Dave Feldman, known as Dave Keto around the internet, is one of our favorite researchers today. Like our host, Geoff, he’s actually a computer engineer by training. With a systems engineering approach to the human body, Dave has one of the most interesting and nuanced ideas around metabolism, lipidology, and cholesterol.
With years of rigorous n=1 self-experiments around low-carb and ketogenic diets, Dave is helping drive a new conversation around cholesterol and challenging the traditional lipid hypothesis.
I think there's a lot of ways we can take this program, but I think I'd like to start from our backgrounds. I think we're cut from very similar cloths, and hopefully, I'm not too arrogant to presume a similar background, but I know that we're both computer scientists and engineers by background, and I would say sort of apply the engineer systems thinking mindset to the human body. I think that's the way I like to describe myself at least, and I would say that my story, I came at it from more of a human performance perspective. How do we take someone that's healthy, how do we make them better? And I think you came from more of a health or a medical perspective. How do you get someone maybe that's not looking healthy or preventing disease, how do you get someone from a not-so-healthy outlook in terms of health span and lifestyle and bring that back to something happier.
So, from that lens, I think my audience and I think all listeners would love to hear a background story of how you as a software engineer by training became, I would say, one of the most well-read and cited researchers and scientists at the edge of low-carb research. I don't mean that lightly. I think when you talk to a lot of active academics, you know your stuff. You're very well-read on literature and very deep on that. So, how does that from software guy to you kind of have an encyclopedia on all the latest on cholesterol, keto, low-carb?
It is funny because I'm just barely three years into. When you go back three years and a few months, and I don't know anything about cholesterol and lipids or any of that, but to your point, before going in a low-carb diet, nobody would've considered me sick, including myself. No way, and so, this is where it's interesting because we see a lot of this nutrition science advancing from one of these two fronts, right? A lot of people go on low-carb, really, I would say probably most people go on low-carb because of a health crisis or because they're concerned about losing the weight. It's only really been kind of a more recent, modern phenomenon that a lot of athletes are saying, "I want to try something really new, and I have a friend who has been doing this," and so forth, and they observe it happening. This is where it kind of gets very related to my research because those people who are in the health crisis who go low-carb, particularly if they are starting very overweight, will tend to see their cholesterol drop when going low-carb, in general, not always, but a lot of times. Particularly if you're going from, say, obese to overweight but not all the way down to thin.
But you have a lot of people like us who you ate low-carb. Let's say you're very lean. You're very fit, and for that matter, you're full-blown keto. You're really keeping the carbs down. Your chances of seeing higher levels of cholesterol have just jumped up. That's a lot of what my research is showing, and that's what happened to me. My dad and my sister started low-carb around the same time I did because they got inspired by what I was doing. They got their blood work, but I was doing marathon training. They weren't. Their numbers jumped up slightly. Mine jumped up by a lot, and at that time, there was no resources. There was just nowhere to go to find out about what this means. What does it mean to see my cholesterol go up while going low-carb?
Yeah. What triggered that initial experimentation? Was it a personal interest?
Well, this is where being a software engineer really ended up changing the game because, and a lot of times I say this, this isn't false modesty. I think this could have been another senior software engineer, similar to me, that might've ended up in the same situation. You have a lot of free access to a lot of important information, like lipidology, which is the study behind lipids, which are cholesterol, and they're also the fatty acids that move around inside your body to fuel your body, right? That access, I mean, before, you'd have to go to a university. I don't. I can not only go on and read different articles, but I can go on YouTube and so forth. So, I can become pretty self-educated fairly quickly.
Right. You can go on PubMed like every other grad student.
Correct, and then, on top of that, I had this different perspective that you'll relate to in that I'm already used to looking at networks, and pretty much all modern networks have a much more distributed base, as in you don't have one thing that's entirely authoritative and telling all the other things what to do. You can't, not really, because it won't scale, right? So, what you do is you have a distributed object network. So, they're distributed, and basically, you have what would be the intelligence of it spread out over several different things, which is kind of like the brain, right? There's not one brain cell that runs the show and tells all the other brain cells. No, between all of them talking together, just like an ant hill, you have some intelligence, and there may be some areas that are more important than other areas, true, but all things considered, the more that I was getting into lipidology, the more I found that it was like a network, and I stand by that to this day. It was a distributed object network. The code is in the collective, and the very first thing that I noticed that was right there physically in the literature, but wasn't spoken about as such was that it was an energy distribution system.
No, arguably, its primary purpose of these lipoproteins, these lipo-carrying proteins, I mean, had many jobs, but its main job was to deliver these triglycerides, and triglycerides are the fatty acids we're fueled on. So, right now, if you go to your doctor, if you get a lipid panel, right, there's four tests you'll see. You'll see total cholesterol. I'll see HDL cholesterol, the so-called good cholesterol. You'll see LDL cholesterol, the so-called bad cholesterol, and you'll see triglycerides, and really, once you start getting the hang of it, it's actually pretty easy to understand what's going on. These lipoproteins, they're like boats that your body makes to move around these lipids. Well, HDL cholesterol is not really a cholesterol. It's really just cholesterol found on high density lipoproteins, HDL, and LDL cholesterol-
And these are the boats actually carrying the cholesterol, yeah.
Yeah. Your body makes these boats, and they make them. The hull of the boats are the same membranes that line your cell. It's called phospholipids. It's really kind of exciting because you know how oil and water doesn't mix well, right? Well, your blood is water-based. So, how do you move oil in through your veins and your arteries? How do you pull that off? Well, your body is actually a genius about this. It makes these little boats, packs the lipids inside, and it's not just cholesterol. It's not just triglycerides. It's also fat-soluble vitamins. The vitamins that also are oils. Have you ever taken vitamin A, D, E, or K?
Yeah, they're always in fat. They're always in olive oil or something.
Exactly, they're always in a little ... or they're in a little capsule that's soft, right?
It's a soft gel.
It's because these are all lipids. Right. Because your body takes great care because your cells need it. It takes great care to package them into these lipoproteins. So, as I'm learning about this, I'm like, "Whoa! This thing looks so much like a network. I swear it's got to be dynamic." But at the same time, I'm kind of second-guessing myself, like, "Am I just projecting my own profession onto this field of knowledge?" But then, I started rapidly testing. I started taking tests every couple weeks, and eventually, I started testing even every day, and I found that I could move around my LDL cholesterol and my HDL cholesterol, my triglycerides. All of these markers that are in that test, I can move them around very rapidly.
So, you were doing venal blood draws daily?
Yes. This is kind of the story behind that first one. I first had eight data points over three months, brought that to Low Carb Vail, talked to a number of the different doctors there, but in particular, I talked to Ivor Cummins who, of course, everybody knows who Ivor Cummins is, the other engineer who is also into cholesterol.
The Fat Emperor on Twitter.
Yep. And I said, "I'm going to go ahead ... " because the only way I can really feel this out is to just do this over one week. So, over one week, I'm going to eat to a particular food plan and see if I can induce this pattern that I'm seeing, and the pattern, now, is somewhat well-known within the low-carb community, is the inversion pattern, which is to say that whatever your cholesterol levels are at, if your cholesterol is normally at, say, this level, and you eat a lot of fat, it will drop, as in your LDL will actually go down, right?
Which is super counterintuitive, right?
Correct. Let's say your cholesterol is right here. Your on a low-carb, high-fat diet, and you have a lot more fat. You actually eat a lot more fat. Your LDL cholesterol will go down, typically, in response to that, and after I demonstrated this in my first public presentation, I had a lot of people requesting, "How'd you do that?" And I was like, "Well, I actually just ate lots and lots of fat, lots of fatty meats, lots of heavy whipping cream, et cetera." And it basically ended up being called the Feldman protocol, and I wrote it up as something that's now up on the site at cholesterolcode.com, and so, a lot of people have done this in order to drop their cholesterol. It has about an 85% success rate. It's not 100%, but it's striking how common it is, and in fact, we did an experiment about a year and a half ago at Keto Fest, where we had two dozen people do this all at the same time and the same thing, about an 85% success rate for everybody. About, I want to say, 19 out of 22 saw their cholesterol drop somewhere between 5 and 38 percent.
Which is insane and very, very counterintuitive.
Just to underline it for the listeners here, when you talk to typical, trained primary practitioner, when you ask them, "How do I lower my cholesterol?" They'll say, "Eat less fat. Eat more vegetables." Essentially, it's a zero sum game. If you're not eating fat, you've got to be eating carbohydrate or protein, and what you're saying is that your data and the data you've collected from folks around in the community is completely opposite to the recommendations of what primary care practitioners are telling people.
Well, let me caveat real quick because on low-carb, my baseline cholesterol will be higher. So, it's really kind of two time scales, if you will. One is what metabolic diet I am on, and in this sense, the practitioners are right. So, let's say that I decide tomorrow to become a low-fat, high-carb vegan. I'm quite confident that my LDL cholesterol will not only go down, but I know how I could probably get it to well below 100, maybe even like 70, right? But why that is comes back to the central core of my hypothesis, what I had called The Lipid Energy Model, which is the reason for this is that, now, I'm not being powered by fatty acids. I'm being powered by carbohydrates, and if I'm being powered by carbohydrates, it means it's going to get it converted to glucose. It means more of my energy stores are in glycogen, and there's less that's coming in on the fatty acid side. Now, why would this have an impact on my cholesterol numbers? The reason is because the cholesterol found in LDL, LDL cholesterol, that was a boat that started out, most of the time, as a VLDL, very low density lipoprotein, which was bloated with triglycerides. Why did it start out bloated with triglycerides?
Because that's actually where you're getting fueled by fat, quite a bit within the diet. Now, you may be fueled, also, by chylomicrons. That's another lipoprotein from food you just ate, and of course, the one you hear about all the time, which is ketones, which is fatty acids broken down into ketone bodies that don't need to be transported around in these lipoproteins, but here's the secret. The secret is, why would we call it the keto diet? When you really sit down and do the math, actually, we're powered much more by the direct delivery of fatty acids, many of those board these VLDLs, which will then, ultimately, as they drop them off, remodel to LDLs. VLDLs last for a small amount of time because they quickly drop off their energy. LDLs will last anywhere from two to four days because they serve other purposes within the body, and a cholesterol that's found on board of these, that's what they're going to zero in on. So, in a sense, they're right. If I decide to go ahead and get powered by glucose, and therefore powered more by carbs.
So, a high-carb, low-fat diet? I believe you might've inverted that, just to make sure that's not low-carb, high-fat vegan diet. You're meaning high-carb, low-fat vegan diet as an example.
Well, and for that matter, I did a recent experiment. I don't know if you had heard about it, but I really wanted to demonstrate that it wasn't even food quality. So, I ate a diet that I was quite confident nobody would recommend. I had white bread and processed meat. What I did was I isolated down to not just white bread, but I got Wonder bread, which is just trash. I do a lot of these experiments so other people don't have to. So, please don't get inspired by any of the things I'm about to say. I knew if I just gorged on white bread and lean, processed meat that my cholesterol would drop, and I predicted that and even posted it in a video, which I kept private right up until the point that the experiment was concluded, and then, I switched it on. So, it was time stamped. That experiment, indeed, my LDL cholesterol, the start of the experiment, at the point where I finally ramped up to full speed, my LDL was, I want to say, 296, so about 300, and in seven days, I dropped it to 83, from 296 to 83.
Which is massive, yeah.
So, I dropped it, effectively, 213 milligrams per deciliter in seven days, something no drug that I know of on the market could accomplish, right? All I did was I changed my metabolic pathway. I was going from a fat-based energy source to a carb-based energy source. That's it, right? And this is important because I really want to emphasize this. The reason I can feel as confident as I do right now is not because I am certain that the so-called lipid hypothesis is wrong. The lipid hypothesis postulates ... This is decades old. This is the one we all hear about, which is higher cholesterol just means high mortality, particularly from heart disease. It's because what I feel they don't account for properly is the metabolic aspect of this. So, I do think you can have high LDL and it be a bad sign, but I'm very careful with my wording here. When I say having LDL as a bad sign, I don't mean the high LDL is, itself, the causal or the instantiating problem. I don't know that that's ever quite been demonstrated. We can see that it's a part of atherosclerosis, but we don't yet know to what degree it's recruited, for the same reason you coagulate in your blood and so forth, right? There are so many mechanisms that call upon LDL in the point of crisis.
So, this is a distinction between causality and correlation. I think it's another way to look at it.
Exactly. Exactly. If you see ambulances at car accidents, but you don't know anything about ambulances, you could correctly say, "Hey, I see a strong association between these big vehicles."
Wailing red light. Yeah, with red crosses.
Right, and if I told you right now, if I said, "So you know, ambulances are also a death trap. Of any vehicle you can ride, for each minute that you spend in an ambulance, your chance of dying is so much higher than your own car. So, don't ride in one," right?
You know better. You know that there's a good reason why you're more likely to die in an ambulance since because you were probably injured or somehow dying, which is why you're in an ambulance, right?
Okay. So, then, we already know if you and an animal ... They do this all the time in animal models. They will do something called denuding where they beat up, say, the carotid artery on purpose, and that will induce atherosclerosis, atherosclerosis being the buildup of plaque in the arterial wall. We know this is happening because it's a reparative event. As a result, it's attempting to do something about it, and some amount of atherosclerosis can be regressed. Everybody acknowledges that. So, how much of this is a process that's already in place to deal with a problem you brought, such as, say, with smoking, which has nothing to do with cholesterol production, but has everything to do with atherosclerosis and heart disease, right? They have to disentangle that. They have to be able say, "Okay," because you could say ambulances caused traffic accidents. It could be that you've got really poor-driving EMTs and so forth, but first, you have to control for what amount they're helping. You have to be able to isolate. They haven't achieved doing that yet.
So, getting back to why it is that I can feel the comfort level that I do thus far, which isn't saying that I'm 100% comfortable, just more comfortable than probably most people who have higher LDL, is that I see context as being very relevant, and the context that I've seen so far in the literature is pretty strong that if you have high HDL cholesterol, and you have low triglycerides, then your LDL becomes very, very irrelevant whenever they put those three together. When you look at the HDL and the triglyceride ratio papers, when you look at the ones where they have those, the triad I'm speaking of, where it's high HDL and low triglycerides, or for that matter, when you look at the papers that look at it from the other direction, where people have low HDL and high triglycerides, that's called atherogenic dyslipidemia, and it's typically associated with having a lot of small, dense LDL particles. That's the dark direction, right? Now, I'm in pursuit of trying to get more data on this triad to try to see for ourselves, and of course, we have a lot of people who are emerging from the low-carb community who, themselves, exhibit this triad. I have to say, right now, the data looks encouraging. Again, try to be a good scientist, and I don't want to say I know what I don't know, but thus far, it's looking pretty good, and that includes my own CIMT data, which I don't know if you're up to speed on this one-
I am not.
... but I am kind of rambling here, if you don't mind, but CIMT data, on the left and right side of your neck is something called the carotid artery. It gives blood and oxygen to your brain. It's super vital, and what they'll do is they'll measure the thickness of the sides of the walls of this to get a sense of your atherogenic burden. It's not a perfect test, but it's actually pretty decently correlated with what your genuine risk is. While on a ketogenic diet and running at LDL levels above 200 milligrams per deciliter, which is considered super high, and LDL particle count above 2000, which is also considered super high, my CIMT has been getting thinner, not getting thicker. In fact, that's not even supposed to happen. It's supposed to say about the same or progress with my age. It was getting thinner until I did one experiment last year called the weight gain experiment, in which case, it shot up on both sides.
Whoa. And you were eating?
I was eating just bread and fat and pizzas. I was having subway sandwiches...
Okay. So, just over caloric.
Yeah, and I was intentionally trying to gain 20 to 25 pounds of fat for that for other reasons that I won't go into. It's a long explanation, but I was curious what my CIMT would do in the wake of that experiment, and sure enough, it had jumped up on both sides, and just to finish, I've since gotten one more, which was last month in December, and it's regressed again after going back to keto and after, once again, having super high levels of LDL and LDLP.
Which is very cool data. I want to get back on some of the more experiments, but I think what you touched upon, where I think it's very important, I think it's under-discussed, is the differences between someone who's healthy looking optimize their biomarkers, versus someone that's obese looking to lose weight, and I think the energy network model is a very elegant way to describe why you'd expect someone who's healthier looking to get even more fit or even better biomarkers would see an increase in LDL because you're going to be driving moisture and metabolism from fat, and therefore, you need more of these transporters, these boats, to fuel your fatty acids around. That makes sense, I think, if you just look at it from a systems perspective. Here's another perspective on, for obese folks who have probably some broader metabolic problems. Why do you see the LDL going down, and how do you explain the variance there?
So, this is theoretical, to be sure, but my theory is fairly is straightforward, in that you're moving from what is a more metabolic deranged-based state to a metabolically healthy/flexible state. So, you remember how I said a little bit earlier that I do believe LDL can be high for a bad reason? Now, I want to kind of go back to ... because I think this analogy will carry now since I sort of talked about these in terms of boats before, and this will also help as to why having low triglycerides are relevant to this larger equation. So, you have these boats, and the job of these boats, whether you're on a low-carb diet or not, is to be available for your tissues who need the contents inside these boats, particularly those fatty acids. So, even if you're on a high-carb, low-fat diet, there's still some degree, if you're healthy, with where your body fat, during the periods of time where you're fasting, and you're between meals, or you're sleeping, right, that your liver will release these boats, these VLDLs, and they're moving about and whatever tissues are like, "Oh, yeah. I need some energy," they've got receptors that can bind to them and pull the cargo off, right?
So, they're constantly docking and dropping off their triglycerides, and that's why, whether you're on a low-carb diet or a high-carb diet, you should see low triglycerides because it suggests that these boats are finding places to dock and drop the energy off properly. Okay. Now, what if there's a problem? What if you're not dropping off energy? Why wouldn't you be dropping off energy to these tissues? Well, you wouldn't be if they're maxed out. So, if your own personal fat threshold is exceeded ... because you'll hear the terms personal fat threshold a lot. I'm sure you may have even talked about it with guests already. It's a threshold point with where your adipose tissue is maxed out.
We're maxed out. Yeah, we can't hold anymore.
And this is a problem because fat cells don't get the credit they deserve. We'd like to just not have any of them. We'd like to not see them expand and so forth. These guys are pros. These adipose site, they are good at staging and pacing your fat into and back out of. So, I like to liken them to sort of food banks if you will. Imagine VLDLs sort of like the large trucks that unload a whole lot of food into them, and then, there are nearby other tissues that want that fat over time. So, during the fasted period, it's fine. They're slowly sprinkling it out to nearby tissues that can, then, use it, right? But no, in this scenario, you've already maxed them out. You've been eating and eating and eating. You're just chomping down those pizzas. You're chomping down the ... and what happens? You get it so maxed out that even those boats that are supposed to be there, I mean, they're important for your survival, are just packed full of these triglycerides. They've got nowhere to park it, right?
So, what happens in that circumstance is you start developing something call ectopic fat, and ectopic fat, the best way to just ... in layman's terms is it's fat being stored in tissues that weren't designed to store fat. So, you've heard of fatty liver, right? You've heard of pancreas accumulating fat. You've heard of the heart accumulating fat, muscles accumulating fat. Anywhere you're having to put fat where it doesn't belong is another way of just saying your body's ran out of room, and that's a dark sign. You need to go after that, but there's one other thing that can happen now. Those boats that, now, are just trying to pack on the fat wherever they can, there's a lot of them. A lot of those VLDLs end up still becoming LDLs. So, now you have high LDLs-
It's in your bloodstream. Yep.
... for a bad reason, and the bad reason couples with having high triglycerides. You're seeing that. You're seeing these boats all bunched up in the harbors not knowing where to go, right? Now, let me go the other direction to give a nice contrast. Now, instead, you are a lean, mean, low-carb, fat-burning machine, right? So, I'll see somebody. There's an ultra marathoner. I can't use his name because he wasn't to remain anonymous, but there's an ultra marathoner I know, and he has LDL ... Well, I'll just say it's in the numbers that his doctors were freaked out about, but he keeps turning around just great biometric markers. His LDL is super, crazy high, yet, his triglycerides are super low, regularly turning around something in the 30s, which is unheard of, 30 milligrams per deciliter, right? Well, I'm an engineer. What am I doing? I'm looking at empty boats, LDL, that probably started out as VLDL, that probably needed to be at that capacity in order to meet this super high demand of triglycerides because this guy does not run on carbs. He runs on those fatty acids, right? So-
Yeah. No, sorry to cut you off here, but I think that's a super elegant explanation. I think it, also, explains, also, fasted glucose levels. If you're looking at glucose as fuel or sugar as fuel or triglycerides or fatty acids as fuel, it's also the same explanation for Type 2 diabetes where you have so much packed sugar that your fasted sugar starts rising, and that's a sign of Type 2 diabetes as opposed to looking at or prioritizing sugar as a fuel or fatty acids as a fuel. You're saying, "Let's look at the network. Your cells require some energetic demand," and whether that's high sugar or high triglycerides for a bad reason, that means your body's not efficient at processing this extra energy, and that's a sign of metabolic dysfunction, which I think is a very elegant, almost like a physics explanation, as opposed to sort of a small little micro picture that people are looking at, which I think is very well articulated. That makes a lot of sense. Very cool.
Yeah. For me, I was never a deep math engineer. I was always an abstract mechanics engineer. So, I was always the guy in the room who was always looking at it from an architect perspective. I always needed to see, holistically, the larger pattern. I needed to see how it all kind of fit together, right? And per what you're talking about, for me, this is ... I feel like, eventually, everyone will just kind of get it to that sense, if I'm right, and then, past that point, we can start looking at this from a metabolic framework, which I think, if I'm right, is imperative that we start doing as soon as possible, right? But this is why. It makes perfect sense why you would see high glucose coupled with high triglycerides. What's happening is the whole thing is now getting overloaded, and there's nowhere to put the cargo, and we already know that these patterns align in a properly functioning metabolism. They become disparate, and it almost becomes like a spin wheel of choose your metabolic fate as to why things go bad because the system's trying to figure out what it can do, but that, it doesn't have a lot of practice with.
Ancestrally, we don't have a lot of practice with food availability around the clock. We don't have that. We've had plenty of practice with famines and food scarcity, and that's why our body has so many things. It has so many hormones having to do with bringing up energy. It really has just the one hormone, insulin, right, with packing it away, and it's also why insulin, I mean, it's really fascinating because when you learn about the insulin ... You may know this as a software guy. Have you heard the term composite response?
So, a composite response ... I have an analogy for you. It goes like this. Imagine you're running a diner. When you're running the diner, you have opening hours where you've got the customers coming in, and you're doing business as normal, and then, you have closing hours, and during closing hours is when you get stuff done that you can't do while the customers are there, right? But what you do in the after-hours can be multiple different things. So, there's janitorial work, oh, but you know what? Now, you need some people to reset the IT, but that can happen at the same time that the people are doing the janitorial work, or there's somebody who needs to patch some drywall, right?
So, paralyzing some processes.
Right. Right. For that matter, it makes sense for you to try to push everything that you wouldn't want to be a part of the customer experience to be in those after-hours. Therefore, it's a period of time for which there is a possible number of different things you'll do. It's a composite of these things, right? Now, here's the catch to that. There's a downside. What if one of those tasks takes too long? Well, then, it impacts your opening hours, right? The patching of the drywall kind of goes out of control. Well, you don't really have something you can do about that. You've got to just keep the place closed until the work is done. Well, think about this from the body perspective. You have insulin coming in, and it's got a lot of muscle. We're talking sympathetic versus parasympathetic. We've got, "Hey, we need to every time all the cells know it's time to go ahead and grab energy, and we need to also arrange a whole bunch of other things at the same time." It's not surprising that things like the immune response would also piggy back on top of that because it's kind of a conditional event, right? I would call it a composite response.
Okay. So, what, then, happens if you have the response persistently? What happens if insulin remains on, so the shop remains closed? How do you deal with that? And the short answer is you don't, right? You try to work around it, but ultimately, the cells themselves, because they manage their own operations, start trying to ... they bring down their own insulin sensitivity, understandably so, because they have to do some form of autophagy, but for the most part, they're being prevented from the level of autophagy that they would accomplish if they just had less of the insulin. That's why whether you're low-carb or high-carb, I have yet to see anything that provides evidence as to why it would be a good thing for insulin to be persistently high. I don't know of any scenario, even if you're an intense bodybuilder, and you want to have maximum anabolic effect. You should still be able to do that within a limited span of time because that's how the body's built.
Right. I don't think that's controversial. I want to get a little bit more tactical, and maybe this is a little bit more speculative. I know a lot of people in our community are either fasting or eat a ketogenic diet, and I'm sure you hear this a lot. My LDL goes up, and I think you described this as a lean mass hyper-responder. You have high HDL, and you have low triglycerides, but your LDL is up, and usually what I respond is that, one, and I think very similar to how you describe it, it's an irrelevant biomarker. There's not a causative effect for cardiovascular risk. Don't worry about it, or two, maybe recommend, okay, maybe look at more polyunsaturated fatty acids to see if that tempers the LDL side. I'm curious what your viewpoint is on that. Do you just usually recommend or tell people, "Hey, don't worry about it," or should you alter your fat load to try to lower it a little bit?
I pretty much never tell anybody to worry or not to worry. I'm always emphasizing that I won't give medical advice, and I'm upfront about, again, not knowing for sure if the lipid hypothesis is true or false. Yet, I'm cautiously optimistic. That's the wording I use, is I say I'm cautiously optimistic. Now, there's some people, to your point, who go, "I hear you, Dave. Still, it's just a little too high for me to be comfortable with. I can be comfortable with an LDL of 150. I can't be comfortable with an LDL of 300. Dave, how do I change that?" Now, this will change as the data changes. As it stands right at this moment in time, of all the potential solutions on the table of what I think I would do if I were in this spot is I would actually just be more likely to leave keto and stay low-carb. So, rather than being like 15 net carbs, I would say consider being at like 100 carbs. At 100 net carbs, you're now going to be fueled more by glucose, and therefore, filling up your glycogen stores. Again, this is my theory. Your glycogen stores and liver being high enough means it feels less necessity via very many different paths.
To transport fat around.
Right. To mobilize as much fatty acids. Now, that will make you feel better with the numbers. I can't say that ... I know from how me, personally, how I feel and what I also see in my metabolic numbers I don't like how that looks, but that's just me. Now, second to that, I would say consider bringing down saturated fat in favor of monounsaturated fat. It won't have as big of an impact typically. For some people, they say that they've seen a bigger effect, but here's the catch with that. Saturated fat is almost a kind of separate category from the coupling of monounsaturated and polyunsaturated fast. So, oftentimes, if something's high in monounsaturated, it's proportionately a little higher in polyunsaturated. So, to date, I don't yet know how much of the effect we see with higher monounsaturated fatty acids is really just a slightly higher amount of polyunsaturated fatty acids because I will say this. If you do bring up your PUFAs, your polyunsaturated fatty acids, substantially more, pretty decent chance you bring down your LDL, but I just can't recommend that. I really dislike what I know about polyunsaturated fatty acids at those levels, and it's usually because you need refined oils to get to that degree.
Yeah. Let's talk about that. I think that's an interesting topic right now because I think you have, and this is maybe just going a little bit down the keto community or discussion, at least, around going carnivore, which is very high saturated fat in terms of your fat load versus ... you have PUFAs and vegetable oils and refined vegetable oils. I'd love to hear your perspective on omega-6s versus omega-3s. Can we unpack some of the discussion around the different types of fat? If we buy the lipid hypothesis, and the lipid transport model where fat isn't the worst thing ever, okay, what kind of fat should I be considering now?
Okay. So, here's the super brief overview. You have saturated fats, which means ... I'll just tell you the very easy way to think of it. There's no double bonds in saturated fat, right? It's one long strand.
It's like a carbon string and a bunch of hydrogens around it, yeah. It's like a very straight line as opposed to crinkled when you have double bonds and all of that.
Right. The double bonds are where you end up having ... One double bond means it's monounsaturated, mono being one. Poly is multiple double bods, polyunsaturated fats, and both omega-3s and omega-6s are polys. The main thing is that they are essential fatty acids, and so, as the existing literature goes, you do need them. We do find that the body has some particular points of it. It's funny. This is actually a little bit of a side project of mine and that I'm sort of trying to pursue down the exact nature of the delivery mechanism because that part kind of interests me. It's not like it's needed everywhere. It's needed in some areas very predominantly, like in the eyes and so forth, and I'm very curious as to how that process works and whether or not it's actually true that we really cannot make double bond fatty acids within the body. That's what the literature will tell you right now, but I don't know. I'm kind of interested.
Isn't alpha-linolenic acid a precursor for omega-6 and 3?
But yeah, so, here's what happens at high doses of polyunsaturated fatty acids, and actually, I'm not even sure I can qualify what that threshold is for high, but I do know this. There is a greater degree of two things. One is that production, the assembly of lipoproteins themselves are more likely to get stunted and then restarted at a certain threshold of PUFAs in the composition of the lipoproteins. So, this is sometimes touted as a good thing, like, "Oh, good, your liver won't make more of them." Again, it's the engineer in me. The body's trying to do something and failing at doing it, even though it's clear that's what it intended to do. I don't start with the assumption that it's a positive, me, personally. There's also something else that, on the second, is once actually in the bloodstream, they're more vulnerable to peroxidation. Now, why this is relevant is it could be that the reason you have lower numbers of LDL beyond that production synthesis step is that you also have more of them that are in the bloodstream getting oxidized faster and, therefore, removed by scavenger receptors faster. If that's actually how it is that you're ending up with a lower LDL number, no, thank you. I don't want any part of that. I'll let other people do that-
Right. This is kind of like the free radical stuff that's messing up your levels, right?
Yeah. Again, if I saw data that suggested higher levels ... Let me take a step back because this kind of really puts the PUFA discussion into perspective. If you just guzzle PUFAs like crazy-
These are refined canola oil? What are PUFA?
Yeah. Yeah. Seed oils, yeah, just down it, I would bet money that you won't die of an MI, of a myocardial infarction.
You won't die of a heart attack, right. But I believe that you'll die sooner than if you hadn't done it, and that's why the term I always drive everything back to is all cause mortality. Whenever somebody sends me a study, and they're like, "Hey, check this out. This thing, this activity, this medicine, this whatever, it reduced chances of people who took it or reduced the chances of people having, say, a heart attack by X amount." Then, I go, "Great. Now, I want to see the balance sheet. Did it improve their chance to live overall?" Right? And that's probably one of the dark secrets of this larger equation is I wouldn't be standing in front of you today if, going all the way back to November 2015 when I first started all of this, I got to see that seminal study I was looking for. I was like, "Okay, I hear about the heart attack, but that's one particular way to die." It should be that if LDL is deleterious in any for, there's no benefit to it at all, then, reducing LDL should have a net longevity. You should live longer because you can take out the whole cardiovascular component. It's gone, right? Now, you can just focus on, "Hey, I just need to not die of cancer, infection, all that stuff."
Alzheimer's, cancer, yeah.
Right. Now, I know better. I've learned a lot. There's actually an immune response that associates LDL, and it gets back to why I was talking about the ambulances before. So, it seems to be that those medications that radically bring down LDL have marginal or no or detrimental impact on all cause mortality.
Yeah, and there's a understandable selection bias, particularly with drug studies. I say understandable because, of course, if you're running a drug study, and you're seeing a higher all cause mortality from the intervention group, you're not going to take that drug to market, right? And so, a lot of these trials, as they even get to, say, stage two or stage three, they're more transparent in what their outcomes are, and if that outcome doesn't look good, that's considered a failure of that drug trial. So, even though that drug may have succeeded at dropping LDL, but it increased mortality, then it's the failure of the drug and is not to be counted towards the total of evidence with LDL. So, if you ran 20 drug trials, and two of them brought down LDL, and also, brought down mortality-
And killed people.
... even just a little bit. Oh, well then, good. That not only shows that these drugs are successful, it's further evidence that lowering LDL reduces heart attacks, et cetera.
Even if the other 18 showed the opposite.
Correct. So, here's where it gets interesting. If you look at the literature as it stands, all the major statin trials, you would have assumed, even with this natural selection bias, which, again, I think is understandable because it's a business model, you would assume that all cause mortality would look great because they're choosing the best of the best, and yet, it's flat across the board. If there's very few trials ... I want to say I can only think of two that actually had a net benefit in all cause mortality that were primary prevention, which is to say somebody who didn't already have a heart attack, right?
Which is a wild result given how you explain it. If your hypothesis makes sense, which is these are ambulances, LDL is ambulances, and if you just randomly shut down ambulances, of course, you're not going to save people's lives. That's association, a correlation, not a causative factor. So, I think if you take that data into the account in your hypothesis, your theory here, it makes sense.
And that's why I theorize that it's possible ... One of these two things are possible. One, if you went into that statin data, and you stratified for this triad, high HDL, low triglycerides, high LDL, that it may show that statins have no benefit, or ... I hope that this isn't even a possibility, or that, that triad would show that there's a net detriment because that group would be more likely to be on a higher fat, low-carb diet, not even intentionally. It might just be people who normally gravitate towards eating more fat and eating less carbs and are athletic or something along those lines. But I doubt we'll ever know because I doubt that they'll ever stratify that group if it turns out that there's no net benefit for having statins for that group. Why would they do that? Why would they cut out a large portion of the population that would otherwise be taking statins?
Other than doing good science, but that aside, sure. Your argumentation, your data, and your knowledge of literature is very compelling, at least for me. So, why isn't this taking ... I mean, it is taking some storm, but why haven't you knocked on every single AHA, American Heart Association guidelines, all of that? What is the steel man argument on the other side, or does it just take time? What do you think is the blocker here?
No, it's a couple things. It takes time, and there's two different, I guess you could say, platforms. So, right now, the most common answer I would get from a lipidologist, because I have been knocking on their doors this whole time. The most common answer I'd get is, "Well, if you believe this, it needs to be a study," and it's a little bit of a tricky answer because I can't easily turn this into a study because currently, you can't make a study for where people are voluntarily at high levels of LDL cholesterol because that's considered unethical.
You can't get it through an IRB?
So, the guidelines as of just a few months ago state explicitly that if somebody has an LDL of 190 or greater, they should be on the maximally tolerated statin, without any further qualifiers. It doesn't even matter what their triglycerides of HDL is or anything. So, that basically kind of cuts off just observing lean mass hyper-responders and what might be an IRB approved study. Yeah. So, in a weird way, you're prevented from codifying the study in the way that would otherwise be accepted for publication, right? So, that's one platform. This other platform is kind of a platform that, obviously, I'm a big believer in, which is, "Hey, why do we have to follow certain rules of science as they're establishing them if they can't adapt to the new information as it becomes available," right? And so, I tend to call this different things. I sometimes call it open source science or peer-to-peer science or whatever.
Citizen science, biohacking.
Sure, exactly, and they would be right to point out that, "Hey, Dave could be something that's dangerous. The whole reason the have things like IRB is to help prevent people from taking unnecessary risks, et cetera," right? And again, I acknowledge that, but the problem here is that you have a lack of interest in even moving forward with something that everybody consents to in order to get the proper amount of data, right? I could tell, right now, I have a Facebook lean mass hyper-responder group. I could go back to them right now, and I could say, "Guys, I have been informed that I really need to tell you with extra vigor that you guys are all at risk. You should all be on the maximally dosed statin ASAP." I've already had ... There's one guy who was getting tired of me qualifying to him because he has FH. He has a high calcium score, and so, I wanted to be very mindful. I wanted to be like, "Just so you know, a lipidologist, a cardiologist, they would say that what you're doing is very concerning, et cetera, et cetera, and I want to be sure that you get from me a two-sided opinion and so forth," and he basically just said this up front. He was like, "Dave, I don't even care what you say. You can turn into the biggest pro-lipid person. I am about to run a marathon with my son for the first time." The guy was like 62, and he was about to run a marathon with his 40-year-old son, and he was like, "I wouldn't even care if it shortened my life by another 10 years. I've never felt better in my life."
His health span's way better. Yeah.
This all comes back to the same thing, which is we're now, at least, in a new paradigm, and that there's a metabolic thing to consider. I'm already acknowledging that there may be two tracks. One of those being metabolic derangement, in which case LDL may be a bad sign, and therefore, it may get coupled with bad outcomes, but there's also potentially a metabolic benefit, particularly if you're powered fat, for which high LDL makes sense and may even be appropriate.
Yeah. It seems like the momentum is going in our direction here. I mean, there's plenty of academics that know you've spoken to and that we've come on the program that I'm sure would love to run this study. I mean, I'm sure you've talked to a number of IRBs, but I imagine every university has one. There's some independent ones. Have you exhausted all your options? I mean, this is just core science, right? This is actually what science is. You have a hypothesis. It's reasonable given observations from these n=1. This is the purest of pure science as opposed to-
You sound like me 12 months ago. So, look, I can make the impassioned plea. If you genuinely believe ... Let's say you are Mr. Pro Lipid Hypothesis. You're like, "Dave, you are flatly wrong. These lean mass hyper-responders are on their way to the grave," right? You should be my biggest advocate for putting together this longitudinal study, right? You should be the one who's like, "Let's start the clock on them right now. Let's get cardio metabolic markers ongoing. Let's get those CIMTs. Let's see any and all progression of atherosclerosis because I assume it's going to happen. It's going to be happening at levels of FH." That's how you would be. Let's get it rolling, right? Think about it. If you're Ancel Keys, and you're the one proposing this, this group is somebody you've been waiting for forever because lean mass hyper-responders have low cardiovascular risk across the board save the one thing, the LDL cholesterol being extraordinarily high. They're perfect. They're the perfect group to test the lipid hypothesis, and if really believe in the lipid hypothesis, you should be 100% behind this. You should be excited that this group was found and that they'll prove it, once and for all, why everyone should be taking cholesterol-lowering medication.
I mean, yeah, we'll see all these people die, and I mean, I think that will be like, I guess, the steel man, like, "Hey, we as medical experts, you are putting people on a dangerous path. We don't want to risk people dying." But it sounds like there is a cohort of people that's rapidly growing that are seeing benefits. So, it seems like even that steel man argument is getting stronger because people are voluntarily doing it. People are seeking this out, and the corpus of data form these n=1's are positive. So, I think even that steel man arguments doesn't really ring compelling. So, I'm completely onboard with your perspective. I think it sounds like you tried all paths. I mean, it's just like pounding your head against a wall. I'm just curious to hear-
I'm working on it.
I'm working on it. Look, in my brain, there's really just sort of two tracts, if you will. One tract is what I've been doing all along, which is researching, disseminating information as fast as I can. It's this new platform of science I'm talking about, and I'm encouraging other people to be as responsible as they can be, acknowledge what risks that they know they're taking on, but at the same time, as much as I can get them to be, be meticulous, be very transparent, and absolutely concede any and all mistakes. It's all data, right? This is why I like to make hypotheses in advance and publicly, is I'm trying to keep my self to account as well, right? It's not that I'm trying to show off. I'm quite confident my hypotheses will fail plenty of times, right? But to me, this is the scientific method in action, right? I don't.
It's much more pure than I think a lot of academics do, right? They can't publish their nonsignificant results.
You're out there doing, I think, what is more pure science than what "a lot of academic scientists are doing", which is ironic.
And that's why I want the new wave of people to hopefully take on this creed because I think the soul of science, in a sense, is kind of at stake here, in my opinion, is I feel like we can take a new wakening to say, "Look, let's never get back to a point where people run super multimillion dollar trials. Get the data, and then, after they have the data, do things like the p-hacking and the rearranging, and be like, 'Aha! Here's how we can fit the narrative that matches who the people who funded us wanted to see,'" right? Let's, instead, be transparent all the way through. One of the things I wish publications would do, and this is isn't my idea, but ever since researching about it, I feel every publication should do, is they negotiate with the team that's considering a particular experiment, determine the design, publish the design in advance of the experiment, and then, agree to publish the results after it's done.
So, lock it in. So, don't let people fish around afterwards.
It's the only way. Because the problem is, right now, publications ... and this is an open secret. Publications will publish what shows positive findings, and they tend towards those findings that usually match the opinions of the editors.
Yeah, which is not surprising. That's human nature, right? Incentives are for academics that have positive results. You're a journal editor. You want to have papers that people will cite, which means it has to be a positive result. So, I think anyone has bad intentions here. I think if we talked to these doctors, I think they do care about improving outcomes. You talk to scientists. They want to do good science, but in this current infrastructure, the publication...you've got to p-hack sometimes. I get the incentives, and it's-
There's a term that also comes from somebody in the field called white hat syndrome. You feel you're the good guy fighting the good fight, and therefore, maybe the way by which you're coming to the evidence is not the way you would idealize, but it's still the right evidence. You're still helping the cause that you know is the right cause, right? And if something doesn't match your preconceived worldview, you don't want the cause. Besides, you're now second-guessing how you did the design. Maybe I just got too many people in the control group that wasn't right, and now, you're ... and that's why. That's why. The whole point of having these things be transparently executed is because you're preventing your ability to bias yourself, even if it's for the best of intentions of both that you can imagine, right?
Yeah. I want to ask you, then. Do you have an example of where you had a hypothesis, and it was absolutely wrong, and you were like, "I thought this was going to happen, and oops, I fell flat on my face, or have you been spot on?
Well, it's not that I've been spot on. It's that I've been a lot more right than wrong, but that's not a brag. Honestly, a lot of times, I have been surprised myself that I've been right about things. So, probably the one thing ... No, even then, I was a little bit torn at the time that I was doing it. Here's what's funny, this most recent experiment, I was coming off the carnivore diet, and I know you kind of wanted to talk a little bit about that. We'll backtrack to that in a second, but there was an opportunity where, at the very end of the carnivore diet, I was going to be in a controlled diet mode anyway. So, I tested a hypothesis that Paul Mason, Dr. Paul Mason, brought to my attention last year where I would add dextrose, and I did it in the form of Bottle Caps, this Willy Wonka candy, and he hypothesized that this would ultimately lead to a higher insulin response, lead to more LDL receptor production that would be expressed in the liver, and therefore, take down total LDL particles overall. Now, I had already done an added sugar experiment from last year, but it was primarily fructose-based. It was sucrose, I want to say, and it was with Skittles.
By the way, I hope I don't have to do these candy experiments anymore. They're not really that fun. They sound like they're fun from a distance. They're not. They're not fun. But I didn't end up committing. I was trying to think, "Did I actually hypothesize with him?" But I didn't. If you see the video, even though I wanted both of us to hypothesize in advance, I said I was torn. What's funny is I, at first, hypothesize that my triglycerides would go up, but the more I was thinking about it, even while talking to him on the broadcast, the more I was like, "No, I think actually my triglycerides will go down." And so, that's the one is stuck to, and sure enough, I ended up being right about the triglycerides. The reason the triglycerides went down is because of the higher insulin ended up being a result of a net subtraction of the triglycerides off of the boats, if you will, right?
Yeah. Makes sense. You have sugar load. You're metabolizing more on the sugar basis rather than a fat basis. Makes sense.
Right. There's one that I might have ended up being wrong on if my original design had worked, and that was on the weight gain experiment I'd hope that I'd have a stall for a moment after switching from the standard American diet, which was designed to gain weight, over to the baseline diet, which was keto. I'd hope that it'd be stalled at least for a few days so that I could capture that vital lipid data, and I hypothesized that my LDL would go up, but unfortunately, that got confounded because I immediately lost weight. Switching over to keto, there was no stall at all it just ...
Which makes sense, right, because that's what a lot of people's responses are. You lost a lot of water weight and then all of that. Yeah, I'd love to hear your experience on carnivore. I mean, I think that's been, obviously, a fad. I don't know if it's a fad, but it's definitely a topic of du jour in, I would say, the low-carb community in the last six months or so. Curious to get your overall highlights there. I mean, I think the data is interesting, at least from a n=1 side of how people feel like they're resolved some autoimmune issues, but I guess there's also, for more classic ketogenic folks, people appreciate the fibers, the polyphenols from plants. Curious if you had any strong opinions there. Obviously, you just came off of a carnivore diet.
So, carnivore has been a subject of deep fascination for me, and the reason is because from a distance, it's one of those things that seems like it shouldn't work. It shouldn't, right? You naturally think, "Oh, come on. Very low variety of micronutrients. Something's got to give pretty quickly," right? And it led into my doing something very deep investigating on proteins, and when I say depression I mean a few weeks. There's other people like Ted Naiman who can tell you a lot more, but I really wanted to understand why one could have a lot of steaks, which is just muscle meat, right? Why could someone have a lot of steaks and not be feeling a micronutrient deficiency pretty quickly? How's that possible? Because one of the benefits of doing what I do is a lot of people like to send me their blood work to do interpretations, and so, I have a few friends who are a carnivore who I've seen their blood work over the last few years, and I've even prodded them into giving me different tests, as far as nutrients go, because I've been curious to see what would change, and one of them has issues, but I don't know if it's related to nutrients, don't know yet, but the others don't. They look fine, and I think only one of them is eating almost entirely steaks, but even then, they kind of veer out. They do fish and a few other things.
But that haunted me. I kept thinking, "Gosh, how is this possible?" And then, I started learning a bit more about protein. I started learning more about amino acids, which, of course, make up the proteins, and I started to realize, and I'll actually be presenting on this at the carnivore convention that's going to be coming up that piggybacks on this...but I started to realize that, actually, there is something to be said about consuming a lot of native molecules, as they call them. They call them native molecules because they're animal-based, right? It's not that you cannot make use of plant-based composition. It's that the composition is going to be very different from animal composition. When you're having animal, you're having a composition, the composition of amino acids the composition of amino acids that are close to your own signature, therefore, of what you would otherwise be built of. If you're a brick house, right, you still may have a lot of wood and metal and other things inside, but the composition of those different raw materials are going to be comparable to another brick house, right?
Right. I could see how this argument leads on a dangerous path of being cannibals, but please continue.
Yeah, the cannibal diet, I don't know if that's come up yet, but it might be popular. It might be. But truly, the first thing that I noticed after I went carnivore ... because it was a little bit of an exploratory experiment. I wanted to see if I could actually stick to bovine entirely through, so cow only. So, I was mainly just doing beef. I was doing hamburger patties, steaks, and all beef hotdogs, and the first thing that struck me, I mean, struck me, is that my appetite totally disappeared. My appetite's lower on keto, and I'm used to just talking about it that way, but in this case, it was just not there. I didn't even spend much time thinking about food. I quickly realized that if I were to ever want to lost weight, like really lose weight quickly, this was it. This was the diet because again, it didn't take much at all, and I wasn't even thinking about it.
Yeah. It's similar to my experience where, I mean, it's hard to eat more than two rib eye steaks a day. Your appetite is pretty full. It's like, "I feel pretty satiated," even though that's not that many calories. It's probably sub-2000 calories or around 2000 calories.
That and, of course, just about everybody reports, your GI stress, all of that, just disappears, and I don't want to say it's entirely gone. I kept very meticulous notes. I want to say I maybe had two-ish incidents that I journaled, but they weren't anything close to what I'm having eating regular keto, particularly when I have a lot more fiber in my diet, and that's another thing that from engineering perspective just kept lingering with me, is I was like, "Wow. There's so little heading to the restroom. Am I really absorbing that much more of what I'm consuming? And if so, what does that mean?" Is this really something my body particularly wanted to have to this degree and has that level or proportionality that's used?
Yeah. No. I think I'm in a similar boat as you. I'm interested just to see how the space evolves. Obviously, pretty early, I would so much earlier in science than keto and low-carb, but the n=1's and the citizen data there, there's something interesting signal there at the very least, I think, is a safe way to say it. It would be, I think, overly dismissive to just say, "Oh, they're a bunch of crazy people doing carnivore. They're full of crap." I think that's overly dismissive.
Well, at a minimum, it's opened some new doors for people who want a sustainable multiple removal diet. So, if you do suffer from wide ... I mean, Mikhaila Peterson is, of course, brought up constantly. Exactly what it is that she has these intensive allergies and autoimmune responses to may be never known past this point, but the fact that they were there and were truly severely impacting her life in a very material way is no question. Nobody argues that point, and this saved her. It's quite a compelling story.
I think this is a really good discussion. I want to wrap up with a couple last questions here, and maybe this is going to be overly fitting your nuance, but I think, given all these experiments and all the data you've collected over the last three plus years now, would you have some overall guidelines for someone to look to have a better nutritional inputs? I mean, could you boil down some guidelines for people as the first part of the questions? Then, two, obviously we're in January of 2019. Hopefully, a very, nice productive year ahead of us. What are some of the big things we should watch out for? Any experiments you're excited about running over the next 10, 12 months here?
There is one that I'm hoping to do next month that if I do, it'll be very explosive, but I have to keep it secret.
All right. We'll stay tuned for that.
Yeah. Keep an eye out for it. As far as just general advice, I mean, here's the thing that I feel I would give that may sound a little more unique to me and not to other people. One, hopefully, anybody who's looked into my research, even if they're not a low-carb fan has at least seen more than enough evidence of how dynamic lipids are. So, whatever your lipid panel is, be aware that it moves, and it can move actually very quickly. I know that the medical community doesn't treat it like that. I certainly do, and it's worth finding out a little bit more about that.
Well, I want to riff off of that, which is interesting because I think people realize that blood sugar moves all the time, right? You eat a sugary thing, boom, your blood sugar's up. You fast a little bit, eat very low-carb, and your blood sugar's down, and given the energy distribution hypothesis, it makes sense that triglycerides and fats also have a dynamicism.
I think what happens is a lot of people treat it as though if your LDL suddenly rose, it's like if there was toxins in the bloodstream or that you got injured in some way that you need immediate medical therapy to resolve, and again, the very first question I'm always going to ask is, is there a potential metabolic rationale for why this happened? If you've had an LDL ... I had an LDL around 130 my whole life. All of a sudden, my LDL is at like 260. Okay, now, wait. Something changed. If that thing that changed explains why it would be at 260, then if my doctor goes, "Oh, this must be genetic," I'm going to push back and be like, "No, I actually changed my diet significantly. I think this may be related to my diet," and as such, we should be thankful that we can actually see that there's this whole other component that may be pretty relevant to us, and that's why I want to say, for a lot of people, just getting that first part is already really hard. That's already a big uphill battle because almost none of us think of it that way. It's already a new paradigm just to get there before even getting onto the energy model.
Now, another thing that I would say that I press upon, and I'm sure you've picked this up, is I like for everybody to constantly challenge whatever their belief system is on a regular basis. Think of whatever you feel the most passionate about, and try to find an opposing voice that'll have a respectful debate with you on it. It's a good thing. It's a positive thing, right? If you're just constantly in that mode, I feel like you can have a lot of personal growth, and I feel like you can really advance knowledge a lot faster for everybody else.
Yeah. It sharpens your tool, sharpens your reasoning.
Yeah, and if I could pick the last one, the last one, I would just say I do a lot of measurements. I get 24, 25 markers now every time I get a blood test. There's nobody, at least I know, who gets as many measurements, especially from blood, as I do on such an intensive basis, but I can tell you there's no meter that's more important than how you feel. People get caught up in diet advice and what they're told to do and will endure feeling terrible in order to chase numbers, like ketone numbers or a particular ... and if that's happening around the clock, look into it, but don't assume that the advice supersedes how you feel because that's the most important meter you have.
A very illuminating conversation. I think it was ... I learned a lot through this conversation, and I hope our listeners did as well. So, how do people follow you? You're on Twitter? @DaveKeto. You're at cholesterolcode.com, and how else do people find you?
I do have an Instagram, DaveFeldmanKeto. I'll concede I'm not that active on it, but that's mainly just because it's very ... Instagram is not desktop friendly. It's very phone friendly, and then, they cut you off at the desktop. So, anyway, I won't rant on that. I'll just say, as a geek, that kind of is a thing for me. Also, I do have a YouTube channel, which is just youtube.com/davefeldmantv, which I am occasionally putting videos up on, and incidentally, I do plan to have a number of short videos, kind of like quick hits, particularly for people on low-carb that are around particular subjects, such as you have high triglycerides and low-carb, what to do about that, and what if you have a low HDL? How much of that is genetic-related, things along those lines, but those are pretty much Twitter and cholesterolcode.com, especially commenting, and cholesterolcode.com's probably the easiest way to reach me if you're trying to.
Awesome. Thanks so much, Dave.
Thank you for having me.
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© 2019 HVMN Inc. All Rights Reserved. H.V.M.N.®, Health Via Modern Nutrition™, Nootrobox®, Rise™, Sprint®, Yawn®, Kado™, and GO Cubes® are registered trademarks of HVMN Inc. ΔG® is a trademark of TΔS® and used under exclusive license by HVMN Inc.
These statements have not been evaluated by the FDA. Our products are not intended to diagnose, treat, cure, or prevent any disease.
© 2019 HVMN Inc. All Rights Reserved. H.V.M.N.®, Health Via Modern Nutrition™, Nootrobox®, Rise™, Sprint®, Yawn®, Kado™, and GO Cubes® are registered trademarks of HVMN Inc. ΔG® is a trademark of TΔS® and used under exclusive license by HVMN Inc.