9/26/18 E57 The Silent Epidemic: Fatty Liver Disease

So with the amount of research Eric does day in and day out (most of which he considers "fun time"), we should probably heed his counsel on what he deems as the next "silent epidemic". Today the guys discuss fatty liver disease - where it comes from and what to do about it. This one is important, so be sure to tune in.

Why is fatty liver disease silently creeping up on us?

How the liver is the "hub" of the body, and what it actually does.

80-100 million people have it (and don't even know it).

Eric gets into the science! - How fatty liver comes about

What effect does ketosis have on the liver?

What are the biggest contributing factors to liver fat?

How Eric has conducted his own case studies based on clients' genetics.

Gotta get that choline! (and where to find it)

And finally, how you can not only reverse fatty liver but also prevent it EVEN when you're genetically predisposed.

Did you know that one of the 5 micronutrients in bioStak is milk thistle? And milk thistle is actually considered the great liver detoxifier! If you haven't ordered your bioStak yet, go to biostak.com to get yours today (and clean that liver!).

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Transcript:

Eric: 00:00 It's sugar, glucose, fructose, same thing. Um, and people just overdo it and it's the same thing. It causes obesity. Same thing, metabolic syndrome, same thing with diabetes. All right. And why in the fifties and stuff you couldn't even find obese people to do really big studies. It just wasn't there. 

Chad: 00:21 They say a journey begins in a single step or in my case, one less piece of bread. My name is Chad and I'm your test subject. I have sought out an expert in the field of nutrition and fitness, so I hoped it helped me feel better. They call him the biohacker, but I call him Eric. I hope you'll join me on a path that leads, you and I to optimal fitness as we live our lives in ketosis. This is the life and Ketosis podcast, a biohackers guide to optimal body performance. 

Chad: 01:04 Hello everyone. My name is Chad and this is my quest to achieving optimal body performance with the man that can get me there. The biohacker himself Mr Eric Bischof. Every episode Eric gives us his crazy intense sciencey knowledge and I break it down with my regular non crazy guy take as we explore the principles of ketogenics and KPR performance training, whether you're just looking for a way to feel better or if you're an elite athlete looking for that edge. We're here to help. And today we're talking about fatty liver disease. Sounds so exciting. Everybody stay tuned in we're going to talk about disease. I don't, I don't mean to make light of it, but, um, I'm actually really excited to talk about this topic. Eric. This is something you and I have chatted about lots, but I still don't really. We haven't had that full conversation about what it is, why we're worried about it, how, how it comes about. 

Chad: 02:05 And so that's what we're going to do today and I'm, I'm stoked on it. I'm ready to have this conversation. How are you doing? Good. Good. How are you? I am fantastic. Back in Washington, right back. I, um, had a, had a week long trip with my 12 year old daughter in Manhattan. I saw that. That was really, really fun. But now we're back at it and I've been, I've been looking forward to this conversation. 

Eric: 02:31 It's good. You got, you got away behind. It's just the two of you, right? 

Chad: 02:35 Yeah, just the two of us there. We have a little tradition in our family, what we started. She's our first 12 year old, so, but where we've started a tradition where at 12 years old they get to pick a trip anywhere in the United States and cheap. 

Eric: 02:50 And she picked New York, Huh? 

Chad: 02:51 Yeah, she did. Yep. So it was good. I saw some Broadway and we ate some good food and walked a lot a lot of miles. 

Eric: 03:00 It had been awhile since I've been in New York, mainly because I didn't leave anything there so I didn't go back. No, no, no, no. I don't know. I just avoid crowds and dizziness and I'd like to be in quiet places because of my age. I guess we all understand. We understand getting old. I'm excited about this topic because it's, it's actually becoming an another. I don't know, another passion of mine. Maybe passions. I have. No. I'm really concerned about this and it's very concerning because it's like, this is a silent, basically had called a silent epidemic and, and I hate using that word epidemic, like it's, you know, the big scare in a word, but it is actually becoming an epidemic. And so we've, you know, we talk about diabetes. All right, we've got a , remember we got like 32 million adults, you know, with a, like 18 and over with, with uh, diabetes and was a core of 20 percent of those don't even know it. And I remember what in 10 year time from late nineties or something, a diabetes increased by 90 percent. So we know this is an epidemic, you know, everybody knows about it. Okay. Then we have obesity epidemic. One out of three are obese. A two out of three are overweight. We have teenagers, adolescents that are obese. So we. So we add that it nowhere in that epidemic, which we are, and now this fatty liver disease epidemic proportion. It really is. And those out there, it's something that you don't even, not even aware of that if you have fatty liver and all, and we're talking 70, 80 200 million Americans have, you know, we call it a Naf ld or whatever you want to call it. It's nonalcoholic fatty liver disease. I'll just use the word fatty liver disease because that's the beginning stage of it. So, and it's like doubled over the last 20 years and it's gonna be, uh, by 2030, even even earlier than that. 

Eric: 05:18 The, the, the stats coming out, is it just very frightening. And even doctors today that I've talked to, I've Dr Friends, they're like, hey, this is an issue and it's great to see the doctors actually, uh, being very concerned about it. And so, you know, think about it, the liver, you know, what's the bottom line is if your, if your livers is, is basically full of cirrhosis, cirrhosis and fibrosis, and it's gone liver transplant. And there's, I, we have a friend that's trying to get a liver transplant and there. So there's only one out of 11 are going to get a liver. So do you happen to the rest? There's just not enough liver so. So it's something real important. That's why I want to talk about it. So obviously, 

Chad: 06:04 yeah, that's very interesting. So I would never, I actually had never, and maybe this points more to my obliviousness than anything, but I had never heard of fatty liver disease until you and I started talking and I find that interesting, especially if it's getting to an epidemic sort of state a state. So what's, why isn't this more talked about? I guess one of my first questions? 

Eric: 06:31 Because no one's really aware of it and they didn't pay attention to because you don't see the symptoms right away. Okay. Everybody is symptom base. All right. You know, you've gotta have something to say, hey, there's something wrong with me. And you go to the doctor. The problem with fatty liver in the beginning, we call that the nonalcoholic fatty liver disease and a lot of people use the word that's been, you know, like the two hits first hit is what we call the non, a nonalcoholic fatty liver disease, which basically you're getting fat accumulating in, in your liver cells, okay. And so we've, we, we don't want fat in the liver cell and a, and I'll say why, but then then what happens in next, we'd call it a second or phase, I call it as Nash. That's a non alcoholic stay outta hepatitis. All right? And that's when it's becoming inflamed. Okay? And there's oxidative stress and there's, there's beginning of the damage and then that leads into cirrhosis, um, and then into a, a fibrosis and then to jaundice. And that's when you really have liver damage is when it went that next step beyond Nash. Uh, we'll, we'll talk about that. And so basically what we got to remember how important the liver is. It's, it's the metabolic hub, and I've used this word a lot. It's, it's the workhorse of the body, you know, and think of all the functions. If we had, let's say, Ketosis, of course we're burning fat for fuel in the liver, which is fantastic. We, it regulates glucose. Remember, glucose always coming from, you know, straight to the liver first via the portal vein. So that tops off the glycogen. Remember, you always have that glycogen reserve for fuel in case you go low for the brain and for other organs, uh, gluconeogenesis making of glucose, cholesterol, it regulates the making and removal of cholesterol. 

Eric: 08:25 It also gets rid of excess nitrogen and synthesizes hormones and fat soluble vitamins are stored there. And, and what? We all know, toxins, it's always there to remove heavy metals, drugs, environmental toxins, pesticides, you know, works in the making a protein. So here we're talking about something that is really, really important. It's like what? Three and a half pounds, I think the liver. And that's because it's got some jobs to do at may age. Yes, that's, it's the hub. Okay. Let's just, you know, and that's why it's so, so scary because what happens, we start getting the, the, the fat cells start accumulating in the liver cells. Okay? Fat Accumulation in liver cells and that changes the function of the liver and you see all these pathways that we're, that we're talking about. Here we go, it's going to interfere with any or all of these pathways. And so, and we all know fatty liver, it's been many years that it increases cardiovascular disease. I think man, it was like three or four times and women more than that. And then by by diabetics. It's like 10 times. So we've, we've, we've known about this, but you know, just like diabetes, just like obesity. Here it is, it, it's creeped up on us. And now 70 to 100, 80 to $100 million Americans have fatty liver. 

Chad: 09:50 That's interesting. Let's, let's dive into what, what we're actually talking about when we say fatty liver disease, right? I mean, you just told us that the fat cells are attaching themselves to the liver cells in them. 

Eric: 10:04 They're going in the actual, the droplets, the lip, a drop triglycerides, triglycerides are being stored in the hypnotic liver cell. Okay? So that's the storage. Okay. 

Chad: 10:17 So what's, what's, I'm assuming this happens to everybody, but at some point it becomes a problem? 

Eric: 10:25 Usually about after five percent to 10 percent. Okay. Of the livers weight okay. Usually when, if you're in that range, okay, but after that, that's when it becomes dangerous. Okay. That's when it becomes an issue. All right? So, so what happens in, in the liver cell itself, all right? Remember we have input, okay? And we have output, alright? So input, obviously dietary, uh, you know, coming in, I'm actually all right, you're going to eat fat, okay? Most of it Kyla microphones gets carried out to your lymphatic and goes that route. But remember we also have fat that needs to be taken out of the liver. All right? And so that's where it comes down to is if you can export the fat out of your liver, okay? Triglycerides. All right? And, and we're doing that the via the Vldl particles. Appleby. Okay. Vldl. And that's what we have to rely upon is how good are we at exporting, distributing the fat that goes to our liver. Okay? So how do we get fat to our liver? And the reason why it's epidemic is what we call de Novo Light Bulb Genesis. Remember we've talked about this a lot, okay? That's carbohydrates, excessive process foods, sugar, fructose, all these things that, that we eat in excess of. Obviously, you know you're, you're gonna have an issue of depositing that and burning it is fuel. 

Eric: 12:01 You get too much. Obviously it has to be done, dealt with, so it goes back to the liver and it's, it's created into triglycerides. All right, so the liver says, Hey, what do I do with this now? And here we have an issue of getting that, export it back out or it can store in the liver. And so there we go. And remember when we talked about spillover and all of a sudden you got to put this fat lipid droplet into a liver cell. It fills it up, it ends up pushing on the nucleus. All right, which is not good. It also squeezes out any chance for glycogen, glycogen storage. And what happens now, we got glucose can't be stored in, is glycogen in the liver, which is a main, a main purpose. Um, so now it ends up in the blood that increases your insulin, you become more insulin resistance and now the pancreas has to kick out more insulin. That liver kicks out more glucose. So this vicious cycle of making more triglycerides and storing it so there it's, it's, it's a vicious cycle and so we've got to do everything we can to make sure we can move the triglycerides out of the liver. All right? And we don't wanna make any more triglycerides. That's at Denovo lipogenesis for eating. You know, we're back to this again, obesity, diabetes. We're eating too much sugar or eating too much fructose. We're eating too much starch where alcohol of course, you know we have that issue so we're, we're, we're not balanced in, in, in our nutrition. And so that's why you look around and people 70 to 80 to 100 million people have fatty liver and they don't even know it. And so there's certain things you can look for that says, hey, how do you know if you have fatty liver? That's probably your next question.

Chad: 13:57 Before we go there though. I think it was interesting as you're talking about these, the hits or the stages yet a lot of them sound very similar to alcohol abuse and some of the stages your liver goes through that in that process. So that's very interesting to me that there's kind of a, I mean obviously they're both affecting the liver, so that makes sense. But like when you talked about jaundice and you talk about, you know, some of these other stages or hits, it's very similar to what it sounds like it is. 

Eric: 14:31 And especially alcohol. We know we have liver damage. We know that. Okay. Just it. Nobody's drinking, but I don't know. It's one of the worst things that kills liver cells but there's nonalcoholic. Okay. The fatty liver disease is the first hit you get, then it, once you get inflammation and oxidative stress we're back to this again. That Causes Nash is what we call it. Okay. And so that, uh, stay out of hepatitis is, is, is the dangerous accumulation because now you've got inflammation, you've got oxidative stress remember, we're back to that lipid peroxidation. Okay. In the, in the cellular membrane, again, we've got free radicals damage going on. We got the cellular membrane damage, we've got the fascial lip, it been damaged, the Mitochondria is now going to be in trouble. And so where are we back to again? We're back to cellular damage. All right, and anytime you have that lipid peroxidation you're going to have damage. Okay. And, and that's what we're trying to do is, you know, always talk about these free radicals trying to counter and of that oxidative stress that oxidative damage by free radicals. And what happens if fat, when you think about you're accumulating fat in, in, in, in the, in the liver cells. 

Eric: 15:53 So you're obviously going to increase the oxidation and you know the lipid peroxidation you're just, you're flaming it. Then you add more omega six fatty oils and different vegetable oils and things like that. We're really creating havoc in our liver cells and that's how the damage ends up getting to Nash, which is the inflammation. Then that gets expedited to cirrhosis. If you don't take care of it. I mean all of this reversible, it is reversible, you know, especially the, the, the first hit even to the second hit when you get inflammation, but the only way you know is well there is a couple like the liver enzymes, alt ast. That's something you can look at, but especially the alt, but it's not really not a good marker because a lot of people have fatty liver and their and their alt is is normal and then if you work out like before your blood tests and we've talked about this, you really hit it hard, hard, hard, that can raise your alt and ast and your liver enzymes, but it has nothing to do with the liver and fat being stored there. That's due to a muscle damage can also increase that. So I think it's a good. Even your gas, it is a marker because remember fructose, if you, if, if fructose, we won't get into it, but fructose is metabolized by the liver cell. That's where it goes. It doesn't go anywhere else. It goes straight from the portal vein, straight to a liver cell. It what it does, it phosphorolates and ATP takes that, breaks it down to ADP, down to amp to all the way down to uric acid. Uric acid can be a test for, for uh, fatty liver disease. So there's, you know, lots of different things. You can look at him, doctors can feel for it. I mean you can, you can actually feel if you liver is getting fat, you can do biopsy, you can do ultrasound, you can do an Mri. So there's ways to check to see if you do have fatty liver and I don't know, Chad if I have fatty liver high, I've never had enzyme issue the alt and the ast or in uric acid issues, but I still don't know. I really don't know. 

Chad: 18:03 There's no way to know unless you get some extensive testing done?

Eric: 18:06 A biopsy would be the best. Okay. Ultrasound would be good too. Okay. Um, but mainly, you know, by your nutrition. Okay. So those that are in keto, you really, you're really reducing your fructose. So you're really reducing your sugar. Obviously your starches, your carbohydrates, those that can go back to the liver. And there's, there's arguments about how much is Denovo Lipogenesis, you know, adding to fatty liver. I'm on the camp that says, Hey, it could be 20, 30 percent. That can be added because if you're obese and your insulin resistance, guess what, you're really increasing your chances of fatty liver that, that liver, the triglycerides are not going to be exported x, export it out of the liver via the Vldl. Not very effective at all. 

Chad: 18:56 What is your, what's your, uh, thoughts like? What's the, the culprit, the biggest culprit? Is it sugar? Is it carbs? Is it 

Eric: 19:07 straight up, processed food? Does it? They just add sugar. Okay. This add sugar and people don't know how much does it perseverative? Yes. Yep. Yep. Yep. And so then basically from that, it's sugar, glucose, fructose, same thing. Um, and people just overdo it and it's same thing cause obesity. Same thing. Metabolic Syndrome, same thing with diabetes. All right? And why in the fifties and stuff you couldn't even find obese people to do really big studies. It just wasn't there. But now you look at it, we got diabetes, we've got obesity, and now we have the fatty liver disease. And what's another portion is now we've got to get into the mechanisms. We have dietaries one nutrition obviously. Okay. And then we have genetic who is predisposed to fatty liver and, and that, and that's critical. 

Eric: 20:01 And so what I did, I just thought, you know what I'm going to. And people you know, and I think people, listeners know that, that I do gene study and I do clients and I look at all their genetics and different, you know, nutrition diseases anywhere from Parkinson's, Alzheimer's, cancer, heart disease, liver. And so what I did, I went through and I pulled up. 

Chad: 20:23 Let me, hold on just a second. I just want to make sure people understand. Yeah, it's really neat for me to have these conversations with you at this point because you have enough time and enough clients under your belt. Then you can actually start doing your own case studies on this kind of stuff, which is pretty phenomenal. The database, you've, you've worked with enough clients that have fatty liver disease, you've worked with enough clients that have diabetes, you've worked with that. You can start seeing patterns and identifying snips and it's just really cool that you yourself rather than just the years of reading studies that you've done now you're actually doing studies in a way like. And I think that's a really cool perspective to come from. So anyway, I'm sorry I didn't mean to cut you off, but I want to make sure people have that legitimate that it, it legitimizes the information that you're giving. 

Eric: 21:18 Yeah. Because you know, and I appreciate you you're doing that because I just thought I'll just keep going. But anyway, I have a different window to look through now. An extra window, a real important window to say, Hey, let me look at this. The polymorphisms, these mutations that would be involved with lip fatty, liver disease, liver disease. Okay. So what I did, and I pulled out 20 clients and pulled out their, their full genetic profile. All right. And so at random I just grabbed 20 and I said, okay, I'm going to take this 20 and I'm going to actually analyze their liver genes. Okay. That would promote a fatty liver or any kind of liver disease. And then go from there. So what I did, I, I pulled out 20 and there's a gene pack that I could upload all these two different analysis, uh, sites and people know there's various ones out there. And so I uploaded it to a gene packet that says here this, this certain pack of genes would be involved with liver disease, fatty liver disease basically. All right? So I took those 20, put them through there. And what happened was out of those 20, which, which I broke everything down, they were graded automatically by a certain, you know, set of um, uh, gene snips and that will be covered. Like I won't go into them. The fruit to the PMA PMT, the stat three, a that PGC one, a TNF, there's more the Vega, the VGF A and l, well there's like 10 or 12, so I can't spend too much time going into them. And I said, okay, let me look at that. And so out of the 20 when I, when I pulled that up, the grades were bad, you know, very bad. Good, very good. 

Eric: 23:08 Okay. So out of the liver, grade, out of the 20 1 was bad. Twelve, we're very bad. Three were good and three were very good. So I'm like, Holy Crud. 13 of the 20 were were bad and very bad and I'm like, that's not good feeling. They're very susceptible. Yeah. Very Sad. Yeah. So they have their liver disease with these genetic snips, polymorphisms and mutations you want to call him are leading toward liver disease? Yeah. Not Good. Not good, but was interesting. There's one and I have all the studies and I won't go. I don't have to go into too much detail with it, but the one of the biggest snips that most, most everyone knows out there that you look at, is that PNP la three. Okay. That's a genetic mutation that mainly that's a protein that promotes the transfer of these essential fatty acids from triglycerides to phospho lipids. Okay. In the hepatic lipid droplets basically, which helps in transport, getting it out of the liver. Okay. That I've already talked about. So there's three of these mutations that were not listed in this. This one analysis that I just talked about. So I said, well, let me go look at those and see what was out of the 20, what issue because those are really critical and there's, I have countless studies downloaded on this mutation about this really leads into, I mean, you read any of the studies, they say this, this a Geno type shows significantly association with nonalcoholic fatty liver disease and Nash fibrosis, Cirrhosis, etc. So the studies are out there to really push it and kind of clarify it. So I went through and I said, okay, who's got this piano? P l a three. And I was shocked out of the 20, 9 were heterozygous. 

Eric: 25:00 Okay. That means you have one of the risk illegals. Okay. Not homozygous where you have both. All right, but you're still heterozygous, which is not good. Out of the 29 were heterozygous and then just under 50 percent and then 10 were all good. They, they did not have the risk of leo. And then one strange person out there, there's three genes that they looked at and everyone that the nine were heterozygous and all three, not just one or two, but all three. And I thought, wow, that is strange. Why are they heterozygous? And all three. And the only one person who was the different person had one good one and one bad one. And that was me. I don't like where did this come from. But everybody else had all three heterozygous. They had the lille, which is, is, is not the is not good. That's the risk of leo. And then 10 had good. But out of all of the, out of all those that I tested, remember when, when they got their liver grade, there was 13 of them were bad. But then the piano, the pla three showed good. So there's a big difference there, you know, because if you would've seen this, she said, oh I'm, I'm very bad on my liver. But then when you looked, you're the pn pla three, they're all good. So now you've got to do your further homework and say hey, that's good. I mean that's a good sign, but anyway, and then so it was just really, it just jumps at me that liver fatty liver disease is an issue and I said, well, there's another factor really important with, with a fatty liver and that's coleen and, and most of people out there and know about coleen and really what calling does it synthesizes fossil turtle, coleen, okay. 

Eric: 26:56 in that cellular membrane to make up that vldl, that exports those triglycerides out of the liver, you've got to have coleen. All right? And I Said, well, let me look at everybody's coleen, and out of theIr snips there's like three. And I think there's like three or four. It's a mthf dijuan, the mtr and of course a p, e, m t is a big player in this. And I said, well, let me say on that, on, on the coleen. And because pmt basically what that is, and I try to keep it short. That's a gene that kind of governs the secretion of, of those triglycerides in the form of vldl, the lipid protein that we talked about and it's very, it. It's always implicated in nonalcoholic fatty liver disease, so remember it's the accumulation of triglycerides in the liver for this fatty liver disease that occurs as a result of the imbalance of fatty acid, Incoming utilization and getting it out as vldl. So what I did, I looked at coleen and out of coleen of all, all those coleen, the very bad were 14. They had the genes of being deficient in coleen and one was bad. 14 were very bad, and then only five were good or very good. So I'm like, oh gosh, these people really coleen, and as far as genetically, they're predisposed to coleen deficiency and it's just like, wow. And that's something that, that, that you've got to pay attention to and that's why I push a eggs and liver to, to all my clients because I want that coleen there to make sure we get the triglycerides out of the liver. But when you look at this in that pmt, I said, all right, let me look at everybody's pmt and see that's a critical one. And out of all those homozygous meaning both risk of deals, 10. 50 percent had homozygous pmt they have an issue with with that fascial tittle, coleen. And then the other were heterozygous 17. Only three had no leo, no risk. Three out of 20. I had no risks with that. Pmt. And I, it really, it, it, it really gave me new insight guys. We've got to pay attention to have you liver disease. We don't. We've got to get on top of it. And so. 

Chad: 29:35 So I think there's a, there's a dolly parton song about coleen, right? Oh no. no, it's. Yeah. Yeah. I'm just trying to break it up here. No, I'm, I'm Listening, but I know, 

Eric: 29:50 I know. I'm sorry I on this, but when I got into the genes, because this is. remember, this is what you're predisposed to. It's not your blueprint. All right? And If you've been living good nutrition and healthy and your lifestyle and even exercise of course plays a big role, but if you're diabetic, you're obese and you, you've abused yourself nutritional wise. and it added a 20. I know I'm going to go further with this and get deeper into it, but when I randomly pulled 20 and it just a big negative picture, I, I was really, really surprised. And, and even I like on mine, I show on that liver one, it shows a plus a and there's a few that I was one of the ones with a plus, but then when it got down to the p and p, l e three, I was the one that had one bad one, one good one. And my, coleen isn't so good. So it was just really, in fact the only two I have to say ran not completely random. I pulled mine out and I pulled my daughters out. And um, so those are the two that, that, that I do know of. Okay. And in her coleen was, was very good and she had no risk whatsoever in her coleen and non in her illegals shooting get. Obviously I have one risk. So she, she got my good one. She obviously had a good one from our mothers. that's what. So she has no risk of wheels and all three. So anyway, that's kind of interesting. I didn't mean to dive into that too deep, but I thought I better share that. 

Chad: 31:26 Yeah, yeah, that's interesting. And what I hear you saying, and maybe if I can just recap it, you let me know if this is kind of the main point you're trying to get across in, in that last place or that last part was this, this understanding these genes and these snips and that kind of stuff is not a destiny. You're not destined to these things. Now you can reverse them, you can modify them, you can put the bad ones to sleep. Um, exactly. As long as you're doing the certain things within your nutrition and exercise and all that kind of stuff and taking care of yourself. These don't need to express themselves. 

Eric: 32:09 No. And, and you know what's in work with your doctor. If you're obese, your diabetes, there's a good chance, you know, I'm just going to say your fatty liver disease, your, what we call the noun. All alcoholic fatty liver disease is, it's there. Okay. I'm, I'm just, you know, I can't guarantee it, but it's an issue. And if you're coleen deficient, just the odds are that, you know, from my stats, I just say, get your cruciferous vegetables, get your, your, your coleen into a eggs and liver. I'm a big pusher of organ meat for coleen and vitamin a and full eight and you know, I won't get into the methylation part of coleen, but that's critical for your methylation. Coleen is a really helps there. And I'll, I won't go down that path right now because we've run out of time, but I have all the studies, um, you know, downloaded everything on the backgrounds and nonalcoholic fatty liver disease as far as the genes and, and it's there. It's there for people to study if they like. 

Chad: 33:17 So dietary, dietary is a big deal. You've, you've mentioned this over and over again. Eggs, I'm organ meat liver and there's frozen vegetables. Coleen supplements. Um, and um, those, those are all really important that I get that we know what that is. What, uh, what about movement? What about, I mean because. SO this is one other thing I didn't want to brush past and maybe I misunderstood, but I want to get some clarification is that I think towards the beginning of this conversation, you said that fatty liver disease relates to cardiac disease in some way. So can you talk about that and then does, does being, does adding movement into your life? 

Eric: 34:05 Yes, yes, for sure. For sure. Because a part of the problem is it in, in inflammation, in especially uric acid and fatty liver disease, we're creating inflammation and we're also losing out on what we'd call them in the, in the coronary arteries is nitric oxide synthase. Okay? What that does, that's your vessel dilator. Okay? And so if you want those arteries to be dilated and when you have a fatty liver and with like diabetes and obesity, you increasing the inflammation. so you're going to have limited amount of nitric oxide synthase. So you're going to raise your blood pressure, you're going to have cardio vascular issues because of that. So like a direct link right there to cardiovascular disease and course you want your, uh, all your arteries and all your coronary arteries and every, all your vascularity to have the nitric oxide synthase because you want it to be dilated. 

Eric: 35:07 So you want to avoid blood pressure, high blood pressure. So that's a group that's one of the big connections right there and your acid and all the rest of it all. It's all connected. And with diabetes you of course, we all know inflammation, insulin resistance, we know the issue of insulin resistance, you know, behind most all chronic diseases and now you just add fatty liver on top of that with, with that inflammation and oxidative stress and everything. Then you're just on your, your cHance for, for issues to have with your health. So we don't need to add this to the plates, but we are. We got diabetes and alzheimer's. That's a different issue, but these are all preventable and reversible type of illnesses that we can take care of through nutrition. Of course, exercIse is key with all of it and that's why I really appreciate ketosis because it's going to lower your sugar intake, it's going to lower your fructose intake, it's going to lower your process, food intake, it just forces it down that path and those are the culprits in kids. Kids are getting fatty liver and, and I didn't even Want to go into that section of my, of, of, of what I studied and that scary. Just think all those sodas and, and, uh, uh, high fructose corn syrup. Ouch. Don't, don't get me on that subject either. But anyway, guys, I apologize if I went a little long on this one. 

Chad: 36:37 Maybe let's finish on this if that's okay. This can be super brief and I don't know how much you've thought through this or not, but if somebody. I mean, if somebody is experiencing obesity, diabetes and even if they're not, but they just know that their diet hasn't been great. They haven't been moving a lot that they think they might be susceptible to or, or might have fatty liver disease. What, what do they do? What I mean? Sounds like first steps are change your diet and your exercise. Change your diet, your exercise, your second. Yep. Secondarily, what? What? What's important? Do they need to be tested? They need to start monitoring it. What's the I.

Eric: 37:22 I would definitely. If you're obese and your diabetes and you're overweight and you're showing some of the signs of inflammation, you're tired, you're fatigued. Muscle. I mean you. You can take this all the way down to some muscle damage. You're going to have those certain marker, especially if they're all high. Okay, you're a gas and then the doctor would say, hey, let's figure this out. Something going on with your liver. A doctor would do that, but sometimes your test will come back totally fine and you still have fatty liver and if you're really interested like I'm going to, I'm going to go ahead and have ultrasounds done and even a biopsy. It depends on the expense of it because I want to know what damage I did to myself when I was, you know, low fat, high carb years. 

Chad: 38:06 Yeah. So are there, are there any medications that big pharma and doctors are trained to push with this? Like I mean, I mean, I know when we talk about the ldl, the lvl, I mean there's, they're, they're pushing statens really, really hard and you've talked very adamantly about that. Like don't, don't let this be your first resource. Is there something like that with fatty liver? 

Eric: 38:31 They have one, they're getting there on somebody. Even metformin seems to help reduce some fatty liver because it, it kind of a, it's kind of fakes you out. Like it's an amp and it says, hey, bring in more sub substrate so I can burn it as fuel. But the metformin has. But these, these issues that there's others that just, they do have side effects and it's not worth it. So if you can reverse, if you're just at a nashville day, you can reverse that and just clean up your nutrition and uh, hopefully we'll export all those stored triglycerides. And there's people that are obese that, and I don't mean all people that are overweight are going to have this because if they don't show them the markers, the biomarkers there, they can be healthy as myself, you know, but they're obese, they just haven't gone into spill over yet. Have that metabolic syndrome forcing fat, you know, the triglyceride liquids to be stored in the liver cell and then causing in and wreaking havoc with oxidative stress and free radicals. So I'm not gonna say all obese people, if you're healthy, obese, I mean, you know, your, your healthy fat, which is great. 

Chad: 39:35 Yeah. And the opposite of that as well as I would say, and I've heard you talk about is you can, you can be seemingly a fit, not even fit but, but, but right, be okay on weight, but still have fatty liver with, with a bad diet, right? I mean, I know people who have terrible diets and they don't, they're not overweight, but they're still really susceptible to this. 

Eric: 39:58 It comes back to that insulin. You can be insulin resistance and be really lean and that's one thing where you have insulin, you know, you can have high glucose, low glucose, and still have high insulin and you don't know that it's the insulin that causes the issues. And even that's why I, I'm a fan of ketosis because you can't have both. So if you're in beta, you're showing beta one point five, whatever, then it's an antagonist to insulin. You can't have both. So if your betas is good, your insulin's going to be down. If you're in your beta is down, your insulin can be up, so that it's a great way to say, hey, I don't know my ins fun. Nobody tests their insulin a, you test your glucose. It's just a great way to, to stay on top of it. 

Chad: 40:44 Right, right. Well, this has been, this is a big deal and this has been an interesting conversation. Um, and I'm, I'm, I mean it's, it's surprising it took us this long to get to this conversation, but I'm just glad we've had it and uh, and I want to remind people, uh, we're available for questions. Um, I mean you've made yourself available to a lot of listeners for any questions. Uh, we're not going to make any health recommendations that need to be made by a doctor or anything like that, but just general information, we are more than happy. You're more than we, I say we, I, w I wouldn't be much help but eric has been so good about answering people's questions and communicating about this stuff. So I want to, I just want to make sure people realize we're not just voices in ear in earphones. We are here and we have resources, we have websites, we have facebook pages and instagram pages where you can reach out to us and talk about some of these things because this is, if you're anything like me, this just get some thoughts firing and like, well, what do you know, what if's and, and that kind of stuff. So, um, just know that we, we want to be more, we want to be a resource more than just voices. Um, so this has been great. Thanks so much for biohacking with us today, eric. No, I appreciate good apps. And, and I also don't want to, I don't want to leave this conversation without saying um, or reminding people bioStaks launch were, were people are getting it. Experience has been amazing. Go to biostak.com. That's again, that's bio stack without a c, so it's b I o s t a k.com. And grab your biostak. This has been really exciting to get the feedback and hear from people and the end to see it go out into the world. So I'm not going to say much more about that. 

Eric: 42:36 In fact I've been working on this. Fatty livers got me, so no has got me so involved I'm actually working on a stack to, to help with fatty liver disease and I have been working really hard on it doing a lot of research and it's a really. I don't know, this, this one's got me nervous about the future for people who really does just by, when I look in the genetic issues of it and those that are predisposed and it just looks tough. It does, but not not trying to scare people at all. 

Chad: 43:10 Yeah so check back with us in three years once Eric has this stack. Ready? No, I'm just kidding. It's not to take that long. I'm just kidding. But seriously, go to biostak.com. You can get tons of information there. Get your bioStak, see how great you feel. Uh, it's, it's, it's been incredible. So anyway, thanks again, eric, for, for all the information today. I think I can speak for a lot of people when I say the work, the amount of time and everything that you put into this research and then now relay the information is just, we're so grateful for it and it's huge. So thank you. Thank you. Thank you. 

Eric: 43:49 Well, I, I keep trying. I don't know everything guys. I just keep trying to learn. That's all I can do and if I make mistakes I'm sure, I say things wrong, but bear with me. I stay on top of it. 

Chad: 44:00 Yeah. And I want to say I want to thank everybody else for joining us on this quest for optimal optimal fitness. If you're ready to begin your own journey and live your life and ketosis, be sure to check out biofitcoaching.com or biofit coaching on instagram and that handles @biofit_coaching. Also if this podcast has helped you at all inspired you and entertain you, we encourage you to go to itunes or wherever you are, wherever you get your podcasts, and leave us a five star rating and a glowing review to help us continue to grow the community. And finally, the greatest compliment you can give us is sharing this podcast with your friends and family, those who are looking for a different way to live. And until next time, stay keto.