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The Lipid Energy Model: Making Sense of Sky-High LDL on Low-Carb Diets | Episode 92
Picture this: you’re lean, active, insulin-sensitive, and thriving on a low-carb lifestyle—yet your LDL cholesterol shoots past 200. Is this a sign of dysfunction, or simply a reflection of how your body fuels itself?
In this episode of The Health Pulse, we unpack the Lipid Energy Model (LEM), a framework that helps explain why some people—known as Lean Mass Hyper-Responders (LMHRs)—see dramatic LDL increases alongside very high HDL and very low triglycerides. Using clear analogies, we break down how your liver’s VLDL “freight trucks” deliver fat, leaving LDL “taxis” circulating in the bloodstream, and why this pattern tends to appear in highly active, carb-restricted individuals.
We contrast this metabolic perspective with the mainstream view that ApoB-containing particles drive atherosclerosis, highlighting why context matters. Advanced lipid testing (ApoB, LDL particle number, particle size), inflammation markers (hs-CRP, homocysteine), and metabolic health metrics (fasting insulin, glucose) all provide a richer, more personalized risk profile than LDL-C alone.
You’ll also hear about practical strategies LMHRs can test with their clinicians—like modestly reintroducing carbs (100–150g/day) to rapidly lower LDL-C without abandoning a low-carb foundation. And we spotlight ongoing research using coronary calcium scans and CT angiography to measure plaque directly in this unique population.
The takeaway? Don’t panic over a single “bad” number—gather context, verify patterns, and track trends. This episode equips you with a clear roadmap to discuss with your healthcare provider.
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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_02:Welcome back to the deep dive. We are jumping straight into uh, well, one of the most perplexing things happening in nutrition right now. Honestly, it can be pretty terrifying for people.
SPEAKER_01:Yeah, absolutely. Imagine this scenario. Maybe it's even you listening. You decide to really optimize your health.
SPEAKER_02:Right. You go low carb, maybe full keto.
SPEAKER_01:Yeah.
SPEAKER_02:And you feel amazing. Energy's great, you're leaner, blood sugar, perfect.
SPEAKER_01:Exactly. So you get a blood test, feeling confident, and the good stuff looks fantastic. Try glycerides, way down, HDL through the roof.
SPEAKER_02:It looks like metabolic heaven on paper.
SPEAKER_01:But then you see it. The LDL cholesterol, the number everyone's been told for decades is the big risk factor for heart disease.
SPEAKER_02:It's just exploded, like maybe over 200, maybe even 300 milliGDLs.
SPEAKER_01:It could be that high, yeah. And that one number throws everything into chaos for you, for your doctor.
SPEAKER_02:It creates this huge conflict. The traditional markers scream danger, but everything else about your health seems great.
SPEAKER_01:Totally. And that specific conflict, that confusion, is exactly why we need to unpack the lipid energy model today, the limb.
SPEAKER_02:Right. Our mission in this deep dive is really to get a handle on the limb. It's this framework that offers a completely different way to look at that high LDL.
SPEAKER_01:A different explanation, yeah. It basically asks is this specific kind of LDL rise in someone who's lean, active, healthy, is it actually disease?
SPEAKER_02:Or is it maybe an adaptation, the body just adjusting how it transports energy?
SPEAKER_01:That's the core question. A shift in energy transport.
SPEAKER_02:Okay, let's dive into that because where this model came from is pretty interesting in itself.
SPEAKER_01:It really is. You know, the lum didn't pop out of some big university cardiology lab initially. No, it was first really described and pushed forward by Dave Feldman, who's an engineer, a citizen scientist. Yeah, him and his collaborators. They were basically seeing all these confusing lab results posted online by low-carb folks and trying to make sense of it empirically.
SPEAKER_02:So it's kind of a bottom-up citizen science thing trying to solve a medical puzzle.
SPEAKER_01:Exactly. Which might explain why it uh sort of rubs up against the established medical thinking so much.
SPEAKER_02:Aaron Powell Okay. That context is important. Now we need to be super clear about who this model applies to. This isn't some, you know, universal excuse for high cholesterol across the board.
SPEAKER_01:No, absolutely not. Crucial point. The LM applies specifically, and I mean specifically, to a certain group. Which is people who are lean, insulin sensitive, and physically active.
SPEAKER_02:Aaron Powell Okay. So lean, metabolically healthy. Maybe they got healthy through low carb and they move their bodies.
SPEAKER_01:Precisely. That profile is key. Because the model is all about understanding the huge shift in energy that happens when you cut carbs drastically.
SPEAKER_02:Right. Because you take away the easy glucose fuel.
SPEAKER_01:Trevor Burrus And the body has to rely much, much more heavily on fatty acids and ketones, too, of course, for fuel. Trevor Burrus, Jr.
SPEAKER_02:So if you're relying on fat for energy, you suddenly need to move a lot more fat around your body, right? It's like logistics.
SPEAKER_01:That's a great analogy. Yeah. The demand for fat transport just skyrockets. If your delivery service suddenly has 10 times the packages, you need more trucks on the road. You need way more trucks. The LEM essentially proposes that this rise in LDL is just a natural consequence of the body efficiently packaging and delivering all this extra fat fuel. The whole system gets ramped up.
SPEAKER_02:Especially in someone lean and active who's burning through that energy quickly.
SPEAKER_01:Exactly. High energy demands, high fat flux.
SPEAKER_02:Trevor Burrus, OK. So if the cause is this shift from sugar to fat fuel, the mechanics inside the body must reflect that. Let's get into how that actually works, this VLDL remodeling thing.
SPEAKER_01:Aaron Powell Yeah, this is really the core of it, section two stuff. It all kicks off in the liver. Your liver is the main packaging plant for fat.
SPEAKER_02:Okay.
SPEAKER_01:When you're restricting carbs, the liver starts packaging up lots of triglycerides, that's the usable fat energy, into these particles called very low density lipoproteins. VLDL.
SPEAKER_02:VLDL, got it. So those are the big freight trucks you mentioned, loaded up with fat energy. Trevor Burrus, Jr.
SPEAKER_01:That's exactly it. Think of them leaving the liver factory, fully loaded, heading out to deliver fuel.
SPEAKER_02:Aaron Ross Powell To the muscles, the heart, all the tissues doing work. Makes sense. So what happens after the VLDL truck drops off some of its cargo, its triglycerides?
SPEAKER_01:Well, it doesn't just vanish, it changes, it remodels itself. As the VLDL delivers its triglyceride payload, there's an enzyme called lipoprotein lipase that helps with this the particle itself gets smaller and denser.
SPEAKER_02:Ah, okay. So it's like the truck is getting emptier and maybe uh shrinking down.
SPEAKER_01:Aaron Powell Pretty much it transforms. As it sheds that fat cargo, the VLDL becomes first immediate density lipoprotein IDL and then eventually. Light LDL. Yes, low density lipoprotein LDL. That's the particle that's left circulating in the blood. It's essentially the smaller, emptier taxi that used to be the big full freight truck.
SPEAKER_02:Whoa. Okay, so the high LDL count we see on the lab report, according to the Lem, it isn't necessarily because the body isn't clearing fat properly like you see in insulin resistance.
SPEAKER_01:Right, that's the usual assumption. Sluggish clearance.
SPEAKER_02:Instead, the LEM says it might just be the result, the byproduct of really high activity in the transport system. High VLDL turnover because the body needs so much fat fuel. Trevor Burrus, Jr.
SPEAKER_01:That is the central LM argument, yes. Because the body is working efficiently, demanding lots of energy, the liver pumps out more VLDL trucks.
SPEAKER_02:That leads to a higher rate of turnover, more deliveries, and more empty taxes, LDL particles left circulating afterwards.
SPEAKER_01:Exactly. So the high LDL count reflects the intensity of the fat transport, not necessarily a problem with it. Trevor Burrus, Jr.
SPEAKER_02:Okay. That makes sense mechanistically. And this process, this specific metabolic state, it creates a very distinct pattern in the blood test, right? This lean mass hyperresponder profile.
SPEAKER_01:Aaron Ross Powell Yes. The LMHR profile. It's a specific signature, and understanding it is key to seeing the context. It's a triad of three things, typically. Trevor Burrus, Jr.
SPEAKER_02:What's the first part of the triad?
SPEAKER_01:Aaron Powell Number one is what we've been talking about, high LDLC. Often dramatically high, like you said, maybe over 200, sometimes well over 300 milliogdl. This is the big red flag for most doctors. Aaron Powell Yeah.
SPEAKER_02:I mean I don't have to jump in there. An LDL over 200, traditionally that's almost an automatic prescription, right? Regardless of anything else. It's seen as immediate, serious risk.
SPEAKER_01:Aaron Powell That's absolutely the standard view. Decades of data support lowering LDL. But in the LMHR profile, that high LDL comes alongside two other factors that are usually seen as protective.
SPEAKER_02:Okay, what are they?
SPEAKER_01:Number two is high HDLC, the so-called good cholesterol, often very high in these individuals.
SPEAKER_02:Aaron Powell Which is the opposite of typical heart disease risk profiles.
SPEAKER_01:Aaron Powell Right. And number three, critically, is low triglycerides. Really low, often under 70 mil GDL, sometimes even under 50.
SPEAKER_02:Wow. Okay. Low triglycerides mean your body is using fat efficiently, right? It's not getting backed up in the bloodstream.
SPEAKER_01:Exactly. That fat is being delivered and burned, not stored inappropriately. Trevor Burrus, Jr.
SPEAKER_02:So that triad, high LDL, high HDL, low triglycerides, it's the complete opposite of the pattern you see in metabolic syndrome or insulin resistance. It's like an inverted profile.
SPEAKER_01:Aaron Powell It's completely inverted. And that combination points strongly towards good insulin sensitivity and very efficient fat metabolism. That the lamb predicts this exact profile because it links the high LDL to that functional need for energy transport, not to dysfunction.
SPEAKER_02:And if the model is right, if it's about the fuel source dictating the transport needs, we should be able to test that, right? Like what happens if someone with this LMHR profile adds back some carbs?
SPEAKER_01:That's one of the key predictions, and it makes the model testable. If you say add back 100 or 150 grams of carbs per day, enough to shift the body back towards using glucose more. Precisely.
SPEAKER_02:So the prediction is LDL should drop.
SPEAKER_01:Aaron Powell The prediction is LDLC should plummet, often back towards or into the normal ranges. And anecdotally, and in some case studies, that's exactly what people observe when they do that experiment.
SPEAKER_02:Aaron Powell Okay, wow. So we have a model, it explains the numbers, it makes testable predictions.
SPEAKER_01:And it's a big butt it's a huge butt.
SPEAKER_02:This model flies directly in the face of decades of cardiology, epidemiology, drug trials, everything we thought we knew about LDL. This is the big controversy, the great divide.
SPEAKER_01:Aaron Powell It absolutely is. Probably one of the biggest scientific debates in this area right now. The traditional view is, you know, incredibly well established.
SPEAKER_02:Simple and powerful.
SPEAKER_01:Simple, powerful, and backed by just a massive amount of data. It states that LDL cholesterol, or more specifically, the number of APOB containing particles.
SPEAKER_02:We'll get to ApoB in a minute.
SPEAKER_01:Right. But that these particles are causally linked to atherosclerosis, to plaque buildup in the arteries.
SPEAKER_02:And causally linked here means based on outcomes. Like heart attacks and strokes.
SPEAKER_01:Yes. Based on huge randomized controlled trials, population studies spanning decades. The evidence is considered overwhelming by the mainstream medical community. Higher exposure to these particles over time equals higher risk, period.
SPEAKER_02:Aaron Powell So from a cardiologist's perspective, seeing an LDL of 300, it doesn't matter why it's 300. The number itself is the risk.
SPEAKER_01:Aaron Powell That's the prevailing view. Every major drug trial, whether it's statins or the newer PCSK9 inhibitors, shows that lowering LDL or APOB reduces cardiovascular events. So for them, a high number is simply a threat that needs to be neutralized. The why is less important than the what.
SPEAKER_02:Okay. So that's the traditional view. High particle number exils inherent risk. The Lang perspective, then, must be arguing that the context changes the risk.
SPEAKER_01:That is the absolute core of the LEM argument. Context is everything. Supporters argue that in this specific metabolic environment, the LMHR triad again.
SPEAKER_02:Low triglycerides, high HDL. Trevor Burrus, Jr.
SPEAKER_01:Right. Excellent insulin sensitivity, often very low inflammation markers. In that context, the LDL particles themselves might behave differently.
SPEAKER_02:Or maybe the artery walls are healthier, less prone to damage.
SPEAKER_01:Trevor Burrus Or the arterial environment is less inflammatory, less sticky. The idea is that something about this overall healthy metabolic state modifies the risk usually associated with that high particle count. The LDL reflects energy trafficking, not the metabolic dysfunction that usually drives high LDL. Trevor Burrus, Jr.
SPEAKER_02:Okay, it's a compelling alternative explanation. But where are we with hard proof? Like long-term outcomes. Has this LMHR profile actually been proven safe over, say, 10 or 20 years?
SPEAKER_01:Aaron Powell And that's the million-dollar question. The honest answer right now. The long-term outcome data for this specific LMHR group is, well, it's uncertain. It's inconclusive.
SPEAKER_02:So we just don't know yet.
SPEAKER_01:We don't. We have case reports confirming the lipid patterns are real. We see people living with these numbers. But we don't have large long-term studies tracking their actual artery health over decades.
SPEAKER_02:Aaron Powell So how are researchers trying to figure this out?
SPEAKER_01:That's where ongoing studies are absolutely critical. Researchers are using tools like non-invasive imaging, things like coronary artery, calcium scans, CAT scores, and CT angiography.
SPEAKER_02:To actually look at the arteries.
SPEAKER_01:Exactly. To directly measure plaque buildup or lack thereof in these LMHR individuals and compare it over time to people with more typical lipid profiles. That imaging data over the next few years is expected to be the real tiebreaker.
SPEAKER_02:Okay, this makes total sense then. If the standard lipid panel, especially just LDLC, might be misleading in this specific LMN context, we can't rely on it alone. We need more advanced testing to build that crucial context.
SPEAKER_01:Absolutely non-negotiable if you're in this situation or advising someone who is. You need more data points.
SPEAKER_02:So what are the key tests? What gives us that context?
SPEAKER_01:Well, number one, and arguably the most important piece of the puzzle beyond the scanner panel is APOLIPOProtein B. ApoB.
SPEAKER_02:Okay, explain APOB again. If LDLC is the cholesterol cargo inside the particle.
SPEAKER_01:Apo B is essentially the protein marker on the surface of each atrogenic lipoprotein particle, VLDL, IDL, LDL. Think of it as the license plate or the barcode on every single truck or taxi.
SPEAKER_02:Ah, so it measures the actual number of potentially risky particles, not just the total amount of cholesterol they're carrying.
SPEAKER_01:Aaron Powell Exactly. And since the traditional view, and even many LEM proponents agree, holds that it's the particle number, the sheer number of interactions with the artery wall that primarily drives risk, APOB is widely considered a much more accurate measure of cardiovascular risk than LDLC alone.
SPEAKER_02:Aaron Powell So in the LEM context, you want to see what the APOB number is doing relative to that sky-high LDLC?
SPEAKER_01:Aaron Powell Precisely. Is the APOB also astronomically high, or is it maybe less elevated than the LDLC might suggest? That particle count is key.
SPEAKER_02:Okay, APOB is crucial. What else? Does the type or quality of the LDL particle matter? Like size?
SPEAKER_01:Aaron Powell It certainly adds another layer of context. This is where tests looking at LDL particle number, LDLP and size come in. Advanced lipid testing, like NMR lipoprofile or cardio IQ panels.
SPEAKER_02:Aaron Powell And why does size matter?
SPEAKER_01:Well, traditionally the risk, especially the risk linked to insulin resistance and metabolic syndrome, is associated more with small, dense LDL particles.
SPEAKER_02:Aaron Powell Right. I've heard those described as being like little hard BB pellets that can more easily get into the artery wall and cause damage.
SPEAKER_01:That's the thinking, yeah. They're thought to be more easily oxidized, more atherogenic. In contrast, these advanced tests can sometimes differentiate between those small, dense particles and larger, more buoyant LDL particles.
SPEAKER_02:Fluffier ones.
SPEAKER_01:Kind of, yeah. Now, a high number is still a high number, APOB tells you that. But the LEM theories suggest that the particles circulating in healthy LMHRs might be predominantly the larger, buoyant type.
SPEAKER_02:Which might be less risky.
SPEAKER_01:Which might be less directly damaging, although this is still debated. But knowing the particle size distribution adds to the overall picture, it provides more nuance than just the LDLC number.
SPEAKER_02:Makes sense. And okay, heart disease isn't just about lipids, right? It's also about inflammation and damage to the arteries themselves. So we need to check that environment too.
SPEAKER_01:Aaron Powell Absolutely critical. You have to measure inflammatory markers. The key ones are high sensitivity, C reactive protein, HSCRP, and maybe homocysteine.
SPEAKER_00:Why?
SPEAKER_01:Because if someone has this incredibly high LDL or APOB, but their markers of systemic and vascular inflammation are rock bottom. Trevor Burrus, Jr.
SPEAKER_02:Well, like their blood vessels seem completely calm.
SPEAKER_01:Exactly. If there's no underlying inflammatory fire, it lends support to the idea that the high lipid levels aren't actively driving a damaging pathological process in that specific individual at that time. Low inflammation is a very positive sign in this context. Trevor Burrus, Jr.
SPEAKER_02:Okay. APOP particle size inflammation. What else? You mentioned the LEM really hinges on the person being metabolically healthy.
SPEAKER_01:Aaron Powell Yes, the entire theoretical foundation rests on good insulin sensitivity. So you absolutely need to confirm that with basic metabolic labs. Right. Fasting glucose, HBA1C, to see longer-term blood sugar control, and importantly, fasting insulin.
SPEAKER_02:Why fasting insulin?
SPEAKER_01:Because it's often the earliest marker of declining insulin sensitivity. If someone's fasting insulin starts to creep up, even if their glucose and A1C look okay.
SPEAKER_02:It suggests the underlying metabolic health, the foundation of the LEM hypothesis for them might be weakening.
SPEAKER_01:Exactly. If insulin sensitivity degrades, the LEM framework may no longer apply, and that high LDL suddenly looks much more like traditional high-risk LDL. Context changes everything.
SPEAKER_02:So you need the full picture. APOV, particle count, maybe particle size, inflammation levels, and confirmed insulin sensitivity. And you need to track it.
SPEAKER_01:Yes. Longitudinal monitoring is non-negotiable. Tracking these trends over time, not just a single snapshot, is the only way to develop a truly personalized understanding and strategy.
SPEAKER_02:Aaron Powell This has been, wow, a really crucial deep dive. So to recap, the lipid energy model offers this compelling alternative lens to view high LDL cholesterol.
SPEAKER_01:But specifically in lean, active, insulin-sensitive individuals on low-carb diets.
SPEAKER_02:Right. Shifting the perspective potentially from automatic pathology to maybe efficient energy transport.
SPEAKER_01:Aaron Powell It definitely challenges the conventional wisdom by highlighting how unique these metabolic adaptations can be. It provides a rational framework for understanding why the numbers look the way they do in LMHRs. But and it remains the critical, but the long-term risk associated with having that sustained high APOB particle number, even in this context, is still the major unanswered question. That's what the current research, especially the imaging studies, is trying to definitively answer.
SPEAKER_02:Okay. So the final thought, the mission for you listening, context is absolutely king in modern nutrition and health assessment. You just cannot afford to look at a single lab number like LDLC in total isolation anymore.
SPEAKER_01:Especially not if you fit this potential LMHR profile.
SPEAKER_02:So if that's you, if you're seeing great metabolic health markers but a shockingly high LDL on a low carb diet, the question becomes how can you use this knowledge? How can you work with your doctor to utilize advanced testing A-pro B, inflammation markers, maybe even SCAC scoring and critical thinking to really understand your individual metabolic health beyond that one single potentially confusing number?
SPEAKER_01:That deeper understanding, that personalized context, that's the real goal here.
SPEAKER_00:That's what we leave you with today.com. Stay informed, stay healthy, and we'll catch you in the next episode.
