In the world of nutrition, perhaps no other topic is as controversial as eggs and cholesterol. On one side of the debate, the plant based community tells us eating eggs are as bad for our health as smoking cigarettes. On the other side, advocates of higher fat diets cite new studies which tend to show that dietary cholesterol has very little impact on levels of cholesterol in the body. Who is right? Should you eat eggs? This episode covers TMAO, the steps you can take to determine whether eggs are a food to keep in your diet, or perhaps whether you’re better suited to a hot bowl of oatmeal for the morning meal.
This Episode Covers:
- Breaking down a big new egg study [9:00];
- ApoE4 and cholesterol absorption [24:00];
- Sitosterol and sterols in LDL-C numbers [32:00];
- TMAO and eggs [45:00];
- Triglycerides, Apoc3 and heart health [55:00];
American Journal of Clinical Nutrition egg study we discuss in the show.
Aaron: The people that you kind of have to get are the one below that level, that they are hyper absorbing, but not to an effect that is immediately obvious in their health, they seem, they feel healthy, but underlying that they’re sort of, they’re potentially absorbing too much cholesterol and they’re just not aware of it, and then it’s going to hit them later on in life. Those are the people who need to take care. And, like I say, the best way to do that is by having, you know, testing for your absorption markers, talking to your healthcare provider.
John: Welcome to “The Gene Food Podcast.” I’m your host, John O’Connor. Hey guys, before we get into today’s episode on eggs, I want to draw your attention to our custom nutrition plan product, I always forget to mention that we do have algorithm that was created by Aaron Gardner, our lead researcher and geneticist on our team, and the algorithm will score you into one of 20 different diet types based on your genetics. You could almost think of it as like the Myers Briggs for nutrition. Helps to solve some of these questions that people like you who are interested in nutrition are always wondering which is, “What is my reaction likely to be to saturated fat? Is saturated fat good for my heart health? Is it bad for my heart health? What’s my blood sugar response?” You know, we touch on issues, histamine, micronutrients, supplements, wheat score, chronotype. There’s a lot of good information in the product and we’re just getting ready to launch a third version of it. So there’s also a meal plan, two-week meal plan that gives you step by step guide about how to eat on the diet that you’re assigned to. So we’re getting good feedback with the product. For the podcast listeners who want to give it a try, you can enter in the coupon code all caps, PODCASTGF, for a 15% discount. So hope you’ll consider that product.
Now on to the episode for today which is a discussion of eggs. Eggs are such a controversial topic. There are people out there who will tell you that eating an egg is going to kill you, it is going to give you cancer, it is going to give you heart disease. There are people out there who will tell you that eating 100 eggs a day is perfectly fine. It’s the best food you could possibly eat and it’s a superfood, it’s healthy. People that are eating egg white omelets are morons because they don’t understand the “new” science on cholesterol. So which is it? How do you decide for yourself whether eggs are a food that is healthy for you or whether eggs are a food that is bad for you? We’re going to dig in we’re going to talk about a new huge egg study, 177,000 people. We’re going to talk about biomarkers you can look at. What lab tests you need to go have done, both genetic, some of those were included in the Gene Food custom nutrition plan, sterol absorption, sorry for the additional plug, but also biomarkers, LDL cholesterol, total cholesterol, and some of these more obscure markers that you can go get tested. Here are the tests you need to do. Here’s the process you need to go through to decide for yourself to finally get past these conversations about eggs are terrible, eggs are great. Let’s get past that.On the other horizon, on the other side of that is your individual response to eggs. We hope that this podcast episode is going to give you the starting point for your own egg enlightenment, your own egg awakening. So here we go. It’s eggs, “Gene Food Podcast.”
We probably should jump in because there’s a lot of stuff to talk about with eggs as it were. So, you said that you are eating eggs right now or you’re not? I mean, you finished your vegan experiment. How long did you do that for?
Aaron: For a month with the caveat that I was having the fish oil and then I have to say it was very good to break out of it on the first of February, so that was quite a nice indulgent day. But, yeah, for this month so we’re going to try out an egg heavy diet really, or an egg-rich diet.
John: Yeah. So for you what is that like? Fourteen a week or?
Aaron: Just one a day, which for me that’s a quite a big increase because probably previously I was on the maybe less than one a week would be my previous sort of special diet. I find that a bit of a struggle to be honest. I’m not a massive lover of eggs. But it’ll be interesting to see if we marry up with the study that we’re going to talk about.
John: Well, so and you got your blood work done after your vegan experiment, and then you’re going to get your blood work done after your egg experiment, right?
Aaron: Yeah. So just maybe become like a monthly thing. And I might try a few different sort of diets and see what sort of effect it has on my blood lipids. Just even out of personal interest, it’ll be quite interesting to see what effect that has on my blood lipids. And I’ve signed up with a new provider as well to one that should hopefully give me a lot more metrics than I was previously getting from my previous report. So be able to dig into things in a bit more detail.
John: Oh, that’s exciting. So you get maybe some LP A, LP little A and…
Aaron: I don’t know if it does that.
Aaron: I have to look in. But I think it’s possibly an option to payback for but I will look into it.
John: Yeah. I was disappointed that getting the full, full, full complement of LP little A snips is so tricky based on what is offered by most labs.
Aaron: Yeah. Probably easier in the U.S. to get a bit more than we can get in the UK but it’s still seems that it was a bit of a dearth of visibility.
John: Yeah. No, I mean in the U.S. you can get LP little A tested if you really try. But the thing that’s funny is the insurance providers a lot of times will push back on that test in particular. But that’s a little bit of a diversion because we’re here to talk about eggs. So the whole genesis for this podcast was we all saw on Twitter, I think I saw Tom Dayspring, who’s a kind of a well-known lipid commentator in the very nerdy cardiovascular health circles. He tweeted out a new study that was done. It was a mixture of epidemiology, food frequency questionnaire study, and some dietary analysis that they did on this other part of the study, which was a drug study.
And it basically found that the top level message was 177,000 people looking at the risk of egg consumption with cardiovascular disease and all-cause mortality. And they found that basically and also the impact on blood lipids, so your total cholesterol, LDL cholesterol. They found no increased risk for eating over seven eggs a week. What was your message on the study? Anything I’m leaving out? You want to talk about how it’s designed, who the groups were?
Aaron: Yeah, so there was three studies that they kind of merged in together. There was this pure study, which is the perspective urban, rural epidemiology study, and that’s from 21 countries, with a sort of lower development indexes, I guess how they would be described. But these individuals were otherwise entirely healthy. And then they also added in two other studies, one called on-nugget and one called transcend. And these two studies multinational. One’s, again, in a more developed country, but in these cases, it was in people with a cardiovascular risk associated with them but not a healthy population. And in both cases, they’ve had their cholesterol measured, their HDL, the LDL, and the total cholesterol level measured, but they also reported their food frequency, so their egg intake,and they were then stratified according to their egg consumption. And then from that they were able to pull out lots of cool stuff that we’re going to talk about.
John: Yeah. One of the most interesting parts of that study was, so I have it, I have the study in front of me. It’s a table two, and they break it out into groups that had less than one egg a week, one to three eggs a week, three to five eggs a week, five to seven eggs a week, and then greater than seven eggs a week. And they break out the pure study, which is the epidemiological study that has the food frequency questionnaires where you’re literally asking people. We’ve talked about there’s a lot of problems with the accuracy of those questionnaires, but it’s still a way that they’re doing nutrition science. It’s one of the, practically speaking you have to do some epidemiology. And they’re tracking their total cholesterol at each egg consumption level, as well as their, as you said, their LDL-C. They even track their Apo B blood pressure, systolic and diastolic blood pressure, and aggregating the data, there’s very little change in any of those metrics.
Aaron: Other than the systolic and diastolic pressure, they see literally no effect. You know, you can look across the numbers for the total cholesterol, less than one egg a week, it’s about 4.9 millimoles per liter, and then you go to seven eggs a week and it’s 4.89 millimoles per liter. It’s literally flat across the board.
John: These are the types of studies that I find so frustrating. Because, if you’re out there and you’re listening and you go back and forth between different sort of ideologically-inclined podcasts, you know, I try to listen to a few different styles of podcasts in the nutrition world, one of which is I listen to some…there’s some plant-based podcast I listened to. And whenever they have on a guest who’s a cardiologist or a plant-based doctor, they’re constantly saying, “Well, if you read the literature, you will understand that eggs are just as bad for you as smoking cigarettes,” or anybody who’s read the data. The data is pretty “clear”, The science is pretty clear that eggs are contributing to cardiovascular disease. And anybody who disagrees is implicitly just not up on the data or the “literature.” But this is a pretty big piece of literature, pretty big piece of data. Is it flawed? I mean, I know this study was funded by the U.S. dairy industry in part.
Aaron: So we talked about this briefly before about the funding source. From my perspective, as a practicing scientist, I always see that as a bit of a red herring when someone flag that up as a reason to distrust the paper. You know, the scientists that working on this, yeah, I just don’t see that they’re being the big sort of shadowy cabal trying to push an agenda. I think the scientists who work on this would have integrity. And then you also have to remember this type of study would have been gone through ethical approval to basically get the participants involved. It would have been reviewed at the journal. And if there’s any sort of sign of inconsistency, it would have been flagged up. So I always find that pulling out the thunder of a study to be a bit of an odd one, personally. There are some flaws with the study. I mean, we kind of we talked about previously, the use of food questionnaires isn’t really great. You know, it’s based on someone’s idealized memory of what they eat. So you often probably get an underreporting of things that people think are unhealthy. But the fact that we just, across this study, you know, someone maybe they might lie and say, “Well, actually, I only eat one to three eggs a week,” whereas actually they eat five to seven. The fact there was flat across the board, even up to above seven eggs a week, is really quite astounding. And those lipid measurements, they’re not like a recall thing. They are accurate measurements that have been taken. So with those we can be quite sure of them. And the fact that it’s so consistent across the population I think is a really, really strong effect.
John: I do too. And I think it’s interesting that they married a drug study, which is, presumably has greater oversight and greater detail, with this epidemiological study. So I thought that was kind of an interesting hybrid. I don’t remember seeing that combination too frequently out there when we look at these studies. I want to get into in a minute here why we could theorize these cholesterol levels and these biomarkers stayed flat across egg consumption. So we’re going to get into a little bit of cholesterol homeostasis. I think it would be helpful to kind of state the rule and then state the exception of the rule, because the exception to the rule is never mentioned. It’s either you get on the plant-based podcasts and all eggs are terrible for you, and if you eat one, you’re gonna die, and then you go into another style that’s a little more kind of like fat-friendly or you could say just call it paleo leaning. And you’re a complete fool if you ever cut out the egg yolks. But we have a study that we’re going to get into here in a second, which is looking at cholesterol absorption markers in APOE4 carriers and talking about how there are genetic differences between people and how they absorb cholesterol, and you need to be aware of that so that you’re not going out and eating 15 eggs a week if your body is absorbing a ton of that cholesterol. Most people probably aren’t. Right? But the thing for me though too is you look at the industry funding. So, you as a practicing scientist, I get where you’re coming from. For me as a lay person I look at it and I say, “Okay. Well, I kind of get why somebody would flag that as a way of discrediting a study.”
A problem that I have is if you get into the weeds on this stuff and you look at an organization like the True Health Initiative, which is this plant-based organization that’s very vocal and trying to set policy towards plant-based eating. And there was a huge controversy recently about them trying to intimidate the “Annals of Internal Medicine” from even publishing a study that showed that there was not significant risk for people in heart disease and a couple other disease markers when they ate a diet that included red meat. And rather than challenging the study on its face, there was a lot of controversy with the fact that they tried to actually intimidate this journal from even publishing that study. And those are the guys that are at Harvard. So it’s like for me as I’m trying to figure out who to trust on these conversations, yes, you have some of these studies that are industry funded. Yes, I’ve seen some of the industry funded studies I’ve mentioned I’ll mention it again because it’s something that pops in my mind, the LP little A study. That was industry funded. You said it was a very good design of study, but I think it looked at the wrong people. I could see how that would be misleading. The problem is the Harvard Nutrition World, they seem just as biased to me as an industry funded study because they’re looking for the same outcomes and they have the same preconceived notions and the same confirmation bias as any other nutrition camp. What say you on that?
Aaron: Yeah, I totally agree. I think the idea of the confirmation bias is definitely too across time. I don’t really know how we can ever really, you know, design that out of our studies, but well, the obvious way is to just basically remove people from the equation and you start having machine-driven studies where there’s no prior assumptions being made on to things like that. That’s going to be the way that we really sort of dial back to it. And I get the point that you’re saying that, yes, these organizations so from the plant-based diet and from animal-based organizations like the dairy organizations. As an organization, they are going to want to have a message that they are going to push out there and they’re going to try and push their agenda. At the level of a scientific publication, I’d like to think, I have to trust and find that there’s enough checks and balances to ensure that the science is getting through is as good as possible with obviously the caveat that you were saying that there is going to be confirmation bias inherently because of what, the type of field that people work in, the exposure that they have to literature, a blitz that’s going to basically drive people in a certain direction. But I don’t think the studies themselves are inherently biased towards a particular outcome.
John: Yeah. I mean, you could envision this scenario where these guys are sitting down to write their conclusions or parse their data and basically like a huge gift basket shows up from the American dairy industry with like all sorts of nice cheese and wine and all that. I mean, I don’t think it really goes like that. Or maybe it does, I don’t know. But in the case of the epidemiology here, there’s looking at the egg consumption, finding no increase in total cholesterol, no increase in LDL cholesterol, no increased risk for cardiovascular disease based on just egg consumption alone, it was spread out across a number of different countries. I thought to myself, “I wonder if that makes a difference.” Because,it’s not just the exits, it’s kind of what you’re consuming the eggs with, athat’s one of the arguments that some of these plant-based groups will make is that if you’re eating zero cholesterol and then you eat some, you’re probably going to see some increase. But like you said, I mean, it’s stratified across such a large group of people eating different amounts of eggs, I don’t see that as being sinking the battleship of the study either.
Aaron: So they actually did try and address that in some way by doing like association studies with other different dietary inputs or things like dietary cholesterol, animal protein fiber, those are the ones that they have listed. And again, they didn’t really see any variation in the response there by eating an increased amount of eggs. So they have tried to account that, again, based on that sort of caveat of it being a food-based questionnaire.
John: Interesting. Okay. And so let’s get it… I mean, so again, top level, you have this pretty big study. It’s inherently flawed because of the food frequency questionnaires, but it’s paired with a drug trial that’s probably a little more precise. They’re finding zero increase in total cholesterol, LDL cholesterol as a result of just eating eggs. Greater than seven a week is the same as eating less than one a week. Scientifically, why is that? Let’s state for the listener. Because what I want this episode to become from basically now forward is rather than just saying, “Okay, eggs are great.” This egg study came out and said, “You should be able to eat eggs with no impact on your lipids. Go eat 27 eggs a week,” or, no, I’d like to have people leave this episode with the tools that we know are available testing-wise to actually try to get an idea and determine whether eggs are good for them. But what’s the general rule? Like could you state basically the rule of cholesterol homeostasis so that people know kind of where, “the science” has moved these days?
Aaron: In relation to whether it’s considered good or bad for your health do you mean?
John: What I’m talking about is let’s say you’re eating a lot of dietary cholesterol, basically, the way it works is you are probably absorbing some of that cholesterol. But to the extent that you’re absorbing that cholesterol, you’re synthesizing less and you’re also excreting some of the cholesterol through bile acids and through your digestive process. So basically talking about how the body in most people will keep cholesterol levels stable. So for these people, I don’t know that these people who kept their lipids stable are not absorbing any of the cholesterol from the eggs. I think rather what’s probably happening as the body starts making less cholesterol, in other words, the synthesis goes down because the absorption has increased. That’s the default rule, right? I mean…
Aaron: And you’ve hit the nail on the head there was saying most people. So, if you increase your cholesterol intake, it’s been shown that it actually has a relatively minor impact on your circulating cholesterol level in most people. So like you say, it’s because the body is adjusting to take account for the fact that they’re getting more in through their dietary intake. So their body synthesizes less or reabsorbs less and more is excreted.
John: Right. Because you’re not just absorbing cholesterol from the food you eat, you’re also absorbing cholesterol as it circulates in your bile acids. So you’re reabsorbing some of the pool of cholesterol that your body has made, and you’re absorbing some of the cholesterol from food. But you could be somebody who’s absorbing a lot of cholesterol but you’re not absorbing a lot of the cholesterol that you’re eating because of the way that cholesterol is structured at a molecular level, but you’re absorbing the cholesterol that’s in your bile acids. So, you’re actually absorbing the cholesterol that your livers making. Correct?
Aaron: Yeah. I mean, so what would have been really amazing for this study, it would have been absolutely impossible to wait for the data. But they guess they would have the data just see the individual responses to people and basically start saying, “Can we assign, are you a hyper absorber or hypo absorber?” And we can basically start categorizing these people, and then seeing if we group them into those different categories of hyper or hypo absorbers, does that then have an impact on the number of eggs that they should be eating, and the impact of egg and take on their cholesterol numbers?
John: Well, that’s a perfect segue because we kind of have that study. I mean, I’m actually much more interested in this Tom Dayspring study. You know, Tom Dayspring tweeted out this the first study we looked at which Aaron described, which is the epidemiology versus drug trial studies, combine the two. But he also tweeted out something that I think is a lot more interesting, which is basically, so you have this default rule and most people are not, to the extent you are absorbing cholesterol in the food you eat, your body is making less, so the levels stay tightly regulated. That’s not the same for saturated fat, though. That’s the thing. You could have somebody who is keeping their cholesterol levels tightly regulated based on the consumption of dietary cholesterol, but what they never tell you is that with saturated fat, just as some people will hyper absorb cholesterol, they’ll absorb more than someone else, both from the food they eat as well as the cholesterol that’s circulating in their body. Some people will have this hyper synthetic response to eating saturated fat. So even though cholesterol might not increase your total cholesterol and cholesterol might not increase your LDL cholesterol, in some people, eating saturated fat will cause an increase in the production of cholesterol. That’s this whole like lean mass hyper responder that a lot of these low carb groups talk about. It’ll increase your production of cholestero,l and maybe you have a genetic variant that has lower ability to clear that cholesterol, the liver is taking cholesterol out of the system, and so therefore you have a net increase in total and LDL cholesterol as a result of eating saturated fat not as a result of eating cholesterol.
Aaron: Yeah, you’ve hit on the head. We talked about the saturated fat angle before, that there’s a certain sub population that if you increase your saturated fat intake, you will see a massive spike in your LDL cholesterol numbers. And those are the people… Yeah. So even if they, they might be able to take in much higher levels of cholesterol and like dietary cholesterol wouldn’t change. But even just a little bit of saturated fat is going to push their cholesterol numbers way out there. And what we’re trying to do is find the particular polymorphisms, the particular gene that might point towards what type of person you would be. It’d be really good to know that you may have those saturated fats but it’s not going to mean that you when you intake saturated fat, you’re going to increase your cholesterol numbers more because then you can avoid saturated fat. But you might also find that you’re fine with cholesterol so you can replace that saturated fat with a different food source and still get the nutritional benefit.
John: Yeah. And in those cases, it’s likely going to be eggs and shellfish. Because, the problem is so many people hear this new thinking and cholesterol, they lump it in with saturated fat and they’re pushing the same message like kind of the Nina Teicholz, kind of crisscrosser side of the debate, they’re all saying, “Well, there’s no reason to limit saturated fat.” Well, maybe in a good chunk of people that’s true. It might only increase your LDL cholesterol in a modest way. But I actually think that they tend to underestimate in the populations just how many people can get in trouble in terms of their cardiovascular numbers by eating a diet that’s really high in saturated fat. Because what people do is they go, “Okay, well…” Nina Teicholz will cite like the Minnesota coronary survey, which was this controlled feeding experiment in this mental hospital, and they gave people higher polyunsaturated fat omega six diet and then they gave people higher saturated fat diet. But it wasn’t like that high of saturated fat. They weren’t getting a ton of, it’s like they were going on this like keto MCT oil diet. People hear that, they don’t get into the details of it and who can blame them, they have to go on with their lives. I mean, parsing this stuff is time consuming. But then they go and they just start crushing MCT oil and crushing butter because they’re told there’s no reason ever to avoid these foods. And then they don’t have their blood work done. Or then they go get their blood work done and it’s it looks really bad. And it’s confusing. And the reason why it’s confusing is because the rules that are enunciated on both sides are both wrong for some people and in many cases for a lot of people.
Aaron: The key thing is to basically find out where you fit on that spectrum, what snips you have, or what are the lifestyle choices you have that are going to influence it and then tie your personal diet according to that.
John: Yeah. And that’s what this Tom Dayspring, this next thing that, you know, like I said, is really interesting. They looked at a laboratory database of people that had their blood work done, 667,000 of them. And they’re looking for the percentile average of fighter sterols in the blood. So the reason why they measure a fighter sterols, we’ve talked about it before in other shows, is that they use these sterols as a proxy measurement for cholesterol absorption. The idea being that you don’t make any of these sterols in your body. The only way they come in your body is if you eat them because they’re native to plants, they’re not native to people. So they measure the sterols and they say, “Okay, well, if you’re absorbing sterols, you must also be absorbing a lot of cholesterol.” I mean, there’s a lot of debate which we’ll touch on here in a minute about whether these markers are actually dead accurate for cholesterol absorption, but it’s the best we have. And so what they found is that actually in people that carried APOE4, which is a genetic polymorphism associated with basically becoming increased cardiovascular risk when eating high saturated fat diet. The APOE4 people are some of the people that are more likely to be these hyper responders who are going to make a lot more cholesterol when they eat saturated fat. And they found that they consistently had elevated levels of these sitosterol, cholestanol, campesterol, and I don’t know about this mesterolone which is this synthesis marker. But what did you take away from that study, Aaron?
Aaron: The really big takeaway for me is some of the studies they found out at the end where they pulled out things like age, you know, that was a really big surprise me the fact that these sitosterol markers are basically dramatically increasing with age, especially in a female population. But as a sort of a genetic blog, we should really focus on the genetic angle of it,and basically the strength of association with APOE genotype. But like you said the people who are carrying APOE2 allele, those are the ones that they tend to have lower levels of absorption markers overall compared to those carrying APOE4 allele. But then when they looked at the really like the hyper absorbers, the ones who absorb absolutely loads of cholesterol, those who had the APOE4, two copies of the allele, they were shown to be really strongly associated with that group. So basically, yeah, if you carry two copies of the APOE4 allele, very significantly likely to be a hyper absorber of cholesterol, which they could measure by looking at these different sterols.
John: Yeah. And APOE4 and then also the what are called the ATP binding because we’ve talked a lot about on the podcast. If people are listening, they may have heard some of the sterol conversations we have. Like, I experimented with [inaudible 00:27:46]. Because basically, at the end of the day, these heart drugs that are out there, you have, statins. Statins block synthesis. So statins are targeted at the people that are making a lot of cholesterol. Then you have absorption. That’s [inaudible 00:27:59] for short. That blocks the absorption of sterol and cholesterol. And then you have the PCSK9 inhibitors and the PCSK9 inhibitors, they tend to try to increase the clearance of cholesterol because PCSK9 is basically like a Pac Man that eats the LDL receptor, which prevents the liver from taking cholesterol out of the system, and so it starts to pool. So if you look at the three drugs, the three biggest classes of drugs give you a real window into how this works. And what they talked about the APOE4 issue is they say, “Hey, some people aren’t really responding and getting their cholesterol levels in range in response to a statin.” And they theorized that the reason why is because their issue is more absorption than it is synthesis. So there’s absorbing a ton of the cholesterol that’s re circulating in their body and they’re also absorbing a lot of the cholesterol that they eat. And so one of the questions I had for you, Aaron, is how reliable do you think just in your own personal opinion having talked about this and looked at this, how reliable do you think the sitosterol, campesterol, cholestanol, those absorption markers are for actually predicting cholesterol absorption?
Aaron: So they break it down in the paper in table two, they show you the sort of the association between absorption and synthesis between like sitosterol and, say, total cholesterol. Sitosterol, it’s okay. It’s about like a 0.25 association. Cholesterol actually…
John: A point what?
Aaron: About 0.25.
John: So what does that mean?
Aaron: If you imagine one molecule of sitosterol and you measure I can tell you a 1:1 ratio, what it’s saying is that for every one molecule of sitosterol that’s absorbed it thinks this is relative to about a quarter of a cholesterol, like a non-zoo cholesterol being absorbed, if that makes sense? It’s trying to say how, you know, for every one molecule of sitosterol that they detect in your blood, how many of the total cholesterol molecules the sort of the molecule that aren’t sitosterol, how many of those have been brought into the same pathways? Trying to work out a ratio between the absorption and the synthesis of the two of them.
Aaron: So basically, if it scored one, it would be identical so that would be a perfect marker. So a score of one, it would mean that sitosterol mirrored perfectly in absorption of cholesterol. So the lower the number, the less closely associated they are.
John: There is a scenario and it seems like this ratio lays that out, there is a scenario where your sitosterol absorption is discordant against your cholesterol absorption. Meaning so you have these pathways that have been, you know, pretty well established in the scientific literature, which is you have the Niemann-Pick C1 like protein, which is basically kind of like the Tom Dayspring analogy is it’s the ticket taker at the bar kinda kind of like let’s everybody in or most people in and then it’s the job of the ATP-binding cassette genes, or decides who it’s going to let in I should say. And then it’s the job of the ABCG and ABCG5 genes, they’re E-flux driven. So it’s their job to see who they’re going to kick out if there’s too many people in the bar. And what I’m kind of getting from this is that even though sitosterol is described as a proxy market for cholesterol absorption, actually, if you’re seeing sitosterol in the blood, it means you’re just getting a lot of that plant sterol in your body, and you could be absorbing a ton more sitosterol than you are cholesterol. Right?
Aaron: Yeah. So the interesting thing they bring out is that they talked about the fact that you shouldn’t just use a single marker like sitosterol, you should basically use a larger panel. So bring in sitosterol, campesterol, cholestanol, and to a lesser extent [inaudible 00:31:59] and basically pull all of those together. Because by adding them all together you increase the ability to be accurate with your measurements for cholesterol, ut looking at it just on a single basis, you’re right. You could just seeing what your blood work with sitosterol could be, you can’t take it as 100% rate for what your actual cholesterol absorption rate is.
John: The thing that’s so funny is this is just like the LP little A situation. It’s like, I mean, even me because of my job at Gene Food, you know, it’s part of my job to do blood work and measure it and publish it, talk about it. People are interested. I think some of these N equals one kind of stories are helpful. Just not because they prove policy or are all that scientific ,but I think they clue people in who may have similar issues. And the LP little A hides out in the LDL cholesterol number. Unless you break it out specifically, it’s just going to hide out in your LDL cholesterol number. And the sitosterol hides out in the LDL cholesterol to a certain degree, so do these other sterols. So nobody is really getting that blood work done. So it’s not really on anybody’s radar. So it’s like you have the people that are out there that are kind of like pushing for the plant-based ketogenic diets, and how many of those physicians are testing for sitosterol? And then also, at what point is this sitosterol if you’re absorbing it become atherogenic? Because that’s something that’s not clear from the studies either is that not everybody agrees that having elevated sitosterol is necessarily bad for you. I think it’s something that’s not on people’s radar because it’s not tested for.
Aaron: Yeah. It’s very difficult to test for is part of the reason for it. I mean, in an ideal world, this study, it would have been based on using some sort of radio-labeled sterols, you know, the types of cholesterol, sterol basically giving those and seeing it if they pass through the intestinal membrane and getting a ratio based on that. But that’s just not going to be possible in people unfortunately. So it kind of the best type of study we have to work out these associations, but it’s not ideal. And like you say, going on into the wider health effects of it, because we can’t measure it as accurately as we want to, it becomes quite messy to try and pick out, you know, what the actual overall, overarching story would be.
John: Yeah. And then just so here’s a question just in the way of converting these metrics. So UG/ML, does that convert roughly two milligrams per deciliter?
Aaron: I’ve to go and do the maths on it.
John: They have a chart that’s pretty interesting. They have all these sterol absorption markers, and then they have this monstro, which is the synthetic marker, and then they show the percentiles, which is actually pretty interesting. So they have like 25th percentile. And they show what the likelihood is of your sterol absorption being normal suboptimal, hyper functioning, all that. I just would be curious to see if that converts into milligrams per deciliter because that’s the way it gets measured in a lot of our tests in the U.S.
Aaron: Yeah, I think it won’t exist. Because you’ve got a couple of different dilution factors there. So the deciliter versus milliliters and then micrograms versus milligram. Yeah, it would have to be adjusted a little bit I think.
John: Okay, we might want to do that because I’d be curious to see…
Aaron: You could work it out. It wouldn’t be difficult to work out.
John: And so at the end of the day, I think what’s…so if somebody is listening to this, they’re interested, you know, “Should I be eating eggs?” We got a little bit kind of technical there with a lot of the sterol stuff, but to zoom back out, if you’re interested in deciding whether eggs are healthy food for you…you go first, Aaron, what would you…if somebody came to you and said, “Hey, I want to eat eggs. It’s easy for me to have them for breakfast, but I’m really worried about my heart health. And I don’t want to jeopardize my health and my future. I want to try to be as healthy as possible and I want to eat the foods that are right for me. Should I be eating eggs?” What would you tell somebody?
Aaron: So unless you have any underlying health issues with your cholesterol, like already very high cholesterol level existing already, I would say that there’s no issue of eating eggs at all. They seem to be an entirely neutral from the point of view of cholesterol and heart health. And then we know that eggs do have a lot of other beneficial nutrients in them that are beneficial for health. So I would say go for it to. Obviously don’t go nuts and eat seven eggs a day, but stay within the guidelines about paper and an egg a day is perfectly achievable and doesn’t look like it would have any impact on your health.
John: Yeah. I would second that as the general rule. And then what I would say is it may be worthwhile to go and find a doctor in your area that’s running a Boston Heart Diagnostics panel and go and see that doctor, have a full panel done, and see whether you have these elevated…you know, like you said, you can’t just focus on sitosterol but see if you have these absorption markers, see if they’re really elevated. And see if you have higher LDL cholesterol. And if you do have higher LDL cholesterol and your absorption markers are elevated, and then you also have APOE4 before and you have some of these at ABCG5 genes, which we report on in our nutrition plans, in that case, you might want to consider curbing your consumption of dietary cholesterol.
But the thing is, is so funny, I just wonder whether, in some cases, these hyper absorbers are actually the people that want to be more vigilant about consuming the “healthy” plant fats. Like I wonder if whether these are the people that actually should be curbing their intake of almond butter and avocado and nuts and seeds. If you look at Caldwell Esselstyn, the surgeon at the Cleveland Clinic who did these heart study protocols that he put people on that they have imaging that reverse heart disease, he’s just as vigilant and it never gets reported. It’s always this simplistic thing of like, “Oh, well, he said cutting out meat.” He’s actually just as vigilant about cutting out the plant fats, the nuts and the seeds in the avocado. Again, for these really sick heart patients, the idea being that they’re probably genetic, they’re probably having a loss of function somewhere and they’re absorbing a lot more of these sterols than a normal person wouldn’t and it’s causing problems for their heart. He cut out all those foods. He cut out nuts and seeds. He cut out avocado ruthlessly.
Aaron: You probably know if you’re one of those people though already, if you are one of those extremes, where you’re in that having a really severe issues because you are such a hyper absorber of collateral, you’re probably already aware the people that you kind of have to get other ones that are below that level, you know, that they are hyper absorbing, but not to an effect that’s immediately obvious in their health. You know, maybe they feel healthy, but underlying that they’re sort of potentially absorbing too much cholesterol and they’re just not aware of it and then it’s gonna hit them later on in life. Those are the people you need to take care.
And like you said the best way to do that is by having testing for your absorption markers, talking to your healthcare provider. And then I guess if you’re a hyper absorber thinking about and you want to control your cholesterol, like you’ve talked about the threebig clinical intervention that you can take, in your case, if you’re hyper absorber, then maybe [inaudible 00:39:23] rather than start into the PTSK9 inhibitors is the way to go.
John: Well, I was looking at that from really from more of the fighter sterol angle than the cluster angle just to reiterate. I’m really interested in the people who have these sterol markers and the sterol markers are really just a marker of absorbing a whole ton of plant fat and not as much cholesterol. You know, part of the deal with the dietary cholesterol thing is the way it’s structured molecularly. It’s not always available to be absorbed. But I guess I would disagree just a little bit with that line of thinking that you just mentioned there. The reason being it’s just because of how long it takes heart disease to develop in somebody. I mean, the heart disease is these incremental insults.
So if somebody who’s in their mid-30s or their 40s and they’re seeing these absorption markers and they’re not sick yet but they’re having these small insults to their body every single day that they keep prevent by changing their diet, I think that’s an interesting case where you might want to say, “Okay, knowing a little bit more about your physiology, you might be able to stave off heart disease or add a healthy decade to your life down the road by taking these precautions now when you’re young because of the fact that heart disease is it’s not like a broken leg. I mean, it’s just the small insults over and over.” So if you maybe if you have a calcium score or getting to the bottom of this I think can be very useful for people that are looking to eat their optimal diet.
Aaron: Oh, yeah, I totally agree. I wasn’t trying to say that you should just not worry about it and that just get your test later on in life. I mean, I think I’m a good example of someone who is proactive and basically try to find out what my blood lipid look like, trying to adjust my diet to stay healthy. And I think it’s definitely something that you say you should start doing when you can basically early on as you can because these things because it’s like a chronic insult over time that eventually becomes acute and if you can basically limit that chronic insult early on in life or dramatically reduce it, then you’re going to probably save that acute event off until way on later in your life or hopefully never at all.
John: Right. And so why do you think that there’s still such fervor out there in the egg conversation? Because most of the plant-based community they’re not backing off of that one bit. I mean, they are still just as adamant that eating eggs causes prostate cancer, eating eggs is just as bad as smoking a cigarette. You know, eating eggs is going to increase your total cholesterol. If you had to just throw a theory out, why are these conversations still so polarizing and so strange from one another?
Aaron: Because I don’t think it’s just about food. It’s all the other stuff that goes with the plant-based diet as well. But I think people just don’t want to accept that an animal product can be beneficial for your health, possibly, or even something that a lot of people eat can be seen as a neutral for your health. I think people want it to be seen that any animal product is unhealthy.
John: And so it’s just you see it as being more ideologically driven?
Aaron: I think there’s a lot of people not just on the plant-based but on some of these extreme carnival-based diets where it becomes more of an ideology rather than a science thing. And when the science backs up what you’re talking about, great. It’s excellent science funded by the way individual. This is the study that we’re going to talk about, something that disagrees with you. “Oh, it’s funded by X, Y, Z organization that they’ve already got a vested interest. The scientist is crap because of X, Y, Z.” Yeah, there’s too much ideology at the extremes of the diet debate and that does muddies the waters for everyone. But when you see big studies like this where they’re looking at lots of people, it becomes very hard to muddy the waters. So if I was going to believe one of the egg studies out there, I’d probably be more inclined to go with this one because they’ve looked at so much stuff and they’re not really making any claim anyway. But you saying it’s a neutral effects basically, which, to me, sounds about right.
John: So in addition to cholesterol, one of the things that you’ll hear out there and it’s based on credible studies too. I think this issue first came on the radar through the New England Journal of Medicine, where they looked at feeding eggs to people who were either put on antibiotics who had had these species of bacteria that produce something called TMAO suppressed or people that hadn’t. And they found that eating dietary coaling, eating dietary cholesterol independent of lipids actually caused the microbiome under certain conditions to create this compound called TMAO. And TMAO is one of the things that you can, first of all, you can test for it. I’ve had my TMAO levels tested when I’ve been eating eggs, when I’ve been eating fish, and it’s come back normal. I think it’s a situation where if you have a microbiome that’s a little bit out of balance there’s specific species of bacteria that produce TMAO. But if you’re looking at whether eggs are good for you or bad for you, in addition to these lipid markers, in addition to the sterol absorption, you definitely want to probably get your TMAO levels tested. What do you think about TMAO in this context, Aaron?
Aaron: Yeah, so it’s a really good one for eggs. Like you say, there’s that cool New England Journal of Medicine paper, where they put people on like a broad spectrum of antibiotics, so basically killing off all of their stomach bacteria. And like a dysregulated gut microbiota And I could see that by getting rid of this gut microbiota, they could deplete the circulating levels of TMAO. Like you say TMAO has been strongly associated with an increased risk of heart disease.
John: And what is it? Can you just say just briefly what it is like the TMAO for dummies?
Aaron: Yeah, yes. So TMAO, it’s Trimethylamine N-oxide and that’s why you shorten it to TMAO for short. It’s basically this compound and there’s two major sources of it. So the first that you talked about is it comes directly from fish, specifically salt water fish and other seafood. And it’s thought to be protective against urea buildup. And to mitigate the effects of precious that’s why it’s called the seafood.
John: That’s why it’s in higher amounts in fish because it is protective for fish when they’re in deep waters?
Aaron: Yeah, something like that.
John: Interesting. Okay.
Aaron: And then if you have too much of it as a human, the idea is that it changes your metabolism or increases your risk of heart attack atherosclerosis type 2 diabetes by the effects it has on your endothelial cells as it’s circulating around. So it’s basically one of these factors that is very predictive for causing heart disease. And then eggs come into it. So that is a major source salt water fish, but the other major source in our bodies is actually the gut microbiota. So they convert things like coli and prostatitis coli, which come from eggs and dairy and carnitine, yes, so red meat. This can also all be converted into TMA and then into TMAO. So TMA is like a precursor of TMAO. So those two are major sources. So if your gut microbiota is out of whack and you eat a lot of eggs or red meat, you could be producing a lot of TMAO, which could be, you know, producing something that’s harmful to your heart health.
John: Right. Okay. And there’s a few things to say there. I mean, you did a great blog on the site that’s basically titled, “TMAO: What We Know And We Don’t.” We won’t get into some of the more sort of obscure genetic stuff there. But I think you found a couple genes that were associated with increased TMAO or increased risk as a result of elevated TMAO, which was interesting, probably beyond the scope of this conversation. And then the debates that go back and forth at each other, you hear people come on, it’s a mechanistic argument. So somebody on the plant-based side of the debate will say, “Well, okay, you want to take the cholesterol feather out of my cap because that’s looking weaker and weaker, especially as applies across the spectrum of people.” It could definitely apply to the APOE4 the hyper absorbers, but it’s not as big of a problem as they had originally sold it to be.
“You want to take that out of my cap. Okay, well, I’ll hit you with TMAO.” And you’re hitting them with the New England Journal Medicine, which is a pretty damn credible source, right? But the problem is, is that then, ironically, the Paleo world will usually come back with a with epidemiology. So they’ll quote epidemiology and they’ll say, “Okay.” And it’s usually, frankly often a lot of times it’s the people that were just kind of crapping in epidemiology on the Walter Willett type studies, but they’ll say, “Well, people that eat fish have a protective impact on their heart. And the people that are eating fish are…and fish is the one of the highest sources of TMAO. So how do you explain that?” And that definitely is an interesting argument.
What I would tend to think is that, you know, if you’re living in one of these Blue Zones and you haven’t had a lot of antibiotics or something like that and your microbiome is generally healthy and you’re eating a diverse range of plant foods, then eating the fish is not necessarily going to be such a problem with TMAO. Whereas if you’re somebody that’s eating a lot of sugar or you’ve taken a course of antibiotics or your microbiome has been disrupted in some kind of a way, then you might be somebody who when you eat fish and when you eat egg sees an increase in TMAO production.
Aaron: Yeah, definitely. And I think that the seafood application of it is possibly like a kind of a red herring. Basically I’ve used that phrase. I think a lot of it’s going to be coming from changes in the gut microbiota, you know, that the dietary intake from seafood is going to play a role, but in a major activity is going to be that dysregulation. And so if you get a test back that shows that you have high levels of circulating TMAO or something that you may wish to consider is basically having someone look at your gut microbiota and see if it’s in sync And if it’s not, you know, is this something that you can do to rectify that?
John: Yeah, I think tests like biome supposedly do that. I couldn’t quote right now which strain of bacteria is that shows up in greater amounts, like putrescine producing bacteria, whatever the case. Just anecdotally, N equals one. I know people in my family who have had their TMAO tested and it’s really high and they’ve eaten a lot fewer eggs and it’s gone a lot lower. It’s gone into range. And then like I said just a minute ago, my experience is that when I’m eating eggs, eating fish, eating some meat, I’ve had my TMAO levels tests and they’re completely normal. So it’s definitely something to look at. If you’re out there eating a lot of eggs and then you go and you get your TMAO levels tested, then you’re probably going to want to cut back on the eggs. But one of the things that I thought about the study that we’ve talked about here is because it looked at outcomes, like cardiovascular disease, mortality, and it didn’t show any increase in those either, I would think that TMAO was kind of baked into that pie, right?
Aaron: Yeah, yeah, definitely.
John: Okay. I think that’s a good rundown. I think just like with everything else, I think the message here is if you have the resources and you’re so inclined and you’re going to eat a lot of eggs, it’s probably not a bad idea if you get a chance to get your TMAO levels tested, see what they do. Just like the stairwells will give you a proxy marker for your absorption of cholesterol rough estimate, TMAO could be something that would not only clue you in about eggs, but it could also clue you in on the state of your microbiome. And I do think that volume, the Naveen Jain startup does actually test for, I don’t know what the state of the sciences on that, but I do know that they do have a predictive tool that they look at the microbiome and they can tell you whether you have the bacteria that are known to produce TMAO.
Aaron: Yeah, those tools are really cool. I think that’s going to be sort of a growing thing. You know, personally, they’re talking about gut microbiota and sort of the role of fiber is something that I’m quite into at the moment. And so it’d be really cool if people can start getting an idea of what’s living inside their gut. Good. I guess the question then comes as to how you can correct that? Is there anything you can do to improve your gut microbiota?
John: I think that’s where the advice is really lacking. I did you biome a few times. I know they’re out of business now. That was an old company that was sequencing and looking at last stuff. I just found the results overwhelming and not that useful. But it was kind of cool to take a look at. I might do Volume Two. Okay, so that that wraps up the TMAO portion. I think for the most part we wanted to be focused on cholesterol, but that I think TMAO was a good thing to mention as well. So I’m glad we touched on that. So TMAO still is for you as you think it’s probably a little bit over sold out there?
Aaron: I think it’s sold in relation to fish. I think that fish angle is there. I think talking about it from the gut microbiota, I think it’s still a good marker for increased cardiac risk. But then there’s lots of other things that are also strong indicators of cardiovascular risk. So it’s kind of pick your battles.
John: Why do you think it’s oversold us to fish?
Aaron: I just think because that the idea of the Blue Zones is a little bit wishy-washy as well, you know, sort of we come out and we say a Blue Zone, but it’s actually quite hard to pin down and define really well what a Blue Zone is. So that’s one aspect of it. And then I think the amount of fish that you would be talking about eating is even in those Blue Zones is quite high. You know, it’s towards the upper end of much normal interval. So I think for most people, you know, which is people who listen to this podcast most I’m going to assume they don’t live in a Blue Zone, they’re not going to be eating enough fish to be getting that benefit from it.
So I think any issues with TMAO are much more likely to come from things like the gut microbiota, and you kind of I know, obviously, it’s like you can’t weigh anything in on it. And you’re talking about your family members dropping eggs from the diet and watching that TMAO go down quite quickly. That’s sort of a good sign to me that it’s more about what’s inside your gut that’s driving GMAO as opposed to something coming like from the amount of seafood that your family was eating.
John: So you’re saying that the epidemiology that shows protective effects for fish pretty consistently for you negates any concern about TMAO?
Aaron: I would say yes. Yeah.
John: Interesting. Okay, cool. So that’s the TMAO conversation. I’m glad we were able to get into that. There’s also the issue to kind of bring it back to the nutrition plans and talk about how we’re trying to score this whole heart health issue for people that are interested. A lot of it comes back to your total particle count, like all the different lipids, all the different life of proteins that are carrying these fats around the body, there’s basically three things that these lipid proteins can carry on the body. You’ve got cholesterol and that cholesterol could in some cases be cholesterol you’ve eaten. It’s much more likely to be endogenous cholesterol, cholesterol you’ve made that the leper proteins are shuttling around to different parts of the body.
Then you have fighters sterols, phospholipids, you know, these plant fats that are trafficked in these lipid proteins and we’ve talked about before about your LDL cholesterol, if you don’t have your sterol numbers, your LDL cholesterol still reflects not just the weight of the cholesterol inside of these samples of lipid proteins, it also reflects the weight of the sterol that’s in there too. So the lipid proteins are trafficking the sterol, they’re trafficking the cholesterol, but they’re also trafficking triglycerides. And so it’s like what I’m really fascinated in right now is if the goal overall and it seems, you know, we’re firmly in the liquid hypothesis camp and not to say that you’re going to have a heart attack if you’ve got LDL cholesterol of 120, but directionally, you want it I think, probably below 100.
I’m really interested in the people that both that have the cholesterol rich particle, which are people that could be the hyper absorbers. You need to find out if you’re hyper absorber. If you’re a hyper absorber, you’re probably not going to eat a lot of eggs. But you could be somebody who gets dyslipidemia to the triglyceride side of the fence too. So it actually could be a situation where if you’re not very insulin sensitive and you’re not doing a great job with carbohydrate fuel, your pancakes could actually spike your overall particle count more than an egg.
Aaron: Yeah. I mean, it’s interesting those cholesterol numbers you’ve sort of talked about easy. Because that egg study as well, they talk about the impact of cholesterol levels on health outcomes as well. And they would actually probably describe a bit of a Jayco response. So they basically have a category of less than 100 in their baseline, which reads as one. And then when you get into the 100 to 200 milligrams per deciliter, you’re actually starting to see a very small. I mean, so it’s very small and it’s not significant protective effect, which then starts to increase again as you get much higher. But it’s interesting to sort of it would be really cool just to drill down onto the exact numbers of where what’s a good total cholesterol number, what’s a good LDL cholesterol number, even before we then started thinking about carbohydrates and sugars coming into the picture as well.
John: Two things to unpack there. One, they were describing a protective effect of your LDL cholesterol, the 115, 120?
Aaron: Not LDL, total cholesterol.
John: Okay, yeah, because that’s a big deal. So total cholesterol I don’t think we’re quite as interested in.
Aaron: They don’t break it down to LDL in the study. But you will come across people who will say, “Your total cholesterol number should level should be several hundred.” And in those instances, you can see that that’s definitely having a deleterious effect on you.
John: Are you hashtagging this LCHF right now? I’m having a really tough time pinning you down in this episode. I kind of hear you sort of having an ideological shift in this episode based on this study. For me, I’m kind of willing to concede the point that you probably want your total cholesterol, you know, south of 200 and you definitely want your LDL cholesterol south of 100. Are you…
Aaron: No, no, I would agree with those numbers still. I would say that yeah. I wouldn’t say it’s given me a like a pause for thought but just the number two on such a large scale study it would be it’s a shame that they don’t break it down into better quintile. It would be good to just to find that real the sweet spot because I feel like with this study, they could actually give us that sweet spot of exactly where the beneficial effect lies. And in my mind that it’s going to be around the sort of total cholesterol that we see between 100 and 200 and then for LDL cholesterol, you know, around 60 to 80. I feel like this study could be the one where they really broke it down they could actually give us those numbers.
John: Isn’t the framing him and framing him offspring and a lot of the stats and trials doing a pretty good job of kind of telling us where the risk levels sit? I mean, would this study be better than some of those JAMA study? You know the JAMA study. I’m going to bring up the one that I always mention, which I because I just thought it was so interesting. For the people that hadn’t heard it…
Aaron: It’s a more up to date study, I feel like it could give us a better readout.
John: Okay. But at the end of the day, you’re still looking at basically…my whole point is, you’re still looking at lowering Apo B in total. I mean, you want to have your particle count be lower. And so if you’re somebody who is getting dyslipidemia to the cholesterol side of the fence, that’s one thing but you might be somebody that’s actually you might be a hypo absorber. You might be absorbing lower amounts of cholesterol. You might be synthesizing lower amounts of cholesterol in response to eating saturated fat. You might have very robust LDL receptor activity. But you also might be somebody who isn’t very insulin sensitive and finds that if you’re eating a whole lot of pasta and pizza, then your triggers get wider range and you basically have triglyceride rich particle.
Aaron: I mean, it’s how it all interfaces together is just really fascinating and try to pick it apart for an individual is tricky. But it’s a worthwhile endeavor if you can figure out exactly which bits are going to cause you to spike or your produce in a particular way. If you can get that information that’s going to be really powerful too.
John: Yeah. Well, speak through the triglyceride rich particle for a minute. I don’t want to just kind of leave that hanging. I mean, you know, clearly you have like the Tim Russert example. In this country you may not have heard of Tim Russert but he’s a very beloved host of “Meet the Press,” which is this TV show that’s been running here in the states for a long time, political kind of commentary show. And he passed away very tragically I think in his 50s. And, you know, one of the things that they found and it’s one of the types of situations that people that are trying to educate the public about the importance of your total particle count will tell you is he had very low LDL cholesterol I think because he’d been placed on a standard but I could be wrong. But he had really, really, really high total particle count because of the fact that he was very insulin resistant. And so his body was basically converting a lot of the carbohydrate and sugar that he ate in a triglyceride fat and then they were trying to put it somewhere. So what about that phenotype?
Aaron: From my perspective, when you talk about people who are becoming dyslipidemia on a carbohydrate rich diet, there’s a couple of things that people can do to try and remedy that. And in some regards, you know, there’s the talking about the type of carbohydrate that you intake. So if you go for a more fiber rich carbohydrate and basically slowdown that processing, I think that can definitely have a beneficial effect on limiting that the occurrence about dyslipidemia, lead generation, those triglycerides and the circulation of those. And they can also help basically with the absorption as well, so we know it can affect gut health.
But then there’s also a couple of markers that people might want to, you know, if you’re worried that you’re falling into that category, there’s a few markers that are of interest that you can get when you have your blood work. So the apolipoprotein CIII is one that you’re interested in. That’s like a major component of the very low density low particle. And it’s basically been shown that it’s associated very strongly in people who have like triglyceride, which particle count. So if you have elevated levels of APOC3 in your blood, it could be a marker suggesting that you’re at risk of this dyslipidemia from cholesterol, you know, increased cholesterol intake, increased carbohydrate intake, carbohydrate intake.
John: Yeah, the idea is that with APOC3, it basically increases the length of time that those particles are floating around in the body because usually their halflife is pretty short or their residence time, the time that they’re actually circulating a shortland and they’re either taken up by a receptor or basically recycled in some way. So with the APOC3, is that a VLDL to basically triglyceride rich cholesterol depleted LDL particle that’s small and dense and when APOC3 is expressed on that particle, its residence time is longer so therefore it’s more prone to oxidation?
Aaron: So two things, I think it’s more prone to oxidation because it is held around longer, but I think you can also participate in this deposition, those sclerotic lesions in your musculature. I think it had quite an important role in that explicitly promoted deposition by glycerides, another lipid particles onto the walls of our vascular system. So they’re both a protein.
John: Yeah. And, I mean, for me, that’s why when I hear these total particle conversations it makes a lot of sense to me because the idea is if you have increase in these particles, that’s bad because the more of them there are, the more they could take a “wrong” turn and kind of deposit something into an artery wall that’s not supposed to be there. And then if you have this APOC3 expression on these triglyceride rich particles, they will live longer and longer and longer. They’re basically a taxi that has more gas that can swim around longer and using that extra gas, there’s more of a chance that they could have an accident. And they could have an accident by crashing into your artery wall or they could have something else that crashes into them like, for example, an oxidized phospholipid or some byproduct of oxidative stress the damages those particles, oxidizes them, makes them that much more dangerous when they do damage basically the artery or the…
Aaron: Your vascular system.
John: Yeah, exactly.
Aaron: Yeah, so they do have quite an important role and basically it’s not just as a particle, they can also influence the character of your endothelial cells while making them more sticky. And that’s part of the reason why you can become more prone to developing new lesions. So it’s a really interesting marker, like you say, for people who feel like they may be at risk about dyslipidemia from carbohydrate intake. I think it’s probably interesting as a whole to everyone. Maybe you can answer this John, re you able to test it out with your testing? Because I know mine don’t currently.
John: Yeah, I think I could ask for it the next time I get blood testing done. I’d like to add to APOC3 snips to the gene food test kits as well. But…
Aaron: We should maybe try and get some blood work from our various diet plans and see…because as me as a quite a sort of flexible and very diet type, I feel like my LDL level is quite low all the time. Never really fluctuates based on my diet. So maybe I’m one of those people that maybe need to pay more attention, like you say, to my particle count.
John: Well, based on the scoring system at Gene Food, you would be somebody who is not likely to have cholesterol rich or triglyceride rich particle.
Aaron: And I know for a fact I don’t really have cholesterol rich ones, but the triglyceride rich one has not been tested previously. So it’d be really interesting to see if that actually marries up with what we’re talking about today.
John: Yeah. I mean, I think so. One of the things we’ve talked about, I mean, I’m in the California Coastal area. And that would predict that I would be more likely to have triglyceride rich particle than cholesterol rich particle. One of the things I’ve decided is, yeah, sure my LDL cholesterol lives like 90 to 110. I mean, I think when you were here in New York, you said it’s just on the verge of healthy but I actually think that when you have an LDL cholesterol of 90 milligrams per deciliter, it can go higher for me too. It can go out of this range. But I actually think that that puts you in like the 15th percentile or something based on the Framingham or…
Aaron: The Framingham thing is off the top my head not on top of my head.
John: I think it’s actually a pretty strong percentile. I don’t think there’s a lot of people that are walking around typically with LDL cholesterol like 50 or 60 or 70 is what I’m saying. I think that based on the you know, what’s out there population wise, it’s pretty good. But then when I have my lipids get out of range, when I see the particle count because I think it’s because those particles are full of triglyceride.
Aaron: Yeah. So if you were saying about 70 or 80, that puts you in the second percentile for LDL C.
John: The second percentile. What is 90?
Aaron: Ninety would put you about 10th percentile.
John: Right. In my case, just to share with the audience, so I’m having when…I’m pretty easily able to get my LDL cholesterol into that 90, 92, 95. If I’m not paying as close attention to what I’m eating, it might go to 110, whatever. But it’s usually in that range. If I really blow out what I’m eating, it might go to 115. It’s never been in the red. What goes in the red for me is triglyceride. If I just abuse my body, I need a ton of pizza mescal, triglycerides go through the roof. And to the extent that I see issues in my labs, there’s a discordance between the particle and the LDL cholesterol presumably because there’s a lot more triglyceride rich particle that’s floating around.
But what’s also interesting is that I routinely see my LDL cholesterol get into the 90 to 110 range, which puts me at the best case at the 10th percentile. But there’s a major discordance between the LDL cholesterol number and the cholesterol numbers and the sitosterol because I’ve seen sitosterol get, you know, like 5.7 milligrams per deciliter in the fours. And that’s why I asked you about this conversion from sitosterol the way that they have it listed in the study to the actual to the milligrams per deciliter the way it’s reported on the Boston Heart Diagnostics because that’s a really interesting thing for people to know if they’re looking at hypo absorption. Their issue might be the sitosterol not the cholesterol. And so that’s one of the ways you can see that. I mean, you don’t want your sitosterol at five, six. And I think if there’s a direct conversion, it puts me more towards like the 70th or 85th percentile, which is like really high absorption of sitosterol.
Aaron: Yeah. We’ll go through and convert them into the sort of standard test format results and then we can rapidly replicate those graphs, which is the sort of the numbers that are actually applicable to people, but they’re actually seeing. That would probably be quite a useful thing.
John: Yeah. Actually, for me, that would put me…So I can get my LDL cholesterol to the 10th percentile, but the ranges that I see out are the triglycerides. And then my sitosterol levels, if this is a one to one conversion, there’s somewhere in that 80 to 90 percentile of levels compared to what the 660,000 samples would have shown.
Aaron: Yeah, so you clearly have issues with your sitosterol absorption. And it’s how you pick that apart genetically then.
John: Yep. Okay, cool. So I guess we’ll just get some charts ready for the show notes and we’ll get this published. Aaron, your final takeaway in eggs is eat them as much as you want, it’s not really an issue?
Aaron: Yep, pretty much. Not as much as you want but within reason, honestly.
John: Yeah. And my takeaway in eggs is find out whether you have APOE4, find out what your ABCG5 genes are. If you really want to know, get a sterol panel done so you can see kind of how much of the finest sterols you’re absorbing and then start testing your blood work and see. And if you’re somebody who is a hyper absorber, especially across all three of the sterols, you know, sitosterol, campesterol, and cholestanol and you have APOE4 and you trend towards higher total cholesterol and higher LDL cholesterol, and I would estimate that this group that I’m describing is probably, I don’t know, 15%, 20% of the population, maybe something like that in that range, I would say for those people you might be better off especially if you are not somebody who is prone towards triglyceride rich particle, you might be better off just eating a bowl of oatmeal than eggs. That’s just my two cents. So, yeah, we’re an hour and 10 minutes in egg convo. Appreciate you joining, Aaron. We’re going to do future episodes. I definitely look forward to doing some episodes on our blood experiments. And you’ve been more vigilant than I have with that but looking forward to that. And we’ll see you on future episodes, my friend.
Aaron: Cool. Speak to you later, John.
John: “The Gene Food Podcast” is our attempt to synthesize the latest developments in the fields of genetics, nutrition, and medicine and offer you practical tips and stories you can use in your own unique health journey. If you enjoy this podcast, you can find more information online at mygenefood.com.