Social media has been going absolutely crazy with the release of a new study that questions the role of LDL and APOB in heart disease. People in the low-carb community say this is a game changer while people in the anti-low-carb community say actually this proves their point. Well, who's right? Let's dive in today to discuss the real findings and what it means for your heart health. Welcome back team to the Building and Life-Long Ethics podcast. Thanks so much for stopping by. I really appreciate it. If we haven't met yet, my name is Jordan Renke. I'm a dual board certified physician in sports and family medicine. And the goal of this podcast is to keep you active and healthy for life through actionable evidence-form education. Today we're talking all about this new study. So let's dive into it here. First, the title is called Plaque Begets Plaque, APOB does not. Kind of interesting. The authors here, the primary author is Adrian Sotomoda with a bunch of other authors as well. And this was published in actually pretty, in kind of jacks of the journal of American College of Cardiology. Their advances, not the main one, but a very reputable source as well. And today we're going through this article. We're gonna kind of go through my take on things. I'll go through the paper first, kind of talk about what it shows. And then at the end, I'll kind of give the highlights and other stuff here. So let's dive into it. So first things first, why was this study done? Well, there's been an increasing popularity in carbohydrate restricted diets and ketogenic diets. So beyond obesity and diabetes, that's the main thing people are doing them for, right? They've said, hey, these may be used for other things as well in terms of some people are claiming for mental health or epilepsy, that's very well known. Other people say maybe it can help neurodegenerative diseases all these other diseases so that a lot more people are using them so they wanna study on it. One reason though that we talk about this is when people go on this, sometimes we're gonna have issues with lipids. So a lot of times you can see increases in LDL or APOB in some people who go on these carbohydrate diets. This is not everyone, by the way, if you go on a low carb diet or keto, some people's lipids and everything goes way down, everything looks fantastic, but there are some people who this goes up on. And that's kind of this population we're talking about here. For a small subset of people, they find that the leaner you are when you go on a lower carbohydrate diet, it sometimes leads to bigger changes. And this is kind of what's known as the lean mass hyper-responder phenotype. So it's characterized by elevated LDL-C, high HTLC and low triglycerides in lean, generalized healthy other people on these carbohydrate restricted model. And then they say kind of the, I did explain this as something called the lipid energy model, which the low carb community, they've been a bunch of scientists saying, hey, this is what's been going on. And the reason we're doing this is 'cause there was concern for when you have elevated LDL, the general idea is that elevated APOB or elevated LDL leads to higher risk of heart disease. And the question they have is, well, in these otherwise these lean mass hyper-responders, so the small subset of people, is that absolutely the case? Where do they have a high risk of cardiovascular disease just because they have higher LDL-C? And so overall the study objective here was to characterize plaque progression in the lean mass hyper-responders, the kind of this phenotype and identify predictors using this CCTA, which is essentially looking at a CT scan, looking at the heart, seeing if plaque is growing there, looking at the main thing here they're looking for though, was in these people who have very, very high APOB, very, very high LDL, and then they scan their arteries looking for plaque and plaque progression, like is it actually worse in these people? Like the standard model would protect. They're saying, hey, general cardiology would say, if you have very, very high numbers of APOB and LDL, you would have progression and it's risky. They're saying in this small subset of people, is that actually the case? That's what they're trying to look at here. That was the overall goal. So moving on there though, the methods, how do they do this? This was pre-registered, which is great. Always love seeing when things are pre-registered, meaning it's clinical trial, looking at it and wanna see how do they recruit them? Recruit them to social media. That's actually like becoming more and more popular. So essentially they said, hey, these people who are self-proclaimed lean mass hyper responders said, hey, do you wanna be a part of study? And so they got them through social media. And who were these people? Well, for inclusion criteria, they had to be on a ketogenic diet for at least 24 months. Their LDL had to be less than 160 before that ketogenic diet. And then after starting the ketogenic diet, LDL had to go up to at least 190. And so 190 was kind of one. And they were saying, hey, we wanna see about a 50% or greater increase in LDL after adopting this ketogenic diet. Also as well, their HDL was greater than 60, triglycerides less than 80, fasting hemoglobin less than six, fasting glucose less than a hundred, and their CRP was less than two, so normal. So pretty much what they're saying is these people are otherwise metabolically healthy, no other underlying conditions, but they have very, very high LDLs after starting this diet. So specifically an increase of at least 50% from starting adopting that ketogenic diet. So a lot of them are way higher than 160, but that was like the goal. And the exclusion criteria are pretty much anything else. If you had high blood pressure, type 2 diabetes, were on a medication for cholesterol, any other stuff, they kind of blocked you out of that. That was kind of what it looked at. And for measurements of, what they were saying is, what they were trying to look for is making sure these people were in a ketogenic diet, right? So they had a dietary adherence was measured by dietary recalls, meaning, hey, what did you eat? But also I thought it was kind of cool daily BHB, so beta-hydroxybutate markers. This is how you are indicating that you're actually in ketosis. So they looked at these daily to make sure, yeah, are you actually in ketosis? Which is kind of cool. And the measurements as well, they got something called the CCTA, which CCTA is a diagnostic test that produces detail, the 3D images of your arteries and kind of to detect abnormalities in either plaque or blood flow and like that. So they're looking at plaque inside your arteries. That's the main measurement looking at there. And they got them at baseline and then at one year. So this study looking at one specific year. They also got EKGs and other things as well. But yeah, they looked inside these arteries looking for plaque and they quantified it. Using an AI, essentially clearly software is what it's called and they also was reviewed by experienced reviewers as well. So essentially they were trying to say, hey, in these ones inside of the lumen, do we have plaque? And if we do, is it calcified? Is it non-classified? How big is it? That's what we're looking for. They also kind of did some additional statistical things trying to figure out a lifelong LDL exposure. A lot of times they say that lifelong exposure to high APOB or LDL or any risk factor, whether that's blood sugar or blood pressure, it's the lifelong exposure. So they tried to calculate LDL lifelong exposure by doing some various statistical analysis as well. And then also going into the stats, they did multiple different things. They had linear models, which kind of looked at things. They had secondary analysis. They were trying to calculate and isolate for things. So that's beyond the scope of this podcast, but they were looking at, hey, how do we make sure that we're looking at just what we're looking for and nothing else? And from a funding perspective, it is worth mentioning that it was, the study was funded by the Citizen Science Foundation, which is a foundation that is really financed by just people on the internet. They kind of donate to it. I will say they have a very historic low-carb leaning. And so it's worth mentioning. I know, I think if this were a pharmaceutical company that did this trial, everyone would rag on it and say, "Hey, this is pharma." So like, and this is, I have to recognize as well, although it is like crowdsource and crowdfunded as well, like a lot of the science is going towards funding low-carb, which is not a bad thing, but I just have to say, hey, if we're gonna rag on people for having biases on one end, then in the other, we have to be aware of that as well. And so just gonna put that out there. So what did they actually find? Well, overall, there were a hundred participants. So that's the hundred participants. The mean LDL-C was 254. So LDL is huge, up there at 254. HDL was about 89, triglycerides, 67. BMI was 22.5. So once again, these are lean people and the average age was about 55. So that's what we got. And predominantly male, 59% male. And yeah, that's kind of what it was. Diet adherence, they were phenomenal. Patients adhered successfully to ketogenic diets confirmed by these dietary assessments and these BHB measurements. And 87% who recorded the BHB where it needed to be on most measurements. So pretty much they're saying like, they're really, really good at adherence, which was awesome. And they wanna mention, hey, were there any significant changes in APOB over the course of the study? No, there were no significant changes in APOB or BMI. They kind of stayed the same. Looking at plaque volume changes, most participants had stable non-calcified plaque. A few did show a decrease in it, but also some did show an increase. The median change though, so on average people did increase their plaque in their arteries. So on average, people did increase the plaque in the artery. That change was 0.8%. And they mentioned they were comparable to other cohorts in previous studies. There's no direct cohort here, but that's worth mentioning. They also looked at the association of APOB and LDL with plaque progression. And they found that neither the change in APOB or baseline APOB were associated with the change in either the NCPV, which is once again, a measurement of how they looked at it, or the TPS, the total plaque score. Those are both kind of looking at the plaque volume inside there. They said there was no necessarily distinct linear association with APOB in there. And association of baseline metrics as well. They did look at, hey, what was your baseline plaque and a baseline CAC score? So that's coronary artery calcium. And a baseline CAC that was elevated, so it was positive showing you did have plaque, that seemed to have the biggest association with an increase of the plaque buildup here as well. That's what they looked at. They also looked at the lifetime LDL exposure, and there was a significant predictor of final increased plaque in a univariate analysis. When you look just at LDL, and they kind of looked at it in isolation and said, yeah, lifelong LDL seems to have a risk when they did other calculations and kind of brought in other variables that seemed to go away as well. But yeah, and up here, there's an image for anybody who's watching, you can see it if you're listening, I'll kind of explain it here. There's a graph showing the total plaque score on the left and the change in the NCPV on right. And graphically it's indicating that APOB didn't have an enormous linear progression like the baseline CAC did. So the right picture shows like pretty steep increase up. What that's showing is that, hey, the CAC seemed to be very highly associated with increasing plaque scores, whereas APOB didn't have it quite as much. However, you will look, if you look closely, you can see that the line is still going up. So it does look like the higher the APOB, maybe a little bit increase there, but it wasn't statistically significant and not like the CAC was. So that's what the general results were. That's what they're saying. There's also a big picture here in the article, which there's about eight different pictures here. I'm not gonna say they go through all of them, but what they're showing essentially the change in the NCPV, the change in the total plaque score, kind of looking at things. And overall, the general trends you'll see is that, once again, baseline CAC, if you had an elevated CAC score, you had a steep increase risk of the NCPV and the risk of the total plaque score. And I thought it was kind of interesting. And the bottom they also showed looking at cumulative exposure of LDL, which didn't really show much association, but then also APOB and saturated fat, which is interesting. And there was heterogeneity everywhere. Meaning like some people, if you ate a lot of saturated fat, you had no real change in APOB, others had the opposite. So once again, a lot of variability. That's gonna be like the big takeaway here. A lot of variability, but we did see a lot of things looking at that. So these charts are something to dig into. Overall, what I wanted to take away was CAC, very strongly associated. Although I did want to mention on the both of the images, the middle images, when you look at the NCPV and APOB, total APOB and the total plaque score in APOB, there definitely looks like there's a trend going up. There was a elevation where as you went up, you did see, yeah, you saw a line going up. So pretty much as you went up with APOB, you did see increase in plaque. It wasn't statistically significant, but you can definitely visually see that that's there. So going on to the discussion, this is once again their discussion. We'll kind of talk about my takes in a little bit there. They said, well, generally independent risk factors for atherosclerosis, like things like LDL and APOB, they thought that maybe, maybe in these specific subpopulation, it's not as linear as they kind of thought it was. That's kind of the big thing. They say, hey, previously studied LDL, APOB, have a pretty good idea that the higher it is, the higher risk you have. They're saying, hey, these people didn't necessarily see that, right? So they have a BMI less than 25, they're otherwise quote unquote, metabolically healthy, then have obesity or insulin resistance. Maybe for these people, this is a little bit different, not quite the whole case. That's kind of what they're saying. They maybe there's this new phenotype where the traditional model of lipid education is not necessarily right. That's something to mention as well. And they kind of were saying this is important because this is the first and only population with independently elevated LDL without genetic costs. So the vast majority of people when they have super high elevated LDL, it's because they have familial hypocholesterolemia, which is a genetic condition, meaning you have lifelong elevated LDL. This is kind of the first population where people are essentially getting themselves into these high levels of APOB and LDL on their own accord. They're saying, yep, I'm gonna go for it, let's do it. And so that's what we're looking at there. And I thought this was novel because these people are out there, right? And this is happening. People feel better on these diets. They're eating, you know, whole diet and they say, hey, I feel good. And so these people are now out there and the cat's out of the bag. Like this is not going away. And so this is a cool study looking at that. And this is also further evaluation of what they call the lipid heart hypothesis, which is the understanding that for maybe this small population, things are a little bit different and the LDL may not react totally the same as it does in a normal population. So that's kind of what we're looking for. And yeah, that's kind of interesting. The big takeaway they said though, is that elevated APOB does not drive out the sclerosis in a dose dependent manner in this population. And they said, yeah, that's one thing. But they did mention though that, and I thought this was really cool that they said these lean mass hyper responders, they're not without risk, right? So we did see kind of the, we did see the score of the plaque go up with pretty much everyone there. There was heterogeneity. Some people stay the same, a couple went down, but then we saw a lot of people on average go up. And it's comparable to other studies looking at this. So we've had previous studies doing the same thing, getting those coronary CTs, looking at people and saying, hey, when you progress over a year, what's the progression? They're saying these people in these lean mass hyper responders responded similarly. So they kind of showed normal pack progression compared to other groups out there, which is kind of interesting. And I appreciate the fact that they said that at least. So that's what they said that, hey, it looked like that. But there was once again, heterogeneity, meaning lots of variability of who went where, was it super intense in one person and the other person didn't do much. So there was lots of differences in variability there, but they did mention that overall progression was similar to other people in other cohorts and other studies. But they say here that overall plaque begets plaque, meaning baseline plaque metrics were the most significant predictor of plaque progression. And yeah, I don't know. It's one of those things, they also talked about potential mechanisms, like why it is. I'm not gonna get into that 'cause that's beyond the scope of this and it's not really that important. But what they're saying here, another takeaway is that they think cardiac imaging is gonna be really important to help stratify people. So they're saying, hey, it's actually the plaque that causes atherosclerosis and not APOB. And so if you don't have plaque based on a coronary CT or something like that, then you're essentially less susceptible to getting heart disease. So therefore you don't need to start like a cholesterol-lowering medication, even if it's very high. That's like what they're saying. A big thing is takeaways. Yeah, we could understand that, hey, maybe we have a more personalized decision, which I'm all for having personalized decisions. That's wonderful. But that's what they're talking about. So that's their discussion. And that's kind of the end of that specifically. They also mentioned some strength and limitations. They said this was a unique population, looked at 100 metabolic outliers with high LDL and APOB due to their own carbohydrate restriction. That was cool, meaning it's a unique population like we talked about as well. They said there were zero dropouts. Can we talk about that for a second? There were zero dropouts in this study. So that's like a pro, but it's also like a con 'cause this is the most intense group ever, which is fantastic and wonderful, but nobody dropped out, which is interesting. And yeah, that's kind of their strengths. They said they had pre-qualified it, they registered it, which is great. Limitations, they said it was just one year. And they recognize that, that they say it should be sufficient to see changes in plaque, but it's still kind of little bit. Also, they didn't have a comparator group. So that's a big limitation they're talking about. They just took these 100 people, looked at them and say, "Hey, this is it." And they went back and said, "Hey, in this other study, "there was a comparator group of this." Like we're using them as a comparator group, which is not the same thing by any means. So, and then they also mentioned that there's no quote unquote normal value for plaque metrics and progression, right? So like how much does it normally change? I don't know, we're not sure. We think we have some previous studies to go off of and that's what we're learning off of. We have no like set number of like, "Hey, this much progression a year is bad or harmful "or anything like that." So we don't have that and I thought it was worth mentioning. But that's what they mentioned for their strength limitations. But now what are people saying? As you can see in the picture here, there's just a big dumpster fire. This thing, oh my gosh. Like when I went, I just see this, I just sit back and I watch people go to town and say, "Hey, like this, it's crazy. "It is really, really bad. "What's going on on the internet right now?" So the reason I love this study so much is because both sides of this camp are going crazy, right? So the pro low carb side is saying, "This is perfect. "Like this validates everything." And the anti low carb says, "No, this is literally validating our idea." It's one of those ones as an outsider, I'm just saying like, "Am I taking crazy pills here? "Like what am I missing that like this group can't see this "and this group can't see that?" So let's walk through what the general consensus is, right? So on each side. So the low carb people are saying, "This changes everything." I'm seeing multiple headlines saying, "This is a game changer. "This changes everything there. "This proves that LDL and ABOB don't cause heart disease." But let's, okay, let's just stop for a second, right? Does this actually prove anything? What can this prove? Well, nothing. This is not an interventional trial. It's an observational cohort of a very, very small, select amount of people, 100 people who have this specific, maybe metabolic profile and phenotype. So this is not proof anything. The vast majority of public, literally we're talking about like 99 plus percent of people this study cannot be extrapolated to because they're not these lean mass hyper responder people. My lean mass, I mean, relatively lean. So the vast majority of our data that we have still applies for most people. And so, yeah, that's the big thing is people are saying, "This proves everything. "Oh my gosh, this changes everything." It's, you know, they're getting clicks, right? That's the big thing. You clicked in this video, I get it. But yeah, that's the big thing that we're seeing. But then we have the anti-low carb, which is saying like, "Oh my gosh, this is actually the opposite, right? "This shows that the plaque progression on keto "and you need to worry about this and it's all bad." And they didn't look at primary outcomes. So let's just take a step back here. There's lots of people in the world saying, "This is an invalid study, right? "We don't, this is poorly done, it's whatever." Like, I think if you were objectively just like remove the fact that we're looking at carbohydrates and just say like, they did a study and they looked at it and it's a piece of information in the pile. I think they'd say, "Yeah, that's reasonable. "It's cool, I'm glad we did this." And so that's what a lot of people are jumping the gun and getting emotionally involved in this. And so I'm trying not to do that. Main arguments I'm seeing from the anti-low carb community say, "Hey, like one person I saw mention, "they didn't look at their own primary outcome." On clinicaltrials.gov, I looked it up, their primary outcome was percent change in total non-calcified coronary plaque volume. And here is reported as an aggregate, meaning reported a median of 0.8. It didn't show necessarily individual ones, which some people were saying, calling the question, saying, "Why are you hiding the individual ones?" That's one thing. Other people have said that keto is even worse than the standard American diet. Meaning that if you look, the comparative group from other studies were unhealthy, meaning eating standard American diets and they had that plaque regression and that's who they're comparing it to. They're saying that, "Hey, this comparative group, "like they weren't healthy at all." And now you're saying like, "Oh, it was, you know, "the progression was similar to other groups." And the argument is saying, "Well, we don't want it to be similar to that group. "That's like a normal unhealthy group." And so what they're saying is essentially, you're pointing to this article and this, you know, increase of plaque in a non-healthy group and you're saying, "Hey, ours did the same thing," but then saying that it's normal where we wouldn't consider it normal. That's one argument I saw making as well. And people, as I said, were mentioning that the plaque progression has swept under the rug and they're saying, "Hey, they're not really "talking about that, saying whatever, "they're kind of poo-pooing it "and just sweeping under the rug." That's what they're generally saying. Let's talk about my thoughts real quick. So we talked about everybody else's thoughts, here are my thoughts. So first things first, let's not show up the Michael Scott meme of, "Okay, everybody stay calm, everybody stay calm "'cause that's what we need to do right now. "We just need to kind of calm down, it's okay." Yeah, take a breath. I think people just get too worked up, man. There's too much free time that they're worried and, you know, this changes their lives or they're worried about this or they're anxious about this. I don't know, just go live your life. But either way, this is one study. One thing I do wanna mention is that is this is one study. I don't think one study should change your life pretty much ever. Regardless what people say, this is just one study. And it's one study looking at 100 people, which is even, yeah, something else different we'll talk about in a future study. But yeah, this is one study and we shouldn't be going bananas over it. There should pretty much never be a time where you read a study and say, "Wow, like that drastically changes "this entire paradigm that we're gonna do." No, if anything, you get a paper and you say, "Hey, where does this fit into the current schema, "the current understanding that I have?" No from there. The problem is a paper like this though, is someone takes it and they have this schema of low carb thinking and they say, "Yep, this fits perfectly. "I love it." And then the other time is, "Hey, I have this schema so it fits in perfectly." I think you have to step back and kind of think, "Hey, what's going on?" I think most people are kind of part right and part wrong about this. I think it's very easy to be in one camp and get emotional saying, "Hey, this is there." I've been fortunate where like, I used to eat a low carb diet. I currently don't, but like I've seen benefits of it. So it's one of those things where I try to get as many tools as possible in my tool belt and I don't wanna poo poo anything like there, but I think they're part wrong. So I think the pro low carb community, I think it showed that in this population, maybe APOB wasn't as directly linked to progression of plaque as we would have speculated. That's not saying it doesn't cause that. I mean, let me be very, very clear about that, but you would expect that, "Hey, with way higher APOB, maybe we're showing that." But there's a couple of limitations to that as well. One, they're probably had a pretty high APOB to start. Right, that's a big thing. So there's no big change. So it's hard to know like, "Hey, from this baseline to this baseline, "is there a big difference?" Either way though, I think it's kind of interesting and cool and unique to say, "Okay, maybe it wasn't, you know, why is it?" Some people who had really high APOB didn't see plaque progression. That's a question I think that's valid and worth asking. I think that's probably the biggest thing from this is like, "Okay, maybe there's other factors going on as well, "but we still saw plaque progression." And so clearly that's something's going on. The anti-low carb group, I do think they have a point in that plaque progression still happened. Like I mentioned, I think that's the biggest thing. I think that the tone though, yeah, I think the tone from the low carb community has been that if you have a pristine diet, right, you're in ketosis, low inflammation, low blood sugars, all that stuff, you can't get heart disease and you can't have it progress. I think this shows the opposite to that. You know, the argument would be that, for most people, probably that these people already had plaque, you know, like, and so that's the cause of it. It's the plaque and not the diet itself. Well, here's my question for you. How do you not get any amount of pre-school plaque in your heart? Like how do you do that? The question is for me, like in the real world, how do you prevent plaque from ever, ever starting in a modern Western diet? That's my midnight question. In the third world countries, that can happen, right? 'Cause we're not overeating and they don't have the resources that we do, like, so that can happen. But in our current environment, how does that happen? How do you prevent any accumulation from childhood on? Do you limit all exposures of foods that you're gonna eat a kid, you're gonna eat a ketogenic diet from the time like literally there's nothing but meat smoothies from as a kid and all that stuff? I don't know. You know, are you gonna limit their exposure to stress, to chemicals, to, you know, the air we breathe, to the genetics they have? Like how do you prevent that? The answer is you can't. You can't prevent that, that we know of right now in terms of avoiding all those things. And so for me, if they're saying the argument is, well, it's the plaque that begets the plaque. Okay, how do we know that we can't get plaque? How do we prevent plaque from ever starting when we have, you know, cadaver studies showing that it can start very like early kids and teenagers and whatnot. So that's for me, it's like most people walking around probably have a little bit of plaque who are adults. That's like, seems to be what the general consensus in the literature is. So if you can have, they have that plaque already and this ketogenic diet doesn't necessarily stop you from getting into progressing it, then we have to kind of think about things. That's kind of what I think about. I think also plaque begets plaque is misleading. I don't like this title. I'll be honest and say that it's catchy. I understand that at all. I get the importance of getting clicks and having important titles. I need you to click on this video so you can watch it. I get that whole idea, but I don't think in scientific literature that's the place for it, right? 'Cause this is not, yeah. I think we're making conclusions way, way, way before we have any evidence or definitively shows anything like that. And also I think it's not an either or situation, right? There's still no proof that you can't get heart disease on a keto diet if you've already had this plaque. And from my understanding, people say, "If you have the plaque, that's the big thing, Jordan." Okay, well show me a population where there's nothing built in already, right? Once again, so for everybody, even in this study, these really, really lean people, there's pretty much no study that shows that you can't have heart disease if you're eating ketogenic diet. And that's the biggest thing I talk about and see is like, "Oh, if your information's low, you can't have it." This shows the opposite to me. It shows that you can still get progression. I don't know. I just see it as a keto diet is not gonna guarantee you that you won't get heart disease. But like most things, there are many, many variables out there and people are gonna have lots of variables. And so everyone's gonna have a different approach, right? So you go on a keto diet, all your numbers look great. Everything's fantastic, wonderful, like that's great. Whereas other people, they go on that and they go through the roof and they still aren't necessarily lean or they have these, that's the biggest thing, right? How do we apply this to everyone else? The answer is you pretty much can't. There's just a very, very small subset. The person who is really not healthy, who has diabetes and is going on a ketogenic diet, having their LDL that high is very, very different than someone who's very lean. Hopefully they get to that leanness and then maybe we talk about it, but yeah, it's just a very, very challenging thing. And so overall, what I'm gonna ask on is, and this is kind of the question I go back to time and time again, are you willing to bet your heart health on this yet? I'm not quite there. I'm not quite convinced that this means nothing, that LDL is gone, it will be doesn't matter. 'Cause I just, it's very hard to generalize to generalize that to everyone else in the population. So that's my personal stance on that. And if you disagree with me, that's cool. I'm cool with that. I'm okay with that. I still respect you and you're a person who deserves love and respect and I get that. So I don't want this to become a war, right? I see people on both sides of the fence. At the end of the day, I don't think this changes a whole lot for my practice. I don't think it should change a lot for your practice either. 'Cause once again, this is one study, just kind of look at it and understanding that most people don't fit in this category. But either way, I do enjoy the challenge of, challenging the status quo, right? This is something that makes us think and help us to think critically. And so I appreciate that opportunity. I think it's cool if nothing more than that regard, but yeah, either way, people just need to calm down. Like I know it's your life and your health and you care about it, but like, man, there's so much more to life than reading studies and getting freaked out about this. And also like, why do you care what someone else does? Like if someone else is getting good results and they're otherwise healthy, like let them do the thing. And I'm never gonna tell someone like, you're wrong, you need to do that. I don't know, that's just my two cents. So sorry, this is kind of a long one, a lot of rambling. It's very emotionally charged for a lot of people. So I wanna step back and try to give a neutral approach. But if you did enjoy the podcast, I would really appreciate it if you liked the video on YouTube or subscribed, or if you sent it with a friend and shared it with them. If you share it with a friend, that would really mean the world to me. It's the highest form of a compliment I can get. But I really do hope you enjoy this, but that's gonna be it for today. Now get off your phone and get outside, have a good rest of your day. We'll see you next time.
