Paul Saladino, MD
👤 PersonAppearances Over Time
Podcast Appearances
Yeah, somebody would consider it high. Yeah. I have the same amount of LDL circulating to my hands, moving through the capillaries, and coming back in my veins. But in me and all humans, we do not see atherosclerosis occurring in native veins. So atherosclerosis doesn't occur in a vein at all in humans. It's because it's lower pressure.
Yeah, somebody would consider it high. Yeah. I have the same amount of LDL circulating to my hands, moving through the capillaries, and coming back in my veins. But in me and all humans, we do not see atherosclerosis occurring in native veins. So atherosclerosis doesn't occur in a vein at all in humans. It's because it's lower pressure.
And when you have lower pressure in a vein, you don't denude the endothelium. You don't create proximate endothelial injury that is necessary to start atherosclerosis. If ApoB-containing lipoproteins, that is LDL plus its cousins, are atherogenic, why don't we get atherosclerosis in veins? They have the exact same endothelial lining on the inside.
And when you have lower pressure in a vein, you don't denude the endothelium. You don't create proximate endothelial injury that is necessary to start atherosclerosis. If ApoB-containing lipoproteins, that is LDL plus its cousins, are atherogenic, why don't we get atherosclerosis in veins? They have the exact same endothelial lining on the inside.
And when you have lower pressure in a vein, you don't denude the endothelium. You don't create proximate endothelial injury that is necessary to start atherosclerosis. If ApoB-containing lipoproteins, that is LDL plus its cousins, are atherogenic, why don't we get atherosclerosis in veins? They have the exact same endothelial lining on the inside.
If you were in a little spaceship like Rick Moranis in Honey, we're like, what is that? Like, you know, inner space or whatever. You know, if you're running through my body in the artery and the vein, if I put you inside a vein or I put you inside an artery and you're looking from the inside of the vessel to the wall, it looks the same. It looks the same.
If you were in a little spaceship like Rick Moranis in Honey, we're like, what is that? Like, you know, inner space or whatever. You know, if you're running through my body in the artery and the vein, if I put you inside a vein or I put you inside an artery and you're looking from the inside of the vessel to the wall, it looks the same. It looks the same.
If you were in a little spaceship like Rick Moranis in Honey, we're like, what is that? Like, you know, inner space or whatever. You know, if you're running through my body in the artery and the vein, if I put you inside a vein or I put you inside an artery and you're looking from the inside of the vessel to the wall, it looks the same. It looks the same.
The inside of an artery and the inside of a vein are the same. The endothelium is the same. Yeah, it's just on the outside of the endothelium, you'll have smooth muscle. Versus, yeah, versus more musculature in an artery to help it contract. And you can actually take a vein and you can transplant it into the arterial circulation. So we do this in coronary artery bypass grafting.
The inside of an artery and the inside of a vein are the same. The endothelium is the same. Yeah, it's just on the outside of the endothelium, you'll have smooth muscle. Versus, yeah, versus more musculature in an artery to help it contract. And you can actually take a vein and you can transplant it into the arterial circulation. So we do this in coronary artery bypass grafting.
The inside of an artery and the inside of a vein are the same. The endothelium is the same. Yeah, it's just on the outside of the endothelium, you'll have smooth muscle. Versus, yeah, versus more musculature in an artery to help it contract. And you can actually take a vein and you can transplant it into the arterial circulation. So we do this in coronary artery bypass grafting.
You can take a vein usually from the leg or other places in the body and you can transplant it into the arterial circulation. So you can take a vein and... and put it in the arterial circulation, and it actually gets atherosclerosis very quickly because it is subjected to higher pressure, and that denudes the endothelium.
You can take a vein usually from the leg or other places in the body and you can transplant it into the arterial circulation. So you can take a vein and... and put it in the arterial circulation, and it actually gets atherosclerosis very quickly because it is subjected to higher pressure, and that denudes the endothelium.
You can take a vein usually from the leg or other places in the body and you can transplant it into the arterial circulation. So you can take a vein and... and put it in the arterial circulation, and it actually gets atherosclerosis very quickly because it is subjected to higher pressure, and that denudes the endothelium.
So when a vein is in the arterial circulation and it has that sort of proximate event, that arterial inner endothelial damage, it will accumulate atherosclerosis, but it doesn't happen in native circulation. And I would argue that is a very strong argument that ApoB is not causal. because I have the same amount of ApoB in my veins.
So when a vein is in the arterial circulation and it has that sort of proximate event, that arterial inner endothelial damage, it will accumulate atherosclerosis, but it doesn't happen in native circulation. And I would argue that is a very strong argument that ApoB is not causal. because I have the same amount of ApoB in my veins.
So when a vein is in the arterial circulation and it has that sort of proximate event, that arterial inner endothelial damage, it will accumulate atherosclerosis, but it doesn't happen in native circulation. And I would argue that is a very strong argument that ApoB is not causal. because I have the same amount of ApoB in my veins.
If it's so bad for my arteries and my veins, if it's so bad for my endothelium, why isn't it damaging the endothelium in my veins? Because it needs a proximate event to have that happen. Now, circle back to humans today in 2024. There are many studies which suggest that 86 to 93% of us have at least one marker of metabolic dysfunction, right? And these are the metabolic syndrome criteria.
If it's so bad for my arteries and my veins, if it's so bad for my endothelium, why isn't it damaging the endothelium in my veins? Because it needs a proximate event to have that happen. Now, circle back to humans today in 2024. There are many studies which suggest that 86 to 93% of us have at least one marker of metabolic dysfunction, right? And these are the metabolic syndrome criteria.
If it's so bad for my arteries and my veins, if it's so bad for my endothelium, why isn't it damaging the endothelium in my veins? Because it needs a proximate event to have that happen. Now, circle back to humans today in 2024. There are many studies which suggest that 86 to 93% of us have at least one marker of metabolic dysfunction, right? And these are the metabolic syndrome criteria.