Dr. Ben Bikman

So the hypertrophic fat cell, in order to ensure its own survival, becomes insulin resistant to prevent further growth, inadvertently thereby flooding the body with free fatty acids to be stored elsewhere, and two, becomes very pro-inflammatory in order to correct its own hypoxia, but in the process flooding the body with pro-inflammatory cytokines, things like C-reactive protein, for example, which is increasingly measured on blood tests.

So the hypertrophic fat cell, in order to ensure its own survival, becomes insulin resistant to prevent further growth, inadvertently thereby flooding the body with free fatty acids to be stored elsewhere, and two, becomes very pro-inflammatory in order to correct its own hypoxia, but in the process flooding the body with pro-inflammatory cytokines, things like C-reactive protein, for example, which is increasingly measured on blood tests.

But the combination of these two things, high free fatty acids and high inflammation is a wicked combination. Because now you start promoting the accumulation of these other types of fats in the body called ceramides within the cells. And when these two signals come to a cell, promote ceramide development or accumulation, now those cells become insulin resistant as well.

But the combination of these two things, high free fatty acids and high inflammation is a wicked combination. Because now you start promoting the accumulation of these other types of fats in the body called ceramides within the cells. And when these two signals come to a cell, promote ceramide development or accumulation, now those cells become insulin resistant as well.

But the combination of these two things, high free fatty acids and high inflammation is a wicked combination. Because now you start promoting the accumulation of these other types of fats in the body called ceramides within the cells. And when these two signals come to a cell, promote ceramide development or accumulation, now those cells become insulin resistant as well.

Whether it's the brain, whether it's the muscle, whether it's the liver, or the blood vessels promoting hypertension. This is why I have a fat first focus, that fat cells are the first domino to fall. That when the fat cells become insulin resistant, that's that earliest stages where the insulin's going up, but it's all still enough to keep glucose in check

Whether it's the brain, whether it's the muscle, whether it's the liver, or the blood vessels promoting hypertension. This is why I have a fat first focus, that fat cells are the first domino to fall. That when the fat cells become insulin resistant, that's that earliest stages where the insulin's going up, but it's all still enough to keep glucose in check

Whether it's the brain, whether it's the muscle, whether it's the liver, or the blood vessels promoting hypertension. This is why I have a fat first focus, that fat cells are the first domino to fall. That when the fat cells become insulin resistant, that's that earliest stages where the insulin's going up, but it's all still enough to keep glucose in check

you know the muscles are still responding to the insulin pulling in glucose the liver is still responding to the insulin pulling in and storing glucose helping blood glucose levels stay low but once the fat cells have become insulin resistant now pro-inflammatory they start spreading that insulin resistance to like for example muscle and liver now you have the glucose levels start to climb so where where you have other people who may promote or advocate an idea that the muscle becomes insulin resistant first or the liver

you know the muscles are still responding to the insulin pulling in glucose the liver is still responding to the insulin pulling in and storing glucose helping blood glucose levels stay low but once the fat cells have become insulin resistant now pro-inflammatory they start spreading that insulin resistance to like for example muscle and liver now you have the glucose levels start to climb so where where you have other people who may promote or advocate an idea that the muscle becomes insulin resistant first or the liver

you know the muscles are still responding to the insulin pulling in glucose the liver is still responding to the insulin pulling in and storing glucose helping blood glucose levels stay low but once the fat cells have become insulin resistant now pro-inflammatory they start spreading that insulin resistance to like for example muscle and liver now you have the glucose levels start to climb so where where you have other people who may promote or advocate an idea that the muscle becomes insulin resistant first or the liver

I don't agree with that, because if that were the case, then glucose levels would start to climb immediately. They don't. Glucose levels stay low because insulin resistance starts in the very low metabolic rate fat cells, and then it spreads to the higher metabolic rate, higher glucose-consuming tissues, like the muscle, for example.

I don't agree with that, because if that were the case, then glucose levels would start to climb immediately. They don't. Glucose levels stay low because insulin resistance starts in the very low metabolic rate fat cells, and then it spreads to the higher metabolic rate, higher glucose-consuming tissues, like the muscle, for example.

I don't agree with that, because if that were the case, then glucose levels would start to climb immediately. They don't. Glucose levels stay low because insulin resistance starts in the very low metabolic rate fat cells, and then it spreads to the higher metabolic rate, higher glucose-consuming tissues, like the muscle, for example.

There are three primary causes of insulin resistance. And by primary, I mean that literally I can cause insulin resistance in isolated cells, in laboratory rodents, and in humans with all three of these. And that is elevated insulin itself, elevated stress hormones, and elevated inflammatory proteins or cytokines.

There are three primary causes of insulin resistance. And by primary, I mean that literally I can cause insulin resistance in isolated cells, in laboratory rodents, and in humans with all three of these. And that is elevated insulin itself, elevated stress hormones, and elevated inflammatory proteins or cytokines.

There are three primary causes of insulin resistance. And by primary, I mean that literally I can cause insulin resistance in isolated cells, in laboratory rodents, and in humans with all three of these. And that is elevated insulin itself, elevated stress hormones, and elevated inflammatory proteins or cytokines.

all three of those things are considered primary in my definition because you can just make insulin resistance happen at the cell in the rodents and in humans all three biomedical models but in as you were kind of alluding to if we were to tell someone all right here but there are others like you said like noxious toxins that can accumulate in fat cells and alter fat cell growth absolutely that is relevant um so i'm not suggesting that there aren't others there are

all three of those things are considered primary in my definition because you can just make insulin resistance happen at the cell in the rodents and in humans all three biomedical models but in as you were kind of alluding to if we were to tell someone all right here but there are others like you said like noxious toxins that can accumulate in fat cells and alter fat cell growth absolutely that is relevant um so i'm not suggesting that there aren't others there are

all three of those things are considered primary in my definition because you can just make insulin resistance happen at the cell in the rodents and in humans all three biomedical models but in as you were kind of alluding to if we were to tell someone all right here but there are others like you said like noxious toxins that can accumulate in fat cells and alter fat cell growth absolutely that is relevant um so i'm not suggesting that there aren't others there are