A Conversation with Dr. Ben Bikman | Jason Fung

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Hey, Ben, good to have you here. Thanks for, thanks for joining us.

Oh, yeah, my pleasure. Thanks, Jason.

Yeah. So Dr. Bickman is a good friend of mine. We've known each other a while and he's one of the smartest guys I know. Honestly. He's really looked at really in a deep way the sort of root causes of disease. And he's not a physician, he's a researcher. And I just want to maybe go back over a little bit of your background about how you sort of got to where you are and then maybe your book why We Got Sick, which is really very insightful about sort of root causes and sort of where we stand because our focus here is longevity. So, you know, obviously trying to avoid why we get sick is so important. So yeah, why don't we start there?

Yeah, yeah. So as you noted, I am a biomedical scientist and a professor. My research focus as a scientist is to study insulin. In. As one main theme in. In addition to that, my lab focuses on mitochondrial function. We do a lot of mitochondrial work, but it's all thematic of trying to get a better understanding of the metabolic influence in chronic disease. You know, for example, you know, we have published a few papers over the past couple years looking at some of the mitochondrial problems in Alzheimer's disease. We have published a handful of papers looking at the differential effects of insulin versus ketones on fat tissue metabolism. So all of these things are just offshoots of our central focus, which is to just understand the role of metabolism in disease and my evolution. You'd mentioned just providing a brief overview. There was actually one that started with an interest in muscle tissue. But then in the late 90s, I stumbled across a paper that had just been published that documented how fat tissue was, as it grew, as it expanded, was capable of secreting pro inflammatory proteins and that these pro inflammatory proteins, called cytokines, were then capable of causing insulin resistance, which was this foundational problem with type 2 diabetes. All of this was a. An app was a total revelation to me that I was certainly aware of the twin epidemics of obesity and type 2 diabetes, but I had not even been interested enough to start to learn about what was the bridge connecting them. What was it about this fat tissue that was causing insulin resistance, the foundational problem with type 2 diabetes, and that there wasn't. There was two things that really set me on the path that I'm still on to this day. One, it was the learning that inflammation had a metabolic consequence. And that was in fact, something that I went on to study for my dissertation work and my postdoctoral work, my fellowship. But at the same time, what blew my mind at the time was learning that fat tissue is an endocrine organization. That was an absolute revelation to me. I'd not been taught that before, even though in hindsight there were hormones that had already been identified from the fat tissue, the most famous of which was, of course, leptin, and still is. But I didn't know that at the time. And it set a curiosity, this burning wonder in me to want to learn more about fat tissue. And so what had started as an academic career that I thought would be mostly devoted to muscle tissue, and we do muscle work, it really quickly became a career that was more interested in fat tissue. And then to kind of really make the long story short, during my postdoctoral work, we had a protocol that required us to be injecting low doses of insulin in animals. And yet they were pear fed. So the animals that were getting the higher levels of insulin, they could only eat as much as the other animals that were not getting insulin. They were just getting like a placebo, a saline injection. So they were eating the exact same amount, and yet they had much more fat than the other animals did. And then I. That was a challenging thing. And I assumed we'd been making. We'd been. There had to have been some mistake that the animal technicians were letting them get more food. And we really had to scrutinize the protocols and confirming in the end that, no, they weren't getting any more food. They were eating the exact same amount of food, and yet they were somehow fatter. And then it was a couple years later that when I got hired as a professor, that someone I went to church with, I was sharing this with them. And he said, you sound a lot like this guy Gary Taubes. And then I read Gary's book and came out of the closet as a calorie Skeptic in that, in that, in the rest is history.

You know, I love that because, you know, I went to medical school in the 90s and that was sort of the prevailing wisdom too is that fat, the fat cell is this sort of inert sack of doorknobs sort of thing. Right. So it's this idea that there's no regulation. It doesn't do anything interesting. You know, it's like if you have, you know, extra doorknobs, you throw them in the sack and you can take them out of the sack, you can put them in the sack, but the sack doesn't actually do anything. And that was the idea with fat cells. Right. And that's, that was the prevailing wisdom and I think to some extent probably is because when you listen to some of the people talk even so called experts and stuff, it's like, oh, they clearly have no idea that the whole thing is completely regulated by hormones, predominantly insulin, because it's not a sack of doorknobs. There are times that it's, the fat cell can store fat and there's times that it can release fat. It can't release fat all the time and it can't store fat all the time. There's a sort of hormone that lets it go in, like, like, lets the energy go in, lets the energy go out. And the fat cell itself has endocrine effects. And that's, you know, that's something that I think is just so important. Like it's, if you don't understand that, that's, that's why there's so much misconception that oh, you can just eat a few more calories and it's just going to go into fat stores.

Yeah. In a certain situation that's exactly right. And people like to assign a certain intelligence to cells. That is not Warran cell doesn't have the intelligence to act on its own and it doesn't know what to do because it wants to play nice with the rest of the body. But how can a fat cell know what's happening in the intestines? Because the intestines will tell it. Or how can the fat cell know what's happening in the blood? There will be a signal. One cell type will tell another cell type. Okay, here's what's going on and this is what I need you to do. And type 1 diabetes is the most unavoidably obvious example because as much as there are a handful, it's a small handful of hormones that do have an influence on fat cells. Thyroid hormone has an Influence. Cortisol has an influence, progesterone has an influence. And yet all of those variables can be present and if we remove only one hormone, none of them matter. And type 1 diabetes is the perfect example. And it also completely breaks apart this whole idea that if there's a lot of energy in the blood, in other words lots of calories, well, the fat cells will just take it in. But so in the type 1 diabetic, if they are, if there's no insulin, there, there's this seemingly impossible situation based on just a purely caloric view. Because the blood is filled with calories, glucose levels, there's 10 times too much glucose free, fatty acid levels in the blood are through the roof. There's even tons of amino acids in the blood which the fat cell isn't going to really use anyway. But suffice it to say, every, the cell, the, the blood is loaded with calories and yet the fat cell can't take in and store a single speck of it because it has to wait. It's an obedient child, which I pretend I have several of sometimes because my kids are so rambunctious. But the fat cell is waiting for its orders. It's waiting to be told what to do. And in the absence of insulin, it cannot, not only can it not hold, pull in and create fat, it cannot hold on to any fat. And so even though the blood is filled with calories, the fat cell just continues to let its own calories out. This is why to me, people want to try to complicate the issue. Now neither of us is saying energy doesn't matter, but insulin is an absolute unavoidable signal that tells the fat cell to store fat. Now you need the calories to create the substance of that storage. You know, you can't have one without the other. If you try to increase insulin without having a sufficient amount of energy, then the person just becomes the central nervous system shuts off because you've locked all the energy away and there's nothing left for the brain to eat. The person goes unconscious. So that's incompatible with life alternative. You can have calories through the roof, and if there's no insulin, you can't store that energy. And once again, it's a death sentence, albeit slightly slower than the other paradigm I just mentioned. So you cannot have obesity without both. But you and I, I know where you and I are so aligned is that we focus, we beat the drum that no one else, that so few are willing to beat, that yes, energy matters. You must have a sufficient amount, but there must be, it must be preceded by a stimulus telling the fat cell what to do with that energy. And that's insulin.

Yeah, absolutely. And the funny part about it is that every cell in the body is the same way, right? Like, no, because, you know, there are thousands of cell, like trillions of cells actually, but thousands, hundreds of cell types. Probably it needs to be coordinated. So therefore you must coordinate it with signals. And most of those signals are hormonal signals, and in this case, it's the insulin. So in type 1 diabetes, of course, there's no insulin. That's the pathology of the disease. And that's where if you don't have insulin, this blood, the fat cell can't take in those calories. And therefore people, you know, even with all those calories, they, they just lose weight. They, they, they become extremely skinny until they die, basically. So what happens in this situation, in, in this situation, the oppos where you have too much insulin? What happens there?

Yeah, so then this is what I like about this segue is that it allows us to present the paradigm that type 2 diabetes is the opposite problem of type 1. That I think it's one of the great tragedies of modern medicine that we have lumped these two total opposite diseases into one family because they share one single thing in common, namely that they both can eventually manifest with high glucose, glucose levels. But how they get there is to exactly opposite scenarios. So it's, it's unfortunate because then we believe they need to be treated the same way, which just compounds the problem. So when there's too much insulin, you now start to create insulin resistance. So I would, I would say there are two things that I, I'd want to emphasize here, and then the conversation can proceed on either of these as you see fit. So on one hand, chronically elevated insulin causes insulin resistance. I have, I've published reports on this. Many other basic scientists have published reports on this. Clinicians have observed this. The, the where with type 2 diabetes, there's, there's. I think it's important to note that in type 2, in true type 2 diabetes, insulin never drops to zero. That does not happen. It has been really, really high. Sometimes it comes down a little, but it is still multiples higher than it ever was before they started on that disease progression. So the idea this, this kind of cleverly false language of insulin production becomes insufficient to control glucose. Well, that's a pretty subjective term. It's. They're still loaded with insulin, and by putting the type 2 diabetic on even more insulin, they become more insulin resistant. So a point that I was getting around to and distracted myself is that every cell type we've used in the lab, muscle cells, liver cells, neurons, brain cells, if they are exposed to even physiological, but higher chronically elevated levels of insulin, they become insulin resistant. You can create all, whether it's cells, whether it's animals. I've done that and published those results. Whether it's humans, that's been published in all three commonly used biomedical models. Cells, rodents, humans, if you increase the insulin and keep it there for a period of time, they become insulin resistant. And lest someone think, well, I'm not a dish of cells or a rodent, I'm a human and I eat when I want. Yeah, but you probably eat a lot of starches because 71% of all calories consumed globally are carbohydrates. And you're probably like the average individual nowadays who eats about six times a day. And considering that it can take insulin up to three or four or five hours to come back down to normal, depending on how much you ate and what you ate and how insulin resistant you. Not a stretch to assume that most adults and children are probably spending every waking moment in a state of elevated insulin because they wake up in the morning, insulin has finally had time to come down overnight, and then they spike it with starchy, sugary breakfast. And then right when the insulin's about to start coming down, they spike it again with a mid morning snack. And that just continues until their evening snacks. And now they're going to bed hyperglycemic and hyperinsulinemic, and they're not sleeping well. But anyway, so one chronically elevated insulin causes insulin resistance.

Let's pause on that for a moment because I think it's a really, really important point because this is the crux of the matter. So. And a lot of doctors simply don't understand this. And I think it's actually crucial. Insulin resistance, we all agree, everybody in the world pretty much agrees is a problem, if you're insulin resistant, then you're much higher risk of all kinds of other diseases, heart disease, cancer, and all this stuff. So if you take the next step and you say, okay, insulin resistance is a problem in everybody, what causes it? And like 9 out of 10 doctors will be like, we don't know. It's like, what the hell, right? You don't know. So insulin resistance being such a huge problem, and it's been, you know, syndrome X. Gerald Reven identified it, like, at least by the 70s. So we're talking about 50 years of sort of medical research and you're telling me that and it's, you know, three, four, five times higher. Diabetes is three, four, five times higher than it was in the 70s in certain countries it's like 10 or 20 times higher. So it's like you have this huge epidemic. You've been studying it for 50 years. You've known it. Insulin resistance is a problem for 50 years. So what causes it? And the answer is we don't know. It's like, okay, well, do you have any idea? And again, I've asked lots of doctors this, by the way. They are like, I have no idea. I asked trainees this and they have no idea because they've never been taught. And I'm always thinking, why don't you actually think about this problem? Because if you think that the problem is hyperinsulinemia, right, which is too.