Cortisol will literally rip the body apart in order to increase blood glucose to the point that it's destroying collagen in skin; it's destroying collagen in proteins from bone. It will strip away any potential source of amino acids to send those amino acids to the liver to active; to use those amino acids as building blocks for gluconeogenesis. So it wants to—it will wreck the body to increase glucose.

Dr. Ben Bman: You really do study insulin a lot. And when we look at the world of exercise, fat loss from exercise performance, what kind of role does insulin play while we're actively exercising? What's it doing?

Yeah, yeah. Well, this is one of the rare moments where insulin actually takes a back seat. Insulin is antithetical to exercise; it has no place in the formula, by design. Insulin's primary action—so we often view insulin purely through the lens of glucose, um, which isn't fair because insulin does a lot, including it literally affects all nutrients. It has a—it has a very powerful influence on fat metabolism, protein amino acid metabolism, and no surprise, carbohydrate glucose metabolism. But in exercise, it has no—it has no place because insulin's thematic effect across all nutrients is that it wants to store them. If there's amino acids in the blood, it wants to push them in; it wants to store them as proteins in a cell. If there is fats in the blood, it wants to pull those fats and store them in fat cells primarily. If there's glucose in the blood, it wants to—to push that glucose into the muscle and the liver to be stored or burned. So the net effect of all of this is that when insulin is up, it wants to be locking in energy; it does not want to be mobilizing energy. Of course, that is, as I said, antithetical to the state of exercise. During exercise, you need to be mobilizing rather than building, which is what insulin wants to do as an anabolic signal. We need to be catabolic during the exercise itself.

So during exercise, one of the reasons we are able to have a higher glucose level is because insulin has bottomed out so powerfully, and there are myriad mechanisms that have pushed the insulin down. But one of them is a direct nervous system effect; that sympathetic nervous system, when it gets turned on, has direct neurons that are innovating the beta cells of the pancreas, and it tells the beta cells, "You keep that insulin locked up." So it's a direct nervous system response that the moment that sympathetic nervous tone is starting to climb with exercise, the ba—the—the beta cells of the pancreas just say, "Okay, it's not my time to shine. I'm going to let these other more catabolic hormones start to come into play," most especially epinephrine, cortisol, glucagon, growth hormone. So these other hormones that are—more people might be surprised to hear me say this—that are more catabolic, yes, even growth hormone is catabolic, um, as an energy controller. These are all hormones that, despite all their differences, the one thing they have in common is they mobilize energy. Every one of those hormones will induce some degree of lipolysis or and glycogenolysis; so breaking down the stored glycogen.

Now, just as a tangent, because I fear people may get upset at me mentioning growth hormone is catabolic, the reality of growth hormone is it does not directly signal tissue growth; it's its product that signals tissue growth, which is the IGF hormones, the insulin-like growth factors. So growth hormone alone is more aptly viewed through the lens of nutrient mobilization; it stimulates lipolysis and glycogen—it basically provides the fuel for what the next hormone does. Because when growth hormone goes up, it tells the liver to release insulin-like growth factors, and then it's especially IGF-1, which then promotes tissue growth, but it's able to do so by relying on the fuel that's been mobilized by growth hormone and others. So to bring that full circle, insulin cannot ex—it cannot dominate during exercise, which is one of the reasons I'm such an advocate of exercise as an insulin scientist. As I'd alluded to previously in previous conversations, one of the true keys to being lean and living long is keeping insulin the majority of the time in a controlled low state, and exercise is a very rapid way to just push insulin down, um, keep it at the bottom because it doesn't fit during exercise. We need to be catabolic; we're breaking down and mobilizing energy. Insulin is the opposite.

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So is there sort of a war that occurs if you're ingesting carbohydrates or fuel during exercise, or is it happening at such like a nano level like where it's—you—you've got an insulin spike a second, or is it because of this kind of insulin-independent glucose uptake where the muscles just suck up the glucose?

Yeah, well, right. Yeah. In fact, you nailed it right there. Yeah, but—but it's—it's a little more complicated in a pretty fascinating way that should give people some pause depending on what their outcomes are. So you—you—you expressed it right that there are, within the entirety of all the complication of the cells of the body, GL—insulin is only actually necessary for glucose uptake into—into just a few of those, like primarily muscle and fat. So muscle and fat have a glucose transporter or a doorway for glucose that only opens when insulin comes and knocks on it, whereas other glucose transporters, like in the liver or the kidneys or the red blood cells, they're just open doors, and if glucose levels go up in the blood, the glucose just comes into the cell; there's no need for insulin to regulate it. Now, insulin still affects those cells in other ways, including even telling them what to do with that glucose, but it doesn't control the entrance of the glucose. Now, however, the muscle is unique because, like, imagine the person—we could imagine during exercise—well, if insulin plummets, how's my muscle getting the glucose? It's as you just mentioned; it basically has a back door. So when the muscle starts to contract—just to kind of be a little precise here—um, the GLUT4 molecule is within the muscle cell, and when insulin comes and knocks on the door, the GLUT4 will come and merge with the surface of the muscle cell and open the doors to allow the glucose to come in. However, when the muscle is contracting during exercise and insulin is low—there's no insulin knocking on the door—during muscle contraction, we're—we start to get higher and higher levels of calcium. Calcium activates an enzyme called calcium-calmodulin kinase, or CaMK. CaMK activates AMPK, which activates another signal, which moves the same GLUT4 out. So we have this—in other words, that's just the complicated pathway of the back door. So when the muscle is working, we have an insulin-independent glucose uptake, which is what you'd refer to. So that helps—that helps the whole dynamic with insulin and glucose kind of playing out the way they do. Um, so it's still GLUT4 transportation; yeah, it is—it is still GLUT4 moving, but you have this insulin back door; you didn't have to rely on insulin to get it done.

Is there a—like a threshold? I mean, to—or like what can you get away with? I've often talked about this insulin-independent glucose uptake as a way for people that are specifically—if they're doing a low-carb—this is the time—like if you want to have some carbs, this is going to be the time. But it doesn't mean that you can go ham on it. I mean, who wants to go ham like that? Was like—you're not going to consume a—you know—

Yeah, no, no, that would make some sense where—where you do have now the ability to pull in glucose without the need of insulin; there's absolutely justification in that viewpoint. The other point I was going to make, and I'd forgotten in the midst of my other long-winded explanation, was—uh, documented evidence in women in particular—that's why I was sort of alluding to at the outset of my answer—it depends on—my view on carb consumption during exercise depends on what your outcomes are. If your outcome is—I'm exercising to improve my insulin sensitivity, just as an example—that's what I study—consuming carbs during your workout is not prudent. The study in women found that when women exercised and fasted, they had a certain degree of insulin sensitivity in the—in the ensuing 24 hours. If they exercised and consumed glucose, that undid the insulin-sensitizing effect of the exercise. So thus, it really becomes outcome-specific. If—if I were talking to a lean marathon runner, okay, eat carb—eat as much as you want, frankly. But yeah, even during your workout, absolutely be getting energy in. Even if I'm talking to a bodybuilder or just a weightlifter who's going pretty hard, if the goal is growth, okay, there's probably some value in consuming carbs. If the point of the exercise—like for me as a middle-aged guy who just wants to stay lean and metabolically healthy—the point is for me to become insulin sensitive and maintain that as much as possible. For me, the carbs make no sense; I don't want to—then I run the risk of happening what—of—of what happens with that study of the women that I mentioned where consuming carbs during exercise undid the insulin-sensitizing benefit of the exercise itself. I don't want that; that's my purpose is to maintain or improve my insulin sensitivity. So I don't, unfortunately, have a clear rule when it comes to carbs and exercise consumption. No doubt the body can handle it better than it would if it weren't exercising. No, that's—out—not up for debate; it's so obvious. But whether or not you want to do it depends on what the benefit is you're seeking. If you're exercising to improve your insulin sensitivity—like I could imagine an overweight type 2 diabetic listening to this—I would say it's not prudent to consume carbs during your exercise. If you are generally leaner, or you're going a lot harder, or you have different outcomes that are more specific for a sport, okay, well, do—do whatever you got to do to perform to your best.

Interesting. Um, you know, one of our mutual friends, Dr. Andrew Nck, up at SDRI, you know, studying—I mean, a lot of times specifically type 1 diabetes, but diabetes research in general—um, I think at the time of the release of this video, it's safe to talk about it; you know, he's publishing a paper that's talking about essentially the only requirement for carbohydrates even during intense inter—endurance activity because, like, right now we're seeing in like the cycling community, like they're trying to push their glucose up to like 180. I mean, they're crazy—keeping it high—keeping it high, which, I mean, with all due respect in that world, like if—if they want to do that, they're moving fast enough; it's probably fine; like it's not having that much of a detriment. But why do we want to have that?

Yeah. Um, essentially they found that all that was needed was 3.4 grams of carbs every 20 minutes; just enough to keep exercise-induced hypoglycemia from occurring; that's all. So it's like—all it was—CU—I don't think people understand fully how little carbohydrates are required to get your blood glucose off. You know, it's like—yeah—like at any moment, we have one teaspoon worth of—of car—of glucose in our blood.

Yeah. I mean, that's such a minuscule amount that you can start to see how a little goes a long way. But also, um, of course, a little can go even further if you have made adaptations, you know, if you've been trained—like you have these incredible exper—uh, stories of athletes, elite athletes even, who are breaking all the rules when it comes to fat burning during higher-intensity exercises. So the classic paradigm had been low—low intensity is primarily fat-reliant, then the higher the intensity gets, the more the body is shifting over to glucose as the primary fuel. That view is not wrong, but if you take an athlete who has done all their training in a ketogenic state, their ability to continue to burn fat at ever higher intensities literally breaks the rules for what we thought we knew about exercise physiology. This was a paper published—I think Tim Noakes contributed to this—a few years ago. They found—and I unfortunately I cannot cite the units—but whatever the previous limit was at the amount of fat that could be oxidized to sustain exercise, let's say it was 1 milligram per minute, it ended up getting like 9 times higher than what they thought was ever possible. And—and that—that sort of breaks the rules of the—the—the fuel utilization during exercise in a very important way because, again, if you've done your training in such a way that if you must be relying on fat as your fuel, you have to have a much higher abundance of mitochondria, because that is the site of fat burning, and you also must have a higher abundance of the enzymes involved in moving in the fat—getting it into the mitochondria in the first place to get to the citrate cycle, then the electron transport, etc. You got to have more of all of that, and you're only going to get it if you pressure it, you know, if you're—if you're pressing that—that process to its limits, the—the cell knows it—learns, "Okay, that wasn't enough. I'm not only forced to rely on fat, but I'm—I'm forced to rely on it at higher intensities than I was previously, so I must adapt," and boy does it adapt. The—during exercise, again, we—we literally are breaking the—off the charts level of fat oxidation in athletes that are forcing their bodies to rely on fat as a fuel. But imagine the advantage in a long endurance event where the main reason people fail or bonk is because they run out of glucose; they can't maintain their—their glucose levels. Well, not only does Andrew's study contribute to what they actually need to do that, but imagine even then how much—much further that glucose is going to get if the person's able to rely on not only fats for fuel, but even ketones, which are a very viable fuel for active muscle cells. Um, so the more the person is—um, pushing the body to challenge the norms of—"I got a carb load every time I'm exercising"—maybe you don't. Again, a lot of it depends on the outcomes, but for the average person listening to this, not only do they not need to carb load, they probably don't even need to be consuming carbs during the exercise in the first place.

Yeah, it's interesting, Ian, and if you're oxidizing fat at a higher intensity, then just by very nature of that, you're going to be more glycogen-sparing throughout the workout, so it leaves you more in the tank for—let's—let's just say hypothetically you get to 90% intensity with fat—it's just purely hypothetical—so that leaves you that final 10% is the only time that you'd start having an—re—over one or start going like—so then at that rate, that's going to be pretty intense, which means you're going to have full glycogen storage—close to full glycogen stores—for that extreme effort where everyone else is dwindling with their last little bit of carbohydrates they have left in the way of glycogen. So you have potentially topped off, or close to topped off—maybe not depending on half the length the exercise—but your glycogen stores relatively untouched—relatively untouched. And important—even in that same—Noakes study—I think it was that same study—when they actually looked at the amount of glycogen in the muscle, even in ketogenic athletes, it's such a testament to how selfish the muscle is that its muscle glycogen levels were totally normal. That if you take a ketogenic-trained athlete as opposed to a high-carb-trained athlete, their muscle glycogen is the same, which means at that last little kick, if you've been able to keep that muscle glycogen untapped, it's hard—I mean, it's easy to see that that could be a potential difference maker.

Well, if we're talking fat oxidation, let's talk uh, you know, fasted training, and you mentioned like creating this adaptation pressure. I've often referred to it as wearing a nutritional weight vest; that's specifically like—Spec Ops communities—that's how I kind of explain that, right? It's like, "Hey, like, you're going into your workout—like how do we sort of induce more fat adaptation? Okay, let's put a nutritional weight vest on you," and that's the—it's a thought process that really clicks for them, right? So it's like we're—we're putting a weight vest on you by training metabolically by putting you in a fasted state. But if we position that discussion to have it surrounding fat loss and where you're really solid in the insulin world, in your opinion—'cause I know this is highly debatable and it's a very hot-button issue for a lot of people—in your opinion, is training in a fasted state burn more fat?

Yeah, so I—I don't think—I think it would be beyond debate to say that yes, during the workout itself, it would burn more fat if you're not putting energy in. I mean, there's a certain kind of priority of—of—like imagine the metabolic bus, and—or—I'm going to—I'm going to be flying home—home later today, and there's priority boarding, or there's sort of your—back in your—different—different zones of boarding—maybe that's the way—that's how we talk about it noways—there's different zones of boarding; different nutrients have different priority boarding zones, or—like for example, ketones—ketones are priority boarding. Um, if ketones are available, they're getting burned; there's no regulation; there's no check to their burning; they are—they bump basically to like the front of the line.

They fly private.

Yeah, that's exactly right. Yeah, I mean, they're just on the plane and gone before anyone else even left the tarmac. So uh, we have kind of different—now it's not quite as simple as I'm laying it out to be, but yeah, if you start to eat nutrients, you are absolutely slowing down the use of your own, or you are replacing those nutrients even in your fat cells shortly after. So to me, during the workout itself, I don't know that anyone could say you wouldn't burn more fat; the question would perhaps then be, "Well, what do you eat after?" Um, for me, as much as I believe fasting is helpful, and I do absolutely—I think that the most important part of a fast is how you end it. As much as we focus when it comes to fasting, we focus on the time—"How long did I fast? Or I did a 24-hour fast, or—yeah, I did a 36-hour fast"—that interests me less than—"How did you break your fast?" That's what matters most is—"What are you eating when you do eat?" Because too often I've seen people who adopt a fasting regiment, and it turns into kind of a glamorous form of bulimia where they—you know, they kind of binge and purge, and I—that's kind of vulgar to say, but they're fasting—fasting—fasting—fasting—fasting—getting hungrier and hungrier minute over minute, and then they just cave in and eat every piece of junk food they can shove in their mouth; they feel full to the point of being sick; they have a lot of shame, which is a very dangerous emotion; guilt is an okay emotion; they have that too, but shame is rarely helpful, if ever, um, and in this case, it's purely harmful, and then—but they resolve to do better tomorrow, and they do the ex—same thing. And that's why I'm such an advocate of saying how you end your fast matters more than how long you fast. Not to have a cop-out here, but I—I think that would apply even to the exercise—the idea of when—more so—

Yeah, yeah, absolutely. But if you exercise in a fasted state as opposed to, say, chugging some glucose source, that to me should be too obvious to even debate about; you absolutely will burn more fat, um, because you don't have a fuel coming in and competing for boarding, you know, as you imagine the nutrients getting on the metabolic plane to fly off the fat—your own body fat is boarding that in the process. But if you are inserting glucose into the mix, it's going to slow down your burning of your own fat. But then again—so during the exercise, that to me should be beyond debate; you will absolutely burn more fat, but then what are you doing for the following 24 hours? Um, because someone who fasted during their exercise—sure, during that 45 minutes they might have burned more fat than the person who is eating a little or drinking something—but maybe that same person who fasted now goes and more than makes up for it by eating uncontrollably something else, whereas that person might have had a slightly better appetite control; I don't know. So it's just too complicated for me to really come down on, but during the exercise itself, 100%, they're burning more fat.

So in essence, I mean, if you can be in control of what you eat afterwards, you could feasibly end up in a better, more advantageous fabric position.

Yeah, I mean, it all comes to me—it all comes down to hunger, like what is the drive to eat something? And—and if a person can break their fast, um, with proteins and fats—so very well-done human study—isocaloric diets matched for protein, and the only calorie differences were shifted in carbs versus fat, and if your first meal of the day was a low-carb version of the meal—identical number of calories—so lower carb, higher fat, you were much less hungry throughout the entire day. That is—that matters. So if you fast through your exercise session, and you know this is what I'm eating when I'm done, and I strongly encourage anyone who has an exercise regiment—have the plan be mostly focus on what you eat when it's time to eat; have that meal laid out, even if in your mind it's ready to go. And if you need to have some accountability, recruit a loved one, a friend, a coworker—"Hey, when it's time for me to eat, gently, lovingly remind me to only eat this because this is what I want to eat," and sometimes we need that external cue. Then if you're hungry an hour later, have another plan for something else, just to put yourself up in a position so that come 8:00 p.m. that night, you don't become a rage monster who is shoving everything they can in their mouth, because that is when we are at our weakest. Um, every person I know—we are the weakest when it comes to food cravings in the evening, and if we have been just mounting our hunger all day long, and that's when we break—uh, we usually break really bad.

I want to pivot.

A little bit, but it's still within the same realm. If we talk about someone that exercises, possibly in a fastest state or not, but I guess in this context, fastest state, like where does the potential for the constrain energy model come in in terms of fat burning? Because the reason that I went this route is because, you know, we're talking about sort of almost this rebound effect of fasting where people just overeat. And I know we've seen it in the rodent model stuff where, like, you know, you have them fast for 24 hours, and then over the next two weeks they make those calories up. Right? It's just like kind of naturally happens anyway, um, you know, unless someone has a plan, that's you're saying, which was the whole kind of point.

But what about, like, say this: we exercise, and then we inadvertently become less active as the day goes on, but we don't really realize it's happening through less non-exercise activity thermogenesis, maybe less fidgeting and things like that? I've asked this question with a couple other guests before, and always get slightly different answers because I know it's it's it's a model; it's not, you know, totally flushed out. But what's your take on that? Like, have you seen that in the lab? Have you seen that before?

Well, I've not seen it in my lab, but guys out of, like, the Pennington, um, and Claude Bouchard, a lot of preeminent metabolic scientists, find this—what do they call it? I think they call it, like, a permissive effect of exercise—where, as you noted, people who are deliberately engaging, you see it actually in multiple ways. You see that not only in exercise, a person who exercises more may be less active throughout the rest of the day. Same thing goes for someone who's deliberately, say, not eating sugar, or they drink a diet soda, like we talked about in a previous conversation, they end up making up for it in another way because they feel like they've earned it or something like that. So there is this desire of the body, certainly when it comes to exercise, where whatever the basal state is that that person has adapted to, any pressure up or down, the body will resist it.

Um, but let's say the person has become accustomed to a higher body fat level, and now they're exercising in order to bring it down. First and foremost, exercise alone will not be sufficient. That has been—even the American College of Sports Medicine has reluctantly admitted, you know, about 10 years ago—that exercise alone is not a sufficient stimulus for weight loss because if you don't control diet, people exercise and they just eat a little more, you know, they make up for it. And so in order to get off that um, plateau, where what has become a new normal, it's an uncomfortable adaptation, um, mostly because they start working against hunger. So if you are limiting the body's ability to mobilize and use its own energy, you will be hungry. You need to have your strategy of, of say, weight loss encompass, or at least start with, um, an intervention that mobilizes your energy, and and that is why I focus so much on the first step of a weight loss journey being: lower your insulin; don't worry about your calories. If you're hungry, eat; if you're not hungry, don't eat, um, and you'll find that easier. We know that when ketones are up, satiety is better. Um, there are studies to show that people, even with eating disorders, find that their relationship to food is better if the brain is fueled with ketones. Um, now that's a that's a tangent, but um, to bring it back to the point, if if they have to get off a plateau, you just don't want to pit yourself against your hunger, because hunger always wins. And in our environment of food where we can get access to anything we want, almost at any time, if you're hungry, you're going to make up for it; you're going to you're going to satisfy that hunger. But if you can start to train your—change your diet in such a way that your insulin comes down, now you're going through this slow and steady adaptation of relying on your own fat for fuel.

You know, I'm coming from the mountains of Utah, and you're here—you have some lovely mountains here. It's not uncommon. Right beside BYU campus is this big—is Y Mountain. We have the big BYU, the Y block letter up on the mountain. Very commonly, people are hiking up to the Y; we call it—I'm always um, amazed and even a little saddened when I see overweight people, or even healthy, relatively lean people who've got, like, energy bars and energy drinks on them just to hike up, you know, about a mile and a bit. You know, it's pretty steep; it's quite a climb. And I think, no, we have energy. Especially if someone's overweight, everything that they can pinch and jiggle, they have hundreds of thousands of calories stored on them as energy, just waiting to be used. But you cannot you cannot open those energy bars of our fat cells until insulin has come down. And so these are people who should have sufficient energy; ironically, they're carrying energy on them, making them work harder on the way up, and and they feel like they have to compensate and eat this external energy. And if if you'll allow kind of an analogy here, it's like the difference between a sports car and a semi-truck, um, or or rather just with the semi-truck and looking at the fuel sources we have: why does that truck, who's hauling a tanker full of gasoline, why does it have to stop and fill up its tank—its own little fuel tank? We have this massive amount of fuel here, and it has just a small little fuel here because its engine is only tapping that small fuel tank, and so every four or five hours or whatever it has to stop and fill it up, when ironically it's hauling around this massive reservoir of energy. Wouldn't it be brilliant—perhaps a bad business model—but if they could rewire that engine, re-plumb the fuel line to be tapping into that, it would never need to stop. That is absolutely analogous to our two fuel sources as humans. We have a little bit of glucose, maybe 2,000 calories worth, and then we have hundreds of thousands of calories stored as fat, even on a lean person. How stupid is it if we're only ever tapping into that modest fuel source and constantly filling it up? This, unfortunately, though, is what happens to the average person. They wake up in the morning, and maybe their glucose and their insulin levels have settled down. First thing they do is they eat a starchy, sugary breakfast; glucose levels spike, and they drop very rapidly, causing hunger. And so that's as if that the the fuel light is flickering, and they feel like they have to refuel, and they refuel that tank, and the glucose comes up, and then it comes down again, which just continues this insanity of this metabolic circus. When if they could give the body a break, ease that insulin down, now all of a sudden you're accessing that fuel that you have to carry around anyway; you may as well use it. And once you start using that, you now have a fuel that is absolute rock steady. You you separate yourself from the highs and the lows of glucose level, of these hyper- and hypoglycemic bouts where you feel lethargic and tired, then you feel crazed hunger, and then you do it again and again and again. The more you have coupled your metabolic engine to glucose, the more you're going to feel frequent hunger and experience the highs and lows in your mood and your cognition and your energy level as the glucose levels go up and down. The sooner the metabolic engine gets coupled to using fat as the fuel, now you have a fuel source that is as steady as the day is long, and you are you have much more stability um, with your energy source and your overall well-being, and at the same time you're improving your metabolic health.

If we were to continue your analogy with the fuel truck, too, the other side of that, or the other continuation of that, is once you were to continue or run a pipe from that other tank to the big tank, it's going to take some time for the body to figure that out, right? And the reason I'm saying that is like we've, in a lot of ways, and I think I see this in the athletic community a lot, and finally people are opening their eyes to it—like, people are really starting to see it now, especially in the endurance world—um, it's still going to take some time. And I call—you know, I can I can say this 'cause I am one—in the meathead world, it's still going to take some time, um, just because like carbs are so precious for anti-catabolic effect. Believe me, I have been the recipient of the fiery darts of those who of those carb advocates. But they get viciously angry at the—but it's also like, I mean, okay, actually touching on that for a second, my theory on this is that if you are more fat-adapted and conditioned to occasionally training or regularly training fasted, you are going to have the systems and processes in place to be protective of that tissue; whereas if you were so enabled using carbs all the time, your muscles have become spoiled little brats that the moment that you don't give them that, they do hit the panic button and do start having issues, and you do become more catabolic; whereas if you paid your debts a little bit ahead of time and developed a level of metabolic flexibility and somewhat fat adaptation, I would argue that you can actually have a muscle-sparing effect because you're not going to hit the panic button; your body's not going to hit the panic button.

Yeah. Oh, I I love that. In fact, even just as evidence in testament to what you just said, just this week, at the time of this recording, a big meta-analysis was published that looked at every available study that compared high-carb diets to ketogenic diets and looked at the building and retention of muscle mass in weightlifters, and shock of all shocks, there's absolutely no difference. So really settling what should be this debate where people say you can't build muscle on a ketogenic diet, you can't keep that muscle on that ketogenic diet. This meta-analysis of several studies proves that idea wrong—that it's if the stimulus is there, the challenge of the muscle and calories are sufficient, then you're keeping your muscle. But I love what you said with regards to ketones specifically. You said, defending muscle—ketones are the great defender of muscle. What do I mean by that? If the difference between—we've been talking about fasting—there's a there's a fine line between fasting and starvation. The line is body fat. The moment a person's body runs out of fat, the fast has ended; now starvation has begun. Now, why is it—what is it about the fat? It's not just the energy, but it's actually what the energy turns into, namely ketones. Because if you have fat to burn, you're making a lot of ketones, especially if you're fasting that long. Ketones tell the brain, leave the muscle alone. But the moment the fat is gone, ketones are gone; now the body starts burning muscle for fuel. That's starvation; that's the difference. So it's fat—it's body fat—and the body fat's ability to produce ketones. That's why Dr. George Cahill and other legendary fasting scientists would say ketones defend muscle because as long as you have ketones being produced from fat burning, the body won't touch its muscle. Most obvious example, and admittedly a dramatic one, was the uh, a case report published of a man in the UK decades ago, morbidly obese; he fasted under medical supervision for 382 days. This is a published report; he would get vitamins and minerals and water, of course, staying adequately hydrated. I think he had coffee and tea, but no calories whatsoever for 382 days successfully. Why did we—why was he not starving to death? Because he had a lot of fat to burn, and eventually he stopped his fast; he started eating again and lived a perfectly long, healthy life, actually, and never gained all the weight back, remarkably. But that was not starvation for you and I; that we're we're dead; we can't live that long because we don't have enough fat to sustain the production of ketones to tell the brain that it can leave the muscle intact. So the moment you run out of fat and ketones are absent, now the mus—the body starts burning its own muscle; now you've entered starvation and all of the misery that comes with it. It—but ketones preserve muscle. Um, in fact, we published a paper in a very obscure journal finding that ketones actually help muscle be more um, stronger in the midst of insults. We were basically challenging muscle cells with these noxious chemicals, and when we had ketones in the mix—in the in the milieu or the the culture medium—they were more robust; they survived better. So there's this literal protective effect of ketones at the muscle. So ketones are the muscle's best friend.

I'm going to pivot a little bit because you said something and I wanted to mention this in another video, uh, because you probably have some interesting stuff on it, uh, when you you mentioned coffee and and tea with that during exercise. Uh, obviously coffee is a strong ergogenic—caffeine is an ergogen—but also influences uh, some more fat burning. Yeah, what have you seen, maybe in your lab or some of the other labs, the influence of like how caffeine actually affects fat metabolism, and is it—I don't want to say a free, but kind of a free ride? I mean, if you don't go and compensate for that additional fat being burned, is it actually like a net fat loss?

Yeah. Yeah. So caffeine, you said it perfectly well; it is absolutely a beneficial molecule when it comes to exercise. So thus we call it an ergogenic. Um, it does powerfully stimulate um, lipolysis, so again that's the breakdown of the fat from the fat cell. At the same time, it stimulates beta oxidation, or the burning of those fats. So it's one thing to move the fat; it's another to burn it. Caffeine actually does both. Caffeine is also, on its own, um, very ketogenic, um, something we've been talking about in this conversation and and others previously, um, and ketones have their own myriad metabolic benefits from signaling satiety to controlling inflammation to defending the muscle. So caffeine does improve or accelerate ketogenesis; frankly, it does so only because it um, accelerates fat burning. When you're burning more fat, you're making more ketones. However, so so calling it a free ride, yeah, probably actually—I mean, it absolutely is is going to help someone burn more fat, no question. Thus, if someone's priority in exercising or just life is to fat burn or keep fat under control, caffeine will help. I don't think that um, is at all question in life. Sorry.

Yeah. Yeah, no, no, no, but it's it's not—it's even beyond question um, that it's so clear, it's such a—it's so obviously helpful in that context. However, caffeine can increase epinephrine; it does—that's one of the mechanisms whereby it does accelerate fat burning. If epinephrine is turned up too much—just to sort of present the other side of this—nothing is ever all good or all bad. Too much caffeine elicits too much epinephrine; too much epinephrine does cause insulin resistance. So that starts to fall under one of the other cardinal causes of insulin resistance, which is stress. Caffeine increases the stress hormone adrenaline or epinephrine, and that can cause insulin resistance if it's elevated too much for too long. So if someone finds that they need kind of a straight source of caffeine too often, I would like—maybe just like a pure caffeinated soda—um, I would say, although coffee and other things like yerba mate, they I kind of like them a little bit too because they have other molecules that will increase dopamine at the same time, and not only does dopamine also have um, a beneficial effect for fat burning, it actually can negate the insulin resistance effect of the epinephrine from the caffeine. So different, like, if it's a plant source of caffeine, it actually usually has other things in there that will keep the the epinephrine in check, which in a good way, um, but if it's a pure kind of soda version, it won't have the other compounds that would have, say, a dopamine effect, and so you're just sort of left to the effects of the epinephrine, which again—of the caffeine stimulating the epinephrine—which you've done too often can cause problems.

Interesting. And lastly, I want to be able to touch on the other—flipping the script side of insulin—for just a second because insulin also has recovery properties to it.

Oh, yeah. And so let's just take a turn for a second and talk about insulin, a little bit of a positive light as far as recovery and exercises concerned, like where could we start there?

Yeah. Yeah. Yeah. So on one hand, it's going to recover any spent fuel, like especially glucose fuel—glycogen. So insulin is necessary to restore the glycogen in the muscle and in the liver; it's it's going to facilitate both of those processes, which is going to prepare you for the next exercise bout later. For reasons that we've mentioned in this conversation, that glycogen—that glucose—becomes a kind of high-octane fuel um, in in anyone, um, but insulin—it's it's important to tease out its effects at muscle because there is some misunderstanding there. Um, it's often—it's interesting for me as an insulin scientist to look at the now abuse of insulin as an anabolic hormone in bodybuilders—in bodybuilding competitions. In fact, you may know more about this than me. It's interesting to view—well, no, no, not the use of the hormones, but you're just more to that community where it's interesting to look at the change in body type and physique, right? If you compare, like, Lou Ferrigno and Arnold, they were very, very tapered. Nowadays, the bodybuilders—yeah, they're more jacked, but they have these enormously distended um, abdomen, and I think that's in part because of the abuse of these other anabolic hormones, like the growth hormone and the subsequent IGFs promoting soft tissue growth and even chronically elevated hyperinsulinemia potentially promoting soft tissue growth and visceral fat accumulation. Um, but insulin does not. So Dr. Shulman at University of Minnesota, I think it was in the early 1990s, published a very, very clear study using muscle cell culture, looking at the degree to which or the mechanisms whereby insulin promoted muscle growth because it does—insulin is anabolic, even at the muscle, promoting the muscle to take the amino acids and turn them into muscle protein. But what Dr. Shulman found was that insulin was not necessary for the uptake of the amino acid and the move—the conversion of the amino acid into into the the the protein. The amino acids themselves could do that. He said—what they found was that insulin promotes muscle growth because it inhibits proteolysis. So insulin, rather than looking at it as a promoter of muscle protein, it's a defender of muscle protein. Now, I don't have my finger on the pulse of this research as intimately as I do other topics; it's possible there are other lines of evidence that have challenged that, but these were extremely well-done studies looking at these labeled amino acids. And again, just to make it clear, they find that the insulin wasn't necessary for telling the amino acids to turn into muscle protein, but the insulin was very helpful at telling the muscle to protect the protein that was there. In other words, don't break down those proteins into amino acids. But that's a problem that you've seen in type one and type two diabetics. A lot of people noticed about 20 years ago that one of the common blood-based features of with type 2 diabetes was chronically elevated levels of amino acids. Indeed, the branched-chain amino acids. So they would see people with type 2 diabetes have this hyperaminoacidemia. So the branched-chain amino acids are higher in the blood. Some people have interpreted that to say that the branched-chain amino acids are causing insulin resistance of type 2 diabetes. I find that view somewhat laughable. I think the more accurate perspective is: as the muscle becomes insulin resistant, now you've lost one of the great defenders of those muscle proteins, and thus the muscle is just undergoing proteolysis more readily in the absence of this defending stimulus, and then it is leaking out more of the branched-chain amino acids into the plasma. Again, not because those are causing it, but they're a consequence of the insulin resistance, which itself is a reflection of the fact that insulin can't keep it in the muscle as well as it used to.

And I mean, would it be so far of a stretch to say that—I mean, if you're getting this anti-catabolic effect with having maybe some carbohydrates post-workout, I mean because of the insulin—like, isn't the protein going to increase insulin enough to probably do that soon? I mean, yeah.

Well, in fact, that that study—that meta-analysis that was just published that I referenced earlier—would absolutely support what you're just saying, where you have someone in a ketogenic diet who is essentially eating little to no carbs, and they have the same muscle growth and strength as the high-carb athlete. So clearly you didn't—you don't need that insulin spike. The fact is, insulin has has a rhythm to it um, throughout the day, even if you're straight fasting and not eating or drinking a single calorie, insulin has a rhythm. And for all I know, it's enough um, to keep that—to keep the normal muscle metabolism in check. But at the same time, there are other signals, like IGF—you know, when we fast, growth hormone goes up. While growth hormone itself is not influencing tissue growth, as I mentioned in a previous conversation, growth hormone will stimulate the release of the insulin-like growth factors—the IGF hormones—and those absolutely promote muscle growth; there's no question. So even if someone is keeping insulin at a relatively low oscillation by a low-carb diet, they needn't look at that and say, ah, great, there goes any of my potential gains. No, because there are other endocrine signals, like IGFs, um, which are powerful stimuli to not only promote but also keep that muscle intact and promote that muscle growth. So, but even then, insulin does have a rhythm, and you're going to get some insulin movement, which is going to help with muscle retention.

Um, one final thing, you know, when I had, you know, Dr. Mike Israetel on the channel, he was was interesting, is he uh, even though he's a fairly high-carb proponent, a lot of the things that he was saying were actually quite reasonable, in actually in line with some of the stuff you and I are talking about. He was—one, he mentioned two things uh, one that I really like that's in line—he's like, carbs are good for muscle building. Okay, why, Mike? Uh, mainly because they trigger your appetite. And like, okay, that's uh, I mean, that's honestly—that was what he fell back on the most. He's like, you know, there's a lot of—it's not wrong about that—make you want to eat more; you want to eat more. Um, but he did say something that was kind of interesting. He said, in many individuals—and you can absolutely go against what he said on this; I I'm I'm open—um, it's—you know, after a workout, bringing your cortisol levels down and getting yourself into a little bit more of a a state where you're a little more recovered and a little less amped up and possibly able to recover better. He said he's found that that's kind of the main reason he would have carbs after a workout. He tends to agree with us on the sense that you—so I'm just kind of curious because I thought, okay, I haven't seen any literature necessarily backing that up. It makes some sense; like, a lot of people feel more calm. So does that have any impact on actual recovery or muscle growth? That I don't know.

Yeah. Well, well, again, um, based on that meta-analysis, I would say that it's not needed for muscle growth because that meta-analysis looked at muscle mass in, again, in the high-carb versus ketogenic athletes and found no difference. So I actually appreciate him invoking cortisol. Cortisol is just like insulin; it is not a uniform villain. If someone has—just to make this clear—if someone has an autoimmune disease where they destroy the adrenal cortex of the adrenal glands and they can no longer make cortisol, they'll die. You need cortisol; it is a necessary hormone. Even if we want to call it a stress hormone, not all stress is bad, right? I mean, stress is how we recover; that's how we improve; that's how we challenge the norm and get better and bigger and stronger; it's through stress. So cortisol is important. However, one thing cortisol does is: if it is chronically elevated—and I can't cite the the the range unfortunately—but if cortisol really goes up, it is absolutely catabolic at muscle.

So I think it is not fair to invoke cortisol at the normal little levels; like let's say someone exercised fasted versus exercised with glucose. No question cortisol levels are going to be a little higher. Um, is that high enough to be pathogenic? No, no way, no. You're not stripping muscle at that—at that modest kind of normal physiological shift in cortisol. But I feel the need to say this, so I don't actually—so I appreciate what he said, but at the same time, I think, yeah, but I'd really need to see a study to prove that, cuz I don't think it exists. But I even still appreciate that for him if he's able to go finish and eat some carbs, he just feels a little better. Hey, you know, good for you. I don't—he also 200 and some odd pounds of solid rock and openly Juiced up, so it's like he's—he's see that when people—not to say this against him, but like we have a lot of health influencers who now are telling these overweight type 2 diabetics that they now need to be eating lots of honey; they need to be eating lots of fruit and this many carbs, and a low-carb diet can damage your body. I think, one, show me the evidence, please cite the studies if you're going to say that kind of thing.

But we're not talking about a lean, ripped influencer; we're talking about an overweight 60-year-old woman with type two diabetes. That is not the same situation, and it's this population that I think of; it's that population that I have in mind when I'm conducting my studies in my lab. It's not the guy with 6% body fat on the juice or not or whatever; that's not who I'm studying because I focus on insulin resistance—again, the most common health disorder worldwide, potentially affecting up to 88% of adults in the US and even more abroad. As much as we think, you know, it's a uniquely American trait to dunk on America and think that we're the worst at everything, and I say that as a Canadian—who—now American who's lived in six different countries and visited dozens more. Um, no one hates America like Americans—um, the way we dump on ourselves. But we even metabolically, we're not even in the top 10 when it comes to the fattest; we're not in the top 20 when it comes to the most diabetic. So this is a global problem. Those are the people I think about—um, the people that are insulin resistant, and I wish that more people with loud voices um, kind of kept that other group in mind and and just had a little bit of caution when you're talking about someone who's struggling with their food addictions. If you're giving them carte blanche, drink as much fruit juice as you want, they're going to go a little too far with it, for example.

Yeah, no, I totally agree, and just to give, you know, and in in Mike's defense, I know that he's that is his inphic, you know, he's—I agree. Yeah, and I don't mean to—I'm not throwing any shade to him. Um, I think for him, he—he can take those—them fighting words; he's able to do a lot more than the other individual would be able to. Totally, man. Well, uh, Ben, where can everyone find you, man? Yeah, yeah, thanks for the opportunity; this is great. Yeah, I primarily put a lot of my content on insulin iq.com, including um, upcoming modules and lessons people can join me with and learn from me, but then my um, Insulin IQ YouTube channel; I have a weekly metabolic classroom. People can find me there and subscribe. Right on, man. Thanks, brother. Thanks, buddy.

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Fat Tissue Scientist Reveals How to Lose Drastically More Fat by Manipulating Insulin - Dr. Bikman

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