But it's very well associated with high cause mortality. A high ApoB isn't good for you.

Well, it depends on the context.

Okay. Tell me more.

Well, it's insulin sensitivity, right, in my opinion. And so if you're swimming in a pool that is dirty people, right? If you're swimming in a pool where the majority of people are metabolically unwell, right? We know from multiple studies in the last 10 years that 86 to 93% of the U.S. population has at least one risk factor of insulin sensitivity, metabolic dysfunction. 86 to 93% of our population is on the continuum of insulin resistance. To some degree, we are swimming in a dirty pond. Of course, ApoB associates with

lower mortality. Because ApoB goes up when you're insulin resistant. ApoB

goes up when you're insulin resistant. And in someone who is insulin resistant, ApoB, I believe, is involved in the cascade of atherosclerosis, but not causal, right? So you can be necessary, but not sufficient. This is dry wood. You need wood to make a fire when you're camping, but wood doesn't cause the fire. And wood is also valuable for humans, right? Woods can be used to make a cabin or a shelter, or wood is used to make things. So lipids, ApoB has immunologic roles in the human body. It's an immune molecule. It's associated with more longevity in people that live to 85. This is the Leiden 85 study. So in many studies, in the elderly, high levels of LDL are actually associated with lower morbidity and improved longevity. So that's what's interesting. But in the interim, yes, if the majority of the population is insulin resistant, and I think this comes back to the inside of our arteries, right? So all of our arteries are high pressure. Our veins are low pressure, but all of our arteries are high pressure, which means that when you are circulating blood through the arteries of your heart, the arteries of your body, you are going to get some denuding of the endothelium, especially at branch points, but even everywhere else. When you are metabolically unwell, your immune system is impaired and you cannot remodel the inside of those arteries as well. And that I believe is the problem. When you don't repair the little cuts and scrapes and bruises that occur on the inside of all of our arteries, just because we have a blood pressure of 115 millimeters of mercury, which is quite a lot of pressure in a healthy individual at systolic heartbeat, you know, if you can't repair that, that is where atherosclerosis starts, I believe. Now, if there's more LDL, there's more LDL moving there. That doesn't mean the LDL caused it because the LDL doesn't injure the endothelium.

It does not. I

don't believe there's any evidence that native LDL injures the endothelium. And therein lies the problem. So the question is, if we are teaching humans how to live long, do we tell them to lower ApoB or do we say, don't be insulin resistant, right? What is the real problem here? And if we're telling them to lower ApoB, how are we telling them to do that? Because you certainly don't eat tallow if you want to lower ApoB, but we talked about all the benefits of eating animals. That's earlier. So there's really, all of it has to make sense if we're going to have a cohesive paradigm of how humans are meant to live. And I think that when you try lower ApoB, whether it's through a PCSK9 inhibitor, a statin, you know, limiting your saturated fat, you can certainly decrease your cardiovascular mortality by lowering ApoB. Will you lower your all-cause mortality? That is much more questionable. And I think that the data that you will lower your all-cause mortality by lowering ApoB is very limited, if not even present, because you will shift it to something else. Like

cancer, most of those stuff.

Like cancer or dementia or something else, right? Some sort of immune thing. So that is the real honest conversation we have to have. And I think there's been a little bit of overemphasis on cardiovascular disease here. Understandably, it's scary to die of a heart attack. But does the data really say that you will live longer if you lower ApoB? I don't think so. I think that the data where the money is, is you're going to live longer if you are insulin resistant, if you're insulin sensitive, right? That is guaranteed. And that's liver fat, right? But that's not the conversation, Dave. The conversation is lower your

ApoB. So what do you say to people who have high levels of insulin sensitivity and low liver fat and high ApoB? Wouldn't a PC inhibitor be a good idea? Oh no. Why not?

Oh no. Because of the side effects of a PCSK9 inhibitor. What's the problem having high levels of ApoB if you're insulin sensitive and you have low liver fat? What's the issue there? Why would you want to lower your ApoB? Then you're going to have all the potential problems of a PCSK9 inhibitor. And if you look at the Mendelian randomizations of PCSK9 polymorphisms, there are potential problems associated with inhibiting PCSK9. There's really nothing wasted in the human body. I think we like to think in pharmacy or in medicine that we can just knock something out. You know, the PCSK9 drug is a monoclonal antibody. You don't need your PCSK9. You can just get rid of that. It's not going to do anything in your body. Just like you don't need your HMG-CoA reductase. You don't need to make cholesterol. It's vestigial, Dave. Nevermind that it's a precursor for your sex hormones and all of the membranes of your body and all of the downstream things that happen from cholesterol, including squalene or coenzyme Q10, which are beneficial. You can just, it's vestigial. You don't need HMG-CoA reductase. You know, you can just knock that out with a statin. This is just like, to me, this is, this is just, this is sort of like prideful, you know, prideful ignorance of human physiology. We're just, we're too quick to assume that there are not going to be any long-term side effects of knocking out PCSK9. So I think, yeah, if you, if your ApoB is quote high and yours probably is, if your LDL is 192. But if you're insulin sensitive, I would argue there's a more nuanced conversation here. And we cannot clearly say that you will increase your longevity from all cause more, you know, that you will avoid. Yeah. Right. And it's like, makes sense. You just want to live well for a long time. Right. We're not just like heart disease isn't the only thing that kills people. Not at all. It's one of the four. Strokes, dementia, cancers. Do you look at the ratio of APOB to APOA? Yeah. I mean, it's an indication of metabolic health, right? Same kind of thing. Triglycerides, all these ratios are interesting. And I think they start to over complicate things. Just look at your fasting insulin. Yeah. You know, it'll tell you 85% of what you want to know. People get really granular. And for what it's worth, I think my ApoB is 110. Yeah. Much lower than it used to be when I was strictly carnivore. So once I started eating carbs, my cholesterol comes way down. My ApoB is still higher than many would quote like it. Yeah. And I just don't see in the literature, there's a clear signal that that's going to decrease my longevity. And as we talked about, ApoB containing lipoproteins have benefits in the human body. They're not just there to kill us, guys. And I strongly object to the notion that they're vestigial or that they, I mean, I've heard discussions online of people saying ApoB is vestigial. We now have antibiotics. ApoB was there to protect us from infections. It's still there to protect us from infections in some way. It does interrupt quorum sensing between bacteria and other pathogens in our bloodstream, almost certainly. And, oh, we have antibiotics now. We don't need as much ApoB. I don't buy it. I don't buy it in any... And I fear that when we lower ApoB long-term, we will see signals of increased cancer, impaired immune surveillance, increased dementia, and other issues in humans. So, like, let your body do what it wants to do, but be metabolically healthy.

That is really profound advice. There's something else I've been talking about for years that I included in the axo.health lab test panel, and it was expensive to do it, but it's LPPLA2.

That's an interesting one.

And like if you're worried about cholesterol or worried about APOB, the lining of the arteries will release LPPLA2, which is a sign it's being damaged. So if there is damage of any cause, that's going to go up. So that means if that number is where it should be and lines very low, then it means whatever my scores are with cholesterol, they don't matter. Do you agree with that? I

think LPPLA-2 is really interesting. So lipoprotein-associated phospholipase A2, it goes up when you give people soybean oil. What damages your arteries? There's a trial in humans that shows this. And Brian Johnson didn't put that in his tweet. Brian's experimenting with a lot of stuff. He's going to come around. I will

bet you money that there will be a time when Brian has ghee and or tallow as a part of his program.

I went forward to it. It takes collagen now. Well, he's taking it the whole time. Yeah, yeah. He's like, I'm vegan, but

I eat collagen. I'm like, I made collagen in a billion-dollar industry. I know why we take it for longevity. And this is important. I don't know if you've seen this. 20 grams of collagen is the right amount.

Okay. And more

than that will drive oxalate formation in the body. It does because of the breakdown, yeah. Yeah. So there's probably a sweet spot. Yeah. So having none isn't a good idea. And it is a signaling molecule like those organs that you make. Collagen, when you take it, signals to your body that there has been damage to your collagen. So then your body regenerates your collagen, even though it wasn't your collagen that was damaged. That's why I realized collagen was interesting. So, and I know Brian's about to launch his collagen brand, which I'm like, go for it, Brian. That's rich. But it's cool. It's like there's one animal food and there's no reason not to add like a healthier mix of lipids. And I'm, you know, I'm on the same longevity journey and I want everyone who is interested in longevity, like get your labs and, you know, personalize your protocol and look at the stuff we just talked about. Paul, you really know what you're talking about. I always love the stuff you share online. We've had similar perspectives during the dark four years when the Fauci overlord ruled our freedoms. I think I can say that without any censorship. I think you can now. And congratulations on your new film as well.

Thank you, brother. I hope people will check it out. It's just a little mini documentary on seed oils, and it's good talking to you always, my friend.