Mind Pump: Raw Fitness Truth - 2630: Fat Loss & Optimizing the Metabolism With Dr. Ben Bikman

Episode Date: June 30, 2025

Fat Loss & Metabolism with Dr. Ben Bikman Challenging the dogma surrounding heart disease. (1:32) Is there a connection between dementia and heart disease? (12:05) Strength training and Alzheimer’s. (17:49) Learning something new helps put off dementia. (22:45) The connection between insulin resistance and your body’s inability to fight off infection. (25:17) We put TOO much attention on total cholesterol. (27:55) Fat cells dynamics explained. (30:13) Why your metabolism is EXTREMELY complex. (44:14) Mitochondrial uncoupling. (48:51) Ketones and athletic performance. (55:39) The problem with DNP. (58:11) Why he is a HUGE advocate of creatine. (1:01:03) The brain loves ketones. (1:04:33) Keep your running shoes in the closet, GO STRENGTH TRAIN! (1:05:32) The metabolic origins of chronic disease. (1:08:10) How GLP-1s are being overused and the proper way to use them. (1:14:48) The resurgence of religion. (1:37:57) As a scientist, did he ever doubt his faith? (1:41:28) The most profound moment of his life. (1:45:51) Related Links/Products Mentioned Why We Get Sick: The Hidden Epidemic at the Root of Most Chronic Disease - and How to Fight It – Book by Dr. Benjamin Bikman How Not to Get Sick: A Cookbook and Guide to Prevent and Reverse Insulin Resistance, Lose Weight, and Fight Chronic Disease – Book by Dr. Benjamin Bikman Unlock sharper focus and support long-term brain health with Ketone-IQ—clean brain fuel for deep work, mental clarity, and sustained energy with no crash. Get 30% off your subscription, plus a free gift with your second shipment at https://ketone.com/MINDPUMP June Special: Shredded Summer Bundle or Bikini Bundle 50% off! ** Code JUNE50 at checkout ** Most heart attack patients' cholesterol levels did not indicate cardiac risk Study: Doubling Saturated Fat in the Diet Does Not Increase Saturated Fat in Blood Insulin signal transduction pathway Mind Pump #1922: Fatphobia & Other Lies That Are Keeping You Fat, Unhealthy & Sick Diabulimia: Why This Eating Disorder Is So Dangerous for People with Diabetes Harris-Benedict equation - Wikipedia Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases DNP (Dinitrophenol): Overview, Mechanism, and Risks Mind Pump #2497: The Amazing & Weird Side Effects of Creatine Muscle strength and fitness linked to reduction in cancer deaths Fighting Cancer By Putting Tumor Cells On A Diet - NPR Healthy Weight Loss Maintenance with Exercise, Liraglutide, or Both Combined Attenuated GLP-1 secretion in obesity: cause or consequence? Mind Pump #2597: Before You Take Ozempic, Wegovy, or Mounjaro Listen to This! Liraglutide modulates lipid metabolism via ZBTB20-LPL pathway Mind Pump #872: Dr. Warren Farrell- The Boy Crisis Mind Pump Podcast – YouTube Mind Pump Free Resources Featured Guest/People Mentioned Benjamin Bikman (@benbikmanphd) Instagram Website Zach Bitter (@zachbitter) Instagram  Thomas N. Seyfried (@thomasseyfriedbc) Instagram Warren Farrell, PhD (@drwarrenfarrell) X/Twitter  

If you want to pump your body and expand your mind, there's only one place to go. Mind pump with your hosts, Sal DeStefano, Adam Schaefer, and Justin Andrews. You just found the most downloaded fitness, health, and entertainment podcast. This is Mind Pumped. Today, we have Dr. Ben Bickman on the show. He's a biomedical scientist and professor at BYU. Now he specializes in the study of metabolic disorders. He's an author of two books, Why We Get Sick and How Not To Get Sick. In today's episode, we talk about the metabolism, fat loss, insulin sensitivity, and the value of ketones. In fact,

today's episode is brought to you by Ketone IQ. You can take this and regardless of whether or not you're on a ketogenic diet, you will have ketones that you'll be fueling your brain and your body. When I use these, I feel sharper in my thinking. I often use them before a podcast. Go check them out. Go to ketone.com forward slash mind pump to get set up by the way that'll get you 30% off your subscription Plus a free gift with your second shipment again. It's ketone.com forward slash mind pump. That's Ketone.com forward slash mind pump now We also have one day left for the June special the shredded summer bundle of programs in the bikini bundle of programs are 50% off. If you're interested, you go to MAPSFitnessProducts.com and then use the

code June50 for the discount. Here comes the show. Ben, welcome to the show. Thanks, Sal. I'm glad to be here. Thank you. So let's start with, so you've got some great information, controversial some of it, because some of it kind of counters what we would consider common medical practices, especially in regards to things like heart disease and cholesterol and stuff. Let's start with heart disease.

We'll go with the easy one. Yeah. What have they got wrong about it? What do we look, how are we treating this in the wrong ways and what can we do about this? Yeah, yeah, so definitely starting with the doozy. But appropriately, heart disease is the leading cause of death. So clearly, I would say what we're currently doing isn't working. So we ought to be challenging the dogma here, right?

This has been the leading cause of death for decades now, all in the midst of vilifying dietary fat and cholesterol. Now, of course, everyone here remembers that I'm a scientist, not a clinician, but that gives me a pretty unique perspective because I'm not going to be swayed by any other influence but the data. And so, my sentiments on this is just born purely from what does the research suggest. So, since the 1950s, we've been embracing a low-fat diet. In the midst of all of this, heart disease has just skyrocketed. Mind you, so has every other problem with chronic disease. What they've gotten wrong primarily is looking at LDL cholesterol as a

singular cause of heart disease. Now, even the most proud cardiologist would have to admit that we don't actually know the step-by-step process of atherosclerosis. That is the term for the blocking, the plaques that accumulate in the vessels of the heart. We don't know. You know, as much as people make these ardent claims of this causes heart disease, actually there's a lot of speculation involved. But the prevailing theory is LDL cholesterol goes up in the blood, it starts to accumulate in the blood vessel wall, and now you have a plaque. And it is just far more complicated than that. But what we know for

certain is that LDL is a terrible predictor of who's going to have a heart attack. In fact, even here in kind of your backyard, at UCLA there was a study done years ago, and they looked at, I think it was over 190,000 people who'd come to the UCLA hospital with a heart attack. You know, a pretty hard outcome, so absolute confirmation that they had heart disease. And then they looked at the LDL levels of these people across this entire spectrum and it was an absolute bell curve with as many people having LDL levels below the threshold that would be considered ideal as there were people who had LDL levels above the threshold, suggesting that it had no predictive power. So for the sake of maybe just

brevity and answering the question quite clearly, the traditional view has been you eat more saturated fat, your LDL cholesterol is going to go up, and thus you have more heart disease. The first part of that assumption is pretty consistent. If someone eats more saturated fat, it's not uncommon that their LDL will go up, but not always.

That's very important. In the context of a calorie surplus, right? I mean, what if you're in a deficit? Yeah, or what if you cut your carbs? So Dr. Jeff Volek, a ketogenic diet expert, he documented in a very compelling study where he was stepwise increasing saturated fat while he was decreasing carbs and the blood lipids of these people looked amazing. Things got better, including the amount of saturated fat in their blood was actually less. We just have a very simplified view of all of these variables. But that last step that the LDL cholesterol is then causing a plaque to form, that's where it just goes off the rails. a plaque to form, that's where it just goes off the rails. If there is, if there's any, again, which is identified or revealed in the evidence suggesting that LDL is not a great predictor of who's going to have a heart attack. Even in someone, if you give someone with a high

LDL a statin, a medication to directly lower their cholesterol, you will, if it is used as a primary prevention, so a person who has not had a heart attack, there's virtually no benefit to that at all. That it doesn't work to just wage war on their cholesterol, but there's a consequence to that because cholesterol is a molecule of life. Every sex hormone comes from cholesterol. Every cortisol comes from cholesterol, which is a hormone to regulate blood sugar levels. Aldosterone, a hormone to regulate body salt and body water. Vitamin D comes from cholesterol. So the more we… it's no surprise that as we have vilified this molecule of life, life gets, I would say, a bit worse in many people. And maybe to have any kind of olive branch on the topic, the only time I believe the evidence suggests that a cholesterol

lowering medication, like a statin, is warranted is if a person has had a coronary artery calcium scan, so a CT scan of their heart. So they lay on the little bed, they got the little camera rotating around them at a high speed, it's taking all these 360 degree images of the heart just to measure the amount of plaque in those heart blood vessels. If they have a relatively higher amount of plaque, statins appear to convey some degree of mortality benefit. But again, that is totally independent of LDL levels. What about the data on, because I've heard this repeated,

that if you've had a heart attack, that then the statins can potentially have an effect. That's excellent. That's a very, very good follow-up from what I mentioned earlier. Where earlier I had said, if it's used as a primary prevention, someone who's not had it, no benefit.

If it's a follow-up, it looks like there is a benefit. But that first point, in women, statins appear to be an overt harm in the case of, like if a guy goes on a statin, yeah, it might not be great for him if he's never had a heart attack. But if a gal goes on it, her risk of developing type 2 diabetes goes up by 50%. Wow. It is a meaningful risk. And so guys, the risk is a little less, although we also have a bigger hit to our libido, which

starts a little higher than in our female counterparts anyway. We feel that hit on the sex hormones a little more than the females do, but they get the hit when it comes to metabolic health. Could it be that, because I've heard this expressed before, could it be that the LDL is not causing things, but rather a symptom? In other words, when you see this plaque build up and then causing a blockage, for example, could the root be something like inflammation?

Oh, yeah. Is your body essentially using it like spackle to strengthen arteries that are in flames? So it's trying to use it as a bandaid. Yeah, yeah. So Sal, just to kind of present a little metaphor to that, this would be, so perhaps the traditional view of heart disease is that, or would be analogous to, we drive around San Jose and we find that every time we drive by a burning house, we see this big red truck with these flashing red lights.

Every time, hey, those big red trucks with the flashing lights must be causing those fires. So that would be analogous to saying, well, we have a plaque and we see LDL, so LDL's causing the plaque. If however, like the fire truck at the burning home, maybe the LDL is there in response to an injury. And so that brings up the idea of yes, inflammation, but also infection. Most people, this is an entire, a legitimate perspective on the origins of atherosclerosis. Remember, we don't actually know how this happens. So there's all these theories. One of the theories is that it's an infection of the

vessel, because if you go in and remove the plaque, you can take it to a lab and find like a dozen infectious bacteria at that plaque. So it's basically an abscess or a little pocket of infection. And LDL has the unique ability to scavenge infectious agents. So LDL literally acts as an anti, not literally, I shouldn't say literally, I'm around 20 year olds too much. It acts a bit like an antibiotic.

It will literally, and now I'm using it deliberately, it will literally bind infectious pathogens like a molecule called lipopolysaccharide, which is something that can invade the body through what we breathe in or more often through our intestines. When people talk about leaky gut, a lot of what's leaky is the invasion of this this bacterial particle that will elicit a strong immune response. LDL will bind LPS and other infectious pathogens, take it to the liver to be dumped out into the intestines. So LDL is acting like this scavenger, in fact a part of this process is called scavenging,

and it will bind these harmful infectious pathogens. What if LDL is there to try to, like you said, to clean it up? Shuttle it out. Rather than causing the problem, maybe it's trying to remove these infectious pathogens out of the plaque. Almost like it's also encasing it to prevent it from going anywhere else or causing any more damage. Yeah, yeah, so we do have an encasing of cells and then the LDL I would say is trying to almost

rotor root it out. To use your example of a fire truck, would this be a good way to explain that? So you keep getting fire trucks, the house keeps catching fire, eventually everybody dies from getting flooded. Because there's too much water. And so like the flood killed everybody. So could it be that the problem, okay yes, the plaque does build up and block you off,

but that's not the real issue. And yes, that did kill you because you were blocked off, but it's the fire truck essentially throwing water on it constantly, now you got flooded. We're not treating the infection. Yeah, yeah, that's right. So there's multiple ways to look at it, but in fact antibiotics use can reduce the risk of infections. Now I'm not recommending people just start wildly taking antibiotics for various reasons, but Sal, yeah, I think there's probably some value in that metaphor, but

again the LDL particles are not actually lining the capsule, there is a layer of smooth muscle that starts to grow over the root or the core of the plaque. LDL is going to be more central to it. If it is anywhere there at all, it's going to be more central, but that's just reflective of LDL's ability to move around and to wiggle through spaces. I have a question I think you'd be a perfect person to answer because

you're talking about this potentially being the root being an infection or bacteria. One theory. Yes, okay. So I'm also reading, yes, a theory. I'm also seeing studies now connecting this to potentially to dementia, Alzheimer's, is there a connection between dementia and heart disease? Do people one or the other have a higher rate of the other one? In other words, because I've also read this that people with gum disease have a higher rate of these things. Potentially the bacteria is entering through the through the gums. Yeah totally. Okay, is there a correlation to them? So that last one you just

talked about is super strong. And it's just for the reason you mentioned, still again playing on the idea that perhaps the origin of atherosclerosis is infectious bacteria, and in this case entering through the oral cavity through the mouth because of infection. That evidence is super strong. And extremely compelling data suggesting

that people who floss have way lower rates of heart disease, and it could just be because they have better oral health. Yeah. Then the connection with heart disease and dementia, that starts to get, I would say there's one layer deeper, but maybe I'm pulling it that way because now I can bring in my real strong suit as a metabolic scientist, and that is probably

a common core of insulin resistance, where you do see these epidemics. What I call the plagues of prosperity, heart disease, Alzheimer's disease, type 2 diabetes, these are problems that were once unheard of and have now, they're the most common causes of death. What they all have in common is this metabolic problem called insulin resistance. And in the case of heart disease, if a person's insulin resistant, they will have more vasoconstriction and they will have a much higher blood pressure with the heart beating harder and faster, which can result in some sheer damage to coronary vessels and other vessels, which starts to create this recovery inflammation

process, which could contribute to the plaque formation. On the other hand, with Alzheimer's disease, which is now increasingly called type 3 diabetes, you guys have probably heard that term. I actually don't love the term. I think it's a little misleading. I appreciate it because it points the finger at a metabolic problem, but the more accurate term would be insulin resistance of the brain. To varying degrees, like muscle, you know, I'm in the right place to talk about muscle. Muscle wants to eat when it's going to play nice with the rest of the body, because there's so much muscle on the human body that if the muscle just ate whenever it wanted to, everything else would starve. So, it needs to be told when to eat, and insulin is a signal that tells it when to eat.

So right now as we're sitting around chatting, if insulin goes up, it tells the muscle, hey, it's time of feast, why don't you get some and I'm gonna feed some other tissues at the same time. Insulin comes down, and then the rate at which the muscle is eating drops a lot, especially with regards to glucose. And so to a varying degree, brain, in the regions of the brain that are involved in memory and cognition, it has the same glucose transporters that muscle has, which is a door waiting to be opened when the insulin comes and knocks on it, and that is the glucose transporter number four, or glute four. So muscle has glute four of these glucose transporters, which will open when insulin comes and knocks and tells it to.

Other tissues, like the liver, will have Glute 2 or the other regions of the brain will have Glute 1. Those are open doors. The moment glucose comes up, it's going to go into those tissues. No matter what. No matter what. Glucose rises, it just spills into the tissue.

Muscle, again, there's so much that if it were able to do that, it would eat it all and the rest of the body would just starve. The brain, again, has a region, has regions that are like the muscle where it will only eat if insulin tells it to eat, but then that gets back to the problem. What do you do if those sections of the brain have become insulin resistant? Now, insulin is knocking on the door of those nerves and telling the neurons, hey, it's time to eat, but the door's not opening. And so the neuron starts to go hungry unless it has something else to eat like ketone. That's the primary other fuel, but I don't want to get off topic. But yeah,

so when you look at the origin of trying to find a connection between heart disease and Alzheimer's, what would seemingly be unrelated, and before we went on, we were talking a little bit about migraines. You guys, you can pick almost every… I don't want to be too dramatic here. Almost every neurological disorder, Alzheimer's disease, and long before it's even Alzheimer's, cognitive decline, we'll say, Parkinson's, epilepsy, migraines, bipolar disorders, and others I'm not recalling off the top of my head. What they all have in common is a phenomenon known as brain glucose hypometabolism. In every single instance, it has been documented in humans that in each of those brain disorders, the brain is not getting and metabolizing as much glucose as it does in the person who

doesn't have those problems. And insulin is the great bouncer, it's the great escort moving the glucose in to the cell to be burned for energy. But unfortunately, in insulin resistance, the overall disease state in the body, that most common metabolic problem, and insulin resistance is the single most common health disorder worldwide. I did my fellowship research in a beautiful country called Singapore before I got hired as a professor at BYU. Why on earth was I in Singapore? Because they actually have higher rates of type 2 diabetes and insulin resistance than we do in the US. And so it doesn't matter where you are, insulin resistance is going to be the main problem and it contributes to even cases of dementia.

Do we see, so does, because I know strength training will get those Glut4 receptors open, does it up regulate those? Does it increase the amount of receptors you have? And if so, how do you do that for the brain? I've seen some studies on strength training and Alzheimer's, actually one of the best forms of exercise it seems to be for that. Is it because that it has a similar effect to the brain when you're strength training? Yeah, that's a great question.

So to touch on the muscle, I'm really, really glad you brought that up. The muscle, when it starts moving, gets so demanding that it has a way of telling insulin, hey, I don't need to wait for you, I'm just gonna take care of this myself, at the risk of sounding silly. You can tell I teach 20 year olds as a professor.

That's right, it's great. Yeah, so yeah, the muscle, its energetic demands go so high that it can no longer wait to be told what to do. It just says, I'm taking over. And it will start greedily taking in anything, especially glucose. So yeah, the moment you have,

in fact, if just for the sake of the, for fun, we can go a little molecular into the muscle, the biochemistry of it a little bit. Normally, when insulin comes and binds to the muscle cell, there are a series of events, what we commonly call the insulin signaling cascade. One protein activates another protein, activates another protein, activates another. You'll eventually get to a protein called AKT. AKT will then, which also actually activates mTOR, which promotes muscle growth, but that's a different pathway. When you get to AKT, you can actually branch into a lot of ways, but there's no mTOR activation if there's no AKT preceding it. So any conversation of mTOR, everyone ought to be thinking about AKT to some degree. But the insulin signal will go to AKT and then it will go to Glut4 and it will tell

Glut4 to move to the edge of the muscle cell and open up the doors and allow the glucose to come in. Now, back to AKT, when we have a lot of muscle contraction and relaxation, you flood the muscle cells with calcium. That's actually how we're initiating the cross-bridge cycle, which I don't know whether you guys have talked about that before, but anyway, the dynamics of contracting and relaxing the muscle. You get a lot of calcium there. Calcium activates its own enzyme called camkinase, which then activates AMPK, the opposite of mTOR,

which activates AKT, and we're right back to AKT, which tells Glut4 to go out. So that's the process of the muscle contraction, which is important. Just as an aside, exercise is antithetical to insulin. When you start exercising, insulin comes down fast, because insulin wants the body to store energy. That's its main thematic effect at every single cell of the body, even tissues where insulin isn't dictating the uptake of glucose like it is at the muscle, it's still telling the cell what to do with the energy. And it's, again, thematic effect is store energy. Well, when

we're exercising, we don't want to store. And you just need less insulin now. We want to be breaking down. Yeah, we don't need the insulin. Because the muscle cells are saying insulin, if insulin's up, it's also going to want to be storing energy in fat cells, because you cannot store energy in fat cells without an elevated insulin. It is impossible. We got to talk about the fat cell, because the whole view is that it's just purely calories. Now we can prove that wrong really easily. But back to the muscle, the muscle doesn't want insulin to feed everything. The muscle wants to eat and it can do it on its own. But now back to the brain, I'm unaware of any evidence suggesting you can force glute

forward to the membrane like you can with a working muscle. But the solution then is, I guess, multiple angles here. One would be to just improve insulin sensitivity. If you can improve insulin sensitivity in the body, then the brain neurons will start responding to the insulin a little better. But at the same time, as you improve insulin sensitivity, your insulin will come down. And when insulin is down, you burn more fat. And when you burn more fat, you make more ketones. And ketones are an unregulated fuel for the brain. As the moment ketones come online into the blood, the brain will immediately start taking it in. And just to put a fine point on that, people have been, we've been trained at a high level to say that the brain needs 120

grams of glucose. That is absolutely not true. Then another lie will be that the brain prefers glucose. Well, that's not true either. Because you can take a human who has a glucose level of about 5 millimolar to use metric units, and then take a... and the ketones will maybe be half that, 2.5 millimolar ketones, and the brain will already be getting two-thirds of its energy from the ketones. So in the presence of... you could have glucose and ketones, your brain's gonna use ketones. Yeah, absolutely amen, exclamation mark. And again, I'm so confident in saying that

because you can take a human body with half the level of ketone as glucose and it's already getting twice as much, twice as much energy coming from the ketone. And again, that's unregulated. The moment ketones go up, the brain just is pulling it in. Could, okay, because we do know that the brain is plastic and it does, for lack of a better term, build.

Yeah. Okay, so learning new things. Yeah. And exercise in general, movement in general, especially the more complex it is, you're gonna create new neural connections or whatnot. Sure, yes. Could that then also, theoretically,

would that open those glute four doors? No theoretically it could I'm not aware of any evidence But if you were to say what is it then been about learning something new that helps put off dementia because it does that's right It does the evidence is really clear these that's where I'm pointing to yeah Yeah, I mean maybe it is because you are getting the sort of brains version of the muscle contracting. I mean, I'll say one of the reasons I started learning to play the piano again, about five or six years ago, was seeing one of my grandparents go through terrible, long, drawn out Alzheimer's disease. It was so terrifying that I thought, all right, I got to start,

I got to start learning Russian again, the challenge of my brain, I got to start learning how to play the piano again, just to find these things. And of course, I want to keep exercising. I would say the main, but even exercise, a point worth talking about is when you are contracting and relaxing the muscle, you have the creation of brain-derived neurotrophic factor, BDNF, which helps with neuron regeneration and strength, just helping enhance the plasticity of the brain. So there are direct connections, I wouldn't be surprised at all,

to find in the coming years that we learn of more, but there are direct hormones that the working brain, what's called myokines, sorry, the working muscle, myokines, these muscle-derived hormones, facilitate improved brain metabolism. Yeah, it's like, BDNF, it's like anabolic steroids for the brain, essentially. Well said. And exercise is a great way to bump it up. You were talking about the calcium process or calcium's role in contracting muscles,

and you talked about how that led to mTOR. Do calcium channel blockers then cause issues with that process? That is a great question. So people will use a calcium channel blocker to control hypertension, for example, because it will make the heart, the myocardium, beat a little softer. You know, I don't know. It wouldn't surprise me. I don't know. The heart does have distinct calcium channels compared to skeletal muscle. Maybe it's specific, but it wouldn't surprise me. I know as a trainer, when you would see someone on a calcium channel blocker, you'd have to be careful with their heart rate because it wouldn't come up as high.

Well, and I wonder whether you got to be careful with just muscle weakness too. Honestly, I don't know. I can't believe I've never thought about that, but it wouldn't surprise me. Yeah, yeah. Interesting, interesting. Okay, so through exercise, you could help this process. We talked about insulin sensitivity, improving that. We also talked about potential theory with bacteria.

Are we talking about potentially a perfect storm then? Because I can't imagine that a hundred years ago we weren't introduced to these same bacteria, but this heart disease explosion happened after that. So could it be just the combination of the two? And what's the connection between insulin resistance and maybe your body's inability to fight off infection? Yeah, yeah, so part of the problem, I'm totally speculating now. This is a great question. Part of the problem could be that perhaps

we're living in a day and age with lower cholesterol levels. As we have become so fatphobic, it's possible that we are getting to a point of too low of cholesterol, and that might be depriving the body of a natural scavenging system like I mentioned. Again, LDL cholesterol does have the ability, in another universe, in another timeline, the scientists who discovered LDL as potentially being relevant in heart disease discovered it in the context of immunity. And it would have been given a different name and it would have been acknowledged because people with the lowest levels of cholesterol die the most from infections and

die the most from anything. Cancer. Yes, cancer, blood-based cancers especially. But the risk of dying from infections goes up like 20 times in people with low cholesterol levels. So maybe part of it is just our fat phobia has resulted in a fat aversion, particularly very nutritious, natural saturated fats, resulting in ever lower LDL cholesterol depriving the body of a natural immune presence. When we combine that with the insulin resistance, which has become again the most common health problem, insulin resistance compounds these issues by, in a handful of ways. I mentioned the hemodynamics, the influence of insulin resistance on blood pressure and the caliber or the diameter of the hemodynamics, the influence of insulin resistance on blood pressure and the caliber or the diameter of the blood vessel, but insulin resistance also does tell the liver

to create a lot of saturated fat. And I am a great defender of dietary saturated fat, but that is not to say that saturated fat in the blood is benign. There's evidence to show that, in fact, one of the biggest cited publications I've ever had as a scientist was a paper that looked at how saturated fats actually promote inflammation. But that has led to some people saying, well, then don't eat saturated fat. Right, but there's a difference. There is a huge difference. Where again, in that stepwise study I mentioned by Jeff Volek's group, even this group was eating about three times more saturated fat in the diet.

And they had lower levels of plasma saturated fats than the group eating the lower saturated fat. Because most saturated fat in the blood comes from what the liver is being told to make. And when is the liver told to make fat? When insulin goes up. Interesting. This is also, I mean, by the way, statins for people who don't know, I mean, it just tells the liver

to make less cholesterol. That's right. Eating dietary cholesterol has very little effect on how much cholesterol. It's like no effect. Yeah, I mean, all it does, if you start eating more cholesterol, it just tells the liver to make less. If you stop eating cholesterol, the liver just starts

making more. Now, what does a guy like me do? Because I eat a lot of red meat. I mean, I have a whole does a guy like me do? Because I eat a lot of red meat. I mean, I have a whole food diet. I exercise regularly, but I eat a lot of red meat, a lot of, you know, saturated fat, no problem. My cholesterol is always low. Yeah.

Do I need to worry? It's like 135 is my total always, no matter what I eat. Should I then be worried because I have such low levels of cholesterol? Yeah, yeah. I mean, no, I don't think so, but there's certainly, my view is we've put too much attention on total cholesterol. Period. Period. In fact, if anyone, if I could give anyone a takeaway, even just from this part of the conversation so far, it would be to look at your most recent blood test and look at a ratio that you're not going to get from the blood test, but you are going to get

the two components of it, which is take the triglycerides number. You're going to have been given your triglycerides in milligrams per deciliter, divide that by the HDL number, which is also going to be in milligrams per deciliter, and that ratio is going to be the single best value for understanding your risk of not only heart disease, but even insulin resistance, where in a Caucasian cohort, if your number is less than 1.5, that's a good sign that you're doing fine. If it's above, that's a warning. If it's higher and higher, up to three to four, then be really concerned. And then in blacks, I think that number is closer to two, that ratio gets to be two. Then in Hispanics and Asians, I think the ratio gets closer to one. So anywhere

between one to two, sort of all the ethnicities are going to fit somewhere neatly in there. The lower the triglyceride to HDL ratio is, the better. Very interesting. Okay. So you said something that I want to go back

to because I think this will be a very controversial topic. You were talking about how insulin plays this huge role in fat storage and it's not energy, not calories. Oh, I was hoping you'd get that. Yeah, so explain this. I put that out there as a teaser.

Explain, yeah, explain this to me, because I'll tell you what my opinion is. Please. I strongly believe, I think that we've oversimplified, completely oversimplified things like the metabolism and calories in versus calories out. I think it's oversimplified. Oh yeah.

I do think it plays a role, but you could take someone, I know this, because I've had many clients do this, you could take somebody, keep them on the same calories, change the hormone profile through hormone replacement therapy, they get leaner. So it's a hormone signal, calories haven't changed, they got leaner, and they built the little muscles. So obviously hormones play a role,

but calories got a two because you can't create energy out of thin air. So am I on the right path here? Oh man, yeah, let me go. Let me unleash me here, yeah. So the fat tissue is the, of all the tissues of the body, that's probably the one I'm most comfortable talking about. Having, like in my lab right now, back at BYU, we have fat cells growing in a little Petri dish. We are studying fat metabolism from the fat tissue of rodents. We even take fat biopsies from humans to study

right from the subcutaneous space of the belly. So I am very comfortable talking about fat cell dynamics. I'm just laying it out there as just to sort of establish some authority on the topic. Let's go back to the fat cells growing in culture, and I promise I'm answering the question in a roundabout way. We will have adipocytes or fat cells in a little Petri dish, sticking to the bottom of the dish, swimming in a sea of calories. They got all the fat, all the glucose they could ever want, and yet they don't grow at all. They're these skinny little fat cells. And then the moment we add one thing into that little culture bath, then they start to grow, and that is insulin. So, maybe one more example just to really put a

fine point on it. There is an eating disorder called Diabolemia. Have you guys ever heard of it? We did. Just about earlier. I heard you speak on a podcast about it. You can hear the word diabetes in there. I told you guys. It is absolute, definitive proof in a human that if you remove one single hormone, it becomes utterly, totally impossible for that body to not

only gain fat but retain even a scrap of it. So in diabolemia, the problem is, and imagine the temptation, everyone listening at home, as I described this, imagine the temptation. Imagine you are a young teenage girl, let's say more susceptible, but even boy, young teenager, you have an insatiable appetite. You can eat whatever you want and you just keep getting skinnier and skinnier. Now you feel miserable, you're peeing all the time and then all of a sudden you get put on your insulin therapy and by the time you leave the hospital, assuming it got that bad, within just days you've've gained so much weight, you can't even wear the same clothes you went in on. And so you learn and you start to look at your insulin shots as your fat shots, which is what some type one diabetics call it. And they learn

that they can eat whatever they want. I mean, thousands of calories in excess, and all they have to do is deliberately under dose their insulin and they can be as skinny as they want. They do, and it's okay, so now I understand the term. And they will! So this is literally an eating, essentially it's a body image disorder. Yeah, yeah, so like a body dysmorphia. Yeah, so you can tell from the term, I tell my students when I talk about metabolism and the nature of obesity,

I, mind you, I have to talk about it carefully because some of the students are stupid and susceptible to dumb ideas, I'll say, you'll look great But you'll die. Mm-hmm, but but you'll look great in your coffin You'll be as thin as you want, but you'll die from hyperglycemia and ketoacidosis Yeah, cuz cuz cuz insulin doesn't just tell fat cells to it shuttles nutrients into me It dictates all of them. That's the thing that people don't appreciate insulin. One of the reasons I'm so devoted to studying it, it is unlike most peptide hormones in that insulin will, again literally I'm using the term deliberately, literally affect every single cell of the body. There are

very few hormones that have that breadth of effect and the thematic effect is telling the cell what to do with energy no matter what the cell is. And so with fat cells, insulin is absolutely essential to the fat cell growing. So the whole idea of thermodynamics is interesting. It's interesting to look at the history of thermodynamics as a discipline in physics. Its origin story is actually in pursuit of a perfect steam engine. That's the origin of thermodynamics. How can we build a steam engine that most perfectly captures the energy, boiling the water, creating steam, turning a turbine and moving the locomotor? How can we do that? So those ideas then started to bleed into biology in an effort to understand how, well, human obesity. And that led to what is

absolutely an oversimplified instance of, well, it's just calories in, calories out. We just disprove that right now, which is if you take out one single hormone, which is just insulin, the human body, it is utter, in any animal, from fruit flies to humans, it doesn't matter. If you take out the insulin in every animal in between, they cannot hold on to their fat. So use this special population. This already proves that's not the case. By the way, side question, they have too low insulin to use any of that energy. Where does it go? Oh, excellent question. So I promised I would get to that. So here's maybe the summary, then I'll talk about how to

reconcile these two things. Because I'm not saying energy doesn't matter. Just like how you kind of pitched the question, and I'm knocking it out of the park here, the energy has to be accounted for. But our view is so simplistic that we fail to have the brain option to account for it. So there must be a signal that tells the cell to store that fat, insulin, but then there must be the energy to store. So insulin is the signal telling the fat cell it's time to store energy. Calories, or more accurately, the carbons that we call calories, those carbons then act as the fuel for that growth. That is what we start to store in the fat cell. If it's glucose, no problem. The fat will turn it into a fat.

If it's straight chains of fatty acids, no problem. The fat cell will just link it up into triglycerides. So regardless, insulin will tell the fat cell to make more triglycerides and to hold onto it. So how do we then reconcile this? If we wipe out the insulin, but the calories are still high, how on earth can we put the fat cell in a state to start to shrink? Where does the energy go? Three mechanisms. If I can

think through these and articulate them as I'm just imagining it off the top of my head here. I'm not imagining them. I'm just going to try to explain it in an articulate way. One would be the impossib- in fact, two levels. One is the fat cell, one is the body, then the body has two levels to it. Energy and ketones at the body. And so, let's start with the fat cell. So, with the fat cell, the biochemistry of the fat cell is such that insulin is necessary to block the breakdown of the fat, that process called lipolysis, what people often call fat burning. That's not fat burning, it's fat breakdown. Insulin stops that, it even modest increases. Even a modest little bump in insulin will tell the fat cell to lock down and stop breaking it down.

And you see this in a blood marker called free fatty acids. If you look at free fatty acids, it's a perfect inverse relationship with insulin. Insulin goes up, free fatty acids, which is the product of fat burning or breakdown, goes down. Insulin comes down through fasting or a ketogenic diet, free fatty acids go up. Okay, now with the whole body, any student listening who is a student of physiology,

you got even somebody, I remember years ago when I got ACSM certified as a personal trainer, we learned about the Benedict equation. The Benedict equation was named after this famous energy scientist named Francis Benedict, and he documented, he outlined this algorithm that could predict metabolic rate. He collaborated in the early 1900s with with Elliot P. Joslin, the godfather of modern endocrinology. I just say that because any students that are listening to this, these are legends. Joslin and Benedict, they came together, they put their brains together in this perfect merger of brain power to study the metabolism in what they called severe diabetes or just type 1 diabetes, untreated

at the time because there was no insulin. Benedict found that in these people with severe diabetes, their overall metabolic rate was about 20% higher than it should be. Interesting phenomenon. So the body was just, the engine was idling a little higher than it should. So everything was just running a little hotter, a little more metabolism, more metabolic rate, for no apparent reason. It's just wasting energy. In the 1980s, I think it was 1984, a group at the University of Minnesota, not a direct follow-up of this study, but it's a good, it is a good follow-up, they took people with type 1 diabetes and first of all, confirmed the finding from about 70 years prior. And then they gave the type 1 diabetics insulin and minute by minute metabolic rate started to drop. So insulin, in other words, has a whole body metabolic effect

at dictating the metabolic rate. Insulin is low, metabolic rate goes up. You're sort of pressing the accelerator. Insulin goes up, metabolic rate goes down. So that's one component that happens at the whole body level. But then the second component is one that no one ever captures, which is the ketones. So when insulin comes down, the overall hybrid of the human body, which is shifting between glucose and fats primarily,

when insulin goes down, fat burning goes up. And when insulin stays at a relatively low level for 12 to 16 hours, the body has begun burning more fat than it knows what to do with, that more than it knows what to do with is essentially ketogenesis, where you have the cells of the liver most especially, it's burning more fat than it needs, but it can't stop burning fat because the low insulin is not letting it stop burning. So that turns into ketones. Now everyone would say, okay, well that's a ketogenic diet. What people don't appreciate is that every ketone has a caloric value roughly similar to

glucose. Now with that view in mind, it starts to create some resolution because when we're in ketosis, you are breathing out ketones and you are urinating out ketones. Think of those as calories. You are literally dumping calories from the body back out into the atmosphere. So being in ketosis results in a, for lack of a better term, faster metabolism? Well, yes, faster metabolism for the reason I mentioned

a moment ago, which is when insulin is low, metabolic rate is higher. Well, you're just burning more because you're wasting more. You're getting rid of more. So there's two. So you're burning more in the context of the body having a higher metabolic rate, and it goes to about 200 calories a day higher. It's a big deal. It is a big deal.

That's 30 minutes on the fricking stair step for hell's sake. I don't want to do that. I'd rather just be in ketosis. But then at the same time, now you're... so that's a higher metabolic rate, but when you combine that with the wasting of the ketones in the breath and in the urine, that's another additive bump. So now you are burning more and you're wasting. And it's the wasting that no one ever talks about or even quantifies. That can be up to a couple hundred calories a day as well. So that's why if someone's on a ketogenic diet, I've been a defender of this term, you have a little more

metabolic wiggle room. And thus attempting to reconcile and counting calories becomes a bit of a fool's errand because mind you, first and foremost, you can never perfectly capture metabolic rate in a human. You can never perfectly capture how much calories they're actually consuming and what's actually getting absorbed and the thermic effect of absorbing it and digesting it. There's so many variables that go into it that my view on the fat cell and obesity is, in fact, I'll articulate it this way. The goal of someone who wants to lose weight is they want to shrink their fat cells because that's weight loss. You don't kill your fat cells, you just shrink them. They have two steps they can take. They can take

the low calorie step, or they can take the low insulin step as their first step. And they're not the same, although they start to overlap a little bit. My problem is the traditional caloric view of obesity is they just say, I'm going to cut my calories without addressing their high insulin. The problem with that view is if you stop energy coming in, but insulin is still a little elevated, which is pushing the energy into storage, your blood nutrients go down. Glucose will go down, ketones will go down. Those are the main fuels for the brain. The brain starts to go hungry, and if the brain goes hungry, the body's hungry, and

hunger always wins. This is why you'll never see a reunion tour of the Biggest Loser game show. That's right. Oh, yeah. They gain it all back. Now, I'm not saying there's no value in looking at energy and scrutinizing it, but it shouldn't be the first step. At least my view is the first step should not be I'm just cutting my calories because

you're going to get hungry and hunger always wins. Let the first step be I'm going to lower my insulin by carefully controlling carbs. Now, I just mean be smart about carbs. Basically, with controlled carbs, the simplest level to that is if it comes in a bag or a box with a barcode, just eat less of it. Whole fruits and vegetables, eat them, enjoy them. Eat them, don't drink them. I mean, depending on where you're starting, you know, if I'm talking to an overweight, type 2 diabetic, eat those fruits and vegetables, don't drink them. I mean, depending on where you're starting. If I'm talking to an overweight type two diabetic, eat those fruits and vegetables, don't drink them. If it comes in a bag or a box with a barcode, don't do it.

So lower your insulin, which is going to not only improve your insulin sensitivity and reduce your risk of heart disease and Alzheimer's disease and infertility and whatever, but it will increase your metabolic rate. And it will start making ketones, which you're wasting from the body. And then you'll get to a lower plateau if you need to start controlling calories at that point to get further fat loss, alright now let's start looking

at your... And or build muscle. This is such a perfect segue for and you're the perfect person to have this conversation with. We have this ongoing debate with people online and it drives all of us crazy. So I can't wait to hear how you articulate this. There's a, there's this argument that, uh, muscle burns about two to four more calories a day per pound than fat does. Yet in our 25 plus years of training thousands of clients, um, we have story after story of the client who comes in who can't lose any weight, only eating 1800, 1900 calories or so, and they need to lose 30 pounds or

40 pounds of fat. We don't move the scale. I dropped that person 15 pounds of fat, add 15 pounds of muscle, their scale doesn't change. That person is now eating 2800 calories. Oh yeah. 15 pounds of muscle, their scale doesn't change, that person is now eating 2,800 calories. Explain that to me and make that rational to the person who is trying to argue that, oh, just adding a pound of muscle is only burning this many more calories. It's not that simple, there's so much more going on.

I've added four pounds of muscle in a client, seen their metabolic rate jump 600 calories from tracking and our argument's always been metabolism is extremely complex. So trying to break this down and simplify it. Yeah. So, okay, let me attempt my own approach to this. So I can state definitively, I mean, we will

literally, from humans, take a fat biopsy from their belly, take a muscle biopsy from the vastus lateralis, put it into a metabolic chamber and literally measure, like at the vastus lateralis, put it into a metabolic chamber and literally measure at the picomolar level, the amount of oxygen it's using, which is to say the finest measurement of metabolism. You put a piece of fat tissue in there, it's metabolic rate, and I'm just going to cite the units we use here. It's using about one to two picomoles of oxygen per second per milligram of protein.

I mean, almost to the point that even in my instruments, you can barely detect it. Like you have to zoom in to detect it. So extremely low metabolic rate. You put that exact same amount of muscle in there, it's easily gonna be 10 to 20, 30 times higher metabolic rate where you have to change the scope again to now measure the muscle.

And so muscle, at that level at least, at a static state, because the muscle's not working, right, because it's just sort of an inert tissue now, I mean kind of dead if you will, we've pulled it out of the living tissue, it is 10 to 20 times higher in its mitochondrial metabolic rate. That is pretty relevant. Now, when you combine that with the fact that fat will never increase its metabolic rate, although let me come back to that because we actually have studies that challenge that, but muscle can. Right now, our muscle mass is, our muscle is burning that, or consuming the oxygen, breathing, or having a metabolic rate at around that 20 to 30 picomoles

of oxygen per second. But if we got up and went to the gym, oh, okay, now we've 10x'd that. So muscle, so all of that just touches on the metabolic grade component. But even aside from that, if we come back to the endocrine or hormone component, if we, if you guys took those same clients at their basal state and then with 10 pounds of more muscle and you had them each eat a bagel and they were wearing a continuous glucose monitor, that's because muscle is hungry. Eighty percent of if someone is wearing their CGM and they see the glucose go up and then it comes back down, that comes back down.

Eighty percent of it's what's going into the muscle. So as the muscle gets bigger, it gets hungrier. And imagine how much easier this person's gonna be at the time they're gonna have controlling their glucose. The more easily you're controlling glucose, the more easily is just another way of saying you're controlling insulin. The more you're controlling insulin, the more your metabolic rate's gonna be high, the quicker you're gonna get into ketosis. And the more people exercise, by the way, the more they have that, again, a metabolic wiggle room.

I've had an Ironman triathlete I knew who would eat 200 to 300 grams of carbs a day and still be in deep ketosis the next day. Because the guy's just burning so much freaking glucose. The muscle's just eating it all. But one other point about the fat tissue, we published a human paper that we found if people were in ketosis, their fat tissue metabolic rate was three times higher than if they weren't in ketosis. So just touching again on this idea of the metabolic rate being higher, which we found was actually a phenomenon of something called mitochondrial uncoupling, that you normally, I don't want to get into that unless you guys want to, but basically the mitochondria

were becoming less efficient. Right. Just burning energy just to hum the engine along. That's exactly how I'm communicating. So Ben, explain mitochondrial uncoupling and what's happening. You said you're becoming less efficient. So is it safe to say your body is less, it cares less about trying to store every calorie and just allows it to burn off as let's say heat? Yeah. Yeah, in fact, everything you just said is spot on. Yeah, so people, in fact, it's a point of amusement for me where you'll hear a radio ad and they'll say, take this supplement and it'll help your metabolism

be more efficient. And I can't help but chuckle because- Make you fat easier. Yeah, yeah, which is just to say, you're gonna be more miserly with your energy and wanna hold onto it. So the whole term uncoupling comes from the two parts of the mitochondria that we often sort of lump together. But at a kind of high level, the one part of the mitochondria is what's called the electron

transport system. That's where you are. That's kind of the receiving end, the ultimate end of burning energy. So when you're burning glucose, you're burning fats, you're burning ketones, all of that when it comes to the mitochondria is giving these molecules, it's going to give the mitochondria molecules that are going to feed the electron transport system. So then you are pumping out electrons or pumping out protons, and you're moving electrons. And then separate from that, but is about to take advantage of all of that, is what's called ATP synthase, the actual metabolic, the enzymatic machinery that's going to create ATP. And every cell of the body that is doing something is doing

that something because of ATP. That is the, we often will say, and I can't help but say it, it's the currency with which the cell is purchasing an action. The muscle and its cross-bridge cycling with myosin and actin, it is going through that cross-bridge cycling because of ATP. The nerves even sending the signal to the muscle in the first place.

ATP is allowing all the movement of the electron, of the electrolytes to move that nerve signal. Every cell of the body is working, is doing it because of ATP. ATP is working because of the electron transport system pumping out protons into the inter mitochondrial space. And so you have a lot of protons that are accumulating in the space and the ATP synthase will say, hey, you need to come back in. And it's almost like a static charge. They're starting to push against each other

ATP synthase will say okay come on in and as the protons come in It's gonna take advantage of that movement and create new ATP. So that is biochemistry right there in the mitochondria fundamental bioenergetics the more so if you have the ATP the cell cell will say, I need this much ATP. And then the electron transport system will say, okay, we're gonna give you this much of the kind of proton movement and electron transport. And so the more that is just kind of tightly regulated,

the more we would say it's coupled. That we have the actions of the electron transport system, this is only working as much as we need ATP being produced efficient Yes, so it's very efficient. No energy waste. That's exactly right. Yep, because we don't want to be wasting it here We're saying it's demand driven. We need this much ATP So give us burn this much energy if you will at the electron transport. This would be Analogous to us sitting in the car and we are in park, we shift it into drive, now we press the accelerator, we see the RPMs go up and

we see the speed go up. Connected. That so they're connected, it is coupled. So the revving of the engine is coupled with the car moving. Now however, what if we put it in park or neutral? Now we're revving the engine, but we're not going anywhere. That is now uncoupling. So now we come back to the same mitochondrial perspective and we say we're still allowing the electron transport system to be burning and getting the energy. But now before those protons ever get to ATP synthase, there's an open door. Now, the protons are getting pumped out,

but before they're getting kind of capitalized with ATP synthase, they just come rushing right back in. And so now, but we're still burning energy, but we're no longer only burning what we need to create ATP, we've uncoupled the process. And again, that is like we're revving the engine, we're burning fuel, the engine's getting hot, but we're not moving, we're not getting any work. In the case, and this is the argument I make when I talk about the benefits of strength

training. In fact, I talked at the National Peptide Congress in Vegas last year, and I talked about strength training and its effects on, in our experience, on people's quote unquote metabolism. How we saw it be so much more effective for fat loss and other forms of exercise. And that's essentially what I said was, I believe very strongly, and I'm glad you're saying this, that that through the process of feeding properly,

eating good protein, building some muscle, teaches your, well it tells your body, doesn't need to be so efficient. So you get this kind of like energy waste. Wait, now is it manifesting as heat? Is that what's happening? Yeah, it would. So uncoupling is heat.

In fact, you can measure this at that microscopic level. In fact, we have a little thermometer in our little metabolic chambers, and you can detect changes in heat. So we published a report finding the human data, I just mentioned a moment ago, if a human's in ketosis, metabolic rate of the fat cell is three times higher,

absolutely because of higher uncoupling proteins. It's actually a protein called UCP-1 that gets inserted and kind of disrupts the process. But we thought, okay, that is an advantage to obesity. So ketones are going to actually help with fat loss, but does that same thing happen at the muscle? Because that would be bad. Right. Like imagine you're in- Not good. Like we have athletes drinking exogenous ketones before they go do their marathons. In fact, the BYU were famous for our distance runners,

and they will drink exogenous ketones before they compete. Well, you don't want to uncouple your muscle. No. Then all of a sudden your muscle's burning energy and you get all flaccid and weak. You can't do anything. Then all of a sudden your muscle's burning energy and you get all flaccid and weak, you can't do anything. We found that not only did the ketones not induce mitochondrial uncoupling at the muscle, it actually

improved the antioxidant capacity of the muscle and enhanced resilience. We insulted the muscle cells with a chemical insult and the muscle cells that had access to ketones actually were more resilient. They survived better. And that's another, just more evidence when people talk about ketones being a defender of muscle.

There's actually a few different levels to that understanding, but at the very level of the cell, ketones make the muscle cell tougher, but no uncoupling. So they help the muscles maintain a high efficiency. What you see in the data for athletic performance is steady state long duration endurance. Ketosis seems to be great. I've experienced this. Power, strength, speed, you want some glycogen for that. So really interesting that you guys are seeing all this stuff. So are these athletes also consuming carbohydrates?

They are. So they're doing both? They are, which I would tell them to. My view, so there's a big, a lot of unknown when it comes to ketone and athletic performance. Most of the little bit of research that is out there, if not all of it, is in the realm of endurance athletes. And in the strength training realm, there might be one paper published on this topic, but I don't begrudge any athlete. Mind you, I don't even ever intend to be an advocate of a ketogenic diet. I'm a defender of ketones as a scientist because I believe they've been vilified and misunderstood. But all the more reason when it comes to an athlete. My view,

like people will often ask me, should I exercise fasted or should I exercise fuel? And I will always just say, as just a scientist, I'll say, well, what's your goal? Is your goal performance? Then you just put anything you can in the tank that's going to maximize your performance. And so these endurance athletes, yeah, sure, they're going to be using glucose. No one ever has a problem using glucose

during athletics, the muscle is just going to use it. Most people won't have ketones and they won't have been training with ketones. So I know a lot of endurance athletes who sort of have a metabolic version of live high, train low, but this idea of they live in ketosis, but they train with glucose. That's how Zach Bitter was. Yeah. Exactly. In fact, when I state this, I think of my buddy Zach and your buddy too, apparently. Yeah, yeah.

I remember he'd find out he would always train, get himself like that, and then when it came to race day, he would utilize carbon. Put it in. Yeah, and why not? The body will never have trouble using glucose. It is such a fuel for literally every cell of the body. In fact, so important that you could stop eating it and your liver's going to make all the glucose you need.

Mostly from lactate, by the way. A lot of people think that the main glucogenic substrate is amino acids from muscle. So it's not from that? No, not even close. Not even close, yeah. In order for that to happen, you gotta be starving. You gotta be starving.

And what's the difference between fasting and starvation? Actually, it's muscle mass and ketones. Like, as a point of a technical term, the difference between fasting and starvation is, are you making ketones? When are you making ketones when you're burning fat? When do you stop burning fat when you've run out of fat? Now once you start cutting into lean mass,

now it's starvation. Yeah. That's why we tell people when they go, am I gonna starve my muscles by fasting? It would take a long time. It would take a long time. It would take a long time. But again, the main substrate for glucogenesis, gluconeogenesis at the liver is lactate.

Okay, so I gotta ask you this, because I don't know if you're familiar with this compound, but bodybuilders, they're like the cosmonauts of using chemicals and stuff, fat burning, muscle gain. I love it, actually. Okay, okay, I was gonna say, you must be fascinated by bodybuilders, because they'll put anything in your body.

Well, I am in multiple ways, but just as a funny little tangent before I let you finish, I admire the self abuse. Yeah. But that sounds like we can laugh. Well, that's a scientist speaking like a scientist. Yeah, but even like the severe,

like you talk to a bodybuilder who's cutting. Oh God. But this is one of the reasons why when we look at these really lean guys who are just these paragons of fitness and strength and they'll say, yeah, just start cutting and eat less. But your mental fortitude is not normal. Like the abuse and what do you, like at any moment,

like they're obsessed over food. Oh, you dream about it. And you take an average person and who doesn't have the, that inherent motivation, let alone the pressure of standing nearly naked in front of 10,000 people. Just take the average middle-aged guy or gal, they're not going to do that.

Hunger's gonna win. Yep, yep, no, so it's so funny. Talking about how complex the metabolism is, the human body is, it's extremely complex. Throw on top of that human psychology, which good luck trying to figure that out. Now you've got the problem of coaches and trainers working with everyday people.

You gotta add all that up. But I need to ask you about this compound. I don't know if you're familiar with DNP. Are you familiar with DNP? Okay, so this is a- DNP? DNP, maybe Doug, look up the chemical. It's been around forever.

Is it an uncoupler? It is a mitochondrial- Is it dinitrophenol? Oh God. DNP? Yes, I think you might be right. Bodybuilders will use this and it's very dangerous. Oh yeah, I'm almost certain.

This is, it is in fact a chemical uncoupler, like Phenformin, sort of one version of it. Yeah, and actually it's a compound in making dynamite. And so these bodybuilders will use it and they'll talk about having a fever and things like that. Oh yeah, it's an uncoupler. Okay, okay. So that is literally just what we were talking about. it's an uncoupler. Okay, okay.

So that is literally just what we were talking about. The mitochondrial uncoupler. So now you have the mitochondria. That's it right there. It's what's called the futile cycle. You got it, dinitrophenol. Dinofetal, dude, that's exactly what I thought. They'll use that to get ripped sometimes.

Yeah, so you'll die. I mean, you literally will burn up. So when the human body gets to a certain temperature, you will unfold proteins and enzymes, so it can kill you, but the reason they feel hot is because they're literally, it's like they're revving the engine. They're seeing the temperature of the engine go up, and yet they're not going anywhere. Now, of course, they will be moving around. The problem with that is you will start to, you could become weaker at the muscle too,

but maybe at the very end they're like, well, to hell with it. I just need to shred these last couple of pounds. Yeah, that's what they would do. They use it for the final. And they don't move. They don't do it and do cardio. They do it and sit in their room and sweat through their sheets.

It's so crazy. All right, so you tell me. But that's an uncoupler. That's a perfect example of what happens. Isn't that illegal? Yes. I mean, who cares? It's the Wild West.

Yeah, yeah, yeah. It's the Wild West. I should hope not. So you're talking about ATP earlier and how it fuels every cell. Ten years ago on the podcast, I talked about creatine and how I thought it was going to be the ultimate longevity supplement. This was ten years ago. Oh man, you were a creation man. 100%. So let's talk about creatine. You must be a huge fan of creatine.

I am. Okay. So why do you like it so much? What does it do for the body then? Yeah. Yeah. So I, in fact, I have used creatine as a professor in a teaching. So I teach, one of the classes I teach is a class called pathophysiology. So, all these future nurses and doctors, they got to come through Professor Bickman. And that means they got to get my metabolic view of disease, which is awesome. Yes. I've had 15 years. I will get emails from students who are working now as physicians and they'll say, Professor Bickman, you changed my whole view of disease. And like, you know, like I look at Alzheimer's,

so Alzheimer's disease, I present Alzheimer's disease rather than a plaque problem, which it is not. It is an energetic problem. The brain is going hungry. And I would cite the robust 10 plus years worth of evidence showing that if you take someone with mild cognitive impairment, early stage Alzheimer's, give them 10 grams of creatine,

you can detect in real time improvements in cognition. You can have them do a series of cognitive tests. I think it's like in five hours. Yeah, just hours later, have them repeat the tests in a placebo group doing the same, the creatine group doing it, they do better. They remember better, they're thinking better. Well, if this was just a matter of plaques,

what the hell is creatine going to do? Nothing. But if you look at it as a problem of that brain isn't getting enough energy. Energy metabolism. At one level because it's not getting glucose well enough. All right, well what if we just kick up its

ability to reproduce ATP by enhancing the creatine phosphate sort of shuttle here? Well then all of a sudden we start to correct the problem. Yeah, so I am a huge advocate of creatine in part because I also want to keep my muscle mass. I'm a middle-aged guy, I'm turning 50, I want to be a healthy grandpa, I want to keep my wife interested, and so I want to keep my muscle, but my brain is my money maker. I don't go on a stage and flex to make my money,

I make my money by teaching, by doing research, articulating these ideas. This has got to be sharp. And so my view is, in fact, I've been quite thrilled to see a lot of people saying five grams ain't enough. We got to bump this up. Yeah, it's like 15 to 15 for the brain. Yeah, I'm thrilled. Yeah, it's so funny. It's the one healthy thing I've done since I was 15 years old and I've been taking creatines since the 90s. Now you're going to be immortal.

And I'm like, it's safe. Yeah, I know. So would a great, okay, so let's just, more speculation, because that's what I like to do. Would a great like brain healthy protocol then be a ketogenic style diet, of course good exercise with creatine? Yeah. Would that just be like great for the brain?

Yeah, so I would say two, one would be the way you just articulated it, which would be a ketogenic low carb diet with creatine. An alternative would be for those, like an exogenous ketone, like ketone IQ or any good exogenous ketone and the creatine at the same time. Those two things. So any way you're going to get those ketones, get them. Indeed, for the sake of the brain. One of the reasons why I beat the drum of ketones,

or rather I defend ketones so vigorously is because the brain thrives on ketones so much. So I defend ketones and even to the point that I think a person would be well served by spending at least a few hours of every day in ketosis. Whether that means you have an intermittent fasting protocol or whether it means you're drinking some exogenous ketones, give your brain a break, give it some ketones. But ketones and creatine is probably the kind of magic sauce. We might make a supplement here. Yeah, even when you're saturated with glucose,

there's value in exogenous ketones? Yeah, yeah, that's a killer question actually, because think about, there's kind of a metabolic anomaly that we've been able to hack here, where normally you're only making ketones if insulin is low, and insulin's only gonna be low if you're not spiking your glucose. So these two things aren't normally gonna play

very well together, but nowadays we can drink ketones. And as far as the brain's concerned, the moment ketones go up uses the brain uses them wow so glad you turned it out that was something that i think we're on tomorrow yeah yeah the brain just loves ketones probably and i'm speaking not very scientific now but i'm going to say it it loves ketones probably more than any other tissue of the body the brain is going to pull in ketones but every cell of the body with mitochondria which is everything but red blood cells is going to use use ketone for a fuel and will do so happily.

Wow. Every muscle cell is included. Okay. So when it comes to exercise, you must be a huge fan then of strength training because of its insulin sensitizing effects. Yeah. In fact, minute for minute, I unapologetically am of the view that if a person is looking at their day and say, I have 30 minutes, should I go on a jog or should I strength train? No question. Yeah.

Keep your damn running shoes in the closet. Go strength train. I want to be kind of delicate talking about this because I don't want to be insulting. I will regularly go into the sauna with athletes at the university. And BYU is, I hate the idea of these guys listening to this because they're such amazing boys, but I will be sometimes with these distance runners and they are so, I'll be really kind, they're just so thin. They're so, so thin. And I'm almost 50 and I'm like, man, I look compared to these boys. Bodybuilder.

I'm like, I'm the one who looks like he's 25. I'm from the neck down, I ignore my freckles and bald wrinkles, but they are built to run, right? And so that's, of course, I want to defend that view. But running, how fast you can run a marathon or 10 miles isn't the best predictor of longevity. It's grip strength and muscle mass. So even just looking ego aside, just looking at how can I be the healthiest grandpa, which more and more is my motivation. I'm years away from that, but God bless me that it may happen someday soon.

I want grandbabies. But I want to be a healthy grandpa. I want to be able to go skiing with my grandkids, wrestle with my grandkids, give them piggyback rides. How fast I can run 10 miles, that's not going to do it. It's going to be, can I get up off the ground? Can I pull myself up? Can I lift something up?

Along those lines, I read some very fast. So insulin sensitivity, we'll get to insulin sensitivity and its connection to cancer risk, because I read some very interesting data. This was a study done on pro bodybuilders, both retired and current. Not a healthy population, okay? Pro bodybuilders don't live. A lot of self abuse.

They don't live a healthy lifestyle. They overfeed themselves, they use lots of crazy drugs to look the way they do. And so when you look at their mortality rate, similar to the average American, which isn't great. Heart disease, a little higher. Liver failure, obviously higher. Cancer risk, far lower.

Pro body was far lower cancer risk. And I'm like, these are some of the most unhealthy people in terms of athletes. They're pumping their bodies full of all kinds of crazy levels of certain hormones. And yet they have lower cancer rates. My speculation was it's the muscle mass. It's gotta be the muscle mass and its protective effects all kinds of crazy levels of certain hormones, and yet they have lower cancer rates, my speculation was it's the muscle mass. It's got to be the muscle mass and its protective effects from maybe an insulin

sensitizing effect. So let's come back to the insulin in just a second because there's and I gotta there's a bit of a black box here for me and I wouldn't be surprised if other scientists can articulate this better. There, I will never forget, there is there was an in vitro, so a cell culture based study I saw one time. They took the blood of people exercising and put it on cancer cells and they died. And so I believe they implicated some of these myokines. So myokine is the term to refer to hormones from the muscle. The muscle is a very active endocrine organ. It pumps out tons of hormones. Some of these hormones may have these anti-cancer properties that are, it was literally, if you looked at the population of the cancer cells in the petri dish, it died, they died. Much, much more than the normal, which was just them surviving. So there

is probably a connection from the working muscle to the cancer cell that I don't know. But what I do know is the insulin resistance angle. So I'm happy to articulate that a little bit because nothing pains a professor more than saying, I don't know. So let me say something I do know. That makes me feel better. Yes. So with insulin resistance, everyone listening ought to look up the work of a scientist. He's at Boston University or Boston College. His name is Thomas Seifried. I need to mention him because everything I'm about to say is me relying on his data. It is compelling.

What he has done is rediscovered and reinvigorated the research of a scientist who won a Nobel Prize named Otto Warburg. This is the Warburg effect. Exactly. Yep. So, a lot of my students don't even know this. They come to my class in their senior year and I'll mention the war. In fact, I didn't even used to talk about the Warburg effect because I thought they were learning it in biochemistry and no one ever learns it anymore. So, the Warburg effect was this phenomenon observed by this scientist in Germany. Mind you, he was a Jew in Nazi Germany and his accomplishments were so significant that Hitler let him keep a lab. Wow.

I mean, just appreciate that. Yeah, he doesn't think about that for a second. Yeah. Yeah. I mean, pretty impressive fellow. He claimed that the fundamental disorder in tumor cells was the inability of the tumor cells to rely on anything but glucose. It just had an absolute requirement for glucose. And they consume glucose. I mean, that's how you find cancer.

Well, it's like 20 times. That's how you find cancer, right? Give you a little glucose, look at the lab. Yeah, you infuse what we call a radiolabeled or a slightly radioactive glucose molecule. You infuse it and then wait a little while. And you see it just light up the tumor. And you'll say, boy, that thyroid is like the black hole because it's eating so much, or the adrenal gland, or whatever.

Yeah, so you can use glucose to identify the location of a solid tumor cancer, which is proof positive that it's a hungry son of a gun. And what it's hungry for is glucose. So you have, one, the preferred fuel for the cancer is glucose. And then number two, it's very common in cancer cells that among its many mutations is an overexpression of insulin receptors. And what does insulin tell a cell to do? It tells a cell to grow. So in the modern carb obsessed world, and just to put that in perspective, the average person eats six times a day and 70% of all calories consumed globally come from carbohydrates. So we are living in an almost

constant hyperglycemic, hyperinsulinemic environment. Yes, that promotes type 2 diabetes and dementia and fat gain, but it also is the perfect recipe for cancer growth where this insulin tells the cancer to grow, glucose fuels the growth. Now, Thomas Seyfried's work is fascinating, and hopefully I can articulate it well. The traditional view of cancer is that it's purely a genetic mutation in the nucleus. There are cancer genes that are mutated and it's just telling the cells to grow uncontrollably. Okay, interesting. So what Thomas Seyfried did is he took the nucleus from a tumor cell and put it into a healthy cell.

I mean, appreciate just the- So here we go, mutated nucleus theoretically into a healthy cell. Into a healthy cell and the cell stayed healthy. Fine. No problem at all. Then he went and took the mitochondria of the cancer cell, put it into the healthy cell. Don't tell me it became cancer. Cancer. Oh, wow.

So his whole view is this is not a genetic problem in the nucleus, it is a problem of metabolism. Wow. It's an energy problem. And so he is the one really who's been leading the charge to have ketones and ketogenic diets be in the therapy protocol with any cancer therapy. It also makes, I mean, Dr. Valtolongo's done some research on this, and I've seen data on fasting,

like you go into chemotherapy fast that are ketogenic, the chemotherapy is even more powerful, you have to use less of it to kill the cancer, so you've essentially weakened that. That's exactly right, yeah, so the comment I just made about Thomas Seyfried's work is that he says that a ketogenic diet should be, I think they say, a neoadjuvant therapy. Before the chemotherapy drugs come in, kind of prime the body with ketogenic diets.

Yeah. Yeah. Wow. So that's the whole theory. That's the metabolic. But once again, we articulated just in our conversation, the metabolic view of Alzheimer's disease. We used to look at it as a plaque problem. Not so much. It's an energy problem. Cancer, well, it's a genetics mutation problem. Not so much. It's an energy problem. The reason I try to articulate the metabolic origins of disease so thoroughly is because, and indeed wrote a book, plug my book, Why We Get Sick, is all about the metabolic origins of chronic disease. That you can imagine at the end of our conversation,

and I know this is coming from an inflated ego perhaps, someone opens up their medicine cabinet, they pull out their drugs for their type 2 diabetes, they pull out their drugs for their hypertension, they pull out their drugs for their erectile dysfunction, and whatever else. Thinking, because I have different pills for these different drugs, they're all different things

and they're not related to each other at all. Not true. Basically, every chronic disease, to some degree or another, is going to be a result of insulin resistance, but to say it another way, compromised metabolic health. That if you can improve the insulin sensitivity, improve the metabolic health, it is every drug I just mentioned,

he could get off every drug I just mentioned. Indeed, I've seen it happen. Which is a massive case for building muscle. Well, I was just gonna say, it's a massive case for that. So this is interesting because what you're seeing is the rise of several chronic diseases, all kind of rising at the same pace,

they're all exploding, and what you're proposing is essentially a unified theory. Like we're looking for a unified theory. A common soil. A common soil for all of those things. All right, so Adam mentioned muscle. So one of the speculations we have with this, so we have this new medical intervention

that is going to tackle obesity in a way that we've never seen a medical intervention even come close. These are GLP-1s. Mm-hmm. And now, a result of using them, not because the GLP-1 causes this, I'm very familiar with the data, but rather the fact that people are eating way less

and they're not doing strength training, is they're losing muscle. Our speculation is that a lot of our health problems, yes, due to obesity, but also due to being under-muscled in a week. Especially when you look at the grip strength of college-aged males today versus their grandfathers in 1984.

It's like way different. Do you think that a big part of our problem is not just the obesity, it's the fact that we're just under muscle, we're just weak. Yeah, yeah. Well, you guys, you're not going to be able to hold me back from talking about GOP1 a little bit, so let's come back to that in a second. But yeah, with muscle strength, yeah, I mean, it's hard for me to imagine and I can only speculate what the actual connection is. But what is it about muscle mass that results in such consistent longevity? That is clear. The evidence is clear that the more you look at the long-lived people, the more among the very few variables that have predicted it, strength is one of them with muscle mass being right there with it. Part of it could be all the metabolic

reasons we just talked about, the overproduction of myokines to help act as kind of anti-cancer agents, agents to improve neurogenesis and brain health. But with the GLP-1 drugs, let me just share my view on how I think they ought to be used because they are extremely powerful. And I think my view is they're being overused. And the loss of muscle mass is a good example of just how that New England Journal of Medicine paper found that in two years of weight loss, 40% of the weight loss was from fat-free mass. Now that's not to say it's all muscle, but there's some muscle. And when you look at that in light of the fact that in the US 70.1%, it's a very specific number because I remember the study of patients on the drug at two years get off the drug. They

get tired of being on the drug. Also a paper just published within the past six months in the year of 2025, they found that the risk of major depression went up by over 200% on these drugs and the risk of suicidal behaviors went up by over 100%. Now, can I pause you there for a second? I'm going to add some speculation. Do you think that could potentially be, we've worked with lots of clients and we know that abuse of food or the use of food in a way to comfort yourself.

Yeah. Could it be that we just took away their drug? Oh, so my view is we always talk about the sweet cravings. And this is what I'm going to come back to, this paper published in the 90s that I have to talk about with GLP-1. People talk about the food noise is gone. My cravings are gone. Well, what do people crave?

No one craves fats, no one craves proteins. We crave carbs. Yeah, sugars. It's something sweet and gooey or salty and crunchy, not with or without fat. And so, whether they're articulating it this way or not, their carb cravings have just been smashed, which is a good thing. And I'm going to come back to that point in a moment because that's how I view the best use of these drugs. Another view of these drugs could be it's getting rid of your cravings for everything, life included. That you could have a guy who used to enjoy going to the gym with his buddies, he doesn't really like it anymore. Or he'd go play pickleball, he doesn't really want to.

You'd have a girl who used to like going out on a walk with her girlfriends, she doesn't really want to do it anymore. So as much as we look at the reduced cravings for sweet things, even that goes away at two years on the drug, by the way, diminishing returns, the cravings come back even while they're still on the drug. Maybe what's actually happening is their craving for all of their former enjoyable things starts to just kind of fade away. And that feeds right into it. Definitely have reduced like energy and fuel because I mean, so I did this as an experiment on the podcast. So took it not needing one. For science. Yes, totally. And I said, I'm going to remove my trainer brain. So I'm not going to go in knowing

I need to increase protein to keep my muscle mass. I'm going to just feed when I'm hungry, do what I want to do. One of the challenges I had, I remember having this conversation with my wife, like I had to choose, it felt like, whether I was going to motivate myself to go work out or help her around the house. Both weren't happening. No energy. Just did not have the drive and the energy and umph to get up and do both.

I literally had to choose one or the other. And so I noticed that as a side effect of it was just- And you, a guy who's had a life of committed exercise, right? Yeah, I love to work out. Yeah. And what you're saying really does feed into what they're also seeing, lots of anecdotes. In fact, there's studies going on right now

to investigate the use of GLP-1s for other hedonistic behaviors. Yes. People are smoking less, they're drinking less. Drinking less, less sex. Yeah. OK, so then proper way to use them. Yeah, yeah.

Okay, so there was a paper published in 1996 in the journal Gut. It is mind blowing on the dynamics of GLP-1. So my sentiment is GLP-1's primary influence with weight loss is that it tells the brain you don't need to eat. To be more specific, I think it helps the brain at an optimal dose know when to stop eating carbs. Now, why do I state it like that? Because that is where I think it's best used. This paper published in Gut, 1996, they separated these humans into two groups, lean humans and obese humans. Then they had to meet a high-fat meal. And they

found that the GLP-1 effect, and remember, GLP-1 is going to tell the brain, hey, we're done, we don't need to eat anymore. It's a satiety hormone, among some other things, but I believe that's the primary mechanism. So it says, we don't need to eat. The GLP-1 response in the lean and the obese group was very overlapped. It got a little bit of difference at the end where the lean stayed a little higher than the obese, but it was very similar trajectory. In other words, whether you're lean and obese, if you eat a very, very fatty meal, you're going to have a generally equal degree of satiety. And both groups would say, okay, I'm done. Now, however, they had to meet a high carb meal. The lean group had a huge increase in GLP-1. The obese group, no statistically significant difference whatsoever. It stayed basically, it was a little bit of noise, but

no significance. Like a GLP-1 deficiency almost. So, yeah, exactly. So now you can imagine these poor folks who are struggling with their weight, they both go out to eat, the lean kid and the obese kid. They eat the same high carb pasta meal. The lean kid has this big GLP-1 response. He eats it and he says, oh, I'm done. Oh, gosh, I couldn't eat another bite. Obese kid. His obese kid, he didn't get that hit. Now he's looking at that plate. It's empty. He says, uh, can I finish yours off? You know, he doesn't get it. So my view on the drugs is they should be used when we've

identified a person who can't control carbs. So first and foremost, back to the earlier part of the conversation, we would say, okay, you need to lose weight. I want you, before we even give a prescription, we say you got to control your insulin. Don't worry about counting your calories. Calories will kind of work themselves out. You got to control your insulin. How can I do that? You got to control carbs. So here's a prescription, You know, whole fruits and vegetables, that's fine, but lots of fat and protein, enjoy. That'll help your insulin come down. I'm going to see you in two weeks. See you two weeks later. I just can't do it. Every night I got to eat a bowl, I got to eat two or three or four bowls of shredded, frosted mini wheats, which is like crack for me,

bowl, I got to eat two or three or four bowls of shredded, frosted mini-wheats, which is like crack for me. Like personally, like we literally in the Bickman home, you don't bring those frosted mini wheats in the home because I can't control myself. Like my wife will come flick on the lights of the kitchen and I got like it coming out my nose, you know, like I've been caught in the act, you know. So whatever it is, the patient comes back and they say, I just can't do it. It's the pint of ice cream every night. It's the four bowls of cereal. I just can't stop myself. All right, here's a prescription and I'm going to start it at this very, very low dose. So my first view is we should be microdosing or just low dose, way lower than the doses that it's currently used. But there's a problem there because it's

actually a quirk of like drug use where that is not a patented space. And so you have to get it from like a small compounding pharmacy or use it off label, which from what I understand, the FDA is cracking down on it. So put all the politics of that aside, my best use of the drug would be the physician now saying, okay, let's start at this really, really low dose. And we're using it to help you control your carb consumption. I'll see you in a month or whatever. Let's say they come back and they say, oh my gosh, this is amazing.

I've never felt better. Okay, that's one version of this. And then we say, all right, let's dose you down now. Let's cycle you off. And so that's the other component of it, cycling. So micro dose and cycle. Let's cycle you off and let's see whether it's stuck. Maybe two to three months. Maybe one month might not be enough. I'll see you in a month. They come back and they say, now we have the different outcomes. This is still amazing. I'm feeling great. I've

learned how to eat differently. I've learned what it looks like. I've learned the habits and now it's stuck. This is how we've communicated it through our coaches, and this is of course anecdotal, because we've had lots of clients now go through, and that's similar to how we communicate it. Two ways, one, start slow, add strength training, increase your protein intake,

because you're dropping your calories, you'll lose muscle mass, let's preserve that. And then while you're on it, you can create new behaviors and weaken those neural networks for whatever behavior you were doing before and maybe strengthen some other ones and after you come off, then hopefully it kind of sticks. But use it to help develop those new behaviors. Don't think of it as weight loss.

Think of it as I'm controlling, I'm changing my dietary habits. But then let's say the person came back one month later and they said, I'm kind of right back at it. All right, let's cycle you on again. Let's just see how you do with another cycle. And this time when you would normally have that craving and you don't, this is where we teach them to journal or try and look into- It's dynamite. It's dynamite. What is causing that? Because that's the only way they're going to fix this.

And then we've found those are the people that it's life changing for. If it's somebody who is very aware, Adam, I can't just stop the ice cream. I can't stop it. They know they have this pool to something like that. Yeah. And then it interrupts that. That's the first step, but then you're not done yet. Now you got to do the work of what was causing that.

What can I replace it with a better healthy choice? Like, there's two things I want to add too, because the GOP ones seem to show in the literature to have their own independent of caloric intake and food intake, their own insulin sensitizing effects. So there's that. And then also I saw this crazy study, it was on tersepitite, which is a triple agonist, where they took, they controlled the calories. They put everybody in a calorie deficit, they controlled the calories.

It has a muscle preserving effect in comparison to just eating low calories. I thought originally, oh, GOP1 you eat less, of course you're going to lose weight, but there seems to be a muscle preserving effect. Any speculation on what might happen? Yeah. So on the second point, you made a couple points and I've already forgotten the first one. The first one was the effect that you're going to have to.

Oh, insulin sensitizing effect. That's independent. Oh yeah, okay, good. Yeah, so let's come back to that in just a second. So, the second effect, it wouldn't surprise me. We've actually now started in my lab doing some muscle cell cultures, treating with and without semiglutide. What I predict is that it's a dose response. We've found that higher doses, muscle cells do not handle that well. I wouldn't be surprised if there is some other kind of off-target effect at a lower dose, which is preserving muscle.

Interesting. So I can't, that's all I can speculate on that. Okay. Now with the insulin component, GLP, when I first became familiar with GLP-1 drugs, it was in my, my PhD lab 25 years ago, 30, almost 30 years ago, if we're going to say, oh no, 25 years ago. And it was one of the first funded labs to look at some of these drugs. So I've been familiar with these drugs for extremely

long time. They were originally used at a relatively lower dose where it was documented that it just improved glucose levels. So what a lot of people don't appreciate is where they have the beta cell making insulin, you have its opposite, the yang to the yin, where you have an alpha cell creating a hormone called glucagon, and it acts in opposition to insulin. Whereas insulin acts to lower blood glucose, glucagon increases blood glucose. So if we started fasting right now, went on a 24-hour fast, over the 24-hour fast, insulin's coming down, glucagon would be going up because it's acting to tell the liver to make more glucose. In type 2 diabetes, part of the problem with the hyperglycemia is that the alpha cell has become insulin resistant. This is a fantastically

overlooked component of type 2 diabetes. Normally, in these little micro environments of the pancreas, you have the beta cell making insulin and that insulin will tell the alpha cell to stop making glucagon, which allows insulin to win that war of glucose. So blood glucose comes down because glucagon came down. However, the alpha cell starts to become insulin resistant. So now the beta cell is still making tons of insulin, maybe more than ever, but the alpha cell starts to become insulin resistant. So now the beta cell is still making tons of insulin, maybe more than ever, but the alpha cell isn't getting the signal anymore and it keeps pumping out glucagon,

which keeps going to the liver, which then continues to release more and more glucose, thereby increasing blood glucose and thus pushing insulin up even higher. So you get this sort of vicious cycle. At the originally used doses and why GLP-1 drugs used to just be called anti-diabetic drugs as opposed to anti-obesity drugs like they are viewed now, it's because at that lower dose you don't have all the satiety

effects and everything else. You did have, however, an inhibition of glucagon. And so if you look at type 2 diabetes as a problem of too much glucagon because the alpha cells are misbehaving, not responding to the insulin more, then it makes sense. If we have a strategy that can start to bring the glucagon down, now the liver starts to obey and starts to hold on to the glucose rather than dump it out. And so glucose comes down, insulin comes down, and the person's going to have healthy… You know what this reminds me of? This is the pharmaceutical industry, right?

It's like they have a drug that does this thing and then they find that it does this other thing with a way bigger market, like Viagra. Oh, this might lower blood pressure. We're getting boners. That's what we're going to market it for. Boners are way better. Yeah, so it's like we've had GLP ones for a long time. It's good for blood sugar lowering, insulin sensitizing if you will.

But if we give people more, they lose weight. That's what we're going to do. That's right. So what was observed to be a very modest effect, which is, hey, their blood glucose gets a lot better and they lose a little weight. Let's just exploit the, let's leverage the hell out of that thing. And so they literally, the difference between Ozempic, which was the originally used anti-diabetic dose and Mugovia is like just the dose of the same molecule. They just found if they move it up four or five times, now all of a sudden,

it's going to be such an impact that it slows the guts down a lot. So the person starts to have food. I mean, just to mention that, when someone goes in for general anesthesia, I mean, where they're going to be put under, they will have them fast and really clear out their guts so that they don't have a risk of vomiting. Oh yeah. So that they don't like breathe the vomit back in and choke. And what they found though is that if someone was on these drugs at these higher doses, they would have to have them fast for longer or get off the drug because food would still be there 24 hours later.

So normally we go eat a meal, that's's gonna sit in our stomach for four to six hours and then move on into the small intestine and the stomach will be empty, unless you're on the drug. Then that food will be sitting there for 24 plus hours. And so no surprise someone gets the ozempic burps because they have food festering in their stomach, creating these noxious fumes

that are constantly coming out. Yeah, so I believe that GOP1s used properly are gonna be absolute breakthrough. Used properly. Yeah, so I believe that GOP1s used properly are gonna be absolute breakthroughs. Used properly. Yeah, so what are your fears about how they're being used and prescribed now? One of mine is just we're gonna be dealing with an epidemic of muscle weakness, immobility,

osteoporosis, which is already a problem. What do you think? Oh, I couldn't have said it better. Fragility is the perfect way to describe it. And remember, 70% of patients get off the drug of their own volition at two years. Over that same two-year span, 40% of the weight they've lost is fat-free mass. So imagine, if you will, who the biggest market is for these drugs, a middle-aged woman. So let's take a 60-year-old gal who has 30 pounds she wants to lose. Okay, she's lost that but let's say She lost those 30 pounds of fat

She will have lost about oh 12 pounds of lean mass potentially and she didn't have a lot of muscle Exactly, and now she gets off the drug two years later for whatever reason Maybe she's tired of the nausea. Maybe she's tired of the thousand bucks a month, or the mental health problems, which are very real. So she gets off the drug. One of the quirks of human physiology is one of those mass depots is gonna come back very easily. One, in the 60-some-year-old gal, will never come back.

So the 30 pounds of fat, she'll have no trouble gaining that back. Muscles hard. The muscle and bone, extremely hard. Not that it can't happen, but come on. One other overlooked component underlying this entire conversation is that one of the versions of the GLP-1 drugs is a drug called Lira Glutide, which is not semaglutide, the main one used in Ozempic and McGovey. Lira Glutide is another one of it. What I'm about to

describe happens with semaglutide, I don't know. I've not seen studies on it. But there was a paper published in Europe that found when fat cells were treated with liraglutide, it activated a protein within the fat cell called p-par gamma. And p-par gamma is an important regulator of fat cell multiplication. And they found that it activated fat cell multiplication, a process called hyperplasia. And so, now that seems like a paradox. When you first look at it, you think, well that's impossible because I'm losing weight. Well remember, fat loss is coming from shrinking fat cells. But what they have happening now then is that while their

fat cells are shrinking... Well that would be a terrible storm. They could be making, now emphasis could, this is italicized in the script that Doug puts together later. It's italicized, it could, underlined, it could be happening with semaglutide where they have more fat cells than they did before they started the drug. So their potential. That's been observed in post contest competitors because they'll go on an extreme diet and they'll refeed because they'll go on an extreme diet, then they'll refeed because they're like, ah, I'm done.

And it's been theorized that it's the body's attempt to become more efficient at capturing calories. Well, adipocyte hyperplasia is a hell of a way to do it. And so their potential to not only get to where they were but then go beyond it is there. Way higher. Wow. So that is a real study.

Again, it was liraglutide, so that's the aster is there. Way higher. Wow. So that is a real study. Again, it was liraglutide, so that's the asterisk there. We can kind of limit the takeaways, but still, one of the versions of this drug has been shown to do this to fat cells. So what I find very fascinating too about this conversation is because now they've introduced these GLP-1s, the most effective by far medical intervention for weight loss period in the story. Nothing comes close for weight loss like a GLP-1. But now you got the problem of muscle loss

and weakening and whatever. What's probably gonna happen, and I think this is happening, I think they're already doing this, is they're gonna start investing heavily in drugs that preserve muscle, like myostatin inhibiting. This is happening.

Yeah, so they're looking at myostatin inhibitors, they're looking at other peptides that have been leveraged in the past for muscle mass. So this is the new, I was just at a conference, a diabetes meeting within the past 12 months, there were multiple talks about these, the new versions of these, of like, you know, like trazipatide with its threesome molecules, like you just mentioned, adding to the cocktail. But the problem is, this has been, mind you, I mean technology just continues to blossom. This has been a pursuit for decades.

A good way to promote muscle growth without promoting growth of other tissue. Without having to use the endrogen receptor. Yeah, yeah. So there are still complications to preventing it from going mainstream, but it is absolutely a focus. And it'll probably just be a matter of time. But isn't it just unfortunate that, like what you guys are doing, we have, we know what

we need to do. Yes. It's just my one last sort of concern I have with the drugs is it's self-discipline in a syringe. It's this false sense of accomplishment where I worry about any intervention that robs a person of developing habits and yeah, just the self-discipline, the self-mastery, so much of life in my view is what have I learned to do with what my flesh naturally wants me to do? There's a part of me that should be the captain here. And I think we are depriving people, I think it would be like bad parenting, to just be

always intervening and not allowing the kid to develop the habits to get through these struggles. Ben. 100% why we think the journaling process and all that has to happen. That accountability too. You have to. Arthur Brooks, a good friend of mine, he's an expert on happiness and human behavior. I know exactly who you're talking about.

The data is clear. A very important component to happiness is challenge and struggle. You work out for years and you look great and your body's healthy and fit, but that's not all the benefits, not even the tip of the iceberg. A lot of the benefits come from just the process and learning and struggle and discipline. And so what book was that?

That was it a Brave New World where people are walking around and they're just taking pills to be happy. And was it that one? Yeah, so it's like we're moving to that future where we're just gonna pop pills and- Just medicate. Yeah, and just I look like I'm fit and everything, but I never really did anything for it. And I think people are really sad. Yeah, there's a, I agree. There's more that as much as we want,

we want here people to have optimal metabolic health. We want them to be strong. We want them to be healthy. To be happy is not the same that you need. There is that journey. Arthur Brooks, I think, is the one who talked about the second peak that people start to experience. They accomplish one thing and then they're left wondering, okay, what's next? What if the first peak is them losing the weight, but they didn't even earn it? They had a Sherpa carrying them up to the top of the bloody mountain top. That's some of what I worry about when I look at the broad, widespread use of these drugs. And it is global. Within the past six weeks, I've given a talk on metabolic health, including GLP-1

drugs in Europe and in Asia, two in Asia, one in Europe. I just say the word ozempic. They don't need to translate it into mandarin. They don't need to translate it into Czech. They already know what I'm saying because that's a word that just worked into the vernacular of the culture. So I worry that yeah, we're getting one outcome, but so much of what we learn and gain and benefit from is in fact not the end, but the means. Yeah, this is going to be, I mean, I know you're a scientist, but do you think this may be one of the reasons why we're seeing this, seems to be this resurgence with this younger generation in religion? Jared Oh.

Pete We haven't seen this in decades and kids are going towards it. Is it because they're kind of figuring this out? Jared Void of purpose. Jared I think every, so I have a lot of thoughts. I'm very religious and in fact, I'm a professor at a religious university. So, I have seen this and I rejoice in it. It just thrills me. I can't help, but probably some of it is looking for meaning and realizing maybe in a previous generation or two. It's hard for me to kind of know where the generation cutoffs are, and I don't think they matter as much as we sometimes think. But maybe them looking at a more consumption-minded generation, where my generation, I don't even

know what one I am, maybe Gen X born in the 70s. I look at the kind of boomer generation, my dear dad whom I love, again dearly, a lot of consumption, which continues to happen. I think a lot of these younger kids might be looking at the challenges they're facing, like here we are in California. I can't imagine being a 25-year-old trying to find a bloody place to live. Forget about it. Like I was joking with you guys before we went on the air, we have professors getting hired in Utah where they can't afford to buy a home in the city where a BYU is located. And I wonder whether a part of it is this perspective that comes from whether a part of it is this perspective that comes from thinking, okay, my goal of getting a home and being independent is hard and I need help. Maybe there's something to be said for your, it's a little bit more of a humbling circumstance. And so you look to a higher

power. I rejoice in it though. I know within my own church, the number of young people going on on a missionary service, and we were kind of joking these young Mormon missions, LDS missionaries, it has literally reached an all-time high. It has peaked. There's like 90,000 18 and 19-year-old boys and girls. Like what I did in the middle of Russia in the mid-90s, these kids are going out. So that's, I think, just reflective of what you just said, which is this resurgence in faith, which again, it thrills me. As much as I am a scientist, and I love being a scientist, I love studying the natural world in pursuit of truth, but I also believe there's a component of my existence and everyone's existence which cannot be quantified into whatever I can hold in my hand. That there's something else to us, and that to me is where religion comes in.

That as much as I'm a scientist is a seeker of truth. Whether you have a PhD after your name or not, a scientist is a seeker of truth. So all of these silly claims about we believe in science, that is a very unscientific thing to say. To be a scientist, you're prepared to just, you challenge everything you think you know, you're trying to understand truth. Even the idea of truth suggests that there's some absolute influence in the world. That's right. Which is why you have all of this post-truth

or my truth, which is some of the dumbest drivel I've ever heard. But I believe. What a great way to feed a lot of diet. Yeah, yeah, well, and I'm a professor at a university. I'm going to talk about a cesspool. That's where those ideas are born. But to me, there's more to us than these fleshy tabernacles. And I want to try to understand that too. There's a truth that goes beyond this. And that to me is where religion comes in. Absolute, it's faith. Absolutely. And to me, it gives a meaning and a

reason and an order that as a scientist, I cannot explain. Yeah. As a scientist, did you ever doubt your faith? Oh, that's a great question. Never. Because some people will say, well, how do you reconcile the faith with science? Faith is everything.

Like, imagine coaching a client if they didn't have faith that they could predict an outcome, that if they couldn't envision a version of themselves that they'd never seen before, they'd never sign up in the first place. Why even start an experiment if we don't have faith that there's going to be something that happens? So I've never, whether it is just a spiritual gift, I have never since the time I was a little boy doubted, never doubted the existence of God ever, like of a divine creator. One funny thing on my mission in Russia, I was there in the mid-90s right after like post-communism, post-Soviet Union, and where atheism was the religion. I mean guys, this two years of me like approaching people on

the street saying, hey, do you believe in God? Do you want to talk about God? It's a freaking tough job. They would throw you in the gulag just a few years later. Yeah, but what was so funny is that you would ask someone, do you believe in God? Oh no, no, I'm atheist. It would just come right out. And then you would say, well, do you believe that there's a higher power that kind of governs

the universe? Oh yeah, of course. That would just be, just as quick, they say, oh yeah, of course. Well, that's God, our Heavenly Father. Oh, oh, all right. Well, maybe I do believe in that. They just wouldn't have even thought about it. But yeah, I've always known, as much as I can know something, and I'm very careful to use that word, I've always very much believed that there is a higher power and it is God, our loving Heavenly Father. There have been times in my life where I've thought, with my particular faith, the Church of Jesus Christ of Latter-day Saints, where I've thought, man, what if it's just all like an amazing myth? Pete Slauson

Because, you know, I want to be careful and really wonder at how I know and believe things. Even in those moments, which I would say are kind of cynical moments, I look at my life and the order that this organization has given me and just the belief. My mom died when I was a little boy, leaving these nine little kind of red-haired, freckled-faced kids with my dad to raise us alone. And it really kind of galvanized my belief system where I thought, you know, a particular quirk of our faith is we believe that, you know, families are eternal units. And I thought, man, if I ever want to see my mom again, this will be the only way. And so I just thought it better bloody be true and I'm all in.

Yeah. And so your dad raised you guys by himself. Yeah. Wow. How old were you when you actually?'m all in. Yeah. And so your dad raised you guys by himself. Yeah. Wow. How old were you when you actually? I was 11. Wow.

Yeah, I'm a defining moment. But I'll tell you, as tough as it was, you can take any of the nine Bickman kids and put us together and we just get along so well. That's so great. We really kind of rallied around each other. That's cool. It's all about family though, right?

I mean, to just sort of say it all another way, it's just about family. But that's back to my point earlier, that as I look at life, yeah, I love being a scientist, but this is a means to an end. I'm here away from my primary job as a professor and away from my family because it's going to help me sell more books, I'll make a little more money. But even then, it's because my wife and I, when we were dating, and you know, no one marries and has kids like Mormon people do, right? You know what I'm saying? Like LDS guys do. So we really talked about this and knew really well we wanted to have a family.

And I always think of these clever ways to express things. I'm provider and protector. My wife Cheryl is nurturer and nourisher. So she's feeding and raising and helping the kids learn and I'm protecting and providing. This is me providing for the family. And so everything I do, at the end of my life, if I have failed my family, then nothing else has mattered. No success in life will compensate for failure in the home. So first and foremost, I'm husband and father and then professor and scientist. Did you have as many kids? How many kids you have? We only have three. You say that like a let down. I have one. I have one. But within the LDS community, boy, three is like the bare minimum. We had a bit of a late start, which is to say we were 30.

By the time we had our first. What's your oldest? What's your youngest? Yeah. So our oldest Samara is 18. She's going to be a freshman at BYU this fall, which is thrilled. And then we have Lizzie, 14, Asher, 12. Can you recall, so because it's been a while, right? 18 years, how your life changed? Oh, I recall it with perfect clarity. Indeed, it was one of the most profound moments of my life. When I was holding little Samara, it was like, I mean, I remember it, like with crystal clarity, it was, I felt like I was looking in a mirror both, you know what I'm saying, how you kind of have that view when you're in between two mirrors and you can see eternity. Like, I looked at her and thought, you are

my immortality. Pete Slauson Oh, wow. Like I looked at her and thought, you are my immortality. You know, as much as we have these vulgar longevity gurus nowadays who just look like plasticized vampires. I know exactly the one person you're talking about. It is so, and I use the word vampire very deliberately because they are literally taking blood from their own children.

And I think it is a vulgar, vile, disgusting abomination. But it's all this selfish view of how can I live longer? I don't care. I want to live well. My immortality isn't going to be me pretending that there's going to be some scientific discovery that makes me live to 500. That is so stupid. What a waste of time. Not to mention, people don't even think about how potentially miserable that would be. Oh, yes. I look at my kids and think, that's my immortality. So, yes, that moment, and I held little Samara and Cheryl was right there and I'm looking at my wife who just went through hell to bring this new little life into the world, I felt like I was seeing eternity. That's cool.

Yep. That is really what I felt. It really did feel like I was looking at her and that there was this eternal reflection between two mirrors almost, where I thought my children are my immortality. I don't live my life to live to 100 or 200 or whatever these mythical pretenders shills are going to think they're going to get to. I live because I want to raise my children well, I want to see them grow,, I want to see them grow, and I want to be involved with their kids someday. So even now I tell my kids, I love you, you little darlings. I loved you when you were in diapers a lot. Please give me grandbabies and I'll do everything I can to help you give me grandbabies.

It'll be interesting what a different feeling that is because you describing that is an interesting way because I probably felt a similar feeling. You describe it very different than me. For me, it was the most powerful feeling of selflessness I ever felt. At that time in my life, I didn't realize just how selfish I was until I, for the first time in my life, actually loved something more than myself. I had said it a thousand times before. I love my mom, I love my these, I love a lot of things.

No, it changes you. It does. And that was probably the most radical feeling. I was going like, oh no, this is actually what it's like to love something more than me. I think, I was asked one time, which is, what advice would you give a guy to help him be motivated to do what you guys do, you know, helping people. And I would say have a reason. Yeah. Have a reason. And once you have kids, unless you're a bit of an a-hole, that should be a reason. Especially for men when they talk about how much money men earn. They're talking about married men with kids. Single men don't do very well. No. We don't want to grow up. Because you think, I mean you're left to your kind of most base desires, which is give me a TV,

give me a video game system, and something to sit on and I'm good. Go to a 27-year-old single dude's apartment. That's exactly what you just described, is a mattress on the floor. Yeah, a mattress. Pulled out, shared TV with you. And I think one of the things that thrills me, Sal, earlier you mentioned about the sort of discovery of religion, especially when I look at young men. And maybe I have a kinship for young men because I was one, of course, but I also look at these kids at my own university. This will sound a little, I can discuss this here, but I worry that someone listening later is going to

think I'm a bit of a bigot. I promise I'm not. I have daughters. I'm thrilled. I'm married to a beautiful woman. I'm thrilled that they have every opportunity available to them. Women outperform men at every level of academia and training. More girls are going to college than boys. More girls are going to graduate programs than boys. More girls are going to med school, to law school. And yet we still have posters that will go up. Women come to this night of women in science, women in medicine, women in whatever, every university does this. There's whole departments and fields of study to women. And I look at these boys and just want to hug them and just say, you matter. You matter a lot because they're being raised in a culture where they're told they don't matter. I've had

conversations with these boys when these posters are up in all of our buildings promoting women going on to graduate school, which is great. I'm thrilled, but my view is it already worked. It's worked too well. We don't need the posters anymore. Let's just treat everyone the same now. And I will ask these kids and these boys that are trying to get to med school, and they know because of their unique attributes, they're going to have a much harder time getting to that next level. That's the boy crisis by Dr. Farrell, right? Yeah, we've had him on. Have you talked to him?

Oh, I totally know what you're talking about. Yeah, yeah. And young men are just, we've been neutered and pacified with things like pornography and video games. Yes. Like not wanting to accomplish and conquer and even, I mean as a teenage boy, the drive to talk to girls got me out of my room and made me, I had to go be scared and go talk to a girl

and I had to be presentable. And a lot of these young men are just sapped. But as they're discovering religion, I think, and they are, especially young men, young men are really going that direction, which is beautiful to see. My hope is among this is a reappreciation, a renewed appreciation for the family and them wanting to be provider and protector. I basically tell these young men, and even men I go to church with, one of the quirks of the LDS churches are sort of a men's organization in women's. I'm the president of the men's organization in my local congregation and all the time

I use this kind of language where I want them all to be alphas. These good, valiant, faithful men of Christ who are strong physically, strong spiritually, they're involved in the neighborhood, I want them to be alphas, and that has taken on such a negative view. Yeah, it means Andrew Tate now. Yes, they think it's some vile chauvinist. Yes. Like no, a true alpha is a soft-spoken, humble guy

who knows when it's time to fight, and he can, but he also knows when it's time not to, when it's time to be quiet. And he's dedicated to one woman. Yes, amen, amen. Great stuff, great stuff. Yeah. This was a great podcast. Really enjoyed you having you on my friend. We get to end with a banger. As much as I'm a scientist, I think a lot more about family

and faith than I do science. I actually love to talk to, it's been a pleasant surprise for me to meet as many scientists as we have that actually have a faith. Because I feel like early on in my life I thought those were the guys that were out there trying to poke holes in religion as much as they possibly can. And a lot of them actually do spend, that's why I asked the question, spend a lot of their life trying to poke holes and that's what led them to finally believe because they're like, I try to disprove it a million different ways. To me there is no, especially when it comes to humans, maybe one other thought on this, we don't belong on this planet, which is a silly way of saying there's nothing like us.

As a scientist, I cannot reconcile, coming from a department at BYU that teaches evolutionary biology, I'm not, one thing I would say is evolution is a theory. I think everyone needs to just remember that we don't know how we came to be what we are. And when I see scientists or anyone stating it as fact that here's the evolutionary line of humans, no. Talk about faith. That's a declaration of faith. We don't know how we came to be who we are. And I'm left looking at all of nature and all the wonder of life with many conclusions, one of which is we are the alien here. There's nothing like us. So, either we were seeded by some alien species or we had a God create us. There's just, yeah, so even my scientific rational mind, I still am left coming to the conclusion that there is a divine design and a creator behind all of it. And some of the most effective apologists, I guess you would call them, like CS Lewis,

they were scientists and strong atheists, like you search, search, search, search, you'll come to the same conclusion. Do CS Lewis is a hero. I love that you mentioned it. Everyone go read his books. Oh yeah, well thanks for coming on, man. My pleasure. Thank you guys. We'll have you back on Oh yeah. Well thanks for coming. My pleasure. Thank you guys. Well, have you back on for sure. Yeah, my pleasure. Appreciate it. Thank you. at mindpumpmedia.com. The RGB Super Bundle includes maps anabolic, maps performance, and maps aesthetic. Nine months of phased expert exercise programming

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