Is Your Diet Killing You? | Dr. Benjamin Bikman | EP 520

If only people were sitting around on a Friday night listening to us chat and thinking, oh, I really want a stick of butter. They want something sweet and gooey. We crave carbs. And they have myriad metabolic effects, one of which is to spike insulin.

What happens to type 1 diabetics if they eat nothing but fat?

The fat cells get big. They get so big that they have to tell insulin, I'm done. A government issues a mandate telling its people what to eat and boy, they got it wrong.

All those vegetables and fruits have been genetically altered to a degree that's just beyond comprehension.

A purely plant based diet is so deficient in nutrients, it is utterly incompatible with human survival. Studies in men have shown that if man stops eating meat, his testosterone plummets, his sperm production plummets.

Listen to that man. Hello everybody. The first thing I think I'll tell you is that I'm on tour again from February through June through the out the United States, in Canada and in Europe. And if you want more information about that, go to jordanb peterson.com and check it out so that you can come and see me and my wife. And if you're inclined to do that, I'm talking today to Dr. Benjamin Bickman, who's a professor of cell biology at Brigham Young University and a lecturer at Peterson Academy. He's done three courses for us. And we are talking today primarily because I'm interested in, and not me only obviously in the rise of the Make America Healthy Again movement. And I've been talking to the people who are integrally involved in that movement and trying to determine, strategize about the, the direction. And that's very complicated thing to do. And one of the things I want to do is figure out where the most bang for the buck might be had with the least amount of trouble. Almost every problem's like that. There's lots of causes of a given problem, but there's one or two causes that are 90% of the problem. And you want to focus there and maybe have a chance then. And so I talked to Dr. Bickman today about insulin resistance and really, to put that in more simple terms, excess carbohydrate intake. And that's the carbohydrates that are rapidly transmuted metabolically into sugar. And that's pretty much all carbohydrates, by the way. And the fundamental problem with America's health is an abundance of carbohydrates. And so we discussed insulin resistance, which is a metabolic condition that arises as a consequence of too much carbohydrate intake. And then we discuss the multiplicity of cascading catastrophic health effects that produces type 2 diabetes being particularly well known, let's say, as a secondary consequence. But cancer, heart disease, erectile dysfunction, reproductive dysfunction, more generally, high blood pressure, you name it, immunological disease, depression, anxiety. There's almost no serious medical condition that's widespread, that can't be traced to excess of carbohydrate intake. And so obviously, it seems to me, that's where the focus should be. And so we walk through the biology, we walk through the practicalities, we walk through some hypotheses about how that problem might be redressed at the government level, but also at the level of individual behavior. And so this is very important. There's likely nothing you can do that will improve your life more, both in the short run, but even more importantly in the long run than to modify your diet away from high carbohydrate intake. And so we walk through why that is. So join us. So, Dr. Bickman, I've been talking to the Maha people about their plans, and it's clearly the case that Americans, Westerners, more broadly, but particularly Americans maybe, are suffering from a slew of unfortunate medical conditions. So what I'd like to know from you to begin with is if you had to rank order the magnitude of the medical problems that presently confront the west, let's say, particularly the U.S. how would you do that? There's a very specific reason I'm asking.

Yeah.

You know, whenever there's a problem, maybe you can. If it's complex problem, maybe you can point to like a dozen, two dozen causal elements. But if you focus, you'll find that three of those are the major contributors, and you could spend an immense amount of time on all two dozen. Or you could focus like hell, maybe on the worst problem.

Yeah.

And gain 50% of the ground. If you spread your forces out across the entire panoply of problems, you're not going to get anywhere. Like, if there are 24 stakeholders in the system that are making America sick and you take on all 24, all you're gonna do is fight endless battles. So I'm curious, if you had to zero in, you know, to where you'd get the most bang for the buck. When you look at the health of America, what do you see as the major impediments? The major problems?

Yeah. Yeah. By. If you look at the top 10 killers, you can actually thematically lump them all into what I call the cardiometabolic crisis, where that encompasses the problems that are overtly metabolic, like type 2 diabetes, which is a top 10 killer. I think it comes in around number six or seven, but also number one, which is heart disease. And now there are others in the top 10, like Alzheimer's disease, for example, that you wouldn't think. You'd say, okay, well, Ben's not including Alzheimer's disease in these cardiometabolic killers. And yet I actually am. Even certain forms of cancers are viewed increasingly as a metabolic problem. So it might be that I'm the guy with the hammer, and so I see the nail, but the nail is poor metabolic health. And that's certainly the focus of my efforts. But I like how you framed the question as much as metabolic health is an underlying issue or a common soil from which all of these noxious plants are growing that we call diabetes, heart disease, Alzheimer's disease, copd, you know, chronic obstructive pulmonary problems. The alternative view isn't that these are each distinct problems. It's just that there are various manifestations of the same problem, Namely, insulin resistance being the most common disorder within the United States. A study published out of University of North Carolina a number of years ago found that 88% of adults have at least one part of what we call the metabolic syndrome, which is a kind of cluster of complications. Interestingly and tellingly, what we call the metabolic syndrome used to be called the insulin resistance syndrome. And as much as you framed it from a western view, just to help people appreciate this, we aren't even in. We're maybe around in the US number 20 or so with type 2 diabetes worldwide, the Middle east, they're experiencing these problems far worse than we are. Even southeast Asia, these countries where you'd look at the population and think, well, you look healthy, you're only maybe a little overweight. But there are ethnic differences where body fat, which is so important to this, will predispose people to these metabolic problems at varying levels. But to answer the question succinctly, the problem is a cardio metabolic crisis. And at the heart of this is this very poorly understood, well, poorly known, poorly discussed problem called insulin resistance.

Yeah. Okay. Okay. So lay out the relationship between insulin resistance and obesity.

Oh, yeah. Oh, that's a great question. So insulin resistance, it's the most common problem. It's the most relevant for chronic disease, naturally. We want to know, all right, well, where did the villain come from? What is the breaking bad story? I typically describe and teach that there are two paths. There's fast insulin resistance, which has its.

Own.

Noxious stimuli, that it Comes quickly, and it can go quickly, but then there is slow insulin resistance. And this touches on your question, so I'll answer it with that one in mind. One of the ways in which insulin resistance develops is by fat cells that get too big. Now, to really confirm as much as we have an obsession on fat, on body fat, we actually look at it kind of incorrectly. We would say, okay, Jordan has 20 pounds of fat, whereas Ben has 30 pounds of fat. So Ben's naturally going to be sicker than Jordan. And yet it's not the mass that matters most. It's actually the size of each individual fat cell. This is why, in that cardiometabolic crisis, the list of what's killing us, men die more from all of those than except Alzheimer's disease. So if you look at the top 10, nine of them go to men, and it's not even close. Men die more from these problems than women by orders of magnitude, almost. But women are fatter than men, so it's clearly not an issue of fat mass, per se. Yeah, yeah. So if you look at as a percent body fat, a woman's going to be fatter than a man by design. That's supposed to be that way for reasons that we won't get into. But men have less body fat, but we have bigger fat cells. So I promise I'm answering the question. But as a fat cell gets bigger and bigger, it's almost like a naughty little child who's taken the water balloon to the tap. Now they're filling it, filling it, filling it, filling it. Oh, boy. You better take that balloon off or it's going to pop. Now, the fat cell, acting in its own best interests, it has to adapt two ways to ensure that it doesn't pop. It doesn't want to die in the body. We don't want our fat cells. We don't want any cell to die. That's a very messy, very inflamed process. So one thing, the fat cell, as it gets ever bigger, it can't turn off the fuel coming in, but what it can do is change the fuel coming out. So insulin has an absolute chokehold on fat cells. This is a little outside the question, so I won't quite get around to it yet. But insulin is an absolute essential signal. As much as we focus on calories, insulin tells a fat cell to grow. And now the fat cell is growing, and it's telling, insulin, Insulin, I am about to pop. And so I have to stop listening to you. And so I'm going to become deaf or I'm going to become resistant to what you're telling me to do. And whereas earlier insulin was telling it to hold on to all of this fat, now the fat cell starts leaking out f fat, even though insulin was originally telling it not to. This creates a problem that we can refer to as ectopic fat deposition. Because now the fat cell is leaking out these things called free fatty acids at the same. So blood fat levels are going up. Now, that's not normally a problem necessarily, but that should only happen when insulin is low. Now we have this weird state where insulin is high, which should be telling the fat break down to slow down. I'm getting into deep biochemistry actually really quickly. So normally if insulin is up because we've eaten some carbs and stuff, then fat in the blood would be down because insulin would be telling the fats to hold onto it. But now, or when we're fasting or low carbohydrate diet, then insulin is down and now we're mobilizing more fat. So normally the biochemistry in the endocrinology is such that if insulin's high fat fats are down, if insulin's low fats are up, unless the fat cells are overfilled or have undergone hypertrophy or growth expansion, now you have high insulin and high fats. And so the body can't burn that fat, it has to store it. And so now we start storing fat in tissues that are ill suited. Like the pancreas is getting fat.

Why isn't it just excreted?

Wow, that's a great question. So actually, if you'll allow me, I love that you just asked the question why. I tell my students that when you ask a scientist a why question, especially a cell biologist, my answer is God only knows. So I don't know why God designed the system to work that way. Why not excrete the fat? But I can.

Maybe it's because historically the probability of prolonged nutrient availability at that level was like zero.

Oh yeah, for sure. We're living in a very unique day.

So the rule would have been historically, if you have extra food, hold onto it, hold on to it. Oh yes, hard times are coming.

So that is in fact reflective though of insulin's effect. It is so determined to store energy that it will literally depress metabolic rate. It will prevent any wasting of energy. So that's the first problem with touching on the question of what's the connection between obesity and insulin resistance? Because there is a connection. So the fat cells get big. They get so big that they have to tell insulin, I'm done, I can't get any bigger. So I'm going to leak out the fats, even though you don't want me to. But then there's a second feature that just compounds the problem, which is as the cells are getting bigger and bigger and fat cells can grow unlike any cell in the body, no cell in the body is capable of the expansion that a fat cell is capable of, much to our chagrin. But as the fat cell's getting bigger and bigger, they're pushing each other further and further away from capillaries, from the smallest base unit of the blood vessel and all of its life giving oxygen. And as it's getting pushed further and further away, the poor chubby fat cell is becoming hypoxic, or it's suffocating. And in an effort to ensure its survival, it starts slowly dripping out these pro inflammatory proteins called cytokines, basically just hormones that turn on inflammation. And there's a whole bunch of them, dozens of them, but some of them will correct the problem. It's like a trail of breadcrumbs. And rather than Hansel and Gretel coming, it's getting to the capillary and stimulating the growth of a new blood vessel. And so it's kind of the fat cell's way of crying out, hey, I'm lacking oxygen, come feed me. And so we have that happen. So both of these things, the poor, we pity the poor fat cell. It's become so filled because of our lifestyle, which is a whole other topic worth diving into. But it becomes insulin resistant to ensure its own survival, spreading fat to be stored throughout the body, and then it becomes pro inflammatory to try to correct its blood supply. And that then the inflammation is one of the fast causes of insulin resistance that I alluded to a moment ago, that anytime inflammation is turned on on the body, yes, that is an immune system process. But the overlapping of the immune and the metabolic is profound. Just a moment ago, you and I were speculating on why the system may be designed the way it is. One thing we know for certain is that of all the systems in the body, the immune and the metabolic are not only essential to survive times of deprivation and to defend the host, but they work hand in hand. After all, what good is it trying to mount an immune response if the warriors don't have any energy to work with? So anytime inflammation is up and it's staying up, that's going to cause insulin resistance. And indeed, it is one of the main causes of insulin resistance.

Okay, okay.

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Okay, so let's, let's, let's walk through this from stage one and also let everyone know what the health consequences are. So I'm going to start the outline. You tell me if I get it wrong and elaborate wherever you want. All right, so we have access to an endless number, an endless array of carbohydrates, and they're very easily converted into sugar. So we have access to sugar of various forms and to carbohydrates in absolute plenitude.

Yes, Right.

And so that's easily converted. That's very high energy source, very dense energy source, and it's easily converted to fat. And so that's what happens. And the reason that happens is because we're evolved for lean times and we store excess energy like a grizzly bear or a camel, and we do that so we don't starve to death in the winter. And.

And thank goodness for it.

Right, Right. And you see this. I guess some of the proof of that is that islanders who tend to be evolved to get through lean times, they're very, very efficient in their metabolism. If they go on a North American high, high carb diet, they just balloon.

Oh, yes.

Yeah. Okay, so, so now too many carbohydrates and sugars, too much fat. Now, the consequence of the fat is manifold. One of the consequences is you, you alluded to two. One is that insulin resistance increases and the other is that inflammation increases.

Yeah.

Okay. So I think what we should do first is we should outline the role of insulin in bodily metabolism.

Yes.

Okay, so why don't you do that and then tell everybody why insulin resistance is bad? Because what you've done so far is make a case for why it promotes cellular fat cell function, but it also has catastrophic effects.

Oh, yeah.

Systemically. Okay, so talk about what insulin does and then talk about what insulin resistance does. Okay. Because just so everyone's clear, what we're trying to do here is we're trying to zero in on the most egregious of the multitude of health problems that might plague us. And we're making a case for insulin resistance as perhaps the worst. It contributes to all sorts of diseases, but it's also highly associated with obesity, which has a variety of health problems as well. Okay, so let's focus on insulin to begin with. Tell people what insulin does and then what insulin resistance does.

Yeah, yeah, brilliant. Yeah. Insulin is an absolutely essential hormone in the body. As much as I am going to go on in the next few minutes and paint the picture of it being a villain, it's critical. If you don't have it, you have a disease called type 1 diabetes and you will die. Type 1 diabetes used to be a death sentence. In the absence of insulin, the body will not last long. And so think so. It is here for a purpose. We need it. However, we need it to work in our favor, and to do that, we need it to be generally keeping in a normal range. And so you just a moment ago, framed the question by pointing a finger at carbohydrates. I agree with that completely. That's a whole topic. As much as over the past decades, we vilified dietary fat, oh, boy, we got it wrong. And wouldn't you know it, you know, in the first time in history, as far as I know, a government issues a mandate telling its people what to eat, and, boy, they got it wrong. No surprise, right? That has happened so often when you take things to that level. So if we put the blame where it belongs, not only are carbohydrates the only macronutrient that people have an addiction for. No one's addicted to fat. No one's addicted to protein. If only people were sitting around on a Friday night listening to us chat and thinking, oh, I really want a stick of butter. No, no one. They want something sweet and gooey. They want something salty and crunchy. So we crave carbs. And they have myriad metabolic effects, one of which is to spike insulin. So this is answering the question of what does insulin do? Insulin's most famous effect, but not its only effect, and I would even say not its most important effect, Its most famous effect is to look at that rise in blood sugar or blood glucose and say, that's beyond homeostasis. This isn't right. If that stays high for long, it's going to start harming the body because hyperglycemia alone is pathogenic. And so insulin acts as a hero and says, your problem, I'm going to take care of you. It brings the temperature back down like a thermostat. You know, the perfect example of homeostasis brings the glucose back down to normal. And then insulin, having done its job, retreats back into the background, if you will.

What's its chemical role in relationship to the conversion of carbohydrate to energy?

Oh, yeah, yeah, right. That's great question. So glucose, you'd mentioned a moment ago, and as you did so, I sort of couldn't help but think of the kind of a metaphor of, like engines, where the body has two primary fuels. @ any moment, it's either sugar burning, blood glucose or. Or fat burning. One is like a kind of race car engine. Boy, it's going to be really quick. You don't have a lot of fuel and you're going to get terrible gas mileage, but boy, it's going to be a quick ride. The other is like a big diesel engine rumbling down the roads of Alberta, hauling, going across the Trans Canada highway and taking its load. It's going to go forever. It's never going to run out of fuel.

And that's the fat metabolism.

That's fat metabolism. And now the next question is, well, who decides? Insulin decides Insulin. Once again, when it comes to any metabolic effect, you need never go further than insulin. There are other hormones that want to pretend that they matter. Thyroid kind of matters. Cortisol kind of matters. Insulin rules them all. And insulin, if it's up, it dictates it's time for sugar burning. If insulin's down, then the body says, all right, it's time for fat burning. In fact, that's where the whole ketogenic aspect comes from. When insulin's down, it is so incompatible with the body storing energy that it literally begins burning more fat than it knows what to do with. It's met its energy needs already, but it can't stop burning fat, and so it starts burning more than it needs. And that more, if you will, becomes ketones. It's sort of A metabolic release valve, like a pressure release valve of a way of saying I'm burning more than I need. And so I've gone beyond what the cell requires. So ketones are going to become a good alternative, but then back to or transition.

Would you think, would you think that the like historically, again, over an evolutionary time span, easily digestible high sugar carbs would have been essentially non existent. Right.

Imagine what we would have had to do to get them. We either had to prepare for battle against a, a hive of bees.

Right, right. And, and when we could find them.

Yes, when we could find them. Or further when we could find, find a digestible carbohydrate, you know, maybe berries or something. Because people need more tubers. Yeah, that's right. We have to appreciate that what we eat is either going to defend itself by claw or by chemical. And a plant doesn't have the advantage of running away, attacking back. So if we dropped any number of us in the wilderness, good luck.

Yeah, yeah. Well, we have to. Even if you're surrounded by plants, we have to understand too that like we might think that historically human beings existed on the kind of vegetables that we have now, but. Or fruits. But all those vegetables and fruits have been genetically altered to a degree that's just beyond comprehension. I mean if you look at the origin plant of corn.

Yeah.

I mean it doesn't look anything like, looks nothing like even.

Look at an apple. Like.

Right, right.

Look at an apple. 100 years ago it was these teeny little crab apples, sour things. Now they're these big juicy sugar bombs.

Yeah, yeah, yeah, exactly.

But the more we eat these, the more sugar bombs and their like, the more glucose is going up, the more insulin has to come up. And now we've come to what I believe is in fact the main driver of insulin resistance. As I transition to insulin resistance, which is too much insulin. And people may hear that and think, hold on, you're talking about insulin resistance. Too much insulin is the main cause of insulin resistance. And it, lest it seem a little unexpected, it is a fundamental biological principle. Too much of something will cause a resistance to that something, whether it's body or soul. If we are exposed to a stimulus, over time that noxious stimulus, it becomes noxious and we try to adapt.

Well, dose matters, right? There's lots of things that are healthy. That's exactly right in proportionate dose. Okay, so now we're eating carbs continually, all the time. So we're relying on this fast energy source. One consequence of that is storage in fat. Yes, one Consequence of that is if there's too much storage in fat is that triggers its own form of insulin resistance. But you also alluded to an insulin resistance. I believe that's merely a consequence of insulin that spikes too high.

That's right.

So there's multiple reasons for insulin resistance in a heavy carb loaded diet.

Oh, yes, all of them become relevant there. Yeah. So we've now kind of gone to both here. The slow insulin resistance is the slow and steady growth of the fat cell, which we outlined earlier. And that's a consequence of insulin being up, telling the fat cell to grow, and the fat cell saying, okay, insulin, what do you want me to grow with? It's the calories. So you have to have both for a fat cell to grow, an insulin stimulus and sufficient calories to fuel the growth. Then we have the fast insulin resistance, I mentioned inflammation, that is one. And then the other one, that is the main one I argue is too much insulin itself. And then once the body becomes insulin resistant, now you really can start going down that list of chronic diseases that are the top 10 killers and to a one, you can see how insulin resistance is either the main contributor or one of the main contributors. Like all of it. Like type 2 diabetes is entirely a disease of insulin resistance, where over time, if you have two variables, the insulin and the glucose. One of the great tragedies from a metabolic scientist with diabetes, type 2 diabetes, is that we have a glucose centric paradigm. Just to use this as an example of how insulin resistance contributes to disease, the conventionally trained clinician only looks at the glucose. They may not have even ever measured the insulin. And when I give these kinds of talks to physicians, they can't even wrap their head around insulin being a marker that matters. And yet the irony is it's the one that matters most. Because over the life of the person with type 2 diabetes, their insulin has been coming, been going higher and higher and higher, but the glucose is staying normal.

Blood glucose, blood glucose.

And so when they come in for their annual checkup, the physician just says, well, glucose is normal, so you're good, but you have high blood pressure. Well, guess what the leading cause of high blood pressure is? Insulin resistance. Or they may say you have fatty liver disease.

Right.

Guess what the leading cause of fatty liver disease is. You have early signs of cognitive decline or dementia.

Right. None of those are glucose.

Exactly. Right, yes. Where now the brain's becoming insulin resistant. And if we could shift the paradigm to an insulin centric paradigm that they would have detected, and then it's 20 years later where they finally see, oh, your glucose is high. Well, now.

But it's worse than that, I think, if I remember correctly, because. So you said that one of the ways that physicians are marking whether you're healthy is to look at your blood glucose levels. But they age correct those so that the norms for you at 50.

Yeah.

What would be normal at 50 is diabetic at 20. But that makes no sense because if your blood sugar levels are as high at 50 as they would have been in 20 if you would have been diagnosed diabetic, it's just as bad for you at 50. In fact, it's an insane correction.

In fact, it's even more pernicious if you look over time at what the diabetic cutoff used to be over the past 70 or so years since that became a marker. So that's been gerrymandered as well, slowly coming down. And you would say, well, why bring it down? It's because the easier it is for people to stumble over, the easier it is to diagnose, and then the easier it is to say, I need to give you a drug. And that is what I believe is partly at the heart of the glucose centric paradigm. You can't drug insulin. It's too stubborn. There's no drug that's going to push your insulin down, but there are drugs that will push your glucose down. And so it's a hell of a way to diagnose someone with a problem sooner and give them a drug prescription. Multiple drug prescriptions. But the great irony, or I would say irony, as if it's an innocent mistake.

Murderous irony.

Yes. The more the clinician is pushing the glucose down. Indeed, with some medications that push the insulin up even higher, they actually kill the patient more, even though you've corrected their blood glucose problem. Just the wrong marker. Proof. It's not the marker that matters. It's certainly not the marker that's causing disease. So the more aggressively you're giving the diabetic more and more insulin, type 2 diabetic, more and more insulin to push the glucose down, they become three times more likely to die from heart disease. You're literally tripling their risk.

Which drugs do that?

Yeah, that will be drugs like a class of drug called sulfonylurea, which is what's called an insulin secretagogue. It basically takes the beta cells and says of the pancreas that make insulin, say, hey, we know you're already working overtime. It's not enough. We need to put you in the gulag you gotta work double shifts and we've bumped up.

That drives the insulin levels up. That drives the sugar levels down.

Yes.

So again, but it increases insulin resistance across time.

That's exactly right. So they get fatter and they die faster. Cancer risk doubles, Alzheimer's risk doubles. Because those aren't.

How common are those drugs?

Oh, extremely common. Even more common is just giving the type 2 diabetic insulin directly. You're literally giving them more of the very thing that's killing them.

Okay, so distinguish between type 1 and type 2 diabetes. Before we go on.

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Well, you and I can both. There aren't a lot for some Canadians to be proud of. But Banting and Best, two legendary scientists from Ontario, were the first to discover the one hormone that was absent in type 1 diabetes at the time. It was called juvenile onset because it was something that would manifest around the age of 10 years old or so. But in type 1 diabetes, that is when the body has killed its own beta cells. Is that an immune problem, an autoimmune disease?

It's an autoimmune disease. Yep.

So the body has, for some reason said to the beta cells of the pancreas, you don't look familiar. So we're going to kill you. And so the person has no beta cells, no insulin, no way to control metabolism, and they kind of burn to death, if you will, in a way.

What happens to type 1 diabetics if they eat nothing but fat?

Yeah, well, that's a great question. In fact, this allows a Transition into the actual dynamics of fat cells. So if you had a. In fact, if you look at the earliest diet that was given to diabetics, type 1 diabetics, before they started using insulin, it was almost entirely carnivore.

Yeah.

You looked at these old fashioned prescriptions, it was this much fatty meat and it would say, fatty meat, don't eat meat that is too lean.

Right, right.

It's because these are fuels. Fat is a fuel that doesn't need insulin to tell it what to do. It can get into the cells of the body, the brain, which doesn't use fat. It readily uses ketones, which you'll make plenty of if you're burning a lot of fat. And so that would be the best way to ensure the type 1 diabetic lived as long as possible. But the great tragedy, when we discovered what was missing. Professors banting and best by giving these patients insulin, that changed things. Now these people could live a long, happy life. But it shifted the paradigm, which was eat whatever you want and cover it with your insulin. That is a term. Any parent listening to this who is a child with type 1 diabetes will have heard this asinine advice. This is a disease of not metabolizing glucose. Why would we tell them?

And that includes carbohydrates.

Oh, yes, they're converted to glucose. That's exactly. Yes. Thank you. Yes. So all dietary carbohydrates are gonna be converted to blood glucose to some degree or another. Some. A lot like the sugar bomb apple. Some very little like a cruciferous vegetable like broccoli or something.

The inedible vegetables. Yeah, exactly.

The ones that you put in front of a newborn, a young little toddler, and they're going to push it off the plate because they inherently know I don't want this. Yeah. So the type 1 diabetic, what used to be a carnivore diet basically became the same standard high carb diet. But you look at these poor kids with type 1 diabetes, it is a life of constant fluctuations, the constant anxiety. And yet now we know in human studies what happens if you control the carbs, get them off the roller coaster. Sure enough, it flattens, it's a flat line. And their insulin dose just plummets.

Yeah.

And depending on how much you have to pay for insulin, that's a wallet saving therapy.

Let me summarize. So human beings have two metabolic pathways. The one that we relied on until very recently wasn't the carb pathway. That's really an emergency. And windfall metabolic system, quick burning, limited Supply. Yep.

Yeah, I mean we have, we have enough carbs to fast. Like truly, if a human was just relying on their. Even you wouldn't even have to go that dramatic. You have someone fast for 24 hours. They've essentially burned through all of their mobilized carbohydrate storage, their glucose storage. That's done, it's gone. And in fact that's going to coincide perfectly with ketogenesis, with the ramping up of ketones in the blood.

So there's, there's an additional. We'll go, go sideways here for a second. While there's an additional issue there that isn't well understood as I understand it, that historically, again, over an evolutionary time span, there would have been lots of times when we had access to like no carbohydrates. Okay. So now. And maybe some of those times as well, to not much protein and fat. So just not much food.

Yeah.

Okay, so what happens then? Well, you go into autophagy, right? So what happens is your body starts to digest its own tissues. Now those could be fat, the fat, which would be fine because that's what it's there for. But if you go past that, then there are more. There are tissues that are starting to be digested, auto digested, that aren't merely for storage. But the body has a hierarchy of self consuming. So it consumes damaged tissue first, which is of course what it would do because if you digested healthy tissue first, you would just die. So that's a stupid solution. Now the advantage to digesting damaged tissue is that when you have access to food again, you regenerate. And so one of the consequences of being reliant on an emergency food supply continually carbohydrates, is that you never enter an autophagy condition and so you don't repair yourself very well. Well, first of all, do you think that's true? I mean. Oh yeah, I've looked into this and that it looks to me like a carnivore diet mimics autophagy. And maybe that's why they're effective.

In fact, not only mimics, it enables it like just to be clear, but you're, you're touching on like this topic of longevity. Yes, which I have, I have followed the, the modern. I don't want to hijack the question.

Go ahead, hijack away.

Okay, well, yeah, with longevity you'd think, well, what is a metabolism scientist going to say? Everything. I have everything to say about longevity because it is this process of the cell constantly wondering how am I doing? Is it time to Build or is it time to break? And one of the quirks of longevity or aging is that a cell actually needs to go through both that. I have looked, I have looked with. And guess who decides whether it's building or breaking hormones.

Yeah. Well, life is optimized death. Right. You have to die continually. The excess and the. What would you. Everything excess about you and everything is malfunctioning, has to die in order for you to propagate yourself across time. So life isn't life. It's. Life is a balance between growth and death.

Right.

So you want to optimize death.

Yeah.

And you optimize death with autophagy. As far as I can tell, carbohydrates, diet, or a carnivore diet optimizes that or can optimize it.

Okay.

So it takes you out of this emergency food supply.

Yeah.

That makes you fat. I want to ask you about insulin resistance now. Now your insulin levels are chronically too high because you're eating too many carbohydrates. What? And tell me the mechanism for insulin resistance. And then tell me about its cascading effects so that we can understand the relationship between insulin resistance and diabetes and Alzheimer's disease and obesity and heart disease and cancer and pretty much everything is aging, for that matter. Yes, yeah, yeah. Blindness, diabetic neuropathy, et cetera, et cetera. So let's walk through that. Eat too many carbohydrates, Your insulin levels are chronically high.

Insulin resistance follows, then you get insulin.

Okay, how. How does it follow? What happens?

Yeah, yeah. Well, in fact, depending on. So everything you just asked is. Is so substantial that not only did I want to put it into a book, but in even a Peterson Academy course, it is an answer of about seven hours or so. But it is so relevant because again, it's the most common problem. So when insulin is elevated for too long, it literally starts to certain cells, not all cells. And this is one of the reasons why insulin resistance is so pathogenic. It's because some cells become deaf, some cells don't. And so as you have insulin going up higher and higher, to the deaf cells, that's not so much a problem. But to the cells who are as acutely sensitive as they were before, now it's stimulating too much. So one interesting example that we haven't even mentioned is infertility. As a Bible believing fellow, I feel very strongly that it is a commandment to reproduce. So anything that compromises reproduction. As a scientist, I'm quite fascinated by the most common forms of. Infertility in men is a problem called erectile dysfunction. The most common problem in women that's a problem of infertility is polycystic ovary syndrome. Both of them are caused by insulin resistance. But it's a perfect example of the kind of two sided problem where insulin resistance is on one side of the coin, insulin isn't working very well, but you always have the other, which is that insulin is elevated. So these are two sides of the same coin. And these two problems of infertility, which again, we hadn't even mentioned yet, are both a reflection of one or the other. So in the case of polycystic ovary syndrome, most common infertility in women, people don't appreciate that all estrogens. Or maybe I'll back up. In order for a woman to have a normal ovulatory cycle, she has to have a big spike in estrogens. So there has to be a big estrogen spike and then that enables, it facilitates ovulation. If she doesn't have this big spike in estrogens, the eggs in her ovaries are able to grow, but one never becomes the dominant and actually ovulates. And if one doesn't ovulate, all of those eggs stick around, then they become cysts. That is the heart of the problem here. Well, it's the manifestation of the problem. Most people don't appreciate that most all estrogens were once testosterone, that in men and women, all of the estrogens circulating through the body and in the women critical to ovulation have to be converted from testosterone. Well, there is an enzyme called aromatase, and her ovaries have a lot of aromatase, whereas the testes in her male counterpart have relatively little aromatase. He's still converting some of his testosterone to estrogens, but not as much. She's doing it a lot more. Insulin inhibits aromatase. So in her body, her ovaries, which maintain an exquisite insulin sensitivity, are looking at all of this insulin and responding, saying, okay, insulin, among the many things you're telling me to do, you're inhibiting the aromatase, which means I have all this testosterone and I can't convert it to estrogens. So not only will she not have the estrogen spike, thereby not ovulating, but she will also have too much testosterone, giving her some of the other symptoms of pcos, like male pattern baldness or more hair on her body and acne and other problems.

Have people been using low carb diets to treat particularly?

There are case reports published the most Common medication that is given to a woman with pcos, even if the physician doesn't know. To test for insulin resistance, they give a prescription for a drug called metformin, which is the most widely used insulin sensitizing drug. And it will help, although it's not solving the problem, it's just sort of masking it.

So you said erectile dysfunction.

Well, so that's the male counterpart, right? Yeah.

So listen to that. Men who are listening to this program. Because erectile dysfunction obviously doesn't only affect reproduction, it affects sex.

Yes.

And so if you're not able to get it up anymore, one of the ways, in principle you could treat that is by reducing your carbohydrate intake dramatically.

Oh, yeah.

Which would also stop you from dying, which is like a good side effect.

Not only will it be more attractive, but more capable of taking advantage of that physical attraction.

Right, right.

By not suffering from erectile dysfunction.

So really what's happened is we've really, because we've become so a society of such insane abundance, we've deviated from our normal diet to an emergency rare diet. So now we can just eat the diet we would eat in an emergency. That was rare all the time. And it turns out that that's, that's not a good idea.

No, I mean, not for.

In the long run.

Yeah. For the sake of the species. Yeah. And then with erectile dysfunction, it's not a problem of the insulin being high, but, but normal physiology in the man and women in various locations of the body is such that when insulin flows through a blood vessel, if the blood vessel is insulin sensitive, the endothelial cells that line the blood vessel wall, they will see the insulin and it will stimulate the production of a molecule called nitric oxide, which will induce vasodilation, an absolutely critical process for erectile function. But those blood vessels become insulin resistant. And now the normal process of vasodilation in the man having normal erectile function is compromised.

Okay, so let's step back now. So you said insulin levels rise and then a variety of tissues in the body become insulin resistant because they don't. They can't tolerate being overstimulated, but some of them don't. And so they are overstimulated. Okay.

And then you, you, you ovaries included.

Right, right. And we talked about the reproductive consequences. But what other tissues become hyper. Are in a hyper reactive state because of too much insulin?

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Yeah, right. So there are, there are not many. Most of them go the way of the insulin resistance, like the man's side of things. And that's like, for example, what causes Alzheimer's disease, where the brain's becoming insulin resistant. But the insulin sensitive side would be a tissue like the liver, where one of insulin's effects at the liver is to tell the liver to make fat. Now, the liver's more complicated. I kind of joke with my students that when it comes to metabolism, the liver's the soccer mom. It is sort of giving, it knows what to do with everything. You have a problem, the liver can solve it. It is the ultimate handler. It is the nexus of all nutrient metabolism, whether it's lactate or ketones or fats or glucose or proteins, amino acids, the liver handles all of them. It is the soccer mom. It does everything. And when it comes to insulin, one of the many responses to insulin is to tell the liver to make fat. That effect is as insulin sensitive as ever. And so now in the high insulin insulin resistant body, the liver is seeing all of that insulin. And one of its effects is to tell the liver to make more fat.

Thus is that when you get fatty.

Liver, then you have fatty common liver problems.

We also now are seeing signs of fatty liver in children.

Oh yeah.

Which is historically unprecedented. Not only alcohol does that.

Alcohol does, right? But too much fructose, another pointing the.

Finger, like in high, in high fructose corn Syrup, which is subsidized to a degree that's absolutely stunning and which is in virtually every processed food.

Yes, yes. So so much of what I rage against when it comes to the government getting involved is it's happened, it's, it's subsidizing the, the most problematic things like high fructose corn syrup. But even if you and I were drinking orange juice right now, that's a straight shot of glucose or apple juice. You know, if we were meant to drink that fructose, then the, we wouldn't even have to eat it with the apple. You know, you, you think you and I could drink four apples worth of fructose and not even think about it?

Right.

And yet we'd never want to sit there and eat four apples because the fiber and things would want to slow it down and we'd feel a little more full. And so we just, we naturally wouldn't focus as much on it. But this environment that we live in, it's almost like we are eating for winter all the time.

All the time.

Because fall used to be the time of abundance. It was fall when we would reap the harvest. It was fall when the fruits, when the plants would be kind of coming into season and boy, let's get ready.

Yeah, like let's lay on some fat like a bear because winter's coming. But in the north that was not good.

Right. Winter never comes. And so anyway, as we go from top to bottom, you can find insulin resistance. You know, the brain, just to find point on it. The brain is one of the high metabolic rate organs in the body. Right now we're having a stimulating conversation. It is entirely possible. I bet our brain is number two or probably number two. Highest metabolic rate at the moment because it's so hungry, it's so demanding. Even when we're sleeping, it's busy, so it needs to be fed constantly. The brain doesn't burn fat for energy for reasons that we don't really understand. Actually the brain is its own hybrid though. Burning glucose, blood sugar or ketones.

Yeah.

Now there is in fact a man whom I love and admire is a scientist in northern Ontario and Stephen Cunane. He presented this idea of a shore based evolution suggesting that the reasons humans departed, in part, we are the only land based mammal born obese.

Fuller pushed that theory too, by the way.

Really?

Yeah, yeah, yeah. Well, it accounts for lots of things like female fat distribution.

Yes.

Kind of webbed hands and feet, our ability to swim, hairlessness, omega 3, the.

Value of omega 3 fats. You know, eating these kind of.

Well, where else would you live if you could?

Not in the Paris of. No, no.

On a warm beach where there were lots of shellfish.

Absolutely.

That's pretty straightforward.

It would be a good way to do it. So the brain has these two fuels, glucose and ketones. Ketones are utterly unregulated if they're going up. In fact, one of the things I love disabusing my students of is the false idea that glucose is the preferred fuel for the brain.

Yeah, right.

Every sort of knuckle dragging, mouth breathing, professor will just spread. Spout that off without actually knowing a thing about brain metabolism. The reality is, if someone has glucose levels at 5 to 6 millimolar in a normal range, and they're fasted or on a ketogenic diet, even when their ketones get to 1 or 2 millimolar. So, over here, the brain has.