Paul Saladino

And in that subendothelial space, it's almost like Velcro. There's a matrix of proteins called proteoglycans, and the LDL can get stuck to those proteoglycans. And when LDL gets stuck to those proteoglycans, it gets oxidized. When an LDL is oxidized or modified, stuck in an arterial wall, an immune cell called a macrophage comes along and takes it up.

And in that subendothelial space, it's almost like Velcro. There's a matrix of proteins called proteoglycans, and the LDL can get stuck to those proteoglycans. And when LDL gets stuck to those proteoglycans, it gets oxidized. When an LDL is oxidized or modified, stuck in an arterial wall, an immune cell called a macrophage comes along and takes it up.

And in that subendothelial space, it's almost like Velcro. There's a matrix of proteins called proteoglycans, and the LDL can get stuck to those proteoglycans. And when LDL gets stuck to those proteoglycans, it gets oxidized. When an LDL is oxidized or modified, stuck in an arterial wall, an immune cell called a macrophage comes along and takes it up.

And that's the beginning of an atherosclerotic plaque. When those macrophages are full of LDL, they form a foam, a fatty streak, or their foam cell, which is a precursor to a fatty streak, which becomes a plaque, an arterial plaque. That's atherosclerosis.

And that's the beginning of an atherosclerotic plaque. When those macrophages are full of LDL, they form a foam, a fatty streak, or their foam cell, which is a precursor to a fatty streak, which becomes a plaque, an arterial plaque. That's atherosclerosis.

And that's the beginning of an atherosclerotic plaque. When those macrophages are full of LDL, they form a foam, a fatty streak, or their foam cell, which is a precursor to a fatty streak, which becomes a plaque, an arterial plaque. That's atherosclerosis.

What should happen, what happens in normal physiology in a healthy artery that doesn't have damage in someone that's not insulin resistant is the LDL moves in and it moves out of the arterial wall. It can get stuck, but then it gets stuck for a short amount of time and it moves out. I think that what's happening here is that LDL isn't the culprit.

What should happen, what happens in normal physiology in a healthy artery that doesn't have damage in someone that's not insulin resistant is the LDL moves in and it moves out of the arterial wall. It can get stuck, but then it gets stuck for a short amount of time and it moves out. I think that what's happening here is that LDL isn't the culprit.

What should happen, what happens in normal physiology in a healthy artery that doesn't have damage in someone that's not insulin resistant is the LDL moves in and it moves out of the arterial wall. It can get stuck, but then it gets stuck for a short amount of time and it moves out. I think that what's happening here is that LDL isn't the culprit.

LDL is part of the causal cascade, but it didn't cause the fire. LDL is a fireman, right? Essentially showing up to the fire, but they didn't cause the fire. LDL is part of the cascade. We know you need LDL to make atherosclerosis. But I think that LDL actually causes atherosclerosis is very shaky. What does cause, what does initiate it? It's this insulin resistance.

LDL is part of the causal cascade, but it didn't cause the fire. LDL is a fireman, right? Essentially showing up to the fire, but they didn't cause the fire. LDL is part of the cascade. We know you need LDL to make atherosclerosis. But I think that LDL actually causes atherosclerosis is very shaky. What does cause, what does initiate it? It's this insulin resistance.

LDL is part of the causal cascade, but it didn't cause the fire. LDL is a fireman, right? Essentially showing up to the fire, but they didn't cause the fire. LDL is part of the cascade. We know you need LDL to make atherosclerosis. But I think that LDL actually causes atherosclerosis is very shaky. What does cause, what does initiate it? It's this insulin resistance.

Remember I was talking earlier about this metabolic dysfunction, this insulin resistance and how that underlies so many of our diseases. That I think is the problem. When you are insulin resistant, which remember is when your mitochondria don't work real well, you don't make energy well, you don't move things down that electron transport chain. When you're

Remember I was talking earlier about this metabolic dysfunction, this insulin resistance and how that underlies so many of our diseases. That I think is the problem. When you are insulin resistant, which remember is when your mitochondria don't work real well, you don't make energy well, you don't move things down that electron transport chain. When you're

Remember I was talking earlier about this metabolic dysfunction, this insulin resistance and how that underlies so many of our diseases. That I think is the problem. When you are insulin resistant, which remember is when your mitochondria don't work real well, you don't make energy well, you don't move things down that electron transport chain. When you're

insulin resistant, your immune cells don't work well, and you have a more enriched proteoglycan layer in your endothelium, in the subendothelial space. So your arteries are stickier when you're insulin resistant, and the immune cells moving in your artery walls don't work in the same way. You don't repair the endothelium, you don't repair your vessels as well.

insulin resistant, your immune cells don't work well, and you have a more enriched proteoglycan layer in your endothelium, in the subendothelial space. So your arteries are stickier when you're insulin resistant, and the immune cells moving in your artery walls don't work in the same way. You don't repair the endothelium, you don't repair your vessels as well.

insulin resistant, your immune cells don't work well, and you have a more enriched proteoglycan layer in your endothelium, in the subendothelial space. So your arteries are stickier when you're insulin resistant, and the immune cells moving in your artery walls don't work in the same way. You don't repair the endothelium, you don't repair your vessels as well.

So there's more injuries to your endothelium, and the LDL particles are more likely to get stuck. When you eat more seed oils, which are these polyunsaturated fats, the LDL that gets stuck in the proteoglycan layer are more likely to oxidize. We know that for a fact.

So there's more injuries to your endothelium, and the LDL particles are more likely to get stuck. When you eat more seed oils, which are these polyunsaturated fats, the LDL that gets stuck in the proteoglycan layer are more likely to oxidize. We know that for a fact.