 I'm a little more Mike in hand kind of guy. So, yes, this sounds a little bit like hyperbole, an entirely different paradigm for cholesterol, but I'm gonna kind of take you through it. First, of course, my conflicts of interest. I usually get to say none, but because some people have been actually contributing as individuals to a business entity, we've had to accept that through my wife's company, Iron Ninja Technologies, and that makes for some funny bedtime conversation because she'll say, well, you'll need to clean up your nightstander. You won't get funding for next quarter. This is also gonna sound like hyperbole, but I actually record every single thing I ingest, every single thing. In fact, I have a standing rule for every single conference that if you can catch me ingesting something that I didn't take a picture of with my phone first, I'll give you $100. And since my wife hasn't collected on that yet, I gotta say the odds aren't looking good for you. And just this last Tuesday, I hit my 100th blood test in the last 32 months. That also sounds crazy, but no, since November 2015, I've actually had a number of different blood tests. And I'm doing this to really emphasize just how serious I am about the data I'm collecting because what I'm gonna show you next is also going to sound quite outrageous. So I just wanted to show this real quick. This also was a first two days ago. I had to get stuck five times in order to get the A vials. It's almost as if my blood was on strike. So now I'm gonna introduce something that I call the inversion pattern. And you'll know why in a second because when I went on a ketogenic diet, I went low carb, high fat, my cholesterol shot through the roof. And after that happened, I became very obsessed about learning everything I could about cholesterol homeostasis. And sure enough, as a software engineer, I kept seeing a familiar pattern. I kept seeing what looked to me like a distributed object network. Now you don't need to know what that is, but I will tell you this much. It's about different objects talking to each other. And I stand by that original hypothesis all the way to this day, almost three years later. Now what you're seeing is a graph. It's a very special graph that has the first eight data points that I got going all the way back to November 2015 up until a conference called low carb veil. And those eight data points I got over three months time. And they said at that time that that's just way too frequent of testing. Like I'm not gonna get my cholesterol to change. It takes like three months to change your cholesterol. But I'm saying no, no, no, no. It is like a network. It actually changes relatively quickly. And these first eight data points illustrate exactly why. And guess what? We see on that left axis a three day average of dietary fat. But on the right axis in the blue, we see the resulting LDL cholesterol collected the day after those three days. So after that conference, after I presented, I told them in advance, I said now I'm gonna do something pretty outlandish. I'm gonna do one weeks testing where I actually take my blood every single day. And I'm gonna eat to a food plan to try to induce the curves. So that's what I did. You see in the dotted line what I did. I brought down my dietary fat and then I brought it back up again. And so what happened to my LDLC? My LDLC went the other direction. Further moved the inversion. Now of course as an engineer, once you've learned something like this, your next step is to, well go ahead and step on the gas. So at that point I ate a huge amount of fat. What happened to my LDLC? My LDLC dropped to the lowest that I had done since I started my research. Now I'm gonna go ahead and fill in the rest. There's quite a few fun stories past this point. But as you can see, there is quite definitely an inverse pattern. And I'm gonna actually flip that axis on the right side so that you can actually see the inversion very closely. You ready? Now let me go ahead and throw up the Pearson and the regression. And you can see just how tight this relationship is between each other. There's no question. While there are a few outliers that you can see in three different spots. One at the first third and one that's about halfway through and one that's over there for the most part. They don't deviate that far from the mean. So this is what I mean by dietary fat inversion. Basically, right now this is happening on a Thursday morning. If I took my blood this morning, what I would do is I would look back yesterday, Wednesday, the day before that, Tuesday and the day before that, Monday. And from that, I would know what the greatest influence was on my dietary cholesterol, on a ketogenic diet. Well, that's what this graph is. Each of those couplings are the three days before and the resulting LDLC. Let me kind of really drive this home and put this another way. There isn't anything in this graph that represents days four and before. It's only that three day window. So now we look at this in a scatterplot. You can actually see the regression line. You can see for yourself just how tight this relationship is. Now I thought that maybe LDL particle count would go by the same equation. It actually doesn't. And it was that week long experiment that I found this out. It does still have a three day window, but interestingly, it has a two day gap. And I've talked to a number of people about this. I don't have enough time in this presentation to explain what my estimations are, but if you ignore the two day gap and you look only at those three days before that, so like using the same example of this Thursday morning, we'd be looking at Monday, Sunday, and Saturday of the days before, we would get a graph that looks like this. And this is the same 29 data points I showed you from earlier. Only this time, the dotted orange line represents that three, those three days with the two day gap. And the purple line now represents LDLP. And I'm gonna flip that axes again so you can see just how tight that relationship is. And get this, the regression is even a little bit better. On the LDLP. So the particle count is surprisingly also following by the same level of an inversion pattern. All right, so where am I going with this? Well, basically that network that I saw early on, I hypothesized and thus far, I seem to have lots and lots of accumulating evidence. Ultimately comes down to the fact that cholesterol is just following an energy distribution system. That's what it really comes down to. And to unpack this, I'm gonna have to take this back a little bit to the three channels of energy you're already used to hearing about all the time. You're used to hearing about carbs and protein being converted potentially to glucose. And you hear of course all the time about fat being converted to ketones, hence the ketogenic diet. And you can be forgiven if you've thought this whole time that all fat gets converted to ketones in order for you to be fueled by it. But actually no, there's this whole other world by which you get direct fatty acid delivery to your cells. And in particular, I wanna focus on one channel, the channel of triglycerides being loaded up onto these two lipid-carrying proteins known as lipoproteins, the chylomicrons and the VLDLs. Let's break it down just a little bit further. Think of them kind of like boats. It's not really how they look, by the way. But the triglycerides get loaded up in a chylomicron in your gut and effectively end up going into your bloodstream and very quickly drop off those triglycerides to your tissues, lots and lots of energy delivery and very quickly come to chylomicron remnants. And this happens within minutes to hours at the most before it then eventually gets reabsorbed by the liver. Now, here's this other line, this other form of boats that ultimately comes from the liver. From fatty acids you have primarily from storage, from your fat cells, typically from lipolysis. These guys are counterbalancing the brown line, the chylomicrons. That's where ultimately this inversion pattern comes from is if I'm eating lots of fat, there's less of a need on the part of the body to up-regulate as many of the VLDLs. And this is really the story of energy delivery right here at least in terms of lipid-carrying proteins. Now, that's not the only thing that lipoproteins do. There's also this other lipoprotein you've probably heard of HDL, right? HDL is the good cholesterol. Well actually, technically it's the cholesterol found on the lipoprotein for HDL. But there's this other lipoprotein that HDL actually works closely with the more you learn about the lipid system. The bad LDL, right? And when they say LDL cholesterol, what they mean is the cholesterol found on that lipoprotein. Well, when we put this all together because this is the support side of the fence, we're gonna go ahead and draw a dotted line. We see energy deliver is on one side and we see supports on the other side. So, watch closely. Energy delivery, support, energy delivery, support. But now you should have noticed there's only one lipoprotein, one lipoprotein that is doing double duty. The first one, the top line, the chylomocrons, they're mainly just delivering energy. That's their main job. Clearly, HDL, its main job is support. Only VLDLs to IDLs to LDLs are running the gambit of both delivering energy and also ultimately playing a support role. And the reason this matters a lot is I'll show you in the next slide because you probably hear all the time, VLDLs and triglycerides, especially at a high level, tend to be associated with disease, right? Well, they are when they're found lingering in the bloodstream. In fact, it isn't the VLDL and the triglycerides use that is the problem. It is their lack of use. And this is commonly associated with insulin resistance and exceeding one's personal fat threshold. This inability to park the triglycerides necessarily means VLDLs will remain longer in the bloodstream, which is a clear sign of trouble. And I can kind of illustrate this pretty well when you start to realize what the life cycle is for this APOB 100. This VLDL to LDL life cycle. How long does anyone know here right now how long does a VLDL last? Does anyone know before remodels, anybody? All right, it's about three to 60 minutes. How long does an IDL, the intermediate lipoprotein last, anybody? 30 minutes or less. How long does an LDL last? Two days? Two to four days. Let me put that a different way. For 98 to 99% of the life cycle of an LDL, or I should say of an APOB 100 containing lipoprotein, it will be an LDL particle if it's not absorbed by the liver. So with that in mind, here is an example of a high healthy lipid energy trafficking system. High VLDL secretion, trafficking and use, leaving little VLDLs and more of their successor LDLs. So these boats, they've got plenty of places to park, they're triglycerides. These are of course adipocytes, right? They're just anxiously pulling it off. It's all right, the docks are empty, no problem. Let's flip it to a different system. How about instead we have an unhealthy energy trafficking system. Adipocytes are full, there's not a lot of places to park it. So even in low VLDL secretion, if use is lower due to poor uptake, it can result in abnormally long VLDL residence time. So you've got a lot of VLDLs. You've got a lot of triglycerides, they're cargo. You've got a lot of remnant cholesterol, the cholesterol found on VLDLs and IDLs, which are closely associated with disease. So I want you to put your engineer hats on with me here. And let me ask you this very interesting question. What's the key similarity between an adipocyte and a very low density lipoprotein? Similarity is each is primarily staging triglycerides. As fat-based energy to make available two cells on demand. So what's the key difference between these two? Well, an adipocyte is stationary and a VLDL is mobile. So an easy way to think of this as an engineer is a VLDL is effectively an adipocyte on the go. Simple. Now, with all of this in mind, I want to introduce you to lean mass hyper responders. Let's take a step back. If you're going on a paleo diet, if you're going on Mediterranean, if you're going on any diet for that matter, that's low carb and tends to be higher fat, you're gonna find a small percentage end up having high levels of LDL cholesterol, some fraction thereof, right? And we tend to call those, it's not, I'm not sure if it's actually a literature term at this point, but a lot of people would call these hyper responders. This predates me coming into the field. But about a year ago, I identified that there's actually a very specific pattern of people that I call lean mass hyper responders. And I wrote this article on my blog, cholesterolcode.com, and when I did, this was the graphic, which is now kind of a famous graphic. Basically, I was saying, look, you got a low carb diet, lower glycogen stores, right? Lower adipose tissue, therefore lower body fat. And yet you have higher energy demands and there seems to be a tight association with people who therefore have a high LDL of 200 or higher. 200 or higher, by the way, is beyond that which is typically considered those who have familiar hypercholesterolemia. That's just super high, right? But then they also would have an HDL of like 80 milligrams per deciliter or higher. Yet they would have triglycerides of 70 or lower, shows a very, very efficient fat use system. And no surprise, more and more people when they send me their profiles at cholesterolcode.com. I would see these numbers and I would be able to then start guessing. I'd be like, are you lean and or fit? They'd be like, oh yeah, yeah, actually, how would you know that? I only sent you my lipid numbers. It's because lean mass hyper responders, I asked on Twitter for a bunch of people to send me, who are lean mass hyper responders? I asked them to send me their pictures that I could post in the presentation. This is what they look like. I know what you're thinking. You're thinking these guys must be on death's door, right? Yeah, this, by the way, was my favorite one that got sent by Prescott. And sure enough, sure enough, his LDL is 218. I guarantee a lot of practitioners right now would just ignore the HDL and the triglycerides. They go, you need to be on two medications right now. You need to take care of this. By the way, whatever you're doing that's getting you all of these cross country miles, doesn't matter. It's not helping you, right? Okay, so let's cut to the chase. Are lean mass hyper responders at high risk for cardiovascular disease? And really, this is just kind of the overall question. Are you at high risk of cardiovascular disease if you go low carb, high fat? Well, let me show you a special little graphic I made about five months ago. This I call the low carb cholesterol challenge. And I made it fun and friendly. And I really pinged a lot of pro-lippid lowering experts, including like the National Lipid Association and many of the different peoples that are luminaries in the field. And I said, look, look, look. You're telling me that low carb, high fat diets are overly comforted, people are overly comforted on this if they have low triglycerides and high HDL, even if they have high LDL. Well, okay, then submit the best study you can find that shows normal, non-treated, that is no gene, no drug studies, right? Normal non-treated people who have high HDL, low triglycerides and high LDL, who have high rates of cardiovascular disease? Now I'm gonna give you a multiple choice answer. Did I get five studies, 50 studies, or 500 studies in response to this? Anyone wanna guess? Zero, zero, yes, correct. That was a trick question, there's. I did not get a single study that met this criteria. And a lot of people who said, well, come on, all the data is in drug and gene studies, right? No, no, actually, I don't know if you've heard of Framingham. But the Framingham offspring study, this study was just fantastic. They grabbed about 4,000 people who didn't have a history of cardiovascular disease and weren't on lipid lowering therapy, so no drugs, right? And then this is what they found. They found when they stratified by low HDL and high HDL, if you did get triglycerides below 100 and LDL below 100, you got what you expected. The best score on there is 0.6, that's the odds ratio. Looks fantastic. So we would expect if we were to flip this and go for above 100 LDL, then the odds ratio would probably be 1.5 to 2.0, right? No, it's 0.7, the second lowest risk ratio, specifically for cardiovascular disease. Okay, okay, well maybe though, this includes a lot of people who had an LDL of like 102 and 105. Fortunately, they had another risk stratification for people who had an LDL of 130 or above, also 0.7. And then we got another study that I even liked a little bit more. This is low triglycerides and high HDL and they just stratified between those two, right? Observational cohort study with our favorite high risk group men. And age 53 to 74 for that matter. And free of ischemic heart disease. This is now my new favorite graph. I want you to look closely because what's happening is there's stratifying between people who have super high levels of LDL, 170 or below and those who have above 170 over here on this side. If you see the dark bar on the left and the dark bar on the right, they're both HDL above 57 and triglycerides below 97. And they're nearly identical. Even better, you could go to the other side of the strat. And if you see that if your HDL is below 46 and your triglycerides are above 142, it doesn't matter if you get your LDL below 170. It doesn't matter if your LDL is above 170. What matters is your HDL and your triglycerides. The reason I love this study so much is forget even LDL. Let's look at some of the other very clear risk markers. Such as smoking. Which of these groups would you rather be in? In the lower, the high triglyceride versus HDL. How about physical activity level? You actually had people in the low physical activity level with a lower risk of ischemic heart disease. With a lower risk of ischemic heart disease. So long as their HDL was above 57, their triglycerides below 97. Even hypertension. Hypertension is nearly identical. I would rather be a male who's smoking, who's hypertensive and who's sedentary. So long as my triglycerides are low and my HDL is high. So I want to fit this in real quick because I know a lot of you guys particularly are interested on the athletic side. What's really neat is the first nine months of my data. I was in primarily a sedentary lifestyle on purpose because I anticipated probably affect my lipids. Well now that you've seen that I've mapped my inversion pattern. We can actually see a differential when I actually had running that was applied after those nine months and for five months following. So you recognize the inversion pattern from earlier but now we have a whole bunch of new data points that are on the right side and I kind of made them glow for you. We're gonna flip that axes and I'm gonna kind of highlight them so that you can see the high exercise period. And now you see a gap. Against what the original inversion pattern was. And that gap to me is no mystery. You see LDL particles also get endocytost. That's basically another way of saying your cells engulf them to make use of their free cholesterol, their phospholipids, their fat soluble vitamins. They're like a care package basically. And so more of them get removed from the bloodstream in the case of where you have to have more muscle repair and growth. And therefore less LDL particles, less LDLC. Voila, my cold open, which I shouldn't have done by the way. You're supposed to like, if you're working up to a half marathon you should train for three months. I trained for six weeks. So my first week I had a seven mile run cold and it really sucked. And I was really sore. I was really sore and so I wasn't surprised when 48 hours later when I got a blood draw I had very low LDLC. What's that last massive gap? That was following a 5K half marathon and full marathon week. 24 hours after the full marathon. You also see the same thing with the LDLP. And while triglycerides are a lot noisier to track, you know that I've already talked about triglycerides as a source of energy. You're actually depleting the triglycerides on a per particle basis. So what I expect would happen with triglycerides in the bloodstream after I've ran a full marathon? I would expect them to go down, right? Well, so let's flip this inversion pattern so we can see them clearly. And sure enough, the three lowest triglyceride scores in my blood that I've ever had were 24 hours after a half marathon, a half marathon and a full marathon. Not surprising to me at all. I have some breaking news. So when I say breaking, I mean, quite literally, this got handed to me just a few days ago. The first paper for the Lipid Energy Model is actually in development right now. I'm quite excited about this. It will be focusing on the first phase of my data, the inversion pattern. And it will also feature the 10 day Feldman protocol which you can find on the website if you're curious, performed by Craig Moffat and Silvio Furrow as well. And it's being prepared by the Magnificent Tommy Wood. Could you give him a round of applause, by the way? I appreciate all the work he's put into it thus far. I'm paying him the same amount I'm getting paid, by the way. Just so you know. This is what the Feldman protocol is, is that basically you spend a couple days eating low calorie but on a ketogenic diet and then you spend a couple days on high calorie and a high calorie ketogenic diet. And we can see Silvio Furrow's in the first line. We could see mine stratified over here. You saw this from a little bit earlier. And we can also see Craig Moffat's. You can see all of our scatter plots compared to one another. The relationships are quite striking. In fact, they hit it out of the park a little bit better than I did. And these are actually the Tommy-approved bullet points, by the way. And I don't want to run too low on time. So I'm just gonna say that this is something you'll be able to read a lot more here pretty soon because we'll actually have it in a formal paper. But I did want to also fit in real quick because this happened last year, the KetoFest experiment. This won't make it into paper because it was a little more loose. But we basically did the same protocol, just basically what I just now mentioned. Low calorie ketogenic where everybody stayed that way. And then at the beginning of KetoFest, on the morning of Friday, we all took a blood test. And then everybody gorged on fat for three days and took a second blood test. And I posted the hypothesis for this in advance of the experiment, predicting that most people would see their LDL cholesterol drop. And I'm thankful for the folks at PTS Diagnostics who basically covered it. And we got people like this guy, I was one of the two Keto dudes, Richard Morris. And by the way, Amber O'Hearn, who's also here by the way for the conference. And this is the axes. And color coded here, I have everybody's lines. As you can see, almost all of them head downward. It didn't matter where you started. High or low in your total LDLC, you usually saw a decline, 19 of the 22 had a decrease of five to 38% in their LDLC in three days. Whereas just three had an increase and three increases only one to 2%. In fact, this last table, you can really see it. All of those that are in blue, they saw a decline. Everybody else, everybody that's in the orange actually saw a slight increase. So across the board, averaging them all together, it was a drop of 25.7 milligrams per deciliter for the entire group. Now I just wanna finish real quick by thanking my patrons. I am actually only accepting money pretty much directly from individuals. And in doing so, I'm impressed that I've been able to basically be crowd of funded through this research. So I wanted to thank them. And then finally, I wanted to thank you for coming and spending this time with me. Thank you so much. Do we have any questions for Dave? And Dave, if you can repeat the questions so they can pick it up on that. Kate, do you like it? Love it, love it. Here, I'll just give this to you. I've done a lot of research on the effect of visceral fat on LDL small particles. And all this research is done in Japan. And because I have inherited problem with visceral fat, I got interested in it. And they found that visceral fat produces a inflammatory cytokine. IL-6, IL-6 reduces HDL particles. And they found that if you could get rid or reduce your IL-6, HDL-2 particles, HDL-3 particles go up. And they found that those are the two sets of particles that cleans out LDL. And so consequently, their big push in Japan is to reduce your visceral fat to reduce heart disease. Well, I definitely agree with reducing visceral fat. Just real quick, Pearl, what you're talking about, cytokines are a signaling molecule, of course, that's basically a cry for help. And it's true, at a certain threshold of cytokines, the liver actually up regulates LDL particles. And there's my colleague at cholesterolcode.com, Siobhan Huggins, actually gets into this quite a bit. She's even doing a talk this weekend on it. And so for sure, one of the things that I definitely recommend is the reduction of visceral fat, visceral fat being the fat that collects underneath the muscle. And it's actually much more concerning because it can intertwine with the organs and so forth. Bottom line is adipose sites, your adipose tissue is really your best friend for staging and providing energy. It's when the fat is getting accumulated. And that's why I showed that slide from earlier where there's like an accumulation of fat in your adipose tissue where you've like reached your personal fat threshold and you can't find a lot of other places to store it that it has to then get stored in other places. And the reason your body does that is because there is a worse place for it to be stored in, which is in the bloodstream. You shouldn't have a lot of fat in the bloodstream. That's why triglycerides are such a powerful indicator of problems ahead. Do you want us to have any questions? Yeah. Ah. And I noticed because of that, because I've tracked my HDL on the computer, I, the study that came out last year of the University of Copenhagen to the IHDL associated with, I guess, possibly the president. And in your data that you've got on the lean mass hypereresponders, were you able to look at the blood levels or see if there was a wall? Yes. So to repeat what you're saying, you're saying you're a lean mass hypereresponder, you've also seen very high levels of HDL, which is typical of lean. I often see, by the way, HDL and lean mass hypereresponders exceeding 100 all the time. That's right. Yep, and that's actually surprisingly common in this profile. You should, by the way, check out our Facebook group. We actually just opened it last month for lean mass hypereresponders. So, per what you're talking about, and it's kind of ironic because Tommy actually did a podcast, which is sort of how we started up some great conversations, in that there is insurance data that showcases higher, and it's all-cause mortality. Yeah, higher all-cause mortality for those people who have like higher HDL. The problem is is they don't, I don't think they stratify for alcoholism, right? And of course, the other downside is you can't always count on surveys to be honest about the level of alcoholism of the participants necessarily. The problem is is that in order to disentangle the potential alcoholic impact on HDL cholesterol, you have to actually be able to determine that toxicity. And per what you're talking about with inflammation, that typically comes with the inflammation. But there's also something else that's exciting about it. Typically, you find in those people who have very high levels of HDL, who are alcoholic, high levels of triglycerides. And so usually you'll tend to find that there already is some dysregulation that's going on within the lipid system. And that's why you always couple the two. If your HDL is high and your triglycerides are low, it's very likely you are a very efficient fat burner in particular. And you actually don't have a lot, you probably don't have a lot of excessive energy parked in your bloodstream. So the other thing I wanna mention is this is a little bit theoretical. But I actually believe that another reason lean mass hyperepondercy, a higher level of HDL, is because there's actually some degree of peripheral energy distribution on the part of HDL particles that is still relatively new. Like it's, I even almost had in my channel, but it's still somewhat theoretical. But because they have, I'm gonna super geek out for a sec guys, I'm sorry. Because they also can carry the Apolyproprotein C2 as well as being bloated with triglycerides after connecting to a cholesterol-listered transfer protein. I'm sorry, I warned you. They actually, there's a legitimate reason as to why there may actually be a part that they play in lipolytic activity. So, sorry, that may have been a little bit more than you asked for, but that's kind of the gist of it. Me personally, I have a very difficult time thinking that the high levels of HDL associated with being a lean mass hypereponder is independently causal of a problem. It could be indicative of a larger problem, but I'm somewhat skeptical. Yes? Are lean mass hypereponders born that way or do lifestyle choices die up and activity can you become one? I believe it's more the latter than the former. So to repeat your question, you're asking if lean mass hypereponders are born that way, is it genetically determined? Or is it lifestyle based? So I'm gonna say something, you guys have heard about apoE4, for example. Before, when I was starting on this journey, I got a lot of information that suggested that apoE4 is the biggest determiner as to whether you're a hypereponder. I would now almost categorically reject that it's the biggest factor. I believe that the biggest factor is how lean and or fit you are while also being very low carb. I believe you got those three things in common. Your chances of having super high levels of LDL cholesterol are substantially higher, but so too is your chances of having high HDL and low triglycerides. And therefore, as of this moment in time, it could be that there's a gene component that's still associated with who ends up being a lean mass hypereponder who doesn't. But given the fact that the association I see like I just showed, like I wasn't cherry picking those body pictures that I was telling you before, I just told a whole bunch of people to send me those. And I knew they would look like that. And I literally just grabbed a bunch of them and just like threw them up. It definitely looks a lot more like a lifestyle situation. And let me tell you, lean mass hypereponders, I mean, they are probably the most powerful living tester of the lipid hypothesis. Because by all accounts, any conventional doctor right now should say that they are at high risk and they're gonna be developing atherosclerosis at a super high rate. And per the data you were asking for before, not just with inflammation, but I also have a lot of them getting CACs and CIMTs, carotid intermediate thickness. I myself running at those super high levels for the first four tests that I had in my research saw regression. I actually had the most regression on my right side, which was, I wanna say, 685 nanometers, regressed down to 531, up until this most recent experiment. And that was running at super high levels of LDL cholesterol and LDL particle counts through most of my research. That's actually a longer story to unpack for a little bit later. But the point is, is the data as it stands right now is looking very encouraging. Yes. I understand why your data and the studies you highlighted provide considerable comfort for the folks who's LDL particle numbers go through the roof. But we do hear that one of the problems with that is that, and you mentioned the lingering issue, that the LDL particles at those high numbers are more likely to stay in the bloodstream and more likely to become damaged with oxidation. Can you say a little about this matter of oxidized LDL particles? Yes, yes. So to your point, you were asking the question on what about the concern of oxidation? Because as I'm sure a lot of you have heard, if you have like let's say 1,000 nanomoles of LDL particles, that's more preferable to having 2,000 because 2,000 are more likely to be oxidized. And the truth of the matter is that from my perspective as it stands right now, I feel, surprisingly, again, it's an engineer following the data. Mechanistically speaking, I think I would rather have more LDL particles to attack the same level of oxidation. It's the oxidation that is ultimately the biggest problem that we're looking for. And if part of the job of LDL particles are to clear oxidation, I mean, it's part of why they have antioxidants on board. It's part of why I believe that they intentionally get their phospholipid shells oxidized is because it's part of their method of clearance. That's still preferable to the naked tissues of your endothelial cells that line your vessel walls, getting oxidized instead, or for that matter, being exposed to free radicals because that can cause a cascading inflammatory effect. I would rather there be a controlled inflammatory burn than one that ultimately has to get addressed too much later. So in a sense, no, and following the data as it stands right now, all things considered, I think I would rather have more LDL particles than less. Again, to meet with the existing demand against the oxidative stress that there already is. This is one of my problems with people taking on a lot more polyunsaturated fatty acids, especially hydrogenated. You can bring down your LDLC and your LDLP, but there's a lot of evidence that suggests it's with more peroxidation of your LDL particles so that basically they're getting cleared by scavengers receptors. I think a better way to lower your LDLP or LDLC is to just have more carbs if that's what you're into. I don't think it's a good idea to find strategies to oxidize it so that you get a better blood test. This is my two cents.