Live Like a Girl with Dr. Mindy Pelz - Insulin: Everything You Need To Know - With Dr. Ben Bikman

Episode Date: June 20, 2022

For full show notes, resources mentioned, and transcripts go to: www.drmindypelz.com/ep126/ To enroll in Dr. Mindy's Fasting membership go to: resetacademy.drmindypelz.com This episode is about insulin, glucose, and your fasting questions.  Benjamin Bikman earned his Ph.D. in Bioenergetics and was a postdoctoral fellow with the Duke-National University of Singapore in metabolic disorders.  Currently, his professional focus as a scientist and professor (Brigham Young University) is to better understand the role of elevated insulin in regulating obesity and diabetes, including the relevance of ketones in mitochondrial function. Outside the lab, Dr. Bikman is a devoted husband and father and enjoys nothing more than traveling and adventuring with his wife and three children.  Please see our medical disclaimer.

Glucigone is a hormone of the fasted state. And I like to talk about it because in a way, it's such a wonderful opposite to insulin that essentially whatever insulin wants to do, glucagon wants to oppose it. Resetters, Dr. Mindy here. And I am on a mission to teach you just how powerful your body was built to be. This podcast is about giving you the power back and helping you believe in yourself again. Let's jump in. On this episode of The Resetter Podcast, I bring you Dr. Ben Bickman.

Okay, you all loved this episode the last time we did this one last year with him. It has been the highest performing episode of the Resetter podcast on our YouTube channel. And for a good reason, we are going to go down the path of insulin resistance. But here's the really cool part about Dr. Ben Bickman. For starters, he's so great at giving us the science in a very chunked down way. So if you are confused on things around insulin resistance, like how can you be in ketosis with your ketones going up, but your blood sugar is going up at the same time? And another really popular question we get is why does my blood glucose change with my hormones? Is that bad? Or,

do I need to add more muscle to my body to become more insulin sensitive? These are the questions so many of you have asked us. So we brought Ben back so that he could not only answer them, but we can go into a little deeper discussion on insulin resistance, specifically to make it very applicable for you. So I absolutely loved doing this interview. I think you all are going to find great. insight in it. Those of you that are fasting and have been fasting with me, oh my gosh,

he has some really cool things in here about why glucose goes up for a longer period of time after you have been fasting. So many mysteries of the fasting world will be resolved in this episode. And if you are not familiar with Dr. Ben Bickman, he, I love this, this is off his Instagram. He is a metabolic scientist. He is a professor. He's a father. You will hear that in here. We talked about children in insulin resistance. And he is a husband. He is the author of why we get sick. And he is such a lovely heart-based man that is changing the world through his teachings on insulin resistance. And I am so excited to share this with you. So if you love it as much as I love doing it, please send it out. And you hopefully you'll hear in this or in the previous

He has a great new shake that is perfect for the ketogenic style eating. So we will leave a link for that as well if you want to head on over to his web page and see some of the great products that he's got to help us all stay insulin sensitive. Enjoy. I'm really, again, I just want to thank you for coming back. Yeah, yeah. I feel like I've talked about insulin resistance from every angle I possibly can. And I also feel like the world is waking up and they're starting to see that insulin resistance is not just an individual problem, but this is a world problem.

Would you agree with that? Oh, completely. Yeah. I mean, I, in fact, let's make sure we bring that up. I've given talks on insulin resistance literally around the world for good reason. Because as much as we, no one loves to rag on the U.S. as much as Americans do. And that doesn't go, I mean, that even includes things like insulin resistance where we think we're the worst in the world and we are not. I'm not even sure we're in the top 10 when it comes to countries with the worst insulin resistance and type 2 diabetes. Virtually every country in the Middle East is higher than us. Mexico is higher than us. Some countries in Southeast Asia.

So yes, this is absolutely a global phenomenon, unfortunately. Yeah, interesting. It's so interesting to hear you say that Americans, we bash America. That, oh, more than any other. Surprises me. Other country, you know, I've lived around the world. I'm originally from Canada, born and raised,

so I'm able to look at this country with somewhat of a foreigner's eyes and appreciate it. Like, only foreigners can, to be perfectly frank. Americans love to hate their own country, which is kind of remarkable to me. I'm an American now, and I love it. I'm grateful for it. Yeah. I do feel like when it comes. comes to the food industry and what we've done to our health, that that is one of the biggest

things we like to hate on ourselves for? Yeah, well, and rightly so, of course, yeah, I mean, there are all kinds of dimensions to this that go well beyond what you and I want to talk about right now. But absolutely, our, one of the beautiful things of capitalism and democracy, which is these two are always intimately connected, which the United States has been such a beacon of for so long is that there is this relentless pursuit for profit. And that is, I do not say that as a bad thing. Unlike most academics, I am vehemently opposed to communism. But it's a, there is a counter to that or an aspect to this, which can be a little more sinister, which is you don't really, you might not care as much what is happening to when this product is consumed as long as.

as it is, you know, helping the investors, you know, so to speak. But yeah, yeah, I mean, that's definitely something where our innovation in the United States has been so remarkable in so many wonderful ways, but our innovation to make food more processed and more palatable is not one of the things we should be proud of. So well said, so well said. So, okay, so explain to the people who are listeners who maybe didn't hear the first episode when I brought you on last year, and I want to encourage everybody to go back and listen to that. What is insulin resistance? How would we explain that? And then the second part I want to ask of that question, why is it getting so much press? Why do so many people are so many people starting to care about it?

Yeah. Yeah. Insulin resistance. The best analogy I can think of is thinking of insulin resistance as a coin, that I'm holding a coin, and I'm calling this coin insulin resistance, but it has two sides. The first side is, in fact, cells becoming resistant to insulin's effects. Not all cells of the body, though. Insulin resistance in the body is happening when some of the body's cells aren't responding as well to insulin. So that's like specific to the cell, any given cell. However, we flip that coin over.

It's part of the same coin. And then we have the phenomenon of hyperinsulinemia or chronically elevated insulin. Unfortunately, especially in the low-carb realm, people don't realize that these always come together. To make this point perfectly clear, to put as fine a point on this as possible, there is no such thing as insulin resistance in the human body without hyper-insulinemia. There must be elevated insulin. I'm going to say this in reverse now for there to be insulin resistance. You cannot pull the two apart. they are on their own distinct phenomenon.

One, a cell not responding as well to insulin, and two, insulin levels being chronically elevated in the blood. But in the case of the whole body, they are absolutely inseparable. Now, I mentioned that in the low carb community, we get this so wrong. And that's because people have started to invoke this idea of physiological insulin resistance, as if, and they will say a low carbohydrate diet can create physiological insulin resistance, as if they're being clever. Well, they're neither being clever nor informed. It's just utterly incorrect. There is, in fact, such a thing as physiological

insulin resistance. It happens in pregnancy and puberty. And that is when the body has become insulin resistant for a good reason, which is in these instances to facilitate rapid growth. in the case of pathological insulin resistance, which is what you and I talked about on the first episode and everyone go watch it, that's the kind that we're all afraid of, because that's the kind that's contributing to breast and prostate cancers and Alzheimer's disease and heart disease, infertility, and all these other terrible things that none of us want. But even still, as different as pathological insulin resistance is and causing disease and physiological insulin resistance is in helping the body be healthy. and strong, they are both the same thing in that it is both altered insulin signaling at certain cells and to higher insulin levels. Now, to help wrap up my rant as quickly as possible, in the low carb realm, people will say physiological insulin resistance, thinking they're being eloquent and clever when again, they're being neither. They're just wrong. But what does happen, because insulin levels drop precipitously on a low-carp diet. And thus, how can there be insulin resistance?

There is not. And indeed, if you inject that person with insulin, they are so insulin sensitive that they will die from hypoglycemia and the lack of ketones. So it boggles the mind to say this. However, the truth of the situation in where the uninformed think it's physiological insulin resistance is that if you take one person who's eating a standard American diet and have him drink 50 grams of glucose, his glucose levels will come up and assuming he's a healthy insulin sensitive person, which is a bit of an assumption. His glucose levels will come up and down in two hours. A nice, neat curve. However, take another lean, healthy person who's following a low carbohydrate diet and his glucose levels will come up and they'll stay up a little longer and take a little longer

to come back down, which does in fact look like a glucose pattern you would expect in someone who is insulin resistant. But that's not what's happening here. The unique metabolic state in someone who's been following a low carb diet is that they are exquisitely insulin sensitive. They've just become somewhat glucose intolerant temporarily, thankfully, but that has everything to do with the production of insulin. The beta cell, so when someone goes and eats a bagel, they will have,

what's called a bifasic insulin release. There is this immediate release of insulin, and then it starts to curve, and then it's met with a bigger second wave. So there are these two phases of insulin secretion. The first phase is the release of all of the insulin that the beta cells have already made and they have on hand, that they've made and that's packaged up and ready to go the moment there's an increase in glucose. That's the first phase, and the beta cells will run through that very quickly. But at the same time, it's running out of its already made stored insulin. It's already ramped up all of the metabolic machinery in the factory to make a whole new shipment of insulin. And that's the second phase. What happens with either fasting or a low carb diet,

there's so little glucose coming in that there's so rarely any big glucose spike. But the beta cells are looking at all of this preformed insulin that's kind of clogging up, it's cluttering up the cell. and it thinks, well, I don't need all this stuff anymore. I don't need preformed insulin because we consume so little glucose that I can just handle any glucose load by making the insulin from scratch and just shipping it right out the moment it's produced. And thus the beta cell, who is determined to be efficient with its use of space, much to my delight, I'm the same way.

It looks at all the cluttered insulin that says, I don't need it anymore. I'm going to get rid of it. And it simply breaks it down into its basic little protein amino acids and just recycles it into something else. But that's the problem, if you will, where someone who's had been adhering to a low-carb diet, they eat a bunch of glucose and it takes them longer to clear the glucose, not because they're insulin resistant,

but because they have temporarily gotten rid of that first phase of insulin. In that state, they only have the second phase. And so it just takes a little longer for the insulin to get up to where it needs to get and to clear the glucose. But have that same low-carb-adapted person eat that exact same carbohydrate, heavy snack or meal six hours later, and the first phase is back and they'll clear the glucose like gangbusters. How is that for a ridiculously over-explained definition of insulin resistance? No, I have so many thoughts on that. I have never heard. That was way too much, though.

I was like, my brain was like following you every step of the way and going, what? Good, good. So I have two questions that I want to say out of what you just said. One, I can't let the comment go by that we become more insulin resistant at puberty and pregnancy. Yep. Why is that? Yep. Yeah. Yeah.

So those are the two peas of physiological insulin resistance as I like to describe them. And as I teach them to my graduate students. So insulin is anabolic. It wants to promote growth. And so you look at these two stages of what could only be described of just hyperactive, explosive growth. You know, a little kid is growing, growing, growing, growing. They hit puberty and boom. And then they plateau. Well, you take the average

mature woman, like, you know, an adult woman, well, her growth is done, but then she gets pregnant. And all of a sudden, the tissue demands to grow the uterus, to grow a placenta, to grow breast tissue, and even to grow more fat to make sure that there is a kind of a metabolic insurance plan to carry the pregnancy full term and then to breastfeed the baby afterwards. which of course would have been done in nature, or, you know, historically always. So having more body fat is this kind of metabolic insurance in the event that food becomes a little scarce, well, let's just pack on whatever we can right now so that we can grow the baby and feed the baby all the way until the baby's independent.

So here you have an adult female who's totally done growing. And now all of a sudden you have this explosive growth because she has to get ready for this baby and insulin comes up and helps. So in both instances, despite their differences, what they have in common is it is the two periods of the most explosive growth of human experiences. So insulin, by becoming insulin resistant in some cells of the body and by having higher insulin, you can basically direct. So the higher insulin is telling the body to make more stuff and store it.

And some of the body cells are super sensitive to that insulin. And thus, they can experience that explosive, anabolic metabolic processes. You know, this is the thing about the human body that continues to put me in awe, is that it's always doing the right thing at the right time. And yet the symptoms that we get, we villainize. I mean, you talk to any young female in puberty and you're like, hey, you're more insulin resistant. Like, nobody wants to hear that.

Yeah. Yeah. Yeah. Oh, that's right. Well, what's interesting, too, just because we're talking about ladies, is to note the effect of prototypical female sex hormones like progesterone and estrogen on metabolism, where women will commonly think that estrogen is fattening, but that's just absolutely false. Estradial, the main estrogen, is very lipolytic. It's very much preventing the female body from storing too much fat. All estrogens are doing is telling her body where to start. store fat, not how much to store, which is why if I had a man and a woman come into my lab and we did a fat biopsy from the fat by their belly button and put it into a little dish, gram for gram, the fat from the woman is breaking down and burning more fat. I mean, burning is not the right word in this case, but it's breaking down. It's undergoing more lipolysis than the fat from the man is. So this is a very, which is why women tend to have naturally higher levels of free fatty acids in her blood than a man does because she's constantly burning or mobilizing

more fat than the man is an estradiol helps that happen. But in stark contrast, progesterone is a fat that is, well, that is the fat of pregnancy. It's progestation. And it works with insulin to make sure the body is storing more fat. And interestingly, progesterone is so eager to store fat that it will stimulate greater hunger, which is why in a normal menstrual cycle, when progesterone is high, a woman will very, very commonly, and this is not my experience, this is published research. She will, hunger will go up. Hunger will almost exactly match progesterone levels. So progesterone levels climb and then come down throughout the month, normal, normal satiety hunger signals, and then boy, hunger is bigger, bigger, bigger, and then it subsides again.

It just goes with progesterone completely. Yeah, and I speak for every woman out there. The answer to that is yes. Yeah, yeah, yeah, good. Well, I, and Mindy, just so everyone knows, I sometimes get a lot of heat. Like, I've seen people make comments like, oh, great, another white straight man talking about women, you know, whatever. I'm not pretending. I know what it's like. Just so everybody knows, right? Yeah, I know. You know that, but just so everybody knows, I'm not pretending. Yeah. But just based on published research, I can speak on this with some authority.

The other thing I really feel like is that just that comment alone, and it's actually something that I say a lot to my community, which is when you're hungry the week before your period, stop villainizing yourself. Stop. You're not undisciplined. It's because progesterone is going to require more glucose. And so it's natural. Now, let's just pick the right food for you to eat. It doesn't mean you sit on the couch, right? You don't sit on the couch. Well said. But you do have, have give yourself grace because your human body wants more glucose. And I think that's so powerful. Yeah. Cool. Okay. My second question, because we're going to get this a lot, is in the first, in that, the beautiful opening comments you had, if you go on a three-day water fast, if you go on a 48-hour

water fast, something a little bit longer, and your pancreas is getting rid of the insulin it doesn't need. if when you bring food back in, will there be a temporary appearance like glucose is high because of what you said where that insulin system? Yeah. Okay. And how long is it at last? All the more reason. All the more reason to be careful with how you break your fast, which is why I'm always saying how you end a fast is much more important than how long you fast. So don't eat something that demands a dramatic insulin response for two reasons.

One, for the reason we just described, which is you're not going to. to clear the glucose very well, you know, kind of warm up the pancreas again if you're going to get into carb heavy foods, start easy. But then second, this is very uncommon and virtually, I would say probably impossible, certainly unheard of in the order of like a two to even three day fast. But there is a phenomenon known as refeating syndrome. You already, have you already talked about this? No, no, but we talk about breaking fast all the time and how important it is. So please. Well, then this is worth taking a moment to explain. But it sort of follows along with that sentiment just from a moment ago, which is, you know,

you don't expect your pancreas to work too hard and expect it to produce insulin that you haven't been asking it to produce for the last 24 to 48 hours or 72 hours. Because all it takes is about 16 hours of fasting for the beta cells to start scrapping their stored insulin. So this is a pretty quick phenomenon. But when insulin levels start to drop, which they do during a fast, the body starts to more rapidly, I want to make sure I explain this correctly. The body will start letting minerals go. It'll start letting electrolytes leave with the water from the blood. And this is why the person's blood pressure will tend to go down.

Now, of course, if you're taking salt and water, this will help mitigate this phenomenon. but even still, insulin comes down and as it is, the body is more rapidly dumping electrolytes in the urine. It's just a natural phenomenon. However, when you spike your insulin really dramatically, you start not only are the kidneys still dumping some of the minerals, they don't get the message immediately. It takes them a few hours to start conserving minerals again. But what happens when insulin spikes is within seconds of insulin hitting the blood, it now starts pushing particularly potassium into cells.

So as insulin's coming to cells, part of what it's pulling into the cell is potassium. And so the person can actually run the risk of developing hypokalemia or low blood potassium. And that is, in fact, a very lethal, I mean, it can kill you situation. Now, again, this is not common on the order of even two to three-day fast. it's usually this was studied in very long, like week, two week type fasts under, you know, strict kind of academic clinical supervision. But even still, it's nevertheless a reminder for us to not end a fast with an insulin spiking meal or snack because not only is that going to be a challenge on the pancreas in that

moment and make it harder for us to clear the glucose. And so we'll be hyperglycemic for longer. but two, we just start flirting with this potentially lethal imbalance in electrolytes. Yeah, it's so well said. So what would be the ideal meal to break a fast with? Yeah, yeah. So protein and fat at the risk of oversimplifying it. Just because there is one, I mean, from myriad reasons, let's see how many I can think of off the top of my head.

One, proteins and fats are what's essential. So why not end your fast with what you literally have to be eating? essential amino acids and essential fatty acids. And two, you will help mitigate the insulin burden because proteins and fats have little to no effect on insulin, respectively. And so it just helps, you know, kind of wake the pancreas back up and removing it. Because the pancreasin has been a little quiescent or still during the, well, the beta cells have been during the fast because it's the fasted state.

And insulin is not the hormone of the fastest state. it's the hormone of the fed state. So you eat something and kind of warm the beta cells up as you start getting more and more to higher carbohydrate meals. What would you say the hormone of the fasted state is? Ah, that's a very, very good question. So there are a lot of ways I could answer this, but I will highlight one that I think hasn't classically been discussed enough, but I've over the past few years tried to shine

a light on it, and that's glucagon. I think you and I've talked about glucagon before, but glucagon, Glucigone is a hormone of the fasted state. And I like to talk about it because in a way, it's such a wonderful opposite to insulin, that essentially whatever insulin wants to do, glucagon wants to oppose it, in a beautiful yin and yang,

you know, there has to be a counter here, each keeping the other in check. It's a wonderful check and balance. But there are multiple other hormones that also would reflect a fasted state. So as much as I'm mentioning, Glucigone, I could just as much justifiably have mentioned epinephrine or cortisol or growth hormone.

All of those climb during the fasted state because what they all have in common, all four of the hormones I've just mentioned, glucagon, epinephrine, cortisol growth hormone, they are all totally different from totally different cells, move totally differently in the body and affect different cells differently throughout the body. What they all have in common is that they all increase glucose release from the liver, that every one of these through totally different mechanisms come to the liver and tell the liver either to break down its glycogen to release as glucose and or stimulate the liver to undergo gluconeogenesis to basically pull in lactate, which is mostly what it does this with, and turn it into glucose and release it back into the blood. That's an

important thing for us to appreciate because as much as I just said a moment ago that fats and proteins are what's essential, thus implying that dietary carbohydrates are not and they aren't essential, too many people hear that statement and either willfully or ignorantly misunderstand it to imply that blood glucose isn't necessary. That is not true. In fact, blood glucose is so essential that the liver has all of these wonderful signals that force it to make blood glucose, which is proof positive in the fact that we start fasting and all our glucose levels do is go to normal. They just hover around 70 to 80 milligrams per deciliter because the liver is so good at making sure it stays there. And that itself is evidence of the fact that the body is

vigorously defending that glucose range. Whether the glucose is pushing up or getting pushed down, it wants to bring it back into that range. And there are some cells of the body that absolutely have to have glucose. And I'm not going to say the brain, because we don't really know that. We know that the red blood cells, red blood cells must have glucose. There is literally no other option because any other nutrient option can only be burned into mitochondria. Well, red blood cells don't have mitochondria. So they literally can use nothing else, unlike the brain, which can shift over to use.

using ketones and even lactate as a fuel because it is so enriched with mitochondria. But red blood cells, they absolutely have to have glucose. And that's one of at least one reason why blood glucose is so critical. And even, again, stepping further back, why it's such a blessing that the liver has such a profound ability to provide all the glucose the body needs. So does that explain why? And we get this question so often from our community. When people are fasting, they can see their blood sugar go up and their ketones go up.

How is that possible? Yeah. Yeah. In fact, let's just invoke glucagon, because glucagon plays a part in both of those. So too does epinephrine, but I like glucagon more. So glucagon has two seemingly counter-effect. Well, it's actually literally the effects you just mentioned. One is that glucagon will stimulate glycogenalysis at the liver.

thereby breaking down stored glucose and increasing releasing it into the blood increasing glucose, although it shouldn't ever go too high because then insulin starts to work against it to push it back down. So if someone sees an increase in glucose during a fast, that's a little uncommon, a little uncommon, but it might suggest that they're kind of, I hate that I may give birth to a sentiment that lives longer than I ever intend to, but maybe they're a little glucagon dominant, you know, so to speak. Yeah, that could become a word. I know, I know, yeah. But essentially, but even then, remember that there's a lot of hormones that want to do this. But I'm only invoking glucagon

because it's simply relevant to both glucose and ketones. But remember, on the glucose raising side, there's glucagon, growth hormone, cortisol epinephrine. So any one of those could be providing a little too much of an upward pressure on the glucose. But as that's happening, insulin will wake up from its fasted, rested state and start pushing it back down. But even still, glucagon is going to want to increase glucose by inducing glycogenalysis at the liver. It also activates ketogenesis at the liver. Because when insulin is low, and then glucagon amplifies this, the liver is burning so much fat that it actually ends up burning more fat than it needs to meet its, than it needs to meet its own energy needs.

And so here's the amount of energy that the liver cells need. And because insulin is low, fat is basically providing all of that energy. But because insulin is low, it can't stop burning fat. And so now it's kind of surpassed what its actual energy needs are. And that extra, if you will, is what gets kind of shunted into ketogenesis and starts turning into ketones. So are you in ketosis if your blood sugar is going up and your ketones are going up? Well, normally you wouldn't. But if glucagon were too high relative to insulin, like what happens in type 1 diabetes, that's exactly what happens in type 1 diabetes.

Insulin is very, very low. And glucagon is too high because it doesn't have insulin to inhibit it. And then you can have this state where you have both high glucose and high ketones. Okay. And as long as they're not too high, it's not a dangerous place. It's the liver. And it can be looked at as positive because the liver is breaking down the stored sugar, which ultimately allows the liver to function better. Yeah, but Mindy, there is something maybe I should kind of end that answer with, which is if someone notices during a fast that they are getting really high glucose and really high ketones, they might, in fact, want to go get their insulin checked.

That might be a warning that there is, in fact, a defect in insulin production or, you know, even beta cell number, like, you know, hinting at some degree of type 1 diabetes. Because in the average healthy person with no hint of beta cell problem, glucose shouldn't be climbing. Maybe a little, certainly during exercise. It should just be ketones are coming up. If they're both going up and they kind of keep going, go get your insulin check. And is there somebody asked on our, on the Resetter podcast YouTube, channel. Is there a way to measure insulin, a home test? Or is it only a, no. Why not? No. It seems like we should be able to create that. Oh, oh, oh, you can't even, you can't even

imagine how competitive and determined multiple labs are around the world. Truly, truly, truly. To not, I mean, forget about the idea of a continuous insulin monitor. I mean, we're a decade away from that at least. But just to kind of miniaturize the ability to take a few drops of blood on like a little insulin meter like we would have ketones or glucose. Oh, no. No, we are, I'd say we're still, that's probably five or six years away. There are so many technical hurdles with trying to measure a hormone. You can't do that with any hormone. I know that because what I've been saying is they need to do it for women where they put like a continuous glucose monitor on them. If we had something that showed where our hormones were at, oh my gosh. That's.

Somebody needs to come up with that. That would be amazing. Yeah. And then it would send the alerts to the husband's phone. That's right. It would, everybody around you, you could be like, hey, hey, look, progesterun is coming in big today. I'm snacky.

I'm going to the buffet. Have dinner ready. Yeah. Would that be great? Oh, my gosh. Here is. You said it. I'm not being a misogynist.

You said it. And I'm hoping if I can. keep saying it. There's going to be some researcher out there that's going to know. And they're going to be like, yes, let's go make that. So every woman is demanding it. Okay, have you heard of the term fat toxicity? Never, but I can't wait to hear what it is. Okay. I can't wait to tell you. And this is what I learned. It is a doctor's, I don't know his first name, but his name is Dr. Gregory. And this question was actually asked on our YouTube channel. And I went and watched his theory on it. Here's his theory. is that insulin resistance starts in the muscles,

that there is a resistance factor. It doesn't start in the liver. It doesn't start in the pancreas. It starts in the muscles. The muscles become insulin resistant, and then it progresses to the liver, and then it progresses to the pancreas, and then you have type 2 diabetes.

No, no, he's wrong. So I don't know him. So maybe I want to be polite in all sincerity. That's just not true. But even still, before I break that down and point out the flaws in that, where does the fat come into that? Does he say that the muscle becomes insulin resistant because it gets too loaded with fat? That's exactly right. Okay. So what he's doing there, whether he knows it or not, is invoking a principle of what we call in the realm of, like, I've published papers on this, so I can't speak with some authority, what we call lipotoxicity, which is he's just kind of made it a little more of a palatable term because someone might not.

know what lipo means. But that lipotoxicity was this idea born a couple decades ago. And again, my postdoc work focused explicitly on this. It was, and still is one of the more world famous labs studying lipotoxicity. But the idea is that the muscle cell or any cell, I'm not even going to invoke muscle because I'm going to come back to that and pull that idea apart in a second. The idea is a cell accumulates fat and becomes insulin resistant because of it. There is some, truth to that idea, but I don't know if most people appreciate it. So the most common form of storing fat is in the form of triglycerides. And triglycerides will bubble together and create what's called a lipid droplet. And you can detect this, of course, very readily in a fat cell. If you look at a fat cell under

a microscope, like we could walk across the hallway right now to my lab and we're growing fat cells in a petri dish. We could look at the fat cells. And you basically, they look like they're a big bubble because all you see is this huge lipid droplet which consists entirely of triglycerides. And within each cell, you zoom into the cell, magnified as much as you can, it just looks like a big bubble in the cell. It's just a big lipid droplet of triglycerides. Triglycerides can be stored in the liver very, very readily. They can also be stored in the muscle. But triglycerides do not cause insulin resistance. They don't contribute to it whatsoever. They're totally inert. However, there is a type of.

of fat called seramides. And anyone who wants to go to Google type in Bickman seramides, you can find the numerous papers I've published on this topic. Ceremides are a type of fat. But the problem with saying that is there are hundreds of thousands of different types of fats. Really. So there are like seramides are kind of the mother molecule in a family of fats called the sphingal lipids named after the enigmatic sphinx because for so long we didn't know what they did at all.

but we know that seramides will make a cell insulin resistant. But even still, we'd have to say, well, how do the seramides get there? What induces their accumulation? Well, things like cortisol, things like inflammation, things like chronically elevated insulin will induce the accumulation of ceramides in a cell, and then the cell has become insulin resistant. Now, however, to try to point the finger at one particular tissue is very problematic because there are a lot of assumptions that have to go into that.

So his assumption that it starts in the muscle, he can't say that. But there are advocates in my realm as actual practicing biomedical scientists who study insulin resistance. There are pools. There are advocates of this muscle first theory. There are advocates of the liver first theory. Then there are advocates, you know, with who say that it's a fat first theory. but regardless, each theory has evidence to support it.

My evidence is just better than the other guys. But nevertheless, it really does depend on the stimulus. Because if I took a random person and infuse them with cortisol, slowly, slowly, giving them a chronic kind of boost in cortisol levels, I would detect insulin resistance concurrently in fat cells, in muscle cells, in liver cells, in neurons. none would have preceded the other. They all would have gone at the same time.

Similarly, if we took the average individual and started infusing a base level of pro-inflammatory cytokines, of course you have to be very careful doing this, but even still, you would start detecting concurrent insulin resistance throughout the body. There would be no way to say this tissue went first, no, because the same stimulus is happening at all the cells and they're all becoming insulin resistant. my view is very much in the average individual who is becoming insulin resistant through their diet is that it's happening due to chronically elevated insulin. And the elevations in insulin are promoting fat cell hypertrophy.

And when a fat cell undergoes hypertrophy, two terrible things happen. One, the fat cell becomes insulin resistant in an effort to control its own growth. And so it starts leaking free fatty acids. And second, it becomes pro-inflammatory to try to increase blood flow because as every individual fat cell is undergoing hypertrophy, they're getting pushed further and further away from blood vessels. And thus they become hypoxic. And to try to correct that hypoxia, they start secreting a whole catalog of pro-inflammatory proteins, some of which will help induce more blood vessel growth, many of which will simply start

promoting insulin resistance throughout the rest of the body. So to try to point the finger of one particular tissue, you're doomed to be laughed at because everyone else will have evidence. Like I'm laughing at him a little bit. You're doomed. But I very much think the fat cell is the first to become insulin resistant. And then once the, and this is reflected, remember, insulin resistance is when insulin is elevated, but glucose is normal.

And then once the insulin resistance has moved to the liver, the muscle, and the alpha of the pancreas, which start producing too much glucagon, now you can no longer control glucose, and the glucose starts to climb, and now you have transitioned from insulin resistance, which is pre-diabetes, into full-on type 2 diabetes, which is both elevated insulin and elevated glucose. Because in type 2 diabetes, insulin does not become deficient. It does not go to zero. If this is true type 2, insulin has gone like this. They were insulin sensitive and insulin was really low, then it starts to climb up really high, and then it can drop a bit, but it never drops to the level that it used to be.

It's still multiples higher than it ever was before. It just came down from where it used to be at its peak. If it actually goes down to basically zero, they now have actually just coincidentally developed type 1 diabetes later in life, which can happen, which had nothing to do with having had type 2 diabetes. They are two totally separate diseases. So on the topic of muscles, I do want to come at this from a different angle because one of the trends that we're seeing right now is a lot of people increasing protein and they're doing

it to increase muscle. And then when we look at the effectiveness of muscle on insulin sensitivity, the understanding is that there's more muscle you have, the more insulin receptors you have. Is that a good trail of thought? And should we be. Oh, totally. Yeah. Should we be highlighting protein? Is that the hero of the insulin day? Yeah, what a wonderful question. So there's a lot of dimensions to this. One is that no question, having more muscle makes you inherently more insulin sensitive.

Just because muscle is the main, it is the lion's share eater of glucose. So when we've gone and eaten that bagel, glucose has come up. As it comes down, 80% of where that is going is to the muscle. And so if you just have more and more muscle, well, then that just means you're dropping that glucose,

that much faster because insulin starts knocking on any doors it can and there's so much muscle while the insulin's like going through a crowded neighborhood. It's like an apartment building, knock, knock, knock, knock, open up. Here's the glucose, glucose, glucose. And so the glucose drops. The less muscle you have, the longer it's going to take for you to clear the glucose because insulin just doesn't have as many places to tuck the glucose away and out of the blood. Now, then to move into the discussion of protein, I think the conversation has gone too far. Interesting. As much as I am a long advocate of protein, indeed, I was defending protein before many were

in the low carb keto space because I saw the trend to just be eating fat, fat, fat, fat, fat. And I thought that's not natural for everyone to just be drinking MCT oil all the time. In nature, protein and fat come together. We pull them apart sometimes, and I'm not saying that's not warranted. Like in any animal fat like butter or ghee or whatever, we've pulled it from the protein that was meant to come with it. But then the fat from the fatty fruits like coconuts, olives, avocados, of course there was no protein there in the first place and that's just the fat. But protein is not meant to be consumed without fat. In nature, there is zero instance of protein existing without fat.

It doesn't happen. And so in our hubris, we think we know so much. We've pulled the two apart. in our obsession and love of protein. Well, I love protein too, and I get it. And I think we ought to prioritize it. But it should come with the fat that naturally wanted to come with it. When protein and fat are consumed together, we digest the protein better, literally, by using bile acids.

It actually facilitates protein digestion. And second, it's more anabolic. You can grow muscles bigger and faster by taking fat and protein compared to just protein alone. Interesting. So do you say that one gram of protein for every body, pound of body weight is an overestimation of what to take? No, no, that's probably, that's probably okay. Because of I can't, unfortunately, as much as I align myself with the merit in the U.S. Now, I still think metrically because of my Canadian roots.

Oh, yeah. Well, we're a worldwide audience. I should have trained. Yeah, yeah, good. So usually around, yeah, it won't, quite be that high, but about one and a half grams per kilogram of ideal body weight, which is going to, which is almost going to be one gram per pound. That's kind of getting close. And in fact, I would even be fine with that. But yeah, I'm okay with that number. I really am. I would just

emphasize, let the fat come with it. Don't like my fear in us prioritizing protein, which we are justified in doing. Protein's amazing. But I just don't like the idea of people just eating a spoon of weight, you know, or something, there should be fat that is coming with that protein. You will digest it better and it will be more anabolic than otherwise. Interesting. Okay. One of the other questions that was really common on our YouTube channel was about kids. How are we dealing with the obesity issue that we've got growing in kids?

And one of the questions came from a parent of like, and I can say, I mean, my kids are grown now, but the peer pressure, when they're in middle school, high school, they go to everywhere they go as a carbohydrate, sugar-saturated experience. How do we navigate this one? Yeah. Yeah. Oh, I love this because as much as I am a scientist, I am a husband and father light years above anything else by way of priority. So I think about this a lot. And just how easy it is. you know, we want our kids to enjoy life and we want them to be able to have treats. That is totally natural. And moreover, we just get freaking exhausted from all their whining when they want, you know,

a bag of goldfish crackers or whatever the hell they're asking for. But for me, I, in fact, it's funny. We're talking about protein because that's actually how I framed this. I don't, I'm very much mindful of the fact that I have two little daughters. And I never want them to think too much. about food. You know, I never want them to be so obsessive just because of the tendency to develop an eating disorder. And so I never want to, I don't say, no, we can't eat. We don't eat that in our home. We never eat that kind of stuff. No, it's, have you had some protein? That's what I always ask.

Have you, all right, you want a little bowl of goldfish crackers because goldfish is like meth to kids, right? Like, that's okay. Yeah, yeah, you're hungry. You haven't eaten in a while. Sure, you can have some goldfish, but have you had some protein? Go eat some protein. Here's, we got some cheese sticks, we got some beef sticks, we got some yogurt. And each of my kids, some cottage cheese, whatever it is, eat some protein first. And of course, my kids, none of them like the same thing, right? Because that would be too easy. So my one daughter will eat some cheese sticks. My other daughter will eat beef sticks and my son will eat cottage cheese. And each of them thinks any of the others are just utterly disgusting. So you never, never get the wrong thing to the wrong kid. Yeah, right. Yep. But just

Go eat some protein. Okay, you've had, all right, yeah, go ahead. Have some goldfish. I don't care. I do care, but I just mostly care that they learn what real nutrition is. And I'll make sure that I kind of mention that. I'll say, like especially to my son, but even my daughters, hey, you're doing some acrobatics or you got lacrosse.

You really need some muscle. Don't waste your stomach on the junk. Get that protein in there first and you can really get your muscles and bones strong. And then if you need some extra energy, okay, go ahead. So that's kind of how I frame it. And I am in no way this, you know, paragon of good parenting. But that's how I've tried to frame the conversation. And it seems to work.

Great. To be perfectly honest, it does seem to work for the most part. Which again, don't say, no, you can't have that. That's just junk. It's like, all right, yeah, well, that's a treat. Can you have some protein first? Just so your body really knows that it needs to grow some muscle and some bone. And that works.

Yeah, and I would say, you know, my kids are grown now, but we did a lot of those kind of conversations as well as like educating them, but also being very fluid with it because you do not want to have them create an eating disorder. I absolutely want to be too rigid. No, no. What would you say if somebody goes into the doctor's office, they're given a diagnosis of pre-diabetes or type two diabetes and they're told it's genetic? What would you say to that? Yeah. Yeah. I would say it very well could be all the more reason to fight that much harder.

That would be the second part of this because there's no question genetics matter when it comes to insulin resistance in type 2 diabetes. No question. It's very much a fact that if someone has a parent who has type 2 diabetes or insulin resistance, they will absolutely have a higher risk. No question. That doesn't mean you give up. All that means is you have to work a little.

little harder, unfortunately. And that means everyone ought to be very compassionate in this regard, not only never judging the other person, because we cannot know what their genes and circumstances are. Regardless of that, just always trying to be a help rather than a hindrance. But all the more, but yes, a person who has been told us genetics, it probably is, but that doesn't mean it's hopeless. Right. Not at all. So would you buy the theory if you live the same lifestyle as your parents and did, then yes, you're more predetermined. But if you change that lifestyle, yeah, I love that. Totally. Yeah. Awesome. Okay. Last question, because I want to respect your time. And this one has

nothing to do with insulin, although I can talk insulin already without you all day. We are doing a theme of gratitude this year on my podcast. Do you have a daily gratitude practice? And if so, what is it, what are you the most grateful for this year in 2022? Yeah, yeah. So I do. And this is easy for me because I'm a very religious person. And so I very much acknowledge in my faith a higher power. So yeah, I pray, I have personal prayer every day, which is always gratitude and a family prayer, which honestly, honestly, that has been one of the, over the life of our little family now. the most touching connecting moments, just being together, literally kneeling together and praying as a family. The kids, it turns into a spontaneous little wrestling match.

It turns into a game of Uno or whatever. But a prayer is in our home, it always starts with what we're thankful for. And then at various times in my life, I've kept a journal, which is in a way been kind of a gratitude journal as well, just acknowledging. these blessings, as I would call them, or just fortunate events or whatever we want to call them. So yes, I very much have a practice of gratitude, and it's something I believe in for the health and well-being of every soul on the planet, the need to acknowledge the good things in our lives and express gratitude for them to the universe or a higher power when relevant, and then even more importantly, or just as importantly, to individuals in our lives.

And then the second part of your question, what I'm the most grateful for this year, there's, of course, a lot that I would say about my family, but just for the sake of being unique, I won't say my wife and children. I'll say this, I'm grateful for my job, actually. I'm very, very sympathetic to people who don't have the stability that a tenured professor does. I am very, very grateful to have the kind of career I do for many reasons, but in this case, this things are getting so unstable and have been for a while and could very well get worse. To be a tenured professor is a very big thing for me to be grateful for the moment.

That's a very practical point of gratitude, but it's very real. Yeah, and it's a beautiful gratitude. And what I'm going to do is a dump tail on that because this is how we started off this conversation. which is, and does the world need your teachings now more than ever as the world is waking up to the fact that so many people are insulin resistance? So I'm going to encourage everybody who follows me to go follow you because you do an amazing job of explaining insulin resistance and inspiring us. So, Ben, I appreciate it.

Yeah, super grateful for you. And go grab some dinner with your family. and I'm sure we will talk again. I love it. Thanks so much, Minnie. Thank you so much for joining me in today's episode. I love bringing thoughtful discussions about all things health to you. If you enjoyed it, we'd love to know about it.

So please leave us a review, share it with your friends, and let me know what your biggest takeaway is.