Introduction
Dr. Eric Westman: From time to time, it’s my pleasure to interview people who I think are movers and shakers in the low-carb world. Often they’re doctors, but in this case, this is a mover and shaker, not a doctor.
Dave Feldman: No, I’m certainly not.
Background: Dave Feldman
Dr. Eric Westman: Please explain who you are, your background, and as if someone had never heard of you.
Dave Feldman: I’m originally a software engineer and have been pretty much my entire life. In fact, I’ve had very little interest beyond the surface curiosity in science, nutrition, and medicine overall until about nine years ago. For those who haven’t heard of me before, what happened was I’d gone on a ketogenic diet, and I was doing so to avoid developing full-blown type 2 diabetes. I read in some forums that producing carbohydrates reduces glucose, and diabetes is ultimately a disease of dysregulation of glucose, so why not take out the carbs? I know it’s a revolutionary thought these days, but that’s what I was going with. I brought down my carbohydrates, and lo and behold, I just had a new lease on life. I felt like I was experiencing an entirely new phase. At the time, I was training for running, and I was hitting new personal records. I had lost weight that I wasn’t even trying to lose and looked more like I did when I was going into college. Everything seemed to be better.
About seven months later, I got my bloodwork. I’m excited to get my blood work because I just know all my numbers are probably going to be the best, and pretty much all of them were, except for one: cholesterol. My total and LDL cholesterol had shot through the roof. They actually doubled. Before that point, I had fairly average levels of cholesterol. I had about 120 -130 mg/dL LDL, which is in the middle average for someone my age but they had shot up substantially. My LDL had gone to 240 – 250 mg/dL. I’m going to be briefing it up a little bit, but from there I became quite obsessed. As an engineer, I wanted to understand the why – why was this happening?
Dr. Eric Westman: What happened to the triglyceride and HDL?
Dave Feldman: My triglycerides went down, and my HDL went up.
Elevated LDL
Dr. Eric Westman: Do we know what percentage of people have elevated LDLs? On average, in a lot of studies, there’s no change, which means some go up, and some go down. Do you have a good sense of how many folks who do a keto diet might have an elevated LDL?
Dave Feldman: The me of 2024 can give you a very succinct answer. Back then, in 2015, I had no idea. But I heard it was super rare. The same forums I was going to were suggesting I go on keto were saying, “This happens to almost nobody except maybe a few people; super rare.” At that time, there was nowhere to go, there was no literature on it.
Dr. Eric Westman: Why didn’t you just stop that? Didn’t your doctor tell you to get off that crazy diet?
Tests
Dave Feldman: I was telling myself to get off that crazy diet. I remember this Subway sandwich I was looking at the day after I got my blood work because I was very scared, very upset, and – spoiler alert – there’s not a point in this story where I’m completely certain LDL is irrelevant, so just a heads up. I will say this, because of how high it went, I thought, “I have to get off keto; it’s not working.” My dad and my sister had adopted the diet at the same time, but their cholesterol hardly moved. So here I am looking at my Subway sandwich the next morning, eating a few bites of it, and I think, “This is crazy. I’ve been doing so well on keto; there’s just got to be more to this story.” I became a little depressed, frankly, and started to try to learn everything I could about lipidology. As I just mentioned, I wasn’t that much into science or nutrition, so I had to learn from scratch. What I found was that it looked a lot like something I work on in software engineering. It looked like a network. The system that moves cholesterol around in our body – it’s a network of different packets, if you will, that contain the cholesterol but also contain the fat we’re fueled by. I believe to this day that that was perhaps one of the most vital clues.
The next piece is, I got a second blood test, a second opinion, maybe there was an error in that first test. This was after two weeks of being depressed, and so my appetite had gone way down. Since my appetite had gone way down, the amount of fat I was eating had gone way down, which included saturated fat, and the amount of cholesterol I was consuming went way down. If those were the drivers of this super high level of LDL cholesterol, this was a natural experiment, right? If I’m eating less of those components that are driving up my LDL cholesterol, then maybe it will go back down again. It didn’t; it went up.
Dr. Eric Westman: In medical training, one of the things that didn’t sit right with me was the fact that if you go on a low-cholesterol diet, your liver just makes more cholesterol. So the kind of routine teaching didn’t sit well, which made me open to the idea that there might be something else going on.
So, you didn’t stop doing this?
Dave Feldman: No. While that was the second test, I, at that point, really dedicated all of my time to tracking my food and tracking my blood work. I started getting a lot of blood work.
Dr. Eric Westman: Have you counted how many cholesterol tests you’ve had?
Dave Feldman: I have. It’s somewhere between 140 and 150 blood draws. Now, these are blood draws as in I’ve literally gone to a LabCorp and got them drawn. As far as actual cholesterol lipid tests, including home devices such as PTS Diagnostics, it’s probably somewhere close to 800 or 900.
Dr. Eric Westman: Do you remember what year we were on the low-carb cruise together?
Dave Feldman: I think it was 2017.
Dr. Eric Westman: The year is a blur to me, but you came up to me with a stack of data from your blood tests, your cholesterol tests, and you showed me how it changed over the course of the day, a lot. I’m a traditionally trained internal medicine doctor, and I thought, well, it’s unusual that it would go up and down so much throughout the day. We’re not taught that. It was very interesting to see someone take on what had been settled science. I was taught that you check the cholesterol level and you can make a decision to put someone on medicine for life based on one test.
Dave Feldman: That’s the conversation I was having with my doctor at the time. The moment I got that second test, I was going back to my doctor. I was saying, “I know what you’ve told me, and that’s what I also read in the literature, but I don’t think it’s true.” At a minimum, I think there’s a different context here that if you’re predominantly powered by fat, then we’re watching these changes in the trafficking of that fat as shown in the cholesterol, and that, I would contend, has seemed to be the case to this day. That’s what all those experiments were for. It’s not good enough to just get a single snapshot, especially months or even a year apart. You learn more by getting a rapid succession of shots.
Up and down LDL cholesterol
Dr. Eric Westman: So how much can the blood cholesterol, let’s say LDL-cholesterol, go up and down through the course of the day if I took it?
Dave Feldman: Yes, I should show you. I want to share this with you real quick.
Dr. Eric Westman: I seem to remember it’s 50 to 100 points. This would be a decision of medicine or no medicine, having a level up and down.
Dave Feldman: Right now, I’m looking over the course of the day, an experiment that I did in 2021 where I was getting my lipids taken six times a day. I got it when I woke up, at 7:00 a.m., 9:00 a.m., 2:00 p.m., 7:00 p.m., and then one last time at 10 p.m., and I was comparing the exact same diet in two different phases. In phase one, it was eating three meals over about 10 hours. In the second, it was eating three meals in about 4 and a half hours, so it was an eating window experiment.
We’re now looking at this graph. Let me tell you what you’re looking at. The blue line is a 10-and-a-half-hour eating window, and the orange line is a 4.5-hour eating window. This is an average. Each phase was 5 days long, and this is an average of the last three days for each of their respective phases. As you can see, my glucose seems to generally track pretty close. The ketones, I’m not surprised, they diverge because the 4.5-hour eating window is closer. Here’s where it gets interesting, notice how total cholesterol rises much higher before coming back down in the 4-and-a-half-hour eating window. The reason this is important is because these are identical diets, the only difference is that one is compressed in less time, the 4.5-hour eating window. I’m not only eating exactly the same things, I’m getting the same amount of exercise in each of these phases. I’m getting the same amount of sleep; everything is synced up so I can see this key difference. To answer your question, not only are these changing over the day but look how much they diverge even on the same diet based on the timing of when I’m consuming my food.
Dr. Eric Westman: Let this be a great warning or a recapitulation if you want to do a fasting lipid panel.
Dave Feldman: Exactly.
Dr. Eric Westman: Look at how after the course of the day, it might go up, 40 points. 50 points. This is over the day, and yet we assume this is a static number, and doctors make a decision of risk based on that first number. How many times now do doctors say, it doesn’t matter if you’re fasting, right? Total cholesterol, how about the LDL? Because everyone focuses on the LDL down the bottom.
Can you explain? So it would go up maybe 50 points, and down perhaps 60 points through the course of a day?
Dave Feldman: Correct.
Dr. Eric Westman: We’re not taught this.
Dave Feldman: I want to draw attention to this too. Take triglycerides. This is something I hear over and over again, people coming into the groups, and they say, “I thought I might have the triad, but it turns out I have super high levels of triglycerides.” The very first question that everyone in the group asks, and this includes me, is, “Wait a second, when did you get your blood drawn?” They were, “I was visiting the doctor’s office in the middle of the day.” Did you eat recently? Did you eat a high-fat diet since you literally are on a low-carb diet? Yes, then you quite literally installed triglycerides into your bloodstream because that’s what you’re packaging when you’re putting together fat from your meal and putting it into your bloodstream.
If there’s anything you should absolutely take from these seven graphs that I have in front of you is that there absolutely is a very dynamic hour-to-hour level with our lipids, especially if we’re powered by fat.
Dr. Eric Westman: You could argue, and I think I did at first, is, we simplify. We just use the fasting level, and so many studies have shown that if you have a fasting elevated cholesterol level, your risk is up, and if you treat it with a drug, the risk goes down.
Were you less confident in that sort of teaching after doing this? The whole cholesterol idea? Because this variability is not something that we’re taught about.
Dave Feldman: Correct. That was part of what got me more and more interested. You know, as I’m sure you’ve watched in real-time online, there are many different, well-intentioned folks, especially doctors but also lipid researchers, who would insist, “This has already been studied. There are already amazing labs that are out there; all of the work has been done so that there’s not much mystery left on cholesterol dynamics and the metabolically healthy people.” And I, with every ounce of humility I can put forth, would say I don’t feel as though the level of curiosity seems to be here for what we’re trying to bring forward to you. If you’re on a ketogenic diet and you’re powered by fat, there seems to be this emerging context that we should be studying. We absolutely should. But that comes to the next part of my life, which was a bit more challenging.
Dr. Eric Westman: To recapitulate this section, you did a keto diet, felt great, everything got better but the LDL, and I hear this all the time. It wasn’t until 25 years into this that I finally heard myself say, “Maybe it’s good that the LDL goes up because everything else got better. Maybe we have the wrong idea of what LDL is, and maybe because everything else got better, maybe it’s good for LDL to go up.” It’s hard for an old paradigm person like me to believe that because I’ve been taught that it’s such a bad thing.
Did you knock down some doors to find curious researchers?
Dave Feldman: I sought to. I tried to go to the top brass, if you will, the highest luminaries. I wrote to many of them. I’m not going to call them out here, but I’ll just say there are some names you and I would know pretty well. I was saying, “It’s not just me. Many people exhibit what I like to call ‘the triad,’” which is not just the high LDL but, as you mentioned, the high HDL, the low triglycerides. Very early on, I had a graphic that was a challenge, and I was trying to keep it friendly. I called it the low-carb cholesterol challenge because, while there was a lot of talk at that time about the small dense versus big fluffy, at the end of the day, what showed more commonly with pattern A, which is the big fluffy versus pattern B, small dense, didn’t even require an advanced NMR. It really could just look at the existing pattern. If you had high HDL and low triglycerides, you almost always had pattern A. Conversely, the other was already known by the name atherogenic dyslipidemia, which is having low HDL and high triglycerides. Whatever diet you’re on, you typically want to have a higher HDL and lower triglycerides, which means that your body is good at managing those lipids on the inside. So that triad of looking not just at the HDL and low triglycerides alongside LDL, I said, “This seems to be so commonplace.” Indeed, many people like myself have an extreme version of this, not just high LDL, but super high LDL levels we don’t normally see except with some genetic abnormality. So I started to dub this profile, this phenotype, “lean mass hyper-responder.” I called them “lean mass hyper-responders” because they seem to be more commonly leaner people, with a BMI of, say, 24 or lower, and their LDL would tend to go higher the leaner they were and the more low-carb they were.
This takes me back to the point you were making earlier. This was rare before, but I would argue that the reason it was so rare before was because leaner, metabolically healthy people weren’t into low-carb. They were often told to carb-load. They were runners and cyclists. It was anathema to consider a low-carb, high-fat diet. As the ketogenic diet became more and more in vogue and even athletes wanted to try it, well, then all of a sudden more people were exhibiting this extreme triad, this very high level of LDL, high HDL, and low triglycerides.
Checking hour by hour
Dr. Eric Westman: You were checking hour by hour. We saw a graph of how these lipids change throughout the day and how surprised I was to learn that.
Dave Feldman: There’s another graph that is hour by hour. Those were six times over the course of a day. One thing that I was surprised to find, that I didn’t realize until maybe three years or four years into the journey, was something I called the triglyceride carryover effect. What I mean by that is it’s assumed that triglycerides go down right away. As you saw in those graphs, triglycerides will go up, but they go down slowly. I would argue that the reason for that is that when you’re metabolically healthy and on a low-carb diet, there’s not as much rapid turnover induced by insulin. So insulin will hack away those fat stores relatively quickly if you’re metabolically healthy and you’re on a mixed diet that includes more carbohydrates, that includes more fiber, and things along those lines. They can have an impact on potentially increasing your insulin levels.
So here I am, interested in tracking hour by hour because I’m watching the triglyceride levels change, and I call it “carryover,” because I would go to sleep with triglyceride levels that might be, say, in the 200 mg/dL range, for example. When I wake up the next day, you can see that they very quickly drop to under 100, sometimes to 60 by 12 hours fast.
Many might say, “Wait a sec, we have an association between triglyceride levels and cardiovascular disease.” I just finished telling you about the triad, which associates a high HDL with low triglycerides. I think you and I are very keen on emphasizing this, these are fasted tests. It’s extremely important to recognize why there’s a difference between a fasted level and a non-fasted level. The biggest thing is if you fasted, whether you’re on a mixed diet or not, if you’ve spent 12 hours not consuming food, then that is the one time where we expect all of your fuel in the bloodstream will have been packed away. That suggests that your body has a good metabolism that’s very effective in packing it away. But the difference between fat and glucose is the body acts on glucose to hold it to that tighter delta, that range. There’s more of an endocrine action, more hormonal action, between glucagon and insulin to try to hold it there.
With fat, there’s less that it acts on. I think that that’s because that’s the state in which, when we’re fasted, it is not as pathogenic. The range by which fat can be up and down is not as pathogenic. Don’t get me wrong, if it’s like your triglycerides are at very high levels postprandial, probably they were at very high levels when you were fasted anyway, which means that there’s probably a dysregulation.
Curiosity and people helping out
Dr. Eric Westman: When you’re talking to other physicians, other researchers, is anyone curious? I remember talking to my lipid specialist here at Duke, years ago, his first response would be, “No. Cholesterol and fat are raised at the triglyceride level.” And I said, “No, I think it’s carbs that raise the triglyceride level too, at least.” He went to the library and found that, I think there were six people or ten people in this study by Aarons years ago that showed that both high fat and high carb led to high triglyceride levels and that low carb would lower the triglyceride levels. He hadn’t remembered that or hadn’t been reinforced enough because everyone was just focusing on “saturated fat is bad”. I remember he was shocked and a little embarrassed that he had only focused on the fat because he was our local, well-known lipidologist.
When you’re doing physiology and thinking about these things, are you getting some curiosity and people helping you figure this out?
Dave Feldman: More and more. In the very beginning, it was very difficult. And to be fair, I am an engineer so they’re hearing me report data to them that they’re used to seeing in an article, in a journal, but they’re not going to take it quite as seriously because I’m not somebody who’s got it published in peer review. This is my way of trying to give them a little bit of leeway you can say. All of that said, as this phenomenon became more and more prominent, as certainly you and many other low-carb physicians would see, this triad would see this combination more and more frequently.
Here’s the elephant in the room: these aren’t just metabolically healthy people who were trying out keto. This also included several people for which there was special efficacy. They had some kind of disease such as epilepsy or type 1 diabetes, or my good friend and colleague, Nick Norwitz, he has severe ulcerative colitis, where there would be a particular reason, even though they were metabolically healthy, they had a particular reason to use a ketogenic diet to treat their disease. They’re the ones who we should absolutely be getting this research for, to find out if indeed it is higher risk because they tend to have the highest levels of LDL because they are usually the ones who are very adherent to keeping truly low carb.
Dr. Eric Westman: Well said. The doctors still respond with, “You cured your ulcerative colitis. You reversed it.” You can’t cure it, they say. I think you can if you don’t go back to eating that way. They’ll even say, “But you have to get off that unhealthy diet when it just reversed your serious medical condition. And use a medication that has all these other side effects.”
I wonder if medical care today is medication care. Most doctors aren’t taught about diet or know what to say, but they can reach for medicine quickly. How many times have you been told that you ought to be on a statin medicine for your LDL?
Citizen Science Foundation
Dave Feldman: Quite frequently. Here’s one of the fascinating aspects of this. I think I’ve stated this many times. I’ll state it here as well. I think it’s good to be a scientist and express uncertainty where we do have uncertainty and say, “We don’t know. Let’s go get it. Let’s go get this data.” I realize I haven’t shared this part yet, but for those watching who don’t know, that’s literally what I did. I started the Citizen Science Foundation in 2019. It’s a scientific public charity because after trying to get a lot of lipidologists and cardiologists to help get funding together, get a study going, and failing, I said, “Let’s see if I can raise the money from the community, but particularly the low-carb community.” I had no idea if it would work. Perhaps the low-carb community did. We raised the money we needed, and right now we’re completing publication on these lean mass hyper-responders with data of CT angiograms, which are, of course, hard scan data, literally looking at the soft plaque at a very high resolution to see if indeed that they’re going to have a higher residence of plaque and a higher progression of plaque because it’s a longitudinal study. We’re getting two scans per participant.
Research and money
Dr. Eric Westman: So what led you to the study protocol and, the question is what happens to people who have high LDLs and high HDLs? Several of my patients applied to be in the study, but they didn’t meet the specific criteria, the high HDL, and the low triglyceride.
How did you find the scientists to help you? I have to say Dr. Budoff is one of the world’s leading CT angiographers. How did you get interest? Or was it just a matter of having the money?
Dave Feldman: More the latter than the former. Once you’ve got money together and it’s clear that you can pay a research center to actually study this, then that’s one of the big first steps.
Dr. Eric Westman: But a key factor is that he is agnostic in terms of belief in LDL. You would have to find someone who isn’t ethically conflicted because he might be saying that LDL in this certain circumstance isn’t harmful. I think Dr. Budoff will study things that he’s more interested in, like science, rather than the politics or the money behind a drug. Is that your impression?
Dave Feldman: Anybody who’s researching at high levels with CTs, for example, they almost certainly have a client list that includes pharmacological interventions. There was no way we were ever going to find somebody who didn’t in that regard. Here’s the thing about Dr. Budoff that gave me a lot of confidence. One, he has come to findings that were considered controversial within his field. For example, there are some recent EPA studies (an omega-3 fat) that there’s a huge amount of pushback that EPA could be this enormous benefit instead of cholesterol-lowering medications, even though this isn’t the claim that’s being made by Dr. Budoff and others. It’s that EPA does show such strong efficacy. I suspect that this is because there’s a greater deficiency for those people who don’t have EPA via diet, but we’ll set that aside for now. There was another thing that I appreciated about Dr. Budoff, which was the Lundquist Institute, which is his research facility that we were ultimately doing this partnership with, they’ve also published negative findings. It does suggest that he takes it where the data goes.
Something else that I think is also important is there is a sort of different beast to CT researchers in that they are more interested in the outcome than they are in the narrative of the outcome. There is a genuine excitement of, “Let’s just see what the data tells us.” I feel like Dr. Budoff has seemed to have shown that quite a bit in the research thus far.
Dr. Eric Westman: Fast-forwarding, you have 80 to 100 people who were flown to the Lindquist Institute to get a CT angiogram, which is not just the calcium score; it’s actually looking at the artery itself. The initial baseline data were presented to me last fall and in an abstract published just a few weeks ago.
The idea of the study though is to follow these people for a year, get a repeat scan, and then compare in those individuals whether there was a change. One of the strengths is over this year you’re going to be making people check the labs, it’s not just self-reported being on a keto diet. The baseline data is self-reported people being on the diet. Will there be documentation of what they’re eating?
Dave Feldman: Let me describe the design of the study. We’re recruiting a total of 100 folks; they’re lean mass hyper responders and borderline lean mass hyper responders. Here are the cut points for everybody. The LDL needs to be 190 mg/dL or higher, HDL of 60 mg/dL or higher, and triglycerides of 80 mg/dL or lower. Importantly, you have to show us that your new LDL cholesterol level after a ketogenic diet was very different from before; it had to have increased by 50% or more, and you had to have had an LDL of 160 or less combined with the increase of 50% or more.
If you went from an LDL of 150 to 200, even though that hits the low and high cut points, it’s still not an increase of at least 50%.
Dr. Eric Westman: Why do we do that?
Dave Feldman: We wanted to show that there was at least enough of a hyper-response that we could confirm, first of all, that they likely did not have a genetic disposition towards higher LDL to begin with and therefore they were hyper responders per se. Some participants didn’t make it, not because from their understanding they didn’t have those lipid levels that I just mentioned to you now, but sometimes they just couldn’t get access to their blood work. They had to prove to us that they did have that by verifiable blood work. Moreover, we also had other cardiovascular risk factors that they couldn’t have had, such as a prior diagnosis of cardiovascular disease, a prior diagnosis of severe hypertension, a number of these different components, and a lot of that is so that it could also pass IRB review and so that we could get the study approved.
It’s worth emphasizing, though, that all of these are supposed to be irrelevant because it’s thought that the existing lipid hypothesis that high LDL alone will drive the presentation and progression of plaque in coronary arteries very rapidly. And that’s what it’s thought, for example, children born with homozygous familial hypercholesterolemia, as they tend to develop cardiovascular disease very quickly alongside their high LDL, and that’s why it’s been thought this whole time that that’s the case.
Here we have this one corollary where there’s not this genetic abnormality that impairs the metabolism of lipids. Maybe this is the hypothesis: maybe that lean mass hyper responders have a functional lipid metabolism, that this is physiological, but that’s a controversial statement I’m making right now, but that’s what I want to check.
The case of the 3 year old
Dr. Eric Westman: I don’t think it’s common knowledge that the first kind of index case, the little girl who had familial hyperlipidemia, started getting manifestations of atherosclerosis when she was very young.
Dave Feldman: Yes, age three.
Dr. Eric Westman: If the LDL is super high and driving all this, you would have clinical symptoms by three years old?
Dave Feldman: To be fair, they would point out, if memory serves, her LDL was, I want to say, 780. I think many people would say that’s still much, much higher than most lean mass hyper responders. I want to bring up the point, my good friend and colleague Nick Norwitz, he’s got an LDL of 500. I wouldn’t be surprised if you right now have some patients that are in the 500-600 mg/dL range. I’m sure, like me, you’re giving them all the warnings, all of the caveats: “This is uncharted territory. We’re getting the data, but we don’t have the data in hand yet.” That said, it’s true, I would have thought things characteristic of those children Brown and Goldstein were looking at, such as tendon xanthomas, things along those lines, that we would have seen a higher preponderance of and, unfortunately, things like developing stable angina. Don’t get me wrong, this study we’re talking about that we’re doing, I’m not by any means suggesting I think everybody will be disease-free. There’s no such diet; there’s no such population that’s immune from atherosclerosis. The question is, will they develop it at a rapid level that seems different from another population that might be comparable? That’s what the most recent published paper was. We were looking at them compared to another study called Miami Heart.
Baseline data
Dr. Eric Westman: You have the baseline data from the study that’ll go on for a year and then repeat the angiogram, but at the baseline, you compared it to the cohort who had the same test but were healthy, and it just happened to be in Miami; that’s why it’s called the Miami Heart study.
If you look side by side at the figure, it looks like they had a similar amount of relatively minor coronary atherosclerosis. The high was 13 or 15 on a scale of 0 to 45, if my memory serves. The point here is that, at baseline, it wasn’t different from another relatively healthy population?
Dave Feldman: Yes, I should set this up a little bit. As mentioned, we had our baseline scans. I said that there were going to be two scans per participant at the time this analysis we’re describing, which is a separate analysis, was being done. We took all 100 baseline scans of our group, and our cohort, and looked at Miami Heart, and by “we,” I mean the statistician inside of Lindquist Institute. I’m blinded by the data, but the 100 here, it turned out that 80 of the 100 were within the age range of Miami Heart.
Dr. Eric Westman: I see.
Dave Feldman: She took the 80 that were within the age range and then from the pool of 2,400 participants in Miami Heart, found as much as she could, the tightest match between the two groups. This is what’s called a match control. I love match controls. I like them more than doing multivariate analysis with control groups, though there are pros and cons to both. These two groups ended up being a very tight match. They had the same age, which was 55.5 years. They had the same ethnicity. They had the same composition of male to female, which was mostly male, which, frankly, is going to more likely have a lot more plaque. They were very similar in cardiovascular disease, or I should say risk factors, even when they didn’t qualify as full-blown risk factors. For example, A1C was like 5.4, 5.5. Blood pressure was optimal but fairly close.
Lastly, there’s the key difference between the two: our group had an average LDL of 272 mg/dL. For people who don’t know, this is the top 10% of the top 1% of the general population. We might be getting used to numbers like that just hearing them in passing in the low-carb community, but outside the low-carb community, you often hear general practitioners tell people who are coming into the lean mass hyper responder groups, “This is the highest LDL I’ve ever seen.”
Dr. Eric Westman: After reviewing your background and the lean mass hyper responder study baseline data, which is fascinating, that full study will have replication in a year, and hopefully, it will go on further. What’s the next step for the studies on cholesterol? Then we’ve got to go back and talk about how you drove down your LDL by eating more fat, blows my mind, but how about wrapping up on the LDL elevation?
Dave Feldman: Definitely on the research front with the Citizen Science Foundation, we just had a conference in March, and I haven’t officially broken the news yet, but I’ll just share it with you here on the podcast because it’ll probably be public by then, we’re already going to be doing a second conference. CoSci, which is short for Collaborative Science Conference, which is a giant charity event to raise money for the Citizen Science Foundation to do this research. We already completed this original study, and even though we don’t have everything published yet, that’s in the analysis stages right now, but the money we’re raising currently is for a new study, which our code name for now is the Triad study. It’s going to be similar to the current one, except with a few notable differences. One, we’re going to have an attached control group. Two, it’ll be a bit more permissive in its eligibility criteria. The current one, for example, had HDL of 60 or higher and triglycerides of 80 or lower. Don’t quote me on this yet, but, for example, we may have different, more common markers of, for instance, modestly lower HDL, modestly higher triglycerides, and possibly other cardiovascular risk factors that we were a bit stricter on before. As you know, we already knew it’d be a challenge to get this through IRB with the initial study. The difference is that now we’ll have existing data that suggests, I think, we can make the case that this is not as high a risk group as would be thought of before, which will allow us to get larger criteria that will probably encompass more of a generalizable audience.
Dr. Eric Westman: It would make sense, too, if things looked good then, in the first study to expand the criteria a bit. That would make sense from a safety and IRB standpoint. Hopefully, the IRB will see it that way.
Dave Feldman: Absolutely, and it’s exciting because I think we’re also proving something super important, which is we’re proving there are not just two places in town where you can get your research done, which is either through the government or through some kind of attached business model such as a pharmaceutical or a drug testing device or a supplement or something along those lines. Hopefully, many people can do what we’ve done here, which is to go out there and ask and get crowdfunding to get this research accomplished. That’s what I’m really proud of, is that we’ve been able to do this through individuals.
Next conference
Dr. Eric Westman: It’s been incredible to watch. Thanks to your persistence and the advent of the ability to fundraise directly in 5 and 10-dollar increments, or whatever the most common amount was, that is a different model. In some ways, though, it’s kind of discouraging and upsetting and depressing that you have to go out and raise your own money to do a study. I bet once you do it, then other people will start doing it, and, suddenly, they’ll take credit for it. Just be ready for that.
When is the next conference coming up? Will it be an annual thing?
Dave Feldman: We’re hoping it will be. There’ll definitely at least be a second one. We’re in the process of getting it negotiated, I believe it’s going to be the first weekend of February. I don’t want to get the dates wrong, but I think February 7th through 9th. That’ll be in Las Vegas again. I can’t announce the location yet, but we’re probably going to put out a save-the-date soon. It’s going to be great because the last one was, as I like to say, more successful than we had any reason for it to be because we announced it literally two and a half months beforehand. A lot of people told me they couldn’t make it because it’s not enough notice, but we still had 300 people show up, and we still managed to raise $67,000, which, as you know, it’s hard to raise money with conferences. They’re usually a labor of love, and God bless everybody who puts them on. We did it on a shoestring budget. We got everyone to contribute their time and their dime, which includes even the speakers. They came themselves via their own travel, and all of our time was volunteered. It was all to take that money and put it into this new Triad study. Again, we’re showing that it can be done.
Lipid levels and lowering LDL cholesterol
Dr. Eric Westman: I’m already envisioning the David and Goliath kind of cartoons.
Can we spend just a moment, this may seem like old history, but I remember you started testing yourself and looking at lipid levels every few hours or an hour. The next thing I hear is that you figured out a way to lower your LDL cholesterol and that you are going to replicate it at a keto conference among people. Tell me this story again.
Dave Feldman: This was 2017. It was two years into my writing this blog called cholesterolcode.com. and only the small number of geeks who were into this component of hyper responders for those going on a ketogenic diet were able to find this blog and chat back and forth with me. I was known for doing very intensive (inaudible) experiments. I wanted to capture my blood work in real time. One of the first things that I identified that associates back to the lipid energy model, is something a bit unintuitive that actually, while in a ketogenic context, so I’m fully fat adapted, my carbohydrate levels are really low, the first thing I noticed was that if I ate less and less and less, then my cholesterol would go higher, which seems unintuitive because you would think if I’m eating less fat and therefore less saturated fat, if that’s driving the higher cholesterol, then my cholesterol should go down. But it wasn’t. It was going up. So I thought, what if I head in the other direction? What if I over consume my ketogenic diet on purpose and, again, track my cholesterol levels in real-time? And sure enough, it showed that it went further down from my baseline levels. Then I stepped on the gas and really consumed a lot in just a few days, and I found I could drive my LDL cholesterol levels to super low levels.
Dr. Eric Westman: We’ve been teaching, and you’ve been learning, that the more cholesterol you eat, the higher your cholesterol will go.
Dave Feldman: That’s right.
Dr. Eric Westman: You’re finding the exact opposite in your case.
Dave Feldman: Yes, but another thing, at that time and probably to some degree right now outside of the low-carb community, cholesterol levels are thought to be more glacial, that they’re very static, and that genetics are the primary driver as to where your cholesterol levels are. If you want to change them, it’s probably going to take some form of medication or very, very severe dietary change. Even then, the major dietary change, you should celebrate having, say, a change of 15 mg per deciliter or 20, something along those lines, and here I am, seeing that I can shift it by as much as 50 or even 100 milligrams per deciliter in a matter of days. It was something I couldn’t believe because of how much I kept reading about in the literature and something that got exciting enough to where a number of people reading my blog would replicate this themselves and report the data back to me.
Sure enough, as you know, there were the 2 Keto Dudes at the time who were holding their conference, and this was in the summer of 2017. We organized an experiment at that time, which we managed to get two dozen people to participate in. Ultimately, these 22 individuals would do exactly what I just described. They would over-consume their ketogenic diet through Keto Fest. We would get the blood work at the beginning of the conference, which was Friday morning, and then again at the very end, which was Monday morning, and then report back the results. Sure enough, of the 22, 19 saw their LDL cholesterol plummet.
Dr. Eric Westman: How much were they consuming?
Dave Feldman: They each tracked it for themselves. They were often consuming fatty meats, like steaks. Some were consuming huge amounts of salmon. My good friend and colleague, Siobhan Huggins, was downing a lot of heavy whipping cream. But why these levels drop, we would better understand, years later
Dr. Eric Westman: Just to reiterate, people are eating more and more fat and more and more cholesterol in the diet, and how many calories a day was this?
Dave Feldman: Many would say it was double whatever their maintenance level of calories is.
Dr. Eric Westman: If anything, the LDL and total cholesterol should go way up based on traditional teaching, right? It’s in the context of a low-carb keto diet, always have to say that. Basically 19 out of the 22. Just about everyone had a claim that they could lower their LDL by eating more fat.
Dave Feldman: That’s correct.
Dr. Eric Westman: I just want to repeat that for people because it goes by fast, and it’s like the man bites dog story. You don’t expect a man to bite a dog. You don’t expect the LDL to go down. For a while, you were saying if an insurance company was going to give you a hassle for a high LDL, then try this and get your insurance to kind of game the system because the system discriminates against people with high LDLs.
Dave Feldman: It does, and it’s getting more pervasive. For example, pilots can have their license taken away, in some contexts, if their LDL is considered too high.
Dr. Eric Westman: Does this make sense? I didn’t know what to say.
Dave Feldman: Yes, where I’m coming from.
This is why we need to do this research because up until this point in time, as you’ve heard me say in many different lectures, we usually look at higher LDL in the context of some kind of dysfunction or impairment, or some kind of illness. Unfortunately, there are reasons I could point to, which could get a bit technical, and we’re not going to go there as to why they cluster together. Because if there’s some metabolic problem, that can be its own reason for why your LDL can be higher.
This isn’t to say that LDL has nothing to do with cardiovascular disease. That’s not what we’re saying. What we’re saying is, can we at least see with people like myself, like my good friend and colleague Nick Norwitz or Adrian Soto Mota, that have high LDL where it seems to be related to fat trafficking, which is what you can see in my lectures on that, that indeed is the high risk? It’s assumed to be by conventional medical zeitgeist today. I suspect we’re going to find at a population level it is not, or at least at the risk level is nowhere close to as comparable as it’s thought to be.
Dr. Eric Westman: Even look at a study that takes all of these different risk factors, the Dugani paper, being a prospective study with women, and 2 type diabetes was the highest risk. It had 12-fold for the first cardiovascular event, and LDL was down, it was one of the lowest associations, below triglycerides and HDL, below metabolic syndrome. The idea that there may be another way to go about this, we’ve talked about this. We were talking about LDL back then with the flip phones, so there may be a new technology or a new understanding, or a different way to go about things. This incessant focus on just one way makes sense to me that it’s not going to explain everything.
Dave Feldman: And it’s being applied asymmetrically, so by that same token, could I say, should pilots get their fasting insulin tested? I’ll bet you hyperinsulinemia will associate a lot more with a risk of cardiovascular disease and a heart attack.
Dr. Eric Westman: It’s not going to be an acute issue. That’s why they check for alcohol. That’s why some people claimed they were on the Atkins diet and had ketones that made their alcohol level high. For pilots, they should be measuring blood sugar. It makes sure they don’t have high hypoglycemia, but they measure LDL. I’ve often wondered, and I’ve tried to test among my patients and never really got the feedback. I have met actuaries who worked for insurance companies back to that point. Are insurance companies measuring in their own database to see if LDL is a predictor, or are they taking the advice of the experts? This would be an easy thing to resolve if you have an insurance company that has its own data with LDLs and other variables. Have you ever talked to an actuary?
Dave Feldman: I have. I thought that they would probably be the best people to approach since it’s assumed that they are just bean counters, right? But there are other considerations that they shared with me as to why they often go with established guidelines.
Dr. Eric Westman: Guidelines? Oh no. They will ignore what they see in front of their face and go with what the experts make.
Dave Feldman: I’m not going to call out who they are. I’m just going to say I talked to one of the largest in the world. I’ll put it that way. And this was not too long ago. I don’t want to connect too many dots, but I said this exact thing. I said, “If I could show you a cohort of people who, for instance, would like to have life insurance, and we could prove to you that they’re at lower cardiovascular risk with data that we have that’s emergent, right? But it’s against the present guidelines. The present guidelines would say that, no, they are indeed at high risk and they’re classified as such, even if we’ve got real-world data to suggest otherwise, and that the data is specific. Isn’t that exactly what you do?” And his answer was, “Here’s the problem. The problem is we’re still liable for anything that we do that could seem suggestive against present medical care”.
Dr. Eric Westman: Very interesting.
Dave Feldman: If you’re saying this is their position, and it makes sense if they’re saying, “We’ll go ahead and insure against people with high blood pressure in this particular context because it turns out, given our own internal data, that they’re not as high a risk.” And then a lawyer or the family of someone who does get a heart attack says, “My husband was taking action to deal with their blood pressure, and they did, in fact, have a heart attack.” And that heart attack might, in fact, be an outlier or even be unrelated to the high blood pressure, just to use this hypothetical. It will still make the case that the lawyer could then take the insurance company to suit by saying they’re the ones who planted that idea in this person’s head, but the guidelines suggest that the high blood pressure was bad. I am just using blood pressure as an example.
Insurance
Dr. Eric Westman: I could just be an internal black box that you don’t tell other people what your secret formula is, but you use triglyceride and HDL instead of LDL. Thank you for sharing that information.
The other thing that seemed reasonable to me, like Divers Alert Network, DAN, which is an insurance company that insures divers because often scuba divers can’t get insurance, that’s here in Durham, North Carolina. So there may be an LDL alert network. Or some entrepreneur could get insurance based on the idea that these people will live longer. It’s a bit of a gamble. Fascinating to hear that an insurance company might not look at its own data but take guidelines. Wow.
Dave Feldman: That is baked into the pie. It’s baked in from their act, actualization, whatever you want to call it, where they’re calculating what the likelihood is that they would be at risk for liability. If something is well-known enough and, let’s get meta here for a second. How crazy is it that what we’re talking about doesn’t come down to your defense as the truth? Your defense should be, “This is an evidence-based position.” If we have more and more emergent data that is undeniable, that this, and again, I’m not stating this as though I know it’s fact yet, let’s say that more and more of our studies continue to suggest at a population level this is a low-risk population, then they should be insured as a low-risk population would be if that’s what the data show.
If your ultimate pushback on that is, that there’s this larger paradigm of assumption that’s based on statistical analysis of what it’s thought to be based on models, what do you say to that talk?
Where to find Dave Feldman
Dr. Eric Westman: I recall a lot of the conversations we’ve had through the years, starting with, “What are you doing by measuring your blood cholesterol six times a day?” I remember I said, “I don’t know what you’re doing, but keep doing it.” I didn’t want to tell you not to.
Where do people find your latest information, or where would you like people to focus?
Dave Feldman: There’s the cholesterolcode.com that I mentioned before. I will concede we are using this blog less and less and posting more of the direct research to the more official site, which is the Citizen Science Foundation, you can go to citizensciencefoundation.org. It is a bona fide public charity, so any support is appreciated. If you contribute, it is a bona fide 501(c)(3) public charity, so it is tax-deductible. We are raising money for the Triad study, if people can keep an eye on it for updates. It’s also on Twitter @realCSF. I am active on Twitter if you’re trying to reach out to me: realDaveFeldman.
Outside of that, we also have Own Your Labs, which is our blood testing service. You can order your labs for direct blood work. Also importantly, we have an additional feature – we’ve had to put it on pause, but we’re about to bring it back. We incentivize people to also share their anonymized blood work for our open data archive, which we hope to have released pretty soon.
Dr. Eric Westman: I would love to see. So, ownyourlabs.com is a place where you can order the lab, go to LabCorp, I think, have it drawn, and then insurance or other people can’t see the labs. Then you can say what diet you’re describing that you follow. It would be very interesting to see a few of these labs compared, carnivore versus carb eater or keto versus carb eater. Blood ketones are different; it’s abnormal to have blood ketones if you’re not a carb eater. We know that that’s not unhealthy if you’re not a carb eater. How many people have put in their information to Own Your Labs?
Dave Feldman: It’s interesting. Coming up until December, I’m just guesstimating, that it’s somewhere in the neighborhood of 4,000 to 5,000. Since December, there have been 5,000 or more people who’ve used Own Your Labs. We’re growing really rapidly, so thanks again to everybody for their support.
However, the thing that we needed to work out – we had some things we had to work out with LabCorp for the next steps, so we had to pause that part of our model until hopefully this coming month. Then hopefully, we can bring it back online again because that’s really what drove us to want to do this in the first place. We love that we’re very competitively priced for people to be able to get their labs this way. It’s also a way for them to contribute directly to Citizen Science with their own data. There are very few open and available data sets for people on a low-carb diet. We want to make that available. We want people to be able to do both formal and citizen research alike to start doing analyses. To be able to gauge exactly what you were just bringing up – things like how much are the labs different between a carnivore and somebody on keto versus somebody on a mixed diet, for example. We pick up that demographic information—how much does BMI associate with LDL as verified by what they give us in the demographic information compared to their blood work. This time, it won’t be as much like a survey; it’ll be more accountable based on what kind of limits they get, including advanced ones like NMR, for example.
Dr. Eric Westman: Fantastic. We were talking a moment ago. How long did it take for this LMHR study, which is now in abstract form published? How long was this from thinking about it to knocking on doors to reading your own?
Dave Feldman: It was seven years ago this month. It was July. I wrote that article that identified the lean mass hyper-responder phenotype. When I wrote it, I didn’t know how prominent it actually was. I kept seeing the pattern because people were sharing their labs back and forth with me. It made sense with the energy model. For two years, from 2017 to 2019, I kept writing emails to prominent lipidologists that I was finding. I kept pinging them on Twitter, any way I could, to try to get them interested in this phenotype. It wasn’t until 2019 that I founded the Citizen Science Foundation and said, “Let’s just do this ourselves.” I kept thinking that – maybe a year and a half away, maybe two years away, throughout this process. Research takes a lot longer than is often hoped for. But we’re here.
Dr. Eric Westman: Isn’t there a saying that overnight business success is really ten years in the making? I think this is true in every part of the world that is going to change something. Thank you for your persistence and thanks for taking the time to talk about some really important research that you started.
You can watch the full video here.
