Paul Saladino, MD

So if you have diabetes, yeah, don't eat as much honey as you or I, But small amounts of honey, probably beneficial. And honey didn't cause the problem. We have to point the weapons at the actual cause. If you point the weapon at the wrong cause, you're just putting your resources where they shouldn't be. And as we talked about, ApoB, wrong place to put your weapon. Insulin resistance.

So if you have diabetes, yeah, don't eat as much honey as you or I, But small amounts of honey, probably beneficial. And honey didn't cause the problem. We have to point the weapons at the actual cause. If you point the weapon at the wrong cause, you're just putting your resources where they shouldn't be. And as we talked about, ApoB, wrong place to put your weapon. Insulin resistance.

So if you have diabetes, yeah, don't eat as much honey as you or I, But small amounts of honey, probably beneficial. And honey didn't cause the problem. We have to point the weapons at the actual cause. If you point the weapon at the wrong cause, you're just putting your resources where they shouldn't be. And as we talked about, ApoB, wrong place to put your weapon. Insulin resistance.

Glucose, fructose, wrong place to point your weapon. Point your weapon at insulin resistance. The same thing with fruit. If you look at someone who's trying to make a case that fructose is harmful, invariably they will cite studies in animals who don't have the same biochemistry.

Glucose, fructose, wrong place to point your weapon. Point your weapon at insulin resistance. The same thing with fruit. If you look at someone who's trying to make a case that fructose is harmful, invariably they will cite studies in animals who don't have the same biochemistry.

Glucose, fructose, wrong place to point your weapon. Point your weapon at insulin resistance. The same thing with fruit. If you look at someone who's trying to make a case that fructose is harmful, invariably they will cite studies in animals who don't have the same biochemistry.

They do much higher rates of de novo lipogenesis when they are presented with fructose, meaning if you give fructose to a rat, it's making much more of that into body fat than we do as a human. We do 1%. You give a human, 1% of fructose goes to fat via de novo lipogenesis. Most of it goes to glucose, it goes to glycogen, it goes to lactate.

They do much higher rates of de novo lipogenesis when they are presented with fructose, meaning if you give fructose to a rat, it's making much more of that into body fat than we do as a human. We do 1%. You give a human, 1% of fructose goes to fat via de novo lipogenesis. Most of it goes to glucose, it goes to glycogen, it goes to lactate.

They do much higher rates of de novo lipogenesis when they are presented with fructose, meaning if you give fructose to a rat, it's making much more of that into body fat than we do as a human. We do 1%. You give a human, 1% of fructose goes to fat via de novo lipogenesis. Most of it goes to glucose, it goes to glycogen, it goes to lactate.

I mean, fructose doesn't turn into fat in humans anywhere near like it does in animals. So you can't look at animal studies for fructose metabolism because it's completely different. It's completely different. And if you look at human studies with fructose, they are, as you suggest, invariably giving pure fructose.

I mean, fructose doesn't turn into fat in humans anywhere near like it does in animals. So you can't look at animal studies for fructose metabolism because it's completely different. It's completely different. And if you look at human studies with fructose, they are, as you suggest, invariably giving pure fructose.

I mean, fructose doesn't turn into fat in humans anywhere near like it does in animals. So you can't look at animal studies for fructose metabolism because it's completely different. It's completely different. And if you look at human studies with fructose, they are, as you suggest, invariably giving pure fructose.

There's not a single fruit or honey or anything on the planet where you're getting pure fructose without glucose. And in the gut, It's all symporters. It's all transporters that need glucose and fructose to move across the gut lining. And so if you get free fructose in the gut, it gets stuck in the gut. Well, what happens if fructose gets stuck in the gut?

There's not a single fruit or honey or anything on the planet where you're getting pure fructose without glucose. And in the gut, It's all symporters. It's all transporters that need glucose and fructose to move across the gut lining. And so if you get free fructose in the gut, it gets stuck in the gut. Well, what happens if fructose gets stuck in the gut?

There's not a single fruit or honey or anything on the planet where you're getting pure fructose without glucose. And in the gut, It's all symporters. It's all transporters that need glucose and fructose to move across the gut lining. And so if you get free fructose in the gut, it gets stuck in the gut. Well, what happens if fructose gets stuck in the gut?

It causes overgrowth of pathogenic bacteria. And then you get lipopolysaccharide, you get endotoxin. So they've done these studies in animals where they'll give free fructose and they'll give something that blocks TLR4 or 5, toll-like receptor 4 or 5, which is what endotoxin triggers eventually. And the negative effects of fructose are essentially abolished. Wow.

It causes overgrowth of pathogenic bacteria. And then you get lipopolysaccharide, you get endotoxin. So they've done these studies in animals where they'll give free fructose and they'll give something that blocks TLR4 or 5, toll-like receptor 4 or 5, which is what endotoxin triggers eventually. And the negative effects of fructose are essentially abolished. Wow.

It causes overgrowth of pathogenic bacteria. And then you get lipopolysaccharide, you get endotoxin. So they've done these studies in animals where they'll give free fructose and they'll give something that blocks TLR4 or 5, toll-like receptor 4 or 5, which is what endotoxin triggers eventually. And the negative effects of fructose are essentially abolished. Wow.

So the negative effects of fructose at the level of the gut and humans is driven by endotoxin. And we don't get more endotoxin when we eat fruit. In fact, I think you could easily make a case that when you eat a blueberry or you're eating a persimmon or you're eating orange juice, endotoxin, which is lipopolysaccharide, goes down.

So the negative effects of fructose at the level of the gut and humans is driven by endotoxin. And we don't get more endotoxin when we eat fruit. In fact, I think you could easily make a case that when you eat a blueberry or you're eating a persimmon or you're eating orange juice, endotoxin, which is lipopolysaccharide, goes down.