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#09 – Cholesterol Deficiency, Eating for Mental Health, Optimizing the Carnivore Diet, and Benefits of Inflammation with Chris Masterjohn, PhD

Despite a shifting scientific landscape, dietary cholesterol is still a hotly debated topic. Joe Rogan and Chris Kresser eat eggs every day, while the plant-based community still loves to highlight the supposed dangers of dietary cholesterol. High cholesterol has historically been associated with poor health, but is there a range where cholesterol levels get too low? Our guest in this episode of the podcast believes the combination of a genetic predisposition combined with a strict vegan diet caused him to develop a dangerous cholesterol deficiency. A former assistant professor of Nutrition Science at Brooklyn College, Chris Masterjohn, Ph.D. is one of the smartest minds in nutrition.

Chris shares a fascinating story of how going vegan caused him to develop nutrient deficiencies which led to a battle with mental illness and anxiety. Chris’ subsequent focus on nutrient-dense, animal-based foods restored his health and changed his perspective on how the foods we eat play a large role in cognitive function. We cover a wide range of topics with Chris and he takes a number of controversial positions in this episode, including who shouldn’t eat eggs, nutrient deficiencies that are most likely to arise on a carnivore diet, whether “fancy” blood testing metrics like LDL-P are necessary to gauge cardiovascular health, why some people fail on vegan diets and much more.

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This Episode Covers:

  • Chris’ journey into Veganism and battles with anxiety [6:00];
  • Cholesterol deficiency and genetic explanations for Chris’ trouble with a Vegan diet[16:30];
  • The new thinking on dietary cholesterol [24:00];
  • Who shouldn’t eat eggs? [27:00];
  • What is an “optimal” lipid profile? [32:00];
  • Chris’ take on arachidonic acid and the role of inflammation [39:00];
  • How linoleic acid depletes EPA and DHA [45:48];
  • Testing for nutritional status and optimizing carnivore diet[49:00];

Discussion:

There are actually quite a few studies which have found an association between strict Vegan diets and issues with mental health. This is NOT to say that all, or even most, Vegans and Vegetarians are depressed. However, there is growing evidence that mental illness may be a bi-product of Vegan diets for some people. The issue is well summarized in this blog on the Psychology Today website. We also touched on some of these issues in our episode with Dr. Kahn.

This is a good article discussing the concordance / discordance issue for LDL-P and why measuring LDL-P is important.

Here is the commentary I discuss with Chris by a physician who believes LDL-C greater than 190 mg/dl can be a sign that a patient may have undiagnosed sitosterolemia.

Here is a link to sign up for Chris’ Nutrient Deficiency “The Ultimate Cheat Sheet.” Use Coupon Code GENEFOOD for a 20% discount.

Transcript:

John: Welcome to the “Gene Food Podcast.” I’m your host, John O’Connor. Hey, guys. Before we introduce today’s episode, I wanted to draw your attention to our sister site, which can be found at www.leafscore.com. At leafscore.com, we’ve created a database that’s growing every day, we’re publishing new content. We have a lot of the research done and not all the content is live on the site yet, but we’re adding more every day. We’re highlighting non-toxic products. We started doing research for Gene Food on the toxicity levels of products when we learned that the body’s ability to detox certain environmental pollutants and other toxic elements is driven in part by genetics. And so we got really interested in this topic and we started creating a lot of content. That content grew too big for the Gene Food site so we had to move it over to leafscore.com. So, you’ll have everything there from products for the bedroom, clothing, children’s toys, dog toys. We’re highlighting companies and brands that are creating non-toxic products that you can trust and that you can use in your everyday life and use with your family, with some degree of confidence.

With that said, that out of the way, today’s episode is a really good one. We brought on, at the request of our audience after our methylation and MTHFR episode, a gentleman by the name of Chris Masterjohn Ph.D. Chris holds a doctorate in nutrition sciences from the University of Connecticut and he was also an assistant professor in health and nutrition sciences at Brooklyn College. He is undoubtedly one of the smartest minds in nutrition science. He’s a meticulous researcher. He has opinions on all of the controversial issues that come up in the nutrition debates and he defends them with data, he knows biochemistry inside and out. He’s a really fascinating guy to talk to. And in today’s show, he took positions on a whole host of issues that our audience is gonna wanna hear. He talked about how a vegan diet caused him to develop severe anxiety and mental illness and how he was able to effectively cure himself by changing his nutrient intake with certain foods. We talk about lipids, we talk about total cholesterol, and why he felt like a deficiency in cholesterol was actually a problem for him and how he used food to come back from that. We talk about omega-3 fatty acids, who should and should not eat eggs, the carnivore diet, all sorts of stuff with Chris. We’re really happy to have him on the show. So, without further ado, please enjoy. Here is Chris Masterjohn, PhD. I didn’t know you were in New York. Are you visiting or do you live in New York now?

Chris: No. I live in New York.

John: Oh, my God. You’re in the city?

Chris: Yep.

John: We should have done this in person. I had no idea. I thought you’re in Minnesota for some reason.

Chris: Oh, nope. You thought I was where?

John: I thought you were in Minnesota. I don’t know why. I was gonna ask you first off where were you located?

Chris: I was never in Minnesota, but I was in Illinois. 2014 I moved here.

John: Oh, okay. Cool. Where in the city are you?

Chris: I live in Astoria.

John: Cool. We should link up, man. Yeah. I didn’t know we are neighbors. That’s crazy. We could’ve done an in-person show. But in any event, I know we’re gonna have a hard stop here at the end of the episode, so I want to jump right in and…

Chris: Sure.

John: For those people who have not heard of you…I know some of our audience requested that we have you on after our MTHFR episode a couple of back. But for those people who have not heard of you, do you wanna give a brief intro, your background, your website, all that good stuff?

Chris: Sure.

John: And then we’ll get into the meat of the show.

Chris: Sure. So, I’m Chris Masterjohn. I have a Ph.D. in nutritional sciences. I went down the academic route for a while doing research. My doctoral research focused on toxic byproducts of diabetes metabolism and how we can use food and nutrition interventions to mitigate them and improve diabetes function. My postdoctoral research at University of Illinois was into interactions between fat-soluble vitamins and I was assistant professor of health and nutrition sciences at Brooklyn College in Brooklyn, New York for about two-and-a-half years where I continued a little bit of that research and did a lot of teaching. And now I work on my own with my goal being to just immerse myself in really complex science for a long time sometimes, for a short time sometimes, and just come up to the surface with new ideas that people can use to improve their health on a practical level or new ways of understanding and explaining even the complex things to people who need that detail to help on shed new insights and new light and new ways of understanding things better.

So, I like to focus on theoretical and practical stuff, connecting them whenever I can. And the way that I got here was I was always very interested in health, especially since my teenage years I watched my mother go through her own health journey that brought her from the point of pain every night from fibromyalgia that kept me awake, it was so bad, to completely restoring her bodily function to being maybe not completely pain-free, but completely functional, good sleep, not in pain every night. And that had a big influence on me. But being 14 or so at the time led me down a lot of paths of maybe youthful idealism and ignorance before I really understood things. One of my forays was into veganism and that was life-changing in a bad way. When I was a little kid, I had quite a number of cavities, when I was 12 or 13, I developed some significant anxiety problems, had digestive disorders going back since I was a baby. But all of these things got 10X worse when I was a vegan to the point where I went into the dentist and found out in a single sitting I needed two root canals and had over a dozen cavities that needed fillings.

John: Wow.

Chris: During that time, I think a lot of my anxiety problems from when I was 13, 14 traced back to just smoking a lot of pot at that time. I haven’t since I was 15.

John: Yeah. They’re saying now that smoking weed, a lot of weed before age 25 is like that period where you might wanna stay off the pot. Is that your understanding?

Chris: Well, that ship has sailed for me. Yeah. I haven’t looked at the research in detail, but there has been some stuff coming out around when the brain is still structurally achieving its structural organization in the adolescent years, which by some research I guess by inference that process is thought to carry into 25-ish. But while the brain is structurally modeling itself, then you’re going to affect long-term, permanent or semi-permanent structures in the brain, not just acutes effects. So, if your brain is fully developed and you’re using a drug, maybe you’re gonna desensitize yourself to that drug by down-regulating some receptors or maybe even some more synopses or something like that. But if you’re taking that same drug when the brain is achieving its overall structural organization, then you might be affecting the anatomical development and density of certain regions of the brain just in how much tissue is there and things like that. But anyway, I had panic attacks from that and my triggers for panic attacks were basically flashbacks to some of the craziest experiences that I had smoking pot.

John: Wow. Okay. What were some of those?

Chris: Oh, intensely hallucinogenic experiences. The first time that I smoked out is by myself and I think it was laced with something but I don’t know what. Anyway, and I did think that I was gonna die at that point. But anyway. So, the point here is that during my teenage years, the triggers were all about specific experiences that were semi-traumatic for me. With anyone who has panic disorder, panic attacks can lead to agoraphobia, which is being afraid to leave your house because you avoid your triggers and if you avoid your triggers, which this conversation is so intensely socially relevant right now, but with panic disorder, if you avoid your triggers, you will have more and more triggers and you will be afraid to leave your house at some point.

But during my teenage years, before I was vegan, the generalization of triggers was not that extreme for me. It was like smoking pot was a trigger and then I’d generalize that to smelling it. But I could just like not hang out with people who were smoking pot and I was fine. So, that’s an example of generalizing the trigger a little bit. Probably, I should have been able to smell it but that’s a very narrow generalization. In the extreme scenario, after you avoid your second trigger, you develop a third one and then you avoid that one, then you develop a forth one. That’s basically what spiraled out of control when I was vegan. I started being afraid to eat all of the food in my house because I thought that it was tampered with, that it was drugged or poisoned or something like that.

And sort of worst-case scenario to paint for you, I remember one time where I was spending 20 minutes inspecting this seal on my veggie burger and I couldn’t find any evidence of tampering so I kept looking for it. And I looked for it until I damaged the wrapper and then I wondered if it had already been damaged or if I just did that. And then I’d be terrified that it had already been there and it just took me 25 minutes to notice it. And so I wouldn’t eat the veggie burger and then I’d be angry at the veggie burger for not being edible and angry at myself for not being able to eat anything. I’d throw the veggie burger across the room in anger and then I’d go pout on my bed that I couldn’t eat anything.

My memory from that time is pretty bad too. I was talking to my mom recently and she reminded me of the fact that I had gone to the emergency room for panic attacks. I actually even as I’m digging into my memories, I do remember one time, but I don’t remember more than one time. And she says that she brought me to the emergency room six or seven times because I demanded it. And this is not when I was 3, this was when I was 20. So, my memory is really sketchy from that time. In fact, I would say there are two times in my life where my memory is pretty sketchy and one is when I smoking pot several times a day and the other is when I was vegan. Veganism and smoking pot have very similar effects on my brain. But anyway, so, it was pretty bad. This was tremendously worse than I was 13, 14, 15 and borderline like non-functional.

So, the turning point, so there’s an intellectual turning point and experiential turning point. The intellectual turning point was when I was working in the dining hall as an undergrad history major and my boss gave me a pamphlet on raw milk. That pamphlet was produced by a farm who followed the work of Weston Price and it talked about the work of Weston Price and how he had found the cure to tooth decay. And this was right after I had gone into the dentist and found out that I had over a dozen cavities and needed two root canals. So, I’m like, “Freedom from tooth decay,” I want in on that for sure. So I go and I go up to the 24th floor of the UMass Library and find the hardcover second edition, 1945 printing of “Nutrition and Physical Degeneration,” which is Price’s magnum opus.

Price was a dental researcher, the head of the research institute of what became the American Dental Association later for about 25 years looking into the causes and consequences of tooth decay in a laboratory research setting and also in the clinical setting of patients. And then he decided at one point that because…and he was working in the 1900s, 19-teens, 1920s on this. And then in the 1920s, the nutrition in America at that time is so bad, much worse than it is today for all its faults today. Because at that time, two things were…one thing and then a second thing were happening. And so first thing was we were developing the technology to refine foods faster than we were developing a knowledge of what was in the foods that we’re taking out. So, the discovery of the vitamins lagged the refining of foods. And when we first started refining white flour to make fluffy bread with a longer shelf life, we had no idea that we were taking vitamins out of it. In fact, because we didn’t know about those vitamins, we also didn’t know that there was a reason to eat something else besides Wonder bread.

So, initially, the intake of the refined foods is really high, there’s no effort to fortify the foods with things that prevent nutritional deficiencies. That came much later because we didn’t know about those things. And then on top of that, as Price’s research is continuing, eventually the Great Depression hits and now all of a sudden people can’t even afford good food. And so my grandmother during the Great Depression, a typical meal for her was Wonder bread topped with Crisco and sugar.

John: Yeah. Jeez.

Chris: That’s not a meal.

John: It’s not the breakfast of champions.

Chris: No.

John: Your story, to me, is absolutely fascinating for a few reasons. One, for people that have not heard Chris do a previous interview, he’s basically somebody who…he’s an influencer who’s quoted and cited very often by nutrition influencers. So, your name came up in the Joe Rogan debate between Joel Kahn and Chris Kresser. I know Chris Kresser is cited to your work on TMAO and you’re somebody who’s just super credible on this stuff. I think one of the things that’s so cool about the story that you just told is just being, frankly, just brave enough to say, “Hey, this diet didn’t work for me.” Because there’s so much that’s being pushed, especially on kids these days with veganism. Not to say that everybody is gonna have that reaction to a vegan diet, but I feel like stories like yours are almost like if you have the state of the union address and the party that’s in power gets to speak to the congress and then CNN chimes in with the dissenting opinion for a little bit. That’s what your story is to me. It’s like, “Hey, look, this doesn’t work well for everybody.” And knowing how deep in the research you get, the thing that I’ve…as I’ve heard you tell that story before, and the thing that I’ve been fascinated and wished I could ask you was how do you piece together in terms of whether it’s snips, whether it’s biomarkers you were low on? Mechanistically, why do you think you developed this inflamed mental state on a vegan diet specifically?

Chris: I can’t say anything for certain and I’m really looking forward to getting my whole genome sequenced, which I think will provide some insights on this. But I have some ideas and the leading one is cholesterol deficiency. So, I have the most data supporting cholesterol deficiency. So, first of all, I’ve never measured my cholesterol in my life to have the total cholesterol be higher than 160.

John: Wow. Okay.

Chris: When I was a vegan, my total cholesterol was 106. And so I clearly have unidentified genetic factors that lower my cholesterol and a vegan diet clearly lowers them much more than any other diet. When I’m talking about 160, I had my cholesterol between 140 and 160 when I was eating really high fat, high cholesterol animal products, 90% animal product diet.

John: And do you know what your LDL particle count was on that diet as well?

Chris: No. And I don’t give a damn what my LDL particle count is. I’ll probably never measure it because…

John: Okay. Good.

Chris: Why would I care what my LDL particle count was if my total cholesterol was 106? Clearly, the issue…

John: This is why I’m so happy to have you on the podcast though. To me, that’s a fascinating statement that you just made. Riff on that. Why would you not…My understanding is like your LDL particle count, if it gets too high, more taxis on the road, more risk for heart disease. Why?

Chris: Yeah. So, why would I care about that if my maximum cholesterol ever measured is 160 and I tend towards low cholesterol and neurological problems from those?

John: Okay. I got you. So, you’re just saying that as a practical matter, if your total cholesterol is super low, then it’s very likely that your LDL particle count is gonna be super low too.

Chris: I guarantee you if I ever have cardiovascular problems, it’s gonna be from high blood pressure, it’s not gonna be from high cholesterol. So…

John: Cool.

Chris: …who cares about what my LDL particle count is.

John: Great.

Chris: I guess this is…I’m way more concerned that I’m gonna have serious neurological consequences from cholesterol deficiency at this point actually. So, as a followup, the reason that the cholesterol hypothesis has re-emerged…I resisted thinking about it for a long time even though it was the only data point that I had that was convincing. So, obviously, I could point out to you a bunch of nutrients that are harder to get on a vegan diet than on a then on an omnivorous diet or carnivorous diet. But at the end of the day, I was probably taking a multivitamin some of the time. I was definitely taking zinc, I was definitely taking B12. All the key players were things that I was supplementing with that you would expect.

John: What about fatty acids like DHA and stuff like that?

Chris: I often took algae oil DHA. Maybe my arachidonic acid ran low because I wasn’t taking vegan arachidonic acid. You can get that made from some kind of mushroom. I don’t even know if that was available at that time. Yeah. I was definitely taking DHA. I was taking anything that you would really expect. And so the ideal candidate to explain my situation would be something that is very high in organ meats, which is what…And we cut the story short, but the short solution of that story is I started eating a lot of animal products focusing on nutrient density, especially organ meats and everything went away. That’s a short version of it. And so the ideal candidate is something that’s really low in vegan diets, isn’t in any of the supplements I was taking at that time, and is really high in organ meats. And so a defect in this synthesis of something that fits that criteria would be the best way to explain my experience. And I happen to have data showing cholesterol is highly and usually low during every time point in my life and was especially low at that time.

But I think I resisted it in part because it seemed like too simple of an explanation. Although, why would I want a more complicated one if I have a simple one? [inaudible 00:20:58] But then the other thing is the best example of a defect in cholesterol synthesis is Smith-Lemil-Opitz syndrome or SLOS. And SLOS is actually very plausible as a carrier because the carrier rates are in some study 0.5% of the population, which is actually a lot of people, especially if you narrow down the population of people who have unusual problems. At that point, I was in the 1% of people who had strange problems. Other population studies show one to 3% of a certain population. So, being a carrier is pretty plausible. There’s not much research on the health effects of being carrier status except that they have a high risk of violent suicide compared to the general population. So, there’s obviously something neurological going on in the carriers, but no one really cares. And I think that’s very largely driven by the bias towards thinking that cholesterol is bad and we wanna reduce it on a population level. And there’s not a lot of people worrying that people are walking around with a cholesterol of 150. Like if you go into the doctor with a cholesterol of 150, that doctor is gonna pat you on the back and…

John: Say you’re doing great.

Chris: …congratulate you that you don’t need a statin. So, what happened more recently was I developed clear neurological problems when I started taking terbinafine, which is an antifungal drug because I had a fungal infection. I don’t wanna go into detail about why, but I’ve been trying to explain why I had these neurological effects from terbinafine. And so I did some more research on it recently and I found that the way that it acts as an antifungal is to decrease the fungal equivalent of cholesterol in the cell wall of the fungus and it’s 65% effective against the human version of that enzyme. So, it’s theoretically possible that it lowered my cholesterol by 65%.

John: Wow. Okay.

Chris: And the maximum effect of terbinafine on that enzyme is actually…I did these calculations over and over again. I should have someone check them to make sure, but I’m pretty sure it’s at least one or two orders of magnitude under the typical plasma concentrations of the drug. So, when you take that drug, it probably has maximal effect on inhibiting cholesterol synthesis. And so that’s why I started looking into it again. And when I did, what I found was…So, the reason I was dismissing SLOS is because usually to have a clinical effect means probably there’s an abortion of the embryo or fetus and if they’re born, they’re retarded and autistic and really severely injured with physical, anatomical birth defects. Though I don’t have any of those. But I recently found that there have been mutations identified in certain populations including ones that I’m from that don’t lead to any physical abnormalities and lead to very mild effects with cholesterol levels as high as 139 but still lead to social impairment and to eczema, both of which I have, and various other neurological effects from it, and affects the eyes. And so now everything is very plausible. So, that’s where I am right now.

John: Okay. Cool. And so can you educate the audience who’s listening. The thinking in cholesterol has shifted over the years, there’s still such a heavy debate. You have the Dr. Gregors [SP] on the plant-based side saying, “Don’t eat dietary cholesterol. It’s terrible for you.” You have people that are, I believe you’re more part of this camp that are in the Kresser, a Masterjohn camp, let’s say, Peter Attia. The new science is that for most people, you eat dietary cholesterol, you don’t absorb it the way that it’s structured molecularly and eating dietary cholesterol is not gonna raise your serum levels of cholesterol. Synthesize for us the new thinking on cholesterol for people that aren’t familiar with this conversation.

Chris: Well, let me tell you the facts as I see them and then if we wanna unpack parts of those we can. So, the basic facts are everyone absorbs cholesterol. Some people absorb more than others. Most people who absorb cholesterol downregulate their own production in proportion so that their cholesterol levels remain relatively stable. But there’s variation in that and it’s probably about two-thirds of people have very little to no effect on their cholesterol levels when they eat three or four eggs a day. Well, a little less than one-third have a rise in LDL and HDL that doesn’t affect the ratio, and about one 1% or a little less have a really big spike in LDL cholesterol. Now, vegans critique this by pointing out that almost everyone who those studies are done in are already eating cholesterol, at least an egg’s worth a day when those studies are done. And so they’re missing what happens when you drop your cholesterol to zero. And I think they’re probably right about that.

My experience suggests that when I was a vegan, my total cholesterol was 106 and when I was eating lots of animal products, it was 160. That could be from saturated fat and cholesterol synthesis, but it could easily be from dietary cholesterol. So, I think they’re right that you’re gonna have lower cholesterol levels on a zero cholesterol diet. You’re gonna get a little bump from having any cholesterol in your diet. So, if you’re an omnivore, you’re gonna be higher than if you were vegan. And then after that, if you eat one egg’s worth or two eggs or three eggs or four, it’s got a two-thirds chance that it’s gonna practically nothing. It’s got a one-third chance that it’s gonna raise your cholesterol, but not in a way that is thought to directly impact your risk of heart disease. And you’ve got a 1% chance that you’re gonna have a really bad reaction of that cholesterol in terms of your lipid profile.

John: Okay. So, in light of that, we’re establishing this new consensus that for most people, eating eggs is not gonna be something that’s gonna cause disease. But who shouldn’t eat eggs in your opinion, if anyone? And also, what is your opinion on whether and when arachidonic acid is inflammatory?

Chris: Sure. Okay. Those are two completely different questions only connected by the fact that cholesterol and arachidonic acid are both in eggs. So, let’s separate them out. So, the short answer and the nearly complete answer is the people who find that eggs adversely affect their lipid profile in a way that can’t be compensated through other things that are less important than eggs in the diet should not eat eggs. I guess you could identify some candidates based on probability that that would apply to them, but it’s borderline pointless to do that. So, if you have familial hypercholesterolemia, there’s a good chance that this applies to you. There are genetic variations in cholesterol absorption. If you’re a hyper-absorber, it’s probably more likely to apply to you. But these things are like…

First of all, almost no one who has genetic familial hypercholesterolemia has a diagnosis of it because the doctors don’t see the point of doing a $2,000 genetic assay when they’re just gonna put them on a statin. So, you don’t even know that anyway. And then second of all, there’s tests that make inferences about your cholesterol absorption. I think the Boston Heart Lab is one of the major ones that offer these tests. But there’s some…I haven’t researched it intensively, but there’s some questions about how good the markers are. But more importantly…

John: You’re talking about sterol absorption panels. Yeah.

Chris: Yeah. The sitosterol and decimosterile [SP]. And they measure a couple of them. They take some ratios and they make an inference whether you are a hyper-absorber or not or whether you’re a hyper-synthesizer or not. Those kinds of mechanistic things are good for predicting probability and they’re good for explaining outcomes, but they don’t tell you what is, right. So, the thing you really care about is your lipid profile. That’s not the thing you really care about, the thing you really care about is your disease risk. But the best estimate here that’s central to everything that is most closely related to how these things impact your cardiovascular risk isn’t any of those markers or the genetics, it’s your lipid profile. And if we can get better information about how much is oxidizing and stuff like that, that’s closer to the point. But basically, everyone is getting their cholesterol tested. Most people are getting subfraction into at least HDL and LDL, a lot of people are getting particle count and all that stuff. I doubt that it frequently saves any time or effort to try to predict forward based on genetics or absorption markers rather than to just look at your lipid profile, look at some of the five or six big things that affect your lipid profile, try to institute the ones that have the least negative impact on your nutrition, and then use as last resorts something like egg restriction if it comes down to it.

The thing is eggs are really great sources of nutrients and so if you can get your lipid profile optimized without restricting eggs, you should do it. It doesn’t matter if you’re a hyper-absorber or if you have familial hypercholesterolemia, you should do it. If I had familial hypercholesterolemia, probably cholesterol restriction is important, but I’d be restricting it from meats and from cheese first because I just think that eggs have more nutrients that are harder to get it from. And if I was putting butter in my coffee, I’d cut that out before I’d cut cheese out because cheese is more important than butter from nutrition rates. So, look for those super-obvious drivers…or you can probably lower your cholesterol by taking psyllium husk. That’s probably better than cutting eggs out of your diet. So, I think you just have to look at…Basically, in the order of priority, you wanna protect eggs in your diet because they’re very nutritious, but you take them out if it’s the only way that you can optimize your lipid profile without doing anything worse to your nutrition.

John: And before you get to arachidonic acid, so optimizing the lipid profile for you, you said pretty clearly that your total cholesterol 106 for you is sub-optimal, triggered cognitive issues, and you like it, it looks better at 160 or so.

Chris: Oh, I’m probably gonna try to get mine up to 180 or 200. Actually, I’m gonna do some experiments.

John: One-eighty or 200 for you is optimal. So, somebody at home, they’re like, “All right. Well, I’m gonna use this as a framework.” What does an optimal lipid profile look like in your view in terms of the big ones like LDL cholesterol, total cholesterol, HDL, etc.?

Chris: Yeah. So, I’m super-conservative on this. A lot of people are gonna listen to me and then they’re gonna be like, “This guy is an old school quack.” So, I think the most important things are, first of all, huge red flag if your total cholesterol is over 300.

John: Okay.

Chris: If your total cholesterol is over 300, you probably got a thyroid problem or familial hypercholesterolemia and you need to get on that stat. After that, then I think the total to HDL cholesterol ratio is the most important thing to look at in terms of lipids. A lot of people in the low carb community wanna look at the HDL, the triglyceride ratio. It’s a good marker of insulin resistance and I think low carb-ers like to look at it because low carb diets tend to improve that. In the general population where not everyone is a diabetic, it’s not the best predictor, lipid-based predictor of cardiovascular risk, the total-HDL cholesterol ratio is. And I do think that it can be good. Probably everyone should at some point get Apo B and LDL particle size and count and take a look at those. The main reason being to look for the unlikely but possible situation that there’s discordance between the risk estimates.

John: Okay.

Chris: I would say overwhelmingly if you’re flagged as a red on your LDL particle count, you probably have a high total-HDL cholesterol ratio and you probably would have saved some money if you just measured your total to HDL cholesterol rate. So, there’s cases where that’s not true and I think you wanna know when those cases are, but I don’t think for like a yearly or quarterly lipid measurement that everyone needs to get the fancy stuff. I think over 90% of cases, the total-HDL cholesterol ratio is good enough. And I would say that the things I would be looking at would be total-HDL cholesterol ratio should be under 4.0. Ideally, it’s 3.0. If it’s a little under 3.0, that’s really good. And I’d like to see that concordant with the total cholesterol not being that high. So, like I said before, over 300 is a red flag for me. If someone’s got a 375 total cholesterol and their total-HDL cholesterol ratio is 2.7, I’m still concerned. And so at that point, I would start trying to understand why. And thyroid is a big thing to look at, especially if the total is really high and especially if the sex hormones are low.

But inflammation and fiber intake are probably the two and inflammation goes back to exercise, dietary quality…obviously, there’s inflammatory diseases. But outside of specific inflammatory diseases, chronic inflammation I think is mostly about body composition, dietary quality in terms of refined versus unrefined and micronutrient adequacy and fiber intake where more plant fiber is generally…or a higher intake of unrefined plant foods is usually going to be good outside of…there are exceptions like some people, plant foods make their irritable bowel syndrome worse or something like that. So, with specific diseases, there’s that. But I think inflammation, body composition, thyroid, and fiber intake are the big modifiable action items that you can work on if your lipid profile is out of control. And so I would just focus on those key drivers in response to something that doesn’t look good most of the time. And yeah, there’s lots of other markers that you can drill down into. I’m not saying they’re not useful. I just think that there’s a lot of people who think they always need the fanciest stuff and I don’t really think that’s true.

John: A lot of these blood tests are just not accessible to people or they’re just way too expensive. Just for the listeners at home who might have had a little bit of confusion about this whole concordance/discordance issue, what Chris is saying is that there was is the famous Tim Russert case where Tim Russert had really low LDL cholesterol, but he was still at very high risk for heart disease because he had triglyceride-rich LDL particles. So, when he had that test done, it would have looked okay on the LDL cholesterol front, but his particle count was actually much higher than his LDL cholesterol count. So, that’s discordance. So, that’s where you actually would wanna have the LDL particle because it would clue you in that you basically have triglyceride-rich LDL particle.

Chris: Yeah. And I think that’s something where you wanna drill down on that once or twice or three times to make sure you don’t fall in that category. If you do fall into that category, then at that point your LDL particle count, triglyceride-rich LDL particles become your routine marker because you know it’s important to you. But if you do the routine, most accessible, obvious, standard testing all the time and you do the fancier testing a couple of times and you know that everything agrees with each other, then in that case, I think you can mostly fall back on the more conventional markers.

John: Yeah. It can be overkill to get too in the weeds on this stuff. One, just as a side note that I think is interesting is I found a researcher, I forgot the name of the physician but he’s in Utah, and he claims in some of his articles that if you have an LDL cholesterol of over 190 that you’re gonna wanna start looking for sitosterolemia at that point because you could be hyper-absorbing plant sterol that could be adding into that LDL cholesterol number. I know you just said that you think the whole sterile thing is not all that proven in terms of heart disease, but I’ve seen videos you’ve done about the dangers of vegetable oils, oxidized fats. I think that ties in neatly with…given your take on this whole arachidonic acid issue, which I was thinking last night, I’m like, I definitely wanna ask him about that because I wanna know what his take is. So, I wanna give you the floor to just chat for a minute about your take on arachidonic acid.

Chris: Yeah. So, arachidonic acid, your original question was when is it inflammatory? And so first of all, inflammation is a good thing. Inflammation is why we’re not always dead or why we’re not all dead from infectious diseases. Inflammation plays an important role, not just in defending its pathogens, but also in cleaning up gunk, debris of dead and dying cells, restructuring tissues. It’s not a bad thing. So, the question then becomes, when does arachidonic acid contribute to inflammation that shouldn’t be there is probably the more relevant question. But in general, arachidonic acid always contributes to the initiation of inflammation whenever inflammation is present. It’s just that arachidonic does other things too. So, arachidonic acid always, in every instance, is the key thing that shuts off inflammation when you resolve it. And if you try to block arachidonic acid functioning, for example, with Cox inhibitors…Cox inhibitors are most of the non-steroidal anti-inflammatory drugs, the over-the-counter medications you’d use to manage inflammation inhibiting enzyme called Cox inhibitors.

They attenuate the peak inflammation as well as the return to baseline inflammation. So, let’s say you had an inflammatory episode and you didn’t take a Cox inhibitor, you would have higher peak inflammation. So, at the worst point, it would be worse and then you would go all the way back down to baseline and completely resolve it. Take a Cox inhibitor in the same scenario, you don’t get as bad at the peak inflammation. So, it’s the worst case of how red, how inflamed you are, how whatever is not as bad as it would have been without the Cox inhibitor, but you also never fully return to baseline because you impair the resolution of the inflammation as well. What do you wind up with? Long-term, chronic, low-grade inflammation, which is thought to underlie a host of diseases. So, inhibiting arachidonic acid metabolism isn’t something you want.

There are other cases where arachidonic acid is just straight up the anti-inflammatory things. So, in the gut, arachidonic acid metabolized by the Cox enzyme to produce the same exact things that initiate inflammation elsewhere is what allows you to tolerate foods in your gut. So, take the arachidonic acid out of the equation or block its metabolism, you’re gonna wind up with food intolerances. So, arachidonic acid is just, overall, a good thing. I don’t think there’s any situation in which you wanna block arachidonic acid from functioning or lower its level in the diet. And I think one of the important things here is your tissues regulate how much arachidonic acid there is in your cell membranes. The only way you can lower it is to become essential fatty acid deficient. So, it’s just not a sensible way of thinking about how to manage inflammation. And I think there are other things that are relevant to inflammation. So, for example, when you resolve inflammation, you start that process with arachidonic acid, but you also wind up pulling on DHA, which is an omega-3 fatty acid.

Most people in modern population are more likely to have deficient levels of DHA in their cell membranes than they are arachidonic acid. And so focusing on restoring the DHA content of cell membranes is a very sensible strategy because a lot of people don’t get enough. Then focusing on not trying to block arachidonic acid function with Cox inhibitors is actually a really practically relevant strategy because over the counter anti-inflammatory drug is the most commonly consumed drugs in the world. So, most people are inhibiting arachidonic acid function in ways that favor chronic low-grade inflammation. So, restoring DHA and not taking over-the-counter anti-inflammatory medications are probably the two most important things you can do to avoid harmful effects of arachidonic acid in inflammation.

John: So, in your view, it’s not restricting arachidonic acid, it’s up-regulating or eating more DHA, getting more sources of omega-3 fats as opposed to trying to get the omega-6 fats out of the diet.

Chris: No. I think now when we say omega-6, now we’re conflating different fatty acids here. So, I think most people consume too much linoleic acid, which is an omega-6 plant oil. And I think that’s a problem.

John: But doesn’t that convert in the body into arachidonic acid downstream?

Chris: It’s not gonna make any difference in your arachidonic acid levels unless you’re deficient in essential fatty acids. Again, because arachidonic acid levels are highly regulated. So, you basically want your arachidonic acid in your cell membrane basically topped off. If your levels are low in a way that’s modified by your diet, you need more. So, if you eat a really high linoleic acid diet, you don’t get more arachidonic acid in your cell membranes compared to if you ate less linoleic acid but you didn’t have essential fatty acid deficiency. What happens, a couple of things happen. One is, if you don’t have preformed DHA in your diet and you’re relying on plant oils to make DHA, then you will instead make an imposter fatty acid made from the omega-6 fatty acids that displaces DHA in cell membrane. So, the best way to make…for example, the best way to make of the brain of a laboratory animal have low levels of DHA, is not to feed low levels of DHA or even to feed low levels of omega-3 fatty acids, it’s to feed high levels of linoleic acid.

Now, all that changes if you’re eating fish or you’re taking cod liver oil or you’re taking algae oil because you’ll just take DHA and put it in their cell membrane. But most people aren’t. And so someone who doesn’t eat that much fatty fish, doesn’t take any DHA supplements, doesn’t take fish oil or cod liver oil, that person is mostly getting omega-3 fatty acids from converting the omega-3 plant fatty acids in their diet. And if they have a high intake of linoleic acid, it’s gonna directly displace those omega-3s and directly displace the DHA in the cell membrane with omega-6 fatty acids. So, linoleic acid causes omega-3 deficiency basically. That’s one problem with it. The second problem with omega-6 fatty acids is that…or the second effect of them is to increase the linoleic acid itself in the cell membrane. And it depends which membrane you’re looking at, how sensitive that is. The most sensitive tissue is the triglycerides that are stored in adipose tissue. So, if you feed a really high linoleic acid diet, you will increase cell membrane content of linoleic acid, not arachidonic acid unless you’re deficient. But you’ll get a massive increase in adipose tissue linoleic acid content.

That itself is a problem because linoleic acid is highly vulnerable to oxidative damage. You need vitamin E to protect linolenic acid from oxidative damage. If you have a high linoleic acid content in your adipose tissue, your body will suck all the vitamin E that you consume into your adipose tissue to protect the linoleic acid while your cell membranes will become deficient in vitamin E. So, that’s one problem. Second problem is the linoleic acid being in the cell membrane it’s not a bad thing per se, but more linoleic acid means more opportunity for oxidative damage to your cell membranes. And that’s not gonna make that big of a difference if you have a really good anti-oxidant status and you don’t have a lot of causes of oxidative stress. But oxidative stress increases with age and it’s present always. So, there’s always some oxidative damage going on. And the more linoleic you have in your membranes, the greater liability you are for that oxidated damage. Oxidative damage is one of the triggers of inflammation. So, you will wind up with more inflammation but it’s not gonna be because you increased arachidonic acid in your cell membranes, again, unless you were deficient, in which case you would want more arachidonic acid in your cell membranes. It’s gonna be because you increased oxidative damage and that triggered inflammation.

John: Gotcha. And I think that segues nicely the last a bit of time we have here to get into your nutrient cheat sheet, your nutrient deficiency cheat sheet. Chris has…he put together a massive resource that basically gives people…it’s not necessarily meant to be read cover to cover, but it’s a resource that gives people clues as to whether they’re deficient in certain nutrients and it also gives access to different places you can test lab work, etc. And I thought it would be fun at the end of the show to get into that, that nutrient cheat sheet, talk about some of the big nutrients that our listeners will be interested in learning more about, and how to spot the potential for deficiency. Chris, you even have…I think the thing that’s really cool about your style is you have this deep knowledge of biochemistry but you pair it with, like on the MTHFR and methylation piece, the practical tips for preparing green vegetables and leafy greens so as to get the maximum folate in terms of when to rinse. And so can you talk about your cheat sheet, some tips for getting more folate and some of the nutrients that are top of mind for you that people are deficient in, and how to tell that they’re deficient?

Chris: Yeah. So, “Testing Nutritional Status: The Ultimate Cheat Sheet” is basically the way I think about is it’s a system for managing your nutritional status. And that means managing your vitamins, minerals, and essential fatty acids whether you’re looking for deficiencies, toxicities, or imbalances to optimize your health. And basically, it holds your hand and walks you through the steps of first identifying what resources are available to you, for example, do you have a lot of money to invest or not? Do you have time to invest or not? And that guides you to pick one of three approaches. One is a comprehensive approach, one is a cost-saving approach, and one is a time-saving approach.

And depending on what approach you’re doing, you’re collecting data to indicate the probability that something is deficient for you. So, one of that legs of data is to review the signs and symptoms that you have that could be related. There’s an alphabetical list of 180 signs and symptoms where you can just go through the checks and then link to the relevant sections that could be related. And just to name off some from the beginning starting with abdominal pain, acid-based imbalance, acne, adrenal hormones, low adrenaline, allergies, alopecia, which is cause of hair loss, Alzheimer’s, high androgens in women, anaemia, different types of anaemia, anxiety, high levels of arsenic, asthma, and it just goes down the list.

John: Yeah. It’s a big resource.

Chris: It’s a huge list and there’s two things that are really valuable about it. One is that if you are googling what might be this or that, it’s extremely time inefficient but also a lot of this stuff is…I collated what do we know about the well-established signs and symptoms that occur in deficiencies of these things and then also alongside that, based on understanding the biochemistry of how they work, what would we expect to be other possible signs and symptoms? And so I think one of the real good benefits there is that clearly explains the difference between what’s well-established and what’s speculative. But if you don’t know the biochemistry, you don’t have access to 50% to 70% of the really useful information, which is based on what we know about how this works, what are five or six clues that we might have that this is the problem that no one else can see because they’re not thinking of how the system works? So, I think that’s really useful. And then it guides you through lab testing, guides you through dietary analysis and helps you develop an action plan.

So, I think the whole purpose of this is to get away from the idea that we can narrow things down to specific nutrients of concern. So, the opposite approach of this, which I think is borderline useless, is to say, well, in the general population, we can measure nutrient intakes, we can compare them to the RDA, and we can say that magnesium is a nutrient of concern but riboflavin isn’t because 90% of people have double the RDA of riboflavin intake, but X% of people have less than the RDA of magnesium or something like that. I think one of the huge problems with looking at nutrients that way is, first of all, the general population is eating 60% white flour for their diet and that’s the opposite of every single health-conscious population.

So, what do vegans and paleo and keto all have in common? Vegan is health-conscious, whole food, plant-based people, right? What do they have in common? They don’t eat white flour. So, all of a sudden, they’re in a completely different camp in terms of their nutrient profiles and in different directions. So, vegan and keto share in common that they don’t eat white flour, but they don’t share much else. Well, you can do vegan keto. But okay. Vegan and carnivore, right? They share in common that they don’t eat white flour, but otherwise, their likely nutrient deficiencies are in completely opposite directions.

So, I think you could brainstorm what is a vegan most likely to be deficient in? What is the carnivore most likely deficient in? And I think that’s something where people want that kind of information, they really should join my Vitamins & Minerals 101 class. It’s a free class. I go through each nutrient, where it’s found in food, when you should think about supplementing? But also what diets are most likely to be deficient in it? What are special concerns for a carnivore diet? What are special concerns for a vegan diet?

John: What are they? Because we’re gonna have on Amber O’Hearn on the show. She’s head of the Carnivore Diet Conference and we’re gonna chat about that diet. What do you think are the big potential red flags in terms of nutrient deficiency for the carnivore diet?

Chris: The number one nutrient problem would be manganese and the number two would be vitamin C and then a lot of the rest of it depends on exactly how you do it. I think if it’s designed really well, you could take care of most of the other nutrients pretty…and even these, like manganese, you can get enough if you eat a lot of mussels. It’s just like if you don’t eat a lot of mussels, you’re screwed.

John: I just don’t trust mussels from most restaurants. After reading Anthony Bourdain’s book, there’s a very small, small handful of places that I would eat a mussel but that’s a little digression.

Chris: I never eat mussels. Well, that’s not true. Once every couple of years, I eat musses. Most people don’t eat mussels every day. So, a carnivore deficiency probably can be long-term deficient manganese most of the time. I have some guidelines around, in my Vitamins & Minerals 101 class, about how to get enough manganese in a carnivore diet. But it’s basically mussels supply enough manganese in one serving and then there’s a handful of fish that supply enough manganese in two to three servings. I can pull up that list of fish if you want me to.

John: And manganese is a superoxide dismutase co-factor, is it not?

Chris: Yeah. For the mitochondrial version.

John: Okay.

Chris: So, if you wanted to get enough manganese on a carnivore diet that doesn’t include mussels, you’re basically…okay. In two to three servings…no, I’m sorry, not two to three. Three to five servings per day, you can get it from dry salami, dry or hard salami, not the soft stuff, Pacific oysters, freshwater bass, trout, walleye pike, burbot, drum, perch, rainbow smelt, sunfish, and sucker. Almost none of which are the fish that people are commonly eating.

John: Yeah, those are not on the menu here in the city. That’s for sure.

Chris: You should probably just supplement with manganese or eventually transition out of carnivore or do a modified carnivore diet that has a lot of spices in it or something like on a carnivore diet, can you put ginger on your steak? If you can, you can get enough manganese.

John: Yeah. Okay, cool. So, there’s a million more questions I could ask you, but you are pressed for time. For the people that want to follow up and check out this nutrient checklist and the free course that we just chatted about, where can people find you online? I know you’re active on Twitter. What are the best places to find you on the internet?

Chris: Yeah. All my major content is on chrismasterjohnphd.com. I’m @ChrisMasterjohn on Facebook, Twitter, Instagram, YouTube, and occasionally Snapchat. And we’ll throw some links in the show notes for the Vitamins & Minerals 101 free class and for the cheat sheet and I’ll give your listeners a 20% discount. And we can just stick that in the show notes.

John: Cool. We’ll absolutely do that. It’s cool to know that you’re in New York. Hopefully, we can meet up sometime in person.

Chris: Yeah.

John: And thanks for coming on the show, man. A lot of good info. It’s great to have you and we’ll see you soon.

Chris: Thanks for having me. It was good to be here.

John: Yeah. Take care. 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 mygenefood.com.

John O'Connor

John O'Connor is the founder of Gene Food. Read his full bio here.

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