0:00–0:58 Intro

1:33– 18:27 High fat vs. High Carb for Weight Loss

18:29– 28:37 Fructose and Fat Loss

28:38– 49:52 Dr. Fung on Fructose & Uric Acid

49:53 – 55:49 Setting up the diet for weight loss

55:50– 1:00:30 Increasing Metabolism and CICO

1:00:32 – 1:04:15 Mike Israetel on Ozempic

1:04:16– 1:20:35 Pros & Cons of Ozempic

1:20:36 – 1:22:34 Losing Weight w/o Being Restrictive

1:22:35– 1:24:53 Adding Carbs Back In the Diet

1:24:54– 1:31:31 Dr. Mike “Should Everyone be on Ozempic?”

1:31:32– 1:35:19 Final Thoughts

Ethan Wright:
Welcome to the Mike Fave Podcast. I’m your host, Ethan Wright, joined by Mike Fave. 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.

In today’s episode, we are going to dive into bioenergetic weight loss and discuss Dr. Johnson and Dr. Fung’s thoughts on fructose and weight gain. And Dr. Isra tells and Dr. Mike’s thoughts on Ozempic for weight loss. Throughout this process, we’ll be diving deep into bioenergetic weight loss and the strategies that Mike uses and has used to help his clients lose over 10 to 100 pounds without significant losses in lean muscle mass.

All right, Mike, you ready to jump into things?

Mike Fave:
Yep. Let’s jump in. One thing I’ll add is, and also. Without going on it extremely low carb or ketogenic diet.

Ethan Wright:
Yeah. That’s an important point to make or fasting. Right, right. Without any of the stressful forms of losing weight. So the first clip that we have teed up here is one from Dr.

Richard Johnson. And he’s talking about how you won’t gain weight on a high fat, low carb diet, and how carbs are all the cause of weight gain. Um, and some specific things around fructose, I believe. So not surprisingly, right. Cause he’s like

Mike Fave:
super anti fructose. Yeah.

Ethan Wright:
I only, I know him as like the uric acid guy and kind of the purveyor of that theory there.

So. Why don’t we jump into that clip?

Clip: Fructose is the fire. It ignites the fire that makes you hungry. High fat diet is the firewood. You put that on and you get a big blaze. If you’re on a low carb diet, if you’re on your keto diet, you can eat a lot of fat. You’re going to control your weight. You’re not going to be hungry.

And so you’re not going to really gain weight, even though you’re on a super high fat diet because you need the carbs to make you hungry to gain the weight from the fat. Even having said that, the carbs themselves. Well, the fructose, even on a low fat diet, will still make you diabetic.

Ethan Wright:
A lot to cover there.

I mean, the first thing that kind of jumps out to me in terms of like, when I talk to people, there’s a lot of people that have tried low carb diets and like, are either stuck and are gaining weight now or like, um, You know, uh, haven’t been able to lose all the weight they wanted to before running into problems.

Mike Fave:
I think the first part of his statements, I think I would say are throwaways. Like there’s nothing really being said, fructose is the fire, and fat is the firewood. Like, I don’t even understand what the analogy is that he’s trying to make there, at least physiologically. Overall, at the major statements that were made, I would say there was three.

The first one was that going on a low carb diet nukes your appetite, and you’re not as hungry, so you lose weight. Okay, that’s true. Fair point. That you will lose weight because you’re, if you’re on a keto diet or something like this, and your appetite is lower and you’re eating less. You will lose weight that way, for sure.

We’ll talk about satiety and carbs. The next thing is, The idea that carbohydrates or fructose cause diabetes is fundamentally incorrect. And we’ll actually go into the research, so it’s not just going to be my point of view on this, it’s going to be from papers, from trials, in humans. looking at intakes of fruit, because again, in the bioenergetics sphere, at least from my perspective, I’m not recommending that people smash, uh, granulated sugar and, and like ridiculous amounts of honey or maple syrup or anything like this.

The major carb sources that are recommended are fruits, a hundred percent juices. tubers and starch sources that you tolerate, ideally whole foods. We’ll get into that. And the first thing’s first, does a keto diet, a high fat diet, and also a potentially a lot of times this winds up also being a high protein diet for people.

Although there are limits the protein consumption in keto diet diets, because if you have too much protein, you drive glucogenesis, which may affect ketosis or ketogenesis. And the answer is yes, if you’re on a keto diet in general, you will probably have a lower appetite because the fat and the proteins which the meals are mainly situated around are very satiating and also help you to stay full for quite some time.

So protein stimulates a variety of different intestinal components, GLP 1, GIP, from the intestinal amino acids when it gets digested, which increases satiety. Then also the fat delays gastric emptying, which makes you feel fuller for longer. And then it also induces the release of an enzyme, or not an enzyme, it induces the release of a protein called, or a hormone called cholecystokinin, which also induces the feelings of satiety.

So you have GIP, which are all induced by amino acids and fatty acids in the intestine that trigger satiety signaling, on top of the fact that That you, the fat delays gastric emptying. So you’re full for really long. And this is why when people are on these keto diets. They’re like, wow, I had six eggs for breakfast and like a bunch of butter.

I’m just not hungry. I’m not hungry until dinner. It’s like, yeah, that’s a, that is a fundamentally going to be an effect of this diet. Is that mean that it’s magical for weight loss compared to lower fat, higher carb diets? No. Now, if you’re lower fat higher carb diet is tons of just straight juice and granulated sugar and stuff like this and really low fat dairy products, whatever else, like you’re probably going to be hungry.

You don’t have a lot of satiety mechanisms in there. That doesn’t mean that that’s the, that’s the comparison point that you’re looking at. Because you can set up the diet in many other ways. Even, even if your fat intake is say it’s 30 percent of calories, if your total energy intake is managed effectively, which 30 percent of calories isn’t technically a low fat diet, if you’re 30 percent calories of fat, and then even if you’re 40 percent calories of carb, or 50 percent calories of carb, whatever the deal is, You’ll still lose weight if energy is maintained effectively.

Whether you’re high carb, low fat, or low carb, high fat, you will still lose weight. Does high carb or high fat low carb make it easier to be more satiated when you’re trying to lose weight? Yes, in comparison to some of the generally set up low fat high carb diets that aren’t very satiating. But that’s a function of how the low fat high carb diet is actually set up and not specific to low fat high carb being fundamentally non satiating.

If you’re a low fat high carb diet, is, and again, you don’t even have to be low fat. It’s just your total energy intake has to be managed. But just for argument’s sake, if your low fat, high carb diet was whole fruits and tubers, and you had a decent amount of protein intake, whether that was steak, chicken, fish, eggs, if it did have some low fat dairy products, etc.,

and then maybe you had some cooked veg with that, and your fat source was avocado or mac nuts or dark chocolate or things like this, you will still lose weight and you will also be satiated. And I see this with clients time and time again, and this is also born out in the research. I don’t think that there’s a magic to.

The low fat or the low carb, high fat diets in so far that comparatively at least to the low fat, high carb diets, it’s just in general, it’s easier to be satiated on that diet if compared to the standard setup that you see with low fat, high carb diets, hopefully that makes sense.

Ethan Wright:
I think when people come to bioenergetics, a lot of the times the foods that they’ll initially try are ones that aren’t typically like high in fiber or have elements that are super satiating and then people end up snacking and then like.

Getting, you know, it’s a lot of dairy and like, uh, juice and stuff like this. That doesn’t necessarily like fill you up. And next thing you know, you’re at like all these calories where I get, I think like you’re saying, it’s like, okay, there’s these mechanisms of protein and fat and that can make you feel full and you can include those in a diet, like an intelligent setup so that you’re not like constantly hungry and having the snack and having, you know, full meals like throughout the day, because.

Even when I started working with you, that was like kind of one of the things that was initially changed was like, I wasn’t grazing all the time. I didn’t necessarily feel the need to graze because I’m having square meals and I’m hungry at those times that I typically eat that. Exactly.

Mike Fave:
And the other thing is fiber is important too.

So fiber also can induce what’s called the ileal break. So it will slow digestion through the small intestine a bit. Uh, and through a release of some of these same peptide hormones with a GIP, GLP1, some of these same hormones. Again, like, if you set, it’s how you’re really setting up the diet. That’s fundamentally what it comes down to is how is your diet set up.

And you, whether you can lose weight on high fat, low carb, and you can lose weight and, and improve metabolic function. We’ll see that on high carb, low fat and everything in between. There’s some specific targets that are really important to hit, but fundamentally managing your energy intake is the major piece here.

And whether you do it with these different setups, you’ll still lose weight and improve metabolic parameters. Now, from my perspective, I think it makes more sense to actually, have higher carbohydrate intake because of the effects of the mitochondria in terms of NAD plus ADH ratio in terms of reactive oxygen species production in terms of the insulin signaling, which I see as a benefit.

And in terms of the effects on thyroid function and androgens and stuff like this, I see those things as beneficial altogether as well as shifts in the microbiome. Could you do a keto diet and also like a high carb, low fat diet and both and see beneficial outcomes in type two diabetics? A hundred percent.

You can see that. And. We have a quote here. So this paper says impact of high carbohydrate diet and metabolic parameters in patients with type 2 diabetes. They say in patients with type 2 diabetes, whether dietary carbohydrates have beneficial detrimental effects and cardiometabolic risk factors has drawn attention.

Um, They say, uh, let’s see, they say here, In this review, we examined recently published literature on the effects of high carbohydrate diets and metabolic parameters of type 2 diabetes. High carb diets are at least as effective as low carb diets, leading to significant weight loss and a reduction in plasma glucose, hemoglobin A1c, and low density lipoprotein cholesterol levels.

The major concern is that high carb diets may raise serum triglyceride levels and reduce high density lipoprotein, or HDLC levels. Increasing the risk of cardiovascular disease. However, these untoward effects were not a persistent consequence and may be ameliorated with the consumption of low glycemic index low glycemic load and high fiber.

Carbohydrate intake should be individualized and low caloric intake remains a crucial factor to improve insulin sensitivity and reduce body weight. However, a high carb diet, rich in fiber and with a low glycemic load and glycemic index may be recommended, recommendable in patients with type two diabetes.

So this is a paper that directly is saying they talk about a study in here, which I will, I’m going to talk about as well, but they’re saying in this paper, That look we’re reviewing the research and you can use high carb diets in patients with type 2 diabetes. So you have dr Johnson, you’re saying carbs cause diabetes and then he qualifies that further after by saying fructose which we’ll also get into And then we’re having we have research here and we have trials that i’m going to show i’m going to read one of these trials That fundamentally shows That you can have a higher carbohydrate intake and improve metabolic parameters in people who already have diabetes.

That’s something we see in the comments, right? You’re like, oh, if you’re metabolically healthy, then you can have carbs. But if you’re not metabolically healthy, then you can’t have carbs at all. And it’s like, no, they’re literally running studies. And, and people who have type 2 diabetes and finding improvements.

As long, and again, they qualify it here as well on the paper, that how the diet is set up is important. If your diet is going to be granulated sugar and like sticky sushi rice as your carb sources, and you’re type 2 diabetic, you’re probably going to have problems. But if your carb sources are going to be, say you tolerate something like potatoes, or yams, or sweet potatoes, or whole fruits, and you make that the bulk majority of your carb sources, or squashes or whatever else, you’re not going to see the same problems.

It’s a very different effect, especially in combination with adequate protein intake and adequate fat intake, adequate polyphenol intake and adequate micronutrient density in the diet. So it’s not, it’s not a carbs versus fat thing. It’s not about that. It’s how are you fundamentally structuring your diet?

Most important thing. And then in the context of this, we have an energy problem. So it’s how much energy do you need to have on a regular basis? Given your context, given what you have going on, you have a high body fat percentage and you need to take that body fat percentage off while maintaining your lean mass, which we’re going to get into this, then you need to manage your energy intake period.

Because if you’re basically in all of this, in the type two diabetes, obesity, fatty liver, you have a metabolic issue and the, you, if you throw in rapidly digesting carbohydrates and, or even if you overload the system with fats. What will wind up happening is you will worsen that effect the oxidation of both fats and carbs is is problematic in these states And so what happens when you go into a caloric deficit state is you take a pressure, you take the pressure off the metabolic system, and you take the body fat levels down, which is important that you don’t use lean mass, and we’ll get into that, but you’re taking the body fat levels down, and as you take body fat levels down, what happens is you don’t have all the inflammatory amplification and signaling from the body fat tissue, you don’t have the increased conversion estrogens, and you also don’t have the constant release of free fatty acids, from the fat tissue that clog up and gum up the system over time.

So you need to get body fat levels down, maintain lean mass and need to set up a reasonable diet, whether that’s with carbs or with fat. My preference is towards higher carbon take. We talked, we can get into a whole episode on the benefits of carbs and why I shoot for higher carbon take. Cause again, I came from a low carb background.

I did keto. I did IF I did paleo. I did carnivore. I did these things and I settled that the higher carbon take. was fundamentally better for me. There’s problems transitioning between them, but at the fundamentally, I think there’s reasons why the carbs would be better overall as an energy substrate. It doesn’t mean low fat either.

It just means the priority is with carbs. And so again, you could do it with either diet, but they’re fundamentally multiple things have to be changed in a diet. It’s not just carbs versus fat, which is this weird dichotomy that the dietary spheres have gotten into. And I think it’s less It’s not as important as like, how is your diet set up for multiple factors?

Ethan Wright:
And I think the like what you’re saying with keeping preserving the lean mass is really important. That would probably be another nod to why you would want to include carbs in the diet throughout that process. Because you see, I think even people I talk to or even influencers online talking about doing some of the restrictive dieting, whether it’s fasting or even with keto, I think you can see maybe, um, or loss in some of the lean mass stuff.

But another component that people talk about is the fructose thing and, um, Dr. Johnson kind of gives a nod to like fructose there at the end too is like, uh, something specific that could be problematic. Um, so I don’t know if you want to talk maybe a little about a little bit about like the whole theory with fructose and in fatty liver, or if we want to jump into the next clip with Dr.

Fung also kind of. Poopoo’s, uh, the fructose thing. I

Mike Fave:
want to read this study here, which is a randomized controlled trial in humans. There’s actually human studies showing this. So they say here, Larson et al conducted a 12 month randomized controlled trial to investigate the effects of a high carb, uh, or high protein, very low carbohydrate diet in 99 participants with type 2 diabetes in Australia.

Now, low carb advocates are going to say, Well, the high protein, very low carbohydrate diet wasn’t very low carbohydrate because the carbohydrate content was 40%, and you would be 100 percent correct, because that is not a very low carbohydrate diet. The definitions in the research have not been standardized to any large extent.

It’s one of the problems with some of the research. But basically, the two different dietary breakdowns, you have, uh, 55 percent uh, carb, 30 percent fat, or 15 percent protein diet, Versus a 40 percent carb, 30 percent fat, 30 percent protein diet, right? So they’re both have a, still have a decent amount of carbs.

One’s higher protein. Now they say the study consists of two dietary periods, a three month, 30 percent energy, energy restrictions. Only three months of the time was there a 30 percent deficit followed by nine months of energy balance. And both groups were recommended a low GI diet, 18 point. So basically they say here, Um, they say as a primary outcome, hemoglobin A1c decreased in both groups over time with no significant difference between groups.

Both groups also demonstrated decrease over time in weight, serum triglycerides, and total cholesterol with an increase in HDL C. These parameters were no different between groups. So basically, um, this is at 12 months, basically with this study, what we’re seeing is you have people on a 55 percent or a 40 percent carbohydrate diet.

And they, these people are type two diabetics. These are diabetics, and they lost weight, improve their hemoglobin A1C, and they improve their living profile, even though the diet of 55 percent carbs or 40 percent carbs. So it’s like you’re seeing that in randomized controlled trials. They’re running with people with carbohydrates and you’re still seeing a benefit, but they’re managing other components of the diet as well.

That one was higher protein, one was higher carb, and you still saw the benefit and you would still argue that these are relatively higher carb diets than what people are talking about in the low carb sphere, which tends to be ketosis. So we’re still seeing it in the research. That’s something to point out.

So for somebody to come on a podcast and say, you know, carbohydrates cause diabetes. It’s like, where are we seeing that? If anything, we have people who are type two diabetic and it’s improving their diabetic state. You’re seeing the markers that are associated with diabetes improving. So, and cause these are the same metrics that people are going to then use and say like, Oh, look, this low carb diet, improve hemoglobin A1C and this and that.

So therefore it’s useful for diabetes. And then turn around and say, well, all the high carb diets, they cause diabetes. And then when you see the same thing, it’s like, well, what do you, what do you say to that? It’s like nothing. You don’t say anything because both diets will improve it. Whether you’d use carbs or you go on a very low calorie ketogenic diet, or you go on a ketogenic diet, both, and if things are managed appropriately, you will lose body fat and you can improve hemoglobin A and C values, insulin values, blood glucose values, et cetera, assuming all like things are structured appropriately.

So you could see it on both sides. So again, like in the last video, we talked about this. We have people saying like, like you’re like, why do you have to make it in either? Or it’s like, we’re not making it in either or we’re saying you can do it with both diets. And that includes having higher carbohydrate intake in the diet.

And also fundamentally, it’s just, I’m saying like, I’m biased towards a higher carbohydrate intake. I think it’s better, but in general, I, it’s to say that you can have high carb, I higher carbohydrate intake and, and see improvements. And that we’re not seeing that it causes or worsens diabetes, despite what Dr.

Johnson is saying in this clip,

Ethan Wright:
you hear all these sorts of things about carbohydrates. Like when you’re on the internet and the alternative health sphere, and a lot of them are just blatantly false. Like when you look at the research, so just, Us just, in the first episode, talking about some of those things.

It’s helpful to just give context, whatever the person decides to go one way or the other in terms of how to set up their diet. It’s like, just have the information that a lot of these, like, carb fear mongering people are not, um, necessarily accurate with all the statements that they’re making, or there’s more context that they’re leaving out, right?

We’re not

Mike Fave:
even trying to make a camp of either or. We’re just trying, we’re responding to the clip and saying like, look, like this just isn’t like, we’re not seeing this in the research. I’m not seeing this when I’m working with clients that, oh man, this person has carbs and they’re like, their diabetes is getting worse.

It’s like, no, if it’s done appropriately, diabetes, their diabetic parameters are getting better. And we showed exact case studies in the last, In the last

Ethan Wright:
episode, we have with people who have like include fructose in their diet and high carbohydrate. The other thing though is then there’s the focus. Well, okay,

Mike Fave:
you know, and Dr.

Johnson Claire qualifies as you said, fructose. So it’s fructose causing diabetes. Maybe it’s not glucose. Maybe glucose is fine. It’s really that dastardly evil fructose. Embedded

Ethan Wright:
within delicious fruit.

Mike Fave:
We have a couple studies here. That basically show that this is not the case. A higher intake of sugar sweetened fruit juice was significantly associated with risk of type 2 diabetes, 28 percent increased risk, while intake of 100 percent fruit juice was not associated with risk of developing type 2 diabetes.

So there’s not, the P value is not significant for this one for a hundred percent fruit juice. What we’re seeing is that a hundred percent, a hundred percent fruit juice does not cause or is not associated with increased risk of diabetes. And this is a systematic, um, a systematic review and meta analysis that flies in the face of this fructose itself is driving it.

And sugar sweetened beverages, sure. We’re basically you have juice where you add a bunch of sugar, didn’t seem to do as well, but for regular fruit intake, which again, this is the recommendation For what I’m working with clients or what we talk about in the bioenergetics years, have fruit. You’re going to do juice, have a hundred percent fruit juice.

It’s like, we’re not seeing the worst outcomes. And this is why this, that’s the recommendation. So we have another study here. This one is. Fruit intake decreases risk of incident type two diabetes and updated meta analysis. So what they say here, they say that we found that individuals in the highest category of fruit intake had a reduced risk of type two diabetes, um, compared to those in the lowest category with moderate evidence of between study heterogeneity.

There was an evident, a non linear association of fruit intake with type 2 diabetes. A non linear threshold of 200 grams per day of fruit intake was identified and the risk of type 2 diabetes reduced by 13 percent at this cutoff. Our findings are consistent with diet recommendations to consume about 200 grams of fruits to prevent type 2 diabetes.

200 grams of fruit is a, roughly a half pound of fruit per day. decreases the risk of type two diabetes. They say by 13%. So there’s another one. Then we get to this next study here. We say effect of fruit on glucose control and diabetes mellitus, a meta analysis of 19 randomized controlled trials. So this is a using fruit on glucose control in people who are already type two diabetics.

They already have metabolic dysfunction and they’re using fruit with them. They say, 19 randomized controlled trials with almost 1, 000 participants, so 880 participants were included. Fruit consumption significantly decreased the fasting glucose concentration, but it showed no significant difference in hemoglobin A1c.

Subgroup analysis further suggested that the consumption of both fresh and dried fruit decreased the fasting blood glucose concentration. So they’re seeing improvements in fasting blood glucose concentration and at the minimum, no change in hemoglobin A1c. So it’s not making it worse, which is what the claim would be from somebody like Dr.

Johnson.

Ethan Wright:
And then with people that you’re seeing and working with on a consistent basis, like fruit, you would say is a pretty primary part of the diet, whether or not their goal is like to lose weight or move, uh, or like improve metabolic function.

Mike Fave:
If they tolerate fruit, they don’t have problems with it.

Yes. If they do better with starches and we do some starches, And then I’m shifting around the fat and the carb percentages based on what, what they’re tolerating, where they’re coming from, all this type of stuff. It’s a personalized approach to the diet. It’s not like, here’s your keto menu. Just go do this.

Or here’s your bioenergetic menu. Just go do this. It’s like, let’s figure out what works for you. Like that’s the fundamental goal that we’re looking for. And then adjusting the foods from there. And I have people who are type two diabetics with severe blood glucose dysregulation, like fasting blood glucose values in 200s and 300s, where they have dropped their fasting blood glucose value significantly.

Drop their hemoglobin A1C points by mult, not per, not like 0.1 points, like 1, 2, 3 percentage points with having fruits in her diet. Like going from like with carbs in like they have carbs in their diet. Like one person I’ve worked with has, she’s dropped her hemoglobin A1C multiple points and that was with fruits in her diet.

Her major carb source is fruits. There’s no starches, so she’s eating almost all sugar from whole fruits and juices. I think we have between 150 and 200 grams a day of sugar, and she’s a diabetic, but it’s just not granulated sugar, it’s not Cokes, it’s not Pepsis, it’s not Smarties, it’s not, it’s not Honey Buns, it’s melon, it’s dried fruits, it’s mulberries, it’s, it’s, it’s a cup, a little bit of orange juice, like it’s things like this is where we’re seeing the change, it’s not from those other sources.

Ethan Wright:
And then also setting up the diet with the other macros too, intelligently to Dr. Johnson’s point where you can improve satiety and stuff, so it’s Kind of bringing the whole picture together, right? Exactly, and

Mike Fave:
despite being post menopausal, and despite being type 2 diabetic, and despite having carbohydrates in the diet, she’s lost weight!

She lost like, well, she lost like, I think like between 10 and 20 pounds.

Ethan Wright:
Well, that must be an anomaly, Mike, because I think Dr. Fung would have some different things to say about fructose and your ability to lose weight while consuming it.

Mike Fave:
Yeah. So I just want to go through one more and then I promise we can get Dr.

Fung. Okay. This one, the reason why is this one will set us up in the future. There are other things that we’re going to talk about. This study says high intake of orange juice and cola differently affects metabolic risks in healthy subjects. This is a 2019 study. And so they gave people either orange juice or Coca Cola and he looked at what goes on with uric acid and gout risk and type two diabetes and stuff like this.

Um, so insulin blood loose values. So, they say, uh, Fecal microbiota, body weight, basal, and oral glucose tolerance test derived insulin sensitivity remain unchanged whether people had orange juice or Coca Cola. Levels of uric acid were normal at baseline and did not change with 2 week cola consumption, whereas they decreased with OJ intervention, with the orange juice due to increased uric acid excretion.

Compared to OJ, consumption of coal led to a higher day long glycemia, an increase in glucose variability, and a lower 24 hour insulin secretion, which may be explained by a decrease in serum potassium levels. They say despite its sugar content, regular consumption of large amounts of OJ do not increase the risk of gout, but may even contribute to lower uric acid levels.

The etiology of impaired insulin secretion with cola consumption needs to be further investigated.

Ethan Wright:
Well, but my glucose goddess would say differently that they’re the same thing. So I don’t know what you’re reading, but

Mike Fave:
yeah, I don’t know what research papers I’m reading. It must be because I don’t have like, you know, like MD behind my name or something like this that I not allowed to read research papers.

But basically what we’re seeing in the research paper, again, they’re comparing Coca Cola and they’re comparing OJ and they’re finding improvements in uric acid levels with orange juice. And we know in the research vitamin C and polyphenol compounds improve metabolism of uric acid through metabolism of multiple things and shift microbiome.

We know, we know this and we also, the mineral intake is extremely important. Adequate potassium intake, lowering RAS, RAS function, having that good potassium, potassium balance. So it’s like to sit here and say that the problem is just fructose and that’s it. And we need to avoid all pro all sources of fructose.

Is it’s just not true. That’s not true. Does taking purified fructose in a liquid form in high amounts cause problems? A hundred percent. It does. We’re going to see that. But does taking orange juice or eating some oranges or a banana, God forbid you blend it up together. Berries in a banana, that polyphenol oxidase, man, it’s just going to completely ruin the smoothie.

It’s like that’s not going to worsen metabolic function in people, especially if you know you tolerate and especially if you’re a healthy person. If you have metabolic dysfunction, you probably don’t want to smash 60 ounces of orange juice straight off the bat. But if you had, you know, blueberries, banana, and you’re doing fine with it from a blood glucose perspective, fundamentally from the research, we don’t see problems.

And then also, I’m working with clients one to one, I don’t see problems. And if you do have an issue, switch around some of your sources and see what works better for you. So that’s the thing is like extreme perspective. It’s like people are, we’re trying to provide nuance. We’re not even trying to say like, look, take high doses of granulated sugar or fructose.

It’s just, we’re not seeing those same problems of drinking Coke that you see with drinking orange juice. And this will also, this will tie in later on when we start to talk about ozempic and also in this next clip that we’re going to watch here with Dr. Pom.

Ethan Wright:
Yeah, the fructose thing is just something that has like made it into the consciousness, I feel like, of everybody kind of in alt health where it’s like fructose and fatty liver and fructose getting shunted short towards, uh, fat.

It’s just all you hear, like, from a lot of these, um, influencers and whatnot. I think Phuong’s honestly a large part of that too. Because he’s like the researcher behind it, right? It’s Johnson,

Mike Fave:
Lustig, and Phuong was his intermittent fasting research.

Ethan Wright:
Yeah.

Mike Fave:
They’re perpetuating stuff. That’s not realistic.

That’s just not realistic around fructose intake.

Ethan Wright:
And it’s even to the point where like, I love Kelly and Cali means and what they’re doing. And then I like listening to the podcast with them on Joe Rogan. And then it goes to, uh, the, the woman, I don’t know if it’s Kelly or Kaylee, but anyway, she, yeah, it’s too close.

But, uh, and she starts talking about uric acid and she’s citing like Dr. Johnson and making this stuff up about the apple and fructose. I’m like, oh man, what a bummer. The thing

Mike Fave:
is, is like, You have to really look at it in depth because the researchers, even the papers that you look at and what we’re going to see this, they will straight up blatantly say that fructose causes these problems.

And it’s through this uric acid pathway or through fatty liver, like de novo lipogenesis production of fat at the liver. And then when you go look at the papers that they cite and you look at the mechanisms and how they’re done, you’re like, What are you even talking about? This is not a normal consumption that people would have, nor the way that they’re going to consume it, or how their body would be exposed to it.

And it’s like you’re, like, looking at extreme circumstances, and then trying to extrapolate down to, like, the normal circumstances, and that’s not how things work. That’s a logical fallacy. You cannot just say like, if I hit a person over the head with a baseball bat at full force, and then I hit, and then if I hit them in the head with a chopstick, it’s like, it’s going to be the same effect.

That’s the comparison. We have these two massively different interventions in terms of strength. In terms of how, the effect, like what we’re doing to people in the study versus what people are normally doing. And we’re saying, well look, look what happens when you do this crazy thing. And it’s like, yeah, well that’s what, that’s why everybody’s having problems.

It’s just because of the fructose.

Clip: Right.

Mike Fave:
Even though it’s like, in this study, like, they would never have this much fructose ever. Yep, let’s hear from Dr. Fung.

Clip: If you eat, for example, one pound of sugar, you have half a pound of glucose and half a pound of fructose. That half a pound of glucose is used by all 170 pounds of the body.

Okay. But that half a pound of fructose goes straight to the liver, which is like five pounds. So the effect on fattening the liver, the effect on insulin resistance, the effect on obesity is much, much higher for fructose compared to glucose. And that’s why there’s such a huge discrepancy when you compare people who eat a lot of sugar and people who simply eat a lot of other carbohydrates, such as vegetables and root vegetables and bread and all that sort of thing.

So what it means from a practical standpoint is that the very first thing you want to do if you’re trying to lose weight, if you’re trying to reverse your type 2 diabetes, is severely cut back on the amount Added sugars in your diet. I

Ethan Wright:
mean, generally, right? Like the way he ends it with the added sugars thing.

Like, I don’t know, I don’t think that’s bad idea, right. To cut out like added sugars necessarily, but it’s just what that kind of preamble before that with. The fructose kind of being the reason why, you know, first of all, nobody eats a pound of sugar in one sitting period. Like nobody, maybe, maybe, uh, Peter, you might find a Peter on Twitter somewhere.

It’s eating a pound of sugar. That’s okay. Okay.

Mike Fave:
That’s that’s maybe, but that’s a lot. It’s like 450 grams in one sitting. Yeah. So there may be one Peter out there that’s doing that one like pea inspired eateries, lone soldier, mashing, mashing sugars. Yeah. But I would say that yeah. No one’s eating a pound of sugar, first off.

99. 99 percent of people are not eating a pound of sugar. And we know that in the research. Well, I’ll show you there. We have a quote here to support what we’re saying. So that’s the first thing. So like, it’s like, I know he’s doing it for example purposes, but it’s not even fundamentally what happens, right?

Most people are having mixed meals, and the mixed meals will include some starches, some sugars, right? If you get up, even if you get a Big Mac, and you get your 32 ounce Coke or 16 ounce Coke on the side, Right. You’re not going to have like all the carbs in that meal. You have the bun and then you have the, the, the, um, the soda.

The soda is only half fructose and the bun is all glucose. Is it starch? So even then you’re not eating a pound of sugar and you’re not getting even close to as much fructose like 200 and 220 grams of fructose that you would see, even if it’s high fructose corn syrup, it’s still roughly 50 50. It’s like 55 45, right?

55 percent fructose, 45 percent glucose. So you’re still not going to see that level of intake of fructose that he’s talking about. This is an example. So number one, that that’s, I know he’s using it as an example, but that’s not even what happens. People aren’t even approximating close to those intakes.

Um, from the get go. Now, the next thing is, if we look at what goes on with fructose metabolism, right, this, it’s true that the liver will take up the fructose, but it is not true that the rest of the body then doesn’t metabolize the fructose. And the reason why is fructose is taken up by the liver, and then it’s converted into a bunch of other things, including glucose and lactate, and also directly to CO2 and ATP, By the liver, an extra hepatic metabolism, on this graphic here, by the way, is from other tissues.

So, the liver converts the fructose to a bunch of other things, and then those get shot out, and then the tissues use those things. So, whether the liver takes up all the fructose or not, it doesn’t matter, because the fruit, the liver, is converting it to other things, and then the rest of the body is then using those things.

As well as the liver using those things. The conversion of fructose to lipids, which is what Dr. Fung is trying to say here, is that, oh, you know, the fructose at the liver, it’s gonna increase lipids, less than 1 percent de novo lipogenesis. Less than 1 percent converted to lipids. They know this in the research now, it’s like blatantly clear, so it’s factually incorrect.

First of all, nobody’s eating a pound of sugar, so nobody’s getting that high dose of a fructose in one sitting. And then number two, the fructose can be converted into other components, and then the body can still use those components. So it’s not just like the liver gets saddled with all this fructose, and it’s screwed over.

It’s the liver turns it to other stuff, and the rest of the body can still use it. So that’s the next thing. Then the thing after that is that it’s not even converted mostly to fats. It’s converted to glucose, lactate, glycogen, and it also turned into energy. So there’s fundamental issues with that perspective altogether.

Like just looking at this alone and we could talk about uric acid and everything else because if it’s not the fructose being directly converted to fat, the next mechanism that gets promoted, which ties in with phone and also with Dr. Johnson’s perspective that okay, it gets converted to uric acid, but it actually doesn’t under normal circumstances to any significant extent.

And we’ll look at that, but I’ll, I’ll leave the floor here. It

Ethan Wright:
wasn’t hard to necessarily find something like this, right? In terms of the research, like, where is he pulling the fact that it’s going also fat? Yeah. Or what is like the hypothesis that you guys that’s driving that? I don’t know where some,

Mike Fave:
somewhere somebody said it, they talk about it in the research, but the research is pretty clear that fructose doesn’t just get converted to rep.

This is Lustig stuff, right? So Dr. Lustig is the one, the guy who’s saying that, you know, fructose just gets converted to fat. And Johnson’s the one saying, no, it’s the uric acid. And then, you know, so, so like there’s the researchers are like in their individual camps and are trying to like parse out the mechanisms.

But in the, when you go through the papers and broad and you start looking at the mechanisms like the conversion of fructose directly to lipids is not that significant. And then with that, if you were to eat a bunch of butter, right? So say you’re going to smash butter in your meal. If the fructose gets converted into stearic acid or palmitic acid, which the sugars get converted to stearic and palmitic, and then they can be desaturated into oleic and palmitoleic acids, right?

If you’re eating butter, which is palmitic, stearic, oleic acid. You’re just getting those fats anyway. Like, if you were to eat the fat, you would get those fats at the liver regardless. Number one, fructose isn’t converted to fat. If you were to eat a high fat diet anyway, you would be taking those fats and the liver would process them as well, right?

It’s gonna go through the liver to a large extent. Now, it’s not the same in the intestine, so to be clear, to be very precise, carbohydrates get taken up to the portal vein, go directly to the liver, fats get taken up into the lymphatic system through the lacteals and circulate and still make their way to the liver.

But still, if you’re taking up fats, you’re gonna get, you’re, you’re gonna get the same fats that you would make glucose or fructose into regardless. So you’re seeing that regardless. So then the next mechanism that gets promoted here is they start to talk about your, like, then it’s like, okay, well, it’s uric acid.

Because fructose depletes hepatic ATP is what they say.

Ethan Wright:
The idea with the uric acid thing is that it just doesn’t get, like, you end up with an abundance and you can’t clear it. Is that like why it’s problematic or what is the problem that they’re saying with a ton of uric acid?

Mike Fave:
I could show you in the paper directly.

Um, let’s just go to it. Let’s see. So, because I think this will be helpful to specifically describe it. When fructose gets created, it, it gets turned into the same products that glucose does. But glucose has a rate limiting step that fructose doesn’t have. And so, and that this step requires ATP. It’s that fructose kinase, right?

Fructose kinase C. So what happens is fructose gets converted into fructose 1 phosphate, a fructose kinase C, which requires ATP. When you get a bunch of fructose coming into the system, there’s no rate limit on this, like it’s not stopped by anything. So it just keeps getting converted through this enzyme and using up ATP.

And what they wind up saying is, The ATP gets depleted, it gets converted to ADP, and then the ADP gets converted to AMP, and then that AMP gets converted to uric acid. And so they’re saying that the ATP, ATP depletion because of fructose at the liver, and it creates problems at the liver, first of all, and then second of all, that the conversion of AMP to uric acid creates issues, which it does, because xanthine Which converts it’s it’s important in multiple steps in this pathway converting hypo xanthine xanthine and xanthine to uric acid Creates reactive oxygen species.

So create stress, right? So it creates oxygen just so they’re saying that your oxidative stress inhibition of protein synthesis mitochondrial dysfunction so their idea here is that the fructose depletes ATP because of the way that it’s metabolized differently than glucose and Then what winds up happening is it creates uric acid?

You Through, um, the uric acid pathway, right? So through this, this pathway here. So ATP goes to AMP, which goes to uric acid through these steps. Now, the problem is, is that you need a lot of fructose to do this. Like, it’s not just like you have it or like an orange and that this problem starts to happen.

And so, what they say here, and this is what we’re going to get into, they say, this, and this goes to the quote that I was talking about, where I was saying that fructose doesn’t go to, um, de novo lipogenesis. They say, although it has been known that fructose can be converted to both plasma and liver triglycerides, this has been, so that’s fats, this has been found to not be the major factor contributing to fatty liver.

Instead, fat accumulation primarily occurs in the liver as a result of fructose metabolism in the liver, causing impaired beta oxidation, so the burning of fats in the liver, and enhanced de novo So they’re, they’re saying it, that’s the cause, but then they start to talk about why that happens and see that pathway just discussed.

So they say, as the metabolism progresses through various steps, the end result of this pathway, so this fructose metabolism, is the production of glycogen, glucose, and triglycerides. However, so we saw that in the previous picture that I showed, that most fructose is actually converted to glycogen and glucose.

And then they say, however, the decrease in ATP that occurs as fructose finite, fructose kinase C phosphorylates fructose results in the activation of adenosine monophosphate deaminase. So basically it’s waste ATP and an ATP gets converted to AMP. So that results in the transformation of AMP to inosine monophosphate.

This results in nucleotide turnover and subsequent uric acid generation. The consequence of this fall in ATP and elevation uric acid include oxidative stress. mitochondrial dysfunction, which can further lead to obesity, insulin resistance, and fatty liver, eventually culminating in metabolic syndrome.

Furthermore, fructose kinase may also cause hepatic insulin resistance, which can contribute to metabolic syndrome and further progression of NAFLD. Um, it should be highlighted that insulin resistance caused by fructose ingestion is likely due to accumulation of serum uric acid, which can increase oxidative stress and blunt insulin sensitivity.

Um, so basically what they’re saying here with these quotes. is that fructose is metabolized differently than glucose. Just that one step that causes the production or the wasting or utilization of ATP, which drives the production of uric acid. Now that wasting of ATP and production of uric acid are what they say is causing fatty liver, diabetes, insulin resistance, metabolic syndrome.

However, in normal people, Or even in diabetics and type 2 diabetics, we do not see this happen. And that’s fundamentally the problem. So, just going through the pathway really quick again, just so that it’s clear. Fructose does not get converted directly into fat very heavily. Period. This paper saying it, we saw the conversion pathways in the other paper.

So we can throw that out. Dr. Jason Fung is not correct on that. I’m not saying everything he’s saying is wrong. Like, if you’re a diabetic, the first thing you do is stop added sugars. Like, sure, we all agree. Like, let’s shake hands. We agree. We’re on the same page. The description as to why we’re doing that, I don’t agree with, and it’s not because fructose just causes, like, fatty liver because it increases fat production, so it doesn’t.

But what it, there, now the next mechanism, and this goes in with Johnson and, and Fung here, is that it’s through uric acid generation. But the question is, does this actually happen in general? And so, I’m not just gonna tell you that it doesn’t happen, I’m gonna show you that it doesn’t happen, because I think that it’s extremely important that we, like, we show our sources here.

This paper, uh, is called, The effects of fructose intake on serum uric acid vary among controlled dietary trials. So this paper was cited in the previous paper as support for what they were saying. Now, I don’t know why they supported, cited that paper as support, because it doesn’t fully support what the researchers are saying.

And this is where I think that people get a little bit mixed up, because they’re just reading that, like, if you just read that paper that I just read you, then you would think, oh, like, yeah, fructose causes a problem, but then you have to look at their sources. So the source they say here is, the effect of fructose and isocaloric exchange for other carbohydrate on uric acid was not significant in pre diabetic and diabetic participants.

Mean difference was, uh, they say here, negative 4. 09, um, with a confidence interval of negative 23. 7 and 15. 6, and non diabetic participants. So basically, fructose is not significant. And isocaloric exchange. So if you take somebody who has a hundred grams of carbs a day and you keep their calories the same and you switch, you increase their fructose intake.

So that means a hundred grams of fructose or 50 more grams of fructose, but you take out the other carbs, there’s no increases, no significant increases in serum, your acid value. They continue they say the lack of effect was found consistently across trials without any evidence of interest inter study heterogeneity So the studies were pretty consistent and they said systematic removal trials during sensitivity analysis did not alter the conclusions So basically if they start trying to just like pull trials out and see like does that make a difference?

They basically show that it doesn’t all right So if you have the same amount of calories And you have, you exchange with fructose, you don’t really see a problem in normal humans, right? And, uh, not even in normal humans, in diabetic and pre diabetic humans. So people who are metabolically impaired. So you’re not seeing this pathway play out to a large extent, at least based on serum uric acid values, right?

So we’re not seeing this huge bump in serum uric acid. The reason that’s important, again, is because that was described as a major cause. for fatty liver, diabetes, et cetera, et cetera, et cetera. By Dr. Richard Johnson, excuse me. I would give him the credit, respect, et cetera. And then, uh, by Dr. Jason Fung kind of invoked some of this to some extent.

Here’s where we see the shift. They say, so there was a significant effect of hyper caloric. So if you have a 30 percent increase in energy, so you take your regular diet and you eat an extra, you eat one third more of calories and in the form of fructose, That’s pure fructose mixed in water, like liquid fructose drink.

So, there’s a significant effect of hypercaloric plus 35 percent of energy fructose on serum uric acid in participants without diabetes. A large uric acid raising effect of hypercaloric plus 35 percent of energy in the form of pure fructose was seen without any evidence of inter study heterogeneity.

So, basically what we’re seeing is that if you feed people a caloric surplus. So a 30 percent caloric surplus. So if my caloric requirement is 2000 calories a day, I’m going to eat 2, 600 calories a day. Probably actually, probably closer to 2, 700 and I’m going to do that extra 700 calories just to be straight up fructose.

So I’m just going to like smash pure fructose and water like liquid fructose. All right. Now here’s what they say from there. They say the three hyper caloric trials in this meta analysis, Fed fructose at 35 percent extra energy or an extra or a total of 213 to 219 grams per day of fructose in fluid form in non diabetic males for one week, a level of exposure that is more than double the 95th percentile, which is 87 grams per day of fructose intake in the U S.

So they fed people, they fed guys, they don’t have diabetes or anything, but they fed them more than twice as much fructose than what you would see. In a, in the typical diabetic, uh, consuming person at then like the top 5 percent of people in the U S to consume fructose, right? It’s like the people are consuming the most fructose.

They fed them twice, more than twice as much as what those people were eating. And then they said, Oh yeah, I raised serum uric acid. That’s why I’m saying like, if you hit these guys with a bat, is that the same thing as hitting somebody else with a chopstick? Right? Like it’s completely different. The thing that gets even, even better here.

They say at these tremendous doses, the resulting 31 micromoles per liter increase in uric acid has the potential to place many individuals at risk of hyperuricemia. Where the mean, uh, where the mean serum u your urate concentration in US adults are 36 micromoles per liter in men and 290 micromoles per liter in woman.

Um, now what is a 31 micro mole per liter increase in serum uric acid that is roughly a 0.5 milligram per deciliter increase in uric acid. which the reference range for uric acid is 3. 5 to 7 milligrams per deciliter. So if you were at four milligrams per deciliter uric acid and you decided that you wanted to take in 219 grams of fructose a day in the form of purified liquid fructose, at least as a healthy person, you would go to 4.

5 milligrams per deciliter on average on your serum uric acid, which is still completely within range. And it’s below the therapeutic target for treating gout, which is six, six milligrams per deciliter. So, it’s like, number one, you have to really try to, to cause this effect in the liver with really high fructose intake that you wouldn’t normally see in people.

And again, what we saw with the Coke versus orange juice study, the orange juice lowered uric acid versus the Coke. So if these guys took in their 219 grams per day of fructose from orange juice or orange juice plus whole fruits. Are they gonna still see this same bump in uric acid? And I bet you money they won’t.

I bet you money they won’t. We don’t have a study for it, but based on the other study comparing Coke and orange juice, I bet you we will actually see either no effect, either, uh, at the minimum, a very minor effect. And at the maximum, maybe a benefit.

Ethan Wright:
It’s just doing that much fructose at one time would be a recipe for digestive issues too, right?

Mike Fave:
We didn’t even talk about this. Like I talked about it, Jay and I have talked about our energy balance and I talked about it on Paul’s podcast where we did, we talked about lust, dig steak on fructose. And basically what you see is like the human intestine will absorb between 5 and 50 grams of solo fructose by itself.

Ethan Wright:
Yeah.

Mike Fave:
And so you can, basically what happens if you get, say your intestine only absorbs 10 grams by itself, if you take in 75 grams of fructose, you’re gonna absorb 10, and there’s no glucose present. If there’s glucose present, you’ll absorb all of it if it’s one to one. But say it’s just fructose, which is mostly what they’re feeding these people.

You’ll absorb 65 grams of fructose. And the rest of it will sit in your intestine, and the bacteria in your gut will be like, It’s a party, it’s a field day, we’re gonna enjoy all this fructose, and then they’ll produce endotoxin. That’s what you see in the rat studies, is endotoxemia, and then endotoxemia will cause liver problems.

So, is it just fructose, or is it endotoxemia? And also, like, who is doing this? Who, even if you’re drinking high fructose corn syrup slurpees from 7 Eleven at 32 ounces every single meal, you’re still 55 45, uh, fructose to glucose. So it’s still almost 1 to 1. You’re not even getting purified fructose. Now, there’s other problems with those things, so I’m not condoning people do that, but fundamentally, like, This is, like, a weird way to say, like, this is the cause of the problem because it’s not really directly applicable to people in general.

And it also, like, then to extrapolate out that fruit and orange juice is the same, we already have studies showing it’s not, it’s fundamentally incorrect and logically incorrect.

Ethan Wright:
Yeah, and it’s just crazy to think that people will hear Uh, these guys talk online about the problems with fructose and like that will, that will literally make people scared to eat like true.

Um, and it’s like, even if you were doing like, you couldn’t try to eat as much fruit to like replicate this study. And even so, like, maybe you wouldn’t even run into some of the issues that they’re talking about, you know, here, which. Yeah, it kind of really puts the nail in the coffin like between, okay, the fructose isn’t going towards fat.

And then this other thing that Lustig and Dr. Lustig and Dr. Johnson are talking about with the uric acid pathway. I didn’t realize that that was like the path and then why it was like the oxidative stress that’s that’s technically the problem. But yeah, that you don’t even get like a major bump in, um, in the levels.

So yeah, quite, um, that was quite the breakdown. I think that will be helpful for people to see, like, and kind of alleviate their fears when they go to eat their banana or berries or, uh, you know, watermelon or whatnot. So yeah, that’s really helpful.

Mike Fave:
Yeah. And it, and just, uh, just as an example, like both you and I.

Are eating very high fructose intakes. It’s just all from fruit. Neither of us are dealing with diabetes. Mine is, I don’t know your recent lab tests, but for my personal lab tests, like, I, I put them online, like, you can see them. And you also have Paul Saldino has his lab tests, you can see them. And I also know for a fact that Jay is, Jay’s lab tests also support this, and I have other clients as well, but these, like, You, you, Jay, Paul, and I are all public about it.

And it’s like, we’re not seeing, like, super high fasting glucose. Hemoglobin A1C is over refer My last hemoglobin A1C, I think it was like 5. 3 or 5. 4. And then, and not seeing like high uric acid values, not seeing signs of fatty liver, like I, we, I’m going to make a video about this, but I just did a bioelectrical impotence scan to see what’s going on with my, with my body fat percentage.

I’m sub 10 percent right now. I’m not saying that’s ideal, but it’s like my fructose intake is not making me fat, diabetic, obese, et cetera. Although to be fair, it’s coming entirely from fruits, whole fruits, stuff like this, papaya, pineapple,

Ethan Wright:
um, things like this. All these components. Yeah, and I’ll be back in the U.

S. soon. Maybe I’ll get my labs drawn and then, um, we could do an episode breaking down my labs or your labs. Yeah, yeah, that’s great. I’m happy to do that. So, with, with clients though, so you’re saying is even clients that are in like a diabetic state or they’re trying to lose weight, like fruit, fruit juice, fructose and stuff is completely on the table.

As long as their tolerance to it, like digestively, um, and with like blood sugar and stuff like this is managed appropriately. And a lot of the strategies that you’re using to like affect those things or what, what you’re doing with the diet outside of just including the, The fruits or fruit juice or whatnot, like how you’re including fiber in meals, you’re having square meals, you’re having protein, you’re having adequate fat, and all of that is helping to like improve the person’s response to the, um, to the, to the sugars, to the fructose.

And a note that you made when you were covering the fructose in particular is like, If you do have, um, a fruit that’s higher in fructose than, um, glucose, you can pair it with something like rice or whatnot. If the digestive tolerance is a, is an issue and then you can like, um, you know, even out the ratio.

Mike Fave:
So two things I’m going to, I’m going to address them kind of out of order a bit. Okay. So if If you have, it depends on the person, right? Some people can do like 50 grams of fructose without glucose and digest it. But for other people, it’s like five grams and you’re like having a problem. Like if excess fructose in ratio to glucose.

Um,

Clip: okay.

Mike Fave:
So if ideally you want to get one, I try to shoot for one to one in client’s diets, just, just to minimize digestive issues off the bat. And chronometer is really great for this. Cause you can actually see a breakdown of your glucose to fructose ratio. You’re, you can even see a mega three to mega six ratio.

I’ve made videos discussing this. You can check it out on the channel. But basically you can, you’re going to try to manage the ratios. And if you have, say you have something like mangoes or apples or watermelon or pears, which are not really great in terms of glucose, fructose ratio, and it’s not the FODMAPs in them.

The other problem, the fermentable carbohydrates, uh, fermentable fibers are if they’re not the problem, if it’s more the, the fructose content, if you have like to have the watermelon in the meal, that has like some glucose source, potatoes or rice, something like this, You may be fine tolerating it because you have the glucose present, but there’s also like watermelon can, can have FODMAPs which can drive the, like digestive issues, bloating gas, the runs, et cetera, especially in higher quantities because of the FODMAPs and may not even be the glucose to glucose ratio.

So it’s the same thing with apples and pears. Also cooking apples and pears can help make the better. And then like even cooking them with a little bit of fruit juice can make it better as well because it’ll, you know, sweeten it up and then also can help to improve the ratios a bit because the fundamental thing is the ratio.

If you’re really skewed, In terms of fructose, which apples are, pears are, mangoes are, watermelon is, then you can get, you’ll get digestive issues from it. So yeah, so you can, you can balance it, but again, FODMAPs may still be an issue. And then when we’re looking at the diet, it’s, this is the thing is like, everybody’s like carbs versus fats, plants versus animal foods.

It’s like, there’s a ladder of things. There’s a pyramid of things that we’re looking at. What’s your total energy intake? How many calories do you need to eat for your goal? Period. Are calories the be all the end all, like this calories in, calories out stuff? No, there’s fundamental issues with it. But calories are a tool that helps you get an average estimate of what your total energy intake is across different foods that are not comparable to each other.

A steak and blueberries are way different. Like, if you looked at a cow and you looked at blueberries, you’re like, well, tell me the similarities. You say, well, I don’t know, like, they’re both alive. Look, that’s fundamentally it like they’re, so the calories allow you to kind of compare energy composition between them.

And that’s it. So it’s a tool. It’s not the be all to end all. So first is calories. What’s your estimated intake? And we’re talking about bioenergetics here, right? Like we’re talking about energy fundamentally. So calories are helpful because it allows us to know how much energy you need. Are you too low?

Are you too high? Are you just right? And then run from there. Then it’s macros. You want to have an adequate protein intake. And we’ll talk about this. We’re going to talk about an ozempic in just a second. You need adequate protein intake, we’re shooting for that 0. 82 grams per pound. And then that’s to maintain your lean mass.

And then from there it’s fat and carb intake. And then you’re going to figure out how much fat and carbs you want to use. And those kind of slide back and forth with each other to hit your caloric target. So then you’re going from there. Then you have to figure out what foods you want to use to hit those targets.

What foods do you tolerate? What foods do you like? Do you want to prep or do you not want to prep? I’m lazy if my wife’s not here. I know it’s rotisserie chickens and I know it’s whey protein because I don’t have to cook when she’s here. I’m eating good So there’s a lot of factors that come in with that But you know It’s quality of food micronutrient density the foods that you like the foods that your digestive system tolerates and engaging from there and then after that it’s then you Can talk about food quality specifically.

It’s like you probably don’t want to eat like McNuggets for your major chicken source Like it probably be better to just have like regular chicken breasts that you cook up yourself at the minimum, maybe like a high quality rotisserie chicken, or if you go to a restaurant that cooks well and you get the chicken there, or if it’s a steak or something like this, fine, do something like that.

Probably not Lunchables ham slices, probably not a good idea to hit your protein target. You want to have like a good source. You want high quality food and if it’s grass bed, organic, all this type of stuff. Great. Then after that, it’s like micronutrient density. Now, a lot of your micronutrients are going to be covered when you get this other stuff down pat.

But then it’s micronutrients, vitamins and minerals are those topped off. You want to make sure that that stuff is all topped off. And that’s between diet and between supplements. So we’re not just looking at, you know, animal foods versus plant foods, calories in calories out. If it fits your macros, um, carnivore versus vegan, uh, keto versus high carb.

It’s like, it’s, we’re taking a fundamental look at diet. We’re taking principles from all of those things. We’re getting out of these dichotomies and we’re saying, what are the targets across all of this pyramid that we’re going to use to hit your particular dietary requirements. And for weight loss, it’s just managing your energy intake within that whole pyramid.

All of this is important in managing the diet. It’s not these dichotomies anymore. Who cares if it’s high carb or low carb, or if it’s plant foods or carnivore or vegan. It doesn’t matter. Like, that stuff is irrelevant to think about. It’s more, what do you need? In your diet that you tolerate based on your personal context to reach your goals and live a healthy life and

Ethan Wright:
maintain that long term.

One of the things you mentioned there too was that you do have to keep track of your like total energy intake and things like this. Um, I think a lot of people when they come to bioenergetics have this idea that when I start including foods in my diet, like coming out of the restrictive, uh, dieting and I’m eating carbohydrates and orange juice and all these things, my metabolism is going to turn into a firehouse.

And I’ll be able to like raise my basal metabolic rate so high that it won’t matter that I have my Haagen Dazs ice cream, you know, for lunch and dinner, and I’ll just be able to maintain like my lean physique and all this kind of stuff. And so I don’t know if you have any thoughts like the death, like maybe you do have to manage your energy intake.

There has to be somewhat of a deficit. Um, and how you go about that in terms of working with people and getting that idea across.

Mike Fave:
Yeah, that is a bioenergetic myth. It’s a myth, okay. The mythical endless metabolism.

Ethan Wright:
Man, shucks.

Mike Fave:
Yeah, I mean, if you’re coming from a severely restricted background, you will, you’ll find that you could probably eat more over time, especially, again, there’s a lot of factors involved in what you may be eating and still maintain weight and potentially lose weight, depending on what’s going on.

If your thyroid function is low and you correct it, like, yeah, you’ll probably be able to eat more and, like, a lot of things will be better. But can you just eat more and then your metabolism will just massively increase over time or once you become poof or depleted after four years You can eat without as much as you want and then your weight’s gonna just magically come off like that is not reality I haven’t at least I haven’t seen that play out and there is a point in time Where I was like flirting with that idea Like I could just endlessly eat and I won’t gain weight and it’s like there is a point that you will gain weight Like there’s like I gained weight It required a lot of food for me and it was hard for me to do because I limited myself to only eating whole food sources to do it.

And I also was working out and I had a lot high lean muscle mass, so I had a lot of room to go. But if you don’t have a high lean tissue, then your caloric requirement is lower because your lean tissue is going to dictate your business metabolic rate and your activity is going to be the next factor. So you need to know you’re, you want to keep your lean tissue high and then you’re, you’re gauging your caloric intake based on that because you’re a lean tissue.

Your muscle mass, your organs, your bones, your, your skin, your hair, your nails, all this type of stuff is what has the most metabolically active tissue. This is what’s really driving energy metabolism. Fat tissue is not. And so you need to gauge based on that. And so we’ll talk about this when we get into the ozempic stuff here, but if you drop your lean tissue, you’re going to screw your metabolism.

That’s what this yo yo dieting stuff does. And then when you have, and this is, you know, when you start to increase your lean mass or at least maintain your lean mass, you take body fat off, you can still eat quite a bit, uh, or at least the same amount that you were eating without gaining weight, even though your weight is lower because you still have this lean tissue.

So lean tissue is extremely important and there’s, your body is not going to endlessly ramp up metabolism. It will increase metabolism, but we’re not talking like a 200 percent increase. Maybe there’s a 10 percent bump from thermic effect of food, or things like this. Maybe there’s a range with the thermic effect of food.

There’s a bump with activity level, higher lean mass will change these things. Fundamentally, like there’s not this endless spectrum and that’s why knowing your caloric intake is extremely helpful to know why you’re gaining weight, why you’re stressed out, why you’re losing weight, why the scale is not moving, all of this type of stuff.

This is where the energy intake becomes extremely important to understand. Again, it’s not the be all to end all calories in, calories out stuff. That’s not, I’m not saying that that’s what it is, but it’s like that understanding of it, like eat less, exercise more stuff, that’s useless. It’s how much energy do you need as an individual based on your context?

How much exercise do you as an individual need based on your context? It’s not the more you eat or the the better or the less you eat the better or the more you exercise the better The less you exercise the better there’s a specific threshold that you are shooting for There’s a goldilocks zone and that’s what we’re working towards.

That’s what i’m working for with clients trying to find that spot Based on their goals. Somebody like, if you want to gain weight, it’s going to be different for you, Ethan. If based on your muscle mass and your activity level and stuff like this, your caloric intake and dietary setups can be drastically different than a, than a lady that I’m working with who’s post menopausal and weighs, you know, 120 pounds is very low lean mass.

Like your diet setup is going to be very different or in say she’s type two diabetic as well. There’s going to be different adjustments and caloric intakes can be drastically different because of that. And that’s why knowing the

Ethan Wright:
calculation is important. I just think with people who have done the caloric restriction and the keto dieting, if they do it for long enough, they do see like, man, I just, I’m now I’m putting on weight at this level of calories.

I have to go even lower and you have to keep going lower and lower and lower. And. You know, uh, like the idea that it would work in the opposite direction as well, like infinitely would be a nice, um, a nice thing, but I guess there’s a, there’s a limit. Um, so yeah, that’s an interesting point that you make about the lean mat stuff.

Like, Because what you’re saying about the low carb dieting, that is something I hear a lot from people who have been doing fasting and keto is that they are losing muscle, but they’re putting weight around the midsection area. And then they’re also having to simultaneously drop calories in order to, you know, Continue losing weight, but it’s not really like fat loss.

Like, I think that’s an important distinction to make is that what you’re after is actually losing, losing fat and preserving muscle mass. And I know we’ll get into that with the Ozempic, uh, clip here. So maybe we should play that and then touch back on that. Ozempic and all of those drugs

Clip: for almost everyone.

If you don’t want to be obese anymore, you just take the medication and you won’t be. But if you do, you just don’t take the medication and you will be. Why is, why can just one pill or one injection do so much? Because it makes you less hungry fundamentally. And then when you’re not really hungry, you stop eating as much food and all these weird other hypotheses about why we were getting fat.

Ozempic kind of crushed all of them out. How does it just do all that? Yeah. Okay. That’s, that makes sense. I think some people have an issue with the fact that they feel like it’s kind of cheating. You know, I had to get there. The I’d love to tackle that one. Okay. Yeah. Your ability to lose weight can be a test of your willpower or you can take the pill and with no added willpower, lose all the weight you want.

And then you can test your willpower on tending to your family better, being a kinder person to others, coaching little league football and being on time for the kids instead of standing in a Hardee’s line, getting your third cheeseburger for that.

Mike Fave:
Yeah, that is a little harsh. It’s just disrespectful.

Yeah. It’s just super disrespectful. Um, cause it’s like disparaging to people. It’s like, the re this is the same message for people that, you’re just fat. Or you’re just obese. Or you have this problem because you’re just gluttonous. And I think for a lot of people like, it’s a la especially with clients that I’m working with, it’s a lack of understanding of what they need to do to lose weight.

And then the other thing is, to say like you just take this medication and you will just lose weight is false. It’s absolutely false. Period. Period. And it’s known in the research, in the semi glutide study, they had to do 150 minutes a week of exercise, plus a 500 calorie deficit per day, and take the medication to lose roughly half a pound a week.

So like, you just take the medication, you don’t do anything else, and you lose weight, is a lie. The reason the medication works is because it nukes your appetite, so you still have to eat less. If you hop on the drug, and then you just continue to still eat, and eat, and eat, and eat, You’re not going to lose the weight.

It’s just nuking your appetite. On top of the fact that if you then continue to eat and you’re on some of these drugs, you’re just going to get serious digestive issues. It’s condescending to people. It’s a lie that you just take this and you just lose weight. And it also doesn’t talk about a risk reward analysis.

Like this is a really smug way to describe what goes on and is unhelpful to people.

Ethan Wright:
Uh, at least for the people that I talk to, like, they don’t want to go about solving their health issues by taking, um, pills or like, you know, whatever it is that’s being prescribed, whether it’s metformin, or statin, or, or ozempic, and it’s like, every single time they go to the doctor, that’s all they necessarily, they, they get, right?

It’s like, there’s these other, there’s problems with the drugs that you’ve talked about in other videos, and like you’re about to talk about in, with ozempic. . Uh, but it just seems like yeah, like a people’s lack of, um, knowing exactly what to do and like, you can’t blame them. ’cause look, when you go into the nutrition sphere and old health and you got Dr.

Johnson saying Yeah, if you got fruit, like you’re, you’re done. You know, and you’re game over. That’s diabetes. Yeah. Everything. And then lut, it’s like, yeah, fructose just inherently wants to be fat. And so you’re, it’s like kind of like, alright, what do I do? And then I’m doing this low carb stuff. And I got to keep on dropping calories and I’m losing muscle mass and all this kind of stuff.

So it’s confusing. It’s confusing. I watched the video that you did on GLP one agonist on the my fav science channel. And I know you’re going to cover some of this stuff, but it’s like. The, what’s required of you and then what the rebound effects of taking the drug is like an important consideration before deciding to tell everybody that like, if you just want to lose weight, just use those, just like take the pill.

Is it worth it? Like, what are the pros versus cons of using this? I think people are really trying to decide, you know, whether or not this is a viable strategy for them at times if the problem is super severe. So I think it’s important that they have the full picture. Of what, what the outcomes of these things are, what could happen.

Mike Fave:
So this study is agonist for the treatment obesity role as a promising approach. And so we’re going to get down here to this quote. So this is on semaglutide. semaglutide as an example. And if you want the full breakdown of all this stuff, I made a video on the Mike Dave Science Channel going through it for like an hour, all this stuff, but we’re just going to go through it quickly here.

I’d say more than 1, 200 patients with type 2 diabetes complicated with obesity were randomly divided into semiglutide, or placebo and given once a week step 2 research. Uh, they say the weight loss ranges of the two treatment groups were minus 6. 9 kg and minus 9. 7 kg respectively. So these are for the two groups, right?

Now, something to keep in mind. They say here, so this was, this was for the step two, then the other one they, they have here, we’ll talk about this really quick.

They then say, in the step one trial, widening it all recruited 1, 961 non diabetic adults with a BMI of greater than 30. Uh, the semi glutide group once 2. 4 mg, so the 2. 4 mg once a week was treated for 68 weeks. The average weight loss was 53 kg. Um, so basically what we’re seeing is that with the semi glutide.

If you take the 2. 5 milligram dose and you do that for 68 weeks and you’re not a diabetic, right? You’re just, you just have a BMI greater than 30. The weight loss they saw was about 15, 15. 3 kilograms. So that’s 15. 3 kilograms over 68 weeks. So what we’re looking at roughly, and it’s going to be important.

So 15. 3 times 2. 2 is 33 pounds divided by 68 weeks. So half a pound a week of weight loss. Now, what they’re not saying in this paper, and as you have to open up the other paper and look at the step one trial that they cite, you have to go to paper 100 here, you see it’s purple because I read it, and also paper 99, uh, the 99 citation.

What they say in those papers is they say the treatment group was semiglutide plus 150 minutes of exercise per week plus a 500 calorie deficit per day with semiglutide. So you still have to do be on a diet and you still have to exercise, right? So you’re still, you still have to fundamentally do that.

And you’re going to lose half a pound per week taking semi glutide. If you are greater than on app. So roughly have a pound per week on average. If you start out at greater than a BMI of greater than 30. So technically a obesity classification. Now here’s what they don’t tell you, right? This is the next piece that’s important to get into.

So, keep, by the way, keep half a pound per week in mind. This paper is titled, A Review of the Effects of Glucon Like Peptide Receptor 1 Agonists and Sodium Glucose Co Transporter 2 Inhibitors on Lean Body Mass in Humans. Right? So they say, In over half of the studies identified, the proportion of lean body mass reduction ranged between 20 percent and 50 percent of total weight loss, which is consistent with diet induced weight loss and bariatric surgery.

No clear differences existed between agonists and sodium glucose transporter inhibitors. Consequently, the loss of lean body mass and skeletal muscle associated with weight loss induced by the SGLT 2 warrant attention. Strategies to preserve skeletal muscle and improve physical function, for example, through structured exercise are of great importance.

So, we have half a pound a week weight loss with, with the, with semi glutide. It also required That people exercise 150 minutes per week and run a 500 calorie deficit per day. And what we’re seeing is a 20 to 50 percent loss in lean muscle mass, lean body mass with these, with these, uh, with these studies, uh, with these drugs.

It gets even better, gets even better. The next thing here is I have some quotes and we’ll throw them up on the screen. The adherence for these drugs is terrible. So they say here, , the medium time to discontinuation for, for the, the, the study’s talking about the, the, the GLP one drugs was 13 months. The discontinuation rate was 47%, 47.7%, and 70.1% at 12 and 24 months respectively, with difference at 24 months for age and dosing groups.

So basically at, after two years, 77, 70 percent of people hop off these drugs, right? So you may lose a half a pound per week. You’re still going to have to exercise and you’re still going to have to be in a caloric deficit of 500 calories per day. As per that study, and you’re probably going to lose 20 to 50 percent of the weight as lean body mass.

And you’re probably going to quit between one and two years, right? Now, how fast are you going to regain the weight? So, for lyric glutide, they say, in our study, glutide alone was associated with a regain of 6. 3 kilograms fat mass after one year, corresponding to a regain of more than 70 percent of the fat mass reduction after termination of lyric glutide alone.

So, they’re gaining, in one year, you’re going to gain 70 percent of it back, once you stop. Alright? Then the next thing that we run into here is semaglutide. Following treatment with withdrawal, semaglutide and placebo participants regained 9 percent percentage points of lost weight, respectively, by week 120, resulting in a net loss of 5.

6 percent and 0. 1%, respectively, from week 0 to 120. Cardiometabolic improvements seen from week 0 to week 68 with semaglutide reverted towards baseline at week 120 for most variables. So you’re only seeing, you’re only gonna retain, you’re not gonna retain most of the weight loss. That you see even with semi glutide or earlier glutide.

And then the cardio metabolic benefits also go away. So you have to exercise. You still have to be in a deficit. You’re probably going to lose lean mass unless you set things out appropriately. You’re probably going to quit between a year and two, between one or two years after 70 percent of people are quitting at 24 months.

And then you’re probably getting regained maybe 70 percent of the way back within a year. So it’s like, is this worth it? Is this the cure? Did I be it to, to obesity? That Mike is discussed. Just, just take the drug.

Ethan Wright:
Just take the drug. Yeah. That seems like a really bad trade. And then like, Oh, I mean, correct me if I’m wrong, but half a pounds a week for six, 68 weeks.

Is it like a miracle, right? Like, I mean, when you’re working with clients and you’re trying to lose, get them to lose weight, are you, what’s the range you’re typically shooting for? Like weekly?

Mike Fave:
Uh, it depends on the person, but I have, I’ve had people lose one pound a week, two pounds a week, all the way up to five pounds a week.

I

Ethan Wright:
see. And then that like, yeah, that trade is horrible because you have to somewhat do the diet, dieting, right? Because you have to be in a deficit. I guess the idea is that the drug will keep you in a deficit. Like, it just makes it easier to not eat.

Mike Fave:
That’s it. Because, and the reason that you’re not eating.

It’s because it slows down your digestion, makes you throw up, makes you nauseous. But not to mention the side effects of it that again, I refer out to that video because it’s, you know, I don’t want to go too much into it. But as an example, we have studies on exercise plus caloric restriction and it’s likely more effective.

Resistance training effectiveness on body composition and weight outcomes in individuals overweight and obesity across lifespan, a systematic review and meta analysis. All right. They say regarding exercise prescription characteristics. The mean intervention with duration was 14. 6 weeks with a frequency from one to five sessions per week.

So this was like, this is what they did with the studies. So you have one to five training sessions per week. And then the people did this for roughly 14 weeks, right? So what was the next thing is what was the outcomes. So for reducing fat mass, both resistance training plus caloric restriction and combined resistance and aerobic exercise plus core restriction were the most effective with changes of five kilograms.

Um, and 5. 3, so 3 kilograms respectively. So if you’re going to adjust your resistance training and caloric restriction, you’ll, in 14 week time frame, you can expect to lose about 5. 1 kilograms. What does that look like? At least based on these studies. So we have 5. 1 times 2. 2 is 11 pounds, right? Divided by 14, so that’s 0.

8 pounds lost per week instead of 0. 5. When you’re not taking semi glutide, you’re just

Ethan Wright:
doing resistance training and exercising. without the negative side effects of the drug and without getting about like having to take it forever, right? Because you’ll get maybe the bounce back. And it seems like you have to keep like in order to retain muscle mass on ozempic, you have to combine it with like at least some portions of the diet being in place, like having adequate protein.

And then you have to do the resistance training too. So it’s like you’re already like more than halfway there without taking the pill, you might as well just do the rest. Of the organization of the diet, you know, so that way you don’t like get the side effects and whatnot from all the from the dog Yeah, it’s a, and so, so when he’s talking like, and it’s like, he’s making it sound so simple, like, just take the pill.

There’s obviously way more on the other side of the equation to consider before you’re just like, you know, throwing in the towel, like, I guess I’m just a glutton, I have to take Ozempic forever.

Mike Fave:
This is a good point. So we have another study here. Physician’s training prevents muscle loss induced by caloric restriction in obese, elderly individuals.

A systematic review and meta analysis. And they say here in the discussion, the main finding of the present meta analysis was that caloric restriction plus resistance training prevents 93 percent of the lean body mass loss induced by caloric restriction. Although it does not affect, um, uh, body mass and fat body, uh, uh, uh, fat body mass reductions as compared to caloric restriction without resistance training.

So what does that mean? It stopped people from losing lean body mass, but they still lost total body mass and fat body mass. They say a previous analysis showed only 50 percent lean body mass loss attenuation with different types of exercise when different types of exercise were added to caloric restriction in sarcopenic obese individuals over age 50 years.

However, since endurance resistance and combined types of training were included in this analysis, it was not possible to identify which type of exercise led to preventative effects. Resistance training by itself. somewhere between 50 to 90 percent of the lean body mass loss can be prevented. Whereas even in regular caloric restriction, you’re not seeing as much body mass loss as you’re seeing with those with the semi gluteidosymbiotic stuff like this, especially if the diet’s not dialed in, which brings me to the next, the next piece is that, and this is something that you just mentioned, They say here, preservation of lean body mass with caloric restriction could be obtained by additional protein intake.

Long end colleagues have shown that caloric restriction resistant training with high protein consumption induces an increase in lean body mass and promotes larger fat loss if compared to caloric restriction with low protein consumption. The only study that has investigated the caloric restriction effects in combination with higher protein intake, 30 percent compared to 15%, found lower lean body mass loss than others.

So, here they’re saying 1. 3 kilograms Lean body mass loss in the 15 percent protein group compared to only 0. 6 in the 30 percent protein group. So prioritizing protein is going to be really important. Protein and, uh, resistance training. All of these things are going to basically prevent lean body mass loss inside the setup.

Ethan Wright:
So when you’re setting up someone’s like weight loss, uh, goals, like the path, the plan for them to get there, you have them in somewhat of a deficit, right? But how, what strategies. Are you using, like, because ozempic is supposed to make it easier to, to have that deficit. But how are you covering the diet in a way where it’s just easy for them to have the deficit without them really even, um, you know, feeling the effects too much or craving a bunch of food and whatnot?

Mike Fave:
It’s just dietary setup. So, it’s having enough protein in the diet. You don’t have to go super low fat or super low carb. You can have an adequate amount of fat, managing total energy intake, and then switching the fat, the sources around. Are you using whole fruits and tubers, or are you using like straight up 100 percent fruit juice?

If you’re using fruit juice, you’re gonna have less satiety. If, are you using, like, whey protein or are you using steak? If you have whey protein, you’re not gonna have as much satiety, or collagen, you’re not gonna have as much satiety. Now, it doesn’t mean you can’t use those things. You definitively can, but you just have to make sure that you have, um, that you’re like combining them in the meal.

Are your meals combined? Protein, carbs, fat, fiber, all together? So you’re having a whey and collagen shake, plus you’re having bananas and blueberries with that, with a base of coconut water, and then maybe you have, I don’t know, you have some like, I don’t know, you have rice cakes on the side, because it’s an on the go meal or a post workout meal or whatever the deal is, right?

Is that your meal? And then maybe you have some chocolate with that, or you put some avocado on the rice cakes. So you make like avocado toast with a shake, right? If that’s what you’re doing, like you’re not, you’re going to be full off for that meal. So it’s about getting that stuff right and setting up the diet, right?

And most, most people I work with do not have satiety issues. it with the diet that I set up. And again, I’m not doing like a sub 20 percent fat diet. I’m not, I’m not going super low fat. It’s like somewhere around like 25, 30 percent for a lot of people. Some people I try not to get too close to 20 cause you get side effects, things like this.

So I’m trying to like 25, 30 percent somewhere in there roughly. And then a protein intake. High point, 82 grams per pound. And then the rest of the filling in the carbs up to their, their target. So that’s, that’s what I’m up to their caloric target. So that’s what I’m running with. And then I’m choosing the foods wisely.

And the

Ethan Wright:
idea is that with a diet set up like that, too, where you’re including all three macronutrients, you don’t have as many cravings as maybe you would on like a lower carb diet or something like this, right? Or the goal would be to keep the cravings at bay by including foods that are, you know, that will hit those cravings.

Like fats and sugar and whatnot.

Mike Fave:
If you have enough sugar in your diet, if you’re say you crave sugar and say you digest fruits well, if every meal you have fruit and you’re like, you’re having your carbon take requirement is 250 grams a day and you’re eating 250 grams of sugar from fruit, you’re not going to crave sugar.

Promise. I promise you’re not gonna have sugar cravings. If you have a fat craving and your major fat source is 70 percent dark chocolate in your diet, or maybe it’s, it’s, it’s roasted salted mac nuts, or maybe it’s, You’re having like guac with your meals. So you have steak, you have some rice, you have some guac.

Maybe it’s like, uh, uh, rice and black beans with guac and steak, like a typical, a typical, like, um, like Cuban meal. That’s what I get in Miami is something like this. Or like, well, my wife’s family will make, she’s Puerto Rican. They’ll do something like that. Or maybe that’s not rice. Maybe it’s plantains and black beans and guac and a steak, right?

Say you’re having a meal like this. You think you’re going to be, you’re going to have cravings for, if it’s like the sweet plantains for something sweet? No. Are you going to have something craving for something fatty? No. And are you going to be really full? Yeah, you maybe won’t even finish the meal. So it’s how are you setting up that meal is really important.

Now, if your meal is going to be whey protein, honey and maple syrup blended up in coconut water, and your fat source is just like putting in coconut oil, are you going to be hungry really fast? 100%. So there are huge differences in how you structure out those meals. From the components, the food matrix, the fiber content, the types of fats used, the volume of the food, the micronutrient composition, the polyphenolic level.

So it’s not just. Carbs versus fat again, like that’s way too simplistic compared to all the variables that you have to play with. And if you take all those variables off the table and you try to get into these fallacious arguments with like, or these pseudo arguments, like with a really narrow window that don’t apply to reality, then like, then you, then you can start to create like, This like, so sophistry for yourself where you’re not really, like, you’re arguing against things that it’s like, well, you don’t, you know, you don’t have to drink pure fructose in water, man.

Like, you get to have a glass of orange juice if you want. Like, it’s gonna be, it’s all right. You, you could have whole fruit too. That’s not a problem. If you wanna have some berries or banana, that’s fine. You know, that’s okay if you don’t want to do, like, you know, you don’t have to do 500 grams of sugar a day.

If you feel like you do better at 200, 2 50 and maybe you keep your fat around, you know, 80 grams, a hundred grams a day. Fine. Like it doesn’t have to be this whole thing. It’s figuring out what target works for you specifically and then adjusting the foods accordingly. So I haven’t had a problem organizing people’s

Ethan Wright:
diets with satiety with this.

Do you find that when you’re working with people and you’re setting up the diet with them, that they’re kind of surprised with like all the foods that they get to have? Like, because you know, they’re like, wait, wait, wait, fructose. Like there’s this problem with fructose. It’s like, no, no, no, you can have some juice.

You can have some of this. And it’s like, Oh, with the, I’m always craving like French fries, you know, and like, then you can have French fries. All right. All right. Like, it’s just a way different mentality, right? Coming into it. Then I feel like what most, I think the people that I talk to have done, it’s like, I’ve done carnivore for, you know, four years.

Like I can do it. Like, give me the plan. Like I can do it. Then they get the plan is like, Oh, all right. This is not so bad. Yeah.

Mike Fave:
I mean, it’s pretty much like, if It doesn’t even happen when, I don’t know if you’re comfortable with me telling, talking about this with your dad. Oh yeah, yeah,

Ethan Wright:
yeah, he’s good.

Yeah, with your dad, it was,

Mike Fave:
your dad, when we sat down, he’s like, I can have 8 ounces of potatoes, like these air fried potatoes, like I can do 8 ounces of these for dinner? I was like, yeah. He’s like, really? And I was like, yeah. He’s like, that’s amazing. That’s great. And then that, it’s like, yeah, you just, the biggest problem with french fries is you’re like soaking them and saturating them oftentimes at restaurants and highly heated polyunsaturated oils.

But it’s like, you put a tea, two teaspoons of olive oil on your full like, you know, like pound or whatever of, of, of, French fries that you’re putting in your air fryer. Fine. Like you’re basically just starch. It’s just, and the potatoes are a great source of nutrients. Yeah. Yeah. And if it hits you, like you just fit it into your target and that’s it, it’s fine.

It’s not a big deal. And so you have nutrient density benefits on the microbiome and then you have a good source of carbohydrate that if you tolerate it is perfect. So it’s, that’s the, like, that’s, that’s completely fine. And so, yeah, a lot of people do feel that way. They’re like, wow, I can actually, this isn’t as restrictive.

This I’m like this, I’m actually enjoying this. Like I can make recipes again. Like this is, Like, and I’m losing weight. It’s like, yeah, because it’s like, yes, keto and carnivore. You will, you will lose weight. You will improve metabolic markers as you lose weight as well, 100%, but you don’t have to do that to get the outcome.

It’s like very clear in the research that that is the case and again, like it doesn’t mean it’s not carbs are not the problem. It’s not fructose

Ethan Wright:
inherently. Oftentimes, I think with all the fear mongering and the carbohydrates is like they’re kind of hesitant to add them back in if they’re coming from a low carb diet.

Cause like I know like every single time I add in carbs, I do anything like my weight just immediately goes up. And so I’m wondering like how you frame that in people’s minds, like, or how you get them to maybe overcome that barrier and try things out. Cause I think it’s like a huge mental block, even for my dad.

So when we just talked about who was doing the yo yoing back and forth was like, every single time I add an orange juice or I have a, like a banana or something, it’s like, I see the weight go up. And, uh, you know, I don’t know if he’s, I imagine he’s being truthful, who knows, you know, but, um, yeah. I mean, not now.

Now,

Mike Fave:
because like he lost a bunch of weight, you know, and then now he’s on like a, like on a higher carb intake, like much higher than his keto stuff. And he still lost a bunch of weight. Yeah.

Ethan Wright:
Now he’s fine. Now he’s like, you know, trying to eat dried mango and everything. So I know, yeah, well, we talked to me here.

Like we had to talk

Mike Fave:
troubles.

Ethan Wright:
Yeah, yeah, yeah, yeah.

Mike Fave:
But the, um, basically. When you first, when you’re low carb and you first add in carbs, you’re going to refill glycogen. So you’re going to bump up a bit. And it’s usually just water weight. Now, as long as the diet setup, probably depending on your size could be like one, two pounds, you’re a bigger guy, maybe up to five pounds or so.

Cause if you’re going to fill up muscle glycogen again, that’s normal. When you first go on keto, you lose a couple of pounds like the first week because you’re losing glycogen and then you’re losing water with the glycogen. That’s fundamentally the cause period. Like it’s nothing that’s so like, if you’re managing your total energy intake.

Like maybe you’ll shift water around you get constipated your weight will go up as well, too You’re holding stool volume. You’re holding water with the stool volume and all this type of stuff. So like bowel movements glycogen Composition all of this site or glycogen glycogen concentrations or amount that you’re holding all of these things will shift Electrolyte balance all this will shift your weight.

You’ll fluctuate Um, but your total energy intake is what’s going to manage your, and your hormonal state and all this stuff is what’s going to manage your weight, right? Those are the fundamental, most important things. And then, yeah, maybe you’ll gain a couple pounds if you start adding in carbs and you’re like zero carb before, but if your energy intake is solidified over time, like you’ll see this, if you have weight to lose, you’ll see the scale come back down.

If you are continuing to just go up and up and up because you’re coming from this perspective that, yeah, my metabolism is going to endlessly increase, then yeah, you might like, then you need to readjust. But it’s not because of carbs lost a lot of times people who are doing that in my experience I have a high fat and high carb intake and they’re in a chloric surplus, which is no bueno.

It’s not a good place to be Especially coming out of this metabolic hole if you were just like yeah, I’m oh mad one meal a day No carbohydrates just steaks water and salt like hardcore and maybe like not even coffee like coffee’s gone, too And then it’s like, yeah, now I’m going to go add libido on all types of food, like sugar and honey and, and ice cream and chocolate.

And like, just like all this stuff, it’s like, yeah, like you need to be careful with that. That’s a very tricky spot to troubleshoot because there’s psychological components in there. As well as the metabolic profile, as well as like the changing up the diet and all the shifts that are occurring that you need to manage effectively.

Can we talk about that inside, that’s like a whole module inside the course that I just filled out because of how many people struggle with that transition, it’s a huge thing.

Ethan Wright:
Yeah, let’s, um, jump into this last Ozempic clip and see what Dr. Mike

Clip: and Do you think that every patient should be on, that is classified as obese by the American medical standards, should be offered a medication?

I cannot say a hundred percent of, of the patients, but the majority would benefit from the drug. Yes. That’s scary because then we’re saying, Like a huge percentage of the United States should be on these medications. Have we gone that far? I believe so. I mean, it’s predicted that by 2030, half of the U. S.

population will have obesity. Half of worldwide also will have obesity in the next decade by the W. H. O. So. I think we’ve lost the perspective around food, around portions, right? Uh, when you’re on this medication, you really see things differently. It’s like a blindfold was removed from, from, from your eyes.

Mike Fave:
Oh boy. Should the world be on ozempic? To be fair, like this is a way more balanced take than what Mike Isretel’s take was. Like Dr. Mike Isretel’s take was way more like condescending. This is just like, we have an obesity epidemic and like. She, they said, she even said like, she can’t say that everybody should have it, but it’s like, can people use this to improve?

It’s like, she said, yeah, and it’s like, that’s true. Like, if you put people on Ozempic, they’re going to lose weight. And that, but it’s like, it’s just, is that the best way to go? And also, is that fundamentally correcting the underlying problem? This is the thing is, I don’t think it is. We’ve already talked about the problems people fall off within two years.

70 percent of people roughly based on at least some of the studies that we have. There’s lean muscle tissue loss. You still need to be in a deficit. You still need to exercise. Ideally, you’re exercising with weights and you have a high protein intake, which you’ll lose the weight doing that anyways. Like you even need the drug.

But the thing is, is like if people knew what to do, how to eat, how to set up their diet, how to manage this type of stuff. And like, that was a skill that they valued and saw that as the central piece of their health. That is way more important than just injecting or taking this drug. Why? Because if you fall off the drug and there’s a bunch of other side effects that are problematic.

So go check out that video if you’re interested in knowing why it’s on the Mike Baseline channel, I talk about the GLP one drugs, but basically there’s a bunch of other side effects that come with it and. Now, if you’re gonna fall off, like, then what you’ll get, you’ll regain. And why are you regaining?

Because the drug doesn’t fundamentally teach you how to get healthier. It doesn’t teach you how to eat. It doesn’t teach you how to manage your diet. It doesn’t teach you how to exercise. It doesn’t teach you any of this stuff. It just nukes out your appetite so that you don’t eat anymore. So is it a shortcut?

Yes. Can it maybe be a tool if you have a really hard time managing your diet to get things on track? Perhaps. Is it ideal? My perspective, definitely not. And I, I would say like fundamentally just getting your diet and learning how to exercise or move in general property could just be walking. But just do that appropriately, you can lose a ridiculous amount of weight.

And I’ve had many clients who’ve done this, just getting a diet and just walking under control who are type 2 diabetics, postmenopausal, whatever the different category that says, Oh, I can’t do this because of X, Y, and Z. It’s like, yes, you can. I’ve done it with people. You know, getting those things right.

Learning how to do that is way more important than just taking this drug. When you learn how to do that, now you have long term stability with this. You can do this into perpetuity. But if you don’t learn how to do it, it will fundamentally create issues because the drop off rate at the two year mark is high.

And there’s other side effects that come with this drug that are not good, including the lean mass, lean muscle mass loss and stuff like this. So I don’t think it, I don’t think it’s a solution. And also, it’s not addressing why this has developed in the first place. And we talked, we show, I show the graphs here.

I show the graphs here and what’s going on. When we look at obesity inside the U. S., it’s a hockey stick since 1976. Why? Let’s figure out this instead of just saying, yeah, we just need to take this new expensive drug. Look at the obesity trends in the U. S. since the 1980s. Again, it’s almost a hockey stick as well.

We went from less than 8%. Now we’re upwards at 2018 at 14 percent and probably higher. So like, we know what the problem is and we have an idea at least of what the problem is. And we can look at it here. We can get into this. And I talked about this in the mob video. This is the percentage of energy intake from ultra processed foods of youths, children in the U S from 2000 to 2018, across all groups, two years old, all the way up to 11 years old, 60 percent of the energy intake up to 70 percent of the energy intake is ultra processed foods.

It’s like, do these kids need Ozempic? Or do they need to learn how to eat better? What’s going to be a better long term strategy that we also saw was just as effective Ozempic or learn how to eat better. So it’s like do the work and learn how to eat better. It’s not because you’re a glutton or anything like this.

Like we, it’s taking responsibility for yourself, understanding that you need to learn how to eat better and learn strategies to get things under control, to get, to learn, you know, all the stuff that we talk about. This is why we’re putting out the content to try to share the information and see like, well, I’m seeing this with this people in this, how this work and this with the research saying.

And that’s why we’re just blatantly talking about it. So people can take the information and try to put in a place and see how things work for them and kind of cut through the dogma. Because this is, I think, key in my experience with working people, it’s diet, diet, diet, diet, diet, diet, lifestyle, right?

And then you could talk about crazy sups and hacks and all this, all this type of stuff, but it’s fundamentally comes down to what are you doing with your diet? What’s going on with your movement? Are you just walking and out? What’s going on with sleep and lifestyle components? Fundamental things. Bottom of the pyramid.

Absolutely key. I don’t like, could a drug like a Zimbic help you not have an appetite and maybe fix, like fix, like help you lose weight initially? Sure. But if you don’t ever learn how to eat or manage your health or take care of yourself, then I think you’re like, maybe you’re just going to come off the drug and you’re going to wind back up in the same place.

At least the probability is high from that perspective.

Ethan Wright:
Yeah. And it’s not sustainable. That’s the big one for me is like, if the research is even showing that it’s not sustainable, then. It’s obviously not like a great long term strategy if you’re trying to like solve the obesity epidemic or something like this, like the stuff that you’re trying to do with clients is give them like a long term strategy, a plan that they can stick to like indefinitely, um, you know, and, and, and figure it out, not like a quick fix or anything like this.

Um, so I think that’s a important point, um, to really hammer home and like people who are going about trying to solve the issues, uh, for themselves and going online and stuff. It’s difficult because you do see these people, um, creating some problematic ideas around different food groups and promoting certain types of diets and stuff.

And those diets I think, um, are not playing out to be long term strategies as well. Like the restrictive dieting with low carb and fasting, which we’ll do an episode on in the future. Take care. And so it’s, how are we incorporating like the theme of bioenergetics? The theme of, um, with, uh, the stuff you’re doing with clients is how do we incorporate the pros from all these different food groups?

How are we assessing like the risk and benefits of, of different strategies and then personalizing it to, to them? So, um, I think we covered a lot. Yeah. So I don’t know if you have any closing thoughts you want to touch on before we hop off here. I think fundamentally.

Mike Fave:
We, like, to manage the obesity stuff or the disease processes, we need to get, on an individual basis, what’s the person have going on, and start to fix and correct from the foundation upwards, which includes the dietary stuff.

Can you use, is, can you use a bunch of other things to help that process? Sure. until we address his underlying components for all the weight loss things and stuff like this that we people aren’t going to see the level result and maintain sustainability of that result unless that stuff is fully dialed in.

So learning how to eat, learning how to manage your diet effectively, not just I’m keto on carnivore or whatever, but like fundamentally like learning how to make a sustainable lifestyle with this type of stuff. That’s what works for you. Fine. I’m not telling you somebody who’s like, I’m a carnivore and I’m keto.

This works for me. It’s the best thing ever. Please do what works for you. I’m, this is if somebody’s on it and they’re

Why we think that the carbs are better and the rationale and like is fructose really a toxin that’s for people who are interested in this if they’re that’s they want to kind of understand this stuff and like see if they can incorporate it how to make it work that’s what this is about and like weeding through the nuances of this stuff because it’s not so black and white as it seems to be promoted online in a large extent but i think getting the foundations right fundamentally is the the key and then you work your way up from there some people have specific stuff going on that needs to be addressed of course you But a lot of people that I’m working with that I’m seeing on a regular basis, their fundamentals are not dialed in and we need to get the fundamentals right in order for things to work effectively.

If that’s done, you start to see changes across the board, whether you’re dealing with diabetes, obesity, autoimmunity, or whether you’re dealing with a hormonal dysregulations, postmenopausal thyroid stuff. Low testosterone, whatever, you still have to get the foundations right. It’s extremely important.

Then you can get to the more specifics as you go. Because a lot of times correcting these foundational components will change some of these more specific elements

Ethan Wright:
as you work your way up. And if people are interested in working with you, where can they find more? They can find more information on my website, mikefabe.

Mike Fave:
com. And what about you, Ethan? If people want to find you, where can they find you?

Ethan Wright:
Uh, I’m on Twitter and Instagram at Ethan underscore Wright7. And the links to the, like your work with me and everything will be in the description below. Also, the podcast is available on all the, uh, platforms like Spotify, Apple Music.

So the links to those will also be in the description below. Um, but with that said, I think we’ll wrap up here and then we’ll catch you guys next week. Catch everybody next week. Thanks for tuning in.