Ep33 Paul Saladino MD is a Carnivore Doctor What Does His Research Reveal?

The well-researched and articulate Paul Saladino MD – what a great discussion – see index below! 

 Paul is on Twitter as @MdSaladino and his Podcast is “Fundamental Health”  

For full TRANSCRIPT, scroll down below index

00:00:51 Plant-Based good, Carnivore bad – it seems to most doctors

00:04:41 The baddest foods on the planet

00:08:04 Paleoanthropology – and how our bodies function best

00:12:48 The Vitamin C Conundrum – explained

00:18:00 Niacin and B Vitamins – what’s the real deal?

00:20:24 What about the QUALITY of the meat you eat?

00:25:01 Global Warming – where is meat seated in the controversy?

00:29:54 The wisdom of our ancestors

00:32:34 Cholesterol and particle numbers – LDLp and ApoB – is the risk rational?

00:41:17 CAC and really getting to the bottom of things

00:45:59 Thomas Dayspring & the credibility of ApoBB Bullets shooting up your arteries

00:52:40 CAC and the “focal nature of atherosclerosis”

00:54:42 Watch dietary changes on blood markers – but don’t discount carnivore benefits

00:56:49 Mikhaila Peterson, and the power of elimination in these diets

01:00:02 Plants can’t run away – but they do have Lectin Defences

01:03:42 Beans, brains and autoimmune neurological disorders

01:08:05 Rhonda Patrick and the benefits of sulforaphane – or not??

01:11:20 Tucker Goodrich, 4-HNE, seed oils – and the value of plants?

01:14:37 The fiber thing, the Plant Paradox and Dr. Steven Gundry.

01:17:45 Methionine and Glycine balance – and aging mice – what gives?

01:21:15 ApoE4, cheese and tallow – a complex equation

01:25:22 Lipopolysaccharides, plants and autoimmune maladies

01:29:00 A challenge – show me a disease that is not autoimmune that is chronic

01:29:45 The least toxic plant foods – listed in fairness

TRANSCRIPT:

Ivor Cummins 00:00:51 Today, I have the pleasure of meeting with Dr. Paul Saladino, who is not your average ho-hum doctor at all, he has quite unusual dietary habits and some strong views on cholesterol and other things that not every orthodox doctor would share. So great to meet you, Paul, finally.

Paul Saladino 00:01:10 You too, Ivor. I’m a big fan, and I’m so excited about this conversation, about all things, carnivore diet, which many people may or may not be familiar with. But there’s so many interesting nuances here with regard to lipids and autoimmune disease. It’s going to be a great conversation.

Ivor 00:01:27 Yeah. I always love discussing these things, even though they are kind of fringe at the moment. And it might not be for everyone. And some people perceive carnivore as extreme, which is fair enough. But you could also say that vegan on the other end is extreme. So I think it’s all about personal choice.

Paul 00:01:44 You know, if you go to your family physician, whether it’s in Ireland or in the United States, and you say to them, “I’m going to eat a plant based diet,” they’re going to say, “Wow!” They’re going to pat you on the back. If you go to your family physician, “I’m going to eat all vegetables, and no meat, no animal products,” they will pat you on the back right now and send you out the door with just a smile on their face, imagining that you are going to have fantastic health and live to be 120 years old.

00:02:12 If you go into your family doctor and say, “I’m eating a carnivore diet, and I’m not going to eat any plants, I’m just going to eat animals nose to tail, like our ancestors did,” and we can dig into that, they will absolutely lose their shit. They will freak out. They may fall over. They may grab you by the shoulders and shake you and say, “What are you doing? You’re crazy.” I’ve been super fascinated by the evolutionary origins of where humans have come from and kind of this concordance between our book of life, our genetics and the way we’re eating. And I’ve come to believe very strongly over the last year that humans evolved as animal eaters, primarily. I had a really interesting conversation with Miki Ben-Dor who’s a paleoanthropologist, on my YouTube channel. And you can look at these recent studies that have come out looking at nitrogen levels and the Neanderthals and early Homo sapiens from 70,000 – 80,000 years ago, and they pretty clearly suggest that the nitrogen levels were so high in our college and that we were eating, we were high level trophic carnivores.

00:03:15 So the concept of humans as carnivores, or primarily hunters, is only strange to us in the last 70 years as he westernized humans on this planet. I think evolutionarily, there’s an argument and then if we actually look at the biology and why we maybe don’t want to eat all plants, or some people might want to eliminate plants completely, it makes a lot of sense. But it is, it is a pretty radical concept. And I’ll admit that even I, when I first heard about it thought, “That’s crazy.” But as I really dug more into it, I realized that there was a lot of conditioning there and there’s a lot of stuff that doesn’t really hold up to scientific rigor when you look into it for reasons for eating plants, or reasons not to eat animals. So it’s a really fascinating conversation.

Ivor 00:03:55 Yeah, I must say, I’m very drawn to it, even though I’m careful to always stress. I mean, I, I work on behalf of a charity to identify people with heart disease before they have a heart attack. And I think our main message really is no processed food, no sugars, no seed oils, you know, eat a safe diet, especially people with heart disease. But this whole thing about more extreme diets, if you will, is fascinating, interesting. And then it’s an emerging discussion that should be discussed openly regardless. Just for the record, I mean, you’re a full medical doctor with approximately how many years experience patient clinical?
Paul 00:04:35 I mean, at this point over 12. 12 to 13 years. Yeah.
Ivor 00:04:41 And you also, it’s quite clear from a couple of podcasts I saw you on, you do extensive research outside of your standard clinical practice, in lipids, and obviously everything to do with diet and nutrition. In fact, I saw one discussion you had with “Bio Layne” – who doesn’t particularly like me, but that’s okay, I like him 😊 And I must say, you lorded over that conversation with actual data studies, like machine gun one after the other. And we’d probably touch on some of those today.
Paul 00:05:14 I’d love to, I’d love to. Yeah, I think that… I have a healthy obsession with understanding the roots of chronic disease. I’ve always been fascinated by the connections between our diet and chronic disease. And throughout my medical career, I’ve had this kind of suspicion almost from the beginning, not quite from the beginning, but once I got into medicine, and started seeing how it worked in actual patient care, I really had this growing strong suspicion that food is connected with chronic disease, and perhaps one of the most strongly connected things, probably the most strongly connected factor. And so there gets to be this sort of fascinating conundrum, this fascinating puzzle. What are humans supposed to eat to obtain optimal health? Is it different for every human? Where is our user manual? You know? When you guys buy a car, I buy a car in the United States, it comes with a user manual, so that when the strange light goes off on the dashboard, you’re like, “What the heck is that I don’t know what that means.” You look at the user manual. Or you get a flat tire, you look at the user manual. But I really would characterize a lot of this sort of quest of mine. It’s like, I am on the quest for the human user manual. And it may be different for you than it is for me. But I would argue that there’s increasing evidence, and perhaps there’s a fundamental diet that most people can eat. And then we can build on that. And some people might tolerate more things than others. But I think that this quest for the human user manual is so fascinating, because it translates into quality of life for all of us. You know, chronic disease affects many people and I, and I’m sure you, I want to live the fullest life I can, I want to have the highest quality of life at all times. And so I want to know how my how my vehicle, my metaphorical vehicle works. And I want to drive a Porsche. I don’t want to drive a Honda Civic, if I can drive a Porsche. I want this vehicle to work as well as possible so I want the user manual. I want to know what type of gas to put in this car. I want to know how to fix the flat tire when it happens.
00:07:08 We don’t know what that is. And that’s why I love these conversations. But I really appreciate what you’re saying there and I couldn’t agree more. I think that you can create a tiered system or a hierarchy of how people can think about improving their diet. And I think that the first step, I couldn’t agree with you more is elimination of processed food, elimination of sugars, elimination of oxidized seed oils, perhaps all processed sugars. I think that if more people did that, we would see incredible benefits, and then, you know, you can move up the chain. And I’m sort of, perhaps at one extreme, and where I see a lot of patients with really recalcitrant autoimmune disease. And for those people, I sort of think, well, as we’ll talk about later in more detail, “Maybe the elimination of all the plants can improve that. Maybe plants are causing autoimmune disease for some people.” But for the majority of people, I think an amazing first step is just elimination of processed foods, elimination of seed oils, and eliminate processed sugars. That’s going to help everyone. I can’t disagree with that.
Ivor 00:08:04 Yeah, that’s in alignment as well with between all the different, even extremely different camps. So we kind of know, last hundred years, chronic disease came off life and we have massively increasing rates over the century. And we know the things that are new – processed food, seed oils, refined sugars, and refined carbohydrates, but the other things we talk about are not new. And 100, 150 years ago, people had all kinds of diets with real foods without chronic disease. So the big commonality. But we’ll get into, yeah, the carnivore thing. One challenge with carnivore is vitamins, minerals, things like these that you might be missing. So, most people would I agree and all the Paleo anthropologists. I always send on Dr. Michael Eades three blog posts, “Are we meat eaters or vegetarian, part one, two, and three.” And every time anyone asked me about this, whether we evolved in that way or not, I send on those three blog posts. And he has the nitrogen, the carbon and all the evidence. So I agree with you. But that’s where we came from. But nowadays, if you go on nearly exclusively meat, what kinds of things might you be missing, or what are the arguments made as to what you’re missing?
Paul 00:09:23 Well, one of the things that I’ll say is that the carnivore diet is kind of like a keto diet in a sense that… you know, I’m using air quotes here. When people say “keto” you don’t really know what they mean. When people say “Mediterranean,” you don’t really know what they mean. When people say “vegan,” you don’t know what you mean. And when people say, “carnivore,” you have a general sense, but you don’t really know what they mean. You know, a vegan doesn’t eat animal foods. And you know, a carnivore doesn’t eat plant foods. But the way that I would recommend people construct a carnivore diet is different than the way that many others in the space are suggesting people can start the carnivore diet.
00:09:57 The first thing I would say is I want to disabuse people of the notion that a carnivore diet, from an evolutionary perspective is meat only. I think of this very strongly as nose to tail eating. And what that means is that just like our ancestors would have done and just like we see indigenous peoples doing today, when an animal was killed, it’s killed from a respectful place, and they appreciate the sacrifice that the animals made to persist, to give them you know, the ability to continue living and to feed the tribe, and they eat the whole animal, both out of respect and out of nutritional considerations. To not eat an animal nose to tail is to be both disrespectful of the resources that we have on this planet with animals and also to neglect, you know, the granular nutritional knowledge that we’ve acquired over the last 100 years. I mean, we don’t know 100% of what humans need, but we have a pretty darn good idea of the nutrients that a human needs, whether it’s vitamins, minerals, co factors. And what’s amazing to me, as I’ve dug into this nose to tail way of eating an animal is that if you look at an animal and you eat, that entire animal, that animal will provide, animals do provide all of the nutrients that a human needs in the most bioavailable forms in the optimal ratios. It’s this incredible, elegant, sort of paradigm. And the last part of the equation is that without any of the plant anti nutrients or toxins. So I’ve argued this before, I would say that an animal eaten nose to tail is the ultimate multivitamin for a human. And, you know, we can break down specific examples of that. But I don’t think there’s any better food for a human in terms of bio availability, in terms of the proper ratios of nutrients, and in terms of the total cumulative sum of all the nutrients that you can get. And so we can certainly break, I’ll say a little bit about individual nutrients that people worry about. And if you look at an animal, in my opinion, there is nothing missing. And if you just back up a little bit, it kind of makes sense intuitively, that animals, a mammal usually, and it’s very close to the way a human looks. I mean, our biochemistry is not equivalent to a duck or a cow, or a sheep, but it’s very similar. Our biochemistry is much more similar to that than it is to a brassica vegetable, to a mustard plant.
00:12:17 And so the way that that biochemistry works is just like ours. You know, we’re going to get an animal… the animals operating system, I’ve also talked about this is, is essentially equivalent to ours, their biochemical operating system, the way they’re built is very much like a human. Not entirely, but it’s very similar. They’re compatible. But a plants operating system is completely different than a human. And it often doesn’t work well with human biology. And when we eat only plants, we are definitely going to get nutrient deficiencies. But if we eat an animal, nose to tail, we will get everything we need.
00:12:48 Now, as I’m saying that, perhaps the first thing people will imagine is that the nutrient that will be most efficient in would be vitamin C. I did a really interesting conversation with Bart Kay on my YouTube channel about vitamin C. And what we find when we look at animal foods is that there is vitamin C in animal foods (there has to be) and there’s a decent amount of vitamin C in liver, and there’s actually a reasonably, you know, usable amount of vitamin C in muscle meat. And if we look at studies from the 1940s and 1935, 1945, they did these crazy studies that would never have been repeated now on conscientious objectors. And they gave some of these conscientious objectors the disease of Scurvy by completely limiting vitamin C. It took six to eight months for them to develop scurvy. And what we know is that scurvy is essentially a disease of collagen synthesis. In order to make collagen, you take a strand of collagen, which is a single fiber of collagen, and then you have to hydroxylate it then you have to glycosylate it, and then the hydroxylation and glycosylation will allow the collagen to form a triple helix. Well, the first step to the hydroxylation of collagen, it uses vitamin C. So what do we get when we get scurvy? We get all problems with collagens and this is where we get bleeding gums, we get the petechiae which are little red dots on the skin suggesting breakdown of microvasculature. We get problems with collagen everywhere collagen is.
00:14:13 And so because we can’t do that first hydroxylation step of collagen synthesis, what they found was that once they gave these people scurvy, after six to eight months, it only took 10 milligrams of vitamin C a day, and perhaps could have even been less. But that was the lowest dose they gave people to reverse the clinical signs and symptoms of scurvy. And what they found was that there was no benefit to any more vitamin C in any of the metrics that they were checking. There was no clinical benefit. There was no serologic or biochemical benefit, meaning that they couldn’t find any evidence. I mean, this is again, the 1930s and 1940s. So what kind of blood tests were they doing? But they couldn’t find any evidence of any benefits of vitamin C above 10 milligrams a day. So this gets into this really kind of countercultural notion like, “Are we really using vitamin C as an antioxidant as much as people think we are?” This is the Linus Pauling theory that megadoses of vitamin C are good for us, which I would argue very strongly with. And most people when they take vitamin C will take 1000 milligrams, which is potentially, you know, 100 times more than they need in a day and can have serious consequences. For people with G6PD or glucose-6-phosphate dehydrogenase deficiency, we know that that much vitamin C can cause molasses.
00:15:23 We’re getting a little bit granular here, but what we see is that vitamin C can turn into an anti, it can turn into an oxidant molecule rather than an antioxidant high doses. We also know that vitamin C can turn into oxalate when you over consume it. So my argument here is if we look at carnivores living now, you know people in the space, there’s no evidence of scurvy and anyone that I’ve ever seen. We now can look at inflammatory markers, we can look at markers of oxidative stress, DNA damage, 8-Hydroxy, 2-Deoxyguanosine that the peroxides, and if these don’t get elevated on lower than what people would consider to be needed levels of vitamin C, maybe 40, 50 milligrams of vitamin C is what I end up getting in a day from liver and muscle meat. All that antioxidant markers look fine. There’s no scurvy. And as I would argue, in you know, sort of corollary, the higher doses of vitamin C are probably hurting people. So it’s a very counterculture idea. But if you look at the science, it really seems to hold up. And it’s quite a fascinating concept.
00:16:20 So the idea that we need, the amount of vitamin C that you can get in fruits and vegetables or you know citrus fruit is is not true. And there’s plenty in animal foods, other minerals and stuff. Yeah, go ahead.
Ivor 00:16:34 Oh, yeah. And I think as well, well, the requirement for vitamin C while being all much lower than they may believe, also, if you’re not processing a lot of sugars and carbohydrates, I believe there’s a lesser requirement for it again. But there is one thing, if you cook the hell out of your meat, I think you will tend to destroy the vitamin C so you want to be rare? I’m guessing.
Paul 00:16:59 Yeah. I mean that’s the idea, that there are cases of scurvy in Arctic explorers and people who were on ships because they had preserved old meat. So you want to you want to make sure you eat fresh meat but if you’re eating fresh meat, and you’re eating fresh organs, you know, if you’re eating an animal nose to tail and not absolutely making all your meat well done, I don’t think there’s going to be any concern of scurvy or any concern from an antioxidant perspective of vitamin C. There’s no deficiency there. Just what we see clinically and scientifically, I think the evidence is fairly strong. And beyond vitamin C, there’s really no argument for any vitamin or mineral deficiency. I mean, the really, really strong clear case is that animal foods have all the things we need in more highly bioavailable forms than plant foods. If you look at beta carotene, which is a precursor of vitamin A, well, there’s preformed vitamin A in animal foods, which is the retinol form of vitamin A. If you look at iron, animal foods have so much more highly observable form of iron and heme iron in plant foods. Many people get anemic just eating plant foods.
00:18:00 This is the same thing with niacin. It’s nicotinic acid versus niacinamide. And nicotinic acid is found in plants and it’s not processed in the same way as niacinamide, which is found in animal meats. And again, it’s this operating, just some concept that plant foods have different forms of these vitamins, minerals and co factors that are different than what humans use. And we are then tasked with an extra step, we have to convert them into our usable form. And some people don’t do that, well with certain polymorphisms with regard to betacarotene, you know there are probably more prisms than PCMOP. It’s just better to get the animal form. It’s more highly bioavailable. So if you look at the nutrient content, wow, animal foods are clearly the multivitamin. They’re the clear winner in all of these camps, whether you’re talking about B vitamins, whether you’re talking about minerals, whether you’re talking about other things, it’s not even a question. So I think it’s pretty clear people looking at a science that there’s, you’re not going to get a deficiency if you eat nose to tail, meaning it’s important to eat the muscle meat in addition to the organs. I would argue there’s a strong need for connective tissue, which is higher in glycine. And then people need to think about an omega-3 source, which would have often been in the fat of the animals, whether the bone marrow or the brain, or they can eat seafood for an omega-3 source. It’s also important to think about where you’re getting your calcium from, and we can talk about a calcium phosphorus balance as well. But I think a lot of people in the carnivore community are neglecting to think about where their calcium sources if they’re not eating dairy, and that kind of imbalance, calcium and phosphorus ratios. But if we’re eating nose to tail, and eating the bones of an animal or eggshells, we’ll get plenty of calcium.
00:19:32 It all kind of works out. I mean, it’s so amazing. As a physician, I love learning about physiology. And it’s neat to see it all come full circle and say, “Oh yeah, it all worked out just fine. And of course it would because I’m eating an animal that’s essentially very similar to a human in terms of its biochemistry, and its nutrient content.”
Ivor 00:19:47 Yeah, and I’m watching an interest too, because I’ve dabbled a little in the science, not too much actually compared to some of my other specialized subjects. But I’ve been interested to see that largely what you’re saying rings true. And very interesting data around this now emerging from the existing literature, from yourself Amber O’Hearn, and others who are researching it. And yeah, you would look and say, the default assumption would have to be are getting everything unless there’s a compelling piece of data to say there’s something big missing. But that missing data seems to be genuinely missing. So we’ll see.
00:20:24 What about the quality of the meat, because one thing that I’ve discussed with people as if you’re eating grass, reared, healthy animals, properly managed, everything you say, I’m sure rings true. I bought about the whole problem with the massive amounts of factory farmed meat, especially in the US, it’s kind of been a race to the bottom with potentially hormones and feeding with feed stuffs that could disturb those balances of fats. Just that whole area, how important is it to eat good, real food meat as opposed to processed?
Paul 00:21:02 Well, I think there’s no question that we should be eating real meat as opposed to processed meat. You know, the processing of the meat, if we’re talking about like deli meats or sausages, you know, the processing of the meat is certainly going to take away from the nutrients, especially vitamin C, like we mentioned. And I think the discussion around grass fed and grain fed is nuance. It’s very interesting. Certainly, I think that, you know, we have to look at the way that cattle are fed and how they’re fed and what’s on the grains. This is such an interesting discussion. I think that for the longest time, I didn’t understand this, because I’ve never been a rancher and I’ve never been on ranches and seeing the way cattle are raised. But you know, what I was recently educated about from a rancher is that when grass is growing, you know, I definitely think that the best cattle, the ruminant that I would prefer, he would be like a cow been living its life on a very green field for its whole life. I don’t want it to be in a feedlot if I can avoid that. But one of the things that a rancher educated me about was that the grass that they’re eating will often turn the seed at certain times of the year, and so that cows do eat some grain. And it’s a natural thing for cows to eat grain, and that grain is going to be “organic.” You know, it’s not going to be factory produced grain that can be moldy and full of glyphosate and these things. But the idea that cows would eat grain is, it really sort of opened my eyes and I think, “Oh, wow.” Like, “That kind of make sense that a cow actually probably wants to eat grain, because a grain is going to be very nutritious for that cow.” When given the choice, when the grass actually goes to seed, they will eat all the grain off the top of the grass first.
00:22:42 So I do think that when we put cows in the factory farming situations, we have to really be careful about the quality of that meat, the treatment of the cow, and the quality of the grains of the cows are fed. But I would have no problem eating a cow that’s been eating, you know, grain that’s growing on grass in the field, you know. I think I just want to introduce the idea that there’s a little more of a nuance here in the discussion. But yes, I think that the factory farming is probably not great. And I think that the work of Allan Savory is quite fascinating. This gets into kind of the ethical conversation and the idea that perhaps if we allow cows to graze in a more evolutionarily consistent manner, they don’t eat all the grass right down to the roots, they’ll graze a little bit and then move somewhere else and move somewhere else. And when they’re on the field, they deposit manure, and that increases the quality of the soil, which increases the carbon carrying capacity of the soil. People can look him up on YouTube, he’s done a great TED Talk. But the idea which is so counter culture, is that one of the ways that we could increase the carbon carrying capacity of the soils and decrease the overall greenhouse gas emissions that we’re seeing in the world is by having more ruminant animals who are eating grass who are managed appropriately. So I thought this was such a cool concept. And it kind of speaks to this idea. Like, yeah, let the buffalo roam. Again, you know, when the buffalo roam, it’s like that song, you know, in the States, you know, about the buffalo roaming, when the buffalo roam, and you know, when the cows roam, it’s probably going to increase the carbon carrying capacity of the soil and increase the quality of the meat. And so, yeah, I think it’s important to think about the quality of the meat, both from an environmental perspective and a health perspective. Processed meats, probably not a great thing.
Ivor 00:24:2 Yeah. I think the processing of the meats, certainly the deli meats and all heavily processed, I suppose you could consider it cattle are held in pens and fed glyphosate, sprayed grains, way more than they normally would eat, and then they’re injected with hormones and antibiotics. I suppose all of that together adds up to a lot of processing, even though it’s a real animal. But like you say, you know, if it’s done with certain limitations, with clean grains that have not been covered in roundup and other things, that may not be so bad. But this will be debated for a long time, we have to come.
00:25:01 The thing about the environments a big one, because I hear, and even my children hear it in school, in debates around saving the environment. And they sometimes asked me, “Well, how do you speak back to someone who says that the animals are destroying, the farm animals are destroying the environment?” And I say, “Well, basically, you say that there were way more ruminants, you know, and bison than we have now, hundreds of years ago, roaming the earth, and back then there was no global warming.” And if you look at the carbon dioxide and the global warming issue, or global impact, and look at the graph of our problem, and it goes right up from the Industrial Revolution onwards, right, there were more animals grazing before that graph moved. So it can’t be the animals by some definitions.
Paul 00:26:27 I mean, if you look at the studies that are done with greenhouse gas emissions, whether it’s carbon or nitrogen, or any of these other ones, I think most people would have a hard time debating the fact that the majority of greenhouse gas emissions come from industry and technology. I mean, like 70 plus percent, you know? And then if you look at this, if you look at the statistics, and again, these statistics can be massaged and so you have to be very careful how people are massaging statistics. Unfortunately, there’s a lot of political agendas at play here. But the most reputable data that I’ve seen suggests that agriculture, which has combined plant and animal agriculture accounts for between 11 and 13% of the total greenhouse gas emissions. Well, if you break down that amount of agriculture, it’s about 50/50. You know, like, animal agriculture is 4 to 6% and plant agriculture is 4 to 6% in total greenhouse gas emissions. People want to believe that the cow farts are causing an issue. That’s false. That’s just not the case. If you look at the science, it’s just not true.
Ivor 00:27:32 Exactly. And I love that distinction you made there because it’s one thing to say that modern agricultural practices raring animals are problematic. That may be fair enough, and we should pull back all the elements of that. But to actually blame the physical animals for their further fires is absurd, because there were a lot more of them hundreds of years ago and there was zero global warming until we brought in industrial methods, fossil fuels, coal. You know, that’s the big change, if you will.
Paul 00:28:06 And I think if people look at it, it won’t be crazy for them to imagine that. When an animal poops, that’s fertilizer. We use horse poop to make beautiful plants. An animal is depositing back much nitrogen rich things into the soil and that increases the soils carbon carrying capacity. So it’s just crazy to think that it’s cow farts. You know, Bill Gates, and this senator, you know, was talking about this, really needs to be corrected, this is not true. And this is the problem.
00:28:35 So yeah, I think if people dig into the environmental aspects of this, and the ethics, they’ll be surprised. There’s some really compelling arguments that putting more ruminants on the earth will give us a little bit longer time on this earth before the greenhouse gases get to be too accumulated and it will also provide more nutritious food for people. And that’s the other piece of the equation. Cows eat grass, humans can’t eat grass, you know? Like, we don’t need that land, you know? It’s not even tillable land. Cows can pasture on land. That’s rocky, it’s up and down, it’s hilly, you can’t even make crops on that land. So to say that cows are using space that we could use to make other food is wrong. And humans can’t eat grass. And so basically, cows are turning grass into steak, which to me is the most magical thing you can imagine. I mean, one of the most magical things you could imagine. They’re the magical machines, you know?
00:29:25 I was recently talking to a guy who’s from the northern part of Europe, and he was saying, “Yeah, in the winter, the reindeer turn moss into a steak, and it’s like, a human can’t eat moss either.” So these animals are really are really an integral part of our life cycle. And we cannot separate animal agriculture and plant agriculture, we need plants for animals to eat. To just get rid of the animals would be a catastrophe for this planet, in terms of health outcomes for humans, and I believe environmentally would be a big problem as well.
Ivor 00:29:54 Yup . Manage them correctly and properly and ethically and it’s great. The only problem, if any, is modern intensive methods. I was meeting with some artisan farmers a few days ago to tell them all about the calcium scan, and we’ll get on to that shortly, to discuss, you know, real food and its ability to prevent or treat disease. So I fill them in a lot of the science that you might have heard me talk about before. But they went through various methods and farming and they said, it really is a challenge in Ireland now. And one example of many they gave was slurry. Now the word slurry in Ireland is the stinking liquid mass that they spray over the fields to fertilize them. And basically, they’re from penned in animals standing on slats, and all of their stuff, their crap goes down, and they gather it in enormous tanks. And then later, they soak these tanks out into huge vehicles, and they spray it on the land. And it’s a kind of a smell pollution thing. And it can also get run off rolling off into rivers. But the interesting thing was these researchers who were with the team I was with, they said, “If you actually compact the feces with straw, like was all was done in the sheds, and then you take that out into the fields and piles, and you turn it like they used to do to let the air at it, you completely changed the nitrogen that’s in it, the fertilizer into a completely different kind of nitrogen compound.” So the slurry actually ends up with ammonia type nitrogen, which is not a good thing for the earth and can damage earthworms and damage the soil and the liquid feces version that’s been stored without oxygen. But the turned feces mixed with straw and air exposed becomes fantastic for the environment. So, it just shows you that humans can take something fantastic and true intensive methods and practical, optimize methods, turn it into something not so good. But anyway, that’s an aside.
Paul 00:31:58 It’s such an interesting thing. And this is the theme you continually see or I continually see is that there’s so much wisdom in what people were doing before us. We have incredible technology. And you and I are talking over the internet and this magical, you know, we’re talking through the air, you know, this is a crazy thing. This is just my rant. But you know, we shouldn’t forget the wisdom of our ancestors, whether it’s how they raise animals, how they ate animals, how they dealt with animal products. There’s a lot of wisdom there. And if we’re losing that, we’re losing something really valuable.
Ivor 00:32:34 Yeah. Well, I’ll skip skip gears now. We’re going to get into cholesterol and stuff and also how we really identify people with disease rather than going through the tea leaves or the chicken gut in trying to guess from risk factors if someone may or may not have a heart attack problem in the future. And I’ll just qualify as I always do that I work for Irish Heart Disease Awareness. And David Bobbett, who founded that, discovered he had enormous heart disease in 2012, and realized that very few people are using the scan, and they’re using the chicken gut and the tea leaves looking at cholesterol. And we know from the research that these measures of cholesterol and other risk factors are very ambiguous. And we know you’ve got to look to see the disease itself to save people who are at risk. So with that said, there are people who eat an unusual diet, like carnivore or low carb or keto and some of them, their cholesterol does go up. A lot of them it doesn’t and it doesn’t have to, especially older people on low carb, but on keto and hardcore, it often goes up. So maybe a bit of your experience, I think you’ve dealt with Dayspring and maybe Peter Attia’s, researcher talking about this LDL versus whether they really have a risk or not. Maybe a little around that.
Paul 00:33:56 This is a fascinating discussion. And I love that we can get into this because I haven’t really done a deep dive. So maybe we’ll do a moderate dive into LDL and cholesterol here. But I haven’t really done a deep dive in cholesterol in any podcast. So this will be very valuable for people. And I’ve appreciated much of your work on this topic and refer people to many of your videos. It’s a very misunderstood concept.
00:34:17 would agree with you on all of those counts. I do think a coronary artery calcium scan is very valuable for people. And we can talk about the applications of that. And I have seen in my clients and even myself that my LDL number has gone up. So let’s just break it down for people a little bit. At least here in the States, most people when they get a cholesterol panel will get an LDL, an HDL, a triglyceride, a VLDL, and a total cholesterol. And the units on that are milligrams per deciliter, which is essentially a density measurement. You’re looking at mass per volume, which is density. And the problem with that is it doesn’t take into account how many particles make up that density of LDL. It’s just giving us sort of a weight of LDL particles if we’re thinking about LDL, but it’s not telling us how many particles that is. I’ve had numerous conversations with Tom Dayspring and I’ve listened to a lot of Peter Attia’s conversations with him. There’s there’s a push now to look at LDL particle number. The units are nanomole per liter. So a nanomole is 10-9 moles. So, if we get into really some of the granular numbers here, I think people may find this quite interesting. So a mole is based on something a number from Avogadro in chemistry and Avogadro 6.02 x 1023 which is a very big numbers. So when we’re looking at a mole of any elements in the periodic table of elements, whether it’s magnesium or sodium, or whatever, one mole of that element is 6.02 x 1023 molecules or atoms of that, or it could be that you can have a mole of a molecule, which is more complex than the element in the periodic table. So when we’re saying nanomole per liter for LDL, we’re talking about, you know, 6.02 x 1023, time set of the ninth, so you can do the math, you end up with 6.02 x 1014.
00:36:15 So, I would say that, you know, one nanomole of LDL means you have 6.02 x 1014 LDL particles. That’s one nanomole of LDL. animal of LDL. 6.02 x 1014 is a huge number. That is 14 zeros, right? 14 zeros. And that is crazy. But then the numbers we see for LDL, and these particle counts are between 1000 and 2000. I’ve shared on social media, my LDL particle number is between 1600 and 2000 nanomole per liter. Meaning if you actually counted the number of LDL particles in the sample that they’re looking at, they’re getting, in my case, say 1600 x 1014 molecules of LDL, that is a huge number, right? Huge. We’re talking I mean, almost an astronomical number. A million is x 106. A trillion is x 1012. A billion is x 109.
00:37:18 Excuse me, I mess this up. Anyway, people get the idea. We’re talking a big number, more than a trillion. You know, we’re talking thousands of trillions of molecules. Now, the LDL particle number arguments goes something like this, you know, if we look at LDL particle numbers, in some populations, they have been shown to correlate with atherosclerotic coronary vascular disease. However, the problem is that sometimes they don’t correlate with that. As you pointed out, you know, there are populations in the world for who the LDL particle number is higher, and you actually don’t see an increase in cardiovascular disease. And so, we will come back to that idea of how many actual LDL particles there are, because I think it’ll help people understand this. But the other thing I would posit in this situation is that in order to achieve an LDL particle number of 1600 or 2000 nanomole per liter, that’s essentially only possible on a ketogenic diet or with familial hypercholesterolemia. This gets into a little bit of the work of Dave Feldman, and he’s often put out on social media, “Please send me a study that shows that an LDL particle number or that a high LDL in people without familial hypercholesterolemia, with high triglycerides, with high HDL and low triglycerides, actually shows that there’s a risk to this high LDL number.” And no one can show it because the studies have never been done.
00:38:36 We’ve never done a study that I’m aware of, or anyone that I’ve ever seen on social media can point to where we’ve studied a population of people like we see on ketogenic and carnivore diets, that is, people who are insulin sensitive, a low fasting insulin, reflected by usually a relatively large particle size, which is in, you know, a nanometers , at a high HDL, a low triglycerides, but they also get a high LDL. So I would say this is a divergent phenotype of LDL that’s never been studied, but what we are doing is using data from people who have high LDLs in the setting of insulin resistance, or familial hypercholesterolemia, and we are conflating that data as a predictor for these people with high LDL particle number. I’d be curious to get your thoughts on this, but this is just my thinking is that it’s so interesting to me that it’s really hard to get an LDL particle number that’s that high unless you’re doing something like ketosis or carnivore, which I would argue are very evolutionarily consistent things. But you can also arrive at that LDL particle number through familial hypercholesterolemia, which involves a genetic mutation. And it’s a completely different situation. It’s actually pretty hard to arrive at an LDL that’s that high with insulin resistance, but sometimes people do. But I think that what’s happening here is that we have a divergent phenotype of elevated LDL that we need to study. And we need to say is this actually the same thing as an LDL of 1900 nanomole per liter, and somebody with insulin resistance, where you would have a condition of low HDL, high triglycerides, small LDL particle size, they look very different. These are divergent phenotypes and yet, we’re sort of lumping them all into the same thing and saying, “This is a risk for people.” And of course, you know, all these physicians are well meaning. And there’s a lot of litigation in this country and there’s a concern that if we leave people with these high LDLs, are we putting them in the position of being at risk for, you know, coronary events, which is where I think something like a coronary artery calcium scan can be very beneficial in terms of differentiating risk moving forward. As you and I know, if someone has a high LDL particle number for a couple of years, and they get a coronary artery calcium scan and the score is zero, you can essentially say your risk of having a coronary event in the next 15 years is very small. Maybe 1%, something like 1% in the next 15 years, with a zero coronary artery calcium scan.
00:40:51 I think it’s something that we’re going to keep using in the future to generate data, to generate information about these people with this divergent phenotype of high LDL numbers without concomitant insulin resistance. It’s just a strange thing that we’ve never seen before. And I fear that we’re using data, we’re using ideas that are centered around insulin resistance rather than insulin sensitivity on these high LDL numbers. Is that kind of makes sense?
Ivor 00:41:17 Yeah, no, that’s a good summary that essentially, the particle number is a risk factor. It correlates in certain populations with more events. As you said, there are populations around the world who have higher particle numbers on average than Americans. And those populations have almost no heart disease, lowest in the world. And the Americans have the highest heart disease. So there’s myriad exceptions. A more recent ones for me is Dr. Garber, I know is a patient with a 3000+ particle number in animal and has been watching carefully. And what Garber does is he always informs them with all of the knowledge and and then they can make their own choice. So this person chose to continue with their diet, but they’re making an informed choice. Interestingly, the person four or five, six years ago, quite some time ago had a zero score, and recently got one again, and the zero score came back again, and the person is in their 50s. So there are many other examples I won’t get into with serial zeroes in calcification, which is the ultimate test for disease presence in people with very high particle accounts who don’t fit the phenotype of insulin resistance, sad diet, eating, you know, where the high particle count reflects the problems of a bad diet and insulin resistance. So I agree, but the system, the system, like I say, it’s litigators. And also the system screams for simplicity. So the whole medical system seems to have gravitated to, “Well, rather than looking at the complexity of what you discussed, we’ll just say it’s the particle number is the biggest thing and get every doctor to just look at the particle number.” But that’s a disservice, though, to people, when it’s only one risk factor of many.
00:43:11 So I’d agree. I think, absolutely the calcium scan is crucial, because mainly to find the people who have big disease, so we can intervene, and they can lower their numbers or whatever they need to do. That’s the crucial thing. But to reassure people who are in the situation that you describe, and with serial scanning, they can check back in a few years. And if they’re still a low score or no real progression, they know they have very little atherosclerosis inside. And they can’t make the personal decision to continue to have a high particle account. I guess the problematic person is one who, who gets the impression, they can change their diet, their particle can can go up and maybe inflammatory markers, and they’re probably fine, where they might not be . I guess you need some expertise to read the blood markers to ascertain is some people might react badly to an ultra low carb keto diet, and rather being insulin sensitive low inflammatory markers, everything good, except maybe a higher LDL. They might actually get some genuinely bad markers going in the wrong place, might react badly.
Paul 00:44:26 I think that that’s where, you know, a functional medicine physician comes into the equation because I haven’t really seen it in my clinical practice. Generally, there’s something else going on in that situation. But yes, you would when people send me like a panels all the time on social media, and they say, “What does this look like?” And all they send me is LDL, HDL, triglycerides, total cholesterol, in milligrams per deciliter. And I say, “I can’t say anything about it. I need to know fasting insulin, I need to know hs-CRP, I want to know fibrinogen, I want to know your ferritin, I want to know your thyroid.” It’s a very, it’s not a complex. And I love that you bring up this equation, this idea that we are really trying to oversimplify things in medicine. And I think it’s because many of these concepts are quite complex, but it does the patient a disservice. Because people getting put on statins is not a small decision. I mean, statins are real drugs. They are going to have major side effects for many people. I can’t tell you how many people I’ve seen. Before I was a physician, I was a physician assistant in cardiology. And I worked for four years in cardiology, and I saw many patients who had myalgia, memory loss, you know, problems with sexual function withstands. And I’m not saying that statins don’t serve a place and haven’t had some data to show that they improve outcomes in terms of secondary prevention, nor am I saying statins are the worst thing in the world, but I’m saying there are serious drugs. Just like any drug we use, you know, whether it’s a proton pump inhibitor, or a selective serotonin reuptake inhibitor, none of these drugs are benign. And it really kind of irks me when physicians say like, “Oh, this drug is totally safe.” It’s not totally safe.
00:45:59 So to put someone on a statin is a very serious decision that people need to be aware of. And I think that there’s becoming this knee jerk reaction, your LDL is high, you’re going on a statin. Well, in my opinion, that’s a disservice to the patient. And the physician, though they may be very intelligent and well intentioned, not considering all of the risk factors nor all of the data points, which wouldn’t go much beyond the cholesterol, as you’re saying, to give a real sense of what someone’s overall picture looks like. Let’s just revisit the idea of LDL particle numbers. And I think people will understand this. The way that LDL probably forms an atherosclerotic lesion is by moving from the vasculature, meaning moving from the blood vessels space inside the blood vessel to the intimal layer, the sub endothelial layer of the blood vessels, so it’s actually going into the blood vessel wall. Now, an LDL particle is between 20 and 22 nanometers. But if you look at the space between the endothelial cells that line the inside of a blood vessel, it’s about 70 nanometers. So it doesn’t really matter how big our LDL particles are, they’re always going to move into that sub endothelial space.
00:47:04 I’ve heard you talk about this, and I think it’s a great thing to point out to people, it’s not just moving into sub endothelial space, it’s becoming oxidized either in the blood or in the sub endothelial space, and then being retained in the sub endothelial space. This is in the blood vessel wall. It has to be retained there in a pretty a glycan matrix, it has to be seen by a macrophage as an oxidized LDL particle and it has to trigger the pathogen associated molecular pattern receptors, the total like receptor patterns on the macrophage and then get taken up as an invader. So when our LDL is taken up by a macrophage, it becomes a foam cell, which is a precursor of a fatty streak. And that’s what an atherosclerotic legion forms from. So there’s some sort of immunologic thing going on, the LDL has to become oxidized. But the arguments around LDL particle number would suggest that, okay, the more LDL you have in your circulation, the more of it is going to get into the endothelial, the sub endothelial space, space, just by a rule of osmosis, just a concentration gradient. One of the things that speaking with people in the space has really pointed out to me is that that’s a really absurd thing to say, because when you actually look at the numbers, what I was saying before holds true. Think about my LDL particle number – 1600 x 1014 particles of LDL. The difference between if I had an LDL particle number of 1000 or 900, people would say, “You’re not at risk.” The difference between 1600 x 1014 and 900 x 1014 is essentially zero, right? It’s not even an order of magnitude. People need to see how big these two numbers are. Right? To say that that is the basis of atherosclerosis is a concentration gradient. I mean, it’s absurd, like, I have 1600 1014 and someone else has 900 x 1014. It is twice, but the relatives, it’s just insane. Like, we’re talking a lot of zeros here. And either way, even if you have 900 1014, you are going to guess, that’s a huge number of particles. That’s still a huge number particles to get into the sub endothelial space, just in terms of the actual osmotic gradient and the actual concentration gradient. So to say that, that’s what’s going on is absurd to me. It doesn’t really make sense. Like, yes, someone can have a smaller number of particles. But think about it in the grand scheme of things. The scale is just enormous.
Ivor 00:49:30 Yeah. It’s like, the system is supersaturated, because there’s such a vast quantity of them. You’re essentially kind of super saturated and more going in or out when they can freely go in and out. This has been said by Dayspring, “It’s just not going to be the lever.” But you also have to say, well, you have populations where you know they have higher numbers and you know they have the lowest heart disease in the world. And when you start putting these facts together in a logical map, you realize that surely the particle number is overwhelmingly more a reflection of a potential underlying issue, than in and of itself, a concentration gradient. But the problem is that that is more complicated, but it’s awkward. It seems they are screaming for the simplicity, that more particles more problem.
00:50:25 It’s a tricky one. And in your chats with Thomas Dayspring or with Peter Attia, I think you’ve talked with his researcher, did they convince you of anything?
Paul 00:50:36 Well, you know, Thomas, Thomas… Tom is one of the people who is an expert in the field of lipidology. He knows the literature, and he’s very concerned about this. But you know, he freely admits to me, we don’t have the studies on LDL and people who are insulin sensitive, and they probably will never be done. And so his perspective is, “Therefore, we have to go by the data we have.” And my perspective is, “Hmm, I think we need to continue the conversation, and I think the studies need to get done.” And so it’s just a difference of opinions. And he’s right, you know, we don’t have the studies. And he’s trying to say, “We don’t have the studies, therefore, we have to go with the data that we have and make the best decision we can.” And I would say, “We don’t have the studies, we should do the studies, and we should continue the conversation, because I am not convinced.” And, you know, with my clients, I have the conversation with them in a very frank way and say, “Hey, this is what the literature shows. You feel good. We don’t have data here. The data would suggest this is the case, what do you want to do?” And I offer them the decision. And they you know, most of them decide they don’t want to take a stand. But you know, I think that that’s the conversation to have with people rather than to say like, “Your LDL is high, you need to stand.” Like it’s more nuanced. And I think that what we will find, my strong prediction, I’ll put money on it in 30 years if we ever do this study is that, you know, we’ll find that these are divergent phenotypes without the inflammatory markers, without the under issue that you’re talking about that is causing small, dense LDL that is causing the populations of HDL and triglycerides to become disordered. I don’t believe that this LDL phenomenon is the best metric of atherosclerotic potential in people. And like you say, it’s because the system is supersaturated, just because there’s so many particles, even at 900 nanomole per liter. The system is saturated. You are still getting a ton of particles moving in and out, you just can’t convince me that 1600 and 900 is the difference. It just doesn’t make sense to me.
Ivor 00:52:40 And also, the other problem is you have to assume that these evolutionary design, macro molecules are inherently toxic in the machine. They were designed in, you know, over millions of years. Kind of crazy.
00:52:53 I’ll give you another just for fun. There’s so many of these opposing bits of evidence that I actually find quite amusing. But you’ve got someone with a massive atheroma in their artery here. the And it’s just about to burst. Its enormous. It’s catastrophic. Just down a millimeter away, or even across the wall, the endothelium in the artery is in perfect health with no issue. That person at the same LDL particle count. Why is atherosclerosis massively focal? It’s in specific spots. You’ve got the same particle count throughout your whole vasculature, but some certain spots get massive atheroma and right beside them, the artery wall is beautiful.
00:53:38 I mean it just clearly screams that it’s not the big factor, you know? But anyway, the key thing is I think you’ve got a calcium scan to actually look for disease, if you’re not sure. And I guess we need to worry most about the people who have high risk of heart disease who have a high calcium score, and maybe they should tweak their diet to bring down the particles to be safe. That’s their choice. And I do think, myself and Dr. Garber’s Book, “Eat Rich, Live Long,” we put actually a series of dietary tweaks to stay low carb or keto, but to bring the particle number down. And that may be something people want to do, especially if they have a high score. They don’t want to wait for a serial calcification test in a few years, they don’t want to take the risk. And that’s very, very valid. And young [Inaudible 00:54:29] like like Dave Feldman and yourself, you know, on people who are healthy and know they’re healthy, well, they can certainly go with the evidence and say, “No, I don’t think this is a problem. I’m just going to watch over the years.”
Paul 00:54:42 Yeah, watch it carefully, you know? I think we just watch carefully and see what happens. And this is an evolving conversation, because we can’t deny the efficacy, the value of ketogenic or carnivore diets for people. I mean, if you look in the community… I just interviewed at Ob-Gyn in my youtube channel last night, and she noted that she had had PCOS in her pregnancies and was more obese and was pre diabetic. I mean, with regard to diabetes and weight loss and these insulin resistant conditions, it’s very clear that for some people, carbohydrate restriction is curative. It’s just miraculous. So we cannot disavow the value of these interventions of a carnivore diet as well. If you look in terms of autoimmune disease, there are so many cases now of people having incredible improvement in autoimmune disease of the carnivore diet. You know, Crohn’s disease, ulcerative colitis, rheumatoid arthritis, psoriatic arthritis, really bad psoriasis, eczema. We can’t ignore these interventions and we need to continue the conversation around the things that we see with them.
00:55:52 I have trouble believing that something that improves insulin resistance that improves autoimmunity is on the other hand going to be bad for a cardiovascular outcome. I don’t think that’s the case. I think some people would argue, “Well, it could improve one thing, but then it’s going to worsen another thing.” I think that’s bullshit. I think that if the body is getting healthier, I don’t think that’s what’s going to happen. But that’s the conversation. What I just want to see is that we continue the conversation and that people don’t stop thinking about the value of these interventions. Because I’ll tell you what, being in mainstream Western medicine, there are a lot of patients who are not getting better and don’t have anything else. And all that mainstream Western medicine can offer them is symptom focused, pharmaceutical based treatment, which is a real disservice. And these interventions with diet, ketogenic diets, carnivorous diets can really change the problem at the root. And that is miraculous, in my opinion. So stop thinking about how valuable they are and when we can use them as a great disservice to all the patients, you know, everyone in the world.
Ivor 00:56:49 Yeah, good. They’re an enormous tool, and you mix them with some other tools, and they’ll blow away pharmaceuticals on average, in terms of beneficial effects. I mean, we see it everywhere. I interviewed Mikhaila Peterson there, a short while ago in Boulder, Colorado. And we went through all of that. And the carnivore, yeah, it’s fascinating to me. But I view it as the ultimate elimination diet. And yeah, as we talked and you went through, it brings all of the fully formed proteins, amino acids, and much of what we need because they’re similar animals. But the other thing is, it’s the ultimate elimination diet.
00:57:27 I sometimes say to people, “Well, look, plants can be helpful. And that’s fine.” I eat vegetables myself above ground, non starchy. But we’ve got to be cognizant that all known problematic foods for humans, whether it’s celiac, or people having a problem with nightshades, or all the different humans who have an issue with foods, the only commonality with all of the problem foods is they’re all from the plant world. They’re never meat, fish or eggs. And they kind of say, “So look, if you’ve got an intractable problem and there’s anything in diet that can help you and everything has failed, and you want to really try the ultimate elimination diet, well, obviously, it’s kind of meat, fish and eggs, and maybe not even eggs, because some people are allergic to the whites.” “Okay, fair enough. But if you do that for four to six weeks, you’ll really find your best baseline with the least problematic diet in the universe. And then you can go from there.” I mean, that’s the way I view it. It’s not for me, because I don’t need to. But if I did need to, of course, I’d experiment with it if I needed to. Wow!
Paul 00:59:18 Yeah, I think that that is one application of a carnivore diet. I think that people sometimes say it’s the ultimate elimination diet. And I would say, “Yeah, absolutely, it’s a very valuable tool.” And I will admit that many people enjoy eating plants and find benefit from plants. And so I think that if people are thriving and they are kicking ass, and all the ways they want to kick ass, sleep, and energy and mental clarity, and athletic performance and libido, man, I don’t care what diet you’re eating, I’m not going to tell you to change it. But if people are sick, if they’re not doing well, if they’re having autoimmune disease, or sleeping problems or any of these other issues, and they’re not finding relief, then yeah, I think you need to start looking at the foods that are triggering you.
01:00:02 And I would argue, I mean, this is just my perspective, as you know, sort of a carnivore paste position that most people will find improvement on this type of a diet and they can add back plants if they want. Most of the time, they don’t end up adding back plants because they feel better without them. For the people that are that feel like they’re thriving, the other thing I would suggest just generally is that maybe they would feel even better without plants. We didn’t really get into this yet, perhaps we can say a few words about it. One of the premises of a carnivore diet is that if you look at plants, they don’t want to get eaten. I think there are some people who are more tolerant to plant anti nutrients and toxins than others. I believe that most people would feel better without plants in their diet, because of these anti nutrients and toxins. A lot of times people don’t even know how good they could feel. But I’m not trying to convince people to eat a certain way, I just want to offer options for people who are not feeling well or want to improve. But if you really dig into the plant toxins, it’s quite a fascinating realm. If you think about it evolutionarily, you know, plants are rooted in the ground, they can’t run away, animals can run away, that’s their defense mechanism. So animals never evolved toxins in their flesh, except for something like a puffer fish in the ocean. That’s pretty rare.
01:01:18 Most animals don’t have toxins. If you look at animal meat, eating an animal nose to tail, there’s nothing toxic in there. That’s just plain, there’s no toxin in there. But if you look at plants, whether you’re looking at a brassica vegetable, like a mustard seed plant, or kale, or cauliflower, there are many plant anti nutrients and plant toxins in that plant. And some people may be more or less sensitive to those. And that’s why I think for some people, I would argue for everyone, an elimination of all the plants would really give you an idea of how good you could feel. And then you could see if you wanted to incorporate that back in. And a lot of times I get asked by people, “What are the least toxic plants?” I think most people want to eat plans just for social norms and things like this. And I think that’s fine. So I’ll start with, I think the most toxic plants are the seeds of plants. I think that’s where plants put the most anti nutrients, whether it’s lectins or digestive enzyme inhibitors, things that are really going to mess up our digestion, and plant pesticides, they’re in the seeds. I would include in the category of seeds, seeds, nuts, grains, and legumes. And that cuts across a lot of things that are held near and dear to people’s hearts. Most people really like nuts, but nuts or seeds. And if you look at them, there’s lots of toxins in nuts that really mess up our digestion. Seeds are a great example as well.
01:02:39 So what’s in the seeds? Well, first of all, there’s lectins which are carbohydrate binding proteins, which I think more and more people are starting to talk about. And the idea is that these carbohydrate binding proteins in plants look very different than the lectins that are in animals, and they can really interfere with our immune system. There’s been some fascinating research done recently showing that in mice and rats, when they introduce a lectin, I think it’s from a kidney bean or something, and perhaps from the Nightshade family of vegetables, and they irritate the gut, they can actually see that lectin travel up through the vagus nerve into the brain of these animals and cause Parkinson’s like lesions in the striatum, in the substantial niagara of the brain. And so the lectins can travel through the superhighway of the vagus nerve, which goes directly from the gut to the brain and they can be seen in the brains of these animals. So this is a wild concept that perhaps this is a big perhaps hypotheses now that is, “Are lectins contributing to Parkinson’s or neurodegenerative diseases and people who are sensitive?”
01:03:42 There’s a very interesting observational study in Denmark, looking at incidence of Parkinson’s disease and people who have had vagotomy, which is severing the vagus nerve, not to prevent Parkinson’s, but usually for other medical conditions like increased gastric acidity. In the last 30 years, they haven’t surgeries where we would cut the vagus nerve. And in the people who have had vagotomies, there is a 40% less incidence of Parkinson’s disease. And it’s like, “What is going on there?” That is a crazy hypothesis. Is this potentially one of the superhighways by which plant lectins travel up through the gut into the brain, and is it causing neurodegenerative disease? Could it be contributing to Alzheimer’s?
01:04:24 Many of these diseases in the brain are actually autoimmune in nature. And I think that the whole idea around Parkinson’s is autoimmune or inflammatories. They’re all changing, I mean, the landscape is changing. So this idea that lectins can trigger autoimmunity, lectins can trigger inflammation is very intriguing and lectins are in all plant foods. They’re perhaps most strongly in the seeds, that is the seeds, nuts, grains, and legumes, but they’re in all the parts of the plant. They’re in plant stems, plant leaves, plant roots. So the avoidance of lectins could really help people in some situations. And then we move on to things like digestive enzyme inhibitors. I mean, we look at like beans, if you eat a raw bean, you are going to be sick as a dog. I mean, three to four raw beans off the vine will make you vomit. There are all sorts of strong, strong digestive enzyme inhibitors in beans. Beans are highly toxic to humans. The greatest irony is that there’s this wildly inaccurate association with health because of the misunderstanding of blue zones, longevity centers based on what people are eating. If you actually look at the blue zones, they’re probably based on clusters of genetic polymorphisms, which are favorable rather than anything that people are eating. If you look at the blue zones, people are not incredibly healthy. There was recently a fascinating study published looking at the sperm quality of people in Loma Linda and it was abysmal. So, the sperm motility, the sperm numbers were much decreased in the vegetarians and vegans in Loma Linda. So, the idea that blue zones are healthy is just this fallacy. If people are living longer in blue zones, and maybe because of their genetic polymorphisms that give them advantage rather than anything about the food they’re eating. But legumes, highly toxic to people, lots of lectins.
01:06:06 And then you move on to this idea of plant pesticides. And plant pesticides are actually pesticides produced by the plant to discourage animals from eating it. In cabbage, there’s this great article that I always refer to from Bruce Ames. It’s called dietary pesticides. 99.99% all natural. And the idea is that in any given day, most people on the planet consume about 1.6 grams of pesticides that are made by plants, these are plant defense compounds, and that we would consume, .01% of that as things like glyphosate. I’m not saying glyphosate is good, but we need to realize that the relative contribution of pesticides from the plants that we are eating is mostly made by the plant to discourage animals from eating it. A fantastic example of this is the family in brassica vegetables of glucosinolates which are found mostly in the seeds, but they’re also in the leaves. So broccoli sprouts are all the rage and broccoli sprouts are made from a glucoraphanin. Well, that’s not true. broccoli sprouts have a compound called sulforaphane, which is made by glucoraphanin, which is a glucosinolate compound. So there’s been a major misunderstanding here, and it’s quite an interesting story to tell really quickly. So we see this pattern plants where they store a precursor molecule to a toxic molecule. And then when the plant is chewed, an enzyme combines with the precursor molecule to make very toxic molecule. In this case, myrosinase combines with glucoraphanin makes sulforaphane. Sulforaphane is such a strong oxidant that if a broccoli plant had sulforaphane in it, most botanists agree that broccoli plant would die. It couldn’t sustain this. It’s such a strong oxidant molecule. So sulforaphane is never present in a plant while it’s living. It’s only present in the broccoli sprouts or the kale when you chew it. When you chew it raw. It’s a defense mechanism saying, “Oh, you’re going to eat my seeds. You’re going to eat my sprouts, you’re going to eat my leaves, I’m going to make sulforaphane and it’s a toxin, it’s an oxidant.
01:08:05 Now, Rhonda Patrick has talked about this a lot and said that sulforaphane is great because it activates Nrf-2 in the liver, which it does. But here’s the thing, Nrf-2, (this gets into all these different rabbit holes) Nrf-2 can be activated by all sorts of things in the human body. It’s triggers the production of more glutathione which is are endogenous antioxidant. People often misunderstand the fact that sulforaphane is not beneficial. Sulforaphane is a toxin. There is a concept of homeostasis, whereby a small amount of a toxin can trigger the production of increased amounts of glutathione in the human body. But sulforaphane is not directly beneficial to humans. In fact, it’s directly harmful. And I’ll tell you why in one second. But sulforaphane is doing something in the liver by triggering the Nrf-2 pathway that we can do on our own – heat stress, cold stress, exercise, fasting. These all increase our glutathione levels and cause oxidative stress. We don’t need so far thing to have adequate or optimal levels of glutathione so it’s a redundant effect.
01:09:05 Well, where is sulforaphane actually toxic? It can be directly toxic if you eat too much of it and you overwhelm the livers ability to detoxify i. It can become a pro oxidant, and it’s always directly toxic at the level of the thyroid. So this gets back to the idea of plant molecules as toxins. They’re from a different operating system. We see this with all the plant molecules, whether it’s resveratrol, sulforaphane, whatever. Sulforaphane circulates in the human body for a short amount of time before it detoxify, and it competes with iodine at the level of the thyroid. So sulforaphane is one of these family of compounds that are called [Inaudible 01:09:38]. There are a number of [Inaudible 01:09:39] in the [Inaudible 01:09:40], lithium, sulforaphane. They inhibit the production of thyroid hormone at the level of the thyroid. So sulforaphane is actually meant… one of the defense mechanisms that we see with sulforaphane as it goes to the thyroid, it inhibits thyroid hormone production. So all these people just crushing broccoli sprouts, I believe there are thousands of cases or hypothyroidism induced by broccoli sprouts. And if you look at my Instagram, there’s multiple examples of people who have written me after I’ve been writing about this recently saying, “Hey, I was doing Rhonda Patrick’s diet. I was doing the sulforaphane. I was crushing broccoli sprouts and kale green smoothies, and I felt horrible. I got Hashimoto’s thyroiditis, which is an autoimmune disease. My testosterone drops.” So anyway, what we see here…
Ivor 01:10:21 You said to them, “Hey, tell it to Rhonda right? I didn’t tell you to eat that stuff.”

Paul 01:10:26 Yeah, I’ve said to her, I’ve said it multiple times on Instagram and social media, but she won’t engage. I’ve said, “Oh, tell Rhonda, you know, like, I want to talk to her.” But you know, I think that she’s hurting people. I believe she’s well intentioned, and I respect her work, but I think that he’s hurting people with that recommendation. Sulforaphane is a plant compound that is a toxin. It has a redundant effect on glutathione. We don’t need it. And then it competes with iodine at the level of the thyroid and is toxic. Sulforaphane has also been shown to induce tumors in rodents. And then sulforaphane has also been shown to induce the formation of oxidized omega-6 fatty acids, because it’s such a pro oxidant. So things like for 4-HNE and acrolein, which what we talked about with regard to oxidized omega-6 fatty acids, sulforaphane has been shown to oxidize fatty acids in the membrane of cells and potentially even oxidized LDL. So this is a real problem.
Ivor 01:11:20 The way you described out there Paul, I mean, and I certainly had a two hour podcast with Tucker Goodrich there on 4-HNE and seed oils, and then six. Yeah. And absolutely, on the balance of what you’ve described there, I would be zero compelled to take that substance into me. And actually, I’d be strongly against it unless it had some real benefit that was proven. But what is it that people tend to pump plant foods for certain benefits? There’s that tendency, and most people don’t tend to exalt animal foods for their benefits nearly so much. Is it just the world we live in likes the concept of plants are good? That seems to be the way the world is.
Paul 01:12:10 I think so. It’s just a wild thing. And it’s why this carnivore thing is so disruptive and so interesting. You know, it’s the idea that “Wait a minute, think about it.” Plants don’t want to get eaten. They’re full of toxins. And there’s a lot of people that don’t tolerate those toxins well at all. Some people can detoxify them better than others, perhaps. And some people, you know, have a thyroid gland that’s more robust and they may not see as much of an effect when they eat sulforaphane. But the exaltation of plant foods is really evolutionarily. A misunderstanding. I mean, I’ve said this before on my social media. I see animal foods as the optimal human foods and plants are survival food. I really believe that humans are faculty of carnivores, rather than omnivores. This is just a distinction that I would make as a teaching point for people. But I would say that an omnivore is an animal that gets unique nutrients from plants that it can’t get other places. I don’t think that’s the case, I think that humans are most well adapted to eat animals. I think that if we look at the fossil record and evolution, we’ve been eating primarily animals for the majority of human evolution. It’s only within the last 50 to 60 years, since we’ve been paying attention to epidemiology, which is badly confounded and it’s virtually worthless, that people are starting to believe that plants are valuable. And I would say the plants have had value throughout human evolution as survival food. They’re inferior food, we know that we can eat plants without dying. But if you look at plant food, I believe it’s ultimately a net negative. And this is what you see with vegans. And people who only eat plant foods, there’s often an improvement in health at the onset within the first few months, because they’re eliminating something that might be triggering them, whether it’s processed foods, or sugars or dairy. But at long term, within two to three years, that the trajectory for vegans almost without fail is nutritional catastrophe. We can not eat plant foods as a sole source of human nutrition long term as humans. I would argue that point strongly. And you know, the corollary point is that if plants really are just survival food, we can include them when we want to if we enjoy them, but we should realize that animal foods are the real optimal food. And if there’s any part of our life that is not optimal, people should consider eliminating plant foods and seeing if that part improves, because I would say that there are many things about plants that is highly there. It’s there from an evolutionary perspective, to highly discourage animals from eating them. We haven’t even talked about fiber, but we can talk about that as well.
Ivor 01:14:37 The fiber thing, yeah. And there’s one topic actually that occurs to me. It’s Dr. Steven Gundry. He has the Plant Paradox book. I never read it but I would guess as a lot of the lectins in all the other plant problems in those. I do know that the vegetarian or vegan people were not happy with Gundry. But at the same time, even though he did highlight all of the concerns around plant foods, he has also done work and does a lot of work with ApoE4 people with heart disease and inflammation. And he sees excessive meats, fats and cheeses particularly, can make their inflammatory markers go up and go on the wrong direction.
01:15:21 So it’s like, this could be the exception that proves the rule that if you’ve sustained metabolic damage from bad foods over decades, that particularly cheeses and rich protein and fatty foods may not be ideal for you, maybe fish and things like that more ideal.
01:16:00 What he says about animal protein, he’ll say animal protein ages us and he just makes the statement. It’s like, “What do you mean animal protein ages us? How does animal protein any different than any other protein?” Essentially, animal protein, protein is protein. If it’s from a plant, from an animal. And amino acid is an amino acid. So to say that an animal protein ages us is just kind of a ridiculous statement. He refers to mouse studies and rodent studies where they overfed the mice with methionine. And what they saw when they overfed the mice with methionine was they did get a shortening of the lifespan of the mouse.
01:17:45 Well, what you dig into there is this biochemistry around the methionine glycine balance and the idea that subsequently, when they restricted the methionine in the mouse’s diet, they got the mouse live longer. They said, “Ah, see, here’s the thing. Protein ages us. Methionine ages us.” And I think this is his argument that animal protein is higher in methionine than plant protein. Well, this is a misunderstanding of the data. What was really going on there was that by over feeding the animals in methionine, they were in balancing the methionine-glycine ratio. And when they gave the animals a robust amount of methionine, it just gave them glycine at the same time, the glycine extended the lifespan of the mice. So it was the methionine-glycine ratio.
01:18:26 So to say that an animal protein that is high in methionine is going to shorten your life is to completely misunderstand the biochemistry around methionine and glycine ratios. And this kind of goes back to nose to tail eating. One of the things that I say to people who are thinking about a carnivore diet, or or who are eating a lot of meat in general, is that meat is a high methionine food. That you must balance that with high glycine foods. These are the connective tissues of an animal. This is the idea of nose to tail eating, that we must balance methionine and glycine in our diets. And we’re not mice, but our biochemistry is pretty similar.
01:18:58 And so Gundry is misinterpreting the studies here by saying, “Hi methionine, muscle meat is going to age you.” That’s bullshit. It only happens that way if you don’t get enough glycine in your diet. And like I said, there are some really remarkable studies, I’m happy to pull one up and tell people the name of it. There are some really remarkable studies that show that when you actually supplement the diet of a mouse with glycine, they get life extension. And that’s really the issue here. That it’s the methionine-glycine balance that we need to think about rather than the amount of methionine.
Ivor 01:19:34 And actually Paul, I’m glad you went through that because I had heard about the ratio before and that was the explanation for these. And Valter Longo is another guy who’s strongly anti animal foods generally, and the similar arguments that protein drives diabetes and cancer. And I think all of it is, there’s misunderstandings in there as you’ve described one of them, but there’s probably more as well. Yeah.
Paul 01:20:01 There are many there are many misunderstandings, yeah. Valter Longo is I think misunderstanding the equation as well. It’s a disservice because animal foods are so rich in nutrients, and people are limiting them, they’re going to develop nutrient deficiencies. I’ll just mention this paper to people because it’s so striking. That paper is called Glycine Supplementation: Extends Lifespan of Male and Female Mice. It’s in aging cell. It’s September 28, 2018. So people can look up that study as well. It’s just a striking demonstration that… and this is sort of what really frustrates me about the people talking about this is they’ll say this on podcasts and then they never share their data. But if you actually nail them to the wall there, they’re talking about mouse studies with excess methionine. And they say, “Oh, that’s been disproven.” Like, you just need to look at the glycine studies to show that. And actually, from my perspective, it’s beautifully symmetric, because it reflects back to ideas around eating nose to tail and getting enough glycine, a balanced from methionine. So the idea is that Gundry is suggesting around the animal foods, aging humans, they’re just fallacy. It’s such a shame that he’s saying this. And then I would also say that he is underestimating the impact of lectins in many foods.
Ivor 01:21:15 Yeah. Fair enough. And what about the cheese though? I think I always suspected, with ApoE4 people who have metabolic issues and sensitivities, and maybe extensive heart disease, it’s always been cheese and animal products – cheese, and fat and protein. And I’ve met a lot of people and discussed with them this, and if you isolate a cheese, which has the casein and other challenges from the animal foods with the ApoE4 patients that he’s dealing with, I wonder, is cheese carrying a large part of the can for changing inflammatory markers? Because cheese in fairness, what do you think about cheese in general? It can cause reactions, it can cause issues. And maybe that’s what’s causing the effects much more so that they do appear to see.
Paul 01:22:12 Yes. This is the problem with nutritional research. Now, if people will follow me on Instagram, they’ll know that I’m not a huge advocate for dairy for exactly this reason. You know, some people do seem to tolerate dairy, but just like egg whites, you know, there are animal products, not usually not muscle meat, you know, but egg whites and dairy are animal products that do seem to trigger immunologic reactions in people. And ultimately, inflammation is an immunologic reaction. I agree with you here. I have concerns about the immunogenicity of casein and whey specifically A1 versus A2 casein. And the fact that casein can break down into case of morphine, which is an opiate like compound found in dairy, which can change satiety signaling and all these things. And so yes, these nutritional studies are badly constructed and that they often will combine heavy cream, and they’ll use heavy cream or a milkshake or a milk product as the source of either saturated fat in these ApoE4 studies or the source of the fats in these studies.
01:23:15 I’ve never seen this study with tallow. I don’t think most researchers in the company in the country understand tallow, you know, they don’t even know what tallow is. It’s just a rendered animal fat. And I’ve never seen research with people just eating steak. That’s not an intervention. But, you know, if you look at the ApoE stuff, I think it’s a complex equation. But yes, I think that it’s confounded by the fact that for some people, dairy may be particularly immunogenic and what we’re seeing there is a signal related to the immunogenicity of the proteins and dairy rather than anything related to saturated fat. And this kind of segways into discussions around saturated fat, lipopolysaccharide, endotoxin. You know, there’s a lot of people talking about this right now. And I think that the data here is also very confusing. But if you look at the studies in increased levels of endotoxin, increased levels of LPS (lipopolysaccharide) and feeding of saturated fat, you really have to dig into the study to see what type of saturated fat people were actually fed. And almost invariably, it’s dairy. They’re getting heavy cream, they’re getting dairy fat, which brings with it casein and whey and other immunogenic proteins. And so the question is, “When you’re feeding someone dairy and you’re seeing an increase in postprandial lipopolysaccharide, is that due to the saturated fat and dairy, or is that due to the casein and the way causing an immune reaction in the gut potentially triggering leaky gut in these people?” So it’s a very complex equation. Researchers are too hasty to blame saturated fat, because that’s the story that everybody wants to make, even though it doesn’t seem to be very clear, when we look at lots of studies, it’s not clear at all that saturated fat is bad for humans. In fact, in many cases, there’s no evidence of that. But the researchers just want to blame saturated fat. It’s like there’s this bandwagon to blame animal foods, and a plain saturated fats, anytime they can get a result suggests that they jump to that conclusion without really thinking at a much more granular level, and thinking, “Oh, they’re all these other proteins in milk.” Nobody’s actually giving a single saturated fatty acid a very pure experiment. Nobody’s giving tallow or, you know, these things. There are some experiments with coconut oil, which look a little different than the dairy experiments.
01:25:22 The other thing with the experiments with lipopolysaccharide is that they’re often done in people with pre existing insulin resistance. So they’re sort of stacking the deck in their favor. The two studies I’ve seen are on women with PCOS and a mixed population of men and women with metabolic syndrome. So these are people that probably already have leaky gut. They already have metabolic syndrome, and they’re saying, “Oh, when we feed these people with metabolic syndrome dairy, we’re seeing increases in postprandial lipopolysaccharide.” Well, that doesn’t really tell me much. Interestingly in those studies, the fasting levels of LPS are normal in both groups, suggesting that it’s just a reaction to the food, that there’s something uniquely immunogenetic or inflammatory about the food they’re eating. And I would strongly suggest it’s not the saturated fat that’s very evolutionarily inconsistent. It’s probably the immunogenetic proteins in the dairy.
Ivor 01:26:14 Yeah, dairy is an enormous confound, or on average, I’d say. It’s tricky. And I think many of the researchers are simply not thinking in that isolationist way to really isolate the factor is. I just think, not true malice, but I just think they’re happy enough to go in and do a study. That’s a fat study, and just do it and get their data and get published and then move on to some other study. They may not even be aware nearly so much of these factors, like the casein and the other, and the interaction with the immune system. I mean, arguably, many of our diseases, even a heart disease are inherently autoimmune type diseases.
01:27:04 In fact, the autoimmune is enormous. I saw a paper the other day, and I know we have to wrap up shortly. But I saw paper just released a week or two ago, I think. And it was quite fascinating. And I didn’t send it on yet until I read it and go through their data. But the paper proposes by looking and analyzing type 1 diabetics, which is non diet induced, you know, it’s more genetic or older environmental issue, type 1 diabetics. And they found that the percentage of celiac issues in the type one diabetic population was so large combined with other analysis they did, they actually suggested in the paper that gluten and plant components may be a big chunk of the cause for type 1 diabetes. Now, that’s not going to be a popular idea there, right?

Paul 01:27:53 Absolutely. I would argue that plants are the greatest contributor to human autoimmunity. And that’s a radical statement. But I think that we will see more and more data, really supporting that statement in the next five to 10 years. And so I’ll repeat it, I would argue the plants and plant toxins are the greatest contributor to autoimmunity in the human population. And so, we’ll wait and see but I think we see evidence of that gluten, lectins, type 1 diabetes, celiac, these things cluster together. And I would also argue that most human disease that’s chronic is autoimmune in nature, it’s inflammatory, and those are essentially synonyms.
01:28:30 I would argue that psychiatric diseases autoimmune for many people, and that we get inflammation in the brain. I would argue that neurodegenerative disease, Alzheimer’s and Parkinson’s are autoimmune. Atherosclerosis can be conceptualized as autoimmune. Small intestinal bacterial overgrowth, auto immune. Autoimmune attack on the myenteric plexus in the gut changing motility. We know that rheumatologic disease are autoimmune whether it’s rheumatoid arthritis, you know, Hashimoto’s, inflammatory bowel disease. These are all autoimmune.
01:29:00 I would challenge people to list for me a disease that is not autoimmune that it’s chronic disease. I mean, sure, you get a cold; that’s not autoimmune. You get pneumonia, that’s not autoimmune. But a non infectious disease. It’s hard to think of one that you can’t really formulate as autoimmune as our understanding happens. And then the question becomes, “What is triggering all this autoimmunity?” You know, Western medicine might say, “Oh, just bad luck.” I would say, “Bollocks!” “Bullshit!” Bullshit. It’s your environment in the first place you look as food.
Ivor 01:29:31 Yeah. And then you got to decide which foods and everyone has to research themselves. But certainly, Paul, you’ve given a huge amount of information here on some of the foods from arenas that we need to be a little suspicious about and careful with.
Paul 01:29:45 Yeah. And so I’ll just add briefly for people, you know, I would say, I talked about the most toxic foods, I would say the least toxic foods, in my opinion, are probably the non starchy fruits, things like avocado, and olives. Plants don’t really put the same defense mechanisms into the fruit that they do in other parts of the plant. But I think that we must remember that fruits and fructose are not good for humans, generally speaking, and most fruits don’t really have much redeeming value, whether it’s high oxalate, in blackberries and raspberries, I mean, a small amount, they will can probably tolerate. But I would say the non sweet fruits are pretty benign, you know, for people and that’s a good place to start. But be aware of where the toxins may be.
Ivor 01:30:31 That’s a great way to finish the chat, that the safer plant foods… and I always perceive as well, that if someone wants to be really careful, or they have a lot of disease going on, particularly heart disease, well, if you focus more on fish, avocado, olive, these kind of very much less problematic plant foods and ideal animal foods like fish, and grass fed fatty meats like lamb, it would be really good too. In fact, lamb has been called land salmon in Ireland for its very high omega-3 to omega-6 ratio. So, you know, that could be a really targeted diet for someone who’s being extra careful.
Paul 01:31:13 Yeah, I think that that’s reasonable. Yeah, I would just be careful not to exclude the land, the ruminant animal foods. You know, I think that, like you said and like we said throughout the podcast, you know, well raised, well cared for ruminants, whether it’s a lamb or a cow. I mean, in my opinion, that’s a super food, you know?
Ivor 01:31:30 Oh, yeah, yeah, and I guess I’ll include lamb but certainly beef as well, but maybe because of concerns around factory farming antibiotics on anything else that could trigger any immune or hormonal problem, someone with a lot at stake can just pay that little extra to get really well reared meats.
01:31:50 Excellent! So I think that’s probably what I’m going to have now shortly tonight. Though I do have another meeting now before I get to my evening meal. What are you having this evening, Paul? What are you having for dinner?
Paul 01:32:02 It’s morning here, my friend. It’s morning here.
Ivor 01:32:05 Oh, well, okay. But lunch. Do you do a lot of fasting during the day and have a main evening meal?
Paul 01:32:11 I do two meals a day usually. And so I ate before we jumped on this call. And I had two grass fed steaks, about 20 ounces of grass fed organic steak. I also eat salmon roe, which is a great source of phospholipid DHA. And I ate some pasture raised duck egg yolks. I don’t eat the whites, but I ate some pastured egg duck egg yolks raw. And then I had a little bit of extra fat and tallow on my steak with collagen for glycine and sea salt. And then I had some raw, previously frozen liver for all the other complementary nutrients there. So that’s my nose to tail meal. And I’ll probably repeat something like that in early afternoon. And that’ll be the rest of my day. I’ll usually only two meals a day and I’ll do like a 16 to 18 hour fasting window.
Ivor 01:33:02 Yeah, that sounds pretty good. I’m really thinking about food now. I’m sitting here as you talk, thinking of my evening meal, because it’s now I think around probably around 6:30 PM, and I haven’t eaten yet today. So I’m looking forward to something nice.
01:33:23 Great stuff. Hey, thanks a lot, Paul. We’ll talk again and we’ll keep watching the day and we’ll see how this develops.
Paul 01:33:28 I’m so excited. Should I tell people where they can find me?
Ivor 01:33:32 Oh, yeah, I’m going to put some links when I post it, but yeah, go ahead. What’s the main place?
Paul 01:33:37 So I’m a functional medicine doctor here in the States. I work with people all over the world. I’ve got clients in Britain, in the UK and Bangkok. So if people want to work with me, they can reach out to me via email. It’s paulsaladinomd@gmail.com. I’ve got a YouTube channel where I’m sort of developing my own podcast and interviews with luminaries. Hopefully I’ll be able to have you on my channel soon.
Ivor 01:34:01 I thought you said luminaries.
Paul 01:34:03 Luminaries.
Ivor 01:34:04 God! Not me.
Paul 01:34:06 Yeah, sure you are. Come on. So that’s it. Paul Saladino, MD on YouTube. You can find that channel. I’m on Instagram at Paulsaladinomd. I’m on Twitter at MDSaladino. I have a Patreon, at paulsaladinomd, if people want to support me there. People can find more about me at my website, which is paulsaladinomd.com. And I also have a Facebook page at Paul Saladino MD. So there’s lots of places where people can reach out to me. Probably email or Instagram are the best and please check out my YouTube channel, I’m trying to put out lots of good stuff there.

Ivor 01:34:40 Excellent Paul, and I’ll put the link anyway to your main website and that’s going to have all your buttons for your social media too I guess. Super stuff, have a great rest of the day.
Paul 01:34:49 Thank you sir. It’s been awesome.
Ivor 01:34:52 Thanks a lot, Paul. Goodluck now. Bye!

 

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