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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Appearances
The Shawn Ryan Show · #179 Paul Saladino - The FDA Approved Poison You Eat Every Day · 5 Mar 2025
podcast
Like we were, the companies were proud of the fact that they were using these polyunsaturated oils because for so long we have been told that polyunsaturated fats are heart healthy and saturated fats are heart unhealthy. and we've got it all reversed. It's all backwards. It's all backwards.
So the reason it's backwards is because polyunsaturated fats are fragile, and they become incorporated into all the membranes of our cells. And there are multiple studies showing that when we have more polyunsaturated fats in our diet, specifically seed oils, this LDL, which is often termed bad cholesterol, is more likely to oxidize, more likely to become damaged in our bloodstream.
And that leads to heart disease in so many steps. Again, we also have to talk about the cholesterol piece and the heart disease piece with all this. So it's a little involved and it's tricky. The idea is that polyunsaturated fats lower cholesterol a little bit, saturated fats raise cholesterol a little bit.
So we've been told the polyunsaturated fats are healthy, and yet humans are eating less saturated fat, more polyunsaturated fats, and rates of heart disease are still skyrocketing, right? So it didn't do anything, it didn't fix The epidemic of heart disease, clearly we've missed the boat here.
And I would say we went in the completely wrong direction, especially since the 1980s, the consumption of soybean oil is the major seed oil consumed by humans, has gone through the roof. And I mentioned this earlier in the podcast, you can look at human fatty tissue, adipose tissue, and you can see that over the last 60 to 80 years, we are really polyunsaturating ourselves.
When we eat polyunsaturated fat, we hold onto it. Our bodies don't make polyunsaturated fat. Do you remember earlier when I talked about pigs and chickens as monogastric animals? These animals don't make polyunsaturated fats either. Ruminants can make polyunsaturated fats. So they don't hold on to polyunsaturated fats. They can get rid of them and they can make them.
We cannot make polyunsaturated fats. So we need a little bit. And historically as humans, we had a small amount of polyunsaturated fat in our diet, both as omega-3 and as omega-6. And omega-6 is the linoleic acid. Omega-3 is the kind of stuff you get from fish, generally speaking. Omega-6 and omega-3 have different pathways in the human body in terms of the downstream metabolites.
We'll talk about that also. But historically, we never had much omega-6. 1% of our calories. Today, 10% to 15% of our calories is omega-6. Some people have 20% of their calories as omega-6 fatty acids. So we have a historical... inconsistency here in what we're doing as humans. And that should raise the alarm. That should ask us, that should challenge us to ask questions.
But because of the cholesterol piece, because this lipid hypothesis has been at the center of medicine for so long, since the 1950s with Eisenhower, and we've been told that cholesterol causes heart disease, we have really, I think, been, we've been misled. And so the whole thing is kind of this house of cards, in my opinion. When you understand that cholesterol doesn't cause heart disease.
And this pisses people like Peter Attia off. And I would love to debate him on this, you know, because he really believes cholesterol does cause heart disease. All respect to Peter Attia, the whole house of cards falls. And so now let's just pause the seed oil conversation and I'll come back to that and I'll talk about cholesterol. You got any questions so far?
Okay. So cholesterol is a building block for steroid hormones in your body. Testosterone, estrogen, progesterone, aldosterone. These are all... built out of a cholesterol backbone. Cholesterol and triglycerides, which are fatty acids, are packaged into buses in your body that move these things around. One of those buses comes from the liver. It's called LDL, low density lipoprotein.
LDL contains a protein called ApoB100. ApoB containing lipoproteins are felt by Western medicine to be causal in atherosclerosis. Atherosclerosis is the process of plaque formation in your arteries of your heart, right? And I have a couple, I have a lot of problems with this theory. I think that they're close. I think Western medicine is close, but we're missing the mark.
And we're not seeing it because 90 plus percent of people are insulin resistant. And that'll make sense in a moment. So LDL is this lipoprotein particle. It has an ApoB 100 marker on it that says it's LDL. Other ApoB containing lipoproteins are things like VLDL, IDL, LP little a, chylomicron remnants, that's not terribly important for this conversation.
Just know that LDL is thought of as the bad cholesterol. And in most humans, when you eat saturated fat, LDL goes up. But if you look at the saturated fat literature, there was a study published in 2020 in the Journal of American College of Cardiology saying, hey, we looked at tons of studies, it's meta analysis. There's actually no real relationship between saturated fat and heart disease.
So that's the first problem here, is that saturated fat, which raises LDL, is not associated with heart disease. And some saturated fats, like 15 carbon and 17 carbon saturated fats, which occur in dairy, pentadecanoic acid and heptadecanoic acid are actually felt to be protective against cardiovascular disease. So there's lots of inconsistencies in the theory.
But you have LDL going up and mainstream medicine says LDL is causal, therefore the more LDL you have in your body, the more likely you are to get heart disease. but except when it doesn't, right? So if LDL is causal in heart disease, then why don't we get atherosclerosis in our veins and we only get it in our arteries? So veins are the vessels that your body uses to return blood to your heart.
arteries are moving away from your heart to your body. So I have a heart here. It pumps blood through my aorta. My aorta branches into all sorts of arteries. They go down my abdomen into my legs. So I have arteries moving blood from my lungs, which is oxygenated to my body, to my toes. And then in my toes, I have capillaries and then it turns into a vein. It comes back. So in arteries,
humans get atherosclerosis, but we do not get atherosclerosis in native veins. But there's the same amount of LDL circulating in all of these vessels. It's a continuous system. So why is that? Because arteries are higher pressure. And I would argue that you must have injury to the endothelial wall. That is often the beginning of atherosclerosis.
That is one of the proximate events of atherosclerosis. If LDL was causal, And the verbiage here is really, really important. If LDL is actually causing atherosclerosis, it should cause atherosclerosis in my veins. The assumption there is that LDL is somehow damaging to the endothelium, but we know that LDL that's not modified, not oxidized, doesn't damage the endothelium. It doesn't happen.
Atherosclerosis is a process by which LDL particles move into the sort of arterial wall. So in an artery, if you have like a tube and you cut the tube this way, or if you cut it lengthwise, and you look at the artery wall, you see there's an endothelium on the inside of the artery, and the LDL moves through the endothelium to this subendothelial space.
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