree? I wouldn't throw them all under the bus.

You know, that's how science works. I mean, it slowly plods forward. Chris is smiling. Yeah. I mean, it slowly plods forward. Chris is smiling. Yeah. I mean, we were starting, Joel brought up TMAO, and then that's how we got onto fish and diabetes. I think there is no strong evidence that eating fish causes diabetes. There's a lot of evidence that suggests that eating seafood reduces significantly the incidence of cardiovascular disease. And again, if TMAO were a problem, then eating a lot of fish should not have that impact.

And you believe that this is probably, well, I shouldn't say you believe, do you believe this is from essential fatty acids that are found in fish, particularly fatty fish? Yeah, I think that's plausible given what we know about EPA and DHA, which are the long-chain essential fatty acids and their benefits. And it could be fish is also really a great source of selenium, as that one study said. Sixteen of the 25 top sources of selenium come from ocean fish. Fish is a great source of bioavailable protein. There are lots of reasons why fish consumption could be beneficial.

So in your opinion, this sort of highlights that there's a lot of complex, different moving parts that we don't totally understand, and that this is why you don't want to rely completely on just the mechanisms and these things that are occurring in petri dishes or mice studies or things along those lines. Yeah. So going back to the Bradford Hill criteria that I mentioned before, which are ways of kind of determining whether associations that show up in observational studies might be causal. One of the criteria is mechanism. Is there a plausible mechanism that could explain the relationship between this variable and that variable? But there are other criteria, strength, consistency, specificity,

temporality, biological gradient, like a dose response, coherence, experiment, analogy. So, yes, mechanisms are great. It's important to study them. I'm all for that. And we absolutely need to study them. I'm all for that. And we absolutely need to correlate them with real outcomes and real human beings to see both in observational studies that are well-designed and in randomized controlled trials to see if it makes sense. And

TMAO, I think, is a great example of that. Is it fair to say that we really just are looking at a puzzle and we don't have all the pieces? Absolutely. You can say that in many cases, and in this case, for sure. Yeah, I disagree. There's a tremendous group, and you can pull this up if you want, Jamie, called True Health Initiative. It's more than 400, I'd call, world experts on nutrition, very divergent food philosophies, paleo, Mediterranean, plant-based. Specifically, what are you disagreeing with? Well, so that there's no consensus to advise the public on a healthy diet for humans. I disagree that we don't know enough.

That's not what we said. What we said was that it's a complex puzzle and we don't have all the pieces. Well, I agree with that, but we have enough to make recommendations. Then why are you disagreeing? Because we have enough to make recommendations to the public, and the True Health Initiative has crystallized that. Okay, but that's not what we were discussing right there about recommendations to the public. We were talking about mechanisms and whether or not it's understood, all the different moving pieces in terms of how your body absorbs nutrients and food.

It's an endless flow of new knowledge. Right. That's what I said, but why did you disagree with that? I didn't disagree with it. That's exactly what you disagree with. You said, I disagree when he said that that's an accurate assessment, that we don't have all the pieces to the puzzle. We definitely don't have all the pieces. We have enough to make recommendations, and then we'll reevaluate it all. Do you want another new meat problem? It's coolest, latest science. Sure. Okay. Jamie, will you go to, please, meat allergy on Google, University of Virginia atherosclerosis. It's a little tough.

Meat allergy. You wait this, baby. Is this like the Lone Star Tick? Oh, you got it, baby. You are so good, Joe. Alpha galactose? Oh, my. Joe, I am so overwhelmed by your science, and I mean that sincerely.

You see the one that says NIH? It's a number two hit on Google. But this is something that's caused by an adverse reaction to a tick. So you've got a listener here who's in Virginia, maybe. You see a segue? Actually, you can throw that. Oh, this is cool. You actually got the whole point.

The average person should eat meat, though. Well, but if you get bit by this tick, you're fucked. No, but this started with – Yeah, you gotta eat fish. Here, go ahead. So this is – It costs diabetes. I don't know.

Go to the second one. It'll have the picture. Just real quick. Okay. You live in Virginia. You end up on a – Yeah, you're right. Get out now.

You end up on my cath lab table because you're in the emergency room for whatever reason. Okay. I draw a blood sample on you. 24% of those people have an antibody to alpha-gal, which is a carbohydrate found in meat. And that shocks people. There are carbohydrates in meat. And only red meat specifically. And only red meat specifically.

24% of Virginians show the antibody. So that was interesting. And some are now developing anaphylaxis carrying EpiPens because they have a meat allergy. That isn't 2.4%. It's 24% have the antibody. But what was discovered at University of Virginia is if you then look at their heart arteries by ultrasound, the more plaque they have, the higher is their titer of the antibody. Brand new science. It's an association. Nobody knows. There is, of course, the possibility of inflammation from immune activation. That's wild data.

Now, I don't wish that on people. I wish we live in a world where people didn't have nut allergies, didn't have lactose intolerance, and didn't have meat allergies. But the reality is there may be a pathway, previously unknown, that is hot. And this all goes back to your question. Is there any new physiology about this whole topic? Okay, but can I stop you right there? This is a pathogen-activated allergy that's from a— And it's pretty severe.

People don't walk around with this without knowing that they have it. They have severe allergic reactions. It's basically like Lyme disease. I mean, it's a horrible tick-borne disease. It can be anaphylactic. We're not talking about like a mild GI discomfort. We're talking about a— I don't think this is a mechanism that has existed for a long time that could explain anything about red meat.

This is something that's only been discovered over the last couple of decades. Yeah. Of those 24% that have the antibody, very few had the full clinical syndrome, but it's still correlated with heart disease. The point is keep an open mind. I don't see the data accumulating that means getting healthier. Can I ask you this? Do you think that it's because they have a mild case of this tick-borne disease or this tick-borne disease is, like, because it is fairly recent in terms of our discovery of it, is it advancing and evolving and getting more potent?

I doubt, you know, the basic biochemistry of meat and the carbohydrates in meat have changed. Has the Lone Star tick become more frequent? I mean, I don't know. Has it become more potent? Yes. Has it become more potent? Absolutely. As Lyme disease has, right?

Is there a cross-reaction between glyphosate and being bit by a tick and our intestinal permeability? There's all kinds of crazy ideas that need to be pursued because some of them will be right. Which is Monsanto's roundoff. We hate it. We hate it. That's right.

Dangerous shit. It's Bayer. It's Bayer now. It's all Bayer. Correlation is not causation. We, we, I know you agree with this, Joel. We have to keep that in mind. I mean, it's that there's a great study done. One of my favorites that was purposely done to illustrate the danger of assuming that correlation equals causation. It was a study done of the most common diagnoses for hospitalization in Canada, 10.6 million people. And they found that 24 diagnoses were significantly associated with the participants' astrological signs. So people who were born under the sign of Leo

had a 15% higher risk of being hospitalized for gastrointestinal hemorrhage. And Sagittarians had a 38% higher risk of being hospitalized for an arm fracture. Now, remember, the proposed increase in risk for processed meat and cancer is 18%. So these risks are on the, you know, that's processed meat at that same level. So Sagittarian has a higher risk of being, if we believe in this correlation data, you know, you can't assume correlations or causation. I mean, that's basic. And I, and it doesn't, again, there are extent you can use Bradford Hill and other things to strengthen the association, but you need to test it with an experiment or the association needs to be strong.

It needs to be over 100% at least to really rise out of the noise and say, okay, we're really seeing a signal. Let me give you another example. There was a recent study just published that showed that pregnant women with the highest maternal consumption of gluten had a twofold risk of type one diabetes in their offspring and their children. That was a double, that was over a hundred percent. So that is actually worth paying attention to because that's so such a large, you know, increase in risk that it doesn't confirm it by any stretch, but it does mean, yeah, maybe we should look into this further. If that was a 5% increased risk,

I mean, you might as well say that Sagittarians have a higher risk of arm fracture. Is it fair to say that when we're doing all these nutritional studies that you're looking at a poverty of data? Yeah. I mean, John Ioannidis had a quote. Let's see if I can quickly find it. Because we're comparing all these different studies. And I mean, obviously, Joel thinks one thing. You think another thing. So here's the Ioannidis quote.

Moreover, given the complicated associations of eating behaviors and patterns. Oops, lost my place. Given the complicated associations of eating behaviors and patterns with many time-varying social and behavioral factors that also affect health, no currently available cohort includes sufficient information to address confounding in nutritional association. So he's saying, you know, lay person translation, there's so many factors that affect our health from our sleep to our physical activity, to our, whether we smoke, whether we drink, you know, our social relationships. There was a study that I think I talked about on one of my previous appearances that shows that not having enough good relationships will increase your risk of death more than smoking 15 cigarettes a day. No studies are controlling for that. Right. Um, gut microbiome,

we now know is really important for our overall health. Are any studies comparing for people, you know, actually controlling for people's, the state of people's gut microbiome? Absolutely not, which is a problem with the TMAO research. So, again, it doesn't mean that observational studies are not useful. It means we have to take them with a huge grain of salt. And the fewer things that are actually controlled for, the bigger the grain of salt will be. Joel? I kind of hear a sense that it's so overwhelming and there's so many spots in the data that we're unable to advise the public again. I don't agree with that. I think we have more than enough data. You can go to Michael

Poland, eat food, not too much, mostly plants. Everybody loves it because it's consistent with the overwhelming 50,000 level look. You can go to True Health Initiative that says- 50,000 level look? Yeah. The whole level of biology, basic science, centenarian, randomized clinical trials, epidemiology. You've got to talk to a patient Monday morning. I don't want to get mired in confusion. I'm going to tell that patient, eat real food, don't eat too much, and eat mostly plants. Because that is a synthesis of 50 years of nutritional research.

Are we going to evolve that to something more brilliant? You might add now fast five days a month or don't eat 12 hours a day. We might be able to refine it with some of the new science on using fasting intelligently, but that's pretty strong. When I go to a true health initiative and say it's all confusing, but 400 scientific international experts say eat locally sourced, close to the ground, plant predominant with water. 400 scientists say that's pretty reasonable. That I can tell my patient on Monday is something they can actually activate.

And we'll figure out TMAO with a block or with fish or with eggs or with choline or whether this tick allergy ends up spreading into Michigan or California. And there's a way to deal with it. But for now, these are critically simple lessons for the public. I'd actually agree with that, including the part about plants. I mean, my recommendation is your plate should be two-thirds or three-quarters plants and then animal products, animal foods. So the question here is not that. Should we eat a healthy whole

foods diet we both agree on that 100 the question is whether animal foods uh should be a part of the diet based on their nutrient density which unfortunately we haven't had a chance to get into yet and their bioavailability and the fact that humans and our hominid ancestors have been consuming them for over two and a half million years. You know, that's my argument is that on that plate, for most people, they're going to benefit from having some animal foods, how much, you know, what proportions of carbohydrate, fat, protein, and all of that, that depends on the person, and you're going to see big differences, actually, from person to person. But, you know, I think today has made it clear there's no convincing data that shows that completely removing animal products from that plate is going to lead to a longer lifespan or significant reductions in disease. Let me put it this way.

What is the benefit of putting that one quarter of your plate, putting animal protein? Like what is the nutrient density of it that makes it? Lots of benefits. Yeah. So animal protein is more nutrient dense in essential nutrients. So making it clear that I support eating both plants and animal foods. Um, so, so making it clear that I, I, I support eating both plants and animal foods. So animals are, animal foods are higher in B12, bioavailable zinc, iron, calcium, uh, choline, taurine, creatine, and not just higher in terms of the actual amounts, but higher in the amount that you absorb. And that's a very key point.

Whereas plant foods tend to be higher in carotenoids, polyphenols, flavonoids, diolosulfides, which are in cruciferous vegetables, and fiber. And those are important as well. well and so to get the best of you know the the most the widest spectrum of nutrient density we want to eat the animals for those nutrients at animal foods and then the plant foods for those other nutrients and what would be negative about removing the animal products from that one quarter of your plate what what could you not fill in with plant protein? Because clearly some people get by with just plant protein. B12 is the biggest issue, for sure. It's not really found in plant foods except for some exotic species of wild mushrooms and nori. And plants and mushrooms aren't really plants. Right. But yeah, in non-animal foods, I guess you could say. But if it's not

just a question of what's theoretically possible, it's a question of looking at the studies that show us what are the average, you know, how common are nutrient deficiencies on omnivorous versus vegetarian and vegan diets. And if you go to kresser.co slash rogan, there's a whole section on that that links to a very in-depth article that shows that, for example, vegetarians and vegans, the average omnivore, the rate of B12 depletion is 11%, and then for vegetarians it's 77%, and for vegans it's 92%. 92%?

Of depletion, which is the first stage. There's four stages of B12 deficiency, and that's the first stage. And the earlier studies that showed less of a difference used only serum B12 as a marker, but it turns out that serum B12 is not a very accurate marker of B12 deficiency, and we need to be using more accurate markers like holotranscobalamin, methylmalonic acid, and homocysteine. And when you use those newer markers, you see those broad, you know, very big differences in deficiency rates. And furthermore, there was a study done in vegans and vegetarians in the Netherlands that were at like a summer camp.

So these were people who were educated vegetarians and vegans. They were really into it. And the average serum B12 level for them, even what was below 200, which is in a deficiency state. And even the people who were supplementing had significant levels of B12 deficiency. And that's probably because studies have shown that the amount that you need to supplement with is about 100 times higher than the RDA. So the RDA is 2.5 micrograms. And you really need 250 micrograms to get your levels up. And if you're deficient, you need 200 times more than the RDA, 500 micrograms. And all the studies are there on my site.

And is the problem that B12 is nonexistent in plant-based foods or that it's not as bioavailable? It doesn't exist. The true cobalamin, absorbable B12 doesn't exist in plant foods. You can get other cobalamides, other forms in plant, even algae. Even algae. Yeah. Most vegans who are educated about this know this, and they take a B12 supplement. But the B12 supplement is probably based on what?

Like what's it coming from? Well, it's not that that doesn't necessarily make the difference. It's are they taking enough to meet their needs? So I hope that anyone who is listening to this makes sure that they're getting enough B12. Right. But what is it coming from? If it's not coming from plants. Bacteria make B12. So if cows are eating dirty ground, they get bacteria.

Cows store it in their stomach. Plants, if you don't wash, will give you B12, but it's the bacteria hanging on the carrot. And we make B12 too, but it's in the colon, and we can't absorb it in the small intestine. But yeah, just making sure that if someone is following this diet, they're getting enough B12 and that they're using the right markers to assess their status. Serum B12 only goes out of range in the final stages of B12 deficiency. And by then it can be too late. Some of the effects of B12 deficiency are irreversible. So it's a pretty serious thing and it's a really important thing for any vegetarian or

vegan to be aware of given those big differences in depletion between the populations so joel if you've been a vegan since you've been 18 obviously you must have been on top of all the supplementation and making sure that you get your right nutrients well it's out number one it's responsible for a health care practitioner to advise somebody eating plant-based to take vitamin B12. Absolutely. There are people that do it because it's fortified in many foods and nori if you eat sushi and nutritional yeast. I don't advise my patients to rely on food because there's a neurologic and hematologic potential for trouble if you don't B12. It actually takes years to deplete your B12.

It's an interesting statistic. I want to come back to humans. 90% of all B12 right now is being given to feedlot cows because they don't eat dirt anymore. They're inside a building that has no dirt. They don't get B12, but the public wants B12 rich meat. So they give B12 to cows to make B12. They're little vegans, these cows. They don't have a source anymore. No animal makes B12. Well, you're only talking about factory farm cows. Factory farming. You know, if you're out there eating dirt in the field, you're going to have a cow rich

in B12. Before you go on, can I stop you right here? Yeah. When you say that, so is it impossible to live a healthy plant-based lifestyle without supplementation? No, many, many people do. But if you're saying you don't recommend it. I don't recommend it, but they should get blood work. Know your vitamin D, know your omega-3, and know your B12. I'm all for optimal health, and I'm practicing high-level

medicine, but I have friends that adamantly show me their blood work. I don't take pills and look at my blood work. I mean, they may sneak by. It's not my medical recommendation. The official recommendation is everybody over age 50 in the United States take B12 for brain and mental health, whatever your diet. And that's a wise advice, whether you take a multivitamin every couple of days like Dr. Longo recommends. There's, you know, this is a real problem. Nobody's denying it. Chris has laid it out well. It's such a simple solution.

I'm going to demonstrate my B12. And what's the source of your B12? It's synthesized methylcobalamin. I just got 1,000 micrograms of vitamin B12 with 400 milligrams of DHA with 2,000 international units of vitamin D3. And that's all vegan? I just did that once a day, and I'm done, you know? And it's all vegan? It has nothing to do with living organisms? Yeah, it's made made how's it synthesized uh b12 is synthesized in labs methylcobalamin

some people believe is the preferred uh choice which i think chris would agree with so contrary to popular belief it can be gotten by completely humane and ethical ways if you're a vegan oh it's algae it's algae for dha It's synthesized for B12. And vitamin D3 is synthesized too. It used to be made from cow's secretion called, sheep's secretion called land limb. It's synthesized now. But it does beg the question of whether we should be following a diet

that can't meet our essential nutrient needs and that leads to deficiencies of many other nutrients much more commonly than an omnivorous diet. And, you know, my position has always been we should get as many nutrients as food as we can, because that's the way that humans are adapted to getting nutrients. There's issues with supplementation sometimes, you know, both like getting too much of a nutrient can be a problem in several cases. That's not the case in B12, which is great because it means people could take really

high doses and it won't be a problem. But as I mentioned, a lot of vegetarians and vegans who are supplementing are still at risk and still deficient because serum B12 is the main marker that is used in this country. And not even most physicians don't test for serum B12. I know this. You probably know this, Joel, from people come in. They've never had a B12 test. But then when they do get the serum B12 test, it's going to miss a large percentage of people who are already in stage 2 and 3 deficiency. I do methylmalonic acid.

So methylmalonic acid and homocysteine are much more important markers. I agree. And homocysteine are much more important markers. I agree. If you look at average homocysteine levels in vegans and vegetarians, they're significantly higher than in omnivores because of this issue, because of the high prevalence of B12 deficiency. And what's ironic about that is a lot of people turn to a plant-based – I don't even want to say plant-based, because I would consider a Nutrivor or a Paleo diet to be plant-based too, but turn to a no-animal-product diet to improve their cardiovascular health, and yet you're seeing much higher rates of homocysteine, like the average in vegans, is 16, which is a rate that's clearly associated with increased risk of not only cardiovascular disease,

but also dementia and Alzheimer's. Chris, I couldn't agree more. I've written many articles. Don't be a dumb vegan. And I don't mean to offend, but we are prone. I mean, there's no bullshit here. This is too important for people. We are prone to have a few holes in the wall that an intelligent person knows how to plug.

It's vitamin D. It's DHA. It's B12. You might go on to say iodine, taurine, vanadium, chromium. I just got those. That's what I do every other day. I'm totally complete. My patients are totally complete. The industry has provided solutions to a relatively simple problem. I don't want- Smallest pills. You got a mouthful of marbles. Let me ask you a question. Is it fair to say that you believe that what the vegan diet is,

it's like you can essentially hack your way to a better, healthier life by just adding a few things like B12, a few other nutrients that you're not going to get from the diet, but with those together, you feel like you're far healthier? Well, because what I didn't get, I substituted, but what I don't want, I'm not taking in, which is animal saturated fat, animal protein. I'm not taking in. So that's the main disagreement here between the two of you is whether or not saturated fat is. Chris and I would both agree as educators, all the public and specifically plant eaters should be aware of nutritional efficiencies. A two-year paleo follow-up study said that people were deficient in iodine on the paleo diet. But vegans have much higher rates of iodine deficiency.

Yeah, they do. But, you know, it's common in America. Vegans have much higher rates of iodine deficiency than paleo people? Unless you eat some nori, some kelp, unless you use iodized salt. So it's a poor argument, though, that the paleo diet is the issue. It just seems like a lot of people have an iodine deficiency. Paleo diet goes back 10 to 12 years in the literature. 2009 is about the first good paleo science that showed up.

And I honor the paleo diet. There is good reason to consider it as a food option, although the U.S. News & World Report does not agree with that. But to say that— Well, what are they basing it on? They're not scientists. Well, they're panel of scientists. They're panel of scientists.

Yeah, and for me, the bigger question— They rate it of scientists. Yeah. And for me, the bigger question is just what's going to happen for the average person who's following these diets. And I agree 100% with Joel that we have to educate people on whatever diet they're on. And I've said this to people. That's why I'm not, I've never advocated strict paleo. I mean, I think that can work for some people, but I've never been ideological about that because I actually think that full-fat fermented dairy is really beneficial when it's well-tolerated. And one of the reasons for it is iodine. Dairy is actually one of the best sources of iodine in the diet. And it's not because the dairy products contain iodine, but they're stored in tanks that – iodophore is the cleanser that's used for the tanks, which is basically just pure iodine.

That's interesting. How bizarre. Yeah. That sounds gross. It's not. It's just like, you know, the iodine you use to clean – it's a natural nutrient. Right. Where do you get it from food, though, outside of that?

So the three top sources of iodine would be, well, iodized salt is the main one. That's why it was added to salt in the first place. But a lot of people on a healthy diet remove iodized salt in favor of sea salt, which I think is a good choice overall. But one of the downsides of that is that they're no longer consuming the main source of iodine. Then dairy products and then sea vegetables, as Joel mentioned, kelp and hijiki and arame and nori, not as much, which is the only sea vegetable that most Americans consume in the form of sushi. So if you take someone on a vegan diet or a paleo diet for that matter, and they remove dairy, iodized salt, and they're not eating sea vegetables, then yes,

that is a risk for iodine deficiency. I have written about that. But let's look at things like calcium. Let's look at iron. Let's look at zinc. Let's look at choline. Let's look at taurine. Let's look at creatine. Let's look at retinol, which is preformed vitamin A. Let's look at EPA and DHA. All of these are shown to be lower in vegetarians and vegans than they are in omnivores. And it just, yes, you can supplement, but it just, you know, do the supplements have the same effect? Like look at calcium. Dietary calcium has inversely related to heart disease and kidney stones, meaning the more dietary calcium you eat, the lower risk of those conditions. But when you look at studies on calcium supplements, the opposite is true. Calcium supplements are associated with an increase in heart disease and

an increase in kidney stones. Associated by epidemiology studies? Yes. But the theory is that with supplemental calcium, it's not the same as dietary calcium. You get a large bolus of calcium that goes into your blood all at once, and then it can get into the soft tissues, which, you know, can make them stiffer, which is, Joel will tell you, is not good for your heart health. And so my point is that supplements don't always affect the body in the same way. That's why I just think it's better to get nutrients from food if you can can because that's the way we've been getting them for millions of years. Let's talk about something I think you guys can both agree on because I am baffled by this carnivore diet.

Yes. I'm baffled. I'm baffled by how many people are clinging to it as a panacea. I'm baffled by whether or not it's a physiological effect or whether there's a placebo effect going on. I have a theory. Please. Yeah. So my theory is that it mimics some of the benefits of fasting, but allows people to persist for longer because it's providing some nutrition. You know, most, if you look in the scientific literature, fasting is like the cure-all for everything.

I agree with you. You can look at any condition and fasting is the cure. We're talking water fasting, so you can do it for two, three, four weeks. The problem is, try that for a year. That will be the cure for life in that case. The longest example is a year of

water fasting. That's that guy that lost, it was 300 plus pounds. Yeah, he was extremely obese. He was living off of his fat stores. The fascinating thing about that was that he actually skin shrank too. Right. Which is really. Yeah, which doesn't usually happen with weight loss.

So this is just a theory. I have nothing to, you know, I don't have any evidence. But meat is absorbed very high up in the digestive tract. And so when you only eat meat, it's a low residue diet and there's nothing left over to irritate or inflame the gut. My theory is a lot of people who are benefiting from this have a really disrupted gut microbiome. Alessio Fasano has argued that leaky gut is kind of a precondition for autoimmunity. And this, the carnivore diet is essentially like a gut rest or a fast. And so I don't, you know, doubt that people are

benefiting from it. The question is, what is the long-term implication? But there is no, I mean, there's a few people that have been doing it. There's some anecdotal evidence of people doing it for a few decades. Well, you know, it's pretty cool. I'm actually going on my homeboy, Sean Baker's podcast in a few weeks. You guys are homeboys? Sean and I started as enemies. We love each other. Sean, I love you, brother.

We're going to have an honest discussion as much as you can to say, why is Michaela Peterson feeling good? And you've got to love that and honor that. If she had done water fasting transitioning to an ultra-clean diet, would she have done as well? Who knows? But to look at Sean Baker's labs and say pre-diabetic, low testosterone, high BUN, I'm concerned, although he just published his coronary artery calcium scan at zero,

and I honor that. He's got little kids. I don't want the guy to drop dead. But, you know, it's way preliminary for the bandwagon that's growing. The problem with the testosterone thing, though, is he said that he had been deadlifting the day before, and the day before he took his test, could that have significantly decreased his testosterone? He said he repeated it a few times and it stayed low, but if your serum totaled... It raised quite a bit.

It could have. I think it raised by 100%. It was like 237. I can't memorize his last, but there's plenty of data. If your serum total testosterone is less than 250, it's an 237. I can't memorize his last. It's low, though. There's plenty of data. If your serum total testosterone is less than 250, it's an adverse mortality predictor. And he wants to be alive. He doesn't need to do it. Michaela Peterson and Jordan might need to do it until they find a better path.

But Sean's adopted it. So the biggest puzzle is, quickly, quickly, one of the things that plant-based eaters and people that fill three-quarters of their plate with fruit and vegetables get way more than everybody else is lots of vitamin C. And vitamin C builds healthy walls and builds healthy immune systems. You love vitamin C. I love vitamin C. I love it from foods. I don't mind it as a supplement.

I don't mind it intravenous. Vitamin C is Linus Pauling. There's so many benefits to the body. Where are these people when every chart says that meat has no vitamin C? Are they eating raw meat, which might have vitamin C? Are they eating organ meat, which might have some vitamin C? Let me stop you there because I'll tell you what the explanation has been to me. The explanation to me has been that there is a decrease in absorption of vitamin C

when you're consuming vitamin C with all these other things, cruciferous vegetables, carbohydrates, all these different things. There's some sort of a, there's an adverse effect. Is that a fact? Well, if you take 1,000 milligrams of vitamin C, you'll absorb a lot of it. If you take 10,000 milligrams, by percentage, you won't absorb as much, but you'll still get more than 1,000 milligrams. But there's also this theory that since you're eating basically a no-added glucose diet,

that there's some kind of competition in us between glucose and C. So even if they get a touch of C, they're absorbing it hyper-efficiently. Nobody knows. They haven't developed scurvy. And then they're getting their glucose from glucogenesis. Internally, right, because they're adding, you know, surely it's a low-carb diet. No doubt about it. It's a zero carb diet

A little alpha gal in there maybe That's about the only curve I think I mean the point is We just don't know We don't know And It seems so risky

I mean as a practitioner myself And as someone who's dealt with chronic illness Who wasn't able to find help anywhere else I mean I do not begrudge people for Sticking with something That works When they've tried everything And nothing has worked And they do this And they feel good find help anywhere else. I mean, I do not begrudge people for sticking with something that when they've tried everything and nothing has worked and they do this and they feel good. I mean, who can blame them? It's really- Well, I've gone to dinner with Jordan,

Jordan Peterson, and he's eating his big giant steaks and he looks great. Well, you know- And he's lighter than he's been since he was 25 years old. That's true. And I'm 100% empathetic with that because I've been through something like that myself. But to then take that and say that we're certain that it's safe is a big leap and the other thing is you know my field atherosclerosis takes years to develop and I wish him well he's contributing amazing

things to the world but unless he's tracking carotid and coronary and doing it year after year after year you know it's an experiment you might not want to run but Sean did run those tests baseline some nutrient deficiencies also take many years It's an experiment you might not want to run. But Sean did run those tests. Baseline. Some nutrient deficiencies also take many years to develop.

So that's another thing to consider. There's another guy that I follow online. I'm sorry I forget the gentleman's name, but he advocates organ meat. And he's saying that organ meat, if you're just eating steak, that you've got an issue. But if you take into account liver and heart, kidneys, that you're going to get all these essential nutrients from that. You're still not getting vitamin C that I'm aware of in any significant amount. You're not getting carotenoids and flavonoids. So how are these people not getting polyphenols?

We don't know. We don't know. Yeah. So, yeah, we don't know is a good summation of is it possible that there's some mechanism that's going on? I mean, absolutely. Sean posted a picture picture he was eating steak and cheese, so it's apparently not an all-meat diet, and I'm not slamming him. I really wish him well, and he can do what he wants. I don't know.

He's a very nice guy. Yeah, yeah. I mean, I'm not slamming him either. The nose-to-tail is important, though, because the organ meats and then, like, the fattier cuts of meat have glycine and other nutrients that are really important. If you're only eating lean meat, I think, yeah, I would be very concerned about that. Children, do not try this at home.

Someone tried to get me. They were saying you should try a carnivore diet for 90 days. And I said, well, the real problem with that would be I eat game. And that's extremely low fat. Very lean, yeah. It's not smart. And I like vegetables and I like vegetables I like to eat them

I eat vegetables with essentially every single meal yeah that's very smart it's an antidote if nothing else but I do think that it's entirely possible that maybe it's people that have this disrupted gut microbiome but that some people might be alert like one of the things

that Michaela Peterson brought up when she was on the podcast, that it might very well be that she's allergic to almost everything. She has some sort of an allergic reaction. You, I think you both think that that could be because of a fucked up gut microbiome. No doubt. Absolutely. She just hasn't had it evaluated. She started to laugh when I talked to my naturopath.

That's what she should have kept on doing, gotten her gut analyzed, gotten her gut healed. I mean, maybe that would have helped her, you know, conjecture. The problem with those naturopaths, it's like good psychics. Can I try to find one? I'll tell you an interesting— Well, and it's also—look, not all problems are solvable. Right. That's a really hard thing to accept.

Yeah. But let's say you get in a car accident and your spine is crushed. You know, most, short of a miracle, you know, that's not, that person's not going to fully regain their 100% of their, you know, musculoskeletal capabilities, right? Right. But we don't have that same understanding with other conditions, health conditions. Let's say I go to Indonesia and I get 10 parasites and then I have to take tons of antibiotics to deal with that. Is my gut ever going to return to 100% of the function that it had before that, even with all the right things?

Maybe not. And so I'm not saying that people should give up hope, but I'm saying that we have to separate between this is helping me and it's making me feel great and nothing else worked. And we know with a hundred percent certainty that this is safe for the longterm. Those are two very different questions. And again, I'm totally empathetic to that, you know, and I would probably do the same thing, especially a person like yourself that has gone through this process of being extremely unhealthy. And I might even say, Hey, you know, if I, maybe I'll die five years earlier, but I'll

enjoy the rest, you know, those years of my life, I won't be in pain and discomfort the entire time, then sign me up. Or I might, I might say to myself, well, wait, it can't be that good for me to be inflamed all the time. And like, you know, that can't be good for me. So maybe even though the all-meat diet might have some downsides, it actually might be reducing inflammation and therefore that will cancel out. We just don't know. But what about an all-meat diet? The thing that gets me is there's no vitamin supplementation. I'm like, what about an all-meat diet with a good supplementation of multivitamins pretty smart idea what about fiber where's omega-3 coming from is fiber essential well it's being questioned i mean it is it as central to health in the medical literature dr dennis burkett from england went to africa described fiber described it reduced all

kinds of chronic diseases. He wrote a book called The Fiber Man and all. It's being questioned now. It's so entrenched. Have we got it all wrong? And only plants have fiber. It's a good question. Where are they getting their fiber? Their meat is sticking in their colon. It's called putrefaction for days and days.

Is it? Yeah, well, that is what happens in a high-meat diet. But is it 100% with every single person? When you chew it well and drink water, does it always get stuck? It's generally thought that it's fiber that is the process of moving abdominal contents, whether you eat an all-plant diet or a mixed diet. I think there's definitely controversy about fiber, but I think the weight of the evidence still does suggest that fermentable carbohydrates, fiber, essentially, are beneficial.

Because they're very important for the microbiome. And we have people like Justin Sonnenberg at Stanford who's done a lot of good work here. Do we know with 100% certainty? No. But we also know that virtually every human population that's ever been studied had significant amounts of fiber in their diet. Except the Maasai, right? No, they did.

They had a very high meat diet, but still. The warriors consumed milk and meat and blood at certain times of year when they were and other times of year they did eat more plant foods. And the wise were eating lots of plants. Even the Inuit, the traditional Inuit, you know, they had during certain times of year, like the winter when the ground was covered with snow,

they had a very low intake of plant foods, but they would still trade for them. And then during the summer when they were able to collect berries and things like that, they would definitely do that. So every culture that we know of that's been studied ate some combination of animal and plant foods. You know, what ratio, what amount, you know, that varies from place to place depending on where they are. But that's what the anthropological data show. There's actually, you know, when you talk about this two super, super cool pieces of data, I'll go quick. There's a professor at University of Pittsburgh, Stephen O'Keefe, who took 20 African-Americans in Pittsburgh eating an inner city, not healthy diet, and 20 rural Africans in South Africa eating from the bush and largely plants, and they switched them for 20 days.

And they measured every single thing they can measure in the microbiome, in their stool, metabolites, TMAO, and all the rest. Your body is so amazing that 20 days on a better diet, what I would call the rural African diet, a better diet, you know, there was incredible changes towards health, making butyric acid, having bacteroides and prevotella, I mean, changes. And the rural Africans suffered American illness in terms of what you can measure within two weeks. Now there's data, I just learned yesterday in Los Angeles, that our microbiome changes in five days. You go to a low-sugar, low-protein plant diet, this is University of Southern California, I can tell you in five days, Michaela Peterson's microbiome would change. Would she feel better? I don't know. I'm just pointing out just the

remarkable resiliency, and that's part of the issue. You can feed a human a whole lot of diets and make it through procreation, which is our main purpose of evolutionary biology to be here. We're talking about from procreation to death for optimal health, longevity, health span. There's more than one path, but let's not beat on our plant-based people out there because we've shown you can reverse atherosclerosis. We've shown you can reverse prostate cancer, University of California, UCSF. And we've shown you can lengthen your telomeres, which may have implications for longevity. Isn't that done through ketogenic diet as well? Doesn't that lengthen your telomeres?

I don't think that's been published um it should be an interesting project you know it takes about three to six months so you'd have to nobody no it's not been looked at yeah and there are there has been we could say the same thing about a diet that is rich in uh you know vegetables and fruits and animal foods you know the powder benefits well you can't reverse heart disease with what you just said. Don't touch that. You cannot reverse atherosclerosis with animal products. It's never been studied. The only thing.

So then how can you say you cannot do it? Well. Do we have studies? What would you tell a patient with the 99% blockages that come to me? Go eat meat? That's being ethical in my life. I would say, do we have studies that show that switching from a standard American diet to a Nutrivor diet? Yeah.

This is a new word, Nutrivor. You coined this? Sarah Ballantyne. Okay. And the idea is just plant-based with meat? Yeah. Yeah. Yeah, it's a whole foods diet with fruits, vegetables, nuts and seeds, some starchy plants and animal foods.

What is the mechanism? Why don't you call that paleo? Well, the problem with paleo is paleolithic people didn't really eat like that. They ate a lot of grains. So when you're- Well, I don't think that's true, Joe. Yeah, but anyway. Go ahead.

What do they eat? For me, neutrovor is a more inclusive term that just means what I said. Some neutrovors might include some dairy products. They might include some grains or legumes. But they're eating whole real foods, and they're including animal foods there, to distinguish that from vegan or vegetarian. Isn't the criticism of the Paleolithic diet or calling it the Paleolithic diet that people in the Paleolithic era actually did experience at least some form of agriculture?

There's been recent data that suggests that grain consumption and legume consumption went back further than it was originally thought it was. Now, whether those were prominent parts of the diet or fallback foods is another question. And does that even matter? I mean, this is why I've argued that the evolutionary perspective is important. It's just a way of generating hypotheses, kind of like observational research. You can't look at what our ancestors ate and say, therefore, that's what we should eat. You can look at it and say, oh, that's interesting. Let's test this out.

Joel, how does it reverse heart disease? Okay. Ketogenic diet and telomeres. There's no science studies out there just to follow up. Okay. I didn't know. How does it reverse heart disease? You go back to Los Angeles, California in 1948.

Dr. Lester Morrison, internist, it's real answer, saw that in the country of Norway in World War II, where they dropped their animal food consumption because of the Nazis, heart disease slowed for those two, three years. He said, I wonder what happens to my heart patients in Los Angeles. He had 100 of them. There was no treatment in 1948. He put half of them on a low animal diet with very high plants, let half of them eat like Los Angeles people. Eight years later, 50% on the high plant, low fat diet were alive, 0% on the standard Los Angeles diet. And then a series of people said, let's start doing that more routinely. Ultimately, there

were randomized clinical studies using cath lab techniques, using ultrasound techniques, using PET scanning that shows it actually causes small decreases in the amount of plaque in your heart arteries, which results in tripling of blood flow because it's fluid physiology that is four R squared. So small decreases in plaque. Nobody ever thought you could decrease plaque with diet and lifestyle, but you can. It causes big increase in flow. So within three, four weeks, chest pain goes away. Within three, four months, stress does get better. And as you keep going, a number of hospitalizations, procedures go down dramatically. To the point, initially small studies got big enough. In 2010, Medicare said, we'll pay for patients to learn how to do this reversal lifestyle.

They don't pay for Mediterranean diet. They don't pay for DASH diet. They don't pay for paleo, keto, Nutri-Vore. They pay for plant-based diets for advanced heart patients. That's only because these concepts of nutravor and paleo have not been around for very long. So all you've said, Joel, is- Do the study. Do the study. Okay. Take care of patients. I don't have the millions of dollars to do the study. But don't suggest you can do it. Be rigorous. So all that you have said, which I agree with, is that a vegan or plant-based kind of diet compared to a standard American diet will reverse markers of atherosclerosis.

That's like, wow, number one in the world. I agree with that statement, but we, there's no, we don't have research. It's not like studies have been done taking people from standard American to neutrovor, paleo, and we haven't seen benefits. We have RCTs that have shown significant benefits in cardiovascular markers. Markers. In neutrovor diets and paleo and low carb, for that matter, and ketogenic. I agree. Your assertion is that the real issue is the standard American diet is killing people.

Oh, yes. And lack of that lack of evidence is not evidence against you know it's it's that we don't we don't that how long have how long have these concepts been around neutrovor paleo how many studies have been done looking comparing for example let's do it would be great if we had a study where you had standard american diet and then you had two different groups you You had a control group of standard American diet and then you had vegan diet and then you had Nutrivor or Paleo.

We don't have that study. So we can't say that eating a diet that's rich in whole foods but contains some animal foods isn't going to reverse atherosclerosis. We can't say that. So I think one thing that we can absolutely agree on is that the standard American diet sucks and that a vegan diet is superior to the standard American diet.

Amen, brother. These two things are agreed, right? If the vegan is supplementing wisely. I just tell you, and this is very subtle, but vegan diet says what you can't do. You can't eat dairy. You can't eat eggs. You can't eat fish. You can't eat meat.

Whole food, plant-based is really the proper medical term. What do you eat? Eat whole food. That's what John Joseph talks about, too. He calls it plant-based. I call it with a bib. Whole food plant-based because you don't want to be just eating pasta all day. Oh, absolutely not.

Junk food vegetarian or junk food vegan diet. So the dispute is whether or not animal protein and organ meats will advance your health and make that it's a superior diet when you add that one quarter of your plate. So yeah, one of the ways to answer this is to look at nutrient density. So I have this study on my website. It's Maillot, I think, Maillot, which is terrible, M-A-I-L-L-O-T. And it's Kresser.co slash Rogan. And he looked at nutrient density of foods and he categorized them based on nutrient density. And he was only looking at, he was looking at essential nutrients.

So all the vitamins and minerals that we absolutely need for health. He wasn't looking at polyphenols and flavonoids and things like that, which are beneficial, but we don't absolutely need. So the number one food in terms of nutrient density, do you want to guess? What? Meat. Organ meats. Score of 754. Next highest, shellfish, 643. And I've often said this to my patients, like If you could be a vegetarian and only eat organ meats and shellfish, you'd be doing really well because of just how nutrient-dense they are.

And that's not really a controversial statement. Let me continue here. Fatty fish, 622. Lean fish is 375. And then vegetables are 352. So, you know, vegetables are on there, But organ meat, shellfish, fatty fish, lean fish are all higher than vegetables. And, you know, grains and legumes don't even really make's a real reason why they're experiencing significant health benefits, particularly if they supplement. Yeah.

Yeah, that's right. That's great. It's just a better – They're going from a highly processed and refined – assuming they're eating a whole foods vegan diet, not just subsisting on baguettes and vegan cookies and stuff like that, which unfortunately people do. A lot of people do. Just like people eat the standard American diet. And for that matter, just like people who go paleo and are eating paleo donuts and paleo ice cream, whatever.

You can do it on any dietary approach. Whole foods. And what I was going to say, I never have proposed except for one small subset that everybody needs to eat a completely plant-based diet. But if they do, they're probably going to have good health. There's a concept called the spectrum. Dr. Dean Ornish, some people beat up on, but he's done all these studies on reversal of atherosclerosis, and he's celebrating around the world, has a book called The Spectrum. Go as far towards it as you can.

I'll love you wherever you're at. You choose. We're not judging you. And that's, I think, the message for your listeners. I mean, when you're eating vegetables or fruit, or maybe it's just vegetables every meal, that's the example people need to hear. And they don't need to abandon everything else. Just don't do it with a donut. Don't do it with a bagel.

Don't do it with these calorie-empty foods. And also time-restricted eating. I think we all agree on that. It's awesome. 12 hours, 14 hours a day. I'm a big fan of four or five days a month lowering calories with low protein, low sugar. Now the science is coming out. Unbelievable. It's right here from Los Angeles. Now, look, I mean, so I want to say this. We're talking about helping people. And I was a vegan

at one point and a vegetarian. And I have friends that are vegans and vegetarians. Again, I'm not ideological about this at all. And so I want to like, to someone who is a vegetarian or vegan, and just to show how nutrient-dense organ meats and shellfish are, if you wanted to be a vegan but you're not, you know, ideologically opposed to eating some small amount of animal product or animal food, you could eat one clam, one oyster, and four grams, which is a tiny amount of liver a day. And you would completely meet your needs for B12, zinc, copper, choline, and many other nutrients with no other consumption of animal foods beyond that.

So this is what I said before. Like the spectrum is large. Some people might consume a higher percentage of animal foods. Some people could consume just that much, and they would still improve their health and well-being by doing that from then eating a strictly plant diet. And one thing that I do have to tell you, Joel, unfortunately, is that you keep saying that Nick and Nate Diaz are vegan, and they're not.

I know. They've fallen back. I don't keep saying it, but they've fallen back. Well, you brought it up a bunch of times. Well, he was when he won the fight. He was. I don't think he was. He was eating fish. He was eating fish and eggs.

It's cool. I worry about his TMO level, but it's cool. No, I'm serious. But, you know, the explosion, the Tennessee Titans and Kyrie Irving and Serena Williams. Serena Williams is a vegan as well? Yeah. She reversed an autoimmune disease called Sjogren's. So is it necessary to be plant-based to be a world-class athlete?

Obviously not. Is it compatible? Do you know who Patrick Boubamian is? He holds the world record for powerlifting. He's been plant-based his whole life. Big, stocky. Look at the guy up. Patrick, P-A-T-R-I-K.

I mean, he's this big, stocky German, but he lifts 1,200 pounds, and he has the world record. He hasn't eaten a piece of meat. Nick Delgado. Nime Delgado. Nick Delgado. Point is, it's an option to be a super athlete without animal products. We're seeing it more and more.

Recovery, which roll on your class. But, you know, it happens. Just stop beating on us because we're doing pretty well. But, yeah, if Diaz has gone back to eating fish and vegetables, it's a whole lot better than the crap American diet that a lot of athletes say. They just cut out all the land animals. Yeah. You initially start doing it to make weight.

Okay. I got it. Got it, got it. A lot of people are talking about quicker recovery. There is some. I mean, there's something like Alex of people are talking about quicker recovery. There is some. I mean, there's something like Alex Caceres. He's a world-class fighter. He's completely vegan.

Sean O'Malley was for a while, but he found himself to have much more energy when he started eating meat, but he might have been doing it wrong or not supplementing correctly. Microbiome and supplementation. Yeah, believe it. But it's really cool. I forget the name right now. The chef that cooked for 15 Tennessee Titans. And they're just kicking ass.

And Griff Whalen used to be with the Miami Dolphins. I forget where he is now. Oakland Raiders. A great, great tight end and such. I mean, it's possible that we can say Scott Jurek set the world record for the Appalachian Trail faster than any other person eating beans. I mean, insane level of athletic fitness. The Appalachian Trail? Yeah, it's like 2,400 miles fastest human to ever accomplish it on beans.

I mean, pretty cool. I mean, this was such an amazing thing to watch a documentary. Yeah. Should we wrap this up? Yeah, I think so. I think we obviously, we've left a lot on the table. There's still a lot that's disputed. But I think one thing that we came to a really solid conclusion on is a standard American diet sucks.

And any deviation from it that's a whole food-based diet, especially with proper nutrients that are supplemented, if you're vegan or what have you, is going to be better than a standard American diet. if you're vegan or what have you is going to be better than standard American diet. The dispute is whether or not the nutrient-dense organ meats, shellfish, meat, fish, that these things would benefit you significantly.

And I think that's... Hallelujah. We got through it very peacefully. Just eat real food. Just eat real food. I actually refer people in San Francisco to Chris. I honor what he's doing. I mean, we may have this dispute about saturated fat and cholesterol, and it's

not unimportant, but he's a prime practitioner. He's treating people at the right level. I believe I'm doing that in Detroit and the people that come to see me. You know, we're the solution. We're not the problem, despite the differences. And you're a good man to bring us on and point all that out. Well, you both handled yourself admirably. I mean, this is a very very emotional tightly contested sort of a dispute and i i i

thank you both very much for being here well thanks for the opportunity joe i mean this have the chance to do this for what almost four hours now that's amazing and it serves people because on most tv segments it's like five minutes and you just get the headlines and there's no depth. Or you get these clickbait articles and it's confusing. So thanks for giving us the chance to really dive deeply on it. And anybody that wants more, download Chris's references, go to my website, the Rogan references. You know, read more. Study this.

Educate yourself. One more time. Yeah, drjoelkahn.com. Big red button, Rogan References. You can keep yourself busy. And your Twitter, which is on my page, but you can link it anywhere. At drjkahn, Dr. J. Kahn. And Chris? ChrisKresser.com slash Rogan for all the resources here.

K-R-E-S-S-E-R. K-R-E-S-S-E-R slash Rogan. And then Chris Kresser, Twitter. All right. Beautiful. Thank you, guys. Thank you. It was Chris Kresser, Twitter. All right. Beautiful. Thank you, guys. Thank you. It was really a lot of fun.

Thank you. Thank you. Yay! That was a good one.