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#31 – 21 Eggs A Week Blood Test Results, Cholesterol Hyper-Absorbers, Lp(a), and more with John O’Connor

Nowhere in nutrition are the debates more fierce than with eggs. Some claim eating an egg is like “smoking 5 cigarettes,” while others say eggs are a super food. Who is right? What would your blood work look like if you ate 21 eggs a week for one month? It’s hard to say, but we do know that those of us who are cholesterol hyper-absorbers can see greater changes in blood lipids when eating large amounts of dietary cholesterol. In this episode, John discusses his blood work after a 21 eggs a week for one month dietary experiment. The results, especially for his Lp(a) number are surprising.

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This Episode Covers:

  • American Journal of Clinical Nutrition on eggs and heart disease [1:20];
  • 21 eggs a week diet experiment [5:30];
  • Discussing my APOB result [11:50];
  • Lp(a) particles are cholesterol rich [16:20];
  • Lab tests for measuring hyper absorption [18:00]


The way that advanced physicians in our country right now test people to see why their cholesterol is high is they use sterol panels. So, they use desmosterol and lathosterol at the synthetic pathway. Why do they do that? Because those are molecules that are at the very beginning substrate of a hopelessly complicated biochemical process. Thirty steps on, the body makes cholesterol. So if there’s a lot of desmosterol, it means that what’s happening is the body is making a lot of cholesterol. Welcome to the “Gene Food Podcast.” I’m your host, John O’Connor.

Hey, everybody. Today we are back on the show. I’m sorry there’s been a little bit of a delay in producing new episodes. Today we’re going to revisit the topic of eggs, which is something that Aaron and I talked about in an episode a few back. And we highlighted for our listeners a study that was conducted by the “American Journal of Clinical Nutrition,” which essentially synthesized data that, from epidemiological studies, food frequency questionnaires, and also from a drug trial, and they came to the conclusion that eggs are a food that is not going to move the needle for you when it comes to cardiovascular risk markers. In fact, the authors of the “American Journal of Clinical Nutrition” study said, “Our findings indicate that moderate egg intake, one egg a day, does not increase the risk of cardiovascular disease or mortality among those with or without a history of cardiovascular disease or diabetes. Also, no significant association was found between egg intake or dietary cholesterol and blood lipids.”

And so, Aaron and I talked about this study, and the reason why we did, and for those of you who are regular listeners and are wondering where Aaron is, I’m going to be solo. This is a gene food podcast experiment. I’m going to try to run this episode solo. Aaron has had a new baby and he is fully committed with research and family items, so I’m gonna try to push forward here. And we talked about it because, if you’re listening to this podcast, you’re interested in nutrition. And you are potentially in one of many diet camps, maybe you’re agnostic, you’re looking for answers, you’re trying to figure out what the best diet is for you, trying to figure out how you can eat a heart-healthy diet, and you’re doing your level best to follow the latest research and do what is going to be good for your body.

And you turn on “The Doctors” TV show, or you turn on “What the Health,” or you listen to a paleo-leaning podcast, and you get totally conflicting information on eggs. One side of the coin says, if you eat one egg a day, which the “American Journal of Clinical Nutrition” is saying is neutral, not bad for you, that’s the equivalent of smoking five cigarettes. And they’re saying this with a straight face, and they’re saying this based on epidemiology, a lot of research at Harvard. There’s credible analyses that point in this direction. Whether the data is flawed is up for debate, but there are bodies of literature out there that point in this direction.

And then on the flip side of the coin, you get some really very excellent physicians and commentators, people out there that are very bright and very smart, and they’re saying, look, eating eggs does not cause problems for most people, because of the fact that there’s a rule in the body called cholesterol homeostasis, where our bodies are very good at regulating our cholesterol levels. And the reason why our bodies are really good at regulating cholesterol levels is because they make 80% of the cholesterol. And 80% of the cholesterol in our body is made by our body. It’s made by red blood cells, it’s made by the liver, and, to the extent that you are absorbing any of the cholesterol that you eat in food, which is unlikely because of the molecular structure of that food, the way that the cholesterol in food is structured in terms of its bioavailability for absorption is low.

And that’s something that if you haven’t checked out Peter Attia’s series, “The Straight Dope on Cholesterol,” that’s something I would highly recommend you check out for further reading, and he talks about this and he says, look, you can be absorbing cholesterol from food, but it’s unlikely because of how it’s structured. You can also be absorbing the recirculating pool of cholesterol in the body, because the body is taking cholesterol out of circulation in the liver and then it’s dumping it through the gallbladder into the intestines, where some of that is pushed out when you use the bathroom, and some of it is absorbed. And that’s where I want to focus today, because I did this episode, hopefully as, like, a little mini public service announcement for people that are listening, to reinforce what we talked about in the previous egg episode, which is kind of getting your own health regimen dialed in to see whether you should be eating eggs, if you’re somebody who’s interested in lipids and wants to keep your lipid markers at, you know, optimal range over time.

And what happened to my blood work when I ate 21 eggs a week for about a month, so rather than having, you know, oats or a smoothie or whatever else I would have for breakfast, I specifically had fried eggs, scrambled eggs, sometimes I’d have some potatoes, roast potatoes, but mostly just egg breakfast. And I love eggs. I wish I could have eggs every day for breakfast. What I found, as I went through all of the different markers that the “American Journal of Clinical Nutrition” looked at, because they’re looking at LDL cholesterol, they’re looking at your apo B number, which is your apolipoprotein B, it’s essentially the total number of particles that have the ability be bad for your heart that are circulating in your body. It’s not just LDL. LDL carries an apo B protein, but VLDL also carries an apo B protein.

And so when you’re looking at LDL particle, you’re only seeing the total number of LDL that are on the road in your body that have the potential to take a wrong turn and deposit a piece of cholesterol or an oxidized piece of fat into your artery wall, where the immune system reaction that then causes inflammation that leads to heart disease can begin. There are these other “atherogenic particles,” like VLDL, that are not going to be picked up in an LDL particle count, because they are not low-density lipoproteins. They’re very low density lipoproteins. They’re a subclass, they’re an LDL subclass. And so, we measure, on these more advanced blood tests, we measure for apo B, because apo B does not only give you your, it’s not only a proxy marker for your LDL particle, because there’s one apo B protein in every LDL particle.

It’s also a proxy marker, and [inaudible 00:07:02] just a way of measuring the total number of LDL plus LDL subclass, and the big one’s VLDL. There’s also IDL. There’s chylomicrons. There’s Lp(a). My understanding is that Lp(a), when it’s measured, will actually be reflected in the LDL particle number though. So, from 10,000 feet, the “American Journal of Clinical Nutrition” says, well none of these markers move meaningfully, even when you eat seven eggs a week. Now, I ate 21 eggs a week, but 21 eggs a week is really consistent with somebody who’s trying to get adequate calories and who’s decided that they’re gonna believe in, for lack of a better term, the rule of cholesterol homeostasis. They know that to the extent that their body absorbs cholesterol, and there’s, I think the best studies say that there’s tremendous variability in how people absorb cholesterol. There’s, like, some people absorb 20% of the cholesterol that they eat. Some people absorb as much as 80%.

This affects people differently, and understanding that different people have different metabolic reactions to dietary cholesterol, and eggs are a huge bomb of dietary cholesterol, in our view at Gene Food, as people who are out here and trying to push the envelope on individualized, personalized nutrition, it is important. And so, you have somebody there at home, they’re listening to, you know, the default rule, which is cholesterol homeostasis, and they say, “Well, I’m fine, because if I’m gonna be eating 21 eggs a week, I’m not gonna see any difference in my serum cholesterol.” I didn’t see much difference in my serum cholesterol either in terms of total cholesterol. I’m not gonna see a whole heck of a lot of difference on my LDL cholesterol likely. Maybe it ticks up a little bit if I haven’t been eating any eggs. And to the extent that I do absorb this cholesterol in the eggs, to the extent that the arguments that are being made by the vegan doctors, which are essentially absorption and TMAO, trimethylamine N-oxide, I believe. I wish Aaron was here so he could give me the 100% correct scientific term, but it’s essentially, it’s a metabolite of your gut. When you eat eggs, your gut microbes turn the choline in the eggs into TMAO, and TMAO is something that’s been identified by the “New England Journal of Medicine” as being quite atherogenic, quite bad for your heart.

So they say, okay, well, I have a healthy microbiome. I’m listening to, you know, X and Y influencers, who’s told me that we can identify the strains of bacteria that are responsible for producing TMAO, so I’m putting the eggs into a microbiome that is healthy. Maybe they’ve even had their serum TMAO levels checked, and they’re not expecting that their cholesterol numbers are gonna go up, to the extent that they even care, because that’s definitely a community of people out there that don’t care that their LDL cholesterol is elevated. They think that the lipid hypothesis has been debunked and that there’s other models out there, you know, that explain why heart disease happens, that it’s not, you know, not LDL. We don’t subscribe to those theories here on Gene Food.

And if you’re looking for a really good conversation where there’s sort of a drawing of swords from two leaders of both of those camps, I would highly recommend listening to the Dr. Peter Attia, Dave Feldman podcast interview from a couple years ago. I’ve listened to it probably 10 times, and I think it’s very instructive in terms of listening to two people who are very intelligent, very thoughtful, very well researched people, who are seeing this lipid issue slightly differently. I think it’s fun to watch them draw swords, and my opinion is that it’s very evident in those conversations who has the better of the science and who has the more sophisticated arguments, but I’ll leave that for you to make that decision for yourself.

So, against this backdrop, there’s not a lot of concern. And we go through the markers and they say, okay, well, you know, my apo B might not have even changed, because VLDL is a marker that’s normally gonna shoot up in conjunction with elevated triglycerides, and likely as a result of some kind of insulin resistance. So somebody goes on one of these dietary protocols and they see, look, my apo B is pretty good. The VLDL number being in, towards the floor on a diet that is lower in carbohydrate is not gonna move the needle on the triglycerides, so therefore my VLDL is going to stay pretty good. And then that VLDL number, if it’s really excellent, could overall put the apo B number in the green, even if the LDL particle is slightly elevated.

And this is where it gets interesting on my blood work, because I saw what I first thought was a discordance between my apo B number in my LDL particle, but when I looked at it, they were both, after this experiment, sitting at about 50% by the Framingham, even though you do have this weird situation where my lab, Cleveland Heart Labs, had the apo B number that was in the green, much more liberal with apo B than they were with LDL particle, in terms of what they considered in their risk factors to be low risk and medium risk and high risk. And I speculated, you know, on this blog I wrote about this, that it could be that people, as you have insulin resistance just increasing quite a bit, you’re seeing that people are having higher and higher VLDL numbers, and so they’ve kind of moved the goalposts to make people feel better about having elevated VLDL.

My VLDL was just like the “American Journal of Clinical Nutrition” predicted, really low, and so my apo B was low. Apo B was in the green, I was at, 87 milligrams per deciliter. But here’s the interesting part, and I know this has been technical and, you know, we haven’t done a solo episode, so I’m hoping that you’re following along with me at home, because what I came to next is the reason why I want to do this episode, which is that I didn’t see much in the way of a change in my LDL cholesterol, I didn’t see much in the way of the change of my apo B, which maintained, which was at a level that was just at the very top of what was considered low risk, but I did see a big increase, relative for me, in my L(a) number.

Now, people out there have heard episodes we’ve done in the past with Dr. Joel Kahn. He’s a famous cardiologist and isn’t, he is an advocate for plant-based diets, but he’s written a book called “Lp(a): the Heart’s Silent Killer,” and Bob Harper of “The Biggest Loser,” who is a famous celebrity trainer, he came out and did kind of a public service thing a few years back, and was public about how he’d suffered a heart attack. And then they checked his blood lipid markers and found that his Lp(a) was really elevated. So Lp(a) is a form of genetic bad cholesterol. It’s a traditional LDL particle with an apolipoprotein B protein structure, but there’s something that’s appended to the apo B protein, which, I’m literally saying this because I know that it’s true. I know this is how it’s just described by the biochemists. It doesn’t mean as much to me. I’m not, you know, but it’s a disulfide bond, apparently. That’s the molecular structure of the bond that then attaches an apo A tail to the particle, which makes this mutant particle, and it’s genetically determined.

And the way I think of it is I think of, like, a LDL particle as being like a spherical ball, almost like, let’s say, a basketball. Things can stick to it in the blood and can attach to it. And those things that can stick to the particle, or should the particle itself oxidize, make it particularly dangerous. When I think of Lp(a), and somebody playing along at home who’s, you know, if this is not accurate, please do send me an email, but the way I think about it is is essentially that little a, that tail, that apo A tail, almost acts as something that, like, sweeps things up out of the bloodstream. And one of the things we know from looking at a lot of the studies, there’s a really good study in the “New England Journal of Medicine,” one of the things that Lp(a) has a real affinity for are oxidized phospholipids.

So, you know, you eat some canola oil. It was, the polyunsaturated fats are notoriously delicate. The canola oil was in a heated truck, who was driving across the country. It oxidized. It could have been oxidized and rancid at the time it was made. You eat that oil, and you have some of those oxidized phospholipids in your blood, those oxidized phospholipids bind to that Lp(a) particle. And that’s what weaponizes the Lp(a) particle. The particle floats through your system and takes some of that really bad oxidized sterol, that plant fat, and deposits it in your artery wall. And then your immune system freaks out, and it’s like, “Hey, wait a minute. This isn’t supposed to be there,” and they start attacking that deposit. And then in the attempt to dislodge it, there’s this inflammatory response that happens, and that’s how you get heart disease. That’s my understanding of it. I think that’s the position of the European Atherosclerosis Society and a few others, but that’s how my, you know, nontechnical mind sort of understands this stuff.

And Lp(a) particles, you could think of them as bad, genetically determined cholesterol, they’re very cholesterol-rich. Those are cholesterol-rich particles. And so, my thinking is is because of the fact that I have some mutations in my Abcg5 and ABCG genes, which are a family of genes that we look at in our Gene Food custom nutrition plan, I am absorbing more of these plant fats and also cholesterol. Now, why would I mentioned plant fats? I mention plant fats because the way that the advanced physicians in our country right now test people to see why their cholesterol is high is they use sterol panels. So, they use desmosterol and lathosterol at the synthetic pathway. Why do they do that? Because those are molecules that are at the very beginning substrate of what the body then uses, like, a 30, hopelessly complicated biochemical process. Thirty steps on, the body makes cholesterol. So if there’s a lot of desmosterol, it means that what’s happening is the body is making a lot of cholesterol.

And then conversely, we also test for phospholipids: cholestanol, campesterol, sitosterol. The reason why we test for those phospholipids is because of the fact that if those plant fats are in your blood, it means you absorb them. Unlike cholesterol, which we make. So you can’t tell whether you absorbed it or you made it. You made 80% of it. So it’s all the same cholesterol. So there’s no way to know whether you’re a hyper absorber unless you measure for sitosterol and these other sterols and stanols that are in plant foods, and that your body is supposed to use the Abcg5 nga pathway to kind of kick out.

I think Tom Dayspring, who’s a very famous lipid expert in Virginia, has used the analogy of the Abcg5 and Abcg8 genes as, like, bouncers at the bar. So they’re gonna determine who gets in and who gets kicked out. And, for somebody like myself, who has mutations in some of these pathways, and I believe, just as an aside, that this is essentially the path to diplomacy in cholesterol. I think in the future, what you’ll look at is there won’t be these ridiculous conversations just pushing these statistical averages back and forth at people.

I think you’re going to have people who have identified these pathways. They can say, look, well, I have a mutation in this, you know, I have this variant in my Abcg8 and Abcg5 genes and so, therefore, that’s why, for me, you know, eating eggs is potentially an issue, but for you, it’s not.

And so, they’re measuring for these sterols, and the sterols are gonna be a proxy marker for cholesterol absorption. And the sterols tie back into the Lp(a), because as we just said, they bind, and they make them particularly dangerous. So to kind of bring it all together, for me, I have these genetic pathways that are of an issue. I’ve seen that corroborated when I do get sterol panels done. But, I mean, it’s really a rare physician who orders these sterol panels. It’s a really a rare thing for somebody to have access regularly to their desmosterol and their sitosterol panels to get an idea of what’s happening here. Is this a synthetic issue or is this a absorption issue? And so, that’s one of the ways that we add value on the Gene Food custom nutrition plans, is you can get an idea.

It’s not going to be the end all be all, but it’s going to give you an idea of where you sit in terms of these absorption and synthetic pathways, what your predispositions could be. Our algorithm is scoring that. Now, you could say, well, we could just get that from blood work. Well, yeah, you could get that from blood work, but also you can have momentary lapses in nutrition give you outsized reactions in blood lipid panels, and in other blood tests as well. They could go back to normal once your lifestyle goes back to normal.

If you know the genetic information at the start, you know that there’s something foundationally that you should be looking to. And so, at the end of this egg experiment, I see my Lp(a) goes from what had been 80 nanomoles per liter to 113 nanomoles per liter, which is basically the equivalent, I think of, like 59, 60 milligrams per deciliter, which is getting into a place…you know, I’ve always had mildly elevated lipoprotein(a), but it’s getting to a place where that’s not in a zone where you’d really necessarily want it. You want it lower than that. And so, long, long, long analysis here, concluded is that what I have is I have a situation where my apo B stayed the same eating 21 eggs a week. My total, my LDL cholesterol stayed basically the same, my total cholesterol stayed basically the same, all predicted by the “American Journal of Clinical Nutrition.”

But I saw my particle count go to like 1443, and my Lp(a) go to 113 nanomoles per liter. And because of the fact that my VLDL, which is that insulin resistance marker, was so low, I’m positing that the 1,443 LDL particle, juxtaposed against the apo B, was cholesterol-rich particle. I’m thinking that because I saw an increase in Lp(a), and I saw my LDL particle go to over 1400, eating this many eggs is something where, you know, that’s an increase in cholesterol-rich particle. There’s no way to know for sure. My understanding is that it’s really, there’s not technology out there that can identify exactly what’s in these particles, so you’re kind of left guessing to a degree. But what I want to close with is to say that there’s the possibility for some unique things happening in your body as a result of eating dietary cholesterol, and that sometimes, with dietary fat and cholesterol, there is a tendency to want to make it checkers, but in a lot of ways, it’s chess, because if you’re hyper absorbing cholesterol, that’s one thing, but if you’re hyper absorbing cholesterol and you have elevated Lp(a), that’s another thing, because of the fact that you’re not only worrying about the cholesterol coming into the system, you’re worrying about the sitosterol levels getting too high.

And those plant fats, they get into the system, whether they’re pre-oxidized in the form of vegetable oil before you eat them, or whether they, for whatever reason, oxidize when they’re in your body, and then make their way into contact with an Lp(a) particle. That to me seems like a phenotype that needs to watch out for cholesterol, sterol, and especially oxidized fats. And just as we don’t know, I don’t think, usually what’s inside of an LDL particle, I don’t think there’s a ton of good tests out there on the market for oxidized phospholipids, but I think if you have hyperabsorption of cholesterol issues, it means that almost by definition, you’re probably absorbing sterol. And if that’s true, I think knowing your oxidized phospholipid levels would be pretty interesting as well, because I think that that would speak directly to the atherogenicity of the Lp(a) particle count.

So, that is my egg experiment. I was pretty much chalk until I hit LDL particle, and most especially, Lp(a). That’s my biggest Lp(a) number I’ve ever had. And so, because of the fact that, and I recognize this is very far from a peer-reviewed study, so this is totally anecdotal, but I can look back on my best ever lipid numbers, and I know that there was not just an avoidance of sugar, but there was also an avoidance of dietary cholesterol. And it seems to me that my Lp(a) ebbs and flows a little bit based on my status as a hyper absorber of cholesterol.

So, our first solo episode, maybe the last, I’m not sure how you enjoyed that. I think it went okay. Let me know in the comments, and thank you for listening, and we will see you on future episodes. Have a great day.

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 enjoyed this podcast, you can find more information online at

John O'Connor

John O'Connor is the founder of Gene Food, a nutrigenomic startup helping people all over the world personalize nutrition. John is the host of the Gene Food Podcast and a health coach trained at Duke's Integrative Medicine Program. Read his full bio here.

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