Dr Bikman: #1 INSULIN Trick Proven To Burn Fat Faster [EAT THIS]

If you just remove this one single variable, namely insulin, then it becomes completely and totally impossible for a human to hold on to any amount of body fat. So rule number 1, control carbs.

Dr. Benjamin Bikman is a leading metabolic scientist.

Today he's exposing why calorie counting backfires and the switch that forces your body to burn fat. If insulin's elevated, the body is sugar burning. If insulin's down, the body is fat burning. So if your weight loss strategy is based on hunger, which which the low-calorie approach is, you're going to lose. It doesn't work. And we found that in humans that had elevated ketones and lower insulin, their fat tissue metabolic rate was 3 times higher.

How about apple cider vinegar? Does that help lower insulin?

Yeah, it does. You can take 1 or 2 tablespoons and significantly reduce the insulin and glucose response due to changes in digestion.

But if somebody does these steps, how quickly can they see a lowered insulin?

Within just days to weeks.

Counting calories is quite possibly the most effective way to ensure that you stay fat forever. As a health researcher, I've spent years digging through all the noise of the weight loss industry, and that search led me to one person, Dr. Ben Bikman. Now, he's a world-renowned metabolic scientist whose work inside the lab focuses on the literal life cycle of the fat cell, uncovering the molecular on switch for fat burning that most doctors are completely missing. Today you're about to learn the insulin trick to flip your body into a permanent fat burning state, why your fat cells actually become insulin resistant before the rest of your body. But here's the weird part: why butter might actually be the key to fixing your metabolism while diet soda might be stalling it. And if you finally want to take control of your health when doctors can't, a very easy step is to hit the subscribe button because you're not going to want to miss out on my deep dive with Dr. Jamnadas all about fasting next week. So, Dr. Bikman, my first question: you are a metabolic scientist, so you've helped so many people lose weight. If somebody's coming to this, they really want to lose weight, especially belly fat, they have diabetes, maybe they have high insulin— why do you think that person should first focus on their insulin?

Yeah, I would say two reasons. One, because of insulin's relevance to the topic in the matters that you just mentioned, as well as the fact that it's so often not going to be acknowledged. So that's a particular irony here where insulin is arguably the most important part of the discussion, and yet it's completely overlooked in most conventional conversations. Just to, at the risk of getting too deep too quickly, when it comes to understanding fat cell dynamics, or to say that another way, to understand how a person can make their fat cells shrink. You really, as much as we have had a caloric-centric paradigm, that is incomplete. That's not to say that calories don't matter, that they don't have some value. They do. But in the absence of an insulin signal or in the absence of insulin telling the fat cell what it ought to do with those calories, then the fat cell will not store it. And just to really put a fine point on that, we need look no further than a person with type 1 diabetes. That in a person, this is one of the reasons I am so adamant about insulin's relevance when it comes to understanding body fat control, that this is a person who has perfect control over how much insulin is in their blood. And if they are deliberately or accidentally underdosing insulin, or heaven forbid, they stop injecting the insulin entirely, they could eat an unlimited amount of calories, 10,000 calories a day, and it will be impossible for them to get fat. So as much as the conversations with body fat regulation have focused on myriad variables, calories and different types of fats and oils, Um, we have con— a confirmation that if you just remove this one single variable, namely insulin, then it becomes completely and totally impossible for a human to hold on to any amount of body fat.

I wanted to ask you a question because many people, they understand now that we have to focus on the hormone insulin and not just the calories. So that's a very important distinction. I want to ask you, as a metabolic scientist, if somebody knows that they have high insulin for a long time, how does that go into a state of insulin resistance?

Right, I love that question because you are touching on the two parts of insulin resistance. The first part, when people hear the words insulin resistance, there isn't— the one thought comes to mind, which is that the hormone insulin isn't working as well as it should. That's the insulin resistance part of it. But every time you invoke the term insulin resistance, you must also appreciate that blood insulin levels will be higher. And so that comes to your, to the heart of your question. I, I maintain that elevated insulin is the primary driver of insulin resistance, that the average individual who's struggling with insulin resistance and all of its consequences, which are myriad and terrible, then, then elevated insulin is the primary driver of all of that process. However, it's not the only driver where there are two other, what I call, or we could consider cardinal causes of insulin resistance, namely stress and inflammation. They each can cause insulin resistance very rapidly through, through their own pathway, their own mechanism that is independent of too much insulin. But Even in those two distinct causes, if they cause insulin resistance, now the elevated insulin is going to be a consequence of the insulin resistance. So we still end up with this two-part pathology where insulin isn't working very well and insulin levels are higher. Whether the insulin is the cause or whether the insulin is the consequence, it doesn't matter. You will always see these two things come together. There is that, that's very important to understand just by, for the sake of being thorough. But beyond that, it helps us appreciate when the word insulin resistance is being invoked properly or not, where people will like to describe a state of physiological insulin resistance when describing adaptation to a low-carb or ketogenic diet. All right. Does it meet any of those definitions? And in fact, it doesn't meet either of them, to be frank, but that's a topic that goes beyond the question you just asked me. But what, but there is instances of physiological insulin resistance and it has nothing to do with diet because it doesn't, in which is pregnancy and puberty. That is when the insulin resistance is serving. A beneficial physiological purpose. And in that case, it's to help the body grow, whether it's mom's body or baby's body or the teenager who's explosively growing. The insulin resistance is serving a good purpose and insulin is elevated. So anytime a person wants to invoke the word insulin resistance, the words, they should, they would be well served to ask themselves, is insulin higher? If it's not, then it is not insulin resistance.

Wow. Okay. I just thought I'd ask that question because we hear so many different terms on the internet, and to understand the difference between insulin resistance, which Dr. Ken Berry says there's no such thing as insulin resistance, it's hyperinsulinemia, high insulin, which you just mentioned. Is that correct?

Yeah. I mean, I, with nothing but love and affection for Dr. Ken Berry, whom I really do love and respect, there, there is, I think I appreciate what he is saying there, but just to really clarify, there absolutely is a phenomenon of insulin resistance where if you were to take two people, one person who's insulin sensitive, one person who's insulin resistant, and give them an injection of insulin and then measure what happens to their blood glucose, just as an obvious outcome, you would see a difference that the person who's insulin sensitive, in response to that insulin bolus would have a significant reduction in blood glucose levels, whereas the other individual might have a very modest reduction. So insulin resistance is a real phenomenon, but I appreciate what Dr. Berry's saying, which is that it's hard teasing them apart. That, which I very much appreciate, that these are two things that are always going to go together. Again, whether the elevated insulin is the cause or the consequence. They're always going to come together.

Okay, got it. So somebody needs to really focus on their insulin if they want to fix a chronic disease or they want to lose fat, visceral fat, and fat that we don't want in our liver, etc. So a lot of people are going to say, but Dr. Ben Bikman, my blood glucose is excellent, I'm in really good metabolic health. Why do you think the current paradigm of a glucose-centric model is a problem?

Right. Yeah, thanks. I love that question because it allows us to better understand the problem that we do have a glucose-centric view of metabolic health, that you'll have a clinician who is just doggedly determined to not only measure the glucose but lower it at all costs, which comes with serious consequences. And I'll hopefully get around to articulating that in just a second. But when we talk about insulin resistance, we need to have an insulin-centric paradigm. And that's really the heart of the answer to your question, that the problem with our glucose-centric view is that we don't detect insulin resistance as accurately or as promptly as we could. Where you have a common scenario is that a person is struggling with insulin resistance over the years. And so here's their insulin levels and here's their glucose levels, and the insulin levels are getting higher and higher and higher, but it's working well enough, especially at the muscle and the liver. To keep the glucose in check. But when those tissues, most especially the muscle and the liver, when they start to become insulin resistant, now you have the blood glucose start to climb. And this is an event that can happen years, even decades after the body has been struggling with the elevated insulin and the insulin resistance. And this state that we can just call insulin resistance is what's driving chronic disease in, in many instances, not all instances, but high blood pressure that's heavily driven by insulin resistance, infertility, cognitive decline, fatty liver disease, and so many other problems. These are driven by the insulin resistance. Those are not driven by hyperglycemia. And so by waiting until the point that the glucose starts to climb, we have Lost years of, of the person not only experiencing the misery of the insulin resistance and its consequences, but lost, lost time where we could have intervened and stopped the process much sooner. But then one final concern with our glucose-centric view is that the clinician has not only detected the problem too late or later than they could have when it was just elevated insulin. Now it's elevated insulin and elevated glucose. Our glucose-centric paradigm will tell the clinician. We just need to lower that glucose at all costs. And they may be tempted, and indeed it's often done, where they just give the patient an intervention to increase their insulin even more. That will lower glucose, and thus with the glucocentric paradigm in mind, it's considered a success. And yet, tragically, an objective review of the evidence finds that the more aggressively you're giving— you're increasing insulin, order to correct the glucose, the more you're making the patient fatter. They gain weight very, very quickly and you're killing them faster. Their risk of dying from cancer effectively doubles. Their risk of developing Alzheimer's disease doubles. Their risk of dying from heart disease triples. So by increasing the insulin in order to push down the glucose, again, the tragedy is we make the patient die faster. If too much insulin is the primary driver of insulin resistance, how can we expect to actually improve the problem when we're giving them more of the very thing that caused it in the first place?

You mentioned that most doctors are focused on lowering the glucose, which is therefore increasing the insulin very slowly, very steadily. What are doctors or experts recommending to push down the glucose?

Anytime a type 2 diabetic is given insulin therapy, it's, that's terrible because they already have a lot of insulin. The nature of type 2 diabetes is insulin resistance. So they have high insulin and you're pushing it even higher. And there's an entire class of drugs that are often prescribed to people with type 2 diabetes in the family called sulfonylureas. Those are what's called insulin secretagogues. They push the, the beta cells of the pancreas to make more insulin, all with the intention of lowering the glucose. But then there are also other interventions that just want to lower the glucose, like drugs that will force the glucose out through the kidneys into the urine. Those actually can help some health outcomes because if you're forcing out glucose, then you're gonna lower the insulin. So in that regard, it can actually help. With the insulin levels and the insulin resistance. But then there are other consequences like the person needing to urinate all the time. And by dumping a lot of glucose into the urinary tract, you are basically, you're feeding a lot of bacteria. So the person is much more likely to have very frequent and severe urinary tract infections. It's like you're giving, it's like as the bacteria are trying to run a marathon up into your bladder, You're basically giving them Gatorade or some sports drink on the way up. You're helping them run the race better. So no surprise that those complications are more common.

Yikes. I think people are thinking right now, what? My doctor is prescribing me insulin medication. I am type 2 diabetic and I should not be doing that. Let's try to understand the root cause of the problem when it comes to lifestyle and the things that we're doing to ruin our insulin levels and our health. The role of carbohydrates. Now, you co-authored a study in 2022 It was discussing the role of carbohydrates in adipose tissue mitochondrial respiration. Dr. Bikman, that's a mouthful. So my question for you is, how does too many carbohydrates affect the ability for a person to burn body fat?

I love it. Yeah, so you're referring to a study that I published with Dr. David Ludwig at Harvard. We had published— that study came from a paper we had published about a year prior, which was looking at the differential effects of insulin and ketones on fat tissue metabolism. So just to set the stage a little bit more, I've already alluded to the fact that in type 1 diabetes, if a person's not treated with insulin, they have no insulin in their body. That's the nature of type 1 diabetes, and they cannot get fat. At the same time, over 100 years ago, two legendary scientists published work finding that in people with uncontrolled diabetes, and that's type 1, their metabolic rate was way higher than it should have been. When I learned of that study, I was fascinated, um, to try to understand the mechanism. Um, so why is it that in, when in a person with type 1 diabetes, when they're not on insulin, their metabolic rate is really, really high. When you start treating with insulin in minutes, this, you can detect a steady minute-by-minute reduction in metabolic rate. It's— that to me was fascinating. And so my lab had published a paper which I'm extremely proud of, and I'm not proud of much of my work. I think it's all just perfectly fine. It's very conventional and average and just me playing the game. But this one I'm very proud of because we, we looked at 3, all 3 commonly used biomedical models. We were growing fat cells in a little petri dish. We were using animals and getting out the fat from animals. And then we conducted fat biopsies from belly fat in humans. And in all three models, we found that if ketones were elevated, the metabolic rate was accelerated in fat tissue. And fat tissue has a metabolic rate. And that comes back to the study you'd mentioned where, where you'd mentioned in that, in that cumbersome title, the, the mitochondrial respiration, that basically is a fancy way of just saying metabolic rate. And again, fat tissue has a metabolic rate in a, even in a normal weight person, fat tissue accounts for about 8% or so of that total body metabolic rate. So it's a very meaningful contributor. And we found that in humans that had elevated ketones and lower insulin because of their adherence to a low carb or ketogenic diet, their fat tissue metabolic rate was 3 times higher. Than it was in those on a conventional high-carb diet. And that was supported to varying degrees in the animals' data and in the fat cell, cell culture data. So in all three models, we found that if, if insulin was down and ketones were up, then the metabolic rate was much more active in that fat tissue than it was otherwise. And that was the heart of the finding in that particular paper. But it, it does come back to sort of how I started a little bit, but, but reconciling the, the caloric view of obesity and the endocrine view or insulin view of obesity, that where I said that I'm not trying to make the claim that calories don't matter. Of course they do. And we need to account for those carbons. That's, that's actually what, of course, we're consuming. We're not consuming units of heat, which is what a calorie is. If you'll pardon a little tangent here, we're consuming carbons, just like an engine that takes gasoline. Gasoline and can combust those carbons. The gasoline is, is, those are carbon molecules. We have our own version of that fuel in the form of, of, of the carbons that we eat, whether it's from carbohydrates or fats. And then we combust them. We burn them like an engine in our cells. Insulin allows the engine to be revving or burning through fuel just for the sake of, well, insulin and ketones. The difference is how we reconcile it is that insulin basically makes the engine more frugal. It won't waste any energy. That whole body metabolic rate will go down when insulin is up with the intention for the sake of storing more of that energy in the fat cell. In contrast, when insulin's down and when ketones are up, now the body is more frivolous. It's just wasting energy. It's burning energy, including from our very fat cells, just to create more heat and waste energy as heat. Rather than storing it. So insulin— the insulin theory of obesity and the caloric theory are not at odds with each other, that, that you actually do need to consider both in order to truly understand the dynamics of, of why fat cells may be getting bigger or smaller.

Okay, got it. So basically, we should not be eating too many carbohydrates, and we should do anything that we can to boost our ketones. So if somebody's watching this and they're eating bread, pasta, rice every day, Dr. Ben Bikman, and they're like, why can I not lose fat? Could that be the reason why?

Oh yes, most certainly. Yeah. If a person is, even if they are starting to restrict their calories, one of the reasons I don't love just a purely caloric approach to obesity is that if a person is overweight, they, and obese, they have higher insulin. That's what's facilitated the body storing those calories in their fat cells. If they simply restrict calories, without addressing their elevated insulin, that, that Dr. David Ludwig, my colleague in that paper you mentioned, he has found that that's a scenario which lowers the total energy availability in the blood. That mat— in other words, the, the, the kind of cumulative amount of energy that can— the calories in the blood, the brain is constantly sensing the energy that's available because it can't store a lot of energy like our fat cells can, or even our muscle or our liver. The, those are tissues that can store a lot of energy as glycogen and fat. The brain doesn't have that storage capacity, so it must primarily rely and constantly rely on the energy that's available in the blood. So if you start to cut calories, but your insulin is high, that ends up lowering the total amount of energy that's available in the blood. The brain senses that energy reduction and starts to panic, if you will, and send this hunger signal. So if we just start by, like the person you mentioned, they may be cutting out fatty foods in an effort to reduce calories and in the process are focusing more on carbohydrates, which per gram will have fewer calories than fat will. But unfortunately, they're also now increasing their insulin. They are putting themselves into an energetic oddity where the calories coming in are maybe dropping, but by increasing insulin, you're forcing those calories to be stored in the fat cells. The brain is relatively getting less. And so any victory they have with fat loss is going to be very short-lived. They'll lose a little bit of pounds over that 1 or 2 weeks where they are white-knuckling and gritting their teeth to get through that hunger. And then hunger always wins. So if your weight loss strategy is based on hunger, which the low-calorie approach is, you're going to lose. It doesn't work. We've been giving that advice for well over 60 years, 70 years now, I think. And, and if it worked, we would not have the obesity crisis that we do. And so as much as I want to embrace the idea that calories do matter, don't focus on them first. The person who wants to lose weight would be better served by having their first step be I'm going to lower my insulin, I'm going to control my carbohydrates, and then I'm going to be more liberal with the other macronutrients, fats and proteins, because they won't increase my insulin like the carbohydrates will. And then a person will start to lose weight, and it doesn't have to be based on hunger, so their long-term success is just going to be much more likely.

Now, as we've discussed, most of us need to lower our insulin levels to fix our metabolic health, and this includes reducing the carbohydrates and fasting. But there is also one natural compound that we can add to boost our energy, our focus, and our strength. And even Dr. Boz recommends it as the number one supplement for her patients. And as you know, my father passed away from dementia last year at 71 years young, so anything I can do to protect the brain is deeply important to me. And that supplement is creatine. Now, creatine has long been thought of as just a bodybuilding supplement, But new research from experts like Dr. Darren Kendall suggests that there is powerful benefits for the brain. Now think of creatine as a natural compound in the muscles and brain that helps your cells produce energy fast. It boosts ATP, which is the fundamental fuel that your body runs on. Now, while you can get some creatine from meat, especially if you're on a carnivore diet, usually around 1 to 2 grams per pound, The latest science from Dr. Darren Kendall and Dr. Rhonda Patrick suggests we actually need 10 grams for cognitive protection. Now, the quality of creatine is the most important, and that's why I'm proud to have Create as a sponsor of today's episode. Create uses third-party tested, highest quality Creapure creatine monohydrate from Germany. It's designed in the USA to be easily stacked so that you can hit that 5 10g maintenance dose. Now I take half a sachet of this unflavored powder in room temperature with water with breakfast and the other half with dinner. And over a month, I'll increase this to 2 sachets a day to reach the full 10g. And since I've added this to my routine, that mental fuzziness has lifted. I feel sharper in my conversations and more present. And honestly, I'm seeing my strength numbers go up in the gym That gives me so much more confidence that I'm building a body and a brain that will last. So if you want to try a proven high-quality creatine, just head to trycreate.co/primal and use code PRIMAL to get 20% off your order plus free shipping when you hit the subscribe button. Step 1 is to control your carbohydrates and then look at your other macros, protein and fat. And that goes into the conversation around fat. What are your thoughts around saturated saturated fat and its effect on insulin?

Yeah. Yeah. Thanks for asking that question. It's, it's been interesting for me to see the conversation around saturated fat in part because some of my most cited scientific manuscripts, in fact, probably my single most cited scientific manuscript was one that I published during my postdoctoral fellowship days. And it was looking at the role of saturated fat. As a driver of insulin resistance. And I thought I understood the topic at the time, these, these 17 years or so ago. And in the ensuing time since my postdoc days to now being an old wise professor, I have had time to reflect on what that study found and what it did not find. What it did find is that when you expose cells directly to saturated fat, especially not all saturated fat, mind you, but palmitic acid, palmitate, the most common. But you don't see it with stearic acid, which is a saturated fat, but less common. But with palmitic acid or palmitate, you can treat cells or expose cells to palmitate and they will become insulin resistant within just a few hours. However, the mistake in taking it is when people extrapolate. Then they start to— they look at that finding and then say, thus we should not eat saturated fat. Those are not the same thing. Dr. Jeff Volek, who's at Ohio State University here in the US, he had an extraordinarily fascinating paper that I think is underappreciated in these kinds of conversations. And so I'm going to appreciate it. He found that they could manipulate the dietary carbohydrates and in so doing almost perfectly control the amount of saturated fat in the person's blood. And to, to put, to state that more clearly, they could increase carbohydrates. And they found that as they were through a stepwise fashion, increasing carbohydrates, the actual amount of fat in the blood that was saturated went up, even as the amount of saturated fat in the diet went down. So saturated fat in the diet went down, carbohydrates went up, and saturated fat in the blood went up. So it was tracking with the amount of carbohydrate. In contrast, if carbohydrates were low, even though the group was eating 2 or 3, I think it was 3 times more saturated fat, they actually had less saturated fat in their blood. That matters so much because it's, it's the It's on the blood side, of course, where the cells are seeing those saturated fats or not. And then the person listening astutely is going to wonder, well, if they're not eating those saturated fats that appear in the blood, where are those saturated fats coming from? They're coming from the liver. The liver is the primary source of the saturated fats that are floating around in our bloodstream. It's not the fats we eat. Those get taken up by the liver and then reprocessed rehandled, burned, uh, for energy or burned for ketones or converted into other molecules to store as triglycerides. Most of the saturated fat in our bloodstream is coming from what the liver is releasing, and the liver makes those saturated fats in response to one humble little hormone, namely insulin. So if a person's worried about the saturated fat effect, on insulin resistance, then they should be worried about insulin because insulin's going to be the primary driver of all the saturated fats that are in their blood. And if someone wants to learn more, they can just look up studies that explore the role of insulin in a process called de novo lipogenesis. That's the name, the term for what the liver's doing when insulin is high. When insulin's high, it tells the liver, make saturated fat.

Okay, that makes sense. So if somebody's coming to this and they, they would say, what does that mean? Does that mean that somebody could eat more butter, lard, ghee, avocado, olive oil, and then not have the bread, pasta, and rice and see their saturated fat levels actually coming down?

Yes.

Okay, because I think that takes a little bit of understanding to learn that plasma saturated fat, the fat in your blood saturated fat, is not the same as eating dietary fat, which you explain very eloquently on your YouTube, uh, video, which has got a lot of educational series. Damn great content, Dr. Bikman, exciting content. Um, I want to move on to— so that we understand it's carbs, it's not saturated fat. This is very interesting, which is understanding the Randle cycle. And you say we try to simplify it, but it's quite complex. This is trying to understand that when you eat a fuel source, like for example glucose or fat, bread or butter. Now, if— how does the body burn each fuel source? So maybe try to explain the Randle cycle and how the body will prioritize glucose over fat, and then also ketones and lactate.

Yeah, I think the, the Randle cycle, it's interesting for me to see how, um, popular it's become. I remember when I first learned of it back in my student days, it was almost as a, it was just an interesting aspect of metabolism, of cellular metabolism. But it's also just, I think, I think it's quite simple in, in, in its, in its relevance, which is we, we have this old adage I'm sure everyone's heard, which is you are what you eat. Well, that's not true. The better version of that adage is you burn what you eat. And, and so if a person is, if, if a cell has relatively more glucose coming into it than fat, no surprise, it's generally going to burn that glucose and not the fat. If in contrast, if there's more fat available in the form of fatty acids coming into the cell, as opposed to glucose, then it naturally, it's going to rely on that fat. I think any effort to try to base a diet on the Randle cycle is foolish, that it, it's, it's not going to lead to any constructive application. It's just more of an academic point. It's just an interesting aspect of cellular metabolism. Now, having said that, I think where, where people have not appreciated some of some aspect of the Randle cycle, even the, the, the person who gave birth to the idea of the Randle cycle mentioned that insulin plays an important part. That if you focus, if you zoom out from the level of the cell and look at the whole body, we can measure the, the, the Randle cycle at a whole body level by measuring something called the respiratory exchange ratio. The RER is a measurement that allows the, the scientist to understand, is the body relying primarily on glucose or is the body relying primarily on fat? And insulin can flip that switch within minutes. You can have someone who is, in fact, insulin is the switch. Just to put a very fine point on that, if insulin's elevated, the body is sugar burning. If insulin's down, the body is fat burning. And This is reflected in just normal life where if you eat a mixed macronutrient meal, you got carbs and anything else coming in. No surprise, you shift to carb burning, sugar burning. As that meal is processed a few hours later and as the insulin has come down, we shift into fat burning, the fasted state of fat burning. That makes all the sense in the world. Now, there are some fuels that I say demand priority boarding. That if they're elevated, the body will not be in a position to store them. Ketones is one of them. Ketones are a fuel that once either made, if you make a ketone, you are generally not going to turn that back into a fat from whence it came. Or if you are taking in a ketone, you're not going to, through an exogenous ketone like go BHB, you're not going to convert that into fat, that thus it must be burned. And so that's why I, I say this, that it kind of has priority boarding. It gets to go right to the front of the line to board the metabolic bus. Whereas now the other fuels are going to be delayed in their burning. But I'm back to the Randle cycle and to kind of finish maybe my meandering answer. I appreciate it, but I think it's limited and people should just view it as more of an academic interest that it, it, it isn't really relevant when it comes to someone trying to change their behavior beyond what we've already discussed, that if a person has more fat on their body and they want to burn that fat, well then back to my adage of you burn what you eat, that if you're relying more on a diet that's based on fat and fewer carbs, you're burning more fat and that will include burning your own fat and you're gonna burn more of it than you would otherwise. Because if insulin's come down and ketones have come up, your metabolic rate has gone up significantly than it would have otherwise. So it's helping your body burn more fat. In contrast, if you're eating more carbohydrates with the subsequent insulin spike, then you're gonna be burning less fat and you're burning more of what you're eating, namely those carbs. That to me, I, I think that's the simplest approach when it comes to the Randall cycle.

Okay. Cause there was a reason why I asked that question, cause I was thinking if somebody has high insulin and they eat a mixed macro meal, so carbs and fat, and usually a carb and fat meal has very less protein. I was curious to know what would happen to that meal and how it's broken down in a person that has high insulin. From what you're saying is they would store it as fat, so they'll try to break down the glucose, try to— and a few hours later try to break down the fat. So it seems like in this conversation, don't think about the Randall cycle in terms of diet, like carnivore, keto, low carb. Just bloody drop the carbohydrates, don't eat too much of them.

If you'll allow me to— earlier I had mentioned where I think here is an interesting opportunity to bring back the ideas of physiological insulin resistance, where I just rail against the improper invocation of the terms when it comes to a ketogenic diet. Some people have said a ketogenic diet will cause physiological insulin resistance, and sometimes in so doing, they're invoking the Randle cycle. That is just not true. It is not accurate. The, what, what this, this myth or mis— or this error is born from glucose tolerance tests. And let me just clarify because there's an, there's a beautiful nuance here that's totally overlooked. But there's a lot of thoughts jumbling around my brain. So let me try to articulate them very succinctly. When we, we often use the term metabolic flexibility. And that's— I like that term. It's a term that comes back to this idea of fuel burning in the body, that a body should be able to shift to sugar burning when it's eaten carbs. But then after the body has processed those nutrients, it should shift back to fat burning during that fasted state. That's metabolic flexibility. The fir— the term metabolic inflexibility was born from work in the, I think, late '90s. At the University of Pittsburgh, where they found that there were a group of people who would, yes, be in sugar burning or glucose burning after a meal, but when they had shifted into the fasted state hours later, they weren't shifting metabolically, that they weren't really getting back into fat burning. They were still kind of stuck in a glucose burning mode. That was the term metabolic inflexibility, referring to basically the problem of elevated insulin. There is an inverse phenomenon that's associated with long-term adherence to a ketogenic diet where the person essentially gets not stuck, but, um, that's not the right way to say it. But because I said stuck earlier, I'm going to say it. They're kind of locked in. I'll say it that way, to a fat burning mode. And, and so their body has become so accustomed to burning fat for fuel that they're not burning a lot of glucose, that if you suddenly load the system with a lot of glucose by eating a very high-carb meal, and then you're measuring the rate at which the body's clearing that glucose, it will take longer than expected. But that's not because they can't burn the glucose. It's because they have so little insulin. And so to really bring all this back to one kind of crystallized thought where people say that a ketogenic diet causes physiological insulin resistance. It doesn't at all. It's totally fake. Not true at all. Neither definition of insulin resistance or neither component is there. They're exquisitely sensitive to insulin and there's very low levels of insulin. So there's no definition met here when it comes to trying to invoke insulin resistance, but they are a little temporarily glucose intolerant. That's not the same thing. What that means is if you load their body with glucose, it will take them longer to clear that glucose, but that's not because they're insulin resistant. It's because their beta cells have adapted to the low insulin requirements of that ketogenic diet. This is something that happens so quickly that even if a person fasts for 24 hours and they go in and take a glucose tolerance test at their clinic, They may fail that not because they're insulin resistant, but it's because the beta cells are so efficient with their insulin handling that even after 20 hours or so, if there hasn't been a big glucose spike, the, the beta cells will get rid of all of their preformed insulin. And that's important for people to understand because when you eat a, a carbohydrate load, insulin comes out in two phases. There's a first phase and then a second phase. The entire first phase of insulin release, which helps the body clear that glucose so quickly, is coming from insulin that the beta cells have already made, that they have produced and just have packaged sitting on the shelves in the beta cell, ready to go the moment the glucose comes in. And then while that preformed insulin is coming out of the beta cell, the beta cell is busily making more.. And that's that second phase of insulin secretion to just really fine-tune the glucose and bring it right back to where it needs to be. In a person who's been fasted for a few hours or adhering to a ketogenic diet, the beta cells have long gotten rid of all of that preformed insulin sitting on the shelf. It basically is looking around, the beta cell is, and says, well, we don't need all this insulin. Let's just get rid of it. It's cluttering up the space. And so the preformed insulin goes away. Now, when the person takes that big bolus of glucose, they don't have the first phase, they have the second phase. So, and so it just takes a little longer to clear the glucose. But this, all of this means that if a person who is adhering to a ketogenic diet, let's say a pregnant, a woman who's pregnant and is going to go in for an oral glucose tolerance test, a way to make sure you are ready is just to eat some carbohydrates. About 8 to 10 hours or 12 hours or so before you take that blood test, that will remind your beta cells or just kind of warn your beta cells, hey, beta cells, there's gonna be a glucose load coming. I need you to fill the shelves with some preformed insulin so that I can have both that first phase insulin and that second phase insulin. And now I can pass that glucose tolerance test with flying colors.

When would somebody have a glucose tolerance test?

Yeah, the most common is the one I mentioned, which is pregnancy, because the clinician wants to monitor any risk for gestational diabetes. Otherwise, it's almost unheard of to do. Now, they used to be more common. Glucose tolerance tests used to be more common until the rise of hemoglobin A1C. And now clinicians— that there was actually a paper that expressed a dismay that I echo, which is that with the increased focus on A1C, we have started to no longer do glucose tolerance tests, which is very unfortunate because the glucose tolerance test is an incredibly useful intervention, but it does take more time and, you know, means where the person has to sit around and the clinical staff has to be there for those 2 hours while they're going through the tolerance test. So nowadays, The only time you ever really see it, but although increasingly less common because of A1C, is during pregnancy.

Got it. Okay, let's move on to the practical tips to lower our insulin levels. Everyone can do this at home. Step 1 is what you eat. What do you think of a higher fat, lower carb diet to fix your insulin levels?

Oh my, I think that is step number 1. That, uh, I think it's the simplest approach. But that doesn't necessarily mean it's easy. I really want to make sure I add that caveat, is to control carbs. That is always for me, rule number one, that we live in a culture that is constantly consuming carbohydrates, that, that by some estimates, one being the Global Nutrient Database, up to 70% of all calories consumed globally come from carbohydrates. And we now have culture globally where we eat 6 or 7 times a day. And if we're not eating, then we're sipping on something with carbohydrates in it that we have a high carbohydrate breakfast, and then we have a mid-morning snack and then a high carb lunch, et cetera. So the average individual is spending every waking moment of the day with elevated insulin because of our constant carbohydrate consumption. So rule number 1, control carbs. Now, I said that that is a simple idea. Why I make a point of stating that it's not so easy is because we also have carbohydrate addictions. That is known to be addictive to people, that in all of the neurobiology of addiction, when it comes to food, there's always one macronutrient that's the culprit, and it's only ever carb. Now, I shouldn't say only because sometimes people find that, well, carbs and fat is more addictive than carb alone, but it's never fat alone. It's never protein. And, and so no one's ever sitting around craving a bunch of hard-boiled eggs. It doesn't happen. Never. We want something sweet and gooey or salty and crunchy, and it's going to be carbohydrate. So with, with that idea, control carbs, I, I respect that for some people, while the idea sounds simple, it is not easy to do. And, and so I, I want people to know that I don't mean to minimize how difficult that can be to actually do because I know it can be struggling, a struggle. And this is where, by the way, I think GLP-1 medications are at their best to help people control their cravings for carbohydrates. Now, I know that's a huge tangent, so I won't get into it necessarily right now, but that's the first rule. Back to the question and how you Presented it. Yes, control your carbs and let those carbs be replaced by the other macros, certainly fat, and then the protein that comes with that fat when, when available.

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Yeah, yeah. Allow me to answer that question in two ways, which is one, um, as from the perspective of my children and then my own approach as the husband and father within the home with my kids. As a, as a university professor, I have had the great fortune of just teaching thousands of darling undergraduate students. In the midst of those students have been many young women who've struggled with eating disorders, and my heart has always ached for them. And I've wondered at the origins of those eating disorders. So I've been always extremely mindful of what I might say or do, the culture I might create in my home that would perhaps drive you needing disorder with my daughters, maybe even my son. It's more increasingly common for young men to have these problems too nowadays, but it's generally been a female problem historically. And so I've looked at my daughters and thought, how can I talk about food in a way that won't drive them to an eating disorder?. And so rather than just vilifying sugar and carbs, what I've tried to do is say, have you had any protein yet? I've tried to focus on what I want them to be eating rather than what I don't want them to be eating. Just to not vilify, although they, some foods need to be vilified and we don't sugarcoat it, but we, I want them to have a culture more of focusing on not restriction and deprivation, but rather what should I eat for the sake of my growing healthy body? And that's, that's, that's worked pretty well. I mean, my kids are all healthy, thankfully. And, and of course genetics matter. You know, there are circumstances that matter here and I want to be sympathetic to that view too, but where a parent can have an influence, I think it's best that you're not just wagging your finger and saying, don't you eat that garbage. They need to, maybe it would be, they'd be better served by saying, hey, all right, hey, you want that snack? No problem. Have you had some protein first? And so in our home, we have lots of beef sticks, beef jerky. We have cheese sticks and cottage cheese. And depending on the kid, my kids are all fantastically different from one another. Just is to me absolute proof that when they come into our hands from heaven, they come with their own personalities and the environment can only mold them so much., but you know, they'll, they'll, they'll, you know, one of my kids likes the cheese sticks, one likes beef sticks, one likes cottage cheese. And, and so that's what they'll go to. And then they'll have that carb snack or food that they, they want. And again, that's worked, I think, pretty well. Now for me, I'm not growing anymore. I'm done growing. I know a lot about what can happen in the body. I am concerned about my own metabolic health and being a healthy grandpa someday. So my own approach is I am extremely strict and eat little to no carbs for breakfast and lunch. And then I will eat carbs at dinner with my family. We have dinner together. I want, it's most important to me that I'm just visiting with my family and that if my daughter wants spaghetti for dinner, then I'm eating that spaghetti with my family. Maybe I'll eat a little less than if it were a big juicy steak, but I just don't care. I don't think about it. I just enjoy dinner with my family and then I do my very best to stop eating after dinner because for me personally, and I don't think I'm the only one, evening is when my cravings get the worst. Where I can have been disciplined and strict and not even tempted by certain sweets and junk food all day, but about the time of 7 to 9 PM, it's like some beast awakens in my soul and it starts craving all that garbage. And so I try to have a family, my home, not have my indulgences on hand. If there is some ice cream in that freezer, I'm probably going to eat it. If there is some delicious cereal that I love so much, I'm probably going to eat it. Even though I don't want it because I'm a little bit of an addict when it comes to some of those foods. And so moderation won't work for me as much as I wish it would. But some of us, when it comes to carbs, that's back to some of my empathy when it comes to the difficulties of controlling carbs. But yeah, in my own home, I approach it as both a father and then as my own approach as a metabolic scientist.

I think that's really important because I think people can appreciate all the wonderful information that you're giving about how the body works. But practically speaking, it's hard. It's a little bit hard. Like, even if you have ice cream in the fridge, it's like, that's gone. If I have pretzels, bagels, pasta, it's gone. So we need to control our environment. Diet Coke, that doesn't have any calories. Does it spike insulin?

No, it doesn't.

No.

And so my— I want people to know, when I, when I talk about sweeteners, I'm presenting my ideas purely from the perspective of a metabolic scientist. Now, others may say, well, what about the cancer? What about the blood-brain barrier? I actually still think a lot of those concerns are overhyped, frankly, that I don't think there's compelling human evidence to support those concerns. But be that as it may, the sweeteners that are found in diet sodas or the zero sodas, they do not increase insulin whatsoever. And so, I actually personally have a pretty, if not apathetic, pretty close to apathetic view when it comes to diet soda. Now, having said that, there is an animal study that found that if you manipulated the gut microbiome, you could affect the insulin response to those sweeteners. That there, I think, is an opportunity for us to have a little bit of nuance in this conversation, that some people might have some kind of response to that sweetener, whereas another person may not. Perhaps based on their inherent differences in their microbiome. Now there's no human evidence to support this. So I'm stating all of this with a heavy dose of speculation. I think an easy way for a person to determine whether they are a responder or not is to monitor their hunger. That if a person drinks that diet soda and then a few hours later they find, or even shorter than that, they really start having cravings for other foods. I would suggest you probably had an insulin response. If however, the person is able to sip on that diet soda and find that they're perfectly content, they probably did not have an insulin response. And so I think we, I think there's room in this conversation for a little bit of personalized approach and hunger post the diet soda is probably the best metric. Hmm.

I think there's going to be some varying opinions. Somebody is going to say that diet soda doesn't cause them to get hungry, it's totally fine, I lose weight. Somebody else, I absolutely cannot have it. I'm on the camp that I probably cannot have it. Sparkling water I can, but diet soda probably not, and not ice cream. Um, so step number 2, after controlling the carbs and the not having, or maybe having the diet soda but it doesn't affect your insulin, step number 2, um, how about apple cider vinegar? 1 teaspoon, does that help lower insulin?

Yeah, it does. Yeah, there's very compelling human evidence to show that acutely and long-term there are benefits. So acutely you can take 1 or 2 tablespoons with a carbohydrate load and significantly reduce the insulin and glucose response due to changes in digestion from that carbohydrate. So acutely it can work. That might be something someone keeps in mind if they know they're going to indulge in some carbs. Well then take a shot of apple cider vinegar in some sparkling water. That's how I like to take it. It's, I think it's delicious. And then second, I mentioned more long-term data. There are studies in people with type 2 diabetes to show that adding apple cider vinegar to a daily normal diet can improve glucose levels over time as well. So I do think there is justification to have apple cider vinegar in your fridge, ready to go whenever you feel the need for it.

Is that before a meal or after a meal?

Before.

Got it. 1 or 2 tablespoons mixed in water.

That's right. Yeah. You don't want it concentrated just because it is very acidic and you don't, you necessarily don't want that on your teeth chronically, but if you're sipping it in water and diluted, it's not going to be a problem. But even having said that, there are some people I know, dentists who will say, well, it's better to drink it through a straw because then you're bypassing the teeth and just going straight back to the esophagus. That there, there might be a case for that, but I'm, I'm not really aware of it.

Okay, next one, point number 3, fasting. Now you say how you end your fast matters more than how long your fast is, so we don't need to be doing 18, 24, it's just how you end it. Why is that so important?

I appreciate you mentioning that kind of mantra that I have. I am an enormous advocate of fasting, and anyone who's curious about it, I, I have to mention my good friend Jason, Dr. Jason Fung. He is the godfather of the modern fasting movement. I don't think we, you and I would even be talking about this if it weren't for him. He really just brought it back into the conversation. I say back because of course it's something that has been around us humans since time immemorial. He's made it more part of the modern conversation. So I'm an advocate of fasting. I'm a great defender of it. I think it's profoundly therapeutic. My statement about the importance of ending the fast is born from me having seen people who experiment with fasting and do so in a way that I think is, um, net— is a net negative, where they fast, let's say, just a 20-hour fast, and they're getting hungrier and hungrier and hungrier, and they have no real set plan for what they do when they're done their fast, and they end up just binging garbage and, and they overeat. And so I'm using the word binging quite deliberately, they make themselves sick on just garbage junk food. And then they feel very ashamed and very guilty and have a lot of self-hatred for it. And then they end up saying, I'm going to do better tomorrow. And they do the exact same thing, the exact same cycle. So some people, I worry, use fasting as a bit of a binge purge cycle. So it becomes kind of an eating disorder. That's why I say that don't focus so much on the length of time. Have more of a plan for when you're done. So just tell yourself, okay, this is the meal that I'm going to eat when I finish my fast. And then 1 hour later, maybe if I feel like I'm still hungry, then this is what I'm going to eat. That I think is a better way to structure a fasting protocol than just focusing on the time alone. The time is important, it, it does matter, but in some instances I think it'd be better for a person to maybe end their fast at 16 hours if they can, if it makes it easier for them to stick to that very set meal than it would be to do a 36-hour fast and then just binge garbage and eat themselves sick.

I guess I would've thought that people would think what they would eat towards the end of the fast because I just do this all the time and have these conversations, but You know, of course, like, you understand the ideas of people, and maybe they don't think about what they should be eating at the end. So think about what, what you should eat, and probably protein and fat, I'm assuming. Is that correct?

Absolutely. Yes. Yes. And just to really help people appreciate the importance of managing your macros at the end of your fast, there is a known phenomenon in the biomedical literature called refeeding syndrome. I invite anyone to look it up for more detail. But this is a known consequence of fasting for an extended period of time and then eating something that spikes your insulin considerably over, and it can kill you. It's an actual lethal event where as you fasted for several, for an extended period of time, and this is typically going to be, you know, when you get to, you know, 2 days or so of fasting, which people do nowadays very commonly. Your kidneys have made some adjustments with potassium excretion where the overall shift in insulin has actually really affected, not in a harmful way, but it's changed the way the cell is moving potassium. And that in turn changes the rate at which the kidneys are excreting potassium. And there, to be specific, the kidneys begin excreting more potassium. That's perhaps an encouragement to be focusing on your smart salts and supplement your electrolytes during your fast. But as the kidneys are excreting the potassium more readily, the overall amount of potassium in the body has come down, which again is not inherently pathological yet. But if you rapidly spike insulin, now you have rapidly accelerated the rate at which the cell starts pulling in potassium. Which leaves the blood or the extracellular potassium to drop precipitously, that can cause something called hypokalemia, which can make the heart basically stop beating and the person dies. And so the worst way to end a fast is with something that spikes your insulin considerably. And yet, back to my earlier point about the problems with the binge-purge form of fasting, that's almost always how they end their fast, with, uh, an insulin-spiking carbohydrate, because that's what they start craving more and more as their hunger gets worse and worse. So yes, it's most prudent to end your fast on the macronutrients that not only spike insulin the least, namely fats and proteins, but also happen to be the macronutrients that are actually essential for human survival.

How do you see fat fast? If somebody was just to eat butter, lard, fat, is that really good to drop your insulin?

I'm actually an enormous advocate of these fat fasts, as you just said them. I love those ideas. And that's frankly how I do it personally, for what it's worth. Now, people should always take what I do with a grain of salt because not everyone wants to look like an old, freckled, wrinkled, bald man.

But oh my God, Ben Bikman, you look amazing. People are gonna say that you are very handsome. I'm telling you, it's gonna be in the comments.

Right. Good, good. Well, heaven knows I need it. So, But, but having said that, when I want to do a longer fast, I will do that, that I will, my drinks as I'm sipping on drinks, there'll be a hot drink with a hearty dab of butter or tallow in it. I actually just prefer the taste of the butter more, as much as I'm an advocate of tallow. I just like the butter taste better, but I will, I will add butter and it makes the fast almost effortless. And, and it's, I think, a very healthy way to have a fast without Letting your hunger get the better of you.

But just to clarify, a fat fast does not mean that someone's gonna eat 5 sticks of butter. It's controlled. Is, is that correct?

Yeah, I think so. Yeah. I mean, I, I think it'd be hard to overeat the butter because there's nothing craving about it. You know, I mean, that I, I just, it's hard I think to overdo it when it comes to pure fat. We have such a satiety response to that fat. That it would be very difficult, um, to really go too far. But yeah, I think for the most part it's just going to be a dab or two of butter when you're drinking something warm a couple times a day. That for me is sufficient.

Got it. All effective tools. Okay, so that's kind of like what to eat, how to break a fast. So I want to get into more specifics. Creatine, does that in any way help lower insulin?

Um, no, no. Creatine will be inert when it comes to insulin. Um, But that's not its benefit. The benefit of creatine is, of course, the ability of a cell to recycle ATP faster. It's just so people really understand that creatine is not a nutrient. You don't burn it to make ATP like you do. Say, like, if we focus on the brain, if you'll allow me to focus on the brain in the context of creatine, because that's where the hottest research is these days. The creatine has been shown to help mitigate the cognitive deficit from sleep deprivation. It has been shown to help the cognitive deficit of just early-stage Alzheimer's disease. There is incredibly compelling data, but of course you have to take much higher levels than you would just normally from, for the muscle dose, you know, up to the range of 15 or so grams per day of creatine. That appears to be the kind of requisite amount to get kind of into the brain. But so what the creatine is doing is helping the brain recycle its ATP faster that your, your hungry brain, is breaking the ATP in order to think and function and animate the body and do all of the functions we need the brain to do. The, the creatine is helping the brain take that broken ATP and rebuild it. Now, when it comes to the brain getting new energy, that's where I think BHB or the main ketone becomes so relevant to the brain. The brain, if the brain has any preference for fuel, it's ketones, not glucose. When given equal access to ketone and glucose, we have human evidence to confirm that the brain prefers the ketones and will rely on, on that BHB more than the glucose. But regardless, the brain will take those nutrients and burn it to create new ATP. And then the creatine just again helps the body, helps the brain, those cells recycle the ATP faster. Now, having said all of that, it's possible that a person— I say possible because I'm not aware of a study that has confirmed this, but now that I'm stating it, it makes me wonder whether there are studies on this. I can't help but wonder the degree to which creatine supplementation may help control hunger. Back to that earlier description earlier of hunger that I gave where the brain is constantly— it's a very energy-hungry organ. And if it's energy, if it's sensing an energy deficit, which is less ATP, then it will drive hunger. Maybe creatine supplementation helps the brain recycle energy faster and better. And thus is less likely to experience hunger, there might be something there. In fact, if no one's published that paper, maybe my lab's got to be the one to do it.

Um, so you co-authored a study in 2025, uh, it's a new study, Exogenous Ketones Provide a Muscle-Sparing Effect, um, while also helping somebody lose fat. Why is that important?

Yeah, yeah, I think that was, that was an interesting study where we had the subjects follow a typical lower calorie diet and nothing significant, but enough to induce regular weight loss. One group got placebo every day, one got several grams of, of BHB in the form of GoBHB. And we found that they, they had a relatively greater preservation of muscle mass. That's important because any time you're losing weight, you have the risk of losing some lean mass at the same time. That's just a consistent feature of weight loss of almost through any intervention. And, and the, the BHB has, is, has previously been shown to defend muscle protein in other studies where they were looking at BHB infusions. I would invite people to look up the work of, of Dr. Nair, N-A-I-R. I think he was at the University of Minnesota where his, his lab found that BHB was defending muscle protein. And our, that finding from the study that we did just sort of supports that with a kind of real-world scenario. Where I think that's important is that if a person is adopting, or the person is interested in weight loss, whether it's through just purely dietary means or whether it's through the use of GLP-1, I very much think there's a case to be made for supplementing with BHB. Now, one comment on that: as exogenous ketones have become more popular, it's very important for people to appreciate what they're actually getting. Some supplements market themselves as ketones and they are not. My lab just published a report on this, and Dr. Dominic D'Agostino at the University of South Florida— that if Jason Fung's the godfather of fasting, Dominic D'Agostino's the godfather of exogenous ketones. And we have both found that one of the more popularly marketed exogenous ketones is, is actually this molecule called 1,3-butandiol, which is not a ketone at all. It's actually an alcohol that the liver will convert into BHB. We found that it— Dom's work found that it hurt the liver, and my work found that it damaged the liver mitochondria. And so people need to buyer beware that if you're looking for an exogenous ketone, you just want something that just has straight beta-hydroxybutyrate in it. And Usually that's going to be coming in the form of, of GO-BHB. So simply just look for that on the ingredient label and you're gonna be getting something that's actually ketones.

That's super important. Next one is caffeine, yerba mate. You love it. Why is that really good to lower insulin?

Yeah. Yeah. So yeah, it's, it's, I, I do enjoy yerba mate and enjoy it sort of modestly or moderately. I don't wanna overdo it with that in part because I don't wanna overdo it with any stimulant. But yeah, these, um, yerba mate has these compounds like chlorogenic acid that has been shown to act almost like apple cider vinegar, where if you're sipping on that drink, and coffee has chlorogenic acids to a degree, yerba mate has more. Um, when you're sipping on this, it actually has that same effect as the apple cider vinegar to diminish the glucose and the insulin response to a carbohydrate load. So it has that acute benefit. And then you could say that there's a long-term benefit because some of the other molecules can accelerate fat burning. And so there are other studies to show that yerba mate consumption can help with fat loss as well.

But if somebody does these steps, which is the caffeine, controlling carbs, exercise, exogenous ketones, et cetera, et cetera, how quickly can they see a lowered insulin?

Oh, oh, very quickly. We, within just days to weeks. And in fact, my lab, a few years ago, working with a local clinic, we identified, working with this clinician, 11 women with newly diagnosed type 2 diabetes, full-blown type 2 diabetes. And within just 90 days with no medications whatsoever, there was not a single clinical marker of type 2 diabetes remaining in the, in all 11 women in this case series. That we reversed every clinical marker of type 2 diabetes. So that's, I've always been comfortable mentioning the 90-day number just because our work supported that so heavily. And yet anecdotally, I've seen people, even type 2 diabetics who are on insulin therapy, their need for insulin drops so significantly that they get off their insulin within just a couple weeks.

Oh, okay. So we've spoken about the practical tips to lower insulin. Now this is to understand if your insulin is actually lower. What are the metabolic markers that one should test and look at?

Yeah, if you have access to a blood test, of course you want to look at your insulin. Other markers would be things like the triglyceride to HDL ratio. I focus on that one a lot because most people are going to get that— those numbers, the triglycerides and their HDL cholesterol. With any blood panel. Anytime they get any fasted markers done, they're gonna get those ones. And so you probably have access to those. Now, in much of the world, those numbers will come in the form of millimolar, which is gonna shift it a bit. I'm in the US, so that's, we measure it in triglycerides per deciliter. So with those numbers in mind, with those units in mind, if your triglyceride to HDL ratio is less than about 1.5, that's a very good sign. That you're metabolically healthy. But there are others like the triglyceride glucose index or the, um, adipose insulin resistance index, which looks at insulin and free fatty acids. So for the sake of simplicity and practicality, the triglyceride to HDL ratio is probably the best. But then beyond clinical or lab markers, a person could just look at other features like their blood pressure. Hypertension is most commonly driven by insulin resistance.. So as the insulin resistance gets better, you should expect the blood pressure to get better. And indeed, that's another one of those medications, hypertensive medications that are often deprescribed within just weeks to months of a person adopting a low-carb diet.

So if somebody's watching this, as a last question, is there anything that we didn't cover pertaining to insulin resistance, belly fat, losing weight that you want someone to know? Yeah.

You know, you mentioning belly fat tickles my brain in a way to mention one other thing, which is visceral fat, which we commonly call belly fat. Everyone remember that belly fat can be a mix of both of those, both the visceral and the subcutaneous fat. So the fat that you can pinch and jiggle on your belly is the subcutaneous, which is generally relatively benign. Subcutaneous fat is generally benign fat. It's healthy. Fat in a way. It's a healthy place to store fat, which is why women can have more fat than men and be healthier, because on the female body, most of her fat, it's overwhelmingly subcutaneous because of her sex hormones. In contrast, in a man, while he certainly can have a lot of subcutaneous fat, he will have relatively more visceral fat because he doesn't have the estrogens to basically have it all be stored subcutaneously. But visceral fat is the most problematic fat. And one effective way to burn that is actually anything that increases your epinephrine or adrenaline levels. So yes, that can be exercise, but everyone always thinks that they need to exercise more. So I'll mention an uncommon one, which is, um, cold bath or cold immersion, that when you do an ice bath, you are activating your sympathetic nervous system. You're getting an increase in adrenaline. And that, that adrenaline is going to relatively push more visceral fat burning than subcutaneous fat burning. That if, if you take visceral fat and visceral fat and subcutaneous fat and expose them to epinephrine or adrenaline, the visceral fat is more responsive. It will actually burn faster than the subcutaneous fat will. So in addition to all the other things we've mentioned, if a person's looking for just one more thing to do, it could be cold exposure.

What would you say to somebody right now? Just, just one thing to do today to fix their visceral fat, lose belly fat, et cetera, et cetera. Just one thing.

Control carbs. I long maintain that's the single most important thing. And I would say, especially for breakfast, that don't start your day off. You know, you've been, you've been fasting while you've been asleep and your insulin has finally been coming down. Don't spike it right back up first thing in the morning. Try to go as long into your day as you can, keeping your insulin low to not only be helping your insulin sensitivity, but also just be longer in that fat-burning state. Make a little more ketones to fuel your brain a little better than it can get with glucose. So control carbs and let it be earlier in the day. And if you want to have carbs, let that be in the middle of the day as much as you can, even though I just said earlier that I eat mine for dinner. But if, if you can, and you need to have some carbs for any reason, I'd say let it be in the middle of the day and start to taper off.

Very simple advice. Dr. Bikman, thank you so much for your time. All your links will be in the show notes.

Wonderful, my pleasure.

I hope you enjoyed this episode. Check out this one again with Dr. Ben Bikman. It is all about how to burn your belly fat using science. I'll see you guys next week.