E23 Keto and Cholesterol: The Real Story

For years cholesterol has been labeled as the silent killer, but what's the real story? And what does the keto diet have to do with it? On today's episode, the guys tackle the myth behind "high cholesterol" and discuss how the keto diet can actually help compliment healthy cholesterol levels. This wide-ranging convo also delves into Chad's creeper beard and Eric's porno stache, so you won't want to miss it!

How cholesterol is both the substance of life and death.

The debunking of the low-fat hypothesis.

How your body regulates healthy cholesterol homeostasis.

Why your body depends on cholesterol.

Eric gets his science in! Learn everything about how cholesterol travels through the body (literally everything...)

What are LDL receptors and why are they important?

Best question of the episode goes to Chad: "Can we prevent oxidation if we just stop breathing?"

Eric shares his own blood work numbers.

How the keto diet improves the way our bodies interact with cholesterol.

Learn the truth behind one of your body's most important building blocks: cholesterol. Who knew right? Including data that shows that higher cholesterol levels correlate with LOWER mortality rates. Lots of science in this one as Eric separates fact and fiction.

Also, be sure to listen until the end to hear about some exciting free gifts coming up for podcast listeners!

Don't forget to check out the podcast recording on YouTube to get the behind the scenes look: https://youtu.be/SapybVuNUJ4

If you have any questions on this episode (or any questions in general) don't hesitate to reach out to us at bioteam@biofitcoaching.com.

And If you're interested in starting your own journey, you can find out more information at www.biofitcoaching.com or on Facebook at www.facebook.com/becomebiofit.

Transcript:

Eric: 00:01 I had a mustache for a lot of years just from an apartment house, and so my kids will keep calling upon our stash and I'm like, ah, yeah, you guys kind of creepy looking like the 70 porn movies or something. I finally agree with this, but I. I did say that when you see those guys pictures of the creepers in, you know, they get arrested. It's all going on. Same. Yeah. I appreciate it. They say a journey begins with a single step or in my case, one less piece of bread.

Chad: 00:49 My name is Chad. I'm your test subject. I have sought out an expert in the field of nutrition and fitness who I hoped would help me feel better. They call him the biohacker, but I call them parents. I hope you'll join me on a path of leads, you and I to optimal fitness as we live our lives in ketosis. This is the life in Ketosis podcast, a biohackers guide to optimal body performance.

Chad: 01:17 Yes.

Chad: 01:25 Hello everyone. My name is Chad and this is episode 23 of my quest to achieving optimal body performance with the man that can get me there. The biohacker himself, Mr Eric Bischoff every episode, I will be sharing my actual results, both successes and failures as Eric teaches me how to apply the principles of Ketogenic and functional movement to look and feel fantastic. Just as a reminder, the first five episodes of this podcast are foundational episodes. That's where you get your foundation in knowledge of Ketogenic Diet and functional movement that we talk about here on the podcast. So if you had to listen to those, go ahead and push pause right now. Go listen to them and then join us back here. And today we're talking about a widely misunderstood topic, right? Wouldn't you say? Yes. Clean Myself. Very blessed are all cholesterol. So let me just give you a quick little history with me and cholesterol. It's very short. It's not a long history at all. Um, but basically I, I have lived my life thinking cholesterol was always a bad thing. Um, that's what kills people. That's what clogs arteries. That's what gives people heart attacks. I don't know, I just, you know, you hear high cholesterol, you hear cholesterol, blah, blah, blah, blah foods. For awhile it seemed very popular to come out and say, you know, whatever. No cholesterol or cholesterol or it was not on like the cheerios box.

Chad: 02:56 So what's the big hubbub about cholesterol? Well, cholesterol is

Eric: 03:00 it, it's a big topic. It's an important topic and it really is because that's the big concern that we have out there. OK, if you think about cholesterol, we could call it and the substance of life. OK? And we've talked about cluster and we've talked to how, you know, it's a precursor to sex, a steroid hormones in a lot of that stuff and I won't go back until that, but it is the substance of life. But then again, it's actually a substance of deaths, but it is the substance of atherosclerotic cause of death. OK. Heart attack or cardio vascular disease. And it is because bottom line, it's where we got to talk about cholesterol and obviously it's a sterile. OK. So what is the big concern and what's the fear is like you had and others have. And what the US dietary guidelines taught us 40 years ago is that cholesterol is bad because it's going to increase your risk of cardiovascular disease, a atherosclerotic plaque, which would cause blockage in the heart attack and die.

Eric: 04:11 OK? So that's the fear that's out there. So it is the sterile from the cholesterol that's going to penetrate your endothelial cell wall. OK? The artery, and we've talked about this before, is the stairwell from the cholesterol that will go what we call the Sub Industry Leo in to the space behind it. And that's where it starts to create the plaque. And of course it calls in the immune system. The macrophages come in. Then we have a phone sale and we create that plaque issue there. OK? So it is from the sterile, but we need to talk about cholesterol in another way because cholesterol, you have to, you can't live without cholesterol. So it is, it is what will cause the atherosclerotic plaque. But it will talk about it further, but it's not. It's a great thing. Cholesterol, we have to have it to live. You didn't have it.

Chad: 05:05 When you say it's a sterile, what does that mean?

Eric: 05:08 A lot of it, we call it a little bit, but it's actually in the alcohol family. That's a sterile. OK. But you know, we'd classify as a limpid because remember in cholesterol and a lot of us already know this is where do we get cholesterol from? What you were talking about was what we call exile genus. And that's a big word now out there because everybody knows the word because we're talking about anxiety as ketones is Beta hydroxylated molecule. All right? So this is basically something from the outside coming in.

Chad: 05:08 Something foreign.

Eric: 05:39 Yeah. foreign . Dietary. We call that exogenous. OK. So they were trying to tell us and they've taught this and it's really sad. It really is because they, they were adamant because of without any good clinical studies or data behind it, they, you know, go into all the, the fat hypothesis and you know, I'll, you know, we've talked about before but

Chad: 06:01 we try to avoid the political topics on there.

Eric: 06:04 But, but the fear was that dietary cholesterol, exogenous, when you eat it, it's going to raise your cholesterol. All right, so that's when they said 200 milligrams. Then they said, ah, let's move that up to 300 milligrams. Oh good. Now you have an acre and a half you can eat per day, and, and that's, and that's what we live by and everybody was low cholesterol, but then all of a sudden the proof starts coming out. The clinical studies and, and this isn't like new stuff. I mean this was back in the early 19 hundreds. They were talking about cholesterol not being bad. I mean in different studies, you can go back quite a ways, but they now the proof was coming out and saying, hey, maybe it's not the dietary, the exotic and his cholesterol that's causing the issue with any type of atherosclerotic issues, you know, heart disease, et cetera.

Eric: 06:58 So it's now it's, it's sad to say that the US dietary guidelines now, and you may, you may not know that whereas our cholesterol limit today, it went up to 300. OK, but where is it today? Today, the US and [inaudible] actually, they said there is no upper limit on your cholesterol. So what does that tell you?

Chad: 06:58 It tells me the government tries to regulate everything.

Eric: 07:29 I think they couldn't, you know, because remember it's about saturated fat is going to raise your cholesterol, raise your cholesterol, is going to raise your scrotum, plaque, your diseases, cardiovascular disease, etc. Without really studying cholesterol and how the different types of cholesterol, the, the light bulb proteins that carry it. And you knoW, we gotta break it all down. Ok? So the dietary that you were concerned with is no longer a concern, but I still have biofitters and those out there to say, hey, I think I'm eating too much and eating too much of this or that and I'm getting too much cholesterol.

Eric: 08:04 And then I go, ah, then we've got to have a podcast like this.

Chad: 08:08 yeah, we're eggs, the big cholesterol foods.

Eric: 08:11 And that was a big. Oh yeah, cause you can get 200 milligrams a, uh, from an egg. Ok? And most people that was your limit was 200. And so it just like the saturated fat hypothesis. And then you have the sodium hypothesis and how you had the cholesterol hypothesis. They're all, they're crumbling, crumbling quickly, but in a way if you think about it, the low cholesterol foods and then the saturated fat, which we'll talk about that a little bit because that's the cobra. They say, eat more saturated fat, you're going to raise your cholesterol, but the saturated fat, the food industry was just responding to what they were saying. Then the food said, hey, well if we we've got to go low fat, so what are we going to do?

Eric: 08:51 We're going to create low fat foods, and so they had choice. They went that way because every instructor, that's what the government said. So you can't blame them in a way I do now because they're not getting off that train. And more and more though you have people out there, you hear it all the time about cholesterol and saturated fat,

Chad: 09:12 So is low cholesterol and low fat related, or are they. Are they synonymous? Wha. Why? Why do you talk about both of them in the same way?

Eric: 09:22 It was ok, but you can actually see studies, clinical studies on a low fat. There was one, they did a 50 day study, if I remember correctly, I'm 50 days and it was very, very strict. Ok. They, they went to, they had him on a low fat and high fat and they checked their baseline cholesterol levels. Ok, so in the test itself, they stayed there. They, they, they resided there. They were fed there. They literally made sure of their, their intake, their meals were completed, everything. They gave him a diet that didn't raise their, their weight or lower it and you to just keep the way that the low fat and high fat baseline levels of costume.

Eric: 10:11 And so what does that tell you about the low fat when you go low fat, what do you, as we talked about before, what do replaced that with

Chad: 10:22 You're getting more processed foods, more processed and more carbs.

Eric: 10:28 You know, the issue of triglycerides and they actually, they show that you can actually with a high carbohydrate diet, ok, process that, that triglycerides you're eating. If you're eAting too much of it, you're going to do what as we talked about, you're going to convert those triglycerides, access to the fact your liver is going to have no choice. It's going to have to store that because you're not burning it. So then we get into what we're talking about light bulb proteins, because we're going to talk about a little bit about how, how it's carried around and, and, and the importance of it because there's different. And you know, we've talked about [inaudible], l, l, v ldl, ok, triglycerides and the ratios.

Eric: 11:16 We've talked a little bit about that, but when you eat a dietary cholesterol or even yet or fat, ok, you're eating a meal. You've got to get it into your, into your body. So how much dietary cholesterol that you eat actually gets absorbed by the body. Very little, very little, ate. Most of it gets extra fired and excrete it, ok? Because it's competing with. Remember your liver sending cholesterol, you know, through bile acids to your stomach, and that's what emulsifies the fat that you eat. SO you have cholesterol in the bile acids, but you're going to regenerate that when the, when the body needs it, it's going to say, hey, stumble. So let's taKe this back into your internal sites. Ok, bring it back in. Ok? So this stuff you're eating is going to be excreted. I can. Your body makes almost all of your cholesterol.

Eric: 12:10 your liver makes 15, 20 percent. Then all your cells and your tissues make its own cholesterol. Then you're really generating it from the bible. when the liver says, hey, let's get, you know, it's taking cholesterol out of your blood, making biles, getting it out of your system. Then it as it needs it. So it's in control. I mean it's a fine line, but, but your body is always, you know, you're going to hit that homeostatic state basis and just keep it equal. At least work towards it will probably show that dietary cholesterol. If someone tells you that and convinces you, doctors will still say, watch your cholesterol. And I'm like, are you serious? It's really not the problem. The problem do still teach that because that's all you know.

Eric: 12:54 But we're going to talk about the problem, right? There's two things. There's two main things I want to talk about in this podcast. The first one is we order whatever order makes sense for you. But first one is when does cholesterol become bad? Right? And what do we watch for and how do we, how do we fix that? Second one is why is cholesterol good? Why does our body created? What is it necessary for? um, but before we go there, dId you notice that I shaved? Yeah.

Chad: 13:25 Last week we sat down for the podcast and we're in a route that was good for eric told me I had a creeper beard down. A little bit of a neck beard going on. So those of you watching on youtube, or if you're not, if you're just listening to the podcast and go on youtube, you can see my clean shaven shelton. Could we get a close up on my face?

Eric: 13:45 So I didn't mean that in a bad. But here I had a, I had a mustache for a lot of years just on an apartment that was in 80 seven. And so my kids will keep calling it a porno and I'm like, yeah, you guys can increase [inaudible] porn movies or something. I finally agree with this. But I, I did say that was kind of. But you see those guys pictures of the creepers and, and you know, they get arrested that going on. He looked better.

Chad: 14:27 I appreciate it. I do that for you. Think she appreciates nothing worse than a cooker husband. So where do you want to start? Do you want to start with the good? The, tHe bad? The bad is, is

Eric: 14:39 concerned about really? Ok, because we've talked about the good quIte a bit. So when you eat saturated fat that you're taking in dietary wise, in your cholesterol, obviously you're going to move the fatty acids into your system, ok? So obvIously you're going to digest it. You're going to have those bile acids there. And most of the fatty acids, those, your triglycerides that you're eating, ok, they're going to break down going to the burial site, ok? Then that's going to combine with cholesterol, but to move, these are fat, fat. So they're insoluble, ok? They're, they're hydrophobic means they don't like water. So you've got to move that into, you know, into your bloodstream. It's gotta be moved to your liver, it's got to get to your organs, your tissues, your adipose tissue, on your muscles, right? So it gets packaged and what we call kyla microns.

Eric: 15:27 So this is coming from the stomach. Ok? Kyla microns, that's a light bulb. Protein and everybody, if you think about it, we need something to carry that triglyceride and the cholesterol and phospholipids are in there and some fat soluble vitamins because they got to get through the blood and water. I mean it's, it's not going to make it through it unless it gets carried through it. Well referred to fat. Yeah, light bulb and proteIn. So there is a protein, lipid protein. It's a mixture of two. Ok, good call. All right, so the protein part, we'll call it, it's what we call an apo b. Ok? Apo lipoproteins. And we have different cognitive april be a poet, but what's going to carry the chylomicrons that's coming from the stomach. Ok. Exotic and exciting that's coming through is going to be [inaudible] we call [inaudible] 48. Ok, that's just its percentage length of apo b. One hundred that carries from your liver.

Eric: 16:21 Ok, I'm going to get to. You told me don't go science and somebody just get left. The thing that I don't let eric ramble a little bit stuck already. Let eric though. let them go. All right. Well anyway, so we've got to get that out your stuff and we've got to get it into your system. Ok? So what it does, obviously it's going to go through the lymphatIc system. Thoracic duct, which is a chylomicron is going to go. So it's going to package it up and get that triglyceride and, and that cholesterol just a little bit, but maybe it's not coming from your dietary cholesterol is coming from that bile acid that we generated because the cost. Because liver says, hey, I need some. Ok, cause it delivers the boss. All right, it's the matter of all the cup. All right, so you're going to bring that in.

Eric: 17:07 The first place that goes, that fatty acid, that triglyceride chylomicron, I'm going to travel to the heart first. Ok? Heart doesn't need it. And as far as energy source. So what's that's doing? That's packaging the triglyceride. Ok? The purpose of it, most of it's triglyceride, it's a big molecule, is to get the fatty acids to what? To your muscles for energy or if not adipose tissue to store it. All right? So what that does that goes through the system. Heart does a heartmate. [inaudible] heart loves fatty acids. Ok? So what happens? It'll stop wherever it needs to go. And we call that the lipoprotein lipase in the lpl. They come out in the capillary. I won't to go science-y, but that's what it says. That's a signal to say, hey, give me some of that fatty acids because I needed it for energy in the muscle or I'm going to store it. So that's there. You're just in the capillaries. It'll say, hey, break it down. Give me the triglyceride. Gave me that. Let's roll. Let's break that down. If I need some fat soluble vitamins or whatever, so it dissolves the fat.

Eric: 18:07 So that it becomes like, how am I going to get smaller and smaller, obviouslY then the reminisce will go to the liver and then that'll go through a process. But the difference is, remember we have two sources now, ok? That's exhaustion is coming in. But what about indogenous? Your body makes it ok? So we go to the liver now, now we talk about what we've heard a lot about as a v, ldl, very low density light bulb protein. Cause remember we got the word out there is it gets to the ldl, which we've everybody likes to call that the bad cholesterol and the age deals. The good. Ok? So here we are, the [inaudible]. The liver makes that via ldl and its purpose is to say, hey, I've got triglycerides coming from the adipose tissue that I need to package up, ok? Or I'm got it from excess carbs that I'm creating a triglyceride.

Eric: 18:59 How? Ok. so it packages up on the ldl, that's the carrier you want to call it a boat or Bus a ship, whatever. ThAt's that protein's going to carry that, um, that, that'd be deal. It's got to terry the, the triglycerides and cholesterol. Ok. So it will push that out. And that's carried by april. Be ok. That's the [inaudible] protein. So that's coming from the liver. YOu can have some kyla migrants coming from the stomach. Bottom line is we've got to get fatty acids, triglycerides out there as an energy source. Cholesterol is just not a lot of it because it delivers, not producing that much, but the cholesterol is getting attached there to and some fat soluble vitamins or whatever are going on the ship or carrier, whatever you want to call it. So it's, it's on it too. And so that goes out. And then that gets used up by muscles and tissues and obviously it that the ldl or get broken down, just like the kalo micron.

Eric: 19:55 You'll take the triglycerides and then eventually it'll take the cholesterol. And so what we work on our way down is we're going to the ldl, then it breaks down to what we call intermediate, a low density. Ok? And then, uh, then we'd go to ldl, low density lipoprotein. Ok. So we have intermediate density lipoproteins and then we have a low density and that's ldl. That's the one we, that's when we're concerned about. Ok, that's the issue is ldl is what everybody, when you have your cholesterol checked and there's markers that we look at to say, hey, you're at high risk of a cardiovascular disease. Ok, they really going to look at your l, d, l not ldl cholesterol because that is a certain number that you have on your, on your basic blood lipid, but is how many of those particles is what we're after.

Chad: 20:49 And the health system in your blood system.

Eric: 20:55 Yeah, cause your liver. Ok. What happens is when that member. We've talked about these ldl receptors and they've been on podcasts, we've talked about, your liver is the largest spot for your ldl receptors. That's your main area that takes the cholesterol out of your blood. Ok? All right? So we need good ldl receptors. When yOu have high cholesterol, high ldl, any of these issues with lots of ldl particles, why is it stain? Why you have so much staying in your blood member? It's maKing its rounds and hopefully it's all getting taken out and goes back to the liver and the ldl receptor takes it out. Ok, but why is it not taking it out? Why is the ld And they get smaller and smaller? Remember we've talked about the small dense ldl particles. See we got a certain amount of ldl particles and now we have different sizes and there's science out there says, ah, it's just the ldl particle count.

Eric: 21:49 That's bad. You got to get as low as you can because that means remember it's the ldl, that little sterile from a very small, dense ldl particle that will oxidize and get into your cells endothelial cell and start the atherosclerotic plaque. That's the danger right there. So you don't want a lot of ldl particles circulating, getting smaller and smaller. They oxidize the phospholipids in the in the cell membrane gets oxidized, so that makes it smaller. Ok? Because you're getting rid of the polyunsaturated fat will cause that some number and the festival limits to oxidize and it gets small. We don't wAnt small dense ldl particles are getting smaller and smaller. You gotta get them out of the blood, so what takes it out? The ldl receptors you have on cells that they'll take it. Ok, but the main one is the ldl receptors in the liver.

Eric: 22:43 It takes the ldl particles out. Ok. And the cholesterol moves it to bio or, or regenerates it and uses it again. So it's your ldl receptors we have to talk about. That's what keeps your ldl particles down.

Chad: 22:58 So can we get the ldl particles to stop oxidizing if we just stopped breathing?

Eric: 23:03 Yeah, that's the key. You're done putting oxygen in your body. No more cellular respiration, no more free radicals. You're good to go. Don't eat too many poly unsaturated and polyunsaturated fats. We've, we've talked about that before where, you know, they say, hey, increase your poly unsaturated fats because that lowers your cholesterol. Well it does because what it does, it [inaudible]. I mean, cholesterol delivery will have an phi with a polyunsaturated fat. That means it's, it'll bounce buying to it is still there. It's in A bound form, but it does lower your cholesterol count a little bit.

Eric: 23:41 Ok? So they'll say, oh, look at that. And my cholesterol is down, but no, not really. You're still in there, but it's off to other tissues and stuff. So it does lower the costume count, but not in polyunsaturated fats have their own story or their own, which we've talked about in mortality rates and different clinical studies show that. And an increase of polyunsaturated fats is not good for your mortality rate and we won't go into that science, but it is good science. But overall the key is I know a lot of out there fear high cholesterol. Ok? And counts in. And I brought my uh, uh, bloodwork is we, we test everybody's blood lipids because I want to see what your blood lipids are. I want to see where your cholesterol is. Our, I want to see your ratios. So we do a basic blood lip and I think everybody out there and when before you start keto or any type of program going get your blood lipids checked.

Eric: 24:33 Ok? Because if you're going to increase your fat intake, because keto , we do. And let them say, oh, you raised your saturated fat, you're going to raise your cholesterol. No, no, no, no, no, cause in saturate, if you increase your saturated fat, you do get some ldl increased cholesterol, but it's the larger ldl and, and there's a lot of lip ecologists that I follow and I read and it's, it's a safer ldl, you know, we have different sizes of ldl, large and small. The small one is what we're running from, ok, this is what we're trying to get that out of, out of the blood so they don't get smaller. So when you eat saturated fat, you actually raise your ldl, but it's actually the larger buoyant ldl plus you raise your html, which is, which we could call that. People don't like to call it, but it's a good cost straw.

Eric: 25:20 That's what's going to hcl high density lipoprotein will take, go by the sales and don't actually take any excess cholesterol out of that cell because you don't want too much cost. You can damage iT. It'll get it back to the liver and take it out. It's kinda like mops it up and kinda goes down. Just scavenge it. Then if you have a plaque issue where the, where it causes the immune system, the macrophages loading up with the phone cell has got a lot of cholesterol hgl that lipoprotein will take that out and move that back to the liver. So that's a good thing. [inaudible] a good thing and like mine, if I, if I read it to you and I read it to my doctor and he's like, oh my gosh, he had mountains statins before I even got through half of it here. He said, know your status.

Eric: 26:03 Of course it resulted in a 40 minute argument. But I had my genetic test here, my polymorphisms and show them all that stuff. He didn't know anything about it but he's a good guy. He really is. He just didn't know a lot about it but, but my, my total cost of [inaudible] and you know, you tell it to anybody, you hit 300, they're like a stat statins ok right away. But my hd was 1:50 and they're like, what your [inaudible] that high 1:50. And, and those are out there. I, I have my, all my snips done, my polymorphism, and I don't handle any of those variants with high hcl issues or, or familiar hypercholesterolemia. I don't have those variants. Ok. So if I did then you can say, oh, that each. because obviously we have this station right now and it's strange because my triglycerides were 38 and my ldl was 92, my ldl cholesterol.

Eric: 26:53 So you're like, oh my gosh. And anybody would definitely say you're a statin candidate, but when you do the ratio is, remember we talked about a big indicator of cardiovascular disease is you want to take your total cholesterol divided by your hcl and then you have a number of their ratio. If you're under three, you're doing really good. Ok, mine's [inaudible]. Oh great. Another great test is triglycerides divided by [inaudible], which I think that's a better indicator of cardiovascular disease. And I was [inaudible] ok. And, and so, um. Oh no, no, I'm sorry. I was point two five [inaudible]. What's the, the total hcl, but the triglyceride. I was point [inaudible] you want to be under one point [inaudible]. So look at my ratios. I mean, look, I mean there's only, so literally the overall numbers would scare anybody.

Chad: 27:46 So the hdl is working with the ldl. Oh yeah. So create that homeostasis as you talk about both numbers  can go up together.

Eric: 27:53 Yeah. Yeah. And, and hel you want that higher number. Ok. In a bet, a better indicator also of cardiovascular disease. If you have a real low hcl number and a high triglyceride number, then you say, oh, we've got issues here to worry about. So there's a lot of different variants, you know, besides this, if I, if you look at this and if I had any of the metabolic syndrome, ok, if I had hypertension and high insulin resistance, my waistline was getting bigger and I have all these, you know, the, the metabolic syndrome issues, ok, then you'd say you better take all this in, you know, in, in together and say, hey, you might have some issues here, but I don't have any other metabolic syndrome issues at all. So I'm just going straight here. But I've had my, my, um, what we call mobility.

Eric: 28:42 I've had that done where they count your articles, your ldl hcl particles, gave you the sizes and the accountant and those are all good. So with these numbers and whatnot with the, and I recommend that if anybody's, you know, with statens if you're going to get a prescription, I would say, hey, let's do my ldl particle count and that's what they call eight bob, you know, and then it's going to do your sizes of your hcl size of ldl particles and then you can really put the puzzle together. You know, how many small, you know, you really want low ldl particle count. That's what the goal is. But I also like to look at the sizes. It's just some other science that some believe in the sizes and I'm one of those,  well that's the science that we have available to us to figure this stuff out and do like at a personal level.

Chad: 29:33 The science that is available to us. We can go get tested. Was there, you said, um, was there anything else you wanted to talk about? The ldl receptors? I mean, we're, we're, we're running little bit too long.

Eric: 29:42 I mean, there's a lot of the markers that you got to be careful of that ldl receptors are affected by a lot of things. Thyroid can affect your, they always happens in and your cholesterol, inflammation can, insulin can, um, you know, and, and you've got to pay attention to what your cholesterol level is in your liver because that's what gonna, you know, that's what status do they say, hey, ldl receptors, uh, let's bring in more cholesterol. Exactly. Ok. And so before you know, and I'm not against statens, I am not. Fortunately I, it, it could save lives and I think it's just too many given out there like a supplement right now. That's what they do. 300 statins. And there's other ways to say, hey, let's start looking at other avenues to bring down our, our ldl.

Chad: 29:42 Its not the only place that medications are in overuse.

Eric: 30:34 And we talked about that before on hormones, thyroid hormones, on the,

Chad: 30:38 So lets leave on the positive, what is, what is cholesterol? At what role does it play in our Ketogenic lifestyle?

Eric: 30:43 It is a major role because number one is it's in the cellular membrane. Ok, so would you need cholesterol in there to make it more fluid, flexible, more. There's more of a signaling of proteins that happen in there. You've got to have cholesterol and endless. I them for the integrity of that cellular membrane. You've got to have it. And cholesterol is also a big issue as far as as what we talked about. Or are steroid hormones. Ok? Because your adrenals and your gonads zone really produced the cholesterol. You've got to get it from your, the ldl particles and what's delivering cholesterol. They're ok to, to that, to the sale, ok, you got to take it in.

Eric: 31:25 And that's the precursor cholesterol to remember a pro. None alone. Progesterone, dhea, testosterone, estrogen. So that's key. Cholesterol is key and it, it's, it's, it's basically the substance of life that I've mentioned. You've got to have cholesterol, but the dietary, you don't have to worry about that stodginess because your body's going to make it ok? And you know, it's interesting. Science, you know, even the older, remember heart at 95 percent of guests that come from a cardiovascular disease, heart attack or whatever is, what's the biggest factor? Ninety five percent happen after age 55, you know, but the problem, why does it happen after 55 is what's going on since you were a teenager all the way up. What's going on on that sub, you know, ab, luminal side, you know, where the plaque starts. You don't see it with an angiogram, it's not visual. Something's happening.

Eric: 32:26 There could be. So it takes many years to finally come out and express itself, which comes through. And then you have plaque.

Chad: 32:33 Thats the plaque buildup on the outside of the artery

Eric: 32:36 Ok, on dublin. well, that's what you have to watch out. You don't, you can't see it. They say up to 30, 40 percent it happens out there. And then it starts to come through the practice breakup and calcium. And we can go into that science. But that's where you got to watch it now.

Eric: 32:51 So how does the keto, the ketogenic diet, um, how does it improve the way that our body interacts with cholesterol? Right?

Eric: 33:02 It does it and it's important because it is. The scary part is everybody thinks they're going to be eating more fat, more saturated fat. Like I do, I do. You know, I've, I've increased my saturated fat, my mono, which is, you know, there's, you just don't do the saturated fat, you know, and you have certain metal poof us which are important and essential that you got to have.

Eric: 33:19 And so in, in, in increasing your fat intake, you want to say, oh, ok, I've got to make sure what's happening as far as my cholesterol count. And like I said, when you increase your saturated fat, your triglycerides drop because you're not eating a lot of carbohydrates anymore and your hgl comes up. Ok, so you get a low ldl boost, but that's the larger buoyant and everybody will talk about it. Then when you go keto, your cholesterol numbers get really. they get good. Ok, there might be a little higher, but remember it's not relative. Yeah. Then that ldl cholesterol, that total isn't the important thing. It's the important thing is how am I. Those particles are there. Ok, that's what you're going after because remember that's all it's about is that little sterile and it's going to get in that art arteriole wall sooner or later if it's keeps floating around and getting smaller and smaller and what oxidizes that is a polyunsaturated fats, so you gotta be careful with your polyunsaturated fat intake so you don't oxidize that festival live but in the cell membrane to make that thing smaller.

Chad: 34:21 So my pseudoscience comment earlier about not breathing isn't true. Actually. That's not what oxidizes is.

Eric: 34:26 is it? Yeah, but don't run from dietary cholesterol. I'll go around from saturated fat, fat your friend and I got big numbers here and I share that with a lot of people and they're like, no way. You know, you're still with us still. Yeah, I'm still there, but science has shown and there's a lot. I'm reading a new book. I read this book a while ago that the older you are ok, when you get my age. All right. The higher cholesterol numbers are right or showing longevity and less mortality. the lower numbers are showing higher mortality and higher cardiovascular disease events.

Chad: 35:08 Well, that makes, that makes sense to me. If, if cholesterol is that one of those major building blocks of the cell wall or you know, the sales structure, obviously you need it. So as long as your numbers are increasing together, you know, in a relative way. I mean, yeah,

Eric: 35:25 there's so much to crush so we Could talk for hours about it and since I don't have any notes or anything you keep, you know,

Eric: 35:31 something must reminds me of something else. I'll jusT keep going. It's a lot without notes

Eric: 35:38 and stuff. This is just my blood test and they say where do I notice? But I'm older and I don't have the retention, but I get, I'm booting up my beta a little bit so I get more cognitive, more memory. so I'm up for the challenge.

Chad: 35:49 I love it. I love just sitting here and soaking in the knowledge. You are, you and I love these conversations and uh, it's, it's helping me and I think it's helping a lot of other people.

Eric: 36:00 I hope so, you know, and, and I got a lot to learn. I don't know it all, but I'll share with you, with what I do know and, and if I don't know it, I'll figure it out. I'll learn it.

Chad: 36:11 I hope. I hope our listeners understand how much of your time and effort and passion and heart is put in to the material that you come to the table with every single week. And it's pretty incredible. Um, so thank you so much for that.

Eric: 36:28 And, and I do, the biofitters. I want their lipids. I want their blood markers. I, that's what I do. I want to say, hey, how can I help your thyroid? How can I help your adrenals? Let's get your g. I just had another biofitter. They just emailed me today. I got her 23 and me report. So now I have some time to spend a mile to go over that and look for some of the snips that, that I, that I want to give her a baseline on. Just justin. I want to be. I'm going to just want to be safe.

Eric: 36:56 Yeah, that'd be safe. Yeah.

Chad: 36:58 Well that's incredible and I'm excited because we have some exciting things planned for the podcast coming up. We have some really cool guests coming on that I'm not going to say too much about, but that are presenting topics that we are kind of quick.

Eric: 37:13 I have taught dress and I cut myself. I'm always talking about testosterone and not estrogen and I'm always talking about a male [inaudible] I, I, I'm sorry.

Chad: 37:23 Yeah. So we're bringing some women's. We're bringing some, some quito women to perspectives. And also another exciting thing. Next week I'm going to plug this. We're actually going to release next week's podcast a day early, um, because it is a. Sorry this is in two weeks. It's going to come a day early because it's a valentine's specific episode where we're going to give people ideas for valentine's dates so it's going to have some information about eating out. It's going to have some information about cooking, a nice dinner at home, all that kind of stuff. So we want to give some people some tools. We want to give our listeners some tools through these holidays and through, you know, that's been one of our biggest efforts. You and I spend a lot of time. How do we help people live functionally through ketogenics and you know, the ketogenic diet. So some cool things coming up that. Yeah, I like that.

Eric: 38:18 Now you just told me it takes a little pressure off of you today. won't forget valentine's day. I've known for that. Your anniversary with. No, so yeah, we forgot about it, but no, it's actually my wife

Eric: 38:32 didn't. Never celebrated before. When I up on her first valentine's with all the stuff, she's like, hey, what's up? And I had all this stuff and I'm like, happy valentine's day goes, oh, you're kidding me. Don't cheat on my ex. My ex husband, I, we never celebrated valentine's day, so anyway.

Chad: 38:48 Well thanks so much for biohacking with us today or not. We really, really appreciate it and I want to thank you for joining us on this quest for optimal fitness. If you're ready to begin your own journey and live your life in ketosis, be sure to check out biofitcoaching.com and biofitcoaching on facebook. We have some great conversations going on there. You know what I'm loving the most lately about our facebook page, our new bio fitters going on there and doing their pledge videos. Their commitment videos is so cool to get to jump on there and see these people who are committing to making a huge change in their life. I mean, that's a brave step. It's a very public accountability system. Accountable. Yeah. That is cool though. Also, if we've, if we've created any value for you in your life and listening to this podcast, we really encourage you to consider going on itunes and leaving us a review and a rating. IT really helps us get the word out that most people know what the podcast is about and that eric is legit and giving us some good, good information. So if you wouldn't mind consider doing that. We would. We would be really grateful. And until next time, Stay Keto.