Paul Saladino's Ultimate Carnivore Q&A

What is up you guys? It's good to be here. Thanks to Ben Greenfield for having me back on the podcast. This is going to be a monologue, it's going to be a soliloquy. And I am also recording video for this podcast. So if you guys want to check that out on YouTube, you can do it there. Hopefully Ben will post that to his YouTube channel as well. And we'll put notes for all the papers that I mentioned in this podcast in the show. Notes. I'm also going to post this podcast on my podcast, which is Fundamental Health. As many of you may know, Ben and I have a bromance going. We've been friends for about the last year. I first was on Ben's podcast in March of this year talking about the carnivore diet. That was an awesome show. I encourage you all to listen to it if you have not heard that show. Ben and I did another show about mid year. If you guys are interested in hearing more of what we talk about when we get together. We might have talked about poop and other things. We definitely talked about Ben's carnivore experience during that podcast. But today I'm going to be answering your questions. The questions that the very astute, very intelligent, very biohacking savvy diet savvy radical athletes that generally listen to Ben's podcast have submitted for me. And I'm super excited to dig into all of this with all of you. So let's just get right into it. I wanted to start. One of the best questions that was submitted, or one of the most sort of fundamental questions that was submitted was how would you define a carnivore diet? Paul and I think this is an important one. It seems like a very interesting question, or at least a very simple question, but it's important to define. So at a very broad level, I think of a carnivore diet as a diet that emphasizes animal foods. That is a diet that focuses on animal foods and understands that the majority of our nutrients are coming from animal foods and consumes either no plant matter or plant matter with attention to a spectrum of plant toxicity. And I'll talk about that more in a moment. But I think that the definition of a carnivore diet is loose. Technically speaking, it's no plant matter and that excludes things like coffee. Though some people who eat a carnivore diet would still drink coffee. We can talk about coffee in this podcast a little later as well. That will be kind of a hot topic, maybe a little controversial, but Generally, technically speaking, a carnivore diet is a diet that excludes plant matter and focuses entirely on animal foods. But I would expand the definition and also refine the definition. So the expanded definition is what I was just saying that I think generally a carnivore diet could almost be a carnivore ish diet, which is focusing on animal foods for the majority of our nutrients, realizing that if we're hoping to get vitamins and minerals, the absolute best place to get those is from animals, hands down, bar none. In terms of bioavailability and raw amounts. Vitamin C is the only exception to that. I can talk about vitamin C later in this podcast, but generally speaking, with vitamin C, I think that there is good evidence that doses beyond 70, 50, 70 milligrams are not beneficial for humans. And we can easily obtain 50-70mg of vitamin C eating animal foods, nose to tail. So that is how I would think about a carnivore diet. And then when you're going to eat plants, if you're going to eat plants, you are thinking about those plants on a spectrum of plant toxicity, thinking which plants are the most toxic and which plants are the least toxic. In my book, which is coming out in February 2020, called the Carnivore Code, I have a whole spectrum of plant toxicity. Also in my book, I go through and I give detailed explanations of different tiers of carnivore diets, tier 1 through 5. In the book, I describe tier 1 as carnivore ish, which is what I'm talking about. Now get your nutrients from animal products. Think about plants on a spectrum of toxicity, which are the most toxic plants, which are the least toxic plants? So I'll answer that question because I know you guys are all curious about that. Most toxic plants, in my opinion, in my estimation, based on the research I've done and what I've seen clinically, are things like seeds, which would include nuts, seeds, grains and legumes. Grains and legumes, we're quite familiar with excluding on paleolithic diets, but nuts and seeds are often included by people. But I think that these can trigger many folks because of phytic acid, oxalates, digestive enzyme inhibitors. When we're thinking about plant foods and what plants are doing, they generally don't want their seeds to get eaten. So the seeds are often highly defended. And I think that seeds can be a very common trigger. In seeds, I'm using the Royal seeds quote, unquote, which includes seeds, grains, nuts and legumes. They're all plant seeds. And then also on sort of the toxic end of the spectrum, I would include most leafy greens. I think things like brassicates have isothiocyanates. We're going to talk about those today. And I think they're pretty toxic for humans. Spinach is very high in oxalates. Pretty toxic. I don't see a whole lot of redeeming value in leafy greens. This may be radical for some people to hear, but it's one of the contrarian notions that I think about and advance in my work. I don't think leafy greens are very beneficial for humans. I think you could get some less toxic leafy greens like arugula or lettuce. But generally speaking, things like spinach, chard, the brassica, leafy greens, these are not beneficial for humans. And I think that the risks far outweigh any potential benefits therein. Other foods that I would consider to be highly toxic would be high oxalate foods. The biggest ones would probably be things like almonds, which are technically a seed. Already talked about that. Root vegetables, specifically sweet potatoes, are moderate. Perhaps the biggest offender is spinach. Beets are also high in oxalates, so I would be careful about those in general. I would put them on the more toxic end of the spectrum. In the middle, I think of other tubers that are. That are less high in oxalates. Sweet potatoes, like I said, are kind of moderate. You might think of berries in the middle and then the sweet fruits I generally think of in the middle of the equation, but I'm not sure they serve a real role in our diet. There's plenty of good evidence that overconsumption of fructose in any form is going to spur de novo lipogenesis, probably trigger insulin resistance through a couple of mechanisms we might talk about in this podcast if I have time. But I'm not a big fan of fructose over consumption either. In the form of honey, table sugar, which is fructose and glucose together. High fructose corn syrup, no surprise there. Or overconsumption of fruit? I think small amounts may be evolutionarily consistent at certain times of the year, but over consuming fruit is not a good thing. So what are the least toxic plants? I would think of those as things like berries and non sweet fruits. Things like avocado. Olives. Yeah, olives have a little bit of oxalate, but it's not that much. Avocado have salicylates. They can still trigger some people, but I think they're Fairly benign on the scale. And I would also put squash on that non toxic end of the spectrum. Obviously squash has carbohydrates, but I don't fear carbohydrates per se, nor do I think that a carnivore diet needs to necessarily be ketogenic or that a carnivore ish diet necessarily needs to be ketogenic in any way, shape or form. And we're going to dig into that in a moment because that is a very interesting nuance. So that's kind of my spectrum of plant toxicity. I think that if we try and think about which plants might be more toxic and less toxic and we focus on animal foods, we're really eating a carnivorous diet. This is pretty similar to the diet that Ben eats right now. Ben provided a chronometer summary of a daily diet that he was eating for this podcast. We're going to talk about Ben's diet later and I'm actually going to dig into his FTO polymorphisms and saturated fat. So many good things I'm just teasing you guys with right now. But one nuance of a carnivore diet that I want to explain to people is also the nose to tail aspect of it. When we are eating animal foods, we are not just eating the muscle meat. I think it's very important. And we will see this later on in this podcast when we are discussing ph and acid base balance to eat nose to tail. And as a teaser for that, we will see that if we are getting minerals that are found in bones, we can easily normalize our body's overall ph balance. And that is important to get from those sources of the animal that are beyond muscle meat. We will think about potential renal acid load, which is called prowl, or the net endogenous acid synthesis, which is the NEAs. And I will discuss some papers regarding overall body acid base balance. And what we will see is that when we are eating minerals like calcium, manganese, magnesium, boron that come from bone, we can really balance the overall acid base equation in the body and see normalization of urinary ph and serum bicarbonate. So we'll get to that. That's a teaser. But the important thing when I'm thinking about which animal foods we are eating is that we are eating these foods nose to tail. This is so important. You guys have heard me talk about this before. If you've heard any of my work, this includes eating organ meats because that's where all of the complementary nutrients come into play. And the other thing That I think about with a carnivore diet is getting adequate protein. I think most people are not in danger of getting inadequate amounts of protein on a carnivore diet. But what is nuanced here is that in the studies that we'll talk about in the next question with athletes, many ketogenic diets don't get enough protein. And I think that if you are doing a ketogenic diet and limiting the protein, that is going to have performance athletic consequences. I recommend, I think that the best way to construct an animal based diet like a carnivore diet is to get adequate protein, which I would say is about 1 gram per pound of body weight. So it's more than most people would say. But for me, I'm 170 pounds, so I'm really usually getting about 170 grams of protein per day. And in the faster study, which we're going to talk about in a moment, which Ben was actually in, as was Zach Bitter, looking at ketogenic athlete performance performance versus high carb athlete performance, the amount of protein was pretty much on par with that. It was 2.1 grams of protein per kilogram, which is about one gram per pound of body weight. And we'll see that when you eat that much protein, the glycogen stores are full and athletic performance is not compromised at all, which is what's so fascinating. So when we are thinking about carnivore diets and ketogenic diets, I don't really like to lump them together because most of what we see in the research is traditional medical ketogenic diets, which are a 4 to 1 ratio of fat to protein. And when we're doing that for epilepsy in kids, generally the protein is inadequate and there can be problems with acid base balance and other issues in the body, which we will talk about. But what I would say a carnivore diet is like a low level ketogenic diet, it's a mini ketogenic diet, it's a soft ketogenic diet, meaning that when we are eating that amount of protein, we're probably going to be out of ketosis, have serum ketones around 0.2 or 0.1. When we have bolus meal of meat and fat and organs, et cetera. And then overnight we will deplete liver glycogen, we will trigger higher levels of ketogenesis, we'll turn on autophagy and then we will kind of cycle in and out of low level ketosis. In the faster study, as we'll see the the average ketones I think were between 0.5 and 0.8 millimolar. So these athletes eating a robust amount of protein, which is what I would recommend, are not in, quote unquote deep ketosis. This is not extreme ketosis and I don't think that that is a good place for us to be most of the time. But I think that low level ketosis appears to me to be a sweet spot for many of us. This means ketone levels between point 1 and 0.8, which is what you're going to cycle between on a carnivore diet or a carnivore ish diet when you are eating adequate amounts of protein and filling glycogen. So I think that it's very important that we not always conflate or confuse research based ketogenic diets done with 4 to 1 fat to protein ratios and a carnivore diet which is going to have a little more robust amounts of protein, a little less fat. What I recommend is 1 to 1 fat to protein with 1 gram of protein per pound of body weight. So it's a real simple equation. One gram of protein per pound of body weight, one to one fat to protein. For me that means 170 grams of protein a day, give or take. And around 170 grams of fat seems to be the sweet spot for me. So that is my long winded explanation of how I would define a carnivore diet. It's a diet that focuses on animal foods that takes into account a spectrum of plant toxicity, that gets adequate amounts of protein, that is probably low level ketogenic, but doesn't have to be on a carnivore ish diet. Like I said, you could even include things like squash, which I would consider to be lower toxicity carbohydrates. You might even throw white rice in there. Technically that's a seed. People might react to it in different ways. I think squash is probably the cleanest carbohydrate that I've encountered. Again, this is all just my opinion in clinical practice and we're all trying to navigate this, but that is my conception of a carnivore diet and that is the framework with which we will operate through all of the discussions of a carnivore diet in the rest of this podcast. So hopefully that helps you guys. The second question, which is awesome and I provided some teasers for in that first question, is how is a carnivore diet going to affect athletic performance? And could a carnivore diet be used for optimal athletic performance in endurance, sprint or strength sports. So this is a huge, really important question. I know a lot of you guys are athletes and that you want to know what is going on here. So let's dig into this as well. So what is so interesting in this question is that this has really been studied in detail on a number of occasions. And we will link to all of these papers in the show notes for you guys. And the first one I would like to share with you is the Faster study. The title of the paper is Metabolic Characteristics of Keto Adapted Ultra Endurance Runners. It's Finney and Volek, two of the godfathers in the realm of ketogenic science and research. Now, as I mentioned earlier, Ben Greenfield was actually in this study. He was one of the ketogenic athletes in the study, as was Zach Bitter who recently set the record, the world record for the 100 mile time around a track. I believe he ran it in something like 11 hours for 100 miles. He had a pace that was around maybe a little over six minutes a mile for 100 miles. So Zach Bitter is a very well known ultra endurance runner who practices what I would say is a carnivorous diet. And Ben has, I think, at least in our conversations, been doing a carnivorous diet much of the time as well. He was not doing a carnivorous diet when he did this study, but he was doing what I would consider to be a low level ketogenic diet or an easy ketogenic diet. We need better words here. But you guys get the idea. This is not a medical ketogenic diet. So I'll just cut straight to the chase with this one. So they had two groups of people. These were 10 athletes in each group. They were keto adapted, meaning they had been doing a high fat, low carbohydrate diet for between six and 12 months. The keto adaptation period is very important when we're thinking about athletes and athletic performance. But the high fat low carb group was keto adapted and they compared the two groups in exercise tasks so they had 2010 of each. Elite ultramarathoners and ironman distance triathletes. They performed maximal graded exercise test and a 180 minute submaximal run at 64% VO2 max on a treadmill. And what they found in the study was that there was no difference in the glycogen utilization, storage or repletion in either of these two groups. There's a fantastic graph. In this group they did muscle biopsies between these two and what you see is that the high carb and low carb groups look equivalent when it comes to the amount of glycogen that is in their muscles before exercise, the utilization of glycogen when they do exercise, and then the replenishment of glycogen post exercise, eating their respective diets. Meaning that the low carb group ate low carb after exercise and in this keto adapted state was able to replete glycogen at the same rate in the same way as the high carb athletes. So it's a pretty striking finding. There's a very illustrative graph in this study that shows these equivalencies. Now, what's fascinating about this is it really argues a number of things. It argues that if our glycogen stores are full on what we could consider to be a low level ketogenic diet, meaning a ketogenic diet that has a lot of protein. Right.

Why would we have any compromise in our muscle? Because exercise, whether it's endurance, sprint, high intensity or strength, the performance is really a function of two things. Creatine stores, which we know will be maximal on a diet like this, or a carnivore diet, which I would say is pretty similar because there's tons of creatine and meat. And if we have adequate full glycogen stores in the muscles, there should be no decline in performance. And the next two studies I will show illustrate that exact point, that in high intensity exercise there is no decline on these sort of low level ketogenic diets with adequate protein. So quite an interesting finding. The other thing the faster study found, and this was repeated in the next two studies we'll talk about, is that maximal fat oxidation was much higher in the low carb group, which probably improves many things. It certainly changes respiratory quotient, probably improves efficiency and increases endurance at the same time. And these athletes are less likely to bonk. They are tapping into fat stores while they are exercising rather than relying primarily on glycogen. As you will all know, the glycogen stores in the human body are limited. They're quite limited. And if you can tap into the fat, you are going to be able to go much longer, much more easily. So that's an adaptation that is beneficial. There is a table in this paper, table 2, where, which describes the protein percentage, like I said, it was 2.1 grams per kilogram in the low carb diet, which is 1 gram per pound of body weight. Super interesting. Also interesting and a little more foreshadowing for this podcast is that the saturated fat grams in the low carb diet were 86 plus or minus 22, so quite a bit higher than the high carb diet. We are going to talk about APOE4 and FTO polymorphisms later in this podcast with regard to saturated fat, but most ketogenic diets do have higher amounts of saturated fat. Certainly in this study it doesn't implair athletic performance and we will dive all into APOE 4, FTO and other cardiovascular implications of higher saturated fat shortly. But that is the faster study. Again, there's a really cool graph on one of these pages which shows pre and post utilization. The last point I'll make about the faster study is that.

In ketogenic athletes, in low carb athletes, what we generally see if we're looking at the enzymes of glycolysis is that PDH is down regulated, so pyruvate dehydrogenase is down regulated. But what's fascinating is that the utilization of glycogen is equivalent between the two groups, arguing strongly that the rest of the glycolytic enzymes are not down regulated in this state. We don't want to shunt the we don't want to make acetyl COA out of glucose and shunt it in the same way. When we're doing this type of physiology, we just want to do the beginning of glycolysis to generate the reducing intermediates to generate the nadh NADPH that we're going to use in that process if we don't have adequate oxygen. So we're not going to do full glycolysis, we're going to do the majority of glycolysis. PDH is down regulated, but the fact that glycogen is utilized in the same way means that we are still doing glycolysis. Glycolysis doesn't shut down on a low carb diet, you're still utilizing glycogen in that way. It's a fascinating thing and it means that hey, you can still access glycogen in the same way. Performance shouldn't suffer at all. So the other two studies I want to highlight here are quite interesting. The effects of a four week very low carbohydrate diet on high intensity interval training responses. This is a fascinating study. They looked at total time to exhaustion, maximal VO2 maximum and what they call a performance graded exercise test and HIIT sessions which were 5 by 3 minutes work rests 2 to 1 passive recovery, total time 34. So it's almost like an interval session. So what they found was that total time to exhaustion, maximum VO2 in the GXT, which is the graded exercise test, increased in both groups and between group changes were trivial and not significant. Between group differences in fat oxidation was significant. And again the low carb group increased that significantly more. As would be expected, the respiratory exchange ratio or the respiratory quotient went down in the very low carb high fat group. This is what happens when we are low carb high fat. It moves to around seven depending on how much of the carbohydrates are in our diet. This is what's called the respiratory quotient. So in this study on the high intensity interval training with a very low carbohydrate diet, there was no difference in the performance of these athletes. And the last one I want to show you guys is called keto adaptation enhances exercise performance, body composition, responses to training and endurance athletes. And what was fascinating in this one, there was no significant change in the performance of the 100 kilometer time trial between the groups. The sprint peak power increased by 0.8 watts per kilogram body weight in the low carb ketogenic diet group versus A minus 0.1 watt per kilogram reduction in the high carb group. So pretty fascinating. Peak power on what they call CPT, which is the critical power test, decreased by 0.7 watts per kilogram in the high carb group, increased by 1.4 watts per kilogram in the low carb ketogenic diet group. So their conclusions were compared to a high carb comparison group. A 12 week period of keto adaptation and exercise training enhanced body composition, so it led to more fat loss and enhanced fat oxidation during exercise as we've seen before, and specific measures of performance relevant to competitive endurance athletes. So this is more of an endurance study, but similar performance benefits were seen. So I think this is a really fascinating nuance to discuss regarding these low level ketogenic diets. This is, this is not medical ketosis. And I think the problem that many people run into on ketogenic diets in general is that if they're not getting enough protein, if they're chasing ketones, their glycogen stores are not going to be full in the muscle and performance certainly will suffer. But in this case what we find, and a carnivore diet is totally in line with this. If we fill the glycogen source by giving our body enough protein, around 1 gram of protein per pound of body weight, performance will not suffer in glycolytic type activities. We will still do the majority of glycolysis, even though PDH may be down regulated. Pyruvate dehydrogenase, we're doing the other things, restoring glycogen we're utilizing at the same rate. But there's a nuance there, right? We got to get enough protein, fill those glycogen stores. Which means we're not going to chase ketones, we're not going to see ketones of 4, we're going to see low levels of ketones, which is fine because we're not chasing ketones in this space. What we're going to see is ketones will rise overnight, kind of come down after meals. That low level is probably the sweet spot I believe for most of us, long term and totally sustainable. So that to me is a very interesting question. I appreciate that one and hopefully that helps you guys with athletic performance. The other thing I would say on these low carb type of diets is that if you are not performing at the level you think you should be, check your salt. We're going to talk about the mineral balance shortly. But sodium, we know that more sodium wasting happens especially early in the process of transition to a low carb diet as insulin falls. And I have found in my work with people and myself that unless I am getting 10 grams of sodium per day, excuse me, 10 grams of salt per day, which is at least 5 grams of sodium, I am not going to perform to my best and I don't feel as good as I could should would if I got more salt, which is sodium chloride. So I think the sweet spot for salt on all these low carb diets is 10 plus grams a day, which is 5 plus grams of sodium per day. There's a very often talked about study that I can also try and link to in the show notes. It's epidemiology, but it actually shows that the best survival is in people who are eating around 5 grams of sodium a day, which is 10 grams of sodium chloride per day. I think that any on any given day I'm probably averaging closer to 15 grams of sodium chloride per day. One of the other questions that was asked in this podcast was where do you get your iodine? So I'm going to skip to that one because this is a good segue. So you guys may be familiar with Redmond sea salt. They're out of Utah. What's cool about Redmond is they're mining the salt underground. So it's an inland salt deposit, which I think could have multiple benefits. One of those benefits is there are no microplastics because it's not a real quote unquote sea salt. It's probably an inland, quote, sea deposit. But there's no microplastics because it's not contaminated. It's from the ground. It's ground salt. And in Redmond sea salt, if you do the calculations, 10 grams of Redmond sea salt, which to the lay person may sound like a very large amount, but it's very easy for me and other people to obtain on low carb diets. That has about 150 micrograms of iodine, which is the RDA of iodine. Even though this is technically not a quote unquote iodized salt.

This has trace amounts of iodine. And when we're getting 10 grams of this salt per day, we will get 150 micrograms of iodine. So that is one source of iodine that probably even gives us enough iodine. There's a small amount of iodine in muscle meat, which will add onto that egg yolks, which I eat probably 4 to 6 of those a day. Later on in this podcast, I'm going to go into detail in my diet, so stay tuned for that. But egg yolks have about 20 to 25 micrograms of iodine in them as well. So even without eating any seafood, I can easily meet the RDA for iodine between sodium from Redmond sea salt, four to six egg yolks a day. I'm going to talk later about why I only do the egg yolks and not the egg whites. Just a personal preference, but as you'll see, the egg whites may be triggering for people as well. I can get four egg yolks, 100 micrograms of iodine, 10 grams plus of Redmond sea salt, 150 micrograms. I'm easily getting between, I would say 250 and 300 micrograms of iodine without even eating seafood at all. We're going to get into EPA and DHA and phospholipid derived things with this. We're going to talk a little bit about salmon roe in this podcast as well. There are lots of sources of iodine and seafood if you choose to include that in your diet. But basically I don't think iodine is as much of an issue as people have thought it is. Unless you are eating. You might want to know how much iodine is in the salt you're using. Again, using Redmond kind of solves the problem. So that's the iodine Equation. The flip side of the iodine equation, I'll just add a word of caution for people is I don't think you want to do excess iodine. I am not a fan of Lugol's iodine solution. If you do the calculations, one or two drops of Lugol's is a milligram plus of iodine, which is whole order of magnitude more iodine than I'm talking about getting per day. I don't think humans should be getting milligram quantities of iodine per day. I think it's too much. And there's some evidence that it may raise tsh, that it will change thyroid physiology potentially negatively. There are some, I believe, observational studies suggesting that higher doses of iodine are associated with more Hashimoto's or autoimmune thyroiditis. I think if we put too much iodine in our body could be a really bad thing. So I would not over supplement with iodine. I think that most of us are getting plenty of in our diet, but it's good to know where all these nutrients come from. So hopefully that's helpful with regard to the athletes stuff and the iodine. And we will move on to the next question. All right, so the next question is a really good one that'll be fun to dig into briefly. As you guys may have known, may have seen, I talk fast, I'm hopefully talking a little bit slower than I did the first time I was on the podcast with Ben. But I get excited and I just roll. And I also have a lot to say about all these things. So I will move faster through some of these other questions and we'll get into all the stuff. So the next question is about sustainability and whether or not every person on the planet could eat a carnivore diet. So before we dig into this one, I will just say that I think this is a valid question, but I think it's the wrong question to be asking at this time. And I think the questions that we have to ask before this one are these. Is the current agriculture system that we are using to feed the United States right now sustainable and working for us? And I would say the answer is resoundingly no. We can think in terms of the US and we can think in terms of the world, but there's a bigger sociopolitical context when we're thinking about the world. So let's just think about the U.S. let's just think about could we do.

Grass feeding, grass finishing. And what I'm going to talk about is very interesting to Me, regenerative agriculture in the US and feed everyone a carnivore diet. Hypothetically, I think that technically speaking, everyone in the US is never going to eat a carnivore diet. This is never going to happen. Vegetarians, I think are 15, 10% of the population at the most. I think that animal based diets, even carnivore ish diets, are probably only ever going to be 15% of the population. So I don't think we need to really be able to scale this to the grand population, 100%. That's never going to happen. But for the sake of discussion and academic experimentation, thought experiment, let's just dig into it. So the first question I asked is, is what we are doing now sustainable and good? The answer is resoundingly no. What we are doing now is primarily mono crop agriculture. This is a really bad thing. When you're growing one crop in a plot of land, you deplete the soil, including the topsoil of nutrients. There's no animals on that land grazing and eating the the plants in an ecosystem. This is not an ecosystems based agriculture. It's a monocrop agriculture that depletes the soil of nutrients. There's erosion and basically we are running out of soil in the United States to grow plants in because it is so depleted, because there are no animals on that land to poop and pee and to die. Like the buffalo have returning nutrients to the soil. It's a cycle, it's an ecosystem. If we want to grow plants, we need to have animals with those plants. We can't just have animals on a plot of land. We can't just have plants on a plot of land. This is intuitive. We get this. And I'm not an advocate for factory farming, for CAFOs. If we just want to have animals on a land, they'll die. But we are all sort of seduced or told that mono crop agriculture is okay. You know, we drive through the center part of California, what we're seeing is just plants on land. Well, that's just as bad. To me that is feedlot feeding of plants. Because when you put plants in a feedlot or plants in a cafo, again, I'm mixing the terms here, but if you put plants in a concentrated environment, they will deplete the soil. If you put animals in a feedlot, that's a really bad thing for those animals too. So both of those are equally bad in my opinion. So what is the answer? The answer is regenerative agriculture, which is ecosystems agriculture. What am I talking about? Here, basically I'm talking about grass feeding and grass finishing of animals in ecosystems, meaning multiple animals together on one piece of land, multiple species. This is what we're talking about. This is where regenerative agriculture goes beyond simple grass fed grass finishing. I think most of us will understand that if we're going to animals, grass feeding, grass finishing is the way to do it, both in terms of greenhouse gas emissions, which we can talk about, and also caring for the land, less toxins in the animals, probably very little toxins in the animals, depending on the quality of the grass, the quality of the land the animals are on. One of the problems I have with feedlot feeding of animals is increased levels of persistent organic pollutants from the feeding troughs. And the grains which are sprayed with things like atrazine, glyphosate, 2, 4D, they can also be moldy grains with mycotoxins like humosonin or others, all sorts of molds that can be on those grains that lead to the cattle becoming sick. Intramuscular fat in beef is an indication of essentially cow diabetes, cow insulin resistance. Right. Humans don't have intramuscular fat unless they have insulin resistance. We also should not have visceral adipose tissue, which is quite inflammatory. Well, if we're seeing intramuscular fat in an animal, a marbled steak that is from an animal that is grain fed, that is unhealthy, people will sometimes complain that grass fed steaks are leaner, but that's because they don't have intramuscular fat in the same way, because the animals are actually healthy. That's what happens when animals eat the way they're supposed to. So what is cool about regenerative agriculture? This type of agriculture has actually been shown to be carbon negative, meaning that because of animals living on the land, in an ecosystem with plants, they poop on the land, they pee on the land, they enrich the soil with nutrients, specifically phosphorus, nitrogen, other things which are needed for plants to develop big root systems. When plants have bigger root systems, they can fix more carbon dioxide from the environment into the roots. And that is part of the carbon cycle. That is how carbon gets pulled out of the environment into the roots, into the ground. And carbon emissions can be net negative, meaning that though ruminants may burp, which is the primary source of methane emissions from a cow, the plants will sequester more carbon into the soil than the ruminants are burping. It's carbon negative. There's a great farm that I'm associated with in White Oak Pastures. I recently went there. We had an event called White Oak Chella. We're going to do it again in May of 2020. I hope you guys will all come to Bluffton, Georgia. They do regenerative agriculture in the way that Alan Savory recommends. I would recommend you all check out Alan Savory's video on YouTube, on Ted Talks, he's kind of leading the charge in terms of this regenerative agriculture, which is basically raising cattle in a way that mimics an ecosystem. It mimics bison on the plain. Bison move around the plains. They don't stay in one place. They impact the land extremely heavily in one spot. Pooping and peeing there. They eat the root, they eat the grass down to the nub. And then the grass is fertilized and it grows right back after they leave. And they can rotate around the grazing lands. And this is what they've always done for millions of years. This is what we're trying to mimic with regenerative agriculture. Places like White Oak. There are other farms like Bel Campo in California doing the same thing. White Oak has 130 acre paddocks that they move cows around. They move animals every day. The other cool thing about regenerative agriculture is that they put multiple species on the same plot. What's cool about this is it interrupts parasite life cycles, just like would have happened evolutionarily from, from an ecosystems perspective. There is a worm that affects sheep called a barber pole worm, and a worm that affects cows called a brown stomach worm. When you put the two animals together, the life cycle of those parasites is interrupted. They don't co infect the other animal and neither animal is affected by the parasite. Because if we're just putting one species on a spot of land, then that worm can do its life cycle like it wants to. But if you put a second species there, like sheep, they're not infected by the brown stomach worm from cows. And this happens in all animals throughout the world. So it sounds gross, but there are parasites all over the place. But what happens, what's so interesting is that in ecosystems, in the natural world, animals interrupt the parasite cycles of other animals. When we put one species of animal on a land, that species of animal is going to be susceptible to parasites because there are no animals to interrupt those parasitic life cycles. So what's so cool about regenerative agriculture is that not only can this way of farming animals lead to healthier animals and a healthier environment because of carbon sequestration, it interrupts those life cycles. And overall the animals are healthier and happier in that type of a setting, and it mimics the natural world. I think the only way that we are going to get back to an overall healthier planet. It's a total buzzword, but it's true. It's cliche. The only way we're going to get back to that is by recreating ecosystems that are natural. We need to go back to bison ranging on the plains, or the closest thing we can do to that, which is regenerative agriculture. So the question was, is this way of eating sustainable? Yes, I believe it is. I think it's the only answer for our planet is to really nudge farming, nudge agriculture back to creating actual full ecosystems. It will sequester greenhouse gases. In terms of land management, what I believe we need to do is eliminate monocrop agriculture. We can still grow plants, but let's do it all together. You know, let's. Let's grow plants in some spaces that are not monocropped. We need to create ecosystems. Let's put a lot of animals and plants together on land. And that, I think, is the only way that we are going to generate the land, the quality of the soil, and keep our environment going for many generations. If we want our kids, kids, kids to have earth that's inhabitable, we need to do something else because what we are doing now is not sustainable. So we need to put our heads together and figure this out. But I think that regenerative agriculture is the start to this equation. So that's a great question. I appreciate you guys asking that one. All right, so let's get to some heated questions here. The next two are about hormesis and xenohormesis, which are pretty interesting things. I definitely feel differently than the mainstream with regard to these. So I'll read the next question. I think that this person is challenging my implication. Quote the implication that you should have only one type of hormetic stressor, either exercise plus cold hot. But if you add the hormetic stress from plant intake to it, it becomes too stressful for the body. And so what he's saying here, or he or she is saying is, couldn't we. Does it create an overload? And then I'm quoting the rest of this question. Doesn't excess exercise also have the potential to cause hormone imbalances? Why don't we just throw exercise under the bus too, while we're at it? So I think what this person is saying is in response to me suggesting perhaps on a previous podcast, that plant stressors could overload our body in terms of hormesis. And this isn't quite what I was hoping to communicate. So perhaps I did not do the best job of communicating this. On the first Ben Greenfield podcast, let's talk a little bit about plant hormesis and xenohormesis. Plant molecules are molecules. They're essentially plant pharmaceuticals. And I've talked about this in my book as different operating systems. And I think I talked about this on the first podcast with Ben. I really see plant biochemistry and human biochemistry as independent, unique things. Plants make molecules for plant biochemistry, not for human biochemistry. What we know is that many plant molecules do have medicinal pharmaceutical value in humans. Metformin is derived from a French lily. There are many others, digitalis.

From another plant, which is known as digoxin. So there are plenty of pharmaceuticals that we are aware of. Aspirin is acetylsalicylic acid from willow bark that we use. But what we have forgotten, if you go to the pharmacy and you get a synthetic pharmaceutical like metoprolol, for instance, which is a beta blocker, the pharmacist will give you a package insert which has all of the side effects, right? There is an intended effect of metoprolol, and then there is all of the side effects that may come with metoprolol or metformin. Metformin is a good example, right? Metformin is a molecule that can affect the amplified SO AMP kinase pathway, but it also has side effects including lactic acidosis, B12 deficiency, and others. It seems to inhibit the first complex of the mitochondria at least partially. And so we are giving metformin to affect glucose sensitivity or insulin sensitivity by affecting AMP kinase. But it has a side effect which is B12 deficiency, lactic acidosis, and potential mitochondrial things which may or may not be part of the actual effect of mitochondria long term. The actual effect of metformin, long term. What we forget about so many plant molecules is the package insert that never comes with the plant molecules. Whether we're talking about resveratrol or curcumin, which I'll dig into in a moment, they all have package inserts. They all have side effects that we are not told about or are not emphasized. I fear the mistake we are making when we think about plant molecules is we forget that despite some demonstrated beneficial effects, we are forgetting about the package insert. We are forgetting about the side effects of these molecules which invariably appear to be damaging because they're from a different operating system. And again, this is an oversimplification And I use it as an illustration to help people kind of grasp this concept. The question that I would offer to all the listeners is why use. We don't use pharmaceuticals if we can correct the root cause? Why would we use plant molecules if we can correct the root cause? Both pharmaceuticals from synthetic sources and from plants are going to have side effects. On the first podcast with.

Ben, we talked about the collateral damage, which is essentially the same thing I'm talking about here, the fact that plant molecules have collateral damage. Now, this isn't exactly what the person in this question is asking, but I wanted to lay that groundwork that I think that plant molecules can have benefit, just like synthetic molecules have benefit. And those benefits in plant molecules are often correcting a symptom or something that has another root cause. Plant molecules are different than vitamins and minerals, right? We're talking about polyphenols or isothiocyanates or other what would be considered phytonutrients, and I would say are just phytomolecules. We're not talking about the vitamins and minerals in plants, which are often similar to the vitamins and minerals, animal foods, though sometimes in different forms. Beta carotene versus retinol, vitamin A, et cetera. That's a whole different discussion. What we're talking about here are plant molecules that are not vitamins and minerals, and they're essentially plant pharmaceuticals. Why would we use a plant pharmaceutical to treat a problem if we're not getting to the root cause? The only time we would do that is like we would ideally do it in medicine when we actually can't correct the root cause or the symptoms are so severe that we absolutely have to treat the symptoms. But the overarching ethos in medicine, we hope, though it isn't always this way, is that we should correct the root cause. And too often I think we get confused or sold this false narrative that plant molecules are correcting the root cause, when in fact they're really just ameliorating symptoms. They're affecting symptoms in a certain way, and they're going to have side effects, just like pharmaceutical molecules that are synthetic have side effects, which is my main problem here. So if we can correct the root cause of an illness, whether it's autoimmune or inflammatory, I think the plant molecules become redundant. And I'll get into more of this in the next question as well. But this person is saying, if they're asking me basically if plant molecules are additive to environmental hormetics, and that you're overwhelming the system of hormesis. This isn't quite what I meant to say. So environmental hormesis, as this person is correctly noting, are things like heat, cold, sun. You can even suggest that hypoxia could be an environmental hormetic. What's different about these hormetics is that they don't really have a package insert. They don't really have side effects. They affect damage in the human body. They create some oxidative stress with like small damage to DNA, which triggers the NRF2 system in the body, or oxidative stress, and then you get more glutathione. And there's a very interesting paper that I don't think I talked about in the first podcast with Ben title. This paper is uric acid and glutathione levels during short term whole body cold exposure. In that study, they looked at cold water swimmers in Berlin and what they found was that the cold water swimmers in Berlin who were swimming for an hour a day or multiple times a week in the winter, had levels of glutathione that were higher than regular people, meaning they had had hormesis, environmental hormesis. You go in the cold water and what they show in the study is they check glutathione levels before and after a cold water swim and they see glutathione levels go down. Specifically, they see reduced glutathione levels go down and oxidized glutathione levels go up, meaning that they are oxidizing glutathione and they are having oxidative stress, meaning glutathione is doing its job. And so what they're seeing in the swimmers is that overall they have higher levels of glutathione because they're exposing themselves to an oxidative stress. Frequently they have hormesis and they illustrate that hormetic effect, or they illustrate the oxidative stress specifically when these people swim. So you can look at the graphs in there and see that this is very different than something like sulforaphane, which also activates the NRF2 system. Now, sulforaphane has been touted as a molecule that can do this, that can activate nrf2 and increase glutathione in the short term. But it has a package insert. Well, swimming in cold water doesn't really have a package insert. Well, what's the package insert for? Sulforaphane? Ah, this is what's so interesting to me. And we're going to get into this in detail in a separate question. But the package insert for sulforaphane and all of the isothiocyanates is that they affect iodine at the level of the thyroid. They've been shown to damage cell membranes by being pro oxidants. They are creating things like 4Hne, and they can interfere with this iodine metabolism at the level of the thyroid and do other negative things in terms of oxidative stress in the body, other places. And they can potentially turn on and off genes in a way that we don't want to happen. So these are kind of the side effects, like the metformin side effects, the sulforaphane side effects. And my argument, my hypothesis, the premise that I'm advancing is we don't need sulforaphane to get enough glutathione. And this has been shown repeatedly over and over in fruit and vegetable depletion studies and inclusion studies, which I'll review in a moment. That when we include fruits and vegetables in our diets and we look long term, there's no difference in antioxidant stress markers, oxidative stress markers, antioxidant capacity, DNA damage or inflammation in a lot of these studies. So where are the benefits to sulforaphane? I would say that if we are doing the things we should be doing, if we are living a radical life, this means hot, cold, swimming in cold water, right? Exercise, sun, maybe holding our breath, free, diving with friends and being safe about it, or other environmental hormetics that our body will be able to manage antioxidant status, ideally without the plant molecules. We don't need the plant molecules. They have side effects that are overall negative, I would say, and they're redundant. They have these collateral effects that are damaging. So it's not so much that exercise is good or bad. Exercise is a hormetic. And exercise can absolutely impair hormonal function if we overdo it. I'm not throwing exercise under the bus and I'm just highlighting that exercise doesn't have a package insert exercise. These are environmental hormetics. We versus molecular hormetics. The molecular hormetics have a package insert. They have a list of side effects that we need to be aware of. And I think that all too often what I've seen is that we don't need these molecules. And this will segue into the next question as well. We don't need resveratrol, we don't need curcumin to be optimal. If we are doing the other things, if we are doing heat, cold exercise, breath holding all the awesome stuff that you guys do. So hopefully that helps answer that question. Alright, so this is a great segue to the next question, which is a really good one. Dr. Saladino, you assert that human biochemistry does not directly utilize plant molecules and that the benefit of polyphenolic molecules and compounds and other such things are only in their role stimulating the human body's own beneficial pathways, albeit with potential unwanted effects from those plants. So I'm quoting now from the question and that's, that's exactly what I was talking about before, albeit with unwanted potential side effects. This is the package insert, hopefully that was clarifying for people and not more confusing. This person goes on to ask, under this paradigm and following a carnivorous diet, how are these desired pathways activated? Are all of these really possible to activate just from heat, cold therapy, exercise, ketosis and such? So this is a fantastic question and the short answer is yes, this is exactly what I was talking about with molecular hormesis. We are able to activate all of these pathways that I am aware of, that I think we are generally aware of with those molecular, excuse me, environmental hormetics. And the one that this person listed that I did not list in the answer to the last question was ketosis. I want to talk about this as well. We've kind of set the stage for ketosis earlier in this podcast with low level ketosis and kind of these moderate levels of ketones. But what we know that when we are in ketosis this can affect epigenetic mechanisms. It is ketones. Beta hydroxybutyrate specifically is an HDAC inhibitor, meaning it's a histone deacetylase inhibitor, meaning that just it affects the turning on and off of genes. Histone, the deacetylation of histones is one of the ways that we epigenetically control which genes go on and off. And we can talk about which genes go on and off in ketosis in a moment. But even with low levels of ketones, BHB 0.2 to 0.8, we are affecting epigenetic mechanisms. So this is a great question. What are the mechanisms that we are aware of that plants can affect in a positive way? The NRF2 system is the big one. We talked about that with regard to sulforaphane a little bit in the previous. There are many polyphenols which can affect Nrf2. Resveratrol affects Nrf2 as well. And we're going to get into all this in detail, but we know this is exactly the same thing that's happening with the the cold water swimmers. And there's other good research showing that exercise affects NRF2, heat affects NRF2, we know that cold does with the Berlin cold water swimmers. And ketosis can also affect the NRF2 system in the liver. NRF2 is a transcription factor in the liver that turns on genes involved in antioxidant response, generally upregulates glutathione levels, so that we can do more molecular policing of free radicals in the human body. So, absolutely, with regard to NRF2, we know that all these molecular hermetics can do this easily. And also there are other toxins in our bodies that can do this, or toxins that we might encounter that can do this. Specifically things like smoking, alcohol, lead, heavy metals. There are many toxins we encounter that can do this. But what is the level of toxicity and do they have a beneficial effect? I don't think anyone is arguing for low levels of lead, though. I interviewed a gentleman for my podcast yesterday, James Clement, who suggests that intermittent hypoxia may have benefits to people and that there are some supercentenarians that smoke low levels of cigarettes. I would never advocate for that because I think of all the negative damaging effects of the tar and the other things in there. But maybe we should all be doing some breath holding. Who knows? Maybe there's a benefit to what Wim Hof is saying, although he's doing really forced respiratory alkalosis, which is a little different. It's not hypoxia, it's low carbon dioxide as you blow off your carbon dioxide. Totally different. But modulating the breath may have a hormetic effect in humans. But with regard to the NRF2 pathway, absolutely, we know that we can affect that with molecular hormesis and that fruit and vegetables really do not give a clear signal that they are affecting that above and beyond what we can do in our normal life. And I'll talk about some of those fruit and vegetable studies in a moment. The other pathway that is often talked about is the sirtuins. So in terms of longevity genes, people are always talking about NAD and NADH and the sirtuins. Now, resveratrol is a molecule that activates the sirtuins. I did a whole podcast with David Sinclair all about this. But as I talked about in that podcast, we know that nutritional ketosis can also turn on the sirtuins because of the way that being in low level ketosis or any level of ketosis affects, affects the NAD to NADH ratio in the human cytoplasm of the cell. So there's a couple studies I'll point out here. Ketogenic diet modulates NAD dependent enzymes and reduces DNA damage in the hippocampus. This is a rat study, but they saw that a ketogenic diet in rats increased the activity of the PARP enzymes, PARP1, which is the polyADP ribose polymerase 1, and also turned on sirtuin. Run sirtuin 1 in the rat hippocampus as the NAD to NADH ratio change. This is what we're trying to do with nad. When we give ourselves nad, we're trying to turn on the sirtuin enzymes. Well, what we know is that those enzymes get turned on when we are in ketosis. Another study, nutritional ketosis increases NAD to nadh ratio in healthy human brain. An in vivo study by P31 magnetic resonance spectroscopy. So we've seen this happen repeatedly. Another one that has to do with this is ketones improve APOE4 related memory deficiency via sirtuin 3. We're gonna get into APOE4 later in this podcast, but it appears that ketogenic metabolism or beta hydroxybutyrate changing the NAD to NADH ratio in the cytosol because of the differential sort of biochemistry of these. I'm not going to get into all that right now. Can affect positive things on learning and memory. That study was also in mice, but it turned on Sir 2 and 3. So in answer to this question, yes, I absolutely believe that we can turn on all of these pathways that are beneficial from plants that we're aware of with these molecular, excuse me, these environmental hormetics. We don't need molecular hormetics. FoxO3 is one of the genes that is turned on by beta hydroxybutyrate. And Foxo3 is one of the two genes that is most associated with longevity. The other one is IGF1. So gain of function mutations in FoxO3 are associated with.

Longevity and loss of function mutations in IGF1 are associated with longevity as well. So those. I'm not going to go into detail about both of those, but beta hydroxybutyrate ketones turn on Fox O3 as well. If any of you have done your genetics, you can look at your Fox O3 genotype and see if you have a polymorphism that is associated with more longevity as well. But super interesting stuff with regard to those. That's a fantastic question and the answer is a resounding yes. It really appears that we can turn on all of those pathways without any of those plant molecules and therefore get all those benefits without any of the package insert side effects. Okay, so I've talked about these fruit and vegetable depletion studies a couple of times. I just want to share with you guys these in detail because I think they're quite interesting and they argue against the notion that fruit and vegetables are clearly beneficial for humans. So there are a number of these that I talk about in the book and at the. I don't want to belabor this, so I'll just talk about two of them. The first one is called the effect of increasing fruit and vegetable intake by Dietary intervention on Nutritional Biomarkers and Attitudes to Dietary Change. A randomized trial. In this trial they had 19 men, 26 women with low reported fruit and vegetable intake. Less than three portions a day. They either consumed their usual diet. So this is not a carnivore diet. They're eating a usual diet which is probably standard American. This study was actually not done in the us it was done in, I believe, Scotland. So this is a standard Scottish diet, a standard English diet, which might not be any better than a standard American diet. So people, half of the group consumed their usual diet, the other half supplemented with an additional 480 grams of fruits and vegetables, which is more than a pound and 300 milliliters of fruit juice for 12 weeks. And at the end of the study they measured markers of antioxidant capacity, DNA damage and inflammation and there was no difference between them. So the conclusion was while increasing fruit juice and vegetable consumption increased levels of circulating carotenoids, there was no beneficial effect. They say a 12 week intervention was not associated with effects on antioxidant status or lymphocyte DNA damage. So where has the fruit and vegetable benefit gone in this trial? If we don't see it there? And there are multiple studies which show this. This is a 12 week trial, so this is three months and there's no benefit there. I think that I don't know what the lifestyle of these people in this trial were like, but it suggests that, hey, we can really do just fine without these things in our life. Another thing that was quite interesting about this study that I will point out is that the intake of vitamin C increased from 70 milligrams a day to 250 milligrams a day in the intervention group with no change in antioxidant capacity or DNA damage. And so I think this is super fascinating and a bit of a hypothesis generating study to say, hey, we probably don't need that much vitamin C to have optimal antioxidant function. What does vitamin C do? It is involved in the formation of collagen, the hydroxylation of the single strands of collagen which form a triple helix and that is the prevention of scurvy. But it is also known to serve some role in aqueous fraction of the cell regenerating NADPH and glutathione, thereby regenerating glutathione by regenerating NADPH and vitamin E that is in the membrane. And so what we could look for to see if we have adequacy of vitamin C is antioxidant markers, glutathione levels, DNA damage, levels of vitamin E that are not oxidized. And at least in those metrics that have been studied in this study, tripling quadrupling the level of vitamin C from 70 had no change. My hypothesis here is that humans need vitamin C. Absolutely believe that. I just don't believe we need mega doses or the mega doses have any benefit. They can potentially have harm. I'm going to release a podcast soon with James D. Nicolantonio. I talked about that with him. I'm not going to go into that in detail now, but in terms of benefit I think it's pretty hard. There are many interventional trials in humans which do not show a benefit to vitamin C in supplemental form. And so I think that probably my hypothesis would be that humans need vitamin C, but the doses that are easily obtainable eating nose to tail that is 50 to 70 milligrams a day are more than adequate to maintain ideal antioxidant status in the human body. I'm not saying we don't need vitamin C, so that's an interesting kind of contrarian idea. Another study, no effect of 600 grams fruit and vegetables per day on oxidative DNA damage and repair in healthy non smokers. Very similar trial.

They measured levels of strand breaks, endonuclease three sites, formamidopyridine sites, sensitivity to hydrogen peroxide in mononuclear blood cells. And they also measured 8 hydroxy 2 deoxyguanosine in the urine and.

Looked at expression of excision repair complementing one DNA repair genes by real time PCR and MRNA expression in two groups of people who were 24 days. One group high fruits and vegetables. One one group no fruits and vegetables. And can you guess what they showed? They say our results show that after 24 days of complete depletion of fruits and vegetables, complete depletion or ingestion of 600 grams of fruits and vegetables, that's a pound and a half or the corresponding amount of vitamins and minerals. The level of oxidative DNA damage was unchanged. And their conclusion is really fascinating. This suggests that the inherent antioxidant defense mechanisms are sufficient to protect circulating mononuclear blood cells from reactive oxygen species, which is really the heart of this excellent question from one of the listeners. Do we do enough? Can we activate these pathways normally? Do we need plants for hormesis? My answer is yes, we can protect ourselves without any fruits and vegetables. They don't really show a clear benefit in these studies at all. And I think we can activate all the pathways we want to activate just by living a radical life and then not get any of the side effects from plants. So that was a long soliloquy monologue about those. But that is one of probably the most important points that I make in my work because if fruit and vegetables have benefit, we should be eating them. And the carnivore diet doesn't make a whole lot of sense. My hypothesis, my premise is that it's not really clear that they have benefit. I think some people can tolerate them better than other people, people. But in general it's fascinating to me these studies that show that, hey, we can probably get optimal antioxidant status and do just fine just by living a radical life. Heat, cold, exercise, ketosis, low level ketosis, we don't need these plants and then we have potentially avoided many of the toxins. So hopefully that helps clarify many of those points. Before we move on, I just want to highlight a few studies that actually show some of the negative effects of resveratrol and curcumin molecules that I referred to a little bit. So resveratrol, though it can activate the sirtuin genes, has also been shown to decrease androgen precursors and has failed multiple clinical trials. So resveratrol reduces the levels of circulating androgen precursors is one of these studies, but has no effect on testosterone, DHEA, PSA levels or prostate volume. 4 month randomized trial in middle aged men. Again, we're going to put all these in the show notes. And what they saw in this study was that daily administration of 1000mg of resveratrol for four months significantly lowered serum levels of androstenedione, DHEA and DHES. I don't know about you guys, but I don't want to lower my androgen precursors. That doesn't sound very good to me. Another trial where resveratrol failed placebo controlled randomized clinical trial high dose resveratrol treatment for non alcoholic fatty liver disease. Basically the conclusion is that in this placebo controlled trial, high dose and long term study, resveratrol treatment had no consistent therapeutic effect in alleviating clinical or histological nafld. So that's non alcoholic fatty liver. And so that's a big deal. Like resveratrol really failed there. And then there is one more trial that I can put in the show notes where resveratrol actually worsened metabolic syndrome. So these are the package inserts for resveratrol, right? It doesn't help nafld. It worsens androgen precursors. Resveratrol we know, acts as a xenoestrogen like many of the flavonoids in plants do. So it'll lower dhea and it actually worsened fructosamine and many of the other markers of metabolic syndrome in a metabolic syndrome trial. So resveratrol can also damage membranes. We know it activates NRF2, which may be good or bad. And we don't need the effects of resveratrol because we can activate the sirtuins by affecting the NADH or NAD to NADH ratio with ketosis even if it's intermittent. Right. So this is a perfect illustration package insert why do we need this drug? It has side effects. The essential medicinal chemistry of curcumin and and the dark side of curcumin are two papers I would point out to people that highlight the package insert side effects for curcumin, which is the molecule found in turmeric. So.

Quite concerning. So I'll just read a sentence from this one. A relatively high number of reports suggest that curcumin may cause toxicity under specific conditions. In 1976, Goodpasture and Origi found that turmeric caused a dose and time dependent induction chromosome aberrations in several mammalian cell lines. These alterations were observed at concentrations of 10 microgram per milliliter. Accumulating data have demonstrated since then that curcumin can induce DNA damage chromosome alterations in both in vitro and in vivo concentrations similar to those reported to exert beneficial effect. For instance, curcumin concentrations of 2.5 and 5 microgram per milliliter were shown to induce DNA damage to both mitochondria and nuclear genomes in cells. These reports raise concern about curcumin safety as the induction of DNA alterations is a common event in carcinogenesis. The authors go on to note that the presence of two alpha beta Unsaturated ketones in the chemical structure of curcumin could be causing a problem by participating in a organic chemistry reaction called a Michael addiction addition. Not a Michael addiction, a Michael addition. This reaction may explain, I'm quoting now, for instance, why curcumin generates reactive oxygen species by irreversibly modifying the antioxidant enzyme thioreduxin reductase, why curcumin induces topoisomerase 2 mediated DNA damage, and why curcumin inactivates tumor suppressor gene P53. So what I'm highlighting for you with both of those articles on curcumin is the package insert. These are the side effects. I'm not denying that curcumin has benefit for some people as an anti inflammatory. But the question then becomes, where does the inflammation reside? What is the root of the inflammation? Should we be using a pharmaceutical to get rid of the inflammation? None of us would really use a pharmaceutical without some concern or without some appreciation for its potential side effects like ibuprofen or aleve or aspirin. But many of us are using curcumin in large doses and supplementing that with piperine in a dangerous way, increasing the absorption in a negative way by inhibiting UDP glucuronic transferase. And it has all these side effects. So if we can correct the root cause of the inflammation, we're going to be much better off. Plant molecules have side effects. Let's try and figure out the root cause. Hopefully that helps illustrate all that stuff for people. All right, so the next question is really an awesome question. Due to the high protein intake, doesn't one's PH go to acidic on a carnivore diet? So the answer to this one is yes, it can go too high on a carnivore diet. If we don't construct a carnivore diet properly, if we don't construct a carnivore diet, nose to tail, getting all of those other important minerals. So the answer to this question, I'll try and make it as simple as possible. It's kind of complex. So the way that acid base balance works in humans, I will try and explain. The blood acidity doesn't really change no matter what when we eat food because the PH of the blood, which is a measure of the acidity, generally stays between 7.35 and 7.45 all the time. If it goes to below 7.35 or above 7.45, we are in dire straits. Or there's something really Wrong. So blood levels of ph are not a good indication of overall acid load in the human body. And this concept of acid and alkaline foods has been bandied about a lot. There actually is some truth to this. Different foods affect the acid base balance in the body differently. And our body has a way to buffer it. There are a lot of minerals in the bone that can be pulled out to buffer lots of acid. The thing is, we don't want to pull minerals out of the bone to buffer the acid unless we absolutely have to. It's a temporizing measure. The bone is a huge reservoir for these minerals, but we don't want to be pulling these minerals out. So how does this work and how do we keep this normal on a carnivore diet? Can we keep it normal on a carnivore diet? I believe we absolutely can. The overall acid load of a human diet is based on two sides of a seesaw. One side is protein. So it is true that the more protein we eat, the more of an acid load we are going to get in our body. That is absolutely true. But there are other things in our diet which balance it. These are the alkalinizing minerals. What am I talking about? Magnesium, potassium, calcium, iron is also an alkalizing mineral. These are the big ones. Right. So if we are getting enough calcium, enough magnesium, enough potassium, enough iron, they will balance the protein acidity in our diet. Now the problem is that a lot of people who are doing carnivore diets don't get enough calcium. They may be getting some magnesium, they may be supplementing with magnesium. But a lot of people on carnivore diets don't think about bones. A reservoir for goodness. And this is what's so interesting to me about eating nose to tail. Like there are many minerals that are only present in bones that are so valuable for us as humans that we cannot neglect eating an animal based diet, nor should we neglect in general, no matter what diet we're on. I'm talking about calcium, manganese, boron, those are the biggest ones. But there are other strontium. So how do we get those minerals? You can get those minerals either by eating a low metal bone meal, you want to make sure it's tested, or a bone broth is probably the easiest thing. So I'm going to talk about all that in detail, but let's just back up and talk about how we estimate the amount of acid in the diet. So there are a few papers that are technical. The first one is estimation of the renal Net acid excretion by adults consuming diets containing variable amounts of protein. And you can see they have what are called NAE values, the net acid excretion values. And there are the way that these are calculated. We don't have to go through the exact calculation, but it takes into account sodium, potassium, calcium, magnesium, chloride, phosphate, sulfate and organic acids. Or specifically it's a balance between the alkalinizing minerals that I was talking to you guys about and protein. There's one other paper where, which makes it a little bit easier to look at in terms of an equation that they actually talk about in the paper, and that is this paper. I will find it here. There's another paper, potential renal acid load of foods and its influence on ph. And basically what you'll see in the calculation of prow, which is the potential renal acid load or the net acid excretion, the nae, sometimes called the NE A C, is that we balance protein by including these alkalinizing minerals in our diet. So there's a couple of fascinating studies that I want to tell you guys about. Effect of a low carbohydrate high protein diets on acid base balance, stone forming propensity and calcium metabolism. And so what they found in this study was that A baseline urine pH, which is a good indicator, was 6.09, which is usual, and it decreased to 5.56 when the amount of protein was increased in these people's diets without increasing the amount of calcium. This is what we want to avoid. But what we can take away from this study is that if we increase the amount of calcium in our diet commensurate with our intake of protein, we can normalize our urinary ph. And so how do people know if they're getting enough alkalinizing minerals on a carnivore diet or a car carnivorous diet, or in general, you can check your urinary ph and your serum bicarbonate. I've observed the same thing in myself and my clients, that if someone is not getting enough calcium, magnesium and potassium in their diet, the alkalizing minerals, the urinary ph will drop. I don't like to see urinary pH drop below 6. I don't like to see serum bicarb drop below 23 or 24, the body will buffer. And you can see these things happening. What's the solution? Calcium. Some people can tolerate dairy, which is a great source of calcium, or we can include a high mineral bone broth, which I will talk about how to make in a Second, interestingly, many people associate phosphorus as an anion, as a acid inducing anion, but it's actually not the phosphorus, it's the cation, the proton that often comes with the phosphorus in different media. So in general, phosphorus intake is not acidic. I don't think milk is going to be super acidic. But if you look at the calculations of the prow, the parl or the neac, cheese looks very acidic. Milk, not so much. Milk is actually going to provide some calcium to balance the phosphorus that is in it. And something about the composition of cheese, probably because it's higher protein than milk, maybe I'd have to think about that increases the acidity of the cheese, cheese relative to that. But what we need to do, the takeaway here from this study, what we saw was that people, this other one that I was talking about, people had calcium of 889 milligrams. And when they increased their protein from 91 to 164 grams a day, which is about what we're probably going to do depending on our body weight, and their calcium stayed the same, it actually went down slightly to 805 with a standard deviation of 359. Then the prowl increased, the NEAC increased, the urinary ph decreased to 5.5. So that's interesting. So that's exactly what we don't want to happen if we are going to increase the amount of protein in our diet. We can maintain acid base balance by eating nose to tail. Getting more calcium in our diet either from dairy if we tolerate it, or from a bone meal if it's low Lead bone meal, you got to have it tested. And I'll tell you guys, the one that I generally used is traditional foods market or you can. The easier thing to do would be to get bones from somewhere you know, are really good, like white oak pastures and grind them up yourself or make a bone broth which should be simmered for 12 hours in an acidic medium. So I want to tell you guys about this other study with bone broths and then I will talk about a mineral addition study which normalized ph, so essential and toxic metals in animal bone broths is the study. What they found was that reducing the ph of the broth from 8.38 to 5.32, which we can do by adding something like vinegar, significantly increases calcium and magnesium extraction by factors of 17.4 and 15.3 respectively. They found that the amount of lead and cadmium were minimal when they did this. And so basically what we need to do to make Our own bone broth is make it acidic with vinegar. I would use just a white vinegar. They cooked it for greater than eight hours and had significantly greater extraction of the minerals. So if you want to have a high calcium bone broth, you have to add some vinegar and you have to cook it for at least eight hours and you'll get more calcium and magnesium, which will be alkalinizing minerals. I think this is probably what our ancestors would have done. I don't know if they would have had vinegar, but I can imagine them cooking bone broths for days long amounts of time. I don't think that the bones would have been wasted. I definitely think this is something that we're missing. Bone broth is kind of in vogue now. So many of you are probably already using bone broth in your life, but you just have to make sure that it's good quality bone broth and that it actually is a high mineral bone broth that is done with an acidic medium. 5.38. I think if you're doing 2 to 3 tablespoons of vinegar per liter of broth that you're making, you will achieve that ph. And you can kind of go by taste. But add acid to the bone broth, make it for a long amount of time and you'll get minerals in your bone broth. So the first study I was talking about were people who increased their protein from 90 to 165 grams and saw a decrease in the urinary ph and probably a decrease in the bicarb. What I said was that we can check our urinary ph very easily. They make very cheap strips online and you can check your serum bicarb very easily. Now the other study I want to tell you about is one called Effects of a supplement rich in Alkaline minerals on Acid Base balance in Humans. And what's cool about this is it shows that if we supplement with minerals, we can affect acid base balance positively. So this was a study with 25 people and they gave them a multiple multi mineral supplement rich in alkaline minerals that we were talking about. Calcium, magnesium, et cetera, potassium. And they found that the blood PH didn't change much, 7.4 to 7.41, but the urinary pH increased from 5.94 to 6.57. And that's what we want to see. Somewhere in that 6 to 7 range of urinary ph is probably fine. And this is what we can do with either a multi mineral supplement or just eating nose to tail with the proper amounts of organ meats and bones and bone meal. So this is a really great question. It acid base comes up all the time with regard to carnivore diet. It's absolutely something we need to think about. We should be checking urinary ph. We should be thinking about the amount of calcium in our diet. I think it's how we balance it. And it's totally doable, nose to tail. And it's not a reason not to eat a carnivore diet, but it's a reason to keep track of labs and not to ignore a bicarb of 16 or 17, et cetera. So I did a debate with Chris Masterjohn. We were talking about this as well. He was arguing that ketones increase the acidity of the blood. And I think that the levels of ketones that we're getting on this type of a carnivore diet with adequate amounts of protein are pretty meager, pretty minor. I don't think that's going to affect overall acid balance in the body negatively. But ultimately we can check those things very easily.

With these metrics with urinary ph, which is probably the best indication of that, and with serum bicarb, and I've been able to normalize those in myself. My urinary ph is about 6.5 as I'm getting these bone broths, and my serum bicarb was 24. A little later in this podcast, I'm going to talk about my blood work. Somebody asked about that. We'll go into detail. But I just want to let you guys know that there is a consensus statement from the European Society for Clinical and Economical Aspects of Osteoporosis that said that high protein diets, and they're not as high as we're talking about, but they're talking about higher protein intake greater than or equal to 0.8 grams per kilogram of body weight. We're talking about two. But they're saying higher protein intake is associated with higher bone mineral density, a slower rate of bone loss and a reduced risk of hip fracture, provided that dietary calcium intakes are adequate. So if we give our body enough calcium to balance the protein intake, we will get stronger bones. And one of the things that's missing in osteoporosis literature and osteoporosis teaching in medicine is a focus on protein. I think we're getting so much osteoporosis in the population now because people are not getting enough protein. We need to balance it with calcium. If we're eating plants, we're going to get these alkalizing minerals and it probably won't be a problem if we're not eating plants because we're trying to be carnivore or super awesome.

I'm speaking tongue in cheek now, but I really don't think we need the plants. We can get those minerals from bones. Bones are our mineral source, one of our major mineral sources on an animal based diet. I think it's totally viable and works great. So hopefully that answers that question. I think that's a really important one. We covered a lot there. All right. I always have so much fun doing these that I go on and on. And we've already done more than an hour. I know Ben's podcasts usually don't go this long, but I'll try and get through some of these questions a little faster. I want to cover most of this stuff for you guys. So interesting for me to do this again. I hope you guys are digging this one. So, next question. You talked about not worrying about IGF1 and MTOR because of the beneficial effects when in ketosis. Would you worry about this for people who don't go all the way with a carnivore diet approach and therefore aren't in ketosis but are eating a high amount of animal protein? So again, you guys, I just probably when this podcast comes out, I've probably already released the podcast with James Clement. On my podcast, which is Fundamental Health, we go into this in detail and we talk all about what James calls the switch, which is mtor. Basically, the deal is this. If your liver glycogen is depleted, you are making ketones. When you are making ketones, your MTOR isn't really on in the same way that it is all the time. We can trigger MTOR with exercise, but when we are making ketones, when liver glycogen is depleted, MTOR is kind of off most of the time. So I think that it has to do with intermittent feeding, feeding windows, and you can really check your IGF one. And James and I talk about that on the podcast. If we're thinking about MTOR. In IGF 1, there are two or three metrics that are important to measure. So it would be fasting IGF1 in the morning, which you'd want to see below average because you think average is standard American. We want to see that below average. And I generally do see that in carnivores. I will often see an IGF one less than 100, around 90 or 120. I think the average is 140. You'll see a standard deviation below which they report as a Z score. So you can check your IGF one and you can also check your fasting levels of ketones. So if you wake up with ketones in your blood, you probably triggered some autophagy overnight, which is a good thing. We don't want to wake up with no ketones in our blood every day. That's probably not a good thing or healthy for anyone. Whether or not we're eating a low carb diet or not, if we're waking up with no ketones in our blood, your body really didn't do any house cleaning, at least in terms of liver autophagy and liver triggering them to There's MTOR everywhere, liver, muscle, brain, everywhere. But we can tell when the liver is glycogen depleted because we'll be making ketones and that's different than the muscle levels of glycogen. Right, because we were talking about athletic performance and glycogen earlier. And when we deplete liver glycogen, we'll make ketones, but that we can still have lots of glycogen in our muscles for exertion. So there's a difference in the space there. So what I would say is I don't worry about animal protein consumption or excess protein consumption of animals, even if you're eating a high carbohydrate diet or a higher carbohydrate diet. But we know that a higher carbohydrate diet is really going to activate MTOR and animal protein is going to activate mtor. You're going to get a big push of mtor, which is great if you want an anabolic stimulus, but we probably need to balance that with some periods of lower anabolic stimulus. Whether that's complete fasting, time, restricted eating, or periods of less carbohydrates, we can leverage that all pretty easily. It's a pretty, pretty straightforward switch. The one thing I will add here is that if people are trying to gain muscle, you can do that on a carnivore diet by eating more frequently. I did a podcast with Gabrielle Lyon recently. She's great in the muscle centric literature with regard to or medicine sort of space thinking. She's a pupil of Don Layman and it's interesting. It looks like you need about 2.6 grams of leucine to trigger muscle protein synthesis. Well, we can get 2.6 grams of leucine from whey protein. If we tolerate it, we can get a strict leucine supplement or you can eat about 4 ounces of meat. So if you really want to grow muscle on a carnivore diet, you want to get 4 ounces of meat 3 to 4 times a day or 5 times a day. Now, this is the opposite of what you want to do if you're trying to trigger autophagy. Right. We know that if we're growing muscle, we can't really have both sides of the coin. It's pretty hard to do autophagy and cellular house cleaning and grow muscle. So you can do one or the other. You might be able to do intermittent fasting. You could eat five times a day and then have a compressed window. But you're going to need to eat that triggering amount of leucine, which is about three to four ounces of meat, three to four times a day, to get maximum muscle protein activation and synthesis, and then exercise with resistance exercise. I think you absolutely can with gain weight on a carnivore diet. You can gain muscle on a carnivore diet. I know when Ben was doing his carnivorous diet, he gained a lot of muscle. So next question is.

One big lingering question some of us have. Is the interaction of a carnivore diet with an APOE 4 status any reason to think that Alzheimer's is much less of a concern on this diet than a standard paleo diet high in saturated fat? You guys, this is a big one to unpack. I'm going to try and do it. Let's dig into it. Okay. What is Apoe 4? Apoe 4 is a variant of apolipoprotein E, which is an apolipoprotein that is in the membrane of lipoproteins in our body and is used as a carrier, a transport molecule, for cholesterol, specifically in the brain. APOE is very important because it transfers cholesterol between astrocytes and neurons. So I did a whole podcast about Alzheimer's and APOE 4 and how we don't need to worry about this unless we're insulin resistant with Tommy Wood on my podcast. So if you guys want to go deep on ApoE4, listen to that podcast. Here are the takeaways. ApoE4 is an isoform, a polymorphism in the ApoE4 gene that has been present throughout the entirety of human evolution. The ApoE4 isoform is the most ancestral isoform, meaning that ApoE3 and ApoE2 only arrived on the scene 200,000 and 80,000 years ago, respectively. For the majority of our evolution as humans, we all had APOE 4. And as I suggest in my book, there is very good evidence that for the majority of our evolution as humans, we have been eating lots and lots of meat. In fact, the hypothesis, the premise that I advance in the book, is that it was eating meat that made us human. So to suggest that there is an evolutionary mismatch between eating meat and Apoe 4 doesn't really make sense, evolutionarily speaking, in terms of our history, because we've always all had APOE 4. It would have been not advantageous for humans to have problems with APOE 4 eating saturated fat from animals for the entirety of our existence if this were a problem, because we all have APOE 4 ancestrally. Well, we did. Most of us now have APOE 3, or some of us have APOE 2. But the transfer of cholesterol between astrocytes and neurons in the brain is really important to know about. Why? Because the brain can't really transport cholesterol across the blood brain barrier. It has to make its own cholesterol and then move it between astrocytes and neurons. So what we're seeing in a lot of people with Alzheimer's is that insulin resistance in the brain makes something about that transfer between the astrocyte and the neuron more difficult. That in people who are insulin resistant, ApoE4 works even worse. But does everybody with an ApoE4 polymorphism get Alzheimer's? No. And are there populations in the world who are not insulin resistant, who don't demonstrate an increased risk of cognitive decline with APOE 4? There are, and this is what is so fascinating. So there are two populations that have been studied in detail that I want to tell you guys about. They are the Bolivian Simain, the Nigerian Yoruba, and in both of these populations, where there's a high proportion of APOE4, this genotype, this polymorphism, is protective against cognitive decline. So the studies I want to highlight for you guys are these inflammatory gene variants in the Simaine, an indigenous Bolivian population with a high infectious load. And they said that the carriers of Apoe 4 had lower levels of CRP and IL6, so they had lower inflammation. And there's a separate study in the Semain which shows that they have improved and maintained cognition. There's another one. Apoe4 is associated with improved cognitive function in Amazonian forager horticulturists with a high parasite burden. These are these Bolivian semenae as well. And I will read this. Older adult E4 carriers with a high parasite burden either maintained or showed slight improvements in cognitive performance, whereas non E4 carriers with a high parasite burden show reduced cognitive performance. Being an E4 carrier is the strongest risk factor to date of Alzheimer's and cognitive decline in industrial populations. It is associated with greater cognitive performance in individuals facing a high parasite and pathogen load, suggesting Advantages to the E4 allele under certain environmental conditions. The current mismatch between post industrial hygienic lifestyles and active parasite rich environs may be critical for understanding genetic risk for cognitive aging. So what is going here? The Apoe 4 story is much more complicated than we have been led to believe. We probably had parasite and pathogen exposure for the majority of our evolution, and APOE4 was probably very beneficial and protective against cognitive decline. But what has happened now? We have a new problem, and this problem is insulin resistance. And what we know is that in settings of insulin resistance, APOE4 appears worse. But if we don't have insulin resistance, APOE4 is probably not a problem at all. And not everyone with APOE4 gets Alzheimer's or dementia. But how much of the population has insulin resistance? A huge amount of the population has insulin resistance. If you look online, you'll see estimates 35 to 50%. But there's an incredible study. Prevalence of Optimal Metabolic Health in American Adults National Health and Nutrition Examination Survey 2009-2016. They looked at very interesting metrics of metabolic health. They defined it as optimal level of waist circumference less than 102 or 88 centimeters, respectively, for men and women, fasting glucose less than 100 milligrams per deciliter, hemoglobin A1C less than 5.7, blood pressure less than 120, 80, triglycerides less than 150 and HDL greater than 40 or 50 milligrams per deciliter%, respectively for men and women and not taking any related medication. And how many of the population met these guidelines? Less than 12.2%. In fact, it was 12.2% only met the guidelines. So 87.8% of the population in the United States can be considered to be metabolically unhealthy.

Jesus, man.

Okay, made a stop. Looks like it paused there for a second. All right, 87.8% of the population in the US can be considered to be metabolically unhealthy. This is crazy. If everyone in the U.S. looks like they have insulin resistance, Everyone in quotes like the majority of people in the US have insulin resistance. Of course ApoE4 looks bad, but in populations that are not insulin resistant, APOE 4 can even confer a benefit. APOE 4 is only an issue if we are insulin resistant. Associations between saturated fat and APOE4 are epidemiology. There's no mechanistic data here, guys. And saturated fat is not bad for humans in and of itself. Anyone that says saturated fat is bad is looking at epidemiology. So why is this misleading? The people who are eating the most saturated fat are people who are insulin resistant because what do they eat the saturated fat with? This is why epidemiology is so, so misleading. And we can't rely on this. Can we see other things which make this seem like there's a discordance? We absolutely can. Here's a case study. APOE 4, the door to insulin resistant dyslipidemia and brain fog. A case study. This is so interesting. So this was a 10 week clinically prescribed ketogenic diet with a 68 year old male heterozygous for APOE 4, had a dual diagnosis of mild Alzheimer's disease and type 2 diabetes. So this is someone with insulin resistance, APOE 4 and cognitive impairment. Because he has mild Alzheimer's, he got 10 weeks of a ketogenic diet which is going to be high in saturated fat. Most ketogenic diets are. And what happened? Cognitive improvements happened and insulin resistance got better. So there is no problem eating saturated fat from animals or coconut or anything with Apoe 4 in the setting of insulin sensitivity. It's only because the entire population looks insulin resistant that we see these associations between saturated fat, insulin resistance and APOE 4 and Alzheimer's dementia. If we can remain in the part of the population that is exclusive, that is elite. This is the Ben Greenfield crew. This is my crew. We are insulin sensitive people. We have all those metrics. We have low fasting insulin, we have regular blood pressure, normal hip circumference. We do not look like the rest of the population. And there is no real good mechanistic or interventional data to suggest that increased consumption of saturated fat with Apoe 4 is a problem. So eating carnivore with Apoe 4, no worries. Your ancestors have been doing it for millions of years. And it's protective in that situation, probably especially if you're out hunting or you're exposed to pathogens or parasites, we're not exposed to that much. But in those situations, in the absence of insulin resistance, there's good evidence that APOE 4 is protective. And in that case study, a high saturated fat ketogenic diet for 10 weeks improved cognitive function in somebody heterozygous for ApoE4. And guess what? Their Insulin resistance got better too. So this is a really, really important point that cannot be emphasized enough and has been widely misunderstood. The association between saturated fat and problems with APOE4 is epidemiology, and it looks like that because 87.8% of the population has insulin resistance. So if you don't have insulin resistance, you're elite and you don't have to worry and you can eat the way your ancestors have been eating, which is carnivore and carnivore ish. The last thing I want to say about ApoE4 is a study. ApoE genotype influences insulin resistance, apolipoprotein C2 and C3 according to plasma fatty acid profile in the metabolic syndrome. Basically what we see here is that people who have APOE4 appear to be more susceptible to insulin resistance. APOE4 is a genotype that makes us much more susceptible to developing insulin resistance when we have a discordance between environment and genetics. This is what I talked to Tommy about. It's probably a susceptibility to getting insulin resistant when we eat standard American meals or combine too much fat and carbohydrate. If we eat in an ancestral way, then we are not going to be affected negatively from APOE 4. But if we have APOE 4, those people look to be more insulin resistant in a standard American diet context. And we can avoid that by living in a way that's consistent with the way that our ancestors were, which is non processed food and I believe mostly animal foods. So let's move on and talk about fto, because we're talking about the two genes here. FTO is the fat mass and obesity gene. And there's a specific polymorphism in this gene that many of you may know about if you have tested your.

Genetics with 23andMe RS9939609A allele carriers have a higher risk of being overweight or obese in population studies. And this is where things come from with fto. And the saturated fat association with FTO is based on, say it with me. Epidemiology. It's based on epidemiology. So the study it's based on is high dietary saturated fat intake accentuates obesity risk associated with the fat mass and obesity associated gene in adults. So the question I got was what about doing a carnivore diet with FTO mutations? The standard thought is to limit saturated fat and get more fat from olive, avocado, etc. Or perhaps to get less fat. And the person also asks, and also the idea if you're an overmethylator. Should you avoid lots of meat? So I'll address both of those quickly and we'll move on. We've already done a lot in this podcast today, guys. Basically, I don't think there's any problem with saturated fat and fto. And I will illustrate this with my case and Ben's. Ben sent me his genetics, and guess what? Ben Greenfield is homozygous for the A allele at that RS location on the ftog, Ben has an FTO polymorphism that predisposes him to obesity. Well, guess what? Ben usually eats a lot of saturated fat, and I eat a lot of saturated fat, too. Animal foods are about 45% saturated fat in the fat. They're not all saturated fat. They're mostly Mono and about 45% saturated and a little bit of polyunsaturated. So we're getting a mix of fats and animal fat, whether it's tallow or suet or whatever. Coconut oil is about 85% saturated. It's a little different chain length. We're Talking about Palmitic versus Lauric versus Myristic, depending on the C14, C16, C18, how many chains are in it. But in terms of pure saturated fat biochemistry, coconut oil is higher saturated fat. So Ben eats a lot of coconut oil. Ben eats a lot of saturated fat from animal foods. In fact, Ben provided a chronometer for one of his days, and this was December 27, 2019, and on this day, Ben ate 46.2 grams of saturated fat. Ben is not obese. I am not obese, and I eat. I probably ate double that amount of saturated fat. So the FTO polymorphism is widely misunderstood, and I don't think we need to worry about saturated fat and obesity in any way, shape or form. On a carnivore diet, if we have an FTO polymorphism, I think what we're seeing here is insulin resistance and the fact that the epidemiology is so misleading because what do people eat with saturated fat? Well, first of all, where is the most of the saturated fat in the diet coming from? From people in the standard American diet. It's probably coming from either it's being counted as saturated when it's actually trans, or it's junk food, or they're eating hamburgers with French fries. In the podcast I did with James Clement on mtor, we talked about this in detail. There's actually, there are studies that show the people who eat more animal products eat more of everything. So this is what's so misleading about epidemiology with animal products. People who eat more animal products eat more bread, they eat more vegetable oils, they eat more processed carbohydrates. How can we say it's the animal food? Why are we blaming meat for what the bread did, or the processed vegetable oils did, or the oxidized vegetable oils did? This is what's so hard to tease out of epidemiology. We can only generate hypotheses. But if Ben and I are any indication, two individuals who are eating a lot of saturated fat with homozygous polymorphisms for the A allele at that locus on the FTO gene having no obesity. This is much more complicated. FTO is a gene that has important roles. If they do knockouts in mice, it's a real problem. It's involved in RNA processing, I believe. So FTO doesn't just exist to make us fat, but it's important to know that the associations between this are all epidemiology. And we must not be misled by this. There's not an interventional study. If you guys are curious what Ben ate in a day, he has a grilled ribeye, he has Wild Planet Sardines, he has a cup of canned pumpkin, GTs coco yo living yogurt, Brazil nuts, vital proteins, collagen, creatine. He's got some red wine, a little dark chocolate, chlorella, olive oil, Primal Kitchen mayo, sea salt, some organifi juice, some more Wild Planet Sardines and a baked sweet potato kettle and fire bone broth. And he walked some. He did some other exercise. Now maybe this is a good segue for what I eat in a day. It's similar to Ben, but it's different because I don't eat any plants right now. So this morning for breakfast I had about 16 ounces of grass fed organic steak from White Oak Pastures. I also had about, I would say 85 to 90 grams of suet, which is kidney fat that I mix into a bone broth that I made myself. And then I had about four or five raw egg yolks, which are soy and corn free. They're organic pastures egg yolks with a good amount of salt. I probably had about 5 grams of salt this morning for breakfast. So that was my breakfast, that's my carnivore breakfast. And then for lunch or dinner, I'm only going to have two meals today. I'm going to eat in about a six to seven hour window. I'm going to have about the same. I'm going to have about another pound of meat. I'm going to have two, two ounces of liver, maybe two ounces of kidney. I've got some brain in the fridge. I know you guys are all going to get all grossed out about that. I usually get lamb brain. I've got some brain in the fridge and I've also got some heart that I'm going to cook up tonight. And I'm probably going to have about another 80 grams of suet or trimmings with dinner and a little more bone broth and salt. It's going to vary for me day to day. Sometimes I'll eat chicken, sometimes I'll eat fish. I do try to select low mercury fish. Sometimes I will eat turkey or bison or other meats, but I'm eating animal foods. I'm getting calcium to balance the protein and I'm thinking about getting organs and I'm going about 1 gram of protein per pound of body weight and about 1 to 1 fat to protein, so hopefully that helps. And I appreciate Ben very much providing his chronometer and sharing with us all that stuff. So the FTO stuff, do not worry about this, you guys. This is just epidemiology, which is quite misleading. And there are many people who are extremely fit eating tons of saturated fat. Saturated fat does not cause obesity directly. Don't worry about it. It's good for you. The last part of that question that I want to address is the overmethylator part. I don't believe in over and undermethylators. I think we have genotypes that affect our MTHFR status. I did a whole podcast with Ben lynch where I talked about that and I am mthfr homozygous@677ct, which means my mthfr enzyme only functions at about 40 to 35 to 40% of normal, maybe less. But what has been shown in multiple studies is that if I eat enough riboflavin, then my homocysteine will normalize and that MTHFR functions normally. Riboflavin is the key. We also need folate, not from a folic acid supplement, but from food. We need B6 and we need B12 and we need enough riboflavin. Well, where do we get riboflavin? Organ meats and heart, these are the best sources. You really cannot get enough riboflavin. You'd be hard pressed to get enough riboflavin from steak. Organ meats are much richer, specifically liver and kidney and heart. So you really can't get a whole lot of organ Meat. Excuse me? Riboflavin from plants either. You probably need 2 to 3 milligrams of riboflavin a day to have your MTHFR work. Normally, I don't supplement with L methylfolate and my homocysteine is consistently 7. It's been as high as 14 in the past when I didn't have enough riboflavin in my diet. And I've lowered it by taking L methylfolate. But I don't like to take methylfolate because it kind of messes with our biochemistry. I would much rather get this from food. Good luck getting that amount of riboflavin from plants because you can only get that in like a pound plus of broccoli. A pound of broccoli. That's an insane amount of broccoli to get that much riboflavin, maybe even more than that. And then you're going to have all the isothiocyanates, etc. Etc. So another question that someone asked was, what do my labs look like? I did a whole podcast about labs on my podcast. You guys, my labs look great. I check them all the time. Somebody said, oh, Shawn Baker's labs don't look good. My labs look nothing like Sean Baker's. I do not eat a carnivore diet like Shawn Baker. He's a good friend of mine. But we do not see eye to eye in terms of nuance in a carnivore diet. I'm not overeating protein, I'm balancing with fat and I'm eating organ meats. So in terms of basic labs, my inflammatory markers always very low. I've had CRP less than.03, HSCRP less than 0.03 times 7 over the year and a half that I've been doing a carnivore diet. I've checked F2, isoprostane, creatinine ratio, myeloperoxidase, ferritin and other inflammatory markers, and they're all very low. None of them are elevated. ESR, etc. Fasting insulin usually runs around 2, GGT is around 12, AST and ALT are around 20. What else? My hematocrit is fine. My other liver enzymes are normal. I talked about AST, ALT, GGT, alkaline phosphatase, my serum bicarb is 24, my urine pH is 6 to 6.5. Trying to increase that with even more bone broth. My serum calcium is normal, my BUN is normal, my creatinine is normal. I've checked cystatin, C as well, multiple times, which is another measure of function. What else have I checked? My thyroid hormones are all normal. I've checked TSH free T4 free T3 antibodies, all within normal. So basically, I've also checked urinary and blood levels of mercury, cadmium, arsenic and lead. They're all very low. I keep an eye on those. I've done gut flora stuff. In the first podcast that Ben and I did, I talked about this. My microbial diversity is very high. It's in the 85th to 90th percentile. When I did this a few months ago. So the idea that we need plant fiber to increase the microbial diversity is false. I've talked about on other podcasts. I won't go into that here today. Then the cholesterol is interesting, right? I've done many podcasts on my podcast about the fallacy of looking at LDL myopically. We have to interpret lipids in the context of insulin sensitivity. And I think the most accurate measure is triglyceride to HDL ratio. Mine is usually 0.5, meaning that my triglycerides are usually about 45, and my HDL is usually about 90 or 95. So that, I think is a very good indication. Do LDLs rise on a carnivore diet? Yes. Do LDLs rise on a ketogenic diet? Yes. Acetyl, COA and ketones, cholesterol and ketones share a common pathway in biochemistry. And I see this all the time I talk about in my book. I don't think high LDL in the setting of insulin resistance is a problem. It's nuanced. I have a whole huge chapter on it in the book. But basically, if we stratify studies like Framingham and look at insulin sensitivity with HDL as the metric, there is no correlation between rising hdl. Excuse me, rising LDL if you have a high HDL and cardiovascular disease. So I'll say that again, no correlation in the Framingham study, when we stratify by L hdl, when LDL rises, there is no increase in cardiovascular disease risk. If HDL is high as a proxy for insulin sensitivity, Again, triglyceride to HDL ratio would be a better proxy. But in terms of that metric and a Framingham study, which I've done in my book, I stratified them all and show you that there's a difference there. There is no correlation. So it's a quite nuanced thing, but I really believe that in the setting of insulin sensitivity, if we are in the 12.2% of the population that is insulin sensitive. LDL is probably protective and there are many studies which show show that as we age, the higher the LDL means we live longer. Probably because LDL has many important immunologic roles. So I'd encourage you to listen to all the podcasts I've done on cholesterol with Dave Feldman, Nadir Ali, my Lipid podcast, or the podcast where I detailed all of my labs in detail. You guys, there is a veritable goldmine on my podcast. I've discussed all of this in detail previously, so I want to run through the rest of these questions as we wrap up here. What's the minimum time to be on the diet to see if it's helping my ailments? Can I do cheat days? I'm going to loop these together. I'm not a fan of cheat days because I think it positions the cheat foods as reward and I think we should need to reframe food as abundance no matter what we're eating. I would say that if we are eating animal foods, we are eating the best foods on the planet and I don't think we should position junk food as a reward food. I'm not a fan of cheat days and cheat days are going to interrupt any immunologic progress. A lot of what's beneficial about a carnivore diet is from an immunologic perspective and the removal of triggering foods. If you cheat every week, you're never going to give the immune system time to rest. And so I recommend people do at least 60 days on a carnivore diet. In the book I talk about a clean carnivore reset, like a clean carnivore cleanse. Give it at least 60 days with no cheats to let the immune system calm down to really know how you're going to feel if you do five days and then eat something else. It's kind of like it is with celiac disease. If you trigger the immune system every five days, you're never going to get it to be quiescent. The immune system has a memory and it's about 21 days if we're thinking about the four and a half or if we're thinking about the half life of an IgG antibody. So some people would even say that you need more than 60 days, perhaps 90 or 120 days if we're going to think about it from a pharmacokinetic perspective. Four and a half half lives to get rid of IgG antibodies. So that means if you eat a food generate an IGG antibody to it. It's going to take four and a half lives, four and a half times 21, to get that antibody out of your body to get that reaction stopped. So if we have eczema or any inflammatory disease or joint pain that's related to a food trigger, we need to get rid of that food for probably 90 to 120 days to get the full immunologic quieting. So at least 60 on a carnivore diet and cheating is going to interrupt that. I think cheating is going to position those junk foods as reward foods. That's just going to sabotage our efforts long term. And I'm not a fan of that at all. Somebody said, would I recommend eating chicken? What about eggs? I think chicken is fine. I think chicken is generally less fatty, it's very lean and I think it's less nutritious overall, though dark meat chicken is quite high in vitamin K2. Animal foods in general are very high in K2. Do not be misled by stuff online that says that animal foods are low in vitamin K because they are only measuring vitamin K1, which we know is nowhere near as effective in cardiovascular disease prevention, at least in epidemiology studies like the Rotterdam study. What about eggs? I think eggs are fine. I prefer the yolk only. I don't do the white. I think I react to the albumin and the egg white and I'm not a fan of that at all. I think it triggers a lot of people. Are there any animal parts or groups of animals that are best avoided for consumption? I would not eat adrenals. Adrenals are very high in vitamin C, but they are also going to have many glucocorticoids in them and can cause problems. And I would be very careful with adrenal desiccated supplements. I talked about my diet.

And they asked if I take any supplement with anything ever. I have in the past. I don't now. Unless you consider salt to be a supplement. But I make my own bone broth. I don't take any, any mineral supplements beyond sodium chloride, which is a rock salt from the earth. I don't take magnesium, I don't take potassium. I don't take anything else right now. I get the boron from the bone broth and I use spring water from a good spring nearby. So I don't take any supplements right now. And I don't have scurvy. My gums are fine every time I've checked my inflammatory markers. I've also checked things like 8 hydroxy 2 deoxyguanosine lipid peroxides normal on a carnivore diet. So that looks good to me. Somebody said I've heard some women have trouble keeping their cycle regular on a ketogenic diet. They need to incorporate refeeds periodically. Would a woman going on a carnivore diet need time for her body to adapt to the acute stress of fat adaptation for her cycle to become regular again? Why would a woman's cycle become inconsistent on a ketogenic diet? Would consuming thyroid help? Also, is a carnivore diet advisable for pregnancy, breastfeeding and children? So many questions here. I think that if women are having menstrual irregularities on any diet, there's something that's a little off. A lot of times on ketogenic diets it might not be enough protein or it could not be enough calories. I recently released the podcast with Jamie Seaman. We talked all about women's hormones. There are many examples of women with PCOS and insulin resistance related menstrual irregularities having significant improvements on low carbohydrate diets like Carnivore specifically. So it's not going to destroy the period. You don't need carbs to menstruate. I think you need to give your body a fed state signal and that comes from adequate calories and adequate protein. You need your glycogen source to be full from time to time. I don't think you want to deplete your glycogen in your liver all the time. You need to give your body enough calories and enough protein, which is I think you'll get fine if you do 1 gram of protein per pound of body weight and about 1 gram of fat fat per protein. Obviously it's going to be individual based on your goals and women need to know that if you're trying to lose weight, caloric deficit will affect hormones negatively. In the short term. It's okay, you want to lose the weight and that's a good thing. But if you're trying to lose weight and you're purposely creating a caloric deficit that is going to affect hormones negatively in general. So there's a lot of things wrapped up in this. I think that those are the main answers for why a women's cycle may become irregular on a carnivore diet. I don't believe there's an absolute necessity for carbohydrates. There are many women that I know and have spoken to on the podcast who do low carbohydrate diets who cycle regularly. Jamie Seaman, this OB GYN is one of them. There are many in the community that don't have any problem with this at all. So I think it's individual. It's probably absence of adequate calories or protein. I don't think any thyroid for that. And I also don't think that there's any solid evidence that we need carbohydrates to make active thyroid hormone. We need insulin maybe, and we need glycogen or we need to signal that we're fed, which we can get with enough protein. But there's. Even though fasting insulin is low on a carnivore diet, there is still a postprandial insulin release. It's not that insulin completely goes away on this type of a diet. And the last one is also is a carnivore diet advisable for pregnancy, breastfeeding and children? So I think it's absolutely fine. I'm not going to be strict about it. I know a lot of people who feed their kids mostly carnivore and then give them some squash and they do carnivore ish on other days or a little honey as treats. I think carbs are fine for kids. I think kids are going to crave carbs if we give them to them. I think animal foods are more nutrient dense than carbohydrates and should be the foundation of a diet for a child. But their carbs are okay from time to time, if you want. Having said that, I don't think we know whether kids need carbohydrates. I think we can get the same fed state signal if we give kids enough protein and calories. But we're still learning and I think it's the same for breastfeeding. As long as a breastfeeding mom is getting enough calories, she'll be fine. I don't think there's an absolute need for carbohydrates in the human diet at any stage of the lifecycle. But I'm open to all of this and I think it's a fascinating discussion and it's individual. I also don't think that carbs are necessarily damaging at any stage in the lifestyle. We just need to know what our goals are. For a lot of people, carbs bother their gut if they have overgrowth, etc. Things that come with the carbs. I think that it's probably going to be obesogenic if we combine carbs and fat if we are eating excess calories and liver glycogen is Full, we will get a signal to do de novo lipogenesis. Carbohydrates may get turned into fat, although that's nuanced as well. I don't think that's a good thing. I would not. Overeating carbs and fat together is going to make us obese probably regardless, so we should be careful of that. But I don't think carbs are necessarily bad. I function better without them and I don't see a decline in any performance because I'm eating enough protein. Presumably my glycogen stores are full. This goes back to the previous discussion of glycogen in athletes, etc. So hopefully that helps. Alright, two more questions and we'll wrap it up here. This is a long one. If you guys held on this long, you are champ. So the first question is about phospholipid forms of dha. And the person asking the question cites a study which shows no statistical significance between them. In that study there is a trend toward increased absorption of DHA in the phospholipid form. We have a special transporter in our gut that pulls in the phospholipid forms of omega 3s that can actually form a micelle. So it's a much easier way to absorb them. So if you look at the studies, there are studies which show equivalent levels of omega 3 raising or equivalent levels of omega 3 when krill oil supplements are used at much smaller doses than fish oil supplements, which are usually ethyl ester or triglyceride forms. I think there's lots of evidence that phospholipid derived omega 3s are much more absorbable and much more utilized in the brains. Some of the studies were done in piglets, but presumably it's the same. And there's actually a special transporter called MFS2DA in the brain that pulls phospholipid omega 3s into the brain. So where do we get phospholipid omega 3 in food? The omega 3 in salmon and salmon eggs is phospholipid. When we take it out of salmon and we make it into triglycerides or ethyl ester, they're processing it and I think it's much worse. In fact, I am not a fan of omega 3 supplementation outside of food because it's often very highly oxidized. I think Omega 3 is something we're learning a lot about. I don't think we actually know what the ideal ratio of three to six is. Clearly we need some three and we do not want to have an excess of oxidized 6. And I think that if we get 2 much 6 in our diet, it's a problem. There's evidence that LDL that's enriched in linoleic acid, which is the main Omega 6 might be more highly oxidizable. And I think that a regular reasonable amount of omega 3 from pastured animals is going to be fine. I get the majority of my omega 3 from pastured egg yolks and probably some from grass fed animal fat, but I don't take a fish oil supplement. I will occasionally eat fish and seafood, but that's where I get my Omega 3 from. And I think it's fine on the labs that I've done on myself. When I check my omega 3 index, it's about 6, which is a sum of EPA and DHA. Some people will use DPA in there as well. So docosa pentaenoic acid in the omega 3 index. But when I've looked at my metrics for fatty acids on the diet, I have pretty low omega 6, pretty robust levels of omega 3, kind of in the middle 7 to 8% of the omega 3 index and then higher levels of saturated fat because probably because I have more in my diet and I think that's fine. I would not recommend getting Omega 3 from supplements. They're highly oxidized. I think we should get it in our food and we also don't need to over consume. I don't think we should over consume omega 3s, you guys. It creates a big stress on the body to keep those polyunsaturated fatty acids from becoming oxidized. We need some, but I think we can get it from food. Egg yolks, grass fed animal fat is fine. Occasional seafood. I think you'll be fine on omega 3s. I would not recommend supplements. So I think it's pretty clear that the majority of the omega 3 that we should be getting is from a phospholipid form, whether it's salmon roe or whatever. I like salmon roe because it will give us Omega 3 in a concentrated form without as much metal deposition. Because it's a concentrate, you can get like half a teaspoon of salmon eggs, has a lot of DHA and the phospholip form way better than a processed krill oil supplement. And you're getting a, you're not getting really any significant amount of metals because you're eating such a small amount. I don't think everybody needs to eat salmon roe. I don't think you need it all the Time. I think it's an ancestrally treasured food that we should be aware of and it's quite valuable. Okay, last question. We're going to wrap it up here. Where is the evidence that cruciferous vegetable consumption at any remotely normal level causes hypothyroidism? This is an interesting question, you guys. So I think that there are tons of studies throughout the world, if you're curious. There is a paper called endemic goiter iodine deficiency disorders. Again, we'll link to. Is well known throughout the world that in regions in which people consume goitrogenic foods, specifically cassava and foods with large amounts of isothiocyanates, of which there are many, even beyond sulforaphane, that endemic goiter is common and is a problem. So what is going on here? Isothiocyanates do impair absorption at the level of the thyroid. This is not debated, but this person is making a very good point. Are isothiocyanates a problem or sulforaphane a problem? And I would say that we need to widen our lens to think about isothiocyanates. Is this a problem if we have enough iodine? I think if we're getting lots of iodine, it's less of a problem. But what else are these compounds doing in the human body that is damaging? And we know that they are interfering with the thyroid. I think we need more research here, but I want to highlight a few research articles that I have found for my book. I go into detail on this. I have a whole chapter on isothiocyanates. So concentrations of thiocyanate and goitrin in human plasma, their precursor concentrations in brassica vegetables, and associated potential risk for hypothyroidism. Again, we'll link to this study. What they found was that collards, Brussels sprouts and some Russian kale contained significant goitrin to potentially decrease iodine uptake by the thyroid. So goitrin is another isothiocyanate that I haven't really talked about before. It's different than sulforaphane, but they say radioiodine uptake to the thyroid is inhibited by 194 micromol of goitrin, but not 77 micromol of goitrin. So they're saying that collards, Brussels sprouts, some Russian kale, actually contain amounts that are enough to do that. They say, however, turnip tops, commercial broccoli, broccoli rabe kale belonging to the Brassica oleraceae contain less than 10 micromol of goitrin per 100 gram serving and can be considered mineral risk. The problem is that all of these are contributing a little bit and it will be have to be interpreted in the context of our overall thiadine thyroid health and iodine consumption. So the question is why would we purposefully consume something that is inhibiting iodine uptake of the thyroid? This is clearly a negative toxic mechanism for sulforaphane and other isothiocyanates. I don't think there's a benefit to these in humans. And a lot of the time we're cooking them which may degrade some of these. Fermentation of these plants will degrade the glucosinolates which, which are the precursors like glucoraphanin for sulforaphane. But this paper is quite interesting because it shows that some of those foods have another isothiocyanate called goitrin, which can be a big deal. And the other concern I have or this study is interesting, this is a study in Melanesia, the role of dietary iodine and cruciferous vegetables in thyroid cancer. A countrywide case control study in New Caledonia. They found high consumption of cruciferous vegetables was associated with thyroid cancer among women with low iodine intake. In terms of anthropologic surveys, or at least population surveys, it's well known to do this. In the book I mentioned multiple other studies that talk about cassava doing this as well and being a goitrogenic compound. I'll mention a couple other studies. The estrogenic effects of extracts from cabbage, fermented cabbage and acidified brussel sprouts on the growth and gene expression of estrogen dependent human breast cancer cells. MCF7 cells.

You can basically get that from the title. But it says study demonstrates that cruciferous vegetables act as bifunctionally like an anti estrogen at low concentrations and an estrogen agonist at high concentrations. There's a lot going on here. These compounds appear to be affecting estrogen signaling as well as in humans. One other study that I think is quite interesting. A couple more here. The genotoxic effects of crude juices from Brassica vegetables and juices and extracts prepared from phytopharmaceutical preparations and spices of cruciferous plants origin in bacterial and mammalian cells. They said in sister chromatid exchange assays, positive results were measured with juices. The genotoxic effects seen in mammalian cells were paralleled by a pronounced decrease in cell viability. What they found was that in bacterial assays all Juices caused genotoxic effects in the absence of metabolic activation. The ranking order being brussels sprouts, greater than cabbage, greater than cauliflower, green cabbage, kohlrabi, broccoli, turnip, black radish. So basically it has to do with the amount of these broccoli extracts, which could be potentially genotoxic in humans and others. One more genotoxicity studies of organically grown broccoli and its interactions with urine. Excuse me, urethane methylmethane sulfonate and 4 nitroquinoline 1 oxide genotoxicity in the wing spot test of Drosophila melanogaster, which is a fruit fly.

The fresh market broccoli juice extract produced a damage increase in the wing spot test in Drosophila. So I guess what I'm saying here is that I am not convinced that broccoli and brassica loves us. I think that kale doesn't love us back. I think that occasional broccoli and people who have adequate source of iodine might be okay. But I think it's very clearly a food that is encouraging us not to eat it. And it has been shown to inhibit absorption.

Iodine at the level of the thyroid, specifically the goitrin sulforaphane appears to do this as well. I think we need more studies there. And then the other compounds are estrogenic and genotoxic in some assays. So these are not foods we should have in our diet, in my opinion. I don't think they give us anything that we can't get from animal foods. But there's a whole chapter on isothiocyanates in my book. All right, you guys, I'm going to wrap it up. This was a marathon. I think we did a lot of great stuff today. I appreciate you all listening to this one. Check me out. My website is CarnivoreMD. You can subscribe to my newsletter there. All of my social media is there. I'm linked on Instagram and Facebook and all that stuff. It's all CarnivoreMD. I got a book coming out in February. It's called the Carnivore Code. You guys, this is my opus. It's, it's 400 pages. It's 650 references. It's got graphics. I know the carnivore diet is controversial. I try and always show up with lots of science and that's what I tried to do in this book. It's also very practical. It has how to do the carnivore diet. And I can't wait to get it into your hands, to get into Ben's hands and to share it all with you guys very, very soon. Thank you for listening to this podcast. Check me out on my podcast, which is Fundamental Health. And I can't wait to talk to you guys soon.