Jay Feldman  0:06  
There are a number of critiques against the lipid energy model, but do they hold any water? And do they mean that lean mass hyper responders are actually at an increased risk of heart disease? We'll be answering these questions in today's episode, episode 116

of the energy balance podcast, a Podcast where we explore health and nutrition from the bioenergetic view and teach you how to maximize your cellular energy, to maximize your health. In today's episode, we'll be going over the validity of the counter arguments against the lipid energy model. We'll be discussing whether the lipid energy model means that high LDL does not increase cardiovascular disease risk. We'll be talking about how thyroid and metabolism relate to high LDL on a low carb diet, what the lean mass hyper responder phenotype means in terms of metabolic health and whether low carb diets are ideal for cardiovascular health and health in general. As always, to check out the show notes for the episode, where I'll link to the studies and articles and anything else that we reference throughout the episode, you can head over to Jay Feldman wellness.com/podcast,

and with that, let's get started.

All right. So in the last episode, we went over, kind of the broad physiology of what's going on in the lipid energy model. And this is something that Dave Feldman proposed quite a while ago. And during this time, there's been a lot of critiques against it, people who are resistant to this idea. Of course, you know, any new or alternative idea will have those sorts of critiques. So we wanted to talk through just some of the main ones, which at this point, with some of the recent research that's been done have really, I mean, there's a lot of evidence to support the lipid energy model and a lot of evidence against these counter arguments. So we wanted to highlight that, especially with some of these new studies that have been put forth

evaluating and looking into the lipid energy model and lean mass hyper responders. So there are two main kind of counter arguments that we're going to start with. The first is basically just that the lipid energy model is not actually accurate. It's not a good representation of what's going on. Instead, the high LDL that we see in these people is due to basically just increased cholesterol production due to increased saturated fat intake on a low carb diet and, or there must be just reduced clearance and and high VLDL, as opposed to lots of VLDL being converted to LDL. So, and the basic idea is just that this differs from what we normally see in someone who's insulin sensitive, so this can't be the case. That's kind of the argument against or one of the first arguments that we'll be talking about it on the saturated fat role. And then the second thing we'll be discussing is whether there is what the evidence shows in terms of the effects of the lean mass hyper responder phenotype and similar phenotypes in terms of cardiovascular disease risk. Do you have anything to mention, Mike, before we dig into the first one here? No, I think we should just, we should just jump in and get into the major points here. Cool. Okay, so yeah, this was, again, there are a number of critiques, a number of people critiquing the model. One who's kind of been pointed to very frequently is Peter Attia. He did a podcast with Dave quite a while back several years ago, and basically put forth some of these arguments that essentially are suggesting that the presentation here is not due to the lipid energy model. It's not due to this increased lipid transport system and increased conversion from VLDL to LDL. But instead, we just must have excess cholesterol production due to increased saturated fat. And of course, those things are bad. And with the with the fact that these people present in this way, it must just be something genetic. There must be something unique about these people. There's no way that it is just being able to be something that can be explained by something like the lipid energy model or a metabolic shift. And of course, the kind of next argument that we'll get to is with those things in mind, and just knowing that there's increased LDL, this has to lead to increased cardiovascular disease risk. So there are a number of at this point, especially, and even at the time, but, but now especially, there's some good evidence against these ideas. There's good evidence supporting lipid energy model and showing that this is actually what's going on. The first of these is basically the fact that BMI is such is so strongly associated with the lean mass hyper responder phenotype, more than anything else, including saturated fat. And what that means is that this is a population that is more metabolically healthy and is just have seeing increased turnover of VLDL to LDL because they're using more triglycerides. So this supports the idea that this is just a metabolic shift, and this is not just saturated fat. So there's a study as.

A large meta analysis that was done in support of this idea. And the title is increased low density lipoprotein cholesterol on a low carb diet in adults with normal but not high body weight, a meta analysis. And they state 41 trials with 1379

participants and a mean intervention duration of 19.4 weeks were included in a meta regression accounting for 51.4%

of the observed variability on low carb diets. Mean, baseline BMI had a strong inverse association with LDL cholesterol change, whereas saturated fat amount was not significantly associated with the elder with LDL cholesterol change. And they have some good kind of graphs and like 3d depictions of this in the paper. It's worth looking at, but it basically shows very clearly that this is, and we'll go through more lines of evidence, but states very simply, right? This is something that is directly correlated with BMI, suggesting that it is actually a lipid energy model. It is actually a different presentation due to the shift metabolically and the increased utilization of fat, as opposed to it being some genetic issue or some sort of

results of the saturated fat, which they've looked at, both of those things in these studies and and found that really BMI is the best correlate, which is some clear evidence here.

Mike  6:14  
Yeah. And I think overall, the other thing we see is the lipid profile that we're seeing with these people in lean mass hyper responders is significantly higher than people are just having a higher saturated fat diet. So we're adding saturated fat into the diet. We're not seeing people go up to 400 500 milligrams per deciliter total cholesterol, or even higher values, or even really, really elevated LDL values. Maybe you're seeing a bump 2040, 50 points, but you're not seeing this huge shift upwards, and even if it's 2040, 50 points in people. So I think that's that's a big piece. There is like, you're not, we're not really seeing this, this, this change with people adding saturated fats to their diet, like butter or coconut oil or beef towel or something like this. And so to just even proposition it that way, it's like, you know, I guess it's helpful that that Dave and his team are doing all these studies, these meta analysis and these different components. But it's like when you when you see people, and you, you you're working with people, and you're seeing them change or die, and you're seeing them have add in saturated fats versus, you know, let's say they're really like monounsaturated fat. You're not seeing shifts like this. You're not seeing massive shifts like that. And so something interesting in the this meta analysis are saying that for you're seeing a drop of 2.5 milligrams per deciliter of cholesterol for every BMI unit, so every point in BMI, so it's a pretty basically, every drop in BMI by one point, you're seeing a corresponding negative 2.5 or a drop in 2.5 milligrams per deciliter of cholesterol. So they actually gave us a relationship here, which is pretty cool to see. And the other thing I want to point out is there's been like, stats on Twitter, to some extent, are in different places where certain individuals have been like, oh, we this. Like, we need the highest quality evidence. It's like, yes, here's a meta analysis showing that, like, it's actually related specifically to lean body mass and not directly to saturated fat in the diet or something like this. Yeah, absolutely. And a very clear one. And, and so that brings us to again, another piece here, which is, yes, it's not saturated fat. And instead, we can show very clearly that as soon as you shift back from using lipids to using carbs, it fully, not fully it dramatically shifts the lipid profile. And that is, again, more very clear evidence for the lipid energy model. And this is something that really can't be explained elsewhere or through some other mechanism. And to be fair, I have personally seen this with many clients coming out of a low carb diet. Who are they? They're working with their doctor, and they can't figure out why their levels are high, and they don't want to go on a statin. And then it's like, yeah, just add in some carbs, and then you add in the carbs, and the lipid profile comes down. A lot of other things improve as well, because there's some problems with, you know, just relying on fats. But that's, you know, beyond the scope of what we're going to talk about here, at least at this point. So yeah, I mean, I've seen it in practice. Many times. Dave and Nick have seen it as well, and they've proved it. We're going to get to this right now. So it's, you know, and I think that also would invalidate some of the genetic ideas as well. And there's case studies that we're going to go through where we see that these individuals have normal cholesterol values when they have carbs in their diet, and it's only when they go on they're very lean and they go on these high fat diets that you start to see these changes.

Jay Feldman  9:37  
Right. And they also rule out for those sorts of genetic things. Because, again, the argument could be made. Yeah, they have normal cholesterol normally, but there's some genetic reason why they're prone to this happening on a low carb diet. Again, it can always come back to some sort of genetic gymnastics. It's always a cop out answer, because we don't know all the genes and all the the multi polymorphisms that can relate to this enzymatic fungus.

Mike  10:00  
So it could always be genetic. It's like, okay, fine, that like, because we can't figure that out right now, we don't have the answer. Let's try to exploit explore options that are actually under our control, instead of have, like, some cop out answer that gives us no agency, right? Well, and looking at that previous study we mentioned with BMI, suggest that this is not genetic, right? This is something that you're going to see as someone, as leaner. And not only have you and I seen this with clients, but I also saw it myself, and I the few cholesterol tests that I got when I was on very low carbon and keto didn't fit me fully in the lean mass hyper responder phenotype like it didn't exactly fit the above 200 LDL, the above adhdl and things like that, but I was close and heading in that direction. I bet if I continued, I probably would have, and that's the other thing too. Is that by showing the incremental shift with BMI, it shows that this is a spectrum. They're focusing on just the population with those really extreme values, just as an example. But the idea is that this is a spectrum that's happening as you shift toward the lipid energy model, which, again, it just makes way more sense than this being a unique genetic population that is separate from anyone else on a low carb diet. Instead, it's not it's just, how much are you shifting toward that lipid energy, transport and utilization? That's that's really the the driver here, of how much you're going to see the phenotype. So speaking of more evidence, we have the Oreo cookie study. Mike, do you want to go ahead and share this one? Sure. So this study has been trending up for like across YouTube in all different areas. And just a preface here, they're showing that Oreo cookies were or outperformed statins in terms of lowering the cholesterol here, which is the reason this is valuable to the models. If, basically, the Oreo cookie they're providing like the worst quality carb source, or one of the worst quality carb source you can see. And there's basically showing that it's literally the carbs are actually making the effect, despite, you know, some of the negative values here. So,

yeah, let's jump in, and let's, let's read the quote. So they say this single subject crossover experiment aimed to test hypothesis that adding in carbohydrates in the form of oral cookies to lean mass hyper responder subject on a ketogenic diet would reduce LDL cholesterol levels by a similar or greater magnitude than high intensity statin therapy. The study was a diet designed as follows after a two week run in period on a standardized keto diet. So the individual was doing a keto diet for two weeks. The study arm consisted with supplementation of 12 Oreo cookies, providing 100 grams per day of additional carbohydrates for 16 days. So it was two weeks of keto, then 16 days of adding in Oreos, 12 Oreos, to get 100 grams of carbs. Throughout this arm, ketosis was monitored and maintained at levels similar to the subject standard ketogenic diet using supplemental exogenous d

beta hydroxybutyrate supplementation four times daily. So during the process, the individual was also taking ketones to maintain the same blood ketone levels. So we're not seeing that the effect is just because ketones have been dropped or some some mechanism there, and then, they say, following a discontinuation of oral supplementation, the subject maintain a stable ketogenic diet for three months, and documented a return to baseline weight and hypo, hyper cholesterolemic status. So after they did the Oreos plus ketone supplementation, they went back on a ketogenic diet for three months, so no more Oreos, and then they basically wound up being hypercholesterolemic Again, so their cholesterol levels increased that during study two. During study arm two, the subject received rosuvastatin, 20 milligrams daily for six weeks. Lipid panels were drawn water only, fasted and weekly throughout the study. So following the ketogenic diet of that three months, they went on six weeks of resuvastatin, so astaxanthin, which will lower cholesterol levels by blocking hmga, hm, g CO a reductase, which is the enzyme that produces cholesterol. Then they say, baseline LDL C was 384 milligrams per deciliter and reduced to 111 milligrams per deciliter, a 71% reduction after Oreo supplementation following the washout period. So they were on keto, they added in Oreos. When they were on keto to start, LDL was 384

when they added in Oreos, LDL went to 111

so it was like, literally, 1/3 of what it was before. Then after they did the washout period, the individual returned back to a keto diet, the so no Oreos anymore. The LDL returned to 421

milligrams per deciliter and was reduced to an ADR. So the lowest point was 284 milligrams per deciliter with 20 milligrams of resuva status therapy, so 32.5% reduction. So we see 384, milligrams per deciliter on keto. Add in some Oreos, 111 milligrams per deciliter. Then they go and they do. They go back to keto. We're now at 420, milligrams per deciliter, LDL, and then statin only lowers it to 284, while the individual is still on keto. So they say, in conclusion.

In this case study experiment, short term early Oreo supplementation, lowered LDL C more than six weeks of high intensity statin therapy in a lean mass, hyper spawner subject on a ketogenic diet. So basically, adding it 100 grams of carbs in the form of Oreos, it probably could have been carbs in any form it like could have been any sugar source, or even star source, whatever the deal was, basically lowered cholesterol in 1/3 of what it was, versus somebody having high cholesterol and taking a statin, and the statin directly blocking enzymatic function, which this is providing evidence the idea that the shift here is from shifting substrate, shifting fuel. So when you have adequate carbohydrates, when you replete liver glycogen, when you start to increase insulin signaling again, you start to see a lowering of the cholesterol very directly. Because now you don't need this cholesterol to oxidize or to provide or transport fats to tissues to oxidize, because you have more carbs on board, versus in the state where you're still oxidizing fats, you're just taking the statin, you're blocking the production of cholesterol, and it's not able to effectively lower the cholesterol to the same extent of the carbohydrate. And I would argue that using a statin in this way, when you have this this high fat, low carb diet, and you're using the cholesterol to transport things, is probably not a good idea, because you're basically blocking your your transport mechanism, for your energy substrate, for your energy source. Now, the individual who did this study like was doing this for a reason, so he's doing this to show, to make a point, to show what was going on, but essentially, you're seeing that this mechanism is directly related to switching the fuels. And Jay, I don't know if you want to chime in and talk about the fact that, like this, really wasn't related to saturated fats based on the variables that he changed,

Jay Feldman  16:50  
Right, right. And it was Nick norwitz, by the way, who did the study, and he's one of the researchers who's been working alongside Dave Feldman and a number of others on the lipid energy model and lean mass hyper responder phenotype. And just to echo what you're saying, of course, statins would not be a good idea in this scenario, right? Something that would really handicap you in terms of your fuel transport, assuming that it would impair VLDL production and but of course, I think, and we talked about this before, statins, in any case, generally, I think, are questionable. So I'll link back to previous episodes where we've talked about that. And yeah, they don't get at the underlying issue, whether you're on a low carb diet or not and all that so but yeah, as you were saying, we know, based on other aspects of the study here that it was not a saturated fat issue, and the reason for that is because, and this was, again, very well,

very carefully done or created or developed. The The idea for the experiment because adding Oreo cookies was done on top of the diet. So there was no reduction in calories or displacement of calories, or displacement of fat. So instead of it being something where we added 100 grams of carbs and took out an equivalent 400 calories of fat, instead, they added, or Nick added the Oreo cookies, which was, it was 12 cookies. So, so I'll just kind of state the quote here with all the information the dose of 12 Oreo cookies, which is four servings, 640 calories, 28 grams of which are fat, eight grams or saturated fat. 100 grams was carbohydrates, and there was four grams of protein, so that was added per day split between two meals. They were saying that was chosen to add the 100 grams per day of carbohydrate. So again, a very good choice, because you're adding calories, adding carbs, and you're adding saturated fat. So there's, I don't know how you could probably possibly make the argument that anymore, that this phenotype is coming from saturated fat, because obviously we added saturated fat, and LDL drops 70% so we know it's from adding carbs, not even that many, only 100 grams, and that was enough to really shift away from a fat based transport system in the lipid energy model. So this is some pretty good support for the lipid energy model, very good support that this is not a saturated fat related phenotype. And also very good support that this is not just due to cholesterol production, right? Because if it was just if the lipid, if the lean mass hypersponder phenotype, was just due to excess cholesterol production from a low carb diet, from high fat, from unsaturated fat, then a statin would have been more effective for preventing this effect, because it's blocking the ability to produce cholesterol. So it's it's a really great study for those reasons. And I think part of why it's getting so much notoriety is because of how dramatic it is, right? Just adding Oreos in and dropping dropping LDL 70% whereas the statin only dropped to 32 and a half percent. But despite that, there are people who, again, have been

criticizing the model, criticizing the idea that there's ever a case where LDL is increasing. LDL is not a bad thing. This must be due to all these other reasons. And then they come out and say things like, Yeah, they did this study. It kind of doesn't matter. It's just a one off thing. It doesn't actually suggest.

Anything. There's someone in particular I'm thinking of which is Dr Allo, who had, he's a cardiologist, and had this cholesterol debate with with Paul Saladino, and he was one of the ones who kind of mentioned it, and was just like, yeah, it's kind of like, worthless. It doesn't really mean anything. It doesn't change our view of anything. But if it's pretty strong support for the lipid energy model.

Mike  20:21  
And I think to like, discount it is really problematic, because the it's in my mind, it means the individual doesn't understand the what this, this whole model means altogether, because the general lipid model, the like the lipid hypothesis, so not the lipid energy model, the general lipid hypothesis, that LDL is just causing heart disease, we just need to lower at all costs. Well, the question is, why is LDL raising, even in that own its own hypothesis there and then, now we're starting to see, well, there's different contexts where we could see LDL raise, and the lipid profile is different, and there's different mechanisms undergoing on as to why, mechanisms that are occurring, as to why this, this is happening. And then if you have this hypothesis, which we'll get to, where you have these drastically elevated levels of LDL, and then you're not seeing the cardiovascular disease, then that brings into question the entire lipid hypothesis altogether. Is like, is it really just LDL, or is there some other factor that is raising LDL, and then you're having a bunch of things going on with LDL, oxidation, immune response and the this triggering event that is leading to the cardiovascular disease, we need to shift our focus from just lowering LDL to actually trying to affect that response. So this hypothesis is helpful, because it allows us to see this context, like, oh, we have this really high LDL. It's not causing cardiovascular disease, or we don't think it's causing cardiovascular disease, and the LDL, the cholesterol, is being elevated for this specific effect as a transport mechanism. So to just discount it, and to just start to discount the idea that these guys are showing, or the information that these guys are showing that it's not driven by saturated fat here, that it is driven by the shifting in substrate, and that the it's not driven by an increased cholesterol synthesis. It's it with by showing that the stand stop blocking it is like it, I don't know why you would want to discount it. It's providing quite a bit of valuable information and valuable context for us to actually get closer to the truth and understand what's going on with cardiovascular disease and with the lipid profile, and get closer to understanding what the triggers are. So it's actually anti intellectual and anti science and anti truth, seeking to just discount this piece of information that is paradoxical to the established consensus. We want to understand all the things together and not have paradoxes. We want to understand why. So in this context, why do we have this? In that context, why do we have that so we can extrapolate patterns and principles and then use those going forward to improve people's health, improve people's function and minimize cardiovascular disease, prevent it, treat it, cure it, etc. So it's like to not look at this as like, wow. Like that is that is really problematic to just like, completely discount it off the bat, and not really dig into and try to understand what's going on here, especially when it has extended ramifications overall. So for me, that's, yeah, that's highly problematic to discount it. And it's like, could there be other mechanisms, sure, but instead of just like, discounting it on on consensus or whatever the arguments are. It's like, Well, why don't we actually figure it out? Why don't we take the time and energy to figure out what's going on? So yeah, I'll leave the floor. I do want to mention one thing before we move forward very quickly, but I want you to give you the opportunity to say any thoughts you had on that. Jay,

Jay Feldman  23:36  
No, I mean, like, I agree with this sentiment entirely. And

it's

there. There's, I mean, we know this. We've talked about this in pretty much any disease process, any diet paradigm, anything like that. Talking about mainstream medicine, there's a lot of dogma. There's a lot of resistance to changing things. Sometimes it's because there's billions of dollars of pharmaceuticals on the line. Sometimes it's because someone's entire career is on the line, and everything they've learned is on the line. It's, I mean, that's that is the nature of things. And obviously something that gets in the way of progression, gets in the way of science. And some people who are going to maybe wait till the final hour of, you know, maybe they can wait five or 10 years from now to see the right data, and then they'll acknowledge that there's actually, like, this is actually legitimate. Maybe they won't, maybe they'll still be resistant to it, and in either case, there's always plausible deniability. But that's, I mean, that's just the nature of the beast. I think, yeah, yeah.

Mike  24:40  
Yeah. The one last thing that I wanted to add to this, and it just bringing up another popular topic, was Dr Sean Baker had actually tried to add in 100 grams of carbs, I think, in the form of apples, and he didn't see a huge shift in his lipid profile or anything like this. And he ran to digest fishies. And so for people who are.

Dealing with the with the this profile, the elevated cholesterol, and they want to add in carbs, it's important to choose your sources appropriately so you don't get the digestive issues. And then the other thing to keep in mind is, if you're a 260 pound man who's exercising pretty religiously and doing things like that, number one, 100 grams of carbs may not be enough to shift your substrate utilization appropriately and refill liver glycogen and things like this, if you are, like, really exercising heavily or trying to hit, like rowing,

like world records and stuff like this. So that's something to keep in mind. And then the other thing is that, if I remember correctly, if you're his, his lipid profile wasn't super high, like the case studies I were reading here. I think it was like 218 or something like this. And then I don't know how lean he was, but if you are like, if you're don't have a super high lipid value, and you aren't super lean, but I think he is relatively lean, then you may not see such a drastic shift. This is specific to people who are very lean who have very low carbohydrate intakes. And you know if it's dependent upon refilling glycogen stores. So again, if you have your 260 pounds, you have a ton of muscle, you have a ton of activity, you may need a higher amount to see a shift. And it also, if your lipid panel isn't super high, then you may not be having this lean mass, hyper responder, response so much, and it would also depend, I think, to some extent, on what's going on with your protein intake. If protein intake is super elevated as well, you could be increasing gluconeogenesis, kicking yourself out of ketosis through this the high protein intake, and that may also shift substrate utilization as well. So there's a couple important factors to make sure are dialed in here effectively for this to work and to see what's going on, and it's related to the actual mechanisms, which Dave and Nick have, like loosed a pretty well in their papers,

Jay Feldman  26:53  
Right. And yeah, so as you're saying, the high protein itself, due to gluconeogenesis could basically prevent the extreme of the lean mass hyper responder phenotype, which is worth saying, of course, less lean people will see it to less extreme, right? It is a spectrum. So this isn't just specific to people who are very lean and seeing it that way. It's just if you're more in the middle of the spectrum, as opposed to at the end, you're not going to see a 70% drop in LDL from 100 grams of carbs. And if you're already eating a lot of protein and converting that to carbs, you're also not going to see as much of a drop for that. Drop for that reason, but it wouldn't have been as increased in the first place, which you're kind of getting at. So the other point that you made here is that this is going to be at least in part dependent on effectively refilling glycogen. But the other thing that's really central to the lipid energy model is the hormone sensitive lipase and lipoprotein lipase, and especially on the hormone sensitive lipase side. This is dictated by the hormonal state. So you need to be able to shift away from the glucagon, adrenaline and cortisol enough and toward insulin enough to be able to see the shift out of the lipid energy model as well. So again, 100 grams for someone who's small and very lean, like Nick norwitz, could translate to 200 grams for someone like, like Sean Baker. So, yeah, definitely great points. There. Also the only reason

it's not like you need to worry about trying to shift out of lean mass hypersponder phenotype for this reason, necessarily it. I think the reason you brought this up is just because that might be why it wasn't seen in Sean Baker's case. But that's kind of it's not like the most relevant thing here. It's not important whether or not you're seeing it. What we're more describing is whether the lipid energy model is valid, why it's worth exploring, and then the we will talk about the ramifications and why. In reality, I would say, as we'll kind of get to we don't think this is an ideal state, but not for the reason that LDL, you know, you're just increasing LDL, and that equals bad. You know, we'll talk about the details there. So the next study I want to share here is again, one basically providing some support against the idea, or support for lip and energy model, and against this general idea that has been put forth. You know that this is not possible. This is very different from what you see in an atherogenic lipid profile and someone who's not insulin sensitive, this must be related to increased cholesterol production, increased saturated fat and all that. So this paper is titled, thyroid markers and body composition predict LDL cholesterol change in Lean, healthy women on a ketogenic diet, experimental support for the lipid energy model. This study is also going to be something we're going to refer back to later when we talk about the role of thyroid here.

But they stayed in this paper. Well, this is what they they looked at. They had 10 lean, healthy premenopausal women who habitually consumed a ketogenic diet for greater than equal to six months engage in a three phase crossover study consisting of continued nutritional ketosis, suppression of ketosis, with carbohydrate reintroduction and return to nutritional ketosis. So very similar to the Oreo experiment here. And what they found was that in an interaction model with BMI and free t3 t3 being the active thyroid hormone, both markers were significant, independent and inner.

Predictors of LDL cholesterol change among lean, healthy women undergoing carbohydrate restriction, body composition and energy metabolism markers are major drivers of LDL cholesterol change, not saturated fat. Consistent with the lipid energy model, as shown in our sensitivity analysis, BMI dominates over saturated fat for determining LDL C change even when greater than 90% of total calories were derived from saturated fat. So very clear evidence here, this is not saturated fat. Instead, we are supporting lipid energy model. You know, this paper is supporting it and showing that this is just due to the shift over in terms of

utilization of fuels, and we're seeing free t3 correlate very well here, as well with the change in LDL, and correlate with getting into ketosis, you know, decreasing the the free t3 so that's something we'll come back to later.

Mike  30:50  
Yep, yeah, and we've talked about this at length before, the effect of low carbohydrate diets on thyroid hormone. And people say, oh, you know, you don't, it's not causing hypothyroidism. Is hypothyroidism like you're seeing TSH jump up or something like this, and it's like you're seeing t3 levels drop, which is actually the most important area to focus on with thyroid function, because that is the main hormone that's having the effect. That is the active thyroid hormone. So I think it's important to hone in on that we're seeing a lowering of thyroid hormone, with the lack of carbohydrates, you're all seeing the lowering of insulin. And these things aren't ideal, because you start to upregulate those stress hormones that we're talking about, glucagon, adrenaline, cortisol, things like this to basically drive the ability to oxidize fatty acids. There's a whole hormonal and metabolic shift to push things in the right direction. And you know, it's good to see here that it is not related to saturated fats. It is specifically related to the shift in hormones and the shift in substrate. And the beautiful thing about this entire hypothesis that it aligns very well with the bioenergetic point of view. It is like it goes hand in hand what we've discussed at length across the podcast and in other videos where we're saying that, yes, when you don't have carbohydrates, you're going to shift these this hormonal profile, you're going to upregulate fatty acid oxidation, and you're actually going to, you're going to drive that fatty acid oxidation. And that's what we're seeing here with this profile. So I think that context is important understand, and I think it's super important that it is related to the fuel shift. And they're basically showing with the research here that it is not the saturated fat perspective, which, again, you're not going to see these huge changes in LDL cholesterol with saturated fat alone, like you're not seeing that in the studies where they add saturated fat either. So these guys are going doing extra work to basically show, yeah, this is really not saturated fat related. But if you looked at any of the studies where they added saturated fat, you're not seeing LDL go to 405 100 because somebody added saturated fat in their diet,

Jay Feldman  32:52  
Right. Yeah, absolutely. And I think these previous studies have really shown that, and I'm gonna cite a couple more, there are basically some pretty clear case reports showing that, you know, they basically had situations where people had this lean mass, hyper responder phenotype and were told by their doctors, or in this case, just for the sake of the experiment, to try to lower their saturated fat, to try to lower their LDL. And what they found was, again, this was not saturated fat related. And so I'm just going to cite these in the in the show notes, so that we don't take too much time kind of repeating the same thing. But again, some very clear support for the lean mass hypersponder phenotype and the lipid energy model underlying it as the driver.

Mike  33:32  
The one thing I want to point out with those studies, Jay just briefly, is that in those studies, the individuals were on high monounsaturated and to some extent polyunsaturated fatty acids in their ketogenic diet, because they were doing like a Mediterranean ketogenic diet. So it's mostly olive oil, which is very low unsaturated fats. And even so in those studies and research, when you're looking at saturated versus monounsaturated polyunsaturated fats, saturated tend to increase lipid profile. Monounsaturated tend to be relatively neutral, and then polyunsaturated tend to decrease lipid profile. But here you're seeing studies where individuals are on high mono and polyunsaturated fats, and their lipid profile is still reaching the levels that we're seeing with people who are doing the lean mass, who have a lean mass, hyper responder phenotype, and are having saturated fats in their diet, which is another basic, basically, piece of evidence that we're showing, that you're citing, that Dave and Nick and their team have showed what that the effect is not related to saturated fats. It is related to the the shifting of substrate the lipid energy model.

Jay Feldman  34:37  
Yep, exactly. Yeah. With that in mind, assuming that now we have support for the lipid energy model, this is actually what's going on, and we'll continue to talk through that. But the other piece of this is, how does this relate to atherosclerosis and cardiovascular disease risk? Because that's the other point that's levied against this idea. Is that which, by the way, as we talked about last episode, Dave Feldman is open to the possibility of this happening. He is not.

A dogmatically low carb, saying that there's no way that this could lead to anything negative. Rather, he's saying it's a question that's worth answering, as opposed to dismissing it and saying this is either too different to be valid, which we already discussed why that's not the case. And you know, it's so different from someone who's insulin sensitive on a normal, mixed diet, so this can't be happening. We already described why that's not the case, and also that this is something that's actually correlated with lower BMI, assumingly, better metabolic state, better metabolic health, though, maybe it goes to reason. Understands, to reason that in this case, the LDL is not actually driving cardiovascular disease risk. It's a good question that Dave has asked, and he is not dogmatically saying there's no way it does. He's saying, let's explore it. Of course, some people on the other side are not even open to the idea of exploring it, and instead, feel like this needs to be dismissed and shut down, because there's just no way it can be explained and so, and there's also no way that it can't increase cardiovascular disease risk. It has to, right? So let's explore that idea a little bit. There are, I think, you know, this is something again. Peter Attia has levied most standard cardiologists and lipid researchers have been making this argument at least early on, although a lot of the or at least some of the more prominent lipid researchers have actually shifted over to the to being open to this lipid energy model, being accurate, and maybe being a situation where this doesn't necessarily confer cardiovascular disease risk, so there is a bit of a shift. Of course, it takes time, and that's okay and expected, but yeah, I think because of that, it's worth digging into and digging into some of the recent research that's been going on here now to kind of just set the stage, and we did this a bit last episode, the general lipid hypothesis suggests that the one of the main drivers, something that's necessary for cardiovascular disease and plaque formation, is the LDL itself. And with the next state step of that, or in the next part of that, is that inherently, increased LDL levels in the blood is going to contribute to increased plaque formation and increased cardiovascular disease risk. And that's really the question here, is, is that always the case, or is that and then the flip side is, is that just correlation? Right? In most cases, when LDL is increased, there's poor metabolic health? Are we just seeing this as a marker rather than a causative factor? And that's basically the question that's being explored here. And the people who don't want this to be explored further, we'll say we already know the answer this is not there's there's no need for this, because we already have the meta analyzes and whatnot, even though I would say there are lots of flaws that will leave for another time. We're not going to dig into those in this in this podcast and derail it down that tangent, but rather just focus on the kind of recent evidence and information here. So with that in mind, we have this question of whether the increase in LDL here is actually contributing to increased plaque formation, increased atherosclerosis, increased cardiovascular disease. So we're going to talk through that a little bit. What I do want to mention before we do is that

we'll talk about why LDL may not be a concern if you're on a low carb diet that is increased LDL. But there are other reasons, as we've alluded to, for which the low carb diets might not be ideal for our overall health, and we'll discuss those in more detail. But with that in mind, if you are looking to switch to a diet that does include animal protein sources and saturated fats along with carbohydrates and actually leads to different lipid profile and also different effects health wise, in this case, we're talking about a more bioenergetic approach. Then you're going to want to download the energy balanced food guide. The energy balanced food guide will help you determine exactly what to eat to optimally support your metabolism and help you lose weight, improve your digestion, get amazing sleep, boost your energy and more. It's a one page infographic, and it organizes foods on a spectrum based on how effectively they support your metabolism. And it also has a separate spectrum that adjusts the scale for you in the case that you're dealing with various digestive symptoms. So the food guide makes it extremely easy to get started with a bioenergetic approach to optimizing your health. And you can go ahead and download it for free at Jay Feldman wellness.com/guide

so there's one other thing I want to mention here before I let you chime in, Mike, and that's just again, when we're talking about LDL and the lipid hypothesis and cardiovascular disease, and this question of, are we seeing something that's just correlating versus causative? One of the things that is always mentioned by the people that are saying that it is clear LDL and increased levels directly causes cardiovascular disease. Directly causes atherosclerosis. It is important. One thing that they'll say is that it is known, it is acknowledged that LDL and APO B containing lipoproteins are necessary and therefore causal. Or what they'll say is they'll say necessary and causal for cardiovascular disease necessary, but not sufficient. And it's important to acknowledge that just because it is necessary doesn't mean that increased levels are going to increase risk, or that it is, I would say, causal in a more colloquial sense, so necessary is considered a type of cause when we're talking about the science in this way. But that doesn't.

Don't think it confers the actual idea that most people are are suggesting here. And what I mean by that is that, and Dave put this really well with a good example, which is talking about macrophages, right? So macrophages, macrophages are necessary for the formulation of plaque, and therefore you could say also causal using this nomenclature. But that doesn't mean that more macrophages is increasing your risk of atherosclerosis. It doesn't mean that lowering macrophages is inherently going to reduce your risk of atherosclerosis. It doesn't mean that's a good thing or something that's worth doing, because there can, there are definitely going to be trade offs if you take out all of your macrophages, for example. So

you can draw a very clear parallel here with LDL and APO B as, as Dave is suggesting, and that's essentially the question we're going to be exploring. Yes, it can be necessary. That doesn't mean that it's causal in the way that most people mean causal. And that's, I think, an important distinction.

Mike  40:54  
Yeah, I think the major piece to get at is like, what is triggering the rise in the LDL particles and then also oxidation of LDL particles, and then the immune, immune recognition of the particles, and then their movement into the arterial intimal space. So it's the question is, what is the major element that's creating this consortium of factors to occur? And not just, oh, LDL is high, and, like we see it in heart disease, and so it's direct, it is directly involved. But it's like, that doesn't necessarily mean that it is driving the process, even though it is like, the the piece getting deposited into the arteries. There's like, there's certain things that have to go on to the LDL particles, and certain things that need to go on at the vasculature for the LDL particles to move into the into the vasculature and actually start to develop, create black formation. It's like, what is the trigger for these things to occur? That is the most important question, and I think that gives the best way forward in actually creating treatments and strategies to solve cardiovascular disease. Then, while we just see all the L so let's just lower it. It's like, it's almost like a cop out answer in terms of, like, what are we, what are we actually going to do with this specific problem? So for me, when I'm looking at this, that's what I'm trying to figure out, is, what is driving this process, what is triggering this process? And the other thing is, it's, there's this is why this, this lipid energy model is so helpful is because they're saying, Okay, in this state of the low carb diet, we see this shift in hormones, and we see this effect of lipoprotein lipase at the cell, and we see this effect on the lipid profile. And the triglycerides are this, the HDL is that, and the LDL is this. It's like, why is it that? The question is, why not that? Is that it's, why is it that? And so that's the question that we need to be asking with cardiovascular disease as well. Why are we seeing small, dense LDL particles, elevated triglycerides and low HDL inside cardiovascular disease, or atherogenic dyslipidemia? And it's like, largely, I think, a large portion of this, especially because we tend to see this in fatty liver disease and diabetes and obesity, is it is driven by metabolic dysfunction. It is driven by a lowering of lipoprotein lipase at the cell, an inability to oxidize substrate that includes fats, that includes carbohydrates, and there's general mitochondrial dysfunction going on with elevated reactive oxygen species and upregulated inflammatory response with macrophages and an oxidized, oxidized LDL. And it's okay, okay, so we see the metabolic dysfunction. The next question is, what is driving that metabolic dysfunction? And this is why this is so important inside the the bioenergetic view, and why this hypothesis is so relevant to the bioenergetic view, because it's starting to give like, point out the different context, discuss the different components that we're talking about, and start to point us in the direction of answers, besides just statins, just yeah, just take your statin, lower your cholesterol, and you should be good to go. And it's like we've already, as you mentioned previously, Jay, we already talked about the tenuous components or the tenuous benefits of statins under most circumstances, it's looking at this one factor in terms of lowering cholesterol. Even with the statins, there may be other effects of the statins, like like blocking inflammatory pathways or inhibiting LDL oxidation, and not just necessarily lowering the cholesterol. And so it's like we need to actually determine what's going on. And the perspective of, you know, let's not even look at this. This isn't even relevant. We already know that. It's LDL. We just need to use statins. Like that is not progressing us towards actually finding legitimate answer, because there's many people who are on statins, who are still getting heart attacks, who are still having a variety of cardiovascular disease and different issues, and it's like it's not solving the problem. It is managing the process. At best, we need to start to get to the root of the problem, start to address that specifically, and then go from there.

Jay Feldman  44:56  
Yeah, I think even saying it's managing the processes is.

Being generous, and,

yeah, it's and of course, not without significant side effects and all that. But yeah, we've, we've discussed that in the past. I'll link back to those episodes. And I do think that, you know,

it's worth it's worth mentioning that, but yeah, so as you're saying, as you're getting at, the increased LDL, in most cases, is going to be a marker of metabolic health, because if, again, you're eating a mixed diet and you have high LDL, it typically means there's excess lipid floating around, meaning that you're not using the fuel that's coming in, there's extra you're often storing body fat, or you're just in a poor metabolic state. And so because of that, you're going to have this as a

as an associative factor, that's an indication that you're going to be in worse metabolic health, you're going to have increased oxidative stress, you're going to have an increased inflammatory state, you're going to be having poor endothelial function. Oftentimes, this is going to track with higher blood pressure, which makes sense. You know that that's to be expected, but that is very different from saying that the increase in the LDL particles is directly causative, or I should, again, when we say causative, I'm making that in a different way from the idea like the types of causes that are put forth in science. And again, Peter Attia loves to say that, you know, LDL causes cardiovascular disease. But what he is saying, He's saying that in the context of meaning that it is necessary, but not sufficient, and that is a type of cause, it is considered to be a type of cause to be necessary. But it's like arteries are also necessary and causal for cardiovascular disease and atherosclerosis in the same way, right? They have to be there, or else you can't have atherosclerosis. That doesn't mean that arteries are bad. So that doesn't mean that increased arteries, or having more surface area of arteries, or something is worse or better functioning arteries, or anything like that, like that is those are all downstream applications. So be very careful when somebody is using causal in different ways, like that, and using it in the strict scientific sense, but in the more colloquial sense, I would say there's a difference, you know, from what we mean by saying just increased LDL particle number increases the causer at risk or drives atherosclerosis, versus it just being a bystander, it just being a marker of a worse state. And again, to explore all of the studies there, all the information there, that is a different podcast. It's a much larger conversation. We talked about part of it in those previous episodes, so I'd refer back to those. But we're really wondering about here is the lean mass hyper responder phenotype as an example, as as evidence for what we're saying right now, for this idea that it is just a marker, and what it would require to show that is that you have these people who have higher LDL and are on low carb diets and are metabolically healthy and low BMI. And you study them over time and see that there's no increased plaque formation, no increased atherosclerosis, no increased cardiovascular disease. And that's essentially what they have tried, have started exploring, and I mean, they've been doing it over some years now, and now has some data to share. Of course, it is not

the end all be all. We need more time for you know, if you want to be very, very careful and say we need to look at this over 50 years. Yes, it's going to take some more time to find people who are this presentation on a ketogenic diet for that long. But we do have some good data here as a starting place to suggest that this is not an issue, an issue in terms of cardiovascular disease risk, and this is from the Keto trial. Do you have anything to mention, Mike, before we dig into that?

Mike  48:29  
No, I think, I think the way to explain the I just want to clarify what you're saying with the causative piece. So I think the way to think about it in normal terms, not by the research definition is LDL cholesterol is involved in cardiovascular disease, but it is not the direct cause of cardiovascular disease. There is something that is leading to the elevation and leading to these variety of factors that is allowing or pushing LDL cholesterol into the vascular space and forming and allowing for the plaque formation. So that is the call, that factor is the cause. LDL is directly involved. And I think that's the important distinction to understand. And so the thing too is because, like, even, even in Peter Attia'

s podcast, where he talks about Dave Feldman, or he interviews Dave Feldman, he's like, he has a lot of, I think he said something online. He's a lot of disdain for people who say LDL doesn't cause heart disease. And it's like, we're not even saying that it's not directly involved. That's the thing, that it doesn't cause it from this, from the scientific terms, exactly, we're just saying that there's some triggering factor, and that is more important to focus on than all these other probabilities and statistics and associated values of just LDL. It's like, what is this underlying driving factor? Maybe those things can help us to understand what, why, why the association is there, why this is involved directly. But to just like, focus on the LDL as the target, I think you're you're focusing on a sim.

Them, you're focusing on a signal and not the trigger, not the actual driving problem, and that is the most important thing. And I think a lot of people do understand that. To large extent, it just like, maybe they're maybe the terms that they use aren't up to Peter Attias preferences that he doesn't like their semantics, or something like this. But I think a lot of people do start to understand this and see this like, there's more going on to the picture than just LDL cholesterol. And they in that sphere, they're focusing on APO B, apo B, cholesterol, cholesterol. It's like, Okay, what about the immune response? What about the inflammatory profile? What about the metabolic dysfunction at the cell? What about the lipid peroxidation? What about the high amount of linoleic acid inside the plaques, oxidized linoleic acid and linoleic acid, cholesterol esters, cholesterol, lineal eight. What about these things? Are these things involved or in these driving factors? I think those are more important than just like, yeah, April B cholesterol, it's like, yes, we see that. We see it's elevated at this point. We see that's going on. But why? Like, we need to know why. And that's, that is the primary question. Again, this starts to ask, to answer these questions, and what we're starting to see, or what we see at overalls, there's different context for this to occur. Hypothyroidism can drive limit, profile up. Is the problem? Cholesterol as a problem? LDL, no, it's poor thyroid function. Infection can drive LDL, up. Is there the problem? LDL? No, the problem is the infection and cytokine response. And this is another circumstance. Another context we see is a low carb, high fat diet and a lean individual driving cholesterol. Yes, is LDL the problem here? Probably not. It may not even be a problem in this context. This may be par for the course, given that specific context, and that's what we need to get to, is this contextual understanding, instead of like, yeah, LDL, for all these contexts, it's just a problem. We just always need to lower it. And in this case, we're even seeing like, maybe lowering it is a bad idea, if that is the way that you're shifting all of your energy to your cells because you don't have carbohydrate available. And that's This is the importance of understanding context and understand, distilling principles out and applying them to different contexts. And just like, yeah, LDL, bad, statins, associations caught, and it's causative from the research sense, it's like, that's not that's not helpful. That is, I think, overall net negative. And I think that's why there's still controversies, because how these things are being thought about is poor quality in terms of the way it's being thought about, not that the research is bad, but how we're thinking about these things is not helping us to solve the question that needs to shift. And Dave Feldman, Nick norwitz and our team are shifting how it's thought about, and I think that's also why they're getting such huge pushback, is because it really is turning these these dogmas and consensus on their head.

Jay Feldman  52:41  
Yeah, absolutely. And just to clarify a couple of things, and the and Peter T is positioned to an extent, he does acknowledge that there is more than LDL involved. He's not saying this is just an LDL problem. And he does also think that it's worth asking the question of, Why, what kinds of things increase LDL. The real distinction, the real thing that we're that is trying to be parsed out here is, is the LDL itself? Is increased levels of LDL a driver, versus Is it a bystander? Is it just a marker, an indicator of poor metabolic health being the larger driver and or not even the larger driver, but the driver and increased LDL is not actually contributing as a driver? That's that's the kind of more particular question that's being asked here, and that the lean mass hyperresponder phenotype is potentially providing evidence

against in terms of LDL being a driver. And again, when we start talking about necessary causes, people will often misunderstand by again, because, for most people, yes, something being necessary doesn't mean that it is causal. In the same way that you could say that, like, paint is necessary for car accidents because there's paint on cars and cars getting car accidents. But that doesn't mean that the paint is causing the car accident. That's That's, again, very, very crude, but general idea for for understanding that the other thing too, as you were saying, is lowering LDL on its own could be bad if you know, if it is just a marker, we're focusing on the wrong thing. But also, and we talked about this in those previous episodes, it can be a bad idea for other reasons too. LDL can have a protective effect. It's something that protects us, and it plays a major role in our immune function. Also, the cholesterol in there is needed to produce steroid hormones. Again, there are a lot of negative side effects that are seen with using statins. And you basically see what happens when you just reduce cholesterol and reduce LDL. So that is, again, something we talked about prior. Just wanted to make a note there. And then the last thing you were talking about trigger, a trigger of cardiovascular disease. And just to clarify, you're not saying there is a that there's just a moment that matches lit and everything, and then you go from zero to cardiovascular disease. You're just saying that there are other drivers here that are actually worth considering. And the question is, is the LDL level on its own, a driver, as opposed to, you're not talking about like a momentary trigger, of course, this is a process that.

Happens over time, and it's a spectrum and all of that. So again, in terms of answering that question of is LDL driver, which, as we've kind of explained, we don't believe it is the case. There is this keto driver that was done by the team here in terms of the people on the lipid energy model, lean mass, hyperspan, or phenotype group, and it was presented in a presentation. The trial is not published yet, but it was presented recently by Matthew Budoff in a presentation titled the Keto trial. Carbohydrate restriction induced elevations in LDL, cholesterol and atherosclerosis. And what they looked at was the lean mass hyper responder cohort, cohort that had very high LDL, very high HDL, and very low triglycerides. And compared that with another group that just had average levels of LDL as an average group, and their LDL levels were way lower, around 120 compared to the average levels of 272,

in the Lean Mass Hyperresponder group and looked at things like calcium scores and calcium artery scan. They also did a CCTA, which is a better way of looking at plaque, it's a little bit more accurate and precise. And so they used both of those and compared these two groups. And what they found, you can see here, was essentially that there was no and the two groups were pretty well matched in terms of age and things like that. And they basically found there was no significant difference between the two in terms of plaque burden, where, again, on one group, you had the mean LDL of about 123, it looks like. And then another group you had 272,

calcium artery score, or calcium scores. There was no difference, total plaque score. There was no difference. And what that suggested was that there was no relationship. Based on looking at the data, there was no relationship between the LDL cholesterol numbers and plaque, which is a pretty notable finding, and the opposite of what many of these people would be saying. And this was looking at people who I believe were on this ketogenic diet, with the with the high LDL for, I want to say at least five years or so, or it's in the first statement there.

Mike  57:07  
So it says match mean age was 55.5, years. Mean LDL was 272 with a max of 590 and the mean duration of the ketogenic diet is 4.7 years. And I think that they, the people that they took were on the ketogenic like they didn't put them on the ketogenic diet for five years. They took the study, and the people had already been on average on the ketogenic diet for five years. So they didn't, this is people who were like, doing this by themselves, this they didn't put an intervention in place. They were just looking observationally, if we have these people who have this specific criteria in their lipid profile, with LDL of x, HDL of x, triglycerides of x, and they've been on a low carb diet, what's the difference between this? And I think it was like looking at the my hand Miami Heart Study and saying like, Well, what do we see here, with their the Miami Heart Study, with their coronary plaque burden in it with their average LDLs of the the 123, uh, versus these, these keto individuals, where, what's their plaque burden with their LDL is 272, so you're comparing these to this specific group, to this specific group, and you're actually, you're seeing, wow, there's not a difference, even Though the LDL value on average is is more than two times as much the amount which you should see a signal. If LDL is the driver right, that would be the idea,

Jay Feldman  58:31  
exactly, right, exactly, and, and, yeah, so. And they didn't see that. And we see that here as well, where they plot out the LDL, LDL levels versus the total plaque score. And you basically see, as these graphs move to the right, these, these are the people who have the most plaque in each group. And there was no correlation with the LDL levels, and then vice versa, no correlation. And that was, again, basically what they found, and it shown very clearly in the graph. And there was a there's another part of this presentation we'll get to in a moment. I'll let you share as far as the Western Denmark heart registry, but yeah, essentially, we're seeing this very clearly. And again, this is just the beginning of the trial. They're going to look at this over time, but this is just the preliminary data. One of the things that has been mentioned is that, you know, five years isn't long enough. We need to see this over a lifetime, and these scans are not going to be able to pick up on the small changes and things like that. Of course, they are pretty good measures. This is not perfect. Science is never perfect, and things take time. And so if you want to be on the side that we need to wait till we have the actual, actual, like absolute perfect evidence, looking over 20, 3040, years, and using every possible scan to see any possibility of plaque? Fine, you can, you can do that. But I would say this is some pretty good evidence so far, and definitely not evidence for the idea that there's a relationship between LDL and plaque or atherosclerosis, and also in the people with the average LDL of 123 to see that there is no correlation there. And these are people who presumably.

Their whole lives have been doing whatever they're doing, and you see it in the lean mass hyper responder group as well. It would be one thing if you said this doesn't tell us enough about being on a low carb diet and having this this lipid profile, we need to look again over 80 years. Otherwise we can just discount all of it. Fine. That's how you want to, like consider things. That's fine, but you would still expect to see a correlation between LDL levels and and plaque. And of course, you don't

Mike  1:00:28  
yep, yep. And I mean that they are planning on checking this over a longer period of time as well. This was just this first thing I he mentions this in the there's a bunch of doctors at the end of the video who are asking him all these different questions, not about the biases, and, you know, the different areas that they may or may not have, like, missed with this. And he's saying, Look, this is just observational, like, we're literally just taking and seeing, you know, what these people's LDL levels are, you know, they're, they've been, they're in this particular criteria, and then what's their plaque burden? And then we were comparing it to this other, this other group we're comparing it to, and now they're going to keep checking these people over time. That is something that they plan to do going forward. So they are looking to that. But then this brings us to the next study. Here is that they do have some studies looking over a longer period of time in the the Western Denmark heart registry, and basically seeing that we don't actually see the correlation with LDL and people who don't have any

who have a coronary artery calcium score is zero. And so what they say here is they say, in this large cohort of greater than 23,000 middle age symptomatic patients undergoing CTA, the LDL C levels were strongly associated with five year myocardial infarction and the cardiovascular the atherosclerotic cardiovascular disease events and those with evidence of coronary atherosclerosis, ie, if their coronary artery calculatory score, coronary artery calcium score was greater than zero, whereas no significant association was found among those with coronary artery calcium, without coronary artery calcium, these results were similar among the multi ethnic study of atherosclerosis participants with 16 years of follow up. So basically, what they're showing here is that if your coronary artery calcium score is zero, what you're you're seeing is that the LDL didn't actually really matter that much, versus if the coronary artery calcium score is greater than zero, then the LDL actually started to become important. And they saw increased risk of different disease processes, atherosclerosis, et cetera. And so things like this start to bring into question, like, is LDL the driver? So is it involved? We already know it's involved. That's known, that's not, no one's debating that at all. The question is, just, is it driving the process? And when you see this, it's like, Okay, we have people who don't have atherosclerosis and they have a variety of LDL values, and we're not seeing an association. We're not seeing a trend in their LDL values. But if we have people with atherosclerosis and as their LDL values increase, you're seeing worse outcomes, then the question is, okay, well, what drove the atherosclerosis, and is the process that's driving the atherosclerosis? Is that triggering the changes in these LDL values and and that's worsening the processor or, or is there some process underlying and with the LDL present, it makes it worse. And so that's the those are things that we want to know, and that's the whole, that's the whole point of this is, is like, that we we don't think that LDL is the driver of this. It's involved in some underlying pathology. And so the question is, like, you know, what is that underlying pathology? Obviously, we've talked about this before. I've talked about this before in other videos on my own channel as well. And so, like, those are the things I think to focus and hone in on

Jay Feldman  1:03:41  
right Right, exactly. And what we're seeing here is that LDL is a good correlate for those other factors, those other things that are driving cardiovascular disease. But in the case that you don't have those other factors suggested by a coronary artery calcium score of zero, LDL is not actually showing any causative role here. And that's important. And again, the people who are saying that the coronary artery calcium scans aren't accurate enough, and whatever, I mean, you can see it here. It looks like it is showing very clearly, correlating very well with with cardiovascular disease, atherosclerosis, at least that's, I mean, you can see that elsewhere, but what you're seeing here is the, I mean, there is a very clear indication with coronary artery calcium and myocardial infarction and atherosclerotic

cardiovascular disease, that's what they're they're looking at. So it is a good enough marker. You can see that here, and when you don't actually have the underlying metabolic issues, but your LDL is high, it doesn't matter. And this is looking at people who have an LDL level above 193 versus below 116 and there is so what they're basically saying, let's just round to like 201 100. Basically, if you have a coronary rd calcium scan of zero and your LDL is 200 versus someone else who has a scan of zero and their LDL is 100 it makes no difference in terms of cardiovascular disease risk. That's essentially what's being said here.

What's being shown very clearly in the table that is directly refuting This is evidence directly against the idea that the LDL is driving cardiovascular disease risk. So I think it's it's a great presentation, and some very clear data there that I would say some pretty good evidence against. I mean, bold little bit energy model for the lean mass hyperbonder phenotype, not being just genetic and things like that, and against the idea that when you go on a low carb diet and your LDL is very high, that necessarily means you're at increased cardiovascular risk or increased risk of atherosclerosis. So that's great. I think you know, as the data keeps coming, you'll continue to show that and and that's absolutely worth acknowledging. Now, there are a couple of of extrapolations and other areas that I think are worth discussing when it comes to this model and this phenotype, in terms of what it means for lipids in general, how we should be interpreting them, or whether we should be interpreting them, and then also whether this just because, let's assume that there is no increased risk of atherosclerosis due to this mechanism. Does that still mean that these are ideal diets, like a low carb diet, which I think is the Yeah, that's the last question we'll answer here. Yeah, yeah. So

Mike  1:06:16  
the one thing I want to mention, just briefly jumping back is Dave and Nick in their paper actually discuss why we see changes in the in the lipid profile in an atherogenic dyslipidemia, and they describe those mechanisms. And so I think that is something that's important to hone in on. And one of the things that they hone in on, and it's this goes directly with the the bioenergetic point of view is that in atherogenic dyslipidemia, there's a decreased uptake of substrate in the form of fats at the tissues. Also there's all we know, there's insulin resistance, so we know there's a decreased uptake of glucose as well of carbohydrate. So this is highlighting, overall, I think, a problem with energy metabolism in creating the L the elevations in LDL. So this is why it's important to understand what is driving up the LDL is, are you having more coconut oil in your diet? As you're going to show us, Jay with the catavince, is it? Is it that they're just having more coconut oil and so they have a bit more LDL cholesterol because of the effects of saturated fat versus monounsaturated and poly plus. Something to note is that the polyunsaturated fats are lowering the lipids via kind of like a pharmacologic mechanism, by triggering the PPARs and things like this. So it's like, is it just elevated because you have the saturated fat? And then you know, if the LDL is not the problem, then the saturated fat, elevating the LDL also shouldn't be the problem. The question is, then, okay, or is it because you don't have carbs, so you just don't have enough carbs, and then that's elevating your LDL levels like, Well, yeah, if that's the reason why, then there's probably no issue with it. But what they're showing at is, if you have metabolic dysfunction, and it's backing up all the lipids into your bloodstream. And so the VLDL is coming out, the cells are not taking up the triglycerides off the VLDL, and then they're being redistributed around the HDL and LDL levels, the regular LDL levels. And now you have a bunch of VLDL, you have a bunch of HDL, you have a bunch of you have a lowered HDL, you have a bunch of LDL, and you have a bunch of triglycerides floating around. It's like, yeah, that's a problem, but it's like, is it a problem because they're all floating around, or is it a problem because they can't get in the cell and be used and now, and it's because of the metabolic dysfunction. And so this is where you This is why I think you see something with this western Denmark Heart Study, where if somebody has atherosclerosis, they are they probably already are having metabolic dysfunction, and that's leading to the elevations in their LDL, whereas somebody who doesn't have the metabolic dysfunction can have a wide range of different LDL going on. And it could be, you know, maybe they just have a more monounsaturated fat diet or a lower fat diet, or the other the individuals are, you know, maybe they have a higher fat diet, they're eating more butter or something like this, and then they're seeing this higher LDL value, but because they don't have any metabolic dysfunction, it becomes relatively irrelevant to the overall picture. And I think that's that's why we can that explains some of the differences that we see between these two different states. I think that's pretty important. And Dave and Nick in their paper, where they go through the mechanisms, actually describe the mechanisms of why they think you're seeing this profile and atherogenic dyslipidemia, and the major piece is that the cells are not taking up the lipids. And it's like the question becomes, why? And that's something that you and I have discussed. It's like metabolic dysfunction, mitochondrial dysfunction, and they talk about some of the things inside the paper as well. Very interesting studies inside the paper as well.

Jay Feldman  1:09:38  
Yeah, yeah, exactly. And so what you're getting at is, when it comes to looking at a lipid profile, we want to actually understand what is underlying it, especially assuming that the lipid profile itself can't tell us anything about atherosclerotic risk inherently without knowing some other things. So let's so you had alluded you know.

You mentioned the Catawbas, and so the way, like just to we'll share their, some of their, the data on them in a second. But in general, what I would say here is that, and as as was suggested by this data, just looking at LDL levels is not going to tell us much about metabolic health or atherosclerosis. And the same would be true about just looking at HDL, just looking at triglycerides, really, just looking at any marker. We always, you know, we talk about this all the time, needing to understand the context, needing to look at multiple markers all together, plus the individual, what is their experience like? What's their day to day life like? You know, what is, what are they noticing in terms of symptoms, and putting that together to try to understand what's actually going on, as opposed to the simplifying of your triglycerides are this. So this is what you need to do. This is bad. This is good. Your LDL is this. Let's get you on a statin, or let's cut the saturated fat right. Like we want to consider these things in a much more complex and accurate context. And the ketamine are another good example here, where and a very different example too, they're not showing a lean mass hyper responder phenotype at all, and they're also eating about as opposite of a diet as you can get to other than the fact that they're also eating a high saturated fat diet. So the ketamine have essentially an absence of cardiovascular disease, an absence of metabolic syndrome. Instead, they're known to be extremely metabolically healthy and extremely insulin sensitive, and yet their lipid profiles look kind of like an atherogenic lipid profile, or dyslipidemic lipid profile from someone on a Western diet. So what you see, and this is some data from a study, and they looked at a bunch of different you know, they gathered a bunch of data about the ketovans, and they looked at lipid profiles. And so when we look at the men, on average, they had a total cholesterol of 181 which is not elevated. Their triglycerides, on average, were 151 which is elevated, non HDL. Cholesterol was 139 HDL was 43 which would generally be considered low or borderline low, LDL of 108 which is considered elevated. Normally wanted to be below 100 according to the kind of conventional standards and ranges. And yet they have an insulin level fasting insulin of 4.0 which is very good, one of the pieces of evidence showing that they're very insulin sensitive. And in the women, we see total cholesterol level of 224 still elevated triglycerides, but they're at 115 so not considered to be out of the range. Their HDL is about the same at 46 and their LDL is up at 155 so considerably higher, and their insulin is about the same, 4.8 but so in this population that's eating very high carb, high saturated fat, they have a lipid profile that most I mean, especially for the women, you know, there definitely would be put on statins if they were in the States, for sure. And probably the men, too, considering their LDL, or at least, you know, it'd be considered borderline. They'd be told to avoid saturated fat and get a lot of fish oil in, you know, to help their LDL and HDL. And yet, this is a population that's very, very healthy, very, very healthy, metabolically and in terms of cardiovascul

ar health. And this is just another good example, similar to the lean mass hyper responder phenotype. That suggests that we the context that that suggests two things. One, these are markers, these are indicators, and that we can use them. We can draw information from them to understand what is going on metabolically, metabolically for someone, as opposed to taking the marker as the disease. And yeah, I would just kind of leave it at that. I think, you know, on my end, I think that that's clear. And Mike, feel free to go ahead and comment,

Mike  1:13:22  
I think the way that is helpful to look at this type of stuff is to understand that these are trafficking networks. So these things are showing how fuel is being distributed and used across the body as kind of indirect values. And so when we're looking at this, we want to have this understanding of it. And this is what Dave was doing when he describes it, and as an engineer whatnot, is that he was looking at this as a distribution network, and the the lipoproteins actually being carrier components, which is actually what it is. So when you understand it in this context, things start to change. When you understand the that you have the liver, you have, what the food coming in from the gut you have the liver, you have this distribution mechanism to the tissues. And then all of these things are carrier proteins or carrier components, or even blood glucose or insulin are basically ways to in the blood glucose and blood insulin levels are ways for the body to transport the carbohydrate in this different fuel substrate to the tissues. And then you're seeing things back up or change based on what's coming in and how these things are being used, and then what's going out. And so when you understand it in this perspective, the question is not, oh, you set up in this particular stratified group, so then your x it's like, here we have a triangle block. We just put it in the triangle hole, and we don't ask why? The question is, why are these things moving the way that they are? What is, where's the where's the log jam? Where's the backup? Is there problematic things coming in from the diet? Is there something going on, specifically at the cells that where they're not You're not taking the substrate of the fuel source?

Services or the components and using them effectively. Is there some other problem going on somewhere at the liver or at the pancreas or something like this? The question is, what is going on in all of this altogether? Why are we seeing these changes in these transport mechanisms and these components being moved in the blood, these signaling molecules? So we want to understand it in context and understand why. And it's something that Dave has done, and he talks about in his model, and that's also why I think it's so effective to understand things, because the context and frame with which he's trying to understand it is super valuable. And he's asking the question, why? Instead of saying, Well, we have these series of associations and we have these cutoffs, so based on these cutoffs, we just do x, and we don't really understand why we see these things, but we've developed these cutoff systems that have these associations, and we just go from there. And I think that this, like algorithmic approach, there's some value to it, and there's some there's some value to understanding or associations and relationships. But I think the under, under, the over, the underlying piece that we always want to understand is, why is this occurring? Why are we seeing these shifts? What's the context in which these shifts are are developing? So that we can start to hone in and find the highest leverage piece to change what's the highest leverage problem, so that we're not spending all of our time fixing all these symptoms. It's like, if you have metabolic dysfunction and LDL levels are high, it's like, yeah, we could focus on LDL, or we could just try to figure out and fix what's going on at the cell so that metabolism is working well,

Jay Feldman  1:16:27  
right, right, yeah, and then LDL would be lowered.

Yeah, yeah, absolutely. And this is all as you're getting at this is why these are questions that should be encouraged to be asking, as opposed to, you know, being dismissed and critiqued for even being asked. So there's one other kind of small aside I just want to mention when talking about lipid profile and markers equal disease state equals degeneration, whatever it is, because the same thing is done on the flip side, when people go low carb, and then they see insulin levels drop and glucose drops and a 1c drops, and then we also see, you know, lipolysis increases and fatty acid oxidation increases. And when we look at someone who has diabetes, they have the, well, they actually already have high lipolysis and high lipid oxidation. But if we just focus on the earlier markers, you know, they have high a 1c high glucose, high insulin. So lowering those by low carb must be good for that same reason. And we want to it's just important to highlight that is the exact same logic that people will say that you are going to get atherosclerosis and heart disease on your low carb diet because of your high LDL. And so I think that is another piece that, again, we've talked about it quite a bit, but it's really worth acknowledging that the high glucose, for example, in insulin resistance and diabetes, is a marker, and it's not a driver, just like the high insulin, just like the high A, 1c these are indicators of insulin resistance. They are not the cause of insulin resistance, and we don't want to make that mistake in the same way that other people make that mistake with lipids and so yeah. I mean, maybe I'll just kind of leave it briefly at that. We just did several episodes talking about insulin resistance, what actually causes it? Why carbohydrates not only are not a driver, but actually help to fix the problem. So I don't want to go too in depth at that, but just wanted to highlight that here, because it's a very clear example of this thought process. And yeah, I think we want to look at these things critically. We want to understand the physiology, and so with that in mind, let's treat insulin resistance the same way. The other piece, again, talking about lipolysis and lipid oxidation, the idea that just burning more fat and releasing more fat from the fat stores equals fat loss is just as reductionistic as again, these other things that we're talking about, and I would definitely recommend caution there. When you actually look at what's going on in these metabolic Ward studies, and looking at low carb versus high carb, the increased lipolysis, increased fat oxidation, lower insulin does not mean loss of body fat. We've talked about the issues. That's called the, basically the carb insulin model of obesity, and it, there's a lot of evidence against it. I would say it's not supported at all. And I would just, I'm just going to link back to some other episodes where we've talked about that, and I would highly recommend looking into that research and treating that objectively in the same way that that you would with your high LDL on the low carb diet.

Mike  1:19:12  
Yep. And to be fair, to in in the lean mass hyper responder model, they do actually show in the model that the fatty acids that are being released from the fat tissue are being circulated to the liver, being turned into VLDL, and then the VLDL is also the redepositing fats back to the fat tissue. So you you're still seeing an increase in or maybe an increase in fatty acid deposition, but you're also seeing an increase in fatty acid release. So it's this constant process of release and deposition, release, deposition, release, deposition, release, and it's depending on what's going on in the fasted versus feeding fed state. Because if you're taking in a large amounts of fats from the Fed state, you can, you can arguably increase your fatty acid deposition more so than you actually.

Do your your fatty acid release, and that can put you in a overall net positive state for fatty acid accrual. And then you can see things like that, you deposition the liver, deposition in the fat tissue, etc. So in a lot of the studies with the Keto, low carb and even for high carb diets, for the metabolic dysfunction, or for obesity, or things like this, they actually create like, it's important that a deficit is created so that you're not continuing to accrue. And it's related to the idea that whatever substrate you use, you can you'll be increasing deposition and utilization depending on what you have going on. Even with carbs, you can increase deposition to fats, and then with fats, you can just store the fats. So these things I think are really important understand. I don't even think that the idea that if I'm just burning fats as my major carb source, or my major fuel source, that I'm going to lose more fat. I don't even think that it's reductionistic. I think it's just a lack of understanding of the complete picture. The people just not getting that. You also have the same thing, right? Yeah, I guess so, yeah. But it's like they're just not understanding, oh, there's also deposition going on. It's not just about burning, it's about deposition as well. And, like, the other thing changes in the metabolic rate and all these components that become important in the overall picture. And so that's that for me, that that's kind of, you know, that that's my two cents there. And then with the the insulin sensitivity piece, or, like, the insulin, hemoglobin, a 1c values things like this, even inside the research, where they're looking at meta analysis of the effectiveness of keto diets on diabetes, and they're making their cut off things like hemoglobin, a 1c less than x percent, like 6.5%

we need to understand, you know, what is hemoglobin A1c a marker of? Hemoglobin. A1c is a marker of three months average of blood glucose. If you don't have any glucose coming in that, then sure hemoglobin, A1c is going to be lower. But that doesn't mean the metabolic dysfunction has been corrected at the cell. You just haven't eaten carbs. So we need to be really careful at the values that we use to determine cutoffs for function, especially if they're indirect. We want to actually understand things in that context, and those the all of the values, whether you're looking at cholesterol on a high fat diet, or you're looking at insulin, blood glucose, etc, on a on a metabolic dysfunction individual, we want to make sure we're understanding what's going on and why we're seeing these changes and how these interventions are affecting these things. Even when we look at catawns, we want to look at the Catawba and say, okay, they have this higher LDL cholesterol. Why? Well, a large portion of their diet is coconuts or or a fatty acid source like that that has a higher saturated fat intake. So is it there is their lipid profile elevated because they have metabolic dysfunction? No, they're just eating more coconuts. It's like, that's that's normal, that's par for the course in that context. So those are the things I think are. That's the importance of understanding things in context, which is a huge tenant of the bioenergetic sphere.

Jay Feldman  1:22:50  
Yeah. And just to go back real briefly, to the idea of the body fat lipolysis as a aspect of the fuel distribution center by the lipid energy model, as you were saying

that. So the idea that that is, there's going to be more fuel leaving and more fuel coming in, is, is just more flux, right? We have more flux through the body fat stores, because that is now our main fuel. And so more flux doesn't mean more loss. We have to look at the net, right? We have to look at how much is coming out versus how much is coming in. And in the same way, we have a lot more coming out. There's a lot more coming into the body fat, too. So it is not like this magic there's there's like magic effect where you just start burning lots of fat, and you just lose all these pounds of fat every day. Of course, you can lose fat on a low carb diet. We've talked about that a ton that we're not saying that, but it is not just because you have increased hypothesis. In the same way that if you think of a carb based diet, or a diet containing carbs, you're gonna have a lot more flux with your glycogen stores, right? You're gonna have more glycogen deposition, more glycogen release. If you just focus on the release side, you would say, well, your glycogen is gonna get depleted on a higher carb diet. And it's like that doesn't doesn't make any sense. You can't just focus on the release side. You have to focus on or you have to look at the entire balance there of coming in, coming out, or motor regulation, metabolic state, all those things. So yeah,

I don't think anyone, I don't think there's ever going to be a point where people stop saying that you have more fat burning on a low carb diet and that leads to fat loss. I don't think we're ever going to be able to stop that from happening. But anyway, we'll, we'll keep trying. So that leads to the last kind of question here that we want to answer, thing that we want to explore, which is, let's take on the assumption that this lipid profile is purely based on lipid energy model does not confer any increased atherosclerotic risk or risk of cardiovascular disease. Does that now mean that a low carb diet is healthy? And we had alluded to two major concerns. I mean, we've talked about these ad nauseam in previous episodes that I'll link to, but in the last episode, we talked about two primary concerns here on a low carb diet that are acknowledged in the lipid energy model. One is the shift toward higher levels of stress hormones, a shift toward less insulin relative to glucagon, epinephrine and cortisol and.

That is something that is basically integral to the model, because it's required for the increased hormone sensitive lipase activity, which is a central part here, and the other is decreased thyroid activity, as is seen by low t3

in a number of these studies, and something that Dave and Nick both acknowledge that they've seen in themselves, they both have low t3 and again, in that previous study looking at the lean, healthy women that are lean mass hyper responders, we saw this clear relationship with t3 where when you drop the carbs, t3 went down, when you increase the carbs, t3 went back up. And

the what I would essentially say, to keep it simple and just based on the things, just based on these two things, not exploring in more detail, which we've done previously, but just based on those two things, elevated levels of stress hormones and decreased t3 are generally not ideal things, generally not things that we would want long term and that will come at a long term cost. And I'll link back to articles. Let me back to the to the episodes where we've talked about this in detail, and essentially what we would say is, long term, that is going to lead to a worse metabolic state, because it is a signal that your body is viewing this state as basically starvation and famine and other stressful scarcity type environments, which is why you see the same thing whether you're on a low carb diet or you just don't eat at all. It's why those things mimic each other, and as a result of that, our bodies want to then conserve energy, and they will favor, kind of the maintenance of the most important organ systems and things like that, at the cost of others. And over time, we'll see a decrease in terms of our metabolic rate and other symptoms that come along with that, and also other symptoms of the elevated stress hormones. We work with people all the time who are coming from these sorts of diets and are seeing those symptoms that cropped up over time in most cases, sometimes it's months, sometimes it's years before sleep starts to deteriorate, testosterone starts to deteriorate, skin, hair and nails start to have issues. You know, energy starts to crash. Yeah, definitely. Thyroid dysfunction, energy is crashing.

Mike  1:26:57  
Mood dysfunction, poor exercise recovery, constant feelings of stress, all this type of stuff,

Jay Feldman  1:27:03  
right? Right, exactly. And

the, again, we are not saying that short term, you might experience benefits in all those areas, because a lot of people do. There's reasons for that. Again, we've discussed these so many times, where you reduce endotoxin production, and if you're poorly oxidizing glucose, and you shift toward fat, you can have a lot of benefits there, or shifting toward ketones in a brain that can't effectively use glucose. There are a lot of reasons why you might have benefits short term. That does not mean that these are optimal diets long term or even short term. It just means in the short term, the benefits might outweigh the negatives, and over time, the negatives will outweigh the benefits. We would recommend not taking that approach at all and instead trying to fix the actual underlying drivers of this state that are actually leading to those sorts of symptoms and issues in the first place. Obviously, that's what we focus on throughout the podcast and all of our content. So that's the the general kind of concerns I would have with this diet, even if it is not contributing at all to cardiovascular disease risk, which we both don't think that it is so, yeah, do you have any anything you want to chime in with there?

Mike  1:28:04  
The only quick thing that I would add overall is that, and it's just kind of mirroring what you said, because that, I think that you had some great points there, that we agree on is it doesn't mean that these diets aren't effective to, you know, make changes in people, help them to lose weight, etc. It's not a statement on that. It's just like it, because there's some downsides to these. So there's pros with the diets, with the Keto, with low carb, with this type of stuff, and there's also cons. And so while the pros do have benefits in certain contexts, and you see outcomes and things like obesity, people can lose weight on them, you see outcomes and things like epilepsy, like that. The benefits of the ketones, specifically, this doesn't we're not arguing against that. It's not arguing that these things can be effective in these circumstances. The argument is in a long term outcome, if you want to optimize health, the some of the downsides of these diets make them less ideal. They make them less ideal for optimizing health. And so ideally, we want to be in a circumstance where we can oxidize carbs effectively, and we don't have we don't have to rely on a low fat a low carb diet and push fatty acid oxidation, because there are downsides to oxidizing fats in the mitochondria compared to carbs, and there are also downsides on the hormonal profile to not having adequate amounts of carbohydrates in the diet. And so it's a very these arguments are important, because people like, well, keto did this for me and and keto solved that for me. And it's like, yeah, no one's denying that you got benefits. That's great. It just there are some detriments that you should be aware of, and we can tell you how to adjust them, fix them. What are the ways to address it, so that you can still keep the benefits of your keto diet and a lot of the components from keto like, it's not like the diet itself, a lot of the components, the protein intake, the types of fat sources, the focus on nutrient density that start to look into the idea of the microbiome and things like this, we're like, Sure, those are all great tenants. Let's take those things and let's just add in a bit of carbs so that you're not running in this famine state, this stress state, and you're having this effect in the mitochondria from prioritizing fatty acids.

oxidation, etc. And so that's it. It's like, it's just a one, it's a shift over. It's like, okay, you have this therapeutic intervention for these certain contexts now. It's like, you could go about it in another way as well. And there are some downsides to that therapeutic intervention. And so it's a nuanced perspective and a nuanced shift. Not all keto and all low carb is terrible and it doesn't have any benefits, and everybody's wrong. It's like, no, there's, there's tons of studies that we can pull up, that we cite, that we talk about, that show these benefits, but it's like we need to also be aware of the detriments. Because a lot of us go into it, like you and I went into the Keto stuff and had problems. We wound up having problems like, why is this occurring? And we start to look in the research like, Oh, this is why my thyroid profile looks like this. This is why I'm having X, Y and Z issue. And then we started to troubleshoot, and a lot of that involved bringing in carbohydrate and so that that is, that's basically it. That's the general idea, not optimal for health. I think in the long term, because of some of these downsides, we can easily correct these downsides without having to reinvent the whole diet, but there is effects of these diets, as in therapeutic context, and they do indeed work in those contexts. It doesn't mean they're the only intervention that works, but they are one intervention that can indeed work,

Jay Feldman  1:31:13  
right. And as we're also saying, this doesn't mean they are the ideal intervention, and ideally we would have an intervention that actually addresses directly what those underlying causes are without the cost, right? Well, and also, while still getting to enjoy carbohydrates, which is nice, and I think most people appreciate that too. So yeah, and you mentioned epilepsy. We just, you know, semi recently did an episode talking about that. What actually is why exactly the ketogenic diets are beneficial there, and again, how we can get those same benefits without needing to shift into a ketogenic diet with those inherent negatives. As you said, we experience those ourselves. And we work with clients all the time, and have you know, clients in our programs and everything that are largely coming from this place and recovering from it. So yeah, I would, I would say that I think that's a pretty

I think that really wraps it up. I think that that's, that's a really

good way to encapsulate it and close things out, unless you have anything else to mention. I think that's, I think that's great. I think we can wrap up the episode,

perfect. In that case, Mike, can you share with the listeners where people can find you?

Mike  1:32:18  
They can find me at my website, Mike, fave.com, and also, if anybody is transitioning from low carb or moving from carnivore or keto and is struggling some of those issues, they can check out my nutrition blueprint on my website. It's a free PDF and video course that walks them through starting to set up their diet and start to bring in carbohydrates into their diet and implement them effectively, without the weight gain and without the blood sugar swings and things along these lines,

Jay Feldman  1:32:42  
awesome, awesome. All right, so if you did enjoy the episode, please leave a like or comment. If you're watching on YouTube and if you're listening elsewhere, please leave a review or five star rating. All of those things really do a lot to help support the podcast, and are very much appreciated. To check out these show notes for today's episode, where I'll link to the studies articles and anything else that we referenced, head over to Jay Feldman wellness.com/podcast

and if you're looking to optimally support your metabolism and lose weight, improve your digestion, get amazing sleep, rebalance your hormones, boost your energy and so much more without needing the low carb diet, with actually being able to include carbs and doing all that with clear action steps and strategies alongside personalized guidance from me. Then head over to Jay Feldman wellness.com/solution

where you can find all the information for the energy balance Solution Program. This program includes customized health coaching, a video library with videos on how to regulate your blood sugar, how to restore gut health, how to lose weight without destroying your metabolism, as well as how to boost your metabolism, how to get amazing restorative sleep, how to rebalance your hormones, and tons more. It also includes resources like a sample meal plan and supplement guide, as well as a private community so head over to Jay Feldman wellness.com/solution,

to check out all the details. And with that, I'll see you in the next episode. You.