October 1, 2025 • 17 mins
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.
📞 Need lab work done from the comfort of home? QLM offers fast, reliable mobile phlebotomy services—no clinic visit required.
📅 Book your appointment or learn more at:
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Disclaimer: The information provided in this podcast is for informational purposes only and should not be considered medical advice. The content discussed is based on research, expert insights, and reputable sources, but it does not replace professional medical consultation, diagnosis, or treatment. We strive to present accurate and up-to-date information, medical research is constantly evolving. Listeners should always verify details with trusted health organizations, before making any health-related decisions. If you are experiencing a medical emergency, such as severe pain, difficulty breathing, or other urgent symptoms, call your local emergency services immediately. By listening to this podcast, you acknowledge that The Health Pulse and its creators are not responsible for any actions taken based on the content of this episode. Your health and well-being should always be guided by the advice of qualified medical professionals.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
SPEAKER_00 (00:00):
Welcome to the Health Pulse, your go-to source
for quick, actionable insightson health, wellness, and
diagnostics.
Whether you're looking tooptimize your well-being or stay
informed about the latestin-medical testing, we've got
you covered.
Join us as we break down keyhealth topics in just minutes.
Let's dive in.
SPEAKER_02 (00:25):
Welcome back to the deep dive.
We are jumping straight into uh,well, one of the most perplexing
things happening in nutritionright now.
Honestly, it can be prettyterrifying for people.
SPEAKER_01 (00:34):
Yeah, absolutely.
Imagine this scenario.
Maybe it's even you listening.
You decide to really optimizeyour health.
SPEAKER_02 (00:42):
Right.
You go low carb, maybe fullketo.
SPEAKER_01 (00:44):
Yeah.
SPEAKER_02 (00:45):
And you feel amazing.
Energy's great, you're leaner,blood sugar, perfect.
SPEAKER_01 (00:49):
Exactly.
So you get a blood test, feelingconfident, and the good stuff
looks fantastic.
Try glycerides, way down, HDLthrough the roof.
SPEAKER_02 (00:58):
It looks like metabolic heaven on paper.
SPEAKER_01 (01:00):
But then you see it.
The LDL cholesterol, the numbereveryone's been told for decades
is the big risk factor for heartdisease.
SPEAKER_02 (01:08):
It's just exploded, like maybe over 200, maybe even
300 milliGDLs.
SPEAKER_01 (01:12):
It could be that high, yeah.
And that one number throwseverything into chaos for you,
for your doctor.
SPEAKER_02 (01:17):
It creates this huge conflict.
The traditional markers screamdanger, but everything else
about your health seems great.
SPEAKER_01 (01:23):
Totally.
And that specific conflict, thatconfusion, is exactly why we
need to unpack the lipid energymodel today, the limb.
SPEAKER_02 (01:30):
Right.
Our mission in this deep dive isreally to get a handle on the
limb.
It's this framework that offersa completely different way to
look at that high LDL.
SPEAKER_01 (01:38):
A different explanation, yeah.
It basically asks is thisspecific kind of LDL rise in
someone who's lean, active,healthy, is it actually disease?
SPEAKER_02 (01:49):
Or is it maybe an adaptation, the body just
adjusting how it transportsenergy?
SPEAKER_01 (01:55):
That's the core question.
A shift in energy transport.
SPEAKER_02 (01:57):
Okay, let's dive into that because where this
model came from is prettyinteresting in itself.
SPEAKER_01 (02:01):
It really is.
You know, the lum didn't pop outof some big university
cardiology lab initially.
No, it was first reallydescribed and pushed forward by
Dave Feldman, who's an engineer,a citizen scientist.
Yeah, him and his collaborators.
They were basically seeing allthese confusing lab results
posted online by low-carb folksand trying to make sense of it
empirically.
SPEAKER_02 (02:21):
So it's kind of a bottom-up citizen science thing
trying to solve a medicalpuzzle.
SPEAKER_01 (02:25):
Exactly.
Which might explain why it uhsort of rubs up against the
established medical thinking somuch.
SPEAKER_02 (02:31):
Aaron Powell Okay.
That context is important.
Now we need to be super clearabout who this model applies to.
This isn't some, you know,universal excuse for high
cholesterol across the board.
SPEAKER_01 (02:42):
No, absolutely not.
Crucial point.
The LM applies specifically, andI mean specifically, to a
certain group.
Which is people who are lean,insulin sensitive, and
physically active.
SPEAKER_02 (02:54):
Aaron Powell Okay.
So lean, metabolically healthy.
Maybe they got healthy throughlow carb and they move their
bodies.
SPEAKER_01 (03:02):
Precisely.
That profile is key.
Because the model is all aboutunderstanding the huge shift in
energy that happens when you cutcarbs drastically.
SPEAKER_02 (03:10):
Right.
Because you take away the easyglucose fuel.
SPEAKER_01 (03:12):
Trevor Burrus And the body has to rely much, much
more heavily on fatty acids andketones, too, of course, for
fuel.
Trevor Burrus, Jr.
SPEAKER_02 (03:18):
So if you're relying on fat for energy, you suddenly
need to move a lot more fataround your body, right?
It's like logistics.
SPEAKER_01 (03:23):
That's a great analogy.
Yeah.
The demand for fat transportjust skyrockets.
If your delivery servicesuddenly has 10 times the
packages, you need more truckson the road.
You need way more trucks.
The LEM essentially proposesthat this rise in LDL is just a
natural consequence of the bodyefficiently packaging and
delivering all this extra fatfuel.
The whole system gets ramped up.
SPEAKER_02 (03:44):
Especially in someone lean and active who's
burning through that energyquickly.
SPEAKER_01 (03:47):
Exactly.
High energy demands, high fatflux.
SPEAKER_02 (03:50):
Trevor Burrus, OK.
So if the cause is this shiftfrom sugar to fat fuel, the
mechanics inside the body mustreflect that.
Let's get into how that actuallyworks, this VLDL remodeling
thing.
SPEAKER_01 (04:01):
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 packagingplant for fat.
SPEAKER_02 (04:08):
Okay.
SPEAKER_01 (04:08):
When you're restricting carbs, the liver
starts packaging up lots oftriglycerides, that's the usable
fat energy, into these particlescalled very low density
lipoproteins.
VLDL.
SPEAKER_02 (04:19):
VLDL, got it.
So those are the big freighttrucks you mentioned, loaded up
with fat energy.
Trevor Burrus, Jr.
SPEAKER_01 (04:23):
That's exactly it.
Think of them leaving the liverfactory, fully loaded, heading
out to deliver fuel.
SPEAKER_02 (04:28):
Aaron Ross Powell To the muscles, the heart, all the
tissues doing work.
Makes sense.
So what happens after the VLDLtruck drops off some of its
cargo, its triglycerides?
SPEAKER_01 (04:38):
Well, it doesn't just vanish, it changes, it
remodels itself.
As the VLDL delivers itstriglyceride payload, there's an
enzyme called lipoprotein lipasethat helps with this the
particle itself gets smaller anddenser.
SPEAKER_02 (04:52):
Ah, okay.
So it's like the truck isgetting emptier and maybe uh
shrinking down.
SPEAKER_01 (04:56):
Aaron Powell Pretty much it transforms.
As it sheds that fat cargo, theVLDL becomes first immediate
density lipoprotein IDL and theneventually.
Light LDL.
Yes, low density lipoproteinLDL.
That's the particle that's leftcirculating in the blood.
It's essentially the smaller,emptier taxi that used to be the
big full freight truck.
SPEAKER_02 (05:14):
Whoa.
Okay, so the high LDL count wesee on the lab report, according
to the Lem, it isn't necessarilybecause the body isn't clearing
fat properly like you see ininsulin resistance.
SPEAKER_01 (05:24):
Right, that's the usual assumption.
Sluggish clearance.
SPEAKER_02 (05:26):
Instead, the LEM says it might just be the
result, the byproduct of reallyhigh activity in the transport
system.
High VLDL turnover because thebody needs so much fat fuel.
Trevor Burrus, Jr.
SPEAKER_01 (05:35):
That is the central LM argument, yes.
Because the body is workingefficiently, demanding lots of
energy, the liver pumps out moreVLDL trucks.
SPEAKER_02 (05:43):
That leads to a higher rate of turnover, more
deliveries, and more emptytaxes, LDL particles left
circulating afterwards.
SPEAKER_01 (05:51):
Exactly.
So the high LDL count reflectsthe intensity of the fat
transport, not necessarily aproblem with it.
Trevor Burrus, Jr.
SPEAKER_02 (05:56):
Okay.
That makes sensemechanistically.
And this process, this specificmetabolic state, it creates a
very distinct pattern in theblood test, right?
This lean mass hyperresponderprofile.
SPEAKER_01 (06:07):
Aaron Ross Powell Yes.
The LMHR profile.
It's a specific signature, andunderstanding it is key to
seeing the context.
It's a triad of three things,typically.
Trevor Burrus, Jr.
SPEAKER_02 (06:15):
What's the first part of the triad?
SPEAKER_01 (06:16):
Aaron Powell Number one is what we've been talking
about, high LDLC.
Often dramatically high, likeyou said, maybe over 200,
sometimes well over 300milliogdl.
This is the big red flag formost doctors.
Aaron Powell Yeah.
SPEAKER_02 (06:27):
I mean I don't have to jump in there.
An LDL over 200, traditionallythat's almost an automatic
prescription, right?
Regardless of anything else.
It's seen as immediate, seriousrisk.
SPEAKER_01 (06:36):
Aaron Powell That's absolutely the standard view.
Decades of data support loweringLDL.
But in the LMHR profile, thathigh LDL comes alongside two
other factors that are usuallyseen as protective.
SPEAKER_02 (06:47):
Okay, what are they?
SPEAKER_01 (06:48):
Number two is high HDLC, the so-called good
cholesterol, often very high inthese individuals.
SPEAKER_02 (06:53):
Aaron Powell Which is the opposite of typical heart
disease risk profiles.
SPEAKER_01 (06:57):
Aaron Powell Right.
And number three, critically, islow triglycerides.
Really low, often under 70 milGDL, sometimes even under 50.
SPEAKER_02 (07:05):
Wow.
Okay.
Low triglycerides mean your bodyis using fat efficiently, right?
It's not getting backed up inthe bloodstream.
SPEAKER_01 (07:11):
Exactly.
That fat is being delivered andburned, not stored
inappropriately.
Trevor Burrus, Jr.
SPEAKER_02 (07:15):
So that triad, high LDL, high HDL, low
triglycerides, it's the completeopposite of the pattern you see
in metabolic syndrome or insulinresistance.
It's like an inverted profile.
SPEAKER_01 (07:24):
Aaron Powell It's completely inverted.
And that combination pointsstrongly towards good insulin
sensitivity and very efficientfat metabolism.
That the lamb predicts thisexact profile because it links
the high LDL to that functionalneed for energy transport, not
to dysfunction.
SPEAKER_02 (07:40):
And if the model is right, if it's about the fuel
source dictating the transportneeds, we should be able to test
that, right?
Like what happens if someonewith this LMHR profile adds back
some carbs?
SPEAKER_01 (07:51):
That's one of the key predictions, and it makes
the model testable.
If you say add back 100 or 150grams of carbs per day, enough
to shift the body back towardsusing glucose more.
Precisely.
SPEAKER_02 (08:11):
So the prediction is LDL should drop.
SPEAKER_01 (08:13):
Aaron Powell The prediction is LDLC should
plummet, often back towards orinto the normal ranges.
And anecdotally, and in somecase studies, that's exactly
what people observe when they dothat experiment.
SPEAKER_02 (08:22):
Aaron Powell Okay, wow.
So we have a model, it explainsthe numbers, it makes testable
predictions.
SPEAKER_01 (08:26):
And it's a big butt it's a huge butt.
SPEAKER_02 (08:27):
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, thegreat divide.
SPEAKER_01 (08:37):
Aaron Powell It absolutely is.
Probably one of the biggestscientific debates in this area
right now.
The traditional view is, youknow, incredibly well
established.
SPEAKER_02 (08:45):
Simple and powerful.
SPEAKER_01 (08:46):
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 (08:55):
We'll get to ApoB in a minute.
SPEAKER_01 (08:56):
Right.
But that these particles arecausally linked to
atherosclerosis, to plaquebuildup in the arteries.
SPEAKER_02 (09:03):
And causally linked here means based on outcomes.
Like heart attacks and strokes.
SPEAKER_01 (09:08):
Yes.
Based on huge randomizedcontrolled trials, population
studies spanning decades.
The evidence is consideredoverwhelming by the mainstream
medical community.
Higher exposure to theseparticles over time equals
higher risk, period.
SPEAKER_02 (09:21):
Aaron Powell So from a cardiologist's perspective,
seeing an LDL of 300, it doesn'tmatter why it's 300.
The number itself is the risk.
SPEAKER_01 (09:29):
Aaron Powell That's the prevailing view.
Every major drug trial, whetherit's statins or the newer PCSK9
inhibitors, shows that loweringLDL or APOB reduces
cardiovascular events.
So for them, a high number issimply a threat that needs to be
neutralized.
The why is less important thanthe what.
SPEAKER_02 (09:45):
Okay.
So that's the traditional view.
High particle number exilsinherent risk.
The Lang perspective, then, mustbe arguing that the context
changes the risk.
SPEAKER_01 (09:54):
That is the absolute core of the LEM argument.
Context is everything.
Supporters argue that in thisspecific metabolic environment,
the LMHR triad again.
SPEAKER_02 (10:04):
Low triglycerides, high HDL.
Trevor Burrus, Jr.
SPEAKER_01 (10:06):
Right.
Excellent insulin sensitivity,often very low inflammation
markers.
In that context, the LDLparticles themselves might
behave differently.
SPEAKER_02 (10:14):
Or maybe the artery walls are healthier, less prone
to damage.
SPEAKER_01 (10:17):
Trevor Burrus Or the arterial environment is less
inflammatory, less sticky.
The idea is that something aboutthis overall healthy metabolic
state modifies the risk usuallyassociated with that high
particle count.
The LDL reflects energytrafficking, not the metabolic
dysfunction that usually driveshigh LDL.
Trevor Burrus, Jr.
SPEAKER_02 (10:33):
Okay, it's a compelling alternative
explanation.
But where are we with hardproof?
Like long-term outcomes.
Has this LMHR profile actuallybeen proven safe over, say, 10
or 20 years?
SPEAKER_01 (10:44):
Aaron Powell And that's the million-dollar
question.
The honest answer right now.
The long-term outcome data forthis specific LMHR group is,
well, it's uncertain.
It's inconclusive.
SPEAKER_02 (10:52):
So we just don't know yet.
SPEAKER_01 (10:53):
We don't.
We have case reports confirmingthe lipid patterns are real.
We see people living with thesenumbers.
But we don't have largelong-term studies tracking their
actual artery health overdecades.
SPEAKER_02 (11:04):
Aaron Powell So how are researchers trying to figure
this out?
SPEAKER_01 (11:07):
That's where ongoing studies are absolutely critical.
Researchers are using tools likenon-invasive imaging, things
like coronary artery, calciumscans, CAT scores, and CT
angiography.
SPEAKER_02 (11:19):
To actually look at the arteries.
SPEAKER_01 (11:20):
Exactly.
To directly measure plaquebuildup or lack thereof in these
LMHR individuals and compare itover time to people with more
typical lipid profiles.
That imaging data over the nextfew years is expected to be the
real tiebreaker.
SPEAKER_02 (11:35):
Okay, this makes total sense then.
If the standard lipid panel,especially just LDLC, might be
misleading in this specific LMNcontext, we can't rely on it
alone.
We need more advanced testing tobuild that crucial context.
SPEAKER_01 (11:48):
Absolutely non-negotiable if you're in this
situation or advising someonewho is.
You need more data points.
SPEAKER_02 (11:53):
So what are the key tests?
What gives us that context?
SPEAKER_01 (11:56):
Well, number one, and arguably the most important
piece of the puzzle beyond thescanner panel is APOLIPOProtein
B.
ApoB.
SPEAKER_02 (12:04):
Okay, explain APOB again.
If LDLC is the cholesterol cargoinside the particle.
SPEAKER_01 (12:08):
Apo B is essentially the protein marker on the
surface of each atrogeniclipoprotein particle, VLDL, IDL,
LDL.
Think of it as the license plateor the barcode on every single
truck or taxi.
SPEAKER_02 (12:21):
Ah, so it measures the actual number of potentially
risky particles, not just thetotal amount of cholesterol
they're carrying.
SPEAKER_01 (12:26):
Aaron Powell Exactly.
And since the traditional view,and even many LEM proponents
agree, holds that it's theparticle number, the sheer
number of interactions with theartery wall that primarily
drives risk, APOB is widelyconsidered a much more accurate
measure of cardiovascular riskthan LDLC alone.
SPEAKER_02 (12:42):
Aaron Powell So in the LEM context, you want to see
what the APOB number is doingrelative to that sky-high LDLC?
SPEAKER_01 (12:49):
Aaron Powell Precisely.
Is the APOB also astronomicallyhigh, or is it maybe less
elevated than the LDLC mightsuggest?
That particle count is key.
SPEAKER_02 (12:56):
Okay, APOB is crucial.
What else?
Does the type or quality of theLDL particle matter?
Like size?
SPEAKER_01 (13:02):
Aaron Powell It certainly adds another layer of
context.
This is where tests looking atLDL particle number, LDLP and
size come in.
Advanced lipid testing, like NMRlipoprofile or cardio IQ panels.
SPEAKER_02 (13:15):
Aaron Powell And why does size matter?
SPEAKER_01 (13:17):
Well, traditionally the risk, especially the risk
linked to insulin resistance andmetabolic syndrome, is
associated more with small,dense LDL particles.
SPEAKER_02 (13:26):
Aaron Powell Right.
I've heard those described asbeing like little hard BB
pellets that can more easily getinto the artery wall and cause
damage.
SPEAKER_01 (13:33):
That's the thinking, yeah.
They're thought to be moreeasily oxidized, more
atherogenic.
In contrast, these advancedtests can sometimes
differentiate between thosesmall, dense particles and
larger, more buoyant LDLparticles.
SPEAKER_02 (13:46):
Fluffier ones.
SPEAKER_01 (13:47):
Kind of, yeah.
Now, a high number is still ahigh number, APOB tells you
that.
But the LEM theories suggestthat the particles circulating
in healthy LMHRs might bepredominantly the larger,
buoyant type.
SPEAKER_02 (13:58):
Which might be less risky.
SPEAKER_01 (14:00):
Which might be less directly damaging, although this
is still debated.
But knowing the particle sizedistribution adds to the overall
picture, it provides more nuancethan just the LDLC number.
SPEAKER_02 (14:09):
Makes sense.
And okay, heart disease isn'tjust about lipids, right?
It's also about inflammation anddamage to the arteries
themselves.
So we need to check thatenvironment too.
SPEAKER_01 (14:17):
Aaron Powell Absolutely critical.
You have to measure inflammatorymarkers.
The key ones are highsensitivity, C reactive protein,
HSCRP, and maybe homocysteine.
SPEAKER_00 (14:28):
Why?
SPEAKER_01 (14:29):
Because if someone has this incredibly high LDL or
APOB, but their markers ofsystemic and vascular
inflammation are rock bottom.
Trevor Burrus, Jr.
SPEAKER_02 (14:38):
Well, like their blood vessels seem completely
calm.
SPEAKER_01 (14:40):
Exactly.
If there's no underlyinginflammatory fire, it lends
support to the idea that thehigh lipid levels aren't
actively driving a damagingpathological process in that
specific individual at thattime.
Low inflammation is a verypositive sign in this context.
Trevor Burrus, Jr.
SPEAKER_02 (14:54):
Okay.
APOP particle size inflammation.
What else?
You mentioned the LEM reallyhinges on the person being
metabolically healthy.
SPEAKER_01 (15:00):
Aaron Powell Yes, the entire theoretical
foundation rests on good insulinsensitivity.
So you absolutely need toconfirm that with basic
metabolic labs.
Right.
Fasting glucose, HBA1C, to seelonger-term blood sugar control,
and importantly, fastinginsulin.
SPEAKER_02 (15:14):
Why fasting insulin?
SPEAKER_01 (15:15):
Because it's often the earliest marker of declining
insulin sensitivity.
If someone's fasting insulinstarts to creep up, even if
their glucose and A1C look okay.
SPEAKER_02 (15:25):
It suggests the underlying metabolic health, the
foundation of the LEM hypothesisfor them might be weakening.
SPEAKER_01 (15:30):
Exactly.
If insulin sensitivity degrades,the LEM framework may no longer
apply, and that high LDLsuddenly looks much more like
traditional high-risk LDL.
Context changes everything.
SPEAKER_02 (15:42):
So you need the full picture.
APOV, particle count, maybeparticle size, inflammation
levels, and confirmed insulinsensitivity.
And you need to track it.
SPEAKER_01 (15:51):
Yes.
Longitudinal monitoring isnon-negotiable.
Tracking these trends over time,not just a single snapshot, is
the only way to develop a trulypersonalized understanding and
strategy.
SPEAKER_02 (16:01):
Aaron Powell This has been, wow, a really crucial
deep dive.
So to recap, the lipid energymodel offers this compelling
alternative lens to view highLDL cholesterol.
SPEAKER_01 (16:10):
But specifically in lean, active, insulin-sensitive
individuals on low-carb diets.
SPEAKER_02 (16:15):
Right.
Shifting the perspectivepotentially from automatic
pathology to maybe efficientenergy transport.
SPEAKER_01 (16:21):
Aaron Powell It definitely challenges the
conventional wisdom byhighlighting how unique these
metabolic adaptations can be.
It provides a rational frameworkfor understanding why the
numbers look the way they do inLMHRs.
But and it remains the critical,but the long-term risk
associated with having thatsustained high APOB particle
number, even in this context, isstill the major unanswered
(16:43):
question.
That's what the currentresearch, especially the imaging
studies, is trying todefinitively answer.
SPEAKER_02 (16:48):
Okay.
So the final thought, themission for you listening,
context is absolutely king inmodern nutrition and health
assessment.
You just cannot afford to lookat a single lab number like LDLC
in total isolation anymore.
SPEAKER_01 (17:00):
Especially not if you fit this potential LMHR
profile.
SPEAKER_02 (17:03):
So if that's you, if you're seeing great metabolic
health markers but a shockinglyhigh LDL on a low carb diet, the
question becomes how can you usethis knowledge?
How can you work with yourdoctor to utilize advanced
testing A-pro B, inflammationmarkers, maybe even SCAC scoring
and critical thinking to reallyunderstand your individual
metabolic health beyond that onesingle potentially confusing
(17:25):
number?
SPEAKER_01 (17:26):
That deeper understanding, that personalized
context, that's the real goalhere.
SPEAKER_00 (17:31):
That's what we leave you with today.com.
(17:54):
Stay informed, stay healthy, andwe'll catch you in the next
episode.
Welcome to the Health Pulse, your go-to source
for quick, actionable insightson health, wellness, and
diagnostics.
Whether you're looking tooptimize your well-being or stay
informed about the latestin-medical testing, we've got
you covered.
Join us as we break down keyhealth topics in just minutes.
Let's dive in.
SPEAKER_02 (00:25):
Welcome back to the deep dive.
We are jumping straight into uh,well, one of the most perplexing
things happening in nutritionright now.
Honestly, it can be prettyterrifying for people.
SPEAKER_01 (00:34):
Yeah, absolutely.
Imagine this scenario.
Maybe it's even you listening.
You decide to really optimizeyour health.
SPEAKER_02 (00:42):
Right.
You go low carb, maybe fullketo.
SPEAKER_01 (00:44):
Yeah.
SPEAKER_02 (00:45):
And you feel amazing.
Energy's great, you're leaner,blood sugar, perfect.
SPEAKER_01 (00:49):
Exactly.
So you get a blood test, feelingconfident, and the good stuff
looks fantastic.
Try glycerides, way down, HDLthrough the roof.
SPEAKER_02 (00:58):
It looks like metabolic heaven on paper.
SPEAKER_01 (01:00):
But then you see it.
The LDL cholesterol, the numbereveryone's been told for decades
is the big risk factor for heartdisease.
SPEAKER_02 (01:08):
It's just exploded, like maybe over 200, maybe even
300 milliGDLs.
SPEAKER_01 (01:12):
It could be that high, yeah.
And that one number throwseverything into chaos for you,
for your doctor.
SPEAKER_02 (01:17):
It creates this huge conflict.
The traditional markers screamdanger, but everything else
about your health seems great.
SPEAKER_01 (01:23):
Totally.
And that specific conflict, thatconfusion, is exactly why we
need to unpack the lipid energymodel today, the limb.
SPEAKER_02 (01:30):
Right.
Our mission in this deep dive isreally to get a handle on the
limb.
It's this framework that offersa completely different way to
look at that high LDL.
SPEAKER_01 (01:38):
A different explanation, yeah.
It basically asks is thisspecific kind of LDL rise in
someone who's lean, active,healthy, is it actually disease?
SPEAKER_02 (01:49):
Or is it maybe an adaptation, the body just
adjusting how it transportsenergy?
SPEAKER_01 (01:55):
That's the core question.
A shift in energy transport.
SPEAKER_02 (01:57):
Okay, let's dive into that because where this
model came from is prettyinteresting in itself.
SPEAKER_01 (02:01):
It really is.
You know, the lum didn't pop outof some big university
cardiology lab initially.
No, it was first reallydescribed and pushed forward by
Dave Feldman, who's an engineer,a citizen scientist.
Yeah, him and his collaborators.
They were basically seeing allthese confusing lab results
posted online by low-carb folksand trying to make sense of it
empirically.
SPEAKER_02 (02:21):
So it's kind of a bottom-up citizen science thing
trying to solve a medicalpuzzle.
SPEAKER_01 (02:25):
Exactly.
Which might explain why it uhsort of rubs up against the
established medical thinking somuch.
SPEAKER_02 (02:31):
Aaron Powell Okay.
That context is important.
Now we need to be super clearabout who this model applies to.
This isn't some, you know,universal excuse for high
cholesterol across the board.
SPEAKER_01 (02:42):
No, absolutely not.
Crucial point.
The LM applies specifically, andI mean specifically, to a
certain group.
Which is people who are lean,insulin sensitive, and
physically active.
SPEAKER_02 (02:54):
Aaron Powell Okay.
So lean, metabolically healthy.
Maybe they got healthy throughlow carb and they move their
bodies.
SPEAKER_01 (03:02):
Precisely.
That profile is key.
Because the model is all aboutunderstanding the huge shift in
energy that happens when you cutcarbs drastically.
SPEAKER_02 (03:10):
Right.
Because you take away the easyglucose fuel.
SPEAKER_01 (03:12):
Trevor Burrus And the body has to rely much, much
more heavily on fatty acids andketones, too, of course, for
fuel.
Trevor Burrus, Jr.
SPEAKER_02 (03:18):
So if you're relying on fat for energy, you suddenly
need to move a lot more fataround your body, right?
It's like logistics.
SPEAKER_01 (03:23):
That's a great analogy.
Yeah.
The demand for fat transportjust skyrockets.
If your delivery servicesuddenly has 10 times the
packages, you need more truckson the road.
You need way more trucks.
The LEM essentially proposesthat this rise in LDL is just a
natural consequence of the bodyefficiently packaging and
delivering all this extra fatfuel.
The whole system gets ramped up.
SPEAKER_02 (03:44):
Especially in someone lean and active who's
burning through that energyquickly.
SPEAKER_01 (03:47):
Exactly.
High energy demands, high fatflux.
SPEAKER_02 (03:50):
Trevor Burrus, OK.
So if the cause is this shiftfrom sugar to fat fuel, the
mechanics inside the body mustreflect that.
Let's get into how that actuallyworks, this VLDL remodeling
thing.
SPEAKER_01 (04:01):
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 packagingplant for fat.
SPEAKER_02 (04:08):
Okay.
SPEAKER_01 (04:08):
When you're restricting carbs, the liver
starts packaging up lots oftriglycerides, that's the usable
fat energy, into these particlescalled very low density
lipoproteins.
VLDL.
SPEAKER_02 (04:19):
VLDL, got it.
So those are the big freighttrucks you mentioned, loaded up
with fat energy.
Trevor Burrus, Jr.
SPEAKER_01 (04:23):
That's exactly it.
Think of them leaving the liverfactory, fully loaded, heading
out to deliver fuel.
SPEAKER_02 (04:28):
Aaron Ross Powell To the muscles, the heart, all the
tissues doing work.
Makes sense.
So what happens after the VLDLtruck drops off some of its
cargo, its triglycerides?
SPEAKER_01 (04:38):
Well, it doesn't just vanish, it changes, it
remodels itself.
As the VLDL delivers itstriglyceride payload, there's an
enzyme called lipoprotein lipasethat helps with this the
particle itself gets smaller anddenser.
SPEAKER_02 (04:52):
Ah, okay.
So it's like the truck isgetting emptier and maybe uh
shrinking down.
SPEAKER_01 (04:56):
Aaron Powell Pretty much it transforms.
As it sheds that fat cargo, theVLDL becomes first immediate
density lipoprotein IDL and theneventually.
Light LDL.
Yes, low density lipoproteinLDL.
That's the particle that's leftcirculating in the blood.
It's essentially the smaller,emptier taxi that used to be the
big full freight truck.
SPEAKER_02 (05:14):
Whoa.
Okay, so the high LDL count wesee on the lab report, according
to the Lem, it isn't necessarilybecause the body isn't clearing
fat properly like you see ininsulin resistance.
SPEAKER_01 (05:24):
Right, that's the usual assumption.
Sluggish clearance.
SPEAKER_02 (05:26):
Instead, the LEM says it might just be the
result, the byproduct of reallyhigh activity in the transport
system.
High VLDL turnover because thebody needs so much fat fuel.
Trevor Burrus, Jr.
SPEAKER_01 (05:35):
That is the central LM argument, yes.
Because the body is workingefficiently, demanding lots of
energy, the liver pumps out moreVLDL trucks.
SPEAKER_02 (05:43):
That leads to a higher rate of turnover, more
deliveries, and more emptytaxes, LDL particles left
circulating afterwards.
SPEAKER_01 (05:51):
Exactly.
So the high LDL count reflectsthe intensity of the fat
transport, not necessarily aproblem with it.
Trevor Burrus, Jr.
SPEAKER_02 (05:56):
Okay.
That makes sensemechanistically.
And this process, this specificmetabolic state, it creates a
very distinct pattern in theblood test, right?
This lean mass hyperresponderprofile.
SPEAKER_01 (06:07):
Aaron Ross Powell Yes.
The LMHR profile.
It's a specific signature, andunderstanding it is key to
seeing the context.
It's a triad of three things,typically.
Trevor Burrus, Jr.
SPEAKER_02 (06:15):
What's the first part of the triad?
SPEAKER_01 (06:16):
Aaron Powell Number one is what we've been talking
about, high LDLC.
Often dramatically high, likeyou said, maybe over 200,
sometimes well over 300milliogdl.
This is the big red flag formost doctors.
Aaron Powell Yeah.
SPEAKER_02 (06:27):
I mean I don't have to jump in there.
An LDL over 200, traditionallythat's almost an automatic
prescription, right?
Regardless of anything else.
It's seen as immediate, seriousrisk.
SPEAKER_01 (06:36):
Aaron Powell That's absolutely the standard view.
Decades of data support loweringLDL.
But in the LMHR profile, thathigh LDL comes alongside two
other factors that are usuallyseen as protective.
SPEAKER_02 (06:47):
Okay, what are they?
SPEAKER_01 (06:48):
Number two is high HDLC, the so-called good
cholesterol, often very high inthese individuals.
SPEAKER_02 (06:53):
Aaron Powell Which is the opposite of typical heart
disease risk profiles.
SPEAKER_01 (06:57):
Aaron Powell Right.
And number three, critically, islow triglycerides.
Really low, often under 70 milGDL, sometimes even under 50.
SPEAKER_02 (07:05):
Wow.
Okay.
Low triglycerides mean your bodyis using fat efficiently, right?
It's not getting backed up inthe bloodstream.
SPEAKER_01 (07:11):
Exactly.
That fat is being delivered andburned, not stored
inappropriately.
Trevor Burrus, Jr.
SPEAKER_02 (07:15):
So that triad, high LDL, high HDL, low
triglycerides, it's the completeopposite of the pattern you see
in metabolic syndrome or insulinresistance.
It's like an inverted profile.
SPEAKER_01 (07:24):
Aaron Powell It's completely inverted.
And that combination pointsstrongly towards good insulin
sensitivity and very efficientfat metabolism.
That the lamb predicts thisexact profile because it links
the high LDL to that functionalneed for energy transport, not
to dysfunction.
SPEAKER_02 (07:40):
And if the model is right, if it's about the fuel
source dictating the transportneeds, we should be able to test
that, right?
Like what happens if someonewith this LMHR profile adds back
some carbs?
SPEAKER_01 (07:51):
That's one of the key predictions, and it makes
the model testable.
If you say add back 100 or 150grams of carbs per day, enough
to shift the body back towardsusing glucose more.
Precisely.
SPEAKER_02 (08:11):
So the prediction is LDL should drop.
SPEAKER_01 (08:13):
Aaron Powell The prediction is LDLC should
plummet, often back towards orinto the normal ranges.
And anecdotally, and in somecase studies, that's exactly
what people observe when they dothat experiment.
SPEAKER_02 (08:22):
Aaron Powell Okay, wow.
So we have a model, it explainsthe numbers, it makes testable
predictions.
SPEAKER_01 (08:26):
And it's a big butt it's a huge butt.
SPEAKER_02 (08:27):
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, thegreat divide.
SPEAKER_01 (08:37):
Aaron Powell It absolutely is.
Probably one of the biggestscientific debates in this area
right now.
The traditional view is, youknow, incredibly well
established.
SPEAKER_02 (08:45):
Simple and powerful.
SPEAKER_01 (08:46):
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 (08:55):
We'll get to ApoB in a minute.
SPEAKER_01 (08:56):
Right.
But that these particles arecausally linked to
atherosclerosis, to plaquebuildup in the arteries.
SPEAKER_02 (09:03):
And causally linked here means based on outcomes.
Like heart attacks and strokes.
SPEAKER_01 (09:08):
Yes.
Based on huge randomizedcontrolled trials, population
studies spanning decades.
The evidence is consideredoverwhelming by the mainstream
medical community.
Higher exposure to theseparticles over time equals
higher risk, period.
SPEAKER_02 (09:21):
Aaron Powell So from a cardiologist's perspective,
seeing an LDL of 300, it doesn'tmatter why it's 300.
The number itself is the risk.
SPEAKER_01 (09:29):
Aaron Powell That's the prevailing view.
Every major drug trial, whetherit's statins or the newer PCSK9
inhibitors, shows that loweringLDL or APOB reduces
cardiovascular events.
So for them, a high number issimply a threat that needs to be
neutralized.
The why is less important thanthe what.
SPEAKER_02 (09:45):
Okay.
So that's the traditional view.
High particle number exilsinherent risk.
The Lang perspective, then, mustbe arguing that the context
changes the risk.
SPEAKER_01 (09:54):
That is the absolute core of the LEM argument.
Context is everything.
Supporters argue that in thisspecific metabolic environment,
the LMHR triad again.
SPEAKER_02 (10:04):
Low triglycerides, high HDL.
Trevor Burrus, Jr.
SPEAKER_01 (10:06):
Right.
Excellent insulin sensitivity,often very low inflammation
markers.
In that context, the LDLparticles themselves might
behave differently.
SPEAKER_02 (10:14):
Or maybe the artery walls are healthier, less prone
to damage.
SPEAKER_01 (10:17):
Trevor Burrus Or the arterial environment is less
inflammatory, less sticky.
The idea is that something aboutthis overall healthy metabolic
state modifies the risk usuallyassociated with that high
particle count.
The LDL reflects energytrafficking, not the metabolic
dysfunction that usually driveshigh LDL.
Trevor Burrus, Jr.
SPEAKER_02 (10:33):
Okay, it's a compelling alternative
explanation.
But where are we with hardproof?
Like long-term outcomes.
Has this LMHR profile actuallybeen proven safe over, say, 10
or 20 years?
SPEAKER_01 (10:44):
Aaron Powell And that's the million-dollar
question.
The honest answer right now.
The long-term outcome data forthis specific LMHR group is,
well, it's uncertain.
It's inconclusive.
SPEAKER_02 (10:52):
So we just don't know yet.
SPEAKER_01 (10:53):
We don't.
We have case reports confirmingthe lipid patterns are real.
We see people living with thesenumbers.
But we don't have largelong-term studies tracking their
actual artery health overdecades.
SPEAKER_02 (11:04):
Aaron Powell So how are researchers trying to figure
this out?
SPEAKER_01 (11:07):
That's where ongoing studies are absolutely critical.
Researchers are using tools likenon-invasive imaging, things
like coronary artery, calciumscans, CAT scores, and CT
angiography.
SPEAKER_02 (11:19):
To actually look at the arteries.
SPEAKER_01 (11:20):
Exactly.
To directly measure plaquebuildup or lack thereof in these
LMHR individuals and compare itover time to people with more
typical lipid profiles.
That imaging data over the nextfew years is expected to be the
real tiebreaker.
SPEAKER_02 (11:35):
Okay, this makes total sense then.
If the standard lipid panel,especially just LDLC, might be
misleading in this specific LMNcontext, we can't rely on it
alone.
We need more advanced testing tobuild that crucial context.
SPEAKER_01 (11:48):
Absolutely non-negotiable if you're in this
situation or advising someonewho is.
You need more data points.
SPEAKER_02 (11:53):
So what are the key tests?
What gives us that context?
SPEAKER_01 (11:56):
Well, number one, and arguably the most important
piece of the puzzle beyond thescanner panel is APOLIPOProtein
B.
ApoB.
SPEAKER_02 (12:04):
Okay, explain APOB again.
If LDLC is the cholesterol cargoinside the particle.
SPEAKER_01 (12:08):
Apo B is essentially the protein marker on the
surface of each atrogeniclipoprotein particle, VLDL, IDL,
LDL.
Think of it as the license plateor the barcode on every single
truck or taxi.
SPEAKER_02 (12:21):
Ah, so it measures the actual number of potentially
risky particles, not just thetotal amount of cholesterol
they're carrying.
SPEAKER_01 (12:26):
Aaron Powell Exactly.
And since the traditional view,and even many LEM proponents
agree, holds that it's theparticle number, the sheer
number of interactions with theartery wall that primarily
drives risk, APOB is widelyconsidered a much more accurate
measure of cardiovascular riskthan LDLC alone.
SPEAKER_02 (12:42):
Aaron Powell So in the LEM context, you want to see
what the APOB number is doingrelative to that sky-high LDLC?
SPEAKER_01 (12:49):
Aaron Powell Precisely.
Is the APOB also astronomicallyhigh, or is it maybe less
elevated than the LDLC mightsuggest?
That particle count is key.
SPEAKER_02 (12:56):
Okay, APOB is crucial.
What else?
Does the type or quality of theLDL particle matter?
Like size?
SPEAKER_01 (13:02):
Aaron Powell It certainly adds another layer of
context.
This is where tests looking atLDL particle number, LDLP and
size come in.
Advanced lipid testing, like NMRlipoprofile or cardio IQ panels.
SPEAKER_02 (13:15):
Aaron Powell And why does size matter?
SPEAKER_01 (13:17):
Well, traditionally the risk, especially the risk
linked to insulin resistance andmetabolic syndrome, is
associated more with small,dense LDL particles.
SPEAKER_02 (13:26):
Aaron Powell Right.
I've heard those described asbeing like little hard BB
pellets that can more easily getinto the artery wall and cause
damage.
SPEAKER_01 (13:33):
That's the thinking, yeah.
They're thought to be moreeasily oxidized, more
atherogenic.
In contrast, these advancedtests can sometimes
differentiate between thosesmall, dense particles and
larger, more buoyant LDLparticles.
SPEAKER_02 (13:46):
Fluffier ones.
SPEAKER_01 (13:47):
Kind of, yeah.
Now, a high number is still ahigh number, APOB tells you
that.
But the LEM theories suggestthat the particles circulating
in healthy LMHRs might bepredominantly the larger,
buoyant type.
SPEAKER_02 (13:58):
Which might be less risky.
SPEAKER_01 (14:00):
Which might be less directly damaging, although this
is still debated.
But knowing the particle sizedistribution adds to the overall
picture, it provides more nuancethan just the LDLC number.
SPEAKER_02 (14:09):
Makes sense.
And okay, heart disease isn'tjust about lipids, right?
It's also about inflammation anddamage to the arteries
themselves.
So we need to check thatenvironment too.
SPEAKER_01 (14:17):
Aaron Powell Absolutely critical.
You have to measure inflammatorymarkers.
The key ones are highsensitivity, C reactive protein,
HSCRP, and maybe homocysteine.
SPEAKER_00 (14:28):
Why?
SPEAKER_01 (14:29):
Because if someone has this incredibly high LDL or
APOB, but their markers ofsystemic and vascular
inflammation are rock bottom.
Trevor Burrus, Jr.
SPEAKER_02 (14:38):
Well, like their blood vessels seem completely
calm.
SPEAKER_01 (14:40):
Exactly.
If there's no underlyinginflammatory fire, it lends
support to the idea that thehigh lipid levels aren't
actively driving a damagingpathological process in that
specific individual at thattime.
Low inflammation is a verypositive sign in this context.
Trevor Burrus, Jr.
SPEAKER_02 (14:54):
Okay.
APOP particle size inflammation.
What else?
You mentioned the LEM reallyhinges on the person being
metabolically healthy.
SPEAKER_01 (15:00):
Aaron Powell Yes, the entire theoretical
foundation rests on good insulinsensitivity.
So you absolutely need toconfirm that with basic
metabolic labs.
Right.
Fasting glucose, HBA1C, to seelonger-term blood sugar control,
and importantly, fastinginsulin.
SPEAKER_02 (15:14):
Why fasting insulin?
SPEAKER_01 (15:15):
Because it's often the earliest marker of declining
insulin sensitivity.
If someone's fasting insulinstarts to creep up, even if
their glucose and A1C look okay.
SPEAKER_02 (15:25):
It suggests the underlying metabolic health, the
foundation of the LEM hypothesisfor them might be weakening.
SPEAKER_01 (15:30):
Exactly.
If insulin sensitivity degrades,the LEM framework may no longer
apply, and that high LDLsuddenly looks much more like
traditional high-risk LDL.
Context changes everything.
SPEAKER_02 (15:42):
So you need the full picture.
APOV, particle count, maybeparticle size, inflammation
levels, and confirmed insulinsensitivity.
And you need to track it.
SPEAKER_01 (15:51):
Yes.
Longitudinal monitoring isnon-negotiable.
Tracking these trends over time,not just a single snapshot, is
the only way to develop a trulypersonalized understanding and
strategy.
SPEAKER_02 (16:01):
Aaron Powell This has been, wow, a really crucial
deep dive.
So to recap, the lipid energymodel offers this compelling
alternative lens to view highLDL cholesterol.
SPEAKER_01 (16:10):
But specifically in lean, active, insulin-sensitive
individuals on low-carb diets.
SPEAKER_02 (16:15):
Right.
Shifting the perspectivepotentially from automatic
pathology to maybe efficientenergy transport.
SPEAKER_01 (16:21):
Aaron Powell It definitely challenges the
conventional wisdom byhighlighting how unique these
metabolic adaptations can be.
It provides a rational frameworkfor understanding why the
numbers look the way they do inLMHRs.
But and it remains the critical,but the long-term risk
associated with having thatsustained high APOB particle
number, even in this context, isstill the major unanswered
(16:43):
question.
That's what the currentresearch, especially the imaging
studies, is trying todefinitively answer.
SPEAKER_02 (16:48):
Okay.
So the final thought, themission for you listening,
context is absolutely king inmodern nutrition and health
assessment.
You just cannot afford to lookat a single lab number like LDLC
in total isolation anymore.
SPEAKER_01 (17:00):
Especially not if you fit this potential LMHR
profile.
SPEAKER_02 (17:03):
So if that's you, if you're seeing great metabolic
health markers but a shockinglyhigh LDL on a low carb diet, the
question becomes how can you usethis knowledge?
How can you work with yourdoctor to utilize advanced
testing A-pro B, inflammationmarkers, maybe even SCAC scoring
and critical thinking to reallyunderstand your individual
metabolic health beyond that onesingle potentially confusing
(17:25):
number?
SPEAKER_01 (17:26):
That deeper understanding, that personalized
context, that's the real goalhere.
SPEAKER_00 (17:31):
That's what we leave you with today.com.
(17:54):
Stay informed, stay healthy, andwe'll catch you in the next
episode.
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