Why We Get Sick: Insulin Resistance and Chronic Diseases by Benjamin T. Bikman | 2020
Benjamin Bikman argues that insulin resistance, not high blood sugar, is the root cause of most modern chronic diseases. He presents data showing 88% of U.S. adults are metabolically unhealthy and explains how insulin resistance develops at the cellular level. Bikman recommends measuring fasting insulin, intermittent fasting, low-carb eating, and prioritizing protein and natural fats as more effective than medication.
Chapters
Worldwide, we are dying from diseases that were really once unheard of. Just a couple generations ago, people weren't worried about heart disease, they weren't worried about diabetes, even much less worried about cancer, certainly less worried about things like obesity. Why is it that we get so sick now, um, from diseases that were unheard of, that our great-grandparents would never have imagined or certainly never worried about? Well, that's what I want to take the time with you to explore— why we get sick and really highlight the relevance of metabolic health. You'll be surprised at just how relevant it is, and the theme that we'll come back to, as you see, here on this, on this introduction is something called insulin resistance. Now let me just paint the picture just to emphasize really the scope of the problem. At the end of last year, a study was published from the University of North Carolina Chapel Hill School of Public Health, and they found in this study that 88% of adults in the US were considered metabolically unhealthy. That's a shocking number. In fact, they used the word alarming. Uh, the number of people that were metabolically healthy or had good metabolic health was alarmingly low. This metabolic health was gauged based on 5 factors, and these 5 factors are typically what constitutes something called the metabolic syndrome, and I'll come back to that idea in a moment. But essentially what they found was that only 12% of adults in the US could check the box, if you will, on all 5 of these factors: that they had an acceptably low waist circumference, that they had good blood pressure, good blood glucose, and they had good blood lipids, namely low triglycerides or high HDL cholesterol. So only 12% of adults— again, to repeat that and reiterate it— were able to check the box on all of them. And 88% failed at least in one of these categories. So the absence— if this, these being good, so to speak, with these 5 pillars constitute good health, then it's the absence of these that ends up creating poor metabolic health. Now these may all seem kind of distinct. You would look at them and say, well, yeah, they're all kind of related to metabolic health, certainly. Well, one strong connection, a common root across all of these, is something called insulin resistance. Now insulin resistance really is the epidemic you've never heard of. And I say this in the midst of, of an epidemic where insulin resistance is the single most common health disorder in the world. Now, let's shift topics just for a moment. And this is admittedly a bit of a tangent, but I promise it's relevant. We are currently, of course, afraid of something called COVID-19, this viral disease that is spreading around the world. Unfortunately, this disease is part of the new global ecosystem. And we should and we can make efforts to control the spread of this disease. We are hearing a great deal about wearing masks and social distancing. And hopefully we have an effective vaccine, and I emphasize hopefully. But even the most effective vaccine is not going to be perfect. Even our best efforts to socially distance will not completely prevent the spread of the disease. So we should focus on the variables that we can to make sure that once we do get infected, which is very likely, the infection will be as minimally effective or affect us as minimally as possible. So that we can shrug off this infection and come out perfectly fine on the back end. Now, what is so interesting about this viral infection is who it affects. And based on evidence published from New York, we found that a significant number, 94% of everyone who came to the hospital with a COVID-19 infection, so in other words, the people whose infection was sufficiently serious, that they had to go to the hospital, 94% of these people had at least one preexisting condition. 88% of them had two or more preexisting conditions. Now, what were the preexisting conditions? Well, it might be a little surprising. The single most common preexisting condition was obesity, so someone having too much body fat. The second most common is hypertension, and the third most common was diabetes. Now, all of these are metabolic problems, and in fact, they all have a single very strong cause that is common across them, and that is namely insulin resistance. Insulin resistance is linked in driving obesity, and it is linked in, and hypertension and diabetes. But the problem actually doesn't stop there. While these are the 3 most relevant insulin resistance-related problems in the context of COVID-19, the context is actually much broader. The relevance is much broader, where insulin resistance is known to be causal in driving fatty liver disease, which is the single most common liver problem in the world. Insulin resistance actually also affects fertility in men and in women. In women, insulin resistance is directly responsible for a condition called polycystic ovarian syndrome, where the insulin resistance is affecting the ovaries' ability to create the proper balance of hormones in order to facilitate fertility in a woman. In men, insulin resistance affects blood vessels that prevents, that causes erectile dysfunction, the most common form of infertility in men. So both in men and women, insulin resistance is causally linked to both of the most common forms of infertility. And then the problems continue where, and I promise I won't go into too much more detail, where we have musculoskeletal problems like muscle wasting and arthritis, and then even neurological disorders like Alzheimer's disease. In fact, Alzheimer's disease is considered insulin resistance of the brain. So I hope I'm really painting the picture of why insulin resistance matters and how it's relevant in why we get sick, all of these non-infectious and even nowadays infectious diseases that we all have a healthy respect for and maybe we're even a little afraid of. Now, should you be afraid? Should you be concerned? Let's just see. I'm going to pretend that I'm your professor for the next few minutes anyway, and I want to ask you, are you insulin resistant? Are you or a loved one insulin resistant? Look through this little quiz and just sort of quiz yourself. Do you have high blood pressure? Do you have high blood triglycerides? You know, last time you went to the doctor's office and had a blood test done, were you told that your triglycerides were too high? Do you have a family member with type 2 diabetes? If you were a woman, did you have gestational diabetes when you were pregnant, or have you had PCOS, polycystic ovarian syndrome? If you're a man, do you have erectile dysfunction? In fact, there's a study that the title of the study, it goes something like, "Is erectile dysfunction the earliest sign of insulin resistance in men?" Do you have fatty liver disease? Now, all of these may seem kind of obvious, and the last one is a little surprising, but it's actually the most obvious to see, and that is your skin. Do you have these things called skin tags or dark patches of skin? And skin tags are small little actual bumps, raised little bumps of skin that someone can get around folds of skin, perhaps around the neck or the armpits or groin, elbows, knees, where the skin would fold in. Someone can get these little kind of stalks of skin called skin tags. And the same goes at those same areas for something called acanthosis nigricans. This is when someone starts to develop a more coarse, rough, darker skin, a more pigmented skin at these same areas. Those are both signs of insulin resistance. So in a way, the skin is a metabolic, is a window into the metabolic soul. It allows us to understand someone's metabolic health. Now if you answered yes, in some instances even to one, but I'll be generous and say if you answered yes to two, at least two of these questions, then you very likely have insulin resistance, or the loved one that you have in mind, another person that you might be concerned with. And remember, most people with insulin resistance, potentially up to 90%, are undiagnosed. They won't know they have insulin resistance. What they might know is that they have one of the other problems I mentioned earlier, like fatty liver disease or infertility or hypertension. Now, I've been talking for now a few minutes about this villain, insulin resistance. Well, nowadays it's all the rage to explore the origin of a villain. Every villain gets an origin story, and we'll do that now. So what is insulin resistance? Who is this villain? To understand insulin resistance, it's best looked at at the level of the cell, and that's what I'm presenting here. So here we have a cell, and then we have insulin flowing past the cell, which it's doing all the time. Insulin is flowing through our blood all the time, and it's constantly passing all the body, all the cells of our body. And importantly, every cell in the body has insulin receptors. I mean every cell, from the bottom of the, of our feet to the hair on the top of your head. Every cell has insulin receptors. And an insulin receptor is essentially a door where insulin can come and knock on the cell. And so insulin is passing by a cell, it stops and knocks on its door. Again, that's something called the insulin receptor. Once it knocks on the door, something happens in the cell, and I'm just calling this action. A cellular event takes place, and I have to be kind of ambiguous, and simply because insulin will do different things at different cells, and so I couldn't hope to convey all the thousands of things insulin does, so I'm just going to call it an action. Now, over time, for reasons that I'll get to in a moment, this action can become diminished. So once upon a time, insulin could come and politely knock on the door of the cell, and the cell would just respond. It would do what insulin wanted it to do. However, again, for reasons I'll get to, eventually the cell will stop responding to insulin the same way. And so insulin's polite little knock on the door isn't sufficient anymore to get the response that insulin wants. And so what happens is the body starts pounding on the cell, so to speak. So we have more insulin, and we have more insulin coming to the cell, and what was once, again, a nice little knock is a pounding. And to a degree, and depending on the cell, it works. The action is returned. We sort of, we see this kind of thing all around us, where we constantly are getting bombarded with something, some signal, some stimulus, and we just stop responding to it. And I'll come back to that idea in a moment. But there are two essential features here that I've mentioned that you have to understand in order to understand the villain, in order to understand insulin resistance. And the first of these two is that in the body, in insulin resistance, some cells of the body have stopped responding to insulin the way they should. Not all cells, but some cells. And then second, and this is important, the body has more insulin in it than it did before. More insulin is flowing through the blood, and that is a condition called hyper— insulinemia. Hyperinsulinemia—more insulin in the blood. So those are the two aspects of insulin resistance, the two definitions. Now let's put this in a slightly different context. Let's imagine someone who's aging, and we're following this person throughout their life, and they're sort of progressing towards metabolic problems like type 2 diabetes, which is really the most common. That's the most often sort of progression of insulin resistance. Something will start as insulin resistance and eventually it progresses to type 2 diabetes. And so as you can see here, glucose starts to climb over time. And that is the main clinical marker that conventional medicine will look at. They track the glucose. Every time you go to the doctor's office and get a blood test, you're going to get your glucose measured, or your blood sugar. They're gonna tell you that number. Now unfortunately, by focusing so much on the glucose, we have overlooked what I argue is the more relevant marker, and that's insulin. And insulin is going to look something like this, where insulin is spiking earlier in the life of this person, indeed before glucose even changes. And then the body gets so resistant to its own insulin, insulin can no longer lower blood glucose as effectively as it could before, and then the glucose starts to climb. and it climbs even faster as insulin starts to come down. Now, there are two important time points I want to indicate as we look across this person's life. The first is, in fact, insulin resistance. And importantly, as you look at the variables here in that span of insulin resistance, you'll see that insulin resistance is defined as a period when insulin is elevated. Insulin has to work harder, but it's able to do some of what it wants to do, like in this case, keep blood glucose levels normal, because one of insulin's main actions is to lower blood glucose. So this, this is important because if we are looking at glucose, we miss the fact that there's this war being waged behind the scenes, the silent war of insulin having to fight more and more and more in order to keep, for example, the glucose levels in check. But it can it works. And then potentially, if this does, if this goes unchecked, up even decades later, now the glucose starts to change. And so then it becomes clinically obvious because we look at the glucose exclusively. Now we detect the problem because as this progresses towards type 2 diabetes, now we have elevated insulin, which again is often missed, not even measured. And then now we have elevated glucose, which is always measured. Never missed. Now again, I mentioned this a moment ago, the problem with this paradigm is that by failing to look at insulin, we missed detecting the disease as early as we could. Indeed, if we look at the insulin, we can detect the problem potentially decades before the glucose changes. That's an important paradigm. Again, we need to focus on the insulin if we hope to to catch or detect insulin resistance with any degree of sensitivity. Now what can you do there? Here is already a takeaway, and I'll emphasize this again at the end of my talk. 6 microunits per mil. Microunits is the common units measured to measure insulin when you get a blood test, and they measure your insulin levels and give you that number later. People who don't follow a Western diet, and I won't say the standard American diet because Western diet really is more accurate. Even that actually is maybe not totally accurate. It should be the global diet now as we are obsessed with eating all the wrong foods, very processed foods. People who eat a non-Western diet, so people who focus on— you consume an indigenous diet, their fasting insulin levels are going to be around 4 microunits and importantly, they have no hint of metabolic problems in these cultures. Here in the US, our average insulin level is 9 microunits. Now, based on conventional medicine, that would actually still fit in a good range, which I resent, because the average American, as you saw, is considered metabolically unhealthy based on the data that I showed you at the beginning of my talk. In this case, we don't wanna be average. We want that insulin level to be around 6 microunits per mil or lower. And again, I'll emphasize that again at the end. So now you know who insulin resistance— what it is, but where did it come from? This is another part of the origin story here. How do we get insulin resistant? Now importantly, I'm going to superimpose on this same figure, the same paradigm I showed you earlier. Insulin resistance generally starts at the level of our fat cells, and in physiology, fat is called adipose tissue, and the individual cells are called adipocytes. So I may mention those terms later, but it's— when that— if you hear me say adipose or adipocyte, just think fat cells and fat tissue. So often the problem will start at the fat cells. The fat tissue falls first, and then as it falls, it starts to spread this insulin resistance throughout the body to places like the muscle or the liver or even the pancreas, driving— in this model, pushing the person more and more towards type 2 diabetes. But we could think of it as problems like like all those I mentioned earlier, fatty liver disease, Alzheimer's disease, et cetera. And I'll touch on that again in a moment. Now, one of, so how does it start? If often it starts at the adipose tissue, if it starts at the fat cells, what starts it? What lights the fire? What comes and sparks the fuse? Here are 3 causes. One, I mentioned a moment ago, is hyperinsulinemia. So too much insulin itself is a cause of insulin resistance. And that can have a direct effect at the fat cells in our body. Stress, importantly, can also drive insulin resistance. And when I say stress, what I actually am referring to are the stress-related hormones. The main ones are cortisol and epinephrine. Those two represent really the, the poster children, so to speak, of stress. When someone's experiencing stress, whether it's an emotional stress due to relationship problems, a physical stress due to exercising too much or sleeping too poorly or being too sedentary, paradoxically, so covering quite a span, those would all be stresses that could start to drive insulin resistance. Importantly, under this topic, someone could also be taking a cortisol-like molecule as a drug in order to control autoimmune conditions, things like prednisone or dexamethasone. They also cause insulin resistance because they utilize the same biochemical processes that I'm alluding to when I'm mentioning stress. And then lastly, inflammation. I mentioned autoimmune diseases a moment ago, and they create a pretty compelling example where there are human studies that find if you look at someone who exper— who has an autoimmune disease you can track their insulin resistance status, and it will follow the status of the activity of the autoimmunity. Now, by that I mean, let's, for example, take someone with rheumatoid arthritis, because there is in fact specific data on that autoimmune disease. When someone has an active phase of the rheumatoid arthritis, they're really feeling the aching. That is inflammation. That is immunity kind of gone awry. And as the inflammation is climbing during that active phase of the disease, the insulin resistance climbs as well. As the disease subsides and the autoimmunity subsides, so too does the insulin resistance, and the person becomes more insulin sensitive. Now, of these three, all of which are relevant, one stands supreme, and that is namely hyperinsulinemia. I emphasize this one due to the strength of the data that indicate its relevance And the— in fact, let me just mention, going back, all of these little numbers I have right here, these are the identification numbers for peer-reviewed published studies that you can go and look at. You can just go to your web browser and do a search for these, and you will find the studies that I'm referencing here. Now, I'm submitting, I submit to you that hyperinsulinemia is the main driver. This might seem a little strange. At first glance, but it won't, it won't much longer. Essentially what happens in the body and the cells of the body, that as the cells are swimming in the sea of ever-rising insulin, the body stops responding to it. And this is kind of analogous to what I see in my own home. My sweet wife is home with our little children all the time, and when I'm home with them, I notice something interesting. I will hear, I'll be in the other room, for example, and I'll hear my little son calling to mom, "Hey mom, hey mom, hey mom," and I can hear him getting louder, louder, louder. And my sweet wife is just deaf to his nagging. She's so used to it. She's so used to hearing that that it doesn't always connect. There isn't always the response like you'd think, or what I referred to earlier as the action. Now, I'm not home as much. I don't constantly hear. I'm not swimming in a sea of all this kind of these beautiful little cherubic complaints and whining that my wife has to hear. So I am very sensitive to those calls for mom's attention. And so I'll be calling out from the other room, "Hey, leave mom alone and just come here and let me help." Of course, they only want mom anyway, so it doesn't work. But I hope you're getting my analogy here. This is reflective of a fundamental biological principle. Too much of a stimulus will result in a resistance to that stimulus. We see this, I believe, in every aspect of our existence. If we are exposing ourselves to a stimulus, we need more and more of that stimulus to get the same response as we did before. That is an important, and I believe even eternal, truth. In the case of insulin resistance, in order to maintain a high degree of insulin sensitivity, In order for insulin to continue to work the way we want it to, we need to keep it low. When insulin has been too high, it's like the little voices that are shouting for our attention that become easy to ignore. Now, we see this in humans very quickly. I'm mentioning one study here where they took healthy college-aged men, you know, the most insulin-sensitive people you can imagine, and by just infusing them with a small amount of bumping their insulin up, their insulin levels up just a little bit, they became significantly more insulin resistant in just a couple days. So this is a phenomenon, this is a cause, hyperinsulinemia, that can drive insulin resistance very quickly and without too much stimulus. You know, it's surprising just how quickly it can happen. Now what happens? How does hyperinsulinemia drive the fat cells to become insulin resistant? And it really has to do with insulin promoting the growth of a fat cell. In fact, one way of looking at this relationship— but I won't elaborate, this is not a talk about fat tissue per se, it's not a talk about obesity— but insulin being elevated is absolutely essential to a fat— to our fat tissue getting bigger. Insulin is like fertilizer, it stimulates fat to grow. And in fact, I'll I'll mention that now. How does it do it? Insulin actually activates two processes when it comes to a fat cell. So when insulin comes to the fat cell and starts knocking on the door of the fat cell, it's going to start promoting two events, telling the cell, these fat cells, to do two things. And it won't always tell them to do both of them. It can be one or the other. Specifically, it can activate something called lipogenesis or adipogenesis. Lipogenesis is when insulin tells a fat cell to make more fat within itself, so the fat cell starts to get big. Adipogenesis is when insulin tells the fat cell to start making more fat cells, and so we start to proliferate. Now, we can identify this in some clever scientific terms where when the fat cells are just getting big, that is called hypertrophy, or we have hypertrophic fat cells. When we are multiplying the fat cells, when we're getting more and more of them, that's hyperplasia of the fat cells, or hyperplastic fat cells. One of these is good, hyperplasia, and one, hypertrophy, is not good. Now, what do I mean? How could I, how could I say that with such confidence? Because I am quite confident about that. When we allow fat cells to grow through hyperplasia, when they can multiply, the fat cells always have vacancy. They're never full. They always have more room to be pulling in more fat. So when insulin comes to a fat cell and tells it to start making, getting more fat, it can continue to do that because if it starts to get a little full, it just makes another, we just get another fat cell kind of recruited into that area. So we constantly, we're just sort of building more space by making more fat cells, and so none of these fat cells ever get too big, and they maintain a very high level of insulin sensitivity. Insulin can continue to come to those cells and tell them to store more fat. In contrast, in the case of the hypertrophic fat cells, it's like the fat cells get too big. There is no vacancy, they are too full. And so they have to stop responding to insulin because insulin would want to continue to tell them to grow and grow and grow. And so it's almost like this self-preservation where the hypertrophic fat cells become insulin resistant in order to avoid getting so big that they cannot contain themselves and they would theoretically burst, you know, pop. And so what happens, they become insulin resistant, they stop listening to insulin. Insulin would tell a fat cell to pull in fat and store it and not share it. Importantly, by becoming a little insulin resistant, these fat cells can, one, stay alive, but they also— they stay alive partly by becoming leaky. They start to release their fat in the form of what's called free fatty acids, and importantly, they start to release these things called cytokines. And cytokines are little proteins that cause inflammation. Now that would sound like it's a bad thing, and in this context it's not great. But in defense of the hypertrophic fat cells, one of the things the hypertrophic fat is trying to do by releasing inflammatory proteins is actually recruit more blood vessels. Because when the fat cell starts to get so big, it actually gets too far from blood vessels to help maintain healthy function. To pull in oxygen and to give up carbon dioxide. And that's one of the many things it would need from the blood or need to exchange with the blood. So when the fat cell is getting too big, one of the reasons it might be releasing these proteins, these pro-inflammatory proteins called cytokines, is just to try to make new blood vessels. But it's a lost cause. It's a Sisyphean task. It's trying to fix the problem that can't be fixed because the insulin is always too high and it keeps pushing it up. Making the fat cell just maintain it too big of a size. So these— the, the hypertrophic fat cell is leaky. It's leaking free fatty acids and these pro-inflammatory proteins called cytokines. Those two things are essential components of the equation for causing insulin resistance throughout the rest of the body. So earlier I said fat falls first. It's like the first domino. Once it tips, it starts bumping into the next dominoes. By becoming leaky with these two molecules and then causing insulin resistance everywhere else throughout the body, like for example, muscle, liver, and brain. And let's look at this in more detail for just a moment. But let's not end with just these three organs. Let's add a couple more: ovaries and even blood vessels. Now, what was it— what would insulin resistance do at each of these things? At the muscle, when the muscle becomes insulin resistant, it actually makes it harder for insulin to help the muscle keep its protein. You know, our muscles function because of the incredible amount of protein in them that allows the muscles to contract and relax. As a muscle is becoming insulin resistant, it can't do that as well, so we start to lose the protein from the muscle, and the muscle starts to shrink. It wastes away. That's something called sarcopenia. In the case of the liver, insulin has a very strong hold of what the liver does with lipids, namely triglycerides and cholesterol. And so dyslipidemia is a term to describe an unhealthy change in blood lipids. And specifically, insulin resistance at the liver will increase triglyceride release from the liver, which is not good. It is not good to have high triglycerides. And it will reduce HDL cholesterol. It will diminish the liver's ability to make HDL cholesterol, which is typically considered the good cholesterol. Cholesterol. At the brain, it's quite fascinating actually. I mentioned earlier that insulin resistance is a key driver of Alzheimer's disease, indeed, to the point where many Alzheimer's scientists refer to Alzheimer's disease as a form of diabetes, like an extension of type 2 diabetes, specifically when the insulin resistance is affecting the brain. And briefly, and this would be a topic unto itself, What, what is part of the problem in Alzheimer's disease is that the brain can't get enough energy. The brain has a high metabolic rate, it has a high energy need, and glucose will typically fill much of that, if not all of that energy need. Now I will say, at the risk of going on a tangent and introducing an unwanted character into the story, there's another fuel called ketones that can help fill that energetic gap, but that becomes the problem. If the brain is totally reliant on glucose, as the brain becomes insulin resistant, the glucose can't provide all that energy. It can only provide this much. And so there's an energetic gap that must be filled. And again, things called ketones can fill it. There is in fact published human evidence to support that. But in this case, with the insulin resistance, putting ketones aside, there's an energetic gap. That is something that can be detected long before the person's obviously suffering from cognitive decline, but it is extremely consistent across people with Alzheimer's disease, this energetic gap known as brain glucose hypometabolism. The brain can't use glucose or can't get enough to fuel itself. Now, I mentioned problems at the ovaries before. I'll just mention this again. Polycystic ovarian syndrome is the most common form of infertility in women. And it is at its core a disease of insulin, insulin causing a problem in sex hormone production from the ovaries. Briefly, the ovaries will take things like testosterone, it'll take testosterone and it will turn it into the estrogens that a woman needs in order to have a normal menstrual cycle for normal fertility. Insulin stops that conversion. It doesn't allow the ovaries to convert testosterone into estrogens at the proper amount. And so the testosterone ends up being too high and the estrogens end up being too low, and then the menstrual cycle is disrupted, fertility is disrupted. But at its core, PCOS is a metabolic problem. And then lastly, although I could go on for hours, with blood vessels, when the blood vessel becomes insulin resistant, it cannot dilate as well as it could before. If we were looking down the length of a blood vessel, it can't get bigger to allow the blood to flow more readily. And when it— when that happens, of course, as the dilation occurs, blood pressure goes down. Well, it doesn't happen when the blood vessel becomes insulin resistant. The blood vessel stays narrow, it stays constricted, and pressure then is higher than it should be. Indeed, almost every instance of hypertension at its core will have some insulin resistance component to it. Now I've kind of made the case that we have a global problem, insulin resistance, and I've introduced to you— you're now an expert in how we become insulin resistant. What can we do about it? And that's, that's the nice thing about this talk. It's like I've been telling a horror story and now I'm giving you the happy ending. So if it was a horror story, the upside is there's a happy ending because we can fight insulin resistance exquisitely well and I'll give you— I'll arm you with some tactics on how to do that. The single most relevant variable that we can control is lowering insulin. Now, like I said, there are other things to do, other things to keep in mind, like stress and inflammation, for example. But lowering insulin, I submit to you, is the single most relevant step you can take to either prevent insulin resistance or start to rapidly reverse it. Now then, how can we lower insulin most effectively? There are 3 things I'll highlight, in some instances briefly: drugs, diet, and exercise. Now, with regards to the drugs that you would be prescribed by your physician, please note this is the gospel according to Ben Bikman here. This is my view on the insulin drugs, the insulin-related drugs that you can get that will commonly be prescribed clinically. I've broken them up into just two categories, and I'm not going to go into too much detail, but I consider some good and others not so good. Now, on the good side, we have two, two categories really: metformin and then anti-inflammatory medications like aspirin. Aspirin works. It can improve insulin sensitivity, but of course there's a downside, which is the problems long-term that it can have on our intestines. Metformin is worth noting simply because it is the most effective drug at improving insulin sensitivity, and not surprisingly, it is the single most widely prescribed anti-diabetic drug in the world. It works, and the side effects tend to be kind of minimal. Now, lest you think I am too enthusiastic about a drug intervention for improving insulin sensitivity, let me emphasize that even this best of all drugs is only half as effective as changing someone's lifestyle. So if you're wondering how to improve your insulin sensitivity and you're tempted to take the easy route and get a prescription from your physician, let me temper that enthusiasm by just emphasizing that it will at its best be half as effective as even just modest lifestyle changes. Lifestyle is the culprit or the cure when it comes to insulin resistance. And I'll get more into some of the strategies in just a moment. Now, the not so good. Let me just mention this one in particular before I mention the bottom two. Thiazolidinediones, or TZDs, are a very interesting anti-diabetic drug. They work very well. Let me just say that on the outset here. TZDs, thiazolidinediones, work well. And you will be intrigued at how they work. In fact, in a moment you'll understand how these drugs work better than most people do who, who use them frequently. Remember, I mentioned to you before that one of the most common origins of insulin resistance will be hypertrophic or bad fat cells. What TCDs do are actually push the fat cell from being so big into being more modest size but having a lot more of them. Now, what is so interesting about the situation— it's two, and it seems like a bit of a paradox. One, you have improved the insulin resistance. The person's insulin levels will get better, their insulin sensitivity will get better. And then the paradox is that they get fatter and fatter because you continue to allow the fat cells to proliferate or to undergo hyperplasia. You keep getting more and more fat cells, so the person gets fatter and fatter. Typically, the individual will stop taking the drug because they gained 30 pounds in 6 months and they say, "This isn't worth it. I don't want to take this drug anymore." They go right back to, of course, in fact, even worse than before because they are fatter than they were before. Once the cells aren't being pushed through hyperplasia, they start to revert back to storing fat through hypertrophy, and then the insulin resistance comes raging back. That's why I have this on the not so good. Now, the bottom two are worth special mention: sulfonylureas and insulin itself. Essentially, it's like we take this same paradigm I showed you earlier where the insulin has started to come down, but importantly, even in the midst of full-blown type 2 diabetes, the insulin is still higher than it was before the person started on that metabolic descent into madness. You need to remember Even in type 2 diabetes, insulin is still higher than it was before at the beginning, but it might have come down from where it was at its peak. Now nevertheless, because we look at type 2 diabetes and even insulin resistance through the lens of glucose, it's such a glucose-centric paradigm that we look at this high glucose and we think, well, let's just, let's just lower the glucose by spiking the insulin up even higher. And so we either give the person direct injections of insulin or we give them sulfonylureas, which is a drug that will force the, the pancreas to make more insulin than it did before. In either case, we are pushing up the insulin higher than it was before, and indeed, if we only care about glucose, I would say it works. If you push up someone's insulin, glucose will come down. Now, there are some important considerations that I believe are too often overlooked. One study I'm mentioning here emphasizes that there is no evidence of long-term efficacy or long-term benefit. And in contrast, there's evidence of clinically relevant negative impact of treating people with insulin in, in an effort to try to improve the metabolic disorder. And to go even further, with both insulin and sulfonylureas, we have human evidence to show that it increases the risk of cancer. And increases the risk of heart disease. So we are improving their glucose all while we are making them potentially sicker than they were before. And because you know the origins of insulin resistance, let me just ask— and I wish I could do this face to face with you to hear your shouted answers— but what will this elevating insulin do to insulin resistance? Remember, One of the main causes of insulin resistance is too much insulin, and now we're pushing it even higher. You're right if you speculate that this will make insulin resistance worse. It does. And that is why when we put a type 2 diabetic on insulin therapy, they need to take more and more and more of it as they become progressively more and more insulin resistant. So these drugs, I will state conclusively, will never solve the problem. It's only treating symptoms of the problem. We need to go right to the origin of the problem and address lifestyle. Now, exercise. I'm a huge advocate of exercise, so don't let the brevity here mislead you. Exercise is important, and I very commonly am asked, and I commonly think, well, what's the best exercise? How could we maximize our time to make the body as insulin sensitive as possible? Well, here is my incredibly informed and scientifically justified answer: the best exercise is the one you will do. It doesn't matter. You start where you are. If it's walking around the block or if it is engaging in very high-intensity resistance exercise at, at some flashy gym, just do something. And let me just add, don't follow up your exercise with an insulin and glucose spiking treat. This is evidence to find that when someone ends an exercise bout, they are more insulin sensitive than they were before, even into the next day. But if they exercise and then drink some sugary drink or some sugary energy bar or something, it actually offsets— it undoes the insulin sensitizing benefit of the exercise. So just because you exercise does not mean you now have room to indulge. In so doing, you have undone much of the benefit, but that is commonly done, unfortunately. Now let's talk about the main one, really addressing the elephant in the room, and that is the role of diet. Um, mentioning diet, I want to highlight 3 strategies in improving insulin resistance. The first one is intermittent fasting. This is a topic that should be familiar generally to all of you. It is, after all, a fundamental part of our faith. Fasting is incredibly beneficial to the body and the spirit. And this study highlighted a series of case studies, clinical, like, patient case studies, that engaging in intermittent fasting was so effective at improving insulin sensitivity that these insulin-dependent type 2 diabetics were able to stop their insulin based on communicating with their physician, which of course you would do as well. I'm not prescribing anything here. I'm just sharing the information. Intermittent fasting was so effective, it was so at reversing, so effective at reversing their insulin resistance, that they were able to start weaning themselves off of their insulin therapy in these insulin-resistant type 2 diabetics. That's all I'll say about that. Now let me introduce another one, and indeed the absolute most popular of all dietary strategies, the low-fat or the low-calorie paradigm. This is, again, without a doubt, the most commonly given advice when someone is being told what to do to improve their metabolic health and risk of all those related diseases. They'll say, well, you need to eat less, and they'll say exercise more, of course. There are problems with that. But I will say, to be fair, I'll highlight the problems in a moment when we compare it to the alternative method. To be fair, if someone shifts from the typical Western diet, high fat, high sugar, and they start to eat less food in general, the insulin will come down just because they're eating less, and then they will start to have an improvement in insulin sensitivity. But we shouldn't just stop there. What we should do, I believe strongly as a scientist, we should survey all the evidence. And then especially compare the low-fat model, which is the most common, to the alternative model of an intervention, which is low carbohydrate. Now let me just kind of present the, the background or the context or justification for a low-carbohydrate diet. And let me do that by highlighting what happens when we eat the 3 macronutrients. So fat, protein, and carbohydrates are the 3 macronutrients in the human diet. And macro— these are the main parts of our diet. The main stuff that we eat comes from these 3 things. When we eat fat, we have no effect on our insulin. When we eat pure protein, we have a modest effect, and that depends on some other variables that I don't have time to get into now, but that can be higher or lower, but there will certainly be some effect on insulin. When we eat pure carbohydrate, we have a substantial release on insulin, even to the point where it's potentially 10 times higher, and it will stay higher than baseline or pre-eating levels, and it can stay elevated for up to 3 or 4 hours. And of course, the more insulin resistant someone is, the higher that will get and the longer it will stay elevated. Now, lest you think I am demonizing one entire class of macronutrient, I will emphasize that that not all carbohydrates are created equal, or in other words, not all carbohydrates have the same effect on our insulin. They won't all spike insulin to the same degree. In fact, not at all, and I'll come back to that idea. Now let's compare these two dietary strategies, one being very common, the advice we get for a low-fat diet, and one being less common. It is spoken of in hushed tones, and that is a low-carbohydrate diet. Let's look at what happens. I'm only highlighting a few studies here. Please understand I could highlight dozens. I'm just picking some clean ones that allow me to present the data very effectively. So here I'm going to show you, as we go through this, these two diets and what they do to glucose levels, to insulin levels, and then to insulin resistance as it's measured. In this study that I'm citing here, and the identification of the study, that number is down in the corner as, as usual, What they found was that on the low-fat diet, glucose had an insignificant reduction to 2%. It was not significant. In contrast, the low-carbohydrate diet had a 15%, a meaningful reduction in fasting glucose levels. Insulin similarly changed modestly in the low-fat group. It went down by 16%. In the low-carbohydrate group, it went down by about 50%. So it went down to about half of what it was before. And we see a similar outcome when they actually, when the scientists actually measured insulin resistance. It went down by about 16% in the low-fat group and went down by over 50% in the group that was just simply scrutinizing their carbohydrate and controlling, eating less of their carbohydrates. And I'll define all that. I'll define a low-carbohydrate diet in a moment. Now let's shift. This study was really interesting, published in a very good journal. Called the New England Journal of Medicine, and they took people and split them up into 3 groups of a typical low-fat diet. So that was low-fat and low-calorie. And then they had another group eating a so-called Mediterranean diet, which was a little higher fat, a little less carbohydrate, and once again it was low-calorie. So they told the people to eat less. And then lastly, it was the low-carbohydrate group, which had a, an unlimited calorie. They could eat as much as they wanted calorie-wise, but they had to keep their carbohydrate down to a low amount. Now, to my frustration, they shifted the carbohydrate. They put the group at first, they started on a very low carbohydrate diet, and then actually they lost so much weight so quickly, and I don't show those data here, but they shifted them up where they increased it up to about 120 grams, which is not particularly low. Nevertheless, what happens if we compare these groups? Well, in these normal patients, in every instance, the low-fat diet was the worst and the low-carbohydrate diet was the best. It lowered glucose the most, it lowered insulin the most, and improved insulin resistance the best. Pretty, pretty clear evidence. All right, another study here. I'm showing you the, the average, the beginning numbers, right? Right here. So the groups, as they were split up into diets, the common average glucose was 86 milligrams per deciliter. And it didn't change significantly in either group. None of these changes was statistically significant with glucose. Then insulin, they started at around 41 picomoles. Now that's a different unit than I showed you earlier. That's an international unit, like what we'd see in Canada or Europe. It's not the microunits per mil that I'd mentioned earlier, which is how we measure it in the US. But nevertheless, we can use that number as, as a gauge for what happened. In the low-fat group, insulin tended to increase up to roughly 50 picomoles. In the low-carbohydrate group, insulin appeared to come down slightly, down just a few points, down to 37. Insulin resistance was actually a stronger change. They all started at this score of 1.28. Now very briefly, if you, this score, you could look this up. It is, they're measuring something called the HOMA score. HOMA is an acronym, H-O-M-A. You can look it up. So it started at 1.28. In the low-fat group, it got worse. It went up to 1.63. That's not a good thing. When you look at HOMA, bigger is not better. So the insulin resistance got worse as this group was shifted to a low-fat diet. And in contrast, the insulin resistance got better when they consumed a low carbohydrate diet. Now let me show one more study. This study is really compelling because it helps us understand some of the nuance in human physiology. We are, after all, complicated, complicated animals. What they did at the outset of this study was split the people up into two groups based on where they started. There was an insulin-resistant group because these people were insulin-resistant, and then the insulin-sensitive people were put in— lumped into their own group as they studied them. And these differences were immediately reflected in the insulin levels. And this is back to the U.S. system of looking at microunits. In the insulin-resistant group, their average fasting insulin was 16 microunits per mL. In the insulin-sensitive group, it was 5. And you'll notice That's below that cutoff that I gave you earlier of 6 microunits per mL. What happened then as they put these groups at different times on the two different diets is quite compelling. When both of these groups were eating a low-fat diet, we saw a very modest change in each of them. The insulin resistance tended— the insulin levels very slightly, a slight tendency to reduce in both. On the low-fat diet. And you could say, well, it's partly because the insulin-sensitive people were already low, they didn't have as much room to go down. Yep. But in the insulin-resistant people, they had a lot of room to go down. Why didn't they go down more? Well, remember, on a low-fat diet, by cutting the fat, we're having the person eat more carbohydrate relatively. And remember, what does carbohydrate do to insulin? Well, it spikes it quite a bit. And if someone's inherently, if they're already insulin resistant, we're just spiking their insulin all the time. Even though they're cutting their fat in their diet, low-fat diet, they've now shifted to the one macronutrient that has the biggest effect on insulin. And in an insulin-resistant person, that's maybe not the best strategy. And indeed, it's not, as these data indicate. When you had these subjects shift over to the low-carbohydrate diet, In the insulin-sensitive people, they didn't really change. And why would we expect them to? If they're insulin-sensitive, that is the person who can eat a carbohydrate and their glucose comes up after eating the carbohydrate, like a bagel, and the insulin comes right up and is so good at working, it lowers the glucose quickly and the insulin comes back down quickly. Maybe it's come up and back down in 90 minutes or so, never really even needed to get that high. But in the insulin-resistant person, by telling them to control the insulin-spiking carbohydrates and focus on the two macronutrients, fat and protein, that have the least effect on insulin, look at the change. They dropped down to roughly 10 microunits. So they were, that was, you know, about a 40% reduction in their insulin levels. It dropped by about 6 microunits per mL, a very significant reduction in insulin. So when we look at the, like I said, the nuance, Some people will respond better to this low carbohydrate model or system than others, and that's because some people just don't handle their carbohydrates quite as well. That's kind of another way of looking at insulin resistance, a carbohydrate intolerance almost. Now, how does this look if I've convinced you that in insulin resistance, scrutinizing carbohydrates is a prudent and justified strategy, how might you— what could you take away for practical advice? Well, I'm all about practical advice. I believe there are 4 pillars to controlling insulin through dietary intervention the best. 1, control carbohydrates. 2, prioritize protein. 3, don't fear fat. And lastly, watch the clock. Now let's go into each of these in a little more detail, very briefly. With control carbohydrates, I don't mean for you to take away from this that I'm demonizing carbohydrates. I'm not. I believe they can be absolutely part of a healthy diet. We just need to be smart about the type of carbohydrates we eat. Essentially, if it comes in a bag or a box with a barcode, it's likely one to be careful with. If it's a natural source like a fruit or a vegetable, although we humans have changed them somewhat. But in general, those are going to be ones you can focus on. But eat them, don't drink them. Now these two come together because in nature protein and fat come together. And let me emphasize that they do. The best protein sources are dairy, beef, or meat and eggs. Those are unequivocally the best sources of protein. All of those come with fat. Fat naturally comes with protein, and so we shouldn't fear that fat. We shouldn't be worrying about the fat that's coming with protein. Indeed, I believe it's very nutritious and necessary. There are such things as essential amino acids that come from protein, and all the animal proteins, animal source foods, give us those essential amino acids. And there are such things as essential fatty acids and all animal-sourced fats give us those essential fatty acids. The more we avoid animal-sourced foods, the more deficient we will become. Now let me, let me just elaborate on the protein for just a moment, although I didn't intend to. I appreciate nowadays there is an incredible obsession with plant proteins, things like proteins from peas or soybeans. Those Ought to not be the sole source of protein because they do not contain the full complement of amino acids that help a human body thrive. But they also contain these things called anti-nutrients. That almost sounds like I'm making it up, but these plant proteins can contain things like tannins or lectins or phytic acids or trypsin inhibitors. And you can look all these things up, please. They actually block the body's ability to use those proteins from the plants. And lastly, plant proteins can be high in, in heavy metals like lead and arsenic, because when you try to get all your protein from peas, you've got to take, you know, 1,000 peas and concentrate them to get a serving of protein. And the protein is what you're intending to concentrate. The unintended product of all this is that you're concentrating all of the metal that is naturally in plants albeit to extremely low levels, you've concentrated these things. So be careful of plant proteins and eat the way our ancestors did. Imagine our grandparents 100 years ago, or ancestors 100 years ago, trying to get their protein from peas and soybeans. Of course, it would be laughable. Now, as I— before I leave this thought behind, and specifically the don't fear fat aspect of it, let me emphasize one, one angle here that is worth considering. And I submit to you that we should focus on healthy natural fat, and that industrial seed oils are not natural. Let me emphasize one, and this is a study that you can look up to see what I mean here. In our modern diet, the single most common source of fat is something called soybean oil. This was a fat that 100 years ago was not even— there was no speck of it in the human diet. And within 100 years, it has gone from being non-existent to, again, the single most common source of fat in the diet. In other words, we eat more of our fat from soybean oil than any other source. That is not good. The primary fats in soybean oil are not healthy. When we overload the body with them, and I I beg your pardon that I can't elaborate on this more. You'll just have to do some of your own homework here. For now, take my word for it, soybean oil is not a fat that we should be consuming very much of, if at all. Now intermittent fasting, I will show no more than this. Here are different strategies that I have here where it can be something called time-restricted eating, where someone has a fasting period and then an eating window within the course of a day. Or they can do a 1:1 where there's a normal day of eating and then a day of food fasting, so drinking water. Or an alternative method that has been shown effective in human studies is a 5:2 where they are fasting on weekends but eating normally during the week. There are many ways to do this. I am not prescribing any of these to you, but I do just want to emphasize that intermittent fasting is something that has a tremendous effect on improving insulin resistance. And then at the end, please get your insulin measured. Next time you're going in through, uh, for, for a health check with your physician or your clinic, ask them please to measure your insulin. Increasingly, this is something that you won't meet much resistance on. Indeed, some of you may already know, um, but it, I will— it wouldn't surprise me if you ask to get your insulin measured and you get a little bit of resistance. That's just because insulin is not in the limelight. It's not at the forefront of clinical thinking. I am wanting it to be because I believe it's very justified. We ought to be scrutinizing insulin, and maybe it'll start with you. Get your insulin levels checked the next time you go in for a checkup at your clinic. And then in conclusion, let me just remind you, insulin resistance has its hand in virtually every chronic disease. All these diseases and disorders that really terrify us Cancer, like the most common cancers, breast and prostate cancers, are very linked to insulin resistance. Insulin resistance making the cancer more aggressive. The most common forms of infertility, the most common forms of dementia, the most common forms of fat, of liver diseases, all of these are either caused by or exacerbated by insulin resistance. And thankfully, that is something we can do a lot about. Now, we've had a pretty productive time. You've learned what is insulin resistance, what it is, the single most common health disorder in the world. You've learned all the diseases that are derivative of insulin resistance. You've also learned the origins, how we get insulin resistant. And by understanding insulin resistance, you have an understanding also now of what you can do to improve it, to reverse it, or even prevent it. Thank you all so much for listening. I hope this has been productive. I certainly enjoyed the opportunity to share this with you.
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