Mark Bell's Power Project - EP. 423 - Cholesterol Debate ft. Layne Norton and Dave Feldman

Episode Date: August 27, 2020

Dr. Layne Norton is a professional natural bodybuilder, powerlifting world record holder, 2x USAPL National Champion, powerlifting and bodybuilding coach, as well as an entrepreneur. Dr. Norton is the founder of the Carbon Diet Coach App, Outwork Nutrition Supplementation, and BioLayne. Dave Feldman is a senior software engineer and entrepreneur. He is the founder and creator of CholesterolCode.com, and the Feldman Protocol. Subscribe to the Podcast on on Platforms! ➢ https://lnk.to/PowerProjectPodcast Support the show by visiting our sponsors! ➢Piedmontese Beef: https://www.piedmontese.com/ Use Code "POWERPROJECT" at checkout for 25% off your order plus FREE 2-Day Shipping on orders of $99 ➢Icon Meals: http://iconmeals.com/ Use Code "POWERPROJECT" for 10% off ➢Sling Shot: https://markbellslingshot.com/ Enter Discount code, "POWERPROJECT" at checkout and receive 15% off all Sling Shots Follow Mark Bell's Power Project Podcast ➢ Insta: https://www.instagram.com/markbellspowerproject ➢ https://www.facebook.com/markbellspowerproject ➢ Twitter: https://twitter.com/mbpowerproject ➢ LinkedIn:https://www.linkedin.com/in/powerproject/ ➢ YouTube: https://www.youtube.com/markbellspowerproject ➢TikTok: http://bit.ly/pptiktok FOLLOW Mark Bell ➢ Instagram: https://www.instagram.com/marksmellybell ➢ Facebook: https://www.facebook.com/MarkBellSuperTraining ➢ Twitter: https://twitter.com/marksmellybell ➢ Snapchat: marksmellybell ➢Mark Bell's Daily Workouts, Nutrition and More: https://www.markbell.com/ Follow Nsima Inyang ➢ Instagram: https://www.instagram.com/nsimainyang/ Podcast Produced by Andrew Zaragoza ➢ Instagram: https://www.instagram.com/iamandrewz #PowerProject #Podcast #MarkBell

i've never heard you beatbox i can do a little bit you know we'll be here and there we'll be here and there we're not recording but i'm recording so maybe i'll throw that in still in the beginning of this this episode we'll see. Okay. All right, Mark, after your drink, what's going down today? Today we got Dave Feldman on the show along with our boy, Lane Norton. Dave Feldman's been studying cholesterol and I guess not cholesterol. That's not a really good way of putting it. Like just your lipid profile in general for many many years now and uh lane norton as you guys know he has a phd in case you guys didn't know and every time we say

phd you got to take a shot so by my count we're already two shots into the podcast but lane also has a world record in the squat i think the world record has been broken in the IPF. Very accomplished power lifter, silver medalist in the IPF. And then Dave Feldman actually comes from a different background than what Lane is in nutrition. Dave is an engineer, but Dave has really broke down lipid profiles and done so much testing on himself. That's what I really find fascinating is how much testing that Dave has actually done

on himself and also has had a lot of other people kind of follow in his footsteps and get his blood work tested as well. But he's had these huge ranges of cholesterol test results within just a couple of weeks, just within a couple of months, sometimes from doing something like eating tons of bread or sometimes by eating certain foods, he's been able to manipulate that structure. And so I think what we'll get into today is we'll talk about, you know, how is the blood lipid profile as it relates to calories, because that's the drum that Lane is always beating is about is about calories. And I don't think that these guys and they can speak for themselves when they hop on here. But I don't think they really disagree a lot.

I don't think we're going to see these guys, you know, try to beat each other's ass with words. These guys, you know, try to beat each other's ass with words. But I do think that it'll just be a great topic, great conversation. And the way that it kind of kicked off was they were just going back and forth a little bit on Twitter. But it wasn't like a Twitter battle. It wasn't like a Twitter fight. It was more like, hey, I think this. Oh, what about this? It was kind of they were going back and forth.

So we'll get it from these guys today. Dave, how are you doing? I'm good. I'm good. Thank you for having me on.. So we'll get it from these guys today. Dave, how are you doing? I'm good. I'm good. Thank you for having me on. Yeah, we really appreciate it. I've been watching a lot of your stuff for many years now. I really appreciate all the work that you've been doing.

If you could fill us in and try to sum up what are some of your findings over the last several years as you've been diving into this complicated blood lipid profile world, I guess you'd say. Yeah, of course, as time passes, that gets to be harder and harder to summarize quickly. But I guess for anybody who's not familiar with my work, I'm actually a senior software engineer and entrepreneur and had absolutely no interest in medicine or nutrition or biochemistry or any of that five years ago when what happened was, is I'd gone on a ketogenic diet. I saw my cholesterol skyrocket. And then I became obsessed with learning everything I could about lipidology because it turned out that there were some patterns in how lipids work that I found to be

very relatable as a software engineer, because in many ways, I think it functions as a network. And I stand by that to this day. That gets a little bit deeper into the conversation. But basically, what I've come to hypothesize, and it's certainly something I'm doing a number of experiments around personally, is that actually, if you're choosing to be powered by fat, then in choosing to be powered less by carbohydrates, then that will have an impact potentially on your cholesterol numbers. Because after all the cholesterol that's being moved around the same system that moves cholesterol around in your blood is also involved in moving around fatty acids in your blood. And I guess since then, there's certainly been a lot more that I've wanted to pursue and whether or not this is associated with risk. And so I've sought

to see how much these profiles that are related to those people going on a low-carb diet, not just with their LDL cholesterol potentially going up, but also with their HDL cholesterol, the so-called good cholesterol, and triglycerides, the measure of fat, the HDL going up and the triglycerides going down, which, of course, I regularly call the lipid triad. And that's a lot of where, you know, debate gets a bit more contentious because there's a lot of people who are concerned, and I think our good colleague Lane Norton might chime in on this one, concerned for those people who do go on a low-carb diet and do see their LDL cholesterol go up, whether or not they're

at a greater risk. Yeah, that's... Go ahead, Lane. Oh, no, I didn't know if it was being thrown to me or if I should wait. Yeah, yeah, it is being thrown to you. Thank you guys both for spending the time today with us. I really appreciate it. Lane, I know we already heard keto, so I think we've got to take a shot for that. I think every time we hear PhD, we need to take a shot. So we're going to be pretty hammered by the end.

No drinking games today. Play it straightforward. But I want to get you some of your thoughts on this because you've worked with so many people over the years you've helped people diet for bodybuilding shows and we can kind of debate on whether even that's even healthy but what have you seen in general i guess let's kind of kick it off with when you assist assist somebody in losing weight have you noticed uh any particular particular trends in their blood work or in their blood lipid profile that would lead you to believe that they're healthier, they're doing better, or maybe even what you've seen in your own self? Yeah, so there's a lot to unpack with what Dave just covered and then obviously what you just asked.

lot to unpack with what Dave just covered and then obviously what you just asked. I think we have to clarify a few things here first, because people tend to think in black and white. So just for our listeners, keep in mind when we discuss risk, saying something is a risk factor doesn't mean that that is going to ultimately that you're going to have this outcome. That's not how statistics work. Statistics means that there's, you know, increased risk. Low risk, additionally, also doesn't mean no risk. And that's important to keep in mind. It's also important to keep in mind what is an independent risk factor versus things that

are just associated with some kind of disease state and process. So with that being said, based on the question you just asked, Mark, because I'm sure we're going to get more into it, and I'll just stay right up front. And I'm not a lipidemiologist. I'm not an expert in blood lipids. I think I got a pretty good grasp of it throughout my academic training and then obviously reading research papers. But, you know, I think one of the things that I try to emphasize is that a lot of the discussion around diets tends to be what is the absolute best diet, you know, physiologically for X, right. Or for overall. And one of the things I've always said is like, listen,

the best diet for heart disease is like listen the best diet for heart disease might not be the best diet for something else um the best diet for diabetes might not be the best diet for cancer like i don't know that to be true i'm just saying that we have to keep ourselves open to the idea that you know all like there might not be this one kind of zen diet okay and even if we're going to have that conversation we also need to walk that back in terms of what can we actually get people to do okay this is a huge huge huge point of contention of people some things people don't understand with me when i look at the research data and i look at the meta analysis

of dietary data and the systematic reviews and all that kind of stuff what you see is that you can improve your blood markers with a lot of different kinds of diets if you sit if you're so there's two things to keep in mind here obviously somebody like dave is not overweight or overweight or obese i don't know if Dave, were you previously? You know, I don't know that I'd say that I was, uh, overweight, but I want to say my BMI before I'd gone keto was 26. So right there at the edge, I think. Okay. So I would say for you, probably for that particular instance, probably less of an application, but if we're talking about overweight people or obese people, the pathology of just having too much adipose tissue and what that does to metabolism in terms of your adipose secretes adipokines, which can impair all different

kinds of things, raises levels of inflammation, those sorts of things. Just losing weight, and we have now several meta-analyses that show this, regardless of the way you do it, pretty much improves markers of health. Now, if we're talking about a situation where we're looking at energy balance, let me backtrack. People have taken that, what I've said to say, Lane's saying that only calories matter, that we can just eat pop

tarts and whatever that's not what i'm saying um there certainly appear to be some things that are independent risk factors for disease possibly and um one of the other things i would like to to point out is that when it comes to like my background, because people will say I'm a shill for big sugar or whatever. I think it's important to point this out. I came from a lab that was actually doing like, not like super low carb, but reduced carbohydrate research.

Like I came from Don Lehman's lab, which basically was, you know, we test, if we test the high protein diet, it was kind of a zone Mediterranean style diet. It was like, you know, we test, if we test the high protein diet, it was kind of a zone Mediterranean style diet. It was like, you know, at most 40% carbohydrate. Um, so I'm definitely not a pro carb person. Um, I'm kind of a, what can we get somebody to stick to and be adherent

with? And if, you know, somebody says, hey, here's what tends to happen a lot. People really mistake physiological superiority for actual psychology. So they find something that they like, that they're able to adhere to really well. It oftentimes doesn't even feel like a diet because it feels so easy to them. They'll lose a lot of weight and then say, see, I tried every diet and this is the only one that worked for me. That's probably true. But then they do kind of mental gymnastics to try to physiologically describe why that diet is so superior to other diets when in fact they should just say, hey, I just really like this. And that what I call it triggers the compliance algorithm with people is very different

from person to person. I've met people who said, you know, when I eat a high fiber, high carbohydrate diet, I don't feel like I'm dieting. I'm very satiated. I'm very full. I've met people who said when I'm on a keto diet, it feels easy. I like these foods, you know, that sort of thing. So I think in today's discussion, what we're probably going to dive into with blood lipids is, okay, if we're doing a high fat diet, are there some independent risk factors? Are there some things that we need to be concerned about when it comes to blood lipids and probably particularly cardiovascular disease risks? I think when we spoke on Twitter, I was just asking for a point of clarification from Dave with a point somebody else raised, and that kind of brought

us here. So yeah, I actually came from a lab where my advisor was very much, I think saturated fat is overblown. I think cholesterol is overblown, those sorts of things. So that's my background in it. And so any other kind of stuff I've looked up has been on my own from that sort of bias. Dave, what's some of your perspective on like after diving into the blood lipid profile so strongly and looking at triglycerides versus HDL versus LDL and looking at all the different particle sizes and all this stuff, how important is this stuff when it comes to maybe, in particular, cardiovascular disease? Like, does it really seem to matter that much? Or what are you finding? Or what are you seeing? Oh, well, before I answer that, I actually want to add that, Lane, you probably find it pretty boring to debate with me on nutrition, because I think I agreed with just

about everything you just said. I think that there are multiple ways to health. And I've said this many times before on Twitter and on social media, you won't be finding me saying like, for example, the low carb ketogenic diet is independently superior to all other diets. In fact, I probably would be a little bit annoying because I really actually feel like the level of true empirical hardcore evidence that we have for what is truly a more superior diet among the ones that we know about right now, I think is lacking. I think that most of what the benefit we're seeing from just about

any diet that arrives is most of it, I think probably 70, 80% of it is just getting off of the standard American diet. So that's that. I just want to throw that qualification out now. Yes. To the point that you're saying, this is where we can kind of tie it all together. So some people are going on a low carb diet and they're feeling exactly like Lane just described. For example, let's say somebody goes on a carnivore diet and they're feeling great end to end. In fact, they may, like I did when I went on a ketogenic diet, they may assume that their blood work's just going to look as amazing as they feel. they may assume that their blood work is just going to look as amazing as they feel. And then all of a sudden they get there and, you know, their doctor comes into the door and they're concerned because right there in bold or sometimes even highlighted in red,

they have LDL cholesterol that sometimes the doctor themselves says is higher than they've ever seen before. Sometimes it's an LDL of 200 or even 300 or 400. We see these lipid panels all the time. And to be very upfront, and I say this all the time, I like to say that I'm cautiously optimistic about there being a high LDL in the context of being fat adapted. That is to say that I believe that there is a difference between these contexts, that you can have high LDL for bad reasons. And usually the tip off are things like if it's an inflammatory response, or if you have something known as atherogenic dyslipidemia. And atherogenic dyslipidemia is almost the reverse of the triad. It's low HDL and high triglycerides. And typically that comes with a preponderance of

a larger proportion of small dense LDL particles. Now, I've sought to look for all data for which we see high HDL and low triglycerides alongside high LDL, which is that triad that we're talking about. And thus far, every study I've been able to find actually shows that it's a low cardiovascular risk. Now, Lane, part of what did get us talking was, and excuse me in that, I think when I was responding to your retweet, I was actually responding more to what the content of the tweet was that you're retweeting. And I think it came off as though as responding to you in this regard. The person who is tweeting it actually was using a modified graphic that included like keto magic on it. And the, like the, you know,

last I want to say five or six conversations I've had with that individual. Unfortunately, they've always taken it towards the personal. And I just want to have more of a discussion on reasoning and data. And I was feeling pretty confident that, you know, if we got on the show today, or pretty much like any other time I've seen you on a podcast that's on a debate, that we'd probably be able to do just that. But all of that said, right now, I do feel that level of cautious optimism, given the amount of evidence that I not only see with the prior research when looked at in that context, but also in what I've been able to see by being in

constant contact with these people who have high LDL. I constantly emphasize I'm not a medical professional and I'm not giving medical advice. I emphasize what things that I think are concerning to watch for, such as development of a stable angina or xanthomas, which are very common for people who have that level of LDL that comes from the genetic disease of familial hypercholesterolemia, and that they should consider physical tests, such as getting CIMT, such as getting a CAC. But, of course, what's better than them all, or at least the one that I like the most is a CT angiogram. So, yeah, I think as far as debates go, I usually try to keep it civil as long as it's kept civil and as long as people don't engage in cognitive dissonance.

If one of those goes out the window, then all that goes out the window for me. But so I think I want to walk back again. So when I talk about this stuff, and there are going to be some things Dave and I disagree on based on what he's just said, and that's fine. When I talk about this stuff, again, I'm not saying that no one should do a keto diet. And I'm not saying, for example, that saturated fat is the devil. But I'm also going to walk through the research and talk about it. And as somebody who, you know, I consume, I actually run a little bit high LDL traditionally in my family. We just seem to run a little bit higher LDL, traditionally in my family, we just seem to run a little bit higher LDL. So Dave talked about the fact that there's this kind of blood lipid triad, I believe they call it,

where you have high TAGs, low HDL, high LDL. And this was kind of from observational epidemiological studies, which is where a lot of this data is derived, which makes it, you know, epidemiology is very limited in what we can actually show because we can't show causation. People try to make it causation all the time. We can come up with like confidence levels and even dose curves, you know, based on epidemiology. But at the end of the day, people who have, you cannot separate one aspect of a diet from another aspect of a diet. What I mean by that is, for example, if you are over consuming one food, it probably means that you're displacing another. Okay. So like, for example, one of the things I've said about, I'll get people on here and claim I'm bought by big sugar.

One of the things I've said about sugar is the fact that, well, one, you're eating more energy. People who eat high sugar don't actually lower their calories proportionately. And when they do, when we see that randomized control trials, we don't really see much morbidity in terms of sugar intake, but they also tend to eat really low fiber. And I think the fact that average person in America's fiber intake is six grams per day. So oftentimes more fat too, right? Not just, sorry, Mark. I was gonna say oftentimes more fat as well, kind of accompanying that sugar, like something like a donut. So yeah, you can't separate those two, right? Like it's, it's not, they're not just doing people who, who get in these studies aren't just doing one thing.

It's not just like, well, you know what? I think I'll eat high saturated fat, but I'll also eat a lot of fiber and low sugar and control my calories, exercise every day. Now, there are some people who probably exist like that, but it's a small subsection. So, and the problem is, is that when we're

talking about something like cardiovascular disease, we're talking about the risk over the course of a lifetime. So our ability to detect that in randomized control trials is extremely limited because we can only assess biomarkers essentially in randomized control trials. Because if you put a few people on a few different diets and you're waiting for them to have a heart attack i mean you could be waiting you know 30 years and we just don't have that long of a time to run tightly controlled randomized controlled trials so what i think is some of the best evidence out there is what's called mendelian randomization studies and mendelian randomization studies. And Mendelian randomization studies essentially look at it from this point of view. Meiosis or the distribution of genetics when you are born

is random. Okay. So, I mean, obviously you have your two parents, but how they get disseminated in the alleles and whatnot is relatively random. And you have people who will be, for example, higher secretors of LDL naturally, people who are lower secretors of LDL, and they don't affect any other blood markers, right? They don't affect other blood lipids. You also have that for HDL. It's out there for a lot of stuff. You can find it for almost anything you want to measure now. So what's cool is now you've almost got like a lifetime randomized control trial, because these people are naturally secreting different levels of, or I don't want to say secreting. They have higher blood levels because you could argue that it's not just secretion,

it's also clearance when it comes to blood cholesterol. So when we look at those, what we see is people who, if you look at low cholesterol, LDL cholesterol specifically, versus high LDL cholesterol, you still see a really significant association between that and cardiovascular disease. And that kind of suggests that there is a causal link. And we do know that LDL cholesterol, unlike VLD, I'm sorry, not VLDL, unlike, for example, chylomicron. So when you eat fat in your diet, for example, some people would say, well, if, you know, this cholesterol is so bad, how can we ever justify eating any fat? Because it's just going to go right into our arteries and fat will clog our arteries. That really doesn't

work that way because chylomicrons are so large that they can't penetrate the wall of the artery. Whereas LDL can and has been shown to do so. Now, you brought up the point of small, dense particles versus larger particles. It looks like particle size does play a role, but here's the caveat to particle size. So when you have small particles, they more easily penetrate the wall and can get into the arteries and be atherosclerotic. Sorry, I pronounced that incorrectly. But they contain less cholesterol overall. Large ones don't get in as easy, but they contain more cholesterol. The net effect appears to be pretty minimal between the two,

if that makes sense. Because small ones are getting in easier, but they just don't carry as much cholesterol. Large ones don't get in as easy, but they carry more. And then you can, you know, when it comes to the triad, you know, for, for, I think when I was in grad school, actually the talk was, well, we really should be focusing on HDL because, you know, people have low HDL, high LDL. It's probably the ratio that makes the most difference. As a marker of health, I think HDL is probably very valid.

Unfortunately, it has not really panned out as anti-atherosclerotic. And what I mean by that is when you look at the Mendelian randomization studies, there's not really so in, sorry, let me back to back up in epidemiology, people who have high HDL have lowered risk of, of CVD, but in Mendelian randomization, where they start from the beginning of life like that, and it's random, other than just their different levels of HDL, that and it's random, other than just their different levels of HDL, you don't see a protective effect. And in fact, actually, higher levels of HDL had a small association with like breast cancer and some other stuff. Now, I'm not saying I'm worried about HDL causing breast cancer, but like it's important to point these things out. So based on those, I would say that yes, LDL cholesterol is an independent risk factor and probably causative for CVD. That being said, a lot of that, by far the most powerful driver

of LDL cholesterol levels is your saturated fat intake compared to your PUFA intake. So your polyunsaturated fatty acids. So you can be on a ketogenic diet and dietary fat doesn't necessarily, in fact, dietary fat itself is probably the most powerful nutritional modifier of CVD risk in terms of if you adjust your PUFA to saturated fat ratio, you can drastically reduce your risk of heart disease. Because, for example, the Mediterranean diet, they don't eat low fat. They eat high fat, but it's quite a bit of polyunsaturated fat and monounsaturated fat, which may have a protective effect, but the data is a little bit more modeled. So, Lane, you hit a lot of great points. I definitely want to jump into the first one because Mendelian randomization was actually one of those areas

that I got very excited about because I too would think that it would be extremely compelling if there were certain genes that had varying levels of LDL and would likewise have varying associative levels of atherosclerotic outcome. And one of the more fascinating things is that, and I talked a little bit with Peter Attia about this, I really wanted to drill into the biochemistry aspect of where nucleated cells are also affected beyond just hepatocytes, the liver cells. Cells like, say, endothelial cells and immune cells may, in fact, have some kind of differences between those who would have these genetic abnormalities. And there's recent studies. I'm not sure if you're familiar with them, but I'll mention one.

We can actually just Google together if somebody's watching at home. It's risk of premature atherosclerotic disease in patients with monogenetic versus polygenetic familial hypercholesterolemia. And what they're doing is they're looking at basically two categories. One is sort of what I like to call the big three, which is LDL-R, ApoB, and PCSK9. You could basically call them genetic mutations given how extraordinarily rare they are, but they have enormous effects on your LDL levels. And then there's basically the rest, if you want to call it that. It's this category of, I want to say it's 223, of what they would put in the group of polygenetic familial hypercholesterolemia.

Now, the assumption is when you hear about Mendelian randomization, you think that it's kind of a mix and match. You can kind of, you know, put in some that have a big effect, some that have a small effect, and you can compare the groups amongst each other and end up with an effect size that has some predictability against the atherosclerotic plaque buildup over time. But that's really not the case in these two categories. The monogenetic and the polygenetic are very different. Even though the polygenetic, you can actually get to LDL levels that are in the 95 percentile or higher of the population, and you still will not have a comparable level of risk at the same levels of that LDL versus

somebody who has one of these big three. And it gets substantially worse if you combine the two. But one of the more fascinating things is after that, after they calculate for that, they additionally look at it against people with an unknown factor for their cholesterolemia. So they have high levels of cholesterol, but they have no known genetic reason for that. And those have like the lowest risk factor. To be intellectually honest, I'm sure Polly, who we're, you know, we both know and are good friends with, he would probably jump in and say, well, that's probably because those people who have an undetected genetic, a non detected genetic aspect, but a resulting cholesterol.

They may not have had it their whole life. But the catch is all of this is still somewhat speculative. We need longitudinal data. We need to actually be capturing the data over time in snapshots between all three of these groups. We need to be able to see those people with monogenetic, those people with polygenetic, and those people with no known genetic to really know. But already we know that there's an enormous difference between those first two groups. And that already is moving against the consistency aspect of the Bradford Hill criteria for making the claim of causality. And actually, this is kind of exciting because I can share just a little bit extra if

you guys don't mind me indulging. As I was talking about with Peter Attia from before, I kept digging and digging, and I finally found I kept focusing a lot on endothelial cells in particular. But then I started focusing on immune cells, and I was happy to find that there is a study, and I'll go ahead and mention this one as well. It's macrophages of genetically characterized familial hypercholesterolemia patients show upregulation of LDL receptor related proteins. And I don't want to lose the whole audience by getting into LRPs, which is, you know, it's part of the super family of LDL receptors. But here's the bottom line. The bottom line is those people with the monogenetic version of familial hypercholesterolemia, they literally have differently functioning immune cells, particularly macrophages. And I know, Lane, you would appreciate this. Macrophages are, of course, integral to foam cells. They're very much a part of that very process. So if the common denominator can't be ruled in as cholesterol levels and allowing us

to rule out all other aspects of lipid or lipoprotein metabolism from the cells that are literally involved in atherosclerosis, then we have a problem. We should at a minimum try to exclude those. And that's why there's 28 SNPs that my colleague Siobhan and I helped to identify that we've gotten from other studies that exclude out the other lipid markers. You mentioned how some of these don't have other effects on other lipid markers. So of course of interest are triglycerides and HDL. And so we managed to find 28 for which they don't have an impact on those. They may have an impact on total cholesterol, but that's okay. That don't impact lipid metabolism.

We'd love to do an MR on those. The problem is they're not closely studied. And my concern is that they may not be because those genetic variants don't have that much of an impact on atherosclerosis. And if I could just fit in one more thing related to that, here's a great example, glycogen storage disease. Glycogen storage disease can result in hyperlipidemia and not just in cholesterol, but even in high triglycerides. And it's a big target for a lot of studies because guess what? They don't have resulting atherosclerosis in spite of their high levels of LDL and triglycerides. In fact, there's, and I don't have those in front of me, but I have some studies I could send your way, Lane, that I think you would find interesting. I think it's GSD1A, I think, is the one that's probably the most studied.

It's the most common of the ones that are there. So, yeah, I think the genetic story is a great one, so long as we can exclude those factors that are likewise able to impact the progression of atherosclerosis. You had mentioned a couple other points, if I can just hit them real quick. You mentioned lipid size. So here's the thing with lipid size. I actually don't put a lot of stock into the small dense versus big fluffy. We haven't had a chance to get into my general philosophy, but it's different than even a lot of low carbers. I believe that your lipid profile is much more a reflection of your health state or your disease state, or of course your metabolic

state. And that it's much more reflection than it is a driver. I'm sure you've known, like say family members or friends who became say obese or type two diabetic and their lipid profile changed. And now all of a sudden they have atherogenic dyslipidemia. So then the question becomes, okay, is it that the atherogenic dyslipidemia drove their atherosclerosis that resulted after they got that profile? Or was it really the atherogenic dyslipidemia drove their atherosclerosis that resulted after they got that profile?

Or was it really the root cause being that which brought them to type 2 diabetes and a type 2 diabetes itself? I'm more inclined to say it's the disease that created the lipid profile. Say it again, Dave. Say that last part again one more time. So the diseases that can result in changes to your lipid profile, I think, have to be disentangled in order for us to determine the causality direction of the lipid profile causing the disease. in a higher level of chronically of chronic sorry let me restate this does atherogenic dyslipidemia result in a higher level of ldl than you would otherwise have had okay if that's true then whatever the root causes of atherogenic dyslipidemia such as type 2 diabetes being associated with cardiovascular disease whether you have high ldl or not should we then remove that from the equation to examine how much the LDL does in fact cause

atherosclerosis? Because it very well could be the case that if you're not willing to change your lifestyle and you have atherogenic dyslipidemia and you take a statin, that that's a net benefit overall. But that doesn't answer the bigger question I'm wanting to drive as, which, okay, what if you don't? What if you don't have type 2 diabetes? And what if you do have this different lifestyle, but you do have higher LDL? Let's look at that context because that lipid profile reflects a different health state, a different disease state. Wouldn't you agree? Yes, I would.

So I think the thing to tease out here is two things. One, we've got to remember we're talking about with longitudinal data, it would be great to have, but we're also talking about a lifetime exposure risk in terms of cardiovascular disease. So that's very, very, very tough to get that kind of longitudinal data because you could be talking about 10, 20, 30, 40 years, if not more. And then I think one of the other things that has to be mentioned is the fact that low risk or reduced risk doesn't mean – you can be at lower risk for a cardiovascular disease even by having an elevated independent risk factor, because as you said, your other lifestyle stuff is good. So for example, if I look at, if I take somebody,

let's assume, just play this exercise with me, Dave, I know you may not agree. Let's assume LDL is causative in atherogenesis, but I have somebody who also exercises a lot. They control their food. They manage their weight. They don't smoke. They don't drink. Are they, and I don't really answer this, but I'm going to guess they are probably less likely to have a heart attack than the person who doesn't exercise smokes and has low LDL. Right? So I agree with what you're saying insofar as this is a overall lifestyle sort of problem that you cannot disentangle. And I agree with that. I think that you can still hold that belief and also acknowledge the fact that there is quite a bit of data to suggest that LDL is causative to some degree in it.

And especially when we look at like even the Framingham study, where when you stratify, like, for example, low HDL and high HDL. Yes, with high HDL, it is a reduced risk of heart disease. But amongst people who have high HDL, those who have low LDL versus those who have high LDL, the people with low LDL still have a lower risk compared to those who have a high LDL, both having high HDL, right? And you see, you also see this with inflammation. So people who have low inflammation have reduced risk. I'm actually looking at a study. Let me see here. One second. Just got to find it because I don't want to miss cite it. It's the Fourier trial.

I think I'm saying that correctly. Inflammatory cholesterol risk in the Fourier trial. And they basically stratified people into different levels of inflammation as assessed by CRP versus LDL and looking at their risk for a cardiovascular event. And what you see is, of course, people who have the highest level of inflammation and highest level of LDL have the highest risk. But even in the lowest level of CRP, which is I think under one milligram per liter, you still have almost a linear increase in risk going from under 20 milligrams per deciliter of LDL, which is ridiculously low, all the way up to, they looked up to 100 or over 100 milligrams per

deciliter. So basically, even in this situation where you're kind of looking at, okay, if we have inflammation low, if we have HDL high, it still appears to be an independent risk factor. Now, I want to quantify that with the difference know, the difference between going from a LDL cholesterol of under 20 to over a hundred takes your risk from 5.3. If you're low CRP, that is in this trial took the risk from an absolute risk of 5.3% to 7.7%. So it's not, it's not like, again, people kind of have this black and white mentality where when I talk about that, it's like, okay, if you have high LDL, Lane's saying that you're going to have a heart attack tomorrow. No, that's not what I'm saying. You may have high LDL and live to be 80 years old.

That is a very distinct possibility if you have a lot of other factors that are in check. However, what the research suggests is that if you also lowered LDL, would you be a little bit better off? Yes, the research does tend to suggest that. So when I talk about independent risk factor, that's what I mean. If we're trying to equate as many things as we can, as Dave pointed out, you can't do it for everything. Even Mendelian randomizations has its limits. But when we look at the consistency of, okay, we have epidemiology, that's one step. We have systematic reviews and meta-analyses. We have animal research. We have mechanistic data. We have the Mendelian randomizations. I would kind of say say how much evidence, what would be for you, Dave, what would be the level of evidence that you would require where you would say,

okay, I do think this is an independent risk factor versus these other things. Because like you point out, your LDL is high, but I am not like personally attacking you saying, well, you're going to drop dead tomorrow, right? Because that's not necessarily the case at all. Because if you're otherwise healthy, I think that your overall risk is pretty low. But you may not be as low risk as possible as if your cholesterol was lower, if that makes sense, or your LDL specifically. So can I confirm something? When you say an independent risk factor, are you saying saying so on balance, if I reduce that risk factor, there will be no tradeoff in risks of any other kind of disease? No, I'm saying that in terms of cardiovascular disease, specifically here.

I think I know where you're going to this, but go ahead and go there. I know you know where I'm going to this. Let's set it up for the audience, right? Yeah, it'll be a good discussion. So this will be good. I hope people will record this clip because I seem to make this point a lot and people seem to miss it, which is that if I wanted to keep from dying of cardiovascular disease in particular, I would do everything in my power to get my LDL as low as possible. I would do everything in my power to get my LDL as low as possible.

So I would be on a high-carb, low-fat diet. I'd be on enzetamib. I'd be on a statin. I'd be on PCSK9, all of that. But recognize that that's the equivalent to saying I am also going to improve the chance that I die of something that is not cardiovascular disease. So we need to be sure that there's a trade-off, right? Like, I mean, I think most people would agree that when you hear I'm going to reduce the risk by X, that they assume that there's no net trade-off at all. I just want to butt in real quick, just so since we're doing the pretext of it, I would agree as long as we're not talking about an underlying, like if we know somebody is predisposed to, say, much higher risk of cardiovascular event versus cancer based on family history and makeup and that sort of stuff.

Then in that case, even if, for example, you knew that something could increase your risk of say breast cancer. I'm just picking something. If you had no history of that in your family, but you had a distinct history of, okay, your dad, your grandfather, their grandfather, you know, died of a heart attack at age, you know, young age, then it may still make sense. Even if there was a trade-off, does that, does, I just wanted to throw that in there in terms of what I would agree to. But otherwise, all things being equal, I agree with you. You don't want to trade one thing and then die from something else. And again, it may still be worth the trade-off. It may be that what I do to reduce my LDL, let's say I reduce my LDL to 80. And in doing so,

I ultimately find out, let's say it's 50 years from now and you and I meet in you know a future bar and I'm like dang it turns out that yeah it would have been better for me to reduce my LDL to 80 because yes I did get an increase in my risk for cancer but that increase netted out on the cost-benefit analysis to where it was still a benefit in the cost of cardiovascular disease risk outcome. So of course, you know, I'm going to come to my favorite metric of all, which I sometimes use as a nickname, and it's all-cause mortality. I like to see data that looks at the whole balance sheet. I think if you're going to make a claim of a mortality benefit, you absolutely have to confirm that whatever intervention you took that reduced the risk of you dying by disease X,

it did not increase the risk of you dying by non-disease X, whatever that category is, right? And I realized, and, you know, I 100% concede regularly and constantly, as you know, I like to look at the NHANES data, which for those who don't know, it's open and available from the CDC, and you can look through it. It's a very large data set. It's like, I want to say, 40,000 people in total. And I by no means am an epidemiologist or a statistician, and I don't claim as such, but you can just look right now.

You can pull it down and look at what the association is between those people who have, say, higher LDL in their 50s, 60s, 70s, and what their likelihood is of still being recorded as alive a decade or a decade and a half later. And the reason I bring this up is not because I believe epidemiology is good at causing things, although I know, Lane, you and I probably would agree a lot more that that comes up in the nutrition space all the time. But it is good at knocking down claims of causation. So you have to have something baked into your hypothesis to help explain

why it is that those people would say a high LDL in their 80s are going to live to 100. And I'm perfectly happy to entertain the concept of reverse causation. So if I can jump ahead and make the case for you, what a lot of people will say is, Oh, you know why that is is because at the snapshot moment that you got people's lipids, those who had extremely low LDL were already in some kind of disease state where the disease state caused both the lower LDL and that new association

with them dying. That said, that's why I like longitudinal data. And I wish more of it was available. I wish there was an enhanced version of longitudinal data. I know we've got it with Framingham and I'd like to get a hold of it, but I'd like to see those people. Cause look, this is just a general complaint I'm going to have overall. My general complaint, Lane, I hope you agree with me on this is we spend way too much time studying sick populations. We should be putting much time studying sick populations.

We should be putting more time into healthy populations and particularly for getting things like high frequency blood tests and, you know, more robust longitudinal data from non stakeholders, from people who don't already have a stake in what the outcome of that data is going to be. And then I think we'd settle so many more of these arguments that are happening, especially in this space? Well, I personally think that most people get way too caught up in the details. And if I had to give my top six recommendations on how to live really long, it would be number one, exercise regularly. Number two, don't smoke number three don't eat like an asshole number four get enough sleep number five limit your stress and number six limit your alcohol and i think if you do that you're probably about 95 of the way there okay but um when when it comes to this kind of stuff i think it is important to to, you know, I'm, I always tell people like, I'm not married to any one hypothesis. I always tell people I'm going to get, hopefully

I don't get in trouble for this statement. I think it's, it's funny. Anybody who knows nineties rap will get that. I'm not being a misogynist by saying this, but I think it's important to date your beliefs, but don't make that hoe a housewife. Okay. So you want to date your beliefs. You don't want to be married to them because you never know what's going to happen. Um, so I see, I think you guys like that comparison. Um, thanks Tupac. Uh, I got, I got to kind of butt in here for a second and it sounds to me like, and maybe you guys can correct me if I'm wrong, but it sounds to me like if you can control your weight or if you're currently heavy and you can figure out some sort of way towards losing weight, we don't really have to worry about a lot of the things that you guys just mentioned. Lane, you brought up some very good points about sleep and general health practices. I think a really something that is very hard for a lot of people to do is to figure out

how in the hell can they regulate the overall amount of food that they take in per day. It's been my own experience through my own journey that I have done keto in like a, what I would consider to be a safe way, but I also done it in a, in a way that wasn't very safe and wasn't very smart because I was like, Oh, I'm going to eat all this fat and this is going to work really well because I'm just going to magically produce a bunch of ketones.

Cause I didn't understand how it worked at first. And I did lose weight and I did, I did take some of that information at times and share it with other people because I was excited because I lost weight. But then I also got stuck. And then I'd also have times where I'd have cheat meals or kind of fall off and then eat an abundance of calories. And these are the things that we don't know. And I can't agree more with Dave on his comment about trying to study these healthier populations, because I think there's a lot of people that are probably well-meaning, but they're probably doing some, a lot of damage and they're not really paying attention. And I think if we can continue

to figure out a way to communicate to people like, Hey, this is, this is a long haul. And when we talk about overeating, we're not necessarily just talking about per meal or per day because it doesn't really erase to zero per day. You have energy throughout your entire life, right? And it's a weekly battle, monthly battle, yearly battle. We need to have a lot of consistency with all this. We know that you can't, we know that it's very difficult to out-exercise a bad diet. out exercise a bad diet, but it's also very difficult to, it's also very difficult to not have any exercise in your life and be able to eat the correct amount of calories because your calories might have to be really, really low if you're super sedentary. So we run into some of

these issues and these are some of the main things that I see really messing with people in terms of people that are trying to get healthy, but they self-sabotage themselves just a little bit with some drinks on the weekend, maybe some junk food at night while they're watching some Netflix and things of that nature. Well, I think, you know, this, again, the larger discussion, I would consider this, you know, if you inject me with true serum, do I think LDL is a causative factor for cardiovascular disease? Yes. That being said, this would be like the surgeon in the scalpel. And I think what most people need is the chainsaw. And what I mean by that is if you've gotten everything else taken

care of, like you can, you can chase the rabbit hole of markers and do it in the wrong way insofar as you make it worse. Okay. So if you're so focused on LDL that you're, you know, okay, I'm just going to give it as low as possible, you know, but you're, you start eating a diet where you're eating less saturated fat, you're eating more PUFAs, but you're overeating, right? For whatever reason, that diet, you can't maintain it. You start putting on body fat. Well, now you're elevating other risk factors, right? And you might even still elevate your LDL because of it. But if all things are equal, I think it makes sense to work towards it. I think I'm going to go back to what Dave was bringing up because there is actually a very strong association between low LDL and the risk of developing cancer. And that's kind of your

hypothesis why in all-cause mortality studies, you don't really see this association with LDL and all-cause mortality. And I think what I would come back to that is we acknowledge the limitations of epidemiology, right? That's, that's a, that's a big part of it. Okay. Did, and you even said it, Dave, right? Like, is it the cart or the horse? Is it the chicken or the egg? Did they, did they have low LDL? Because we do know in several disease states, it causes your LDL to drop. Now, and again, like you even kind of made the case that is the dyslipidemia a response to the atherosclerotic disease? Is it a response to that? Great, great, great point. And we can't separate those things. So what I would go back to is since we don't have that longitudinal data, I think Mendelian randomizations is one of the best things we got. And there was actually a

study where they looked at low-density lipoprotein, LDL, and the risk of cancer. And it was a 10,000 participant Copenhagen city heart study, or sorry, 59,000, or sorry, it was a subsection of 59,000 total participants. So they looked at people who developed cancer and they were genotype for PCSK9, which seems to be the main one that a lot of people look for, as well as other polymorphisms, which are associated with reduced LDL plasma cholesterol. And what they found was the association with the incidence of cancer, of all cancers, completely went away when they medallion randomized, meaning that it appears that it's more of an association thing, that whatever produces cancer also tends to drop your LDL. And keep in mind that cancer

itself is an, and I don't know that this is the mechanism, but cancer itself is an extremely metabolically greedy tissue. You're going to see it rob nutrients out of the bloodstream. And so that could be part of the reason why I don't know exactly why I'm just kind of speculating. But again, it takes a really robust, it's actually really shocking how closely associated it is with cancer in terms of LDL cholesterol, and basically shows that there's absolutely no association when it's randomized. So again, you know, I'm not dismissing epidemiology because again, like there's uses for epidemiology, but when we put epidemiology up against, you know, essentially a randomized

controlled trial, we tend to err towards the more tightly controlled study, I would suppose. I'm actually really glad you brought that up because this is something I've chatted back and forth with Avi about because it would stand to reason that if, and let me be very specific about what you were talking about, the gene in question, PCSK9, just for those people who don't know, PCSK9 is a protein that attaches to the LDL receptor and kind of marks it to get degraded. So people who have a genetic abnormality where they make less of the PCSK9 are therefore marking less LDL receptors to be degraded. Therefore, there's more LDL receptors and therefore there's more removal of LDL particles. And that's why they tend to have very low levels of LDL.

Now, forget about cancer. Let's just talk about all cosmetology. It's the whole point. The very first thing I did when I found out about this PCSK9 loss of function is I went to the literature in any data set I could find that would show that those people who did have PCSK9 loss of function would indeed live longer than the mean average of the population. Now, Avi and I talked about this at length, that the one study that was actually a full study that I was able to find,

and that he actually had me read it. I kind of chatted back and forth with him on it. But ultimately, it didn't show a difference in all cause mortality later came back with an abstract, but it wasn't a full study for which it claimed that it did. And to which I said, okay, reach out to the authors. I would find this data compelling. I'd retweet it. I'd put it up on cholesterol code. I'd be very interested in it because any, any genetic abnormality that results in substantially

lower LDL and that shows greater longevity, I would consider it to be very compelling data. But as of yet, I've not seen it anywhere. And I mean, even trust me, I'd be a dog with a bone that existed. I'd want to go get it because I think that would be some of the most compelling data you could look at. And to round out your point, it doesn't matter if it's cancer. It could be infection. It could be lower respiratory diseases. It doesn't matter. The point is we would expect that if low LDL reduced cardiovascular disease with no other tradeoff, then we should see a likewise drop in all-cause mortality.

And this is where amygdala randomization could help us out if that's exactly what it showed. Yeah. So we don't have that data yet, which is, you know, that's one of the things, maybe we will have it in time. But it's one of the things where I think the point I would come back to is I'm not really making claims about all-cause mortality, but more so about it being an independent risk factor for CVD. That being said, I think this highlights in something I've been saying for a long time, and I think these guys over here can vouch for that, is that I take a much more 10,000 foot approach to nutrition, right? And acknowledge the fact that, hey, just because I'm saying something's an independent risk factor doesn't, again, because I don't want people to strawman my argument, which gets made all the

time. Just because I'm saying it's independent risk factor doesn't mean I'm saying that somebody who has modestly elevated LDL or even elevated LDL is going to die earlier than somebody else necessarily. There's a lot of stuff that goes into that, right? And when it comes to all-cause mortality, you're taking already messy epidemiology and it's making it really messy, right? Because we can correct for some confounding variables, but a lot of it we can't. So yeah, that's one of those things where we really don't know yet. It'll be interesting to see what happens. But it's not something we all care about. Yeah, no, I agree.

Like, if you said, hey, I'm going to give you a pill that will prevent you from dying of cardiovascular disease, which you will die of at 70, and the way it does is it gives you cancer at age 68, then I don't want to take that pill. That's not what the research shows in terms of, we're talking about statins or that sort of thing. It doesn't show that. If you're making kind of a hypothetical argument, I see what you're saying. You don't want to chase a rabbit hole. I think what I would say is it certainly doesn't show it people dying earlier, right? And I think when it comes say is it certainly doesn't show it people dying earlier. Right.

And I think when it comes to all cause mortality, because it is so messy, because it is so complicated and because we're living so much longer than we ever had before, and you have to die of something, um, what it takes to extend the lifespan is probably not going to be one thing. Right. extend lifespan is probably not going to be one thing, right? So if we're just being honest and somebody says, hey, I got this person, their blood markers seem pretty good, but they do have high LDL, they're taking a statin, but they're not exercising, they're not sleeping well, they're not monitoring their stress. Well, do I think that the statin is going to extend their lifespan? I'm not really sure. I think it's probably going to take a myriad

of different approaches. And I will tell you, like I said, I run a little bit high cholesterol or a little bit high LDL. I manage that through dietary fiber intake, as well as trying to limit saturated fat intake. And I've been able to control it with that. But that is a byproduct of, oh, hey, by the way, since I eat low saturated fat and high fiber, guess what I have to eat to get that stuff? A pretty healthy overall diet, right? That's pretty devoid of a lot of processed foods. And again, I don't want people to strawman what I say about processed foods. I just, I don't want people to strawman what I say about processed foods. I just, I try to be very careful because I see the demonization out there of individual nutrients. And I think one thing Dave and I would both agree about is that it is the

overall milieu of what you're putting in your body. And, you know, but I just don't want to demonize things because it's convenient. And what I mean by that and what people will call me out on is, oh, Lane, you're saying that it's okay to consume junk food. That's not what I'm saying. What I'm saying is if you are eating some junk food in a small amount in energy balance or in a deficit or whatever, and you're doing all these other healthy behaviors and you're, and you're not overeating on calories, do I think that little bit of junk food is going to cause you to fucking die? No, I don't. And I'm sorry, the research doesn't support that it will, right? And that's what I mean by, okay, I think it's important to look at the overall picture, which I think Dave and I would both be in agreement about.

But when I look at the individual stuff, if I look at the data that's out there and I say, okay, do I think LDL is a risk factor for cardiovascular disease independently? Do I think LDL is a risk factor for cardiovascular disease independently? I do. But like Dave said, it's going to be interesting to see if we get more detailed all-cause mortality over the coming years. Because in the end, that is what we care about. The problem with all-cause mortality is it may take a much more robust amount of interventions to actually affect it currently is there is currently is there a direct link between um nutrition and how long we live like as far as i know we don't have like that much proof of it i mean we can use some common sense and say hey like if you don't eat if

you don't eat a lot of crap and you don't overeat that you are probably better off than somebody that balloons up to 400 pounds or something like that. But it's really hard to even quantify even just that statement that eating healthier will add up to a longer, healthier life because we don't know of the other factors that the person might not be adhering to. I think we definitely do see it in the short term. I've certainly myself have, in fact, I joked about being on the COVID diet because when this all went down, you know, I was getting a lot less sleep and my diet was not as stellar as it normally is. I was staying up late researching all sorts of stuff. I can say in the short term, my health from a

pretty independent standpoint was definitely worse. So, and of course I've seen this with likewise family members in that if all of a sudden they're not paying that close to their nutrition, you know, clearly it has a very big impact on like hyperinsulinemia and their gut sizes, all other factors with metabolic syndrome. I think to Lane's point, it's true. If you're going to do something like say, oh, if you're advocating for having a Pop-Tart, you know, a week is, is it, you know, a cheap meal or something like that. And that's going to shave a year off your life.

Well, good luck coming up with the data for that. I have, yeah, you're going to, you're going to parse that out. Right. with the data for that. I have no idea how you're going to parse that out, right? But I do want to get back to your point, Lane, on the all-cause mortality. This is why I bring up the direction of causality and why epidemiology, I think, is good for at least field testing that. One of my frustrations when the reverse causality argument is brought up, not because I don't like it being brought up, I think it's a good thing to bring up. One of my problems is that there are so many lipidologists I know who bring it up in passing, who I say, wait a sec, if you believe that there's

such a wide girth of people who, if you see very low levels of LDL, it's indicative of an underlying condition or problem, why aren't you using it prognostically? Why aren't you? Because we've seen this. We've seen acute drops with either LDL or HDL. And we usually say, look, you may want to consider some wider spectrum testing because it could be a problem, right? Now, those are rare cases. And I don't want to go into those too much, but I will say when your lipid values change substantially, particularly towards the low at a very fast rate, that's something that I think is worth some extra consideration. Now that said, again, being able to disentangle it,

this is one of the problems I have with being able to approach Mendelian randomization is we need to likewise get the longitudinal data alongside Mendelian randomization as well. Unfortunately, I feel that there's a little too much that's supposed right now about the year-to-year differences going all the way back to when you're a toddler. And unfortunately, there's not a lot we can do about that because you don't want to be taking like, say, yearly blood tests from, you know, children quite as easily but we do know with those monogenetic factors they are if if if a child unfortunately gets born with say homozygous fh which is to say they have the two alleles they're in deep trouble they the case that got brown and goldstein started they're famous for i'm getting the nobel prize for discovering the LDL receptor. It was a little girl who had a stable angina at age three and xanthomas at age three.

And she had her first MI at age six. It's terrible. And that's what got a lot of this, a lot of the movement started to be interested in this. Now, part of the reason I'm glad to bring that up is I would be interested in what your guys' prediction is and Lane's prediction. As you guys may know, I'm right now working with Spencer Nadalsky, who has a very different opinion than I do on the limit hypothesis, and Dr. Tommy Wood. And we're putting together a study to test for those people who are on a low-carb diet who has extraordinarily high levels of LDL. Odds are all four of us know many by this point

called lean mass hyper responders. And we're looking at a cohort of people that are, that have excellent cardiovascular markers across the board. I mean, not just the high HDL, low triglycerides, but low inflammatory markers, none of the metabolic syndrome, et cetera. And we're going to get a hundred of them. And then we're going to take CT angiograms at the start. And then one more time, a year later, we were originally going to make it five years, but the luminary that we're connecting with says for sure, we should be able to see the geographical changes in their, um, in their arteries in one year, given the effect size, given just how high their LDL is. So right now, my prediction is I think we're not going to see a substantial

increase in LDL as would be expected if they had homozygous FH, like I was just mentioning with, say, the little child. Spencer Nadalsky would say that we will, that we will see a rapid progression of atherosclerosis. So what would you guys guess? Me first or these guys? What would you guys guess? Me first or these guys? Well, I would say that my concern would be whether or not a year is long enough, but I understand you have to make a certain time point for it. You can't just – I don't want to be one of those people who say,

well, why don't they do it for 10 years? Because obviously more time is more money. I guess what's your control group? There's not a control group. Lean mass hyper responders, again, we're going off the advice of this luminary. I can't mention this person's name yet, but I can tell you they're very, very high up and respected in the field. And at the point where the IRB is approved, everyone will know and then it'll get the chat. But he's the one who convinced us to not do five years that we would have more than enough data at one year given his existing experience with those who have FH and who have LDL at this level. He says the CT angiograms

should show a statistically significant increase. Do you know what the average LDL approximately is going to be amongst participants? My guess is you haven't really recruited subjects. No, we can't recruit until we have the IRB. And I don't even want to guess yet, of course, because… Well, you're going to have inclusion criteria, right? Like there's got to be a minimum that they've got to be above. What's your inclusion criteria? What's your inclusion criteria? I don't think I'm allowed to say that either. Here's what I am going to tell you. I'm going to tell you that the existing lean mass hypersponder phenotype, as I've defined it from the 2017 article, are those people with an LDL of 200 or higher.

Which, of course, in the existing guidelines means you should be on the highest tolerable dose statin. An HDL of 80 or higher and triglycerides of 70 or lower so i can't say this much it's probably if it's not that it's probably going to be something like that um and i will say that in the groups and between the sites and everything else we know several people that are we know like for example we know 50 people that are say um an an LDL of 400 or higher, for example. And again, at 400 or higher, we're talking homozygous FH levels. They should right now be showing very high prominent levels of xanthomas or stable anginas and so forth. Because getting back to what you were talking about with the Mendelian randomization,

unlike the little girl who just came out of utero, right? These are people who would, in theory, have the lifetime burden. So if you're, say, 40, and you get the same levels of LDL as that little girl who had homozygous FH, you have that whole balance sheet of the 40 years prior as part of the existing atherosclerosis right yeah what um okay let me ask why did you call it lean mass hyper responder i assume there's there's something with that it was it was observational if i could go back in time i would have called it something different it just happened to be that it was generally people were very lean and didn't have a lot of fat mass so a lot of the kinds of people you would,

I'm sure see and work with, although generally, generally it it's, um, they're less likely to be, um, uh, bodybuilders. So it's, there are certainly some who are bodybuilders, but, and you may already be aware of this, uh lifting resistance training especially uh is also an ldl sync you and i i believe a lot of this comes back to endocytosis for muscle growth and repair and so forth but you take for example the keto gains group they're like median ldl levels for even people who's carnivore might be say 160 180 right but those people are more like, say, cyclists or yoga instructors or runners. Those will be the ones who can have like super, super high levels of LDL. And this all fits the energy model.

I don't know if you had a chance to look through the energy model, but basically the gist is if you're having to traffic more fatty acids around as triglycerides, you're going to have more turnover. But the more lean mass you have relative to fat mass, it makes sense that that speed of recycling has just got to be at a higher rate. Therefore, you're going to have more remaining LDL particles and therefore more resident LDL-C. And that's how you end up with these levels. But they look like unicorns in that lipidologists around the world don't know what to do with them because typically you don't see that level of LDL without likewise, say, higher inflammatory markers like you tend to see with FH, sometimes higher levels of triglycerides, et cetera. They're very unusual in that regard.

So what I would say is, and this isn't meant to be a cop-out response. This is just meant to be a complete response, is that it's hard to answer that question. And trust me, I understand limitations more than anybody having done those, not these sorts of studies, but studies in general, it's hard to answer that without a control group where you've got people who are similar phenotype, but also lower LDL, right? So the question, now the question you asked me is, do I think you will see increased, what was the measure you're going to use again? Increased atherosclerosis.

CT angiogram. CT angiogram. Okay, cool, cool, cool. Yeah. So do we think we'll see increased buildup? If LDL is an independent risk factor, you would expect yes. However, when you're also dealing with people who are lifting weights or exercising and, you know, have all these other healthy behaviors they're doing, I'm not sure. And like I said, what needs to be, what would hopefully be a comparison would be where you do the same thing, but with people who have one group, similar everything, LDL, other groups or everything, low LDL, obviously very difficult to recruit for very difficult to find.

Because I don't think it would be hard for me to recruit for and find, just help me raise another couple hundred thousand dollars. Yeah. I would love to do it. Right. Yeah. That's what I mean by hard to recruit for hard to find because money, when people ask about, and again, Dave, I think it's great what you guys are doing because you're actually trying to answer some questions. And it's like people ask, well, why didn't they do the study for this much time? Why didn't they use this?

Money, money, money, and money. I don't know. I was in a debate on Twitter. I don't want to call it a debate. I don't want to I was in a debate on Twitter. I want to call it a debate. I don't want to fight with that. Where somebody was like, nobody should ever charge for any nutritional advice or weight loss advice. It should be free. And I'm thinking, do you work for free?

Like all these researchers, they got to, they got to make a living. They have to make some money. Like they have bills like the rest of us. I think when we think of scientists, think that like you know it's like this um benevolent you know person sitting in a lab and just you know their food and their cell phone bills and everything's taken care of no no they're probably getting paid you know maybe 60 grand to be there and they're just trying to they're just trying to make a a living and you got to pay those people do the research. That's, that's the equipment costs money. The medical equipment costs an enormous amount of money. So I think what you're doing is great. Um, what I would say is you, like, I wouldn't be surprised if you see, so for example, let's take the reverse. Okay.

Let's say you have these people, they've had this burden over their entire lives but now recently they've been getting healthy they are they've been you know controlling their calories they've lost weight they're exercising well maybe you'll actually see less over time but what's hard to know is what's that the lipid hypothesis would push back on that, that you're not going to get regression. That's true. Yeah, that you wouldn't have regression. And listen, to your point, we have a good analogy, which is smoking, right? So if you are a three-pack-a-day smoker, you're like, it's okay, though, because I run five miles a day and I eat right and all of that other stuff.

Sorry, you get another cohort of people just like you who don't smoke three miles a day and I eat right. And all of that other stuff, sorry, you get another cohort of people just like you smoke three packs a day and they're not going to drop dead as fast. Right. And that's, and that's, I think, I think a valid point. And it's why I don't, a lot of people who are good friends of yours are concerned that we get to the other end of this. And if it doesn't show a huge effect size that I'm going to suddenly walk out and declare, Hey, the lipid hypothesis is over. This disproves everything. It doesn't.

This is the beginning of a conversation, but it's, I think the beginning of an important one, because I know that you, as much as I know the low carbers get on you, you, you do, as you mentioned, your app, for example, has a keto setting. get on you. You, you do, as you mentioned, your app, for example, has a keto setting. You do have people you talk to and coach in the low carb who want to go on a low carb lifestyle, right? Those, those people, there's so many people who I think don't have as much of a choice about how they deal with their type two diabetes. They instead have type one diabetes, or they have epilepsy for which there's a much more clear association of reduction of carbs to potential benefit. Yeah, sure. I think, I think for those

people, if they're one reason to not take these steps when they see otherwise excellent benefits is cholesterol. That's what keeps me up at night. That's, that's why I worked so hard at trying to get this. So I think that's, you know, a little bit of teaching people about false equivalencies, you know, and that sort of thing. Because, you know, if you have epilepsy and you're worried about your risk of, you know, of a heart attack, you know, 40 years from now, I think you're missing the forest through the trees in terms of like what benefit you can get. Because the first, you know, real benefits shown to the ketogenic diet were for epilepsy. I mean, it seems to be very good

at being able to control epileptic seizures. So yeah, I mean, as you pointed out, Dave, I kind of take the Michael Jordan approach of Republicans buy sneakers too, my man, where, you know, we have, we have a keto setting on our app, but I don't hate keto. I mean, Dom D'Agostino is a good friend of mine and we've been on Joe Rogan together talking about keto, energy balance, all that kind of stuff. But one of the reasons, actually somebody asked me like, how can you be friends with Dom? I'm like, because Dom doesn't say stupid shit. Like he doesn't say things like calories don't matter. Like he acknowledges this, you know? And I think that that's just the tough conversations that we have to have is that, you know, a lot of people will listen to you and I on this conversation.

And they'll probably get pretty frustrated by it because nobody's making like really extreme claims. It's a lot of nuance. There's a lot of stuff to dig through. And you're probably, if you're looking to walk out of this and be like, okay, who spiked the football and you know, do I need to worry about LDL or not? Well, it's a really long conversation. And you know, again, it's one of those things where like, I guess, so I don't want to dance around your question.

So I think you may see a little bit difference. But if these are otherwise healthy people, it wouldn't shock me if you didn't see much difference, if that makes sense. And that in itself would be very relevant. um and that in itself would be that in itself would be very relevant like it's even if it's some something in between even if there's some progression of atherosclerosis that's of some statistical significance but it's still when compared to an fh group uh it's nowhere close to that that at least gets us some data to get the ball rolling to better understand, you know, what the real difference is on diet induced hyperlipidemia versus a genetically, you know, induced hyperlipidemia. And I think that that's relevant. And I think, you know, this points to a larger discussion also of

understanding the difference between something being, being an independent risk factor and understanding that that doesn't mean it's going to kill you tomorrow or that it could kill you at all. So, for example, you can have the what the health, right, where one egg is the equivalent of smoking six cigarettes. I still don't understand the mental gymnastics they went through to be able to justify that. don't understand the mental gymnastics they went through to be able to justify that. But it's almost like these diet groups get so encamped. And one of the reasons I agreed to come on here with you today is because I don't think you fit into this. I would disagree with some of your hypothesis, but I don't think that you are married to your beliefs yet anyway but um you know if if i've had these times in my own career for example i mean it's something completely unrelated but

where i had to question okay is my hypothesis correct so i used to be somebody who ate eight small meals a day because the idea was you keep amino acids high, keep muscle protein synthesis going. And then we got some data back out of one of my experiments where I looked at that and I go, well, shit, I really can't justify doing that anymore. So I had to decide, do I believe my own data? Right. And, um, I think one of the problems is people get so entrenched in their beliefs and they marry their beliefs. They get married to their beliefs. And then once you're married to it, it becomes very hard to divorce those beliefs, right?

It's very painful. So I think, like I said, one of the reasons that I don't advocate against any particular diet, and you can watch my Twitter, you will see it one week, the vegans are giving it to me. And the next week, it's the, you know, the orthorexics, the clean eaters, or the no, we know non processed food next week, it's people who ate fructose. And the next week, it's the keto people giving it to me. And I think that's just because like I said, I don't, I'm all for if somebody says, hey, a ketogenic diet helped me control my calories and get my weight down.

Then, hey, if you did have success with another approach, it's probably a perfectly viable approach. Just because you might get conferred a little bit less risk if you were able to get your LDL cholesterol a little bit lower, that doesn't matter. If you're not able to stick to that diet, you end up overeating and putting that weight back on like that. That's a, that's a much more important thing to think about is just the overall effects of what you're doing and your overall lifestyle. Actually, I don't know if you saw it, Dave. It's kind of a little bit outside this discussion, but there was a really good

meta-analysis that just came out looking at not just meat and processed meat, but also different quartiles of fruit and vegetable consumption. and basically showed that with processed meat, yes, there was still an association with, I believe it was cancer. But when you came to unprocessed meat, at the highest level of processed meat intake, if you also had a high level of fruits and vegetable intake, there was zero association with cancer when you got fruits and vegetables that high. And again, that points to the fact that we really, a lot of nutrition people out there, we want to get really reductionists, but it's hard to get reductionists because all this stuff exists in the continuum. And like I said, if you're eating really high something,

you're probably eating really low something else and vice versa. And we, it's really hard to disconnect those things. So I would say to people at home is like, let's not get too reductionist with stuff, right? If you're worried about the fact that you have, you know, an apple because there's fructose in it, you're really worried about the wrong stuff. Now, if you're worried about having five Cokes a day and overeating your maintenance calories by 500, 600 a day, yes, that's worth worrying about. So I realized I went on a long diet right there. Lane, I know you have to bounce on out of here, but before you take off, I'd love to know,

why do you think you get so misunderstood? Because I think that your message is, it's, I haven't really seen it change. I haven't seen your message change. You always kind of revert back to the same, you know, one or two or three principles and people still get confused or mad or triggered. uh, confused or mad or triggered. I have a theory. Go ahead, Dave. I, I think to put it in Dave Feldman like language,

I think you're very colorful on Twitter. And so I think probably people find more, uh, like if I could distill down what you say, cause I started following you after that Joe Rogan with with Don DiAgostino, and you made a lot of points that I was like, these are not only some points that I agree with, I've not been hearing anybody else make these points. And I think I tweeted back to you the one where you like, I want to look the best who could appreciate your content more would take more opportunities to watch something like this because I have and having watched you uh doing interviews like this and I don't see any of the colorful language I see on Twitter I just feel like Twitter is sort of maybe a place where you find some kind of therapy with sort of I don't know that's that's my theory roasted I don't know.

That's my theory. Roasted. Well done. So this just turned into the lane's going to lie on the couch moment. Everybody's going to psychoanalyze them, huh? That's right. I'll be real. So I think that everyone likes their message a little bit differently.

And there are a lot of people who really resonate with the fact that I will boldly call out BS. Um, but if, but that being said, if you look at when I call and it's not always sometimes I am aggressive and probably not maybe more so than warranted and I usually if I'm called on it I usually walk it back because I think it's important to own your shit when you're wrong or when you've when you've been overzealous right but usually if people are respectful to me I I'm respectful for them. The problem is on Twitter, not very many people are respectful. Um, but yes, I use colorful. I actually had a, a Doug Coleman, who's actually a colleague of mine. And I, I liked Doug quite a bit.

He's in the ISSN, but I said something to the effect of, oh, if you ever feel the need to like tell someone how they should eat unsolicited, just stop and ask yourself why you're being such a fuck face. And, you know, like basically like if it's notolicited, just stop and ask yourself why you're being such a fuck face. And, you know, like basically like, if it's not solicited, just close your mouth,

you know? And he was like, did you really need to include that kind of language? I'm like, it's so much more fun. It reads so much better with fuck face in it. Doesn't it? Like it's so much better that way.

So I, I think that part of it is, I actually talked to my wife about this one night because my wife is very much like, Holly is like the most cordial, polite, you know, I'm like, it's good. I have you because you can be good cop and I'll be bad cop. But she is so cordial and polite. And I said, but that's great because you can convey our message in a way that is going to capture the audience that I never can. But I'm also going to capture a certain percentage of audience who's tired of hearing everybody pussyfoot around it, who's tired of everybody just kind of giving the politically correct answer and who wants to hear somebody who's going to, you know, go after it a little bit more. So I think there's definitely like, I had this also discussion with Greg Knuckles. He's like,

you realize you're never going to change the opinion of the person you're arguing with by arguing with them that way. I said, that's true, Greg, but the likelihood that I'm going to change their opinion, even if I'm nice to them is probably also very low. I'm not doing it for their benefit. I'm doing it just to plant that little seed of doubt in somebody who's, who might be watching. And I can't tell you how many people I get who actually messaged me and say, Hey, I used to hate you. And then as I followed you more and more and saw you deconstruct these arguments, I realized, Holy shit. I actually, he's actually right. So, um, I actually, he's actually right.

I'm going to call you on that though. I'm going to call you like right now, we're having a pleasant conversation. Let's rewind time and imagine instead you were Twitter you in this thing. I don't think your message would have resonated as well as it does now. So it's true. I think it helps when you adapt to what you believe

the receptiveness of the other person is. Oh, but that's the difference, Dave. That's the difference is you're being very respectful and nice, and you're also not engaging in logical fallacies, right? So that's like in previous debates, if somebody is being respectful but engaging in logical fallacies, I'll also get frustrated. Dude, there's a new guy on – there's a guy on Twitter right now that's trolling you hard. I've been seeing over the last four or five days. Is that the bacon guy? I can't even remember his name, but I was like, wow. And he just keeps saying one dumb thing after another.

I'm like, oh, my God. This is the guy that believes that essential amino acids are not actually a thing. That your body can make all the amino acids that you possibly need, and you don't need to eat protein that's what i saw that's right yeah so in his hypothesis it's a testable hypothesis yeah so i said so his his uh basic premise is that okay if we need if if the human body is tens of thousands of grams of protein, I know, so more than that, right? Like the average person, if you're 50 – well, actually a lot of it's water. But let's say you're like 20, 30 kilograms of protein.

How is it you can survive with only 50 grams of protein per day as a baseline requirement? And I said, well, I think you probably don't understand the fact that your body does this thing called amino acid recycling, where seven out of every eight amino acids that are incorporated into new proteins are from old proteins that have been degraded. So you don't actually have to just like eat your entire body weight in protein every day. But yeah, apparently he is a, I don't want to demean people who work at this job, but he works at Costco and believes that he has discovered that the nutritional narrative of the world is wrong and that people like me are not. So actually, this is interesting, Dave.

People have looked at nutrition as a second science for a long time. for a long time. So I think people think that all PhDs in nutrition do is pull out a chart of the food guide pyramid and just stare at that motherfucker for about six years. And then when we're done staring at it for six years, they hand us a PhD. And the fact is we have to take a lot of biochemistry, a lot. I've taken, you know, analytical chemistry, organic chemistry, two semester biochemistry, nutritional biochemistry, physical chemistry, instrumental chemistry, inorganic chemistry. Like my degree is basically a chemistry degree. It's just with regards to food chemistry. at like dieticians who are very clinical in how they apply their knowledge, they think that most nutritionists are behind the times and that it's kind of a second science. So to your point, Mark, that's, that's the guy who's trolling me. And, and, and he's been, he's been, he's been fun. Lane. Thank you so much for your, uh, by the way, I come from engineering, particularly in

software engineering. We don't care what paper you walk in the door with. We want to see your work. We want to see what you've accomplished. We want to review your code, right? I don't care whatever somebody's education background is. What can I observe that they accomplish? What things do they say that make sense and so forth? And so in that regard, I likewise dislike when somebody assumes credentials are not at least a head start.

I think it's 100% fair to call out when somebody who does have a degree is saying things that are, you know, clearly not reflecting the effort. But that said, it's just like I would go to a doctor if I was hurt. They've got the head start for me on whatever it is that I think there's going to be a problem, and I want to see how that plays out. Now, again, at the end of the day, though, I'm still an engineer. So I'm going to start from a skeptical standpoint, but I will also be open-minded to wherever a source of information comes from if I think they're making a valid point. That's the catch. So I think just to wrap this up in terms of like, you don't want to make an appeal to authority, right? So where I tell people, because people say I appeal to authority because I talk about

my education, but that's not exactly correct. Because if I was only appealing to that and not providing empirical data, that is an appeal to authority, right? But if somebody, so it's okay to talk about, hey, I took this, this, this, and this, if you're also providing empirical data based on a claim. What's not okay is to use a degree as a shield. And when somebody questions your claims, say, well, what the hell do you know i did a phd in x right that's not okay uh and i there are people who do that and i tell people listen people go well if you have a phd you got to know what you're talking about i'm like probably um so all degrees do and we see this with medical doctors who say insane things. Um,

all a degree does or an advanced degree is increase our confidence that that person probably knows what they're talking about. They probably should get a little bit more leeway. You probably should value their opinion a little bit more, even if there's no data to back it up. But that being said, some turds just don't flush. And so I've seen PhDs who couldn't logic their way out of a paper bag. There's definitely some people who have degrees who don't know what the hell they're talking about. And I feel bad for the average person because they have to wade through this soup of experts really trying to figure out who knows what they're talking about. So I'm with you, Dave. If somebody, I've hired people in my company who don't have a degree in nutrition and they're really, really good nutrition coaches. But I also saw their work. I saw their

logical process, that sort of thing. That's what I care about. Now, if somebody comes to me and they're really good and they have a degree, great, awesome, even better, right? But at the end of the day, agreed. If you can provide evidence to support your statements, that is what we should be valuing above all else. Dave, I'd love to get your perspective on how you manipulated your cholesterol levels with, I think at one point you did it with bread, and another point you did it with extremely high amounts of fat. And Lane, if you need to go, that's fine, because we're just going to talk poorly of you,

and we're going to talk about the superiority of the ketogenic diet. I've got about seven minutes left. Okay, cool. So I'll write it out. All right. If you haven't heard about this experiment, Lane, you might actually find this to be adventurous. I did this, I think, two years ago. It's colloquially known as the white bread and processed meat experiment.

And this is effectively what I did, I was getting, it's getting to a point where I really wanted to really draw emphasis in the energy model and how I really do believe it's very much associated with metabolic pathways and not with the food quality choice. Because unfortunately, a lot of people who are pushing for the high carb, low fat diet are coming at it from the perspective of it's, you know, it's fiber, it's having particular nutrients content, something along those lines. And it's not so much that I don't think that that's a potential value. It's that I really wanted to draw forward that no, this is really about both metabolism and existing energy status, particularly having glycogen stores in the liver.

I believe that that's a very major factor as to how much the body will traffic more fat. And just to give the quick like one or two sentence biochem reason that I may lose a lot of people on, but then I'll take it back. I believe it ultimately comes down to if your glycogen, your hepatic glycogen stores get low enough, it's going to activate greater hypoleptinemia, which will further activate the HPA axis, which will activate greater lipolysis, which means that your fat cells are going to be overall dumping more lipolysis at a lower rate. Or sorry, at a higher rate because of higher glucagon, lower insulin, but especially the hypoleptinemia. higher rate because of higher glucagon, lower insulin, but especially the hyperleptinemia. And that starts this higher cycle of more throughput going back through the liver, packaging more of those back up into triglycerides, exporting them out as VLDL,

which hardly hang in the system for very long because you've got higher turnover in periphery. Okay. That's the big bio geek explanation. So what did I do? I said, all right, I'm going to intentionally pick a diet nobody recommends ever. And that's going to be white bread and processed lean meat. And I specifically wanted to pick meat because a lot of people feel that meat is the reason for which you're ending up with higher levels of LDL. And no, it's not. I ate loads of lean processed meat along with loads of bread. And what happened was my LDL at the start of the experiment was 296. So at 296, I'm 50% higher than even what that max range is against the guidelines. And in seven days at a rate of around, I want to say 40 milligrams per deciliter, my LDL was dropping, dropping, dropping until it hit 83. So drop of 213 milligrams per deciliter in seven days. And yeah. And why do I think I did that? Well, I mentioned the system that I was just

talking about before that I flipped back the other direction, obviously eating all that bread, I make myself hyperinsulinemic. So I'm clamping off the lipolysis big time, but I'm also further filling up my glycogen stores. And without question, I'm telling the body, we're replete with glucose. We got plenty. There's no reason for you to turn over a lot of these VLDLs. And guess what? While my LDL dropped, as I expected, my HDL went to a record low of 38. And my triglycerides jumped up to,

I want to say 220, something along those lines, which by the way, I think is worth emphasizing because a lot of people believe that if you overeat on carbs, because there are these overfeeding studies. And I think Lane, you may be familiar with these, for which there wasn't a higher rate of de novo lipogenesis. I believe that I, that was very compelling to me that indeed, I was at least getting some reasonably large degree of de novo lipogenesis to get to those levels of triglycerides, unless they were all just resonant through the full seven days. So granted, I would have liked to have done more sophisticated testing to better suss that out. And there's an experimental lab test I may be able to eventually get where I can

actually look at the composition of my VLDL a little bit closer, and that'll help me better understand how much that was recently secreted versus just held up and captive, if you will. But the bottom line is, I would much rather have the lipid profile that I had at the start of the experiment with the high LDL, high HDL, low triglycerides than what I had at the end. And I'm sure if I continued eating like that and continued to have that lipid profile, I would have probably had a worse health outcome over time. It's hard to know, but let me ask you this. Do you know your caloric intake and

your total fat intake during that time i do you know what um i'm just going to tell you right now you could go to cholesterol code right now and it's under uh white bread probably just search it and there i have all the data for that experiment laid out yeah it's tandem drop experiment part two and i guess it was on november white bread yep white bread and processed meat and yes i think to where you're going i was definitely hyper caloric i was definitely what i would say above maintenance yeah what was your what was your uh total fat intake but not by much my fat so my fat was 13 34 50 50 56 56 46 these are in grams so roughly roughly 50s i want to say okay so i'll address the denofal epigenesis part real quick, and then I've got to go.

Basically, the research shows that in overfeeding studies, if you're overfeeding carbohydrate, what tends to happen is you don't really store that carbohydrate. You kind of just burn it, you use it, and you store the fat that you're taking in. However, there is evidence that if you're on a very low fat diet and calories are high enough and carbohydrates are high enough, your body can ramp up de novo lipogenesis to account for a decent amount of fat. And that makes sense. I mean, you wouldn't want to just waste, like if all you had available was carbohydrate, but you were in an energy surplus, you wouldn't just want to waste it and not be able to capture that energy. So do I know whether or not that's specifically what happened in this case? It's hard to know without a tracer study, obviously, but it's certainly

possible. And Dave, thanks for talking with me guys. Thanks for having me on. If anybody wants to follow me, I'm at bio lane on all platforms and i sell some shit uh i sell books uh i saw i have a book fraud fraud yeah uh fat loss forever and i also have a nutrition coaching app that as dave said has a keto setting on it um and it's actually been tested uh dom digustino actually uses our app um said he loves it. So that's cool. You got supplements too, right? What's that? You got supplements that you're selling now too, right?

Yeah. So, well, we had our pre-sale. The line should go live here in about eight to 10 weeks, depending on when we get inventory in. It's going to be called Outwork Nutrition. So yeah, check all that stuff out. But definitely, guys, check out our Carbon Diet Coach app. It's an amazing app. Um, we have over 15,000 users.

Now we have a 4.8 star rating in the app store, which is really hard to get. Uh, and it's 10 bucks a month for customized nutrition coaching that goes on this guy right here, which, you know, if you can afford a coach, great. But if not, we're a really great option. We're on iOS and Android. Thanks for having us on. That's my 10 second give me money pitch thank you lane really appreciate it thanks guys dave if we can keep you on for just a little bit longer i'd love to dive into this a little bit more so i also understand that you took in like enormous amounts of fat at one point too and got

your cholesterol readings right like with three or four hundred grams of fat every day or something like that right yeah so i've actually done this several times in fact it's colloquially called the feldman protocol in fact if anybody wants to go to the site they can they can click on feldman protocol it kind of outlines it and this is really what sort of kicked off all of my research was that this is what happened play by play. I get the initial cholesterol test. I flip out and I didn't start learning everything I can about lipidology. But in the two weeks after I'd gotten that initial test, I was like, you know, I'm going to get another test just to confirm just to confirm that this is what it is. But in that span of time, I was very depressed and my diet kind of fell off. And I said, you know what, I'm only going to eat if I'm like really hungry. And I started becoming hypo caloric. I started just eating less

and less and less. And then I get the second test. And as I, it happened at the same time, I'm learning about the lipid system, but I'm also saying, you know what, what i'm not i think this may be more of an energy distribution system more than anything else that may explain this so that when i got my second test i was actually excited because instead of my ldo going down from how little i was eating and how much my saturated fat went down, it went up. It skyrocketed. It went up to, I think, 400. And the lady at the counter who was handing it off to me saw, she had already seen me two weeks prior get the lab, and I was clearly dejected by it. And so I could tell she was already afraid to hand it to me this time

because she remembered me from last time. And she's handing it to me, and I at i was like oh actually she didn't know how to read my reaction because i seemed genuinely excited to get it because at that moment in time i was like you know this is only two data points but i'll bet this is an inverse pattern and so after that i started my diet started to ramp back up and sure enough my cholesterol started going down so that they go inverse from each other. The more fat I eat, the lower my LDL goes. And vice versa, the lower fat I eat, the higher my LDL goes. So I figured out that it's this window.

It's about three days. It's about three days. If you are fat adapted, that indeed, if you eat at a hypercaloric level, if you consume a lot of fat, you'll see your LDL drop generally. It's about an 85% success rate so far for everybody that's done it up to this point. There's now, I want to say 250, 300 people before we lost count. For a little while, I was trying to get everybody to report in what it was. And now it's just too many people. It's actually the second most visited page, I was trying to get everybody to report in what it was. And now it's just, it's just too many people.

It's actually the second most visited page, I think on the site. So, but yeah, it, and it fits with the energy pattern. If I can just tell you the quick biochemistry behind it in, in general,

if you're consuming fat, it packages it in these boats, these lipoproteins called Kyla microns. Lane mentioned that a little bit earlier. They're really big and they've got a lot of triglycerides from the food you just ate. The triglycerides are packaged in there and they're in your gut. They go from your gut into your bloodstream and they very quickly dilipidate and get smaller and then your liver takes them up right away. They're constantly being counterbalanced with the fat your body is supplying

in another kind of boat called a VLDL, very low density lipoprotein. And that's strictly from the liver. And if this is high, you're getting a lot of fat from this and you're fat adapted, then this will be lower. Because why supply from your fat stores if you're already getting a lot coming from the diet? But if you switch it and now, oh, I'm not getting a lot of fat from the diet. Well, then your body through the glucose and insulin axis, so forth, activates more lipolysis that packages into VLDLs. And here's the key difference.

Chylomicrons, they get taken away right away. What happens to VLDLs? When they get dilipidated, they become LDLs and they remain in the bloodstream for two to four days so that's why if you eat a lot of fat voila you actually end up with lower vldls and therefore lower successive ldls did that make sense hopefully i absolutely now i'm curious about this because when when i was wondering about this when you guys you and lane were talking when someone that's listening to this let's say they're starting their whole diet journey and um they are not in the most healthy place so they are at risk for cardiovascular disease

and they're really wondering well you know this is the first step for me is to choose the diet i'm going to do obviously you know we we figured that you want to choose the best diet that you're going to be able to adhere to right so whether it's keto whether it's we figured that you want to choose the best diet that you're going to be able to adhere to, right? So whether it's keto, whether it's low carb, etc., you want to be able to choose the best diet you're going to adhere to. But also, what do you think would be the, I guess, ideal diet for them to try to start with being at risk for cardiovascular disease, not having the healthiest habits just yet. And just trying to figure out where to begin, right? Because if they were to start with like a keto or low carb, just kind of higher fat diet, maybe they'd be afraid that that would increase their likelihood for that as they start to trend down in terms of body fat, weight, their exercising, etc.

I was curious what both of your takes would be on that for where the starting point would be versus when they are a little bit healthier and they could venture off into trying whatever diet they want to do. So, yeah, well, first of all, as I was kind of saying from earlier in the podcast, I don't ascribe to any diet being the clear and obvious choice, the superior choice. For people starting out, I will say I can only speak to my own friends and family. Part of the reason I practice and enjoy keto is it's just been the easiest for me, really. I mean, all other things considered that I've tried, I've not really been a big dieter per se, but this has just been an easier lifestyle. Now, my dad and my sister of my immediate family, they were inspired to do so shortly after I started. And they had been

trying different things. My dad was down the road on type two diabetes, and he's now functionally cured it by going on this diet, which he cared a lot about. My sister mainly just wanted to lose weight, but she also suffered from hypertension. Both of those have been helped by going keto. But her daughters, two of her daughters, my wonderful nieces, wanted to be plant-based. And I've helped them as best as I can to try to at least make good decisions there. They've asked me point blank. They've said, hey, wait, are you only an advocate for keto? And I say, I'm, you know, to sound like Lane, I'm an advocate for what works for you. If you, if you can be plant-based and be nutritionally complete, because this applies

to all diets, you need to be sure that whatever you're eating, you find a way to get the other things that you need in the diet so that you will be okay. And plant-based, of course, I talked to them about B12 and DHA and so on and so forth. That said, I will say if I were to give general advice, if you're worried about cholesterol in particular, and the things we've talked about here today, there's, of course, the group called Virta that you may have heard Sarah Hallberg's connected to, Steve Finney's connected to, and so forth. They, I think, had an average BMI of like 45 or 50 to start. So they were certainly out there on the obesity side. That group, this tracks with the energy model.

When they go on a ketogenic diet and they lose a lot of weight, but they're still overweight. So they haven't actually gotten to say our levels. You tend to see cholesterol levels either stay around the same or go down or go up slightly. But all of these other factors, such as metabolic syndrome, a lot of those tend to improve. But again, it's not a panacea. Your results may vary. But I think for people who are interested in, hey, is this a trade-off? Do I have to get higher cholesterol to improve these other things? Well, again, going from obese to overweight, I tend to find that's more likely the pattern. Conversely, though, if you're going from overweight to lean, then it's a little more likely that you're going to see the higher uh ldl the higher total and ldl cholesterol but this is this one thing that does frustrate me there's not enough emphasis placed

on other cardiovascular risk markers that get better with health improvements period it does frustrate me how much focus there is on LDL. Assume the lipid hypothesis is 100% right, and that total in LDL cholesterol does cause atherosclerosis. If you do have it higher, you will have a higher risk for it, and you quantify that into a list of one. You have this other list of hypertension, waist-to-hip ratio, blood sugar, hyperinsulinemia.

All of those are cardiovascular risk factors. If the LDL is keeping you from what is clearly a much longer list for which you could quantify to be so much better, I think you should at least put that on the table. That's all I'm saying. That's all I'm saying. Yeah, it probably doesn't do any good to have somebody come into a doctor's office with a waist measurement of like over 50 and then be talking so much about their LDL cholesterol and just prescribing a statin. But that's what we see happen often, right? That's definitely what I've seen in my family. family, there's a few challenge cases that it's been tough on me emotionally because keto was working for one of the challenge cases and they found that they could be on it easily. And then ultimately their doctor talked them into getting off of it. And at the time of talking,

I said, it's cool if keto doesn't work for you and you want to do a different diet, but for what it's worth, I hope you have another place to go. I hope you're not just going to quit. I hope you're not going to feel that diet isn't an important thing you need to change to improve your life and your health outcomes. Cause I see their blood work and it scares the heck out of me. And it's unfortunate because I do, I'm sure you guys deal with this yourselves, particularly when it comes to things like working out and training and so forth. People can't help but want to find the excuse to stop the momentum. And a lot of times the momentum is what keeps you going. The momentum

is what takes you into an entirely new life, an entirely new you. And a lot of times that, you know, the inner us, we're kind of reaching for the excuse not to put in the work to get that momentum going and to keep it going. Now, actually, I wanted to ask this too, because this is going to be the next part of what I wanted to kind of get from you. When an individual, let's say they go to their doctor, because I have friends that have come to me with this question. Um, and I also have clients that this has happened to them where you're relatively healthy. Um, you are on a low carb keto type diet, but now your doctor is telling you your LDLs

are high. You need to increase your grains and your fiber intake and your carbohydrates. Um, but they're relatively healthy individuals at this point. And now it's in their head and they're worried and they want to switch up their diet, even though they're feeling great. Now, what I wanted to know is other than LDLs, you did mention a few other markers that people should look at. Now, can we clarify what other things that they should be trying to pay attention to other than their LDL cholesterol? I certainly have my favorite list. I actually call it the big three for me. I look, I look, I especially want every test, every blood test to include fasting insulin,

fasting C-reactive protein. And unsurprisingly, I like a lipid panel. Lipid panel actually can tell you a lot about your health status, particularly if your triglycerides are super high. All three of these though, you need to be fasted. And it's not the common advice. What commonly happens is people are told they don't need to be fasted for these tests. And I have more than enough data just on my own tests. I think I have something like 129 blood draws since November, 2015. And I can tell I can tell you I've done, I've done tests, for example, where I took, I want to say it's been at least seven or eight times. I've had a blood draw 24 hours after either a half or a full marathon. And all of them included a C-reactive protein.

And my, my CRP C-reactive protein is usually under one or a little above one which is typically normal except for those days and i've had it as high as 52 following a half marathon i've had mine be through the roof i've had mine be through the roof as well after uh working out and my doctor like freaked out he's like what, what, you know, maybe you're sick. Or I was like, well, I did train really hard the day before. Because you are inflaming your body. When you, when you work out, look, listen, you die. You did not have inflammation. Inflammation is often, inflammation gets a bad rap.

Inflammation is really the healing process. So when you have inflammation markers that are elevated, it's not telling you that your problem is inflammation. It's telling you, I mean, it can be if it's an autoimmune thing, but generally speaking, if your inflammation is high, there's something that's happening that's activating it, especially if it's chronic that you should look to, you should try to resolve. And that's why I like C-reactive protein. chronic that you should look to, you should try to resolve. And that's why I like C-reactive protein. C-reactive protein is what they would call a non-specific acute phase reactant. And

that's a good thing. It's kind of a general alarm and it can give you false positives. Like we just talked about, like you worked out and, you know, it just reflects you working out, but I'm okay with that because when it's low, because you made sure you controlled for all of that, you didn't do a workout. You weren't sick. If it's extremely low, it actually rules out a huge number of problems altogether. Now, fasting insulin is another one. There's no good reason that I've ever seen for chronically high fasting insulin full stop for sure you want insulin to be high enough post-prandial so like just after you've eaten food to help shuttle energy away and insulin is part of for example how you build muscle right to an extent but high fasting insulin

like you've just slept all night and you're waking up and your cells right now should be fully into, um, uh, into autophagy. They should be getting their housework done, but you are still ringing the bell with insulin because it's so anti-catabolic. There's no good reason for that. I think that that's why we'll find so much diseases associated with that. The more that we make that a standard which it should be should be a standard and getting to lipid panel of course there's not really a good reason to have high levels of triglycerides especially fasted triglycerides but there is one caveat i've got to throw in there you're more likely to have a longer lasting level of triglycerides the lower carb carb you are. So the more you're powered

by fat, the lower your basal insulin levels are. And therefore the longer the triglycerides will last in the bloodstream. Um, just real quick, I've seen this with carnivores. If you ever talked to any carnivores or very low carbers who say, I don't understand my triglycerides are super high. I actually have a whole article on what I like to call the triglyceride carryover effect, which is you could, for example, eat, you know, a steak at say 7 PM, go to sleep at 11 PM, wake up. And if you got your blood test at six or seven, well, I guess this doesn't work for that example.

It'd have to get, it'd have to be before 12 hours. You can have high levels of triglycerides because it's actually still carried over from when you were sleeping, but that's because you actually haven't had much of an insulinemic effect from the food you were eating. And by the dawn phenomenon, everything else it's, it's shuttled back to under, you know, a hundred. So for example, I'll have triglycerides of say, uh, 200 at eight hours fasted. That's then 60 at 12 hours fasted. Those, those numbers change pretty quickly. And your glucose levels could be high if you're on a lower carbohydrate diet. Sometimes we see that when somebody gets their fasted glucose, is that right?

That's right. And this is actually something I'm a bit vocal on. You take that same person, you put a continuous glucose monitor on them, and it doesn't look like a diabetic at all. It's like a flat line. It's like a a tight Delta of what I believe is adaptive glucose sparing. There's a higher affinity for fat in those people's systems so that it can spare that glucose for obligate tissues. Like your red blood cells, they, they can't process the fat. They need to be using glucose to some degree. It could be your brain. And to some degree, of course, it could be also your muscles, especially if you're like, say, working out in the morning and you do more explosive exercise. Again, all of this just makes engineering sense to me. It's frustrating how high glucose levels are so closely tied to type 2 diabetes where they won't differentiate with the hyperinsulin with the hyperinsulinemia having high levels of insulin because i'd be willing to bet well actually there's a disease that that illustrates this perfectly there's a disease i forget what

the origin point of why this is but they they have generally higher fasting glucose levels comparable to someone with type 2 diabetes but same thing tight homeostasis and none of the issues that you see with somebody who has uh diabetes they don't have any of the things that tend to be associated with sky-high levels of glucose so i myself i'm not that concerned with the higher levels of glucose that we see in carnivores or just super low carbers But what about trying a diet that's a little bit higher in protein and leaning a little bit more towards something like protein leveraging, which I texted you a little bit about? It seems like carbohydrates can be problematic,

and it seems like to some extent fats can be problematic, but it seems like protein maybe doesn't seem as problematic, but maybe I'm uninformed. So it seems like if we can eat a good amount of protein to satiate the body and to keep our muscle mass, then we can just select and pick what other energy source that we want to bring in, whether it be carbs or fat or some combination of them. But it seems to me like it's a lot easier to balance your energy when protein's kind of the base. Have you seen anything in some of the stuff you researched, whether it be blood work on yourself?

Have you noticed any negative impact from trying to eat more protein? Have you had any experience with that? Well, for sure, I think that you have to meet your protein needs. That's like a no-brainer to me. And yeah, I think that the energy substrate you get, I will say this, and again, I try to avoid the diet debates, but I will say this. bit like Ted Naiman here, the big risk is when you've got a combination of fat and carbs and very low protein. All of those foods tend to have bad outcomes associated with them, donuts and things like that, right? So I do like the concept, especially if you're doing a lot of athleticism, if you're exercising a lot, of being very aware to meet your protein needs and to sort of treat the energy that you're

going to get it from fat or carbs as certainly very relevant, but not something that you're trying to meet the macros with quite like you do protein. That's kind of my default position anyway. A lot of the issue that I think I would say gets a benefit from being low carb specifically is when you already have a problem with carbohydrates. And I think a lot of the debate right now is at what point do you create that kind of intolerance to where now you have a good reason to be low carb? And a lot of the people that I know that are very athletic who are doing low carb right now, I don't know that they actually would have a problem with, for example, adding in more carbs or something along those lines, because I don't know that they ever reached that point we're talking about where, for example, you know, your pancreatic beta cells are burnt out or whatever reason there is that drove you towards type two diabetes. But all of that said, protein can't get around that. There's not going to be a

low protein diet. That's going to, uh, become a thing., can't get around that. There's not going to be a low-protein diet that's going to become a thing. I'm pretty confident in that. I think my problem with carbohydrates is more psychological. Like once I start to eat them, I find myself wanting to eat more and more of them. So I have to kind of pick and choose about how many carbs I eat. If I'm going to have, you know, a serving of carbohydrates, I might have a cup of rice. I might have a potato. I might have, you know, in the same day, I might have a piece of fruit, but that's usually it. I try to keep it pretty

low. And that's just for my own sake, because I know that if I, you know, start eating carbohydrates in the morning, it just, for me personally, it tends to entice me to want to continue to eat them and then to go really off the rails and eat stuff that is a fat and carbohydrate combination like pizza, donuts, ice cream, all that good stuff. I experienced the same thing. My wife doesn't have that problem. She can have, she's low carb, but she has like a cheat day. And for her, she'll have that cheat and that will be it. And it will oftentimes just be a single cheat meal. And I joke – it's not entirely a joke.

I joke that, oh, if I ate that, I wouldn't stop. I would eat that and then I'd eat that 10 more times or a hundred more times before I had to get out of it. So there's some things that are sort of low carb, but not really bad for me per se, but still not ideal that I would consider a cheat. But there are other things, for example, I haven't had French fries since I went keto. even when there's been experiments that allowed me to be able to have carbs for the purpose of experiments just the waking experiment i know there's no i treat it like it's alcoholism if i have any fries it could be all downhill i loved fries like what happened to dave like he ate french fries, man. He told us, he warned us on the show. He told us about it.

Exactly. You know, you mentioned that you, uh, you talked to Peter at T about stuff like this and I listened to his podcast a bit and, um, I haven't found recently that he's mentioned anything about it, but the last time I heard him talk about like utilizing fasting within what he does, he had a frustration with that. He couldn't necessarily prescribe it in any type of specific way. Um, that would be, you know, you should do this to yield this type of result. He just knew that it was generally like a good thing to do, but he didn't know how to prescribe it to the population necessarily. Now you, um, in terms of using

fasting and, you know, using it to test your blood work um do you have any general um i guess information on how fasting can be prescribed to individuals for their benefit of health uh or is it just you know do it as you feel that it helps help you restrict calories etc i myself am not that good at fasting i wish i were better usually the one time i'm a guaranteed 14 hours fasted is when i know there is a blood test coming and so i'll be sure that i do the overnight fasting to do so but i will say this autophagy is definitely real. And autophagy is reliant on there being, I have kind of an analogy, and the analogy kind of goes like this. You have the opening hours of a restaurant where the customers are in there and they're eating. And then you have the closing hours. And in the closing hours, things can get done, a variety of things can get

done. There's the janitorial, there's maybe some Wi-Fi needs to get installed. Maybe there's some patchwork that has to happen out on the floor, right? That's how I think of cells. Cells systemically all have their opening and closing hours. And ideally you want them to do whatever they want to do on their own as much as possible. And so part of the reason I do like from a systems management standpoint, why I like low carb high fat is that it's because of that lower basal insulin or really a lot of hormonal influencing of these cells you're kind of leaving them on their own to do their own thing and in that regard i do think that it somewhat emulates fasting in fact i just got done with the presentation on how much fasting has in uh common with the

lipid energy model as it associates with being low carb, high fat. And so there are a lot of things that they have in common as far as like glycogen stores and all of that. But I do believe this and it's a hypothesis, but I believe these lean mass hypersponders I talked about earlier, I believe they're enjoying a higher overall rate of autophagy when compared to people on a mixed diet. And that's because I believe that even though they may not be fasting consciously that much, it's actually very hard for them to fast for like multiple days compared to other people. They're basically in a blended fasted state from their body's perspective. They're operating at the super, super low level of

basal insulin. They have, I believe, not just the autophagy, but also possibly enhanced aphrodisitosis. I think, and it's very anecdotal, but I think given some of the athletes I've been working with, they may have actually better recovery time. And that could be related to that. Again, I don't want to make wild claims, but again, systemically, this all kind of makes sense. Dave, thanks so much for your time. I really appreciate having you on the show. We'll have to connect with you again at some point. Great information. And I think for those people that want to dive deep into it, they got a lot of great information. Where can people find you? Well, of course, I'm very active on Twitter as Dave Keto. You can also come to our website, which is cholesterolcode.com. Also, if you're somebody who's gone low carb and you've seen your cholesterol levels rise beyond just those resources, we also have two Facebook groups.

There's one, you can just do a search for cholesterol code in Facebook. There's also one for lean mass hyper responders, and both of them are getting larger than I thought that they would have. So there's a lot of people who can further communicate their experiences and share ideas and so forth. So always good to come there as well. That comment about Twitter being therapy for Lane is, was, was spot on, was dead on. That was amazing. I know, I know that you were, you were playing nice, but I think that that was fun and funny. And I think that he found it to be funny. So thanks for that. Appreciate it. Anytime we can roast Lane, he's been a friend for a long time. Anyway, anytime we can beat him up and rough him up for in favor of it. and like i said to him i think

it's important for people to kind of see this side of him too i i thought this was a very pleasant exchange that we had and and i hope we continue the conversation yeah i've had him debate some other people on the show as well and he's kind of always been the same way like every time it's not you know i think people are expecting this you know a hostile thing to happen and it's usually uh it's usually just some back and forth and we move forward from it so it ends up being beneficial for everybody thanks again i will say this i will say that we need more of this one of the problems is there's too much talking past each other there's too much of these community tribalistic things that I, again, I know you followed me for a while. I am, I am very proactive about trying to connect with people of different, different opinions and trying to have respectful debates, discussions, discourse. And so I applaud you for not only, you know, mentioning this and getting us on here, but I hope you have many more.

Awesome. Thank you so much. Have a great rest of your day. Thank you, sir. That was some awesome information, man. There was a lot of stuff where, you know, I've been following some of this information for a long time, but there's a lot of stuff where I'm like, man, I do not know what a lot of these words mean. I know that some of you listening maybe in the same category,

but maybe if you're listening at home and you're not understanding what's going on, maybe you can highlight some, you know, a couple of words and start to search for them on your computer as you're listening to this. But I'm really, really, I really dig that whole conversation because I think it cleared up a lot of stuff for a lot of individuals as far as LDL is concerned, because especially when you go on a high fat diet and it's, I get this message a lot. A lot of people have talked to me about this that aren't clients at all. They're like, it's like my doctor says I have high LDLs, but everything else is great. I feel like, but they're, they're, they're scared and they want to switch. You know, if this can give them confidence, um, that you're on the right path, you don't have to make that switch because like when an authority tells you that it can be kind of scary, you know? So I'm really happy that they helped clear that idea for some people. But it was complex.

Yeah, I was listening like, okay, I need to look this up. I got to look this up. Got to look this up. It got to be a little a little crazy a couple times, but really just if you bring it back every single time to the point of if you can figure out a way to not overeat then you should be okay so how do you how do you do that you know can you i i think occupying your time is huge like trying to figure out how can you occupy your time for me um because i do like to fast if i can just wait to eat till i get home from here, which sometimes is two and sometimes it's not till like four or five. That helps a lot because now I can have two big meals.

I like to eat kind of a good amount of food. I like to feel full and that works great for me. And maybe, maybe somebody else has to find a different way to occupy their time. Maybe, you know, maybe they want to eat in the morning and then eat when they come home from work and kind of fast through the middle of the day. Or maybe they want to try to simply just track, you know, you can track your calories. You could try to up

your protein. I think that upping your protein can really drastically help you to eat less, eating more fiber. The walks again, walking is just going to occupy your time. Lifting, lifting crushes your hunger. Sometimes it makes you a little more hungry, but usually like when you're done training, a lot of times for me anyway, it seems to occupy enough time as well. But sometimes it's 20 minutes, 30 minutes to a gym and then you train for an hour. So that would be, you know, a two hour time slot that you're just not eating, you know? So what are some things that you can do that don't involve you eating all the time, whether it's hanging out with friends or being in front of your computer or being in front of your TV screen, you know, try to make some rules for yourself.

So you're just not overeating. Cause if you don't overeat, I don't think it matters that much what it is that you eat. Obviously, if you're going if you're eating like junk all the time, then we can make a rational claim that we don't think that that would be a great idea. But for the most part, I like what Lane said, too, because of his condition, because of his cholesterol. Personally, he cuts saturated fat down. He tried and he tries not to overeat so what does he end up with any plus he's trying to eat enough protein because he's into working out so everything all his bases seem to be fairly covered yeah and lane did mention like uh i don't know i forgot what his six things were but keep stress low don't eat like an asshole so don't eat a surplus all the

time get enough sleep i don't know if he did mention exercise like an asshole. So don't eat a surplus all the time. Get enough sleep. I don't know if he did mention exercise. He said, don't smoke, don't drink. Don't smoke, don't drink. There was something else. Yeah, I think sort of exercise. But like, yeah, if you really do live that way, the big aspect of it being interesting, if you can find a way to maybe eat in a deficit quite a bit, like those concepts will get

you healthy and in shape without having to dig into the weeds this much. And so, like, how hard or easy is it to get into a deficit by just working out? Because I feel like a lot of people, like, they just heard Mark say, like, oh, I actually let Mark trains in order to fast a little bit longer. But I know there's people that are thinking, no, I'm going to be burning calories. So I'm going to need some calories to work out or else I'm going to feel like crap, I'm going to be burning carb or burning calories. So I'm going to need some calories to work out or else I'm going to feel like crap or I'm going to perform like crap. Um, it's, especially if you don't have your food handled and you're eating, you just kind of eating like an asshole or not really paying attention to that. Um, just going to the

gym and lifting weights probably isn't going to put you in a deficit of calories. Even if you add in an hour of cardio into the mix, you're probably not going to be put into a deficit of calories. I mean, that is one of the big reasons why myself and I believe why Mark also mentions why fasting is so beneficial. Just because it's so much easier for me to be, for you to be in a deficit of calories because we're not spending most of the time eating. Like if I were to eat breakfast and all this other food that generally most people do, they eat breakfast, a snack, lunch, another small snack.

They have calories in their drinks, dinner. If you're going to be in a deficit, those are all going to be very small, non-substantial meals, which for most people, they don't do. Most people have very substantial meals for all their meals because they want to feel full and satiated. Let's say that I'm allowed to eat, I don't know, 3,500 calories a day approximately or something. I don't even know what it would be, but let's just say that, right? So if I start my day off with like, you know, if I start my day off with 700 calories and I have another, you know, X amount of calories and I, and I already, I already used up like 1500 calories. Well, now I have 2000 calories for those last two meals and that may be enough for me.

But, you know, I, like I said, I like to feel pretty full. I could just save all my calories for later on in the evening and I can probably run a pretty good caloric deficit for many, many days on end and not even like without really barely noticing it. Obviously during the day, like 11 a.m. comes and like sometimes a little earlier, but it's usually like around 10 or 11 and around like one or two where I'm like, I'm pretty hungry. But once one or two rolls around, I'm like, I'm eating in like an hour. That's not a big, I'm like, this is not a big deal.

This is not that hard. And, you know, for other people that might have a different schedule, you know, just set your timing up accordingly. But I usually do what I call like a double dinner. I eat about two or three hours before dinner. Normally, the way it works is as soon as I get home, I start to cook something. I eat, I take a shower, and then my wife is home, the kids are home. We kind of all hang out and we just cook again. So, but one of the keys with fasting though, is you have to act as if it

never happened. So you, it's not, now it's not time to make up for lost times, you know? Because I mean, if I start throwing heavy whipping cream in my protein shakes and stuff, like it's, it's just completely, it's fairly useless. Like somebody might be able to say, oh, well, fasting has these other properties or whatever, but I just don't think it really, you know, for long term success and for long term health, I don't really think it works that way. Yeah. And like the point that I'm like really trying to point at is, you know, we hear you can't out train. You OK over there? Yeah.

I just found I don't know if I've grown this very long hair or if it's a stray hair. Just it's really long. Oh, yeah. I'm sorry. That's all right right it just caught me off guard oh but we hear you can't out train a bad diet but i think you know there are people that like no i'm low carb and you know they will have the heavy cream and the coffee and then you know they'll have like the i'll just go to wendy's and have like four or five patties with extra cheese it's like okay your diet isn't bad per se because you are low carb or whatever, but you're still having like 5,000 calories and it's not even dinner time yet.

So, by the time you get to that workout, that workout's not going to burn nowhere near that, right? It's going to burn off like one of the, you know, pieces of cheese that you had. So, they say, you know, you can't outwork a bad diet. Right. But I think the flip side of that is really important, too, that you and I just wrote this down because this is from Ted Neiman. And I just think it's amazing. But he said you also can't out diet, no exercise like that's huge.

Like you can to some extent. You can't. I don't want to say. That's huge. You can to some extent. I don't want to say it's impossible. But if you don't do much, then you don't need much. And it's like you could kill that at one trip to McDonald's. Easily.

Yeah, you get a quarter pounder and some chicken nuggets and a large fry and a big chocolate shake. And it's like if your body just doesn't need that many calories because you're just, you don't have that much muscle mass and you don't move around a lot and you do that every day. Yeah, I mean, and I would imagine that you'd probably eat something else other than that, but that's a fairly dense meal. And if you do that two, three times a day, along with the first thing that you have in

the morning is a big bowl of cereal or something like that. I just, you're just, you're probably going to be in trouble. You're probably going to be behind. And once you get behind, it is really, really, it's really easy to accumulate body fat. Once you start getting your body a little bit behind and you teach your body, hey, this is what we're doing. This is how it works every day. We're going to store a little bit of this fat every single day.

You're going to be overstressed pretty much all the time. You're going to be behind a little bit every single day. You're always going to be a little bit tired. What happens when you're tired? You're not motivated to do anything. You're not motivated to even stay on the very diet that you wrote down or you talked about. You're not motivated to go to the gym. You said you were going to go to the gym and then you're, and then you're asking a question, Hey man, how do I stay

motivated? Well, it's like stay on top of your shit and you'll always be motivated. You like the best thing for motivation. I always think is to eliminate it as a factor. Let's fucking get rid of it. Just be diligent. Just do your stuff. Like do your stuff when it needs to be done. Some, sometimes the urge to actually do something, nobody wants to like wash the dishes. Nobody wants to scrub out their pan right after they cooked. But if you do it immediately after you just cooked, it's clean the next time. You know what I mean? Like it's all a small life lessons that will really add up over a period of time and allow you to make those leaps forward.

Yeah. But there should be no reason why you don't exactly resist the strain like i think the really cool thing that he said is like uh like uh for for athletes that do weight train it's like an ldl sync like even if they um compare it to individuals that do like you know heavy cycling etc that have the same types of diets. Individuals who do exercise with weight training have lower LDL levels. I think that is pretty cool. Like doing 30 minutes of weight training or whatever can be super beneficial. The gym doesn't have to be that hard either. You know, like it might be challenging while you're there. Like some of the stuff that you do might be, you know, today I did, I

pretty much just try to pick one body part. I did chest. I did cable crossovers. I did some flat bench. I did some incline dumbbell bench. I did a machine and I did one extra set of cable crossovers on the way out the door to get that pump. And it's like, you know, four or five exercises, you know, and if I was pressed for time, could

I do two less exercises? Yeah, of course. Yeah. And still have a good workout. Could I go back and forth between doing pushups and bench press for five sets and even have even have just that be a good workout. Fuck. Yeah,

I can. That'd be great workout. I'd be smoked. Maybe even do like jumping jacks in between just to keep that heart rate elevated. It's like, that's going to be a tough ass workout. So,

you know, it'd be tough, but it'd be simple to do. It won't be, it's not complicated. I guess is my main, my main point with it, but amazing having those guys on the show today.

Appreciate Lane Norton, Dave Feldman. They gave us a lot of info, a lot of insight. I liked it back and forth. I think that we should have Lane on more because I think that he is a good antithesis to whomever else that we have on the show. So that was awesome. I had a lot of fun with that. Yeah, it was. Lane was really nice.

I like Lane. I haven't seen that side of Lane on the podcast outside of this podcast room. Like when he's here, he's pretty chill. He's awesome. But the past two times we had him on, I think he was pretty fired up. He was. But that's nice to see too. I think he's getting a better, I think he's getting in a better place though.

Could be. I think it's just exactly what I just talked about. You know, people feel like they're kind of always behind. I think he's getting a better. I think he's getting in a better place, though. I think it's just exactly what I just talked about. You know, people feel like they're kind of always behind. I think he's getting ahead. You know, I think it's I think it's hard. You know, when you you go to school, you get a Ph.D., you work your ass off and you're kind of you're climbing that ladder. But now he's got supplements. He's got an app.

He's got a lot of people on there. He's getting you know, he's getting recognition. He's starting to get paid well. Like all these things are kind of like falling into place and it won't be too long before he, all the anger is wrung out of him at some point. So this may make, it'll be making that money. He won't care anymore, but maybe not. I don't know. He'll still have a twitter for his therapy that was amazing that was pretty funny take us on out of here andrew awesome thank you everybody for checking out today's episode um if you found any benefit into this uh today's debate even though it was like a it was a very uh gentleman-like debate uh smash that thumbs up button for us give us a like

subscribe to this youtube channel if you're watching on youtube um if you're on itunes drop us a review that would be super beneficial to the to the podcast and also please make sure you're following uh at mark biles power project on instagram at mb power project on twitter give us a shout out let us know that you guys are listening to the podcast tag us do whatever you got to do to get our attention uh my instagram is at i am andrew z and sema where you at? I am Seema Inyang on Instagram and YouTube and Seema Inyang on Twitter.

Mark? 20 years. 20 years of marriage. And while I was training today, Tom's like, oh, what are you going to do? Like, 20 years. You got to do something big.

I said, I'm going to fucking kill myself. I'm going to go throw myself off the nearest bridge. No, just kidding. It's been an amazing 20 years. Thank you so much, Andy Bell. Can't wait to hang out with her tonight. We're going to go out to eat, have a good time, and then in a few days, I think we're

ready to go to Tahoe and celebrate up there. That should be pretty cool. But I made it. I think you get, like, once you get to 20 years, I think you get think you get like a year off right yeah you have to do whatever you want to do that yeah you get a year off and then you get a gold jacket wait but she doesn't get to do whatever she wants right yes she does actually no that's not that's kind of how it works you're not married so you're not that wouldn't that wouldn't work out so good for me i don't think you're coming back right yeah i don't think i would do so well

anyway strength is never weakness weakness never strength catch you guys later