Jay Feldman 0:04
Welcome to Episode 83 of the energy balance podcast, where we teach you how to live without constant hunger and cravings, fatigue, brain fog, poor sleep and other low energy symptoms by maximizing your cellular energy. I'm Jay Feldman. I'm a health coach and independent health researcher, and joining me again today is my good friend Mike Fave. Mike and I have been studying health and nutrition together for a long time now, and Mike also draws on his experiences from working within the healthcare industry. Today's episode will be focused on how nutrient partitioning affects eating behavior and fat loss, and this includes more specifically, how our bodies partition nutrients and why this matters for optimizing our health, why hyper palatable food and stress eating are not the primary drivers of overeating, how being sedentary can mimic starvation and excess stress, how excessive fat burning causes metabolic derangement and overeating, and why an energetic deficit is not required for fat loss and instead causes fat gain. This episode will be a bit of a different format, where we'll be walking through one study in particular and evaluating its claims and then extrapolating based on those claims. So you'll have to let us know in the comments what you think of this style of episode. And if you'd like us to do more of these episodes or other styles instead, to check out the show notes for today's episode, you can head over to Jay Feldman wellness.com/podcast where I'll link to the studies and articles and anything else that we reference throughout today's episode, and if you are dealing with any low energy symptoms, maybe those are regarding regulating cravings and hunger and trying to prevent overeating or trying to help with weight loss or supporting your energy and reducing fatigue. Or maybe it's other low energy symptoms, like various gut symptoms or brain fog or trouble sleeping or hormonal imbalances, or any other symptoms or chronic health issues that really come back down to that cause of a lack of energy. Then head over to Jay Feldman wellness.com/energy where you can sign up for a free energy balance mini course, where I'll explain how these different symptoms and conditions are really caused by lack of energy, and I'll also walk you through the main things that you can do from a diet and lifestyle perspective to maximize your cellular energy and resolve these symptoms and conditions. So to sign up for that free energy balance mini course, head over to Jay Feldman wellness.com/energy, and with that, let's get started.

All right, so we are trying a bit of a different format or different topic type approach. Today, we're going to be digging into a few studies and really kind of picking them in part, going through them step by step, pulling out the pieces that we think are most valuable, most worth discussing, and we'll kind of, yeah, just go over them and share our thoughts, and hopefully that will provide some value and insight into both the value and what these studies are actually providing, but Also just how we're looking at at research and how we evaluate and interpret studies as we as we read them, when we're, you know, trying to research any particular topic.

Mike 3:32
Yep, and some of these studies are from, uh, previous episodes that we've done or things that we have mentioned in the past. So right? Think we'll be going through with these episodes, some new studies, and then also studies that we've done, we've referenced and talked about in other episodes, but didn't bring them up fully.

Jay Feldman 3:53
Yeah, yeah, exactly. And I know the studies I'll be bringing up today are ones that I've used, like, things that have inspired articles or supported aspects of articles that I've written, you know, things that I've been citing. And same with podcast episodes, you know. And as you're saying, these are things that we reference. But I think you know, with that too, whether it is reading an article or listening to our podcast episodes, I think there's so much value in looking through what we are citing. I think it really does add a lot of depth to understanding, and that's how we get to the understanding that we have at the time, is by going through these things and putting those pieces together. So for anybody who is really interested in learning and understanding these things, I think going through those studies like we will today is really essential, all right. Well, let's dive in then. So the first study I'll be bringing up is titled cell specific competition for calories drives asymmetric nutrient energy partitioning obesity and metabolic disease. Diseases in human and non human animals. So I'll pull that study up in a second. But just as a brief kind of overview, what this study is, kind of review article is kind of getting at is a couple of things. For one, it's opposing the simple calories in, calories out idea and bringing in this concept of what they call energy partitioning. It's kind of also fuel partitioning, or I probably argue that it is fuel partitioning as opposed to energy partitioning. We'll talk through that in detail. But this is something that we've discussed when talking about calories in, calories out, talked about in terms of weight loss. And then the other piece of this is what actually drives our desire to eat, and what drives eating behavior beyond just calories and calories out again, there are a few aspects of the study that I don't fully agree with also, and so I'll kind of touch on those, you know, if they come up. But yeah, it talks, it's kind of looking through a lens of competition between the different tissues, between the different cells in the body. And so I think that they talk about a cooperative aspect as well. And I think that that one is a much more helpful lens, much more accurate way to view it, as opposed to actually looking at it as competitive, where it's all done with the entire organism in mind, and in a very constructive way. So that'll, you know, that's an aspect I don't really agree with and there's a couple other things too, that they really focus on as causes of obesity and weight gain, being the number of fat cells, and that being largely genetically driven, or driven by the by the mother's nutrition when the fetus is developing. And they also talk a lot about exercises, again, basically being the main driver or determinant of how obese or not obese somebody is. And so those are some things that we've talked about why I don't you know why we don't really fully agree with them, and there's some issues there. And so maybe we'll dig into those as well. There's two figures I want to bring up before jumping into this study that I think will help to lend some context as well. And these are, these are from another study that I've brought up in the past discussing weight loss, you know, in the discussion of weight loss and energy. And this idea, the the kind of note, this notion that a, gaining body fat involves excess energy, and B, the idea that eating too much is what causes weight gain. And so this study kind of breaks not this study will be talking about that just reference, but there's two figures from a previous study that I think are worth looking at really quickly, just again, to provide that context, I'll pull those up real fast. So this is that first one, and what we're seeing here in this figure is the basically separation between food and body fat and energy. And so what they're showing is that, basically, when we take in food that acts as fuel, and there's two places for that fuel to go. It can either be stored as body fat, or it can go to produce energy. Of course, there are other places that can go as well. You know, it can go toward muscle mass or repairing any certain organ or tissue, yeah, glycogen storage. So there's other areas as well, but they're just kind of delineating these two and saying that there's this notion that if you're gaining a lot of body fat, you also have a lot of energy. But what they're showing very clearly in this very simple diagram is that the fuel has two places to go. It's either going to fat or it's going to ATP to energy. You can't convert ATP or energy to fat. That's not like we don't have the capacity to do that, and so it's not something that happens physiologically. So generally, and this is something they point out throughout this paper, is that if a lot of fuel is being converted to fat, and somebody who is gaining weight or is obese or anything along those lines, that means much less is being converted to energy.

Mike 9:00
So it's a shunting of sorts.

Jay Feldman 9:03
Yeah, exactly. So that's kind of the first piece of context that I want to add. And the second piece is the relationship between food intake, energy, body fat gain or loss, and how that affects hunger and eating behavior. And so this is a second figure from that study. And so what they show here is that when you have a situation where that food is being stored as body fat and it's not being converted effectively to energy, so this is someone who's gaining weight or is overweight, that leads to they just they show here, then you have low ATP in the liver, and you also have low ATP in the brain, and that activates a signal to eat when we have a lack of energy in the liver, lack of energy in the brain, that causes us to want to continue to eat because of that lack of energy. It's the whole point of eating is to, you know, among other things, to restore, you know, restore energy availability. And so despite. Despite the fact that you have an increase in fat storage, which would generally increase the hormone leptin and tell you not to eat, the lack of energy overrides that signal. And so this is, again, another piece of context, I think, is important when we go into the next this next study, it really corroborates this, and talks a little bit about the details here of these, yeah, of these mechanisms and how this actually plays out.

Mike 10:23
Before you, before you go this, this idea, or this paradigm, gets rid of the perspective, or challenges of perspective that people talk about, of like leptin resistance, as if the body just develops resistance to some particular hormone. Or even to some extent, I guess it'll come. You will. Probably won't discuss it here, but even questioning the underlying ideology behind insulin resistance overall becomes more if moves it into the perspective of an actual cellular energetic deficit, or issue with cellular energy, rather than, and then that being the cause of some type of resistance, rather than you just developing resistance from exposure which are very I think the second argument, or the first argument, which is not the is the one coming from, like a cellular energy deficit. It's much more eloquent and also simple than than the like kind of basic argument of, oh, it's just like too much exposure, or some idea of, like, receptor up regulation or down regulation, yeah.

Jay Feldman 11:28
And that's something that's talked about exactly in that paper, basically, that this idea of leptin resistance, as you're saying, is not just a situation where the cells get tired of responding to the hormone. Instead, the lack of energy is a stronger, more important signal that is increasing the eating behavior, as opposed to leptin, which would decrease it. And as you're kind of getting at, the same thing happens in other situations of hormone resistance, like insulin resistance, but the insulin resistance is not caused by the cells just not wanting to respond to insulin anymore, because they've done it so many times and becoming resistant to its signal, but rather, it's because the thing that is trying to be signaled can't happen right? There's, there's an issue with the glucose oxidation. You have a buildup of glucose in the cell. The cell is full of glucose. It can't take up more, even though insulin is trying to tell it to take up more, so and, yeah, and that's that specific example I'll link to situations when we've talked about that, because we have dug into that a bit well.

Mike 12:25
The the pathway is mapped out right, because for the fat, for you to start to increase large amounts of fat production and not have glucose oxidation or oxidation in general, you get a backup what, I think, what was citrate, at the elect, at the at the in the mitochondria, or at the mitochondria, and then it starts moving substrate towards that so literally, like, that's directly what's happening is you're you're shunting away production of energy, and then you're moving that energy towards the production of fat and fat storage.

Jay Feldman 12:57
Yeah, yeah, yeah, exactly. And you mentioned the citrate buildup, there's a handful of other, a handful of other things that happen as kind of adaptive responses, changes in NADH, NADH, NADH ratio, buildup of other intermediates that all have those same kind of signaling effects. So, and that's kind of exactly what this, this paper, is more or less getting at is that, just like with insulin resistance, and they actually talk about this, so I'll just kind of pull it up in a second, but in these scenarios, this is not a situation of malfunction or maladaptation. This is the nor this is not, I shouldn't say normal. This is the cohesive, systemic, adaptive, intelligent response, like this is what is supposed to happen because of the inputs that are being given to the system.

Mike 13:47
So it's genetics.

Jay Feldman 13:50
Exactly, all right, let's, let's dig into the actual study. So as I mentioned, the study is titled, cell specific competition for calories drives asymmetric nutrient energy partitioning obesity and metabolic diseases in human and non human animals. So the first piece here that I think is worth discussing or highlighting, I'm going to read this this quote, and then we'll kind of dig into it, but kind of is exactly what we were just discussing. They lay out this premise, which is the same premise that we've discussed throughout this podcast. They state, we posit, that the mammalian body is a complex physiologic ecosystem in which survival and health are determined by metabolic flux, ie, the flow of energy through living cells. An organism's metabolic flux is determined primarily by the energetic demands of the constituent population of cells, energy intake behaviors, and the availability of nutrient energy to meet metabolic demands. So again, just creating that general framework that we're working from with. Is that, and that this paper is focusing on, is that energy is that underlying currency that is determining health. They the second part here, I don't agree with the 100% where they said that the metabolic flux is determined primarily by energetic demands. But that's not, not entirely worth taking into. But we've talked about, you know, the availability of nutrients, hormone hormonal state, sunlight, activity, so many things will determine metabolic flux beyond just energetic demands, and there's a lot of things that will drive an increase in energy. In fact, I would even say that's the default, without needing to add any demands, and just a question of whether things are blocking that process. The other thing I wanted to mention real quick here is they talk about nutrient energy. And I think, uh, what they because they kind of use that term of nutrient energy throughout this paper, and I would really compare that to just saying fuel, like they're kind of referring to the potential energy in a macronutrient that is taken in. So when they say that later, I'll, I might just use fuel interchangeably with it, because that's it gets complicated when you don't create that separation between the fuel and energy.

Mike 16:15
I just want to end here just briefly that this I would, I would guess that this paper you started looking at when we were talking you and I were having conversations about the idea that, like, people talking about the Randall cycle, where it's like, Oh, if you have eat too much fat, then you'll be internal resistance. You can't have carbs. And then we were kind of talking about, well, there's like, however many trillions or billions of cells in the body that all require nutrients. And the nutrients, whether macro or micro, are required for different functions. For example, fat doesn't isn't only a nutrient substrate. The same thing with carbohydrates, they can be used for different processes. So to have to worry about so or to think put things in the perspective of, I'm just going to have carbs for in this meal, and fat in that meal, because Randall cycle, it doesn't take into consideration the fact that you have all of these different cells that have multiple different functions simultaneously, and have different nutrient requirements and needs simultaneously, that are able to take up and use these things at different times where, and then the metabolic dysfunction not being a cause for that Being a cause of something else.

Jay Feldman 17:21
Yeah, yeah. 100% I think that's a really helpful layer to add as we go through this. Is that kind of idea, again, with nutrient like with the partitioning of energy, or, really, what they're talking about is the partitioning of fuel, as you said, that can involve moving different fuels to different areas depending on need. And you know, we've talked about how, for example, the brain is always going to be a great something that will always be uptaking carbohydrate, whereas something like the muscles can take up whatever's needed, whether it's carbs or or fats. So moving on to the next piece. Here, I tried to just pull out the most important parts of this study that are worth discussing. Because if we they spend a lot of time kind of laying out some of the just some of the basics of of their, I don't know, of their this kind of hypothesis, theory, these things that they're putting out. It's like a 22 page paper. So it really wasn't worth going through some of those initial pieces. So as I was saying, one of the things that they discuss is the idea of this all being a cooperative strategy, where the different partitioning of fuels, at the very least, is something that's done in an adaptive way to support the organism as a whole. And so here they're talking about this in terms of insulin resistance, which is what we were just mentioning. So they state, at the cellular level, we posit, that insulin resistance is the predominant cooperative strategy and operates by increasing the availability of serum glucose to other cells, for example, as the level of stored energy within hepatic and skeletal muscle cells increases, such as glycogen saturation and lipid accumulation, insulin sensitivity and the ability to store serum glucose, as glycogen decline, the concomitant reduction in the competitiveness of insulin resistant cells increases the availability of nutrient energy substrates to other cells, especially those that remain insulin sensitive. So what they're talking about here is that insulin resistance in a particular cell or a particular tissue is a way of stopping the further influx of fuel, because that tissue is already saturated, as they said, whether it has enough glycogen or has enough fat, whatever it needs. And so the insulin resistance is a way to essentially prevent the uptake of more fuel. And then, as they say, this increases the availability of, they say, nutrient energy substrates. Again, it increases the availability of fuel to other cells, especially those that remain insulin sensitive. And this is how you can have that situation where you take. Carbohydrates. And let's say they're just going to certain tissues, they're just going to the liver, they're just going to the brain, because the muscle glycogen is full, or they're going to go to those places first. And if the muscle is still insulin sensitive and and the there's no glucose left, or not much glucose left, then maybe they're taking up the fat that's that's available at the time.

Mike 20:18
And you can see this too with like how the different glute receptors work, right? Glute four, which is where you it's muscle and liver and fat, all require insulin, whereas the other glute receptors don't require insulin to function. And the other glute receptors are expressed in the brain, the red blood cells and other organs. And so essentially, those tissues are always taking up glucose. They're always they're always taking glucose, whereas the muscles and the liver and the fat tissue take up glucose with meals. So when they haven't the insulin spike, which happens with carbohydrate rich meals, and then those are the tissues that you start to see the increase in insulin resistance. And that's where you start to that's what they even talk about in the research, is like hepatic insulin resistance versus adipose insulin resistance versus, like a muscular insulin resistance. Then it makes sense, right? You top off your glycogen in your muscles, and it's like, now you have more nutrient for other areas.

Jay Feldman 21:15
Yeah, yeah. And why would you want the muscles to continue taking up that substrate, and again, it's, it's kind of the, I think such an important point here is recognizing insulin resistance, not as pathology, so to speak, but just as a normal response to that situation.

Mike 21:33
Yep, and the pathology that they see within insulin resistance, where you have diabetes, obesity, etc, is coming from other factors that are triggering that response. Rather than the insulin resistance being the direct problem, it's what is causing that underlying insulin resistance that is the pathology, and the insulin resistance in the bot and everything else that comes with that is the body's response to these pathologies. And then obviously, over time, with that chronically happening, you are going to have a degradation. As you degrade the structure, or as you impair the energy production, the structure will continually degrade.

Jay Feldman 22:09
Exactly. And as you were saying, those blocks, those factors, let's say it's endotoxin, for example. So the problem is not that now you're insulin resistant, in that case, that this is caused by endotoxin, and so you shouldn't take out carbs, but rather that there is this endotoxin issue that's impairing energy production. And so the natural response is to, well, I'll mention this in a second, of what that natural response is to a stressor like that. So in the paper, they then state hepatic and skeletal muscle cell insulin resistance is induced in numerous contexts, including the elevated levels of fatty acid oxidation induced via hypocaloric feeding, fasting or starvation. This cooperative strategy diverts nutrient energy substrates against fuel to other cells, such as neurons, and allows for their survival of all cells in the body, as we posited previously, the naturally occurring insulin resistance of pregnancy is a cooperative strategy that draws nutrient energy against substrate or fuel to the fetus. Thus, in contrast to the current consensus on the pathological nature of insulin resistance, we posit that insulin resistance is an essential feature of mammalian metabolism, and our frameworks of competitive and cooperative strategies explain the evolutionary benefit of this cooperative strategy in the mammalian ecosystem. So kind of summarizing exactly what we just described, and they gave a couple of nice examples there, right of hypochloric feeding, fasting or starvation. Of course, you can also throw low carb diets in there. They mentioned that these, that these are all signified by elevated levels of fatty acid oxidation and that driving insulin resistance. Again, the people who are in the know who are suggesting low carb diets, ketogenic diets, whatever it is, discuss that those cause physiological insulin resistance. I think a lot of people who are following those diets don't recognize that, don't really understand that. But that's like the people who are aware of the physiology, like there are, you know, will acknowledge that they have to make they have to then make the argument that this is beneficial as a whole, which I think is where the problem comes in. But again, this is the normal response, whether it's against starvation, fasting, hypochloric, feeding, excessive exercise, any situation of low energy where you are diverting substrate to other areas that need it to allow for basically overall survival. They compare it to the same thing that happens during pregnancy, where basically the the substrate needs to be diverted to the developing fetus.

Mike 24:36
And it's genius, because the release of excessive amounts of free fatty acids from the adipose tissue triggers metabolic responses in the cell that signal that starvation state. Right? They've causes adaptations to trigger the starvation state. And then you have, you develop like insulin, you develop that insulin resistance that then spares glucose for the nervous system. So you're all the other. Tissues are starting to move towards beta oxidation, so, and that glucose is, you have that ready for the nervous system. So it's, it makes sense, and they literally, they say it directly there, that it allows for the survival of all of the cells in the body. So there's a, there's an intelligent prioritization and hierarchy and of utilization of different substrates in different contexts. And so what is our what does that mean for us is we have the ability to alter the context and therefore alter the effect, and that's through base. It's not through, it's not through low dose Metformin or resveratrol. It's through. It's through dietary and lifestyle modification. Supplements are a part of that. But the foundation for this type, for these signaling is going to be clearly dietary intervention.

Jay Feldman 25:53
And another parallel piece here is kind of bringing this back to to the issues with calories and calories out is that this sort of effect can be brought on, as we said, from anything that will increase fatty acid oxidation, whether it's any sort of diet, excessive exercise, or a low carb diet. And so these are things that will dramatically affect where fuel is partitioned, even if you're taking in the same number of calories, you know, and the the flip side of that is, is if you were to have a high carb diet, that's also going to change how things are are partitioned, because of these adaptive effects. And there's another study that I was thinking of going through, and kind of decided against it, just talking about what happens in starvation and in these stress states. And in addition to just partitioning the nutrients or the substrate to the areas that are absolutely essential, like your as you said, like your nervous system, and diverting it away from the things that are not essential or not as essential, like reproduction, we see that in starvation, we also see a decrease overall in metabolic rate. We see a decrease in body temperature. And these are other strategies that our bodies use in a parallel way to allow for as much, you know, as greater chance, as great a chance of survival as possible.

Mike 27:09
And the last point here, very brief, but I just want to point out, I think is really interesting, is the idea, and this is something that I that, that Dr Pete had mentioned, but it's also, I think, known in the like in the mainstream, that that mothers who have digestational diabetes, I think they can tend to have macro is it macrosomic or macrosomic babies, or very large babies? And what they're saying here is that it's an adaptive strategy to drive glucose towards the fetus. And I think Dr Pete had mentioned something along those lines as well. So I think, you know, from a low carb sphere, or keto perspective, here, mothers need to be on low carb diets to avoid gestational diabetes. No, I think that looking at, you know, if there's not a pathology with the gestational diabetes. You know, if the mother's not having an issue, perhaps that's actually a beneficial response for for the fetus overall. But you know, really depends on the context too. If there's, like, pre eclampsia or something else going on, obviously that's a different story, right? Then just just, it also depends on how it's defined, right? If you're just because it's like, is there just elevated blood glucose in that situation? That situation, and there's no other symptom, then it's like, okay, well, is it really a problem? And I right, you'd have to look into that a little bit more, but still interesting thought process. ,

Jay Feldman 28:33
Yeah yeah. And I think what it's kind of alluding to, too, is that when when you are in a sub optimal state, and maybe there is not enough nutrition to go around, right? There's only so much available for you in the fetus. Then that is when you tend to see this sort of insulin resistance to divert the nutrients to where it's most important, right? It's like when you're seeing the equivalent of a starvation state, when you're seeing that stress where there's too high of an energy demand and not enough needs. This is just suggesting that when that's happening in pregnancy, the fetus is favored, and it's done through that sort of insulin resistance. So I think it can still be a sign of pathology or or a sign of of less than optimal function, but still be, of course, an adaptive response.

Mike 29:16
Ideally you'd want the mother to remain insulin sensitive and still have enough substrate to go for the baby.

Jay Feldman 29:25
Yeah. So moving on here to this. This next part that they discuss, they call it effective calorie intake, and I'll let them explain it. So they say the framework of effective calorie intake describes the amount of nutrient, energy or substrate or fuel available to constrain energy intake, food intake, I'm going to restate, I'm going to restate this with my own terms, because I think, again, throwing around the word energy like this is something that is just a personal something that bothers me, personally, yeah, pet peeve, because I think it's really sloppy and. Inaccurate and leads to the idea that calories equal energy and all that, all that..

Mike 30:05
Conflation, a lot of conflation. Yeah, yeah.

Jay Feldman 30:09
So the framework of effective calorie intake describes the amount of fuel available to constrain food intake via the inhibition of the sensory motor cells that govern ingestive behaviors, ie energy sensing, appetite, appetite of neuromuscular networks in the liver and brain. So I'll just finish reading this, and then we'll kind of break it down. They then state, we posit that the availability of fuel to each cell is constrained not only by ingested behaviors and total food intake, but also by the context dependent asymmetric competition between individual cells. Thus, when our energy sensing, appetitive cells in the liver and brain are out competed by other cell types such as fat and or muscle cells, the effective caloric intake of a meal is diminished, and total food intake will be increased to compensate for the deficit. So to put that in a little bit more plain English, what they're basically saying is that we have the main areas that control our appetite and our hunger are in our liver and brain. And they're basically saying that when they have enough fuel available, that's when our appetite and hunger turn off, and then vice versa. And so they were saying that the this is not only affected by the amount of food we take in, but also whether these areas are getting enough fuel and are able to produce enough energy. So this kind of part they say at the end, is that if the these areas in the liver and brain are out competed, they don't have enough fuel, or they don't have enough energy, then the what they call is the effective calorie intake of a meal is diminished. And so it's another way of saying is that the body remains hungry with the same amount of food coming in. And so they then say that the total food intake will be increased to compensate for the deficit. It's kind of a backwards way of of evaluating how a meal works. But what they're kind of saying is that the meal will be less satisfying. It'll create less satiety. And so you'll want to keep eating if these areas are not satisfied, as far as energy goes. And yeah, it kind of goes exactly hand in hand with what we were like those figures I brought up earlier. That's why I wanted to bring them up, is because, yeah, the whole idea of calories and calories out has completely ignores this fact, and completely ignores what drives appetite and food coming in. And it's not hyper palatable food, not that that doesn't have any effect. But it's not hyper palatable food. It's not stress eating. It's not any like the main driver of how much food you're going to take in is how much energy you have, especially in the areas that are most sensitive to are made to be most sensitive to that energy availability, which is the brain and liver.

Mike 32:52
And I think that the stress eating is a great explanation of this, where the in the situations of stress, which you've defined before, and we've we've discussed at length before as like, essentially a lack of energy based due to the energy demand on the body in different circumstances. So with the lack of energy, your body will give you cravings for energy rich foods. Now, the one thing to keep in mind here, and I think it's important to put it into context, is especially if you look at this over time as obesity and being overweight and all these metabolic disorders did not become a thing until the advent of industrial food and and the industrial food And so calorie the industrial food is lacking in or at number one, is lacking in nutrients. Overall, it has macronutrients of often poor quality and in forms that can cause issues, particularly in the microbiome, but and then also additives that can cause issues. So you have that problem. But then on top of that, it's the calories in, calories out. Model has been created at or can arguably have been created depending on some of the some, depending on what you look at and some of the journalism that you look at to deflect from the the understanding of that this food is basically nutrient poor. So the argument, and we talked about this before, and I don't want to go too far into it, so the argument has become one of has become one of your gluttony, rather than the fact that the food supply is crap and it's calories in, calories out, is a great deflection for that. It completely don't worry about the nutrient quality of the food. Don't worry about what it does in the microbiome. It's just worry about calories. Just worry about energy intake, because when you shove this, when you shove this food into your system, it produces energy, and that's in the form of calories, and that's it. And basically what we're saying is that entire middle section of the equation of your body has to digest it without having bacterial issues from it. And the study. That I'm going to look out a sec will will actually bring this into play, and then also bring that into the system. Use different nutrients, vitamins and minerals, to take the energy and then convert it into to take the substrate and then convert it into energy. So if you're deficient on any of those, you're not going to produce energy from the substrate. If the food is causing problems in the intestine that's blocking energy production, you're not going to get going to get any energy from the substrate. And then, if the food is of poor quality, garbage laden with a whole bunch of different toxins, whether that's peroxidized fatty acids from being high in PUFA and vegetable oils, that's going to block your energy production. So it's like all that middle equation has been, has been subs, has been cut out and they just put in their gluttony. It's pure gluttony. It has nothing to do with all these other known, documented physiological factors. It's just that you eat too much.

Jay Feldman 35:51
Yeah. 100% and they, I think I'm pretty sure it's in this study we'll see toward the end. I'm pretty sure they talk, they describe exactly a couple of things you said, where they're like, we're missing some big pieces here when it comes to obesity. And again, they're, they're focused here on the competition between tissues, and that, of course, can be part of it, right? That there's areas outside the liver and brain that are competing for the substrate, and that's a part of it. But I think what they're not acknowledging here, which that other paper that I, that I brought those figures up from in the beginning really touches on is that one of the bigger problems is converting that food to energy. And as you're saying, issues with digestibility, lack of nutrients, the presence of PUFA, bacterial toxins, those things are going to block our ability to produce energy from the food. And that's not going to allow for those safety signals and there's satiety signals, and then you're left just living your whole life hungry and restricted or gaining weight because you're not actually converting that food to energy. Yep, all right, so moving on a little bit. So they talk a little bit, yeah, I'll let them kind of get into this a little bit more in terms of the effect of calorie intake, and we'll kind of build on it so they say the disproportionate disposal of nutrient energy or fuel reduces the effective calorie intake of each meal by lessening the absolute amount of fuel available to inhibit the sensory motor cells in the liver and brain that govern ingestive behaviors, this reduction in available energy leads to compensatory increases in food intake to overcome real or merely apparent deficits, while physical activity engenders a real perturbation in energy homeostasis, ie, a true signal that necessitates an increase in total food intake to ensure survival, excessive fat cell hyperplasia leads to an apparent deficit, ie, fall signal that drives increments in ingested behaviors and overconsumption of calories. And so I mentioned this before that they're really hyper focused on physical activity and then fight fat cell hyperplasia as like, the only two factors that can that are like driving this difference in partitioning. But an interesting piece here, and something we've talked about a lot, is that one of the main things that drives food to the fat stores is stress hormones, specifically, specifically cortisol. Again, it's very apparent when you look at Cushing syndrome, right a situation of excess cortisol. And this is something I'll be talking about in one of the next studies, and so forgetting fat cell hyperplasia is the only reason for increased storage of fuel is fat. But if you have all these signals that are preventing fuel from being converted to energy and also partitioning it toward the fat storage, that is another scenario where you're left with less fuel for the brain, less fuel for the liver because it's, it's all being driven to fat as a defensive reaction to the starvation, to the stress, to whatever it is, and so that that's kind of what they're it's kind of, yeah, an extension of what they're discussing here.

Mike 38:52
Yeah, the other thing too I want to mention, and this is something that we talked about in previous podcasts, recent previous podcasts, where even with physical activity, it's not a linear there's not a linear relationship. Physical activity, at a certain point starts to it's not that you can just make it up with food intake. There's only so much that you can recover from. So the physical activity itself will start to pull energy from other systems, and it actually, and then, yeah, exactly. Or fuel, yeah. And then, in the long run, this can cause, and this, this can cause basically a issue hormonally, or it's not an issue. I'm only the hormonal system is signaling the issue that leads to up regulations and cortisol, etc, that puts you in a Hypo metabolic state and predispose you to essentially developing other issues that can include metabolic issues, and you can see that with, you know, the the female athlete triad, and different things with overtraining and hypogonadism in men, and responses to overtraining, things like that. So there's a there's definitely it, it's there's not a. Linear response with exercise, but you you have exercise can divert and or substrate or fuel away from other systems. So that's something it's also something to keep in mind. So there's obviously a a limit there, because it's the the perspective here that I get from them, or at least the the feeling I get from them, is that there's this idea that it's kind of linear, like exercise will just increase your energy intake. But I also think it's really important here to mention the secondary is that they're talking about an actual energy deficit due to a fuel shunting to the fat stores. That's quite an interesting concept that you know, I think a lot of common people, regular people, non research people understand this, like, I've heard this from people before. It's like, oh, they're just, they're people are obese because they're eating the wrong foods, and those wrong foods they don't have nutrients. So it's just leaving them like they're always, they're still hungry for those nutrients. There's like, a perspective that I've heard before from people, and this is, this is a little bit more in depth on that perspective, but it's, I think that's something interesting to consider.

Jay Feldman 41:06
It's nice that you've heard that I normally just hear that people are gluttons. Yeah, I think there's the there's, I guess, what I hear is less even of a focus on a lack of the good things that are needed. But rather, people are gluttons, and they're eating a lot of fat and sugar. And again, not, you know, they're like, that is, I don't know it's here. So here in Ecuador, all of the labels, the only, the only like, piece of advice, or thing that they describe, or like, it's a super big part of the label, and it tells you how much fat is in there, and there's like, a meter green, yellow, red, and how much sugar. And that is, like, the only important pieces of information for you to know about any food nutritionally is the fat and the and the sugar.

Mike 41:47
Here, it's plant based. Everything that has a label that it's like, it could be like cheez, its it's like, plant based, whatever it is, whatever brand health is. Now it's healthy because it's plant based, which doesn't mean anything, you know, even things that, like, they're gonna start labeling bananas plant based, and then, just as like, a marketing gimmick is gonna be things that are always have been plant based, are now plant based. Yeah.

Jay Feldman 42:13
I mean, they do that with, they do that with gluten free, right? Like, things that would never even have, like, like fruit, you know, it's never going to have gluten but I've seen that with, you know, labeling things as vegan or vegetarian that are just like, there's nothing in there that wouldn't be.

Mike 42:30
yeah, it's insane. It's insane. Like, your your orange juice is gluten free now, like, right? Oh, really, now it is before it wasn't. Yeah, exactly. Did you need a certification for that.

Jay Feldman 42:44
Yeah, yeah. So moving on. Here they state, to be precise, we do not argue that decrements in effective calorie or caloric intake are the only mechanisms that drive energy intake or food intake. However, we argue that the asymmetric competition for new for fuel, and concomitant reductions in the inhibition of energy sensing, appetitive cells in the liver and brain are the primary drivers of habitual food intake above basal metabolic energy requirements. So again, this is kind of what I was saying earlier. They're acknowledging that there are other factors that can drive eating behavior, but this is just the primary one. Thing I did want to mention, also, Mike, you were talking about the physical activity situation and this paper's view on it. I don't think I really highlighted any of those points, because I felt like it was kind of beside the point. But interestingly, the main thing they focus on from the physical activity side is just not being sedentary. They basically said that, as long as you're not sedentary and you're getting some amount of flux through the muscles, as far as fuel and the production of energy, you're fine. And the other the point that they don't touch on, as you're saying, is that there's a certain point where exercise really starts causing some problems, because we are limited in our capacities, and so you have to start pulling that energy and fuel from elsewhere. And so that was something you were touching on that they don't acknowledge. But it's not, you know, at least one nice thing about this paper is that they are not just saying more and more and more exercise, and you need to exercise a lot to get the benefit. They really just say, Don't be sedentary. And I think I don't know, I may or may not highlight some of those points, so we'll see if those come up.

Mike 44:14
I do want to mention, really quick with that too, is that there's this idea of with exercise. There's an idea of, like, how many calories you burn with exercise. And if you looked at how much calories you had to burn, like, if you want to burn how much exercise you needed to burn, 1000 calories, it's a ridiculous amount of exercise. It just it never works out, especially considering that there's other effects besides, and I think this is extremely important. There's other effects that exercise have besides just using energy. And this is, I think this is largely not discussed in that calories in, calories out, sphere bodybuilders discuss this, right? You talk to a bodybuilder, you ask him some of them will? You ask them some of the best ways to be. It's like have a high amount of muscle mass, because then you can increase your metabolic rate, and you have more tissue to put substrate in it, from this perspective, to put to store substrate, etc. And then you also elevate your basal metabolic rate, and you have essentially more disposal areas. Is kind of what some of the bodybuilders will talk about, which is not necessarily, and it's kind of tangential to the point of view that we're discussing. But yeah, yeah, there. And then you also have the hormonal effect, which is discussed, like the bodybuilders will a bodybuilder will tell you to do, or some of the bodybuilders will tell you to do squats, do these heavy lifts, because you'll tax X number of amount of muscles, and then you'll have this hormonal response. They're not saying, Oh, you need to burn X amount of calories, like we want the hormonal response. Hormonal response, which I think I've discussed before, as being significantly more important, or significantly more powerful than this calories and calories out stuff, you know, you there's a study that, you know, maybe I should one day, I'm, I'm gonna, I'll bring it up. But it was, the study is talking about where they gave body, they gave sedentary men testosterone, and they build more muscle mass just taking the exogenous testosterone than the men who were exercising and not using exogenous testosterone. So it's just something interesting. And I think I saw recently on the forum, there was a study showing that men in Europe who were given, uh, they were given testosterone for five years. Over the course of those five years, they were obese men when they started lost, I think, like 50 pounds just from taking the testosterone, not even looking at whether they exercised or not, which is, again, just indicative of the power of hormones and the signaling of hormones, which, again, the signaling of hormones comes down to what's going on energetically at the cell, and what are you doing diet and lifestyle wise, right? If you have an excessive amount of PUFA in your testicles, you're not going to be able to produce the testosterone that you want. So just those, just one basic example of them.

Jay Feldman 46:52
eah, yeah. And I know you've mentioned, I think that study with the usage of testosterone versus exercise, I think you've mentioned it before, but yeah, we haven't.

Mike 47:01
We haven't never, like gone through it like this. It's an easy study to go through it, but yeah.

Jay Feldman 47:08
All right, so moving on talk a lot about their previous research was kind of what they referenced earlier on, talking about what goes on in the mother during pregnancy, and the diversion and partitioning of fuel in that situation. So they talk a lot about that. And they talk also a lot about so that is like a predisposing factor for obesity, by causing potentially increased amount of fat cells in very early on. You know, very early on, they also talk about genetic factors and a lot of inherit, inherited type things. So not really worth discussing. This is just just mentioning this. So this is that I wasn't going to, but you were just talking about physical activity. And so here they talk about how, here's this metabolic tip, tipping point where. So here's sedentarism on the on the left, and they say, as long as you're past that point, you're and you're in the, quote, physical activity range, or physically active range, you'll be neutral as far as what they call energy balance. But they're really talking about fat balances, and you're not gaining weight. And they do actually talk about the extreme physical activity causing, well, actually, they're talking about it causing weight loss, which obviously does, but it just comes at a cost. Yeah. So just just interesting that they did at least acknowledge, acknowledge that you just don't want to be sedentary. Yep. Again, talking about energy balance, which, again, one of my pet peeves there is describing calorie balance as energy balance, describing fat balance as energy balance, when really those are calorie balance or fat balance. And there is a difference between those things in energy but anyway, all right, so here we're talking they actually talk about, you know, the physical activity and the sedentary zone and the problems that it causes here, they say, We pause it. This occurs because as hepatic cell metabolic flux declines, these cells become saturated with glycogen and metabolites from fatty acid oxidation. So this is what I was mentioning earlier, where they're just there's a focus on flux through the liver and fluxive muscles, which I don't really agree with but they bring up another point right after this, I think is worth discussing. They say this leads to decrements in insulin sensitivity and metabolic flexibility, ie, the ability to alter substrate oxidation as substrate availability changes, as discussed previously, the only context in mammalian evolutionary history in which hepatic cells experienced elevated levels of fatty acid oxidation would be starvation and or chronic elevated physical activity, given the fact that these contexts induce the initiated, the initiation of ingestive behaviors and energy intake and a reduction in basal energy expenditure to ensure survival, we posit that physical inactivity, ie low metabolic flow. X provides a full signal that drives increments in energy intake or food intake with concomitant decrements in energy expenditure. So what they're saying is that, and they're using, again, the kind of, you know, evolutionary context, which I think there's, you know, there's just kind of some misguided, it's a misguided thought process. But they're saying that the only context in mammalian evolutionary history in which hepatic cells experience elevated levels of fatty acid oxidation, so the only situations where you see elevated fat oxidation would be starvation or chronically elevated physical activity. Obviously, these are situations of intense stress. And they're saying that these are also situations where you see a reduction in basal energy expenditure to ensure survival, as well as increases in appetite. So they're just talking about those effects of fat fat oxidation, of course, another kind of strike against low carb diets and the idea that we just want to be fat burners. And then they're basically saying that physical inactivity mimics those states. And I think that there's something there. I don't think it's just because of a lack of flux that causes buildups of metabolites of from fatty acid oxidation and saturation with glycogen. I don't think that that's really a reasonable explanation for what's going on there, but I do think there is something there, as far as sedentarism actually mimicking the effects of excess stress or starvation or excess activity even.

Mike 51:28
So basically, what they're saying is that, since the muscles and glycogen will be full the muscles and liver, the glycogen in the muscles and liver will be completely full. Then the substrate coming in will lead to elevated free fatty acids, and so that SIG that produces a signal of akin to starvation or extreme stress, that has a whole host of these other triggering pathways. And they're just saying, they're saying sedentarism causes that to happen because you're not burning through those stores. Which Right? Right? I don't know if I 100% agree with that. I know you don't either. I think that that's a little I don't that's there's more to that, especially based on my experience where I've have people who adjust their diet to better diets overall, and are still relatively sedentary. You know, it's not that they're just sitting down and doing nothing all day, but they're not going to the gym. They're not, they're not doing any of these structured exercises like work and then whatever else, and they still are able to lose weight or and not, and especially not gain weight. I think there's other much more factors at play. Still think that's too simple of an explanation, especially because there are studies looking at the activity levels between some of the hunter gatherer populations and the Western populations, and finding them to be equivalent. Yet changes in diseases and obesity are extreme, and so I doubt it's I highly doubt that it's related so heavily on physical activity. I think physical activity plays a part. But I would say that there's much more involved with diet than just, than just physical activity. And perhaps the researchers, at least, this thought process is a very mechanical thought process, like an engineering thought process, putting the body into a mechanical engineering perspective. It's just fluxes of these, of well, these are full, you know, these containers are full, so nothing else can go in. So then we're just gonna have this excess stub straight in the body, and all that triggers the signal, and then that, therefore, that's obesity, like, it's very mechanical.

Jay Feldman 53:32
Yeah, and there it's a little bit more intelligent, like there's an added layer beyond the calories in, calories out, right? They're, they're exploring the relationships between different tissues and fuel needs and everything and adaptive responses, but only so much as you're saying. But what I liked here is that they're talking about fat oxidation being that signal of a problem. The other piece, what was it was, oh, talking about things that they ignore. They act as though muscular activity, like physical activity, is only way to deplete liver glycogen, as if the brain doesn't exist and doesn't consume a huge amount of carbohydrates every day. So I think that's like, you know, another area where they're just completely missing the mark. But I think, as we've talked about, one of the things that you see when there is a disruption in proper energy production, proper glucose metabolism, is the shift to fat oxidation. And so I think that, and all of the plethora of possible things that can cause that is the equivalent of this state. And as you're saying, it's not just physical activity or inactivity that causes that. There's a plethora of things. Physical inactivity tends not to help, but it's really largely beside the point, especially when you're just looking at it from a depletion standpoint, of just depleting substrate being the difference, especially when they say that that is the true signal, right? They talk about that as being the the true signal, as opposed to the false signal. Or, I don't remember what the Yeah, they say instead of. Signal and yeah, so I think there should. Why is there not a true signal when you're not active? Also, like both of those are true signals. So, yeah, I don't even think it fully holds up from what they're describing themselves. But again, the reason why I wanted to share the study and also bring those things up was because of this added layer that they that they bring in on top of calories and calories out. And the this idea of partitioning, that I don't think is talked about.

Mike 55:27
Its also is somewhat contradictory, as far as a solution for somebody who is overweight or obese. Because if you're in an overweight and obese state and you're shunting your you're shunting your your food, your fuel, into your fat stores, and then you go and exercise, you're already at a deficit as far as energy goes. So then is exercise going to increase your deficit on the cellular level of energy, and then trigger an increase in food consumption, and it gets shunted more into the fat stores like it doesn't. It doesn't solve the middle piece there, still.

Jay Feldman 56:00
Yeah, from their nomenclature, you're just adding a true signal on top of a false signal. So you're just adding the equivalent amount of hunger to make up for the fuel used, the energy expended from exercise, so you've still got the same amount going to fad. It doesn't actually change that. And you just added a little bit more food and added a little bit more activity. Yeah, it doesn't even make sense.

Mike 56:19
But make the but you're making the energy deficit worse because it's being shunted to the fat. So that's arguably worse from this perspective.

Jay Feldman 56:29
Yeah, yeah. So it's definitely a missing piece there, for sure, a handful of them, yeah. So this is the part at the end. I think this is the last part that I highlighted to discuss, yeah. Okay. And so this is kind of coming back to what you were talking about earlier, about earlier, about what is, you know, on the larger societal level, what's actually causing obesity, and, you know, and is it just as simple as eating too much? And so they point out a couple of the problems with that general idea of it's just eating too much. And they say, so this is their second point. They say simple carbohydrates, such as dietary sugars or including dietary sugars and starches and fats are often presumed to be causal factors of obesity. Yet there are populations that consume substantial, substantial amounts of these macronutrients with very low prevalence of obesity and metabolic diseases, and they cite a, you know, a handful of papers that are, that are showing those populations again, this is, this is not like an in depth explanation, physiologically about why these things are not problems, which we have have offered, you know, a lot of previous episodes. But just looking at it on the simple observational level, if it was as simple as sugar, you know, simple carbohydrates and fat causing obesity, of course, you would see it in these populations that that consume large amounts of those things, and that you don't see it. And so obviously there have to be at least other factors at play. And then last or the last point, I want to highlight their fourth point. They say there's no evidence that chronic positive energy balance, again, they're talking about weight gain is driven by the widespread availability of inexpensive, highly palatable foods and beverages. If this speculation was true, all humans in high income nations would be obese because these foods and beverages were ubiquitous from multiple generations, as such fat cell hyperplasia and or physical inactivity. Eat low metabolic flux induced increments and energy intake behaviors provide a more rigorous, mechanistic explanation for over nutrition. It's funny that they're highlighting how there's how their explanation is more mechanistic, but yeah, so ignoring that last piece there again, they're just saying, again, just the very simple idea that the availability of inexpensive, highly palatable foods and beverages, the idea that that would cause obesity, obviously, is not the case. Because everyone who would have those available, and would, you know, eat them in some amount, would become obese. Obviously, every like, whether the people eat them often or regularly, everyone has tasted these things, you know, and so if some, so there's Yeah, again, these are very like, it's kind of a very simple point against it. It's not really arguing in depth or touching on the physiology, but it's not very strong, yeah, yeah, not very strong arguments. But I just thought there were little things worth, worth highlighting, yeah?

Mike 59:13
I just, and I also like, it's like, since that hypothesis doesn't make sense, ours, obviously, is the one that like ours, ours is more mechanistic and more rigorous. So therefore, like we have a this is a better eye bosses, because this one doesn't make sense for this reason is very weird argument, very weird arguing

Jay Feldman 59:33
Yeah, and obviously that I highlighted two of their last now to six reasons or something, and obviously those other ones were not even worth mentioning.

Mike 59:43
There's definitely a good the article has good perspectives, like the perspectives, the the movement in the direction I going, I think is great, but I think that, like, then their extensions from that are like, it's, it's, it just becomes, oh, it's just because you're not moving enough. It's the argument comes from. You're eating too much, and you're just eating too much, just too much calories in, too much calories, and not enough calories out. And then they're like, Okay, it's not about that. But then it's like, Oh, you just need to move more because of this energy, this this, uh, fuel flux between the the liver fat and the rest of the body. It's like, they like, start to move in the right direction, but then it's just not. Then at the end, their extensions of it are just like, Yeah, not really. There's probably way more to the picture than that.

Jay Feldman 1:00:30
Yeah. And how myopic to say like, there is this whole piece of fat loss physiology that people are not talking about, the partitioning that can occur regardless of the amount of food coming in, or even considering the amount of food coming in, but it can regulate in so many ways. And then to only talk about physical activity and fights, fat cell hyperplasia, meaning increased numbers of fat cells, not even to talk about hormones, right? They didn't even touch on glucocorticoids, thyroid hormone, you know, hormones like, how can you talk about this sort of fuel partitioning and not even mention those things, it's and again, not and the hormone still being a layer above what's, you know, really going on underneath, just kind of being a reflection, as you said, a signal of those things. So yeah, certainly, a lot of pieces that are missed.

Mike 1:01:14
But, well, I didn't even go into Cellular Physiology and the differences right and signaling between beta oxidation versus Yes, versus carb oxidation, or anything like that. So they're like, it's purely just like, it's like classical, like some of the classic obesity researcher work, which is just like some argument about calories in, calories out, and you need to eat less and exercise more, and you need to, like, eat better, like your fruits and vegetables, like some, there's so many papers on PubMed like that, and then just describing some generic answers about these things, instead of trying to, like, look in it to the from these multiple layers and angles, etc. So because, because you, if we're going to talk about obesity or or diabetes or chronic disease or overweight, you have the perspective of okay, of endotoxemia from the gut. You have the issue of polyunsaturated fatty acids. You have the issue of nutrient deficiencies. You have the issue of like peripheral serotonin from coming from the gut. You have the you have arguments around around cortisol signaling, not only your elevated glucocorticoids and elevated estrogen, particularly in an elevated estrogen, overall lowering of steroids. But then you also have what we're talking about on the on the cellular level now, where you have the 11 beta HSD, one and two, and changes which, which adjusts the production of active cortisol versus cortisone, which is the inactive form of the glucocorticoid, having adjustments of those ratios. And then, like, there's so many different layers and angles to look at from this, and they all work together nicely in the same system. And these are kind of like surface level arguments, and they're almost like, they're almost like philosophical arguments to some extent, about the physiology, or like, in the sense that it's, it's like trying to think of, how are we thinking about this, rather than getting into the like, into any of these other mechanisms. But when you start to get into some of these other mechanisms, and some of these the other things that you look at, like, for example, Cushing's disease, as you mentioned, you start to get this perspective that changes how how you it, changes how you think about it. When you start to go in depth.

Jay Feldman 1:03:22
Definitely. Yeah. And you need to have the type of paper, the types of papers that are looking at things philosophically, right, you said, or from a bird's eye view, and trying to put those pieces together, they're just missing a lot of pieces. Yeah, yeah, yeah, yeah. I don't have anything else to add from, from that paper to you.

Mike 1:03:43
I think it started off well, and then the back end just was the their concluding point that you at least the fourth one that you read there was disappointing.

Jay Feldman 1:03:53
And obviously, like, you know, I skimmed over almost all of the points that they brought up regarding the whole idea of of fat cell hyperplasia and low physical activity driving these things because of that, because it really felt like it was those. Those were not valuable parts from the paper.

Mike 1:04:11
Yeah, yeah, yeah. Overall, I think that's nice to see the perspective changing.

Jay Feldman 1:04:17
Yeah, yeah. Still blaming people just being I'm being inactive.

Mike 1:04:22
Yeah, you're sitting down too much.

Jay Feldman 1:04:26
Yeah, but I guess it's better than I don't know. But the other thing too is, at the end there, they basically, you try to make the argument that it still doesn't matter what you eat, right? Like they were talking about sugars and fast snapping the issue a little bit earlier. I didn't highlight it, but they said something about, maybe I can pull it up, but they're just talking about how, yes, they state, thus, it is not what is eaten, ie, diet that engenders health or disease, but what one's body does with what was eaten. IE, nutrient metabolism, therefore, macro and micronutrients cannot have health effects independent of the metabolic phenotype of the. Consuming individual dietary components per se cannot be the determining factor in obesity and metabolic health. Thus, obesity and type two diabetes are not dietary concerns, but are metabolic ones. And then they cite their evidence. They say evidence in support of our argument is found across disciplines. And then they go on to state those six points, and it's like the there, there's a complete ignorance that diet and the nutrition that's coming in can also affect metabolic health and can affect the food partitioning and can affect everything else that is that confers health and metabolism. And so there's, again, just a highlight of how ignorant this paper is to those things.

Mike 1:05:47
Well, yeah, well, it's hilarious. That's actually hilarious. That is extreme ignorance, especially when you consider that like it's for example. So the drugs that we take that come from sometimes come from the foods that we eat. They don't have any effects. It's just, it's you need to, need to exercise. So your omega threes that lower your triglycerides, not and I'm not arguing in favor of that. They don't have any metabolic effects, right? But they're right that they don't do anything. They're macronutrients, which that is ridiculous, and especially considering that, like, as an example, omega threes are pharmaceutical drugs.

Jay Feldman 1:06:26
Yeah.

Mike 1:06:27
You can't even get more insane than that.

Jay Feldman 1:06:30
Yeah, yeah, it, uh, it's pretty insane. And there's, there's something else that they said, Uh oh. Again, there's so they come back to physical activity, and then this hereditary piece of things, which, interestingly, they talk a lot from the hereditary side, not of it being stuck in set in stone genetics, although they do talk about that as a factor in metabolic phenotype, you know, affecting metabolic phenotypes of things. But they also talk a lot about maternal nutrition, and so I don't know it's like, again, still a weird, weird separation to create, like, nutrition only matters until you're born, and then it doesn't, like, nutrition only matters for the mother until you're born. And then they do talk about during development, like, up until age, I don't know, 13 or something, how that's when mostly your fat cells number is determined unless something major happens or you get obese after that point. And it's like, so nutrition only matters during that period of time, and then after that, nothing matters. Yeah. It's again, kind of ridiculous.

Mike 1:07:33
Well, yeah. And then the same thing too, with like the maternal hyperglycemia or maternal or gestational diet, gestational diabetes, so the fetus essentially gets prioritized for excessive blood glucose. And they were they or excessive glucose, they were saying, then they were saying that that predisposes towards obesity, right, right? Which is so saying the fetus is getting in excess of glucose and that predisposes towards obesity, but diet is not important. Like, macronutrients are not important for your health. It's just, you know, it's just exercise, essentially, and it's the same, it's the same thing. You were making an argument and saying that starvation and excessive exercise created an excessive amounts of free fatty acids, and that triggers this metabolic response. But then it's like, okay, so keto diets, which also do the same thing, doesn't trigger the same metabolic response, like it that's, yeah, that's so it's such an it's interesting that they're holding those, those views simultaneously.

Jay Feldman 1:08:36
Right..yeah. And as you said, like medications are working through the same mechanisms that nutrition is working through like, it's not like there's two separate sets of physiology or three. Like, one is how our fat metal like, how our body fat metabolism works, and body fat physiology of gaining and losing weight, one is nutrition, which is also separate from that. And then one is like everything else that works on physiology, like medications, and those things don't affect each other at all. Like, what a what a weird, foreign concept. The other thing I wanted to add real quick was just that those figures I pulled up earlier, the title of that study was decreased energy levels can cause and sustain obesity. Just for anybody who wants to take a look at that study, it's a it's a good one to look through. Maybe one will break down. If people are liking this style of episodes. Maybe we'll break that down in the future. Because, yeah, it's another one that I think is really, really great, and brings, you know, brings a lot of great things to light. But there is, again, still, I don't think it creates a full picture. They talk about the issue with converting fuel to energy. They talk, I believe, about endotoxin doing that, and excess nitric oxide. But they don't, you know, they, they kind of zero in on just a couple of mechanisms there, and don't really acknowledge others. But anyway, it's a good paper to take a look at as well.

Mike 1:09:48
I think it's uh, I think this is a good point about studies, right? You have, there are studies that say great things, like, there's some points in some in a lot of studies that are amazing. Right, but then there's also, can be a lot of crap that comes with it. So when you're reading a study, if you find some points that are great, it doesn't mean that the rest of the study is right. And on the flip side, just because some of the researchers points are off or you don't agree with them, or they don't make sense, doesn't mean that there are other points in the study that don't make sense, like there is like this goes even outside of studies, like in different dietary camps, right? So like, the Vegan, Vegetarian dietary camp talks about like meat putrefying in the colon and why you shouldn't eat that there's legitimate there's a legitimate perspective there that's been shown that exposing the microbiome to large amounts of animal proteins alone, by the by themselves, can lead to production of certain metabolic products from the bacteria's metabolism that cause issues. That's a great point. There's there's validity there. There's something to take into consideration. It doesn't then mean that no meat is the answer.

Jay Feldman 1:11:00
You mentioned that you mentioned this whole situation and touched on a great study discussing it in our nutrition with Judy, discussion on her thoughts on repeat. And there were comments saying, Oh, we're not supposed to eat meat now. And so I'm glad I think we mentioned at the time that that's not at all what we were saying. I think it's always good to highlight that. But anyway, yeah, so you're saying.

Mike 1:11:24
Well, the thing is, is that there's workarounds for it, right? If, if eating, when you eat meat with polyphenols, different fibers, vegetables, fruits, etc, the production of those compounds are severely limited, severely limited. Plus it's a quantity thing, if you it's a digestibility thing as well. Certain things impair the digestion of proteins, like you're going to eat with a bunch of beans, you may find that you have more protein in your colon, and then you maybe perhaps more of those metabolites. Like there's, there's a whole host of factors that go in there. It you don't need to have such a drastic extension like that. And it's the same thing kind of happened, I think, with some of these researchers perspective, in this past study, where it's like, okay, there's metabolic partitioning. We have the liver, we have muscles, we have fat cells, and then you have all the other cells. It's like, that's another thing I want to point out. And this is a little tangential, and a lot of these studies, like when they talk about insulin resistance and things like that, their only thought process that you hear about, or the only areas you hear about is like, Oh, the liver glycogen, muscle glycogen and then fat. It's like as if those are the only areas, like, yes, where glucose or these substrates can be disposed of. And it's like there's a whole bunch of other areas. It's just insulin is important in those areas, because those are the areas primarily exposed or presenting glute four receptors, whereas the rest of the body is just taking up nutrients, particularly carbohydrates, kind of add libitum as they want, as they need. So there's a, yeah, I think that it like with these researches, it's like we have all these different nutrient partitioning systems. So the perspective then becomes, oh, we need to make sure that those aren't always top topped off. So you need to be moving around. You need to be, like, expending, like, clearing out those stores, essentially, to make more room. And therefore you then you won't get like, a metabolic issue, which is just, it's, it's just like a softer version of calories and calories out that prioritizes exercise, like, Eat less exercise more. They're just like, Oh, you just need to exercise more. They move heavier on that, even though some of their perspectives are bringing to light the ideas that we've discussed before, about the idea that you have multiple cells in your body that have multiple requirements simultaneously, like that. It's, yeah, it's just an interesting extension. It doesn't mean that, like the point that some of their points were good, but then some of the other stuff is that we talked about is like, what is this right?

Jay Feldman 1:13:39
One thing that that makes me think of from this study, which is another really good piece that it brings to light, other than the just the partitioning piece, is that they're saying that weight loss and health, you know, healthy body fat loss does not result necessarily from a deficit, but rather just being able to properly Meet you like to have an appetite that aligns properly with needs. And as we were kind of saying, when you have the larger picture in mind, it always aligns. It's just, what is that need? Is the need to hold on to body fat, or is the need not to have body fat, but or not to have, like, excessive amounts of body fat? But I like that they aren't saying the solution here is just you need to be taking in less than you're eating, or, sorry, taking in less than you're burning. But rather that, they're kind of saying, as long as things are functioning, okay, those everything should line up well, as far as your appetite and your needs, like metabolic needs, and you should be in at a healthy weight. Again, they throw in a bunch of other things that are not that, but that is another piece that they kind of bring to light. And even though we don't fully agree with it, I think it's a way, way healthier approach compared to the...

Mike 1:14:57
The gluttony model?

Jay Feldman 1:14:58
Yeah, just again, just. Just, I know I say it every single time, but I don't know of anything more damaging than telling people that eating less and exercising more is the solution for their for their weight problems. It's, I think it is largely responsible for the destruction of human health, again, in a large sense, again,

Mike 1:15:19
That and the foods that they're recommending to eat,

Jay Feldman 1:15:21
Well, exactly. And that's the extension of it, right? Is it doesn't matter what I eat, so I can eat any like, whether it's vegetable oils or or grains or whatever it is, because all that matters is how much I take in, and I have to make sure I just take in less. Yeah. So, yeah.

Mike 1:15:34
Because there's some professor, right, who ate a bunch of Twinkies, but he ate less than his calories, and he still lost weight. Like that. I hear that all the time. It's like, okay, fine, but I'm sure, like, is the other thing is weight. Is weight the ultimate determinant of health?

Jay Feldman 1:15:49
Right? And obviously you can see weight loss studies where people are losing, uh, fat, free mass, you know, they're losing muscle. There's also the question of, is it sustainable? Does it last for a long time? You know, they start causing various other metabolic problems that down the road will will prevent him from being able to lose weight on his low calorie Twinkie diet. Yeah.

Mike 1:16:10
The other thing too is there are, and this is, this is mind blowing. So everyone just, just be ready. There are people who have normal weights, that have cancer, diabetes, heart disease, etc, I know it's, it's, it's absolutely mind blowing. Is obesity a factor that it exacerbates those situations? Yes, in a lot of times, yes. But there's also the hospitals filled with normal, white people, healthy people, healthy weight. People healthy weight, exactly that eat less and exercise more and still have heart disease, etc.

Jay Feldman 1:16:51
I can't tell you how many times I've had someone tell me that their doctor was so surprised that they had a heart attack because their cholesterol was fine and for you know, their age, their weight was good, and they're active, and they eat well, and they eat healthy. You know, these are not necessarily people like these are not people who eat healthy in the way that we're talking about, right? They're people who do the standard things that they're supposed to do. And everyone's doctor is just always so surprised that all of their healthy patients having heart attacks and whatnot.

Mike 1:17:20
Yeah, yep. It's, yeah, there's no, it's, it's, there's no else to go that. I've seen it too. I have people in there. I have people in the hospital yesterday who I'm looking at their lipid panel, and tomorrow they have to go on to get a heart cath, have stents placed, and their lipid panel's fine, and they've been on statins for X number of years, and they still need to go get stents placed. It's just and, and they have cancer, and they have etc, etc, etc, like, that's an everyday thing you have. I have obese people coming in, guys with these massive bellies coming in, which is that that central obesity, which with high amounts of visceral fat, which is the worst, which metabolically is like one of the worst things, according to the research, at least, or associated data, etc. And their lipid panels look great. Their cholesterol is great. It's excellent. It's below 200 and their triglycerides aren't super elevated. And their hemoglobin, a 1c is is, you know, 5.6 so it's just, it's elevated, but not that much. But they have massive bellies, massive, big, massive, old bellies. They're obese. Their legs are purple because their venous circulation is so poor. They've already had stents placed, and now they're getting more and it's just like, but their labs look great. And then the guy will tell me, Oh, I'm trying to lose weight. You know, for the past X number of months, I've been eating less, etc. It's like they have clear metabolic dysfunction. Regardless of what these things are saying, regardless of what these things are saying, even though they're they're cholesterol is 190 or whatever it is, and they've been on statins for the past 15 years, or whatever it's just, it's clearly more to the picture than those things. But yeah,

Jay Feldman 1:19:06
Yeah, all right, that's going to wrap up today's episode. If you did enjoy it, please leave a like or comment. If you're watching on YouTube and if you're listening elsewhere, please leave a five star rating or a review on iTunes. All of those things really do a lot to help support the podcast, and are very much appreciated also. Let me know in the comments what you thought of this different format where we were kind of walking through this particular study and extrapolating and explaining our thoughts based on that if you'd like us to do more episodes like this. Let us know if you'd like us not to do more episodes like this. Let us know as well, again, either in the comments here on Youtube or at the show notes. You can leave comments as well. And the link for those show notes is Jay Feldman wellness.com/podcast and if you head over there, you can also take a look at the studies and articles and anything else that we referenced throughout today's episode. And if you are dealing with any low energy symptoms, maybe those are related. To the topic we were discussing today in terms of regulating hunger and appetite or preventing weight gain or allowing for weight loss, or maybe it's other low energy symptoms like fatigue or digestive symptoms like bloating or brain fog or poor sleep or hormonal imbalances, or various other symptoms or chronic health issues. Then head over to Jay Feldman wellness.com/energy, where you can sign up for a free energy balance mini course, where I'll explain how these different symptoms and conditions are really caused by lack of energy, and I'll also walk you through the main things that you can do from a diet and lifestyle perspective to maximize your cellular energy and resolve these symptoms and conditions. So to sign up for that free energy balance mini course. Head over to Jay Feldman, wellness.com/energy, and with that, I'll see you in the next episode.