Speaker 1People don't crave fat. They don't crave protein. There's zero evidence in humans to support that. They crave carbs. And so that's what these medications can help with.
Speaker 2You are tuned into The Dr. Tina Show with Dr. Tina Moore. For more, visit drtina.com. On this episode of The Dr. Tina Show, I am so excited. I got to have Dr. Ben Bickman join us for this episode, and I could not be happier. Dr. Bickman is an expert in metabolic health and insulin resistance. He wrote the book, Why We Get Sick. Wonderful read if you haven't read it yet. He's a professor at BYU, and the man knows his shit. And I missed him. I missed my opportunity to have him on the show months ago when my Instagram got taken down and I was so heartbroken. So we finally got him on and we had the most spectacular conversation. I know you're going to love it. We even talked about GLP-1s, and I think I maybe taught him a few things that he's going to look into in his research at BYU. So stay tuned. Anyway, without further ado, let's jump in. Dr. Ben Bickman, I am so excited to have you on The Dr. Tina Show. I have tried and tried, and I messed up with our last appointment, and we didn't get to have our interview. So thank you so much for making the time today to be here.
Speaker 1Oh, my pleasure. Yeah, I'm glad you finally got done standing me up. It's time we got together.
Speaker 2I know. I know. To my defense, I was deplatformed from Instagram that week, so I was having some drama. Yes, there was like, you know, the cortisol face you see on the internet. People are like, that's not real. And there's videos of me from that week. I'm like, there's your cortisol face. I'm round as round can be from stress. So you are just a legend in my book, and I love everything that you say. And you really tease out the nuance of things, and you're not ever painted one way or the other. You're just a really good professor. So let's start with that. You're a professor. Where do you teach? What's your background?
Speaker 1Yeah, yeah, right. Yes, I do love being a professor. I'm in the cell biology department, and I have been at BYU, Brigham Young University, tucked up in the Rockies of Provo, Utah for almost 15 years. And I do love being a professor. And in particular, I like being a professor at a private religious university, not for the reasons people would think. Yes, I'm religious, but I actually like being at a private religious university because I can just teach science. I don't have to worry about the infusion of any kind of religion. I don't have to worry about the political ideology or not worrying about being beholden to any state funding. It's just teach science, teach the topic, and that's what I get to do. And I really do enjoy it.
Speaker 2Yes, and you are always so diplomatic and just objective, and I think it's beautiful. I know I bring a lot of fire and passion to my opinions, and I can't help myself. But truly, I was trained. My degree is my bachelor's in biology from U of O, and I am a biology geek. And so I do get impassioned because I feel like the last several years, basic sciences has just been thrown to the wayside and redefined with dogma and ideology. And my heart broke a little bit over the last few years watching that happen, a lot actually, because I just truly believe in good old basic sciences. And there's good and bad to a lot of what we're hearing on the internet, and you always just bring the straight facts. So thank you for that. Well, good. You're welcome.
Speaker 1Yeah, no, we're totally aligned on that.
Speaker 2Yes, awesome. Okay, so you have written a book called How to Not Die, right? Is that the title?
Speaker 1Well, yeah, so a couple of books. Yeah, first, Why We Get Sick was basically just meant to be a primer on insulin resistance, something at the time no one was talking about. And I'm thrilled that it's become so much more common of a topic. And then there was a follow-up called How Not to Get Sick, was essentially just implementing some lifestyle changes to help address insulin
Speaker 2resistance. Yeah, yeah, good. And you really break it down in there. I think that even your opening chapter of the Why We Get Sick, I mean, you, within a chapter or two, you're just, you dive right into the cardiovascular impacts of insulin resistance, which I don't think people appreciate truly. And this is something my mentor taught me about insulin resistance way back in the early 90s. And so I have been beating this drum with my patients and with the, you know, my fledgling online following when I first started, and nobody wanted to hear it. Nobody cared. And so I've been doing this for a long time. And I've been doing this for a long time. And I feel like I can't believe it's been this many decades that people are finally starting to get it. He was teaching me to keep your waist circumference low, to not eat, you know, loads of carbohydrates at lunch. He told me in 1995, he told me to bail on so much cardio and start lifting weights. Wow. Yeah, really ahead of his time.
Speaker 1Yeah, yeah. But just as a testament to what you're saying with regards to the disregard for the topic, when I was even proposing, and this was about 2018, I had a variety of titles for the book, including just sort of insulin resistance, what it is and why you should care or something like that. But I knew no one would care. People see the word insulin and immediately just think, well, I'm not diabetic, so that doesn't apply to me. Little knowing that now this is the single most common health disorder worldwide, not just an American problem. And so I had to think of something a little more provocative just to get people to stop and actually be interested in the book.
Speaker 2Yeah, yeah, no, it's perfect. It's great. It's a great read for anyone who hasn't read it. It makes all the sense in the world and it breaks it down for you in a really digestible way. So why don't, I know I've probably beat this into my listeners way too many times, but in your definition, can you describe insulin resistance?
Speaker 1Oh, yeah, my pleasure. Yeah, I think it is, there's an obvious component to it, and then there's a less obvious component to it, but they are both components. You cannot have one without the other. And it's important just to state this up front. Because people may hear other instances where insulin resistance is invoked improperly in various contexts where it has no business being brought up. So with all of that weird preamble in mind, we can think of insulin resistance as a coin with two sides or a pathology with two parts. On one hand is the obvious aspect, which is that the hormone insulin isn't working quite as well as it used to. Now, I'm deliberately being a little soft on that. I'm very soft in my language because there are some tissues or cells of the body that are still responding to insulin perfectly well, but then there are others that are not. And that's where the insulin resistance component has come in, where some cells are indeed resistant to the hormone insulin's effects. And insulin does a lot of things throughout the body. Literally every single cell of the body has insulin receptors. So it does more than just control glucose, which is all some people, even very well-trained clinicians don't know. That insulin does more than regulating glucose levels. That's just its most famous effect, but even far from its most important. Now, that's one part of insulin resistance. And again, the most obvious for something called insulin resistance. But the other part is very important to really understand why insulin resistance is so problematic, which is hyperinsulinemia or elevated insulin. The reason, whether it's pathological insulin resistance, like we're talking about when it's causing diseases, or whether it's physiological insulin resistance, which is when the body's become insulin resistant for a purpose to fuel growth, like puberty and pregnancy, even then, if it's insulin resistance, you will always have elevated insulin. And then just to really put a fine point on that, bringing these both together, one of the most compelling examples is the fact that insulin resistance is so problematic. Now, the other part of insulin resistance is looking at infertility, just to use it as an illustration here, where in women, the most common infertility is polycystic ovary syndrome. Well, one of the interesting features here is that the cells, the theca cells and the granulosa cells of the ovaries that are responsible for making estrogens, the female sex hormones, of course, your audience, I need not go any further into that topic. You guys are so well formed, informed because of what you've taught them. So estrogens were once androgens or testosterone. And there's an enzyme called aromatase that will mediate that conversion. And those cells maintain their insulin sensitivity. And so as insulin levels have been going up in insulin resistance throughout the entire body, those ovarian cells are responding really, really well to it. Now, we would say they're responding too well. Insulin's inhibiting the aromatase, which is preventing her body from converting testosterone into estrogens, and thus her estrogens don't go high enough to have a normal ovulatory cycle. Now, on the other hand, though, is the most common form of infertility in men, which is erectile dysfunction. In that instance, it's actually less a problem of the hyperinsulinemia like PCOS is. And now it's really a problem of the insulin resistance. But in this case, it's because his endothelial cells have become insulin resistant. So the cells that line the blood vessels, normally insulin will tell those cells to dilate. Now the cells aren't listening. So in the case of male infertility, it's actually the resistance part. In the case of female infertility, the most common form in both, now it's a problem of the hyperinsulinemia. But both of them happen in a body that is experiencing insulin resistance.
Speaker 2Wow. I had never thought of it that way. I wish you were my professor in undergrad.
Speaker 1Well, I'm delighted to be your honorary professor for the next hour or so and everyone listening.
Speaker 2I know. I woke up and I was like, I get to interview Ben Bickman and my husband knows nothing. And my husband's like, "Who's Ben Beckman?" And I'm like, seriously, I could talk to this guy for like six hours if I could just co-op his time, like pull him over here and say, give me the download. We could nerd out. Yes. Okay. So I think that folks, I'm guessing my audience has a general idea of why insulin resistance is a problem. Can you give us the kindergarten version? And then I want you to share what happens when you have all this excess insulin floating around in the bloodstream and what it does to fat cells.
Speaker 1Oh, yeah. I'd love to get onto that topic. Yeah. So insulin resistance, to help people appreciate why a scientist would devote his career to it, why your mentor focused on it well ahead of his time, I would say, 30 years ago. No one. I thought people weren't talking about it 10 years ago, let alone 30. So insulin resistance is the most common health disorder, like I mentioned. Evidence within the U.S. suggests that potentially up to 88% of all adults in the U.S. have some disorder. And that's a very high degree of insulin resistance manifest based on markers of the metabolic syndrome, these five features that clump together. Well, the metabolic syndrome used to be called the insulin resistance syndrome, and I wish it still were because it's a more accurate name. Now, I've found as a Canadian American, I've found that no one disrespects America like Americans. You know, Americans want to think that America is the fattest, dumbest, worth living. You know, Americans want to think that America is the fattest, dumbest, worthless country on the planet. And as a person who's traveled the world and is not born here, that couldn't be further from the truth, even metabolically. So, in fact, the most insulin resistant countries on the planet, more than the U.S., are actually several countries through the Middle East and Southeast Asia. So as bad as we think we have it, you know, we don't actually take top spot. We're not even in the top 20, probably, to be perfectly frank. So, nevertheless, it is an extremely common problem. It is probably the leading contributor, if not one of the main leading contributors, to virtually every chronic disease. Heart disease, you mentioned, Alzheimer's disease, fatty liver disease, the most common liver problem, type 2 diabetes, of course, and infertility and so on. So that just helps people put things in perspective. Now, to my great delight, one of the topics that my lab has focused on, like literally growing fat cells in Petri dishes right down the hallway in incubators in my lab right now, it has been to focus on the variables that influence fat cell dynamics or what is it that makes a fat cell grow. And then when we know that, we can appreciate the variables that we can leverage to help fat cells shrink. So there are, in fact, two essential variables. One is a variable that is the only one anyone has ever heard about, namely calories. And energy does matter. Those little carbs. Those little carbons that we call calories, which don't even get me started on why we ever invoked thermodynamics in biology. I think it's one of the dumbest, most egregious directions biology ever took. We're not eating units of heat. You know, we're eating carbons. And so why are we calling them units of heat? Why are we calling them calories? Anyway, it is the game that we're playing. And so we'll play along. So we eat calories and calories do matter. However, the calories need to be told. What to do at the fat cell or to say that all another way in order for a fat cell to grow, it must be told to grow and then it needs to have the fuel for that growth. They're not the same thing, Kate, for example, just at the level of the cell, we have fat cells if they're they can be swimming in a sea of calories, lots of glucose, lots of fats, and they stay skinny little small fat cells. They don't even look like a fat cell until. We start spiking in a little bit of insulin, then we can check four hours later, they're bigger, check four hours later, again, they're bigger, still check 24 hours later, and they're big, fat, juicy fat cells, just like you'd think about now, even at a human level, we see this, albeit somewhat tragically, there are people who get diagnosed with type one diabetes when they are in their early teenage years, when we're very fragile emotionally, we're very prone to being susceptible to peer pressure. People learn that they can skip their insulin injections and be as skinny as they want. This is in fact so effective and so common that it has a name called diabulimia. Anyone can look it up. This is absolute proof that there is another component to why fat cells get big in addition to just calories because these people can literally eat 10,000 calories a day of pure chocolate cake. They don't have to throw it up. They don't have to starve themselves. They can eat it and enjoy it, and they just look at that needle. I mean, imagine the temptation. They look at that little syringe and say, you know what, I don't want to poke myself with you right now because I want to be skinny. Now, there's a metabolic storm raging in their body because of this, and it is very harmful and lethal, and yet by directly controlling their insulin levels, allowing it to stay low when it should have gone high, they cannot store fat. So as much as we ardently pound the table and claim that calories are all that matters, no, I can prove that wrong, and I just did. All you do is wipe out the insulin, and the human body has no potential to store fat. So the relevance of insulin with the fat cell is that it's like the fat cell is like a naughty kid. It has all these calories around it, and it doesn't know what to do with it. It needs to be told. Insulin is the signal that tells the fat cell it's time to grow, but then the fat cell says, okay, I'm ready to go. But with what? Okay, now I pull these calories in. If you have one variable up without the other, it's death. It's incompatible with life. That's why insulin, for reasons that, for the sake of time, perhaps I won't get into, but I'll follow your lead, but that is why insulin is referred to as the hormone of the fed state. When Dr. George Cahill, famous fasting starvation physiologist, was asked about the difference between the fed and the fasted states, he said it's all a matter of insulin. If insulin's high, it's the fed state, and in a fed state, the body, the fat cells will say, all right, hey, there's energy to store. I'm going to hold on to this because we might need it later. When insulin is low, even if calories are coming in, the fat cell doesn't know it. In the absence of an insulin stimulus, the body thinks it's still in a fasted state, and thus cannot, the fat cell is going to say, well, I'm not going to store energy if insulin isn't telling me to because I don't want to be pulling it in if other parts of the body, if we're fasted. Then we need to be mobilizing energy, not storing it. So that's a long-winded way of answering your question about the relevance of insulin on the fat cell, and the short answer is it's utterly critical.
Speaker 2Yes. This is why I say that when middle-aged women start getting the middle-aged middle, and they go from that gynoid, curvy shape to that android shape, that is insulin resistance starting. Oh, yeah. That is when we have to nip it in the bud, and we live in a society where we have normalized that. Because the estrogen is waning, so they're becoming more insulin resistant, and society is like, oh, just, you know, we don't do anything until people get into some severe state or until these secondary pathologies start showing up, you know, like the cardiovascular disease and the, you know, all of it. It's just bizarro land why we don't address these things. You know, going back to what you said about metabolic syndrome, my mentor taught me about that when it was called Syndrome X. Yeah, that was the very first title. Way back when, and he diagnosed me. My tiny little petite mom just gained a bunch of weight out of nowhere, seemingly nowhere. It was menopause. And he was like, hey, we've got insulin resistance here, you know, and that's when I learned about it. And it's just, it's been mind-blowing that all these years have gone by, all these decades. I really thought that during the past few years with the virus that shall not be named, I really thought that people would take it seriously because I was like, you guys, metabolic disease is what's driving the poorest outcomes with this, and we need to take it seriously. This is something we have control over. This is something we can do something about. And through trying to educate people, I was just heavily censored. And that's when I knew. I was like, something is awry because I was telling people to go for walks outside in the sun, eat meat, and lift weights, and I was getting censored.
Speaker 1Yeah, in fact, I couldn't, even to this day, I'm surprised that the role of the fat cell hadn't come up more. There are multiple reasons just to touch on this topic lightly, just like you are, and I appreciate that. But in order for a virus to work, it needs to get into a cell. And one of the ways in which the unnamed virus gets into cells was through a receptor called ACE2. And guess which cell type expresses more of that than almost any other cell type? The fat cells. And so it stood to reason that if someone had more fat cells, there were more potential factories to pull in and start reproducing the viral part of the virus. So, yeah, there was a huge, from the very, very beginning, we knew of that. And yet, you're right, you could not talk about it.
Speaker 2No, no. God forbid we empower people to. Yeah. Take their health into their own hands. Treat them like adults. Yes, exactly. All right. So we've talked about insulin resistance. We've talked about fat cells. Let's talk a little bit more about fat cells. So it's the big, inflamed, full fat cells that are the problem, right?
Speaker 1Yeah, yeah. It's the hypertrophy. That's exactly right. Yeah. So there are more and more, as I think about insulin resistance, I think that I ought to have, if I could make one edit to my Why We Get Sick book, I would have described insulin resistance kind of along two paths. Fast insulin resistance and slow insulin resistance. insulin resistance. So this is literally the first time I've ever articulated this in public because I've just really been wondering how I can present these ideas in a more precise way. So there are these, the fast causes like too much insulin, stress, inflammation, those are things that will cause insulin resistance literally within hours. But as the stimulus goes away, so too does the insulin resistance. So it's fast on, fast off. Then there's a slow insulin resistance that will settle in over time and take longer to go away and that's the fat cell. So even the example you just mentioned where, what is it about the woman going through menopause where she goes from the gynoid fat pattern to the android fat pattern and that happening to, I basically say that when a woman goes through menopause, she becomes a metabolic mortal that prior to that, she's sort of bulletproof. She's a superhero when it comes to metabolism. The chances of a premenopausal woman getting things like heart disease and type 2 diabetes are so fantastically lower than her male counterparts as to make her almost a demigod. But with the loss of the sex hormones in her favor, now she becomes a mortal if you will. And a lot of that is, estrogens have myriad metabolically favorable effects. One is to tell her where to store fat and now back to the fat cell. When we store fat subcutaneously or beneath the skin and more of the gynoid pattern, that is a healthy place to store fat because those fat cells have the ability to multiply. In part, thanks to estrogens and progesterone and that means that the potential to store fat is higher but it means also that the size of the fat cells are smaller and that's what matters most. People like to focus on fat mass, no, it's the size of the fat. The problem with the male pattern of storage, android, particularly fat that is stored within the abdominal space is that those fat cells will almost only grow through hypertrophy. So that brings us to the size matters here. Small fat cells are very anti-inflammatory and very insulin sensitive. Big fat cells are, in fact this is worth elaborating because it's just so fascinating, there's two things that go wrong. So firstly, as the fat cell is getting bigger and bigger and it can get like 20 times bigger than the small fat cell. There's no cell in the body that is capable of this much growth. But it's almost like a balloon. The kid's been filling the balloon on the tap with making a water balloon. Now it's reaching a point of maximum dimension but they're still dripping in water and so rather than bursting, the fat cell says, "You know what, insulin, you are high, that's why you got big in the first place. I can't listen to you anymore. If I continue to be insulin sensitive, I'm literally going to burst my membrane." Because like a balloon, there's only a finite capacity for a volumetric expansion. And so it says, "I have to stop listening to you. I'm going to become insulin resistant," and it starts leaking out its fats. So that is one of my favorite clinical tests that can measure this right at the level of the fat cell. It's not easy to do because you have to do two uncommon tests. One is to look at the insulin and to look at the free fatty acids because free fatty acids or non-esterified fatty acids, NEFAs or FFAs, and they can be measured in a blood test. It's just kind of very rare and a little more expensive. If you see that insulin is high, which should be inhibiting the release of free fatty acids from the fat cell, but if insulin is high and free fatty acids are high, that is proof positive that the fat cell is insulin resistant, so you're getting it right at that kind of first cell level, and that's a test called the Adipose Insulin Resistance Index or SCORE. But nevertheless, so that's one thing that happens. Now where you have the fat cell leaking out its fats with all these free fatty acids going into the blood and the high insulin, now the body can start to experience a high degree of ectopic fat storage, so tissues like the liver or even muscle or the pancreas are starting to store a lot of fat, and you'd say, "Well, why don't they burn it?" because high insulin, they don't let them burn it. Insulin is forcing other tissues of the body to store it. So that's one thing that is wrong. It took me longer than I intended to explain it. Then the second thing is totally unrelated, which is that as the fat cell is getting bigger and bigger, remember, like 20 times bigger than it used to be, it starts to push fat cells further and further away from blood vessels, from capillaries. And in so doing, the cells start to become hypoxic or they start to suffocate, they're too far away. They're too far away from the blood to get that life-giving oxygen, and in order to try to correct that problem, the hypertrophic suffocating fat cell starts leaking out these pro-inflammatory cytokines, which are basically just pro-inflammatory hormones. Because some of those, among the dozens of pro-inflammatory cytokines being released, some will get to the capillary and tell it to follow the trail of breadcrumbs and start butting off. So it's a new capillary in order to feed the big fat cell so it doesn't have to continue to suffocate. So it's a way, so in both instances, now this inflammation though, of course starts to lead to this subclinical chronic systemic inflammation, which contributes to increased heart disease and insulin resistance in type 2 diabetes, but lest we blame the big fat cell too readily, we have to have some sympathy because both of these things, becoming insulin resistant, becoming pro-inflammatory, are efforts of the fat cell to prevent its own death. That it's becoming insulin resistant so it doesn't burst, because that would be very messy for the body to have to clean up, and then second, it's becoming pro-inflammatory to once again prevent its own death to try to correct the lack of blood flow. It's just that the rest of the body ends up paying a metabolic or cardiometabolic price in order to keep those overfilled fat cells alive.
Speaker 2This is what I call fat cells gone rogue. Because your immune system gets completely screwed up in this process and it all just kind of goes to hell in a handbasket. It's a big mess and it's hard to come back from. This is one of the places where I really think that appropriate low personalized dosing of GLP-1s can start to clean up the milieu and pull people back from the brink of this edge because people just don't understand it, this whole, "Oh, it's just calories in, calories out. Eat less and move more." That whole group on the internet, I'm like, "Tell me you don't understand metabolic health." That is a difficult place for some folks to come back from, and I'm all for giving folks a leg up to get them to start unwinding that and obviously bringing in. You and I both talk about this, like you have to do the lifestyle stuff or it's a moot point, but I do think.
Speaker 1But you have to do it the correct way. Like you're just saying, as much as you and I both are beating the drum, lifestyle, lifestyle, well, the conventionally trained individual, including with illustrious degrees after their name, when they hear lifestyle, they think, "Eat less. Exercise more." Just to really help see how wrongheaded that is and to help us have some empathy for those who've tried it and failed, if Tina and I, everyone listening, if we were hosting a really amazing buffet lunch and we had the best chefs in the world and there's going to be tons of food for people to come and eat, and we tell people, "You're going to want to try some of everything. Come really hungry," what are you going to do? Everyone listening, think about what you do before you go to a Thanksgiving dinner or your Christmas dinner. You do two things. You eat a little less in the days before, or at least the day before, and you exercise a little harder, and it will work. You will go to that event very, very hungry. Well, why then do we expect any different outcome when we give people that advice who have been struggling with obesity for decades? We tell them, "Eat less. Exercise more." Sure, you're going to lose a little bit of weight in the very, very short term, but that is the perfect recipe for hunger, and hunger always wins, and so on that long journey of weight loss. There are two variables. Those two variables that both cause fat cells to grow are the two variables you leverage to get the fat cell to shrink. Rather than having the first step be the low calorie step, if you haven't addressed your high insulin, that's going to make you very hungry very soon and you'll fail. Right before you know it, you'll be right back where you started. So take a low insulin approach, control carbs. First and foremost, don't count your calories. That will start to take care of itself, and then you'll start to go further down the road. Metabolic rate will go up. When insulin comes down, which it does, you'll start making ketones. Every time you're breathing or urinating, you're getting rid of the calories that come with those ketones, and so you're literally wasting energy from your body, further reconciling the calorie problem, and then eventually, if you need to, then you can start looking at your calories through some sort of structured fasting. But even then, so I'm very much an advocate of people getting the right information to help them. But as simple as that sounds, control carbs, unfortunately, all of the research into the neurobiology of addiction in humans suggests that humans display addictive tendencies towards only one of the three macronutrients. It's not fats. It's not protein. It's carbs. And so as simple as the idea sounds, control carbs, it's harder to implement than it would seem because that's what some people may have an addiction for, and that's where you and I are very much aligned on this, that's where I believe GLP-1 receptor agonist medication comes in in my view it's essentially a way of saying you're an addict to carbs and as much as you know you should be stopping them you just can't stop this is going to help because one of its effects is to act centrally to reduce cravings and again people don't crave fat they don't crave protein there's zero evidence in humans to support that they crave carbs and so that's what these medications can help with i'll be like like you though the lowest possible dose combined with the proper nutritional coaching and you and i are again aligned on this doing anything you can to keep your muscle mass
Speaker 2yep and just move i mean that's yeah at this point i just want folks moving and it does seem to get folks moving it's one of the i don't i don't entirely understand the mechanism but it's something that my friends who my clinician friends who are prescribing it and i've got a lot of folks who are in my course now that are health professionals that are working with people on glp ones or they're prescribing glp ones and they have concluded with me that there's something about it that in the brain centrally gets people wanting to move more i don't know if it's the anti-inflammatory mechanism and it's decreasing pain because i'm hearing crazy amazing stories on its reduction of pain for all sorts of different types of conditions but it gets people wanting to move and once that starts to me it's all about instincts i think if people's instincts turn on they start to make better choices but sometimes it's really hard to reset that lever to get those instincts to turn on because it could even be epigenetic they could have been bathing in insulin in utero and and come out just marked for you know it's just marked for obesity the thermostat gets
Speaker 1set uh in utero no doubt about it and that's why i would hate for anyone to ever hear me talk about this kind of thing and think that i'm just an absolute ball-busting authoritarian i actually have a lot of sympathy because people's genes and circumstances matter enormously and and that's why as much as i'm glad i don't feel like i need any kind of pharmaceutical help i'm not going to begrudge someone else if they do need it yeah talk
Speaker 2about that study you brought it up on one of your reels it's one of the first ones i found when i i have a theory about functional glp1 deficiency but that's a whole other conversation um i mean i just really think that just like functional hypothyroidism functional uh hypoadrenal functional i mean you can you can sort of eat and lifestyle your way into your hormones not working correctly and whether it's them being produced correctly or them converting correctly or them being received correctly i think that you can functionally get yourself there and i've always supplemented hormones on that premise and this is to me just another hormone right the glp1 is a signaling peptide hormone it's not a steroid hormone but i think that that's where i i think it can really sign for folks and then you did talk about this story on a reel about how obese individuals when fed fat had the same glp1 response endogenously but when fed
Speaker 1carbohydrates yes oh i'm so glad you brought that up that was one real you know social media for me is a real chore uh it's just it's just me you know like i sit in my office and the whole reason i even got involved in social media just as a funny little aside and i promise i'll come right back to this um was after i got tenure as a professor i thought i i just was struck by how irrelevant academia is how content science has become to just publish a paper in a peer-reviewed journal and and have no regard or concern for whether that actually is meaningful you know it's it's almost as if publishing these papers which we prize so dearly in academia it's it's like a currency that is fake it's like we're printing counterfeit bills because we go into the real world and try to use this peer-reviewed publication for any value someone would look at and say what the hell is that what am i going to do with this and and so i was very humbled by this a realization that that i didn't want like i literally asked myself looking out the window i said self ben do you actually know a topic that is valuable and and i thought in all humility yeah i think it is valuable i think my knowledge on obesity and diabetes is important and that was a there was a logical follow-up which was is is it sufficient then to just publish a peer-reviewed paper no i have to find another way to share and that was the beginning of the book and social media so that post was one that i i wanted often i don't care i don't really know how to manage social media and i'm not very good at it or i don't really know what to do and i'm bumbling along that was a paper where i thought this is really impactful and it's really important and it and i i worried that it didn't really catch on but it did for you and so now i'm happy to elaborate on it but it was just like you said where if you give as much as we blame fat you take an obese person and a lean person they're both going to sense a satiety from that fat in other words they would equally say i'm done i don't want any more you gave me i i ate i ate a quarter of a stick of butter and i just do not want any more um but give them carbs now all of a sudden that's where the difference is was and and so this is a drum i just cannot beat loudly enough a lean person could be defined by the person who can eat the most addictive of the macros carbs and have at least in one instance a such a sufficient glp-1 response that their brain says i'm done i'm good whereas the obese person one way of defining them could be you eat the most addictive of all of the macronutrients and you do not have an equal glp-1 response and so you're going to crave it more and so you ate that handful of gummy bears or a full half a pound of them whereas the lean person would have stopped at 10 pieces you haven't gotten that signal yet your brain isn't saying it's time to stop and so you just keep going now there's more complication to it than that but that is absolutely a part of it if if we can if we claim that glp-1 is a satiety signal and thus should be leveraged in pharmaceuticals you at the same time have to look at that study and i'm okay making that claim then you have to look at that study and have a lot of understanding for the individual who who literally may not be making as much glp-1 as you and so let's give
Speaker 2him a leg up absolutely that's exactly why i talk about glp-1s to give him a leg up i am one of those people i am a complete carbohydrate addict and i have a very so i used to be an anorexic i i learned i very specifically learned how to control my appetite as a young person and interestingly i lost the ability to have appetite control when i hit perimenopause it was just gone it it was just gone one day and i was like what is happening here what is going on and i know it was the estrogen waning and the shifts and all of that but when i took the tiniest little amount of glp-1 i of course guinea pig myself up first for this experiment and i took the tiniest little bit and boom that appetite control i'd had my whole life that i had ingrained in me was back and not to the point of anorexia of course because i like my muscle too much but i i always tell people i dose to appetite control not appetite suppression i have no interest in suppressing people's appetite for you that is
Speaker 1that's a brilliant way of stating it um because it allows you to help at least prevent some of the reason why lean mass may be so hit with these high doses one of the things i worry about is is the like true malnutrition yeah and so you don't want to get rid of that you still want to have an appetite for eating at least some good proteins and good fats i think that it's
Speaker 2actually a little bit anabolic at tiny doses and i think it's catabolic at high doses that's just my hypothesis and talking to a lot of people because i have a pretty sizable audience so i've heard from a lot of people i've heard from a lot of clinicians i've heard from a lot of folks using it personally and clinically and when given to a metabolically optimized individual such as myself who just was starting to get that little i was just going into that android body shape it's almost anabolic and then when you just a little bit too much can be a lot too much in those folks and all of a sudden you get into catabolic my hair starts falling out i start wasting it's like that so and it's the difference between the most minuscule amount and so i think there's a sweet
Speaker 1spot do you know what you're gonna get a kick out of this so we are we have been growing muscle cells in my lab treating them with doses of semaglutide in part to actually try to find out is it you know with that that paper finding that with the normal dose regimen used that 40 of the weight lost was from fat-free mass which would include some muscle although they didn't measure muscle mass but we're actually trying to determine whether it's a direct effect of the semaglutide or whether it's an artifact of the poor nutrition and so i actually literally just made a note we've been using the high dose that's used in all the clinical studies and so and showing that it's actually this is unpublished data so it's too early to really state this but we're actually trying to figure out what it is but it's not been good for muscle viability um but i we're going to
Speaker 2do a low dose yeah i'm talking low low like a fraction of the starting dose and it really depends on the individual's state of muscle as well so i've talked to some of the more like you know the the gym guys the strength and conditioning guys they might be utilizing it now for because i've consulted with a whole lot of people i'm not treating them but i'm consulting with them because they want my insight and they'll do the tiniest little dose and i have had so many people come back who were already very physically fit they're like they're like you like they're they're cut and they've come back and said it's almost anabolic it's like the same feeling i get when i use testosterone and i was like really and then i think you know there's some data showing that GLP-1s, and I don't know what doses they use, but it'll shut down adipose-derived stem cells. I think that's where we're seeing the ozempic face, the ozempic butt. It's not just weight loss. It's not just rapid weight loss. I think it's actually catabolic at higher doses. And hair fall will happen. The cardiomyocyte study that came out in mice, they OD'd those mice. I mean, severely. We didn't see the dosage, but you know better than I, usually in mice. I mean, from what I could tell, it was like 10, 12 times the regular dose in a human. And then they did it very rapidly. So they induced very rapid, intense weight loss in a short amount of time. And then they were like, oh, their heart cells shrunk. And I'm like, well, no shit. You can't put somebody into this catabolic state. And so that's just what I suspect. And I think it's, of course, different for each individual and depending on what their needs are. And I'm not trying to go against what Big Pharma is saying that we need to do, but I think it's different for each individual. And I think it's, of course, different for each individual. I just really want, my whole goal with this is to get physicians who are prescribing to understand that we need to use a more personalized dosing approach. And you don't just have to keep cranking people up to the highest dose to get the weight to come off. I've got my dad at the halfway point of semaclutide and I just waited. I waited, I waited, I waited, I waited. And about seven to nine months in, the weight just started melting off. And he was having very, very tiny incremental weight loss, which I wanted it to go slow for him because he's really conditioned and I didn't want to have any wasting. But all of a sudden it started, I had to pull the dose back. So I think it, it's a timing thing too. You know, I think it, for me, I have Hashimoto's and I was up to two grains of armor thyroid a day for like a decade. That's how much thyroid I was taking. And I am now barely able to tolerate half of a grain since I've been microdosing GLP-1s. So I think it's healing. I think, and it's time, it's time under treatment, you know, that leads to some of these healing anti-inflammatory regenerative impacts.
Speaker 1Yeah. Well, it sounds like you're doing it the right way, which is a more personalized approach rather than just saying, Hey, everyone just take this one dose without any regard to their individual circumstances. I think that is the best version of using these, these powerful drugs.
Speaker 2Yeah. I, I, I like that with any drug, but particularly, I mean, we wouldn't crank somebody up on insulin and expect great things to happen or leptin or ghrelin, right? So why would we do it if we don't have the ability to use these? Um, okay. So I'm going to jump back for a second, cause we were talking about hormones, uh, menopause and such. You made a great statement. I used the audio on a reel and it really caught fire and not everybody was happy. You talk about how menopause, you actually don't have a decrease in your
Speaker 1metabolism during menopause. Yeah. You don't. Yeah. I mean, don't shoot the messenger. Yeah. So that was Dr. Um, Herman Ponser, wrote that, uh, who was the lead author on that study. Yeah. It, it essentially determined in men and women from around the age of 20 to 60 or so, um, metabolic rate stayed the same. Um, now men have a higher metabolic rate, uh, than women at an absolute level. But when you control for, um, fat free mass, which is, I believe how they did it, it's, it absolutely just leveled right out. And it was essentially a flat line. Now women have like a pregnant woman and even through some of those menopause studies, um, menopause itself, that is like peak metabolic rate. You know, you are literally burning energy for two people. Um, you know, the, the, the busy work of growing a human. So metabolic rate hugely spikes during pregnancy, which is a confounding variable, of course, but yeah, it doesn't, um, it didn't slow down, um, until about the sixties. So yeah, I mean, menopause itself, which would have started well before then did not correlate with a drop off, but it's, it's, this is such a, one of the reasons I found that study very gratifying is because I have long railed against people blaming metabolic rate. Like I'm a college professor. I hear all kinds of silly conversations. One of them between students, uh, an often one is one over one chubby individual complaining about a lean roommate, a skinny roommate who just says, oh, they can eat whatever they want. And yet in reality, when you actually look at what these people eat, they don't eat as much as they think they do. And in contrast, the overweight person usually eats more than they think they do, but they would say, oh, well, this roommate, the roommate would brag. And while I got a high metabolic rate, I can eat whatever I want. No, no, that's just not true. Um, uh, or, or the person that isn't true actually, but I realized I'd kind of gotten onto a different topic, but the person would graduate and I'd see the student 10 years later. And now they're 50 pounds bigger than they were 10 years ago. Oh, well, I got married and my metabolic rate slowed down. Right? No, it didn't. You might've slowed down, but you sure as hell started eating very, very differently. So that's what I, what I don't like. What I found gratifying again is that it, it removes the, the kind of passive excuse of, well, my metabolic rate slowed down. So there's nothing I can do about it. It ends up giving someone an opportunity to not be responsible for themselves. And the study among many other cool findings was kind of a refutation of that idea. It said, to me, no, you can't blame your metabolic rate for gaining weight in your thirties or forties or even fifties, late forties, early fifties through menopause. It's not metabolic rate. Um, it's, I would say it's endocrinology. Uh, it's further evidence that, that our thermodynamic or caloric centric view of obesity is, is wrong that it is not complete, that there is a broader, um, inclusion here that, that absolutely involves hormones. Yes. Most, especially insulin, nothing is as powerful as insulin, but other hormones like estrogens, estrogens are fascinating at fat cells, really accelerating fat cell turnover. Yes. Facilitating the storage of fat, but really facilitating the burning of fat, which is why women at any moment are burning about 40% more fat than men as a function of her body weight. It's all because of estrogens. Then there's the kind of wild card of progesterone, which is basically, the body's way of making a brief check and pausing and saying, Hey, we might've just gotten pregnant. So let's get a little hungrier and store a little more fat. And that's what happens. Progesterone will have a central effect at the brain, telling the woman that she's hungrier than she normally is for that, you know, that period of time when progesterone spikes. And then either there was fertilization and implantation in the words pregnancy. And then that progesterone signal just keeps going, wanting her to store that fat for the metabolic marathon of pregnancy. Or the signal goes away because it says, Oh, actually false alarm. We didn't get pregnant. Let's go right back to normal. And sure enough, she does. So that's my rambling way of just saying hormones matter when it comes to metabolism, which, and that is one reason why as a professor, when the opportunity came up for someone to take over our graduate course in endocrinology, I was willing to burn every bridge with every colleague to just ensure that that became my assignment. Because it allows me, it allowed me to, it allows me to go. I have a whole lecture devoted to the endocrinology of metabolism that these students will have learned some biochemistry. This is lipolysis. This is ketogenesis. This is glycolysis without ever realizing that which of all of those processes is turned on can be completely dictated by hormones.
Speaker 2You need to make that course in the Jordan Peterson Academy.
Speaker 1I'm going to do it on my own. In fact, just kind of early announcement on my benbickman.com site. And I'm actually in the process of making my Metabolic Science Academy. And I'm going to just start taking like the best of my lectures that I've ever prepared and just start offering them there. So that's going to be one.
Speaker 2Yes. I can't wait. That's so great. It's so true. It's just the symphony of the hormones gets completely skewed as we go through big shifts and that impacts the fat cells. Oh, yeah. Yeah.
Speaker 1There are fewer shifts. It's as big as menopause, much to the chagrin of every gal who has to deal with it. Of course, it is. It is a monumental shift. I know as a guy, of course, I observe it just as a scientist. But yeah, I mean, these are extremely powerful hormones. And I meant what I said with the advantage of the female sex hormones. A woman is kind of a superhero that she can handle all kinds of metabolic abuse and kind of shrug it off. But if she what worries me is that if she's if that has enabled her to adopt bad habits, the bill comes due. When those hormones go away, now buckle up because you're in for a hell of a cardiometabolic ride.
Speaker 2So true. I think of it this way. We turn into little potato shapes when we're tweens, when we're pre, you know, we're just in that preteen mode where we're like we haven't really hit menses yet and we're just little potato shaped girls. We go from skinny little girls to potato shaped girls and then we get curvy. And then we go back to potato shape when we hit menopause. And it really sucks because I was a total potato in sixth grade and then I turned into a total potato shaped girl like a year ago. And here's why I again, why I like GLP-1s because if you take a very inflamed, low muscle mass, high adipose, high visceral fat, high inflamed, you know, high body fat, specifically that visceral fat, and you start throwing estrogen replacement therapy at it, you're going to end up with a very inflamed, low muscle mass, therapy at that woman, the conversion into estrone is going to be, it's already happening, right? Because the fat turns the testosterone into estrone via aromatase. And things don't always go down the pathways we want when we put estrogen in that body shape. And so to me, GLP-1s, again, are a beautiful way to clean up the milieu and get some of that body fat and that body composition shifted and that metabolic health revved. And then we add the hormone that they so desperately need because it needs to be in there, but it doesn't always go well if we put it into that.
Speaker 1That's a great way. That's a great perspective. Not only to acknowledge, good for you for acknowledging the relevance of the fat cell in the endocrinology of the menopausal woman, because it does. The adrenal gland and the fat cells essentially start to try to pick up the slack, albeit poorly, from the ovaries. But yeah, I mean, if a woman has expanded her fat too much, then it's not going to cooperate like she thinks it is.
Speaker 2Yeah, yeah. And then I would see on labs, you know, I'll do, I'm not a huge fan of the Dutch test for diagnosing or for finding out base levels, but I think, or baseline, but I think that it's great to see what pathways things are going down. And I just think, you know, it's the estrone is the problem. It's the problem child in the equation. And menopausal care up until recently has really been led by too many, and no disrespect for you for being a guy, but too many old guys saying, oh, well, you've got your fat to convert into estrone, so you'll be fine. You don't need any HRT. Well, I mean, I've been on the women's health initiative, obviously, just through a wrench and everything. And I never stopped prescribing. My mentor taught me how to do it right. And we knew that that study was busted. So I've been prescribing HRT for two decades with no problems, but I think that it really does matter the body you put those hormones in, right? We really, we need a metabolically sound body to get the optimal effects and pathways going.
Speaker 1Well, I think you're doing it perfectly.
Speaker 2Thank you. Thank you. That means a lot, actually. Okay. Let's talk about, another subject which you and I were talking about offline, AMPK, SIRT1, mTOR. Will you please explain, because I know you can do this better than I, what those pathways are, why they're important, and then why it's so important to have them in balance because we see so many influencers or supplement companies trying to drive one end or the other.
Speaker 1Yeah. Yeah. Boy, what I like about that question is it brings up the whole, whether people acknowledge it or not, it really touches on the deeper. question of longevity because those are the targets, the oft-invoked targets of longevity in one way or another. So to put it succinctly, AMPK and mTOR represent, they each represent the opposite of the two features of metabolism. So metabolism is the sum of all of the biochemical reactions in the cell. In those biochemical reactions, the metabolic reactions can be broken up into the reactions of the cell. So the metabolic reactions can be broken up into the reactions of the cell. Breaking things down or catabolic or building things up, anabolic. So metabolic is both of those things. AMPK is the penultimate catabolic signal. If AMPK is turned on, the cell is breaking things down. Now that is not a bad thing because that's, for example, activating autophagy. So it's just wanting to take all the things that are built up, including fats and glycogen, and start breaking it down and burning it, activating autophagy to clean some things out. So it's the process of breaking down and cleaning. Whereas mTOR is the penultimate or the poster child signal for anabolic, promoting the building up. Unfortunately, mTOR has become a villain. The bordering on bizarre longevity gurus that we see out there nowadays will be doing everything they can to vilify mTOR and keep it down, including taking drugs like rapamycin. Well, if you are inhibiting mTOR too much, it's no surprise that you're going to have a hard time building things up. And that's why in human studies, people who are using rapamycin, they find that in response to protein, their ability to induce or activate muscle protein synthesis is demolished. Or what about workouts? After a workout, you normally have a period of building back up unless you're on rapamycin, because then that effect is inhibited. So now someone may hear that and think, well, okay, then I want mTOR too much. But if you're on rapamycin, you're going to have a hard time building things up. After a workout, you normally have a period of building back up unless you're on rapamycin. Well, okay, then I want mTOR too much. But if you're on rapamycin, you normally think, well, okay, then I want mTOR turned on all the time. Well, that's a good way to cause a cancer because then it's just never ending growth. And so the balance of these two, it's really an elegant kind of yin-yang variable where you, in order for proper growth, which is what we care about, you and I share an affection for building and maintaining muscle. If you have too much mTOR activation, you actually start to get diminishing returns and you have an mTOR resistance or an anabolic resistance. But of course, if you have too much AMPK, you're going to have a lot of you have no growth. It's constant breakdown. And so you need to have these periods of going on and off, on and off. That is the key in order to have sustainable muscle growth and bone growth and maintenance. So you need to be able to turn mTOR on. Insulin will turn mTOR on, but so too will amino acids. And I would argue that amino acids are going to be a better signal because it turns mTOR on and then it allows it to turn off. The problem with insulin is that we, we eat an overwhelmingly carb-heavy diet. We eat every two hours. Insulin is never allowed to come down during the day for most people. And so insulin is activating mTOR every waking moment of the day. So we don't want an insulin-induced mTOR activation because it may go too long. We want a protein-induced or amino acid-induced mTOR activation because it'll turn on to facilitate muscle protein synthesis, and then it will turn off to facilitate autophagy and fat burning and glycogenology. Dr. Justin Marchegiani: And then later on, we'll turn it back on. And so to me, the ideal method of maintaining muscle, which is critical to longevity, critical. I mean, just to add one more comment on that, when I see older people just jogging, jogging, jogging, I put my head in my hands. That is not, it is, that is, how, how quickly you run 10 miles is in, on no radar of longevity by way of predictors. How strong you are and how much muscle mass you have, every single study on longevity shows that those are significant variables in predicting. So you want to, longevity. So you want to do whatever you can to build and maintain muscle. So you do need to work out, but you may as well get as much help as you can by making sure you're activating mTOR with a workout and some good protein, and then you're turning it off by doing generally low carb or some fasting, et cetera.
Speaker 2Dr. Amy Moore: Yeah, I love this. That's, that's a great way to explain it. I was taught a long time ago to keep mTOR activated after a workout. So don't go drink alcohol after you lift weights, because you'll shut off mTOR and you'll shut off that great building response. Make sure you get enough protein around your workout so that you have that mTOR, but you don't want mTOR on, you know, nonstop. Going back to GLP-1s, it drives AMPK, SIRT1 pathway. So maybe that's why it's causing why I think it might be. Dr. Yeah, just like you said earlier, when
Speaker 1it gets too high and it goes, it's too catabolic, it's shifting that balance. So the whole metabolic system is shifting more towards catabolic than anabolic when it goes too high, which isn't surprising. I mean, the poison is, the dose makes the poison here. And as much as GLP-1 is a good thing, insulin's a good thing, leptin's a good thing, but when we have too much of a good thing, it's become a bad thing.
Speaker 2Dr. Absolutely. No, 100%. Okay. I think I, cause that was my last question was problems with rapamycin. It's funny, I've never wanted to take that and I've been asked by so many people my thoughts on it and I'm like, I don't have a lot of good thoughts on it. Dr. I feel like messing, I feel like the whole metformin, rapamycin, I feel like messing with all of that is not my fave thing.
Speaker 1Dr. Oh, no, no. In fact, yeah, even metformin, thank you for mentioning it, where even in metformin, a very compelling study published out of Colorado State University found that people who exercised, in this case, aerobic, they did aerobic exercise, looked at muscle mitochondrial function and biogenesis and found that no surprise, it went up. But when they took metformin, it totally negated it. It literally wiped out all of the mitochondrial adaptations of the exercise. And so those two should never go together. If someone's on metformin, I'd say as you start to be able to exercise more, not that I'm giving any medical advice here, but talk to your clinician about weaning off the metformin, cause those two do not play nicely. But it's been a bit of a kind of dark humor for me to see some of these longevity gurus who go on rapamycin thinking they're being so clever only to find out that it's actually destroying their body. And then to make a thoughtful post about my clinical team and I have really looked at this and decided I shouldn't be taking it. Yeah, you think? Just eat some meat, get this guy a steak and he's going to be just fine.
Speaker 2Dr. Always. Steak and dark chocolate and deadlifts. Those are always the solution. And sunlight. I mean, you're probably not loving the sun as much as I do.
Speaker 1Dr. Well, I'll say this. When you have my complexion, a little bit of sun goes a long way.
Speaker 2Dr. I just had a basal cell carcinoma taken off from here, but I think that was from all the tanning beds in my teenage years.
Speaker 1Dr. Well, in fact, what's so funny is I had one taken off my head about a year
Speaker 2ago. Dr. Oh, man. It's just a bummer, right? To hit this age and you're like, oh, I guess this is when we start carving. Dr. Yes. Dr. Okay. I want to leave the men with something. You always sum it up so beautifully in all of your content. Talk about one of the easiest ways to increase natural testosterone. free available testosterone. Like what are some of the top ways that you like
Speaker 1Yeah, well, I appreciate you bringing this up. I just had made a mention of this recently, and I think that's on your mind. Yeah, so I've been always, once again, kind of found a grim amusement in the radio ads, in the ads, men, are you overweight? You're low T. You need to increase your testosterone. And I always sort of chuckled at the order of events. As a scientist, I always want my students and myself to be thinking of the pathway. What is the series of events? What is the domino that's falling into the other that's falling into the other? And the traditional view of obesity and testosterone in men, or just metabolic health and testosterone in men, is totally backwards. The traditional view is your testosterone's low, and that's making you gain weight. Now, to be clear, if a man actually does have hypogonadism, it will facilitate weight gain. It will make it harder for him to be metabolically healthy, but that's not common. What is much more common is that he's eating a lot of insulin, spiking foods with sufficient calories to tell his fat cells to get big. And like you'd mentioned earlier with menopause, when fat cells get big, they actually start to act like ovaries. And so now he has fat cells that are, it's literally taking in his testosterone and converting it into estrogens. That's not a good change for a dude. And it's going to make him start to store fat in an uncomfortable way, and he'll get man cans or man boobs, potentially. But also he. He's going to feel lower energy, his drive, his libido, all of these. Which women also benefit from when it comes to testosterone, mind you, of course. Both sexes have both of these sets of hormones, just in different ratios. But yeah, as much as the man may be told he has low testosterone, before you go on a therapy, not that I'm opposed to pharmaceutical help in this regard, but I do think it's in his best interest to say, well, how can I just give my testes a break? And let the. Testosterone that they're making just stick around a little longer. And that is just getting the fat cell out of the way. So the fat cell is almost working against the testes in this case. And the smaller the fat cells get, the more they have retreated, and the testes are allowed to win the war for testosterone and do what they want to do, which is make a manly man more manly.
Speaker 2That's a really great way to put it. I make all of my male patients sign a contract if I give them TRT, saying that they will eat a low-carbohydrate diet, that they will. They will strength train. Good for you. several times a week. Who knows if they follow it, that they will not consume a lot of alcohol, because it's just. It's not a get-out-of-jail-free card. None of these are. GLP-1s, none of them. You don't just get to, like, shoot your T and it's all good. Because what I have seen clinically is these men, if they continue down that aromatase pathway, and their estrogens start going up, and they start becoming very difficult. That is a very interesting behavior that comes out of these men. So they start. That is where I see the aggression of testosterone. When people say, oh, roid rage. It's not. It's actually, they just get kind of bitchy. I hate to say it, but it's like an aggression with sort of a bitchiness. And that's a really difficult patient to deal with. So I share that because it's true. And I think for women, I mean, just if we want balance, we have to have muscle mass, and we have to have our adipocytes smaller, you know, a little bit smaller, at least in that. Midsection of the body. We have to be cognizant of that if we want our hormones to work right.
Speaker 1Yeah. Yeah. Well said.
Speaker 2Amen. Awesome. Okay. Well, I want to be respectful of your time, and I could ask you questions for hours, but we'll do that another time. Where can everybody find you? Your Instagram is phenomenal. I'll just say that right now. Everybody go follow him. It's phenomenal information. Every single day I wake up to like a little awesome biology lesson. So where else?
Speaker 1Well, if I only knew how to manage it better. Yeah. So I try to be active on social media. But yeah, more and more I'm trying to create a central hub for my content, and that is now just benbickman.com. And Bickman is B-I-K-M-A-N-O-C. Benbickman.com, where I have different levels of kind of access currently than like I mentioned earlier. I'll be starting to release lectures, basically series to try to give people as much education as they want on all things metabolism.
Speaker 2Awesome. Well, I will send everybody to the right places in the show notes. I am so honored you came on and that you spent time today. And after I, after I stood you up, especially after I stood you up. Thank you, Ben. Thank you so much for coming on the show today. My pleasure. Thank you. Thanks for listening to the Dr. Tina Show. This is a Wellness Loud production produced by Drake Peterson and mixed by Mike Fry. Theme song is by John the Guilt. You can watch the full video version of this podcast inside the Spotify app or on YouTube. As always, you can email the podcast at podcast at drtina.com. That's D-R-T-Y-N-A. And if you like this episode, please rate, review and subscribe on your favorite podcast app. You can also find all of my offerings on my website at drtina.com. For more shows by my team, go to wellnessloud.com. See you next time. And thanks for listening. This podcast is for general informational purposes only. It does not constitute the practices of medicine, nursing or other professional healthcare services, including the giving of medical advice. I am a doctor, but I am not your doctor. No doctor patient relationship is formed. The use of this information, and the materials linked to this podcast is at the user's own risk. The content on this podcast is intended not to be a substitute for professional medical advice, diagnosis or treatment. Users should not disregard or delay in obtaining medical advice from any medical condition they have, and they should seek the assistance of their healthcare professionals for any such conditions.
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