Nicolette: 0:01

Welcome to the Health Pulse, your go-to source for quick, actionable insights on health, wellness and diagnostics. Whether you're looking to optimize your well-being or stay informed about the latest in medical testing, we've got you covered. Join us as we break down key health topics in just minutes. Let's dive in.

Rachel: 0:25

You know, for the longest time, the story we all heard about heart health was well, pretty simple, wasn't it? High cholesterol clogs your arteries. End of story.

Mark: 0:34

Right, like it was just plumbing.

Rachel: 0:35

Exactly, but lately the science seems to be pointing to, I guess, a much more dynamic picture, maybe even surprising.

Mark: 0:43

Absolutely yeah. We're doing a deep dive today based on this really fascinating article the Truth About Cholesterol and Atherosclerosis Debunking Old Myths with New Science.

Rachel: 0:54

Okay.

Mark: 0:55

And it really does challenge that old simple idea and brings out some crucial new insights.

Rachel: 1:01

So if you're listening and you want to really get what's going on with heart disease, you know beyond just that one cholesterol number, but without needing a PhD.

Mark: 1:09

Yeah, without getting totally bogged down in medical jargon.

Rachel: 1:12

Then you're definitely in the right place. Our goal today, our mission, is to pull out the key knowledge from this piece what really drives atherosclerosis, according to this newer science?

Mark: 1:22

And I think the most important thing to grab right off the bat is this Atherosclerosis isn't just about how much cholesterol is like floating around. It's about the bigger picture. It's about inflammation levels in your body, how your body is actually handling the fats, the lipids.

Nicolette: 1:37

Yeah.

Mark: 1:38

That context, it's everything.

Rachel: 1:40

Okay, so let's break that down. Atherosclerosis 101. And it sounds like it's way more involved than just, you know, pipes getting clogged with gunk.

Mark: 1:48

Precisely yeah, the article really stresses that it's an active process. It's deeply tied into inflammation and your immune system's response. It's not just passive buildup. Often the first domino to fall is some kind of problem with the inner lining of your arteries. That's called the endothelium. Think of it like the smooth nonstick coating inside a pan getting scratched up Right.

Rachel: 2:12

And what does the scratching? What damages that lining? Well, a few things.

Mark: 2:15

High blood pressure is a big one. Insulin resistance, you know where your body isn't responding well to insulin. Okay, smoking, obviously, and even just sort of general wear and tear from the things like oxidative stress happening in the body.

Rachel: 2:26

Oxidative stress like rust.

Mark: 2:28

Kind of yeah, it's chemical damage, and when this lining, this endothelium, gets damaged, it becomes leakier, more permeable, and that allows certain fat carrying particles from your blood, especially the ones that have a protein called ApoB on them, to kind of slip through into the artery wall itself.

Rachel: 2:47

ApoB. Okay, we'll need to circle back to that one we will, and LDL, the one everyone calls bad cholesterol.

Mark: 2:53

that's a major type of these ApoB particles.

Rachel: 2:55

So, okay, these LDL particles get inside the artery wall. That's the cholesterol we've always been told is the bad guy.

Mark: 3:02

Well, ldl's actual job is just carrying cholesterol around, which your body needs. It's essential. The trouble really kicks off when those LDL particles get trapped in there, in that subendothelial space Trapped, and then they undergo this process called oxidation. Basically, they get damaged. They react with other molecules. It's like metal rusting when it's exposed to air and moisture.

Nicolette: 3:21

Gotcha.

Mark: 3:22

And this oxidation gets ramped up by things like inflammation and just poor metabolic health overall.

Rachel: 3:27

And this stuff, the oxidized LDL or ox LDL. That's the real problem, child.

Mark: 3:32

That's what the article really highlights. Yes, ox LDL isn't just, you know, inert fat. Sitting there it becomes highly active, it triggers inflammation, it promotes the whole atherosclerosis process.

Rachel: 3:42

How does it do that?

Mark: 3:43

Well, what's really interesting is how it acts. Like a flare signal, it attracts your immune cells, specifically macrophages, a type of white blood cell, to come to the site of injury.

Rachel: 3:54

Okay, so the body's trying to clean it up.

Mark: 3:56

Right, but that's where things go wrong. These macrophages start gobbling up the oxidized LDL, and in doing that they transform into these things called foam cells.

Rachel: 4:06

You might have heard of them. Foam cells yeah, I think so.

Mark: 4:09

They're a key feature, a hallmark of the very early stages of plaque development in the arteries. Okay, but it doesn't stop there. This ox LDL also signals smooth muscle cells in the artery wall to migrate and lay down more sort of structural material which helps those early fatty streaks grow into more complex, hardened plaques. Wow, the article even mentioned some research identifying ox LDL as a key initiator and actually a pretty strong marker of cardiovascular risk.

Rachel: 4:38

Okay, so we've got the damage lining LDL gets in, it rusts, gets oxidized and then attracts the cleanup crew, the macrophages which turn into foam cells and build up plaque. Okay, but the article also mentioned red blood cells. That felt like it came out of left field.

Mark: 4:56

Yeah, that's a more recently understood part of the story. It seems red blood cells become particularly important later on, in the more advanced stages. We're talking about plaques that are more vulnerable, the ones that might become unstable and rupture. Sometimes bleeding can happen inside these plaques. It's called intraplaque hemorrhage.

Rachel: 5:15

Bleeding inside the plaque.

Mark: 5:16

Exactly, and when that happens, red blood cells get into the plaque structure.

Rachel: 5:20

And why is that a problem? They just carry oxygen, right.

Mark: 5:24

Normally, yes, but when they break down and the term is hemolyzes, they release stuff that makes the situation worse.

Rachel: 5:31

Like what.

Mark: 5:32

Well, one thing is free hemoglobin. That actually contributes to more oxidative stress right there on the plaque.

Rachel: 5:38

More rust.

Mark: 5:39

Pretty much. They also release iron, and iron is a big deal because it acts like a catalyst, like a turbocharger for oxidizing even more LDL through these things called Fenton reactions.

Rachel: 5:52

OK, so it speeds up the bad process.

Mark: 5:54

Massively. And finally, the membranes of those broken down. Red blood cells release phospholipids which can attract even more macrophages to the area, leading to more foam cells.

Rachel: 6:04

So it's like a feedback loop from hell almost. The plaque gets damaged, it bleeds, the red blood cells break down, releasing stuff that causes more damage and oxidation.

Mark: 6:12

Which then weakens the plaque further.

Rachel: 6:14

Exactly. The article really emphasizes how these processes amplify the oxidative damage and, crucially, weaken the fibrous cap.

Mark: 6:22

The fibrous cap. That's like the protective shell on the plaque. That's right.

Rachel: 6:26

It's the layer holding it all together, keeping it stable. If that cap gets weak and thin, it's much more likely to rupture, and that rupture is what triggers heart attacks and strokes.

Mark: 6:35

Yeah, there was some important work cited that really brought this red blood cell connection to light. It just underscores again that atherosclerosis isn't simple. It's this complex, multi-step thing involving lipids, yes, but also inflammation, oxidative stress, immune cells, even red blood cells and vascular injury.

Rachel: 6:54

Man, that old clogged pipes idea really does miss almost all of that complexity. So, given all this, where did the traditional focus on just total cholesterol or LDL-C actually come from? What did it get right, maybe, and where did it fall short?

Mark: 7:09

Well, the article does acknowledge that focusing on LDL-C, especially lowering it, has definitely helped. It has reduced cardiovascular events, particularly for people already considered high risk.

Rachel: 7:18

Wait, so it wasn't totally wrong. It helped some people.

Mark: 7:21

Not totally wrong. No, it correctly identified that LDL can be atherogenic, meaning it can contribute to plaque, especially, as we now know, when it gets oxidized Right. And yeah, plenty of studies showed that lowering LDL-C, often with statins, does reduce the risk of future events, especially in what we call secondary prevention, people who've already had an event.

Rachel: 7:41

Okay, so that's the what it got right. Column. Now the big question OK, so that's the what it got right. Column. Now the big question what did it miss? What are the key things this new science highlights?

Mark: 7:50

OK, this is where our understanding has really shifted. The article points out several critical things. First, the number of LDL particles in your blood might actually be more important than the total amount of cholesterol inside those particles, the LDL-C number.

Rachel: 8:06

The number of particles versus the amount of cholesterol, explain that.

Mark: 8:10

So you could have someone whose LDL-C level looks, you know, normal or even good, but they might have a really high concentration of small dense LDL particles.

Rachel: 8:19

Ah, smaller particles, but lots of them.

Mark: 8:21

Exactly Each one of those particles. Even if it's carrying less cholesterol than a big fluffy one can still get into the artery wall, get oxidized and contribute to plaque.

Rachel: 8:29

And a standard test wouldn't show that.

Mark: 8:31

Not usually. Your LDL-C might look fine. You'd need to measure something like ApoB, which we mentioned.

Rachel: 8:35

The protein marker Right, or the actual LDL particle number, ldl-p, to see that hidden risk. That makes a lot of sense.

Mark: 8:47

More potential troublemakers, even if they're smaller. What else did the old model kind of overlook? Another big one is the ratio of your triglycerides to your HDL cholesterol.

Rachel: 8:52

Triglycerides to HDL.

Mark: 8:54

Okay, a high ratio there often signals underlying metabolic stress, things like insulin resistance, maybe elevated levels of other fatty particles called VLDL remnants, and often an overproduction of those small dense LDL particles we just talked about. This whole metabolic picture is really pro-atherogenic. It fuels the fire.

Rachel: 9:14

And HDL itself, the so-called good cholesterol. Is it always good?

Mark: 9:19

Well, that's another nuance. The article really stresses that just having a high level of HDL cholesterol, a high HDLC number, isn't automatically protective.

Rachel: 9:28

Really.

Mark: 9:28

Yeah, what matters more is how well that HDL is functioning. Is it actually doing its job effectively?

Rachel: 9:33

Which is.

Mark: 9:34

Its main job is reverse cholesterol transport, basically grabbing cholesterol from the artery walls and taking it back to the liver. But if your HDL is dysfunctional, how does it get dysfunctional? Things like oxidative stress, again damage from high blood sugar, glycation or just general inflammation can make HDL less effective. So the quantity on the report might look good, but the quality might be poor. It's not doing its protective job well.

Rachel: 9:57

OK, quality over quantity for HDL Got it and we keep dancing around it, but inflammation seems like a massive piece. The traditional model maybe didn't emphasize enough.

Mark: 10:07

Absolutely huge, you could argue. Cholesterol, or maybe oxidized LDL gets the process started, but inflammation is what really drives the plaque's progression and, critically, its instability.

Rachel: 10:18

Instability, meaning likelihood to rupture.

Mark: 10:21

Exactly Markers in your blood like HSCRP, high sensitivity C-reactive protein, or others like IL-6, TNF-alpha. Studies show these correlate with higher risk of heart attacks and strokes, even in people whose LDL-C is technically well controlled.

Rachel: 10:34

Wow, okay, and we talked about red blood cells earlier. How did the old model miss their contribution?

Mark: 10:39

Yeah, for a long time they just weren't really seen as part of the atherosclerosis story directly. But, like we discussed, when they break down inside those unstable plaques, the hemoglobin and iron get released Right and that massively promotes LDL oxidation and foam cell formation. Plus, the leftover membranes from those broken red blood cells can actually stimulate more inflammation and even encourage new leaky blood vessels to grow within the plaque itself.

Rachel: 11:06

Which just makes it even more unstable.

Mark: 11:08

Precisely it adds fuel to the fire.

Rachel: 11:10

And what about the structure, the physical structure of the plaque itself? Did the old model miss something there too?

Mark: 11:15

It didn't really get into the why of plaque rupture as much. Now we understand that inflammation activates certain enzymes, like MMP9 is a key one.

Rachel: 11:24

MMP9.

Mark: 11:25

These enzymes basically act like molecular scissors. They chew up the collagen and elastin, the stuff that gives that fibrous cap its strength and integrity.

Rachel: 11:34

So inflammation weakens the cap from the inside out.

Mark: 11:37

That's a good way to put it Makes the plaque fragile, much more likely to break open.

Rachel: 11:41

And one last thing the article mentioned was phytosterols plant sterols Aren't they supposed to be good? You see them added to foods.

Mark: 11:47

That's a more nuanced point. They can help lower LDL cholesterol for many people, that's true, but but there's some emerging evidence, according to the article, suggesting that for certain individuals maybe people with a genetic condition called cytosterolemia, or just people who absorb these plant sterols unusually well high levels of specific ones, like campesterol and sidosterol, might actually get incorporated into the vessel walls. Uh-oh and potentially contribute to endothelial dysfunction and maybe even plaque instability. It's a complex area still being researched.

Rachel: 12:19

So even good things aren't always universally good for everyone.

Mark: 12:23

It's a reminder that biology is complicated and context matters.

Rachel: 12:27

Definitely so. Okay, it's abundantly clear. The picture is way more intricate than just high cholesterol is bad. This brings in particles, inflammation, metabolism, structure. It's a lot. Let's really dig into one key piece you mentioned.

Nicolette: 12:40

Yeah.

Rachel: 12:40

ApoB. The article called it a better marker of risk. Why? What makes ApoB so important?

Mark: 12:46

Right, apob or apoliprotein B. It's such an insightful marker because it's basically a protein tag found on every single potentially harmful atherogenic fat-carrying particle in your blood.

Rachel: 12:56

Every single one, like LDL, VLDL.

Mark: 12:59

LDL, yes, but also VLDL, IDL, which are sort of intermediate particles, and LPA, another important one, all the ones that can contribute to plaque.

Rachel: 13:08

Okay.

Mark: 13:08

And here's the crucial part Each one of these potentially harmful particles carries exactly one molecule of ApoB on its surface. Just one.

Rachel: 13:19

Ah, so it's like a direct count.

Mark: 13:20

Exactly when you measure ApoB in the blood, you're essentially getting a direct count of the total number of these atherogenic particles floating around.

Rachel: 13:28

OK, so LDL-C measures the amount of cholesterol inside the LDL particles.

Mark: 13:32

Right the cargo.

Rachel: 13:33

But APOB tells you how many actual vehicles, how many particles are out there that could potentially deliver that cargo into the artery wall.

Mark: 13:41

That's a perfect analogy and that's why it's often considered a more accurate, more direct measure of your actual risk than LDL-C alone.

Rachel: 13:48

Because someone could have normal LDL-C.

Mark: 13:50

Right, but still have a very high number of those smaller, denser LDL particles. Each one carries less cholesterol, so the LDL-C might look OK.

Rachel: 13:58

But the ApoB count would be high because there are just so many particles.

Mark: 14:02

Precisely, the ApoB test would likely pick up that increased particle burden, that higher traffic, whereas the standard LDL-C might give false reassurance.

Rachel: 14:12

And is there research backing this up? Does ApoB predict risk better?

Mark: 14:17

Oh, yes, the article mentions. Numerous large studies have consistently shown that ApoB is a stronger predictor of future heart attacks and strokes compared to LDL-C or even non-HDL cholesterol.

Rachel: 14:28

That makes sense. Intuitively. It's the particle getting in that starts the problem. Right, it's the particle number in that starts the problem.

Mark: 14:32

Right, it's the particle number, the concentration, that dictates the likelihood of hitting the artery wall and getting trapped.

Rachel: 14:38

And is the medical world catching on to this? Is ApoB testing becoming more common?

Mark: 14:43

It definitely is gaining traction. The article cites a 2021 consensus statement from the American College of Cardiology. Ok, that actually recommended considering ApoB as a primary target for assessment, especially in people with insulin resistance metabolic syndrome or high triglycerides situations where LDL-C can be particularly misleading.

Rachel: 15:01

Right, those situations where you might have lots of small dense particles. Exactly so. How does ApoB compare to that other test you mentioned, LDL-P, the particle number test? Do they tell you the same thing?

Mark: 15:17

They're both aiming for the same goal of testing the number of LDL particles and generally, both are better predictors of risk than just LDLC. Okay, but APOPE often has some practical advantages it tends to be less expensive. It's more widely available on standard lab panels. Now, good points Doesn't always require fasting, which is convenient, and it's increasingly being built into risk calculators and treatment guidelines.

Rachel: 15:38

So easier to access and use clinically often.

Mark: 15:42

Often yes.

Rachel: 15:42

And the article specifically mentioned times when checking ApoB is really crucial.

Mark: 15:46

Yes, it emphasizes its value, particularly if you have normal or even low LDL-C, but your triglycerides are high.

Rachel: 15:53

Okay, the discordant pattern.

Mark: 15:54

Exactly Also for anyone with metabolic syndrome or type 2 diabetes. People with elevated LPA.

Rachel: 16:00

Which is that other genetic risk factor particle.

Mark: 16:02

Right, and just generally, anytime there seems to be a mismatch between someone's LDL-C level and their other risk factors or family history. If things don't seem to add up, APOV can provide a lot of clarity.

Rachel: 16:14

Are there target levels for ApoB?

Mark: 16:16

The article mentioned general targets, ideally aiming for below 80 mL of GDL for many people and perhaps even lower, like below 65 mL of GDL, for those considered at very high risk.

Rachel: 16:27

Okay, that really clarifies the ApoB story. Now let's pivot back to inflammation. The article didn't mince words calling it the real catalyst of plaque formation. Why such a strong focus on inflammation?

Mark: 16:39

It's a strong statement, yeah, but the science really backs it up. Think of it this way Cholesterol, maybe, specifically oxidized LD, the gasoline poured on the fire. It's what transforms a relatively stable plaque into something dangerous, something prone to growing rapidly and, most importantly, rupturing.

Rachel: 16:58

So how does inflammation do that? What's the mechanism?

Mark: 17:00

Well, we touched on parts of it. Remember the damaged artery lining lets LDL in. Once that LDL gets oxidized, it's a huge red flag for the immune system. It attracts those monocytes which become macrophages.

Rachel: 17:12

The cleanup crew that turns into foam cells.

Mark: 17:20

Exactly. But as they engulf the ox LDL, they don't just sit there quietly, they start churning out a whole bunch of inflammatory signals, molecules called cytokines, things like IL-6,.

Rachel: 17:26

TNF-alpha MCP-1. Glyndals that call in reinforcements.

Mark: 17:29

Pretty much. It creates this self-perpetuating cycle More inflammation attracts more immune cells. It promotes the growth of those leaky new blood vessels within the plaque which can bleed Right, causing more problems. It fuels more oxidative stress and, as we discussed, it activates those MMP enzymes.

Rachel: 17:45

The molecular scissors.

Mark: 17:47

That degrade the plaque's protective cap, making it weak and unstable.

Rachel: 17:50

So inflammation is really driving the danger aspect of the plaque's protective cap, making it weak and unstable. So inflammation is really driving the danger aspect of the plaque.

Mark: 17:54

That's the key insight. It's less about the sheer size of the plaque sometimes and more about how inflamed and unstable it is.

Rachel: 18:00

And can we measure this inflammation? Are there tests?

Mark: 18:03

Yes, definitely. The article mentions several key ones. High sensitivity C-reactive protein, HSCRP, is probably the most common.

Rachel: 18:10

H-CRP.

Mark: 18:11

Elevated levels, say above 2.0 mL, signal higher cardiovascular risk, even if your LDL looks great.

Rachel: 18:18

Wow Okay.

Mark: 18:19

Interleukin-6, IL-6 is another important one. Higher levels predict future heart disease and it's actually being explored as a therapeutic target, itself Interesting. And there's another called LPPLA-2, which seems more specific to inflammation happening within the blood vessels and unstable plaques. So HSTRP gives a general systemic inflammation picture, while IL-6 and LPLA2 might offer more targeted insights.

Rachel: 18:44

And wasn't there a big study mentioned that really drove this inflammation point home.

Mark: 18:48

Absolutely the CANTOS trial from 2017. It was a real landmark.

Rachel: 18:52

What did they do?

Mark: 18:53

They used a drug called canakinumab, which specifically blocks one of those inflammatory cytokines, il-1. They gave it to people who'd already had a heart attack and still had high HSCRP levels indicating ongoing inflammation. And the result. The remarkable finding was that the drug significantly reduced their risk of having another heart attack or stroke. And here's the kicker.

Rachel: 19:13

Yeah.

Mark: 19:13

It did this without lowering their cholesterol or lipid levels significantly.

Rachel: 19:18

Whoa how it was purely targeting the inflammation.

Mark: 19:26

Exactly. It was really powerful proof of concept that targeting inflammation directly could reduce cardiovascular risk independent of cholesterol lowering.

Rachel: 19:30

That really changes everything, doesn't it? So what are the implications? How should this change how we think about our risk?

Mark: 19:36

Well, the article strongly suggests that if you have, say, normal LDL numbers but your HSCRP is high, or if you have metabolic syndrome or diabetes. Right, or even chronic inflammatory conditions like rheumatoid arthritis or lupus. You might actually have a significantly higher vascular risk than a standard cholesterol panel would suggest.

Rachel: 19:56

So the standard panel could be misleadingly reassuring for those people.

Mark: 19:59

It could be. The recommendation is that these individuals could really benefit from a broader risk assessment, looking at inflammatory markers alongside lipids and focusing on lifestyle changes that tackle both.

Rachel: 20:10

This really drives home that it's not just the stuff floating in the blood but the whole environment which leads perfectly into the next piece Diet, insulin resistance and overall metabolic health. How do these tie in?

Mark: 20:23

Fundamentally, the article frames the metabolic environment as basically setting the stage shaping your cardiovascular risk, and insulin resistance is a key player here.

Rachel: 20:35

How does being resistant to insulin mess with our lipids and inflammation?

Mark: 20:39

It throws a lot of things out of whack. Your liver starts pumping out more VLDL.

Rachel: 20:43

Which raises triglycerides.

Mark: 20:44

Exactly and also promotes the formation of those small dense LDL particles we keep talking about. Okay, insulin resistance also tends to lower your HDL levels, the good cholesterol and makes the HDL you do have less functional. Impairs that reverse cholesterol transport.

Rachel: 20:58

Double whammy.

Mark: 20:59

Yeah, and high insulin levels themselves can contribute to other problems like activating the sympathetic nervous system, causing sodium retention and directly damaging that endothelial lining.

Rachel: 21:10

So it hits on multiple fronts and you mentioned a marker for this earlier.

Mark: 21:13

Yes, that triglyceride to HDL ratio. The article highlights that again. A ratio over 2.0 using MGDL units is a really potent indicator of underlying insulin resistance and higher cardiovascular risk, even if your LDL-C looks perfect.

Rachel: 21:29

So simple yet powerful, and diet obviously must be a huge lever here.

Mark: 21:33

Absolutely massive. The types of food you eat directly influence these lipid dynamics and inflammation.

Rachel: 21:38

What kind of diets are problematic according to the article?

Mark: 21:41

Diets high in refined carbs, added sugars, processed seed oils. These tend to crank up triglycerides, promote those small LDLs and fuel inflammation.

Rachel: 21:51

Makes sense.

Mark: 21:51

Also, getting too many omega-6 fats without enough balancing omega-3s can contribute to oxidative stress and endothelial issues.

Rachel: 21:58

Yeah.

Mark: 21:59

And just consistently eating too many calories overall, regardless of source, tends to raise insulin and ramp up fat production in the litter.

Rachel: 22:06

Okay, so that's the bad news. What about the good news on diet? What helps?

Mark: 22:09

Definitely good news too. The article mentions patterns like low-carbohydrate diets or Mediterranean-style diets.

Rachel: 22:15

Why those?

Mark: 22:15

They've generally been shown to lower triglycerides, improve HDL function, reduce those small dense LDLs and lower inflammatory markers. Things like time-restricted eating or intermittent fasting can also be beneficial for some people. They can help lower fasting insulin, improve lipid profiles, reduce oxidative stress and, of course, focusing on fiber-rich whole foods, healthy fats like monounsaturated fats from olive oil, avocados, getting enough omega-3s these all support better lipid balance and help keep that endothelial lining healthy.

Rachel: 22:47

So, bottom line, the same LDL-C number on a lab report could mean very different things depending on someone's insulin sensitivity, their inflammation levels, their diet.

Mark: 22:57

Precisely. That's why looking at LDL-C in isolation can be so incredibly misleading. You really need to assess for insulin resistance. Maybe look at inflammation markers. Understand the dietary context, especially if the numbers are kind of in that borderline zone.

Rachel: 23:11

Which brings us right to personalized risk. How do we put all these pieces together? When should an elevated LDL really worry us, and what are the key tests beyond the basics to get that fuller picture?

Mark: 23:23

Right. The article stresses that a single cholesterol number just isn't enough. Risk is contextual pull. It depends on that whole metabolic, inflammatory and even structural picture in your arteries.

Rachel: 23:34

So when does a high LDL become more concerning?

Mark: 23:37

It's more concerning if it's paired with other warning signs, for example, high ApoB level, say over 100 milligdl, or a high LDL particle count LDL-P. That tells you the particle burden is high. If you also have insulin resistance, metabolic syndrome or type 2 diabetes, that's a major red flag.

Rachel: 23:54

Makes sense.

Mark: 23:55

Elevated inflammatory markers like HSCRP or IL-6, a high LPA level. That genetic factor Got it A strong family history of early heart disease or personal history and, importantly, if there's already evidence of plaque held up on imaging like a coronary artery calcium or TAC score over 100, that shows the process is already underway.

Rachel: 24:14

So what are the key tests the article recommends to get this deeper insight? Let's recap those.

Mark: 24:19

Okay, beyond the standard lipids, apob is probably top of the list for measuring that total atherogenic particle number.

Rachel: 24:25

ApoB got it.

Mark: 24:26

LDL particle count. Ldlp is another way to look at particle quantity. The triglyceride to HDL ratio is crucial for metabolic risk, ideally aiming below 2.0.

Rachel: 24:36

DGHDL ratio.

Mark: 24:37

Check high-sensitivity CRP. Hscrp for systemic inflammation ideally below 1.0 mil-GO.

Rachel: 24:45

HSCRP.

Mark: 24:46

Fasting insulin and maybe a home IR calculation to specifically check for insulin resistance.

Rachel: 24:52

Insulin and HMI.

Mark: 24:53

Lepoprotein or LPA to assess that genetic risk. Maybe even things like ferritin and GGT which can give clues about oxidative stress and liver issues impacting lipids.

Rachel: 25:03

Ferritin GGT.

Mark: 25:05

And then there's imaging the coronary artery calcium CAT scan that directly measures plaque burden and is a very strong predictor of future events.

Rachel: 25:12

CAT scan. Wow, that's a comprehensive list.

Mark: 25:15

It gives you a much, much clearer picture than just LDL-C alone.

Rachel: 25:18

And the article had an example to drive this home right, Comparing two people.

Mark: 25:22

Yeah, it painted a picture. Imagine two 48-year-old men, same LDL-C level on their report. Looks identical.

Rachel: 25:29

Okay.

Mark: 25:29

But man A has a much higher ApoB level, a poor TGHDL ratio, high HSCRP and high fasting insulin. Man-b has good levels for all those other markers.

Rachel: 25:40

So even with the same LDL-C.

Mark: 25:42

MAN-A is at significantly higher risk. The article makes that point very clearly. Their underlying metabolic and inflammatory health is completely different. That's why this personalized approach, looking beyond just one number, is so critical for accurately understanding risk and tailoring the right interventions.

Rachel: 26:00

This has been incredibly eye-opening really changes the perspective. So let's try and wrap this up. What are the absolute key messages, the main takeaways from this deep dive into the newer science?

Mark: 26:09

I think the biggest one is yes, cholesterol is involved in atherosclerosis, but it's not just about the amount, it's about the form, like oxidized LDL, the particle number, apob, small dense LDL. The overall context, inflammation, metabolic health, those are way more critical.

Rachel: 26:22

Context is king.

Mark: 26:23

Exactly. High ApoB, or lots of small particles, means high particle burden. Oxidized LDL is what really triggers the inflammation. Inflammation is what makes plaques dangerous and likely to rupture.

Rachel: 26:36

And underlying issues like insulin resistance fuel the whole fire.

Mark: 26:40

They absolutely accelerate the whole process, and we even learned that red blood cells in advanced plaques can contribute significantly to oxidative stress and instability through hemoglobin and iron release.

Rachel: 26:52

So for people listening, what's the actionable thought here? What should we be thinking about differently?

Mark: 26:57

It really comes down to looking beyond that standard lipid panel. Talk to your doctor, ask about measuring ApoB. Ask about HSCRP. Understand your insulin sensitivity, maybe through fasting insulin or that TGH deal ratio.

Rachel: 27:09

Get the broader picture.

Mark: 27:10

Get the broader picture and never underestimate the power of diet and lifestyle. Those are your primary tools for influencing not just your lipid numbers but that whole crucial inflammatory and metabolic environment.

Rachel: 27:21

So the provocative thought for everyone listening might be stop fixating on just that one cholesterol number.

Mark: 27:27

Yeah, ask yourself what's the rest of my story. What's my ApoB, what's my inflammation level, what's my metabolic health really like?

Rachel: 27:33

Exploring those other markers can give you a much truer sense of your actual cardiovascular risk.

Mark: 27:39

Absolutely. That empowers you to take more targeted action.

Rachel: 27:42

This has been just fantastic A really important discussion, I think. Thank you so much for breaking down all that complexity.

Mark: 27:49

My pleasure. It's crucial information.

Rachel: 27:50

And just a final essential reminder for everyone listening the information we've gone over today is purely for educational purposes. It's crucial information. And just a final essential reminder for everyone listening the information we've gone over today is purely for educational purposes. It is definitely not a substitute for professional medical advice.

Mark: 28:02

Absolutely Always. Always consult with your own doctor or qualified health care provider for any questions or concerns about your specific health situation.

Rachel: 28:12

Couldn't agree more. Get personalized advice from your trusted professional.

Nicolette: 28:22

Thanks for tuning into the Health Pulse. If you found this episode helpful, don't forget to subscribe and share it with someone who might benefit. For more health insights and diagnostics, visit us online at wwwquicklabmobilecom. Stay informed, stay healthy and we'll catch you in the next episode.