Speaker 1: 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.

Speaker 2: 0:26

Welcome back everyone. We are diving deep today into, well, one of the most, I'd say, disruptive things happening in personalized health. Right now we're talking about low-carbohydrate eating. Now, for many of you listening, the benefits are probably pretty familiar Easier weight management, maybe fantastic improvements in insulin sensitivity, lower triglycerides, higher HDL cholesterol. You know it sounds like a total metabolic win, but and this is the key thing there's this counterintuitive surprise that pops up for a really specific group of people, often lean athletic types. For these individuals, their LDL cholesterol, you know, so-called bad cholesterol it just shoots up dramatically often into numbers that, frankly, make most doctors pretty nervous. So today our deep dive is all about the lean mass hyper-responder, or LMHR, phenotype. Our mission is to really understand this group, look into the controversy around their super high LDL and figure out what kind of monitoring you really need. And the big question, the really high stakes one, is this does having sky high LDL in this specific metabolic context carry the same cardiovascular risk as it does for well everyone else? Let's unpack that.

Speaker 3: 1:30

Yeah, it's absolutely critical we figure this out because, look, if the answer is no, then we fundamentally have to rethink how we assess heart disease risk. But if the answer is yes, then this group, despite looking healthy on paper otherwise, might need, you know, pretty immediate intervention.

Speaker 2: 1:46

OK, let's start with the basics. Who exactly are we talking about here? This term LMHR. It was coined by researcher Dave Feldman and his team right.

Speaker 3: 1:55

That's right, and it describes people who are typically already lean, physically active and this is important highly insulin sensitive, before they even start cutting carbs.

Speaker 2: 2:05

Got it, and their response is defined by a specific lipid pattern, a triad, you call it.

Speaker 3: 2:11

Exactly a triad, Three specific markers that, when you see them together, kind of fly in the face of the traditional high risk profile. So first they have really high LDL cholesterol LDL-C we're talking often way past 200 milligrams per deciliter, sometimes even over 300.

Speaker 2: 2:26

Wow Okay.

Speaker 3: 2:27

Second, their HDL cholesterol HDL-C the good kind is also very high, usually, you know, above 70 milligdl, sometimes much higher. And third, their triglycerides TG are super low, typically under 70 milligdl.

Speaker 2: 2:40

That's the paradox, right. Normally, if someone walks in with an LDL of, say, 250, you expect to see high triglycerides and low HDL, maybe issues with blood sugar insulin resistance.

Speaker 3: 2:52

Precisely. The standard picture of high risk often includes what we call metabolic syndrome high triglycerides, low HDL, often central obesity, higher blood pressure. The LMHR is the complete opposite. They have that sky-high LDL, yes, but everything else looks well, pretty much perfect Normal blood pressure, great glucose control. They're lean, low inflammation.

Speaker 2: 3:12

They're metabolically healthy by almost every measure, except that LDL number.

Speaker 3: 3:15

Exactly.

Speaker 2: 3:16

And just to be clear, this pattern mainly shows up when people go on really strict low-carb diets like keto or carnivore.

Speaker 3: 3:23

Overwhelmingly yes, it seems to be a direct result of that drastic carbohydrate restriction interacting with their specific physiology.

Speaker 2: 3:30

OK, so it's not just about eating more fat. Something fundamental is shifting in how their body works when carbs are taken out, If they're already lean and insulin sensitive. What's driving this huge LDL surge? Where's it coming from?

Speaker 3: 3:44

Yeah, that's the million-dollar question, isn't it? And the answer seems to be tied into how their body transports energy when glucose isn't the primary fuel. There are basically three main ideas floating around. The first is what's called increased fat flux, so without much glucose, the body runs on fatty acids. The theory goes that LMHRs are just incredibly efficient at pulling fat out of their storage even their limited storage and getting it into circulation. And when you mobilize fat like that, the liver has to package it up into lipoproteins like LDL particles to ship it out to muscles and organs that need energy. So more fat mobilization might mean more LDL trucks are needed.

Speaker 2: 4:23

Wait a second. If they're lean, wouldn't they like run out of fat stores pretty quick? Shouldn't the LDL then drop?

Speaker 3: 4:29

Ah well, that actually leads right into the second proposed mechanism high energy demands. Because LMHRs often don't have much body fat to begin with and they're frequently very active Right. Their bodies are constantly screaming for fuel delivery, so their reliance on these circulating lipoproteins, these LDL delivery trucks, might be amplified because their other fuel depots are low. The idea isn't necessarily that the LDL particles are bad or damaged, but that they're being actively used, maybe turned over really quickly, to deliver huge amounts of energy all over the body.

Speaker 2: 5:01

So they're basically running this super high volume, maybe hyper efficient energy shipping operation.

Speaker 1: 5:05

OK.

Speaker 2: 5:06

And the third idea links this to genetics.

Speaker 3: 5:09

Precisely. There seems to be a strong component of genetic predisposition. We know there are specific gene variants related to how we handle lipid stink genes like APOE, ldlr, pcsk9. It's possible that certain genetic profiles make people hyper-respond metabolically when they switch fuel sources so drastically. The low-carb, high-fat diet is the trigger, but maybe your genes decide if you get this dramatic LDL surge.

Speaker 2: 5:32

So it's not just the diet alone.

Speaker 3: 5:34

No, the key takeaway here really seems to be a crucial gene diet interaction. It's the diet hitting a particular genetic setup that likely creates this LMHR phenotype.

Speaker 2: 5:45

All right, Now we're getting into the really tricky part, the gray area, the controversy. Yeah, Because, look, we have mountains of evidence, decades of it, saying high LDL is a cause of atherosclerotic cardiovascular disease, ASCVD, you know, the plaque buildup leading to heart attacks and strokes. So when someone in the LMHR community says, yeah, my LDL is 300, but hey, my triglycerides are 50 and my HDL is 90, the medical world gets well divided.

Speaker 3: 6:12

It's a real clinical puzzle. On one hand you have the conservative view. This is often the stance of mainstream lipid experts. They argue, based on huge population studies, that LDL is inherently atherogenic. The higher the number, the more exposure your arteries have over time period. They see an LDL of 300, and regardless of other markers, they think risk and usually recommend getting that number down. Sometimes aggressively, they treat the number itself.

Speaker 2: 6:35

Okay, that's one side. What's the counter argument from the LMHR perspective?

Speaker 3: 6:39

They argue for what you might call the metabolic context view. They say hold on, you have to look at the whole picture. They point to their low triglycerides, high HDL, low insulin, often zero inflammation, their leanness and they ask does this unique metabolic environment change the nature or the function of those LDL particles? Is an LDL particle floating around in that clean environment the same risk as one in someone with metabolic syndrome, where particles might be small, dense, maybe oxidized or glycated?

Speaker 2: 7:07

That's the crux of it, isn't it? Are these LDL particles, even though there are lots of them, somehow less dangerous because the overall metabolic health is so good, or does the sheer number still cause plaque buildup over time?

Speaker 3: 7:18

And this leads us straight to the major evidence gap Right now. Today we just don't have the large-scale long-term studies specifically following LMHRs to see what actually happens to their hearts and arteries over decades. We don't know definitively if they develop atherosclerosis faster, slower or at the same rate as someone else with a similarly high LDL but a different metabolic profile. They really are in a kind of cardiometabolic blind spot. We need solid proof, not just plausible theories.

Speaker 2: 7:46

Which means until we get that proof, we have to be cautious. So okay, let's talk practicality. Since this high LDL is almost always tied to the very low carb diet, what can you actually do if you identify as an LMHR and you're concerned about that number? What levers can you pull?

Speaker 3: 8:01

Well, if the primary goal is simply to lower the LDL number, the most direct route is often a dietary adjustment, because the whole thing seems driven by this massive fat mobilization for fuel. Reintroducing even a moderate amount of carbohydrates maybe say 50 to 100 grams per day often signals the body to switch back towards using glucose. Anecdotally, this frequently brings the LDL-C down significantly and for many people they can do this while still keeping blood sugar stable and maintaining many of the other benefits that they got from low-carb.

Speaker 2: 8:31

So you don't necessarily have to completely abandon the approach, maybe just tweak it.

Speaker 3: 8:36

Exactly. Another potential tweak is fat source alteration. Sometimes the LMHR response seems more pronounced, with very high intakes of saturated fats, things like butter, fatty red meat cream. Some find that shifting the fat focus towards more unsaturated fats like olive oil, avocados, nuts, fatty fish, can also help lower the LDL-C, even while keeping carbs relatively low.

Speaker 2: 8:59

Interesting. But regardless of whether someone tweaks their diet or not, monitoring seems absolutely critical. And you're saying a standard lipid panel isn't really enough here. We need more advanced tests.

Speaker 3: 9:09

Absolutely non-negotiable. And, yes, the standard panel can be misleading. It usually measures LDL-C, which is the weight or the mass of cholesterol carried within the LDL particles, but what seems to matter more for atherosclerosis risk is the actual number of potentially additives. Atherogenic particles bumping against your artery walls. Think of it like traffic.

Speaker 2: 9:30

Okay, traffic analogy, let's hear it.

Speaker 3: 9:31

All right, ldlc is like measuring the total weight of all the cargo being carried by trucks on a highway. But what causes traffic jams and potential accidents isn't the weight of the cargo, it's the sheer number of trucks on the road.

Speaker 2: 9:43

Gotcha More trucks, higher chance of collision.

Speaker 3: 9:50

Precisely, and that's why we need tests like opal lipoprotein B or ApoB. Apob is a protein found on every single one of these potentially atherogenic particles VLDL, idl and LDL. One ApoB molecule per particle. So measuring ApoB basically tells you the total number of these particles, the total number of trucks on your highway. It's considered a much more accurate marker of particle burden and risk than just LDL-C alone.

Speaker 2: 10:10

Okay, APOB counts the trucks. That makes sense. What else?

Speaker 3: 10:13

Well, many advanced lipid tests, sometimes called NMR, laco profile or cardio IQ, will also directly report LDL particle number, ldl-p. It's another way of quantifying the number of LDL particles. Specifically For an LMHR, it's crucial to know is there high LDL-C mass due to having a few really large fluffy LDL particles packed with cholesterol, or is it due to having a huge number of smaller particles? The latter is generally considered higher risk.

Speaker 2: 10:41

Right, so ApoB and LDLP give you the particle count. What other tests are important for context?

Speaker 3: 10:47

You definitely want to check lipoprotein or LPA. This is a completely separate risk factor, mostly determined by genetics, not diet. If it's high, it significantly adds to overall cardiovascular risk. No matter what your LDL is doing, you need to know your LPA number.

Speaker 2: 11:01

Okay, check LPA.

Speaker 3: 11:02

And keep an eye on inflammation markers like high sensitivity C reactive protein, LHS, CRP. You want confirmation that the underlying metabolic environment is indeed calm and not inflamed, which usually is the case for LMHRs. But you have to check.

Speaker 2: 11:16

Makes sense. And then there's imaging. You mentioned coronary artery calcium scoring the C-score. How does that fit in?

Speaker 3: 11:22

The CAC score is really interesting here. It's a CT scan that looks directly for hardened calcified plaque in your coronary arteries. It doesn't measure risk factors in the blood. It measures the actual presence of disease.

Speaker 2: 11:34

So it shows if damage is actually occurring.

Speaker 3: 11:36

Exactly For LMHRs grappling with high LDL or APOP-E numbers, a CAC score can be incredibly informative. Many are using it often serially over time to see if their high particle count is actually translating into plaque buildup. Getting a CAC score of zero is generally very reassuring, suggesting very low short-to-intermediate-term risk. Even if the LDL is high, it provides a piece of direct evidence about what's happening in the arteries themselves.

Speaker 2: 12:04

Wow. Okay, that seems like a critical piece of the puzzle while we wait for more long-term data.

Speaker 3: 12:09

It really is, and it all underscores the need for truly personalized nutrition and monitoring. We can't just use blanket guidelines here. It has to be tailored, using these advanced tests.

Speaker 2: 12:18

Okay, let's try and wrap this up. What's the main takeaway for you listening?

Speaker 3: 12:23

The LMHR phenomenon. It's really shaking things up in metabolic science. It shows just how powerfully diet can change our biomarkers, sometimes in really unexpected ways, like driving LDL sky high even while fixing almost everything else.

Speaker 2: 12:37

And until we have that definitive long-term evidence about the actual risk and I should say studies using imaging like CAC are underway right now. Looking specifically at this group, the safest approach seems clear. It's careful, close monitoring with advanced testing Get your ApoB checked, know your LDL-P, find out your LPA, track inflammation and seriously consider a CAC score and, importantly, work with a doctor or healthcare provider who actually understands this specific metabolic situation.

Speaker 3: 13:05

It's really quite something. One set of markers looks amazing, another looks potentially alarming, all from the same dietary shift? Yeah, it is. And maybe the final thought, the provocative question for you to mull over, is this If we zoom out, does the very existence of the LMHR group suggest that our future models for predicting heart disease risk need to evolve the full metabolic picture, the triglycerides, the HDL, insulin sensitivity, inflammation, leanness rather than focusing so heavily, almost solely sometimes, on the quantity of LDL cholesterol alone? Answering that could fundamentally change preventative cardiology as we know it.

Speaker 1: 13:45

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