June 19, 2025 • 19 mins
In this episode of The Health Pulse Podcast, we challenge one of the most entrenched narratives in modern medicine: that LDL cholesterol is the primary cause of heart disease. Inspired by the work of Dr. Paul Mason, we explore a compelling new framework that puts the spotlight on inflammation, insulin resistance, and metabolic dysfunction as the real culprits behind cardiovascular events.
We unpack why nearly half of heart attack victims have normal LDL levels, and how focusing solely on cholesterol may overlook the deeper, root causes of arterial damage—like oxidized cholesterol, endothelial dysfunction, and systemic inflammation triggered by modern diets high in seed oils and refined carbs.
🎧 Tap play to explore why it’s time to shift from outdated cholesterol models to a more nuanced, root-cause approach to heart health—and how this could transform prevention, testing, and treatment strategies.
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Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Nicolette (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.
Mark (00:27):
Welcome to the Deep Dive.
So for decades, right when wetalk heart disease, there's been
this one main suspect everyonepoints to LDL cholesterol.
Rachelle (00:36):
The bad cholesterol.
Mark (00:40):
Exactly.
It's been painted as you knowthe primary villain and that
idea shaped everything our diets, medical treatments, huge
public health campaigns.
Rachelle (00:46):
Absolutely.
The advice was always prettystraightforward Get your LDL
down, lower your risk Simple.
Mark (00:52):
But what if it's not quite that simple?
What if that's actually wellmisleading?
What if LDL isn't the main badguy?
We're seeing this growing groupof researchers physicians too
challenging this whole idea,suggesting maybe we've been
aiming at a wrong target.
Rachelle (01:08):
It's a really fascinating challenge to the
standard thinking, and one ofthe key voices here is Dr Paul
Mason.
He's an Australian sports andexercise physician with a well,
a pretty compelling alternativeview.
Mark (01:19):
OK, so what's his core idea then?
Rachelle (01:21):
His hypothesis basically suggests the real
driver isn't just cholesterollevels.
It's more complex.
It's about inflammation,insulin resistance you know,
your overall metabolic healthand atherosclerosis, the plaque
buildup.
He sees that as a response toinjury in the blood vessels,
damage and oxidative stress, andit's the oxidized LDL, not just
(01:41):
any LDL, that plays theproblematic role there.
Mark (01:44):
Oxidized LDL.
Rachelle (01:45):
Yeah.
Mark (01:45):
Okay, that's a key distinction and that's exactly
what we're getting into today.
We'll explore the roots of thetraditional lipid hypothesis,
unpack Dr Mason's perspective,look at the science behind both
sides and really figure out whatthis means for you, for your
health, and how maybe you cantake a smarter approach to
thinking about heart risk.
Rachelle (02:03):
Yeah, get ready to maybe question some things we
thought we knew for sure.
Mark (02:06):
All right.
So to really grasp Dr Mason'schallenge, we kind of need to
set the stage first.
What's the conventional viewhe's pushing back against, the
one we all sort of grew uphearing?
Rachelle (02:17):
Well, for more than half a century, the dominant
idea has been the lipidhypothesis.
The core premise is simple HighLDL cholesterol in your blood
leads directly to fatty plaquesbuilding up in your arteries.
Mark (02:28):
And that goes way back, doesn't it?
Rachelle (02:30):
Oh yeah, it really gained steam.
Mid-20th century Ancel Keys,his seven-country study.
That was hugely influential.
It linked dietary saturated fatand cholesterol levels to heart
disease deaths.
Mark (02:42):
Right, I remember hearing about that one and that study.
It really set the direction forpublic health.
Rachelle (02:47):
Massively.
It led to widespread dietaryguidelines you know, low fat,
everything.
And then, by the 80s 90s,statins arrived.
They became the go-toprevention strategy.
All built on this assumptionlower LDL-C, lower your risk.
Tools like the Framingham RiskScore basically codified that.
Mark (03:04):
So OK, there must be some evidence supporting this
traditional view right.
What are its strong points?
Rachelle (03:14):
Oh, definitely there's epidemiological evidence.
Look at familialhypercholesterolemia.
That's a genetic thing wherepeople have incredibly high LDL
from birth and they do have amuch higher risk of early heart
disease.
That's a clear link.
Plus, you have the big statintrials like 4S, Jupiter.
They showed clear reductions inheart attacks and strokes when
LDL was lowered.
You can't ignore that.
Mark (03:29):
Okay.
So there's some solid backing,but, like we hinted at, there
are also gaps, inconsistencies.
This is where it starts gettingreally interesting, I think.
Rachelle (03:37):
Exactly.
This is where the plot thickens.
A really striking fact is thatalmost half the people who have
a heart attack actually have LDLlevels considered normal.
Mark (03:46):
Half Wow.
That alone seems like a majorproblem for the hypothesis.
Rachelle (03:51):
It is.
And then there's the nuance ofLDL itself.
We're realizing maybe it's notjust the amount of LDL, but the
particle size and density thatmatters more.
Mark (04:00):
Smaller denser particles being worse.
Rachelle (04:02):
Precisely, and often other things high triglycerides,
low HDL, signs of insulinresistance.
These turn out to be muchstronger predictors of heart
problems than LDL alone.
Mark (04:12):
And inflammation markers too, like CRP.
Rachelle (04:15):
Yes, C-reactive protein, CRP.
That might actually track theatherosclerotic process better
sometimes.
There was a review back in 2018, BMJ Evidence-Based Medicine
basically saying focusing onlyon LDL-C oversimplifies a very
complex multifactorial disease.
Mark (04:29):
So these aren't just minor quibbles.
They're pretty significantholes in the story.
We've been told If the old maphas flaws, who's drawing the new
one?
Enter Dr Paul Mason.
Rachelle (04:39):
Right and his hypothesis is a genuine paradigm
shift.
He basically takes thespotlight off LDL levels per se
and shines it onto the metabolicenvironment.
Mark (04:49):
The environment meaning.
Rachelle (04:50):
Meaning the overall state of your body's metabolism.
In his view, cholesterolbuildup isn't the starting point
.
It's a consequence of injury tothe blood vessel wall and that
injury driven by inflammation,oxidative stress and, especially
, insulin resistance.
Mark (05:05):
Okay, so step one is damaged the vessel lining the
endothelium.
How does that kick things off?
Rachelle (05:10):
Basin argues that atherosclerosis starts when that
lining gets damaged or inflamed.
That makes it leaky, basically,and then oxidized molecules,
crucially oxidized ox, ldl, canget through and start
accumulating.
Mark (05:23):
Ah, there's that oxidized LDL again.
Yes, and he has this greatquote.
Rachelle (05:26):
something like LDL is not the enemy unless it becomes
oxidized.
The real trigger is damage tothe endothelium that allows
oxidized LDL to enter itcompletely reframes LDL's role.
Mark (05:37):
It does.
It's not the villain, maybejust caught at the scene of the
crime after the real damage isdone.
Rachelle (05:43):
Kind of Maybe even a necessary part of the repair
crew.
But it gets problematic whenit's damaged, itself oxidized
and the environment is unhealthy.
Mark (05:51):
Got it.
And insulin resistance wheredoes that fit in?
You mentioned it's key.
Rachelle (05:55):
It's central to his model.
Chronically high insulin levels, the hallmark of insulin
resistance.
They wreak havoc.
They increase oxidative stress.
They make smooth muscle cellsin the artery wall grow too much
.
They mess with nitric oxideproduction.
Mark (06:10):
Nitric oxide helps blood vessels relax right.
Rachelle (06:12):
Exactly so.
Impairing.
That is bad news.
All these things damage theendothelium, creating that
initial injury that lets theprocess begin.
Mark (06:19):
It feels much more like a systems view, doesn't it?
Not just zeroing in on onenumber?
Rachelle (06:24):
It really is.
It connects chronicinflammation, oxidative damage,
even mitochondrial function, andstresses from our diet,
especially, he points out, seedoils and refined carbs.
Mark (06:36):
They all converge to harm our blood vessels.
So in this picture, high LDLmight just be a sign that the
body is responding to injury,not the root cause itself.
Rachelle (06:43):
That's the core idea.
An elevated LDL might bereflecting a deeper problem, a
response to tissue damage,rather than being the primary
driver.
Mark (06:51):
Okay.
So if this framework holdswater, what's the big
implication for how we thinkabout heart health?
Rachelle (06:58):
It means the whole lower LDL at all costs.
Mantra might be misguided.
The focus should shift, perhapsdramatically, towards fixing
the underlying metabolic health,controlling inflammation.
That might be the real path toreducing risk.
Mark (07:12):
So if cholesterol isn't the main driver, what is?
Dr Mason points to chronicinflammation and insulin
resistance as the primaryengines.
Right, Not just side issues,but the core problem.
Rachelle (07:22):
Exactly.
He argues it's the quality ofyour metabolic environment that
dictates whether atherosclerosisgets a foothold.
Mark (07:28):
Let's unpack inflammation first.
We hear that word a lot.
How does chronic inflammationspecifically damage arteries?
Rachelle (07:34):
Well, inflammation is normally a good thing, a healing
response, but when it's chronic, low-grade simmering all the
time, that's different.
It starts to degrade theintegrity of that endothelial
lining.
Mark (07:45):
The lining inside the arteries.
Rachelle (07:46):
Right.
Think of the cells lining yourarteries as being held together
by tight junctions, like seals.
Chronic inflammation loosensthose seals.
That allows things thatshouldn't be there, like
oxidized LDL, to slip throughinto the artery wall.
Then immune cells rush in, tryto clean up the mess, but it
starts this whole cycle ofplaque formation, foam cells,
fatty streaks, the beginning ofatherosclerosis.
Mark (08:09):
It's almost like the inflammation opens the door for
the cholesterol problem to evenstart.
Rachelle (08:18):
Precisely.
There was a big review inNature Review's Cardiology back
in 2017 that essentially calledatherosclerosis a chronic
inflammatory disease, not just alipid storage problem.
Mark (08:24):
Okay, that makes sense.
So if inflammation is a keyproblem, what's fueling it in
our modern world, particularlydiet-wise?
Rachelle (08:30):
This is where Dr Mason really emphasizes something
often overlooked our massiveoverconsumption of omega-6
polyunsaturated fats, pufas,specifically linoleic acid from
common seed oils.
Mark (08:43):
Soybean oil, corn oil, sunflower, safflower, the ones
in practically everythingprocessed.
Rachelle (08:48):
Those are the main pulpits.
Yeah, we need some omega-6, butour modern intake is way out of
balance with omega-3s.
And this excess, Mason argues,creates a highly
pro-inflammatory state.
It primes the body for thatendothelial damage.
Mark (09:03):
How does linoleic acid specifically cause problems?
Rachelle (09:07):
Well, linoleic acid is quite unstable.
It oxidizes very easily,especially with heat, like in
processing or cooking.
When it oxidizes, it createsthese reactive byproducts.
Mark (09:20):
These nasty little things can get incorporated into LDL
particles themselves, making theLDL itself more prone to
becoming that harmful oxidizedLDL.
Rachelle (09:25):
Exactly.
It makes the LDL particle muchmore vulnerable.
These oxidized byproducts alsodirectly damage the endothelium
and create systemic oxidativestress.
There was a review inAntioxidants in 2021 linking
these oxidized linoleic acidmetabolites OXLAMs, directly to
plaque development.
Mark (09:43):
So the type of fat you eat literally changes the nature of
your LDL, making it potentiallymore dangerous before it even
gets near an artery wall.
It's like silent oxidationsetting the stage.
Rachelle (09:52):
That's a good way to put it, and it connects back to
insulin resistance too.
Some evidence suggests excessomega-6 can worsen insulin
resistance, affecting glucoseuptake, promoting liver fat,
causing inflammation in fattissue.
It just feeds that whole cycle.
Metabolic dysfunction leads tovascular damage, leads to
oxidized LDL, causing moreproblems.
Mark (10:12):
Wow, okay.
So let's talk more aboutinsulin resistance as that
silent accelerator.
How does it drive vasculardamage?
Rachelle (10:19):
Chronically high insulin just disrupts so many
things.
It ramps up oxidative stress,damaging cells.
It activates the sympatheticnervous system which can raise
blood pressure and, crucially,it changes the type of LDL your
liver produces.
It favors those small, denseLDL particles, the SDLDL we
mentioned earlier.
Mark (10:36):
The ones that are more likely to get stuck and oxidized
.
Rachelle (10:38):
Exactly.
And high insulin also messeswith triglyceride clearance, so
fats hang around in your bloodlonger.
Mark (10:43):
And all this creates that classic metabolic picture.
You see, yeah, hightriglycerides, low HDL, the good
cholesterol, maybe high bloodsugar, high insulin, high CRP.
Rachelle (10:53):
That's the signature, yeah.
And studies like one in LancetDiabetes and Endocrinology in
2018 found that insulinresistance was actually a
stronger predictor of coronaryartery disease than LDL
cholesterol was in middle-agedfolks.
Mark (11:08):
So the bottom line for someone listening, just focusing
on your LDL number might meanyou're completely missing these
huge underlying drivers likeinflammation and insulin
sensitivity.
Rachelle (11:19):
That's the core argument.
Address the inflammation, fixthe insulin resistance and you
might lower your actual risksignificantly, even if your LDL
number doesn't plummet or evenif it stays a bit higher.
This is huge for people withnormal lipids but underlying
metabolic issues.
Mark (11:34):
Which leads us right back to LDL itself.
We've called it bad cholesterolfor so long, but maybe we need
to reconsider its role entirely.
Rachelle (11:41):
Absolutely.
First off, ldl isn't inherentlybad, it's essential.
It's like a delivery truck ittransports cholesterol, yes, but
also fat-soluble vitamins,antioxidants.
It's vital for cell membranes,hormone production, even immune
function.
Mark (11:53):
So calling it bad is an oversimplification.
Rachelle (11:55):
A massive one.
Dr Mason puts it nicely LDLcholesterol is essential to life
.
We don't just make it, wedepend on it.
So just blindly trying to crushLDL levels without
understanding why they might beelevated could be
counterproductive.
Mark (12:09):
And this is where that idea of particle size comes back
in Small dense versus largefluffy.
Rachelle (12:14):
Yes, exactly.
The research Dr Mason points toshows those small, dense LDL
particles, SDLDL, are the realtroublemakers.
They slip into the artery wallmore easily, they oxidize faster
, they stick around longer.
Mark (12:27):
And that shift towards smaller particles often happens
when someone is insulinresistant.
Rachelle (12:32):
Very commonly yes, Even if their total LDL number
looks okay on a standard test.
A study in Circulation way backin 2002 flagged SDLDL as a
better predictor of heartdisease than just total LDL-C.
Mark (12:44):
So what about this idea that high LDL might not be risky
if inflammation is low?
Yeah, that seemscounterintuitive to everything
we've heard.
Rachelle (12:51):
It does, but there's growing evidence.
We see this sometimes in peopleon well-formulated low-carb or
ketogenic diets.
Their LDL might go up,sometimes quite a bit, but often
their inflammation markers likeCRP stay low.
Their HDL goes up,triglycerides plummet, their
overall metabolic health looksgreat and, importantly, measures
of actual plaque like coronaryartery calcium scores SRE scores
(13:13):
often remain stable or evenimprove.
Mark (13:16):
So the context matters immensely.
High LDL in a sea ofinflammation and insulin
resistance is bad news.
Very likely yes, but high LDLin a metabolically healthy, low
inflammation environment mightbe benign or at least much less.
Rachelle (13:29):
Concerning that's what the emerging data suggests.
The Framingham Offspring studyeven showed that high LDL wasn't
linked to more heart eventswhen triglycerides were low and
HDL was high signs of goodmetabolic health.
Mark (13:42):
This completely changes how we should think about risk
assessment then Just looking atLDL-C seems way too simplistic.
Rachelle (13:48):
It potentially is.
Dr Mason and others argue for amuch more nuanced approach.
Look at fasting insulin orcalculate home AR for insulin
sensitivity.
Look at the triglyceride to HDLratio.
That's a powerful, simplemarker.
Check HSCRP for inflammation,Maybe even measure oxidized LDL
directly.
And then there are advancedtests like APOB, which counts
(14:10):
LDL particles, lipoprote proteinA and definitely CAC scoring to
see actual plaque burden.
Mark (14:15):
It pins a much fuller picture of what's actually going
on.
Rachelle (14:18):
Exactly.
To wrap up Mason's view on LDL,it's not the particle itself
that's inherently bad.
It's what happens to theparticle in a damaged, inflamed,
metabolically unhealthyenvironment that makes it a
threat.
Mark (14:30):
Okay, so let's talk practicalities, clinical
implications.
If this hypothesis Mason'shypothesis is closer to the
truth, it means a pretty radicalshift from lower LDL at all
costs, right.
Rachelle (14:40):
A huge shift.
The focus moves away from justmanaging a number LDL and
towards identifying andcorrecting the root causes, the
metabolic issues that damage theblood vessels in the first
place.
Mark (14:50):
So how does that change dietary advice?
The old low-fat watch yourcholesterol advice seems
completely off, if this model isright.
Rachelle (14:58):
It really does.
Mason argues that low-fatadvice is outdated, maybe even
harmful, especially for peoplewho are insulin resistant.
His approach is quite different.
Mark (15:07):
More like low-carb, ketogenic, nutrient-dense foods.
Rachelle (15:10):
Precisely Low-carbohydrate, focusing on
whole nutrient-dense foods.
Precisely Low carbohydrate,focusing on whole nutrient-dense
foods, and criticallyeliminating those industrial
seed oils packed with omega-6linoleic acid.
So getting rid of the soybean,corn, sunflower oils.
Mark (15:23):
That's a big change for most people's kitchens.
Rachelle (15:25):
It is.
The emphasis shifts to wholefoods, ditching refined carbs
and sugars, and maybe usingthings like intermittent fasting
to boost metabolic flexibility.
It's about fixing themetabolism first.
Mark (15:37):
And there's evidence supporting this.
Rachelle (15:38):
Yeah, studies like the Virta Health trial showed
impressive results withcarbohydrate restriction,
improving insulin resistance,lowering inflammation markers
like CRP, even reversing type 2diabetes, often while reducing
or eliminating medications.
Mark (15:52):
Okay, so diet changes.
What about testing?
How should doctors monitorpatients differently?
Rachelle (15:56):
Well, instead of just the standard lipid panel, you'd
prioritize tests that reflectmetabolic health and
inflammation.
Fasting insulin, heir thetri-HDL ratio definitely HSCRP.
Mark (16:07):
Maybe oxidized LDL or APOB .
Rachelle (16:09):
Yes, those add valuable detail, and coronary
artery calcium scoring gives youa direct look at existing
plaque.
It moves beyond just predictingrisk based on cholesterol to
actually measuring underlyingphysiology and disease burden.
It allows for much morepersonalized care.
Mark (16:26):
What about statins, then?
Where do they fit in this newpicture?
Their benefit might be moreabout inflammation than
cholesterol.
Rachelle (16:32):
That's a key point.
Statins do haveanti-inflammatory effects
independent of lowering LDL, andthat might explain a
significant part of theirbenefit.
So the thinking isn'tnecessarily never use statins
but rather be more selective.
Right For someone who ismetabolically healthy low
inflammation, good insulinsensitivity, high HDL, low
triglycerides even if their LDLis high.
(16:53):
Dr Mason might question thenecessity or the degree of
benefit from a statin,especially compared to
addressing lifestyle first.
The absolute risk reductionmight be small.
Mark (17:02):
So the big takeaway from Mason's model is almost
paradoxical A normal LDL insomeone who's metabolically
unhealthy could actually be moredangerous than a high LDL in
someone who's metabolically fitand has low inflammation.
Rachelle (17:14):
That captures it perfectly.
It flips the script.
The context is everything.
Mark (17:19):
So optimal prevention isn't just about lowering a
number.
It's about improving insulinsensitivity, cutting out
processed foods and seed oils,monitoring inflammation,
managing stress, sleep the wholepackage.
Rachelle (17:32):
Exactly.
It's about treating the terrain, the whole metabolic
environment, not just chasingone specific marker like LDL.
It's a comprehensive strategyfor metabolic health which
ultimately protects thecardiovascular system.
Mark (17:44):
Wow, okay.
So, as we wrap this up, we'vereally looked at two very
different ways of seeing heartdisease.
There's the traditional lipidhypothesis.
Ldl is the main villain.
Rachelle (17:53):
The standard story.
Mark (17:54):
And then Dr Paul Mason's alternative view, focusing much
more on inflammation, insulinresistance, the quality of the
metabolic environment and therole of oxidized LDL.
It definitely seems the oldmodel is well incomplete at best
.
Rachelle (18:07):
Yeah, the evidence challenging the simple
LDL-centric view is becomingharder to ignore.
The real takeaway seems to bethat the future of heart care
might not just be about chasinglower and lower cholesterol
numbers.
It might be more about diggingdeeper, identifying the root
metabolic problems that actuallymake cholesterol dangerous, and
focusing on restoring overallhealth vascular, mitochondrial,
(18:28):
metabolic health through smarterlifestyle choices.
Mark (18:32):
It's a profound shift.
So the final thought for you,the listener, to chew on, is
this how might rethinking badcholesterol change the way you
look at your own diet, yourdoctor's visits, your health
priorities?
Rachelle (18:45):
Are you focusing on the LDL number or are you
addressing the potential rootcauses like inflammation and
metabolic dysfunction?
Mark (18:52):
Something definitely worth considering.
We hope this deep dive gave yousome food for thought.
Keep exploring these ideas anddefinitely talk with your own
healthcare provider to figureout the best approach for you.
Nicolette (19:07):
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.
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.
Mark (00:27):
Welcome to the Deep Dive.
So for decades, right when wetalk heart disease, there's been
this one main suspect everyonepoints to LDL cholesterol.
Rachelle (00:36):
The bad cholesterol.
Mark (00:40):
Exactly.
It's been painted as you knowthe primary villain and that
idea shaped everything our diets, medical treatments, huge
public health campaigns.
Rachelle (00:46):
Absolutely.
The advice was always prettystraightforward Get your LDL
down, lower your risk Simple.
Mark (00:52):
But what if it's not quite that simple?
What if that's actually wellmisleading?
What if LDL isn't the main badguy?
We're seeing this growing groupof researchers physicians too
challenging this whole idea,suggesting maybe we've been
aiming at a wrong target.
Rachelle (01:08):
It's a really fascinating challenge to the
standard thinking, and one ofthe key voices here is Dr Paul
Mason.
He's an Australian sports andexercise physician with a well,
a pretty compelling alternativeview.
Mark (01:19):
OK, so what's his core idea then?
Rachelle (01:21):
His hypothesis basically suggests the real
driver isn't just cholesterollevels.
It's more complex.
It's about inflammation,insulin resistance you know,
your overall metabolic healthand atherosclerosis, the plaque
buildup.
He sees that as a response toinjury in the blood vessels,
damage and oxidative stress, andit's the oxidized LDL, not just
(01:41):
any LDL, that plays theproblematic role there.
Mark (01:44):
Oxidized LDL.
Rachelle (01:45):
Yeah.
Mark (01:45):
Okay, that's a key distinction and that's exactly
what we're getting into today.
We'll explore the roots of thetraditional lipid hypothesis,
unpack Dr Mason's perspective,look at the science behind both
sides and really figure out whatthis means for you, for your
health, and how maybe you cantake a smarter approach to
thinking about heart risk.
Rachelle (02:03):
Yeah, get ready to maybe question some things we
thought we knew for sure.
Mark (02:06):
All right.
So to really grasp Dr Mason'schallenge, we kind of need to
set the stage first.
What's the conventional viewhe's pushing back against, the
one we all sort of grew uphearing?
Rachelle (02:17):
Well, for more than half a century, the dominant
idea has been the lipidhypothesis.
The core premise is simple HighLDL cholesterol in your blood
leads directly to fatty plaquesbuilding up in your arteries.
Mark (02:28):
And that goes way back, doesn't it?
Rachelle (02:30):
Oh yeah, it really gained steam.
Mid-20th century Ancel Keys,his seven-country study.
That was hugely influential.
It linked dietary saturated fatand cholesterol levels to heart
disease deaths.
Mark (02:42):
Right, I remember hearing about that one and that study.
It really set the direction forpublic health.
Rachelle (02:47):
Massively.
It led to widespread dietaryguidelines you know, low fat,
everything.
And then, by the 80s 90s,statins arrived.
They became the go-toprevention strategy.
All built on this assumptionlower LDL-C, lower your risk.
Tools like the Framingham RiskScore basically codified that.
Mark (03:04):
So OK, there must be some evidence supporting this
traditional view right.
What are its strong points?
Rachelle (03:14):
Oh, definitely there's epidemiological evidence.
Look at familialhypercholesterolemia.
That's a genetic thing wherepeople have incredibly high LDL
from birth and they do have amuch higher risk of early heart
disease.
That's a clear link.
Plus, you have the big statintrials like 4S, Jupiter.
They showed clear reductions inheart attacks and strokes when
LDL was lowered.
You can't ignore that.
Mark (03:29):
Okay.
So there's some solid backing,but, like we hinted at, there
are also gaps, inconsistencies.
This is where it starts gettingreally interesting, I think.
Rachelle (03:37):
Exactly.
This is where the plot thickens.
A really striking fact is thatalmost half the people who have
a heart attack actually have LDLlevels considered normal.
Mark (03:46):
Half Wow.
That alone seems like a majorproblem for the hypothesis.
Rachelle (03:51):
It is.
And then there's the nuance ofLDL itself.
We're realizing maybe it's notjust the amount of LDL, but the
particle size and density thatmatters more.
Mark (04:00):
Smaller denser particles being worse.
Rachelle (04:02):
Precisely, and often other things high triglycerides,
low HDL, signs of insulinresistance.
These turn out to be muchstronger predictors of heart
problems than LDL alone.
Mark (04:12):
And inflammation markers too, like CRP.
Rachelle (04:15):
Yes, C-reactive protein, CRP.
That might actually track theatherosclerotic process better
sometimes.
There was a review back in 2018, BMJ Evidence-Based Medicine
basically saying focusing onlyon LDL-C oversimplifies a very
complex multifactorial disease.
Mark (04:29):
So these aren't just minor quibbles.
They're pretty significantholes in the story.
We've been told If the old maphas flaws, who's drawing the new
one?
Enter Dr Paul Mason.
Rachelle (04:39):
Right and his hypothesis is a genuine paradigm
shift.
He basically takes thespotlight off LDL levels per se
and shines it onto the metabolicenvironment.
Mark (04:49):
The environment meaning.
Rachelle (04:50):
Meaning the overall state of your body's metabolism.
In his view, cholesterolbuildup isn't the starting point
.
It's a consequence of injury tothe blood vessel wall and that
injury driven by inflammation,oxidative stress and, especially
, insulin resistance.
Mark (05:05):
Okay, so step one is damaged the vessel lining the
endothelium.
How does that kick things off?
Rachelle (05:10):
Basin argues that atherosclerosis starts when that
lining gets damaged or inflamed.
That makes it leaky, basically,and then oxidized molecules,
crucially oxidized ox, ldl, canget through and start
accumulating.
Mark (05:23):
Ah, there's that oxidized LDL again.
Yes, and he has this greatquote.
Rachelle (05:26):
something like LDL is not the enemy unless it becomes
oxidized.
The real trigger is damage tothe endothelium that allows
oxidized LDL to enter itcompletely reframes LDL's role.
Mark (05:37):
It does.
It's not the villain, maybejust caught at the scene of the
crime after the real damage isdone.
Rachelle (05:43):
Kind of Maybe even a necessary part of the repair
crew.
But it gets problematic whenit's damaged, itself oxidized
and the environment is unhealthy.
Mark (05:51):
Got it.
And insulin resistance wheredoes that fit in?
You mentioned it's key.
Rachelle (05:55):
It's central to his model.
Chronically high insulin levels, the hallmark of insulin
resistance.
They wreak havoc.
They increase oxidative stress.
They make smooth muscle cellsin the artery wall grow too much
.
They mess with nitric oxideproduction.
Mark (06:10):
Nitric oxide helps blood vessels relax right.
Rachelle (06:12):
Exactly so.
Impairing.
That is bad news.
All these things damage theendothelium, creating that
initial injury that lets theprocess begin.
Mark (06:19):
It feels much more like a systems view, doesn't it?
Not just zeroing in on onenumber?
Rachelle (06:24):
It really is.
It connects chronicinflammation, oxidative damage,
even mitochondrial function, andstresses from our diet,
especially, he points out, seedoils and refined carbs.
Mark (06:36):
They all converge to harm our blood vessels.
So in this picture, high LDLmight just be a sign that the
body is responding to injury,not the root cause itself.
Rachelle (06:43):
That's the core idea.
An elevated LDL might bereflecting a deeper problem, a
response to tissue damage,rather than being the primary
driver.
Mark (06:51):
Okay.
So if this framework holdswater, what's the big
implication for how we thinkabout heart health?
Rachelle (06:58):
It means the whole lower LDL at all costs.
Mantra might be misguided.
The focus should shift, perhapsdramatically, towards fixing
the underlying metabolic health,controlling inflammation.
That might be the real path toreducing risk.
Mark (07:12):
So if cholesterol isn't the main driver, what is?
Dr Mason points to chronicinflammation and insulin
resistance as the primaryengines.
Right, Not just side issues,but the core problem.
Rachelle (07:22):
Exactly.
He argues it's the quality ofyour metabolic environment that
dictates whether atherosclerosisgets a foothold.
Mark (07:28):
Let's unpack inflammation first.
We hear that word a lot.
How does chronic inflammationspecifically damage arteries?
Rachelle (07:34):
Well, inflammation is normally a good thing, a healing
response, but when it's chronic, low-grade simmering all the
time, that's different.
It starts to degrade theintegrity of that endothelial
lining.
Mark (07:45):
The lining inside the arteries.
Rachelle (07:46):
Right.
Think of the cells lining yourarteries as being held together
by tight junctions, like seals.
Chronic inflammation loosensthose seals.
That allows things thatshouldn't be there, like
oxidized LDL, to slip throughinto the artery wall.
Then immune cells rush in, tryto clean up the mess, but it
starts this whole cycle ofplaque formation, foam cells,
fatty streaks, the beginning ofatherosclerosis.
Mark (08:09):
It's almost like the inflammation opens the door for
the cholesterol problem to evenstart.
Rachelle (08:18):
Precisely.
There was a big review inNature Review's Cardiology back
in 2017 that essentially calledatherosclerosis a chronic
inflammatory disease, not just alipid storage problem.
Mark (08:24):
Okay, that makes sense.
So if inflammation is a keyproblem, what's fueling it in
our modern world, particularlydiet-wise?
Rachelle (08:30):
This is where Dr Mason really emphasizes something
often overlooked our massiveoverconsumption of omega-6
polyunsaturated fats, pufas,specifically linoleic acid from
common seed oils.
Mark (08:43):
Soybean oil, corn oil, sunflower, safflower, the ones
in practically everythingprocessed.
Rachelle (08:48):
Those are the main pulpits.
Yeah, we need some omega-6, butour modern intake is way out of
balance with omega-3s.
And this excess, Mason argues,creates a highly
pro-inflammatory state.
It primes the body for thatendothelial damage.
Mark (09:03):
How does linoleic acid specifically cause problems?
Rachelle (09:07):
Well, linoleic acid is quite unstable.
It oxidizes very easily,especially with heat, like in
processing or cooking.
When it oxidizes, it createsthese reactive byproducts.
Mark (09:20):
These nasty little things can get incorporated into LDL
particles themselves, making theLDL itself more prone to
becoming that harmful oxidizedLDL.
Rachelle (09:25):
Exactly.
It makes the LDL particle muchmore vulnerable.
These oxidized byproducts alsodirectly damage the endothelium
and create systemic oxidativestress.
There was a review inAntioxidants in 2021 linking
these oxidized linoleic acidmetabolites OXLAMs, directly to
plaque development.
Mark (09:43):
So the type of fat you eat literally changes the nature of
your LDL, making it potentiallymore dangerous before it even
gets near an artery wall.
It's like silent oxidationsetting the stage.
Rachelle (09:52):
That's a good way to put it, and it connects back to
insulin resistance too.
Some evidence suggests excessomega-6 can worsen insulin
resistance, affecting glucoseuptake, promoting liver fat,
causing inflammation in fattissue.
It just feeds that whole cycle.
Metabolic dysfunction leads tovascular damage, leads to
oxidized LDL, causing moreproblems.
Mark (10:12):
Wow, okay.
So let's talk more aboutinsulin resistance as that
silent accelerator.
How does it drive vasculardamage?
Rachelle (10:19):
Chronically high insulin just disrupts so many
things.
It ramps up oxidative stress,damaging cells.
It activates the sympatheticnervous system which can raise
blood pressure and, crucially,it changes the type of LDL your
liver produces.
It favors those small, denseLDL particles, the SDLDL we
mentioned earlier.
Mark (10:36):
The ones that are more likely to get stuck and oxidized
.
Rachelle (10:38):
Exactly.
And high insulin also messeswith triglyceride clearance, so
fats hang around in your bloodlonger.
Mark (10:43):
And all this creates that classic metabolic picture.
You see, yeah, hightriglycerides, low HDL, the good
cholesterol, maybe high bloodsugar, high insulin, high CRP.
Rachelle (10:53):
That's the signature, yeah.
And studies like one in LancetDiabetes and Endocrinology in
2018 found that insulinresistance was actually a
stronger predictor of coronaryartery disease than LDL
cholesterol was in middle-agedfolks.
Mark (11:08):
So the bottom line for someone listening, just focusing
on your LDL number might meanyou're completely missing these
huge underlying drivers likeinflammation and insulin
sensitivity.
Rachelle (11:19):
That's the core argument.
Address the inflammation, fixthe insulin resistance and you
might lower your actual risksignificantly, even if your LDL
number doesn't plummet or evenif it stays a bit higher.
This is huge for people withnormal lipids but underlying
metabolic issues.
Mark (11:34):
Which leads us right back to LDL itself.
We've called it bad cholesterolfor so long, but maybe we need
to reconsider its role entirely.
Rachelle (11:41):
Absolutely.
First off, ldl isn't inherentlybad, it's essential.
It's like a delivery truck ittransports cholesterol, yes, but
also fat-soluble vitamins,antioxidants.
It's vital for cell membranes,hormone production, even immune
function.
Mark (11:53):
So calling it bad is an oversimplification.
Rachelle (11:55):
A massive one.
Dr Mason puts it nicely LDLcholesterol is essential to life
.
We don't just make it, wedepend on it.
So just blindly trying to crushLDL levels without
understanding why they might beelevated could be
counterproductive.
Mark (12:09):
And this is where that idea of particle size comes back
in Small dense versus largefluffy.
Rachelle (12:14):
Yes, exactly.
The research Dr Mason points toshows those small, dense LDL
particles, SDLDL, are the realtroublemakers.
They slip into the artery wallmore easily, they oxidize faster
, they stick around longer.
Mark (12:27):
And that shift towards smaller particles often happens
when someone is insulinresistant.
Rachelle (12:32):
Very commonly yes, Even if their total LDL number
looks okay on a standard test.
A study in Circulation way backin 2002 flagged SDLDL as a
better predictor of heartdisease than just total LDL-C.
Mark (12:44):
So what about this idea that high LDL might not be risky
if inflammation is low?
Yeah, that seemscounterintuitive to everything
we've heard.
Rachelle (12:51):
It does, but there's growing evidence.
We see this sometimes in peopleon well-formulated low-carb or
ketogenic diets.
Their LDL might go up,sometimes quite a bit, but often
their inflammation markers likeCRP stay low.
Their HDL goes up,triglycerides plummet, their
overall metabolic health looksgreat and, importantly, measures
of actual plaque like coronaryartery calcium scores SRE scores
(13:13):
often remain stable or evenimprove.
Mark (13:16):
So the context matters immensely.
High LDL in a sea ofinflammation and insulin
resistance is bad news.
Very likely yes, but high LDLin a metabolically healthy, low
inflammation environment mightbe benign or at least much less.
Rachelle (13:29):
Concerning that's what the emerging data suggests.
The Framingham Offspring studyeven showed that high LDL wasn't
linked to more heart eventswhen triglycerides were low and
HDL was high signs of goodmetabolic health.
Mark (13:42):
This completely changes how we should think about risk
assessment then Just looking atLDL-C seems way too simplistic.
Rachelle (13:48):
It potentially is.
Dr Mason and others argue for amuch more nuanced approach.
Look at fasting insulin orcalculate home AR for insulin
sensitivity.
Look at the triglyceride to HDLratio.
That's a powerful, simplemarker.
Check HSCRP for inflammation,Maybe even measure oxidized LDL
directly.
And then there are advancedtests like APOB, which counts
(14:10):
LDL particles, lipoprote proteinA and definitely CAC scoring to
see actual plaque burden.
Mark (14:15):
It pins a much fuller picture of what's actually going
on.
Rachelle (14:18):
Exactly.
To wrap up Mason's view on LDL,it's not the particle itself
that's inherently bad.
It's what happens to theparticle in a damaged, inflamed,
metabolically unhealthyenvironment that makes it a
threat.
Mark (14:30):
Okay, so let's talk practicalities, clinical
implications.
If this hypothesis Mason'shypothesis is closer to the
truth, it means a pretty radicalshift from lower LDL at all
costs, right.
Rachelle (14:40):
A huge shift.
The focus moves away from justmanaging a number LDL and
towards identifying andcorrecting the root causes, the
metabolic issues that damage theblood vessels in the first
place.
Mark (14:50):
So how does that change dietary advice?
The old low-fat watch yourcholesterol advice seems
completely off, if this model isright.
Rachelle (14:58):
It really does.
Mason argues that low-fatadvice is outdated, maybe even
harmful, especially for peoplewho are insulin resistant.
His approach is quite different.
Mark (15:07):
More like low-carb, ketogenic, nutrient-dense foods.
Rachelle (15:10):
Precisely Low-carbohydrate, focusing on
whole nutrient-dense foods.
Precisely Low carbohydrate,focusing on whole nutrient-dense
foods, and criticallyeliminating those industrial
seed oils packed with omega-6linoleic acid.
So getting rid of the soybean,corn, sunflower oils.
Mark (15:23):
That's a big change for most people's kitchens.
Rachelle (15:25):
It is.
The emphasis shifts to wholefoods, ditching refined carbs
and sugars, and maybe usingthings like intermittent fasting
to boost metabolic flexibility.
It's about fixing themetabolism first.
Mark (15:37):
And there's evidence supporting this.
Rachelle (15:38):
Yeah, studies like the Virta Health trial showed
impressive results withcarbohydrate restriction,
improving insulin resistance,lowering inflammation markers
like CRP, even reversing type 2diabetes, often while reducing
or eliminating medications.
Mark (15:52):
Okay, so diet changes.
What about testing?
How should doctors monitorpatients differently?
Rachelle (15:56):
Well, instead of just the standard lipid panel, you'd
prioritize tests that reflectmetabolic health and
inflammation.
Fasting insulin, heir thetri-HDL ratio definitely HSCRP.
Mark (16:07):
Maybe oxidized LDL or APOB .
Rachelle (16:09):
Yes, those add valuable detail, and coronary
artery calcium scoring gives youa direct look at existing
plaque.
It moves beyond just predictingrisk based on cholesterol to
actually measuring underlyingphysiology and disease burden.
It allows for much morepersonalized care.
Mark (16:26):
What about statins, then?
Where do they fit in this newpicture?
Their benefit might be moreabout inflammation than
cholesterol.
Rachelle (16:32):
That's a key point.
Statins do haveanti-inflammatory effects
independent of lowering LDL, andthat might explain a
significant part of theirbenefit.
So the thinking isn'tnecessarily never use statins
but rather be more selective.
Right For someone who ismetabolically healthy low
inflammation, good insulinsensitivity, high HDL, low
triglycerides even if their LDLis high.
(16:53):
Dr Mason might question thenecessity or the degree of
benefit from a statin,especially compared to
addressing lifestyle first.
The absolute risk reductionmight be small.
Mark (17:02):
So the big takeaway from Mason's model is almost
paradoxical A normal LDL insomeone who's metabolically
unhealthy could actually be moredangerous than a high LDL in
someone who's metabolically fitand has low inflammation.
Rachelle (17:14):
That captures it perfectly.
It flips the script.
The context is everything.
Mark (17:19):
So optimal prevention isn't just about lowering a
number.
It's about improving insulinsensitivity, cutting out
processed foods and seed oils,monitoring inflammation,
managing stress, sleep the wholepackage.
Rachelle (17:32):
Exactly.
It's about treating the terrain, the whole metabolic
environment, not just chasingone specific marker like LDL.
It's a comprehensive strategyfor metabolic health which
ultimately protects thecardiovascular system.
Mark (17:44):
Wow, okay.
So, as we wrap this up, we'vereally looked at two very
different ways of seeing heartdisease.
There's the traditional lipidhypothesis.
Ldl is the main villain.
Rachelle (17:53):
The standard story.
Mark (17:54):
And then Dr Paul Mason's alternative view, focusing much
more on inflammation, insulinresistance, the quality of the
metabolic environment and therole of oxidized LDL.
It definitely seems the oldmodel is well incomplete at best
.
Rachelle (18:07):
Yeah, the evidence challenging the simple
LDL-centric view is becomingharder to ignore.
The real takeaway seems to bethat the future of heart care
might not just be about chasinglower and lower cholesterol
numbers.
It might be more about diggingdeeper, identifying the root
metabolic problems that actuallymake cholesterol dangerous, and
focusing on restoring overallhealth vascular, mitochondrial,
(18:28):
metabolic health through smarterlifestyle choices.
Mark (18:32):
It's a profound shift.
So the final thought for you,the listener, to chew on, is
this how might rethinking badcholesterol change the way you
look at your own diet, yourdoctor's visits, your health
priorities?
Rachelle (18:45):
Are you focusing on the LDL number or are you
addressing the potential rootcauses like inflammation and
metabolic dysfunction?
Mark (18:52):
Something definitely worth considering.
We hope this deep dive gave yousome food for thought.
Keep exploring these ideas anddefinitely talk with your own
healthcare provider to figureout the best approach for you.
Nicolette (19:07):
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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