Steak & eggs?
Try liver, kidney, heart, & bone marrow. A meat-only eater, Dr. Paul Saladino specifically recommends a "nose-to-tail" carnivore diet over the traditional focus on muscle meat.
Dr. Paul Saladino is a leading voice on the science and application of the "nose-to-tail" carnivore diet. He has used this diet to reverse autoimmunity, chronic inflammation, and mental health issues in hundreds of patients, many of whom had been told their conditions were untreatable.
Dr. Paul Saladino, really great to have you in the program.
Good to be here. Thanks for having me on.
I first got on to your program and your podcast and a lot of your YouTube videos from my friend Brian, who's one of our investors at H.V.M.N. He's been one of my favorite biohacking human performance star partners exploring diet, different exercise with different devices and gadgets. As our regular listeners know, we have a lot of the carnivore thought leaders on the program. We've had Shawn Baker and Mikhaila Peterson and Travis Statham and that crowd. I found that one, there's more and more evidence believed upon the carnivore diet.
Two, I thought that your articulation, your data, your way to presenting that that corpus is very, very compelling. It's succinct and compelling. Really fun to have you on the program and talk about all of that.
Thanks, man. It's been a fun journey. It's been a really, really cool rabbit hole to go down, for sure.
Maybe as a quick brief, it would be helpful to get a sense of how long you've been on the carnivore diet and your journey from, I presume more of a standard American diet or standard Western diet and how quickly that you go from a standard diet to this nose to tail carnivore that you've really been a proud exponent of.
I've been on a nose to tail carnivore diet. We can define that later on in the podcast for a year solidly right now.
Zero plant products for a solid year at this point. Prior to that, I had espoused a organic Paleo diet for quite a long time. 12 years, I was organic Paleo. I thought that was a really good incarnation of diet. I still think that's a very good incarnation of my dietary plan. One of the things for me was that I had eczema. It was on my elbows, on my knees. At certain times, in medical school, it got worse. It caused impetigo, which is a super infection of the skin. I got septic at one point. It was just continually clear to me based on my recurrent flares of eczema over that decade on an organic Paleo diet but something was still wrong.
My immune system was still being triggered in some way. I kept trying to refine it and I kept trying to take things out. I kept trying to think about it. Is it histamine? Is it oxalates? Is it this? Is it that? Is it lectins? I had various experiments where I would do low lectin Paleo and then low histamine Paleo and then low oxalate Paleo and then I did them all at the same time. The eczema still continued. Perhaps, it would get better and wax and wane at times, but I would still have it from time to time. I thought is it dairy? At that time, I wasn't really hip to the idea of A1 versus A2 but I tried no dairy.
I incorporated dairy back. Anyway, the iteration continued around the idea of what is going on with my body? Because I think that unlike mainstream Western medicine, when I see something like that, I think there's something out of balance here. My immune system is still triggered and I need to correct it because it's going to have other effects elsewhere in my body. That was eventually how a light bulb went on and the carnivore diet became my focus. I heard Jordan Peterson on Joe Rogan talking about his daughter, Mikhaila. Her autoimmune issues, his autoimmune issues and there were improvements from this meat diet. My first thought was that is crazy.
I think it's most people thought because we come up against so much conditioning when we're talking about these types of diets and so much narrative connected with the idea that we've always been told that plants are so good for us. As I thought about it more and more, I thought, okay. This actually makes some sense. Perhaps, there is something triggering autoimmunity in myself with this diet. I dove into it and as I got deeper and deeper into it and quickly saw that it was creating really good results for me and started using it in some of my clients and then started reading more about the anecdotes and the case studies that were happening with the carnivore diet.
I thought, well, this is the beginning of something really big. This is just the tip of the iceberg but there are so many questions. Because when you tell people or you suggest that eating animals nose to tail is an ideal diet or one of the optimal diets or perhaps the optimal diet for humans, you run up against so many long held notions. That this is cannon in nutrition. Over the next few years, I just can't wait to see what happens in nutrition. I think that as the carnivore diet gains momentum and gains scientific reputation and backing, we certainly may have to rewrite the nutrition textbooks. It's a crazy potential. It's going to be tectonic.
Not to make this overly dramatic but I think there's something there. I remember a year ago is I think when more and more people were thinking what the carnivore diet. It was visceral gut punch to most people. They're like, "What? You're insane." I think within relative in the last month or two or some recent conversations, I think people are trying to be more and more open with it. Perhaps, I think it would be a good way to start the conversation around being good scientists and assuming or not assuming a null hypothesis. Let's just assume that the traditional nutritional guidelines are correct and go down the list of some of the major critiques of the carnivore diet.
One piece of literature or a corpus of literature is around epidemiological data around how red meat is associated with elevated cardiovascular disease risk and increased mortality. How do we address that? How do we debunk that broad epidemiological point?
We see those epidemiology studies almost on a daily basis now. It's interesting. It used to piss me off and now, it just makes me excited. Because I think, okay. The more fuel for the fire. It's going to be a big bonfire when this goes up. Because there's lots and lots of detractors and lots and lots of people who are arguing against it. I think when people realize that there's merit here, it's going to be a really big, warm, bright fire that's going to be historically quite memorable. The epidemiologic data is intriguing. I love that you bring this up to start because I think it's so important to keep examining this for people who are listening.
Most of your listeners will be familiar with the details of these studies and will understand that these are epidemiology rather than interventional studies. Oftentimes in the mainstream media, there's a great disservice here because the mainstream media just says one half a serving of red meat per week decreases your life expectancy by this much. These sensational headlines, there's no discussion of how they're arriving at that postulate or what's going on there. It's really misleading to the public, so much so that I would argue it's pretty much propaganda at this point. It's quite disturbing. As your listeners will most likely know, these are not interventional studies.
This is not a study where they gave people half a serving of meat and followed them for 50 years. It's nothing like that. In fact, it's nothing even close to that. These are studies that are based on surveys and they're food recall. They can be prospective or retrospective. Meaning, the investigators asked people what they eat and then they follow them in five to 10 years. Most of these studies are done on a retrospective basis, which means they look back at mortality and people's lives and the quality of their life. Usually, they're just looking at mortality ratios or death rates. They'll say, "What did you eat? What things do you include in your diet?"
They're all based on memory, number one, of what we eat. They're trying to distinguish whether it's like, "Oh, you're eating more eggs? Therefore, you're having more atherosclerotic coronary vascular disease." That was a big one. That came out a few years ago. You're eating more bacon and then you have more of these diseases. The first problem is that these are recall studies, which we know are inherently flawed. People don't have a great recall to the amount or the types of foods they've eaten.
Do you even remember what you ate for breakfast or what you had for lunch yesterday? People don't really even know.
Two weeks ago. These are asking in the last 10 years.
If they're doing a prospective study, they'll ask someone, "How are you eating now?" Then they'll follow them five to 10 years later or two or three years later. How they might have been eating then might not reflect how they're eating now. The whole basis of these studies is flawed. Oftentimes, we'll say, "Oh, it's the best we've got," but it's not really that good to begin with. There's a much discussion around the basic garbage nature of epidemiology in the fact that it's really not that valuable. I think the problem with epidemiology is that it was designed to generate hypotheses. Those hypotheses were supposed to be tested with interventional studies.
Now within Western medicine, we're using these hypotheses generating studies as cannon. That's a huge mistake. The other thing that happens with these studies and there is a large body of epidemiological literature to associate increased consumption of red meat or animal products with increased cardiovascular disease and shorter life span. That is not able to be argued. However, that is primarily within Western cultures. The idea here is that this is probably or potentially reflecting healthy user bias. When we're looking at epidemiology, we cannot infer causality. Correlation is not equal to causation.
A correlation between an increased consumption of red meat and a shorter life span does not mean that red meat causes a shorter life span. In many of these studies, we also do not know in which direction the arrow of causality may go. This is something we could talk about with regard to the epidemiologic studies with TMAO or Trimethylamine N-oxide, which is something that people love to criticize in a carnivore diet about.
Yeah. I just want to bring that as point two but I'm glad we're touching on that.
The idea of correlation not being causation is something that probably will not be foreign to your listeners but yeah. You can associate all kinds of things that are clearly not related.
There's a great association between the amount of cheese people eat and a number of people that die getting tangled in their bedsheets. There's a great correlation between Nicholas Cage movies per year and the number of deaths by homicide. There are all sorts of correlations out there that may not be causative. Do we think Nicholas Cage is causing violent homicide? Probably not. Is cheese causing death in the sheets of your bed? Probably not unless you're eating cheese in your bed but it's unusual.
This is the problem with epidemiology is it requires so much intellectual archeology and so much digging to really say, "What are we looking at here? What do these statistics actually show us?" We can get some clues by looking across cultures because if we look at epidemiology surrounding meat and longevity or meat and cardiovascular outcomes or meat and cancer in Eastern cultures, specifically in Asia, we see a very different picture than we do in the West. In fact, the people that eat the most meat in Asia live the longest.
They have the lowest rates of cardiovascular disease if we're looking at populations of men and they have the lowest rates of cancer if we're looking at populations of women. How does that jive? How could red meat be toxic in the West and then it's actually health food in the East? We could make arguments about the quality of the meat in different places but presumably, it's essentially the same. It's not that much different that it would in one place kill you swiftly and the other place actually be helpful for humans. The more likely explanation is, this is all around narrative.
This is the James Dean concept that we've been told in the Western United States or the Western world that over the last 70 years that if you eat red meat, you're doing a rebellious thing. You are doing a bad thing for yourself. Who eats red meat? People who have very dangerous behaviors or more rebellious behaviors, these are the James Dean types. The people that smoke, drink, they exercise less. They have often a lower socioeconomic status and they're more likely to engage in poor health behaviors or not engaged in healthy behaviors. Getting out of the sun, exercising, things like that.
There's a really interesting study called the UK Shoppers study, which illustrates this very clearly. In this study, I'll back up for one moment. If we look across populations of the Westernized world, people will often say, "Vegetarians have the longest life expectancy. Vegetarians have lower all cause mortality." That may be true relative to the general population. What was so cool about the UK Shoppers study is they looked at two studies, an omnivore vegetarian study and another study of healthy users. What they found was the death rate ratio, meaning the all cause mortality, the rate at which people were dying between vegetarians and people who had healthy behaviors was the same.
eople who were non-vegetarians, so we're talking about vegetarians versus omnivores with healthy behaviors, same death rates. Vegetarians versus general population, general population dies sooner. That's clear. This study suggests and again, this is an epidemiology study but this study brings up the idea. Maybe it's not what we're eating or not eating in these studies that's showing us these data points. Maybe it's actually the healthy behaviors that are helping the vegetarians be longer lived and the people who are eating meat be shorter lived. They're not doing the healthy behavior. This is where the epidemiology gets so murky.
It's an interpretation problem. Essentially, are you detecting the signal of healthy user behavior? Are you detecting the signal of vegetarianism?
I think it's also interesting and especially in the culture of context in the Western diet when you're eating meat, it's oftentimes you're having a beer with burgers. You're eating a lot of fries. You got the Coca-Cola with you. Again, are you detecting the signal of meat? Are you detecting the signal of alcohol, sugar? That is not a question that epidemiologists can detect. I think you've hit it exactly on the dot. It's Statistics 101. Correlation and design equal causation. I think that for better or for worse, there's not a lot of understanding of that basic core concept there.
You said it well. Epidemiology cannot answer this question. If I were king, I would outlaw the media sharing studies that can't tell us the thing that they're trying to study. These are hypotheses-generating studies.
The other side of this coin or the further down this rabbit hole is the interesting notion that there have been a few actual interventional studies with meat or with animal proteins. These I think are so seldom done that they should be highlighted. The results are quite striking. There have been comparisons of animal protein and plant protein given to various populations of humans. This is actually an interventional study.
A randomized controlled trial.
Yes, it's a randomized controlled trial that can't be blinded all the time but sometimes, you're blinded. Generally, in the interventional trials or I should say, across the board in the interventional trials, they're usually giving isolates of milk protein or beef protein to people. I don't know if they've ever done a study with the steaks but they do not see animal protein being inflammatory. There's no evidence. There's no interventional evidence that animal protein is inflammatory towards the immune system. That animal protein causes DNA damage. There's a great study that looked at all sorts of different markers.
They look at markers of gut inflammation. They look at markers of GI health. They look at markers of DNA damage. They look at markers of immunologic signaling. They don't see any signal in an interventional sense when they give people meat protein versus plant protein. The flip side is also true. We can discuss this later. They don't see a lot of inflammatory signals for plant protein but I will mention that in that study, the cow Protectin was higher in the plant group. The cow Protectin is an inflammatory marker that signals inflammation in the gut. That really raised my eyebrows. I thought that's interesting.
I think it almost reached statistical significance. I'd have to go back and look at the study but the cow Protectin was higher in the plant group but across all the other measures, the meat group did not show any change in inflammation relative to the plant group. Where is the actual interventional data that meat is bad for us? It doesn't exist. It just doesn't exist in the scientific literature. We're always told about epidemiology.
You're right that I haven't seen any data on the inflammatory markers but there is some study on interventional basis showing that there's increase in LDL with meat versus plant-based protein. I think that unlocks another whole can of worms around is elevated LDL cholesterol a problem in and of itself? Is that a cap to the full health of someone's metabolism? I think one, let's address that but two, I think some of the interventional studies, I'm quite positive. I think one of the things that I thought was interesting was that red meat consumption increases telomere length.
Right? I think not even is this poor or comparable to plant-based protein. There was an interesting data point suggesting this could be superior to plant-based proteins. I think it is worth addressing the LDL question because I think again, with the whole dogma, I think there's an open discussion and we've had conversations with folks like Dave Feldman and Ivory Cummins around this whole LDL cholesterol question. Is this of concern? Can I just get your perspective such from a carnivore lens on the LDL cholesterol question?
The red meat and telomeres is quite interesting because red meat I think was the only thing that lengthen telomeres that we know of. If you look at that study, they say, "The only thing that did this was red meat. We're not aware of anything else that can do that." Perhaps there's other things out there but I've never seen anything else have that result. It's quite a unique finding for telomeres. The reproducibility and the accuracy of the telomeres measuring is a little sketchy from time to time but I think that the take home message there is that red meat probably is a unique food in that sense. Have you ever seen those cans? I think they use them in the circus. They have this compressed snake. You open the can and the snake just goes boom and explodes out?
That's what you just did with LDL. You just opened the snake can where it's like, boom.
Huge can of worms but we can dig into it. I've talked about this at length on my podcast as well, which is Fundamental Health. I had Dave Feldman on there.
Nadir Ali, so yes. There is evidence that red meat, specifically saturated fat, well-raised LDL. There's also evidence that ketogenic diets can raise LDL. I don't think we fully understand all of the nuance there. I've heard Dom D'Agostino talk about dairy fat raising LDL more than other fats. I have a relatively high LDL. I've seen a high LDL in quite a few carnivores who don't eat any dairy. I think that's pretty clear that a ketogenic diet for mechanisms that we can discuss and the saturated fat in general will raise LDL. Then people run around screaming and they're just like, "Oh, my God. This is such a big deal."
I think again, this is a little bit of a disservice to the message here because we haven't fully unpacked it. That assume so that is predicated on the fact that LDL is a bad molecule or that LDL cholesterol is actually going to be an issue when it's higher. I would say that that discussion hinges on the question of whether LDL is directly toxic to the endothelium or not. Within mainstream lipidology, that would be people like Tom Dayspring, Peter Attia. These are people who are well seeped in the lipid literature and would espouse the mainstream perspective. They would say that the best theory is called response to retention.
The response to retention model posits that when you have more LDL, there will be a higher propensity just because of a numbers game for the LDL to get retained in the subendothelial space. That would suggest that LDL is directly toxic to the endothelium or that LDL is somehow triggering its own retention. I think that that is where I disagree with this hypothesis. I do think that retention of LDL is the key event in the initiation of atherosclerosis. What I'm talking about now is the retention of the LDL particle, which is a lymph protein particle that circulates in our bloodstream.
In the subendothelial space onto a proteoglycan layer, Ivor has done a great job talking about this proteoglycan layer in the subendothelium and how LDL getting in there isn't the problem. Because we know that happens all the time. The LDL moves in and out of that space. It's when it gets stuck. It's like if you have a ball with Velcro on it. If you throw it against the wall and it doesn't stick because there's no Velcro on the wall, it's not a big deal. If there's Velcro on the wall, it sticks. From the literature that I have seen and I plan to have Spencer Nadolsky on my podcast. He's one of this mainstream lipid guys and have a little discussion with him.
Perhaps a friendly debate about this but from what I've seen, there's a real diversions of phenotypes here. I think this is again where the issue becomes confused. I don't think there is robust enough evidence to implicate LDL as directly toxic to the endothelium. I think that instead, what we see is that states of metabolic syndrome and insulin resistance, this would be metabolic dyslipidemia are really what is causing this subendothelial proteoglycan layer to become more sticky. We know that insulin resistance can increase the amount of APOC3 on the LDL particle. That also makes the LDL stickier. I think there's a large amount of evidence now to suggest that number one.
Insulin resistance creates a stickier subendothelial space. Number two. That LDL is probably not directly toxic to the endothelium. Let's just examine the second thing in a little more detail. The idea that a molecule that we have evolved with for millions of years would be toxic to our bodies doesn't make a whole lot of sense to me just intuitively. LDL has all of these valuable functions in the human body. LDL is an immunologic mediator. We know that it affects core by bacteria. When bacteria invade our body, they put all these molecules to communicate to other bacteria saying, "Hey. It's okay. Come in. Invade." LDL mocks those up.
LDL can also be involved directly in the immunologic response. LDL carries cholesterol to the testes and the ovaries. These are tissues that potentially don't make their own cholesterol and so, it's invaluable. That cholesterol backbone gets delivered so we can make sex hormones and be healthy individuals. LDL also carries molecules that are involved in energy production among other roles. LDL is a crucial, crucial player in the human body. Just at a basic level, why would such a molecule be bad for us? Why would it hurt us? These arguments, they don't really make sense to me. Some of the most compelling examinations are around the actual numbers of these things.
When you look at an LDL number on a general cholesterol panel, it's a milligram per deciliter. There are these more sophisticated LDL panels now, which can get those numbers in nanomole per liter, which is an actual particle count. When you have nanomole per liter, you can do the math with Avogadro's number and actually calculate the number of LDL particles in your body or my body. People will probably be shocked to learn that even an LDL of 100 milligrams per deciliter, generally speaking, assuming an average particle size, you have one times 10 to the 18th particles of LDL in your body. That is 18 zeros. That is a very, very large number.
When you have an LDL of 300 milligrams per deciliter, you have three times 10 to the 18th particles of LDL in your body. Now granted, that's three times the other number but one times 10 to the 18th particles of LDL is still a huge number. How could something at one times 10 to the 18th not be toxic to our endothelium? At three times to the 18th be suddenly toxic to our endothelium? At what point does this happen? The lipidologist might argue. It's a gradual progression.
That's bologna in my opinion, too because there are trials like the Fourier trial, which is a combination of statins and PCSK9 inhibitors that got the LDL down to 30 milligrams per deciliter, which is probably not even high enough for people to make sex hormones or let alone live a healthy life. They still had a very large number of cardiac events when the LDL is at that number. In my opinion, it's pretty clear that it's not the number of LDLs. No matter how much LDL you have on your lipid panel, you have a really boat load of LDL particles in your body. I would argue though I haven't done the quantum physics or I haven't done the actual numbers in physics, I'd love for somebody to do this with me.
I believe that one times 10 to the 18th, the brownie in motion of the LDL particles in and out of the endothelium is probably saturated. I don't think there's anymore LDL particles. You could do a tracer study to prove this. I don't think there are any more LDL particles getting into the subendothelial space at three times 10 to the 18th relative to one times 10 to the 18th. If that's the case, the whole argument falls apart because I would argue that one times 10 to the 18th or even three times 10 to the 17th, which would be an LDL of 30 milligrams per deciliter, that system of LDL or that flux of LDL into the subendothelial space is probably saturated.
That's not the key issue here. It's whether or not the LDL gets stuck because of all those numbers. You still have a colossal amount of LDL moving into the subendothelial space. The other thing that people forget is that our HDL exists in our body at two orders of magnitude higher than the LDL. If you look on an NMR profile, the HDL is measured in micromole per liter, not nanomole per liter. The HDL is around 10 to the 20th. HDL is not an atherogenic particle. HDL carries 30% of the cholesterol in our bodies but it's not an atherogenic particle. How did the cholesterol hypotheses people explain this?
Because HDL is also moving in and out of our subendothelial space. Yet it's not an atherogenic particle. It's like there's a huge amount of HDL particles. There's a huge amount of LDL particles. We know that insulin resistance makes the LDL stickier. If you look at data like Dave's data and much other data, you can stratify and see that when you correct, when you look at people who are insulin sensitive versus insulin resistant, there's a clear divergence in how that LDL affects their cardiac risk. One of my favorite slides from Ivor is that he did a re-analysis of the Framingham data. He sub grouped those people into high HDL and low HDL.
That HDL metric is probably a proxy for insulin sensitivity. When people become insulin resistant, their HDL generally goes down. The low HDL group is a proxy for insulin sensitivity or insulin resistance. A higher HDL group is probably more insulin sensitive. What did he find? He found that as you go up an LDL number according to the Framingham data, if your HDL is high, there is no increase in cardiac risk. As you go up an LDL number with a low HDL, there is an increase in cardiac risk. That makes sense. In an insulin resistant state, if your LDL is sticky and your subendothelial space is sticky, then yeah.
If you put more LDL around, it's probably going to be a problem. Without insulin resistance, without a sticky subendothelium, I don't think there's really any compelling evidence to suggest that we should be worried about higher levels of LDL.
Most people on these ketogenic and carnivore diets, pretty darn insulin sensitive. There's not a whole lot of insulin resistance in this community.
Yup. I think it reminds me of our initial conversation around epidemiology and correlation is not equal to causation. I think a lot of the infringed around Framingham is that these are epidemiological studies. Retrospectively trying to correlate these things. Again, I think the potential flaw of logic of standard practice is that are the LDLs causing this? I think that's a question that is being unpacked now. I think one of the best I've ever heard is that ambulances are correlated with people dying at an accident scene. Are the ambulances killing people? Are they just a part of that response process?
It's interesting when I think about LDL. Is that the ambulance or is that the person that ran you over? I think that question hopefully will be resolved and people will have a better understanding of consume diet.
I think that the other thing with LDL not to belabor this point is that most of the LDL supporters or most of the people that espouse the conventional view of LDL as atherogenic or toxic would often point to GWAS. They'll point to genome wide association studies. If you exclude genome wide association studies, you see a whole different picture. Genome wide association studies are surveys of people who have genetic polymorphisms, which cause them to have a high LDL. This isn't the same thing. Perhaps this is the fundamental flaw that most of these people are making and they're thinking.
]For that assumption to be valid for the rest of us, that has to be the same condition as a high LDL on a ketogenic or a carnivore diet, which is not the case. You have a genetic mutation, a genetic polymorphism in CETP or PCSK9 or one of these other LDL receptor. These are the familial Hypocholesterolemia people in some sense but there are genetic polymorphisms, which cause people to have a high LDL. They'll say, "Oh, look. There's a linear progression in the amount of coronary events in the LDL in the GWAS in the people that have these polymorphisms."
I say, "That is not representative of the generalized population. Those are people who have broken cholesterol metabolism because they have a polymorphism." We would never do that anywhere else in medicine. We'd never say, "Hey. This genetic mutation, this genetic disease gives you this condition. Therefore, we're going to just expand that and apply that to everyone else in the population as a blanket statement." That doesn't make any sense.
That's a little spurious, yeah.
It is a little spurious. People need to be very careful. Again, this is where I think the onus is on the investigators and people are not doing a very good job of communicating what is GWAS. What is Mendelian randomisation? The other studies are the Mendelian randomisations.
These are all genetic people. These are people with genetic polymorphisms that affect the LDL metabolisms. Dave has talked a lot about this.
Dave has issued a challenge. It is impossible to find a study in people who did not have a genetic polymorphism that causes their LDL to be high that shows that a high LDL in the setting of low triglycerides and high HDL have an increased risk of cardiovascular disease. That study does not exist.
Before forgetting about TMAO, let's address that point really quickly around TMAO, it's associated with cardiovascular risk. People say that red meat has a lot of TMAO but it's also interesting to notice that fish and different other animal products and things considered classically heart healthy also have high TMAO.
I recently did a podcast with Steven Gundry and he's been a proponent and said, "TMAO is a bad thing for a while." I wish we'd gotten more time on that podcast to really duke it out. TMAO is Trimethylamine N-oxide. It comes from a molecule called Trimethylamine. Red meat doesn't have TMAO or TMA and it has precursors for TMAO specifically choline and carnitine. You're absolutely right. Fish do have approximately 40 times more TMAO in a pre-form state than what might be made out of an equivalent amount of choline and carnitine found in the same amount of meat as fish. A six ounce piece of fish is going to have 40 times more TMAO approximately.
I think that's about the right number. A six ounce piece of fish is going to have 40 times more TMAO than the amount of TMAO that you would make from a choline and carnitine in six ounces of meat. Again, this goes back to the thing we were talking about in the beginning. This is epidemiology. I was trying to unravel the TMAO story and I thought, where are the mechanistic studies? Where are the interventional studies? They don't exist. This is all epidemiology. This is another fascinating rabbit hole to go down. It really recapitulates everything we've been talking about in so many ways.
What you see here is people with higher TMAO levels do tend to have higher rates of cardiovascular disease. As you suggested, correlation is not causation. As I mentioned, we do not know in which direction the arrow of causality may go. I would say this is pretty much clear now. Anyone who knows the TMAO literature would have a hard time debating what I'm about to say. This is not conjecture. What we've seen now with TMAO is that the formation of TMAO in the liver is under the control of an enzyme called FMO3. I think it's flavin monooxygenase 3. That enzyme is under the control of insulin. People who are insulin resistant have higher levels of insulin and make more FMO3.
It would follow that those who are insulin resistant would have a higher level of TMAO. Now, Eve's getting a high level of TMAO from insulin resistance the same as getting a high level of TMAO from choline and carnitine. Not in this bod, no way. No way. This is the same thing as the LDL story. Is getting a high level of LDL related to insulin resistance the same thing as getting a high level of LDL related to a ketogenic or carnivore diet? Nope. Not the same phenotype at all. These are divergent phenotypes. There was a great study that came out recently. I think it was a Mendelian randomisation. It was statistics.
It was epidemiology but what they were able to show in that study was that elevated TMAO was likely being caused by diabetes and caused by kidney disease suggesting what we would call reverse causality. In the studies that associate high TMAO with cardiovascular disease, it's not that TMAO causes cardiovascular disease. It's that insulin resistance associated with cardiovascular disease probably causes a high TMAO. This is the problem with epidemiology. This is why everyone is so off the mark with this. As you suggested, we had a sense this was a fishy story, bad pun for a while. Because fish has not been associated with cardiovascular disease historically in epidemiology studies.
Yet fish has 40 times more pre-formed TMAO. The other piece of the equation is that we know that these compounds, choline and carnitine are crucial for normal healthy metabolism. Choline is a precursor for phospholipids, membranes, choline, supplementation has been shown to improve outcomes. NAFLD, which is non-alcoholic fatty liver disease, choline has been associated with improved outcomes in terms of psychiatric things because it's also a precursor for acetylcholine.
Carnitine is only found in meat and is clearly beneficial for us in terms of antioxidant response and it's been associated with improved response to other psychiatric things as well. We need these things in our bodies to limit choline and carnitine out of fear for TMAO is to move the health of the population in a clearly negative direction. We will have worsening of non-alcoholic fatty liver disease that would be a travesty. These are not the things which cause heart disease.
I think we're just starting to address all the bricks that people commonly throw at the carnivore diet. I think the last brick that people like to throw is the methionine content. Again, very tight. It's a core component of red meat or animal protein and methionine being associated with high mortality risk. I think this probably goes into your nose to tail discussion where glycine supplementation or glycine content, which is found in collagen basically reduces that issue where glycine supplementation basically resolves any of the methionine concerns. Any additional play of color there?
Those are concerns that I believe were originally raised in the 1950s and 1960s based on rat studies. That's exactly the case. That when they gave rats a high methionine diet and they eliminate glycine, they saw a life span restriction. They saw they died earlier. When they took the methionine out, they said, "Oh, they live longer." Then people stop and they think, "See? Rats live longer when you limit their methionine. Therefore, we should never eat meat."
We should all be skinny and never have any anabolic processes. It doesn't make any sense. We would never have gotten to this point in evolution by avoiding methionine. The third experiment is the one that people often forget about but it's the most important experiment, which is where they added glycine in to the diets. They saw lifespan extension because it was more about the methionine glycine ratio than the actual burden of methionine. You're right. As we know, it's fairly easy to obtain methionine in a nose to tail carnivore diet by looking for a connective tissue.
That's found in bones. It's found in skeletal, tendons. It's found in collagen, collagenous tissues, chewy bits. As Westernized Americans, we don't really want to eat these but we can get collagen supplementation, etc. etc. or just pure glycine as an amino acid. It's probably beneficial in most contexts.
Yeah. I think all the common concerns that folks might have with the carnivore, I think we've addressed a lot of that. I would say that okay. We have established that it is not clearly obviously stupid. People might say, "Okay. Vegetables are great because there's polyphenols. There's fibers. If you're eating 100% carnivore, 100% animal-based, you're not getting the fiber. You're not getting this polyphenols." Things like Resveratrol, Sulforaphane, these popular antioxidant polyphenols that are hypothesized to contribute to longevity. What are your responses or thoughts in terms of both the fiber story and the polyphenol story?
Another big, big can of worms. I'll sign on packet in a clear and concise matter. Let's address fiber first. In the fiber story, there are a number of sub headings, which we can address quickly. The evidence for fiber as preventative for colon cancer does not exist. That is not a debatable statement. If you look at the studies from the New England Journal of Medicine, from '99 and 2000, there is no evidence in the medical literature at this point in time that fiber supplementation either from fruits and vegetables or we brand fiber supplements changes your rate of recurrence of colonic adenoma or pre-cancerous lesions.
That idea that we need fiber to prevent colon cancer is a fallacy. In fact, there were some studies that showed an increased rate of tubular adenoma recurrence in people who were given essentially psyllium husks, which are metamucil. The fiber and colon cancer doesn't exist and then there's fiber in constipation. That's another fairytale unfortunately. If you look at the real literature there, there's a really great interventional study that's often quoted in which the complete removal of fiber resulted in total resolution of idiopathic constipation. I think each group was about 20 to 40 people who were divided into no fiber and some fiber or regular amount of fiber.
All the people in these groups had idiopathic constipation, which means doctors didn't know what was causing their constipation. In the zero fiber group, every single person in the group had resolution of their constipation. The idea that we need fiber to fix constipation would be completely contrary to the results of that study. In fact, the removal of fiber resulted in resolution of constipation. Even furthermore with regarding constipation, if you look at the literature, it's pretty clear. Fiber does not change the quality of stool, the pain with passing stool or the need to use laxatives or the amount of bleeding that people get with stool when they have constipation.
Fiber will increase the stool bulk and perhaps might increase the number of stools but constipation is much more than that. Constipation is hard stool, which is difficult to pass requiring the use of laxatives, often resulting in hemorrhoids or fissures from bleeding. Qualitatively, fiber does not relieve the symptoms of constipation. If you ask people with constipation, I hear this all the time. They say, "It's even worse when I ate fiber because then my poop just gets even bigger and it hurts more to pass it." It's just more painful and it causes more problems when people get bigger stools. Fiber doesn't really help constipation.
There's diverticulosis, which people have probably heard me talk about a lot. There's no evidence that fiber improves diverticulosis. That is a misconstrued story from a surgeon named Burkett in the 1960s. If you look at the data, actually in terms of case series, which are based on food frequency recall questionnaires with colonoscopy, people that ate the smallest amount of fiber had the lowest amount of diverticulosis. In interventional studies and further colonoscopy studies, there's never been shown to be a correlation between diverticulosis incidence and the amount of fiber that people eat. It's pretty clear.
Fiber doesn't prevent diverticulosis, which is the out pouching of the colonic mucosa through the muscular layers. It's a small blind pouch, which can get infected and form diverticulitis. Fiber doesn't prevent that. Fiber doesn't prevent cancer. Fiber doesn't prevent or treat constipation and perhaps, the last piece of the fiber equation is the microbiome. This is the murkiest discussion. My good friend, Tommy Wood has enlightened me regarding the word tasseography, which is reading tea leaves. What I would say about the microbiome is at this point in time, it's mostly tasseography.
Many of the claims regarding fiber in the microbiome I would say are overblown and they are extrapolations. I don't think that there's evidence that we really know what a healthy microbiome is and which organisms we should have in there. There are thousands and thousands. They are commensals and there are fungi and there are viruses. There are protozoa and there are worms in some people. Maybe they're good. Maybe they're bad. The idea that we absolutely need plant fiber to create a healthy microbiome is something I've heard repeated on many podcasts and I always kind of bristle and think. How do you know that? Because clinically, we see the opposite.
Anecdotally, we see the opposite. There are plenty of anecdotes, plenty of what will hopefully soon be case reports or case studies of people with bad GI issues. Meaning, either an inflammatory bowel disease that would be Crohn's or ulcerative colitis. Also, irritable bowel syndrome, which is probably synonymous with small intestinal bacterial overgrowth. Many of these people have complete resolution or significant improvement in their symptoms when they eliminate fiber from their diet. If it were true that plant fiber weren't necessary or requisite for an ideal, healthy microbiome, why would we be seeing those things clinically?
Because those are conditions that people would then link to a microbiota issue. People are trying to treat Crohn's and ulcerative colitis with probiotics. They're trying to treat that with fecal microbiota transplant or trying to modify the gut flora to treat those diseases. If it were true that the lack of plant fiber would really cause the colonic microflora to become totally dysbiotic or even the small intestinal microflora to become totally dysbiotic, we would be seeing something very, very differently clinically. The other issue, which I'll just touch on briefly is the colonic mucus. I am patiently waiting for Rhonda Patrick to debate me on this. I respect her work and I disagree with her with this extremely.
She's in San Diego.
Yeah, I know. I'm hoping to see her on each one of these days. I'm just going to get my buddy to film us having a throw down right there. It's Rhonda Patrick. I went on Steven Gundry's podcast. I'm friends with him but I disagree with his repetition of the study as well. There are many people in the functional medicine space that will repeat the notion that plant fiber is required for a healthy gut mucus layer. I think what are you talking about? That doesn't make any sense. The studies that support that are really not present. There's one study from 2016 in the journal Cell, that I believe everyone is quoting. It's a mouse study.
They are not a biotic mice meaning they're bred without any bacteria in their guts. They're inbred mice. They're given a 14 species, 14 human-like microbiome. It's a contrived version of a human-like microbiome. It's not a real human microbiome and it's not even a human. The species that they're given are fiber-loving species. The mice were divided into two groups. One group is fed a high fiber diet or a carbohydrate-based diet. Another group was fed a zero fiber diet. What they see is that the colonic mucus layer is a little bit smaller in the zero fiber diets but when they looked at the histology, that is the actual gut epithelium under a microscope, they look at immune cells.
They find no pathological changes suggestive of inflammation in the zero fiber group. The whole thing to me is just like, where have people gone with this? Where are people getting the notion that you need to have plant fiber to support the mucus layer in your gut? I just scratch my head and think, I am waiting for someone to help me understand that. Because again, clinically, that's not what we see.
It's also a very contrived setup because obviously, if someone is eating more carnivorous diet, they're with a very different microbiome than someone's eating a very plant-base diet. That won't even necessarily be useful in the field, in clinics. Yeah.
There are many bacteria which can metabolize fat, protein and animal-based collagen. That's the thing I think that most people are missing. That our gut microbiome can shift. There's a study where they put people on what I would consider to be a very poor version of a carnivorous diet and they compare it a plant-based diet. What they see is a divergence in the gut flora within a week. The animal-based eater, again, it's not an ideal diet. The animal-based eaters had more bile acid tolerant organisms and more organisms to ferment fat and protein. They made isobutyrate and they made acetate and they made propionate as short chain fatty acids.
The plant-based eaters made butyrate as a short chain fatty acid and had different colonic and small intestinal microflora. The investigators in that study jumped to the conclusion. Look, we know what's going on with the gut because they have this organism. What's worthy of biophilia or they don't have this organism. They clearly have an unhealthy gut microbiome and I think that is an extrapolation. We do not know that. Clinically, nobody is assaying anything clinically in that study. They didn't do inflammatory markers. They didn't follow those people moving forward. It was almost like a setup. They were just trying to prove that these bile acid tolerant organisms would show up when they gave people a bunch of foods, which promote the formation of bile.
Okay, sure. Yeah, of course. How does it track longitudinally and etc. etc. I think that the microbiome is where everyone tries to strum in carnivore with regard to the fiber thing. I would say that it's not a fair critique. Clinically, we just don't see it.
Why aren't we getting better?
Also, I think the fiber, I think you covered really, really nicely. I think it's interesting that look at the history of why fiber even being popularized. It was a patient with Mr. Kellogg who just had they just call it reduced libido in the population. It's a very interesting start of that hypothesis generation. Thus far done in interventional studies hasn't been very compelling. I think from a microbiome products perspective, I think as we're looking at some of the literature, just very, very early and very, very speculative. I think people are very aggressive. They're saying, "Okay." We know what the optimal microbiome is. We're going to feed you this stuff and you'll get there. It's like, "There's no idea there."
We also know that fiber inhibits the absorption of nutrients and it's going to decrease micronutrient availability.
Why you would want to eat foods with fiber and not get all the nutrients is beyond me but that's what people are advocating for.
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Polyphenols is an interesting question where moving from folks that might have insulin resistance or metabolic syndrome moving now towards professional athletes where people want to get the most of the day. There's reasonable data around polyphenols. What do you think of that? Is that more of a hermetic effect? Do you think there's some value? I think there's been interesting propositions. Say that we adopt the carnivore point of view. We can say that meat is food. Maybe plants are medicines. Plants might be useful for tweaking and optimizing things here or there. What are your thoughts there?
When we say polyphenols, what we're actually probably saying is phytochemicals because there are many chemicals, which are not technically polyphenolic in structure like Sulforaphane that get included in this group.
Okay. Basically, plant molecules that seem to have some good effect.
Plant molecules that we've been told have magical benefits, yes. Yes.
If we just back up for one moment and think about the context of this, I believe it's revealing. These are molecules that plants make for their own biochemistry or defense. Most of these molecules are phytoalexins. They are plant defense molecules. They are molecules plants make in response to fungal or herbivorous attack. Resveratrol is a great example. Resveratrol is made in response to a fungus attacking a plant. Resveratrol is not made by a plant in order to help humans. None of these chemicals are. People need to just think about that. Sulforaphane is an isothiocyanate that is not a polyphenol but it is made in response to animals eating plants.
Sulforaphane exists in a precursor form called Glucoraphanin, which combines with an enzyme Myrosinase only when the plant is chewed. Sulforaphane is a molecule that doesn't actually exist in broccoli. If you look at the mechanism, Sulforaphane is very clearly a defense molecule. It's a booby trap. It doesn't even exist until the broccoli is dead and getting chewed. That's the context. Now, if we really believe these molecules are magically beneficial for humans, that would be an incredible evolutionary accident. These are different operating systems. Plants and animals have diverged evolutionarily 500 million years ago.
From Bell's advocate perspective, a lot of drugs come from plants, aspirin. Okay. They seem to be reasonable in terms of what they do for medical purposes.
There's a difference between using plants as medicine and using plants as food. I think what we know and this is one of my gentle criticisms of naturopathic medicine sometimes is that molecules are molecules. I think that whether the molecule is from a plant or the molecule is from a pharmaceutical, we know that it can have effects on the human body. I'm not denying the notion that a molecule from a plant could affect the human body. What I'm suggesting is the position that molecules from plants perhaps very similar to pharmaceuticals are not all good. The pharmaceuticals is a very good parallel here. If I told you, "Hey. I'm going to give you a drug."
Say, you're my patient. I'm going to give you a drug. It's a Statin, which I would never give you. In fact, if you were my patient, we would probably never be having a conversation about drugs because you're healthy and I don't like to prescribe drugs. Hypothetically, if a physician is talking to a patient and they're prescribing a drug, whether it's Metoprolol, which is a beta blocker or Statin medication or an immunologic drug given for a rheumatologic condition. They should say, "This is what the drug does. Here are the side effects." This is exactly the same with plant molecules because just like pharmaceuticals, these molecules are not native to the human body.
This is a really simple idea. If our body doesn't make the molecule or use it as a vitamin or a mineral, it's probably going to have a side effect somewhere in the human body. This is what has been forgotten time and time again about plant molecules in our, I would argue, over zealous intention to lift these molecules up as magical. We forget that just like aspirin, which is acetylsalicylic acid, just like that molecule, which is actually derived from White Willow bark but made into a pharmaceutical, there are side effects. The non-steroidal anti-inflammatory drugs are a great example in comparison to Curcumin.
When I give someone or again, I don't give this medication but when people take Ibuprofen or Naproxen, which are Motrin in the leave or take another non-steroidal anti-inflammatory drug like Diclofenac, they are often told by the physician, "This is going to have side effects. It can hurt your kidneys because it affects the formation of prostaglandins and it can affect the way that the afferent and efferent arterials in the kidneys work. It can decrease the mucus layer in the stomach. If you take too much, you can get an ulcer but it's also going to decrease your pain." People always know there's a trade off.
When we think of Curcumin and this is again my gentle critique of naturopathic medicine. We forget that Curcumin has side effects, too because in fact, it's just a molecule. It's really the same as the pharmaceutical molecules. Certainly, between molecules, what we're trying to do is maximize the benefits and decrease the side effects. What we would continually forget or what supplement manufacturers and people don't ever tell us is the side effects of the plant molecules. There's no FDA requirement on the inclusion label of Resveratrol or Sulforaphane or Curcumin to say, "Hey. Here are all the side effects." There are side effects.
This is I think where people are misled. If you look at the literature on Curcumin for instance, Curcumin probably has an anti-inflammatory effect. There haven't been a ton of double blind placebo controlled randomized trials but there have been a decent number of trials, which show an ant-inflammatory effect of Curcumin. Ibuprofen also has an anti-inflammatory effect. Ibuprofen has side effects. Curcumin has side effects. That's well documented in the literature. That Curcumin can affect DNA replication. That Curcumin can be toxic to native human cells. That Curcumin can affect potassium channels called the hERG channel and that Curcumin can damage DNA directly.
I'm not saying that Ibuprofen is better than Curcumin or that we shouldn't use Curcumin during some applications. I'm just reminding people that all the molecules that are foreign to the human body that are outside of our operating system have side effects. My overarching perspective on Curcumin is that we're overusing it. That it's used too often to fight inflammation, which we're not getting to the root cause of. That's a whole separate conversation.
We see the same thing with Resveratrol and Sulforaphane and any plant molecule. Nobody tells us about the side effects. Resveratrol is actually a molecule that's been a great failure. If you look at the trials with Resveratrol, it extended life span in lower invertebrates like sea elegans which is a little worm and perhaps in yeasts. It had some data in mice which were compelling but in humans, it's failed miserably. Yet it's still on many shelves and grocery stores and it's a multi-million dollar industry. It's failed in trials of non-alcoholic fatty liver disease. It's failed in trials of metabolic syndrome.
In fact, in metabolic syndrome trials, it actually worsened dysglycemia. It worsened glucose control. What are the side effects of Resveratrol? Well, it also happens to be estrogenic so it's going to decrease your androgen precursors. That's not a good thing for men or women if we're inhibiting DHEA and androgen precursors and it's going to lower your testosterone. Sulforaphane is exactly the same thing. It's been shown in studies to decrease DNA damage working through the Nrf2 pathway because it's a prooxidant. We can talk about hormesis because it's a prooxidant that will increase your glutathione. Sulforaphane has side effects and nobody talks about these.
It can compete with iodine at the level of the thyroid and cause thyroid issues for people. Sulforaphane also is known to induce prooxidation of lipid membranes, creating 4-HNE in Acralyn. There's some evidence that Sulforaphane can even be inflammatory to the immune system. This is a big thing. Then people will say, "Okay. The plant compounds are better than the pharmaceuticals. The risks are worth the benefits." I would say, "That's where I differ." This is my concept. This is my shtick. I say, "You don't actually need those. Why don't we talk about the benefits here? The benefits of Sulforaphane are glutathione."
It's been very clearly demonstrated repeatedly in studies that we can maintain an adequate level of glutathione and oxidative defense without plant molecules. We don't need molecular hormesis to get enough glutathione. Why would we do something that's redundant and suffer the side effects? A physician isn't going to give someone medication they don't need because there's going to be side effects but that's what's happening with these plant molecules.
People are taking them via supplementation or they're believing that they're getting a benefit from eating plants when in fact, their redundant effects that I don't think have ever been shown to do anything unique for humans with the side effects that are often ignored. Is that making sense?
Yeah. Such a complex network and you're pushing one lever here. It's hard to tell that you're not just fighting one localized end point that you're controlling. You're pushing a lot of different things. I think when you're talking about Resveratrol, obviously there's well-credentialed people still talking about it like David Sinclair over at Harvard still promoting it. It reminds me of some of the arguments around things like Metformin or Rapamycin, these anti-aging drugs where you might get some longevity increases but you're also pushing a lot of marketers that you might care for as well in terms of Metformin potentially reducing testosterone.
I think it's a complicated story. I think you're making a very good analogy towards looking at plant molecules almost as a pharmaceutical. There might be one localized end point that you want to be optimizing for. If you have a specific goal to optimize for that, maybe that could be useful for you but don't forget there are side effects. I think with the drug industry, at least there's more discussion around side effects. Where with plant foods, it's just so indoctrinated that plant foods are just generally healthy. That we don't even talk about side effects. I think that's interesting perspective.
People will tell the benefits of Metformin. I think that Metformin has benefits in the setting of a standard American diet. If you're an obese rat or you're an obese human who won't change their lifestyle, yeah. Metformin is going to be beneficial for you. The risks probably are outweighed by the benefits. If you are a human that makes intentional choices with their diet, I'm not aware of any benefits to Metformin that you cannot achieve through intermittent fasting, ketosis, if we're talking about genetics, if we're talking about HDAC, if we're talking about Histone deacetylase inhibition. The benefits of Metformin on the kinase system are generally achievable in a ketogenic state.
You don't have the side effects including lowering testosterone, B12 deficiency, lactic acidosis. This is really a perfect illustration of the concept I'm trying to communicate to people here. Why would you do something that has a redundant benefit for the risks when you can just live your life well? The conversation changes completely when it's not you and I talking. When it's a patient that comes to anyone in office and says, "Hey, doc. I'm never going to change my lifestyle. What's the best medication you got for me?" "Well, here. Here's some Metformin. Sure."
That's a completely different conversation than most of your audience and most of the people that are interested in a carnivore diet. I don't even know the man or woman on a carnivore diet that's not trying to optimize their life in other ways. If people are making intentional choices, they are aware of this. They're cognizant but yes. There are benefits to molecules, molecules derived from plants, molecules derived from pharmaceuticals, molecules derived from bacteria in the setting for medicinal uses. Especially there are benefits to molecules for people that are not able or willing or aware of the importance of changing their lifestyle but that's a very different conversation.
It's very clear to me and I think you would agree with this. Lifestyle is the biggest lever. In that collection of tools of lifestyle, food is a big, big wrench. Changing what you eat is going to be so much more powerful than Metformin, Resveratrol, Sulforaphane, any of these molecules. In people that are trying to optimize, I don't think we need any of these molecules to be optimal. I think there actually going to be a decrease because of the side effects.
I think that's where optimal is an interesting definition. I'm just thinking again back to performance athletes. I would say that even athletes that are amenable to low carb ketogenic lifestyle will have carbs, fast carbs before their Olympic race or their event. I think the lanes in optimal needs to be more clearly defined because what's optimal for you might be for health span and longevity or for someone who's more of a productivity office worker. Okay. I want to optimize my brain power and my health span but someone who's trying to optimize to win the gold medal for power lifting, it's like, okay. I'm going to take off my health span maybe but that's a fair trade.
I think perhaps that's more of an engineering concept versus more of a medical concept. Okay. There is trade offs for every single position. These plant molecules or just having carbs right before a race is not necessarily optimal for my metabolism and my metabolic health but it's going to help me win that race. I think you would agree with that as well. Just curious in a sense of how dogmatic are we around defining optimal for everyone? Versus can we have a nuance discussion realizing that some people's optimal is different given your baseline and what your goals are.
I totally agree with you. I've talked about a quality of life equation in the past and the idea that every person has a ability to find their highest quality of life at any moment. Who am I to say what that is? You're right. Most of what I'm talking about now assumes the metric of optimal as health span and lifespan. I'm not an Olympic athlete. I think I always wish that I was but I never got even close. I'm a surfer. I hit the punching bag. I do jiu jitsu casually now. I'm not going to the UFC. I'm never going to be a pro surfer but yes, absolutely. There are times in people's lives where optimal will sacrifice lifespan, health span, mitochondrial health.
In those situations, yes. Molecules, whether they're plant-derived or synthetic, can have a benefit and can get them to optimal. I think that most of the discussion of a carnivore diet is in the context of optimal health and lifespan but you're absolutely right. There are exceptions. There is nuance when we're looking at these edges of performance. These are unique. You bring up a fantastic point, which I would totally agree with. If someone's going to run a marathon, you're going to benefit from carbohydrates. Any activity that you do that's going to deplete your glycogen, that's more than an hour and a half or two hours at a certain percentage of your VO2 max, you're going to need carbohydrates to fuel for that.
Personally, I haven't found that my performance suffers with intervals on a punching bag or jiu jitsu or surfing for a few hours because those are decreased levels of exertion. They're not crazy. They're not crazy long. My friend, Zach Bitter who's a world class ultra marathoner eats mostly ketogenic or fat-based diet and then uses carbohydrates in training and during his races. That's super smart.
That's the way he does it.
I think there are a lot of athletes that do eat keto and low carb. I think again, you might be able to pull it off but you're not necessarily trying to win that gold medal. You probably want to have as much substrate in all types of forms. It's not just ketones. It's not just carbohydrates. Everything all at once going.
The faster study, which is Phinney and Volek study, I'm sure you're familiar with them is something I keep coming back to. If people are not familiar, they tested the metabolic engines of carbohydrate and fat-burning athletes that is ketogenic athletes after the athletes have become keto adapted. What they found was that the rates of glycogen storage and replenishment were equivalent between the two groups. This is pretty contrary to popular thinking that even in the ketogenic athlete, you are replenishing glycogen, which is pretty wild.
You are making glycogen. In the short term, we will deplete our glycogen as we are becoming keto adapted. In the long term, it appears that even ketogenic athletes have glycogen. The other thing that's an advantage is that in a ketogenic state, we burn more fat. That it was some astronomical number, two to six times more beta oxidation in the ketogenic athlete. You're burning way more fat. From an endurance perspective, someone that's keto adapted has a clear example because you have a much bigger tank of fat.
That's a really interesting thing. Perhaps I think that in my mind and this is an interesting idea. It almost seems like the ideal athlete would be someone that's keto adapted and then uses carbohydrates for their event. I think there are some nuanced conversations about would you find benefit from training with carbohydrates? Maybe not. Maybe the idea is to be keto adapted in your training and then use carbohydrates targeted for specific events but we don't know.
I think it's a super open inquiry. In a lot of our conversations, there's a lot of periodization and cycling both on training and on diet. You would cycle your training protocol and your diet protocol in different ways of optimize and peak for different events. Exactly. Sometimes, you want to be training fasted or training keto. Sometimes, you want to be training fully fueled.
I've actually heard that cyclists in long races, say there's a Tour de France can become ketogenic when they deplete all the glycogen.
At the end of the race, they'll have ketones in the blood.
Yeah. I'm not a serious endurance athlete but I'll generate ketones after a long ride. Absolutely. We're doing 100, 150 miles a day, that kind of intense exercise, yeah. They're definitely in ketosis towards the end of that race.
From that perspective, you would want to have developed that machinery prior.
Because if you don't have that machinery, you're in trouble. That's that metabolic flexibility people talk about.
Yeah. One of the things that I think has been most interesting following your work is that I would say that most carnivores' articulation of what to consume seems very simple. People talk about just eat a bunch of ribeyes. That might be fine. It seems that some people are doing that. I think Shawn Baker is someone who goes more of a simple way of just consuming meat. I found that your articulation around looking at salmon roe nose to tail, making sure you get all the organ meats as really well reasoned, well articulated. I'm curious to introduce that concept to our audience. When you talk about carnivore, this is not just the kind of the cave man that will just eat a bunch of steaks. There's a more nuanced way to do this. Can you talk about that?
I think that the cave man approach is the right one. I think that the subtlety there is that the cave man, we're not just eating a bunch of steaks.
Fair enough, yeah.
The Flintstones didn't just eat steaks. If you think about it, the most plausible explanation is that our ancestors were eating the whole animal. Based on first principles, when we think about human nutrition, there is this overarching context that human nutrition requirements definitely change in the state of ketosis. All of that aside, if we're looking at all the vitamins and minerals that a human needs to thrive, I don't see any downside to getting a larger variety, a more robust collection and a larger amount of vitamins and minerals. That I think is exactly where the nose to tail carnivore diet comes in.
Entirely meat-based diet, I know Shawn is a good friend of mine. He eats salmon occasionally and some eggs. Without including organ meats, I do think there are minerals and vitamins that he is falling short on or could get in more robust quantities. If we're thinking about how to get the maximum amount of micronutrients, I think that that is eating a whole animal. This is challenging for people. People need to ask themselves what are my goals with a carnivore diet? Is it a 30-day cleanse? What is my context? Am I super busy? Do I just hate organ meats? Is this a long term thing? I think there are different levels of a carnivore diet.
I think an introductory carnivore diet for 30 or 45 days could be just fine with meat and eggs and some fish and maybe a little bit of liver. A very simple collection of foods. If people just wanted to see how they would feel and maybe see if some of their autoimmune issues or dermatologic issues or inflammatory issues or mood issues would resolve. When people decide to do a carnivore diet long term or decide to use it more frequently, or if people are just looking for higher nutrient density, nutrient content foods, I think inclusion of a nose to tail perspective is very valuable. That's certainly what I do personally.
This is really just the concept that if you and I are out hunting and we kill an animal respectfully and we're appreciative of this animal and how it's going to fuel us, we're going to eat the whole animal. It's so interesting because when you look at the nutrients that a human needs to function and thrive, they're all in the whole animal. Many of them are missing from the simple short term diet. In the bones, you're going to have calcium. In the bone marrow, you're going to be getting higher amounts of DHA and perhaps unique neurologic factors, neurotrophic factors. We know that bone marrow and brain are prized by indigenous people.
The bones are often ground up and eaten later. I don't think indigenous people they're eating them for calcium but that's good source of calcium. There's great fat. There's unique qualities of fat in the bone marrow and the brain. Then you look at the connective tissue. This goes back to our methionine and glycine conversation around the connective tissue is where the glycine is. They're going to eat all the animal. They're going to eat all the tendons, all the grizzly bits. Maybe they'll boil them so they're softer. This is tendons. I've had pho at Asian restaurants and there's tendons that's quite delicious when it's boiled. It's connective tissue.
You'll find these things in other cultures but Westernized cultures have just stripped them all away. Of course, there are the organs. The organs are where there's a lot of unique micronutrients. Meat is very rich in about half of the B vitamins and some of the minerals. If you look at liver specifically, it's an incredible compliment to that. Meat is high in zinc. Liver is high in copper. You need both.
If you over consume zinc without consuming enough copper, whether by supplementation or perhaps by eating meat without eating any copper containing foods, you can become copper deficient because of the way that zinc and copper are stored in the small intestine, in the Metallothionein protein and they're sloughed off together. When people are consuming zinc supplements without copper, they can get copper deficient, which is a big deal. That causes neurologic symptoms that mimic B-12 deficiency.
The same is true with B vitamins. There are some B vitamins in meat but there's not a lot of folate and not a lot of riboflavin. Where are those? There's some in eggs but they're mostly found in liver. Liver's a fantastic source of riboflavin. I had a really interesting discussion with Dr. Ben Lynch on my podcast about MTHFR. One of the more compelling things that we know about this MTHFR enzyme, which is Methylene tetrahydrofolate reductase, most of your listeners will probably be familiar. It's an enzyme that makes 5, 10- Methylene tetrahydrofolate into L-methylfolate. That enzyme can be polymorphic.
If we don't give our bodies enough riboflavin specifically, then people with polymorphisms and that enzyme can have dysfunction of the enzyme and not make enough L-methylfolate, which leads to rising Homocysteine. Now, it's really easily remedied. People will take L-methylfolate but I think that the better way to fix it is to eat foods that are high in riboflavin because there's good evidence that if you have adequate riboflavin that's being three to five milligrams of riboflavin per day, someone with even a 677 c/t polymorphism that's homozygous just like myself can have a normally functioning MTHFR just by getting enough riboflavin.
It's the binding site for riboflavin that is affected by that polymorphism. You just need a little more riboflavin. You're never going to get three to five milligrams of riboflavin eating steak. It's really, really hard but you're going to easily get it eating liver and egg yolks help. There's a few other foods that are high in riboflavin but this is the idea that we just create this really elegant balance of nutrients when we try and eat the organs, the connective tissue, some bone material and some real animal fat. Brain, bone marrow, suet, which is kidney fat, etc. Eating the whole animal gives us a more robust collection of nutrients. Like I said, I just can't see how that's a bad thing.
Yeah. It just makes sense from a visceral kindergarten level. It's like, okay. There's an animal and you want to eat as much components of it because I'm more like an animal than a plant. Me turning this grain of leaf into human seems more complicated than turning a cow with this brain, the eyeball, the gut, the liver and the tendon into human. You mentioned that MTHFR notion. Actually, I think this is a good segue into more of an audience Q&A with some of our friends and listeners we actually wrote in. I mentioned my friend, Brian who got me on to the nose to tail carnivore and got me looking at all of your stuff.
He actually wrote in about your conversation with Ben Lynch asking about different genetic polymorphisms that people should be concerned about that might not do well on carnivore. Is that something you've looked at? Do you think almost everyone regardless of different polymorphisms could do well on a carnivore diet?
One of the podcasts that I'm going to do in the future is an ApoE4 podcast. I think that these questions are interesting. At this point, I've not come across evidence that there are any polymorphisms that I'm aware of. My knowledge is still expanding.
There are no polymorphisms, not ApoE3, not ApoE4, not FTO that make it so that people will not thrive on a carnivore diet. I could be wrong about this. I'm still learning. I think it's a fantastic question and there is some nuance. As I mentioned, I'm going to be talking to Dom D'Agostino later today for my podcast. One of the questions I have for him is if he's aware of any polymorphisms that don't really make ketogenic diets so good for humans either. That would almost contain the same question.
That's overlapping, yeah.
Yeah, because a strict nose to tail carnivore diet would be ketogenic. Perhaps there are some people that don't do as well on ketogenic diets. That would be trial and error. There are ways to make a carnivore diet non-ketogenic with honey. You could do a carnivore-ish type of diet where you're most eating animal products and including some squash or some sources of carbohydrates that we think probably have less plant toxins. There are ways to do it but yeah. It's a great question. It's well-considered and it's part of my evolving understanding. There's nothing that I'm aware of now. People will always cite FTO.
I'm just not convinced by the studies around FTO and saturated fat. I'm not convinced by the literature on ApoE4 and saturated fat either. That's something I have to dive into much more. I'm going to do a podcast with my buddy, Tommy Wood in the future and we're going to go into ApoE4, saturated fat and what it all means and how to do it all. At this point, I haven't seen it. I'm open to the possibility there may be out there and there's more to learn there. Perhaps Brian has some suggestions for genes we could look at. The ones that I've seen people say like, "Oh, I have FTO. I can't eat saturated fat." I think I'm not buying that one. If you look at the literature, it's not that convincing.
The ApoE4 specifically says what Alzheimer's and neurologic conditions and it sounds like the main concern there potentially might be more from an insulin problem than from a saturated fat problem. Again, back to the LDL and that whole story. Brian also wrote in asking seems to be an avid follower here that you've recently increased your fat intake up to 75%. You must be in ketosis.
Certainly. I did one the other day. It was probably an hour and a half post prandial and my glucose was 64. My ketones were 2.3.
In nutritional ketosis.
Yeah. I did a podcast with Ted Naiman on better, stronger, faster.
We went back and forth a little bit. Ted is a great guy, super smart. He's a family doc in Seattle where I just left. We had a round table discussion about benefits of higher protein, benefits of higher fat. My perspective is that if you're trying to lose weight on a ketogenic or carnivore diet, you may want to increase protein relative to fat. Make the ratio something like a little more protein and fat in grams. If you're trying to do performance activity or if you're trying to maintain body composition, which is where I'm at, I feel best and I think most of my clients feel best with more fat. It's not a small amount more fat. It's a significant amount more fat in terms of calories and grams. I think that there's a sweet spot for protein for humans and that beyond a certain amount, we just don't use it for building muscle anymore.
I think that was his question. I think his questions were on in terms of protein content, how much protein on a carnivore diet you want to maintain some anabolic function?
I don't think we should be doing low protein. I think that moderate protein is ideal for humans. I think that for most people, depending on what they're doing, that's going to be about .7 to one gram per pound of lean body weight per day, which is a lot more than most people would think of. Now, there are a lot of carnivores eating twice that amount. If you eat five ribeyes a day, you're going to be getting four or 500 grams of protein a day. I think that's more than anyone needs and my concern is that actually is damaging. That creates a stress on the urea cycle and requires the liver to turn all of that nitrogen into urea.
We know there are polymorphisms in genes like Ornithine transcarbamylase or OTC that affect our capacity to turn nitrogen into urea. I happen to have an OTC polymorphism. I'm probably not a great converter of nitrogen into urea. My upper end of protein is probably a lot lower than other people's.
You can look at tables and charts and stuff and what I've noticed is I think that for me, the ideal, if you're trying to maintain and perform is get the amount of protein you need to maintain your lean muscle mass and then don't eat anymore protein. Because protein is building blocks. Protein is not really fuel. You should be fueling your body with fat beyond that. That's how you're going to feel best. Don't make your liver convert it into urea. We can do it but at some point, we hit that upper end. There is absolutely the ceiling to what our liver can convert. I think that some people on carnivore diet are probably beyond it or right up against it. I think they feel better with more fat.
Mental calculation here. Even if you're doing 25, 30% protein and the rest in terms of fat, say you eat 3,000 calories a day, that's still 750 calories of protein, 800 calories from protein, which is upwards of 200 grams of protein, which is going to be more than enough for any use case for anabolic function. The typical minimum RDA is .8 grams per body weight of kilogram. If you're an 80-kilogram guy, 176-pound guy. That's around 75, 70 grams of protein a day to just maintain. You're getting more than double that.
Even with a 25, 30% macro of protein.
Yeah. I'd probably get around 150 a day.
Yeah. Somebody like Mark Bell, he's 250 and he probably has 220 pounds of lean muscle mass. He might need a little more protein. I think that actually that hearkens back to Brian's first question. The context of the carnivore diet will be important. What is your Ornithine transcarbamylase? How well do you process nitrogen? What's your upper end for protein like? Maybe you're hitting that.
I think people could be eating less protein than they think and still functioning just fine.
I think they feel better on more fat and I also think that there is a bottom end to that. At which point they're eating not enough protein. That's not a good thing either.
Just knowing Brian, he's a strong fit guy. It sounds like it's don't worry about getting too little protein here.
Even if you're doing 25, 30% protein, that's going to be plenty. I think just that back of the envelope math, that's plenty. Pete Jacobs who is a 2012 Iron Man Champion who's recently on our program and he's now shifting on to carnivore actually has a question for you. He asks about low stomach acid from a process plant heavy diet, low protein diet. Older people might have this issue. Have you had stomach acid issues when you're switching people to a carnivore diet? What are your thoughts about that question?
Often, what I see is a zinc deficiency. If people are concerned about low stomach acid, I would recommend a micronutrient panel to make sure that they have adequate micronutrients. If we're zinc deficient, we do not make acid in the parietal cells very well. That can be a problem. I think that in the short term, yeah. If people are not digesting the food well, perhaps some HCL is beneficial. I do not recommend long term Betaine HCL in people. I think that if they're eating meat, they should be zinc adequate and you shouldn't need it. I think if people are nutritionally deficient, it could be a problem.
That would be a reason to work with a functional medicine doc and make sure you're okay. The best test of this called The Heidelberg test. I think that's more and more will do pH capsule endoscopy for people and actually prove they have low stomach acid. My suspicion is that a lot of people think they have low stomach acid and it's actually something else. They end up taking a lot of Betaine HCL or a lot of bitters or a lot of other things. Pancreatic enzymes that they don't need and I'm always a fan or parsimony and avoiding extra supplements and stuff.
Do you feel like autoimmune issues have propped up more in recent years because of a change in environment, change in diet? Two, how do we change the culture around this notion that plant food is healthy and meat is unhealthy? I think that story's been conflated with a couple reasons. I think there's a moral question there. I think it's an environmental question there. I think there's the health question there. I think the health question you've addressed really, really tightly in this conversation where clearly, it's not going to necessarily be bad for you. It might actually be optimal for you.
I think the environmental question I've seen some of your conversations around that. It's not that clear that agriculture is much more efficient than animal husbandry. I think there's a real academic debate to be had there. I think the moral question is probably the strongest argument around mass farming, factory farming, other mammals as food. I think on the other side of the story is like, okay. Nature is metal. Lions eat zebras. Nature isn't this happy zoo where everyone is living off of plants necessarily. I don't know what's the best approach in terms of opening people's minds around some of these concepts.
Kind of a convoluted two-part question. First part, why aren't there just more autoimmunity? Do you think it's more awareness around lectins and autoimmune issues? Has that always been a part of human nature? People just doesn't realize it? Can we talk about how you break down the cultural philosophical aesthetic moral questions around animal consumption?
It's pretty clear that conditions like autism, celiac disease, autoimmune issue in general are increasing in incidence. It's not just detection. It's increased incidence. That's pretty clear. There's a very compelling hypothesis around the assertion that this is due to our environment. There are many things in the environment, which could be triggering this. Toxins, pesticides, glyphosate, many things, which are creating hyperpermeability to the gut epithelium and foods. I think that our food habits have changed. Even if you go back 70, 80 years, I don't think people ate vegetables the way they eat vegetables now.
Everything looks a little different. People would definitely eat vegetables but I think that even four or five generations ago, people really understood that meat and animal products were the reason that we were healthy. That if we didn't have enough money or we couldn't obtain animal products, we would eat things like potatoes or bread or other things. Generally speaking, I think that our not too distant ancestors really understood that animal products were vital and crucial. One of the nuances that we haven't really talked about is I do think there is some genetic variation in our individual human ability to tolerate plants.
This goes back to Brian's question, which is well taken. Are there polymorphisms that affect carnivore diets for all people? I'm not sure yet. One of the things that I've mentioned recently in my interviews is that I would hypothesize that a carnivore diet is the basic diet for all humans or let's say the vast majority of all humans. That based on our evolutionary history and our biochemistry, that I think the vast majority of humans will thrive on a nose to tail carnivore diet. There is individual variation in how many plants we can tolerate on top of that.
Like I said, I'm not convinced that plants really represent a beneficial addition to that beyond entertainment and social norms, which is not trivial. I think there are some people who can tolerate more plants or less plants without becoming sick or manifesting illness more swiftly. Mikhaila's a great example of that. I seem to be an example of someone that doesn't tolerate plants very well in terms of eczema.
I think for myself, I've done lots of six weeks of carnivore and then I eat some salads or I eat some noodles at a pho restaurant for example. I don't really see much real change in terms of any of that.
I think I have a little bit more tolerance towards these carbs or these vegetables.
Yeah. Jeff Volek has talked a lot about the carb tolerance. His idea is that perhaps only 30% of the population is carb tolerant. You bring up a very important point there that for a lot of people, a moderate amount of carbohydrates is enough to create insulin resistance. There's definitely some genetic variability at play here. I don't think that everyone needs to eat a carnivore diet to thrive or to be optimal. I think that for some people, it can be an incredibly valuable intervention when other things have failed. I think that for most people, a carnivore diet will create pretty darn amazing health.
To which they can add plants if they would like to depending on how they tolerate them. Having said that, I do think that there is a higher incidence that we're both detecting and seeing more autoimmune disease now. Because of changes in food, changes in food structure, changes in pesticides, toxins, all these things. Continuation of our interaction with the environment as humans.
The moral question, I think that I understand what you're asking. Whenever I hear that, I think a couple of things. The first thing is like you said, nature is metal is one of my favorite Instagram accounts. I think it's true. We have become separated from hunting animals. We don't really understand what it's like to hunt animals. I think that's a tragedy actually because my limited experience hunting animals was quite profound. Really taught me to respect the animals and to be more appreciative of the food I was eating. I will admit that when I eat food that I pull out of the fridge, I don't respect it nearly as much because I forget what that food came from.
It looks like a steak. It doesn't look like a cow or a deer. When I bow hunted a few years ago and I killed a deer with my friend, every time I ate that meat, I know that deer. I saw that deer. Most people would say, "That's super sad. We shouldn't do that." Yes, none of us were trying to kill animals and this is the way the world works. In order for something to live, something else must die. I think all life is sacred. I think the killing of animals actually results in a very clear imperative to live our lives well as humans. It's a reminder everyday that I don't know how long I'm going to live. Maybe I'll live another 50 years if I'm on Dave Asprey terms, maybe I'll live another 100 years.
I'm going to consume a lot of calories in that amount of time. There's just no way around it. I haven't figured out a way to do internal combustion or nuclear fission. The calories are going to come from somewhere. As has been described by many people with regard to the environmental arguments, plant-based agriculture results in the loss of life as well.
I would argue that plant-based agriculture results in more loss of life and more detriment to the overall ecosystem of the earth, which I would consider to be one large living, breathing organism than animal agriculture because of the loss of top soil, mono crop, agriculture depletion of nutrients from the soil and by kills, animals that are killed in the processing of these foods. We're in a bugaboo. We cannot avoid impacting the earth by living on it. I think that respectfully harvesting animals in my opinion and the opinion of many others is the most spiritually compatible way for me to live. I think that it's in no way, shape or form disrespectful. I have never seen any evidence to show that a plant-based diet is more compassionate in any way either. I do not think that factory farming is the way to do it.
Yeah, exactly. I think that's the most compelling point from that moral standpoint is this essentially the current generation's form of slavery. Where just enslaving and factory farming these poor mammals.
I'm not a fan of that. The question not for me, for an agricultural scientist is how do we do more pasture-raised animals? Perhaps that will be something that I address. I've seen some discussions of it on social media spheres. People say, "We could do animals grass-fed." Other people will say, "That's impossible." I think whether it is or it isn't, it's a conversation that we should have. We are where we are. We can't change it. There are 7.8 billion people on the planet or something like that. I don't have 7.8 billion kids. I just showed up here, man. There's a lot of people. We just find ourselves in this predicament.
I think that animals are the most nutritious food for humans even if they are factory farmed. I'm not advocating for that. I don't want animals to suffer in those settings. I still think animals are the most nutritious food for humans. I think that if we want humans to be healthier and we want humans to solve problems and we want less of a burden on our economies by health, we will feed people well. That will result in greater health and a population results in greater problems solved.
Greater solutions and so that's the way I see it. Feed the people the best food you can. If the best food that they can get is factory farmed animals, then fine. Let's figure out a way to not factory them anymore.
Yeah. Let's bend our dollars towards things that are more sustainably raised or more humanely raised and bend more of the industry to follow suit.
I think that's the best we can do at this point.
You can't tell people, "Hey. Just go for sub optimal health. We're going to pay that cost in the backend when everyone's obese and has diabetes." You got to pay somewhere.
I think especially we're humans. We've got to optimize for other fellow humans. Let's bend the happiness of all life in the medium long term when we have more and more resources and education to do so.
Yeah. Yeah, I agree.
Last question. I always like to ask this question. If you have infinite money, infinite resources to run a study, how would you structure it? Obviously, there's a lot of questions to be answered through an interventional well run carnivore diet. Curious if that would be where you would be going. What would the arms look like? What would some influence be that you would be really excited about or focused on
That would absolutely be the study. That would be such a game changer. One study to point to, I think there would be a nose to tail carnivore diet arm. There would be a ketogenic arm. There would be a paleo arm, standard American diet arm. Give it a vegan diet arm. Give it a vegetarian diet arm to really highlight it. Make some plant-based stuff in there and then look at metrics. Look at hormones. Look at insulin sensitivity. Look at inflammatory markers and follow people long enough. This is why the study would be very difficult to see the arc of chronic disease. Look at micronutrients.
Look at micronutrient sufficiency because I think the plant-based diets will quickly reveal themselves as problematic in that respect. I think that what we will see in a little bit longer event horizon is that the carnivore or less antigenic diets will result in better outcomes in terms of immunologic measures, inflammatory measures, psychological, mental health measures, psychiatric measures, these kinds of things. Yeah. I think most people in the world want to know how to eat. Let's do a study where we just really follow it carefully overtime.
The flaws of the study would be that people have individual genetic variation but I think that if you could show that an animal-based diet is healthy, I think it'll very clearly show that inflammatory markers are lower. GI issues are lower. People might say, "Wow. Maybe we should put more people on that." Ultimately, it's just about people trying and seeing how they do.
Well said. Not much to add there. Really great conversation. Really fun to chat with you, Paul. Where do people find you? Where do people follow to learn more about your practice and your content? I know you have a Twitter, YouTube. What else do you got?
I've got a podcast. It's called Fundamental Health with Paul Saladino, MD. People can check that out. That's on all the outlets. I repost it to my YouTube channel. YouTube channel is just under Paul Saladino, MD. My website is carnivoremd.com. I see patients throughout the world and then I have Instagram, which is @paulsaladinomd and Twitter, @MdSaladino. If people want to get in touch with me directly to become clients, they can find that information on the website.
Awesome. Thanks so much, Paul.
Thanks for having me on.
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