Ep. 86: Robb Wolf on Ray Peat and the Bioenergetic View: Stress & Blood Sugar 

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In this episode we discuss:

  • Whether it’s stressful to be in a fat-burning, keto-adapted state
  • How blood sugar is regulated when we’re not eating carbohydrates, and how this impacts stress hormones and thyroid hormones 
  • Whether having stable blood sugar levels on a low-carb diet is a good thing 
  • The problems with elevated levels of glucagon, which occurs when someone is on a low-carb diet   
  • Why glucagon is a stress hormone and its impact on thyroid hormones 

4:30 – why we wanted to discuss Robb Wolf’s perspective of the bioenergetic view  

8:25 – Robb’s main points against the bioenergetic view

9:52 – whether fat-burning and being keto-adapted is stressful and how blood sugar is regulated in these states 

31:29 – the problems with elevated levels of glucagon, which occurs when someone is on a low-carb diet 

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Jay Feldman 0:04
Welcome to episode 86 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. In today's episode in this series, we'll be discussing Robb Wolf's perspective on the bioenergetic view and explain or clarify some of the misunderstandings of the bioenergetic view, as well as trying to bridge the gap and find some common ground, while also explaining some of the key differences between our views. And before we dig into this episode or get into this episode, I do want to clarify, make it clear that this is, of course, not personal at all toward Rob. And as I was saying, we are really trying to bridge the gap here and maybe allow this to be the beginning of a longer conversation or discussion together. And with this in mind, with this series, we wanted to dig into some of the points that he brings up in an episode where he was asked about his thoughts on the bioenergetic view. And part of the reason for this is because these are points that we've heard to be brought up pretty frequently, especially from people who are either newer to the bioenergetic view, newer to this podcast, or who are coming from an ancestral health, carnivore, low carb, paleo, primal way of thinking, and so that's why we wanted to dig into the responses or the thoughts from Rob. And we also had tried to keep this rather quick. We tried to keep this as a shorter response, but as is typical for us, we ended up getting into the weeds a little bit. And so this became a two part episode, but again, I do think it was worth it, because we did dig into some pretty important points here and some pretty common, again, misunderstandings, I guess you could say, of the bioenergetic view. So with that in mind, in today's episode, we'll be talking more specifically about whether it's stressful to be in a fat, burning, keto adapted state. We'll be talking about how blood sugar is regulated when we're not eating carbohydrates, and how this impacts our stress hormones and thyroid hormones. We'll be talking about whether having stable blood sugar levels on a low carb diet is actually a good thing. We'll be talking as well about the problems with elevated levels of glucagon, which occurs when someone's on a low carb diet, and why glucagon is a stress hormone as well as its impact on thyroid hormones. If you are new to this podcast, then after listening through today's episode, I'd highly recommend you go back and listen to episodes one through seven, where we took some time to dig into and explore the foundations of the bioenergetic view of health. 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 these are symptoms you've tried to rectify with a lower carb diet or a primal approach, or carnivore type diet, or maybe these are other low energy symptoms. Again, this could be anything from chronic cravings and hunger, low energy or fatigue to joint pain, weight gain, digestive symptoms like bloating or constipation or any other gut related issues, brain fog, poor sleep, hormonal imbalances and on from there, any of those low energy symptoms, or if you're dealing with any chronic health issues that, again, maybe you've been trying to resolve from these or through these different approaches, 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 a 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 menu, course, head over to Jay Feldman wellness.com/energy, and with that, let's get started.

All right, so we have been sent over this clip from Robb wolf discussing his thoughts on the bioenergetic view and Ray peats work on his podcast very briefly, but he had gotten a question about, you know, what he thought about it. And so we figured, you know, someone had sent this over, asked our thoughts on it. We figured we would share our thoughts. And there was a few reasons why we wanted to discuss it. For one, I think that there are some very common kind of misunderstandings or misrepresent. Presentations of the bioenergetic view from Rob's response. And I think it's really common from the people who are in that camp to have this view of, kind of the bioenergetic space, or perspective on health. And so I felt like we felt like it was worth kind of dispelling some of those misunderstandings, or kind of bridging those gaps. And I think the other reason why it's important to do that is because the view that we have in the, you know, of the bioenergetic view, I think, is actually a lot closer in some ways, to the alternative health views than is sometimes thought, because the actions tend to be very different. But I think there's a lot more overlap than there isn't. And of course, the part that isn't overlapped, I think, is really, really important, and that's what we'll be discussing today. But yeah, so those are some pretty, you know, key differences. I want to point those out, but also I think there's more overlap than is realized, and with this as well, I mean, I'd like to kind of bridge that gap, maybe find some common ground. And you know, we'd both also be happy to discuss this further further with Rob. So, of course, no no disrespect to him or anything, just kind of wanted to discuss the differences, and if he's open to it, maybe we'll discuss it on his podcast, or podcast or something like that. Is there anything else you wanted to mention before we dive in Mike?

Mike 6:16
Yeah, this isn't a there's no ad hominem here. This isn't a personal attack. This is literally just talking about concepts and ideas and trying to create an understanding for things. I feel like there's also in the lower carb aspect of things, perhaps there's a maybe not a full flushing out of what we're talking about with the bio, bio energetic idea. And I think part of this was evidenced in some of like the statements, and no, you know, not trying to call out Rob or anything like that, but it's we want to kind of clarify what some of those statements are, or what some of the perspectives are in the bioenergetic camp, so that there's no discrepancy in what, or at least our perspective of the Bioenergy energetic camp. There's no discrepancy in what we're discussing. There's no, like, you know, false idea of what we're discussing. And then kind of bring together some basic ideas, or some some counter arguments to some of the points that are proposed in opposition to what was claimed to be the point of view, or the bioenergetic point of view altogether. And I know that who in this, in the point of view, Rob was kind of discussing Ray and Matt Stone, so I don't know what this their what specific views he was pointing on those, but we're going to talk about, like the general overarching ideas here.

Jay Feldman 7:37
Yeah, yeah. And of course, that kind of Yeah, not being necessarily a clear representation of where I think this space is at, but that's, I think, reflected right in some of the points he describes in terms of the bioenergetic view. And of course, for people who aren't aware, this is a view that we subscribe to, that we kind of view things through. I know we're kind of separating ourselves from that, and I think that that's just helpful, because I think it's helpful to separate yourself from the views that you hold, as opposed to identifying with them and then being offended or insulted when someone you know has an issue with that view, or anything like that. But just for people who are maybe new to the podcast, this is the view that we that we hold in terms of health. So that's part of why we're more or less defending it or, again, just trying to bridge the gap here. Yep, perfect. All right, so I'll just start by summarizing a few of the points that Rob made, and then I'll, you know, we'll, these are the few points that we'll be dispelling. So the first is essentially that he's saying that low blood sugar is not a problem if you're fat or keto adapted, and so in those states, it's not stressful. It's not stressful to be keto or fat adapted. And this is in opposition to the general view from the bioenergetic standpoint, that low blood sugar is a problem and drives stress. And even if there's not consistent low blood sugar seen in these states, these are stressful states. So we'll explain the details as to why that is. He also a couple other kind of points he made. One was that, in reference to the bioenergetic view, being a view where we're trying to increase the amount of energy available to the organism, Rob mentioned that he feels like, or he's of the belief that most people are not actually lacking energy, so we don't need to focus on increasing it. And he used, you know, the evidence of obesity and people being overweight, and we'll explain why. That does not mean that people are actually lacking or that people are not lacking energy, and this doesn't mean that they have excess energy. So we'll dig into that. And then the last is this idea that the bioenergetic view ignores evolutionary biology and is ignoring what has gone on ancestrally. And we'll discuss why that's not the case. There's just some differences in our view of that evolutionary biology and what that means for us physiologically and nutritionally. Yep, awesome. So we'll dig in with that first one, basically this discussion that low blood sugar is not a problem or. I guess what he says is that low blood sugar is a problem when you're a sugar burning machine, but if you're reasonably fat adapted or keto adapted, low blood sugar is a non issue. Just doesn't happen. So being fat or keto adapted isn't stressful. I'm paraphrasing here, Mike, I know you had some direct quotes on if you wanted to. I can read them if you want. Yeah, just like kind of the main one or two that kind of encapsulated that.

Mike 10:23
So there's a there's a couple points he brings up. There's the he does acknowledge here that he says early in the Keto adaptive state, cortisol is elevated, epnephrine is elevated, if one is properly electrolyte, that is largely mitigated. So he acknowledges first that in the early stages of keto there is stress. And then what he winds up going and also discussing now, these aren't chronologically in order. These are just his direct quotes, kind of out of order from the video, but low blood sugar is absolutely a problem. When you're a sugar burning machine, if you are reasonably fat adapted, and particularly if you are keto adapted, low blood sugar is a non issue. It doesn't happen. And this is one of the things that I think the ray PD and folks just don't get. There's a very different scenario, or if you are even marginally fat, fat adapted. He also says here, you look at CGM so continuous glucose monitor traces of people on a ketogenic diet, particularly people on a carnivore diet, it doesn't change. It's just rock solid. And because the body can produce glucose from a whole host of things, gluconeogenesis, from amino acids, from the glycerol backbone of fats, or triglycerides, more specifically, and that is not inherently a stressful process. So we're gonna the last piece. I think that's helpful here says so I think that these folks, the rapedian folks, are being really selective, that they're taking the hypoglycemic state of somebody who's carb dependent, primarily carb dependent, and they're applying that scenario in which people are carb independent effectively. And so he says, It concludes all these things. Leave me saying it's kind of that you're just going to paint low carb diets uniformly as some sort of stressful situation. They're not appropriate for all people. So those are the main quotes that we're going to be parsing out. We're gonna Claire, we're. Those are direct statements from Rob in the podcast. Those are not paraphrased. They're not in necessarily in order. I, when I we pulled them out together, we tried not to, like, leave out any section to mischaracterize what Rob was saying. That's why they're kind of dense quotes. So they're, they're, that's specifically indirect what Rob said in multiple elements in regards to the low blood sugar piece. Now what we're going to do is we're going to talk about why the you don't see low blood sugar inside the Keto and carnivore diets. Why that? What's the mechanism behind that? Why that mechanism is stressful, and then what our actual position is from the PDN sphere, or the bioenergetic sphere, however you want to, whatever you want to term it in terms of low blood sugar, because we're not just talking about low blood sugar. Where you in. You eat carbohydrates. Your blood sugar peaks up an hour later, and then two hours later, comes back down. And now you need to use glucagon, adrenaline, cortisol, etc, to bring that blood sugar back up to a normal level. We're talking about like even in those situations where blood sugar isn't having peaks and troughs, as you see in carnivore and keto, what mechanisms are behind that consistent blood sugar and how is that problematic? So we're gonna kind of go through all of that and parse all of that out. So it'll involve a steel Manning to steal Danny, one of Danny's favorite words, and then also, like a discussion of the mechanisms behind and why it's problematic.

Jay Feldman 13:29
Right? And and this is part of the reason also why, at least personally, I don't normally use the nomenclature of low blood sugar being a problem in terms of these states, because it's, as Rob is saying, it's not actually the blood sugar, right? Blood sugar is very, very stable when you're on a low carb diet. He referenced ketogenic diets. He referenced using this for people of Yeah, Carnival, but he referenced using this for people who have type one diabetes, and that is really easy for them to manage the exogenous insulin that they need, because their blood glucose is really predictable, very, very stable. And he also mentioned just kind of another and this, I don't remember what the phrasing was, but he mentioned that you don't see Cushing syndrome in ketogenic diets as well. And this was part of what he was saying, like, how can it be stressful if you don't see that? So we'll kind of talk through that as well. But the as we're kind of getting at in the initial phases, in the initial shift into a low carb, fat adapted, ketogenic adapted state, if you want to put it that way, there are dramatic increases in stress hormones, namely, as you said, glucagon, adrenaline, cortisol, growth hormone as well, which all of those help to increase blood sugar. When blood sugar is decreasing, and you'll see major increases in these and that's in the short term. Then after someone has really adapted, you don't see the dramatic increases in those things at baseline, other than glucagon, which we'll discuss. And that is why, and because of that, you see very stable blood sugar, or, I guess, as a kind of a result of the stable blood sugar, basically what. Happening is you're not having blood sugar fluctuations based on carbs that are coming in, but rather, you're producing the carbohydrate endogenously through gluconeogenesis, and this is driven largely by glucagon, and so you have pretty stable blood sugar. But our The problem with this, I think, is kind of twofold, but one is that we don't want to just look at this endpoint. And we do this a lot, right? It's talked about a lot with cholesterol, you know? You don't want to, just like, paint high cholesterols as the problem. We want to consider why it's happening. Same goes for blood sugar, where high blood sugar is not the problem in insulin resistance and diabetes, but rather, it's a symptom of underlying issues that we'll talk a little bit about, and have talked about extensively before, and I'll link to. And by that same kind of thought process, the idea that any time blood sugar increases is bad, is based on that same reasoning, and so definitely don't agree with that. And the flip side, again, is just because your blood sugar is extremely stable doesn't mean it's always good, and by stable, we mean not really fluctuating. And in this case, that's because that blood sugar is driven that is kept stable by a steady production of glucose through gluconeogenesis, which requires glucagon, and that comes at a major cost. And I'll get to that in a second. Mike, I know you were going to chime in..

Mike 16:17
Yeah. So the one thing I want to just give people an idea of before. Like to give a context for everything that we're discussing. When you eat carbohydrate, you have a raise in blood sugar. Your blood sugar elevates, and then your body will release insulin, etc, and then you basically will see that blood sugar come back down. So the general glucose curve, or glucose area under the curve, is peaks in an hour, comes back down two hours later. Now, on a low carbohydrate, ketogenic diet, carnivore diet, anything with a very large, low amounts of carbohydrates, you don't see these curves. So that's that's the difference that we're talking about here. Now, in order, when, when in a regular situation where you have that peak, and then two hours later you're coming back down to a baseline blood glucose level. You have to elevate these adaptive hormones, adaptive or stress hormones, and they're the reason we they turn them adaptive is because they're helping you adapt to the current situation that you have in that moment. So in the moment where you've eaten your meal, it's about three hours later, your blood sugar's coming back down to baseline and is still continuing to drop. You don't have adequate amount of blood sugar available, so your body uses glucagon to break down some of, at least initially, the glycogen that you have stored inside your liver to then maintain blood sugar. So the raising of that blood sugar initially and then it coming back down, is a normal process. It should happen it you, and it's mediated by a series of effects, but largely insulin is released in response to the carbohydrate. And an insulin is a master signaling hormone, and it's an ANA, very anabolic hormone. That's saying, Hey, we have a lot of nutrient, specifically carbohydrate, on board. We don't need to keep breaking down or catabolizing Being in a catabolic state of our glycogen, our protein tissue and our fatty acids to create more glucose to flood the bloodstream with pre fatty acids. We have it coming in exogenously. Let's build back our stores. Let's, let's, you know, replace what we just broke down, etc. Now that creates the curve. Now, at the bottom of that curve you you will then activate glucagon again, which is basically saying, Hey, we don't have enough. We're going to start breaking stuff down again to make to maintain an adequate blood sugar, because maintaining adequate blood sugar is extremely important for essential nervous system function, for other tissue function as well, like the testicles, the red blood cells, etc, the some of the cells within the kidney are all directly require blood sugar. Now, on the low carb side, when you don't have those carbohydrates coming in. You don't have that insulin response. You don't have that drastic increase in blood sugar, and then it raised back down the baseline. You just have blood sugar being maintained through the catabolic, catabolic process of glucagon, growth hormone, adrenaline, cortisol, to some extent, mostly glucagon, after your fat adapted on a perpetual basis, you're not seeing the curves. So whether the curve is there or not is like kind of irrelevant to the argument. The main point of the argument that we want to get to is you the period where blood sugar is being maintained at a low enough level that you need to trigger these hormones. And that's where the really important piece gets get situated here.

Jay Feldman 19:42
Yeah, and so, so kind of key points here that obviously regulating blood sugar is extremely important. That blood glucose is absolutely necessary for us to live. If we can't trigger these stress hormones in order to bring our blood sugar back up, when it drops, we'll die like we need to have enough blood sugar in the blood at all times. Is because it's massively important for the brain. Even if you're keto adapted, you're still using considerable amount of glucose there you mentioned some other areas as well. So it's very important. That's why we have these counter regulatory hormones, normally deemed a stress hormones. And the reason why they're also called stress hormones, and this is important because we'll, we'll be talking about this in a moment, is because they're released under stress. And that's because stress puts us in an energy deficit, which often typically involves drops in blood sugar, because the glucose in the blood is being used to produce energy, and so as it gets depleted, it triggers the release of these hormones. Now drops in blood sugar are not the only thing, so you can have maintained blood sugar at slightly higher levels, but increased stressors, so increased energy demands, and that will cause the release of these stress hormones as well. So the stress hormones are directly tied with the energy availability at the cellular level. When there's not enough energy there, they're released, they help to increase fuel availability by raising blood sugar, and that, ideally, will prevent the continued lack of energy. So that's why they're deemed stress hormones. I think in the low carb space, we were definitely of this belief at the time. We just thought of those as things that increased when you were psychologically stressed, or maybe physical, physically stressed as well. But it was never really pointed out the direct tie with energy availability and the direct tie with blood sugar. So those are really important, I think, important to highlight, especially for somebody listening to this who is not already familiar with that perspective. And I'll link back to episodes where we've discussed that in more detail in articles as well. So coming back to this state, as you're saying, when we're not taking the carbs in, we have to maintain our blood sugar on an ongoing basis using gluconeogenesis. And initially, the initial drop in blood sugar when we're first shifting in will lead to major releases in the stress hormones. But over time, we don't need as deep of the stress hormones just to maintain baseline gluconeogenesis, partially because our glucose needs go down, because we start using more fat and ketones, and partially also because there's some adaptation to to the stress hormones, and actually an increased sensitivity to that which we'll get to so when we're in a fat adapted to keto adapted State, and we need ongoing gluconeogenesis. This has to be performed under the presence of glucagon, that is the the stress hormone that is needs to remain elevated in order to keep a constant flow of gluconeogenesis. And that gluconeogenesis can be coming from amino acids, whether that's from protein we take in, or protein that's broken down from our muscles. Can also use the glycerol backbone from fat and as well as stored glycogen. But at this point in a keto diet, you're not really tapping into that as much, because you're not refilling it as much. So what I think is an important piece here, from Rob's view, from the low carb view. Generally, the idea is gluconeogenesis is a normal process. We've evolved to have this process. How could it be stressful? How could it be a problem to be relying on gluconeogenesis for our carb availability? And we'll kind of dig into this a little bit later. But just because we have processes doesn't mean that we want to be relying on them. Of course, if you rely on things that lead to the production of cortisol for excessive amounts periods of time. We know that's not a good thing, and what we're basically saying is that relying on this process of gluconeogenesis to provide your carbohydrates does a similar thing on a smaller scale, but it builds up over time, and largely that's mediated by glucagon, since that is the main hormone that's at least required in that state if you're not dipping in and out. Side note, for the people who are dipping in and out of ketosis, that means you're relying on those other stress hormones every time you go in and out. So I think you can argue that that's worse, and if you're Yeah, I mean, I would kind of leave it at that. But So the important piece here is that we are going to make the argument that gluconeogenesis is inherently a stressful process to further, to use an ongoing basis, yes, to maintain blood sugar. There's a few reasons for this. And well, there's one underlying reason, and then there are the kind of reflections of that reason in terms of hormones. So the underlying reason is that producing glucose from other substrates is not very efficient, and so I'll share a study here in a second that basically shows that it's 30% less efficient than just using glucose to produce energy if you wanted to convert amino acids to glucose to energy, it's 30% less efficient because of This inefficiency our bodies, and essentially this is wasting energy, wasting 30% of the amount of energy that you would need if you're producing energy from glucose. The our bodies don't favor this process because they need to, or they favor processes that are energetically efficient so that they can have as much energy as possible. We'll kind of get to that in a little bit. And because of that, our bodies don't favor this and they will when they have to rely on this process, they will signal it as a means of stress, or as a sign of stress, as a sign of a less than optimal environment where they have to operate under less efficient means. And we'll. Describe in a second how this ends up decreasing our metabolism overall, causing long term issues. And this is a protective mechanism, because our bodies know that they can't sustain the same energetic requirements when they're getting their glucose from through this inefficient gluconeogenic process. So I'm gonna share a quote from this study describing this inefficiency. So the study is titled gluconeogenesis and energy expenditure after a high protein carbohydrate free diet, and high protein was around 30 ish percent and maybe 35% of of energy, and that was the age condition that they're referring to. So they state that energy expenditure, or resting metabolic rate was greater in the H condition than in the n condition. The increase in energy expenditure was a function of the increase in gluconeogenesis. The contribution of gluconeogenesis to the change in energy expenditure was 42% so that was the change in gluconeogenesis was responsible for 42% of the increase in energy expenditure, and it says that the energy cost of gluconeogenesis was 33% and that's relative to glucose. I don't know if I cut that part off in the quote, or if that was later on in a different quote, but that 33% is relative to just using glucose to produce energy. Is there anything you want to add in about that Mike?

Mike 26:19
There's a couple things that I wanted to point out. It's the the overarching pitching picture with the gluconeogenesis process is that you were rather than having to dip into a stressful situation periodically with taking carbohydrate and then having to upregulate the counter regulatory hormones, to some extent, because..

Jay Feldman 26:40
You're saying, if you go too long without eating carbs after being on a car, like having carbohydrate rich meal?

Mike 26:46
I'm saying, if you don't have carbohydrate on a regular basis, if you move into that low carb, keto, carnivore, etc, sphere, then you're relying on the stress process perpetually, rather than just running, relying on a small function of glucagon in between meals on or or on an overnight fast on a smaller basis, because you still have gluco you still have a glycogen available. So rather than just having a like even though, with the blood glucose swings, as they would call it, in the lower carb sphere, you have to rely on glucagon in the other in the on the flip side, without adequate carbohydrate on a regular basis, you're just relying on glucagon all the time, especially in the initial period when you start to deplete glycogen and all and, uh, glycogen on a regular basis, and you have to upregulate free fatty acids and fatty acid oxidation. Well, then you're driving adrenaline, cortisol, growth hormone, etc. So you're rather than just like having to dip into glucagon, you know, periodically in between meals with adequate carbohydrate. You're just running on it perpetually now. So it's actually can, at least from, I would say, from our perspective, worse. And then, not only that, while running through gluconeogenesis, as you just pointed out, in comparison to to glucose, you're in a situation where you're you're having to spend or you're having to spend more energy to get the same outcome that you would if you just had glucose you have a the with gluconeogenesis, you're actually you have a less efficient energy production process. And the other thing to point out here is the gluconeogenesis can occur through multiple mechanisms that we kind of glanced over really quick. So you have the glycerol backbone from triglycerides, which is essentially just stored fatty acids, and then you have amino acids, and you have glycogenolysis. So breaking down glycogen glycogenolysis after a period of time on a low carb diet is probably minimal, minimal input to the to the system. It's largely going to be through amino acid catabolism, and then also fatty acid catabolism. Now, something that's not that's directly showed, that we're going to talk about in a few minutes, is that running heavily on amino acids actually, like on a high protein, low carb diet is worse hormonally than being on a lower protein high fat diet, because you have this map the with with a utilization of amino acids for energy production, you up regulate ammonia production. So you really have to be running ketogenic, like a high fat, moderate protein, low carb diet, and to not argue against the high, elevated stress hormones over a long, longer period of time. So you have...

Jay Feldman 29:19
You're just saying, because of the ammonia production in that state, you would still have high glucagon, whether or not you're eating high protein.

Mike 29:26
Yes, but in that state, you have high cortisol as well, right? And so the initial argument for Rob was that you would like in these low carb states, you don't see long term high cortisol, but it's only in the low carb moderate protein ketosis states that you don't see these hormonal problems. And that's bore out inside the carnivore keto research, and also inside the groups where it's like, if you're not doing well in keto or carnivore, you need to eat more fat and less protein. And so that's, I think, a primary point overall, is that the high. Protein and using utilizing amino acids as a substrate for gluconeogenesis. There's a limit to that. It becomes problematic. So you're relying largely on fatty acids, and then with the fatty acid piece, glucagon does drive the gluconeogenesis to a large extent, but involved in that process of liberating free fatty acids is cortisol, adrenaline and growth hormone. Now, once your fat adapted, you're not going to see you know, these massive, out of range stress responses, but you still have to drive these hormones in that system as well. And we'll touch on that in a bit. In a couple minutes, you still have to drive these hormonal cascades to continue to liberate substrate from your tissues to turn into glucose because you don't have adequate glucose, as opposed to just giving your system glucose. So it's a very it's like a very roundabout way to get adequate carbohydrate on board, and it is driving stress processes overall, which is like counter to what his initial statement was about it not necessarily being stressful, and especially if you're a fat burner, like as a fat burner, you are just driving the stress process on a continual basis. Rather than having to use some glucagon when you have a dip in blood sugar, you're driving it perpetually. So you're going to see it a flat curve on your glucose, sure, but that doesn't mean anything that it doesn't have up and ups and downs. You're still using the counter regulatory hormones. The problem is the counter regulatory hormones have to up regulate on the down.

Jay Feldman 31:31
Right, right and so at baseline, as you're saying, high glucagon is going to be present. Fat adapted, keto state. Anytime those demands are increased, you're going to then dip into the cortisol and adrenaline much quicker than if you're on a higher carb diet, where you would hit the glucagon first. So another way of saying that is that when you're in the low carb state, you're already a step into stress. You're already a step into the stress state, which is the spectrum, right? You have different depths of levels, and you see this in terms of the blood sugar response. First you have glucagon released, and then adrenaline and then cortisol. If it dips even further, it's kind of our last ditch effort. And so when you're already relying on glucagon, you're already a step into that process, and you're much more prone to the adrenaline and cortisol releases when you increase those energy demands. And so we'll share a couple of studies on that here in a moment. One thing I did want to mention, I pulled up that study, and there was another quote just a moment later, describing that it states that the cost of gluconeogenesis was 33% of the energy content of the produced glucose. So just for reference, that one actually has the comparison there and explaining that you're using up a third of the energy that you're going to be able to produce from the glucose anyway, just by using the gluconeogenic process, which is a huge amount. And that's why we don't favor gluconeogenesis. That's why it activates stress. If you want to zoom out and look at the evolutionary biology context, which we'll dig into more later. In terms of of running on this process, it's much less energetically favorable, and our bodies favor more energy in in terms of their signaling, and when there's not enough energy available, on the stronger side, you get cortisol. But even on the weaker side, you get something like glucagon. And as evidence of this, I want to dig into some of those effects of glucagon, and this is largely responsible for a lot of the effects that you see in low carb diets in terms of thyroid activity. So the first thing I want to touch on here is that glucagon is largely the hormone responsible or driving insulin resistance and diabetes, and so much of the time we're focused on insulin is as if excess insulin is the problem. We've explained extensively why that is not the case, and that excess insulin is only occurring because there's an issue with energy production in the first place, and with that because you already are in this energy deficient state, which, again, we'll get to in a little bit, as far as what that actually means, we're not talking about calorie deficient, but energy deficient. When you're in that state, you that is what triggers the release of the stress hormones. So when someone who is insulin resistant, they're not producing energy efficiently from glucose, they're in an energy deficit, and so they're producing excessive amounts of the counter regulatory stress hormones, including glucagon, and that's largely responsible for the hyperglycemia that's seen. And so got a couple of quotes here describing this, unless there's anything you wanted to touch on real quick before I share those quotes. No, go ahead. Okay, so this first quote is from a study titled glucagon and type two diabetes, the return of the Alpha cell. And they state that patients with type two diabetes suffer from fasting and postprandial hyper glucagon EMIA, meaning excess glucagon, which stimulates hepatic glucose production and thus contributes to the hyperglycemia characterizing these patients, it has become apparent that suppression of glucagon secretion or antagonization of the glucagon receptor constitutes potentially effective treatment strategies for patients with type two diabetes. So just describing that glucagon is contributing. Reading to the hyperglycemia, both fasting and postprandial, and that blocking this effect either the production of the glucagon or the effect of the glucagon is very protective in these states. Another quote here from a study titled pancreatic Alpha cell dysfunction and type two diabetes old kids on the block is very much related, and they state that recently, numerous findings indicate that the defects of glucagon secretion get involved with development and exacerbation of hyperglycemia and type two diabetes, aberrant Alpha cell responses exhibit both fasting and postprandial states. Hyperglucogenemia contributes to fasting hyperglycemia caused by inappropriate hepatic glucose production and to postprandial hyperglycemia owing to blunted Alpha cell suppression. Yep. So again, seeing a very similar thing in this in this quote, as well showing the issues with excess glucagon production and type two diabetes, and that this is happening both in the fasting and postprandial state, and is what contributes to the hyperglycemia that's seen. And they describe it as inappropriate hepatic glucose production, but I would really say it's extremely appropriate, considering the energy deficit that's there. And this is the exact adaptive normal response that should happen, because our body is trying to recover its ability to produce energy as much as possible, and that's what these stress hormones are there for. It's just not working, which is why it continues on into a pathological state.

Mike 36:26
Yeah, and the energy deficit. So I'm going to add some quotes to that, but just to touch on it briefly, we're going to cover the energy deficit piece specifically with in talking about the obesity reference that will that Rob had talked about. So we'll we'll read his quote in a second. We'll talk about that in a couple minutes. But the diabetes and obesity often go together, and they're characterized together by an energetic deficit at the cellular level, with an over with a lot of substrate floating around inside the vasculature. And one of the main or key features of diabetes is this extreme production of glucagon. It regardless of the regardless of whether you're fed or not. So usually insulin or having carbohydrate will lower that glucagon secretion. It'll it'll shut down this production the insulin race as you stop undergoing gluconeogenesis and use creating glucose from fatty acids, from protein, etc, and then putting it out into the to the blood as as glucose insulin will shut that process down. Now there's a little there's talk about regulation. I'm going to discuss that in just a second, some of the regulatory mechanisms there. But in diabetes, that doesn't happen. You just have this constant, consistent effect of glucagon still undergoing gluconeogenesis, regardless of whether you eat or not. And the parallel here that I just want to tie in is in the low carb keto carnivore states, it's basically up regulating glucagon in a similar fashion that you would be seeing with diabetes, where you're constantly relying on glucagon to put out this this glucose output. Now, it's not exactly the same. I don't want to mischaracterize the state, but you have a situation where you're constantly relying on glucagon to increase blood glucose and upregulate free fatty acid oxidation and other tissues and spare that glucose for the central nervous system, you kind of have a similar process going on inside diabetes as well, where a lot of the tissues are actually oxidizing free fatty acids, and much of the gluco the glucose that is be created, being created from gluconeogenesis, is coming from triglycerides. So it's a there's very significant parallels between the states, and that's why we're discussing the glucagon, the hyper glucagon, anemia, state of diabetes here, because it's, it's a mirror state to some with some differences that we'll discuss between, um, the low carb ketosis, carnivore states and diabetes. Um, now the quote that I wanted to share here

Jay Feldman 38:59
To interject real quick, right before you get to that quote, you touched on something that I think was really important and probably would have been a nice thing to mention, that kind of precedes the blood sugar situation. You know, we've been talking about this energy deficit that is what leads to the production of these hormones in the state of a low carb diet. An energy deficit is what drives all these responses. It's what ends up driving the increase in stress hormones, what ends up it's what ends up driving the ketogenesis, the reliance on fatty acid oxidation, is the lack of glucose leading to in if you're shifting in an immediate, short term energy deficit, when you're shifting into a low carb state, and then basically an ongoing one that's forcing the ongoing production of glucose. That is why we need glucose. That's why we use glucose. Is because it's really great for producing energy. That's why our brains can't use fat for fuel. Yes, they can partially use ketones. We've discussed this before. I know that it's there's a lot of discrepancy here versus what's talked about in the low carb space. So I'll just refer to some previous episodes where we've discussed this in more detail, in terms. Of the details of why glucose is way more efficient at producing energy than fat, but that is what's responsible for a lot of what are said to be the benefits in ketogenic diets is all of the oxidative stress, the reactive oxygen species production driving the hormetic responses. We've talked extensively about why this is not ideal to be driving these stress responses, but this is what is underlying this constant need for glucagon and gluconeogenesis is an energy deficit just brought out by the lack of carbohydrates. To compare that to type two diabetes and insulin resistance, and this is what you were saying, was there's a little bit of a difference here. Is that the problem in those states is not that there's not enough glucose available, but that it's not effectively being able to to be used to produce energy. It's a separate but related issue in which both cases, you're not able to produce energy effectively. But the reason why there's a difference here is because in one case, you're just avoiding the carbohydrates. Of course, avoiding the carbohydrates doesn't solve that issue, but in both cases, the commonality is the energy deficit and the driving of glucagon, and then the reliance on free fatty acid production and oxidation of fats. So I just wanted to draw that parallel, because you had brought it up, Mike. And I'll let you go ahead with the quote.

Mike 41:11
Yeah. So now I have a couple things to add. The first piece I want to show is that in animal models, basically abolishing glucagon directly eliminates the the diabetic state. So what they did here is they have, I'm going to read this, this section here, they say experiments performed in mice deprived of glucagon receptors by genetic modification. So glucagon receptor knockout suggests that glucagon is essential for the development of metabolic anomalies and diabetes, the destruction of pancreatic beta cells in control mice by streptosoin injection, induced in 24 hours, the appearance of severe hyperglycemia and the metabolic manifestations of diabetes. In contrast, no hyperglycemia occurred and glucose tolerance remained normal after streptosoin injection in mice deprived of glucagon receptor, the glute, reintroduction of a glucagon receptor and liver of gluco glucagon receptor knockout mice with an adenoviral vector induced a marked hyperglycemia and a glucose intolerance after streptosis and injection. These experiments clearly show that the presence of a normal glucagon action in the liver was necessary for the the apparition of diabetes and type one diabetes. So what they're and this, this goes hand in hand with diabetes type two, but there's a little bit of different mechanisms there. But essentially what they're showing is that so in diabetes type one and type two, type one, you have a loss of beta cells, which are insulin producing cells. Type Two, you have some loss of insulin producing beta cells, but what you more have is a resistance of of the body's tissues to insulin, so it doesn't effectively respond to insulin, and some of the mechanism we'll talk about in a sec. And what you're seeing here in these states is if you induce type one diabetes in rats by streptosins, a bacterial toxin that they inject into the rats, and it basically destroys the beta cells of the pancreas, so they don't have cells that can produce insulin anymore. If you eliminate the glucagon receptor in these mice, they don't get diabetes. They don't get the manifestations of diabetes. Now, if you then give them a virus that that codes for the glucagon receptor. And so basically, the virus will inject that gene into the genome to to create the glucagon receptor in these glucagon receptor knockout mice. Do you find that this? The Diabetes features of hyperglycemia, insulin resistance, etc. Is it reappears. So what's what's starting to be discussed? And there's a hypothesis by, I forget what it's called. Let me see if I can find it here. The hypothesis is from these researchers. It's acid and Unger, and they propose the BI hormonal disorder, which is essentially low plasma insulin, and then high plasma glucagon. And so what there's what they initially discussed, is the absence of insulin is responsible for the increase in lipolysis and proteolysis, or so, which is a breakdown amino acids, and then glucagon excess is responsible for the increased hepatic glucose production and ketogenesis. So the fate, the state of diabetes, is a state not only of insulin resistance or lack of insulin, it's a state of excessively chronically elevated glucagon, regardless of the context. So you have lack of insulin allowing for the upregulation or the basically, a lack of anabolism, a lack of tissue building, so a breakdown of proteins and fats and then glycogen initially, and then you have glucagon, which is driving the process of taking these broken down substrates from the tissues and then diverting them into the production of glucose. So it's a it's the glucagon is essential for driving this. Eight. And the piece that's quite important here is that in these low carb, carnivore keto diets, et cetera, in order you need glucose, there's not a question of whether or not the body needs glucose. It needs glucose to such an immeasurably important extent that it'll break down its own tissues to produce glucose, which is counter to the idea that glucose or carbohydrate is not required for human functioning, like those ideas that come out of the low carb sphere, it's like it's so important.

Jay Feldman 45:29
Go ahead, they say that it's essential and it's an essential nutrient which doesn't actually have anything to do with or that it's not essential, right? They say carbohydrate, glucose is not an essential nutrient. That doesn't mean that it is not essential to our physiology. It means that you don't need to consume it, because you can produce because you can produce it. Fat is also not essential. It's just that you can't create omega threes and Omega sixes, which, if you argue, if you want to make the argument that those are essential, it's like point, you know, like point 5%. Of your diet would have to be made up of those. So largely, fat is not essential either. By that same definition. It's people get confused and kind of use the wording in a in like a misguided or or a misleading way to make it sound like that means that your body doesn't need carbohydrates. It does. It can just produce them on on their own. But as you're saying, this is the fact that our bodies do that is actually evidence that these are extremely important, required nutrients that we need, because we'll go to great lengths to produce them if we don't have them. Also. By the same token, same thing with fat. Fat is essential too. If we don't take it up, we'll produce it from carbohydrate. So this is not a question of, are either of these very important to physiology. They both are. But yeah, there's kind of a little side note there, because there is that misleading claim that people say that carbohydrates aren't essential, as if that means anything about this physiology.

Mike 46:40
Yeah. And the other question that, and we'll get to this with the evolutionary stuff, is an idea of essential versus optimal. Just because something is a like, just because something isn't necessarily essential, doesn't mean that consuming it or using it, it doesn't make it optimal. So those are those that's a very like. It's easy to conflate the those those things, and it's important to not conflate those things so but overall, what we're what we're essentially getting at here, is that in both ketosis, carnivore low carb diets and the diabetic state, you have this, this consistent elevation of glucagon and then elevation of gluconeogenesis at the liver. This also explains why you see these prominent keto people, carnivore people, etc. And then also tons of clients that we've worked with come and they have this elevated fasting blood glucose because they're chronically elevating their blood glucose levels on these diets with glucagon. You don't need to have carbohydrate to elevate your blood glucose. And then in the diabetic state, it's the same thing. The elevated fasting blood glucose that you're seeing with people is not because they're eating too much carbohydrate on a regular basis. It's because glucagon is driving gluconeogenesis to a large extent overall. And then on top of that, when they're eating carbohydrate, gluconeogenesis is not being shutting shut down. So they have an elevated baseline of of glucose in their bloodstream from gluconeogenesis. And then the carbohydrate that they eat on a regular basis is additive to that, and then their insulin insulin resistant, so they're not taking up the carbohydrate and target tissues. Something I do want to point out here that is quite important is the your tissues in your body don't need insulin to take up carbohydrate, only certain tissues require insulin to take up carbohydrate over baseline levels on a regular basis. That's going to be your liver, your fat tissue and your muscles, and that's because those those tissues have a glute four receptor which takes up the carbohydrate. So those tissues are what becomes insulin resistant, under under the under these states. Now the other thing to keep in mind, though, is that even if your carbohydrate, and you see this in diabetes, if you don't have a lot of carbohydrate on board, and you start drastically ramping up fat oxidation, you become insulin resistant, even in non target tissues. And if you have carbohydrate going to non target tissues, then what happens is pruvate dehydrogenase can be shut down, and you start pushing things into lactic acid metabolism, because you cannot, and you cannot bring the carbohydrate into the Krebs cycle as well. So it's a slightly tangential feature of these states, but it's also a problematic state, because you're forcing the rest of the tissues of the body to not use carbohydrate to run on fatty acids, which there's a problem with running on the fatty acids. And then you're driving glucose production through gluconeogenesis, by breaking down proteins and fats, so essentially breaking down your stores, and then driving that to using that specifically for your brain function. So you're driving a glycolytic carbohydrate metabolism in a high fat state by lowering pruvate dehydrogenase function. You're driving fatty acid oxidation, which comes with Ros, etc, and then you're you're taking down tissues and fatty acids and protein, and even some of the protein and fats that come from the diet. And. You're then trying to turn that into glucose to provide a substrate for the brain. Ketones can also be a substrate for the brain, but only up to 60% and so, and then, then it's an inefficient process overall. So it's like you're relying on all these backup pathways to try to produce this glucose, and then, and and, like, it's an inefficient process, and there's problems with it overall. And then it's also the feature that you see in the diabetic state. And then you're also seeing trends in people who are running this long time where it's like, yeah, their blood glucoses are elevating. They're getting large amounts of free fatty acid in their serum. They're having high amounts of glucagon, and then they're having physiologic peripheral insulin resistance. So it's like, you're driving similar path. You're driving similar states. Now the kicker is, what's going on at the cell in terms of between diabetes and and the low carb keto individual, right? I think that there's a difference there, where somebody who's on low carb and keto, they can probably come off low carb and keto after a period of time and be able to to not be diabetic, whereas a diabetic may have a hard time coming, like just getting off of being a diabetic and then, and then using carbohydrate effectively. So there's differences in the pathology there, but overall, you're driving similar pathways. And then, as to mention there, you're also with that you pointed out, Jay is that you're already one foot into the stress doorway. So when you start to move further into stress, when you get exposed to another stress, you you can start driving these other hormones more easily. And you see that, and we'll discuss that with exercise in these states.

Jay Feldman 51:33
Yeah so that's that context. And so to kind of wrap this, this up in terms of glucagon, I wanted to a just mention in terms of that study you mentioned showing, and the studies I referenced, too, that the glucagon is the driver of the diabetic state, as you were saying, it is the driver of the hyper glucose, the excess glucose, not the insulin resistance, right? The insulin resistance is really a misnomer. We actually have inhibited glucose metabolism. It's really is little to do with insulin, but rather, is driving a state where a the cells are filled with excess glucose, so they can't take up more. And that happens even without insulin, also even in those in those tissues that have glute four, there's still just concentration gradients will allow them to uptake glucose. But that can't happen when they're full of glucose. They're not converting because they're not converting it to energy. So we have an energy deficient state, which is triggering stress, triggering this glucan glucagon, which is causing the increase in blood sugar. To make up for it, the blood sugar is not being used, and that is what triggers excess insulin to be produced. It's a response to the glucagon. It is not the glue. It's not the insulin first, and then the glucagon is the glucagon first. And so you referenced, you know, we've both referenced some of these researchers talking about this. There's some really great research on the insulin side talking about this as well, from a researcher with the last name sunkson, S O n, k, s e n. I've referenced his studies in the past, but he basically talks about how when insulin is administered, he talks about this whole process from the same perspective. And when insulin is administered in these states, it's not working by increasing glucose uptake, necessarily, it does a bit, but largely by opposing the effects of glucagon and inhibiting hepatic glucose production. And that's what's helping to decrease the fasting blood sugar. So and again, the name for that insulin effect, in that way, is, it's kaolonic. It's called a Kalon. And so he talks a lot about that, some interesting research that I'll reference. But to kind of wrap up this glucagon piece, the point that we're getting at is glucagon is not benign. Is the feature of the stress response. We see it in these states where the reason why we're bringing it up, that it's has this huge role in insulin resistance and diabetes, is because that is a very clearly metabolically deranged state that is driven by the presence of this glucagon, which is, again, also driven by the inhibited glucose metabolism, but that this is not a a hormone that we want to be driving, and is a part of the stress cascade. A couple other important points here to note as far as glucagon goes. Just to wrap up that part is that another way that we another piece of evidence that suggests this, that this glucagon is directly anti metabolic and stressful is that it inhibits the conversion from the inactive t4 the inactive thyroid hormone t4 to the active thyroid hormone t3 this largely happens in the liver, and so the glucagon directly inhibits the diode denace enzymes that allow for that conversion, and along the way, it'll then lead to lower t3 and increased reverse t3 what this basically means is it puts you in a state where you have low active thyroid hormone and you have a lower metabolism. And again, you won't see this short term, because short term you're you have all these stress hormones that actually increase your energy expenditure through very stressful means, not something including glucagon, right? Including glucagon, and then, of course, adrenaline and cortisol and massive amounts. But over time, you get this thyroid suppression that leads to a low metabolism in the long run that causes major issues. And there's a ton of research showing this happening in low carb diets and in excess glucagon states, or by administering glucagon. So that's saying very clearly. And again, the. The these normal responses, these adaptive, evolutionarily consistent responses to a low carb diet, are what caused that situation. And again, just kind of using this as evidence for a reflection of the fact that this is driving a stress state that is not ideal, unless you want to argue that a low thyroid state is ideal, that's kind of a separate argument. And we'll talk, I guess, a bit about that in terms of energy and evolution, but we are certainly arguing that that's not a good thing. And Rob didn't mention that. He's arguing that it's a good thing either. Some people do argue that, and that's, again, a different conversation, but at the very least, if that's happening, we have to acknowledge that just the lack of carbohydrates puts us into that sort of state. Yeah, the last thing I was going to mention, just to wrap up the glucagon piece, before talking about the excess stress that we also see in other contexts of low carb diets, is that glucagon, and we've been talking about this because it drives the production of glucose from amino acids, also from glycerol backbones, from from triglycerides, it will lead to muscle wasting if there's not enough dietary protein coming in. And so you see that in states where we not only don't have carbs, but we don't have protein, you see muscle wasting, for example, fasting. And a lot of the research looking at fasting now is suggesting that we're seeing this muscle wasting, this loss of fat, free mass, and that is coming because you're putting yourself in a state where you need to rely on these stress hormones, and you don't have protein available to produce the glucose, which is still stressful as it is, but because you don't have that available protein from your diet, you're pulling it from your muscles. So that's another piece here, and we'll kind of talk about this in a moment. We'll come back to just this fact that we have to like, when you're in that state, you're also much more prone to muscle catabolism.

Mike 56:35
Yep, the piece I was going to add here, so there was two pieces I want to add, specifically about the the thyroid piece. First, a lot of people will say that they don't get and this was something that Judy, I think, had discussed when we were talking about we did our podcast and on her article, but that they're not hypothyroid because their TSH wasn't elevated, and their t4 wasn't wasn't low, or something along those lines, and just a specific, more nuanced discussion, or more like a further step from what you're saying, The deiodinase enzymes convert t4 to t3 by removing an iodine group. Now, in these low carb states, there's an adjustment in the deiodinase enzymes function or expression. So some of the diode nice enzymes will increase the conversion of t4 to active t3 but others will increase the conversion of t4 to reverse t3 so what, what I've seen with clients, and I think you've seen as well, is that TSH and t4 can be fine. Maybe they're completely in range. Maybe there's smack in the middle of the range. And then when you start, when you start to get into t3 you start to see a lower t3 and you start to see a higher reverse t3 if you're testing t3 so, and this is extremely important, because t4 is not active thyroid hormone, and TSH doesn't tell us anything about what's going on with thyroid hormone at the cellular level. So you could, you know, if somebody comes to me, I'm freezing cold, I'm having insomnia, and you know, I'm tired all the time. I'm fatigued. And then you go and you and you look at their thyroid, well, with my thyroid hormones, fine. And then it's like, no, your TSH. A low TSH doesn't mean anything. It doesn't tell us much of anything. A high TSH can tell us hypothyroidism, but a low TSH doesn't tell us anything about hypothyroidism. What? What? And the same thing with t4 you can have a a normal t4 but if your conversion at the at the cellular level, what's going on specifically at the cell, is low, from t4 to t3 then you will still be hypothyroid. And so there's, there's quite a few interesting studies about this, but you really need to look at the entire system. And with the low carb piece, you're not seeing overt, traditional hypothyroidism, with a high TSH and lower t4 and t3 you're seeing perhaps a normal TSH, perhaps a mid range, or low to mid range t4 and then you're seeing a high reverse t3 and then you're also seeing a lower t3 or perhaps mid range t3 and that's and then you're seeing classical symptoms of hypothyroidism. And it again, the the state, the glucagon is adjusting the the signaling for the deiodinase enzymes at the cell and at the liver, so that it's driving this, the this, you're basically in a state. You're triggering a state that's saying, Hey, I don't have adequate energy on board, and carbohydrates and thyroid hormone directly relate together. I don't know if you want to say anything about that.

Jay Feldman 59:29
Yeah. So as far as the TSH goes, I just wanted to mention also that it can not only be normal because maybe there's normal t4 but not enough t3 but also the excess stress hormones, not necessarily glucagon, but cortisol, especially will also suppress TSH. So you might see a very low TSH. In a low carb state, might see a lot of signs of high cortisol. And you know, maybe regardless of like you'll see fine TSH, whether it's because of what they'll call you, they call it you thyroid six syndrome, which is where you're not converting the t4 to t3 and only. They only identify it and like really severe illness and hospitalized patients, but it exists in people who are semi functional and just, you know, having typical hypothyroid symptoms. And so that is that will lead to just normal TSH, but still hypothyroid states, but also you'll see suppressed TSH from cortisol, which, again, this is why, what you were part of why, or another reason why low TSH does not mean that thyroid activity is okay, because it can be suppressed by these stress hormones. So I just wanted to add that piece in.

Mike 1:00:30
And then the other thing that I wanted to just drop in here is there's some information basically showing that, and I'm going to pull it up right here in a sec that glucagon is directly involved in the stress cascade. So it is a stress it is like a typical stress hormone, and it's elevated in the same in the same situations that you would see catecholamines and and the glucocorticoids. So I'm just going to read something really quick here, and it's basically just going to we're basically showing that glucagon is a classic, or can possibly considered a classical stress hormone. Here we go. So they start here. Basically they say, recently, there's been an interest in the in the finding that glucagon increases energy expenditure. This observation produces a conundrum, why does a hormone that counteracts hypoglycemia, a state of energy deficiency, also increase energy expenditure? This could be explained by a more wide ranging role that includes aiding and physiologic stress responses to stress. Then they come down here and they talk about glucagon in stress and animal models, large elevations in plasma glucagon are observed immediately after acutely stressful stimuli. Hyperglucogenemia is well recognized in patients under a range of physical stress states, including trauma, burns, surgery, sepsis, hemorrhage, acute myocardial infarction, cardiac arrest and hypoxia, including in neonates. Very high plasma glucagon concentrations are seen in diabetic ketoacidosis and contribute to hyperglycemia in the setting and all these pathologic scenarios, hypoglycemia is not a primary driver for glucagon secretion, and instead, other provoking factors must be thought Now, the reason this is important is because the when you're looking at like there's an idea already that you don't want to elevate cortisol and adrenaline on a long term basis. But when we, when you, when we recategorize what the idea of stress is, when we define stress as this energy deficit, and you basically the stress hormones are trying to correct that energy deficit, what you're seeing is that glucagon is directly involved in that same definition. So it's the same thing. It's, it's glucagon, adrenaline, growth hormone. Now growth hormone does have other effects, but there's, there's nuance in there. But glucagon, adrenaline, cortisol, growth hormone, etc, are all involved in mustering up. This the stress response, and we discussed that in in a recent video we did, discussing what's it called, discussing the mitochondrial responses to stress, and then like seeing the 200% increase in energy metabolism during stress, with that largely increasing the the fatty acid oxidation and decreasing oxygen or decreasing carbo carbon dioxide production, so overall, decreasing the respiratory quotient. So you're seeing in these states, which, again, that's also another pathological feature of a high carbohydrate or low carbohydrate high fat diet is a lack of CO two production, which decreases the boron Haldane effects and delivery of oxygen and nutrients to the mitochondria and is part of a slowing of the system on top of this, but it that's a little bit tangential. Overall, what you're seeing is that the glucagon is part of that stress cascade. It's involved in mediating a lack of a lack of immediate energy availability with the catecholamines and the glucocorticoids, and being in a low carb state, regardless of whether or not you're having blood sugar ups or Downs is relying it's chronically putting you in a state of an energy deficit, requiring the use of these hormones to correct that energy deficit. And then there's backup pathways built in so that you, like, for example, utilizing ketones and whatnot, or fatty acids for gluconeogenesis, et cetera, so that you don't have like, complete muscle and body catabolism.

Jay Feldman 1:04:28
Yeah, absolutely. And as you were saying, we talked about that in the in the response, you know what you were saying earlier, in terms of the energy expenditure that's increased in response to stress. We talked about that in that study. And of course, glucagon playing a big role there. There's also some research showing that the release of calcium is necessary for that stimulation of energy production from glucagon, again, just showing that that is something that only happens in an energy deficit, and we're doing it through these backup means. You mentioned fatty acid oxidation and all the costs that come with that. Yeah. So yeah, very important points there. All right, we're going to end this episode there and pick back up in part two, where we'll be discussing whether low carb diets increase cortisol over time, whether tolerance to stress is improved on low carb diets, why being overweight or obese is not a sign of excess energy, how the bioenergetic view incorporates evolutionary biology and how this differs from the ancestral health model. And we'll also discuss what we think of Paul saladinos interpretation of the quote, repeat diet. If you did enjoy this episode, please leave a like or comment if you're watching on YouTube, or leave a review or five star rating on iTunes, if you're listening elsewhere, all of those things really do a lot to help support the podcast and are very much appreciated. To check out the show notes for today's episode, you can head over to Jay Feldman wellness.com/podcast you can take a look at the studies and articles on anything else that we referenced throughout today's episode, and if you are dealing with any low energy symptoms. Maybe these are related to the blood sugar regulation that we discussed today. Maybe you've been dealing with various issues since going on a low carb diet, or, you know, trying to resolve any of these issues using a low carb diet. Maybe you've had some success. Maybe you haven't, either way, if you're dealing with any of these low energy symptoms or issues, things like chronic cravings or hunger, low energy or fatigue, chronic pain or joint pain, weight gain, digestive symptoms, brain fog, poor sleep or insomnia, hormonal imbalances, or any other low energy 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 a 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. 

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