Cholesterol Is Not the Problem – What It Reveals About Inflammation, Metabolism, and Vascular Health | Inflammation | E133

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Your body needs these fats to survive. And if you go on a low or no-fat diet, you will suffer and your body will start to churn out more of what it needs. Liver production will go up and it ain't going to be the good stuff. It's going to be whatever it can make.

Welcome back, everybody. We are back and excited about today's conversation.

Yep.

We've been talking about metabolic health in terms of people's arteries. You know, something I like to tell people is you are how old your arteries are. If the arteries to your brain are 80 and you're 50, guess what? You're 80.

You're 80, yeah.

If you're 60 or 70 and the arteries to your brain, your heart are 30, guess how old you are?

You're 30.

You know, and you're going to live, you know, you're going to be doing a lot of stuff. And so, when we talk about metabolic cardiology, we're literally talking about this idea of the ultimate biohack, the ultimate anti-aging thing, which is can be measured by hard data points, you know, calcium scores, obviously coronary catheterizations and CT PETs and all these fancy things the cardiologists do. But then things we do, you know, looking at vascular markers, looking at, you know, Lp-PLA2, which is a marker for unstable plaques, looking at carotid intimal-medial thickening, a lot of cool things. But I want to talk about one that's a little bit of misunderstanding that people are confused about. And it's kind of funny because as we're recording this, literally a week years ago we flipped the food pyramid upside down. Now fats are back.

Fats are back.

Fats are back. And we're going to talk about cholesterol. Yeah. You know, we're at— talk with patients. There's about 300 things, more than 300 things we can measure to measure your vascular age, risk for strokes, neurovascular, cardiovascular stuff. But the standard is blood pressure, you know, weight, sugar, A1C.

Are you diabetic? Do you have dyslipidemia? Do you smoke? Do you have family history? Hypertensive, sedentary?

And we look at maybe 15. We'll be generous. Let's say 30, right?

I mean, that's really generous.

And we ignore the other 270.

Yeah.

And so what I want to do is I want to give people a window to what we do and what this metabolic cardiology thing is and pick a super basic thing everybody thinks they know about, but they don't, which is cholesterol.

Yeah.

And so we're not going to— we'll probably veer because we always veer, but stick on cholesterol. LDL particle, HDL.

I saw what you did there. Stick on cholesterol.

I like it. Stick on cholesterol because the point is that there's 300 things. We'll pick one and we're going to blow that up.

Yeah.

It's cool what we can do. It can be complicated. But the point is, is that there are options, things out there. So that's the point. Yeah. Is that what we do is not just high cholesterol, here's your statin. Yeah. High A1C, here's metformin or GLP-1. But it's actually looking why is it high? And then dealing with it.

So understanding how it's affecting you.

Yes.

Is it affecting you?

Yeah.

Negatively, I guess is the point, right? Correct. Because you need it and we're gonna talk about that. But is, is your cholesterol or your lipid panel or your lipid profile, however you wanna say it, is it a risk factor? Is it currently contributing to, to disease or disease that's present? Is it making it worse or is it a non-issue based on everything else that we're seeing and something that can be not necessarily ignored, but not necessarily prioritized either.

Yeah.

Or what it means for you.

Or are we focusing on the wrong things?

Yeah.

So let's start with the first wrong thing we focus on. Yeah. Cholesterol.

Cholesterol.

What is an optimal cholesterol for all-cause mortality? You want not just heart attack, not just stroke, dementia, not just cancer, because there are numbers that correlate with all these. Yeah. For living for as long as possible, what's the range you tell people? I have a range I tell people. What's the range you tell people?

Yeah. So the range that conventional sets up is they want your cholesterol below 200, right?

Yeah, yeah.

So for me, if your cholesterol is below 150, 160, it's problematic. It's actually too low. So my low range is about 150, 160. I might go as 140, but it really depends on other factors. What's their brain function? What's their hormones look like? What the vitamin D status is? All things that cholesterol is going to be needed to make. And therefore, if you're seeing suffering in those downstream metabolites, markers, et cetera, then clearly that number might be too low. And then I don't have a problem with cholesterol being over 200. I think up to 240 is fine. I think even 250 is fine depending on the way that everything else looks.

That is what, okay. I thought we were gonna disagree about something here. 'Cause big Japanese study, 80,000 people, there's a, a J curve, right? So if it's less than a certain number, your risk for dying goes up. If it's greater than a certain number, your risk for dying goes up. I was actually talking with Sally Fallon who wrote the book Nourishing Traditions, and she was like, gimme that data. So I was like, so I did my little thing looking for the data and I couldn't find that data point, but I found 3 or 4 other massive Asian studies all saying the same thing, 220 to 240, you know, maybe 210 to 235. But the idea is that if you want to all-cause mortality, living for as long as possible, as healthy as possible, the range is actually higher than standard of care.

Yeah.

That's the first data point I want to throw out there. The second one is, so what do you do with, you know, cholesterol, LDL, HDL? So let's, why don't you like break down cholesterol for us? Sure.

Like, okay, cholesterol, what is cholesterol?

What is triglycerides, LDL? What's this HDL-P thing that might correlate with HDL functionality? Like, why don't you just give us the 3-minute, 10,000-foot view of— I know I'm putting on minutes.

Yeah. So first and foremost, I'll start with a basic lipid profile that most people are comfortable and familiar with. And that's essentially total cholesterol that we were just talking about, LDL cholesterol, which is notoriously called bad cholesterol, HDL cholesterol, which is notoriously called good cholesterol, and then triglycerides. Those 4 markers, each individually seen on a traditional lipid panel. You go for your physical, that's what your doctor's checking when you're getting fasting labs. Total cholesterol, we just talked about, is not the bad guy. Total cholesterol has been demonized. Total cholesterol is normal in 50% of patients with coronary artery disease. Total cholesterol, when too low, creates problems. Total cholesterol, when too high, can also create problems, but there's a sweet spot, and it's higher than you would think it is, and it's dependent on the individual and what else is going on. Taking it a step further, when you're looking at triglycerides, triglycerides Triglycerides are basically more, for me, a tell of what's going on metabolically with regards to their insulin flexibility. Are they insulin resistant? Are they insulin sensitive? If someone is pre-diabetic, pre-diabetic or insulin resistant, their triglycerides are going to be higher. If they're eating a lot of carbohydrates, simple carbohydrates, sugar, triglycerides are going to be higher. Other things can contribute to that familial hypertriglyceridemia. So that's more what's going on with the metabolic component, maybe not so much the lipemic component, although they're tied together. Then we have good and bad cholesterol. LDL and HDL. The problem is, is that LDL is not all bad and HDL is not all good. LDL itself is necessary for life. LDL is something that is important for fighting infections, controlling inflammation, managing oxidative stress, supporting the biological body functions, supporting cell membrane integrity, coating the brain the same way cholesterol does. All these things that are important— LDL is important, as is HDL. But if LDL is glycosylated, so sugar slapped on it, or oxidized, so damaged, or it's a high particle number and they're small dense particles that are easily getting stuck on things, then it's going to become problematic and eventually lead to potential plaque and then eventually coronary artery disease. HDL, on the other side, is more of the kind of molecule that's good cholesterol that cleans out the blood vessels, that's reparative. However, there's such a thing as dysfunctional HDL, meaning HDL that functions like bad LDL. And there's no direct way to measure that, but there are indirect ways to measure that. And HDL2b is one of these markers that you can get through certain labs, not many, but also looking at HDL particles, looking at other factors like myeloperoxidase and ApoA-1. These are the, the kind of risk stratification panels that when we expand out, we're not just taking something basic, but rather saying, hey, your basic panel conveys more information than you know. When we're also looking at these other parameters. So LDL, when bad, is bad. LDL can also be good. The other constituent of LDL is apolipoprotein B that goes along with that molecule, and then Lp(a), which is more of a genetic one. I kind of think about it in the way I explain to patients that it's akin to a tennis ball that's fresh out of a tennis ball can. So just imagine a yellow tennis ball fresh out of a can. The whole tennis ball is the LDL cholesterol molecule. The white stitching is the ApoB, and then the little fuzzy yellow stuff is like the LDL particles. And so if you were to shrink your tennis balls down, lower LDL-C, then particle number and ApoB will kind of follow suit. But it doesn't always correct the problem altogether. So you have to factor in other ways to manage that. You have to make sure you're fluffing those particles out. You have to make sure that Lp(a) is accounted for, and then HDL on the other side of the coin, if it's dysfunctional, you have to work on making it functional. How do you do that? Manage oxidative stress, control inflammation, improve them metabolically, make them more insulin sensitive. Maybe it's a gut microbiome issue, maybe it's chronic infection, maybe it's toxins like heavy metals. There's so many layers to it. This is just kind of like a really quick 50,000-foot view, but it's not as basic. It's not as simplified as people think it is.

And one thing I wanted to mention towards the beginning that I didn't mention is that the 3 causes, you know, depending on what you read, I always quoted 80%. I was at the lecture with one of our mentors, Mark Houston.

Yeah.

Probably the top metabolic cardiologist in the world, wrote the textbook of this product on this topic saying maybe 90%+ of cholesterol is actually made in your body. Yeah. Your liver and your cells. So, when you see an elevated cholesterol, what does it mean? You know, there is a genetic component, which is a I've yet to have a patient of mine with familial hypercholesterolemia. Yeah, same. Yeah. And so it's 3 things. It's your macro and micronutrients. So what you eat and nutrient deficiencies or, you know, processed food thing, toxin exposure and infections. So when someone has a cholesterol that doesn't go down and they've done a lot of stuff, the question is, well, your diet macros and micronutrient stuff, do you have toxin exposure and you have infections? And the answer is Usually, yes. Yes.

I just had a conversation with a patient today because she's fit, she's metabolically flexible, at least we're working on that, but she's not overweight. She doesn't have high visceral fat. She doesn't have a lot of adiposity. She's active. She is managing her stress, although not great. And we talked about that a bit. She eats super clean. So you're taking someone who's little, who's not overweight, who's active, who eats clean, and yet her lipids are still high. But she's a postmenopausal female whose stress is high, whose gut microbiome is off. And we literally just had the conversation where I said, look, a third— the numbers that I've seen— a third of your lipids are, are affected by your diet. Two-thirds, maybe as high as 80%, are coming from within, meaning made by the liver in response to something else. What's that something else? So we're diving deeper. In her case, it's, are your hormones optimized? Can we get this stress under control? Do we need to look for chronic infections? Let's recheck your gut and see if the microbiome is better than it was previously. And as we unlayer these things and reveal them, ultimately this is going to get better. But it's not a you're eating the wrong foods and you're not exercising enough situation for her. It's other things nobody else really would have been paying attention to.

And something, you know, 80% of my patients I'm seeing right now are women coming to me with a whole host of issues. And for women in this situation, this was published from an NIH study the fall of 2024. So a little over a year and change ago, you can predict a woman's risk for 30-year cardiovascular mortality based on 3 markers. It was LDL-P. So it's a particle number, which we'll talk about in a second. hs-CRP, which is an inflammatory marker. Lp(a), so which is the little fuzzy, the little thing you're talking about. And so that's a 1 data point. The other data point is that— and it was interesting, you know, learning this during November timeframe— if a female comes into you with high blood pressure, high cholesterol, and she's in menopause, what is the number one intervention you can do in her that will lower her risk for heart disease 50%? If you treat her high blood pressure, it's 38% roughly. Hormones will reduce her risk for heart disease 50%. 50%. So all of a sudden, in a menopausal female who's worried about her heart stuff, you'll get a bigger bang for your buck not treating cholesterol not treating your blood pressure, though standard of care would say do that.

Yeah.

Is actually addressing your hormone replacement, which, oh, by the way, as of November 2025, we can do again, right? Yeah. Which we've been doing for years, right? Yeah. Still never stopped. Yeah. So the point is that it's more than that. So going a little deeper, oxidized LDL, you mentioned. Yeah. LDL that's burnt. It's an analogy I give people. It's like you toast bread and it burns, caramelizes. You roast your coffee.

Ages. Will age you. Advanced glycation end products.

Yes. That's what that is. The LDL particle number is a little different. As that number goes up, that's a risk for heart disease. And that's something we order routinely, especially if they're small dense, right?

So hard to see these, not beach balls.

Yes.

Because again, if the LDL particle number is high but they're big fluffy beach balls, less risk.

Big fluffy, good. Small, babies, bad. Yeah. To caveat, we now have access to order the HDL function test. Cool. Through Cleveland Heart Labs, through Quest.

Great.

Which is where we work first. I got the information literally last week.

HDL2b?

No, it's HDL function.

Oh, the function test.

Yeah. Okay, great.

Awesome.

That's like $85. Cool. Okay. Probably not covered by insurance. But what I learned from Dr. Houston last year was that the LDL particle number correlates with your HDL function. It's a 0.8 or 0.9 correlation, which is pretty good. So, we already have that number in our advanced lipid profile.

Yeah.

That tells us rough guesstimate of HDL function. And many people who come in at, you know, half of all people who go to the ER, this is where you cut your teeth, right? You go to the ER with their first heart attack, half of people there will have a normal cholesterol number. So what's the problem? You look under the hood, you'll see LP(a) up, you'll see dysfunctional HDL. And so all of a sudden knowing this becomes important for interventions we'll talk about here because we can actually get these things to go up. Yeah, those things or go down.

Go down. Yeah.

LP(a), let's talk about that a little bit because I feel like that might be a little misunderstood. I'm hearing very deterministic things about it, like if you have it elevated, You are going to have heart disease.

Yeah.

And yet I have patients who have come here from other countries. One actually is from the Caribbean. His grandma's in her 90s, cholesterol 240s, 250s. She's fine. Mom, same situation. He's like, you know, 30s to 40s, high cholesterol, has this thing being elevated. He's like, oh my gosh, you know, familiar. Have heart attacks or strokes. What do I do? And I'm like, your grandma has it. She's fine. Your mom has it. So Even things like that amplify, I call it like it's throwing gas on the fire. If you don't have inflammation, if you don't have all these other things, they're not determinative. And I think that's something that people need to keep in mind that when you look at these things, you can have 3 or 4 of these, 5 of these.

And still be okay.

Still be okay. And so why don't you talk to that a little bit? 'Cause I feel like people get these ApoE4s, I have an ApoE4 gene. Oh my gosh, I'm gonna get dementia and heart disease. And it's like, well, have you heard of the Nigerian paradox where the whole population of Nigeria has the highest instance of this in the world, they have no increase for those two things. Yeah. Talk about that.

Yeah. So Lp(a) is genetic, and if you have it, if you don't, you don't. So you test it once, and if a patient doesn't have it, you don't have to test it again. Usually if it's elevated, then it's something that you probably had passed down and you have to pay attention to it to the extent of is this contributing to disease? So when you have an Lp(a) that's elevated, depending on the extent of elevation and the cutoff, I believe is less than 75. So, I mean, if it's like 80, if it's like 90, it's probably not problematic. If it's 300, 400, you already have a CAC CT that shows plaque. It's probably playing a role, but you have to play the card of what else is at play. Is it just this? Is this the isolated risk factor? And if so, do we even see disease? And if not, then how can we say that this is as big of a risk factor as somebody else might tell you it is? It doesn't genetically guarantee that you're going to have vascular disease. It just puts you at risk for it. There has to be other players in place, and that's situation-specific and individualized, that eventually lead to the final common pathway of all vascular disease that we touched on in other podcasts, which is those three finite mechanisms of injury: inflammation, oxidative stress, and vascular immune dysfunction. If you're controlling for those despite this abnormality, this number, then you're not going to get vascular disease. It's notoriously difficult to treat, but you can treat it. There are no drugs on the market yet that are directed at it, although there's one in the pipeline that I hear about that apparently that apparently targets Lp(a) and can lower it by as much as 80%. When that gets released by the FDA, who knows? But right now, the best case scenario is off-label use of, of a PCSK9 inhibitor like Repatha or other drugs like Leqvio. And, and really statins, which are the standard of care, will paradoxically raise Lp(a). And so you take someone who's got Lp(a) that's maybe not even the problem and it's mildly elevated, and you see that, you get emotional about it, and their other lipid profile, cholesterol, LDL, et al., are slightly elevated. and now that person gets put on a statin to feel better about themselves. They lower cholesterol LDL and they raise their Lp(a), and now that's creating a problem. That doesn't sound like good medicine to me. So you have to look at all these parameters and figure it out. Lots of nutraceuticals can help. I've had really good success with things like niacin, high-dose niacin, as long as they can tolerate the flush reaction or it's not too demethylating or it's not driving their blood sugar up. I've had good success with NAC. I've had good success with high-dose vitamin C, fish oils. Like there's just many things that you can use to bring Lp(a) down.

Have you heard about the Linus Pauling?

Linus Pauling?

Yeah. Hydroxyproline. Hydroxyproline. Well, hydroxyvitamin C. Proline. Well, NAC. Lysine. This is for Lp(a)?

Yeah.

What I heard about was NAC, hydroxyvitamin C. It's like 5 grams twice a day. And then the last one was like pomegranate. So there's probably some variations of it.

There's a variation on it where you add proline and lysine as well, because vitamin C does better in those situations where you're getting those. So I think like either way, they're all working towards the same mechanism.

But I've had people with Lp(a)'s 300— sorry, one was 420— come down to 210. Now, still really high.

Yeah.

But the 50% reduction, I mean, I'll take that.

Yeah, huge.

And I'm looking at these other markers. So, let's keep on moving. We could talk about this for a long time. I wanted people to get an idea. Again, the idea is that 300 markers, cholesterol, we're blowing that up and then dissecting that. And this is kind of what we do with all that stuff. HDL, you kind of allude this when you first talk about the big ones, you know, cholesterol, triglycerides, HDL, is the triglyceride to HDL ratio, which if you say your triglycerides are 150 and your HDL is 50, that's a 3. And that's going— goes more towards a metabolic kind of concern issues. Traditionally, both those ranges was considered okay. And you can have someone with a triglyceride of 100 and their HDL is 30, still at risk. And so all of a sudden you can take some of these and look at ratios, look at a non-HDL, which is your total minus your HDL. And that number, if it's over 160, is an indirect marker of the particle number. So there's different ways to kind of divide this up that people have been doing for years. But the point is that it's not just one number, it's not just two numbers, it's a bunch of things.

Things and then ratios to get insight in things that aren't being directly measured. It's just, it's being scientific and methodical about it. What's your ideal HDL triglyceride ratio?

I like it less than 2.

Yeah.

Personally, I want mine personally to be like 1.5.

I like 1 to 1.

Yeah.

I love it when the panel comes back and it's like, your triglycerides are 70, your HDL is 70. Yeah, well, that's, that's, that's awesome.

I haven't seen that myself. My cholesterol runs high, runs about 210, 220, and my HDL runs really high as well.

Yeah.

HDL function. Let's talk about that briefly because I feel like that is like the disrespected uncle no one talks about, you know, Rodney Dangerfield, whatnot.

Yeah.

But incredibly important. And you can have a normal HDL of 45 and be a male, 50 in a female. And yet if you have dysfunctional HDL, Just like a bad LDL. Yes. So talk about that. Well, we kind of briefly talked— talk about that briefly and what would you do about that?

Yeah. So HDL again was just like ignored and always just assumed to be good. And if you didn't have enough, then that was the problem and you need more and more and more. And then that meant better. And that's not necessarily true. And notoriously, and this is across the board, females tend to have more HDL. I just see that. I don't know if that's statistics or, or anecdote, but either way, most females coming through have a higher HDL than the guy patients. And it doesn't always mean that it's protective. It doesn't always mean that it's beneficial. And I have some women that HDL comes back and it's 100 and they're patting themselves on the back, but it's dysfunctional HDL and it's actually carrying risk that they're not aware of. And no one ever told them that that's even a possibility. So if that HDL molecule is dysfunctional, that means it's not protective. That means it's not sweeping through the blood vessel, cleaning out like a larger particle LDL would. The whole point of beach balls, not BBs, is that they sweep through— these molecules sweep through the blood vessel, kind of cleaning out the perimeter, picking up plaque, picking up debris, and just keeping it nice and patent and open. And when they're small and damaged, they're stickier. And when they're stickier, they stick to areas of damage or to sticky plaque that's already there. When you're measuring these things, you're measuring what's in the bloodstream. You're not measuring what's in the wall or what's in the the lumen of this blood vessel that's seen radiographically or on a catheterization or in future ways of testing. That being said, when HDL is dysfunctional, you have to work hard on the metabolic component more than anything. Is this person overweight? Is this person inflamed? Is this person oxidative? What's their redox poise or balance like? Does this person have a gut microbiome issue? Is this person have fatty liver disease? Is this person insulin resistant or pre-diabetic or diabetic? When you handle those components, I see HDLs transform. HDL and triglycerides to me go hand in hand with that picture. Cholesterol and LDL cholesterol are a little bit different. Collectively it's the package, but you have to look through it through kind of almost like subtopic lenses to kind of figure out what to do for these patients.

Yeah. And it's interesting cuz with that you mentioned niacin, pomegranate extract.

Mm-hmm.

Very, very powerful for that. There's actually a product, Cardiolux, which is actually super concentrated. Yeah. Of pomegranate. So endothelial dysfunction, inflammation, immune dysregulation. So let's notch this down even a little deeper. Yeah. Inflammation, hs-CRP, fibrinogen, oxidized LDL, elevated ferritin, a white count over 8,000.

High platelets.

High platelets.

High interleukin-6, high TNF-alpha.

Oh, you're getting really fancy with cytokines now. Yeah. Yeah.

They're all inflammatory.

So what are the favorite inflammatory markers, I guess Lp-PLA2 technically, would that be, 'cause that's, that's a marker, that's a, it's an enzyme. So I guess technically it's not inflammatory molecule. Yeah. But what are your favorite inflammatory molecule markers to look at when you're looking at risk for heart disease? Yeah.

So for inflammation, hs-CRP, I think, I feel like that's one that just is a slam dunk. Everybody needs to get one of those. Not CRP, not C-reactive protein, but high sensitivity C-reactive protein. It's, it's kind of like boiling it all the way down and just getting that little first bit that's super high sensitivity. Sensitivity. So HSCRP, everybody should know what theirs is, and the goal is less than 1, as low as possible, right? And then ultimately after that, it depends on the individual. I like fibrinogen. I like fibrinogen a lot in patients that are chronically ill and post-infectious. I see those go up post-COVID. Those, those went up quite a bit. They were responsible for a lot of the kind of micro clotting symptoms that people were having. I'm short of breath, but I don't have a PE on a CT. You have these neutrophil traps or nets, you have fibrinogen elevation. Like, that's how that whole infectious inflammatory component plays a role. But fibrinogen, HSCRP— I check sed rates on a basic CBC. If their platelets are up, that's called thrombocytosis. That could be due to inflammation. Ferritin is an acute phase reactant. If ferritin is high, I'm obviously going to rule out iron overload. But if their iron and their percent sat and their TIBC is normal, and we've already done genetics and they're not a hemochromatosis carrier or have hemochromatosis, then I'm going to say you're inflamed because your ferritin's high. I think uric acid is an inflammatory marker indirectly, although it's metabolic. It's indirectly showing metabolic dysfunction, which to me means metaflammation. On a chemistry, basic chemistry, an A/G ratio, albumin to globulin. If your A/G ratio is elevated, you have metaflammation. Other than that, you can get a little fancier like interleukin-6, TNF-alpha. These are inflammatory cytokines and you can kind of expand out and then you kind of cross the threshold of inflammation into oxidative stress. Oxidative stress would be a little bit different where you'd be looking at things like oxidized LDL, 8-OH-DG, F2-isoprostanes. Like these are things that are telling me that this person is oxidative, which basically means that they are having damage to their cell, damage to the cell membrane, damage to different structures in the body. It's just kind of when you hear about antioxidants and why plants and and fruits and vegetables are so good for you, and vitamins or antioxidants are so good for you. Get your antioxidants. It's the opposite of an oxidant. An oxidant is going to damage, an antioxidant is going to protect. The goal is balance, because we need an oxidative burst to kill things. We need an oxidative burst to, to be able to balance our immune response and fight infections. Our body makes a version of bleach that just releases from cells, but you, you want to have it balanced. It's called redox poise. So there's inflammation and there's antioxidant oxidant and, and, and redox boys.

And then the F2-isoprostane tends to do more, elevate more with inflammation in the fat membrane compartment. Yeah. And the 8-hydroxydeoxyguanosine more through DNA.

DNA damage.

Yeah.

And then I like myeloperoxidase is another one to check.

That's a good one. Yeah. Yeah. 'Cause that means you tend to have more elevated white cell.

Yeah.

Meaning just potentially infections going on.

It's usually the macrophage-mediated foam cell deposition.

Yep.

Into the cell membrane to the vascular lining.

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Yeah, my fibrinogen went up.

Yeah. And so that's a marker that I do on patients. It can go up as you age, which is a mark of us all getting—

D-dimer is a good one, by the way.

Get inflamed. Typically with every decade you get over 50, it tends to go up. So, like, 0.5 is normal if you're 50, 0.6 is normal.

For the D-dimer?

Yeah.

Yeah. So, you just age-corrected. Correct. Correct.

Yeah. And then, blood— interesting, blood donation. You know, I remember reading this data point 15 years ago. If you're a male and you donate your blood twice, 2 or 3 times a year, no other data point being looked at, you actually lower your risk for heart disease 20 to 25%. And, like, why? Is it addressing iron overload? Is it detoxification? Is it removing some of these inflammatory markers? So, A lot of these things we've known indirectly forever. It's just now in our world, it's like we have things to do for it. So, inflammatory markers, endothelial dysfunction. I think about ADMSAS.

ADMA, SDMA.

What are some other endothelial markers for looking for that idea that the inside of your arteries are dysfunctional, which is literally where this stuff kind of begins?

Yeah, ADMA is a good one. Probably my go-to stalwart. For me, that stands for asymmetric dimethylarginine. And so it's kind of like, the way that I explain it is it's the, it's like the leaky gut marker for the blood vessel. When your ADMA is up, it means that your blood vessel is leaky and that you probably have some endothelial damage and impaired nitric oxide production. So eNOS, your ability, iNOS, your ability to make nitric oxide through nitric oxide synthase is impaired. So you're not going to dilate the blood vessel well. That could be problematic, especially if it's already stenotic or tight. Lp-PLA2 as like a black at-risk-for-rupture marker. Myeloperoxidase plays a role there too, because again, keeping in mind that we talked about those finite mechanisms of injury where you have either inflammation, oxidative stress, or vascular immune dysfunction, when there's damage from one or all of those to the blood vessel and that glycocalyx, that lining, that protective coat is stripped and the endothelium is exposed, and then there's damage to that, and then all of a sudden a white The white cells come in, that's the macrophage that turns into a foam cell. That's where that myeloperoxidase and other things are kind of playing a role. That's where plaque deposition begins. It's the body's response. It's a biological bandaid. It's, hey, this is bad, let's do something about it. Now all of a sudden you have an area where there's debris and cell response and immune response and stickiness and maybe created self-induced inflammation that will regress over time if you get the problem sorted out, if you get the risk sorted out. Or it will progress and get worse if you don't. So my go-tos are Lp-PLA2, ADMA, myeloperoxidase, and then again, inflammation and oxidative stress markers indirectly. And then imaging, CIMT, CSCT, if you can get a CLIRLY study, that kind of stuff. Because if they have plaque, they clearly have endothelial dysfunction.

Yeah. And that's, it takes decades sometimes. I remember learning this in medical school during the Vietnam War, young guys coming back home, getting autopsies, and these 18, 19, 20-year-old kids already had fatty streaks in their aorta. And so it starts decades, decades. So if you have an elevated calcium score, it's not, oh my gosh, I'm going to die tomorrow. It's like, this has been going on for decades. Yeah.

You know, one more albumin in your urine. If you have, if you have albumin in your urine and your kidneys are leaky, your blood vessels are leaky. Like, let's be real. So I think urine microalbumin is a good one as well.

Yep. That's tested on everybody comes in, gets that, that one done. One data point I remind people of in 1900, the most common cause of heart disease in our country was infections. You get strep and you develop rheumatic heart disease, you get a valvular issue, you get typhoid and you get an aneurysm, right? So before the antibiotic era, the most common cause of heart disease in our country were actually infections, acute things. And now—

Endocarditis, myocarditis.

And now we've replaced it with these low-grade things from dental plaques, infected root canals, gut issues. I mean, a whole host of things. So this, this concept that we're talking about here is actually over 100 years old. It's not new. It's just below the hood or below the surface, so to speak.

Yeah.

So let's transition a little bit because we could keep on talking.

Yeah. It got lost in the shuffle.

Yeah, I know. To talk about therapies and treatments. So if it's 3 causes, the macro, micronutrients, infection, and then inflammation, obviously diet, we're not going to spend time talking. Everybody knows you should eat clean, avoid processed foods.

Through a lot of mono and polyunsaturated fatty acids. Get your omega-3.

Healthy, healthy, healthy fats.

Yeah.

In balance, right? Yeah. I was just listening to an individual talk about our food system and how chickens and eggs eat lots of corn and soy, and those chickens are super high in omega-6s and we eat them. It's one of the things that drive Americans' inflammation is just the fact this stuff is buried in our food system.

You are what you eat. Yeah. But I would like to touch on that just for a split second because Again, if, if your diet is influencing this, and most people feel like they know what to do, great. But the one thing that I think flies under the radar a bit is, again, fats have been demonized for so long, and people are learning the difference between healthy and bad fat, but even then shy away from eating too much of the healthy fat, thinking like that's going to create a problem. Your body needs these fats to survive, and if you go on a low or no-fat diet, you will suffer, and your body will start to churn out more of what it needs. Liver production will go up and it ain't going to be the good stuff. It's going to be whatever it can make. And it's— I've seen this over and over again, and I don't know if there's a study that supports this, but I've seen a lot of female patients that have had cholecystectomies, had their gallbladder removed, and then they were told, don't eat fat because you can't handle it anymore. And then all of a sudden they present with dyslipidemia and they never had it. And the only difference was that they stopped eating fat. And then I have to convince them to eat fat to treat They're high fats and they're just like, huh, you're crazy. And then they do it because they believe the crazy. And guess what happens? Their lipids get better because they're controlling the narrative. They're eating healthy fats in moderation and their liver's not churning out LDL like it's its job because it's fighting inflammation and infections and all these other things that we then get that under wraps and then everything gets better. And if you need bile salts, you take bile salts, but you don't tell somebody don't ever eat fat again. That's just insane.

Yes. So let's transition. That's a perfect segue because we'll talk, we'll start there to like, how do we treat some of these numbers? This is not comprehensive. What we do is individualized, personalized. We do people's blood testing. We ask them about their diet. We ask them about their environment. Is there mold in the environment? How's your gut doing? All that kind of stuff. But so this is, we're just kind of skimming the surface. But to your point, lipid therapy, that's something we do here all the time.

Yeah.

I know. Oh yeah.

I think, you know, I just had a 2-hour IV of IV PC, IV phenylbutyrate, like just awesome.

Awesome stomach goodness. But, the idea of healthy fats, particularly phospholipids are like soap. And, there's one called PlaqueX that has been studied overseas in Europe to actually dissolve this gummed-up stuff in people's arteries. Omega-3s, omega-6s. One of the things about making bile, it's how your body detoxifies. And, if you don't make adequate high-quality bile, your liver won't function optimally. TUDCA, which is a fancy version of ox bile. Yeah. Ursodiol, which is a fancy version of ox bile, is being used to treat autoimmune liver diseases. There's actually an FDA-approved product to treat symptoms of ALS, which has this in it. These bile salts production are important part of how our peroxisomes work, which is these little small organelles, these little organ-like things inside of our cells that burn off toxins. So, all of a sudden, if you're not getting the healthy fats, the way you detoxify bad fats in your body, It's through healthy fats. And to your point, if you're not getting healthy fats in, all you've got left is the bad fats. Bad fats.

And you need an oil change.

And you recycle them. Yes. And so how do you do an oil change? You puncture some holes in it.

Yep.

Binders in the gut. You rev up your engine to burn it off. That's your butyrate, TCA. And you pour in healthy clean, clean, which is your PC kind does a little bit of everything. It's the healthy fat. It also helps. It's like soap.

PC is phosphatidylcholine.

Phosphatidylcholine. Yeah. And so, All of a sudden you can use, you know, omega-3s.

Yeah.

Extra virgin olive oil. I've talked about a bunch. I love it. I eat it.

Quality 6s.

Yes.

Because they're a necessary evil.

Well, you know, the thing about it, unfortunately most Americans, we have way too much. So it's an issue of doing a balance of a 1:1 to 4:1 and letting your body do the rest.

Yeah.

Because we, the average American has way too much.

Way too much. You need 6s.

100%.

So necessary. Too little is a problem, but most people have too much, which are inflammatory. There are some versions of omega-6s that are anti-inflammatory, but the body has to convert those and it's GLA converting into DGLA, and the only way you're getting those without that conversion is through like borage oil or evening primrose oil or blackcurrant oil. But the reality is, is that 6s and 3s share a common desaturase enzyme to convert from one to the next to the next. And if there's not a balance, one's going to hog it and one's going to take all the enzymatic activity and the cofactors that go along with it, and you're going to have an imbalance, which creates metabolic disarray, cell membrane disarray, et cetera. The other thing is that you need. Liver support. You need colagogues. You need protein to have glycine to make bile. So it's all the things, right? It's eating fats, it's eating protein, it's eating cruciferous vegetables, it's getting antioxidants, it's doing the things you were just talking about. But like, that's like the part that, that no one's really talking about or focusing on. And, and that I think that now that we're honing in on it, we should really honor and speak about.

Well, it's interesting because there's Omega-6 called conjugated linoleic acid. Yeah, that's ridiculously important. And the main source of that for our diet is actually ruminant milk from ruminators. You mentioned healthy fats, you mentioned adequate protein. And so I'm not trying to get in a debate about the new food pyramid, which has its faults, but overall it's like better adequate protein. I mean, it doesn't need the big old hunk of red meat on there, but adequate protein, mainly plant-based. Healthy fats. Like, that's what we're talking about. And the other thing I like to think about in regards to all of this is how many times have you had a patient, you do an organic acid profile because I know you like doing your organic acid profiles and they come back and the amino acid levels are low. And you're like, you're eating 80 grams a day and you have multiple low amino acids. You have an amino acid, a protein deficiency, and that's, you know, Phase 2 detoxification requires amino acids. And so even our patients, I have one young lady I'm thinking about particularly who she loves organ meat. She's eating like 130, 140 grams of protein a day.

And still deficient.

So, so I did a, a NutrEval on her. Her organic acid levels were like in the low normal range. But I'm like, well, she, maybe she's producing too many nitrates, right? So I looked at the nitrogen acid, the amino acid cycle, and it was low normal. So I was like, wait a second, we did a GI effects. Look at that.

She's not absorbing it.

She's absorbing it all.

Oh my gosh.

Her 1-methylhistidine, 3-methylhistidine, normal. She has high need.

Yeah.

And I was like, I'm double checking, triple checking, quadruple checking. She's taking so much, eating so much, and it took her—

Did she have that much of a deficit or—

This was over 3 years to get her to the point. Before it was all low, low, low, low, low, low. This last time, which was this past— to 2025. We got the stuff to come in. The point of that is, is you hear these recommendations, like ultimately you have to individualize.

Yeah, it has to be personal.

And I, when I was talking with her, I'm like, I don't believe my eyes because I believe you, I trust you, you're doing— she's thriving, doing great, her hair's gorgeous, she's like amazing, super healthy, takes her liver, freezes it, and yeah, great. But it's like, and still like just in the normal range.

You would have never guessed that without testing it.

Yeah.

And the thing is like, you don't know in that situation, So basically what Dr. Hartman is explaining is like, this is a person who's eating more than enough protein, clearly more than what suggests further recommendation, and ultimately still almost has a deficiency in amino acids. So the first thing that would come to my mind is this person's not breaking it down, not absorbing it, but he checked her gut because that's what a good clinician does. And it was fine. She was absorbing it. So it's a need. It's a metabolic need either for this individual creating, filling the gap that been there for so long and getting that deficit back to normal, or there's ongoing overutilization, right? Like if she didn't feel well, but her gut was fine, it was why is she utilizing so many amino acids? Does she have a lot of DNA damage from oxidative stress and she's using it all for repair? Is methylation an issue? Is, are toxins an issue? So that's the kind of detective work that we're talking about. Like in those situations, you have to boil it down to what am I seeing and what does this mean? And then look at that patient clinically and say, what am I going to do about it? Because it's not one size fits all and you have to tailor it to the individual. Otherwise you're gonna hurt 'em or not get 'em better.

So fats, so something, you know, particle number's high, LDL particle number's high, total cholesterol's high. Yeah. HSCRP's up a little bit, you know, and those individuals I tend, again, diet and environment. Yeah. Gut, we're already doing all that stuff. Yeah.

Foundational stuff assumed.

100%. Yeah.

Work on stress, prioritize sleep, move your body. Yeah. Eat clean.

Yada yada. For those individuals I like, you know, balanced omega-3s.

Mm-hmm.

Using vitamin E, particularly your alpha delta tocotrienols, liposomal vitamin C, NAC. Those are a few basic interventions. You can see those things lower. I use those routinely for those numbers. Your hs-CRP is up, you have an infection. I've had multiple patients where I've had to, you know, dental issues, nothing works. You do a round of doxycycline for some oral thing. All of a sudden, their hs-CRP comes down. You're like, okay, you need to work with your periodontist because all that scaling stuff you think is not a big deal, is a big deal. You know, individualizing all this to people is super important. What are some of your favorite go-tos for some of these numbers? Yeah, when you see people.

So I start with, again, foundational stuff, and then fiber and fish oil, fiber and fish oil, fiber and fish oil. You know my go-to. So I check an OmegaCheck on every patient. If their OmegaCheck is low, we're working on that first. And I want their OmegaCheck not to just be normal but optimal. Optimal for me is greater than or equal to 8. Normal is above 5.4. and that's an OmegaCheck that you can get at Quest LabCorp. Actually, LabCorp doesn't do it, so Quest. And OmegaChecks are showing you 3s, but you also get 6s in that ratio. If you want to take it a step further and look at a full fatty acid profile to see about their sat fat, their 7s, their 9s, the breakdown of the 6s, the desaturase activity, just do an organic acid testing, right? Like with the fatty acid profile, do a NutrEval, do a Metabolomics or whatever lab you like. But I'm going omega-3s first and foremost. Fiber. Nobody eats enough fiber. Fiber is such a broad sort of intervention because you can address inflammation, you can address a microbiome issue, you're ramping up detox, you're blunting that glycemic punch, so you're going to get a bit more insulin sensitive. You're just— you're taking care of so many facets that are going to indirectly affect that dyslipidemia that sometimes that's just enough. Then it goes the next step, like, depends on what I'm trying to address. If you're maximizing fiber, which for me is 30 to 40 grams grams a day minimum, slowly. If you start really, really low, like if you're only doing like 9 grams a day, don't go to 40. And then the omegas, the next step would be like, maybe I'm going to use red yeast rice in that patient. If I think that they're absorbing a lot of cholesterol in their gut, a rapid absorber, I'm going to use a plant sterol, right? Like drugs on the market that are used by pharmas— by cardiologists like Zetia. What is that? It's just basically a prescription plant sterol, right? Decrease intestinal absorption, give some plant sterols. If you want to decrease production, give an HMG-CoA reductase inhibitor. That's a fancy way of saying Red yeast rice or the trademark pharmaceutical name statin, right? So I do a little red yeast rice or I might do some plant sterols. I like berberine. If this is a cardiometabolic presentation, if this person is a little bit overweight, if they have dysbiosis in their gut, if they have insulin resistance and dyslipidemia, berberine is a nice broadsword to use for that patient. You're, you're doing all those things with just some berberine. I like niacin in the individual, especially if they have Lp(a) elevation. And HDL suppression, niacin will revamp an entire lipid profile. It can lower cholesterol, it can lower LDL, it can raise triglycerides, it can raise HDL, it can lower Lp(a), it can lower LDL particle number, it can fluff out particles. So like, niacin's nice. I don't use it a ton, but you can use pantothenic acid, which is vitamin B5. You can use, you know, I don't know, there's like a host of things. It's just like so many things like NAC, like you said, vitamin C, vitamin E. Aged garlic extract. There's just like so many different things that you can layer in. It just really depends on the individual. I'll use aged garlic extract if they have oxidative stress and they already have plaque, cuz it's got good data on plaque regression as well as dealing with mitigation of some of that oxidative stress. Makes the blood a little slippery. Also can help with some of the gut bug stuff. So I like aged garlic extract for that.

I use a lot of K2 MK7.

Yeah.

Yep.

Yep.

Calcium. What, 720 micrograms a day or higher if you've got elevated calcium score.

Mm-hmm.

The one thing about the OmegaCheck, the omega-3s, I remember Rhonda Fitzpatrick was talking about this at the A4M Conference a year and change ago. And just the data point stuck in my head that if you have a low omega-3 level and you're not a smoker, you're not a smoker, your risk for heart disease is the same as a smoker with a normal omega-3 level. And all of a sudden, it's like literally just getting my omega-3 levels normalized is like I quit smoking.

Yeah. That's profound.

It's profound. And then the whole, you mentioned rapid cholesterol absorbers. There's a test you can actually do for that. But then the treatment is plant sterols or they absorb. So removing those, doing things to block the absorption of those. So we could keep on rambling. Yeah, I love it.

I love this stuff.

The point is, is that this is just cholesterol and the pantheon of these 300+ things and individualizing, personalizing it, getting someone's data sheet. Where'd you grow? What's your job? What's your gut look like? What are your hormone status? Do you have sleep apnea? All that stuff. And then when you get the numbers back, You really, that, this really enables us to 100% individualize someone's program and we get really good results.

Yeah. And you establish targets and you, you discuss those with the individual. Here's what your number is. Here's what your risk stratification looks like. Here's what your disease profile looks like. This is our treatment plan. Let's track these numbers over time. These are our targets. And if we don't hit our targets, then we go ahead and we modify the plan. Or if you feel like what you're supposed to do, you gotta dig deeper. Like, am I looking at heavy metals at this point in time? Have I looked at chronic infections yet? Is this a CIRS patient? Is this— and you just keep asking questions until you find the answer.

Yeah. We'll end with this data point because you, you, you said it, the very— you mentioned the word heavy metals. According to the, I think it's, I believe it's USPFTF or NHANES data, one of the two national things, 30% of all heart disease in our country is directly related to lead exposure. 30%. Wow. This is government data. So if, and who is this? This is people before born before 1991, you know, leaded gasoline, paint in '76 and then the '80s, you store in your body, half-life of bone is 17 years. But if someone has heart disease, they always get a lead level. And the question becomes, how often is their lead level zero? In my clinical practice, they often have some number.

Yeah.

And so all of a sudden, again, we didn't go down the heavy metal pathway during our conversation. But again, another data point.

Yeah.

That for some people, depending on what your job was, where you live in the country, can be really important.

If you breathe, if you drink water, if you eat food.

Yeah, yeah.

I mean, I get urine provoked on all my cardiovascular patients. I get urine provoked, um, metal challenges and see what their body burden is, check serum, and just correlate till we get it as low as possible. There's no biological purpose for these things, like, so there shouldn't be an acceptable range. There is an acceptable range. I don't know who established it, but the reality is, is that the acceptable range Zero.

It used to be, it used to be higher. It used to be 50. Yeah, it used to be higher. Like in the '70s.

It's better. I mean, it's getting better. I'm not trying to be mean to anybody, but come on.

It was 10. It was 10 when I started my training. Now, it's 5. Yeah. And the question is what's the— Progress. What's the— Well, 50 to 5 is a big drop. Yeah. And the question is what's the lead level that you have the— What lead level affects IQ in a fetus and a kid's answer is Any lead level? Yeah. It's not a safe lead level for a developing brain.

Yeah.

So, I hope this information was helpful. If it was to you, like, share, subscribe. That's how we get this information out there. All this stuff was for educational purposes only. You should, of course, always discuss this with your own personal healthcare provider. And with that, we will sign off and we'll see everybody next time. See ya. My daughter was never supposed to walk, talk, or crawl. And today, at 19, she's thriving. And guess what? We ignored every single thing the specialist told us to do. Hi, I'm Dr. Aaron Hartman, MD, and I wrote Incurable: From Hopeless Diagnosis to Defying All Odds so you don't have to navigate this alone. In it, we share the secrets that she and thousands of my patients have used. Grab the book or Audible wherever books are sold, or you can find it in the link below.