HOW TO REVERSE INSULIN RESISTANCE | WHY WE GET SICK WITH DR. BENJAMIN BIKMAN

Now, the average individual listening to us right now may say, well, I don't eat soybean oil. Yes, you do. If you're eating the bulk of your calories from foods that come from bags and boxes with barcodes, it is exceedingly likely that you're like the average American where you're getting most of your fats from these refined seed oils. Most. The average American gets more of their fat calories from soybean oil and shortening than literally any other fat in their diet. And these are rich with these omega 6 fats. And among the many, many things omega 6 fats do, they can drive insulin resistance at the level of the fat cells first, and then other tissues start to follow.

Human metabolism and its role in chronic disease. In addition to his research and teaching, Dr. Beckman actively serves as a research mentor to undergrad and graduate students. He and his students frequently publish their findings in national publications, and he lives with his wife and three kids in Utah. I have to be honest with you. Chronic dieting will not work for sustainable weight loss. The only way to lose weight, keep it off, and prevent disease, which, hello, that's what I'm all about, is to live a low insulin lifestyle. I know that might sound strange to you, but it's true. When how will this affect my insulin becomes your new litmus test. Instead of how many points or calories does this have? Weight loss clicks into gear. It becomes so much easier. I know for most people it's a paradigm shift. You've been fed bad nutritional advice then that advice has been reinforced by government recommendations and billions of dollars in marketing by big food companies. This misinformation is not your fault, but your health is your responsibility. And when you accept full responsibility for your health, you can expect get results. That's why I'm so proud you're here with me today. This is a huge win because you're about to learn life changing information. So give yourself a little round of applause for being here, for showing up and for learning. I'm honored that you're spending your time with me today. Knowledge is power, and Dr. Beckman is about to impart decades of wisdom in one short interview. You're going to learn what insulin is, what causes insulin resistance, how to know you have it, and how to reverse it. We also touch on major diet myths and mistakes that everyone deserves to know. I know that you're going to walk away with simple, actionable steps to start lowering your insulin. And when you do, the weight will come off, your blood pressure will go down, and Your blood work will improve. I know because that's exactly what I teach in my program, Weight Loss for Health. And I hear stories like this all the time from my members. I know that these kinds of results are possible for you. With the right information and the right strategy, I am confident that you can reach your weight loss and wellness goals. Let's go ahead and dive into this interview. Hey, Dr. Morgan. Here. If this is your first episode, you may not have heard about the brand new quiz I created called the weight loss plateau quiz. If you've been struggling to lose weight, this 60 second quiz is what you need. Did you know that there are different types of weight loss plateaus? It's true. If you want faster, more effective weight loss, you'll need to identify what's holding you back from losing weight, why you hit a plateau. That way you can create a targeted strategy that actually works. I created this quiz to help you get to the root cause of your weight struggles. Whether you're not seeing weight loss or you lost and then regained, this quiz is for you. No matter how old you are or stage in life, no matter if you've been diagnosed with disease or just have a little bit of weight to lose, I'm confident that your success is inevitable. You can lose weight, but you've got to believe in yourself and you've got to take action. If you haven't already, go take this quiz today right now@weightlossforhealth.com quiz that's weightlossforhealth.com quiz. All right, let's get started with today's interview.

Dr. Bickman, thank you so much for joining us today on the Reshape your health podcast. We are so blessed by your presence and I know this is going to be a great interview.

My pleasure. Please call me Ben. This will be great.

Oh, good. I want to start with your personal story. I think that I've done a lot of research into you, but I think listeners haven't. You know, you might be new to them. So can you tell us about your personal story with health and weight loss and wellness and just what drove you to do so much research on the field of insulin resistance?

Yes, it was something I never would have imagined studying as a young undergraduate. I didn't even know what insulin resistance was, which isn't surprising. A lot of people don't even now. My evolution to become the scientist that I am now did start from a long held interest in the body. I was just raised in a generally healthy home, my dad especially, who largely raised us Alone. After my mom passed away, when we were quite young, he was just always focused on making sure we got our vitamins and that we had a good hearty breakfast. It was never cold cereal. So generally just raised in a home that prized health and that interest just sort of grew. When I was an undergraduate, I just wondered what do I really want to spend the rest of my life doing. And I was in a class as an undergraduate and I was taking a class physiology class from a professor who was an actual scientist as well. He had an NIH funded lab here at the university where I'm back now at byu. And I was just amazed that there were still scientists studying the body. I'm embarrassed to admit this, but I as a 21 year old at the time, I started a little late after high school I served a two year mission for my church. So I was a little late starting my undergraduate in the first place. But I was amazed that there were still scientists studying the body. I just assumed, we're done, we know everything, there is no more science, there's no more questions to ask. But that, that planted such a seed of interest in my mind and I really appreciated the work life balance that he seemed to have, that this was a guy who had freedom of his schedule and freedom of thinking, which of course is something that is so precious in academia and may it always be that way. And that planted the seed. And then I stuck here at BYU to get my master's degree in exercise physiology in part because I knew I wanted to continue in academia, but I didn't know what to do yet. And I was close enough to finishing my undergraduate that I just sort of needed an immediate step. And so getting a master's degree, I'm not too proud to admit that was really just a way to hold off a bit more before I committed to a PhD because I just didn't know enough yet. But it was towards the end of my PhD. Sorry, towards the end of my master's degree, which was an exercise physiology. So it had me studying the muscle and cardiovascular fitness. That was the focus of my thesis. But I stumbled across a paper that had been published a few years prior to that. So this to me was in the early 2000s. The paper had been published in the late 90s which detailed how fat cells produce and release pro inflammatory proteins or hormones. And that was such a fascinating discovery in my young mind at the time because it showed to me that fat cells are far more involved in the body than just storing fat and that they may be the connection between obesity and diabetes. And that was something I've been hearing a lot about this confluence of these twin epidemics. Diabesity had been coined kind of a term in the early 2000s. So a lot of people were talking about it. And the idea that the fat cell could be releasing these pro inflammatory proteins and that then is what's driving the type 2 diabetes. It blew my mind. And of course, what was inserted in that paradigm, the fat cell is producing more inflammatory proteins that then would result in something called insulin resistance. And that was the foundation of the type 2 diabetes. So that was the beginning of my interest in insulin resistance. And it represented a total shift that I've never really turned back from, which was my interest pivoted away from muscle cells. Not that we haven't studied muscle cells in my lab, we have as my. With my own lab. But I am much more interested in fat cells now. And that was the subject of my dissertation and my PhD and the focus during my postdoctoral studies. And now with my own Lab these past 10 years, it has been to continue to dive into insulin resistance. And then one last comment on that, because I'd be remiss not to state it. Once I received my teaching assignment as a professor and I was given the assignment to teach a class called pathophysiology. That's the sick body. That's when the body systems aren't working well. I was just amazed at how frequently insulin resistance was relevant to one of these pathophysiological conditions where I'd be teaching the students a lecture about fatty liver or liver disorders and fatty liver disorders. Fatty liver is the most common liver disorder. And wouldn't you know it, insulin resistance is the most. Is the implicated most common cause. And the same thing would go with Alzheimer's disease and heart disease and infertility and hypertension, all of these chronic diseases that we're afraid of. Insulin resistance to some degree was causing this problem. And that was very wonderful for me as a professor because it let me bring up a topic that I'm an expert in from time to time. But it also changed the way I looked at the research that I was doing. I saw a value in what we were studying that I didn't quite see before. I saw a scope that I couldn't ever imagine. I thought that me studying insulin resistance was only relevant to type 2 diabetes. And then it was this wonderful realization that actually it's relevant to virtually every chronic disease or what I like to refer to as the plagues of prosperity. And so that's My long winded answer, How I got to being a naive but interested undergraduate, to being totally committed professionally to understanding what is the most common disorder and one of the least known.

Absolutely. And you wrote an amazing book. I always say it's the book that I wish I could write. Meaning I wish I had the expertise and writing skills and everything that goes into writing a book. Why We Get Sick. It's an amazing book. I highly encourage every single person who hears or watches this interview to go read it. I read it. Pretending that you were on a pedestal, especially for the first half. And you're like, insulin resistance does this and it does this and it affects diabetes and heart disease. That's right. That's kind of how I read the book. I loved it. I soaked it in. I shared it with my members of weight loss for health. And I really want to know what drove you to take on that huge undertaking, which it was. This is a very dense topic and you made it very understandable.

You know what, Morgan? Thank you. That's all very nice of you to say. Let me dispel some of the myth. It was easier than I thought. And it's not because someone would say, oh, well, it's just because, Ben, you're such a gifted writer and I'm a decent writer. But I had just. I had been kind of synthesizing this idea for so long that once the time came for me to actually spit it out onto paper, it just gushed out. But nevertheless, my university here, every summer they do something called Education Week. And it's basically one week where the campus. There's no students. It's kind of in this break at the end of fall semester and before. Sorry, at the end of summer semester and before fall semester has started. So the campus is empty for a couple weeks. And so the university kind of took advantage of that time to create this Education Week. And this is something for just anyone, not students, anyone from the community can come sign up for a series of classes on all kinds of topics, all kinds of topics. And this would be taught by professors generally teaching their areas of expertise, but of course, very much to the. To the level of the public audience. And I had thought this was probably about five years ago. I thought this, what a fun challenge this would be for me to take everything that I kind of sprinkle over an entire semester, four hours a week, a four credit class, and then condensed it to one week, you know, five hours, one hour a day. What a fun challenge that would be. And so one spring, I submitted this application or this idea. And the university loved it. And they said, yep, do it, please. You got the green light. Send us your kind of teaching plan. And so I did it. And at the end of this week, it was absolutely mind blowing to me. They had me in a pretty good sized room, and I think the room could fit about 200. By the end of the week, they had moved me into a room that could fit 500 and there was standing room only. By the time I got to that Friday class, I was just amazed that people would be as interested in this as I was. And at the end of this week, dozens of people came up and just asked, where can I get your book? And I thought, I really ought to write a book. And that was the moment that class ended, that first year, five years ago. I immediately started writing the book. But oh my heavens, though, Morgan, let me now explain what is difficult. I'd written the book in about eight months. From beginning to end, I wrote the whole book. And I was so naive. I thought that just like when I published some of my scientific manuscripts, I thought I could put together a manuscript and then submit it to. You know, when we publish a manuscript in the science realm, we write a manuscript, we submit it to a journal, the journal gets reviewers and they review it and they tell you whether it's acceptable or not or whether you need to make some edits. I just thought it'd be the same thing with a book. I just need to contact a publisher, say, hey, I've written a book. Do you want to publish my book? No, you have to get an agent. And it took me eight to 10 months to find an agent. And then even after I had my agent working with her, it took us another almost year to find a publisher who wanted to publish the book. It was such a hassle. So writing the book was a piece of cake. It was actually trying to get the whole process of getting the book published. And during this time I was tempted, I confess, to just self publish, because you can do that these days. But I am so glad I didn't. Anyone who's tempted to do that, I'm so glad I didn't, because working with the publisher made this book so much better. Just having an outside set of eyes tell me what was good, what was not, what needed to be expanded, what might not be the best fit for the book at the time. It became such a superior product. Nevertheless, I've gone a little off topic. The book was born from my seeing how interested people were in this topic and how generally unfamiliar they were with it. And I just needed to get this on paper and kind of leave my mark that if there was one thing I would want someone to know that represented the sum of everything I know and what I care about it is that we don't know of everything I know. And what I care about it is that we don't know. The public, the average person does not know enough about this thing called insulin resistance, and that is making them fat and sick.

Well, and then in the introduction for your book, which was written by Dr. Jason Fung, and I talk about his work a lot, the obesity code, the diabetes code, the cancer code. I was. I thought, how did he get Dr. Fung to write an intro for his book? But that's probably another conversation. Anyways, he said up to 85% of American adults have insulin resistance and most of them have never even heard of it. And I'll be honest, throughout my physical therapy education and even my geriatric residency, I don't think I ever heard the term insulin resistance. It wasn't until after that, when I had seen so many people suffer from amputations and neuropathy and cognitive impairment from diabetes, I thought, how can we prevent this? And that got me down the research rabbit hole, landed on insulin resistance. And like you, I thought, how do we not know this? How is this not mainstream knowledge? And it kind of became my mission then to help people learn how, what it is, how to lower it so that they can lose weight, keep it off and prevent disease. How on earth are we here where 85% of adults have it and don't know it?

How are we here? What a wonderful question. It is a very, very sobering statistic. And lest anyone think this is a particularly American problem, that is far, far from the truth. I have done. I did my postdoctoral work in Southeast Asia, in Singapore. There is massive insulin resistance statistics in Southeast Asia. I have given talks in the Middle east. And there is an incredible burden of insulin resistance in the Middle east, even worse per capita than we have here in the US Mexico is as bad or worse than the US is. So this is not a problem that is unique to the United States. This is a global problem. And how we got here in part is because we did what we were told. That seems a little maybe mean to say, but I think the. The dogmatic view of nutrition has in part led us to where we are, where we have been told with the best of intentions perhaps, that we need to avoid fat and we need to focus on carbohydrates. And now More and more these days, we need to avoid animal proteins, which I know is something that we'll get to later, and it's something you're passionate about. We basically started eating a diet that was protein deficient. And in our efforts to avoid, well, in our efforts to avoid fat, it became protein deficient. Now, protein's been vilified for other reasons nowadays, but it led to us eating more and more fake foods because real food has fat in it and of course, protein. And so our avoiding. We were told to eat a high carbohydrate diet and avoid natural fats, which is what saturated fats are, and to eat several little meals per day. Basically, we were given a prescription when it came to our diet that would result in the average individual having elevated insulin levels every waking moment of the day. Because we wake up in the morning, we've been told that we ought to eat this big, hearty whole grain cereal or bagels or bread or whatever, and orange juice. Our insulin, our glucose is going to spike dramatically. The insulin is going to stay elevated for perhaps in the average person, it could stay elevated for two to three hours easily, easily above average, above what it was before the meal. And then right around then, they'll think, well, now it's time for my mid morning snack. And so they bump it up again. And so every time throughout the day, before insulin ever has a chance to come back down to normal, we've bumped it back up. And that is one of the key drivers, insulin resistance. There are other inputs involved, no doubt, but one of the key causes of insulin resistance is chronically elevated insulin. In fact, you cannot have the insulin resistance without the chronically elevated insulin. They must be viewed together hand in hand. They go hand in hand.

Yeah, I'd really like to. Before we dig too deep into it, I think that we need to take a step back and realize most people listening and watching have no clue what insulin resistance is. Can you please start from the starting line and explain what insulin resistance is and what are the signs of insulin resistance?

Yeah, yeah, excellent. I'm very glad to start there. So insulin resistance is a coin, and it has two sides. On one side of the coin, it is that insulin isn't working as well at some cells, at some tissues in the body as it used to. Now, that is very, very important for me to make clear because you have to understand that some of the body's cells are responding to insulin as well as they ever have. And that becomes very relevant when we talk about the other side of the coin. In A moment. But some of the cells, like muscle cells, for example, aren't responding in fat cells, which constitute a fairly significant part of who we are, our muscle cells, especially in our fat cells, depending on how fat we are. So these cells aren't responding to insulin as well as they were before. So insulin isn't working as well as it was before at all cells of the body. That's one part. That's the insulin resistant part. Some cells are resistant to insulin. The other side of the coin is the one I just mentioned, which is chronically elevated insulin or a condition called hyperinsulinemia. And again, that matters because some cells have a perfect responsiveness to insulin. They're still totally insulin sensitive. Now, however, this chronically elevated insulin level is overstimulating these cells. It's making these insulin sensitive cells do too much. And we have to appreciate both sides of this coin that we call insulin resistance in order to understand how insulin resistance is so involved in the origins of so many chronic diseases. Because while it may be the insulin resistance part that is making someone's blood sugar levels rise and becoming more and more diabetic, it's the hyperinsulinemia part that is making someone have hypertension and making the woman have polycystic ovary syndrome. So there are different pathologies or different disorders that are going to be a result of one or the other or.

Both side of the insulin resistance coin, right?

That's right.

Okay. And then for those who aren't familiar, can you just explain what insulin is and what it does?

Right, Yeah, I should have even so one step further back. I should have started there. Yeah. So insulin is the hormone from the pancreas that we all have flowing through our blood, unless we are a type 1 diabetic. Then you have to inject the insulin because you have to have insulin. Insulin is a hormone of life. You must have it. You cannot survive without it. So insulin is. Does all kinds of things. Literally every cell in the body will respond to insulin literally. And I know the kids these days use that term not literally. I do mean it literally. Every single cell in the body has insulin receptors. So every cell will respond to insulin. And because every cell does different things, insulin tells different cells to do different things. The most common effect of insulin, or how it's most commonly viewed, is because is by through the lens of what it does to glucose. So when someone eats a starchy, sugary meal, of course blood glucose levels will spike. That is unhealthy, in fact, even lethal if it stays high for too long. Insulin comes in to save the day, where in the pancreas will sense this elevated glucose, it will release insulin and start making more insulin. And that will open the doors to allow the glucose to move from the blood into some of the body's cells, like muscle and fat cells, for example. And that would then lower the glucose levels. And insulin, having done that particular job, will also come down. But again, insulin does something to every cell, even those cells where insulin isn't necessarily stimulating glucose uptake, it's still telling the cell to do something. And so if I had to define insulin in a whole body term or a thematic effect of insulin, I would say insulin tells the cells of the body, every single cell of the body, what to do with energy. So it tells the cells whether to grow or to shrink. It tells them what to do with the nutrients that they have. And the theme of it all is to store energy. Insulin wants the body to store energy. It abhors wasting energy. It wants to dampen metabolic rate. It wants to prevent any breakdown of fat, for example. It just wants the body to store stuff.

Okay, I think that's a really good starting point. And building on that, you know, with both of us really passionate about preventing chronic disease, getting the word out there, let's talk about heart disease. February, we had it a couple months ago. It's National Heart Month. I had some posts about how to prevent heart disease and one of them was an interview with Dr. Nadir Ali. And he talked about why LDL goes up on a low carb lifestyle. And I really like how you explained this in the book. For people who are concerned about heart disease, sometimes their doctor might recommend to lower their LDL and they, they blank. They put a blanket statement on it that it's bad. And I thought you did a good job explaining LDL and how we can determine, you know, a better way to determine your risk of heart disease in the book. So can you elaborate on that?

Yeah, yeah. So I would say any. Definitely. If anything I say is incongruent with what Nadir Ali says, defer to him. He is the expert and I'm not a lipidologist. But the little bit that I do know is this, that LDL is not the villain that we believe we've believed it to be. And that very much plays into us erroneously vilifying saturated fats. The whole reason we're afraid of saturated fats is because it can impact, it can increase LDL in some people. But when I talk to someone who has a high LDL and they're very worried because in part their physician has made them worried. They've told them they need to be worried. I will very quickly ask did you get a pattern or an LDL diameter test to know whether you had pattern A or pattern B? And basically, and if you guys already, if you already had nadir on, then this has been stated before. So I'll do a brief version of it. But if LDL matters at all, and that is a big if, there is no causal evidence in humans to confirm that it does, there's just correlational evidence. But let's say LDL does contribute to plaque formation in blood vessels. What seems clear is that the type of LDL matters or the size of the LDL matters. And we define that based on the diameter and we put it into a spectrum or a pattern. Are you pattern A which means your LDL lipoproteins are big and fluffier, or is it pattern B which is when the LDL is actually tighter and more dense. The pattern B is more associated with atherosclerosis, whereas pattern A appears not to be. And again, this is all correlational, but the idea is perhaps that the more dense and tightly packed the lipoprotein is, the more likely it is to bump into blood vessels and then potentially even invade those blood vessel walls, thus perhaps making it more prone to develop an atherosclerotic plaque. And again, that's all the theory, that's all the theory of it. However, this. So that's one, one nuance that I think someone could take away from ldl which would be, well, what is your pattern? If you have a higher ldl, but it's this pattern A or the bigger, fluffier kind, then it appears that you have very little to worry about. If anything, what's interesting about LDL is just how often we fail to appreciate its healthy aspect where we need. And I'll come back a little more to atherosclerosis and blood lipids. But LDL is absolutely fundamental to human immunity. And this could be why individuals with the lowest LDL levels are significantly more likely to die, especially from infections and blood based cancers. Their risk of dying from infections and like leukemia cancers, I think it's 15 times higher if someone has very low LDL than if they have high ldl. So when I'm talking to someone who has high ldl, I often will say, congratulations, you're probably going to live longer. Because there are studies that the Shanghai, what was that study? There's the Baltimore Longitudinal Study, the Honolulu Heart Study, The Shanghai Aging Study or something like that. One of the themes of these very different areas of research is that the people with the highest cholesterol, including ldl, tend to live longer. So I say if you have high ldl, then look at your other lipids, particularly your triglyceride to HDL ratio, because that is a much better predictor of heart disease. If you have lower, relatively lower triglycerides and relatively higher HDL cholesterol, and that results in a triglyceride to HDL ratio that's somewhere below 1.5, then I would say that is when I especially say, congratulations, you're probably going to live longer than average. But then to sum it all up, I just strongly encourage people to pay the 60 or 65 bucks, depending on where they live, go to a radiology clinic and get a coronary artery calcium scan, a CAC scan, because that's something that can actually tell you the degree to which you have plaque in your heart vessels. And this is what all these blood lipids, ldl, triglycerides, hdl, they're only surrogates of what the CAC scan can actually tell you. So if someone has high ldl, but they have a zero CAC score, then they have nothing to worry about.

Yeah. That's what Dr. Ali really said was the gold standard as well. So I'm happy to hear you confirm that. I want to talk about people listening to this. Between 8 and 9 out of 10 of people listening or watching have insulin resistance. They probably have never received a fasting insulin test. Like they have maybe fasting glucose test. I want to talk about. How does somebody know if they are insulin resistance? Insulin resistant. Let's start with the blood test and then go on to some signs and symptoms that they can use if they don't want to get their blood tested.

Yeah, yeah. In fact, you'd mentioned signs earlier and I failed to get around to it. So this is good time.

Okay.

Yeah, yeah. So if someone can get their blood test, I would say there's two nice things you could do. Well, one, actually, three. One is the triglyceride to HDL ratio that I just mentioned. If that ratio is below 1.5, that is a very good sign that you're insulin sensitive. If it's above 1.5, that's a good sign that you're insulin resistant to a fasting insulin. If you can get a fasting insulin measurement and it's at 6 micro units per mil or less. Now that is the gospel according to Ben. There is no unfortunately, we have so chronically overlooked insulin as a clinical value that there are no clear cutoffs. And I would say I wouldn't trust them anyway because the average American is insulin resistant and they're going to have higher than normal levels of insulin anyway. So my views, and I base this on evidence, is that six micro units is a good cutoff. If you have a fasting insulin of 6 or less, that's a very good sign that you're doing great. Maybe I could even almost be a little more liberal and say that if it's under 10, that's good just to kind of make a nice clean cutoff. If your insulin is up into the teens, that is, that's a warning sign. If it's, you know, say below 15, between 10 to 15, if it's above 15 ish, I would say that's a bad sign and you probably are insulin resistant. I allow that academically, I allow that kind of wiggle room in the low teens just because like every hormone, insulin has an ebb and a flow. And it's very possible that someone goes in and gets their fasting insulin measured, but they happen to catch it at a peak, at a flow rather than an ebb. And all the more reason then to look at the triglyceride to HDL ratio. So I'm always quick to bring that one up after the fasting insulin because while the fasting insulin can change and that is a problem, the triglyceride to HDL ratio isn't going to go in that same kind of dynamic pattern as quickly. And then lastly, and this would be considered a gold standard, if anything is that's available to the individual, if someone can do an oral glucose tolerance test and then get their insulin measured at every 30 minutes, that might be a bit extreme, so I'll do a simpler version of it. But if someone can do 0 minutes 30, 60, 90, 120, and at the simplest way of interpreting this, if they have a peak at 30 minutes and then every subsequent time point is lower than the 30 minute time point, that's a very, very good sign. And then lastly, with that same kind of challenged pattern of insulin or an oral glucose tolerance test, you want to make sure that at that two hour time point, if your insulin is below 30, that's a good sign that you're insulin sensitive. If at 2 hours your insulin is above 30. So even if someone just measured insulin at time point zero and time point two hours and didn't wasn't able to do all those intermediate time points to get the whole pattern. If your insulin started, you know, at a good number issue, say, below 10 to make it a little generous, and it was below 30 at two hours, that's. That's a good sign.

And you said a glucose tolerance test. Can you explain what that is?

Yeah. Right. So that is something that a lot of people can get done at a clinic where you go in and you just drink a little solution of pure glucose, 75 grams, and then you sort of feel a little sick, and you, you know, you go in and get your blood drawn. So any gal whose. Most gals who've been pregnant have had this done.

Yeah, I refused it. Yeah. I have a.

Well, my wife failed it.

I failed it with my son, Dawson.

I'm not surprised. Part of my problem with this, and I teach this to my students, who are all future nurses and doctors, I say, you can't assume, if someone fails that it could be a false positive, so to speak. Where we have standardized this, we have every single woman drink the exact same amount of glucose. And if you have a petite, thin gal, like, say, my wife is, and compare her response to a woman who's 6 foot 2 and weighs 100 more pounds than my wife does, you know, my wife's going to get a false positive because she's so petite. That's a significant amount of glucose for her little body to metabolize. This other gal, who's a big, husky woman, she can metabolize it much more rapidly. And even though she might actually have a problem, she's just so much bigger that that amount of glucose is nothing to her bigger body. So she may get a false negative. So I don't think that test is used very wisely, frankly. I think if we're going to use it, we need to have a way of basing it on body weight to some degree.

I think that makes sense. I refused it with my daughter.

She'll be one in May.

Just because I didn't want to put that much sugar into my body. I knew other signs of, you know, of issues which we can talk about next. And I thought, I am not. I'm not going to have gestational diabetes. I'm not going to expose my body to that. And I. And I really tell people, advocate for what you want. You know, doctors give recommendations, and you can give recommendations, too. So can you talk about other signs of insulin resistance besides blood work?

Yep. That's great. Yeah. So. So the blood work is, of course, the most obvious way to find this out, but people would be surprised at Just how obvious some of the non blood work signs may be in indicating insulin resistance. At its simplest, I think if someone is a little overweight, that's a little subjective, of course, but I'll leave it there. If they're a little overweight and they have high blood pressure, I could almost say we're done. Because it is so unlikely that someone's going to have hypertension and it not be caused by insulin resistance. Or I'll say that another way. Insulin resistance is almost always the cause of hypertension. Now people can have. That's why I emphasize the overweight. I know in myself. I will check my blood pressure here in my office. I have a little automatic cuff just from time to time. And I noticed that for me, if I have a bad night of sleep, my blood pressure is absolutely higher, even significantly higher than when I sleep well. And so I have to qualify this. If someone consistently has high blood pressure, you could say, well, they're just consistently bad sleepers. But if we combine that with the fact that they're overweight, then I would say we've gone beyond bad sleep. That is very, very likely confirmation or indication that the person has insulin resistance. And then I would add maybe just one more with regards to signs and symptoms, and that's the skin, where the skin is incredibly responsive to insulin and thus can reveal insulin resistance quite well. There are two things. One is skin tags. If someone has skin tags at their armpits or around their neck or around their groin or around the backs of their knees, these are any, generally any area where their skin is rubbing against itself, say, well, they're just consistently bad sleepers. But if we combine that with the fact that they're overweight, then I would say we've gone beyond bad sleep. That is very, very likely confirmation or indication that the person has insulin resistance. And then I would add maybe just one more with regards to signs and symptoms. And that's the skin where the skin is. If a person has skin tags, that's a very, very strong sign that they have insulin resistance. And then less common than that, skin tags is more common. Less common is another situation called acanthosis nigricans. And that's when a person will have like dark spots. Now I'm covered with dark spots called freckles, of course, and that's not what I mean. I don't mean these distinct little freckles. I mean like actual kind of sections of skin where it's darker and may even feel a little differently, a little rougher, more velvety than the rest of the skin, that is, that is a very, that's almost absolute confirmation of insulin resistance. If someone has either of those, but especially the acanthosis nigricans, it's. I would, I would bet everything that's a person who has insulin resistance. It is so tightly connected with it.

And I love that you said somewhere in the book that, you know, if you have diabetes, you are insulin resistant. I think we focus so much on blood sugar. So if someone is prediabetes, can we assume. Has prediabetes, can we also assume that they have insulin resistance?

Oh, at 100%, prediabetes is. Yep. Prediabetes is synonymous with insulin resistance.

Yes. So here's something. This is a selfish question and it's a rabbit hole that I went down when I read your book. And we have companies nowadays that do continuous glucose monitoring, which is fabulous. Right. I think that that's very helpful in so many ways. But I'm more interested in insulin. Why, why is that not invented yet or is it and I just don't know about it?

Oh, it's not. Oh, believe me, Morgan, can we do.

That and be millionaires together?

Oh, my goodness. You, you, you would be amazed at how many groups are actively attempting to do this because of course, the utility goes far beyond insulin. The moment you can create a continuous insulin monitor, you can pick any other hormone. So it is going to, once that dam breaks, it's going to break and it'll be wonderful. And I know groups that are actively studying this, including a guy named Tom. So at Stanford, at Stanford, a genius bioengineer, but they're actively working on miniaturizing these kinds of devices that would allow, I mean, imagine the value, of course, insulin. That's what we're talking about. It would. Once we can do insulin, then you can have a little patch that's telling you not only your insulin levels, but it could be, it could be your cortisol levels, your, your epineph or your adrenaline levels, your glucagon levels, the sky, growth hormone. The sky's the limit at that point. But it is technically fantastically difficult. So my view is that in the next couple years we will have at home insulin tests, you know, something like. But it won't be exactly like this, but just how someone can make a finger prick and measure their glucose or their ketones with a little meter. It won't look like that. It'll be something different, I believe. But there will be some at home test in the next couple years for people to measure their insulin levels. And then I would say in 10 more years, then we will get to the point of continuous hormone monitoring, including insulin. So it's technically just fantastically difficult to. But that is also why I believe we look at diabetes type 1 and type 2, strictly through the lens of glucose, in part because we have been able to measure glucose for 100 years. We've only been able to measure insulin for, say, 40 years or more than that now, 50 years. But even then, more often than not, even nowadays, it is a radioactive test. So you have to have approval to handle these little, very, very mildly radioactive molecules. But it's not easy to do. You have to have a whole blood sample and you have to take it to a lab, and it's an extensive process. So just measuring insulin is still a challenge. And that's partly why I think we look at type 1 diabetes and type 2 diabetes as a family of problems, because of what they have in common, which is the elevated glucose. But that is such an unfortunate paradigm, because if we could have looked at the two from their origins as insulin diseases, then we would see that they're not at all related. They are exact opposites. Type 1 diabetes is a disease of too little insulin. Type 2 diabetes is a disease of too much. We shouldn't lump them together. And I think that we only do disservice well to both groups, frankly, when we do so, especially type 2 diabetes, even type 1. But type 2 is just so much more common. We need to look at it through the lens of insulin. And once we do, we can detect it much sooner, because in the average individual who's progressing towards through prediabetes and type 2 diabetes, we define it on the glucose levels. And so we've been waiting for years and years and years for the glucose to finally start rising. But if we'd been looking at the insulin years before the glucose ever moved, the insulin would have moved, and then we could have detected the problem.

10 years. We're waiting too long. I heard this analogy once that, well, James Clear, I don't know if you've read Atomic Habits. I really like his work. And he has this analogy that bad habits have the reward in the present, right? If you want to smoke, if you want to eat a donut, you get that instant reward. And the negative impact of the bad habit is delayed until the future. And so we tend to just kind of ignore it or not worry about it or not recognize it. Whereas a good habit, you know, the penalty, so to speak, is in the present. We skip we skip the donut after church. You know, we might feel restricted then, but the reward is in the future. And I think that is the beauty of the continuous feedback monitoring is to bring that, you know, negative or positive impact of a habit to the present so that you cannot ignore what you're doing to your body. And I think that that's a nice thing to pivot into. How does insulin resistance start? What are, what. What are people doing that's causing insulin resistance without even knowing it?

Yeah. So I touched on the most, what I believe is the most relevant, which is chronically elevated insulin. And that is entirely a matter of what we're eating. So where someone's eating high carbohydrate foods and they're eating every two to three hours, that absolutely is going to be driving insulin resistance. Too much insulin causes insulin resistance, and this has been shown in humans. This has been shown in laboratory rodents and in individual cells at all three of these biomedical models. I could cause insulin resistance in each of them by just increasing the insulin. Humans as well. So chronically elevated insulin is a big one. Now, there are two more that I think are worth emphasizing because they've also been shown to cause insulin resistance in these same three biomedical models. So I just have to mention them. One is inflammation. Inflammation itself can drive insulin resistance. And this is. I don't emphasize this one at the first because it's harder to really know, well, how can I control my inflammation? It's easy to know how to control your insulin because it really is just a matter of control your carbohydrates. Inflammation is a little more subtle, but it is a driver of insulin resistance. And this is most obviously relevant in people with autoimmune diseases, when people have an active phase of their autoimmunity, because autoimmunity also tends to come and go. You can track the insulin resistance with the autoimmunity. When, say, the rheumatoid arthritis is active, the person is more insulin resistant. When the rheumatoid arthritis has subsided for a time, well, then the insulin resistance does too, and they become more insulin sensitive. So inflammation is another one of these big three. And then the last one of the big threes is stress. The prototypical stress hormones are hormones called cortisol and epinephrine or adrenaline. That's another name for it. Both of those, they mediate the stress response in the body. So when someone's feeling stressed, part of what they're feeling feeling is the consequences of the elevated epinephrine and cortisol. And or cortisol, depending on the time of the stress. Both of those hormones have totally different effects throughout the body. But one of the effects they share is that they both increase glucose levels. And that is why they're called insulin antagonists. So they're trying to increase glucose, insulin is trying to lower glucose, and so it puts them at odds. So if someone's experiencing stress and the stress hormones are up, then it just means the body, insulin has to work a little harder. And so the body's becoming more insulin resistant. So those are the big three that have been shown to cause insulin resistance in cells, rodents, and humans. But I have to add another one that I think is very relevant, which is the excessive consumption of omega 6 rich seed oils like soybean oil and canola oil. Now, the average individual listening to us right now may say, well, I don't eat soybean oil. Yes, you do. If you're eating the bulk of your calories from foods that come from bags and boxes with barcodes, it is exceedingly likely that you're like the average American where you're getting most of your fats from these refined seed oils. Most. The average American gets more of their fat calories from soybean oil and shortening than literally any other fat in their diet. And these are rich with these, these omega 6 fats. And among the many, many things omega 6 fats do, they can drive insulin resistance at the level of the fat cells first and then other tissues start to follow.

Yeah, I think in your book, didn't you say linoleic acid is the most readily oxidized fat and that oxidation then leads to inflammation? And like you just said, inflammation is a root cause of insulin resistance. Is that kind of the link between them?

Yeah, yeah, that's so one. They do become, in fact pro inflammatory molecules, but also they make the fat cells grow through a process called hypertrophy. And when each individual fat cell hypertrophies, it becomes insulin resistant. So it basically forces the fat cells into this insulin resistant pathway.

Now, I read a lot of different books. Was it in your book where you talked about hypertrophic versus hyper hyperplasia of fat?

Can you explain that? Talked about it too. Yeah.

No, I think it was from your book and I thought that was fascinating. We weren't planning on talking about this, but let's go down that rabbit hole really quick. Explain, explain that difference.

So gladly. It's very, very relevant. So when someone I will sometimes be asked, including in from my own students, where does insulin resistance start? There is no definitive answer to that question. There are theories that it starts in the liver or the muscle or the fat cells. I am firmly in the camp of the fat cells. I firmly believe the fat cells fall first. They're the first domino to fall, and that starts to spread the insulin resistance throughout the body. And basically what happened. It's a fascinating series of events and part of why I love the fat cells so much, because it's really a case of the fat cell trying to ensure its own survival that causes the problem. So very briefly, and I will try to be brief because this is a topic that I devote an entire graduate level course to. If you had two people getting fat, they're each gaining 10 pounds per year, they could actually be getting fat through totally different processes. On one hand, we could have a fellow who's getting fat through a process called hyperplasia. This is when each individual fat cell grows just modestly, and then it recruits a new fat cell, and then it recruits a new fat cell. So they never. No fat cell ever gets very big. All the fat cells are very modest in size. But what's so interesting is that there's almost a limitless potential to continue to make new and new fat cells. So hyperplasia is like a hotel that the moment it gets full vacancy, it just builds another room. The moment each of the beds is filled, it just adds new rooms to the hotel. So no individual room is ever too full, but the hotel itself just continues to grow. In contrast, another fellow could be getting fat through hypertrophy. And this is when the number of fat cells is set. And this is most people, most people get fat through hypertrophy, which is why we have such a problem with insulin resistance. And in this instance, this is when the fat cell number is set. So this is like the hotel that cannot create any new rooms, but it just keeps packing people into the rooms. So each individual room is getting more and more stuffed, or back to the fat cell. Each individual fat cell is getting fatter and fatter, and then it gets big enough that it reaches a point where it essentially tells insulin, because insulin is the signal that's telling the fat cell to grow. Or it's the individual, the hotel employee, that keeps shoving new more guests into each individual hotel room. The fat cell reaches a point of maximum dimension beyond which it cannot grow, lest it burst and then really hurt the body and make the body very, very sick. So the fat cell basically tells insulin. Well, it does two things. One, in order to ensure that it doesn't get any bigger, it stops listening to insulin because insulin is trying to tell this hypertrophic fat cell only store fat, don't let any out. But insulin keeps pushing more fat in, and now the fat cell starts to break the fat down, which is something insulin would normally inhibit. So the fat cell has become insulin resistant and is now leaking fats in order just to ensure that it doesn't explode or burst. Second, though, and this is equally relevant, as each individual fat cell is getting so big, it's pushing the fat cells themselves further and further away from the blood vessels and within the fat tissue. So each individual fat cell is getting pushed further and further away from capillaries. And thus each individual fat cell is becoming more and more hypoxic. It's starting to get deficient in oxygen. And so the fat cell, in order to try to get more oxygen and more blood, it will start secreting pro inflammatory hormones, some of which can be used to increase new blood vessel growth, so it can start to try to grow new capillaries. So both of these processes, the fat cell becoming insulin resistant and the fat cell becoming pro inflammatory, are both.