Paul Saladino
speaker
961 appearances
2 recordings
2 series
first heard Jan 2025
last heard Mar 2025
Paul Saladino’s voice in public audio — every appearance, attributed to the second.
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The Shawn Ryan Show · #179 Paul Saladino - The FDA Approved Poison You Eat Every Day · 5 Mar 2025
podcast
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.
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.
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.
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 you have LDL that's more fragile, full of polyunsaturated fats, getting stuck to a proteoglycan matrix because you're insulin resistant. You're getting injury to the endothelial wall that we all get when we are... living our lives that doesn't get repaired because the insulin resistance impairs your immune function that repairs those endothelial walls. But LDL didn't cause any of that.
It's just getting caught up in the process. So this is the major problem with the theory for me is that there are plenty of examples of people with high LDL that don't get atherosclerosis or that don't get atherosclerosis at the rate that they should. And there are examples of people with low LDL who are insulin resistant who get lots of atherosclerosis.
So there are so many inconsistencies in the theory that I think what's going on here is we have conflated LDL as causal when it's actually just part of the causal cascade. So I'll just resume way out for people. I think about this like wood and fire. If you're going to build a campfire, you must have wood, right? You have to have wood, but wood didn't cause the fire. Right? Gotcha.
But wood also has other valuable things. If you get rid of the wood, you won't have any fire. You can lower someone's LDL and they will have less atherosclerosis, but that doesn't mean the LDL caused the atherosclerosis. If you lower wood, if you take away wood, if you have a forest that's been decimated by a forest fire, it's going to be hard to find wood to make a fire.
But that doesn't mean wood caused the fire. It was the lightning that caused the fire, right? You need the spark to cause the fire. So what's the spark? It's the insulin resistance.
It's the mitochondrial dysfunction leading to extra damage to the endothelial wall, leading to immune cell impairment, leading to LDL that's more likely to oxidize, leading to more proteoglycans in the matrix in the subendothelial space. The other thing, and where the metaphor extends, is that wood is also valuable. If you're living in the woods, you can build a house from wood.
In the human body, LDL is valuable. LDL serves an immune role. We've often been told LDL cholesterol is just there to kill us, which makes no sense evolutionarily. Sometimes you hear this explanation that like, we don't need LDL anymore because now we have antibiotics. But I think that's a little bit, that doesn't really jive with me. Historically,
All throughout our time as humans, LDL is an immune particle. It interrupts infections in our body, whether viral or bacterial. Bacteria and viruses communicate with each other using something called quorum sensing, and LDL particles and other lipoproteins can interrupt that. So LDL has value in the human body.
And it's probably not surprising then that if we look at some of the longest-lived people, they often have elevated levels of LDL. because they're not insulin resistant. So my assertion, and this is very controversial and I'm happy to defend at any time in the right forum, is that if you are insulin sensitive, if you are metabolically healthy, LDL is good for you.
It's an immune particle, it's valuable. It's when you become insulin resistant that it becomes a liability because it's part of the causal cascade. What is a problem if you live in a place with a lot of lightning storms and you have a bunch of dry wood around? If you don't have lightning storms, wood is great, right? You want to build things. I can build a canoe. I can build a fishing rod.
I can build a house. You don't want to get rid of all your wood. And we know that when you lower LDL, there are potential problems in humans. Now, The data around lowering LDL becomes muddy because drugs that lower LDL can have side effects.
But for instance, statin drugs, which lower LDL by interrupting their synthesis in this cascade of cholesterol synthesis, they're HMG-CoA reductase inhibitors. They inhibit an enzyme in this cholesterol synthesis pathway. They're associated with slightly increased rates of diabetes, dementia, myalgias, lower libido.
lowering LDL, lowering cholesterol production is not always, it's not without problems. And to think that historically or by design or evolutionarily, that LDL is just there to kill us, that doesn't make any sense. And that eating a food that is at the center of the human diet for all of human history, like red meat that has saturated fat,
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