Jay
Welcome to the energy balance podcast, a podcast where we explore health and nutrition from the bio energetic view and teach you how to maximize your cellular energy to maximize your health. Today's episode is part two of my followup from my debate with Dr. Eric Westman on Ben Greenfield's podcast. And I'll be digging into a number of our disagreements and some other comments that Dr. Westman made that I didn't have a chance to discuss or address on that debate.

And that includes whether you should be concerned about low T3 or high glucagon on a low carb diet, as well as whether insulin resistance is a problem of excess glucose metabolism or excess fat metabolism, whether a low metabolic rate allows you to live longer, whether high carb diets cause overeating and insulin resistance, whether you should be concerned about glycation on a high carb diet, as well as a handful of other points that Dr. Westman brought up throughout the debate. As always, to check out the show notes for today's episode, link to the studies, articles and anything else that I reference, head over to jfeldmanwellness.com/podcast. And with that, let's jump right in. 

All right. So in part one of this followup, we dug pretty deep into the bioenergetic and hormonal effects and concerns regarding a low carb diet. And in this episode, we're going to dig into a number of the other points that were brought up throughout the debate and some of our disagreements and kind of get into the details and, you know, refute a number of the points that.

Dr. Westman brought up. First one I want to dig into here. Dr. Westman mentioned or brought up this paper a handful of times. was a paper written by Isabella Cooper and the title is Ketosis Suppression and Aging, the Effects of Suppressing Ketosis in Long-Term Keto-Adapted Non-Athletic Females. And we're just going to touch on this briefly. I don't think it's particularly relevant to the discussion we were having.

And it also wasn't a hundred percent clear as to what he was trying to suggest with this paper. I don't think he really described that exactly. It seemed like he was bringing it up to suggest that in the same way that we see negative effects going from a high carb diet to a low carb diet, like increased stress hormones and inflammatory effects, things like that. You also see negative effects going from a low carb diet to a high carb diet. And people will say, you know, the fact that you see these negative effects going from high carb to low carb suggests that high carb is the kind of natural state. Whereas low carb diet is an unnatural state. And so it sounds like he was suggesting, well, you see the same thing going the other direction. So maybe low carb and ⁓ ketogenic diets are actually the natural state of the body. And we'll talk about that conclusion, but first it's worth just touching briefly on what exactly was studied or discussed in this paper. So the paper was pretty similar to one of the other studies we looked at from Isabella Cooper and some of the same other authors. So in this study, they were looking at 10 pre-menopausal women who were on a ketogenic diet for an average of 3.9 years, we'll call it an average of four years. And what they did was they went for three weeks on a controlled ketogenic diet, then three weeks on a high carb diet, and then went back to the controlled ketogenic diet for three weeks. Now the high carb diet was not controlled. What happened was they just told the participants to eat ad libitum, meaning as much as they want, according to the UK eat well guidelines.

So according to the generic UK guidelines, much like we have in the United States. And the macro breakdown that they suggested was 55 % carbs, 20 % protein, and 25 % fat. So obviously this would be far different from a ketogenic diet, but we don't actually know anything about what they were eating. If they were eating close to these macros, what foods they were eating, they were just given these guidelines or recommendations and that was it. And what they found was when they went from the ketogenic diet to the high carb diet, there was a clear shift in fuel utilization. So we saw the RQ value increase suggesting that there's an increase in carb utilization and a decrease in fat utilization. We also saw changes in glucose levels, insulin levels, IGF-1 levels, which are all to be expected when shifting into a higher carb diet, especially from a lower carb diet. And they also noticed that there's an increase in weight. There was weight gain when they were on the high carb diet. And we'll be coming back to that. Now they also found that there's an increase in a couple of inflammatory markers and liver markers after the three weeks on the high carb diet. And and those then went back down after, you know, when they went back to the keto diet. ⁓ however, it's worth noting that the majority of inflammatory markers saw no change. was no difference in them. And there's also no difference in some of the kind of bigger picture inflammatory and stress markers like cortisol and CRP things that we do. I mean, cortisol, see universally increase when shifting from a high carb to a low carb diet.

CRP is shown in some studies as well to increase. Uh, but you know, that, that was not seen here when going from the ketogenic diet to the high carb diet. And again, there was a couple of inflammatory markers that increased. And so, as I was saying, it seems like Dr. Westman was suggesting that this is very parallel to what happens when you go from high carb to low carb. So, uh, it doesn't actually point to any negative effects when going high carb to low carb or, know, it's a parallel effect. And there's a number of problems, I think, with that conclusion and really withdrawing many conclusions at all from this diet, at least in terms of shifting from keto to high carb. And there's a few reasons for that. So for one, we're definitely not seeing the same markers shift here. When we go from high carb to low carb, we see major increases in stress hormones like glucagon and cortisol. Those were not seen here. Now, the other thing is there was weight gain seen when going onto the higher carb diet. And that alone is normally something that's going to increase inflammatory markers and lead to some negative health effects, negative effects in terms of the biomarkers. And this is not the case when we go from high carb to low carb. You actually see the negative effects independent of any weight gain. So you're not seeing, you know, someone goes from high carb to low carb, there's all this weight gain and there are negative inflammatory effects. You see these effects even without this major confounding factor in weight gain.

 And so in this situation, there's no way in this study to identify that the inflammatory markers were due to the increase in carbs and rather could have just been due to the increase in weight, which is something that we know to happen. You can gain weight on any sort of diet. And if you're gaining weight, you're going to generally see some negative effects. And then on top of that, another huge confounding variable is that there was no control of the higher carb diet. So we have no idea what they were doing there. They could have been dramatically overeating. They could have been eating extremely unhealthy choices in terms of carb containing foods.

All, we were, they were just given guidelines. We don't actually know what they were consuming during that period of time. We don't know if it was actually in line with the guidelines. We don't know if it was similar at all to the macronutrient ratios that were being given. So that's another huge confounding variable here with the study. It doesn't mean that there's no value to looking at these markers, but it certainly, I would say, doesn't suggest what Dr. Westman was maybe insinuating or, or implying that it would suggest. And it's also worth noting as well. If you take anybody who's following the average Western diet guidelines, whether it's the UK guidelines or the U S guidelines. And then you put them on a controlled diet of any form, a vegan diet, a keto diet, a mixed macro diet, whatever it is, you know, ⁓ higher fiber, higher protein. You're going to see improvements on whatever diet you've changed them to coming from just the standard Western diet. And so you kind of saw that here, you basically saw keto to standard Western diet guidelines back to keto and there was benefits, but that really doesn't say very much about potential benefits of keto or negative effects of a higher carb diet. So, I mean, I don't want to dig into this any further. mean, there's, don't think there's much more to discuss here when it comes to this study, but it was one that Dr. Westman brought up a good handful of times on the debate, if I remember correctly. So, ⁓ just wanted to at least touch on it here and explain, you know, or share my point of view there. Now, as I mentioned in part one of this follow-up, I've seen a ton of people struggle with issues after doing long-term low carb dieting. And I talked about how this happens on the mitochondrial level, the hormonal level, and then how that has downstream impacts on things like anxiety, decreasing energy, decreasing libido, increasing blood sugar levels, causing insomnia and trouble sleeping, decreasing body temperature, increasing weight gain or causing weight regain after people have lost it. And, you know, I've helped a lot of people reverse these issues.

Using a bio-energetic approach. So if you're looking for guidance and understanding how to create a sustainable bio-energetic diet and lifestyle to resolve these issues or any other health issues you might be working on, then head over to jfeldmanwellness.com slash call, where you can sign up for a free call with a member of the J Feldman Wellness team who can provide you with insights on your health issues and make sure that you get the support that you need along your health journey, whether that's one-on-one coaching, group coaching, or our energy balance course. We've helped a ton of people reverse everything from insomnia to fatigue, to brain fog, to severe digestive problems and everything in between. And we'd love to help you do the same. So head over to jfeldmanwellness.com slash call to sign up for a free call. All right. So let's move on to something else that Dr. Westman mentioned, ⁓ during the debate. I have, at least I'm pretty sure if he mentioned it during the debate and I know I've heard him mention it in other videos where he was basically saying, maybe there's low T3 on a low carb diet. And we talked about this in the last episode, you know, there's quite a bit of evidence for that. But I don't care about a number, you know, in terms of the blood work, I care about the clinical relevance. I care about if somebody's actually dealing with a hypothyroid state and you know, the same could potentially be said about elevated glucagon or cortisol, you know, who cares what's on the lab work, you know, if it's not actually affecting someone or if someone's feeling better, what's the difference? And on one hand, I agree with that. mean, when we're looking at someone's health, we want to look at the whole picture and If one marker is off, we don't want to necessarily just treat that marker in isolation if they're not presenting with the issues you might expect from that marker being off. But there are still some concerns here, even if someone sees low T3 and they're not dealing with severe hypothyroid symptoms, A, they're often dealing with ⁓ what would be considered subclinical hypothyroid symptoms. And we'll talk about that in a minute. But also, when we're seeing these values, this can be an indication of what's to come.

When we initially have some stress, even like short-term chronic stress, we don't necessarily see all the deterioration, but you know, we might be feeling okay. We might be getting through it. All right. But we might start to see that things are looking off in the lab markers. And if we keep doing what we're doing, that can then lead to that deterioration that can then lead to those problems cropping up. And that's what we want to be obviously very much aware of. So while we don't want to necessarily treat the marker on its own, we definitely want to understand what is causing those markers to be changed and, and in a negative way what the potential downstream effects of that are and, you know, how we might prevent it and what we want to look out for. And as I've mentioned earlier in this episode, and I mentioned it in the last episode as well, I do see signs of hypothyroidism very frequently in people who are coming from low carb diets. And again, they might not be such intense hypothyroid symptoms that someone's like really sick, but I definitely see things like low body temperature, cold hands and feet, dry skin, fatigue, thinning hair, low mood, joint pain and a number of other symptoms that I've described earlier. And so these are things that we would definitely want to look out for. And, you know, if we're only focused on the scale as our metric, and we're just looking for weight loss, or we're just looking at certain metrics on the blood work, we might miss these things that are actually pointing to some underlying issues. So that would be one thing to consider when we're talking about looking at the person as a whole. It's true. We don't want to just look at the markers. We want to make sure we're considering those different symptoms as well. And then also we want to consider what the long-term effects are of let's say low T3 or high glucagon. And on that front, I've heard Dr. Westman say, at least in other videos, I don't think he actually mentioned it in the debate. And I've heard this mentioned by other ⁓ people in favor of low carb, where they'll say, you're not considering these hormone levels in the context of a low carb diet. Maybe low T3 is normal on a low carb diet. Maybe lower testosterone is normal on the low carb diet. Maybe high glucagon or high cortisol is normal on a low carb diet. How do we know that those things aren't actually supposed to be that way. And we're just comparing this to someone on a high carb diet. And so in some ways, kind of like we talked about last time with the question of maybe everything changes with fat metabolism on a low carb diet. want to consider the question, but we also want to make sure that there's actually some physiological basis to support this sort of questioning. We don't want to just assume that it's likely based on any random possibility that we come up with, there would actually need to be a physiological basis for this. And so In order for it to be true that low T3 is totally fine, would have to have, there would have to be evidence showing that there's no downstream effects of low T3 in a, you know, in someone on a low carb diet that they have way increased sensitivity to something like T3 so that, you know, there's no downstream effects of the low T3 or standing with testosterone. we're seeing low testosterone, there would have to be evidence that there's increased downstream sensitivity to testosterone or on the glucagon side.

Again, you would have to show that the glucagon isn't actually having any of the downstream effects. There's an insensitivity to glucagon. And also you'd have to show that that insensitivity to either of these or increased sensitivity or reduced sensitivity has no other negative side effects. And I don't think there's any good evidence for that. And there's a lot of downstream effects that we should be aware of when it comes to these hormones. They're not just hormones related to blood sugar or just hormones related to glucose metabolism. They have tons of other effects.

We know that excess levels of glucagon is a major driver of insulin resistance. We know it reduces the conversion of T4 to T3, which obviously that's not interfered with on a low carb diet because we see that happening. We know that it increases the stimulation of catecholamines and glucocorticoids. So epinephrine and cortisol, ⁓ which is, you know, goes hand in hand with the stress response. We know that excess glucagon causes immunosuppression by activation of certain T cells.

So we would have to show that there's no immunosuppressive effects of this excess glucagon. We know that it slows intestinal motility and gastric motility. And these are things that are also really common effects on a low carb diet. They also go hand in hand with hypothyroidism, but they can also be driven by glucagon. And so we would have to show that that effect doesn't happen. We have to show that, you know, the other long-term negative effects of excess glucagon, like cardiomyopathy and heart failure, which are shown to be driven by high levels of glucagon also aren't happening.

In this condition, there's some sort of insensitivity that prevents it or some other effect. And that's just glucagon. You the same thing would have to be true for T3. T3 affects the immune response. It affects heart health. You know, low T3 and hypothyroidism, even subclinical levels increases heart disease risk and atherosclerosis and blood pressure. It's also really tightly tied with mood. You know, we can see, we see increased depression and anxiety associated with hypothyroidism. We see fatty liver disease associated, see problems with skin health. see problems with the reproductive hormones. You know, and I mentioned this in that last episode that T3 is the main regulator of what's called the star protein, the steroid ogenic acute regulatory protein. And that's the protein is the rate limiting step of our steroid hormone production. So if you have less of that, you're going to have less prognatholone, less testosterone, less progesterone. And so we would have to show that somehow there's some mechanism that circumvents all of these issues that are associated and driven by low T3 in these contexts.

And there's just no good evidence that I've seen that would support that. And the same would be true of the reproductive hormones of progesterone and testosterone. These aren't just hormones that have effects in the reproductive system. They have effects on immune function, on energy and mood, on mitochondrial function, on insulin resistance, on cardiovascular disease. So we'd have to show that again, there's no downstream effects here that are impacted with this change in hormones in order for it to be true that it's just normal to have high glucagon or low T three on a low carb diet. And if someone wants to say, that's my hypothesis, there's no evidence for it, but that's just, you know, that's a hypothesis I've come up with. That's fine. But there's no reason to put any stock in that. So, yeah, that's just something that, you know, I think we need to consider when it comes to this idea of, not caring about the marker on its own. Obviously I'm not saying that we should just look at an individual marker on the paper and that's it. And that's how we should evaluate someone's health.

Not at all saying that, but obviously we shouldn't ignore that marker. And we should especially consider that with someone's health and the other symptoms that they're experiencing. those are some things to consider when it comes to the changes in these different hormone levels on a low carb diet. All right. So next thing to dig into here, uh, something that Dr. Westman had mentioned interestingly, and I don't know, I don't know exactly where this was coming from, but when we were talking about that versus carb utilization, and I was talking about the fact that we don't see an increase in fat utilization in the brain on a low carb diet. He was saying, well, how do we know that? And I'm not sure if he was just playing devil's advocate,  or just trying to be, you know, adversarial in that way, or if he actually isn't aware of what goes on in terms of fuel utilization in the brain, one on a low carb diet. If he is aware of that, if he is aware of the fuel utilization changes in the brain on a low carb diet, then I mean, it would have just had to have been an argument in bad faith. and if he's not aware of that, then I think that would be pretty surprising as well, because this isn't a new finding, right? We've known what's gone on in terms of, fuel metabolism in the brain again, since the 1960s, from, from Cahill, who's one of the, you his research in fasting was, really pivotal and very, very well known. and then the other thing too, and we'll dig into this is that this is where ketones come in. So I think the vast majority of people on a, you know, who are advocating for low carb diets are pretty aware of that.

The brain isn't utilizing fat. It's that we're producing ketones and those are replacing part of the glucose needs. So we go from, you know, a hundred percent utilization of glucose in the brain, mostly, you know, nearly a hundred percent to 30 to 40%. And then the rest being supplied by ketones.

So, you know, I don't really know where this argument was coming from, but he did mention it. So I figured it was at least worth touching on here briefly. And again, kind like we talked about earlier with this idea that fat metabolism would be different on a high carb diet versus a low carb diet. It's worth noting that there's already fat available on a higher carb diet. We're not talking about a zero fat diet here. And so if there wasn't fat available and we're saying now we're providing this new fuel, maybe the brain uses it. Of course that would make sense, but there's already fat available. There's already free fatty acids available for the brain to use as fuel if it wanted to, if that was a part of its physiology, even on a higher carb diet. And that's not the case. But anyway, looking into know, ketogenic states and the utilization of fuels in the brain. Uh, there's a 1967 paper by Cahill titled brain metabolism during fasting. That's worth taking a look at. And it looked at fuel utilization in the brain during fasting and found that ketones could be used for around 60 % of the brain's energy needs while the rest is fueled by glucose. So someone wanted to look at, uh, you know, just the starting place in terms of evidence for this, you know, you can take a look at that paper and I'll also touch on a couple of quotes here describing this in a way that also factors in a number of the mechanisms we were talking about in the last episode. So this is a paper titled brain energy metabolism, spurns fatty acids as fuel due to their inherent mitotoxicity and potential capacity to unleash neurodegeneration. 

And they state the brain uses long chain fatty acids to a negligible extent as fuel for the mitochondrial energy generation and contrast to other tissues that also demand high energy. Besides this generally accepted view, some studies using cultured neural cells
or whole brain indicate a moderately active mitochondrial beta-oxidation. Here we corroborate the conclusion that brain mitochondria are unable to oxidize fatty acids. They go on to state later, oxidative degradation of long-chain fatty acids is the most potent mitochondrial process for ROS generation. To minimize reactive oxygen species generation, obviously brain mitochondria completely substituted fueling of long-chain fats by that of glucose or of the ketone bodies, beta-hydroxybutyrate and acetoacetate with an FADH2 to NADH ratio of 0.29 and 0.33 respectively. So we talked a lot about that ratio in the last episode where ketone bodies have a much better ratio than fats and especially the long chain fats. Glucose has a ratio of 0.2, so quite a bit less than the ketone bodies, but that plays a major role in the efficiency of mitochondrial respiration when using these different fuels. But in any case, yeah, I think it was something that I don't need to really be touching on here, but Dr. Westman did.

bring up this idea that, you know, question the idea that there's not an increase in fat utilization in the brain on a low carb or ketogenic diet. All right. So let's move on to talking about the metabolic rate on low carb diets, ketogenic diets, starvation and fasting. And so this was something that was brought up toward the end of the debate. And, you know, the idea was,  I don't remember how it was brought up, but basically we came to this idea that, you know, in starvation, of course we see a lower metabolic rate in order to survive for longer periods of time. And that that's what that adaptation is for. And it goes hand in hand with increased fat metabolism and increased ketone production and a lack of glucose and a low carb diet ketogenic diet causes the same thing. It's a fasting mimicking diet. And it seemed like Dr. Westman agreed with that. And he said, well, isn't that a good thing? That's, know,  a low metabolic rate is associated with a longer lifespan.

What he's referring to here is what's called the rate of living theory of aging, which is an older theory coming out of basically the thinking in the industrial revolution, which is that basically the more you use a machine, the faster it wears out and the quicker it, you know, it degrades. And, know, the assumption being the same for humans and animals. And basically when looking at the metabolic rates of different species, what was generally found was that there's an increase when there's an increased metabolic rate by, you know, based on weight, there's shorter lifespan and faster aging. And so that's what this rate of living theory was originally based on. But for anyone who's aware of the aging and lifespan research, the rate of living theory has long been debunked for lack of a better term. so it's really, I mean, there's tons of evidence against this and we've done a prior episode, I've written an article as well discussing this. So I'll just link back to those instead of getting into the details here, but it's really not something that's considered valid for a number of reasons. There's all these confounding variables. And one of the important ones is that there are certain differences between species that confound the changes in metabolic rate. But when you look within a species where a lot of those variables are constant, and one of them in particular is the ⁓ unsaturation index of the membranes, when that's constant, you actually see that a faster metabolic rate leads to a longer lifespan. 

And one of the major confounding variables when looking at this rate of living theory was the propensity toward increased ROS production, oxidative stress, and damage to the structure of the tissues due to changes in the unsaturation index. So I'll again, I'll link back to prior episodes and articles where I've discussed this, but it was also interesting that he brought this up because this is data that's based on animals.

And, you looking at other species, and this was something he seemed to take a huge issue with when I was talking about rodent research, which I think is,  in many cases, very much applicable to humans. And we talked through human research as well in the last episode, obviously we went through all of that, but, know, it seemed like a bit of a, a bit of a double standard where I brought something up related to other species. And of course, in his view, that doesn't apply at all because those are other species. And that he brought on this idea of the rate of living theory, which is also based on research looking across other species.

And yet that was something that he viewed as a good enough argument, good enough support for the idea that a low metabolic rate would increase lifespan. So just an interesting ⁓ situation that occurred on the debate. And interestingly, I then brought that up on the debate. You know, I mentioned a, the problems with the rate of living theory. And as I was going through that, he said, well, why would this be, you know, this wouldn't be valid because it's based on animals. But it was interesting because he was the one who actually brought this up as support for his argument that a low metabolic rate from a low car ketogenic diet would be a good thing. And he seemed to not recognize that this was, you know, I was actually explaining why his argument wasn't supported. he further did, he further invalidated it by mentioning that it's based on animal research, which we shouldn't be considering. But in any case, I'll link back to prior episodes and articles digging into the rate of living theory problems with it and newer theories that are far more relevant and accurate and the evidence for those.

Along with that, why a higher metabolic rate is actually a better thing and why you don't actually want a lower metabolic rate as is driven by a low carb diet. All right. So brings us to another topic here, which has to do with insulin resistance and glucose versus fat burning or oxidation. And there was a point where he mentioned that too much glucose in the cell interferes with fat burning and that this is the state of insulin resistance. And so I think there's a lot of confusion here.

All throughout the low carb space and elsewhere as to what's really being seen in insulin resistance. So we'll dig into that a little bit. And I think one of the biggest sources of that confusion is that in general in insulin resistance, you see a few different features, a few different things going on at the same time. One is that you see inhibited glucose oxidation. So we're not actually efficiently utilizing the glucose inside our cells. But what you do typically see is an increase in glycolysis. Glycolysis is the inefficient utilization of glucose we're converting that glucose into lactate. Sometimes it's called anaerobic glycolysis or aerobic glycolysis if we're kind of forced into this when oxygen is present. But you do see an increase in glycolysis with a reduction in glucose oxidation. And so I think some people get confused about that and they say, well, this increase in glycolysis is actually the problem that's driving the state or they see that and they say, this is a state of excess glucose burning, but it's actually the state of reduced glucose oxidation and poor glucose metabolism leading to increased glycolysis.

And along with that, you actually see increased fatty acid oxidation. So this idea that there's this interference with fat burning and that you have less fat burning in these states is something that can happen in more severe scenarios where there's such impaired metabolism that there's actually reduced fatty acid metabolism. But in the vast majority of cases, and especially in the progression of insulin resistance, you see increased fatty acid oxidation, increased beta oxidation, increased lipid metabolism. So we'll be talking about that, digging into some studies that demonstrate this.

The first one is a study titled Characterization of Cellular Defects of Insulin Action in Type II Non-Insulin-Dependent Diabetes Mellitus. And so they looked at seven non-insulin dependent diabetic patients and they did some different clamp studies. we'll kind of go through these. I'm not going to read the quote all the way through because I think it makes more sense to kind of go in order of the studies. So study one was euglycemic and normal insulin clamps.

They took these people with type 2 diabetes who normally have high levels of glucose, hyperglycemia and high levels of insulin, hyperinsulinemia. When they brought them down to normal levels, what they found was further down they state in study one, glucose uptake was decreased by 54 % in the people with diabetes versus controls. So when they had the same normal levels of glucose and insulin, there was less glucose uptake. They also found that glycolysis, glycogen synthesis and glucose oxidation
were reduced in these patients with type two diabetes. So, partially, of course, this is driven by the reduction in glucose uptake, but we see that there's reduced glucose metabolism and they state non-oxidative glycolysis and lipid oxidation were higher. So basically there's an increased reliance on glycolysis, as we said, and an increased reliance on fat metabolism when we're in this kind of normal state. I'll link back to episodes where we dug into insulin resistance and diabetes and why it's not caused by carbohydrates we talked about that in way more detail in those.

So I'll link back to those, we'll at least go through a little bit of it here. But essentially what we're seeing is that in this normal state, there's impaired glucose metabolism, increased reliance on fats for fuel and also non-oxidative glycolysis. And this is then what drives the stress reaction where the body says, all right, we need to increase the glucose levels so that we have enough fuel and we need to increase insulin levels as well to make sure we're increasing the amount of glucose that gets taken up by the cells.

And so we see a part of that in study two. So in study two, they did hyperglycemic normal insulin clamp. basically kept an insulin at the same level, but increased the amount of blood trigger. And what they found was that in study two, glycolysis, but not glucose oxidation was normal. Non-oxidative glycolysis remained higher and glycogen deposition increased and lipid oxidation remained higher. So what they found here was that there was an increase in glucose uptake and we saw an increase in glycogen deposition and an increase further in glycolysis but there was still not an improvement or resolution of oxidative glucose metabolism. And we still saw increased lipid metabolism, lipid oxidation, fat metabolism. So we look at study three, which was when there was a normal amount of glucose and excess insulin, high levels of insulin, hyperinsulinemia. And what they state was that in study three, hyperinsulinemia normalized glycogen formation, glycolysis and lipid oxidation, but did not normalize the level of non-oxidative glycolysis or the decreased glucose oxidation. Lipid oxidation and glycolysis and glucose oxidation were inversely correlated. And we'll go through the conclusion in a second, but what we have here in study three was that with the increased insulin, there was increased glucose uptake. And so there was normal amounts of glycogen formation. Glycolysis was normal. And then we also saw because of further glucose uptake into the cells, there was less fat metabolism. The glucose metabolism increased enough to lower fat metabolism, but it did not normalize the elevated non-oxidative glycolysis or the decreased glucose oxidation.

So even though there was a decrease in fat metabolism in this scenario, we still didn't see a resolution of the situation. There's still this blocked glucose metabolism and increased reliance on glycolysis. They go on to state that, in conclusion, in type 2 diabetes, market hyperinsulinemia normalizes glycogen synthesis and total flux through glycolysis, but does not restore normal distribution between oxidative and non-oxidative glycolysis. Hyperglycemia cannot overcome the defects in glucose oxidation and non-oxidative glycolysis.

Lipid oxidation is elevated and is suppressed only with hyperinsulinemia. So we get a pretty good scope here of what's going on metabolically in the state of type two diabetes and insulin resistance. And we're going to be looking at this in some other tissues as well that describes this further. And again, we went into this in way more detail in those other podcast episodes. So make sure to take a look at those for more information on this topic. But one thing that was brought up during the debate was the utilization of fuel in the heart.

What I mentioned was that the heart typically relies on fat for 70 to 90 % of its energy needs and glucose for 10 to 30 % of its energy needs. But in the debate, Dr. Westman stated that he is of the belief that the heart should be oxidizing more fat, you 90 % of its energy needs coming from fat as opposed to a bit lower on that scale. But what we actually find is that in type two diabetes, in heart disease and in heart failure, there's impaired mitochondrial respiration and an increased reliance on fat for energy.

And the utilization of glucose is actually reduced by 30 to 40%. So what he's describing here that he is saying should be happening at this is the ideal state is the state that we actually see in type two diabetes or disease and heart failure. We'll go through this in a couple of studies here. The first one titled metabolic abnormalities of the heart and type two diabetes. they state 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 as you have to be fully elucidated, aberrations in cardiac, substrate metabolism and energetics are thought to be key drivers. These aberrations include excessive fatty acid utilization and storage, suppressed glucose oxidation and impaired mitochondrial oxidative phosphorylation. So we're seeing that in this state of type 2 diabetes, looking at the heart and you see this in other tissues as well, you see it in the liver especially, and fatty liver disease, but what they're saying is increased fatty acid utilization, suppressed glucose metabolism and impaired mitochondrial respiration. So we're actually seeing this shift toward increased fat metabolism in type 2 diabetes. And in this study, they talked about it in heart failure and ischemic heart disease as well. This is a study titled mitochondrial fatty acid oxidation alterations and heart failure ischemic heart disease and diabetic cardiomyopathy. 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. So this exact scenario we're talking about increased reliance on fat metabolism, impaired glucose oxidation, and less glucose utilization overall, but increased reliance on glycolysis. 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 mitochondrial 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 there's greater reliance on fat, less reliance on glucose metabolism in this state of diabetes, as we already discussed, and also talking about in these other states like heart failure and ischemic heart disease. They go on to state 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 it's not just that we see this metabolism happening as a result of other problems, but if you actually intervene, you know, using a drug to lower fatty acid oxidation and increase glucose oxidation, actually improves the state of the heart in these different conditions. 

So these metabolic problems are actually contributing to the pathology. The increased fatty acid oxidation is actually contributing to the pathology in these states and lowering it actually helps to resolve the issue. And they talk about that as well in this study. This is a study titled Role of Fatty Acid Uptake and Fatty Acid Beta Oxidation in Mediating Insulin Resistance in Heart and Skeletal Muscle. They state direct measurements of fatty acid beta oxidation in the heart have shown that in most situations of insulin resistance, fatty acid beta oxidation rates are accelerated.

Furthermore, different strategies to inhibit fatty acid beta oxidation in heart and skeletal muscle have been shown to increase insulin sensitivity. So not only is it a scenario where there's underlying pathology driving increased fat metabolism, but the fat metabolism is actually contributing to the insulin resistance to these issues in the heart as well. Now, one thing Dr. Westman mentioned,  I believe he mentioned in the debate was that ketones are beneficial in heart failure. And there's some truth to this or a couple of reasons that is very related to what we're talking about here. So for one, when there is an underlying metabolic problem, we see glucose oxidation is impaired. so providing ketones is the next best option after fixing the glucose metabolism. If you aren't going to fix the glucose metabolism issue, then providing ketones is better than forcing the tissue to have increased reliance on fat for fuel, which is obviously actually contributing to the pathology. So yes, lowering the fatty acid metabolism, whether it's via ketones or increasing glucose metabolism, you both of those are going to be beneficial orders by blocking the fatty acid metabolism directly. That doesn't actually suggest anything different about the state that directly fits in here with what we know about insulin resistance and heart failure and, the rest here. So, ⁓ yeah, just wanted to go through some of those studies and clarify the, confusion in terms of fuel needs in these different states and what's actually driving the pathology. And again, definitely corroborating what we talked about last time in terms of the benefits of glucose metabolism over fat metabolism.

All right. So moving on to one of the next points that was brought up very briefly by Dr. Westman during the debate. was just kind of a, maybe a bit of a throw away. don't remember exactly again. I'm just going off of notes since the debate was, you know, a little bit over a week ago, but he had mentioned that babies are born on ketosis. And I think he was essentially saying, again, how can this be a bad state? And, you know, he pointed at that, at the fact that, you know, all sorts of animals go into ketosis when they're starving, when they're not eating, fasting, whatever you want to call it. So how can it be a bad state? We obviously talked a lot about that and how just because it's something that we do naturally doesn't mean it's a good thing, right? When we're exposed to stress, we increase cortisol, but that doesn't mean we want to do everything we can to increase cortisol. Doesn't mean the stress is a good thing. We just have a response to it that allows us to survive and deal with it. But just because we have a response, doesn't mean it's a beneficial response for our health, especially in the long-term. So we talked about that quite a bit, you know, in the last episode.

And in this one, but,  in terms of this comment about babies being born in ketosis, I wanted to touch on that since it's a little bit of a different situation. So it's true that babies are born in mild ketosis and they remain in mild ketosis while they're, you know, very young and, know, in that stage and breastfeeding, but this is a pretty unique state because they're actually in this state of ketosis, even when they're consuming quite a lot of carbohydrate so when you look at the composition of breast milk, around 40 % of the calories are coming directly from sugar. And normally that would be a state that would very much prevent ketosis. But in this case, we actually see that babies are in ketosis despite consuming 40 % of their calories from sugar. So this is obviously a different physiological state from an adult getting into a low carb diet or an adult consuming 40 % of their calories from sugar. This is very different physiologically and to suggest that because this happens in babies, it would be healthy in adults, I think  there's a lot of leaps in terms of that, that kind of a conclusion, but it's also worth noting that there are very different mechanisms that play when it comes to babies and ketosis, and they're not producing ketones for the same reasons that we do necessarily. And they have other reasons that actually drive them to be more likely to be in ketosis. And part of this comes down to the utilization of ketones for structural purposes in the brain.

It's true that babies are producing moderate amounts of ketones, even though they're still utilizing glucose as a fuel to a large extent. And they're not relying on excessive amounts of fatty acid oxidation. Like we were talking about being a concern on a low carb ketogenic diet. So it's a very different state. But in this case, the ketones are used a bit for a fuel, although the brain is actually still preferring to use glucose over the ketones for babies. You know, it's still, there's still a preference toward utilizing glucose in that state. Again, something that's a little bit different, but the reason for that is because the ketones are largely used for structural purposes in the brain. The brain doesn't really take up fatty acids very well, which also goes hand in hand with its inability to utilize fatty acids. And so the increased ketones act as lipid precursors for the brain, which the brain is made up of lipids. So the provision of the ketones in the state is actually for more structural purposes in the brain. They are used a bit for fuel, but the glucose is used preferentially over the ketones.

So it's really a pretty unique state, obviously something that wouldn't really apply to adults. And obviously if we were to, this is why if we were to eat a 40 % sugar diet, we don't go into ketosis. But so to suggest that because this is happening in babies, a low carb ketogenic diet is healthy for adults. think, you know, there's, there's so many leaps. That's quite a stretch there. And, and, you know, not saying that any production or exposure to ketones is a bad thing. Obviously there are physiological exceptions and I don't think it's bad that babies are producing ketones, but again, this is a totally different scenario from an adult eating a low carb ketogenic diet. Another very common criticism hurled when it comes to high carb diets. And Dr. Westman mentioned this on the debate. He said that, you know, we see an increase in glycation when there's higher blood sugar levels. And this is something that, you know, a lot of people discuss in the low carb space, you know, this concern regarding glycation and carbohydrates.

I'm going to be doing an episode digging into this in quite a bit more detail. So I'm to keep it a little bit more brief now and just touch on a couple of notable points in terms of the differences between low carbon, high carb diets and glycation. And the first is that there's a little bit of a straw man here because I'm not suggesting that it's a good thing to have chronically high blood trigger levels. obviously chronically high blood trigger levels go hand in hand with insulin resistance and metabolic syndrome. And obviously that's going to be correlated with intracellular glycation, oxidative stress, tons of negative effects, tons of inflammatory effects. We know that to be the case. I'm not suggesting that that's a healthy state. And so to say that we see high blood sugar in that situation and increased glycation, you know, I would agree, but that doesn't mean that a high carb diet is actually driving that. So we're going to come back to that in second. It also doesn't mean that a low carb diet can also cause increases in blood sugar.

But just to be clear, I'm not suggesting that we want to be insulin resistant. I'm not suggesting that we should be eating a diet that encourages that. And a high carb diet does not encourage that. And we'll talk through examples of that ⁓ here in a little bit. And that brings us to this idea of glucose and insulin levels increasing after eating on high carb diets versus on low carb diets, because the kind of assumption built in here, and I've heard this stated in many cases that because you have an increase in glucose and an increase in insulin after eating on a high carb diet,
that's basically going to contribute to insulin resistance over time. And that's going to cause the state. And we'll talk about the fact that that doesn't happen, but it's also worth noting that there are considerable increases in insulin and glucose on low-carb diets as well, especially because of the protein that's consumed. And we looked through a couple of studies talking about this. I the first one is just ⁓ looking at the insulinogenic effects of foods. And so this is a study titled an insulin index of foods, the insulin demand generated by thousand kilojoule portions of common foods.

And it's an interesting study to look at because I think a lot of people would be surprised by what they see here. And the reality is that protein is something that largely stimulates insulin release. And what they found is that if you look at isocaloric amounts of fish and beef, it actually increased insulin more than really high carbohydrate foods like oats and pasta. There was a greater insulin release from the fish and beef. And you actually saw that when you compared it to high sugar foods like apples, again, isocalorically, fish and beef caused a greater insulin release or about the same insulin release actually as apples or chips as well. Chips was another one that they looked at and that was about the same as fish and beef. So this idea that you're only getting insulin excursions on a high carb diet is very much not the case considering that protein is a major stimulant of insulin production. And the same can be true on the glucose side as well. You can also see increases in glucose levels on ketogenic diets, even eating low carb meals.

And they show that here in this study, and this was a study that we looked at in the last episode as well. This one is titled glucose and libid homeostasis and inflammation in humans following an isochloric ketogenic diet. It was a metabolic ward study on men without diabetes. did four weeks on a normal diet, which wasn't a low fat diet. It was 50 % carbs, 35 % fat. Sometimes they do far lower fat, which actually further increases insulin sensitivity. And you could even say that that's a bit of a confounding variable, but in this case it was 35 % fat versus a keto diet which was 5 % carbs and 80 % fat. And we showed very clearly, we saw that there was, you know, that the people on the ketogenic diet were in ketosis. They had the increased ketone levels, increased free fatty acids, increased glucagon, and they looked at the effects of eating a low carb meal on glucose levels. And we see that here in figure one, if we look on the left, this was a graph that we looked at earlier, ⁓ showing that on the carbohydrate containing meal.

There was actually a significantly worse insulin sensitivity and we saw increased glucose levels after that carbohydrate containing meal. But when we look at the right here, this is looking at the people who are on the high carb diet, eating a ketogenic meal and the people on a ketogenic diet eating a ketogenic meal. What they actually found was that the glucose area under the curve for the ketogenic diet participants eating the ketogenic meal was actually a little bit higher, not statistically significant, but it was actually a little bit higher than the people on the carbohydrate containing diet eating the carbohydrate containing meal. So what we're looking at here is on the left, have the lower curve, the ones with the filled end squares versus on the right, you have the ones with the circles, the hollow circles. And what they actually found was that the glucose area under the curve was higher on the right for the ketogenic diet people eating the ketogenic meal versus the higher curve diet people eating the higher carb meal. So this idea that you're going to be dramatically increasing glucose all the time on your
 high carb diet, you know, based on eating something with carbs is not actually supported here. In this case, they're finding that eating the ketogenic diet meal led to the same amount of glucose increase as the high carb meal for the people on the high carb diet. So this idea that you're either getting a lot of insulin and glucose excursions after eating versus no insulin and glucose excursions after eating is really not at all accurate as to what's happening. So that's the first thing that's worth noting is that if any insulin and glucose excursions insulin resistance, you would see that on low carb diets as well. But then the other thing that's worth touching on here is briefly touching on the evidence that high carb diets don't cause chronically high blood sugar. They don't cause chronically high insulin levels and instead can and should, you know, have done in a healthy way. They should lead to healthy and even very low levels of fasting insulin and low levels of glucose, low A1Cs and good insulin sensitivity.

And we can see this when we look at native cultures on high carb diets and I'll link to these studies in the show notes so we, you know, don't weigh the episode down with too much of those. We can look at the Katawans who have a diet that's 69 % carbs and 21 % fat. They have very low fasting insulin levels. the average for men was four and for women it was 4.8. We can look at this in the Tuki Senta. This is a group that eats over 90 % of their calories from carbohydrates and they're incredibly insulin sensitive. They have very, very high glucose tolerance, no signs of metabolic syndrome.

And there are other native cultures as well. I'll link to those in the show notes, but these are people who are eating high carb diets for their whole lives. And they're not showing problems in terms of metabolic health or insulin sensitivity or insulin resistance. And we can also see this looking in, you know, studies where they put people on high carb diets, people who don't have insulin resistance and see improvements in insulin sensitivity and weight loss, but then also in people who do have insulin resistance and type two diabetes and see incredible improvements in terms of insulin resistance and weight loss, know, type two diabetes. And again, this flies directly in the face of this idea that consuming more carbs is just going to lead to insulin resistance when the reality is it can reverse it. And so we'll start just touching briefly on the Kempner diet as an example. This is a very high carb diet, as much as 565 grams of carbohydrates a day, very low protein and very low fat. And they use this diet for people who were obese, for people with type two diabetes.

They found that it decreased blood sugar levels, decreased insulin levels. People were able to lower their insulin dosing. ⁓ in some of the studies and one that we'll share here in a minute, 25 % of people who are on this study were able to fully stop their insulin medication. And this was in a study titled effect of rice diet and diabetes mellitus associated with vascular disease. Now in this study,  I'll just kind of touch a cup, touch on a couple of the improvements that we're seeing. We won't go through it in detail.

But they found that there's an average drop in fasting blood sugar by 47 milligrams per deciliter. The average decrease in weight was 7.3 kilograms or 16 pounds. 58 % of the people in the study were able to decrease their insulin and 25 % were able to stop their insulin entirely. Again, this is people with type two diabetes. And they found that these improvements incurred both in patients who lost weight and in those who did not have a significant weight change. So it wasn't just driven by the weight loss. was other, you know, there's direct metabolic effects of this diet that led to massive improvements in insulin sensitivity. So it was the Kempner diet. Another notable one was the Predican diet. And this was a pretty similar diet involved a low fat, high carb, high fiber and low salt diet. The Kempner diet was actually very low in fiber. But in this diet, they were getting less than 10 % of calories from fat, around 15 % from protein and the rest from carbs. So we're talking about a very high carbohydrate diet here. They also made sure to incorporate walking as a part of the protocol.

And they found that people lost weight. were able to get off of their hypoglycemic drugs. They were able to stop insulin. And these effects happened rapidly within just a few weeks, you know, three to four weeks, large portions of people were able to get off of these drugs and lose weight. And then they did studies where they followed these people. You know, they did follow-up studies for a couple of years after and show that the benefits continued as long as they continued with the diet. So I'll link to these studies in the show notes, but again, some very clear high carb diets showing incredible benefits for insulin resistance as opposed to the opposite of this idea that they're causing insulin resistance. Now there's also a number of very well controlled studies showing the same benefits for high carb diets on insulin sensitivity and reversing insulin resistance. So we'll touch on a couple of these. The first one is titled high carbohydrate, high fiber diets for insulin treated men with diabetes mellitus. And in this study, they did two different diets. One was 43 % carbs, 37 % fat and 20 % protein. And then they compared that with 70 % carbs, 9 % fat.

21 % protein. So there's a big change, you know, going to a much higher carbohydrate intake and much lower fat intake. made sure that there was no weight loss in the study. So they made sure that, you if someone was losing weight, they gave them more food so they didn't lose weight. And despite that, they still saw improvements in insulin resistance. People were still able to reduce their doses of insulin. They're still able to see lower blood sugar values. They were still able to stop their insulin medications altogether. So still massive improvements, totally independent of any changes in weight, as was suggested by the Kempner studies.

We have this study here. I'm going to actually share this quote. This is one titled changes in body weight, body composition and energy intake in women fed high and low fat diets. So they had women go from a higher fat diet of 37 % to a lower fat diet of 20%. Obviously high fat diet here is relative. We're not talking about a low carb ketogenic diet, but I'm just using this not to discuss that part as much as just the idea that you can see major improvements in metabolic health on a higher carb diet. And this is not something that's driving insulin resistance.

And what they found in this study was that the women lost weight while increasing their calorie intake by nearly 20 % relative to when they were on the high fat diet. And they state the effects of a 20 % fat diet, low fat diet on total body weight, lean body weight and adiposity were studied in 18 premenopausal women with body mass index BMI of 18 to 44 subjects were fed a 37 % high fat control diet for four weeks, followed by the low fat diet for 20 weeks, total body weight, lean body weight and fat weight were measured.

at the end of the high fat and low fat dietary periods by hydrostatic weighing. Despite adjustments in energy intake to maintain weight throughout the study, subjects exhibited a 2.8 % decrease in total body weight, an 11.3 % decrease in fat weight, and a 2.2 % increase in lean body weight by the end of the low fat period. Similar changes were observed in obese and non-obese women. By the end of the low fat period, energy intake had increased significantly in comparison with the high fat diet to 119 % of the high fat intake.

Results cannot be explained by changes in daily activity levels and suggest that macronutrient composition plays a role in energy requirements for weight maintenance. So what we saw here is a high carb diet. The women lost body fat, gains lean mass in the process, despite eating 20 % more or 19 % more than when they were on the higher fat diet. Moving on to a couple others, this is a study titled effect of high glucose and high sucrose diets on glucose tolerance of normal men. So in this diet or in this study, well, I'll read the quote and then we'll get to it. I'll explain it after. They state.

As the dietary glucose content was increased progressively to 40, 60, and 80 % of calories, gradual improvement in glucose tolerance tests occurred when normal subjects were changed from a controlled diet to one containing 80 % of calories as sucrose, significant improvement in the oral glucose tolerance test occurred. These improvements in glucose tolerance tests 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 led to improvement of the glucose tolerance in normal subjects.

So I'm not suggesting that we should be getting 80 % of our calories from table sugar. Obviously that shouldn't have to be said, but obviously I'll throw that disclaimer out there. ⁓ but we're seeing here is that as the calories increase from carbohydrates, we didn't see worse insulin sensitivity and increase in insulin resistance. didn't see, you know, body fat gain or anything like that. What we saw was that increasing the calories up to as much as 80 % from glucose or sucrose led to an improvement in insulin sensitivity. This was over 10 weeks.

And then last study here improved glucose tolerance with high carbohydrate feeding in mild diabetes. And they found something similar again, this was in people with mild diabetes though, not, you know, in the last one, was men without diabetes and what they state was to evaluate the effect of increased dietary carbohydrate and diabetes mellitus glucose and immunoreactive insulin levels were measured in normal persons and subjects with mild diabetes maintained on basal 45 % carbs and high carbohydrate 85 % carbohydrate diets.

Fasting plasma glucose levels fell in all subjects and oral glucose tolerance significantly improved after 10 days of high carbohydrate feeding. Fasting insulin levels were also lower on the high carbohydrate diet. However, insulin response to oral glucose did not significantly change. These data suggests that the high carbohydrate diet increases the sensitivity of peripheral tissues to insulin. So this was just 10 days. I think we would have seen even more improvements if it was gone on for longer, like in these other studies. But what we're finding is that the higher carb diets
aren't causing high blood sugar. They're not causing higher insulin. They're not causing insulin resistance. Instead, they're actually causing the opposite. Now, again, I'm not saying that if we just took the average Western diet and said, eat more carbs, drink more soda, that's going to be healthier for you. I'm obviously not saying that. I've made this disclaimer tons of times, but I'm not saying that all carbs are created equal or that the carbohydrates that most people in the Western world are eating are healthy foods. But that doesn't mean it's actually the carbohydrates that are the problem. There's a ton of other issues.

With those foods that are entirely independent of the carbohydrates. What we see here in these studies and looking at the native cultures is that eating a high carb diet is actually supportive of metabolic health and insulin sensitivity. We just want to make sure that we're doing it from the right quote unquote sources of carbohydrates. Again, go ahead and download the energy balanced food guide for free at jfeldenwellness.com slash guide to take a look at what I would consider to be the best sources of carbohydrates. All right. So there's one other point that was brought up by Dr. Westman.

which was this idea that carbohydrates can be addicting. And I know he mentioned it at least once in the debate, at least it was in my notes and I'm pretty sure I've heard him describe it elsewhere. And I've heard tons of other people in the low carb dieting sphere basically resort to this argument, which is that basically if we, if we go through all the metabolic effects, we go through the physiology and we find that there's no, you know, we come to this conclusion that low carb ketogenic diets are not actually better for metabolic health or insulin resistance or anything like that.

Then we come to this criticism that people are going to eat more on a high carb diet because carbohydrates are addicting. And the first thing that's worth noting here is that this is a very different argument from the argument that high carb diets inherently cause insulin resistance, low carb diets inherently reverse insulin resistance. It's not due to calorie intake. It's not due to, ⁓ you know, weight changes or something. It's because the carbs themselves are the problem. So we're talking about a very different argument here. We're just saying that basically you're going to eat more on a high carb diet, eating more is the problem. You're going to eat less on a low carb diet.

And that's actually why the low carb diets are beneficial. So it's a very different argument that's being made here. So I just want to make that clear. But then I also want to look at the research that looks at what happens when people have more carbohydrates and whether it's actually a situation that causes overeating. What we actually find is that if you restrict carbohydrates a lot, it will lower appetite. But also if you restrict fat a lot, it'll lower appetite. It'll lead to people eating less. And this has more to do with the fact that we're cutting out tons of problematic foods that happen to have high amounts of carbs and fats. Most of the things that in the low carb sphere, people think about as carbohydrates, like donuts and pizza, you know, are actually very much high fat foods as well. And so if you're eating a low fat diet, you cut those out. If you're eating a low carb diet, you cut those out. So we're cutting out a lot of the foods that are inherently not ideal in the Western diet when we're cutting out carbs or we're cutting out fat and the restriction or any restrictive diet, really, you could talk about a vegan diet or a carnivore diet.

Both tend to lead to eating less because of the restrictive aspect of it. And so we see that here with a number of studies looking at high carb, low fat diets. This is a study titled body weight and low density, lipoprotein cholesterol changes after consumption of a low fat ad libitum diet. And they had people on a 35 % fat diet versus a 15 % fat diet. They were allowed to eat ad libitum and on a low fat diet, they ate less and they lost weight. Naturally they were allowed to eat as much as they wanted. And you know, as long as they kept the fat at 15%, I think the meals were actually provided in this study at 15 % fat and they naturally just ate less and lost weight. This next study, and I'm going to go through these quickly because there's not too much in terms of specifics that, uh, or that, you know, are worth sharing, but I will of course, link to these in the show notes. Uh, this next study is titled weight loss on a low fat diet consequence of the imprecision of the control of food intake in humans. They looked at, um, people on a higher fat diet, or they put them on a high fat diet of 35 to 40% for seven weeks. And then they went on a low fat diet of 20 to 25 % of total calories from fat for seven weeks. They're allowed to eat as much as they wanted and they naturally ate less on that lower fat diet. And that led to weight loss. Next study is a study titled an ad libitum, very low fat diet results in weight loss and changes in nutrient intakes in post-menopausal women. They basically put these women on an 11 % fat diet from a 33 % fat diet, found that it led to weight loss as well. And again, this was an ad libitum. 

All of these are ad libitum studies where they were allowed to eat as much as they wanted. And as they increase the carbs and decrease the fat, they naturally ate less. And we see that in this last study as well. We're going to share a quote from this one too. This is a study titled weight loss during 12 weeks ad libitum carbohydrate rich diet and overweight and normal weight subjects at a Danish work site. And this was a pretty mild fat decrease. So in some of these other studies, you know, we're getting down to 11 % of calories from fat, 15 % of calories from fat. One of the ones that I mentioned was 20 to 25 % calories from fat. not that restrictive on that side. And in this study, they actually just decreased from 39 % fat to 28 % fat and increased carbs from 46 % to 56%. So just a small decrease, know, only 11 % decrease in fat intake. And the fat intake was still not that low at 28%. And what they state was in conclusion, instructions at a work site and ad libitum intake of a carbohydrate rich low fat diet resulted in a significant loss of body weight.

And fat mass and overweight and normal weight subjects. So again, this was just telling people eat lower fat, basically eat a lower fat diet and eat as much as you would normally eat, ad libitum. And they weren't giving them a control diet or anything like that. And they found that they naturally eat less and lost weight. This idea that carbs are so addictive and that, you know, for eating more carbs in our diet, we're naturally going to eat more is very much not the case. I do think for people who are on a carb restricted diet, if you're on a low carb diet, you're going to, in most cases have massive cravings for carbohydrates. And if you do eat a little bit of carbohydrates, you're going to want to eat a ton. It's not because you're addicted to carbohydrates. It's because we have a physiological need for carbohydrates and a physiological desire for carbohydrates. And so if you've been deprived of them and then you eat some, yes, you're going to have a strong urge to eat more. And what we find is when people are not restricting those carbs, cause the only thing that can happen in a and maybe this happened in that, you know, Isabella Cooper study said, if you're heavily restricting carbs and then you eat some, and if you hadn't had them in a very long time, the likelihood of overeating is, is massive. This isn't an addiction because it, well, for a number of reasons. One, we look at these diets and see that it's not something where just eating more and more actually kind of encourages more overeating. It's actually the opposite when you're getting enough, you actually end up potentially eating less. And that's something that's extremely common. People go through these refeeding periods after coming off of low carb diets because they've been restricted from carbohydrates for so long. And during that time, there's a major propensity to quote unquote overeat, but then it normalizes and those cravings go away and you're not constantly feeling like you want to eat sugary or high carb foods. And I've worked with tons of people who thought that they had a sugar addiction. They thought that they had a carbohydrate addiction and you know, they would be on a low carb diet, but then they would go through binges and you know, they would go and grab the ice cream container from the freezer. They would have a bite.

And then before they knew it, the entire container was gone and, or, know, they were at a birthday party and had, you know, they say, okay, the cake is there and I just can't resist it. And they have a bite and then they eat the whole thing and they have two more pieces afterward, or tons of these other scenarios. And they, you know, just resort to saying, I just can't be around it. I have to get it out of my house. I can't control myself. I have a carb addiction, a sugar addiction. But the reality is, and these people who I've worked with, where they think this is the case.

When we get them actually eating a diet that's supplying all of their needs and they're eating a good amount of carbohydrates, they find that this isn't the case anymore. They go and grab the ice cream and they take a bite and they eat a few more bites and they eat a normal portion and they put the rest back. Or they go and get the slice of cake at the birthday party and they eat a few bites and they don't even finish it. You know, they realize that that was all that they wanted. Or on the flip side, they eat a good, well-balanced diet or a good, well-balanced meal and they aren't feeling like they're still craving sugar after or anything after because they're actually fulfilling those needs.

So I think that this resort to this idea of carbohydrates, you know, are just inherently addictive is not at all well supported. And I think it's also a huge derivation from what most people are saying on a low carb diet, which is that there's an inherent metabolic benefit on a low carb diet. But also I just think it's very far from the reality. All right. So that's everything I had as far as my notes from the debate, things that were brought up that I felt like were important to address.

If you have any other questions or if there are any other points that I didn't discuss from the debate that you'd like to hear me dig into in more detail, definitely let me know in the comments. And if you did enjoy these episodes, please leave a like or comment wherever you're watching or listening. And also please leave a review and five star reading. All of those things do a lot to help support the podcast and are very much appreciated. As always, to take a look at the show notes where I'll link to the studies and articles and everything else that I've mentioned throughout today's episode, head over to jfeldmanwellness.com/podcast.

And if you're looking to optimally support your metabolism, lose weight, improve your digestion, get amazing sleep, rebalance your hormones, boost your energy levels, resolve various other health issues, recover from a low carb diet, whatever it is. And you'd like to do that with clear action steps and strategies alongside personalized guidance from me, then head over to JayFeldmanWalnes.com/solution, where you can find all of the information for the energy balance solution program. This program includes customized health coaching and includes a video library with videos on how to properly regulate blood sugar, how to restore your gut health, how to lose weight without destroying your metabolism, how to boost your metabolism, how to get amazing sleep, how to rebalance your hormones and tons more. It also includes resources like sample meal plans that are individualized based on your needs. It also includes recipes, a calorie and macro calculator, a supplement guide and tons more as well as a private community. So head over to JFaldenWallness.com/ solution to check out all the details. And with that, I'll see you in the next episode.