September 23, 2025 • 14 mins
Why do some of the leanest, healthiest low-carb eaters see their LDL cholesterol skyrocket into ranges that would alarm any doctor—while all their other markers look perfect? This puzzling pattern, known as the Lean Mass Hyper-Responder (LMHR) phenomenon, is one of the most hotly debated topics in modern nutrition and cardiology.
In this episode, we unpack the science behind the LMHR lipid triad: extremely high LDL cholesterol, unusually high HDL, and strikingly low triglycerides. We explore competing theories on why this occurs—ranging from increased fat metabolism to genetic predisposition—and ask the critical question: does LDL cholesterol carry the same risk in a clean metabolic environment as it does in someone with insulin resistance and chronic inflammation?
You’ll learn why advanced testing beyond a standard lipid panel is essential for LMHRs, including ApoB, LDL particle number, Lipoprotein(a), and coronary calcium scoring, and how these markers help provide real context while the research continues to evolve.
This conversation pushes beyond conventional wisdom to challenge how we think about cardiovascular risk, diet, and prevention.
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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 1 (00:01):
Welcome to the Health Pulse, your go-to source for
quick, actionable insights onhealth, wellness and diagnostics
.
Whether you're looking tooptimize your well-being or stay
informed about the latest inmedical testing, we've got you
covered.
Join us as we break down keyhealth topics in just minutes.
Let's dive in.
Speaker 2 (00:26):
Welcome back everyone .
We are diving deep today into,well, one of the most, I'd say,
disruptive things happening inpersonalized health.
Right now we're talking aboutlow-carbohydrate eating.
Now, for many of you listening,the benefits are probably
pretty familiar Easier weightmanagement, maybe fantastic
improvements in insulinsensitivity, lower triglycerides
, higher HDL cholesterol.
You know it sounds like a totalmetabolic win, but and this is
(00:49):
the key thing there's thiscounterintuitive surprise that
pops up for a really specificgroup of people, often lean
athletic types.
For these individuals, theirLDL cholesterol, you know,
so-called bad cholesterol itjust shoots up dramatically
often into numbers that, frankly, make most doctors pretty
nervous.
So today our deep dive is allabout the lean mass
hyper-responder, or LMHR,phenotype.
(01:12):
Our mission is to reallyunderstand this group, look into
the controversy around theirsuper high LDL and figure out
what kind of monitoring youreally need.
And the big question, thereally high stakes one, is this
does having sky high LDL in thisspecific metabolic context
carry the same cardiovascularrisk as it does for well
everyone else?
Let's unpack that.
Speaker 3 (01:30):
Yeah, it's absolutely critical we figure this out
because, look, if the answer isno, then we fundamentally have
to rethink how we assess heartdisease risk.
But if the answer is yes, thenthis group, despite looking
healthy on paper otherwise,might need, you know, pretty
immediate intervention.
Speaker 2 (01:46):
OK, let's start with the basics.
Who exactly are we talkingabout here?
This term LMHR.
It was coined by researcherDave Feldman and his team right.
Speaker 3 (01:55):
That's right, and it describes people who are
typically already lean,physically active and this is
important highly insulinsensitive, before they even
start cutting carbs.
Speaker 2 (02:05):
Got it, and their response is defined by a
specific lipid pattern, a triad,you call it.
Speaker 3 (02:11):
Exactly a triad, Three specific markers that,
when you see them together, kindof fly in the face of the
traditional high risk profile.
So first they have really highLDL cholesterol LDL-C we're
talking often way past 200milligrams per deciliter,
sometimes even over 300.
Speaker 2 (02:26):
Wow Okay.
Speaker 3 (02:27):
Second, their HDL cholesterol HDL-C the good kind
is also very high, usually, youknow, above 70 milligdl,
sometimes much higher.
And third, their triglyceridesTG are super low, typically
under 70 milligdl.
Speaker 2 (02:40):
That's the paradox, right.
Normally, if someone walks inwith an LDL of, say, 250, you
expect to see high triglyceridesand low HDL, maybe issues with
blood sugar insulin resistance.
Speaker 3 (02:52):
Precisely.
The standard picture of highrisk often includes what we call
metabolic syndrome hightriglycerides, low HDL, often
central obesity, higher bloodpressure.
The LMHR is the completeopposite.
They have that sky-high LDL,yes, but everything else looks
well, pretty much perfect Normalblood pressure, great glucose
control.
They're lean, low inflammation.
Speaker 2 (03:12):
They're metabolically healthy by almost every measure
, except that LDL number.
Speaker 3 (03:15):
Exactly.
Speaker 2 (03:16):
And just to be clear, this pattern mainly shows up
when people go on really strictlow-carb diets like keto or
carnivore.
Speaker 3 (03:23):
Overwhelmingly yes, it seems to be a direct result
of that drastic carbohydraterestriction interacting with
their specific physiology.
Speaker 2 (03:30):
OK, so it's not just about eating more fat.
Something fundamental isshifting in how their body works
when carbs are taken out, Ifthey're already lean and insulin
sensitive.
What's driving this huge LDLsurge?
Where's it coming from?
Speaker 3 (03:44):
Yeah, that's the million-dollar question, isn't
it?
And the answer seems to be tiedinto how their body transports
energy when glucose isn't theprimary fuel.
There are basically three mainideas floating around.
The first is what's calledincreased fat flux, so without
much glucose, the body runs onfatty acids.
The theory goes that LMHRs arejust incredibly efficient at
(04:04):
pulling fat out of their storageeven their limited storage and
getting it into circulation.
And when you mobilize fat likethat, the liver has to package
it up into lipoproteins like LDLparticles to ship it out to
muscles and organs that needenergy.
So more fat mobilization mightmean more LDL trucks are needed.
Speaker 2 (04:23):
Wait a second.
If they're lean, wouldn't theylike run out of fat stores
pretty quick?
Shouldn't the LDL then drop?
Speaker 3 (04:29):
Ah well, that actually leads right into the
second proposed mechanism highenergy demands.
Because LMHRs often don't havemuch body fat to begin with and
they're frequently very activeRight.
Their bodies are constantlyscreaming for fuel delivery, so
their reliance on thesecirculating lipoproteins, these
LDL delivery trucks, might beamplified because their other
fuel depots are low.
(04:50):
The idea isn't necessarily thatthe LDL particles are bad or
damaged, but that they're beingactively used, maybe turned over
really quickly, to deliver hugeamounts of energy all over the
body.
Speaker 2 (05:01):
So they're basically running this super high volume,
maybe hyper efficient energyshipping operation.
Speaker 1 (05:05):
OK.
Speaker 2 (05:06):
And the third idea links this to genetics.
Speaker 3 (05:09):
Precisely.
There seems to be a strongcomponent of genetic
predisposition.
We know there are specific genevariants related to how we
handle lipid stink genes likeAPOE, ldlr, pcsk9.
It's possible that certaingenetic profiles make people
hyper-respond metabolically whenthey switch fuel sources so
drastically.
The low-carb, high-fat diet isthe trigger, but maybe your
(05:30):
genes decide if you get thisdramatic LDL surge.
Speaker 2 (05:32):
So it's not just the diet alone.
Speaker 3 (05:34):
No, the key takeaway here really seems to be a
crucial gene diet interaction.
It's the diet hitting aparticular genetic setup that
likely creates this LMHRphenotype.
Speaker 2 (05:45):
All right, Now we're getting into the really tricky
part, the gray area, thecontroversy.
Yeah, Because, look, we havemountains of evidence, decades
of it, saying high LDL is acause of atherosclerotic
cardiovascular disease, ASCVD,you know, the plaque buildup
leading to heart attacks andstrokes.
So when someone in the LMHRcommunity says, yeah, my LDL is
(06:06):
300, but hey, my triglyceridesare 50 and my HDL is 90, the
medical world gets well divided.
Speaker 3 (06:12):
It's a real clinical puzzle.
On one hand you have theconservative view.
This is often the stance ofmainstream lipid experts.
They argue, based on hugepopulation studies, that LDL is
inherently atherogenic.
The higher the number, the moreexposure your arteries have
over time period.
They see an LDL of 300, andregardless of other markers,
they think risk and usuallyrecommend getting that number
down.
(06:32):
Sometimes aggressively, theytreat the number itself.
Speaker 2 (06:35):
Okay, that's one side .
What's the counter argumentfrom the LMHR perspective?
Speaker 3 (06:39):
They argue for what you might call the metabolic
context view.
They say hold on, you have tolook at the whole picture.
They point to their lowtriglycerides, high HDL, low
insulin, often zero inflammation, their leanness and they ask
does this unique metabolicenvironment change the nature or
the function of those LDLparticles?
Is an LDL particle floatingaround in that clean environment
(07:00):
the same risk as one in someonewith metabolic syndrome, where
particles might be small, dense,maybe oxidized or glycated?
Speaker 2 (07:07):
That's the crux of it , isn't it?
Are these LDL particles, eventhough there are lots of them,
somehow less dangerous becausethe overall metabolic health is
so good, or does the sheernumber still cause plaque
buildup over time?
Speaker 3 (07:18):
And this leads us straight to the major evidence
gap Right now.
Today we just don't have thelarge-scale long-term studies
specifically following LMHRs tosee what actually happens to
their hearts and arteries overdecades.
We don't know definitively ifthey develop atherosclerosis
faster, slower or at the samerate as someone else with a
similarly high LDL but adifferent metabolic profile.
(07:40):
They really are in a kind ofcardiometabolic blind spot.
We need solid proof, not justplausible theories.
Speaker 2 (07:46):
Which means until we get that proof, we have to be
cautious.
So okay, let's talkpracticality.
Since this high LDL is almostalways tied to the very low carb
diet, what can you actually doif you identify as an LMHR and
you're concerned about thatnumber?
What levers can you pull?
Speaker 3 (08:01):
Well, if the primary goal is simply to lower the LDL
number, the most direct route isoften a dietary adjustment,
because the whole thing seemsdriven by this massive fat
mobilization for fuel.
Reintroducing even a moderateamount of carbohydrates maybe
say 50 to 100 grams per dayoften signals the body to switch
back towards using glucose.
Anecdotally, this frequentlybrings the LDL-C down
(08:24):
significantly and for manypeople they can do this while
still keeping blood sugar stableand maintaining many of the
other benefits that they gotfrom low-carb.
Speaker 2 (08:31):
So you don't necessarily have to completely
abandon the approach, maybe justtweak it.
Speaker 3 (08:36):
Exactly.
Another potential tweak is fatsource alteration.
Sometimes the LMHR responseseems more pronounced, with very
high intakes of saturated fats,things like butter, fatty red
meat cream.
Some find that shifting the fatfocus towards more unsaturated
fats like olive oil, avocados,nuts, fatty fish, can also help
(08:56):
lower the LDL-C, even whilekeeping carbs relatively low.
Speaker 2 (08:59):
Interesting.
But regardless of whethersomeone tweaks their diet or not
, monitoring seems absolutelycritical.
And you're saying a standardlipid panel isn't really enough
here.
We need more advanced tests.
Speaker 3 (09:09):
Absolutely non-negotiable.
And, yes, the standard panelcan be misleading.
It usually measures LDL-C,which is the weight or the mass
of cholesterol carried withinthe LDL particles, but what
seems to matter more foratherosclerosis risk is the
actual number of potentiallyadditives.
Atherogenic particles bumpingagainst your artery walls.
Think of it like traffic.
Speaker 2 (09:30):
Okay, traffic analogy , let's hear it.
Speaker 3 (09:31):
All right, ldlc is like measuring the total weight
of all the cargo being carriedby trucks on a highway.
But what causes traffic jamsand potential accidents isn't
the weight of the cargo, it'sthe sheer number of trucks on
the road.
Speaker 2 (09:43):
Gotcha More trucks, higher chance of collision.
Speaker 3 (09:50):
Precisely, and that's why we need tests like opal
lipoprotein B or ApoB.
Apob is a protein found onevery single one of these
potentially atherogenicparticles VLDL, idl and LDL.
One ApoB molecule per particle.
So measuring ApoB basicallytells you the total number of
these particles, the totalnumber of trucks on your highway
.
It's considered a much moreaccurate marker of particle
burden and risk than just LDL-Calone.
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 quantifyingthe number of LDL particles.
Specifically For an LMHR, it'scrucial to know is there high
LDL-C mass due to having a fewreally large fluffy LDL
(10:34):
particles packed withcholesterol, or is it due to
having a huge number of smallerparticles?
The latter is generallyconsidered higher risk.
Speaker 2 (10:41):
Right, so ApoB and LDLP give you the particle count
.
What other tests are importantfor context?
Speaker 3 (10:47):
You definitely want to check lipoprotein or LPA.
This is a completely separaterisk factor, mostly determined
by genetics, not diet.
If it's high, it significantlyadds to overall cardiovascular
risk.
No matter what your LDL isdoing, 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 theunderlying 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 arterycalcium 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 looksdirectly for hardened calcified
plaque in your coronary arteries.
It doesn't measure risk factorsin the blood.
It measures the actual presenceof 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 canbe incredibly informative.
Many are using it oftenserially over time to see if
their high particle count isactually translating into plaque
buildup.
Getting a CAC score of zero isgenerally very reassuring,
suggesting very lowshort-to-intermediate-term risk.
(11:58):
Even if the LDL is high, itprovides a piece of direct
evidence about what's happeningin the arteries themselves.
Speaker 2 (12:04):
Wow.
Okay, that seems like acritical piece of the puzzle
while we wait for more long-termdata.
Speaker 3 (12:09):
It really is, and it all underscores the need for
truly personalized nutrition andmonitoring.
We can't just use blanketguidelines here.
It has to be tailored, usingthese advanced tests.
Speaker 2 (12:18):
Okay, let's try and wrap this up.
What's the main takeaway foryou listening?
Speaker 3 (12:23):
The LMHR phenomenon.
It's really shaking things upin metabolic science.
It shows just how powerfullydiet can change our biomarkers,
sometimes in really unexpectedways, like driving LDL sky high
even while fixing almosteverything else.
Speaker 2 (12:37):
And until we have that definitive long-term
evidence about the actual riskand I should say studies using
imaging like CAC are underwayright now.
Looking specifically at thisgroup, the safest approach seems
clear.
It's careful, close monitoringwith advanced testing Get your
ApoB checked, know your LDL-P,find out your LPA, track
inflammation and seriouslyconsider a CAC score and,
(13:00):
importantly, work with a doctoror healthcare provider who
actually understands thisspecific metabolic situation.
Speaker 3 (13:05):
It's really quite something.
One set of markers looksamazing, another looks
potentially alarming, all fromthe same dietary shift?
Yeah, it is.
And maybe the final thought,the provocative question for you
to mull over, is this If wezoom out, does the very
existence of the LMHR groupsuggest that our future models
for predicting heart diseaserisk need to evolve the full
(13:26):
metabolic picture, thetriglycerides, the HDL, insulin
sensitivity, inflammation,leanness rather than focusing so
heavily, almost solelysometimes, on the quantity of
LDL cholesterol alone?
Answering that couldfundamentally change
preventative cardiology as weknow it.
Speaker 1 (13:45):
Thanks for tuning into the Health Pulse.
If you found this episodehelpful, don't forget to
subscribe and share it withsomeone who might benefit.
For more health insights anddiagnostics, visit us online at
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Stay informed, stay healthy andwe'll catch you in the next
episode.
Welcome to the Health Pulse, your go-to source for
quick, actionable insights onhealth, wellness and diagnostics
.
Whether you're looking tooptimize your well-being or stay
informed about the latest inmedical testing, we've got you
covered.
Join us as we break down keyhealth topics in just minutes.
Let's dive in.
Speaker 2 (00:26):
Welcome back everyone .
We are diving deep today into,well, one of the most, I'd say,
disruptive things happening inpersonalized health.
Right now we're talking aboutlow-carbohydrate eating.
Now, for many of you listening,the benefits are probably
pretty familiar Easier weightmanagement, maybe fantastic
improvements in insulinsensitivity, lower triglycerides
, higher HDL cholesterol.
You know it sounds like a totalmetabolic win, but and this is
(00:49):
the key thing there's thiscounterintuitive surprise that
pops up for a really specificgroup of people, often lean
athletic types.
For these individuals, theirLDL cholesterol, you know,
so-called bad cholesterol itjust shoots up dramatically
often into numbers that, frankly, make most doctors pretty
nervous.
So today our deep dive is allabout the lean mass
hyper-responder, or LMHR,phenotype.
(01:12):
Our mission is to reallyunderstand this group, look into
the controversy around theirsuper high LDL and figure out
what kind of monitoring youreally need.
And the big question, thereally high stakes one, is this
does having sky high LDL in thisspecific metabolic context
carry the same cardiovascularrisk as it does for well
everyone else?
Let's unpack that.
Speaker 3 (01:30):
Yeah, it's absolutely critical we figure this out
because, look, if the answer isno, then we fundamentally have
to rethink how we assess heartdisease risk.
But if the answer is yes, thenthis group, despite looking
healthy on paper otherwise,might need, you know, pretty
immediate intervention.
Speaker 2 (01:46):
OK, let's start with the basics.
Who exactly are we talkingabout here?
This term LMHR.
It was coined by researcherDave Feldman and his team right.
Speaker 3 (01:55):
That's right, and it describes people who are
typically already lean,physically active and this is
important highly insulinsensitive, before they even
start cutting carbs.
Speaker 2 (02:05):
Got it, and their response is defined by a
specific lipid pattern, a triad,you call it.
Speaker 3 (02:11):
Exactly a triad, Three specific markers that,
when you see them together, kindof fly in the face of the
traditional high risk profile.
So first they have really highLDL cholesterol LDL-C we're
talking often way past 200milligrams per deciliter,
sometimes even over 300.
Speaker 2 (02:26):
Wow Okay.
Speaker 3 (02:27):
Second, their HDL cholesterol HDL-C the good kind
is also very high, usually, youknow, above 70 milligdl,
sometimes much higher.
And third, their triglyceridesTG are super low, typically
under 70 milligdl.
Speaker 2 (02:40):
That's the paradox, right.
Normally, if someone walks inwith an LDL of, say, 250, you
expect to see high triglyceridesand low HDL, maybe issues with
blood sugar insulin resistance.
Speaker 3 (02:52):
Precisely.
The standard picture of highrisk often includes what we call
metabolic syndrome hightriglycerides, low HDL, often
central obesity, higher bloodpressure.
The LMHR is the completeopposite.
They have that sky-high LDL,yes, but everything else looks
well, pretty much perfect Normalblood pressure, great glucose
control.
They're lean, low inflammation.
Speaker 2 (03:12):
They're metabolically healthy by almost every measure
, except that LDL number.
Speaker 3 (03:15):
Exactly.
Speaker 2 (03:16):
And just to be clear, this pattern mainly shows up
when people go on really strictlow-carb diets like keto or
carnivore.
Speaker 3 (03:23):
Overwhelmingly yes, it seems to be a direct result
of that drastic carbohydraterestriction interacting with
their specific physiology.
Speaker 2 (03:30):
OK, so it's not just about eating more fat.
Something fundamental isshifting in how their body works
when carbs are taken out, Ifthey're already lean and insulin
sensitive.
What's driving this huge LDLsurge?
Where's it coming from?
Speaker 3 (03:44):
Yeah, that's the million-dollar question, isn't
it?
And the answer seems to be tiedinto how their body transports
energy when glucose isn't theprimary fuel.
There are basically three mainideas floating around.
The first is what's calledincreased fat flux, so without
much glucose, the body runs onfatty acids.
The theory goes that LMHRs arejust incredibly efficient at
(04:04):
pulling fat out of their storageeven their limited storage and
getting it into circulation.
And when you mobilize fat likethat, the liver has to package
it up into lipoproteins like LDLparticles to ship it out to
muscles and organs that needenergy.
So more fat mobilization mightmean more LDL trucks are needed.
Speaker 2 (04:23):
Wait a second.
If they're lean, wouldn't theylike run out of fat stores
pretty quick?
Shouldn't the LDL then drop?
Speaker 3 (04:29):
Ah well, that actually leads right into the
second proposed mechanism highenergy demands.
Because LMHRs often don't havemuch body fat to begin with and
they're frequently very activeRight.
Their bodies are constantlyscreaming for fuel delivery, so
their reliance on thesecirculating lipoproteins, these
LDL delivery trucks, might beamplified because their other
fuel depots are low.
(04:50):
The idea isn't necessarily thatthe LDL particles are bad or
damaged, but that they're beingactively used, maybe turned over
really quickly, to deliver hugeamounts of energy all over the
body.
Speaker 2 (05:01):
So they're basically running this super high volume,
maybe hyper efficient energyshipping operation.
Speaker 1 (05:05):
OK.
Speaker 2 (05:06):
And the third idea links this to genetics.
Speaker 3 (05:09):
Precisely.
There seems to be a strongcomponent of genetic
predisposition.
We know there are specific genevariants related to how we
handle lipid stink genes likeAPOE, ldlr, pcsk9.
It's possible that certaingenetic profiles make people
hyper-respond metabolically whenthey switch fuel sources so
drastically.
The low-carb, high-fat diet isthe trigger, but maybe your
(05:30):
genes decide if you get thisdramatic LDL surge.
Speaker 2 (05:32):
So it's not just the diet alone.
Speaker 3 (05:34):
No, the key takeaway here really seems to be a
crucial gene diet interaction.
It's the diet hitting aparticular genetic setup that
likely creates this LMHRphenotype.
Speaker 2 (05:45):
All right, Now we're getting into the really tricky
part, the gray area, thecontroversy.
Yeah, Because, look, we havemountains of evidence, decades
of it, saying high LDL is acause of atherosclerotic
cardiovascular disease, ASCVD,you know, the plaque buildup
leading to heart attacks andstrokes.
So when someone in the LMHRcommunity says, yeah, my LDL is
(06:06):
300, but hey, my triglyceridesare 50 and my HDL is 90, the
medical world gets well divided.
Speaker 3 (06:12):
It's a real clinical puzzle.
On one hand you have theconservative view.
This is often the stance ofmainstream lipid experts.
They argue, based on hugepopulation studies, that LDL is
inherently atherogenic.
The higher the number, the moreexposure your arteries have
over time period.
They see an LDL of 300, andregardless of other markers,
they think risk and usuallyrecommend getting that number
down.
(06:32):
Sometimes aggressively, theytreat the number itself.
Speaker 2 (06:35):
Okay, that's one side .
What's the counter argumentfrom the LMHR perspective?
Speaker 3 (06:39):
They argue for what you might call the metabolic
context view.
They say hold on, you have tolook at the whole picture.
They point to their lowtriglycerides, high HDL, low
insulin, often zero inflammation, their leanness and they ask
does this unique metabolicenvironment change the nature or
the function of those LDLparticles?
Is an LDL particle floatingaround in that clean environment
(07:00):
the same risk as one in someonewith metabolic syndrome, where
particles might be small, dense,maybe oxidized or glycated?
Speaker 2 (07:07):
That's the crux of it , isn't it?
Are these LDL particles, eventhough there are lots of them,
somehow less dangerous becausethe overall metabolic health is
so good, or does the sheernumber still cause plaque
buildup over time?
Speaker 3 (07:18):
And this leads us straight to the major evidence
gap Right now.
Today we just don't have thelarge-scale long-term studies
specifically following LMHRs tosee what actually happens to
their hearts and arteries overdecades.
We don't know definitively ifthey develop atherosclerosis
faster, slower or at the samerate as someone else with a
similarly high LDL but adifferent metabolic profile.
(07:40):
They really are in a kind ofcardiometabolic blind spot.
We need solid proof, not justplausible theories.
Speaker 2 (07:46):
Which means until we get that proof, we have to be
cautious.
So okay, let's talkpracticality.
Since this high LDL is almostalways tied to the very low carb
diet, what can you actually doif you identify as an LMHR and
you're concerned about thatnumber?
What levers can you pull?
Speaker 3 (08:01):
Well, if the primary goal is simply to lower the LDL
number, the most direct route isoften a dietary adjustment,
because the whole thing seemsdriven by this massive fat
mobilization for fuel.
Reintroducing even a moderateamount of carbohydrates maybe
say 50 to 100 grams per dayoften signals the body to switch
back towards using glucose.
Anecdotally, this frequentlybrings the LDL-C down
(08:24):
significantly and for manypeople they can do this while
still keeping blood sugar stableand maintaining many of the
other benefits that they gotfrom low-carb.
Speaker 2 (08:31):
So you don't necessarily have to completely
abandon the approach, maybe justtweak it.
Speaker 3 (08:36):
Exactly.
Another potential tweak is fatsource alteration.
Sometimes the LMHR responseseems more pronounced, with very
high intakes of saturated fats,things like butter, fatty red
meat cream.
Some find that shifting the fatfocus towards more unsaturated
fats like olive oil, avocados,nuts, fatty fish, can also help
(08:56):
lower the LDL-C, even whilekeeping carbs relatively low.
Speaker 2 (08:59):
Interesting.
But regardless of whethersomeone tweaks their diet or not
, monitoring seems absolutelycritical.
And you're saying a standardlipid panel isn't really enough
here.
We need more advanced tests.
Speaker 3 (09:09):
Absolutely non-negotiable.
And, yes, the standard panelcan be misleading.
It usually measures LDL-C,which is the weight or the mass
of cholesterol carried withinthe LDL particles, but what
seems to matter more foratherosclerosis risk is the
actual number of potentiallyadditives.
Atherogenic particles bumpingagainst your artery walls.
Think of it like traffic.
Speaker 2 (09:30):
Okay, traffic analogy , let's hear it.
Speaker 3 (09:31):
All right, ldlc is like measuring the total weight
of all the cargo being carriedby trucks on a highway.
But what causes traffic jamsand potential accidents isn't
the weight of the cargo, it'sthe sheer number of trucks on
the road.
Speaker 2 (09:43):
Gotcha More trucks, higher chance of collision.
Speaker 3 (09:50):
Precisely, and that's why we need tests like opal
lipoprotein B or ApoB.
Apob is a protein found onevery single one of these
potentially atherogenicparticles VLDL, idl and LDL.
One ApoB molecule per particle.
So measuring ApoB basicallytells you the total number of
these particles, the totalnumber of trucks on your highway
.
It's considered a much moreaccurate marker of particle
burden and risk than just LDL-Calone.
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 quantifyingthe number of LDL particles.
Specifically For an LMHR, it'scrucial to know is there high
LDL-C mass due to having a fewreally large fluffy LDL
(10:34):
particles packed withcholesterol, or is it due to
having a huge number of smallerparticles?
The latter is generallyconsidered higher risk.
Speaker 2 (10:41):
Right, so ApoB and LDLP give you the particle count
.
What other tests are importantfor context?
Speaker 3 (10:47):
You definitely want to check lipoprotein or LPA.
This is a completely separaterisk factor, mostly determined
by genetics, not diet.
If it's high, it significantlyadds to overall cardiovascular
risk.
No matter what your LDL isdoing, 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 theunderlying 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 arterycalcium 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 looksdirectly for hardened calcified
plaque in your coronary arteries.
It doesn't measure risk factorsin the blood.
It measures the actual presenceof 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 canbe incredibly informative.
Many are using it oftenserially over time to see if
their high particle count isactually translating into plaque
buildup.
Getting a CAC score of zero isgenerally very reassuring,
suggesting very lowshort-to-intermediate-term risk.
(11:58):
Even if the LDL is high, itprovides a piece of direct
evidence about what's happeningin the arteries themselves.
Speaker 2 (12:04):
Wow.
Okay, that seems like acritical piece of the puzzle
while we wait for more long-termdata.
Speaker 3 (12:09):
It really is, and it all underscores the need for
truly personalized nutrition andmonitoring.
We can't just use blanketguidelines here.
It has to be tailored, usingthese advanced tests.
Speaker 2 (12:18):
Okay, let's try and wrap this up.
What's the main takeaway foryou listening?
Speaker 3 (12:23):
The LMHR phenomenon.
It's really shaking things upin metabolic science.
It shows just how powerfullydiet can change our biomarkers,
sometimes in really unexpectedways, like driving LDL sky high
even while fixing almosteverything else.
Speaker 2 (12:37):
And until we have that definitive long-term
evidence about the actual riskand I should say studies using
imaging like CAC are underwayright now.
Looking specifically at thisgroup, the safest approach seems
clear.
It's careful, close monitoringwith advanced testing Get your
ApoB checked, know your LDL-P,find out your LPA, track
inflammation and seriouslyconsider a CAC score and,
(13:00):
importantly, work with a doctoror healthcare provider who
actually understands thisspecific metabolic situation.
Speaker 3 (13:05):
It's really quite something.
One set of markers looksamazing, another looks
potentially alarming, all fromthe same dietary shift?
Yeah, it is.
And maybe the final thought,the provocative question for you
to mull over, is this If wezoom out, does the very
existence of the LMHR groupsuggest that our future models
for predicting heart diseaserisk need to evolve the full
(13:26):
metabolic picture, thetriglycerides, the HDL, insulin
sensitivity, inflammation,leanness rather than focusing so
heavily, almost solelysometimes, on the quantity of
LDL cholesterol alone?
Answering that couldfundamentally change
preventative cardiology as weknow it.
Speaker 1 (13:45):
Thanks for tuning into the Health Pulse.
If you found this episodehelpful, don't forget to
subscribe and share it withsomeone who might benefit.
For more health insights anddiagnostics, visit us online at
wwwquicklabmobilecom.
Stay informed, stay healthy andwe'll catch you in the next
episode.
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