I was trained as a physician. I'm a medical doctor. I eat more than one pound of meat per day. Wait a minute, why are we eating plants in the first place? My most recent LDL was very high, it was 533 milligrams per deciliter. What's normal? Less than 100. Any mainstream doctors who are hearing this are just wanting to throw daggers at me right now. So, several people asked me to comment on this podcast. Yet another Joe Rogan episode that touches on nutrition. Let's take a look. That's an accurate way of describing it, most plants are not edible but almost every animal is edible. Interesting. Yeah, I think about 80,000 plant species are edible, many others are not. What we want to know is health effects. The 80,000 plants that are edible could be the worst foods in the world or they could be the

most health-promoting foods. Same for the animals that are edible. We find out by looking at data on people eating different things, which I'm sure they're going to get into pretty soon. Plants make chemicals broadly called phytoalexins that are meant to dissuade animals, insects, fungi from overconsuming them, and so my fear is that these plant chemicals are not good for us. Okay, so plants make chemicals to protect themselves, so maybe that makes them unhealthy for us to eat. Interesting hypothesis. So, are these phytoalexins harmful? From this paper, not only do phytoalexins have important roles in plant protection against microbes, many of them have potent medicinal activities such as anti-cancer and neuroprotective properties. They continue some alexins are toxic to cancer cells yet promote the survival of neurons. They inhibit breast tumor progression, they inhibit the survival and proliferation

of triple-negative breast cancer. The most famous alexin is resveratrol, which has anti-cancer, anti-inflammatory, and cardio-protective activities. It also protects hippocampal neurons against cerebral ischemia. The authors conclude: the impressive effects of alexins on human health highlight why scientists have suggested mining plants for these valuable molecules. I'm not saying we should eat plants to get more alexins in our system; it's not about that, but if you want to argue against eating plants, this is not the argument you want to use. If anything, it points in the opposite direction. And this paper we just looked at was published this year. You know what's funny? I usually see people using this logic when they're arguing against animal products, like avoid eggs because of TMAO. But that argument is pretty weak now because the most recent evidence indicates TMAO may just be a marker, not actually cause disease per se, so because of those data, I

stopped talking about TMAO as a reason to make a dietary choice in my videos like over a year ago, but I still hear people argue this, eggs are bad because of TMAO, so he just flipped it around. If you're going to say eggs are bad because of this molecule without causal evidence, then I'm going to say plants are bad because of this molecule, alexins. There's a little bit of poetic justice, and I think it's kind of funny. Bottom line is if we're going to argue a food is bad because it contains a certain molecule, we have to actually show that it causes disease in living, breathing humans actually eating that food. Outcome data. Otherwise, it's speculation, and we have to remove all plant foods from our diet because of alexins and lectins and whatever else, and then we have to remove all animal foods because of heme iron and TMAO, and we starve to death. So recognize this

pattern because you're going to see it everywhere. Avoid this food because it contains molecule xyz. The question is always the same: do we have evidence that that thing actually causes disease? In the natural context, not purified a thousand times or in mice or whatever. So yes, it's a very weak argument here, but not fundamentally weaker than when the same logic is used for a thousand other things out there. This is going to sound extreme when I say it, but I'll back it up: there are no nutrients in plants that you cannot get from animal foods in essentially equivalent or more bioequivalent forms. He probably means essential nutrients. I mean, there's thousands of nutrients you can only find in plants; they're called phytonutrients, literally nutrients from plants. But he knows that; he probably meant essential nutrients. The problem is that whether a diet contains all the essential nutrients for me to survive tells us very little about health.

value. I can get all the essential nutrients from a combination of junk food and pills. Doesn't mean it's a healthy diet. So, this is a little reductionist, it's kind of like the bad molecule logic we just saw. It's trying to boil down a food to a few of its components divorced from actual observable health effects, medium and long term, which at the end of the day is what we all care about. We can eliminate all plants from our diet and survive, sounds like he's doing it. We can eliminate all animals from our diet and survive, tons of people do it. The question is health consequences, medium and long-term disease risk. We get that information by studying people on different diets as rigorously as we can. Data. Which I'm hoping they'll get to pretty soon. Epidemiology can generate correlations but we cannot draw a causative inference from

that data, we can have a correlation which we then test with an interventional study. So, this is important, we went over this in a recent video. You can basically split nutrition data into three bags. Bag one is lab data, so data in mice or in a test tube or in a petri dish. Bag two is population studies. So, take a population, look at what they eat, record their health outcomes, and look for statistical correlations. That's what he's talking about, epidemiology, observational studies, they're all names for bag two. And bag three is clinical trials. Take volunteers, split them randomly, assign different diets, and watch what happens to their health. That's the interventional studies he mentioned, they're also called RCTs, randomized controlled trials, all names for bag three. So, there's a certain hierarchy of evidence. Human data weighs more than lab data, and generally speaking, clinical

trials weigh more than correlations. RCTs are not perfect, and epidemiology is informative, but everything else being equal, bag three trumps back two if they ask the same question. So that is the relationship he's alluding to; it's well accepted, I agree with the gist of that. It just makes sense that your body would fare best on the things that it evolved with. I agree with you; I don't. I mean, it's a very compelling idea; it just feels like it should be right. Eat what you evolved on. The problem is lots of things feel right and seem to make sense and then don't pan out when they're tested. It's routine in science. Our ancestors ate very different diets depending on where they lived; some ate a lot of animals, some ate a lot of plants. Early humans ate grass seeds a hundred thousand years ago. Sorghum. That's a grain. Oats, thirty thousand years ago. And get this,

they were using it to make flour in the Paleolithic. So, the actual paleo diet included processed foods. One of the scientists explains: the idea that prehistoric people didn't eat grain is just wrong. It's misinformed. So, does that prove whole grains are healthy because our ancestors ate them? Is it an argument for eating more flour? No, it tells us nothing about long-term health value. Cavemen ate what they found. Here's another quote from that same scientist: people ate what they could get their hands on. Of course, we ate starchy vegetables 170,000 years ago. Basically yams. Our ancestors may have eaten nuts, fruits, seeds, vegetables, and other plants. The findings reflect a varied plant diet and staple plant foods. And from that oats study, the study clearly indicates that the exploitation of plant resources was very important for hunter-gatherer populations. Does

that prove plants are good for us? Again, it says nothing about long-term health value. You see the problem with this logic, just eat like cavemen? It can be used to support any diet we want, including some processed foods. Everybody uses this ancestor diet argument to defend the diet they like. On the game changers, they used this exact logic to defend a plant-based diet, and I criticized it back then because it was a weak argument. Then the movie gets into this question of what our ancestors ate. In my opinion, it's largely a distraction. Our ancestors ate what they had available. What I want to know is health effects of different diets after 60, 70, 80 years. Think about it. We just talked about how epidemiology is just observational, just correlations, needs to be confirmed with a clinical trial. So correlations from a modern population done five years ago, that's not reliable.

but correlations from a hundred thousand-year-old fossils, that nails it. The other caveat of epidemiology is the uncertainty of having to rely on people's recollection of what they ate. It's far from perfect, but fossils aren't any less uncertain, as these archaeologists explain. Our knowledge of the diet of early hominins derives mainly from animal skeletal remains, leading to a bias toward a protein-based diet. Sure, bones preserve much better than leaves or fruit. Even if we knew exactly what cavemen ate, it wouldn't help us. We're trying to dodge heart disease and Alzheimer's and live to 90. Most cavemen didn't make it that long. And these are post-reproductive diseases, so all the selection pressure from natural selection happens before that. The best tools we have are direct comparisons of diets in living people in modern studies. It's the most rigorous, it's the most well-controlled, and it asks the right questions. He basically took

every bad argument from the game changers and just turned it around. In his defense, he's not using a ton of anecdotes, and that was probably the weakest part of game changers. I get hundreds of emails from people who are like, I took your organ pills and I feel better. I'm like... oh here we go! Here we go with the anecdotes! I can't believe it! I love this guy. He just stole the game changers script. Oh guys, I called this a year ago. Their weaker point is the implication that these athletes are not just great but that they are better because of the diet. These are anecdotes and we shouldn't base life and death decisions on arguments like that. The problem with leaning on these too much is that you open the door to all kinds of nonsense because then anything goes as long as you find somebody who felt better doing x. You can always find another subjective report from somebody else who

felt better after eating a ton of meat. Anecdotes are not evidence of the superiority of a diet because we can find anecdotes to support anything: eating only vegetables, eating no vegetables, eating no fruit, eating only fruit. It's not informative. The best demonstration we could have asked for right there. Anecdotes are weak whether they're used to argue for vegan, keto, or eating meat all day long. I am not saying we ignore what happens to our body or how we feel; let's not strawman it. My experience is important to me. It's not a scientific argument. And even for me, it's limited. We have to be careful with this. You're gonna die; you're eating like that; you're gonna die. Why do I feel so good? Something makes me feel good, great. That doesn't necessarily mean it's healthy long term. We can't feel plaque growing in our arteries. We can't feel tumors growing until

it's too late. My personal experience informs me and in light of the science, not instead of it. I completely understand the impulse to reject expert advice if you tried it and it didn't work for you. I've been through that experience in my own family and I've talked about it before. No one's saying you should just do whatever works for most people even if it hurts you and just suck it up. No one's saying that. If what makes you feel good doesn't align with expert advice, maybe it's the only option you have, and if that's the case I don't blame you for doing it, in your shoes I probably would do the same. But maybe there's a way to get the benefits without the risks whether it's weight loss or food intolerances or whatever you're struggling with. Maybe we can get the best of both worlds by both listening to our body in light of what science has figured

out without getting into this rabbit hole of all experts being corrupt and all the science being wrong. When you're only eating meat, you don't eat as much. You're reducing calories just because you're just not as hungry. Yeah, and that probably underlies many of the benefits people report on many of these diets. The weight loss when you cut out 60 or 70 percent of your normal foods. We see this on keto, on whole food plant-based, etc. There are many ways to lose weight, not all are healthy. Losing weight is a good thing, but what's the cost? So, they've done studies with vegetarians and vegans and omnivores looking at the way the brain responds. So, that means that in the deeper brain, they still crave meat. So? People crave junk food, does that mean it's healthy? Whether people are viscerally attracted to a food is not exactly a reflection of its health value, it's almost

the opposite. okay, we're a year in, sorry, an hour in, freudian slip... I'm waiting for them to get to the point, to some actual solid data. This is like a master class in beating around the bush. By the way, this is three hours long. I'll address some of the key points, but if you want a detailed point-by-point fact-check, two scientists, Layne Norton and Kevin Bass, wrote one, long form, so I'll link it below, check it out. Because those are all things that get vilified, right? And I don't believe saturated fat is a villain at all. It's not a villain. Everything has saturated fat. Lettuce has some saturated fat. The problem is too much of certain types of saturated fat. Let's look at the best evidence, randomized clinical trials. Bag three. One way to get a global view

of back three is what's called a meta-analysis of randomized controlled trials, basically combining a number of RCTs together and seeing where the arrows generally point. It gives us more confidence, and it carries a lot of weight. Here's one from 2010. They conclude, Consuming polyunsaturated fatty acids in place of saturated fat reduces coronary heart disease in randomized controlled trials. So, eating unsaturated fats, predominantly found in plants, instead of saturated fat, lowers cardiovascular risk. Here's another meta-analysis of clinical trials from 2017: Randomized controlled trials that lowered saturated fat and replaced it with polyunsaturated vegetable oil reduced cardiovascular disease by 30 percent, similar to the reduction achieved by statin treatment. Taking into consideration the totality of the scientific evidence, satisfying rigorous criteria for causality, we conclude strongly that lowering saturated fat and replacing it with

unsaturated fat, especially polyunsaturated fat, will lower the incidence of cardiovascular disease. Here's another meta-analysis. Came out this year, 2020. Looked at 15 clinical trials put together. There was a 21% reduction in cardiovascular events in people who had reduced saturated fat compared with those on higher saturated fat. The greater the decrease in saturated fat, the greater the protection from cardiovascular events. They also explain: people who are currently healthy appear to benefit as much from the reduction in saturated fat as those at increased risk. So direct tests, randomized controlled trials, not correlations. Dozens put together. This is the highest standard of evidence, and the answer is consistent: you want to go easy on saturated fat to keep your cardiovascular risk low. So do we want to eat zero saturated fat? No, I don't think that's possible. It's definitely not necessary. So how much is too much? The studies also

address this question. The 2020 analysis we just looked at teased out how much saturated fat we can eat before the risk shoots up. They write: The data suggests reductions in cardiovascular outcomes in studies where saturated fat was greater than 10% of calories in the control group and less than 10 in the intervention group. So, when you start with more than 10 in the controls and you lower it to less than 10, the risk comes down. Ballpark. There's individual variation. But it's around 10. Which is exactly what the guidelines say. The USDA dietary guidelines recommend limiting saturated fat to less than 10% of total calories. So that leaves room for some saturated fat richer foods in your diet if you want. What if you don't want to bother with the math and the numbers? Well, your lipids give you a good idea of where you are. If your cholesterol levels are really good, chances are you don't

have to worry as much if your cholesterol is getting high. Chances are you can tweak the saturated fat and see some improvement. LDL is removed from circulation by docking to a receptor, a sort of docking station. Eating too much saturated fat gets rid of the docking stations so LDL can't be removed and concentrates in our blood. Last thing before we move on, there's some nuance here, just like with everything else. Saturated fats are not all created equal. Dark chocolate, for example, is high in a type of saturated fatty acid called stearic acid, which is an exception because it doesn't raise cholesterol levels. So there you go, sometimes science delivers good news. To say that it's saturated fat driving this doesn't make a whole lot of sense; the correlation is with vegetable oil. Right, we touched on this already, so we're not going to dwell too long, just want to point out he's basing the claim on correlations, which is exactly what he told us.

not to do if we don't want to get confused. The way that epidemiology is so misleading for us. I think he said, I don't want to misquote him, I think he said he got this from a blog? So my friend Jeff Knobs let me borrow these graphics from his blog. We already saw that when you look at randomized trials, so actual direct tests, not correlations, replacing saturated fat with polyunsaturated vegetable oils reduces cardiovascular disease by 30 percent. I'm not saying we have to eat oils, it's not an issue, we don't need them in our diet, if you don't want to have oils, don't eat them, plenty of sources of unsaturated fat. Nuts and seeds and olives and a bunch of things. We're just pointing out the confused logic of suggesting vegetable oils are the problem based on correlations when the strongest evidence by his own standards point exactly in the opposite

direction. So, this is another pattern we see all the time when you find conflicting messages. It's usually not the case that one side is just lying or just a pharma shill or something. It's all down to the sources people rely on. What is driving this? What is driving this? Because we were eating more saturated fat in 1900, we were eating way more saturated fat in 1800 or 1840. Let's think about this logic that people are eating less saturated fat but heart disease is still high, so saturated fat can't cause heart disease. Something being a risk factor doesn't mean it's the only cause. I can cut back on saturated fat, and my disease risk can stay high, for example, if I eat something else that's unhealthy instead. This is fairly well understood; it's been teased out by a lot of research. Here's the 2017 meta-analysis we saw earlier, replacing

saturated fat with whole carbs or unsaturated fats lowers risk. To the left of the line is lower risk, but replacing saturated fat with refined carbs, processed foods, does nothing. They're just as bad. They're both risk factors. And replacing saturated fat with trans fats may be even worse. So that makes perfect sense. You can have a population or a country eating less saturated fat and not getting any healthier depending on what else they do or what else they eat instead. This is exactly why clinical trials are important because you change one variable with country data a thousand things change so it's hard to know which is the cause. So it's always the same story, correlations are important, we don't dismiss them but if we get lost in them and forget to check more reliable data we get confused. Hormones are made from a cholesterol backbone and if you did not have cholesterol you would be very sick and die. There's a genetic condition

called Smith-Lemli-Opitz syndrome. A lot of these kids die in utero because they don't make cholesterol. Yeah, our body produces cholesterol precisely because it's an important molecule. We don't need to eat it precisely because our body makes all we need if we don't have one of those rare genetic diseases. Eating some cholesterol is not necessarily a problem either, depends how much and depends on your individual condition. And if we just think about it evolutionarily, why would nature, why would evolution have designed a particle that kills us within our body? Because it doesn't kill us unless it's too high, just like every other parameter in our blood. Nature and evolution also put glucose in our blood, does that mean it's okay to have sky-high glycemia? Sodium, potassium, every metabolite in our body can become a problem if they're too high. LDL and cholesterol are the same. The confusion here is that he's thinking in these simple terms of

good and bad. So, if nature put the molecule in us, it must be a good thing. But if it kills us, it must be a bad thing, and the two don't combine. Of course, the answer is that LDL isn't bad. I've said this before; I disagree with that label. We all have LDL in our blood; we all want to have it. It's having it too high that's the problem. By the way, the point here is not to bash him or to make him look bad or anything like that. I don't have anything personal against him. I don't know anything about him. Seems like a really nice guy, to be honest with you, and seems like an intelligent person overall. He just heard some stuff online, didn't really think them through. We've all done that; I know I have. It's not about him; it's not about me. Next week, it's going to be somebody else online saying

things that are going to confuse you. The only thing that matters here is learning to distinguish confusion and noise from life-saving information. The rest is a waste of time. At a very high level, they would say LDL is bad; you want less LDL. What's the root of this hypothesis? It's a lot of epidemiology, Mendelian randomization, and genome-wide association studies—interesting. So now you understand that; now it's not a bunch of gibberish anymore, right? So what did he say? He said the data behind LDL and cholesterol and heart disease is a bunch of epidemiology, so correlations, and some genetic studies. Both of those things he named are types of genetic studies; we'll talk about that some other time. What did he leave out? Bag three. So the message is that we don't have clinical trials looking at cholesterol and heart disease.

so we can't really be sure. Is that true? This randomized clinical trial done in Northern Europe lowered LDL-cholesterol in over 4,000 people, and cardiovascular risk dropped by 34 percent. This randomized clinical trial done in the UK lowered LDL-cholesterol in 20,000 people. Coronary death fell by 18%, major coronary events by 27%. This randomized clinical trial conducted in the US lowered LDL-cholesterol in over 4,000 people. Major coronary events fell by 24%, strokes by 31%. This randomized clinical trial done in Scotland lowered LDL-cholesterol in 6,000 people. It cut cardiovascular risk by 31% and cardiovascular death by 32%. This randomized clinical trial done in Australia lowered LDL-cholesterol in over 9,000 people. It cut coronary death by 24% and heart attacks by 29%. When you use a drug, it can have multiple effects.

so it's good to see different drugs so you can rule out off-target effects. So in this randomized clinical trial, they used a different class of drug to lower LDL-cholesterol in 27,000 people. It reduced cardiovascular risk by 15 to 20 percent. Here they used a third different class of drug to lower LDL-cholesterol. Cardiovascular risk was reduced by 34%. We could keep going, we've barely scraped the surface, but I'm sure you've got things to do. These are published in the top medical journals in the world. Randomized clinical trials, placebo-controlled, thousands of subjects per study. This is the highest standard of evidence, and they started being published 30 years ago and all the way up to very recently. You can lower LDL-cholesterol with diet. We've looked at the saturated fat trials. The mechanism is similar. The drugs increase the LDL receptor, the docking

station we talked about, so LDL is pulled out of circulation. Going easy on saturated fat does the same thing. It bumps up the docking station. Here's the European Atherosclerosis Society: Perhaps the most compelling clinical evidence for causality is provided by randomized clinical trials evaluating the effect of therapies that reduce LDL-cholesterol on the risk of cardiovascular events. These trials are one of the main pillars of the evidence, possibly the number one pillar of evidence. We can't talk about cholesterol and heart disease and not bring these up; it makes it sound like we just fell out of the DeLorean. Here they plotted everything. Each little square is a randomized clinical trial. So you're looking at bag three, my friends. The higher the LDL-cholesterol, the higher the cardiovascular risk. It's what's called a dose-dependent effect. Here it is together with the other types of studies. Red is clinical trials, bag three. Gray is epidemiology, bag two.

blue are the genetic studies he mentioned. Each dot is a study. So if your LDL-cholesterol is lowered in a clinical trial, your risk goes down. If you have it genetically low, your risk is also lower. Now some of you may be paying extra attention and asking: How come the lines don't all perfectly overlap? Great question. The effect of genetically determined LDL-cholesterol is stronger. The line goes up faster. That's because in the clinical trials, LDL-cholesterol is lowered for a few years. By design. That's the duration of the trials. But if you have the genetics, it's low your whole life, from birth. So this doesn't mean that if you don't have the best genetics, you're doomed. What it means is that the earlier in life you get this handled, the better off you are. This is widely accepted now. So we're going to move on here because I think the point is clear but you

can lower LDL-cholesterol with statins, with drugs that are not statins, with diet, with genes. all consistent, all lower risk. here's the conclusion of this massive analysis: consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes atherosclerotic cardiovascular disease. this is one of the most well-established facts in biomedical science, both because of the scale and the rigor and the consistency of all these different experimental approaches all pointing in the same general direction. to say that this idea is based on weak evidence, that it's all correlations, that there's no clinical trials, no causal data, is not serious. but i'll tell you, i was a vegan. i was a raw vegan. your lab results are very high what about arterial plaque? zero. whoa... wait a minute, why are we eating plants in the first place?

Scientist reacts to Carnivore Doctor on Joe Rogan

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