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The SHOCKING SCIENCE On How To Prevent Diabetes & LOSE WEIGHT | Dr. Ben Bikman

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In this episode of Health Theory, Dr. Ben Bikman challenges the prevailing medical paradigm that frames Type 2 diabetes and metabolic syndrome primarily as a glucose problem. Instead, he argues from his book *Why We Get Sick* that these conditions are fundamentally diseases of profound insulin resistance and hyperinsulinemia (chronically elevated insulin levels). While high blood sugar is acknowledged as pathogenic in acute scenarios like diabetic coma or kidney damage via osmolar gradients, the chronic drivers of heart disease, Alzheimer's, infertility, and erectile dysfunction are attributed to excessive insulin. Bikman explains that current treatments often lower glucose by aggressively pushing up insulin production, which paradoxically worsens metabolic health over time. He posits that shifting focus from glucose management to lowering systemic insulin is crucial for detecting and treating the root cause of these diseases decades before traditional markers like blood sugar rise. The discussion delves into specific cellular mechanisms where hyperinsulinemia causes damage, particularly through Advanced Glycation End Products (AGEs) binding to Receptors for AGEs (RAGE), which triggers chronic inflammation and cell death in nerves and capillaries. Furthermore, Bikman details how excess glucose converts into sorbitol within cells that cannot store it as glycogen; this accumulation draws water into the cells until they burst, leading to tissue degeneration. The conversation also clarifies that not all fat storage is equal: visceral fat surrounding organs becomes insulin resistant to prevent organ crushing, whereas subcutaneous fat in women's gluteofemoral regions remains sensitive due to estrogenic influences and evolutionary pressures related to pregnancy survival. This distinction explains why men typically suffer metabolic consequences from weight gain sooner than women, as testosterone promotes dangerous central storage while estrogen encourages safer peripheral storage. To reverse these pathological states, Bikman outlines four core principles: controlling carbohydrates, prioritizing animal-based protein with fat, consuming high-quality fats like eggs, and practicing intermittent fasting. He asserts that carbohydrates are not essential nutrients for humans and that a vegan diet is incompatible with long-term human survival without expensive supplementation due to inevitable deficiencies in iron, vitamin B12 (leading to pernicious anemia), and essential omega-3s like DHA and EPA. Regarding protein sources, he emphasizes the superiority of animal proteins over plant-based options because plants contain anti-nutrients like phytic acids that inhibit digestion and may concentrate heavy metals. He also highlights a unique physiological advantage in exercise: muscle cells possess insulin-independent glucose transporters activated by contraction, allowing them to clear blood sugar effectively without requiring high insulin levels, thereby lowering systemic resistance after physical activity. The dialogue addresses the limitations of current pharmaceutical approaches for diabetes, noting that drugs which block carbohydrate absorption or force glucose excretion via kidneys often result in side effects like diarrhea and increased urinary tract infections without addressing the underlying metabolic dysfunction. Bikman critiques the medical community's tendency to prescribe medications rather than advising dietary changes, arguing that treating symptoms with pills while ignoring the root cause of insulin resistance leads to a cycle of increasing drug dependence and worsening health outcomes. He shares personal anecdotes regarding diet-induced relief from chronic pain, brain fog, and migraines, reinforcing his view that many distinct medical conditions are merely branches growing from the same tree—insulin resistance—and can be pruned by cutting down this root through lifestyle modification rather than medication management.
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A vegan diet, um, well, to put it bluntly, is incompatible with human survival. [music] Everybody, welcome to another episode of Health Theory. I am here with Ben Bickman. Ben, welcome to the show. Oh, Tom, my pleasure. Thanks so much. Dude, I'm really excited to talk about your book, Why We Get Sick, uh, which is really interesting and it's a take on what most people call metabolic syndrome that I've never heard before. Um, because I would literally, 7 minutes before beginning to research you, I would have said the problem is your glucose levels. And the fact that that is the very thing that you like swat down in the first like six words of your book, um, walk walk us through that. What's the difference? How is it possible that this is not a glucose problem? Yeah, yeah, so glucose, like like I mentioned in the book, glucose is really the sidekick, um, here of the story. And to understand metabolic syndrome, we need to understand the origins of that. Uh, even the term metabolic syndrome used to be called the insulin resistance syndrome. And I I regret that we ever left that title. Um, it's not that glucose itself isn't valuable, but it's that changes in glucose really ought to be viewed through the lens of insulin. And to to to defend that paradigm, let's imagine an an individual who's progressing from perfect metabolic health to um, metabolic disarray. And at the end of that would be type 2 diabetes. Type 2 diabetes really represents the the prototypical metabolic disease, which is itself a disease of profound insulin resistance. Now, to to kind of take us there on that journey through time, we would have an individual coming into the clinic, and year over year, we would be measuring their glucose. And we may see year upon year that their glucose levels are normal every time. And yet other markers of of disease are getting worse. Maybe they're gaining weight, their blood pressure is starting to climb, that is such a common one. Maybe they have some fertility issues. In women that would be PCOS, in men that would be erectile dysfunction. But throughout all of this, the the the physician starts to treat the person's infertility or they start to treat their hypertension, but the glucose stays normal and so they don't really pay that any regard. However, if we had been looking at insulin through this timeline, we would have seen that while glucose levels are staying normal, the insulin levels are going up. In fact, going up by potentially multiples. Where by the time that 10 or 20 years later, when we finally see the glucose starting to change, insulin had changed multiples. You know, it's maybe four or five times higher than it used to be. And if we shift the paradigm away from glucose to insulin, we not only detect the problem significantly sooner, indeed potentially decades, but we also treat the problem much much better because the the prevailing glucose-centric paradigm is that in type 2 diabetes, we have high glucose and we just need to do whatever we can to lower the glucose, including pushing the insulin up even higher than it was before. That works in lowering the glucose, but it reveals the the the problem in that when we lower the glucose, the more aggressively we're pushing up insulin to lower the glucose, the more we're literally killing these individuals. They they get fatter and sicker and die more by trying to push down the glucose while pushing up the insulin. Again, the paradigm should be this is a high insulin state, which is insulin resistance. We need to lower that not and then let the glucose take care of itself. Yeah, so this is interesting because um I'll start poking at the predictions that your hypothesis makes. [clears throat] So, if I could lower sugar without increasing insulin, then I should be able to um abate the problem because I still like glucose is still an issue, I'm assuming, right? Um oh, absolutely. Um and I don't want to I don't want to um derail that the point you're trying to make. Yes, and so I'll keep it brief. Glucose is an issue, but when type 2 diabetics are dying from heart disease and and kidney failure and other diseases and have a substantially increased risk of Alzheimer's, it's not the glucose that's doing that. It's the insulin resistance. But that's not to say hyperglycemia isn't pathogenic. It is, but all the prototypical problems, other than maybe the blindness that we associate with diabetes, those are really insulin problems. So, what's cool about the hypothesis, so um you know, for anybody playing at home, of course the thing I'm talking about to lower your glucose without um upregulating your insulin is diet. So, avoid things that have glucose in them and suddenly your blood glucose goes down. Um so, all right, that paradigm is interesting. So, I can pull my glucose down, it keeps my insulin down, and I'm going to be healthier. So, it'll be interesting to walk through um what the problems are that insulin creates, but first I actually want to understand better what the problems are that glucose creates. So, why is elevated glucose a problem? Why does the body work so hard? Because if I understand right, the difference between uh normal and somebody who's diabetic is a quarter of a teaspoon Yep. of sugar in the bloodstream, which is crazy when you think about how much blood you have in you, and it's that fine finely regulated. So, if my body is willing to pour this ultimately damaging hormone, at least in in um too high a level, what is it that becomes the pathological problem if I just let my sugar be elevated? Yeah, well boy, Tom, you're you're bringing up a lot of very interesting and relevant points here. So, gluco- hyperglycemia is acutely acutely lethal and chronic chronically lethal or long-term lethal. And acutely, um hyperglycemia can cause a coma, a non-ketotic coma it's called where if your glucose levels get too high, and this would it depends on the person, but it's typically around 200 mg per deciliter. At around that range, you are now you have a glucose amount in your blood that the kidneys cannot reabsorb. So, as you have all the blood passing through the kidneys, um the glucose will get filtered out and then it will get pushed right back into the blood. It'll get reabsorbed through these glucose transporters that are unique to the kidney. However, once we've gotten to that, you know, around 200, low 200s, now what gets filtered out into the urine or what would become urine cannot get reabsorbed. And so, now we have created an what's called an osmolar gradient. Basically, this pull pressure, whereas the kidneys are now pulling in too much glucose and keeping that glucose, they are demanding a certain amount of water to maintain a concentration that would keep it somewhat comparable with the rest of the body. And so, now the person starts urinating out profound amounts of of water. It's almost like a pressure valve where the body knows that the long-term consequences of the glucose are going to be disastrous and I'll I'll are they? I I want to really understand that. So, why am I having why am I going into a coma? Like, what's happening at a cellular level? Yeah, so that is the acute one. Um and that is that when when you're urinating out too much water, all of that water's coming from the blood, what's called the plasma of the blood, which represents the majority of of what we call blood. And so, naturally, as volume as the volume of blood starts to go down, so too does pressure. Pressure will go with volume, just that fundamental physical principle. And so the volume's coming down, pressure goes down, and we are a big column of water. And the one tissue that that is most susceptible to reductions in blood pressure is the one tissue at the top of this column of water, namely the brain. If we don't have enough pressure in the in the cardiovascular system, we literally cannot get blood up to the brain, and now the person will go unconscious and will stay unconscious. let me chase that what that hypothesis would predict is if I could somehow keep my blood pressure elevated, I could tolerate um more blood sugar. Is that accurate? You absolutely could. Now, but that would lead us to the long-term consequences, which is the damage to nerves and and and capillaries. There are two distinct mechanisms whereby hyperglycemia or chronically elevated glucose is going to damage cells in capillaries and and nerves in particular. They appear to be very susceptible to this. One is the activation of a receptor on all cells. All cells have this, and it's called the receptor for advanced advanced glycation end products or rage. That's the clever little acronym. Advanced glycation end products are literally just molecules of of taking a glucose and binding it to amino acids that are just circulating in the blood. So what ends up happening is that these advanced glycation end products will bind to these rage, these receptors, and then they activate inflammation. Rage actually is just what's called a pattern recognition receptor. It will recognize all kinds of things that are generally viewed as noxious stimuli. So essentially, rage is just waiting there to be activated if something messy comes around. And then it will say, "Hey, you're Yeah, like like like bacteria. Bacteria are a big one. So kind of infectious or harmful agents in the body. Rage is just waiting there to activate the immune system. And then what happens when we have chronically elevated glucose, we have advanced glycation end products chronically elevated and now the body is is essentially activating inflammatory pathways within cells all the time. And if a cell is activating those pathways for too long, it will activate apoptosis. It'll basically say, I can't I can't do this anymore. I need to die. And the second mechanism is is actually somewhat related to the topic I mentioned earlier about osmolar um gradients and trying to balance fluids. When when you have such a high level of glucose, many cells of the body have open doors for glucose. It where the glucose just comes in. If there's a higher amount of glucose outside the cell than in, then it just can't help but pulling keep pulling the glucose in. But that overwhelms the cells' capacity to burn the glucose. And cells can't most cells can't store glucose like the liver can. It can store glucose as glycogen. The muscle can do that, too. Many cells of the body don't have that capacity. And so that glucose sits around and then it gets converted eventually non-enzymatically. It's just this sort of process of the glucose changing into a molecule called sorbitol. And sorbitol is membrane impermeable. Once you have sorbitol in a cell, it literally can't go anywhere. And so you have more and more of this sorbitol accumulating in say the endothelial cells of blood vessels and then the these cells start pulling in more and more water and then they burst um through this degeneration process. They basically get so full of water that they pop. I love understanding this stuff at the cellular level and look, I'm so wildly ignorant. Like it's crazy to me that I've gotten to my age without having heard any of what you're talking about right now. Um so now walk us through what that looks like as pathology and then my next question will be why the cell cells start to get annoyed and start making it impossible to feed them the glucose. Yeah, yes. That this is great. This is a great progression. One let me make one other comment though that you you'd touched on or we were almost getting to and then you'd mentioned well if if I need ever more insulin to control my glucose, why don't I just put less glucose in the system? That strategy is so obvious that it has led to multiple drugs being developed that do nothing more than there there's two classes of drugs. One, it'll block the glucose from digesting. There there's this class of drug that will you can eat starch and you take this pill and it doesn't allow your intestines to absorb the glucose. And so the glucose stays in your guts and you sure you might get some diarrhea but then it never it never moves the glucose into your bloodstream. Alternatively, in that same family of drug, you have one that you can take that will actually force the kidneys to excrete more of the glucose. It essentially accelerates that natural limit or that that that it lowers that threshold making the kidneys more readily dumping out that glucose. It's not going to mess with my blood pressure though? Well, sure you have to drink a lot more water but it will work. It'll lower your glucose and that helps your insulin come down but Tom, you touched on it so accurately at the beginning. If I'm taking a drug that is going to block my glucose from coming in and give me diarrhea or I'm taking a drug that's going to force the glucose into my kidneys potentially well, drastically increasing urinary tract infections and maybe even increasing bladder cancer because cancer and infections all love glucose. Why don't I just take the rational so obvious approach of just eating less glucose? But that's the one conclusion so many in this diabetes space like genuine and educated and even smart individuals, they they cannot they cannot get themselves to that step. They can nod and write prescriptions for for glucose inhibitors for digestion and glucose pushers into the kidneys and yet never just take a step back and say, "Maybe I should just tell the person to eat less glucose." That is really the logical conclusion that's just being wait it's just waiting for the person to come to. And and you all you've already come to with this idea of frame of reference. Like everybody has a frame of reference and I've heard you speak to this with doctors. You said, "Look, a doctor's job is not to go research all this stuff. A doctor's job is to treat a patient." And when your frame of reference from schooling from just the society that you grow up in is, "Hey, there's a drug for that." That's, you know, that's what you reach for. And that's exacerbated and now welcome to sort of, you know, as as we all have ones that we love that struggle profoundly with um food relational issues. I won't go all the way to addiction, but I think that would be also a fair characterization. Mhm. Um you see them, you know, doing themselves uh great harm in terms of longevity, in terms of quality of life, inflammation, um just the level of adiposity that they're carrying around. And you can tell them, whether you're the doctor or someone that loves them, whatever, "Hey, by the way, just don't eat carbohydrates." And they won't do it. And so I imagine if you're a doctor day after day after day, your frame of reference is already drugs and you see the people, the vast majority just can't or won't make those changes, you just Yeah, there it is. Yeah, no, I think you're absolutely right. And I never intend to to paint all medical practitioners with such a broad in such broad strokes. Uh in fact, that's part of the tragedy of this all, isn't it? Where where we're we're describing this such a such an obvious conclusion, which is just eat fewer carbohydrates. And and yes, that is such a simple idea, but that doesn't mean it's easy to put in practice because to your point, when you start asking someone to change habits, you are probably asking them to do the most difficult thing they can do. It's just so much simpler to take a pill and consequences be damned. Yes, and here's one insight that I think a lot of people don't have. They don't recognize how much of their life is tied to diet. And I recently so I've I've been on that train for 15 years. Thankfully just encountered the right information at the right time. This does not make me clever. It just very luckily got onto that early. And even I about I don't know 12 months ago ish. Um I got into this thing where I was making this like pecan pudding thing. Dude, it was so good and I all of a sudden I was like, oh man, I've got like crazy brain fog and I'm tired all the time, but it was happening at a time where I was stressed and I was just sort of losing my enthusiasm for life. And so I was just like, oh man, you know, I've I've got to change something so we you know, what's going on? What's happening in my life? And I was like, okay, what advice would you give to somebody if they came to you with this problem? And I would say, it's your diet, man. And so I'm like, is it your diet? Like you know about this stuff, but is it your diet? And so I was like, what am I eating a lot of? I'm like, I'm eating a lot of pecans. Let's cut them out. Literally 48 to 72 hours later, gone. So I was just like, oh my god, pain, uh joint pain especially, headaches, fatigue. Man, often times it comes down to diet. And so like, when I hear people who are are in chronic pain, I'm just like, I'm telling you, start with your diet. And so anyway, just super super interesting. I have all the empathy in the world for people struggling with that. Like no judgment, but um you know, I just want to see more of them realize, okay, I can experiment with my diet and make this pain go away. Yeah, yeah, it's this this kind of empowering idea. And that was very much part of my intention when I decided to kind of roll up my sleeves and get that book all together. I I imagined an individual who would be going to their medicine cabinet every morning and they would pull out a medication for their hypertension, a medication for their migraines, a medication for their infertility, and or even their diabetes. And then and at the end of this at the end of this this like this conversation when they realize wait, so many of these problems, literally everyone I just mentioned, but so many of these chronic diseases that we're all afraid of, they seem like they're distinct problems, but to varying degrees they're all trees, they're all branches from the same tree. And rather than continuing to prune these individual branches that all inevitably grow back with the medications we're taking, let's just cut the whole tree down. Let's just get right to the roots of this thing and get rid of the problem. And and so it was this idea that it might be empowering that rather than hopelessly taking medications every day knowing that the only the only future is increasing the dose of those medications, let's actually address the true origins of the problem, which again to varying degrees is often going to be insulin resistance. So now walk me into that pathology cuz this is where the story really starts to get interesting. Cuz so many things that I had no idea were related to insulin are direct results of insulin. Yeah. Yeah, so insulin resistance, which is my focus as a scientist, is is very likely the single most common health disorder in the world. A paper published in 2018 found that 88% of adults in the US were considered metabolically unfit. In other words, they had some aspect of the metabolic syndrome. And again, as I mentioned earlier, that's really the insulin resistance syndrome. So it doesn't take too much of a logical step to say well then 88% of adults has have some manifestation of insulin resistance. So can we make that really simple and say metabolically unfit just means it you're forcing your system to pump too much insulin? Yeah, in fact, exactly. In fact, that's a perfect segue to just defining the villain. So, insulin resistance is the villain and it's all the rage nowadays to have a movie about the origins of of villains. So, let's let's describe it. So, insulin resistance is is two problems. And this is so essential. Those especially for those that are in the low-carb space where the term insulin resistance I believe gets invoked a very inappropriately in certain settings. Um and you have to have both of these phenomena occurring for it to be insulin resistance. One is the insulin resistance itself. And that is defined um at the level of the cell. What is insulin? How is insulin acting at the cell? Once upon a time, one molecule of insulin was capable, say, of of moving this many molecules of glucose into the cell. And that's one of insulin's main most famous actions where insulin comes to the door of a cell, knocks on the door, allows the glucose to then come in once it's opened those glucose doors. Um so so insulin can't do that as well. That's part of the what we call insulin resistance. So, insulin resistance is that some cells of the body, but not all, aren't responding to insulin as well as they used to. And that is a particular problem in light of the second aspect, the second side of this coin that we're calling insulin resistance, which is the hyperinsulinemia, or in other words, the chronically elevated insulin levels. You That is the part that's overlooked. People will only want to mention the insulin resistance part of it, maybe the elevated glucose levels, which again is really selling insulin short as it has its hand in thousands of biochemical reactions throughout the body. But even still, you cannot pull that apart from the chronically elevated insulin. There is no situation of insulin resistance in the body that that lacks the the other side of this, namely the hyperinsulinemia. And that is the pathological side, which we're talking about now, where someone is noticing their blood pressure going up or he's noticing his erectile dysfunction. Those are very much consequences of the insulin resistance. But do we have And that's that's the pathological insulin resistance. But there are states of physiological insulin resistance where the body is deliberately pushing up its insulin and changing the efficacy of the insulin throughout the body in order to do something. So it's serving a useful or a physiological purpose. But that only happens in two instances. It's puberty and pregnancy. In those instances where the the elevated the the substantial increases in insulin are facilitating a substantial growth. And in pregnant mom, it is basically her body's way of saying "I'm about to undergo this metabolic marathon growing this little human in my belly, and I need to make sure I have enough fat to go through that whole process if for some reason food became scarce." And so it really does serve a purpose for mom to get fat in the elevated insulin in that pregnancy-related insulin resistance help that helps that happen. But also mom's elevated insulin helps the baby grow and the baby get fat. And a baby must be fat when it's born to be healthy. In fact, if a baby is too skinny, um it's very likely the baby will suffer from learning um disabilities as the baby grows as he or she grows because a baby In fact, Tom, it's a this I I hate that I'm getting off topic, but you steer me back if we need to. Humans are the only land-based mammals that are born obese. And we are the only animal that is born with a brain and head a skull that is bigger than the birth canal, much to mom's chagrin. But we have these massive metabolic um demands in our brain. And the baby must have enough fat to make enough ketones to feed the brain. And if baby doesn't have enough fat when baby's born, say because baby's premature, um then then we need to make sure we can fatten that baby up as quickly as possible. Otherwise, it's it's very very likely the baby's going to have learning disorders because it just wasn't getting enough ketones to to fuel this incredible growth of the brain during those newborn years. Okay, God, there's so much there. Um I want to go back. You had mentioned that not all cells get insulin resistant. What cells do not get insulin resistant? Yeah, that's a great question. In fact, I I like to present this sort of paradigm when I teach this idea to my students. You have some cells on one end, um like like uh muscle cells. Muscle cells can become very insulin resistant. That's a problem because now they're not pulling in glucose as well. It's a problem because insulin isn't defending the proteins, and now you could be break breaking down muscle proteins, um and then just releasing those amino acids, but for no for no reason. It's just that the insulin isn't working. Then you have a tissue like the liver, um which uh can can some of its aspects become insulin resistant and some of the liver's processes stay insulin sensitive. And then, you have some types of fat cells, like, for example, the the the the fat cells that a woman will have on her butt and hips, the what's called the gluteofemoral fat depot or fat pad. Those are fat cells that will virtually forever maintain perfect insulin sensitivity. Insulin will always tell those fat cells to store more fat. But not all fat cells. So, like a guy, fat cells that where where they're stored more centrally around the abdominal area, or or even more um relevant, the visceral fat cells, the fat cells that are within the abdominal space and behind our behind our abs, behind our muscles, um around our liver and guts and kidneys, those are those are fat cells that can become insulin resistant. But so we have those the glu- the gluteal femoral fat cells, which is which is a subcutaneous fat. That's a fat that you can pinch and jiggle. Um those maintain almost perfect insulin sensitivity forever. And I don't know why it could be that a woman has such a the woman is going to bear the metabolic burden of pregnancy. And so that might just represent a way to ensure that the woman always has a place to store a little extra fat should she need it. And if you think about the cell, the fat cells within the abdominal within the visceral space surrounding our kidneys and our liver and and etc. and our intestines, if we had limitless potential to store fat there, it would literally crush all of those essential organs. You know, it would be expanding so much that it may even start to put pressure on the lungs and the and the heart. And so then we die. So that it's we we it makes sense that those fat cells would become insulin resistant because insulin tells fat cells to grow. And those cells essentially get to a point of hypertrophy where they start to tell insulin, you want me to keep growing, but if I do, we're going to die. So for the sake of the body, I'm not going to listen to you anymore and I'm going to you want me to store more fat, I'm going to start I'm going to become insulin resistant and I'm going to start leaking fat. That actually becomes a problem overall, but I would say it's a it's a problem that we're willing to have rather than, you know, crush our internal organs. But when you look at the the woman on her butt and hips, well, there's no harm in storing more fat there. It is literally not going to get in the way of anything. She might she might curse it, but but it is a nice place to store fat. And women store more fat in the subcutaneous fat depots, the fat beneath the skin that you can pinch and jiggle, than men do. Men store relatively more of their fat, of course, on their abdomen, but inside in the visceral space as well. So if you have a couple they got married in college, now they're both gaining 10 lbs, you know, every year or so, the man will start to suffer from the consequences of that much, much sooner than the woman. Women can just as visceral fat around his organs. Yep, that's exactly right. Women can get than men? Do you think the reason that nature is doing that is because we don't have to bear children? Oh, I I do. Yeah, in in in fact, that that difference in how we're storing fat is entirely under the control of sex hormones. Androgens, testosterone, like, are are promoting the fat storage in the abdominal and even visceral space. Estrogens, in contrast, are very much stimulating the storage of fat um in that subcutaneous space, especially the butt and hips, but also the arms and the breasts and all those prototypical female spots. So, that's under the control of the sex hormones. That's why little Tommy and little Jane, as they grow up through puberty, they start to look so different. It's because the sex hormones are telling the body where to store the fat, not how much, though. Insulin's telling the body how much fat to store. The sex hormones are just telling the body where to store it and how and how to store it, whether to it's growing through making new fat cells, what's called hyperplasia, which is what's happening on the um the fat at the butt and hips, or whether it's hypertrophy, which is usually what's more happening around the abdomen or in the visceral Okay, so now we're back to the uh the pathology of elevated insulin. When you were describing all the things that I just thought of Honestly, I defaulted to thinking of them as a a reaction to elevated glucose. So, um you know, damage to the epithelial lining of the vasculature, like things like that. What what is happening and what is it that that what are the properties of insulin that cause that? Yeah. Yeah, well, it would depend on the specific pathology, but you mentioned the endothelium or the epithelial lining of the blood vessels. So, that's a a really nice um place to to kind of define or identify part of what's happening with insulin resistance. Now, to put all this in perspective um as one step back and then I'll step right back into it. Um insulin has an effect on on literally every single cell of the body. There is not a single cell in the body that doesn't have insulin receptors. Every cell will respond will respond to insulin in some way. Doesn't matter what it is. Now, the endothelial cells are a fascinating example because they have multiple ways to respond to insulin. And and this is um very illustrative of how insulin resistance is virtually in every instance the the cause of hypertension. So, if someone listening to this has been told they have hypertension and they've been struggling with it for years or they're taking a drug for it, I can almost guarantee it's because they have insulin resistance. It is very uncommon for that to be an exception. So, there there are several distinct mechanisms, um but but I mentioned one where insulin will come to the endothelium and it will it will bind to the endothelial cells and it will induce the production of a molecule called nitric oxide. Now, that is not something that happens at other cells of the body. And so, this is just reflective of how unique insulin is at different cells. It will tell different cells to do different things. And so, it comes to the endothelial cells, it stimulates the production of nitric oxide, which will relax the smooth muscles of the blood vessel, and now we have dilation. And so, that's changing the way we're moving blood around. In in systemically throughout our body, that helps the blood pressure be a little lower because the blood vessels are a little wider. And so, now the pressure has gone down, but at the say with an erection, you need that dilation to facilitate greater blood flow into that area. And so, that's that's the problem. And in fact, indeed, that is the problem in in hypertension. Um, chronically, when someone puts on the blood pressure cuff and they see their blood pressure is high, part of that problem is that insulin isn't working well. And insulin used to induce this vasodilation because of nitric oxide, and now it doesn't. Insulin is still there. It's pounding on the door of the endothelium. The endothelium isn't working anymore. So, that's one effect. But then other ways that insulin is affecting hypertension, insulin uh amplifies the sensitivity to catecholamines, like epinephrine. When when epinephrine is high, it will induce vasoconstriction. And it will induce the heart. It will stimulate the heart to beat harder and faster. In in chronically elevated insulin, the insulin is pushing up the epinephrine in the body. So, it's amplifying this this kind of anxious-like state, where the blood vessels are constricting, the heart is beating harder, and then overall, we have an increase in blood pressure. Another, [snorts] maybe one more, um, just cuz I would dominate this for too long. Insulin also stimulates the release of a hormone called aldosterone. And aldosterone is the main hormone that tells the kidneys to hold on to salt and water. And so, if you're eating a diet that's keeping your insulin high, that's going to artificially push up your aldosterone. And the consequence of that is going to be that the kidneys are now retaining too much salt and water. And of course, that means blood volume goes up, and as blood volume goes up, blood pressure goes up. And now our blood pressure is potentially getting high enough that it may hurt, um, blood vessels. So, those are several distinct mechanisms. In fact, I ended up bringing in, you know, multiple different angles. But to varying degrees, you have this happening in the hippocampus, which is compromising glucose use, which is necessary for memory and learning, which is why they call Alzheimer's disease in insulin resistance of the brain. You have this happening to blood vessels in the brain, um, where they don't dilate as well. They don't They're aren't as dynamic and that can lead to migraines. And that is why people who adopt low-carb diets can in many instances have a complete cessation of migraines. They may never have another migraine again. Um and and and and many many more pathologies. Polycystic ovary syndrome, which is one I've alluded to a few times now, which is the most common infertility in women, that is directly a result of too much insulin in the body preventing the ovaries from releasing a big spike of estrogens. And if you don't have that estrogen spike, you do not have ovulation. And so the woman has ovaries that are making lots of follicles throughout the menstrual cycle or the ovulatory cycle getting ready to ovulate, but the insulin is preventing it from actually ovulating. And now all those follicles just stick around in the ovaries making the ovaries get bigger and bigger and bigger. It is It is not to be trifled with. All right, so we have just put told everybody how they're getting themselves in trouble. Now, let's get them out. You do a great job of talking people through this. Diet, exercise, what are what are the keys? Yes. Yes, so in fact, let's start with the simple one, which is exercise. Any kind of exercise is going to be beneficial. And that's [clears throat] because two two reasons. One, during exercise itself, insulin must come down somewhat. It's just It is incompatible even just for survival really to be exercising and insulin staying high. Because the muscles are using the glucose and therefore there's no reason to inject the insulin. Yeah. Yeah, in fact, yes, that's a part of it where if insulin is up, insulin wants to store energy. It is It is not allowing the liver to share its glucose. It is not allowing the fat cells to share their fat. Um and and so that is of course not conducive to exercising. You need those tissues to be sharing their energy so that the hungry muscle can be pulling it all in. And so insulin comes down during exercise. Now, to the to the astute listener, they'd be saying, "Well, wait a minute, Ben. You You and Tom were just saying how you need insulin to move glucose into the muscle." Not when you exercise. That is a genius in the design of the muscle cell. It has insulin-independent doors for the glucose. So, the moment you have a muscle that is going through that dynamic contraction and relaxation, you open those glucose doors without insulin ever having in come ever having come knocked on them. So, it's an insulin-independent mechanism. So, it That Wow, I've never heard that before. So, muscle cells do not need insulin, then why do other cells need insulin? Because is it going back to that sort of idea of like, "Hey, even between men and women, we have to like, you know, move this stuff around differently. So, we need sort of the middle man that's going to, you know, partition this and, you know, send this to the right places?" Yeah. Well, in fact, [clears throat] let's just burst the balloon. Um very, very few cells of the body actually need insulin for glucose uptake. Like the liver that I mentioned a moment ago, insulin will tell the liver what to do with the glucose, but it doesn't tell the liver to take it in. Most of the cells of the body are They can pull in glucose without the need of insulin. And so, that's part of the tragedy of how we define insulin through by just nature of what it does to glucose when the reality is only a handful of cells actually respond to insulin with glucose uptake. Um and that is muscle and fat and heart and then the some parts of the brain. And so, in the grand scheme of things, that's that's a profoundly small number, but the muscle is so hungry during exercise that it just basically tells insulin, "Look, in when I'm and when I'm at rest, you're the boss, but when I'm exercising, I'm the boss. I'm going to get what I need." And so, it basically pushes insulin to the side. And again, that's a good thing cuz insulin comes down. And now that working muscle can clear the blood of glucose. And so, we have that acute benefit of insulin coming down, then we have the long-term benefit, which is at the back end of all of this, our glucose is going to be better controlled because we've been exercising, and now the insulin doesn't have that pressure to be higher as it is. I wore a continuous glucose monitor for, I don't know, probably 6 months. A, it's super fun. Anybody watching this episode, if you've made it this far, trust me when I say you'd really enjoy it. Um and I had ice cream and my blood sugar went from like 85 to 178 in like 20 minutes. Maybe it was a little bit longer, but it was fast. And so I started doing air squats and I must have done close to 300. It It was to the point where I was like, I'm either just going to accept that, you know, I have this crazy uh blood sugar spike, or I'm never eating ice cream again cuz I don't want to do 300 air squats again. It takes hours. Um and but it dropped my blood sugar back down. I think if memory served, it dropped it back down to either right around 100 or even back under 100. I I literally I had heard people say a million times, "Hey, exercise really helps. Like if you're pre-diabetic, go exercise." And it's just like, "Why would that be true?" And in doing that and seeing like, "Oh my god, like my muscles are obviously gobbling up the sugar from the bloodstream." I I was really shocked at how how profound the effect the measurable effect was. Yeah, in fact, I that's that exact phenomenon is why, which plays out in multiple studies in humans, is that's why I recommend that when someone has eaten their most starchy meal of the day, go on a walk. Just get out and do something. Whatever that whatever that meal was or that that treat that spiked your glucose, get out and walk. Just go on a 20-minute walk or something, and you will much more rapidly bring that down. What might be elevated for a few hours may only be elevated for an hour if you get out and do something. Yeah, it's crazy. Um, that's super interesting. Okay, so exercise good, muscles have a unique door that's really going to pull in the the glucose. So, now talk to me about diet. Right. Right. So, this is the elephant in the room. In fact, far far more relevant than exercise. As much as I am an advocate of exercise, there are even exercise studies that find that if you exercise and then you follow that up with high-carb meals, then you mitigate, you undo the insulin-sensitizing effect of the exercise itself. Just touching on the fact that if you try to compare diet to exercise, diet will beat the hell out of exercise as a variable for insulin resistance. Now, when it comes to diet, the principles I think there are, to me, I've I've attempted to sort of distill these ideas to four principles. And they are so simple, but again, at the very beginning of our conversation, we both realized and acknowledged that doesn't mean they're easy. But, assuming that someone would want to hear them anyway, and then they can make their own choice, I would say the very first principle needs to be control carbohydrates. Now, I'm not saying you don't eat any, but carbohydrates are not essential to humans. So, put that in perspective then when when you're looking at a big spread of of carbohydrate-heavy foods, um, this is that is the macronutrient that is the biggest offender. It will spike live my entire life and never eat a carbohydrate and be fine? Are we prepared to stand by that statement? Oh, to 100%. In fact, indeed, Tom, even the most dogmatic dietitian has to even reluctantly admit that. Um, it is it is literally the stuff of dietitian and dietetics textbooks. Carbohydrates are not essential to humans. Again, that's an unpopular sentiment nowadays, especially, but it doesn't change the reality of humans. There is no such thing get unless I eat Well, yeah, yeah, that's a good question. So, there there are certainly and so let me be nuanced here. There are plants that can be beneficial and part of a healthy diet, but that does in no way mean they're essential. There is there there's certainly no such thing as an essential carbohydrate. That's so In fact, we know people, I know I'm friends with Shawn Baker. Everyone knows about him. I mean, talk about a beast. That guy literally eats nothing but steak. Yeah, that's crazy. The the whole carnivore thing is really interesting to me. But all things being equal, I don't care. Right? So, as long as everything's being done ethically and the animals are, you know, treated well and free range and all that stuff. And the only bad day they have is the day they die and you make that as wonderful as as you possibly can. Um I don't care. So, I just want to know what's going to help me be healthier longer. And I know you have some interesting concerns about a vegan diet and I would love to to hear what you think it's missing if anything. I don't want to put words in your mouth. Yeah, yeah. Yeah, in fact, that this plays well still into that first rule with controlling carbohydrates. But a vegan diet Um well, to put it bluntly, is incompatible with human survival. Um and and so I like to get real specific. Yeah, yeah, so now that's not to say there could be a vegan listening to this and they're saying, "Well, forget you, Ben. I'm doing fine." But it is a privilege of the elite. You have to be educated enough to know what your deficiencies are and you have to be wealthy enough to afford the supplements. Now, the deficiencies are going to be iron and someone could say, "I'm getting all my iron from my plants." No, you're not. That doesn't work. You you cannot get iron from from from broccoli to to any measurable amount or even the right kind that's going to influence your iron. So, you have vegans who will suffer from iron deficiency anemia almost all the time. They will suffer from vitamin B12 deficiencies, which are is impossible to get from any plant whatsoever. And and that leads to something called pernicious anemia, and that is something that vegan mom actually can pass on to vegan baby. But the baby will be identified as failure to thrive. If the baby won't be meeting normal kind of growth metrics and and cognitive metrics because of the lack of B12 in mom's diet, which is then passed into the milk or not passed into the milk. But you need vitamin B12 for cells to divide. And so, the newborn baby, which is experiencing such explosive growth, a lot of that growth is happening because of hyperplasia cells dividing. And we The reason we tell a mom to get folate is so that the cells of the fetus, that little growing baby can divide. But if you don't have B12, the folate can't work in the first place. That's sort of the other side of this concern. Folate and B12 work hand in hand to allow cells to divide. And you cannot get B12 from plant sources. It it It's impossible. You have to get it from animal-sourced foods. So, that those So, pernicious anemia and and any disease related to a failure of cells to divide would follow that. And then just one last one would be the essential omega-3s for the brain, DHA and EPA. And and a vegan would say, "Well, I'm getting alpha-linolenic acid or linolenic acid, ALA, which is the the plant-based omega-3." And I would say that's all fine and dandy. You cannot Humans can't convert enough of that over to constitute the omega-3s of EPA and DHA, which are so essential for brain development. In fact, that goes back to the growing baby and the developing baby and baby's brain as well, which has a very high need for omega-3s. Um and so, so there are multiple deficiencies, and those are just um some of the obvious ones. Very interesting. Okay, so we are controlling carbohydrates. We're having some animal protein for sure. Yep, in fact that's the second one. We're getting fat. Yep, yeah, that's the second point. Prioritize protein and it has to come from animal sources. In my mind it's very clear. There's no question animal sources are superior. It is it is I think very unfortunate this growing trend of trying to get protein from plants. Now I know this is delicate cuz some people have a lot of strong feelings about this kind of thing, but the consequences when you're trying to get your protein from plants is you very often will become protein deficient because the plants won't have the full complement of amino acids or in the right levels. Um, they are not as bioavailable. This is documented. You aren't moving those in as well. And part of that could be that plant proteins have honest-to-goodness molecules in them that inhibit the digestion of the proteins. Phytic acids, tannins, trypsin inhibitors, these are things that just occur in in these plants. They're in peas, they're in soy. And when we take a thousand peas and concentrate them to get one serving of protein, the protein's what we want. What we don't want is all the other stuff coming with it. Like these molecules that block digestion. We also get potentially dangerous levels of heavy metals like lead and arsenic because plants, these seeds of the plants, will naturally concentrate these minerals from the ground. Now if you and I just ate a handful of peas, that's in such an inconsequential amount as to not be relevant. But it's also an inconsequential amount of protein. So if we want to try to get enough protein from peas, we end up getting these other things that we don't want. But nevertheless, prioritize protein and then if you're getting it from animal sources it's going to come with fat because in nature the best proteins always come with fat. And that's good because it helps us digest the protein better. And fat and protein are more anabolic than protein alone. So, there's something anabolic about the fat. And so, don't fear fat. And then the fourth principle Really fast before you move off that one and we get to the fourth one. Um where do you come down on eggs? Yeah, so I think eggs are are God's if or nature's most perfectly packaged food. It is a one-to-one mix of protein to fat by mass. And I think that is Well, I joke. It's like it's a divine mix. But, that is the exact mix that this study that I just mentioned showed where they had they had weightlifters take egg white, which is egg white and whey is the best demonstrably the best proteins in humans. And then they had them So, they had them take egg whites alone and detected a significant increase in muscle protein synthesis. And then they had them take the whole egg, which is by mass one-to-one. There's an equal amount of mass of of egg white to yolk. And now they got a significant growth of the muscle beyond just the egg white alone. I eat a lot of eggs. So, I'm I'm very happy to hear that. Um okay, so the fourth pillar bucket Yep. Yep, the fourth pillar is fasting. Um and and this doesn't need to be anything complicated. It's funny how complicated something can be of just not eating. That you know, we've made it so complicated. And so, I I and I don't I don't really try to come down on any particular version of that. Um there are so many different ways to do it. Um full multi-day fasts or just within 24-hour time-restricted eating windows. My only advice is if someone's going to engage in time-restricted eating, like an 18:6 where they fast for 18 hours and eat for 6, I would say when you can, try to push that eating window to the beginning of the day. That is better than pushing it to the end of the day. Um there are metabolic improvements that come with it. There are studies that have compared that. But, also practically speaking, it's just so much easier to indulge in junk food when you're eating in the evening. But, But your eating window has has stopped with lunch, you're you just don't indulge. You're not as you're not as tempted. Um but I appreciate that socially awkward, you know, dinner at least for me. I'm a I'm a husband. I'm a father. Not eating dinner is just weird because I want to have that moment with my family. So, despite me saying that, it doesn't I'm not trying to pretend that it's easy to do. But but if if someone can do it, it's better to have the eating window be earlier in the day than later. Yeah. I have my last meal at about 1:15. Mhm. Yep. Yep. That's a great way to do it. It really is. Honestly, for years I did it the other way and I thought, "Oh, breakfast is, you know, super easy to skip and so I'll do lunch and dinner." And then I just found myself in the mornings I'd be so distracted and I'm like, "Oh, you know, I hope I have like a meeting where I have to be responsive versus where I need to be creative." Because I can do meetings all day in a fasted state, no problem. But I'm not as creative and maybe other people are, but for me it's I'm not. And uh so finally I was like, "Well, wait a second. I start getting tired in the evenings anyway. Why don't I start ending my meal much earlier? So, because of my sleep schedule, I go to bed very early, so I get up really early. So, I don't eat probably for about 4:00 to 5:00 hours in the morning anyway, but I'm still having my first meal at like 9:30. Um yeah. And then I have my That's a great way to do it. 1:15 or so. Yeah, but you came to intuitively is certainly supported by the data. What I came to through a lot of pain and suffering. I am the most [laughter] like I have done everything from a health perspective like the hardest, dumbest way possible. I spent like 3 years in rabbit starvation. I got lean, but because all I was eating was protein, I hurt everywhere. And it was god awful. I mean, it was god awful. I was lean and I looked great, but whoa, I did not feel good. In fact, that is so important because there is I am I am a huge defender of protein, but I I vehemently disagree with the idea that you need to focus on protein at the expense of something like fat. I think that we are denying nature if when we're teasing those two apart. And and I think it's not a it's not it's interesting that our ancestors, even here in the United States, in the early 1900s, we didn't eat chicken. We had the we we didn't If you look at the consumption of meat patterns in the United States, chicken as a meat was almost nothing for for decades decades decades and then it exploded in the mid-1900s right around the time we started vilifying saturated fat and fat in general. And chicken meat is so lean. We didn't used to eat the chickens, we kept them for their eggs. And so when we this modern focus on protein, I I do appreciate really the utility of protein and the value of emphasizing it very much. But to to pull that away from the fat leads us to I think an unhealthy way of eating. So interesting. Ben, you are fascinating. I loved your book. I have so enjoyed my time with you. Where can people follow you, dive in deeper, get more insights? Where's the best place? Yeah. Yeah, thanks so much, Tom. This was great. Yeah, so everyone can check out the book. It's Why We Get Sick. And I am fairly active on mostly on Instagram these days and people can find me there at Ben Bickman, PhD. And then I invite everyone go check out two kind of ventures I'm involved with. One is a coaching platform just to try to create a nice simple online low-carb coaching. I don't do the coaching, but I helped create the kind of the the curriculum, I guess. And people can find that at insulinIQ.com. And then lastly, just a little while ago I started a company called Health Code and health is spelled People can go to that website at gethealth hlt h.com. And that was really just born from my my view that as valuable as a low-carb diet is, it's sometimes hard for people to do it. And we've touched on that even in this conversation. So, I just thought no one had really done a low carb shake that great yet. And so, it's a low carb high fat high protein in that one-to-one ratio, that divine ratio that I mentioned earlier. Um and if anyone wants to make a purchase, please use Ben 10, um my my name Ben 10 for a 10% off the order. Amazing. Dude, thank you so much. This is wonderful. Guys, trust me, his book Why We Get Sick absolutely phenomenal. He's got such a unique take that you guys just went on a ride and got to enjoy. Uh it's amazing. You will be richly rewarded. And speaking of things that are rewarding, if you haven't already, be sure to subscribe. And until next time, my friends, be legendary. Take care. Thank you guys so much for watching and being a part of this community. If you haven't already, be sure to subscribe. You're going to get weekly videos on building a growth mindset, cultivating grit, and unlocking your full potential.