Ep. 114: Fat-Burning Drives Insulin Resistance And Eating Carbohydrates Improves Insulin Sensitivity

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In this episode we discuss:

  • How increasing carbohydrate intake actually improves insulin sensitivity, even in people with type 2 diabetes 
  • The research showing that fatty liver disease and cardiovascular disease are both characterized by excess fatty acid oxidation 
  • The role of stress and excess fat burning in insulin resistance 
  • Why strategies such as intermittent fasting, cold plunges, and OMAD (one meal a day) are not effective for improving insulin sensitivity 

0:00 – intro

1:17 – stress hormones (glucagon, epinephrine, and cortisol) are major contributors to insulin resistance and diabetes 

4:05 – elevated glucagon levels, not carbohydrates, are the driving force behind high fasting blood glucose levels

6:43glucagon is a driver of insulin resistance, while insulin is just a symptom 

12:46 – the research showing that blocking stress hormones directly improves insulin sensitivity 

15:14 – “hormetic” stressors like intermittent fasting, cause insulin resistance

19:30 – fat burning drives insulin resistance and keeps us in a catabolic state, driving weight gain and muscle wasting

22:15 – cortisol drives insulin resistance and why serum cortisol levels don’t provide the full picture

25:00 – carbohydrate intake (even from pure sucrose) improves insulin sensitivity while low-carb diets reduce it

29:40 – decreasing fatty acid oxidation by increasing carb intake improves our ability to tolerate carbohydrates

33:46 burning fat contributes to increased disease processes and does not lead to losing more body fat

38:04 – fatty acid oxidation damages our mitochondria and increases fat storage

46:22type 2 diabetes directly contributes to heart disease by upregulating fatty acid oxidation 

52:05 – how to decrease fatty acid oxidation and improve glucose metabolism

Links from this episode

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Jay Feldman 0:05
Eating carbohydrates improves insulin sensitivity, even if you're already insulin resistant. We'll be discussing why that is in today's episode of the energy balance podcast, a Podcast where we explore health and nutrition from the bioenergetic view and teach you how to maximize your cellular energy to maximize your health in today's episode, which is part two of our two part series, digging into the evidence and studies research supporting the bioenergetic view of insulin resistance, we'll be further digging into some of this research and talking about how increasing carbohydrate intake actually improves insulin sensitivity even in people with type two diabetes. We'll also be discussing the research showing that fatty liver disease and cardiovascular disease are both characterized by excess fatty acid oxidation. We'll be talking through more of the details behind the real causes of insulin resistance and diabetes, and further evidence for the bioenergetic view of insulin resistance and type two diabetes. To check out these show notes for today's episode, where we'll link to the studies and articles and anything else that we reference, head over to the Jay Feldman wellness.com/podcast

And with that, let's dig in to where we left off from the last episode, which is the stress hormones and how insulin is not the cause insulin is not the problem here when it comes to insulin resistance, instead, we've got some metabolic problems and in addition to fatty acid oxidation being a contributor, the stress hormones are a major contributor to insulin resistance and type two diabetes and we'll start by discussing glucagon and so glucagon is something that is going to increase anytime we decrease our carbs. It's also kind of the first stress hormone that's increased anytime we enter into stress and we've discussed this in a previous episode that I'll link back to where we were talking about our disagreements with Robb wolf as far as the bioenergetic view of health goes and as a stress hormone, glucagon will increase glucose release at the liver. It'll increase hepatic glucose production. It'll increase fatty acid oxidation, or fat burning and again, these are things that we always discuss. This is characterization of stress. fat burning is stress. Those three things go hand in hand. Anytime you're under stress, regardless of the driver, it's going to increase fat burning. We've discussed this prior, and we see this especially in insulin resistance, another state characterized by high stress, high fat burning and problems with glucose oxidation. And as we'll get to there is an elevation at glucagon as a response to that as a compensatory mechanism, because if we're not producing enough energy from glucose, we need to get it from somewhere, and we have to do it through fatty acids and glucagon helps us with that, but it comes at a cost. And as a response to elevated glucose or glucagon and any elevated stress hormones, our body will turn down its metabolic rate long term, decreased thyroid hormone production and conversion, decreased sex hormone production, all these other things will be turned down digestive processes get decreased you know, we have to prioritize our vital functions when it comes to stress and famine and scarcity, and that's essentially what the stress hormones signal and so in this paper, it's titled glucagon and type two diabetes, the return of the Alpha cell. They describe this, and they state that patients with type two diabetes suffer from fasting and postprandial hyperglucagonemia, 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 much like we saw earlier, if you can turn off fatty acid oxidation, it will help the pathology, as they're saying here, another contributor is glucagon, hyperglucagonemia, excess stress hormones and excess glucagon specifically. And if we turn that down, or turn down its activity, that will also help with the pathology. It won't fully fix it. It's not going to fix what's causing the problem with glucose oxidation that's underlying, but it is a factor that contributes and makes the glucose oxidation worse.

Mike 4:06
Yeah, and something I think that's really important to point out here is that the low carb sphere is having an uptick in people who are talking about their fasting glucose levels increasing, and especially like when they're especially in the morning, right? And this is a function of glucagon. This is glucagon, and then also cortisol, increasing the production of glucose at the liver, which is increasing blood glucose levels. And the important piece from that study that I that that ties in with this is that most diabetics blood glucose levels are not elevated because of the carbohydrate that they're eating per se, they're already baseline elevated because their glucagon levels are elevated and they're they have a high they have gluconeogenesis, the production of glucose from the liver going on despite eating carbohydrate. and normal people, when you eat carbohydrate that stimulates insulin, that lowers glucagon, and then your body will boost that glucose, and then your blood glucose levels will come back down into a normal range. And type two diabetics, and I see this with clients all the time. They'll have a baseline elevated blood glucose level. Then they eat their glucose goes up. It goes up higher, because they're starting from a higher baseline, and then it comes back down. And where does it come back down? It comes back down to that initial level that they started at, that that could be 150 milligrams per deciliter. That could be 120 that could be 200 depending on the degree of metabolic dysfunction the person has going on. So glucagon is essential to the high blood glucose situation. The the elevated blood glucose levels that you see in all of these states, whether that's diabetes, whether that's obesity, or whether that's pre diabetes, impaired glucose tolerance individuals. In all of these states, you're seeing the blood glucose levels elevated, and that is directly glucagon, that is not necessarily dietary intake of carbohydrate, which is why you see this in low carb eaters who are not eating carbs, and they're like, Oh, I haven't eaten carbs, or haven't I've been on carnivore one meal a day, and I haven't eaten any carbs, and all of a sudden my blood glucose level, oh, it's doubled or oh, I'm I'm sitting at 120 milligrams per deciliter per day. And it's like, yes, because you are running on stress hormones, you're up regulating glucagon, and you're increasing your blood sugar through those mechanisms, which is a central piece of the diabetes and metabolic dysfunction picture.

Jay Feldman 6:20
Yeah, definitely. And, yeah, we'll leave it at that. There's some, some people out there who are suggesting it's other albums has nothing to do with elevated stress hormones and these inherent effects to low carb. But rather, you're just eating too many calories still, or you're eating windows too wide and things like that but yeah, those, those are just ignoring the actual pathology that's being caused there. This next study will further dig into glucagon as a driver here, and look at elevated glucagon in different states and how it actually causes insulin resistance, even when there is an insulin resistance there, just like elevated fatty acid oxidation would I'll let you dig through the first few quotes, Mike, and then I'll go through the next couple because this is a longer, I mean, I don't know about a longer paper, but more quotes that are worth sharing. Here's a lot of really great quotes in this paper, if you want to take on those first

Mike 7:08
few. Okay, so I'll take on these first three, and then you'll get to the the ones after. Okay, yep. So this paper is titled metabolic effects of glucagon in humans, and the first quote here starts off and says, glucagon induced insulin resistance may cause diabetes by itself in patients with glucagonoma, a rare tumor that secretes glucagon patients with total so I guess just quickly, in this in this situation, people who have a tumor that secretes excess amounts of glucagon can actually get diabetes just from that glucagon. So this is one scenario that the paper is describing. Now they're going to go to another scenario here, and they say patients with total pancreatic pancreatectomy lack pancreatic glucagon secretion as a result they exhibit outstanding insulin sensitivity, being predisposed to life threatening hypoglycemic episodes. So in an opposite side of the spectrum, when people don't have a pancreas, they don't have the beta cells that produce insulin, but they also don't have the alpha cells that produce glucagon, and without that glucagon, they're actually extremely insulin sensitive, so much so that they can get life threatening hypoglycemia, so their blood sugar can drop so quickly and so rapidly, because they're so they're so insulin sensitive, their cells can take up carbohydrates so easily that they can actually almost die because the blood glucose levels get too low. So the next thing that they say here is, in contrast, patients with diabetic ketoacidosis. So this is again, another the other, going back to the other side of the spectrum, with excess glucagon, shows strikingly high plasma glucagon levels, and they experience profound insulin resistance that requires high amounts of insulin for metabolic control. So we're seeing multiple different areas here where low low glucagon or lack of glucagon production is actually makes you insulin sensitive, and an excessive glucagon is part of the insulin resistant paradigm. Now the next quote that they we just

Jay Feldman 8:57
before you jump on the next quote, I just want to highlight here. Essentially, what they're suggesting by this line of thinking is that glucagon is more of a driver. It lies underneath insulin, and the insulin, the excess insulin, is being produced as a response to the high stress hormone levels. So if we're going in order, we have impaired glucose metabolism and then a reactive stress response and a reactive fatty acid oxidation, and then on top of that, elevated insulin is well, so then as a result of those, we have impaired glucose uptake and elevated blood glucose levels, and then as a response to that, we're getting insulin. So we've talked about this earlier. We're kind of framing it as insulin is just a symptom here, and it is quite a few layers away from the underlying problem. And this line of evidence is supporting that

Mike 9:41
yes, and it's showing that the stress hormones are directly involved in the pathology as well and drivers of this. So we don't want to be optimizing for these things. Which is what would happen? Increasing them Yes, which would be yes, increasing them, which is what we'd be doing on the low carb diet. So the next thing that they go on to say is fasting plasma glucagon is. Elevated and abnormal patterns of glucagon secretion in response to dietary components similar to diabetes are already present in glucose intolerant patients before the diagnosis of type two diabetes. Fasting plasma glucagon level is higher in obese patients compared to normal controls. In addition, there's a nonlinear relationship between fasting glucagon concentration and insulin resistance, such that more severe fat more severe insulin resistance is associated associated with higher fasting glucagon levels. Furthermore, fasting plasma glucagon decreases in obese subjects after weight loss, both bariatric surgery and dietary intervention result in comparable reduction in fasting plasma glucagon level. So what they're showing now is we don't have the extreme where you have a glucagon tumor, or you have your pancreas taken out, or you're in diabetic ketoacidosis. What you're seeing in just people who are obese and just people who have impaired glucose tolerance, they're not even type two diabetic, yet, they're pre diabetic, or they're not even pre diabetic, they just have their glucose tolerance. Isn't that great. You're already seeing that glucagon levels are rising, and the worse, the higher the glucagon levels are, or the more dysfunctional secretory patterns of glucagon are, the worse the dysfunction is. You're seeing that this relationship bear out now. It's not exactly linear, as they're saying. There's probably, like a threshold point, and then it increases from there. But basically, what we're seeing is even in these more normal middle of the road situations, again, they're not metabolically normal, but it's not as severe as losing your pancreas or having a tumor that's accrued glucagon. You're essentially seeing that the glucagon is driving the pathology and is, or is heavily involved in this pathology as well. So we're seeing multiple scenarios where where glucagon is directly involved as a stress hormone in this insulin resistance impaired glucose tolerance type of state,

Jay Feldman 11:47
exactly. And the clear thing they're highlighting here is you have a spectrum of insulin resistance. As that gets worse, you see elevated those things go hand in hand to just showing a very clear correlation, and which suggests that glucagon is a major driver here,

Mike 12:00
yeah, and that's often not talked about in the the alternative and the mainstream spheres, is the role that glucagon plays. And that's why, as we talked about in our podcast with Robb Wolf, like optimizing for glucagon is our podcast talking about Rob Wolf. We weren't on with him, but optimizing for glucagon secretion through low carb diets is actually maybe contributing to the pathology long term of insulin resistance, where you actually have this dysfunction of oxidizing glucose in these elevated glucose levels, not just the dysfunction that you see in the low carb diet by itself, it may be a driver of the actual full pathology, instead of the physiologic insulin resistance, Say, and I did that with air quotes,

Jay Feldman 12:41
right, right, suggesting that it's not benign. That's what you're saying. Yes.

Mike 12:46
So the last quote that they the last quote that they discuss here, and this is in the same in the same line of thinking, they say monoclonal antibodies that block glucagon receptors are beneficial to control diabetes in patients with type one and type two diabetes. So essentially, if you block the glucagon receptor so that glucagon is unable to bind in and have its signaling effect, you actually see improved ability to control diabetes in both type one and type two diabetics, highlighting the extremely important and essential role of glucagon in both diabetic pathologies and drive which are characterized by type one is characterized by deficits in insulin secretion, which, long term, could cause issues with excess fatty acid oxidation, because again, the glucose the insulin is lowering these stress hormones. And then also in type two diabetics, which is characterized at least initially, by issue or dysfunction at the cell, in terms of oxidizing glucose and so again, in both of these states, knocking out glucagon actually improves control. So we're seeing extreme examples where glucagon is either contributing to diabetes directly and with high amounts, or if you remove it all together, as you're seeing profound increases in insulin sensitivity. We're seeing more middle of the road cases in in more normal people who don't have tumors or have their pancreas removed, where in obese individuals or diabetic individuals or impaired glucose tolerance individuals, their glucagon is directly involved in their pathology. And there's this, this relationship where higher levels equal worse outcomes. And then we're also seeing, okay, let's test this hypothesis. If we block glucagon, what happens? And oh, wow, our glucose control is improved directly. So this is basically creating multiple levels of of evidence that are saying glucagon is directly involved in the pathology of diabetes, insulin resistance, and then even impaired glucose tolerance and obesity as well,

Jay Feldman 14:45
exactly. And as you're saying, not only are they putting out clear correlation, of course, as we know, correlation doesn't equal causation, but then they provide these other lines of evidence, like that. Providing glucagon on its own, in the case of a tumor, drives the pathology blocking the activity of glucagon at the glucagon receptor provides benefits, and lowering glucagon with pancrea tectomy will also improve insulin sensitivity. So we're seeing that this is actually causative, not just correlative, yes, and in these next quotes in this paper, which were important to include, based on everything we're talking about with the typical recommendations for insulin resistance. Well, let's look at things that actually increase glucagon and also further contribute to this pathology. So what we have is a couple of quotes. The first one states hyperglucogenemia occurs in clinical conditions involving adrenergic stimulation and metabolic stress, such as exercise, infections, acute hypoglycemia and starvation to assure, to assure availability of glucose to peripheral tissues such as the brain and skeletal muscle. So what they're saying is any form of stress increases glucagon. It's protective, it's adaptive, to help sure that there's glucose available for the tissues that need it, like the brain, but anything like that will increase it. And that includes fasting. It also includes low carb diets. It includes old baths, all these things that we're trying to do to waste our glucose and increase our fat burning and all that. Those all increase glucagon, which is contributory to this situation, and they dig in a little bit more into fasting, and some short and shortish term fasting, which they're talking about, like one to three day fasts. Here, there's also evidence showing major harms to intermittent fasting, so you know, 16 hour fast and showing that this contributes in the exact same way. But it's even worth mentioning this because some people out there for a decade or more had suggested that we should be doing fast of one day, two days, three days or longer, as a just general, you know, healthy thing to do to increase autophagy and everything. And you know, they've since, most of these people that I know of has since changed their view here quite a bit later, and this is part of the reason, is because it's pretty harmful. So what they say here is that glucagon secretion is a major driving force to the metabolic adaptation to starvation. Plasma glucagon levels increase after 24 to 48 hours of fasting, inducing hepatic insulin resistance that prevents glucose from being stored again. It's also worth mentioning, this will happen in a very short period of time. If you just go without eating and let your blood sugar drop. You know, after four hours, five hours, depending on how well you're using glucose, glucagon will increase, but it'll increase quite a bit at this point. They go on to say glucagon also promotes gluconeogenesis and ketogenesis. The increase in plasma glucagon level associated with starvation persists for several hours after refeeding, glucose tolerance is markedly impaired and healthy and healthy subjects after three days of starvation, the blood glucose concentration averages 210 milligrams per deciliter one hour after ingestion of 100 grams of glucose. So what they're saying is that this is such an intense stress of three days of fasting that glucagon levels are elevated for several hours after refeeding. So after you've already provided fuel that's supposed to turn off glucagon like normally, if you go four hours without eating five hours, whatever it is, and your blood sugar drops, and you increase glucagon as soon as you eat something, that glucagon goes down. That's part of why carbohydrates are so important. It's part of why insulin is so important. It's because it turns down glucose. But you've caused such severe stress by doing something like this that even a meal will not turn the glucose down for several hours, and you're extremely insulin resistant, as they show by the consumption of 100 grams of glucose causing massive increases in blood sugar to 210 milligrams per deciliter, very similar to what happens on an oral glucose tolerance test after a low carb diet of any sort which, of course, parallels fasting. We've talked about this extensively, how low carb intake mimics fasting and causes this sort of insulin resistance as a result of high glucagon, and this is why we don't want to do that. Yeah, and

Mike 18:47
imagine eating one meal a day, doing omad, and then wondering why you have, seriously, you have an impaired glucose tolerance. And it's like whether you're even if you were doing omad with carbohydrates. So omad is one the one meal a day, you would still have glucose intolerance, because for the whole 24 hour window that you weren't eating because you're only eating once a day, assuming you're keeping the same eating window each day, then it actually be worse, because then you're on the days that you had an altered window, you would actually have more than 24 hours so in those circumstances, you would have impaired glucose tolerance just from driving glucose glucagon secretion up in that 24 hour window, on top of the fact that you would also be driving fatty acid oxidation, things along these lines. So in terms of improving insulin sensitivity, this is like, this is not an ideal strategy to do it, because you are driving glucan secretion, you're driving fatty acid oxidation. And that's something I think that's really important as well to know, is that the glucagon is also involved in ketogenesis, which is the only you get to ketogenesis with fatty acid oxidation. So the glucagon is supporting fatty acid oxidation. It's not just about raising blood glucose levels. It's raising blood glucose levels through gluconeogenesis, but it's also driving fatty acid oxidation, which, as we talked about, fatty acid oxidation peripherally, inside the cells, inside the mitochondria, will block glucose uptake, and then the glucagon itself will be increasing blood glucose levels. So now you're actually creating a direct situation for insulin resistance and foreseeing high blood glucose levels and things along these lines, because you're increasing blood glucose and you're making the cells peripherally insulin resistant by driving fatty acid oxidation. And the last piece that I think that's really important to point out here is where is glucagon getting its ability to produce glucose in the starvation or fasting or low carb state, it's getting it from amino acids. So you have to break down amino acids, you have to break down your tissue, or you have to break down the protein that you're eating and convert that into energy in order to get this increase in blood glucose, which you need in these states from glucagon. So it's three it's like a three way terrible thing, right? You're inducing a catabolic state. Then you're making the cells insulin resistant peripherally, because you are driving fatty acid oxidation, and then you're raising blood glucose levels. And again, you need this in states of starvation, because your central nervous system cannot do without glucose or keys or ketones. Ideally, you'd want to be using glucose. So there's obviously specific reason for that, but in these states, like you need that, but it also drives this pathology, which is not ideal. And again, this individual who happened to change their mind on fasting after a 10 year time frame came to this decision under the perspective of, oh, look, I've actually lost lean mass over this time frame. And it's like, well, how do you think you lost the lean mass? You drove gluconeogenesis in your and your fasting states, which broke down your protein tissues and kept you in a catabolic state. So you couldn't put on tissue effectively, because you're using this, the protein substrate, as energy. And you you can't get and you can't signal this anabolic state. So the glucagon is directly driving this

Jay Feldman 21:58
right and the stress hormones, the constellation of glucagon, adrenaline, cortisol, to have direct catabolic effects, partially through this mechanism of just trying to produce gluconeogenesis, but also just a direct effect in terms of their catabolism. So yeah, not a not a good situation to be driving here, and we see this to just the we see the exact same thing play out with cortisol, just in a more exaggerated way. And it's pretty well known that cortisol, of course, is catabolic. But also when it comes to insulin resistance, it's pretty well known that glucocorticoids, the administration of them medically, is a great way to induce insulin resistance, cause weight gain, cause muscle wasting, all sorts of things. So of course, them being implicated in insulin resistance is less uh surprising, but still worth highlighting briefly here. Uh, Mike, do you want to share this quote?

Mike 22:47
Yeah. So what they start to talk about here is they're, they're talking about glucocorticoid specific, glucocorticoids, specifically in insulin resistance. So we just covered glucagon. We're going to cover the glucocorticoids, which is another major stress hormone. So the paper here titled abnormal cortisol metabolism and tissue sensitivity to cortisol in patients with glucose intolerance, they say here, recent evidence suggests that increased cortisol secretion, altered cortisol metabolism and or increased tissue sensitivity to cortisol may link insulin resistance, hypertension and obesity. In summary, in patients with glucose intolerance, cortisol secretion, although normal, is inappropriately high given enhanced central and peripheral sensitivity to glucocorticoids. And I absolutely love this quote, because you and I have been talking about this ad nauseam to the low carb advocates who've been saying, Oh, my cortisol levels aren't high. It's like your serum values don't necessarily indicate the full activity of the hormone. You have to know what's going on in terms of the metabolism at the target, which, again, is the same problem with with what we're talking about insulin and the up when you're in these states, you are driving increased metabolism of cortisol to its active form and increasing the sensitivity these cells to this hormone. So your values can be kind of like they can be in range. But that doesn't necessarily mean anything. You have to take the whole picture into context. So that I love this quote. I think it's, it's super relevant to all to a lot of these different arguments, and I don't have high cortisol things that you hear all the time.

Jay Feldman 24:19
Yeah, yeah. No, it's a great point. And I'll link back also to previous discussions where we've demonstrated that the low carb diet, for example, will increase tissue sensitivity to cortisol and reduce cortisol clearance. And yeah, support exactly what's being said here and you will get to a point, whether it's on those or an insulin resistance, where you will see serum elevated elevated serum cortisol normally, that's even farther down the line when there's even more pathology. But as you're saying, the highlight here is that even if you're not seeing it in the blood, work doesn't mean that it's there's not increased cortisol activity, and that is certainly problematic. You know, you certainly don't want to see that and drives the pathology here in insulin resistance. Yep, yep. All right. Right? So let's dig into a particularly controversial one, one that we've alluded to a few times, which is about carbohydrate intake and insulin sensitivity. And we've talked about this before, but essentially, there is this juxtaposition where low carb diets cause the reliance of fatty acid oxidation and reliance on stress hormones, and those things block insulin sensitivity, they block our ability to use glucose effectively. On the flip side, increasing carbohydrates does the opposite. It actually increases our insulin sensitivity pretty significantly and we see this not only in someone who's insulin sensitive, but even in people who have diabetes and so we'll dig into a couple of papers here that essentially show this and it's also worth mentioning here, and we won't go through these studies, but I'll cite them in the notes that there's a lot of studies out there, I mean, a ton of them showing no association between sugar intake or carbohydrate intake and insulin resistance. So even on kind of the more epidemiological level, or even controlled trials with those things, they don't support this notion that's been this ridiculously oversimplified notion, this carb, insulin model of obesity, that the more carbs you eat, the more insulin you produce, the more fat you store, the less insulin sensitive you are that's just not, it's just not what happens in the physiology. And it's very, very clear, and it's really unfortunate, it's really harmful, that that idea still circulates, still permeates, you know, decades plus, down the line, and honestly, in the alternative world, is still to be prominent theory that's being purveyed so some major concerns there and so before we dig into these studies, I just want to mention that if you are listening and you're looking to reverse your insulin resistance, or even if you don't have insulin resistance, but you're looking to optimally support your metabolism, lose weight, improve digestion, get amazing sleep, rebalance your hormones, boost your energy, and various other you know symptoms that you're looking to resolve, and you're looking to do this with clear action steps and strategies alongside personalized guidance from me, then head over to Jay Feldman wellness.com/solution, where you can find all the information for the energy balance Solution Program. This program includes customized health coaching, a video library with videos on regulating blood sugar, which, of course, is particularly relevant here, as well as videos on restoring gut health, losing weight without destroying your metabolism, how to boost your metabolism, how to get amazing restorative sleep, how to rebalance your hormones and tons more. There's also resources like a sample meal plan and supplement guide, as well as a private community so you can get support from all the other members who are also improving their health and their insulin resistance. So again, head over to Jay Feldman wellness.com/solution, to check out all of those details. And with that, let's dig into this first study here. So this paper is titled, effect of high glucose and high sucrose diets on glucose tolerance of normal men and they were basically looking at diets with different levels of glucose and then comparing that with sucrose. And so they state, as the dietary glucose content was increased progressively. They started at 20% and then went to 4060, and 80% of calories, a gradual improvement of glucose tolerance occurred and when normal subjects were changed from a control diet to one containing 80% of calories in sucrose, significant improvement in oral glucose tolerance occurred. These improvements in glucose tolerance were associated with slight reductions in plasma insulin levels. These studies demonstrate that short term periods up to 10 weeks on a high sucrose diet lead to improvement of glucose tolerance in normal subjects. And what they were essentially finding was the most improvement on the sucrose diet, the high sucrose again, we're talking 80% of calories from table sugar, from sucrose, and this is in a liquid diet. All of these, they're using liquid diets for the non control diets. And so what they found is that, again, insulin sensitivity continued to improve as you increase carbon take from glucose alone, and when you switched it from glucose to sucrose, meaning it contained fructose, then it was even better when it came to insulin sensitivity. And we'll dig into another study right after this, showing that high carb diets also improve insulin sensitivity in people with insulin resistance and and type two diabetes, but we've talked about the benefits of fructose in the past, and this also supports that how much benefit there was in terms of glucose tolerance when you had the fructose component alongside the glucose. And this these ideas that fructose is a toxin and a poison and all of that, which obviously this study suggests otherwise, but we've also gone gone through extensively in previous episodes why that is not the case. The issues with that research why fructose doesn't increase uric acid to a concerning level or really at all, except in really extreme conditions. So I'll link back to those. We won't touch on that now, but it's just worth noting that if you were to change to an 80% so an all liquid diet with 80% sucrose from the control diet that they had, butine increase in improvement in insulin sensitivity. So pretty dramatic findings here. Yeah,

Mike 29:50
basically, what you're seeing is the lower there's two things, more carbs and low or I guess that they kind of go together, but more carbs and lower fat are is improving insulin sensitivity. Improving the ability of the body to oxidize carbohydrate. And this was a normal man curious to see what happens when we get into diabetic individuals. But this is exactly what we're saying. Is as you in, as you lower fatty acid oxidation, and they're doing this through the diet. They're not using insulin, but as you lower fatty acid oxidation, you and you increase, or you try to push an increase in glucose and glucose oxidation insulin sensitivity improves as the cells are improve their ability to actually oxidize carbohydrate.

Jay Feldman 30:30
Yeah, yeah, exactly. It's very telling study here. And do you want to share the next one? Sure.

Mike 30:37
So this study is titled, improved glucose tolerance with high carbohydrate feeding in mild diabetes. So they start off, they say, to evaluate the effect of increased dietary carbohydrate in diabetes mellitus, glucose and immunoreactive insulin levels were measured in normal persons and subjects with mild diabetes maintained on basal 45% carbohydrate and high carbohydrate, which is 85% carbohydrate diets, fasting, plasma glucose levels fell in all subjects and oral glucose tolerance zero to 120 minute area significantly improved after 10 days of high carbohydrate feeding fasting. Insulin levels also were lower on the high carbohydrate diet. However, insulin response to oral glucose did not significantly change. These data suggests that the high carbohydrate diet increase the sensitivity of peripheral tissues to insulin. So basically, what they're showing here is that when they change people, and this include diabetics from a 45% carbohydrate diet to an 85% carbohydrate diet, their fasting plasma glucose levels fell and their ability to actually tolerate a glucose challenge improved significantly just after 10 days on this type of diet. And so the other thing they're seeing is fasting insulin levels were also lower on the high carbohydrate diet as well. So what you're seeing is these people are requiring less insulin to keep their fasting blood glucose levels lower, and then they are requiring less insulin for a carbohydrate challenge, to actually respond to the insulin effectively. And again, this isn't just about the sensitivity to insulin. What is this showing? This is indicating an improved ability for the cells to uptake and utilize carbohydrate, because, as we discussed in the in the previous episode, the ability the cells respond to insulin is dependent upon what's going on inside the mitochondria and with mitochondrial function. And I'm sure a portion of this also involves lowering glucagon, lowering glucocorticoids, as we talked about, with some of the other mechanisms as well in this specific episode. So there's that's exactly what we want to see, and that's one of the strategies that we're talking about, is being effective for improving insulin sensitivity and ability to oxidize carbohydrate is actually oxidizing the carbohydrate, or increasing carbohydrate, not oxidizing or increasing fatty acids.

Jay Feldman 32:48
Exactly? Yeah, exactly. And alongside that, another part that you just mentioned at the end is the lowering of fatty acid oxidation, right? Also being huge here, of course, if you're increasing carbs, I'm assuming that there is a pretty big decrease in fat intake as well. I'm assuming that they weren't actually consuming a 60% protein diet prior or 55% protein diet prior. So yeah, so that's that's huge, right? 45% to 85% this is the opposite of what most of the people out there are suggesting that you do when it comes to improving insulin sensitivity, and yet, this is in people with mild diabetes, and you saw all the most important markers in oral glucose tolerance test, which is typically the gold standard, alongside lower fasting insulin and improvements in fasting glucose as well. I mean, it's, that's exactly what what we're looking for. So, yeah, that's, I think, pretty clear there in terms of the fact that as we increase carbohydrate intake, it actually supports and increases insulin sensitivity. And that brings us to the last area of evidence that we're going to touch on briefly here, which is showing that just like we see this in kind of pure insulin resistance in other disease processes that are directly related, like cardiovascular disease and fatty liver disease, you also see increased fatty acid oxidation as a contributor, and this is happening even alongside the accumulation of fat, even alongside increases in body fat, increases in liver fat. And this is so important, again, something we didn't touch on directly earlier, in terms of misconceptions and things like that, but this idea that burning more fat, you know in the cells means losing body fat, is not accurate. There's some great Kevin Hall studies that show this clearly, where they have a low carb diet increased fat burning, lower insulin and yet less fat loss, compared to a high carb diet with lower fat burning and higher insulin. Now we see this here in the fatty liver state, where you actually see increased fatty acid oxidation and accumulation of fat at the same time. Those things are not mutually exclusive, and that's because of the metabolic derangement due to the issues with mitochondrial respiration. And so we see that here in these papers, the first one states excessive hepatic mitochondrial TCA cycle and gluconeogenesis in humans with non alcoholic fatty liver disease disease, and they state, approximately 1/3 of the US population has NAFLD, a condition closely associated with insulin resistance and increased risk of liver injury dysregulated mitochondrial metabolism is central in these disorders. Individuals with NAFLD had a 50% higher rate of lipolysis and 30% higher rate of gluconeogenesis. This fits in with exactly what you saying before, elevated free fatty acids as a result of lipolysis and elevated gluconeogenesis as a result of the production of glucose at the liver. These are both being caused by stress hormones, and so we're seeing that clearly here, and as they state in the next quote, the strong association between intrahepatic triglyceride content and hepatic oxidative and anaplerotic TCA cycle activity demonstrates the induction of mitochondrial fat metabolism in response to lipid overload during nfld simultaneous induction of pathways of lipid accretion, oxidation and gluconeogenesis oxidative stress, loss of glycemic control and potential damage to the liver during chronic hepatic steatosis. And so what they're saying here is essentially, you have this, this, which we described in insulin resistance, you have these different derangements going on together. This. The ones that they highlight are lipid accretion, meaning that there's a increase in fat stores. There's increase in fat storage. Also lipid oxidation, meaning fat burning and gluconeogenesis, both of those being the result of stress, creating all of this damage in NAFLD and, of course, causing the exact same thing in insulin resistance. And that's why these things go hand in hand. Yeah.

Mike 36:30
And I think the really interesting piece here overall is that the liver is the liver has an increased response to oxygen, or an ability to be damaged when it's oxidizing large amounts of fatty acids. And you're seeing the problem in NAFLD is just this overload of fat. And like, how do we deal with all this fat? The liver cannot deal with all the fat. It can't oxidize through all of it. So it's like trying to burn it, trying to store it. And the biggest problem here, and the I think the reason that you brought this up, is that the oxidation of fat, and the overload of fat is central to the pathology. And that's the same thing that we're seeing in diabetes, and it's the same thing that we're seeing in obesity, and it's the same thing that we're seeing impaired glucose tolerance. Is this, this impaired ability, or this over reliance on fatty acid oxidation, within the impaired ability to actually oxidize carbohydrate and so that. And again, the problem is centralized inside the mitochondria and involves the variety of stress hormones, right? So, glucagon, adrenaline, cortisol, and again, we've talked about this in depth in the fatty liver series, going through the mechanisms and highlighting fatty acid oxidation and also the stress hormones in this process. But the major point here to get across is that we are seeing the same pathology and fatty liver disease play out in diabetes, play out in obesity, play out in impaired glucose tolerance, and these same pathways are the pathways that are being up regulated in low carbohydrate diets and fasting and starvation plans that people are promoting now To solve these exact problems,

Jay Feldman 38:01
right just increasing the pathology. And we had an extensive fatty liver disease series, an eight part series that I'd recommend people check out, where we dug into the fact that the underlying problem there is an issue with mitochondrial respiration, with glucose metabolism, and that's what is underlying all these other things, just like insulin resistance, because they're essentially the same problem. One is just focusing on what's going on at the liver. But yeah, you see it very clearly. And in this next paper, they further describe this if you want to share this quote, it's a brief one, just kind of suggesting or supporting the same idea.

Mike 38:35
So the paper is titled, lipid oxidation products in the pathogenesis of non alcoholic pseudo hepatitis, which is fatty liver disease, this fancy word for it, they say in in NAFLD. So fatty liver disease, both lipid oxidation and the citric acid cycle are enhanced, suggesting that hepatocytes try to counteract excess lipid by increasing the oxidation of that lipid, the higher production of of reducing equivalents by lip lipid oxidation caused. So that's a high amount of NADH and FADH, two we talked about this in the Randall cycle studies. Causes an overflow of electrons through the mitochondrial respiratory chain, resulting in higher free radical generation. This may lead, in turn, to mitochondrial dysfunction, with consequent progression of liver pathology. So this this quote is excellent, because this quote is basically saying exactly what we've been saying throughout this process. Then that driving fatty acid oxidation creates an overproduction of reactive oxygen species inside the mitochondria, and that overproduction of reactive oxygen species these damaging components, the smoke that gets produced in the engine, damages the engine, damages the mitochondria and running this long term, prioritizing this long term, actually damages the mitochondria directly and here they're saying is, what's that is what's contributing to the damage to the liver, not to mention, and Jay, you actually have talked about this in our fatty liver series, is that if you load your liver up. With a bunch of polyunsaturated fatty acids, and then you create a bunch of smoke inside the liver cells by running fatty acid oxidation, you're setting yourself up from a transition from just a fatty liver to now in an inflamed liver where you actually have the hepatitis portion of this that moves into cirrhosis. So the fatty acid oxidation is like the spark, this metabolic spoke the smoke through the production of ROS and this is, again, this is why we don't want to drive fatty acid oxidation and prioritize fatty acid oxidation, and why lowering it is helpful, not just because there's the not just because fatty acid oxidation impairing the glucose oxidation, but also because the fatty acid oxidation over the long term, accumulates damage through producing this reactive oxygen species in this metabolic stress.

Jay Feldman 40:47
Yeah, yeah, exactly. It is a huge contributor to the pathology. This is why fat metabolism is for low energy needs. Because again, like, if you're, I don't know if we're trying to keep the analogies going, if we're in a car, and maybe we can only really need to get, you know, we only need to go slowly a small distance, we can get away with it. But as soon as you actually need high metabolic like a high metabolic rate and high ATP production, you end up with a ton of smoke. As you were saying, it's like the engine is is working with a really low quality fuel. That is great if it's like going really slow, or if we're in a starvation state and want to slow everything down to make sure we can survive. But if we're actually forced to rely on this, it causes major, major issues. So that's what we're seeing here, and they describe it very nicely, discussing the issues with the mitochondrial respiratory chain, the reductive stress, all of that. So yep. So as they were saying in those first two studies, the excess fatty acid oxidation is going on as a response to the pathology and also as something that contributes to the pathology. And then this next study, they state very clearly that despite all this increased fat burning, you're still getting an accumulation of fat at the liver, and most of that fat is coming from fatty acids. It's not coming from fructose glucose. It's not coming from other substrate. It's coming from the fatty acids despite all this elevated fat burning, which again, suggests that just increasing fat burning to try to lose body fat or to try to improve these scenarios is totally missing what's actually going on because you're just focusing on the one side of the equation, which is the fat burning side, and forgetting the fat accumulation side and when you bring more fatty acids into the system, you're also increasing the storage of fat, you know, as well as the increase in fat burning and that's what we saw with that Kevin Hall study, where the high fat, low carb diet had more fat burning but less fat loss and so we see that here in this study titled sources of fatty acids stored in liver and secreted via lipoproteins in patients with the non alcoholic fatty liver disease. And this quote states succinctly, the goal of the present study was to directly quantify the biological sources of hepatic and plasma lipoprotein triglycerides which is triglycerides in non alcoholic fatty liver disease, of the triglycerides or fat accounted for in the liver, around 59% came from Non-esterified fatty acids, free fatty acids. Around 26% came from de novo lipogenesis, meaning from some other substrate, like glucose or fructose, and 15% or 14.9% from dietary fatty acids. So what they're saying here is, of all the fat that's accumulating in fatty liver disease. 75% is coming from fat sources, from fatty acids, either from the diet, which was a smaller percent, about 15% and 60% from the body's own fat tissue due to stress causing the release of fat. And 25% is coming. 26% is coming from some version of carbohydrates that's being converted to fat, or presumably, a bit of protein as well, or amino acids as well. But what we're getting at here is despite all this fat burning, despite this idea that you're deficient in fat burning in this state, would you know, obviously it's not the case we see elevated fat burning and elevated fat storage coming from the fats. This is not a fructose problem. It's not a carbohydrate problem we discussed that extensively in the fatty liver series, and this being a big reason why is that fat is actually the source of fat in the liver? Yeah.

Mike 44:05
And I think what's really interesting here is that they're saying 59% of that is coming from the Non-esterified fatty acids, which are that's not coming from your diet, that's actually coming from tissue stores or from the fatty acids circulating around in the blood, which would again highlight the importance of stress hormones in this pathology, because those stress hormones are actually driving up the release of these fatty acids. So you're, you're pulling, you're, you're pulling all these fatty acids from stores, from tissues, from the blood supply and the liver is trying to handle all these fatty acids and the actual burning of the fatty acids, as we talked about in the previous quote, is inducing damage to the liver directly. So it's, it's the stress hormones are essential or central into this, this specific pathology as well, which is, it's really interesting to see, again, these are all the same mechanisms that we're showing is causing the problems for instance, sensitivity is driving fatty acid oxidation, driving the free fatty acid. To release, and that's through the different stress hormones, glucagon, adrenaline, cortisol, and then the actual effects of fatty acid oxidation inside the mitochondria the cell,

Jay Feldman 45:10
exactly. And just to add a bit of clarification, the fat source is not necessarily from the diet. I mean, 15% of the total fat is 60% is from the body's own fat stores. But as you're saying, that means stress hormones are involved here. And that doesn't mean that diet doesn't play a role. If you're eating a low carb diet that will increase the stress hormones, including glucagon, that will increase the release of free fatty acids, which are the ones that the liver is taking up largely to produce fat. So the diet, of course, plays a huge role here. It's not this doesn't exonerate fat in the diet. It's just saying that the that's not necessarily the main source fatty acids are but most of them are coming from the body's own tissues.

Mike 45:49
Well, and this goes with the Kevin Hall paper that you're saying is that if you are on a really high fat, low carb diet, while you may increase fatty acid oxidation, because like from the facet you're taking your diet, you also increase the the actual storage of those fatty acids as well. And the stress hormones are going to liberate these fatty acids so that you can burn them. So it's, it's like, it's even worse, right? Because you have more coming in from the diet, and then you have more accretion or storage of these fats, and you have the stress hormones you're driving those stress hormones, which are releasing, and you're just creating this overflow of fats,

Jay Feldman 46:21
right? Right, exactly. And as we discussed, a huge driver of the pathology is the excessive fatty acid oxidation and lack of carb oxidation. So yep, that, of course, being something majorly implicated here in fatty liver disease, and if we move on to cardiovascular disease, we see a continuation here in terms of the fat oxidation being increased and implicated. Do you want to start us off with this study looking at the heart in type two diabetes? Sure.

Mike 46:45
So this paper is titled, metabolic abnormalities of the heart in type two diabetes, and what the authors go to say, they say, type two diabetes mellitus escalates the risk of heart failure, partly via its ability to induce a cardiomyopathic state that is independent of coronary artery disease and hypertension, although the pathogenesis of diabetic cardiomyopathy has yet to be fully elucidated, aberrations in cardiac substrate, metabolism and energetics are thought to be key drivers. These aberrations include excess fatty acid utilization and storage, suppressed glucose oxidation and impaired mitochondrial oxidative phosphorylation. So traditionally, heart failure is characterized, or is heavily, usually caused by coronary artery disease. So basically, blockage of the arteries, which blocks blood flow to the heart's muscle tissue, so you don't get oxygen, you don't get glucose, and then basically the heart slowly starts to be suffocated to death. In response to this, the blockage of the arteries. But something that's been known for an extended period of time is that diabetes directly contributes to cardiovascular disease and it doesn't or specifically to heart failure and cardiomyopathy and what they're they're saying is, well, the diabetes is like, while it can increase coronary artery disease, that blockage of the arteries, it also seems to be doing it through this other mechanism we don't like. It's not just this lack of blood supply. Now, what they're saying here is that, well, it's actually this problem with metabolism, and it's the same exact problem that we've been talking about through this past episode, this episode and the previous episode, where, in this diabetic state, the heart cells, the cardiomyocytes, are having, they're not able to effectively oxidize glucose to at a level that would be normal for their for their function. And so they're up regulating their their use of fatty acids, that's impairing their metabolic function, and now you have heart failure again. The heart is failing because the cells are being forced to run on excessive amounts of fatty acids with this metabolic dysfunction, and that's leading to, or it's leading to and a function of the damage to the mitochondria, the impaired mitochondrial oxidative phosphorylation. So it's an energetic problem. So it's not just this lack of blood flow and substrate, oxygen, all cyber stuff. It's like inside the cell itself, with the diet, the diabetic cardiomyopathy, the cells are not having enough energy and having energetic dysfunction characterized by an inability to oxidize glucose and an upregulation on fatty acid oxidation.

Jay Feldman 49:10
Yeah, exactly. It's a great characterization there, or explanation there of what's going on, and we're seeing that very clearly, and this next paper digs into it in a bit more detail and more support showing the influence and as they described in the first paper, the fact that the changes in substrate metabolism and energetics are drivers of the state. Excessive fatty acid oxidation and storage, suppressed glucose oxidation, impaired mitochondrial oxidative phosphorylation, all being drivers of the state and we see that in this paper, where they're digging into it, in, you know, a bit further and in some different versions of heart issues. And so they the title of this paper is mitochondrial fatty acid oxidation, alterations in heart failure, ischemic heart disease and diabetic cardiomyopathy. And they state in many forms of heart disease, including heart failure, ischemic heart disease and. Diabetic cardiomyopathies, changes in cardiac mitochondrial energy metabolism contribute to contractile dysfunction and to a decrease in cardiac efficiency. Specific metabolic changes include a relative increase in cardiac fatty acid oxidation rates and an uncoupling of glycolysis from glucose oxidation. Again, this is describing exactly the state that we described in terms of insulin resistance before where you have high glycolysis, poor glucose oxidation and a reliance on fatty acid oxidation. In Heart Failure overall, mitochondrial oxidative metabolism can be impaired, while in ischemic heart disease, energy production is impaired due to a limitation of oxygen supply. In both of these conditions, residual fatty acid oxidation dominates over mitochondrial glucose oxidation. In diabetes, the ratio of cardiac fatty acid oxidation to glucose oxidation also increases, although primarily due to an increase in fatty acid oxidation and an inhibition of glucose oxidation. So again, in contrast to everything we're told about insulin resistance, being this state of of you know, you're just running on glucose, you're metabolically infectable. You've got to be using the fat. That is what's happening already, the fat is being used, the glucose is not being efficiently used, and you see it in the heart contributing to pathology. And they wrap this up by saying, recent evidence suggests that therapeutically regulating cardiac energy metabolism by reducing fatty acid oxidation and or increasing glucose oxidation can improve cardiac function of the ischemic heart, the failing heart and in diabetic cardiomyopathies. So again, not only do we see the correlation, not only do we see these both, you know, both of these things happening at the same time, but we see this actually being causal. And when you fix the glucose oxidation or reduce the fatty acid oxidation, you get improvement in the state. And again, this is it's just a great example where you see everything play out from you know that we described in terms of its own resistance. You see it very clearly being described here, in this in these multiple different versions or aspects or types of heart disease, where you see the exact effect that we're describing that's going on in other tissues as well, and some resistance, yeah.

Mike 52:05
I mean, I don't have too much to add there. I think you wrapped it up pretty well. I think the central piece for everyone to take away is to just understand that the dysfunction inside the cell in terms of mitochondrial function, inability to oxidize glucose effectively, and then up regulation on fatty acid oxidation with that whole Malu that happens with that, the glucagon upregulation, the cortisol, the adrenaline, all of these stress hormones is central to all of these disease states, all of these pathological states, whether that's diabetes, obesity, heart disease, fatty liver disease, we'll talk about it in cancer, we can talk about a neurological dysfunction In all these different disease states you're seeing this. This is central, this is core across all of these different things. And so it's important to dive in and figure out, like, what how do we address this? How do we fix this specifically? How do we get the system oxidizing glucose effectively? How do we lower the excess fatty acid oxidation? How do we bring those stress hormones down? And it doesn't seem to be through low carb diets, because they are driving this pathology directly. They're increasing fatty acid oxidation, they're increasing glucagon, they're increasing cortisol, they're increasing adrenaline, whether that's serum levels or whether that's local metabolism and effects of the cell, we're still seeing these increases. So we don't want to be optimizing for the things that are driving this dysfunction that we're seeing in all of these different states, and the carbohydrate pieces is essential to this,

Jay Feldman 53:27
yeah, yeah, absolutely and so what that does bring us to is this, you know, we've, I think, elucidated very clearly and gone through the evidence supporting what actually is going on here, and that the impaired glucose metabolism is the cause of this issue in and again, the solution here is not, as you said, avoiding carbs, not bringing in fat, but instead fixing that underlying problem. We kind of alluded to some things earlier that are involved with fixing this issue and that are essentially the solution to insulin resistance but when it comes to the details, we've discussed these again, not only in all the other previous podcast episodes where we discuss how to improve your energy balance, how to improve your metabolism, which is this right? That is fixing glucose metabolism, to fix this issue, but also in the pro the previous episode, not the one directly previous, but the prior episode where we discussed this kind of overview of what's going on in insulin resistance from the bioenergetic view, we went through some specific extra solutions, some things to look to in terms of diet, possible changes to make, some some extras that you might want to look to if you're dealing with insulin resistance, some other kind of avenues and strategies to to take a look at or consider. And so I'm just going to reference back, or suggest that the listeners go and listen back to that episode instead of repeating it all here, since we did cover it in more detail there. So as far as the solution for these issues goes, I would take a look back at that episode, and with that, we'll wrap up here and wrap up the series and so if you did enjoy today's episode and this series, please leave a like or comment if you're watching on YouTube. YouTube, and if you're listening elsewhere, please leave a review or five star rating on iTunes. All of those things really do a lot to help support the podcast, and are very much appreciated to check out these show notes for today's episode, where we'll link to the studies and articles and anything else that we referenced throughout the episode, head over to Jay Feldman wellness.com/podcast and Mike, do you have anything you want to share with our listeners?

Mike 55:23
Yeah. So if anybody's dealing with this mitochondrial dysfunction, trying to get out of excess fatty acid oxidation or impaired glucose tolerance, low carb diets, etc, they can check out my website, mikefave.com where they can pick up the nutrition blueprint, which sets up a helps, gives them guidelines to set up a diet. And then also you can check out my, my website, Mike, dave.com for one to one consulting, if that somebody needs that

Jay Feldman 55:47
perfect Yeah. And I'll mention as well, when it comes to creating a diet. Here, I've got a another resource for people that can be helpful when it comes to improving insulin resistance. And obviously, as we've discussed throughout this episode, there's a lot of conflicting information out there, so I've created this energy balance Food Guide, which you can use to determine exactly what to eat to support your metabolism, lose weight, improve digestion, get amazing sleep, boost your energy. It's a one page infographic, and it organizes foods on a spectrum based on how effectively they support your metabolism. It also has a separate spectrum based on digestive issues. Basically, it helps to adjust the scale as dealing with different gut issues, which, as we've discussed or alluded to here, discussed in the past, are contributory to insulin resistance. So the food guide makes it really easy to get started with a bioenergetic approach to optimizing your health. So head over to Jay Feldman wellness.com/guide to download that free energy balance Food Guide, and with that, we'll see you on the next episode.

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