0:00 Intro

0:55 Low Carb vs. Bioenergetic View of Cholesterol

7:42 Peter Attia on Nutrition vs. Pharmacology to Lower Lipids

10:47 Example Lipid Panel Transformation w/ Diet Alone

23:01 Lab Values Mike Likes to See w/ Clients

27:31 Ken Berry on Carbs Increasing Triglycerides

33:49 Timeline For Temporary Rise in Triglycerides After Adding in Carbs

36:14 Example Lipid Panel Transformation #2

44:06 Thoughts on Exercise

48:48 How to Track Your Progress

51:36 Dr. Lustig on Sugar Raising Small Dense LDL

57:53 Metabolic Function Central to Cholesterol Paradox

1:01:41 Lean Mass Hyper Responder

1:08:42 Mike’s Thoughts on Red Yeast Rice

Ethan Wright

Welcome to the Mike Fave Podcast I’m your host Ethan Wright joined by Mike safe. On this podcast. Mike and I help you make sense of the online health chaos while answering your individual health questions along the way. So if you have any health trends, topics, or questions you’d like to see us cover, please leave them in the comments below and we’d be happy to get them answered on future episodes.

Ethan Wright

In today’s episode, we are going to dive into cholesterol and cardiovascular disease by discussing First Doctor Peter Atlas controversial take on cholesterol and lipid lowering strategies. Second Doctor Ken Barry’s take on carbohydrates raising triglyceride levels. And last but not least, the infamous Doctor Lustig telling us how sugar causes cardiovascular disease. Then from there, if we have time, we’re going to get into rapid fire questions from my clients and private revive community about cholesterol and cardiovascular disease.

Ethan Wright

So before we jump in mic, let’s provide some context based on what you and I are experiencing with the clients.

Mike Fave

Yeah. So I think the overarching journey that I tend to see, and I think you’re when you’re talking to people on discovery calls, what you’re hearing for people specifically around cardiovascular disease and cholesterol is it’s like relatively uniformly amongst people. So we’re seeing a very similar journey amongst all these people. The first thing is now people will come in at different points, but in general it tends to start with you.

Mike Fave

You go to your doctor, you get a checkup. Cholesterol levels are high. Your doctor says, hey, I need you. I need you to go on a stallion. I want you to go on a statin. And so then some people will be like, yeah, okay, I’ll go on this side and they go on a side. Maybe they get side effects, maybe they don’t.

Mike Fave

If they do, maybe they want to change. If they don’t, then they continue or they go and do a little research. They type in YouTube and then usually they’ll find like the, the, the alternative health for the low carb, the keto, the carnivore, these different years paleo. And what they’ll see in these figures is that they see that cholesterol doesn’t cause heart disease.

Mike Fave

You don’t have to necessarily worry about cholesterol. You have to worry about insulin resistance. That’s the real problem. And so then the solution in those fears is this low carb diet, right. You don’t have any carbohydrates and it’s like a funnel. So you start with, you know, lower your carbohydrates, lower your sugar, and then all of a sudden, like a couple months later, now you’re a full blown carnivore.

Mike Fave

I think both you and I had this experience.

Ethan Wright

Yeah, definitely. And I know just in talking with people. Yeah. It is. It’s all or nothing. The doctor wants me to take a statin in the low carb guy saying, don’t even worry about my LDL cholesterol. So it’s a confusing, perspective. It’s a confusing problem that people, I think are trying to tackle. And then, yeah, I think bioenergetics tries to bring some sense to why both camps are saying these things.

Ethan Wright

So maybe you can talk a little bit about like how that problem, that paradox is essentially solved there. That’s going to be the goal, at least on the on the podcast where people.

Mike Fave

I think it gets even more confusing the like before you even get to apologetics. And apologetics is just like by the time people make it to the there at the end of the funnel with bioenergetics, they’re like, I don’t even know anymore. So this I think there’s a step between bioenergetics and the ketone stuff. And that’s when you start to see, you know, people like Doctor Peter Dia, who was a low carb advocate who was doing low carb and keto and stuff like this at one point in fasting.

Mike Fave

And now he’s like, become like a pretty strong, lipid hypothesis advocate where he’s basically saying, like, the major way to adjust the lipid panel and, is to use pharmacologic agents. So other things like statins, Pcsk9 inhibitors is that MI, etc.. And the goal is like for after therapy with these pharmaceuticals to bring your lipid values down.

Mike Fave

And so we’re seeing him talk about that. And it’s kind of weird because he was in the low carb sphere. Like he like he came out of the low carb sphere. But he’s like low carb lipid hypothesis proponent I think that like then it’s like so well, where we yeah. Yeah. With all these different elements. And then you get to the bioenergetics and bioenergetics talks about how metabolism is the central problem, which is, you know, I agree with that perspective.

Mike Fave

And then you actually want to be able to oxidize carbohydrate instead of just, you know, limiting carbohydrate and then just only oxidizing fat. And then if you ever add carbs on board, like, God forbid, the goal is that you actually are able to use the carbohydrate now. But then I think people jump into the sphere, and this is what people are saying is like they jump in there, gain weight, maybe lipids aren’t as good, maybe insulin values or blood glucose isn’t as good.

Mike Fave

It got worse. Stuff like this and like, well, now I don’t even know where I want to be because they’re like, I don’t want to go back to keto. I don’t want to go back to carnivore paleo, this type of stuff. But I also know I can’t stay where I’m at with the bioenergetics stuff and the theory this is what you tell me all the time is like, people are like, well, the theory makes so much sense, but I don’t know how to implement it.

Ethan Wright

I mean, that’s why if you’re in bioenergetics and you listen to all the podcasts and you were low carb beforehand and you start adding in carbs because people on the podcast are saying, oh, you improve your thyroid health and you’re going to lower your cholesterol values. And then you do that and you get your labs drawn again and your cholesterol levels are higher and maybe your triglycerides are higher.

Ethan Wright

Now, that person’s really in the spin cycle. So I think the goal is to bring clarity and try to walk the person through. I’m curious to get your thoughts on the steps that you take with those clients, and like how you get them to do achieve, like the improvements in the lipid panel and metabolic dysfunction.

Mike Fave

I mean, that’s what we’re going to cover today. We’re going to use some interesting clips from like the different speakers to talk about this. But I think ultimately there’s not really a paradox. I think there’s a there’s an ounce of truth in each perspective, even within the lipid hypothesis perspective in terms of cholesterol being involved in cardiovascular disease and then metabolic function being a core like the major driver of cardiovascular disease.

Mike Fave

And then on top of that, like people not who have metabolic dysfunction, having a more difficult time with carbohydrates, I think I also see that. So I think the the all health sphere has, percentage of truth in it. What Doctor Peter Tila is saying to some extent has a percentage of truth in it. And then also there’s a lot there’s a percentage of truth inside the bioenergetics sphere.

Mike Fave

I think in the health sphere, the low carb carnivore, paleo, this type, these spheres. I think the fundamental understanding of insulin resistance and what’s going on with mitochondrial function and oxidization of different fuel sources and stress hormones, I think there’s like a lack of understanding there. I think with Doctor Peter Tas lipid hypothesis, perspective, I think it’s very reductionistic and it tends to heavily focus on LDL as the major factor that we’re looking at.

Mike Fave

And or it will be more specifically instead of and and like maybe not getting to like what are the all of the other components that could be involved with these issues. And then like pharmacologic management being a major treatment and a no bioenergetics for I think part of the problem is the sphere is like, you know, res work is pretty detailed.

Mike Fave

It’s pretty research heavy. And so it’s not really extremely user friendly for a lot of people to read. So I think a lot of people are relying on interpretations of res work instead of directly reading res work. And also res work changed over time. And then the implementation around the bioenergetics stuff is also kind of like all over the map.

Mike Fave

So like people get there and they like get a sense of like, okay, like there’s something here. The theories, the perspectives, they make sense. But then when it comes to implementation, so like it’s flat, like I’m feeling better but I’m gaining weight and I’m not happy about that. And metabolic function is not ideal though. So you can rectify all of these components and hammer out the paradoxes.

Mike Fave

And that’s that’s what our goal is here to do. That is what I want to talk about specifically today, because I think it’ll bring a lot of clarity for people so that they know what to do, which is up to a large extent with diet and lifestyle, and also understand why they’re doing those things.

Ethan Wright

Yeah, why some of the things they may have experienced through the different dietary journey have happened. And that’s going to be important to acknowledge as you come out of that in into like this new perspective. Yeah. With that said, should we jump into the first clip?

Mike Fave

Yeah. Let’s jump in.

Ethan Wright

Nutrition first is pharmacology as a way to lower limits.

Youtube Clip

I believe that using nutrition to solve the lipid problem is not a good solution. I think. Use nutrition to solve the nutrition problem. Use nutrition to address energy balance, protein needs, anabolic structure, energy, all of these other things and let your lipids fall where they may because this is one of the few areas in medicine where we have amazing pharmacologic tools.

Mike Fave

I’m curious, Ethan.

Ethan Wright

And I’m a little I mean, I’m a little confused with the let’s use nutrition to solve the nutrition problem. I’m not exactly sure what he means by that.

Mike Fave

When we’re looking at lipids. Right. Fundamentally, what are what are we talking about? We’re talking about cholesterol and triglycerides. Right? Those are the major components that we’re looking at. And it’s all surrounded by what’s going on with your diet. So to then say like let your like do your diet stuff. Don’t and like let things fall where they may fall.

Mike Fave

Then what we’re going to do is like, we’re just going to strongarm this with drugs because we have really good drugs when the fundamental component that is adjusting what’s going on with distribution of your fuel sources is the fuel coming in, like your diet. It’s just a weird perspective to me. I just it just I, I don’t really disagree with this at all.

Mike Fave

I think that the one of the major drivers that we can look at for shifting a little panel and I have an example here, is going to be diet hands down, are the genetic disorders and diseases that shift things because this specific enzyme doesn’t work. Yes of course. But for the vast majority of people, I think the fundamental problem is lifestyle, diet, metabolic function related.

Mike Fave

And those are the ways that you’re going to fix it, not just like, let me just take all these drugs now, maybe the drugs can help. In the meantime, depending on how it’s working, what its mechanism is, etc.. But I think, like fundamentally the ultimate root cause or root, your barring genetic issues is going to be diet hands down.

Ethan Wright

Right. And like you’re saying, you’ve had a lot of clients who had maybe high cholesterol or high triglycerides and then modify their diet and seen improvement, right?

Mike Fave

Yeah. Significant improvement. So now we can we’ll show an example.

Ethan Wright

Yeah. I mean, I think it would be good to show an example, but that is the first line of defense essentially like or the first plan of attack. Right. Would be to modify the diet. Yeah.

Mike Fave

Stage one like every person that we’re working with, you’re doing a discovery called you. You’re collecting the information where they are with their health. What do they have going on after that? Like I’m looking at lab work, I’m looking at their diet. I’m looking at their supplementation. I’m looking at their movement. I’m looking at the report that you wrote, and then we’re putting everything together.

Mike Fave

We’re hopping on a call. We’re saying, this is the plan. This is the things that we’re going to do to fix these specific problems. You have going on. And the first thing is almost always diet. Now, some people need like at the hundred and 80 degree turn around and some people need like a 10% change to what they’re doing.

Mike Fave

But it’s like step one is always diet.

Ethan Wright

I think it would be good to look at the lipid panel and then maybe talk about the interventions that like were made. Or maybe you can explain like what are the first things that you’re looking at. Is it the carbohydrate total intake. Like the macronutrient ratios to adjust the cholesterol or what are the modifications to the diet?

Mike Fave

Let’s pull up the lipid panel. And then just to answer the second portion of your question, even before you jump in, because I think it’ll be relevant. What gets changed depends on that person’s context. If the person is has metabolic dysfunction versus their hypothyroid versus their keto carnivore, lean mass hyper responder versus they have, you know, like a genetic situation going on.

Mike Fave

All of those things will shift what the recommendation is because you’re like, you have a different cause. So you’re trying to figure out what is the underlying adjustment that needs to be made based on an individual’s context, instead of saying like, yeah, like everybody just needs to go to our carnivore. Like can sound best strategy. It’s like, where are you at?

Mike Fave

What do you have going on? Like with all the information that we can have that you have available, can we sleuth out and figure out what’s going on? And then that’s where the adjustment. So well look at this. This is one case study of a very specific example. So this one is going to be I think pretty shocking for a lot of people.

Mike Fave

This is one of my clients. I have an APB here. The APB at this point in time was 240. Milligrams per deciliter. Now ideally less than 80. So this is three times the target that we would that I would typically shoot for. Apob is essentially the protein that the lipids cholesterol, the fats are encased in. Because basically the fats since they are fats don’t transport and water very well and our blood stream is water based.

Mike Fave

So in order to move these fats around the body, we needed to have some transport mechanism that allowed them to mix. So you have these little particles, these little packages. Apob is the protein that makes is the one of the major proteins that makes these packages. And basically what it does is it it allows you to shift around the LDL, IDL, LDL.

Mike Fave

And so you have one apob particle per like every package of your for the cholesterol. So if you when you’re looking at table B, you’re seeing how many particles, your liver is putting out, how many lipoproteins your liver’s putting out because there’s one table B for every lipoprotein that the liver is putting out. And so it’s telling you how much, efflux, how much output, how many Amazon trucks are leaving your liver at any point in time.

Mike Fave

And so in this case for this individual, the B level here is super high. Like a lot of fat export from the liver, a lot of lipoprotein export from the liver such that it’s three times the target that I’m typically I’m typically setting up for it. Now the next thing I will see is with that the total cholesterol value is 796mg per deciliter.

Mike Fave

Most people, the doctor want you less than 200. This individual is 796. Pretty crazy lipid values on top of that LDL cholesterol by itself. So not even total is 695. So it’s almost 700 for the LDL. And now we’re looking at HDL, HDL 65. So relatively speaking the HDL value in ratio to the health to the total cholesterol onto the LDL is quite low.

Mike Fave

And an even worse than that is triglycerides are also high. So ideally you want to see triglycerides at the minimum less than 150 but ideally less than 100. So or even over the minimum target for triglycerides. This this isn’t technically a lean mass hyper responder profile because of how high the triglycerides are.

Ethan Wright

And for those listening, it’s 189, right? Yeah.

Mike Fave

One 89mg deciliter on the triglycerides, total cholesterol, seven 96mg per deciliter. And then the LDL cholesterol 695mg. That’s it’s almost 700mg per deciliter, just LDL and an HDL 65mg per deciliter. These are things that I look at that can be extremely important when looking at if you just get a standard lipid profile, if you don’t get a job, your doctor doesn’t want to do apob or look at any of this type of software, it’s expensive.

Mike Fave

Whatever the deal is, you can take a standard lipid profile and look at your cholesterol to HDL ratio, your triglyceride to HDL ratio, and then your LDL to HDL ratio. These values are not ideal. So I’m actually going to make a separate video going through the specific values that I look at. So stay tuned for that. Like with all the labs to assess this type of stuff.

Mike Fave

But this is a key example of a starting place. When I first started to work with this individual, this is the lipid panel that we first had to look at. This individual was on a low carb, high fat diet. And there is a potential that this individual had, familial hypercholesterolemia. On top of being on this low carb, high fat diet and the fat sources in the diet here were mostly dairy fats.

Mike Fave

This individual also was not necessarily an older person. This person was somewhere around their 30s, in their early 30s. I don’t want to give out too much personal information about this. This is one of my clients. But in general, this is probably the highest lipid panel that I that I’ve seen. And with the clients that I work with, that people 400, 500, and 600, but this one at 800 was like was like pretty high.

Mike Fave

And the drop that we got was pretty precipitous with just diet. So I want to show that next. But I’m curious, do you have any questions about these lipid values.

Ethan Wright

That’s pretty high. I was curious what kind of dietary set up there on there. But if it’s yeah, low fat I mean no high fat low carb makes sense. You say the first step, right is to figure out like what exactly is is going on. Like what’s the cause? So obviously the low carb diet. But then are you looking at other lab values as well?

Mike Fave

When I first work with somebody, I get the I’ll get like a full health history and I’ll, I’ll look at the diet, I’ll look at their chronometer if they have CGM data. I’m looking at CGM data, what drugs they’re on, what supplements are on, what’s their activity level, what’s their stress level, sleep status, all this type of stuff.

Mike Fave

Age, everything. Family history. Like I’m really trying to look at everything so I can see where are the problems or where are the potential problems. I don’t try to get people to spend like $5,000 of lab testing up front, because that when I happened to me, when I was sick, that like, blew out all my savings, I really just is that so?

Mike Fave

What I usually tell people upfront is like, what lab testing you have? I’ll take a look at that. I’ll see what’s going on. We’ll see what’s going on with lifestyle, diet, things like this. And then we’ll see what further lab testing we need to do based on the information that we’re giving, we’re given. And then we run from there.

Mike Fave

And it also depends on like how much money the person has for the testing, because a lot of stuff’s not covered by insurance. If you’re looking at really in-depth markers. So I’m not really trying to, you know, have somebody break the bank. I’m trying to work with what what they can give me and try to get the outcomes.

Mike Fave

Because just doing the diet and getting micronutrients under control, adjusting lifestyle movement like these things by themselves make a huge shift. And that’s what I did for this individual. This individual did have metabolic dysfunction like outside of the lipid panel. We’re not talking about somebody who’s like a normal healthy metabolism. There are things that were going on there as well.

Mike Fave

And then we still saw the shift even by adding carbs to the diet. So this was the follow up lipid panel. It was about a couple months later. They didn’t get an APB. But what you’re seeing is the previous LDL was 695. Right now it’s 158. So that’s like one quarter of the LDL. There was no drugs used to lower this.

Mike Fave

We just shifted the diet, shifted the fat sources around, brought carbohydrates on board the triglycerides, as an example, dropped from 189 to 74. And then HDL values actually picked up from the the 65 to 122 122. On the higher side, I like to see HDL, at least over 60. But this is like a pretty significant shift, because all those ratios that I talked about drastically shifted this total cholesterol values.

Mike Fave

Now, 291 from the 796. So that’s a huge, huge shift downward from where the previous values were.

Ethan Wright

Well, how long was like did that take to get the reduction.

Mike Fave

This was on the order of months and months.

Ethan Wright

Oh wow. Okay.

Mike Fave

It was literally within a couple months of bringing carbs on board, shifting the diet around. And the thing is, it could have happened sooner. But this was the that was the pre test. And then this is the post test. So this is what like this was the next test that we had. So I don’t know when exactly it shifted.

Mike Fave

That’s just when we were able to get the next lab draw with the doctor. So the person could get it covered by insurance.

Ethan Wright

Using just diet.

Mike Fave

Using diet and then like basic supplementation, like if you’re vitamin D deficiency or if you’re folate or B12 is low, or if you need to bump your zinc up, or if your iron overloaded, like I’m looking at stuff like this, if you’re, you know, seeing what types of fat you’re using the diet saturated versus monounsaturated, how much carbs you’re having, is there issues going on with the liver?

Mike Fave

Is there issues going on with thyroid function? So I’m looking at all is there stress movement activity levels. So I’m looking at all this stuff and I’m just making adjustments to those areas. And a lot of times it’s diet and lifestyle modification. And then targeted supplementation. And I mean I don’t prescribe array drugs. So none of this is drugs.

Mike Fave

All lifestyle diet modification and supplements.

Ethan Wright

In the order. The first two things are adding carbs back in from the low carb diet, and then adjusting the composition of the fatty acids in the diet. Would you say that that’s like the top two things to maybe look at?

Mike Fave

Again, it’s like person contact dependent. And this individual, they were running a lower low carb, high fat diet to just to like minimize how much insulin they had to use. And then it was really driving their lipids up. It was so high. I think it was in the background of like either a heterozygous or homozygous familial hypercholesterolemia. It’s like a genetic predisposition towards high cholesterol.

Mike Fave

And then on top of that, we were trying to troubleshoot a lipid panel because obviously wasn’t great. And the person was concerned, their doctor was concerned. And then we’re also trying to adjust and manage the diabetes simultaneously, because the one of the major strategy we did to bring this down was bring carbohydrate on board. It was like a tight rope to get that under control.

Mike Fave

And then once we got it, it was fine and all this stuff started to really get on it. But this was like this person’s situation was specific. We’d look at the next one, we’ll see that their dynamic is different. And so the strategies were different. That’s why we’re looking at trying to get this full picture to see, like where do we need to make the adjustments?

Mike Fave

Like what are the specific areas that need to be changed for the person. And then and then systematically work through it. So yes, it was diet and then there was some, you know, nutrients, micronutrient status. Is there stuff going on in the gut, what’s going on with hormones, lifestyle components and like try to systematically go about step by step, adjusting those and to make sure the person can do it over the long term, right.

Mike Fave

So they can implement it. They have to maintain it going forward.

Ethan Wright

And to kind of bring it back to that clip. A feeder to what I’m hearing is just there’s so many levers to pull within the diet before you jump to the pharmacological route. Right? So it’s not like, oh, I just I tried low carb and this is the case. This is like where my lipids, you know, fell where they fell.

Ethan Wright

And and I need to go pharmacology. But there’s like an order of things to, to look at. And like you’re saying getting to the cause is, is going to be like the most important thing. And how you go about modifying the diet in that direction. Right.

Mike Fave

Exactly. And it’s it it will be person specific, like so it’s like also ranking and in order of priority on what you’re going to address with, with somebody like where are the biggest areas to get under control is like because it’s not always so straightforward. Like, yeah, I just add carbs in board and it solves all the problems.

Mike Fave

So that’s why when I hear a clip like, like what Peter was saying, where he’s like, oh yeah, like, you know, just do what you’re going to do with the diet. And then we’ll just lower your lipids with drugs. It’s very like, it’s like, that’s very weird to me. It’s a very weird perspective because it’s like you’re talking about a system that’s can that is dependent upon what you’re eating on a regular basis, barring very specific genetic disorders.

Mike Fave

And even then, what you’re doing with your diet is going to have an effect, even in those genetic disorders, on what’s going on with these profiles. First, try adjust what’s going on with your diet. If you have adjusted things with your diet, you looked at all these other metrics and then you get to a point where it’s like you’re how you have an obvious issue and these other strategies haven’t worked.

Mike Fave

Then you go to level ten and then you start talking about medications and components. Obviously, if your doctor prescribes something, please by all means not medical advice, please speak and work with your doctor. But in general, like I’m thinking about things in the tier and I work with the doctors all the time, and I’m working with a person and a doctor, and I like write out the strategies that I’m looking to use with the dietary adjustments and the supplementation.

Mike Fave

And it’s like, look, okay, you know, it’s not coming down. Okay. What is our next step? What is the next option or here to be ruled out? This, this, this this and this. Have you.

Ethan Wright

Ever gotten to the point with a client where you’ve gone through everything and the lipids like still aren’t coming down and then you’re sitting like, oh, maybe there’s a formal pharmacological intervention that’s necessary or do you usually solve things prior to ever getting.

Mike Fave

There? When I’m looking at a lipid panel in general and say, I don’t have ABC, I just have a basic lipid panel, that’s what most people have. I’m looking at what your total cholesterol. Sure. Then I’m looking at what is your LDL cholesterol. Sure. But then the major markers that I’m really interested in. What are your triglycerides. Are they less than 100.

Mike Fave

What is your HDL cholesterol value. Is it greater than 60. What is your ratio of total cholesterol to HDL. Is that less than three. And then I’m saying what is your ratio of LDL to HDL. Is that less than 2.3. And then what is your ratio of triglycerides to HDL. Is that less than 1.9. And then on top of that then I’m saying where’s your fasting insulin value.

Mike Fave

Is that around five. Where’s your blood glucose value. Your fasting blood glucose value is at less than 90. Where is your uric acid value is at less than six. Where your Alt in your AST values are those less than 26. So I’m looking at multiple factors and I’m trying to gauge based on those overarching factors. So if somebody’s like yeah, my LDL is is 220, or not my although my total cholesterol is 220, my LDL is like a hundred and I don’t know, 120 or my HDL is 90 something.

Mike Fave

And then my, my, or another one, another poor markers VLDL, my VLDL is less than 24 and my insulin is five. And my ratio for total cholesterol to HDL is less than three. And my ratio for LDL to HDL is two. And then my ratio for triglycerides to HDL is 1.6. And I’m seeing stuff like this. And the other values are looking good.

Mike Fave

But LDL and HDL are a little bit high. I’m like, yeah, it’s like I’m not as concerned about that value at that point, because all of these other metrics that we have look pretty good overall. And even then, most times I’m able to get people to hit those targets and I’m able to the the one thing that I haven’t always been able to do is get total cholesterol values less than 200, and total LDL values less than 100.

Mike Fave

I be able to skew, shift all the ratios, get the insulin values down, fasting blood goes, but sometimes the cholesterol will hover to 10 to 20, and an LDL be bumped up over 100. And then. But then even then I’ve seen Apple values come down, even though the LDL is bumped up a little bit and stuff like this.

Mike Fave

So there has been times where that hasn’t happened, and it’s up to the person’s like, well, we have all these risk factors. And then you present the report, it’s like, you know, here’s a report like see what your doctor wants to do. Does your doctor want to go with pharmacologic management given these values. Do you want to go with pharmacologic management.

Mike Fave

Given these values and these risk factors like where these components are. And then the you know, then it’s the person’s risk like personal decision on whether they want to move in that direction from that point. And it’s like, well, based on these values, based on where all these things are, okay, these things look good, these are the problematic areas.

Mike Fave

And then also it’s like, can we make further adjustments? Like a lot of times you can make further adjustments with dietary components and supplements and stuff like this. But you don’t always like people like yeah. Like I’m happy. I’m like, I was at 800 and now I’m at like 200 and, you know, 290. And my trend is still coming down on my values.

Mike Fave

So I’m really happy with that. And I, I don’t know if I want, I don’t really want to be on the stat and I understand the risk. And so then that’s a personal decision because ultimately the person’s personal decision between them, they have to make it. They talk to their doctor and then, just all share research studies and papers and go and like, give the analysis on these different data points, say, like, here’s what I think overall.

Mike Fave

And then you got it, you know, presented to your doc. You guys come to a decision on what exactly you want to do.

Ethan Wright

And I think most of the people that we talk to on a consistent basis are less so interested in understanding. And they’re more interested, at least off the bat, right. And more so interested in seeing what they can accomplish using some of the dietary strategies that you’re talking about and positioning it as like, you know, you just do your diet and let everything kind of fall where it falls because you have these awesome pharmacological things that you could implement if things don’t work out, is like kind of taking the ball, like out of their court a little bit, you know, it’s like, no, there’s a lot to try here.

Ethan Wright

Like, let’s run through some of these options, see how you feel, look at these other markers that you’re mentioning before and then get a total assessment of like what’s going on, big picture. And then yeah, I mean, I guess the discussion with you to figure out, like where to where to go from there, but yeah, that all makes sense.

Ethan Wright

So the next clip that we have here is of Ken Berry talking about how carbohydrate raise triglycerides. And I know based on some of the people that I talk to on the calls, they will say that they came into bioenergetics hoping to improve some of the lipid panels and in triglycerides. And then they add carbohydrates in and they see a bump in triglycerides or maybe sometimes even a bump in cholesterol.

Ethan Wright

So let’s get Ken Barry’s opinion and then Mike will get your response on why someone could be experiencing that after adding in carbohydrates and go from there.

Youtube Clip

That’s that’s important because having elevated triglycerides hypertriglyceridemia can increase your risk of heart attack, heart disease, and stroke. If your triglycerides are high enough, they can actually increase your risk of a life threatening condition called pancreatitis. Most important concept that I want you to take away from this video is that eating fat does not raise your triglycerides in specific kinds of carbohydrates.

Youtube Clip

That’s what leads to hypertriglyceridemia. So, tip number one is to decrease your total carbohydrate intake for other people. It’s probably people who have that genetic previous position I talked about earlier. They have to cut the carbohydrates even more.

Ethan Wright

He you. So maybe to start with like why. Well, first of all is fat, like, not going to raise your triglycerides or like, what is the relationship between fat intake and triglycerides?

Mike Fave

Typically when somebody goes on a high fat, low carb diet, triglycerides drop and an LDL and HDL will increase. Again, what’s happening is the body. So triglycerides are fats or fats floating around in the bloodstream. The when you don’t have the carbs coming in, the body starts to use those fats. And then also the body starts to raise the HDL.

Mike Fave

LDL values because it’s starting to transport fats to the tissue from the liver. So yes, triglycerides tend to drop when you go low carb. Now, if you have metabolic dysfunction, even if you go low carb, like say, and you’d say you’re not losing weight with it and whatever. Like you can still see triglycerides high. And I have an example here of a client who was low carb, type two diabetic with high triglyceride values in a, not so great lipid profile.

Mike Fave

So we’ll talk about that now when you switch from a low carb diet to a higher carb diet, you can see a bump in triglycerides, at least initially. And the reason why is because your body starts to use the carbohydrate, which leads to more triglycerides being pushed in the bloodstream. And also the triglycerides can move to the liver, be packaged in VLDL, or the fats that aren’t being used can be removed, deliver packages for LDL, amp up the LDL, at least initially.

Mike Fave

Now, if that’s a when you first switch from low carb to higher carb, you can see that LDL and HDL drop. Maybe the LDL can bump a little bit in triglycerides can bump a little bit. But as things improve, metabolic function improves, those things should continue to come down. So even as an example for myself, my triglycerides are less than 100.

Mike Fave

I think they are less than 70 or 80 on my last blood test, but I’m having 450g of sugar per day, so the idea that get the general idea like, oh, you eat carbs, the carbs are going to create fat production at the liver and in the fat production at the liver is going to the noble label is going to lead to this bump in triglycerides.

Mike Fave

But whether they’re not actually clear on that’s the mechanism, because when they look at the metabolic, the isotopic tracer studies, or they’re looking at when they see people a bunch of carbs, or they’re looking at the panels are not sure, is it because the body starts to oxidize the carbohydrate, and then you get an increase of triglycerides in fats in the bloodstream and LDL.

Mike Fave

HDL do drop when you add in carbs. It’s another thing. Or LDL tends to drop when you add in carbs. HDL may drop depending on the person a little bit when you add in carbs, because now you’re using that carbohydrate instead of this fat, you’re switching your fuel. And then the triglycerides get left in the bloodstream. And then also, you know, they can go to the liver.

Mike Fave

And then the increase in overlap with Genesis, which they don’t see directly from the carbohydrate, could be from the fatty acids going to the liver in the liver packaging up and exporting them back out. So it’s not necessarily that you are that you are seeing, the carbs being converted directly to the fat and then bubbling up triglycerides.

Mike Fave

There could be other explanations for why that’s occurring. When you’re first low carb and you go into higher carb, you can see initial bump. And then as you come back down, as your body’s transitioned into using those carbohydrates. Now, another thing that’s really important to understand here. If you have metabolic dysfunction, right, say you’re type two diabetic, say you’re insulin resistant, pre-diabetic, fatty liver, whatever the deal is you can you will get bump triglycerides, bumped LDL cholesterol bumps, total cholesterol and low HDL cholesterol.

Mike Fave

That is a different profile than the high LDL, high HDL, low triglycerides of a lean mass hyper responder, or even the normal lipid profile. Somebody who’s just generally healthy, not doing low carb or anything like this where you see a normal cholesterol, normal HDL, triglyceride, like everything looks normal across the board. The goal state, from my perspective, is to be able to have a normal cholesterol value, normal HDL, normal LDL, and then also be able to tolerate carbohydrate.

Mike Fave

So you don’t need you want to be in a state where you can’t tolerate carbs and bumping them up. That’s usually indicative of metabolic dysfunction in general. So you see people who are even when they’re like in a low carb diet, they’re still driving, they still have metabolic dysfunction. You can still see, triglycerides bump up. And I seen that quite a few times.

Mike Fave

Now, when you go keto carnivore, whenever you start losing weight because you’re in a caloric devastate because your appetite is knocked out, you’re eating one meal a day, you’re fasting, whatever else. You see improvements in metabolic function. But if you’re on a high carb diet and you also lost weight, you would still see improvements in your your lipid panel, your triglycerides and everything as well.

Mike Fave

So general weight loss and improving metabolic function will fix the lipid panel as well. And then whether you’re high carb or if you’re higher carb, it’ll bring down HDL and LDL. If you’re lower carb, it’ll bring down triglycerides. But there will be a shift because what you’re seeing is a shift in fuel utilization in the body. Because again, blood glucose what that and the arteries and veins, they are basically pipelines to the tissues from the liver.

Mike Fave

And you’re seeing changes in which fuel source is being used peripherally and which fuel source is being distributed based on what fuel source you’re bringing in.

Ethan Wright

And then when you are saying that the triglycerides initially go up after someone adds in carbohydrates, what is the typical timeframe there? Like how long would be considered like a normal response versus, oh, we have a problem.

Mike Fave

Generally, what will happen if you set up the diet appropriately? Not the I’m going to come in to bioenergetics and eat unlimited ice cream and unlimited sugar in the milk. And just like drink orange juice all day long, like every hour, just another glass. Another glass, like stuff like this. And tons and tons of dairy. If you set up the diet appropriately, which why you on the website, there’s a nutrition blueprint.

Mike Fave

This is what we’re doing in the course. All this stuff like very specific in granular detail. What what I do with it, you will see within like you should see maybe an initial bump and then it comes back down. So maybe after a month or so or two months, especially if things are set up well, it’ll come back down.

Mike Fave

Your lipid panel should ultimately drastically improve. And I’m going to show an example here in just a second. But it should it should change very quickly. Especially say you are overweight. You tired your diabetic fatty liver. Whatever the deal is, you start to drop that weight and you start your diet is that I’ll probably have enough protein. You have enough carbs, enough fat.

Mike Fave

It’s not that you have to be low fat. You just have to have enough of each of those things to talk about the targets and the blueprint and whatnot. When that and then say you’re losing weight and metabolic function is starting to improve, you’ll still see triglycerides come down on a high carb diet. And I have example this year.

Mike Fave

And the last one is well the triglycerides were 189 if we look here. So the first triglycerides for this person was 189mg per deciliter. Right. That was on a high fat very low carb ketogenic diet. Right. So still has high triglycerides. Why? Because there is metabolic dysfunction. It’s not because of the fats or whatever else is because of the metabolic dysfunction in and of itself.

Mike Fave

And then when you come back over here and we look at the follow up panel, triglycerides are 74. So they’re less than 100 is ideal. Adding in carbs and things like 200 or 250g of carbs a day in a diabetic. So we’re seeing that improve. So it’s not just that carbs drive high triglycerides, metabolic dysfunction drives high triglycerides, and you can have transient bumps and changes with triglyceride values when you as you change your context.

Mike Fave

And it also even post-meal, you’ll bump triglycerides and stuff like this for your fasting triglycerides. If everything is going well, metabolically will be low. So the fundamental goal is get to a good metabolic state.

Ethan Wright

Okay, so what about for someone who adds in the carbohydrates and maybe their metabolic state isn’t great. So they get the longer term elevation of triglycerides like more than the month, and then maybe even a bump up in LDL. I know it’s probably contextual and how you start to attack that, but what are the things that you would start to look at?

Ethan Wright

You know, given that circumstance.

Mike Fave

This person is a type two diabetic on insulin and hypothyroid and hypo gonadal. Right. So it’s like, oh, you can’t have parts if you have metabolic dysfunctions. Like there’s three types of metabolic dysfunction going on here like C and fatty liver. And so we have diet we know there’s fatty liver right. So this is the initial panel. This was in November of 2023.

Mike Fave

Right. And we see these values are because of what’s going on at the liver. These are liver values. You have alt AST. These are the alt specifics of liver. This person is not exercising. So you’re not seeing this because of exercise. Alpha specific delivers the the albumin globulin ratio. Bilirubin values are at the top end of the range.

Mike Fave

So we’re seeing okay the liver is not super happy here. And we know there’s fatty liver in this context. Then the lipid panel we’re not seeing 900 on the cholesterol but total cholesterol is high. But the big deal here is that the triglycerides are high. The HDL is quite low. And then the LDL is high. So the ratio is pretty bad right.

Mike Fave

The LDL the HDL ratio here is 4.1. We’re look we want that less than 2.3. That is the ideal target. When we’re looking at total cholesterol you have 237 divided by 39. You have a 6 to 1 ratio of total cholesterol to LDL cholesterol. We want it less than three. So even though the total value is not really that bad, it’s all over the target.

Mike Fave

You want to let’s do 100. The ratios and breakdown of this. This is metabolic dysfunction. This is in air quotes. Author. Hygienic dyslipidemia on top of fatty liver. On top of diagnosed insulin dependent type two diabetes on top of diagnosed hypothyroidism. I’m not showing all the values on top of low testosterone or borderline hypogonadism. So we’re seeing all of this and it’s and the this person they were on a, low carb diet, a keto diet for a while.

Mike Fave

And you know, this their you know, their insulin usage, their metabolic function are great. They’re trying to figure out how to add in carbs. So this was like mid range. They were had this profile already. And then the adding in carbs wasn’t going super well with what they were doing. And so then that’s when they reached out to me like Mike, like, what do I do?

Mike Fave

How do I adjust this diet? How I bring the carbs on board, you know, my, my, my insulin usage is not great. My weight is not great. So let’s see the follow up panel. So the follow up panel, we can see this was in May 2024. So you have to set. So we started working together basically in in November December.

Mike Fave

So December January February March April. So five months total cholesterol down to 141 from 237. HDL stayed around the same. We weren’t able to fully bump it up the LDL value down to 81. So the previous LDL value that we had was 100 and 161. And now the current LDL value that we were able to get it down to was 81.

Mike Fave

Triglycerides went to 143, and the triglycerides here were 198. So 50 point drop in Tregs. And then the LDL here was 28. And then here the VLDL, which was 37. So about a nine point drop in VLDL, about, almost 100 point drop in total cholesterol, a significant, 80 point drop in LDL cholesterol, HDL cholesterol dropped by eight points.

Mike Fave

But it’s so basically in ratio, not really that bad overall. And then the the ratios improve. So our previous total cholesterol to HDL ratio I think was 234 divided by 39. So a six this current one is 4.5. So we improved the ratio by 1.5. So we still we still had a ways to go at this point. But everything significantly improved.

Mike Fave

And I want to show here when we’re looking at these values alt ast now and range. So the liver cleared out. We were working on clearing out the fat and the liver. And we’re seeing that alt here is 91 AST here is 42 at the start. And then when we finished Alt or we didn’t finish. But what. And look at this this this halfway point or this three quarters of the way point alt went down to 16 AST went down to 19 alkaline phosphatase.

Mike Fave

Is that 93 here. And the previous alkaline phosphatase is 143. And we’re seeing bilirubin was at 1.12 for total bilirubin. And now the current total bilirubin is 8.5. So the liver function improved. The lipid profile looks significantly better. The changes that we made to their diet here was we added in carbs. We moderate fat intake is what they were doing was they’re eating high fat and they were trying to add the carbs on top and not adjusting the fat intake.

Mike Fave

And then they were already having metabolic dysfunction. They were already overweight at this point. They were already having a higher body fat than was ideal. And then when they saw the panel wasn’t looking good, insulin density wasn’t looking good and adding carbs and thought that that was an ideal. So we figured out what was the caloric intake. They need it now.

Mike Fave

We figured out, how much fat do we want them to run with? How much carb do you want them to run with? We need to clear out the liver. So we adjusted the carb sources overall, and we switched toward some starchy or sources that were higher in glucose. So we didn’t put pressure on the liver with too much fruit juice.

Mike Fave

We still had some present even now, like we have some fruits set up in the diet with tubers and things like this. And then at some points we even had popcorn is just like, not super, like a good quality popcorn. So basically this was how we started to adjust things. And also the person in this time frame where they, the carbohydrate intake, I think was somewhere around 200 to 225g.

Mike Fave

This person had lost, around, I think at this point in time, roughly 80 pounds. So he dropped 80 pounds. We improved the lipid profile significantly, we dropped the insulin usage, and we did this with carbohydrates on board and the triglycerides still dropped even though we bumped up carbs. The initial carbohydrate intake I think was, you know, around 100g.

Mike Fave

We doubled it.

Ethan Wright

I mean, it’s just another example, right, of like how getting the foundation covered can really move the needle. And I feel like in talking with people, sometimes they go, oh, not my diet solid like I do grass fed meat and this kind of stuff. And then when I tried to, you know, probe a little deeper, like, are you tracking the amount, the ratios of macronutrients and things like this?

Ethan Wright

They’re they’re typically not. And then one of the things you just mentioned there was like having the same fat intake that maybe you had on a low carbohydrate diet and then adding carbs in on top of that, but not really realizing that that’s what’s what’s going on is like one of the mistakes you talked about last time.

Ethan Wright

And that’s probably oftentimes, what you see where we’re in a situation like this right, to.

Mike Fave

When the system’s not working. So say, as an example, say you have a car, say the engine on the car is shot like the thing is dead. If I just start, like flooding the engine with tons of gasoline, does that fix the problem now? So I need to try to fix up the areas of the engine that don’t work.

Mike Fave

Get it running again? Don’t flooded with fuel. Try to like put in enough fuel to start to test it. See how it’s going to run, get things working in under control and then move from there. So that’s the that’s what I’m looking to do. It’s not just like, yeah, if you come on board, you slam orange juice and sugared milk and whatever else that, that people are thinking about, like it’s just going to all get better.

Mike Fave

It’s like, no, if things are broken once the system is broken, it more effort, more energy requires more strategies to fix. As things get better and you fix you, you start tolerating these things. Things start getting back to normal. The engine starts to process stuff a lot better. And so that’s the ultimate. That’s what that’s what has to happen.

Mike Fave

You have to put interventions in place to fix things. It’s two times as hard to fix something, and it’s half as hard to maintain something with already good and just maintaining it way easier than a few. That’s broken. And you got to you got to fix all the little broken pieces with it.

Ethan Wright

My next question would be with this person in particular, or any of the clients that are in a similar state, how much of an emphasis are you putting on exercise?

Mike Fave

The first client that we talked about, we just said to do walking.

Ethan Wright

Walking, okay.

Mike Fave

The second client for the first, all the way until May. I don’t think we did any exercise besides, because besides trying to get the person to go for a walk after meals and then eventually we tried to, we did so we could start because like the person had lost significant amount of weight, a lot of body fat. And I wanted to start to build up the lean body tissue, the muscle mass, because it’ll improve insulin sensitivity and improve a lot of these markers as well.

Mike Fave

So then we did the workout routine, but by May, we I don’t think at that point that we really had that much exercise stuff going on, just walks. And then I think also the individuals doing rebounding and stuff like this here and there, but it wasn’t super consistent. But this person had already lost over 60 pounds without doing any like concerted exercise out of gym.

Mike Fave

It was just diet and they were already had type two diabetic on insulin and they were already hypothyroid and like diagnosed hypothyroid, not by me, by another doctor and on thyroid medication on top of on top of using insulin and type two diabetic. So that’s why I’m saying like you can have metabolic dysfunction and just getting the diet and lifestyle stuff dialed in.

Mike Fave

I’m not saying that’s the only thing to do. There’s multiple levers, there’s diet, there’s sleep, there’s SOPs, there’s drugs, there’s hormones, there’s exercise, there’s light exposure. There’s all these things you can do. But just even like for me, it’s diet first, just doing that can make a huge difference and a variety of values. And I mean you saw that here.

Mike Fave

These are two case studies.

Ethan Wright

It’s just interesting to hear that that can be accomplished without having to like kill yourself in the gym or something like this, like you’re losing weight and improving metabolic markers and lipid panels and all this kind of stuff, which I feel like a lot of people may be hesitant to like, start like trying to make progress on this stuff, or maybe just go the pharmacological route because they feel like it’s going to be this massive investment in terms of getting in the gym and doing like lots of cardio to lose the body fat or whatever.

Ethan Wright

And it’s like, what I’m hearing from you is if you set the diet up appropriately, have the foundations in place, and then make it so that you can be consistent with it, that’s how you can achieve the results. And it doesn’t have to involve like doing the StairMaster for hours on end or anything like this. It can be simple walks, and, and things like that in that nature.

Mike Fave

So I don’t even recommend that people go do a bunch of cardio if people are going to go to the gym. My recommendation is to lift to build muscle tissue, not just to go like try to burn calories or something like this to go build muscle tissue. But even then, when I’m building out workout routines, I a lot of people are surprised is like, wait, but I’m not out of breath.

Mike Fave

And it’s like, I don’t feel bad after I feel pretty good after the like. I’m actually enjoying it. And it’s like, because of you again, if you set the diet up, if you set the the diet up appropriately, then what happens is when you’re losing the way you you shouldn’t really feel that hungry. You’re starved. You’re not going to feel starved.

Mike Fave

You shouldn’t really feel maybe you’ll be slightly hungry, but that’s about it. And it just be like one time and it’s not really that big of a deal. Maybe you have some berries or something like this, but you won’t really feel that you’re in a huge deficit and you feel terrible. Let me just adjust like I’m there along the way and then when it when it comes to the exercise, the same thing when you’re looking at certain metrics like how much volume of exercise you need for a week, how many sets her body part per week you need to do in order to build muscle tissue.

Mike Fave

That’s what you need to know. And then the next question after that is how close to failure do you need to get? So how intense those exercises need to be? How frequently do you need to hit those muscle groups, and how much time do you have between them. So we’re looking at these very specific metrics. It’s the same thing with the diet.

Mike Fave

How much calories, how much protein, how much carbs, how much fat. How much are you having per meal? How are you organizing it across the day? Getting into the nitty gritty of that is where you see the progress and the huge benefit, and then the supplements and everything else is additive in to that. So now instead of just relying like, well, yeah, your lipid SoC.

Mike Fave

So just go on this drug regimen. It’s like, why don’t we harness diet? Why don’t we harness exercise. Why don’t we harness, the supplementation. Why don’t we. If you have to harness pharmacology, why don’t you harness pharmacology and take this multi-pronged approach and hit all these things and get them very specifically dialed in and then see, am I getting the outcome and then track the outcome and then see those outcomes improve?

Mike Fave

That’s for me. That’s that’s that’s how I’m looking to gauge things. I’m looking to see. The benefit is like when I when I look at this person, did he lose 70, 80, 90 pounds. Yeah. Did he improve his values across the board. Yeah. Do we still want to see things improve further. Yeah I want better targets. I want those ratios underneath my ideal thresholds.

Mike Fave

And then it’s on autopilot and the person just has to run it. That’s the heart. The hardest part of the whole game is just consistency.

Ethan Wright

So when you are trying to track these things as you’re making the interventions, is there a typical timeline that you like to see to make them make sure things are heading in the right direction? I know you have to take into consideration what’s available to the to the person, but ideally this person comes to you, you make the interventions.

Ethan Wright

Is it? Let’s look at the labs and get them redrawn in three months, two months, six months, like yeah. What would be the ideal timeframe.

Mike Fave

I’m gauging based on how much resources, like how much money do people want to put towards this? I don’t get kickbacks for any of the labs, like there’s no kickback to me. But the lab testing is expensive in general because you want to get a full view of what’s going on. So if the person has a lot of resources and they really want to like, spend the money to figure this out and trend the stuff, then we can do it on a more reasonable time frame.

Mike Fave

You can find a bunch of other metrics to look at that aren’t always lab values. Are you losing weight? Are you sleeping through the night? What’s going on with your blood pressure? How much insulin are you using per day? And you can see, like in the meantime, is all of this getting better? So it’s like looking at things, things like this like very specific for the target and based on the person’s context, adjusting timelines.

Ethan Wright

You want to have the time to see the changes get made right. You don’t want to go be getting labs like necessarily every two weeks or something like that. Give things time to play out. Make sure you’re on the right track. I just think with people, like getting the feeling like they’re moving in the right direction is always a huge motivator for them to be like staying consistent and stuff like that.

Ethan Wright

So having something where they know like, oh, I’ll get these things checked, like on a consistent basis, or even if it’s just like, yeah, how many nights am I taking things like this? It’s helpful to be like, you know, this is like, this is working. I’m moving in the right direction and whatnot.

Mike Fave

When people see that weight move down on the scale, like even if the other lab values are not perfect, like for me, I’ll be looking at like, yeah, your weight came down as great, but like, I really want to see this be here. And they’re like, I look great. I’ll do that one later. Yeah. So there they’re like, if you can’t do labs all the time, find other metrics in the meantime.

Mike Fave

And still trend some progress. If you don’t see progress within a couple weeks and starting to make the interventions, whether that’s in some way of how you feel, how you’re sleeping, your energy levels, your blood pressure, your your weight coming down. Like if you’re not seeing that within a couple of weeks, you need to make a change with what you’re doing.

Mike Fave

It doesn’t need to be a complete 180 degree change, but you may have to make a 5 or 10% change to what you’re doing, because maybe you’re not hitting that threshold that’s required to get the outcome.

Ethan Wright

In the 5 or 10% can make a huge difference, too. And even if it’s diet, diet, or lifestyle, right, like there’s a lot of 5 or 10% adjustments that you can make and dire lifestyle that will really make a massive difference. You know? And it’s not just that, oh, your diet’s good. You guys get like pharmacology boom. Next.

Ethan Wright

Yeah. You know so.

Mike Fave

Maybe we jump into our our last Clif here our last tips here.

Youtube Clip

The day when you measure your triglyceride in the fasting state, you are actually looking at how your liver handles the carbohydrate and in particular the sugar in your diet. Because those VLDL oils, those triglycerides, they are what your liver does with sugar. It turns sugar into fat and packages it as VLDL. And then those fields offload elsewhere and become the small dense LDL.

Youtube Clip

And if the goal is to get rid of the small, dense LDL, that means you got to get rid of the sugar, because that’s what made it so by understanding what each of these species are and how one goes to the other, then you can look at a landslip and understand the evolution of those species in a photograph.

Youtube Clip

And so you can basically figure out what happened, where which process is going on, and therefore what you need to do about it.

Ethan Wright

So I mean, this clip kind of reminds me of the one that you responded to on Paul Saladino podcast where Lustig was talking with Anthony Romine just goes through dishes, wants to be fat. Is like it just yeah, it just craves, you know, being fat.

Mike Fave

The way that he describes the process is not exactly how it works. And I kind of hinted at this already, but I want to show a graphic. You’re really quick because I think this exemplifies things pretty well. These are from, isotropic tracer studies. So basically they give people tagged, carbohydrate like, you know, fructose. They’ll give them a tag bolus this.

Mike Fave

So it’s radio. It’s tagged with a radio label so that they can track where the, the components from the fructose move throughout the body. And then basically what they show is that, you know, most of the fructose gets converted to glucose and lactate, a percentage of glycogen in glycerol, but less than 1%. And the reason I’m highlighting fructose here is because fructose is considered more light biogenic than glucose.

Mike Fave

And that’s the major thing that people like, you know, Doctor Lustig or Richard Johnson, or a lot of the low carb docs rail against, but not of most of the fruit dose is not converted to lipids at the liver. And as they say, the data are obtained within study periods less than or equal to six hours. So this is what’s happening like six hours after you ingest or given fructose.

Mike Fave

So this is between 50 to 150g of fructose. They’re getting really high dosages in these studies basically to see what happens. So you’re not really seeing a lot of fat production from the fructose that even in purified fructose forms in a variety of these studies. Now, the thing though that does happen is you can see, as we talked about the bump in triglycerides and the bump in triglycerides is not necessarily because of fructose just going to the liver and making a bunch of fat.

Mike Fave

But again, we’re talking about shifting fuel substrate. What winds up happening. You’re taking in the carbohydrate the the substrate is being shifted. And you may get more triglyceride being left in the bloodstream. Or you may have, you know, change in and what’s going on with lipid panel and stuff like this because of the change of the substrate. And last, because the fruit was just converted to fat.

Mike Fave

And I want to make a point here. It’s like you’re like, oh, the fructose. It gets converted into fat. It’s like, what is it you convert into like palmitic and stearic acid. So it’s like you are just going to eat that if you’re eating butter anyway. Just going to eat. If the liver is producing that fat, you would be eating that fat if you’re eating the fat anyway.

Mike Fave

And so basically so it’s like a weird argument for me. It’s like, well, don’t eat fruit, Charles, because it gets converted to fat. Just eat a whole bunch of fat that’s already the fat that you that you have. But he talks about how it raises small, dense LDL. We didn’t see that with the with the last client that we had the example from, you can see a bump in small LDL, with metabolic dysfunction.

Mike Fave

So I would say the small LDL with like bump in triglyceride, like, like a high levels of triglycerides in general and super low HDL values, those overall tend to be, related to metabolic dysfunction. And I think that overall metabolic dysfunction is associated with this lipid panel changes and with cardiovascular disease by itself. And so you’re seeing this like hodgepodge mix of things.

Mike Fave

And then in the state of metabolic dysfunction with the shifts in these lipid panels. Now you’re in a state where your metabolism not working well, you have a high amount of oxidative stress. And then you have these these little proteins that are floating around. They’re not being used. They’re sitting in circulation for a longer period of time, exposed to oxidative stress because of the metabolic dysfunction.

Mike Fave

And now you’re getting oxidized little proteins, which can drive being directly a driver and involved in atherosclerosis and it also and metabolic stress. You also have the rise in inflammatory mediators and immune signaling, which also drives atherosclerosis. And you also have a rise in stress hormones like catecholamines, aldosterone, the Ras system and glucagon and stuff like this, which also drives at the cardiovascular disease and atherosclerosis.

Mike Fave

So you’re seeing like all of these things and it’s a whole profile coming together. It’s not so simple. This like very linear logic carbs increase small LDL. And that’s probably a vascular disease. Like that’s not how it works. So I think if you had a metabolically healthy person, they were flowing the fuel through very nicely. The carbs and fats, both of them to ATP.

Mike Fave

When you take it in in a diet, you’re not going to see huge bumps and small, dense LDL. You’re not going to see huge bumps in triglycerides because the substrate is being used perfectly fine. But if the substrate is not being used perfectly fine, then you start to see you’re taking a measure of the fuel in the pipelines and you’re saying, well, look at what?

Mike Fave

Oh, well, let’s see what happened with the fuel. And you’re saying, okay, well this the fuel mixture here doesn’t look good. Like there’s some problems going on. It is damaging the pipeline. And it’s like, yeah, because the fuel sitting in there is not getting turned into energy. So it’s getting old. It’s getting old is getting oxidized and it’s driving.

Mike Fave

It’s driving inflammation and damage to the pipelines. So we need to have the flow working effectively overall and not. And I think the metabolic dysfunction is a primary driver. And again it’s not that the fructose or carbs just go drive liver fat production even in the animal models in order to get fatty liver. It’s not just a high carb feeding, it’s there’s a bunch of factors calling Matheny deficient diet high fructose plus high fat, isolated fructose plus high fat plus calling at this deficient diet.

Mike Fave

So there’s multiple factors coming together to create this problem. It’s a multifactorial issue centered around bottlenecks and problems and metabolism, not just carbs. Small dense LDL boom, cardiovascular disease.

Ethan Wright

And that’s kind of like where the sort of solution, right, to the paradox kind of lies, right, is in the metabolic function now, because, I mean, there’s actually in the in the lean mass hyper responder models. That’s why you see the like triglycerides here, the fatty acids being like use as fuel in that situation. Because that person is somewhat like metabolically healthy.

Ethan Wright

Like would you you would classify that person as metabolically healthy, right?

Mike Fave

I have an example here. This is from a paper it’s called Effects of Dietary carbohydrate and triglyceride Metabolism in humans. They say. Here’s one example. Data from 34 patients with coronary artery disease who are switched to a diet very high in carbohydrates, 76% with almost no fat, 8% of energy. So it’s only basic energy of carbohydrates, 8% of energy fat for the group as a whole.

Mike Fave

The average plasma triglyceride concentration did not increase significantly from the baseline diets, although a highly variable response was noted in the data of individual subjects, those with a body mass index at greater than 28kg/m², so like a high body mass index, a high BMI experience a 30% increase in triglyceride concentration, whereas those with a BMI less than 28 experienced no change.

Mike Fave

These data demonstrate that certain characteristics, e.g. BMI, can make some individuals more sensitive to lipid and lipoprotein changes with dietary carbohydrate increased. Is it BMI or is BMI a proxy marker for metabolic function here? And you’re seeing that when people have issues flowing the fuel sources through and they’re storing it so they’re having higher BMI or whatever the deal is, then you’re starting to see problem.

Mike Fave

Now, if you have a high BMI because you’re Arnold Schwarzenegger and Mr. Olympia, like, that’s very different than a high BMI because you’re holding a large amount of body fat percentage. Now, in this same paper, they go on to say or they say the second source of fatty acids for very low density LDL are very low density lipoproteins and triglyceride synthesis.

Mike Fave

The noble label genesis could be stimulated by an excess flow of glucose through the glycolysis pathway and into the hepatic acetyl coenzyme A pool. So basically the carbohydrate can flow to become acetyl CoA. And these Itokawa can increase through. There’s metabolic pathways there to be produced in the VLDL that the LDL cholesterol and triglyceride triglyceride synthesis. But they say here we measure the contribution of both free fatty acids and de novo label genesis to the production of fats, from carbohydrates to VLDL.

Mike Fave

Triglyceride synthesis in healthy men before and after a five weeks of iso energetic high carbohydrate feeding in which the diet was rich in polysaccharides or complex carbohydrates high in fiber, we found no evidence that carbohydrate induced, hyper triglyceride, high hypertriglyceridemia resulted from elevated free fatty acid flow, or the noble life of genesis. The primary phenomenon of carbohydrate induced high triglycerides could be explained by 37% reduction in triglyceride clearance from the blood.

Mike Fave

So when you switch them to a high carb diet, they stop burning as much fats, which left more triglycerides in the bloodstream. Not that they just started automatically converting all those carbs in the fats and then exporting them out of the liver as triglycerides or VLDL. So again, it’s not as simple as eat carbs, produce liver fat, put it in the bloodstream, it’s eat carbs, use carbs less fat gets burns you back up.

Mike Fave

And then you know you could. That will change things downstream. But you’re seeing in people who are not overweight or metabolically healthy. It doesn’t create a problem. Again, because the fundamental issue is not carbs or fat. It’s not either or. You have people on high fat, low carb diets. You improve metabolic function. You got people on high carb, low fat diets, you improve metabolic function.

Mike Fave

Its metabolic function is the central piece of all of this. And we’re measuring indirect values in the bloodstream. The pipeline is seeing how fuel is being distributed and then trying to see what is it, this one thing or this other thing. It’s like it’s fundamentally what’s going on with metabolism and everything else is downstream or backlogged from that.

Ethan Wright

And that’s why you’re saying there’s the gap in time, because it’s the switching of the fuel sources that has to take place, and the gap is short as long as that person is metabolically healthy. My question would be is like a lean mass hyper responder or phenotype. Like, why would that person be motivated to say like, stop consuming a high fat diet if technically they’re metabolically healthy and they’re transporting the fats through the cholesterol and this kind of stuff, like what is, what would be your case to that person to be like, hey, maybe it’s better to switch fuel sources like to glucose.

Ethan Wright

Are there markers you’re looking at, or is that person technically was in that state with a lean mass hyper responder? Technically B like physiologically insulin resistance, right. But maybe non pathological or how are you looking at that?

Mike Fave

If you have somebody who’s a lean mass hyper responder and like it say they’re oxidizing primarily fatty acids, then yes, they are physical, logically insulin resistant. So if you throw cards in, there’s going to be a period of time where they’re not going to be as good at using them because their body is relying on fats, but it doesn’t mean it’s pathology.

Mike Fave

The pathology is different, though, that when you’re doing a high fat, low carb diet, you get your body’s like, okay, we’re going to do this fat thing. And if you’re healthy metabolically, like you’ll do the fat thing and then probably be fine. A lot of people are, I guess, fine. If you do a high carb, low fat diet and you’re like, doing, like your body is going to get really good at using the carbohydrate if you’re healthy.

Mike Fave

It’s like, yeah, we’re doing the carb thing. When you’re metabolically impaired. This middle person, it’s like they’re not doing anything. They’re not doing the carbs, they’re not doing the fats. They’re like having a problem with all fuel sources. So that’s the that’s the that’s how you rectify the paradox. And you’re seeing all you’re seeing is in the lean mass hyper responder.

Mike Fave

Right. They’re just really good at using the fats now. So they’re like all their systems are geared towards oxidizing fatty acid substrate and the high carb diet. The systems are geared toward oxidizing carbohydrate substrate in the person. Other problem their system is just trying to figure out like what can we oxidize here? Because like nothing’s working.

Ethan Wright

So get it back up.

Mike Fave

Exactly. Carbs are backed up, insulin’s high fats are backed up, glucagon is high. And it’s like the whole system is dysregulated because what’s happened is you have this system where you have hormones, are trying to gauge what’s going on at the peripheral, like the body’s trying to gauge and signal with hormones what’s going on with the cells, what’s going on inside the like, the bloodstream, what’s going on at the liver and what’s going on from the gut and all this type of stuff.

Mike Fave

But what’s happening is the cells are like full, but they don’t have energy. They’re filled with fuel, but they’re not turning into energy. Then the bloodstream is filled with fuel and the cells are calling for energy. And then the liver is filled with fuel and it can’t it’s still calling for energy. So you have this weird hodgepodge of we have all this fuel, but we can’t do anything with it.

Mike Fave

And we’re still calling, we’re still signaling for the fuel because we’re fundamentally at an energy deficit. And so that’s where you get the then the whole system is arranged like the signaling gets to range between insulin and glucagon. The signaling is the range between release of free fatty acids and shutting off fatty acids, and production of glucose from the liver, and the amount of glucose that’s already in the bloodstream.

Mike Fave

And the ATP levels are all this. The mitochondria are under pressure, there’s not enough ATP, but there’s there’s a lot of fuel floating around. So things are broken down. And so you have to there’s a lot of steps that have to go to getting things back on track and a lot of that. Then what happens is the body’s like, right, we’re going to put this in storage.

Mike Fave

And that’s where you see people start. They show that the storage stuff in storage of the storage. And at a certain point it’s like it’s all you have only have so much storage to some extent, and you start leaking all the fuel sources out of that storage. And you have all this inflammatory mediators because the fats amplify that, that inflammatory response.

Mike Fave

And so then you have like at that point now you’re like you’re you’ve maxed out storage, you’re leaking all the fuel substrate and nothing’s being used. And the pipelines are getting backed up. And then since you’re since metabolism is metabolism is messed up, ATP generation is not good. Then you’re starting to see oxidative stress with the fuel. And so it’s like you like have a fire lit in your pipeline with all your fuel sources present.

Mike Fave

So these create huge this is where the problem lies is in this. And that’s why it’s like you need to fix the diet to get and you need to fix what’s going on with metabolism so that you can get this food comes in, digest it. Liver distributed cells use it instead. A few food comes in digest it. Liver doesn’t know what to do with it, tries to distribute it, and cells don’t know what to do with it.

Mike Fave

And then it’s still stuck in distribution. And then the liver gets it back and it’s like, I just sent this out.

Ethan Wright

You’re taking all these like, you know, factors to consider within the diet in terms of how to structure what food sources, ratios, supplements to bring on board lifestyle implementation, stuff to correct that problem, to push towards being able to oxidize the fuel sources. Primarily you would say glucose, probably the one you want to shoot for. So those strategies will be enhancing that.

Ethan Wright

And it’s that’s not a ketogenic diet, a low carb diet or anything. Along the restrictive, side.

Mike Fave

Right. It’s not like a high like this is the diet. It’s like, what is this person as an individual need given their context? You got the outcome. And so say to answer your questions and maybe say you had a lean mass hyper responder and everything was going well. Like all our markers look good and things like are going well overall.

Mike Fave

Like okay. Like I’m not saying you have to switch to a higher carb diet. It’s just from my personal perspective and my understanding of reading the research. Right. I think it’s better to have glucagon lower. I think it’s better Google metabolism levels. I think it’s better to have cortisol lower. I think it’s better to not have the changes that happen in the mitochondria with that oxidation.

Mike Fave

That’s the primary way of oxidizing. You’re always oxidizing carbs and fats. It’s just a slider. As far as percentage, I think it’s better to be oxidizing carbs more so than fats, based on what happens in my understanding of what goes on in the mitochondria, I think it’s better to have a high or higher CO2 concentration based on poor and haldane effects.

Mike Fave

Then if you’re doing the fatty acids, I think you can have a more nutrient dense diet. In general, if you have the carbohydrate sources and if your major energy source is butter or olive oil or something like this. And I think it’s better from a microbiome standpoint to not dump in tons of fats all the time into the GI tract and things like that.

Mike Fave

So like, I have my reasons, I’m like, I have like bunch of rationales on why I think carbs trump fats, but if somebody is doing well on that diet, I’m not sitting here saying, every single person needs to be on this. It’s like from my perspective and my understanding of the physiology and what I’m seeing with clients. And these are components, I think that the carb oxidation is what I would prioritize.

Mike Fave

I think the insulin signaling and the effects on thyroid hormone effects on androgens, the effects on glucagon, the effects on on the mitochondrial changes of microbiome CO2 levels. I think that fundamentally the NAD plus any ratio, that to me would indicate that carbohydrate metabolism would be better than fatty acid oxidation, that that’s my perspective. I’m adjusting based on the outcome.

Mike Fave

People come at me and they’re like, well, you know, our carnivore is the best. It’s like, I don’t care what Di you’re doing. I like it’s not personal for me whether you’re in this camp or that camp, like it’s irrelevant. It’s like, what do you need to do to get your outcome to function better? And how can I help you to do that?

Ethan Wright

So we covered a lot of the questions, from the community within our discussions talking about the clips. But there’s a few that we didn’t get to. So I want to just shoot these off at you real quick and then get your thoughts. The first one that we have is what are your thoughts on cholesterol lowering supplements, specifically red yeast rice.

Mike Fave

Yeah, this is a good one. I mean, the fungus that produces it produces lovastatin in it. I can’t tell anybody not to take a stand, but I think that there would be some concerns with using a stand because you’re blocking this whole pathway, an eight pathway, which is involved in the production of a variety of different components. By blocking this pathway, you’re also blocking a bunch of other things that in a long term could potentially be problematic.

Mike Fave

And that’s why I think there’s potential concerns. And there are known side effects with statins like myopathy, insulin resistance and risks, like this or associations, at least with insulin resistance and diabetes in some studies, increased risk of infection. Some like this. So you have to be careful with what mechanism you’re looking at, even though it lowers cholesterol and can have other downstream effects.

Mike Fave

Also signs of other effects beyond that. So the red yeast rice I’m not a personal fan of because it’s similar to STAT, and if you’re on a side, you probably don’t want to be taking red yeast rice on top of this, and you’re kind of doubling up on the same mechanism. So I would avoid red yeast rice as an option.

Ethan Wright

Okay, let’s jump into the last question here. Why can infections in the gut or infections in general present as high cholesterol?

Mike Fave

When the immune system gets activated, it releases a bunch of components called cytokines and inflammatory molecules. Or, you know, cell signaling molecules. So some of them, like tumor necrosis factor alpha and interleukin six, increase the production of cholesterol at the liver. So you get a heart, it will raise LDL total cholesterol, things like this. Why. Because the lipids bind to endotoxin.

Mike Fave

And then they get brought back to the liver. And in the cells in the liver can actually start to detoxify those toxins. So it’s kind of like it’s like a mopping up effect. So the cholesterol goes and helps, in and it’s involved with the immune response and is involved with detoxifying some of the toxic components. So it’ll bump that up.

Mike Fave

So chronic low grade inflammation or low grade infections can drive up lipid panels by increasing these cytokines. That will increase the cholesterol values overall. And also alter the metabolism of the cholesterol peripherally, by adjusting its uptake and utilization at the cells. So there’s a lot of ways in which the the immune stimulus from infections can lead to the elevated lipids.

Ethan Wright

So it’s like a protective effect essentially. And now maybe another thing to consider when you’re talking about lowering cholesterol pharmacologically is like the cholesterol is there to to protect against infections and things like. That’s right.

Mike Fave

If you have an infection and then you’re just nuking your cholesterol levels like that, probably that could potentially not be a good idea. And if it’s like really high, we see these strong associations. So like the risk is worth the reward to like smash things down. But for me the question is like can I lower it in a way that doesn’t increase the risk with like with the pharma stuff?

Mike Fave

And there is some side effects and risks with the pharma stuff, which is that’s what I talked about in the podcast with, with Paul.

Ethan Wright

And there’s, I think, a litany of things to try before you go that route that we discussed in this podcast. I think we covered quite a bit here. So is there anything you want to finish up with before we before we wrap up.

Mike Fave

Try to see the levers that you have at your disposal. You have pharma, you have supplements, you have diet, you have exercise. And try to pull all the levers to improve your health and get the outcomes that you’re looking for. I think that’s that. That’s what I’m looking at. And then try to figure out what is specifically going on in your circumstance and you know, and get that under control instead of like looking for this.

Mike Fave

Well, it’s keto, it’s bio energetic, it’s carnivore, it’s vegan. It’s like you may have something very specific going on, and you’re going to take a world tour of diets and supplements, whatever else. Instead of saying like, okay, like what? Like taking stock and saying, like, where am I specific issues for me and then trying to address those.

Ethan Wright

And if anybody’s interested in working with you or checking out what else, you have going on in terms of YouTube socials and stuff, where can they find you?

Mike Fave

Of course they could find me here in the podcast. They find me on the YouTube channel. Mike. They’ve just Mike they have YouTube and the website, as always. Mike Viacom and what about you, Ethan? Where can everybody find you?

Ethan Wright

So it’s Ethan underscore right on Twitter and Instagram. That’s usually where I’m hanging out. So you can find me there. And then again, if anybody has any topics they’d like to see us discuss in the future, please leave them in the comments. We’ll get to them. And with that said, we’ll catch you guys next week.

Mike Fave

Yeah. Get you.

Ethan Wright

Actually. All right.