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Interviewee Bio: 

I’m a senior software engineer and entrepreneur.

I began a Low Carb, High Fat diet in April 2015 and have since learned everything I could about it with special emphasis on cholesterol given my lipid numbers spiked substantially after going on the diet. As an engineer, I spotted a pattern in the lipid system that’s very similar to distributed objects in networks.

I’ve since learned quite a bit on the subject both through research and experimentation which has revealed some very powerful data. With this new general theory, I’ve shifted around my cholesterol substantially without any drugs or special supplements of any kind.
https://cholesterolcode.com/
Twitter: @DaveKeto

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Transcript:

Carole Freeman:

Well, hey you guys. We made it. We’re live here broadcasting into our Keto lifestyle crew. And you may be watching us later as well too on YouTube and Facebook. So thank you so much for joining us. I am so excited to be here today with Dave Feldman who is a personal friend, but also an amazing, amazing guy. I call him a cholesterol investigator. He calls himself a senior software engineer and entrepreneur. So welcome Dave. Thank you so much for being here.

Dave Feldman:

Thank you for having me Carole.

Carole Freeman:

I miss … Every time I get to do one of these interviews now in these current times, I miss you guys even more because we can’t see each other in real life. But it’s good to see you virtually. I met you Dave, what is it, going on, five, six years ago at the very first Low Carb USA conference.

Dave Feldman:

Yes.

Carole Freeman:

And my first … I remember you before you even met me because I, at lunch time the first day of Low Carb USA, I’m sitting by myself outside. Would grab lunch at some like randomly. You were at a table next to me. We’d grab lunch at some grocery store or something like that, and you’re sitting at a table with a bunch of guys. And I can overhear you talking about like, “You guys, I think I figured out this weird thing with cholesterol,” and you started sharing the things you’d find out at that point. So that’s my first memory of you. And then we later connected and got to know each other better from then.

Carole Freeman:

Some people watching this may like totally know who Dave is and are huge fans, or on one side of the controversy or not. But let’s just take it back for those people who are like, “Who the heck is Dave? Why should I care who Dave is?” Let’s take it back and just tell us how you got so interested in this cholesterol thing.

Dave Feldman:

Well, mainly it’s because mine jumped through the roof after I went on a ketogenic diet. I started in about April of 2015, and about seven months later I get my blood work back, and like so many others I was like, “Oh, I’m expecting it’s going to be better than I’ve ever had,” because I’d been feeling great, I was setting personal records with my running. It’s just I had every confidence in the world that it was going to be fantastic. I thought there was a chance my cholesterol might go up a little bit, so I was prepared for that, but it had skyrocketed. It had gone up, I think, over 100 milligrams per deciliter.

Dave Feldman:

So here I am. I’m looking at an LDL of like 230, 240, something like that, and I’m flipping out. And after that, I became obsessed about this science that revolves around cholesterol, and really, the overall topic itself of lipids which are just these insoluble elements that your body makes use of that it needs this system to move it around in your body.

Dave Feldman:

And what’s funny about that is, this system in many ways is one I’m kind of familiar with in software. It’s a network. And that’s how I ended up getting so interested in it. I started seeing patterns that I thought were familiar, and then I started doing a number of self experiments which I’m sure you’re very familiar with now where I found I could manipulate the numbers very substantially because basically, and this is kind of my elevator pitch, I posit that our cholesterol levels in somebody metabolically healthy especially are kind of ride sharing with our fat-based energy. So if you’re powered a lot more by fat, it will almost certainly have an impact on your lipids, particularly your cholesterol levels.

Carole Freeman:

Ah. So those of you that are watching right now, I can see that we have some people watching live. So go ahead and just chime in, in the comments, so we know you’re here. Just share with us where you’re watching us from, and feel free to pop questions in for Dave. He’s here to answer questions, but also, if there aren’t questions where I’ve got plenty of questions for him too. So let us know that you’re here and what are your top questions about cholesterol in general.

Carole Freeman:

Let’s go back to like what’s old school, what doctors think of what is cholesterol, and then we can then compare that to what you’ve discovered and over the years.

Dave Feldman:

Well, of course, I believed like so many others before I got into this that cholesterol was just kind of this liquid that’s just traveling through your bloodstream and globbing onto the edges, because I grew up with the same thing I’m sure you’ve seen many times over which is these pipe analogies. You’re seeing glunk like going down and then getting stuck in the pipes, and that’s how you end up with these stenosis that you would see in the arteries.

Dave Feldman:

And over time I found out no, no, it’s actually extremely sophisticated in that your body makes these proteins, lipid carrying proteins which you’ll hear of as lipoproteins, and they’re carriers. They’re carriers for these lipids, and they actually are being made by your body all the time to move them around because really these lipids, they don’t hang out in your bloodstream unescorted. They’re constantly being escorted by these lipoproteins, these boats as I like to refer to them.

Dave Feldman:

And that’s actually one major misconception, is for example, you’ll hear something like LDL cholesterol and you’ll think it’s a kind of type of cholesterol. It’s really only one type of cholesterol. There’s really only one cholesterol molecule. But LDL is really the kind of boat that you find that cholesterol in, HDL cholesterol, the so-called good cholesterol. By HDL cholesterol what they really mean is the cholesterol found in HDL particles. But that’s also another carrier protein.

Dave Feldman:

So these boats, they’re being made constantly up. I’ll share a fun fact with you. How many LDL particles do you think you have in your body right now? Just guess a number out of nowhere.

Carole Freeman:

Oh, me personally, gosh, I don’t even know. This is fun because I’m like, “No, we never talked about this in school. We never learned this.” So I don’t know. I’m going to guess 400.

Dave Feldman:

Nope. You have about a million trillion.

Carole Freeman:

Oh, okay.

Dave Feldman:

So do your best to imagine a trillion, and then imagine a million trillions, right? It’s basically a one … It’s called a quintillion. It’s a one with 18 zeros behind it.

Carole Freeman:

Okay.

Dave Feldman:

So to give you-

Carole Freeman:

We’ve got one a person from California. Hello Facebook person from California. Welcome. Please share. Pop in your questions about cholesterol. Okay. So a number that’s so big we can’t even imagine it. Okay, got it.

Dave Feldman:

But I can give you an analogy, something else that’s measured in quintillions. It’s estimated there’s 7.5 quintillion grains of sand on every beach and desert all around the world.

Carole Freeman:

Okay.

Dave Feldman:

So if you counted every single grain of sand all around the world, it would come to that amount. And that’s about how much your body turns over every two weeks.

Carole Freeman:

Wow. Wow. Okay.

Dave Feldman:

It’s making those and turning them over constantly.

Carole Freeman:

And so we’ve become obsessed with a tiny little number. So the difference between somebody who’s say 90 LDL versus 400 LDL, we’ve associated that with bad things versus I don’t even know what decimal point that would be as far as actual change compared to how much is actually there.

Dave Feldman:

Well, actually, and then I’ll take it to the next step which is for all those boats that are in your system, you might be like, “Wow, that is so many proteins. I mean my bloodstream must just be packed full of them.” Actually I’ve calculated the surface area for what would be. So for example, an LDL particle is around 2.3 nanometers, which isn’t going to mean anything to you. But you can take it as what the fraction of the total blood volume is. So in an adult male there’d be like five liters of blood. So the total amount of that blood volume that’s taken up with these boats if you were to just put them all together is around 1 10,000 to around 1 5,000, somewhere in that range. So about maybe 2% of 1% to give you a sense of it. It’s hardly, it’s … Oh, go ahead.

Carole Freeman:

Oh, I was going to say so the old analogy of cholesterol clogging your arteries is definitely not what’s going on. Like there’s not so much of it in there that it’s just backing up and causing this sludge mess. That’s not what’s happening.

Dave Feldman:

Well, I’m not going to make a true/false answer to that because of course I am going to state plainly. I don’t know if cholesterol causes heart disease indirectly. For example, ApoB containing lipoproteins to just get a little bit technical are participants in atherosclerosis. The bigger question you’re really reaching for is, is atherosclerosis the buildup of plaque in the arteries, is it mediated mostly by your cholesterol levels?

Carole Freeman:

Well, I would more-

Dave Feldman:

That’s the question we have.

Carole Freeman:

Well, and I was more looking at like people visually who haven’t studied biochemistry. They actually have been conditioned. The analogy is like, no, it’s just like this big glob that get stuck in there, so it’s a mass problem, like the …

Dave Feldman:

Yeah, and that’s what I’m getting to, is that original analogy I brought up earlier definitely doesn’t hold, and that it’s not just this goop that’s kind of wandering around and finding its way into your arteries as described. It’s certainly much more complicated than that.

Carole Freeman:

Yes. And we’ll get there. So our Facebook viewer, I’m wondering this … I think this might be Penny, but I don’t know for sure, that hoping will talk about convincing her doc who’s only considering that you need to follow a plant-based diet and then follow up to that was doesn’t believe in any new science. So should we go there now? Should we work our way there?

Dave Feldman:

Yeah. I think, and this is where it gets interesting, because the energy model that I really since you met me was kind of the beginnings of the energy model. And what I mean by the energy model is it’s this sort of larger take, if you will, that I have. And I have a, for anybody following, they can go to cholesterolcode.com/model and there’s a poster. And the poster kind of walks you through these different elements that I’m talking about. So it might make it a little bit easier if you go and visit that.

Dave Feldman:

But the model suggests that indeed, if you’re metabolically healthy, it’s more likely than not, particularly if you’re lean, particularly if you’re like normal weight or even leaner and very low carb that you’ll be trafficking more of these boats, and therefore it’ll be a higher likelihood that your cholesterol levels will be high, not just your LDL but also your HDL. And typically your triglyceride levels are low, and that’s what I call the triad, is those three together, high LDL, high HDL, low triglycerides. And that’s common for somebody on a low-carb diet who is metabolically healthy, normal size to lean. That’s a common response.

Dave Feldman:

Now, this may be surprising if you’ve started out as really overweight and you’ve now gotten to a weight for which you still have a little bit to go. A lot of times those folks will either see a drop in their LDL cholesterol or a slight increase, or that it remains roughly the same. This too actually fits the energy model which I’m not going to go into yet.

Dave Feldman:

But I do want to get into the plant-based scenario where if you are low-fat high-carb, well then, you’re trafficking glucose more in your bloodstream, not fatty acids. If you’re trafficking glucose, you don’t need a carrier. Glucose is water soluble, so it fits right into your bloodstream, can move around just fine. And because of that in the same exact scenario, I would say, I would predict that it’s more likely your cholesterol levels will go down. And that’s why I could see how from a distance it looks like that’s just the most obvious decision to make if you’re wanting to bring down your cholesterol levels.

Dave Feldman:

And, for what it’s worth, if somebody were to come to me and they said, “Look, the only thing I care about is reducing my total and LDL cholesterol levels,” I would say, “Well, yeah, yeah, I mean consider going low-fat high-carb because that will succeed in dropping that down if that’s where you want to take it.”

Carole Freeman:

Well, and even when I was in school all those years ago, I remember our biochem class where our professor explained the mechanism where when insulin was higher, that was a driver of creating cholesterol in the body. And I had a light bulb moment even at that time, long before I’d even started following keto, that like, “Oh, wait a minute. So high-fat diet doesn’t cause like directly this cholesterol to go up automatically? It’s insulin which is high-carb diet is going to cause insulin to be higher and that is going to cause cholesterol be higher.” And I’m like raising my hand. They’re like, “Well yes, but,” and then the recommendations were follow a mixed diet, moderation, never mind the science that we just learned. Let’s go back to lowish fat and don’t try to restrict carbohydrates.

Dave Feldman:

Yeah. Certainly I feel very differently on that in the general view. Again, speaking just as far as being metabolically healthy, insulin typically brings up expression of your LDL receptors, it activates something known as lipoprotein lipase. Lipoprotein lipase is the enzyme that will take triglycerides off and in particular for your adipocytes which are your fat cells. So if you’re consuming a lot of carbs and you reach a point of maxing out your carb storage known as glycogen, then it’s time to store it. That’s why oftentimes you’ll see triglycerides go up in people who are consuming a lot. Whether they’re low-carb or low-fat, if you’re consuming a lot, your body wants to store it because that’s how we ancestrally survived to make it through the famines and so forth.

Dave Feldman:

So that takes insulin. Well, if you’re low, if you’re basically on a diet that results in lower relative insulin, then odds are you’re actually doing the opposite. You’re taking more of the fat out of your adipocytes and out of your fat cells, and you probably need to circulate it more depending on how low your total fat mass is. You may have to circulate it more in a global sense as opposed to in a local sense. That by the way is why the energy model kind of makes sense for when you are of a higher weight. You have more fat mass to muscle mass, and therefore, there’s more, if you will, local availability of those fat cells. You know what I mean? Hopefully that kind of unpacks that a little bit.

Carole Freeman:

So this is Penny that’s questioning here. She’s watching us live. She’s got, yeah, LDL and HDL are high but our triglycerides are low, so that classic high good cholesterol, low triglycerides, but the LDL is the wild card. Let’s start with can you just kind of in a easy for people … That’s one of the things I love about your presentations, is you’re always able to create these analogies that make it easy for people to understand when they don’t even have any science background or nerdy biochem background or anything like that. Can you help people understand? So what is LDL? What is HDL? And then what is triglyceride because people get those numbers on their lab reports and then they just rely on their doctor to be able to interpret those?

Dave Feldman:

Yes. I do have kind of a new analogy I’m going by that’s probably going to make it into our paper. You hear a lot about ApoB. ApoB is short for Apo lipo protein B, but you hear about it as very relevant because it’s on that LDL boat. So ApoB is that protein that carries it around.

Dave Feldman:

Well, you make ApoB in your liver and it’s constantly making these boats that are loaded up with triglycerides and fat soluble vitamins, basically all these lipids your body needs. So that boat, it starts really big, bloated with these things that your tissues need. And its job is to start big and to get small. And there’s really only one way it gets small, which is that it gets its cargo taken off of it. And not to get into the biochemistry of it, but its hull, the outer part of its hull are made of things that are also part lipid and part water soluble, but they have to shed. These are phospholipids. They have to shed as they get smaller. You don’t make things get smaller at these sizes without parts of it being shed. And here’s where it gets interesting.

Dave Feldman:

Correspondingly with ApoB there’s this ApoA1 which is really the species of HDL. And HDL is supposed to start small and get big. And that’s why we see an association with more HDL cholesterol having lower and lower cardiovascular disease, because that usually means HDL particles are being successful. Those boats are successfully getting their cargo. And we won’t get into the where the cargo comes and goes and so on and so forth, but we will say this much. On a constant basis what you want to be seeing in your bloodstream is you want to see those ApoB like VLDL and LDL succeed at dropping off their cargo, and you want to see the HDL succeed at picking it up. And the way that’s happening is at the port.

Dave Feldman:

So where’s the port? The port is any cell that needs it. Whether or not it’s muscle cells or your heart cells or your adipose cells, what’s happening is that the big boats are coming along, they’re dropping off their cargo, the ApoBs, they’re getting smaller and smaller, and at the same time those constituent pieces that are coming off of it are going on to the HDL boats that are getting bigger and bigger. And that’s why two years ago, two, gosh, it’s almost three years ago, I realized that actually so much important information comes from just those three markers together, those simple markers.

Dave Feldman:

Forget about NMRs and forget about a lot of these other things that, granted, I’m very interested in. You know I get a lot of blood tests Carole. Ridiculous amount. But a basic lipid panel actually tells you quite a lot right there with that triad, because when you’re seeing that your LDL cholesterol is high but you’re also seeing your HDL cholesterol is high and your triglycerides are low, to me it’s very suggestive that you have a very functional, very active low-carb lipid system. And it seems to be succeeding because your triglycerides are low.

Dave Feldman:

No doubt Carole, you and I have seen people who go on a ketogenic diet. They have high LDL but they don’t have what I just described. Instead, they have low HDL and high triglycerides. And I often hear from other people who are critics of my work that I’m just fine with high LDL in a ketogenic context. It’s not the case. I don’t care who you are or what diet you’re on. If you have low HDL and high triglycerides, that says to me that there’s a failure of moving that cargo across right. And that in a nutshell is why I started pursuing three years ago in particular this triad, and I even put out a challenge. You may have heard of it, the low-carb cholesterol challenge.

Carole Freeman:

Yes. I’ve been meaning. I can’t wait to ask you about how that went because I often cite that to my clients who they come back and their HDL is high, their triglycerides are in optical range, and then the doctor’s like, “Your cholesterol is through the roof,” and maybe they have like a 200 LDL or something like that. So I often would cite that Twitter challenge that you put out. So would you just reset like what that is for people that you did? And I don’t know the outcome, so I can’t wait to hear the outcome.

Dave Feldman:

Yeah. So I started about, again, it’ll be three years ago this February, February 13th. And what it was is I basically, I just made this image that said, hey, send me the best study that you have that shows those people with high LDL will have higher cardiovascular disease when likewise matched with high HDL and low triglycerides. It’s just very straightforward.

Dave Feldman:

And I said best because I thought I would get flooded. I was fairly new into my research and I thought that there would just be a fire hose of different studies, so I just wanted to see the best ones. And it was just sort of generally ignored, which I was surprised by because I was reaching out in a friendly way to a lot of the bigwigs that were out there, and there were a couple doctors who said, “Hey, I’ve got a study that meets your your challenge.”

Dave Feldman:

And then we went through it. It didn’t actually meet the challenge. But I remained encouraging. I was like, “Okay, this one doesn’t meet it if you look at this criteria. But let’s see if we can get.” And then six months later to the day I said, “You know what? I’m going to put a finder’s fee behind it.” And so I’d put a-

Carole Freeman:

You wanted. You wanted to find the truth. You wanted to see if this information was out.

Dave Feldman:

I do. Yeah. I do. And I really should emphasize this. Like I don’t, I’m not a scientist at a lab where I have access to, or nor am I researcher who has access to all of this data. But I’ve been seeking this data for a long time, particularly these three together. Because I, again, I think that if the LDL hypothesis of it being independently causal towards heart disease is not modulated hardly at all by other risk factors, then it should be fairly straightforward. You should see people with very high LDL, like you just mentioned. People let’s say at 200 LDL, they should have definitely above average cardiovascular disease.

Dave Feldman:

So six months later after I started that, I then put this finder’s fee of like $300. So if anybody could find a study that meets this criteria, and I laid it all out. And I didn’t even want high cardiovascular disease. I said just above average. If you have something that’s just like just above average cardiovascular disease for high LDL when likewise matched with a stratification of high HDL and triglycerides, then I have the reward. And the stratification by the way was like an HDL of 50 and above and triglycerides of 100 and below. And I know Carole, you and I both see people all the time that are way higher each day on way lower triglycerides.

Dave Feldman:

But that said, it’s not been met yet, and I actually brought up to a thousand I want to say six months after that, and it just, it’s been lingering there. I’ve never actually dispersed anything because it’s just, it’s not been met. And like I said at first it got ignored, then it started getting ridiculed, and then it started getting like pushback and so forth. I was like, again, this is me wanting to fund the debunking of this, you know what I mean? Help me disprove my hypothesis in this regard, at least the foundation of how this may associate back to risk.

Carole Freeman:

So originally when did you make the request that’s now a challenge? I missed how many years ago is that now or a year or …

Dave Feldman:

Be three years this February 13th.

Carole Freeman:

Okay. So this, and for those of you that aren’t Twitter people, I got to tell you, like Twitter is the place where people are going to be like, “Oh, I’m going to prove this person wrong, and here’s my proof, here’s the science, here’s the research article.” It’s not just where people argue about things. They actually, there’s a lot of people on there that are backing it with real research articles.

Carole Freeman:

So this means that in three years with a thousand dollar bounty not one person has been able to produce one research article, one study that’s ever been done that shows that if your HDL is in a good range, healthy range, your triglycerides are also in a healthy range, that the LDL number matters one bit. There’s no correlation between heart disease … cardiovascular disease, the broader term for that.

Carole Freeman:

I rest comfortably with that. But I also encourage my clients to make their own informed decisions about how they interpret those numbers. But again, so in three years nobody’s been able to produce even one piece of research that shows that that’s of concern. That says a lot to people.

Dave Feldman:

Well. No, hold on though. I will add a few things. So one, we do have two studies, and the two that I cite frequently that have stratified for it and that do show an association with lower cardiovascular disease. One with I think ischemic heart disease, and I forget what the other one is. But they both, they show near very close to about the same as the optimal levels but with low LDL. But, I’m sure critics, and they have, point out that there’s a slightly higher association with those that have the higher LDL. And I’ll 100% acknowledge that. That’s why I want even bigger data, because both of those studies, I think one was with 4,000 participants, one was with like around 5,000, something along those lines.

Dave Feldman:

So it’s still very compelling in that I can correctly say that every study I’ve looked at, and there’s these two. Technically there’s a third one, the third one, and I try not to talk about statins was on the 4S trial where they also stratified out and found that those people with low HDL and high triglycerides in the placebo group saw the worst outcomes when they did not have the intervention of the statin that was being examined in that study. But that those who didn’t, who were in the placebo group but who had high HDL, low triglycerides. Actually I don’t think it was. I think it was like moderate HDL and moderate triglycerides compared to what our standards are saw virtually no benefit. So technically there’s really three studies per se that stratify out this triad.

Dave Feldman:

Now, I again, I try to be a good scientist. I want to say, “Look, we don’t know what we don’t know,” and that’s why kind of helps me segue into I’m doing this study. This study has been kind of consuming my life, especially in the last year, and that we’re getting a whole bunch of individuals that have this triad at very heightened levels, which is a phenotype I like to call lean mass hyper responders. And we want to get a hundred of them enrolled and followed for one year where we’re going to get CT angiograms at the beginning and at the end of the year to compare with each of these individuals.

Dave Feldman:

But given the existing lipid hypothesis right this moment at enrollment, if we have some amount of time that they’ve already been a lean mass hyper responder to qualify and we will, there should already in that first tranche of data be substantial atherosclerosis. There should already be given how high their LDL levels already are, that should already be obvious, that should already be evident in the initial scans. And again, I want to be a good scientist. I don’t know what I don’t know. We’ll see when we get there.

Dave Feldman:

But I will say that I am at a minimum a little surprised that we’ve had, like certainly I’ve come to know some lean mass hyper responders with extraordinarily high levels of LDL who I’ve told them, “Your levels are comparable to somebody who has a genetic disease known as familial hypercholesterolemia.” Here are the things that they typically see such as tendon xanthomas or of course they may develop an angina at a fairly quick pace. We’ve already seen this with unfortunately small children who had that genetic disease. And that’s part of what’s convinced modern science that it’s LDL that’s doing it, not the genetics.

Dave Feldman:

I may have a different opinion, but again, I think that there’s more to the story at least, I guess you could say. And that’s why I want to find out and that’s why I tell them, that’s why I stay close with these people at the super high levels of LDL as the mass hyper responders to see if they develop these. Now, anecdotally speaking, I’ve not seen a lot that substantiated it, but I can’t say that it’s entirely conclusive that anybody who’s ever become lean mass hyper responders of no concern at all. It’s just, it’s certainly not matching the pattern at a population level that I would definitely expect for people with LDL levels that high, that they compare to those who have familial hypercholesterolemia or FH as they tend to call it.

Carole Freeman:

Oh, the more we talk, the more questions pop into my head. Oh gosh. Well, yeah. Oh, gosh, where do we want to go next? Let’s see. Those of you watching too, like what questions do you have about cholesterol for Dave? Your personal journey or other cholesterol questions too.

Carole Freeman:

Let’s see. So just to clarify then. The three-ish studies that have come up, what did you find as far as like did it meet … So you said two of them met your criteria as far as like optimal levels of HDL? Say again what those showed.

Dave Feldman:

Yeah. So one is the Jefferson study which I believe it separated them out into three groupings. And that one did have relatively high HDL in the smallest tertile, which I want to say was 57 and above I think.

Carole Freeman:

Okay.

Dave Feldman:

I’d have to double check on the triglycerides, but I think it’s something under 100. And then what they did was they stratified them out into these … Really they stratified below 170 LDL and above 170 LDL, which is part of why I liked it, was because 170 is already just about 20 off from the guidelines at the top level. So right now, if you came to your doctor with an LDL of 190, odds are they might diagnose you on the spot as having FH, as having this genetic disease, because how else could you have an LDL that’s high?

Dave Feldman:

I’ve been doing my darndest to stay in contact with the NLA and to emphasize that no, there does seem to be … This is certainly central to my research, this other LDL level that seems to be diet induced. Spence coined the phrase, and I like it, diet induced hypercholesterolemia. And unfortunately it’s not well recognized yet. I wish it would be, because my concern is that I think that there’s a lot of people who are going on a low-carb diet. Their doctor says they have FH, and then makes decisions that are life-long therapy related based on the assumption that they have FH.

Dave Feldman:

And I think it’s not a safe assumption, because if it’s concerning to the doctor and patient, they’re going to take steps to change that medically. They should at least know that dietarily you can change that, getting back to the energy model. You can if you want to take on marginally more carbs and even still be low-carb, but have to take on at least enough that your body needs less reason to traffic the fatty acids. So anyway. That’s kind of the challenge.

Carole Freeman:

And so that study then did show that the over 170 had a slightly increased correlation with cardiovascular events?

Dave Feldman:

Yes. I almost … I’m able to, yeah, I guess I am able to screen share on here, right?

Carole Freeman:

Yeah.

Dave Feldman:

I kind of want to kind of just pull this up real quick because I think I know how I can get to it quickly. Because when I say that it’s an increase, I want to say it’s like less than a percent change.

Carole Freeman:

And that also … Last time I saw you speak, you were talking about all-cause mortality as well as being even more important, right? So a lot of people hyper focusing on cardiovascular. But if you die from something else with a lower number, is that, and your increase of dying of something else is much higher than your risk of dying of cardiovascular, which is more important to you.

Dave Feldman:

Yeah. You’re really teeing me up here because it’s absolutely the case, that I put enormous … Here’s a running joke I’m sure you’ve heard me say many variations of which is what’s one activity I can all but guarantee will reduce your chance of dying of cardiovascular disease by 99%. It’s rock climbing without safety equipment. Another one is playing in the traffic. Another one is skydiving without a parachute. All of these things, you could correctly say they will reduce your chance of dying of cardiovascular disease. Obviously it’s hyperbole. What I’m trying to illustrate is that no, it’s not good enough to look at a single endpoint. You need to be able to see all the endpoints. You need to be able to see and really the ultimate endpoint is all of them together as all-cause mortality.

Dave Feldman:

Now, there’s already existing studies long before I got into this that show that actually high LDL is associated with longevity, is associated with lower all-cause mortality. And there’s additional nuance and context to it. But, as you know, once I finally got a hold of a large data set which was NHANES, I didn’t even bother with cardiovascular disease. I shot straight to all-cause mortality. I was like I want to see how the triad performs in all-cause mortality.

Dave Feldman:

And in the NHANES data, if you extract out, if you exclude those people who are on statin therapy and so forth so you could help to confirm there’s no confounders, it’s actually quite impressive. High LDL, high HDL, and low triglycerides appears to be the best combination you can have of all of those markers, that again, even when comparing high LDL versus low LDL with the same amount of high triglyceride, or sorry, high HDL and low triglycerides, then actually the higher LDL performs better. And granted, this is associational data, can’t emphasize that enough. It’s not necessarily causal, but that’s also part of how the whole model works is.

Dave Feldman:

And Carole, this is kind of the part that I never seem to be good about getting across to people, which is that the existing science, existing literature thinks of these boats, these lipoproteins as the cause of a problem, that they’re the source of the issue.

Dave Feldman:

Now, I do think you can have high LDL cholesterol and high LDL particles and it be for a bad reason. And I think the typical tip-off is the opposite of this triad, is having the low HDL, the high triglycerides. This even has a name in literature called atherogenic dyslipidemia. But I believe that this profile that appears, this low HDL, this high triglycerides, it’s not because the HDL is not doing enough of its job and it’s its own independent cause, and the high triglycerides being these triglyceride rich lipoproteins are independently the cause therefore of atherosclerosis. I would argue, as an engineer, this is kind of like looking at a network and trying to pick out which packets are the worst because you think the packets are the problem. I would say isn’t it possible though that it’s actually that which results in the characters of those packets?

Dave Feldman:

Sorry. That was a little bit geeky because you guys probably know what packets are, but-

Carole Freeman:

There may be an engineer watching here somewhere, so.

Dave Feldman:

Yeah. My point is I think it’s the profile, it’s what the lipid patterns are telling you about the state of the individual, and then it’s like you’re wanting to shoot the messenger. Now, this isn’t to say that it isn’t possible that both are true, that there could be some form of the lipid hypothesis that is in fact true. It’s just that an easy way for us to test that was to go and look at healthy populations with the triad. It’s the easiest possible way to test it.

Dave Feldman:

And that’s why I wanted to get a hold of NHANES. That’s why I like to get a hold of these other data sets, especially if they have longitudinal data, because I posit it and I still do to this day that the triad is going to show generally much more positive results, especially at a population level. And that’s why we’re doing this study. We’ll see. We’ll see with even those people at the highest levels of LDL.

Carole Freeman:

Were you the one that came up with the ambulance analogy where is it, if you look at accidents on a freeway and you look at the number of ambulances responding to car accidents and are you going to blame the car accidents on the number of ambulances there or are you going to blame it on actual accidents?

Dave Feldman:

I’m sure because I think that analogy was used in other contexts so I doubt I’m the one who originated it, but it’s definitely a way for you to recognize cause and effect relationships. So whenever you read a headline on some paper that says such and such linked to such and such, usually it means it’s associated. And an association is important because a basic example that was provided that I still like to this day is they find that people with red cards get pulled over more often. Oh, that must mean if you get a red car, you’re going to get pulled over more often. Is it though? Or is it possible the people who are attracted to buying red cars are already the kinds of people who like to drive cars fast?

Dave Feldman:

Well, science is supposed to be adamant about reducing the likelihood of other things that could confound that. So before you can say A causes B, you have to rule out two other things. You have to rule out how much B can cause A, and you have to rule out other things that can cause both, a C or a D or an E or an F, et cetera. So I think, and I can be wrong, that a large amount of what is the problem of atherosclerosis, this buildup of plaque in the arteries, can result in higher LDL levels as in the case of some genetic abnormalities but also in the case of being highly inflamed. I think you can get this atherogenic dyslipidemic profile, and I think that that can move up your LDL levels, but it will probably do it alongside higher triglycerides and a lower HDL.

Dave Feldman:

Again, this is just my hypothesis, but that’s what I think the data is telling us because in every turn that I’ve been able to find, the triad is associating not just with lower cardiovascular disease in general but with greater longevity, which is like less dying overall. At low levels of LDL you have a higher association for example with cancer. That’s not to say that low LDL causes cancer. But we can’t necessarily rule it out either. That’s why we, again, we just need to follow these individuals more to actually get clinical data to know. Bottom line is, let’s stop testing sick populations to come up with our conclusions. We need to test more healthy populations. That’s for sure.

Carole Freeman:

I’m keeping an eye on time. I know you got to get out of here in about less than 10 minutes, so we’ll make sure we wrap this up for you. I know you said you’ve got … You’ve always got an experiment going on. So can you share us like what you’re personally working on right now?

Dave Feldman:

Yeah. No, no, I started Thursday, did I? Or Friday. No, sorry, I started Friday, and today is the third day. For five days I’m eating my “baseline” diet. There’s a diet that I decided on a while ago because it works for traveling and so forth, but it needed to be very fixed, so that when I had a washout period, I could always check what that blood work was at the end of the washout against other washout periods to know what differences there were. That diet is not going to sound super exciting. It’s just cheese, hard-boiled eggs, and all beef hot dogs. And the reason that was selected was because I can actually get it in probably any place around the United States, and because I travel a lot, or at least I used to before COVID, I knew I could get those products just about anywhere of that particular brand. So I could be confident that it was portable.

Dave Feldman:

Well, I have a multivitamin as well and I also supplement salt tablets. Now, I’m going to have that for five days, and I’m going to eat exactly the same meal at 9 a.m, 2 p.m, and 7 p.m, and that’s what the normal baseline diet is. But starting Wednesday, I will get my blood work in the morning to confirm against that baseline, and for the next five days I will be compressing it to where I’ll be eating at 4 p.m, 5:30 p.m, at 7 p.m.

Carole Freeman:

Oh, an intermittent fasting test.

Dave Feldman:

Exactly.

Carole Freeman:

Okay.

Dave Feldman:

And what I like about it is I’m going a step further. It’s kind of a big pain in the tuchus, but I’m also getting … Six times a day I’m getting both ketones and glucose and lipids. Once when I wake up, once at 7 a.m, once at 9 a.m, just before I eat, once at 2 p.m just before I eat, once at 7 p.m just before I eat, and then finally at 10 p.m before I go to sleep. And I suspect that’s going to yield some pretty good data. So far it already has, and that part I can’t share, but-

Carole Freeman:

Okay-

Dave Feldman:

… it’s pretty fascinating to see the patterns. But I’m interested to see what they look like when I start heading into the intermittent fasting phase. We’ll see.

Carole Freeman:

Okay. Cool. Very cool. And then the research that … the bigger scale research that you’re doing. Is that still in recruitment phase? Can people sign up for that or is that, where’s the stage of that?

Dave Feldman:

We haven’t started recruitment. We’re in the process of drafting the protocol that we then send to the IRB committee.

Carole Freeman:

Okay.

Dave Feldman:

We hope to be submitting that soon. Naturally my partners would get annoyed if I didn’t mention. You can help us out by going to citizensciencefoundation.org. And if you do, know that we’re actually a bonafide 501c3 public charity. So your donation could be tax exempt. Please, see your tax preparer, but typically it is. But yeah, Citizen Science. I mean, we raised the money on this from private individuals because I got tired of trying to go the public route. But I think it’s absolutely crazy to me that these lipidologists in this very field that I’m swimming in, aren’t absolutely over the moon trying to study the same exact thing. It’s just such a big deal in my opinion, but whatever.

Carole Freeman:

Yeah.

Dave Feldman:

Obviously I’m biased.

Carole Freeman:

Like Penny’s doc that’s like, “I don’t want to look at new science. We’ve already got this figured out. So why should I even try to look into it even more?” Well, just in wrapping this up, thank you so much Dave for being here. Just in wrapping this up, any closing thoughts, anything else you wanted to mention real quick before we wrap this up?

Dave Feldman:

Yeah. One, if you see just 1% of 1% of my research, you should at least know that your lipid levels are typically very malleable. I really do feel like if there’s any one thing people should take whether they believe in low-carb or not, it’s that they shouldn’t make life-long medical decisions from a single lipid test, especially if it seems to be something that changed due to diet. So that would be one thing. Two, please be sure you’re fully fasted when you get your blood tests. I know that that’s a change that they’ve made over the last five or 10 years or something like that. But if you are on a low-carb diet and you are powered by fat, you’re almost certainly going to have high triglycerides, even though we just talked about it, if you have a a test that’s not 14 to … or sorry, 12 to 14 hours water only fast. Try to fast for at least that amount of time.

Carole Freeman:

I didn’t even know that they’d made that change in lab recommendations until like I think it was just a few months ago I saw the protocol change. I was like, “What?” So apparently they’re telling people that you don’t have to be fasted for your test now. But it’s like, how? There’s so many things that you absolutely need to be fasted to interpret because we haven’t interpreted information of people who’ve just eaten. So all of a sudden we’re throwing that in the mix? I was just like, “What is this world coming to?” Yeah, nonsense.

Dave Feldman:

Well, and unfortunately a lot of doctors spring in on their patients. Like the patient comes for a visit and they’re like, “Oh, well while you’re here, we’ll just go and get your blood work.” Well, if you just had a big fatty meal three hours ago, you literally installed triglycerides into your bloodstream because that’s, again, just as I was talking about, those are the boats that are dropping it off for you. So my two cents is just be very cautious with that. Make sure you try to get a fasted test, just because it’s the number one thing that comes to our groups.

Carole Freeman:

And water water only for 12 hours, right?

Dave Feldman:

Yes. Try not to consume anything else if you can.

Carole Freeman:

Fasting also includes liquid calories that you drink. I remember looking at people’s labs for so much at Microsoft, and one dude came in and his triglycerides were super high and I was just like, “Oh my gosh, what’s going on? Are you fasted?” “Oh absolutely. Well, I just had coffee this morning.” And I was like, “Okay, so anything in that coffee?” “Oh yeah. I just had a white chocolate mocha at Starbucks, a venti, 400 grams of sugar in it.” I was like, “Okay, so just so you know, I know you didn’t eat any food, but that’s actually still this.”

Carole Freeman:

We’ve got one quick little question that popped in here last minute. Well, how do I get my doctor on board with this information? Any quick suggestions for that Dave?

Dave Feldman:

Don’t underestimate your own ability to bring new information to your doctor. There really are a lot of doctors who, I mean, most of them push back, but there are definitely a number of them that now follow this work, particularly if you’re not the first keto patient, you don’t know if you are, who’s brought this to their attention. Feel free to send them our way to Cholesterol Code. We put special emphasis on responding to doctors who are not low-carb doctors to, and again, in the politest way, try to bring them as much information and dialogue as possible to help answer their questions.

Carole Freeman:

Yeah. And all else fails, there’s new doctors that you can consult with that may be open to this information too. I know you got to run. Dave is so great at actually following very strict protocols. For all of you out there that are saying like, “I’m so bored with my keto foods,” like did you hear what he’s eating for five days? Hot dogs, cheese, and hard-boiled eggs for five days straight, so.

Dave Feldman:

Not for the first time.

Carole Freeman:

Stop complaining about being bored with your keto diet. Anyways. Dave, thank you so much for being here. It’s so great to see you. I miss seeing everybody in person, miss you so much, and thanks for sharing all this. Well, contact information is going to be, all the links that he’s mentioned and all that will be in the notes section here. So reach out to Dave and thanks everyone for watching.

 

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