Latest / Heart Health, Reimagined with Dr. Mona Shah, MD / Your LDL Is Normal. So Why Is There Heart Plaque?
Transcript
- 0:00SPEAKER_00: Your LDL is 90, your doctor calls that normal, maybe even good.
- 0:05SPEAKER_00: You exercise, you eat well, you don't smoke, maybe you're even vegan or vegetarian.
- 0:12SPEAKER_00: And then you get a coronary calcium scan, or even better, a coronary CT angiogram, and you're told you have plaque in your heart arteries.
- 0:22SPEAKER_00: Your first reaction, how is that even possible?
- 0:26SPEAKER_00: I hear this question all the time.
- 0:28SPEAKER_00: And here's the truth: it's not that LDL doesn't matter.
- 0:31SPEAKER_00: The problem is that one LDL number measured today cannot tell you the whole story of what's been happening inside your arteries for the last 30, 40, 50 years.
- 0:42SPEAKER_00: I'm Dr.
- 0:43SPEAKER_00: Mona Shaw.
- 0:44SPEAKER_00: I'm a triple board certified cardiologist specializing in preventive and holistic cardiology.
- 0:50SPEAKER_00: If you've already watched my video on the seven labs I checked beyond the standard panel, you know the standard cholesterol panel is missing the numbers that actually predict plaque.
- 1:01SPEAKER_00: Today I'm going further than that.
- 1:04SPEAKER_00: Five specific reasons a normal LDL can sit right next to real coronary plaque, including a few most people have never even had explained to them.
- 1:15SPEAKER_00: Once we understand why the plaque is there, we can make much better decisions about what to do next.
- 1:22SPEAKER_00: And if you've been with me these last few weeks through the labs, the tests, and the treatment options, this is where it all starts coming together.
- 1:32SPEAKER_00: Let's get into it.
- 1:34SPEAKER_00: Here's where I think a lot of the confusion starts.
- 1:38SPEAKER_00: I definitely review LDL, but if you've seen my other videos, you know I focus more on APO B.
- 1:46SPEAKER_00: So for argument's sake, let's say you haven't had your APOB checked yet, and all you have is your LDL.
- 1:53SPEAKER_00: Then this pertains to you.
- 1:56SPEAKER_00: This also pertains to you if you've had your APOB checked.
- 2:00SPEAKER_00: Your lab may flag your LDL as being a certain reference range, but a lab reference range and the right LDL target for you personally are not necessarily the same thing.
- 2:12SPEAKER_00: An LDL that's perfectly reasonable for a young person with no plaque, no major risk factors, and no significant family history is not necessarily the LDL I want in someone who already has coronary plaque or real additional risk factors.
- 2:28SPEAKER_00: It doesn't mean that we don't start young checking labs, checking LDL and APOB, but we just will handle it a little bit differently when someone's younger than when until they get into their 30s, 40s, and 50s.
- 2:42SPEAKER_00: So instead of asking only, is my LDL normal, I want you to start asking, is my LDL appropriate for my individual cardiovascular risk?
- 2:54SPEAKER_00: Those are two very different questions.
- 2:58SPEAKER_00: Reason one, your LDL only tells me today's story.
- 3:02SPEAKER_00: Let's say you're 58, and your LDL today is 95.
- 3:06SPEAKER_00: Great, but what was it at 25, at 35, at 45?
- 3:11SPEAKER_00: What was happening in the years you weren't even getting blood work?
- 3:15SPEAKER_00: Atherosclerosis, meaning plaque buildup, doesn't build from one cholesterol measurement.
- 3:21SPEAKER_00: It builds over decades of exposure.
- 3:24SPEAKER_00: Think about pack years with smoking.
- 3:26SPEAKER_00: We don't just ask whether someone smoked a cigarette today, we care how much and for how long.
- 3:32SPEAKER_00: Cholesterol exposure works the same way.
- 3:35SPEAKER_00: So a normal LDL today doesn't erase the previous 30 years.
- 3:41SPEAKER_00: That's reason number one.
- 3:43SPEAKER_00: Someone can have a reassuring panel today and still be carrying real plaque.
- 3:49SPEAKER_00: Same goes with APOB.
- 3:52SPEAKER_00: Reason two, the particle count most people never check.
- 3:57SPEAKER_00: Quick recap: if you haven't seen my video on this, LDL cholesterol tells us roughly how much cholesterol is riding inside your particles.
- 4:09SPEAKER_00: It doesn't tell us how many particles you actually have.
- 4:12SPEAKER_00: And it's a particle hitting your artery wall that starts plaque, not the cholesterol it's carrying.
- 4:20SPEAKER_00: That's what APOB measures.
- 4:22SPEAKER_00: I'll link it below.
- 4:24SPEAKER_00: Two people can have an identical LDL and a completely different APOB, one of them building plaque right now, the other one not.
- 4:33SPEAKER_00: Have you ever had an APOB check, not just an LDL?
- 4:37SPEAKER_00: Most people haven't, because most doctors never order it.
- 4:41SPEAKER_00: But advocate for yourself and get it checked.
- 4:44SPEAKER_00: But I don't want you walking away thinking that just having these particles circulating means they bump into an artery and instantly become plaque.
- 4:53SPEAKER_00: The biology is more interesting than that.
- 4:56SPEAKER_00: And once you understand it, you'll understand why this isn't as simple as high cholesterol clogs a pipe.
- 5:04SPEAKER_00: Your artery wall isn't a passive pipe.
- 5:06SPEAKER_00: It's lined with a thin layer of cells called the endothelium, kind of like a protective inner skin.
- 5:14SPEAKER_00: For a particle to cause trouble, it actually has to slip through that lining.
- 5:20SPEAKER_00: This process is called transcytosis.
- 5:24SPEAKER_00: Once it's through, it gets trapped inside the wall itself.
- 5:28SPEAKER_00: That trapping is called retention, and it's the critical step.
- 5:32SPEAKER_00: Once a particle is trapped, your immune system notices cells rush in to try to clean it up, but in the process, they can get overloaded with fat and turn into what we call foam cells.
- 5:45SPEAKER_00: That right there, that's the actual start of atherosclerotic plaque.
- 5:52SPEAKER_00: Not high cholesterol just hitting your blood, a particle getting trapped and your body reacting to it inside your artery wall.
- 6:01SPEAKER_00: Let that really sit with you.
- 6:04SPEAKER_00: If you're sitting there thinking, why has nobody ever explained my cholesterol to me this way?
- 6:09SPEAKER_00: That's exactly why I started this channel.
- 6:12SPEAKER_00: Every week I break down a cardiovascular testing, research into something you can actually use.
- 6:18SPEAKER_00: If that's helpful, subscribe and like this video.
- 6:22SPEAKER_00: It also tells me exactly which topics to go deeper on next.
- 6:27SPEAKER_00: So I don't like the old explanation.
- 6:29SPEAKER_00: Your cholesterol was high and it clogged your artery.
- 6:32SPEAKER_00: That's far too simple.
- 6:34SPEAKER_00: Two things determine whether plaque forms.
- 6:38SPEAKER_00: The particles circulating in your blood and the environment inside your artery wall.
- 6:43SPEAKER_00: Both matter.
- 6:45SPEAKER_00: Neither one alone tells the whole story.
- 6:49SPEAKER_00: Blood pressure matters.
- 6:50SPEAKER_00: High blood pressure, what doctors call hypertension, puts extra force on your blood vessel walls every time your heart beats.
- 6:59SPEAKER_00: And over years, that extra force wears down that protective lining we called the endothelium.
- 7:06SPEAKER_00: Smoking is even more damaging.
- 7:09SPEAKER_00: Vaping, the chemicals in a vape pen, injure that lining directly and flood your body with oxidative stress, which is basically cellular damage building up faster than your body can repair it.
- 7:24SPEAKER_00: Insulin resistance and diabetes do something similar by changing how your blood vessels function day to day.
- 7:32SPEAKER_00: Ongoing inflammatory conditions matter, age matters, and for women, the hormonal and metabolic shifts around menopause can raise cardiovascular risk too.
- 7:44SPEAKER_00: I have a video coming out soon that goes deep on that because it deserves its own conversation.
- 7:50SPEAKER_00: The point is athosclerosis, meaning plaque buildup in your arteries, develops sort of interaction between harmful particles, the artery wall itself, inflammation, genetics, and time.
- 8:02SPEAKER_00: It's not one number.
- 8:04SPEAKER_00: If you want the deeper walkthrough on APOB itself and how to read it, I've done a full video on that.
- 8:10SPEAKER_00: I'll link it below rather than repeat it today.
- 8:14SPEAKER_00: Reason three, the genetic risk hiding behind a good number.
- 8:20SPEAKER_00: The second number most people have never had checked is lipoprotein A, LP little A.
- 8:26SPEAKER_00: It's largely genetic, you can't out-exercise it, you can't out-diet it.
- 8:31SPEAKER_00: About one in five people has an elevated level.
- 8:34SPEAKER_00: And current guidelines recommend everyone get it checked at least once in a lifetime.
- 8:40SPEAKER_00: I've shared before that this one is personal for me.
- 8:44SPEAKER_00: I have elevated lipoprotein A myself.
- 8:47SPEAKER_00: And it's part of why I found soft plaque despite doing everything right on paper.
- 8:53SPEAKER_00: If you haven't seen that full story, it's in the video I just mentioned.
- 8:57SPEAKER_00: Here's what it means for you.
- 8:59SPEAKER_00: If your father had a heart attack at 48 or your mother needed bypass at 55, an LDL of 95 doesn't mean everything is fine.
- 9:08SPEAKER_00: Lipoprotein A may be exactly why heart disease runs in that family, completely independent of lifestyle.
- 9:17SPEAKER_00: Reason four.
- 9:19SPEAKER_00: Insulin resistant hiding behind a normal LDL.
- 9:23SPEAKER_00: This one gets missed constantly, and it's not something I've covered in depth before.
- 9:28SPEAKER_00: I've talked about it though.
- 9:30SPEAKER_00: Insulin resistance can build for years before anyone meets criteria for diabetes.
- 9:36SPEAKER_00: And it quietly changes your lipid or cholesterol metabolism, higher triglycerides, lower HDL, the good cholesterol, and LDL particles that are each carrying less cholesterol.
- 9:48SPEAKER_00: Remember our truck analogy from the APOB video.
- 9:52SPEAKER_00: If each particle is hauling less cargo, you can have more particles circulating without your LDL cholesterol number even looking dramatic.
- 10:02SPEAKER_00: That's another reason APOB matters more than LDL alone.
- 10:07SPEAKER_00: But insulin resistance adds one more layer most people have never heard of, remnant particles.
- 10:15SPEAKER_00: These are leftover fragments of the particles that carry your triglycerides and particle for particle that can carry far more cholesterol than a typical LDL does alone.
- 10:27SPEAKER_00: When insulin resistance pushes triglycerides up, remnant particles usually climb right along with them, and they're just as capable of getting retained in your artery wall as LDL is.
- 10:38SPEAKER_00: Your seeing their lipid panel doesn't isolate this at all.
- 10:42SPEAKER_00: It's baked into the numbers you're not seeing clearly.
- 10:45SPEAKER_00: So I'll have someone sitting across from me with an LDL of 95, and then I find elevated triglycerides, their APOB is higher than I expected, their glucose is creeping, their blood pressure is creeping, maybe there's more visceral fat than they'd like to admit.
- 11:01SPEAKER_00: Suddenly, that LDL of 95 means something completely different than it did on its own.
- 11:09SPEAKER_00: Your doctor is very likely checking fasting glucose, maybe your A1C, both of which can actually look normal for years, while this insulin resistance is quietly happening in the background.
- 11:22SPEAKER_00: Glucose is a late indicator.
- 11:24SPEAKER_00: Ask yourself, do you know your triglycerides?
- 11:28SPEAKER_00: Has anyone ever checked your fasting insulin, not just your glucose?
- 11:33SPEAKER_00: Reason five.
- 11:35SPEAKER_00: Plaque isn't just a lipid problem.
- 11:38SPEAKER_00: It's an inflammation problem.
- 11:41SPEAKER_00: We now have clinical trial evidence that targeting inflammation directly can reduce cardiovascular events.
- 11:51SPEAKER_00: Many without even touching the LDL.
- 11:54SPEAKER_00: But the story here is more nuanced than lower inflammation equals lower risk.
- 11:59SPEAKER_00: And I think that nuance is worth understanding.
- 12:02SPEAKER_00: One landmark trial, Cantos, followed more than 10,000 people who'd already had a heart attack and had persistent inflammation.
- 12:11SPEAKER_00: Targeting a specific inflammatory signal in the body reduced cardiovascular events by about 15% at the effective dose, without even touching the LDL cholesterol at all.
- 12:25SPEAKER_00: But here's where the sign gets more interesting.
- 12:28SPEAKER_00: A newer recent trial called Zeus targeted a different inflammatory signal in patients with atherosclerosis, chronic kidney disease, and ongoing inflammation.
- 12:40SPEAKER_00: The drug substantially reduced inflammatory markers.
- 12:44SPEAKER_00: However, it did not reduce heart attacks, strokes, or cardiovascular death compared with placebo.
- 12:51SPEAKER_00: That's an important lesson.
- 12:53SPEAKER_00: Inflammation clearly participates in atherosclerosis, but simply lowering an inflammatory marker doesn't automatically translate into fewer cardiovascular events.
- 13:04SPEAKER_00: The pathway matters, the treatment matters, the patient population matters.
- 13:10SPEAKER_00: So when I see an elevated inflammatory marker like high sensitivity CRP, I don't treat that number in isolation.
- 13:18SPEAKER_00: I want to understand the whole picture: metabolic health, smoking, blood pressure, sleep, visceral fat, inflammatory conditions, and everything else that could be contributing to vascular inflammation.
- 13:33SPEAKER_00: That's really the theme of this entire video.
- 13:36SPEAKER_00: Atherosclerosis is complex.
- 13:39SPEAKER_00: LDL matters enormously, but one LDL number doesn't tell us everything happening inside the artery wall.
- 13:48SPEAKER_00: So why did the labs miss the plaque in the first place?
- 13:52SPEAKER_00: This is where imaging changes the conversation.
- 13:55SPEAKER_00: A coronary calcium scan finds hard calcified plaque, but not soft, non-calcified plaque, the kind that's actually more dangerous.
- 14:08SPEAKER_00: A coronary CT angiogram gives us a full picture and can pick up both types.
- 14:14SPEAKER_00: So someone's labs can look reassuring and imaging can still show atherosclerosis is already there.
- 14:22SPEAKER_00: If you want to see exactly what that looks like, I got a full video on the scan that shows all your plaque linked below.
- 14:29SPEAKER_00: Biomarkers help us estimate risk.
- 14:32SPEAKER_00: Imaging shows us whether disease is actually present.
- 14:35SPEAKER_00: Once imaging shows me plaque is there, I don't dismiss it because the LDL landed in a normal range.
- 14:42SPEAKER_00: I ask, why is this person developing plaque and what are we missing?
- 14:47SPEAKER_00: So what do you actually do next?
- 14:50SPEAKER_00: If you've been told you have a coronary plaque despite a normal cholesterol panel, remember four steps.
- 14:56SPEAKER_00: Confirm what was actually found, calcified, non-calcified, or both, and how much disease is present.
- 15:03SPEAKER_00: Define your total cardiovascular risk, not just LDL, APOB, lipoprotein A, blood pressure, metabolic health, smoking history, and family history, all of it together.
- 15:16SPEAKER_00: Identify what's actually modifiable for you specifically and set individualized treatment targets and goals.
- 15:25SPEAKER_00: Not is my LDL inside the lab normal range.
- 15:28SPEAKER_00: But given my actual plaque, my genetics, and my risk factors, where should my numbers be?
- 15:35SPEAKER_00: That's a completely different conversation than the one most people are having with their doctor.
- 15:41SPEAKER_00: The bottom line is this normal LDL does not mean zero cardiovascular risk.
- 15:48SPEAKER_00: LDL matters, but it's one piece of a much bigger story.
- 15:52SPEAKER_00: Particle burden, genetics, and metabolic health, as well as inflammation, as well as decades of exposure and what your arteries actually look like on a scan.
- 16:02SPEAKER_00: Now I know that's a lot.
- 16:04SPEAKER_00: Particles, genetics, insulin resistance, inflammation, imaging.
- 16:07SPEAKER_00: If you're feeling a little bit overwhelmed right now, that's completely normal.
- 16:11SPEAKER_00: And that is not what I want you to walk away with.
- 16:14SPEAKER_00: There's a real amount here you can control.
- 16:17SPEAKER_00: Your genetics, your lipoprotein A, your age.
- 16:21SPEAKER_00: That's what you can't control.
- 16:23SPEAKER_00: But there's also a lot you can control.
- 16:26SPEAKER_00: My job isn't to hand you a list of everything that could possibly go wrong.
- 16:30SPEAKER_00: It's to help you figure out which of these actually apply to you and advocate for yourself.
- 16:38SPEAKER_00: Work on yourself through diet, through exercise, sleeping better, stress management, getting on the right supplements, and medication when it's genuinely needed.
- 16:47SPEAKER_00: You don't have to fix everything at once.
- 16:50SPEAKER_00: You just need to know what to look at.
- 16:52SPEAKER_00: And I'm here to help you figure that out.
- 16:55SPEAKER_00: If you haven't already watched my video on APOB and lipoprotein A, watch that one next.
- 17:01SPEAKER_00: And once you understand why plat can show up behind a normal LDL, there's one question left.
- 17:07SPEAKER_00: You found it.
- 17:08SPEAKER_00: Now what?
- 17:09SPEAKER_00: That's exactly what I'm covering in my next video.
- 17:13SPEAKER_00: The one that finally pulls all of this information on this channel so far together.
- 17:18SPEAKER_00: If you found this helpful, subscribe and like the video.
- 17:23SPEAKER_00: And tell me in the comments have you ever been told you have coronary plaque even though your cholesterol was normal?
- 17:29SPEAKER_00: If you have, you're definitely not the only one.
- 17:32SPEAKER_00: I'll see you in the next video.