I found that insulin resistance was a foundational cause to virtually every chronic disease, what I now refer to as the plagues of prosperity.
Today's episode is with Dr Ben Bikman, who is a professor and researcher in insulin resistance, and I think you're gonna find it really informative. We are talking all about insulin resistance and helping you really understand what it is and why it matters. So we do get a little sciency at the beginning. Be sure you stay tuned till the end, where we wrap it up and really give you specific things of what you can do to improve and prevent insulin resistance in your own health. He's got a great book called Why We get sick, and also some really helpful tips on his website, benbickman.com or his social Ben Beckman PhD, I hope you enjoy, heart disease, forms of cancer, the most common liver problem, fatty liver disease, the most common forms of infertility, high blood pressure, or even certain skin disorders that are increasingly Common. As much as these seem like totally distinct, unrelated problems, I found that there was substantial evidence to suggest that they all had one thing in common, namely, insulin resistance.
Thank you so much for being here. It's so nice to meet you and talk with you. Oh, my pleasure. I'm delighted. Well, we're not going to waste too much time here. We're going to dig in, but I do want to tell listeners a little bit about you. So Ben has his PhD in bioenergetics and works currently as a professor and researcher at Brigham Young University, which is also my alma mater, so we're happy to connect. Yeah, go Cougs, yeah, yeah, that's right. Well, let's just go ahead and dive in. Would you start by just hitting us off with why this topic is so important, especially insulin resistance, but the bigger picture of metabolic health, right? Yeah, it? I confess part of my answer is, is, in fact, my own journey, my own evolution, which is this focus on insulin resistance. When I first began my academic career, my pursuit of becoming a scientist and a research professor, I thought I was only going to focus on the connection between obesity and type two diabetes, and the bridge that connects those two phenomena is insulin resistance. So insulin resistance, I considered just to be the great mediator between fat getting too much or too big and type two diabetes. And then as I continued to kind of dive down into that topic, which is what you do with science, you usually pick a field and just go deeper and deeper, I found that insulin resistance was also a foundational cause to virtually every chronic disease, what I now refer to as the plagues of prosperity, heart disease, the most common forms of cancer, the most common liver problem, fatty liver disease, the most common forms of infertility, high blood pressure, even certain skin disorders that are increasingly common as much as these seem like totally distinct, unrelated problems, I found that there was substantial evidence to suggest that they all had one thing in common, namely insulin resistance. So to sum all of that up, insulin resistance is relevant to every non infectious chronic disease. But to make matters even worse, and to justify my own professional expertise, it is also the most prevalent problem where there was a paper published just a handful of years ago that found that up to 88% of all adults in the US have some manifestation or symptom of insulin resistance, like high blood pressure or high blood glucose, or, you know, along those lines. And as much as we like to think it's a uniquely kind of American attribute to think that America is the fattest and the worst, and that is just not true. I've, I've just over the past week, gave a talk about insulin resistance in Morocco and Sweden, and a month before that, I gave a talk in Japan and Thailand. So there, this is an absolute global problem. So global proportions, making insulin resistance the single most common health problem worldwide. And then again, putting it in perspective even further, it then contributes to all of these chronic diseases. That's so helpful. So we are going to be talking about specifically insulin resistance and metabolic health in women, and hopefully by the end of this, people will feel pretty good about knowing how to go about finding out if they have insulin resistance, and have some sort of action strategy for for what to do about it and why this matters so so much. So I'm excited to break it down. I think it's helpful to first clarify a couple definitions, because everyone has heard about this now, but I still think it can be really confusing. Will you break down probably those two definitions to start with, of insulin resistance and metabolic health? Yeah, yeah. Wonderful, right? So let's start with metabolic health, because.
That term gets thrown around very, very readily, and in fact, I would suggest, maybe too readily, at least without people appreciating it. So metabolic health, One common way of defining it would be through the lens of the metabolic syndrome, which is another thing people have heard of. The metabolic syndrome is this clutch, this cluster of complications that kind of always tends to clump together. And this is, you know, having a little too much fat around the belly, high blood pressure, high blood glucose, and then your blood lipids, your triglycerides and your HDL cholesterol are a little off. Those are the things that tend to just come together. However, before it was ever called the metabolic syndrome, it was called the insulin resistance syndrome. That was one of the original terms for this observation, of these problems that clump together and then insulin resistance is really a pathology with two parts, or as I like to say, it's a it's a coin with two sides. One side of the coin is the resistance to insulin, and insulin is a hormone that flows through the blood, and it has the ability to affect every single cell of the body, which is not common, but literally, every single cell of the body has insulin receptors, these little doorways that are specifically designed for insulin to come and knock on The door. Some of those cells stop answering the door. So that's the insulin resistance part. Now, as I noted, that's only one side of the coin to really appreciate insulin resistance, especially with women and fertility, as we'll get to you, have to flip the coin over and consider the other side of it, which is, every time you talk about insulin resistance, you are also talking about hyperinsulinemia, or elevated blood insulin levels. There is no insulin resistance without hyperinsulinemia, those two things are just locked at the hip. They come together. And again, when it comes to female physiology, with pregnancy and infertility, these two opposites, you actually have these unique they are each a unique manifestation of insulin resistance with its two parts. And also, I'll add on to that, menopause, right? We see these rising levels of insulin resistance, then when the hormones go away, that's right, those female hormones, or those sex hormones, are pretty closely integrated with the controls for the insulin, yeah, especially estradiol, the main of the the kind of poster child of the estrogens, estradiol is, I've sort of joked previously that it allows the woman to be a metabolic superhero, that when the estradiol goes away, now she's immortal, like her unfortunate male counterparts, who've always been subject to the frailties of metabolic mortality, but as long as the woman has those premenopausal estradiol levels, she's kind of bulletproof metabolically. Yeah, well, I won't argue with that. I like that definition. So tell us one more time. So the insulin is a messenger, right? And it's going and knocking on the door, what message is it trying to deliver? Because I think when we talk about this, it's really easy to demonize or, you know, to say, like, Oh, I got it insulin, bad guy. I don't want insulin, right? Like, everything, when we talk about anything in the body, basically, it's in moderation, right? There's too much of a good thing or not enough. What is it trying to tell the body? Yeah, I love that. You framed the question that way, as much as I kind of have a career looking at insulin as the villain, it is absolutely a molecule of life, and that the absence of insulin, in other words, an untreated person with type one diabetes, is a death sentence, and that's because of what insulin does. Back to the question, we often look at insulin strictly through the lens of controlling glucose or blood sugar. People, in fact, indeed, even very experienced clinicians, think that insulin has no more relevance than its control of blood sugar levels, which is just fantastically unfair, because insulin will stimulate dozens of different effects at different cells of the body. In fact, the number of cells that will pull in blood sugar or blood glucose in response to insulin is actually just two or three, but all the other cells of the body still need insulin to tell it. And so here's the thematic answer when insulin knocks at the door of every cell of the body, brain cells to bone cells, lung cells to liver cells. The common message is, although it can be personalized to cell type, is I'm here to tell you what to do with the energy that you have right now, and that is out here in the blood with me as I'm coming in. That is the thematic effect of insulin at every cell of the body. It's just saying, Hey, I've got some energy here. And to really put a fine point on it, I need you to store it. That is the thematic effect, even in those cells where insulin isn't necessary for the glucose to come in. And I'll just to be really precise, when insulin comes to fat cells, you.
There's glucose out ready to come in. Blood glucose has gone high. The blood glucose cannot get into those fat cells until insulin comes and knocks on the door, and then the door opens. Now the glucose can come into the fat cell. In contrast, the liver cell, it can pull in glucose the moment glucose starts going up, but it won't know what to do with it. In the absence of insulin, it'll pull it in and let it out, pull it in and let it out. It won't actually hold on to it. So insulin will come and knock on the door, even though there's glucose rushing in, the open door right next to it, and we'll say, Hey, you're pulling in glucose. This is what I want you to do with it. I want you to hold on to it, turn it into glycogen, because you're going to want that later, for when we stop eating glucose. So in a good situation, of course, we want that insulin to tell our cells exactly how to process energy, which is metabolism, right? That's what you're describing. So we get energy in through food, generally through food, and then the insulin tells the cells, hey, good. We've got energy here. Let's save this or use it for the rest of our body functions, for thinking, for our heartbeat, for all of the the functions that are keeping us alive. Now, where does this go awry? There's a cue. Then that cues the insulin to go to start saying that too much. And then, so what is that cue? And then how does that start to cause this cascade of of badness. Yeah, yeah. So, yeah. So transitioning here, then from now that I, you know, hopefully everyone feels like they have a pretty good understanding of insulin and insulin resistance, then it's, it is fun to kind of move into the origin story. You know, if insulin resistance is the villain, how did it break bad? Where did it How did it become such a bad guy. So insulin resistance. Again, this two part pathology, insulin resistance at some cells of the body, not all cells become insulin resistant, but combined with the hyperinsulinemia I generally describe, or my own classification system, has sort of brought me to the conclusion that there are primary causes of insulin resistance, and then there are secondary causes. For the sake of time, we'll just put the secondary to the side. The primary causes are ones that are each capable of causing insulin resistance, not only on their own, so they're each independent, but they've also been shown to cause insulin resistance in every studied biomedical model. Now what I mean by that is, when a biomedical scientist is publishing results from from research, we are using cells that are growing in little petri dishes, or we are using laboratory rodents, or we're using humans. So these three primary causes of insulin resistance have each been shown to cause insulin resistance in all three of those biomedical models. Now with that, as a very long winded warm up to it, there they are, stress and inflammation and too much insulin. And if you'll allow me, I'll just briefly kind of define them. So with stress, I mentioned stress as a professor who teaches a graduate class in endocrinology. So I'm just fascinated by the hormones. And you can't really understand stress without understanding hormones. Stress is hormones, namely epinephrine, also known as adrenaline and cortisol. And there's some other inputs there too, but those are the big boys. They're the main ones. So it's cortisol and epinephrine. Now, as much as we call them stress hormones, they're actually very different. They come from different cell types. They are they come from different origins. They're different types of hormones. They are carried in the blood in very different ways. They actually act on the receiving tissues in very different ways. So they actually have very little in common. The one pronounced thing they have in common is that they both increase blood glucose and do so very, very strongly. That means that they become antagonistic to insulin, whose most famous job, but I won't say most important, whose most famous job is to lower the blood glucose. And so the more those stress hormones are elevated, the more insulin is having to work harder, and we have come to insulin resistance. And this is a phenomenon that happens quite quickly. Each of those stress hormones can have both shared stimuli and distinct stimuli, like too much caffeine is going to stimulate epinephrine. A little more poor sleep is going to stimulate cortisol. A little more fasting is going to be a little more epinephrine at first, and then a little more cortisol. And then those will generally subside. But even still, they kind of play together a little bit. But suffice to say, when those hormones are up, there may be a little bit of insulin resistance, if only temporarily. Then second is inflammation, very briefly, anytime the body has elevated levels of these inflammatory proteins called cytokines, which can be elevated from an illness like infection or an autoimmune disease or.
Inhaled pollutant particles, then that will once again stimulate a degree of insulin resistance. And then the third one is the one I believe is the most relevant in most people, which is too much insulin. And now the astute listener may start to think envision this sort of vicious cycle, and that's exactly what's happening, where too much insulin is both the feature of insulin resistance, but it's also a cause and a consequence. So if your body isn't responding very well to insulin, no surprise that the body starts making more but at the same time, too frequently, spiking insulin levels is a way for the body to just start to become deaf to the signal. It's like the person who's constantly listening to really loud music, you become deaf. That's like the cells that are constantly inundated with insulin. You become deaf to the signal. And that's largely driven to just the way we eat. We kind of have two main problems, and this sort of starts to touch on the solution, but I promise I won't get ahead of the conversation here, but we, yeah, yeah. We just have a culture, particularly where you and I are here in Utah, it really is particularly apparent where we have a constant carbohydrate consumption and we just feast too frequently. So we eat overwhelmingly, what goes in our mouth is refined starches and sugars, whether we're eating them or drinking them, and we're doing it way too often. And that means as we're spiking our blood sugar, we're spiking our insulin, and insulin can take four or five hours to come back down, and long before then we've already spiked it up again. And so we live in a constant we live in a culture where most people spend every waking moment in a state of elevated insulin. From the moment they wake up, they eat or drink something sugary and starchy, and that just sets the tone, the metabolic tone, for the rest of the day and even well into the evening. And so that I leave with, I end with that one, that the most important one I contend is the chronic elevations in insulin. Yes, wow. Such a great a great instruction on all of that, I think, just to reiterate that last part is you, you eat the glucose and the the body's idea is to take that energy and go do something with it. So it's not a flawed system in and of itself. But we eat energy in the body's like, got it, okay? Insulin comes in and says, here's what we're gonna do with this, if we keep giving the body the wrong cues, which is glucose, glucose, glucose, amongst other things. And then it starts to become additive, where you have really processed foods that are spiking glucose, in addition to stress in a different in addition to inflammation, and then you have lack of sleep, which is more stress, and you start having all of these components add on to each other. All of those are just cueing the insulin to go up, up, up. And meanwhile, the cells, like you said, are starting to become deaf. So what happens to the insulin? Then the insulin goes up even further so it can yell to get those cells to respond. And around and around it goes until we get that insulin resistance. Since we're talking right now, do you want to comment? Maybe this is the right time to comment on how the sex hormones, even just briefly, kind of how, what is their role in this with estrogen and lack of estrogen? Yeah, so yeah, estradiol being the main of the estrogens, which is particularly relevant here. But I also have to bring in another one, which is progesterone. And of course, this part of the conversation is very relevant to pre menopausal women, because then with the loss of ovulation comes a substantial change in those hormones. With menopause. To answer this, I almost have to revisit the causes of insulin resistance, because the three primary causes that I described are very acute stimuli like you can take in a human and within 24 hours make them insulin resistant by giving them too much insulin or stress hormones or inflammation. But just as quickly as that can settle in, if you remove that stimulus, you remove the insulin resistance. So it's a very acute on and off. Now, of course, in many instances, it's just chronically on. So to really understand the role of the sex hormones, particularly in women, we actually have to bring in the fat cell, at the risk of making it all a little more complicated, but a little more compelling at the same time, I hope. But the fat cell is the tissue primarily responsible for chronic insulin resistance. So when a person has an insulin resistance that is deeply set in and is now going to take, you know, a, you know, a few months to resolve. At that point, we're really talking about the fat cell. And so briefly, when, when a human gains fat, they can gain fat through two different ways. They can gain fat through a process of the fat cell multiplying, which is called hyperplasia, or they can gain fat through a process of the fat cell number staying the same, just each individual fat cells getting bigger and bigger. That's called hypertrophy. Hypertrophy is the way we most often gain weight and.
And it is the most harmful, because as the fat cell gets bigger and bigger, it starts to become insulin resistant in order to try to stop growing. It's basically like a water balloon that we've had connected to the tap, and we're letting it get bigger and bigger and bigger. We can tell it's going to burst soon. We don't want it to burst, so we turn the tap off. The fat cell starts to reach a point of maximum dimension, and this can be well over 100 times the volume of when it started growing. There's no cell in the body that is capable of growing like the fat cell can grow. Nothing comes even close. So this big fatty balloon is just getting bigger and bigger, almost to the point of bursting, and it's insulin telling it to get big. It is literally impossible. As a brief little aside, it is literally impossible for a fat cell to grow in the absence of an insulin stimulus. You can feed fat cells all or expose it to all the calories you want. And if insulin is low, it cannot get big. It is totally impossible. This is why some type one diabetics tragically learn that if they deliberately underdose their insulin, they can eat as much as they want. And now there's metabolic Havoc as a consequence of this, and it is absolutely catastrophic. But if their only motivation is to be thin, well then they have total control over that because of what's in that little insulin syringe. That's an eating disorder called diabulimia, just as a tangent. So the fat cells getting bigger and bigger, and it starts to tell insulin. If I continue to grow, I'm literally going to rupture, and we don't want that. That's going to be very messy and inflammatory, and it's a bad way to die. None of us want this. So I'm going to become insulin resistant, and I'm going to stop listening to you, and that then through other mechanisms that I won't get into starts to that's sort of like the first domino to fall. And then the fat cell starts to spread the insulin resistance to the liver, to the pancreas, to the muscle tissue, and when those three tissues in particular, start to become insulin resistant. Now we start to struggle with glucose levels, and we start pushing into type two diabetes. Okay, now to bring that back to women really briefly, sorry for the little excursion there, but I think it's helpful. So why did I say earlier that estradiol with the main estrogen? Why does that give a woman kind of a metabolic immunity? It's because estradiol has the ability to stimulate the growth of new fat cells, which a woman may curse, and it doesn't happen everywhere. It is unique to her subcutaneous fat tissue. So subcutaneous is the fat tissue that we store right beneath the skin. Women generally do more of that. That is a very healthy place to store fat. So it's the estradiol that's primarily telling her to store fat in her subcutaneous space. In the male counterpart, it's his androgen levels that is telling him to store it on his belly. Back to the woman, yeah, that's right, in the visceral space, most especially. And then with the woman with her high estradiol levels, when the estrogens are elevated, not only is she storing her fat subcutaneously, but it's also enabling that when the fat cell starts to get a little big before it ever becomes insulin resistant and pro inflammatory, estradiol is saying, okay, you've reached your limit. Let's make another one now and then you are going to help carry so this daughter fat cell is going to help carry the metabolic burden. Whereas in the male, he doesn't have that ability. Generally, genetically, sometimes people do, but more the vast majority of the time he won't. His body is saying your fat cells getting bigger and bigger, too bad, you just got to carry the load, and now you're becoming insulin resistant and pro inflammatory, and now you're in now you have heart disease and fatty liver disease, etc, whereas the woman just continues to get gain body fat and she's perfectly healthy. So that's one component to it, where her estradiol levels are actually telling her body to store fat in a healthy way. But at the same time, this is shocking to most women. Women are fat burning machines. At any given moment, a woman is burning 40% more fat than her male counterpart is. Now she may say, Well, why do I have more fat than him? Too? Estradiol is stimulating the breakdown of fat, and estradiol is actually stimulating the burning of the fat, because those are not the same thing. So estradiol is both stimulating the breakdown of the stored fat from the fat cell, sending it out to a tissue like the muscle, telling the muscle, I've got some fat for you here. You got to burn it. So at any moment, a woman is burning more fat and then a man is in fact, this is so substantial that if you are looking at an uncommon marker in the blood called free fatty acids, which is not the same as triglycerides or cholesterol or anything else, it's uncommonly measured, you have to have a different metric for men versus women, because the woman is going to be like 50.
50% higher than the man, and that's her baseline state. She's just burning so much more fat than he is, and that's all estradiol. Now I'd mentioned progesterone. Progesterone actually starts to complicate it a little bit, and it's that one time of month with during ovulation, where her progesterone levels will go high and then come back down, depending on what happens. If she just has a normal ovulation, without any pregnancy, it went up and down if, of course, there was fertilization and implantation. And now the pregnancy is moving. Now it's staying high, but during that one period of time, for those couple days or few days, progesterone has two effects. Progesterone wants fat cells to stop burning fat, so it starts to offset the estradiol. In that particular effect, they're complementary in other ways. And at the same time, it starts to stimulate hunger. So a woman, it is literally a central nervous system effect of progesterone at the brain, stimulating appetite, promoting hunger, and then at the same time, at the fat cell, telling the fat cells, hey, stop breaking down fat and hold on to it, because we might get pregnant. And once we get pregnant, the whole metabolic milieu changes from one of fat burning to one of storing. And that's of course, because the woman bears the metabolic burden of reproduction, and so that's her way of just, kind of stocking, stockpiling the calories where she's committing to, you know, growing a little human, and then, in ideal circumstances, feeding that little human for up to a year afterwards. And she's got to have a lot of energy on her body, because that is a metabolic marathon. She her metabolic rate goes higher during pregnancy than at any other time in her life,
because she's just so busy growing another human and then feeding that little human anyway. That is a tremendously longer answer than I expected, but it allows us to bring in the nuance of the fat cell, and that's what we have to understand in order to appreciate the metabolic advantage that a woman has in staying metabolically healthy, being very metabolically flexible, being very insulin sensitive. But those are kind of redundant. It's because of what her sex hormones are doing at her fat cells, as opposed to what his primary sex hormones, his androgens, are doing it his fat cells. It ends up giving her the advantage. What? What makes the man bigger, faster, stronger, also makes him more susceptible to metabolic disarray, and what makes the woman more suited to to to have the primary responsibility for reproduction? Of course, it also gives her an immunity to some of that, the necessity of the reproductive metabolic burden, yeah, yeah, which then, of course, if we follow it through the woman's life and she hits menopause now where she's not secreting those normal estradiol levels, then all of those good things you just mentioned go away. And we see that pretty clearly in women's labs results, we see as their estradiol levels fall, we'll see their their metabolic markers, their insulin resistance, frequently go up. And they'll say, I haven't done anything like, why is Where's this coming from? And we'll see the the insulin resistance come up. So in fact, let me just add one final comment about the fat cell. Then is that it's, it's, it's a, it's interesting to me, as a scientist, to note that at around that same time that the woman has is ovulation has ended and she's going into menopause, that tends to be roughly around the same time that we start losing fat cells, which sounds strange, but remember, fat cells are kind of the buffer like if we can store fat and fat cells, we're metabolically healthy. It's when the fat cells start to run out of room that metabolic consequences follow, like insulin resistance throughout the life of a normal person, as we are born, going through infancy, childhood and puberty, the number of fat cells is going up. We're making more and more fat cells until the end of adolescence, so mid to late teens and girls, late teens even early 20s and boys, because boys are just later in this regard, then for the most part, the number of fat cells a person has is pretty static. For the most part. Even in women, there's little changes in fat mask, of course, going up or down, but that's mostly do the size, but women can make more, but it's generally mostly flat line until around late 50s into 60s, depending on the person now we stop during that whole 40 or so years. For every one fat cell that dies, we just replace it, and that's about a 10 year cycle. Fat cells live for about 10 years. They're not immortal, but they're long lived. And then at the end of that time period that I noted, then we don't replace our fat cells, so the number of fat cells we have starts to drop. Now, lest we think that's a good thing, remember, it's the size of the fat cell that matters most. It's not how much fat you have. And so if a person continues to eat.
Live a lifestyle that wanted their body to store that much fat in the first place as we start losing fat cells, and in the case of a woman losing the protective effect of estradiol, in particular, she really that is really a moment to be careful metabolically, because then she has the risk of really growing her remaining fat cells, and the bigger the fat cell gets, the more insulin resistance and its consequences follow. Yeah. So unfortunately, there is just this sort of snowball effect as women go through menopause and and there are ways around it. So it's not a it's not a doom and gloom, but it is worth being aware of that when people feel like, gosh, it feels like my body has changed suddenly. Yeah, yeah. It really has an everything in it has,
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Values. So you go to your doctor, they get a cholesterol panel that one's not a fancy one, that's there, but, but most doctors won't bring up the triglyceride to HDL ratio, but it's right there. If you have an LDL level, it's in there. You can look it up yourself. Totally agree. In fact, I co authored a paper suggesting that if, if Statins have any benefit. I don't mean to be overly controversial here. We have a generally a medical culture, where we just look at the LDL and then just, Oh, your LDL is high. Let's go on a statin. We reviewed the evidence, finding that if LDL was high, but the triglyceride to HDL ratio was low, then the benefit of statins was negligible to nil. Now I'm not giving medical advice, of course. Here you can look at my study anyone who's listening, but it was the triglyceride to HDL ratio that really determined any value of this very widespread medication. So those are a couple blood tests you could do if your blood pressure is high. The most common cause of high blood pressure, this is especially relevant in men, is insulin resistance. And then maybe I'll just transition quickly into one that you can actually see, which is the skin if people, people will probably quickly know what I'm talking about, around the neck, around that kind of collar, line of the neck. You can look for two different skin problems. The most common one, that's a reflection of insulin resistance, is skin tags, these little, kind of teeny, little mushrooms. You know, it's not like a rounded mound or a mole. It's like a little column, a little pillar, or a little mushroom of skin just kind of sticking right up those skin tags, very strong sign of insulin resistance. And then the second, the name of it is called acanthosis nigricans, which is just a phenomenon where the skin starts to feel kind of like tissue paper. I crinkly and it's and it gets a little darker. Now, depending on the pigment of the skin, naturally, you may not be able to see the pigment change, but it gets a little darker and it gets it gets a little kind of crinkly, like you've taken tissue paper and crinkled it up and then spread it back out once again, right along that neckline. That can also happen on the armpits and or the groin. Generally, it's wherever skin starts to kind of rub. But those are, you know, right at kind of eye, eye level observations that you can see. And be pretty confident that if you see those things, you're seeing a manifestation of insulin resistance. And then, as also, most doctors will check a hemoglobin, a 1c right is the name of it. And then a fasting glucose is also somewhat common. It's it's at least easy to access. Are those ones that you recommend looking at? Yeah, yeah, I do, although I just am quick to note that glucose is a later marker that that to really appreciate insulin resistance kind of coming back to the original definition that we outlined or started with. It's when the body needs more insulin, but in the case of glucose, it takes more insulin, but it is working well enough to keep the glucose in check. And so one of the problems with that I have with insulin resistance and metabolic markers is that we have a very glucose centric paradigm that we're always looking at the glucose, but there's evidence to suggest that the insulin can have been elevated for up to 10 or 20 years before the glucose ever changes. So glucose is a very late marker, which is why I generally don't focus on it, because you're always going to get it. But if you're waiting for glucose fasting or a 1c it's it's going to be late that that the person may have already been struggling with high insulin for up to 10 years, and then eventually the insulin starts to lose the war. Now the glucose levels are climbing, so glucose is absolutely going to be a marker, but it's going to be a delayed marker, so all the more reason to focus on the earlier signals, like insulin itself and the triglyceride to HDL ratio. Can you have a falsely negative insulin where it looks like it's normal, but actually it's not.
That's a good question. It would be very, very uncommon only because it's it's generally impossible to have insulin resistance without elevated insulin. Now, again, you could have a state where the person's insulin is so volatile that you just caught it at the lowest of the low and maybe it was in the low teens, which is what I've said before, is it can maybe be good. It's kind of like an orange light or yellow light. Is it actually problematic?
You know, rather than, like, green light is good or red light is bad, but all the more reason to then look at the triglyceride to HDL ratio, or some of these other surrogate markers. Yeah, that's helpful. I think I do the whole constellation of those, and they're a little bit all over the map. They're not, it's not super black and white. Sometimes you have one that looks good, or two that looks good and then two that don't look good. And you really are looking at the whole picture. So it's nice to know which ones to prioritize in that, in the insulin and triglycerides. So now we spend the rest of this talking about hope and what do we do about it? So what are, what are the overarching kind of pillars of lifestyle change that people need to be aware of when correcting and or avoiding insulin resistance? Yeah.
Yeah, yeah, right. It is. It is so nice to be able to kind of transition to the happy ending, because as much as it sounds like a bit of a horror story, if it is, it does at least have a nice resolution, which is that insulin resistance is not only totally preventable, but totally reversible. We published a report with a local clinician, a clinical team here, finding in 11 women was full blown type two diabetes in just 90 days. There in type two diabetes is just the insulin resistance where it's now high glucose too. There the type two diabetes was gone without a single pill popped. No days. Sorry, 90 days in 11 women, I might have said I probably got it wrong 90 days. So it was 11 women, exclusively women, and it was 90 days in 90 days with no medication. There was no amount of clinical evidence anymore of the disease. They had reversed their type two diabetes completely without, I'm assuming, without massive amounts of weight loss. Per se, they weren't, yeah, yeah. Well, only as much as you would maybe get in 90 days, you know, so kind of a modest amount. So just to answer the solution and the prevention, I'll briefly revisit the three causes. And so, of course, there are kind of non caloric, non dietary influences, like sleep. Chronic sleep deprivation can absolutely cause insulin resistance. No question, you sleep poorly. Your insulin resistance is demonstrably elevated the next day. And so that is something to be mindful of. What are your sleep habits? How's your sleep hygiene, inflammation, what is the air you breathe? And these are all they can kind of feel a little overwhelming, and that's okay, because they're also the ones that matter a little less, you know, like, what is your inflammation? Are you eating foods that is that are harming your gut and increasing gut permeability, or leaky gut? Do you have an autoimmune disease? When those things are up, you're going to have a little more insulin resistance. But again, those pale in comparison to the high insulin the main intervention is, how can we lower insulin? And that is entirely what we eat and how often we eat it. So I generally outline,
I guess, four pillars, but you can almost distill it down to two.
The first, I believe, is the most important. So I would suggest starting with it, which is control carbs that now this is not to say we can't eat them at all. I want to be very, very clear, because it seems people are just people are so eager to to kind of be offended at certain ideas these days. I'm not waging war on carbohydrates, not at all. What I am saying is that most people, 70% of all calories consumed globally are carbohydrates. So this is the thing we eat by far the most of unfortunately, particularly in the west and increasingly in the Middle East and East Asia, those carbs are coming from bags and boxes with barcodes, so they're very processed starches and sugars. That's what I mean by control. We've just got to stop getting our carbs from these processed sources. Whole fruits and vegetables. Eat them, enjoy them as much as you want. But note that that's not they're not. That's not the same. It is not the same. Eating whole fruits and vegetables is not the same as opening up a bag of chips or having a bowl of cereal or having a pint of ice cream. Now the tragedy is, of course, of all of the macro nutrients, and I'll get into the other two in just a moment, carbohydrates, proteins, fats, there's no evidence to suggest humans have cravings or addictive tendencies to proteins and fats. It's only carbs, either carbs alone or carbs with fat, but never fat alone, and never fat with protein. We don't have any like no one is sitting around on a Saturday night craving a plate of bacon and eggs. If only that happened, if only I could feel that myself. No, we want something sweet and gooey or salty and crunchy, and that means it's coming from a bag or a box with a barcode. So the first rule control carbs, especially in the evening. As a little tangent, you do not want to go to bed hyperglycemic. If you've spiked your glucose when you're going to bed, you activate what's called your sympathetic nervous system, which is your fight or flight response. And now you're lying in bed, you're hot because your body's amped up, your heart is beating harder and faster, and you're wondering, why are you so anxious? You're not anxious. You just activated your sympathetic nervous system because you went to bed hyperglycemic because you gave yourself fuel, and your body was like too much. And the body's thinking, I need to try to get rid of this. It's time to go for a run or go for a workout. No, it was actually time to go to bed. And you, boy, did you mess that timing up. So control carbs. That is rule number one. And then the other two kind of go together, which is prioritize protein, make sure you're getting high quality protein.
And generally, high quality is going to come from animal sources. And if it's plant protein, then you just have to focus on fermented plant protein, because plant proteins are generally going.
Be a little poorer quality, and I know that's also unpopular these days to talk about, but prioritize protein and then don't fear fat. Don't be afraid of fat. We have a very fat phobic culture. But if the fat is coming from fruits or animals, then we as humans are well suited to eat them. And the fruit fats or coconuts, avocados, olives, enjoy them. Be very careful with refined seed oils, or so called vegetable oils. Those are very harmful in a way that is just too much to get into right now. Just ages the body more. Yeah, it sure does. Yep. And so then the fourth rule once, though, and I do think the timing is important, those you manage your macros first, control carbs, prioritize protein. Don't fear fat. And fat and protein always come together in nature. Well, at least there's no such thing as protein alone. So when I say don't fear fat, largely, I mean don't fear the fat that comes with those proteins. That is, it's designed to come together. When humans eat protein and fat together, we digest the protein better and it's more anabolic. There are human studies to show that if a human eats protein alone, there's a certain degree of muscle growth that can happen following a workout. If a protein, if a person eats that protein with fat, it's even bigger, and so don't fear the fat that comes with the protein. Okay, once the macros are managed, that is going to bring down insulin. Very, very well, then the person can choose whether they go on to that fourth step, which is a structured of a structure of frequent fasting. Now that can mean whatever works for the person. I sometimes am reluctant to even invoke fasting because it elicits an immune response in some people, but it also it's so subject to interpretation. It can, it can, it can really play on eating disorders. And so as much as I'm an advocate of fasting, I will simply say,
as much as people focus on the length of the fast, how you end your fast matters much more than how long you fast. So if person, if a person, has a a habit of 24 hour fasting, and then they just binge on junk food, and they eat themselves sick, they feel ashamed, they feel guilt, self hatred, self loathing, and they just say, I'm going to do better tomorrow, and they do the same thing. It becomes kind of a glamorous version of bulimia, to be very blunt about it, crass, and it's so that's my point. How you end your fast matters much, much more than how long you fast. And so not everyone will find that fasting works for them. I I find it works for me. My wife hates it. She She is no longer having children, but she will say, I wish I were still breastfeeding so that I wouldn't have to feel bad about not fasting. You know, she would sort of joke about it. She hates fasting, and it's very hard for her to do. I can just shrug and do a 36 hour fast, and I barely notice it. Men and women are different. My wife is particularly for her. She's still ovulating. Her progesterone will go up at any moment. Her these hormones are higher than they are in my body. I absolutely believe that while women can certainly fast very, very well. In fact, I think some of the evidence of that is in the fact that when you look at ultra endurance events, this is the one event where women can can consistently beat men. In anything else where it's power and speed, men have the natural advantage. If a person's gone through male puberty, that's an advantage that will never go away.
But when it comes to these ultra endurance events, which is just hugely reliant on fat burning, a woman can perform better than a man and outrun him. And so a woman is built, she's built to be able to fast because she burns fat so well, and fat is such a long fuel. It's like a diesel engine. However, depending on her ovulation state, depending on her menopausal status, which is sort of plays into that fasting can be harder. So I anyway, back to the point I mentioned that fourth point of some structured, frequent fasting, with a little bit of caution and even trepidation, because I don't think it's necessary, and it doesn't really work for everyone anyway. So I really emphasize the kind of manage macros, those first three pillars, the trinity of managing your macros, matters much, much more. And then when it does come to fasting, I just encourage people to be careful, be mindful of your own past, your own eating habits and perhaps struggles. And then really focus on how you end your fast, have that be very structured, if necessary, recruit outside help and say, I'm ending my fast at 6pm
or 8am or whatever. This is what I'm planning on eating. Can you please just make sure I just do this, and then if I'm hungry 30 minutes later, this is what I'll eat after, because it just becomes too easy.
To really turn it into a binge purge cycle. It's, it's a very slippery slope. Yeah, I love that. I just want to reiterate a couple of those things. So the carbohydrates first aiming in. I think when some people hear this, they just want to cut all carbs out, and you will feel terrible, and your body will crave it, and you'll go through almost withdrawals. I like to focus on the second two that you said first, which is making sure that you're getting that adequate protein before you even think about anything else, making sure you're getting adequate fat, and then also getting adequate fiber, with eating the rainbow and getting all those phytonutrients and the vegetables in right? And then come back and switch those carbohydrates from the processed carbs into the fiber rich carbs that we find in plants and and then, really that's where people don't get the sugar cravings and don't get the energy crashes once you're fed. I think oftentimes we focus too much on don't eat not you, but oftentimes we hear a lot of don't eat this, don't eat this, don't eat this. And the point is that the body wants to be fueled. The body wants to be fed. So feed the body, fuel the body, and then cut out the extra and along that same line, I think that's the key with fasting for women, is understanding it's just as much about how you're fueling compared to how you're fasting. You know, you can't fast if you haven't fueled, if you're in a chronic calorie restriction, then you don't get to fast. That's That's just not how it goes. You have to be fueled. You have to be in a state of safety. You can't be running, you know, a marathon, and running a million miles a week and then go fast. You have to understand the right timing and context to bring that additional strain on the body. And it can be really productive, but, but you should, you should think about and understand the nuance with it, and then it can be really, really beneficial. So I love all of those. Yeah, I think it's so important. You have such a perspective that I can't have for multiple reasons, most especially the clinical work, in addition to the personal living here, of course. But yeah, I one of the reasons I focus on that so, so cautiously that fourth step is because women are just so much more inclined to just go too far with it and to take a little bit of a good thing in this one regard. You know, men just, yeah, I'm gonna fast, but I also I know when I'm done, and I don't really want to do it, you know, I don't want to get too thin. I want to keep my muscle
and so yeah, a guy will generally be a little more capable of regulating himself in that regard,
unfortunately. So I do, yeah, I think this is a proper amount of caution. And just understanding the fasting component, while it can be revolutionary in someone's health, it's just such a fine line as well. Yeah, let me just go through a couple kind of rapid fire questions, because I think there are some some things that just come up all the time. And so the first one is diet soda. There's questions about like it doesn't spike insulin, but it's still not good for you with regards to insulin resistance. And we'll keep this just brief, but yay or nay on that big deal? Yeah, yeah. Well, I think it's a small deal. Now, I know people feel very strongly about diet soda and aspartame in particular, I do not I think any evidence of it being like a cancer concern. I personally, as a scientist, believe that is not justified from the evidence that you give that much of anything to these animals that they're all going to get cancer no matter what you're giving them, because it's, you know, such high doses when it comes to an insulin response, aspartame won't have any effect. And frankly, the vast majority of sweeteners don't either. And that's the same approach I take. Is leave it on there, like, if that's what you're drinking, leave it there. Do everything else first, and then, you know, there are other health reasons, but, but it's not a big role in in this this, we'll try to answer it quickly. How much of how much does genetics play a role here? Are there people who just will not be able to do this with medication? Or is it more epigenetics? Is it more the lifestyle than the genes? Yeah, it's definitely more lifestyle than gene, which is both good news and bad, good because it does mean you can do something about it, but bad because it means you have to do something about it if you want change. But there's no question that while, while there is no clear gene culprit to say, Oh, you're more insulin resistant than you that's never been done, there is no question that there is a familial pattern, that if you come from a family where mom or dad had type two diabetes, you absolutely are more insulin resistant, even right now, than your friend who does not have a parent with type two diabetes. So if you have, if you're if you have a first degree relative with type two or gestational diabetes, which is just type two diabetes of pregnancy, basically, then you absolutely are further on that spectrum of insulin resistance than someone else. But again, the good news is you can do something about it, and if anything, I would just hope that that could be a little extra motivation, but it will mean you've got to be a little more diligent. Yeah. Yeah.
Yeah, are you a fan of the five small meals or the two to three regular meals? I hear this a lot, like, make sure you're eating every two hours. I'm not a fan, but I'm not either. No, I think that's a way. I think that actually has is a large degree combined the frequent eating combined with our constant carb consumption is largely what's yep, that's brought us to where we are. The human body is not meant to eat every two hours. We have to have periods of fasting, even if it's just a few hours. And so I am much, much, much bigger advocate of letting your insulin come down. And it to me, I say fasted. And we just got done talking about fasting to to to me an endocrine slash biomedical slash metabolism scientist, I look at fasting as a state of insulin being high or low. If insulin is high, you are in a Fed state. If insulin is low, you are in a fasted state. Even if it's in the middle of the day and it's been four hours since you ate. If you have to have periods of time or insulin comes down, that is the key to healthy metabolism. Metabolism is a term that encompasses both the building up or anabolism and the breaking down or catabolism. Healthy metabolism is a balance of those processes, building up, which insulin wants to do all the time and breaking down, which we can only do When insulin comes down. So I'm much more an advocate of condensing consumption. Yeah, eat a meal and eat a good meal, and then that's right, be done, and then you won't be hungry and you won't have that energy crash. Yep, last couple questions here, CGMS, continuous glucose monitors that we see with the little white circle on the back of people's arms. People are doing it more for biohacking. Big difference. Small difference. Big fan, not a big fan for a non diabetic, yeah, yeah. I am a big fan. I because I have seen so many people who are able to make substantial lifestyle changes on their own without having me or you telling them what to do. They're able to look at their phone and see and and see, oh, my, look at what happened when I ate this or I never sleep very well. And how interesting that now I see my I spike my glucose up to 200 every night when I go to bed because I snack on these things. So the value of the CGM is, I think it gives people a very objective insight into what they're actually doing. Because, as my wonderful father once taught me, humans are great self deceivers. We we trick ourselves into all kinds of of deceit, thinking in in cases of eating that we're doing better than we really are, the CGM sort of wipes out the potential for self deceit. And so in that sense, I think it's tremendously useful. We've we talk about insulin actually being the better marker. Do you think we'll get to a continuous insulin marker? Oh my, oh, Mallory, you have no idea how big that question is. That is like the $1 billion question. So I will say being somewhat connected to that industry, the there are multiple additional analytes that are coming out with continuous monitoring there will there are already continuous ketone monitors that you can get. There are going to be continuous lactate monitors coming out soon too, which I am interested in, the continuous hormone monitors, I'd say that's at least a decade away. Yeah, yeah, yeah. We didn't do justice to the movement side of all of this. Will you just give a real quick like, how should we just be moving in general? Yeah, yeah. Well, you'll pardon me for the answer, right? Saying this, yeah, yeah. I'm often asked, What's the best exercise to improve insulin resistance? It's the one you'll do. Yeah? So it really is important you are just moving. When we move the muscles they they're able to pull in glucose without insulin needing to tell them what to do. And indeed, high insulin is antithetical to exercise. Exercise is I'm breaking down. I want to be catabolic right now, and so insulin has to come down to enable that to happen. And the more you're able to bring your insulin down, the more the body can resensitize to insulin. So I am a huge advocate. But for for this audience of with mostly women, let me just make a plug. Please, please, please, do something that's helping you retain and build muscle, as much as it is the sort of the female default just going to walk or a jog, that's good. It's better than nothing, but spend some time trying to build up your muscle because muscle mass is one of the great predictors of longevity and just optimal metabolic health. Yeah, I 100% agree. I heard a conversation recently between some women, and they were they were discussing sort of the health advice that we hear about, you must do this, and you must do this. And they kind of ended with, like, it's just too much, it's just too much, like, I hear you, I hear it's important. It's just too hard. I'm just not going to do that. I'm not going to do that with my kids. What is your sort of plea or advice to I mean, a lot of these women are very, very busy and busy moms or busy grandmas and have these busy.
Lives. And yet, I think it's a misstep for us to dismiss this health information because it's just too much. What? But I sympathize too, because it is too much. It is hard. What is your Do you have any thoughts on that? Yeah,
right. It can be overwhelming. Absolutely. If I could, I would just say, pick a bookend of the day, pick either your breakfast or your evening and fix it. Just start with just one of those. At the simplest I would I used to always say, just start with your breakfast. But more and more, I actually think it's probably more prudent if you can control your evening snacking. That is the hardest time, at least for me. Maybe it's a little too much confession in Old College habits where you would eat three bowls of cereal and just sort of shrug it off. I like, I'm a cereal addict. I cannot moderate I can't it is this like descent into metabolic mayhem if I try to convince myself, Oh, I'm just going to have a little bit. I'll just have a half a bowl. No, I can't. I cannot. It is easier for me to never even pour a single piece of cereal in the bowl than to stop at a half of one bowl. If I start, I don't stop until I'm sick, like a true addict. And so maybe I'm a little revealing, a little too much here, but I'd say pick one part of the day, either breakfast to fix that will be easier, because most people really aren't too hungry at breakfast. And so if that's the easier one, then start with that one, but, but, or maybe even a little harder, start with your evening and just wipe out evening snacking. I guarantee you'll sleep better, and maybe that will lend itself to just having a better day the next day where you feel like you also have a little more control. So just pick one of those times of the day to fix. Start with that one. I love that. That's the same advice I give. And just saying it again, the more fueled you are, the better fed you are, the easier that's going to be if you're starving, it's going to be really hard not to go eat that thing that sounds amazing to you. So fuel yourself when at the best time that you can get the food in and then go from there. Okay. Last question here is, is there any final kind of wrap up that you would want to give to the women listening about insulin resistance, metabolic health? Just sort of a summary, kind of just a final thought, yeah, yeah. I would, I would just say, kind of be, take, if you're anything anyone listening, sort of like my wife or my sisters, one of men's superpowers is we're not as hard on ourselves,
that we're sort of okay with our foibles and and so I would perhaps just stay at the risk of sounding kind of cheesy, you know, like be be kind with yourself, and be kind even with your with your fat mass. That I'm amazed at the way, how self critical my wife is, and I'm looking at her thinking, you know, bring that body over here, sweetheart, you know. So
I don't know that sounds kind of silly now that I'm singing out loud, but I would just try to, you know, accept the reality that the WIMP the female body is is literally designed to have to have a have more fat on it, and that is for a beautiful reason. It is literally for the good of the species. It is, it is entirely for reproduction. You have to have more fat to maintain your health, to maintain your bone mass, as much as we look at leptin as only a satiety hormone, that is not at all true. And leptin comes from fat tissue for normal fertility and sexual function, you got to have high leptin for normal bone mass. You got to have high leptin for good mitochondrial health. You got to have high leptin. Leptin comes from fat. Women need more fat than men. So maybe I would just say, as much as we paint the picture of, you know, helping control fat mass, which is necessary also, you know, maybe try to be a little more forgiving of what you've got, because I guarantee your male counterpart isn't upset about it, for what that may be worth, that's terrible to say. No. Thank you so much. Your perspective is really helpful, and you've taught us so much. I think it's been a really nice overview, and with a lot of detail about insulin resistance. And I hope women do feel empowered, and kind of both feel the nudge. You know, there is some amount of urgency. We can't We can't dismiss it, and we can't really make light of it, because it's too consequential. But it's doable. It's very, very doable. So it sure is, yeah, and so just bring it down to the smallest size, start with those kind of manage macros and pick one part of the day to do it. Yeah, awesome. Well, thank you so much for being here My pleasure. Thank you so much for tuning in to today's episode. A huge thank you to our guests for sharing their insights and time with us. We are grateful for the incredible support from our sponsors and to all of you listening. We couldn't do this without you. If you enjoyed this episode, please consider subscribing on your favorite platform. You can find us on our website, uplift for her.com, YouTube, Apple podcast, Spotify, or wherever you love to listen. And if you found value here today, please share this episode with someone who would benefit from it. Leave us a comment or.
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