What They Aren't Telling You About Glucose and Insulin Resistance | Dr. Benjamin Bikman

We're eating carbs continually, all the time. So we're relying on this fast energy source. One consequence of that is storage and 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. Yes. 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 then the fat cell saying, okay, insulin, what do you want me to grow with? Ah, 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, 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 them, 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, 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. 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. Yes. Where now the brain's becoming insulin resistant. And if we could shift the paradigm to an insulin centric paradigm, they would have detected. And then it's 20 years later where they finally see, oh, your glucose is high.

But.

Well, now.

Yeah, 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, it, that, that makes no sense. Because if, though 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. Oh.

In fact.

So that's. 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.

Yeah.

Over the past 70 or so years since that became a marker. So that's been gerrymandered as well, coming down. And you would say, well, why bring it down? You. 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 glucocentric paradigm. You can't drug insulin. It's too stubborn. There is no drug that's gonna 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 smart 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, and they become three times more likely to die from heart disease. You're literally tripling their.

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 got to work double shifts and we've bumped up.

It 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 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.

Yeah, good. 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. 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. 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 look at these old fashioned prescriptions, it was this much faster, 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. This is a term. Any parent listening to this who has 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 going to 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 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. And depending on how much you have to pay for insulin, that's a wallet saving therapy.

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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, 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. Hormones.

Yeah. Well, life is optimized. Death, right?

Well said.

You have to die continually. The excess and the what. What do 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.