August 8, 2025 • 18 mins
Half of all heart attack victims have normal cholesterol levels—a fact that’s reshaping everything we thought we knew about cardiovascular disease. In this episode of The Health Pulse, we explore the science pointing to inflammation—not just cholesterol—as the true trigger of atherosclerosis.
We break down how inflammatory damage to arterial walls transforms cholesterol into a threat, and why standard lipid panels fall short in identifying those at risk. You’ll learn about the advanced lab markers that offer a clearer picture: hs-CRP, oxidized LDL, lipoprotein(a), and others that reveal your real cardiovascular risk—even if your total cholesterol is "normal."
We also examine the powerful role of diet, insulin resistance, gut health, and lifestyle in driving or reducing arterial inflammation. Most importantly, we offer actionable strategies to lower inflammation, reverse damage, and restore vascular health—with guidance rooted in the latest science and supported by advanced lab testing from services like QuickLab Mobile.
If you’ve ever been told your cholesterol is fine but still wonder about your heart health, this episode is essential listening.
📞 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:
👉 Quick Lab Mobile
📧 Contact us: info@quicklabmobile.com
💬 Enjoyed the episode? Leave us a review and let us know what topics you'd like us to cover next! Your feedback helps us bring you the content that matters most.
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 to the Deep Dive.
We're your shortcut to beingtruly well-informed.
Today we're diving intosomething pretty fundamental
about heart health, Somethingthat might just change how you
think about it.
Get this stat from the AmericanHeart Association Nearly half
the people who have a heartattack they actually have
cholesterol levels considerednormal.
Speaker 3 (00:47):
Yeah, it's a statistic that really stops you
in your tracks, doesn't it?
It challenges well decades ofthinking.
For so long, the story was allabout cholesterol, specifically
LDL, you know the bad one.
But the science, the newerresearch, it's giving us a much
more complete picture and,honestly, a more hopeful one too
.
It's giving us a much morecomplete picture and, honestly,
a more hopeful one too.
It's really pointing towardsinflammation as the actual
underlying driver behindatherosclerosis.
Speaker 2 (01:09):
Atherosclerosis.
Ok, that's the plaque buildupinside your arteries.
Speaker 3 (01:12):
Exactly that slow, progressive buildup and
inflammation seems to be thereal spark.
Speaker 2 (01:17):
So if it's not just about cholesterol, what's
actually happening?
This is already making merethink things.
Speaker 3 (01:23):
Right, it's not simply about high LDL numbers
floating around causing troubleon their own.
Atherosclerosis really seems tostart when inflammation damages
that delicate inner lining ofyour blood vessels.
It's called the endothelium,and that damage it sort of
creates the sticky surface,almost like Velcro.
It lets cholesterol particles,yeah, but also immune cells and
(01:44):
other debris latch on, and thatkicks off a whole cascade of
immune reactions.
It lets cholesterol particles,yeah, but also immune cells and
other debris latch on, and thatkicks off a whole cascade of
immune reactions.
It's like starting a fireinside your arteries.
The result is those hardened,narrowed vessels, and that
explains why someone can havesignificant heart risk, even
with normal cholesterol.
Speaker 2 (01:58):
Okay, right, let's really dig into this then.
This deep dive is all aboutgiving you the insights to
understand what really drivesheart disease.
So we're going to explore whatatherosclerosis truly is, how
inflammation sparks it and whatmakes it worse, which lab
markers you might need to gobeyond just the standard
cholesterol test and, maybe mostimportantly, how you can start
(02:20):
addressing the root cause, notjust chasing a symptom like high
cholesterol, because if you'veonly been focusing on
cholesterol numbers, you'reprobably missing a huge part of
the picture.
We want to help you see itclearly.
Speaker 3 (02:30):
Absolutely.
Let's start with that basicidea.
Atherosclerosis it's just themedical term for that plaque
buildup inside arteries.
Think of your arteries like Idon't know clean, flexible pipes
that carry oxygen-rich bloodeverywhere in your body.
But over time this plaquebuilds up, it narrows those
pipes, restricts the blood flowand that dramatically increases
(02:50):
the risk for things like a heartattack or a stroke.
And it's not just a simple blobof fat either.
It's this complex sticky mixcholesterol, sure, but also
calcium, dead immune cells, fats, other cellular junk, all sort
of sticking together.
And you know this doesn'thappen overnight.
It's a slow burn.
It can start silently, maybeyears, even decades, before you
(03:11):
feel anything.
Speaker 2 (03:12):
And for so long the old view was pretty
straightforward LDL cholesterolthe bad stuff was the enemy.
Just lower it, maybe withmedication, and you reduce your
risk.
Simple Seems simple, but here'swhere it gets tricky and, like
you said, maybe more interesting.
Up to half of people havingheart attacks have LDL levels
that are technically normal oreven optimal.
Clearly, that old view justdoesn't capture everything.
Speaker 3 (03:33):
Exactly, and what's really fascinating is how the
modern view has shifted.
It's quite different Now.
Atherosclerosis isn't reallyseen as starting with
cholesterol.
It starts with damage to thatinner lining, the endothelium,
and that damage it's oftencaused by things like chronic
inflammation, yeah, but alsohigh blood pressure, toxins from
the environment, even justfrequent blood sugar spikes.
Speaker 2 (03:56):
Ah, okay, so the lining gets damaged first.
Speaker 3 (03:59):
Right.
And once that barrier iscompromised, then LDL particles
can slip into the artery wall,but it's in the wall that they
become oxidized.
Think of it like they rust.
They rust.
Yeah, essentially.
And that oxidation that's whattriggers the big alarm for your
immune system.
It calls in immune cells.
Think of them like tiny cleanupcrews, macrophages mainly.
(04:19):
These cells then gorgethemselves on this damaged,
oxidized LDL and they becomethese bloated things called foam
cells.
Speaker 2 (04:26):
Foam cells I've heard that term.
Speaker 3 (04:28):
And those foam cells.
They're basically the firstbuilding blocks of plaque.
That's why atherosclerosis isreally being recognized more and
more as an inflammatory diseaseat its very core, not just a
simple cholesterol storageproblem.
Speaker 2 (04:41):
So, wow, it's less about just having cholesterol
around and way more about how itgets changed or transformed by
inflammation.
That feels like a criticalturning point.
It's like, ah, cholesterol ismaybe the bricks, but
inflammation is the architect,the construction crew and maybe
even the fire that hardens thestructure.
(05:01):
Is that a fair way to thinkabout it?
Speaker 3 (05:03):
That's actually a great analogy, a really powerful
one.
Modern cardiology, you know thethinking now widely accepts
atherosclerosis as thisimmune-driven inflammatory
process.
Every time that endothelium,that lining, gets hit with high
blood sugar, oxidative stress,toxins, high pressure, it gets
injured, it gets inflamed.
Speaker 4 (05:40):
And this triggers the release of inflammatory signals
.
Things we can actually measurelike high sensitivity C-reactive
protein or HSCRP.
Speaker 3 (05:46):
Also specific cytotimes like IL-6 and and over
time the whole process leads tothicker artery walls, less
blood flow, higher risk of clotsforming and eventually a higher
chance of that plaque rupturingand causing a heart attack.
So it sounds like we reallyneed.
That is a crucial distinction.
(06:07):
Yes, not all LDL is inherentlybad or created equal.
The real troublemaker isn'tjust the LDL molecule itself.
It's what happens when it getsoxidized and that oxidation
process.
It's heavily fueled byinflammation, often from a poor
diet and general oxidativestress in the body.
This oxidized LDL is highlyatherogenic, meaning it's very
(06:28):
good at causing atherosclerosis,and you almost always find it
in those unstable plaques, thekind most likely to break open
and trigger a heart attack.
Speaker 2 (06:35):
That makes so much sense now.
Speaker 3 (06:36):
Yeah, and it explains why you can see patients with
perfectly normal LDL numbers,but if their inflammation is
high, they still develop seriousheart disease.
Just focusing on totalcholesterol or even just
standard LDL, it completelymisses this root issue and it
raises a really importantquestion, right?
If atherosclerosis isessentially a chronic immune
disorder you know where theimmune system is constantly
(06:56):
reacting to what it sees as aninjury inside the arteries well
then, our prevention strategiesneed a fundamental shift.
Speaker 2 (07:03):
That is a huge shift, wow.
So, instead of just lowercholesterol, lower cholesterol,
it sounds like we need to bethinking about calming the
immune system down, reducingthat inflammation, protecting
that vascular lining, and Iguess, for those wanting to
track our own risk, the standardcholesterol tests just aren't
going to cut it, are they?
Speaker 3 (07:20):
You're absolutely right.
If you're only testing totalcholesterol and maybe LDL, hdl,
you're really only seeing a tinypiece of the whole
cardiovascular puzzle.
So many people with normallipids still develop heart
disease precisely because theirinflammation markers are high,
and those markers are what trulydrive the process.
Functional and preventativemedicine labs offer a much
deeper look under the hood, soto speak.
(07:41):
For instance, hs-crp, highsensitivity C-reactive protein.
It's a well-known marker ofjust general systemic
inflammation, and elevatedlevels correlate really strongly
with heart risk, even in peoplewho have normal LDL.
Speaker 2 (07:55):
OK, so HS-CRP, what level should people aim for?
Speaker 3 (07:59):
Ideally you want that below 1.0 milligel.
Lower is generally better.
Speaker 2 (08:03):
Got it Below 1.0.
What else Beyond HS-CRP, whatgives us that fuller picture?
Speaker 4 (08:07):
Well, we can actually measure oxidized LDL directly,
which, as we've been saying, isthat more dangerous form,
strongly linked to those on thestable plaques.
Then there's LPA, lipoprotein.
It's kind of a tricky one.
It's not so genetic, it's anLDL-like particle, but it not
only promotes inflammation, italso makes your blood more
likely to clot.
Oh wow.
Speaker 2 (08:27):
A real double whammy then.
Speaker 4 (08:33):
Exactly, it's a real double whammy for heart risk.
Speaker 3 (08:34):
And guess what?
It's not even included instandard cholesterol panels, but
having high LPA significantlybumps up the risk of early heart
disease, especially if you alsohave high CRP or high oxidized
LDL.
Speaker 2 (08:44):
Okay, lpa, that feels really important to know about,
especially if it's genetic.
Speaker 4 (09:08):
Stay even lower, maybe seven or eight.
Speaker 3 (09:11):
Then there's fibrinogen.
That's a clotting factor.
High levels can indicateincreased risk of thrombosis,
blood clots, but also coinstowards inflammation.
And you know, for digging evendeeper into metabolic health,
which is often driving theinflammation, we look at markers
like fasting insulin andcalculate home AIR.
These directly measure insulinresistance.
Speaker 2 (09:32):
Ah, okay, because insulin resistance is a big
driver of inflammation itself.
Speaker 3 (09:36):
A major driver.
Yes, and for the most advancedpicture, you can even measure
the direct signals of immuneactivation specific cytokines
like IL-6 and TNF-alpha.
These basically tell us howloud those inflammatory distress
calls are inside the body.
Speaker 2 (09:51):
Wow.
So these labs, they go waybeyond just seeing if
cholesterol is building up.
They help show why it might bebuilding up and like how active
that whole inflammatory fire is.
It really changes theperspective.
And this all comes back to well, our daily lives, doesn't it?
Our choices, especially diet, Iimagine.
Speaker 3 (10:07):
Oh, absolutely.
Atherosclerosis doesn't justhappen in a vacuum, and one of
the most powerful drivers maybeone we underestimate is diet,
specifically a diet heavy inrefined carbs, added sugars and
certain processed seed oils.
These foods directly fuelinsulin resistance, oxidative
stress and immune dysfunction.
They basically create theperfect storm for inflammation
(10:29):
inside your arteries.
Speaker 2 (10:31):
So OK, those sugary drinks, the white bread, the
pastries, the processed snacks,they're not just about weight,
they're actively fuelinginflammation in our blood
vessels.
Speaker 3 (10:39):
That's exactly it.
Think about it Meals high insugars and refined starches
cause these big blood sugarspikes.
Your body pumps out insulin tohandle it, but over time, doing
that again and again leads toinsulin resistance.
Your cells just stop listeningproperly to insulin, so you end
up with high, fasting insulinlevels, chronic, low-grade
inflammation.
Your body starts producing moreinflammatory cytokines like
(11:02):
IL-6 and CRP, and it leads tomore oxidation of those LDL
particles we talked about.
In fact, studies clearly showthat people who are insulin
resistant tend to have moreinflamed arterial plaques, even
if their LDL levels are exactlythe same as someone who isn't
insulin resistant.
Speaker 2 (11:18):
That's huge.
That insulin resistance pieceseems absolutely critical.
Speaker 3 (11:22):
It's a massive piece of the puzzle.
Speaker 2 (11:23):
Yes, and I keep hearing more and more about gut
health being connected toeverything.
Does the gut play a role heretoo?
Speaker 3 (11:30):
It absolutely does.
It's a critical connection.
Your diet doesn't just messwith blood sugar, it profoundly
shapes your gut microbiome andyour gut bacteria are major
players in your cardiovascularhealth.
Speaker 2 (11:41):
How so.
Speaker 3 (11:42):
Well, when your gut gets out of balance maybe from
too much sugar, alcohol, stress,processed foods, antibiotics
that protective gut barrier canweaken.
It gets leaky and this allowsbacterial toxins, things like
lipopolysaccharides or LPS, toleak from the gut into your
bloodstream.
Speaker 2 (11:58):
Leaking from the gut into the blood.
That sounds bad.
Speaker 4 (12:01):
It is.
The process is called metabolicendotoxemia.
Think of it like a slow,constant loop of inflammatory
triggers coming from your gutand circulating throughout your
body, including your arteries.
This is now recognized as areally significant contributor
to atherosclerosis, especiallyin people who aren't
metabolically healthy.
That LPS triggers immuneactivation, ramps up vascular
(12:24):
inflammation and can even makeexisting plaque more unstable,
more likely to rupture.
Speaker 2 (12:28):
Wow, it really is all connected, isn't it?
You've got health directlyimpacting your heart risk.
Yeah, who knew?
And I guess if we're eating alot of those highly processed
foods, we're probably notgetting enough of the good stuff
either.
Speaker 4 (12:40):
That's spot on.
Diets high in processed carbsand sugars are almost always low
in key anti-inflammatorynutrients, Things like omega-3
fatty acids, magnesium, vitaminD, antioxidants like CoQ10,
glutathione.
These nutrients are vital.
They help reduce oxidativestress.
They improve insulinsensitivity.
They protect that delicateendothelial lining.
So yeah, the bottom line ispretty clear you really can't
(13:03):
separate your diet frominflammation and you can't
separate inflammation from yourcardiovascular risk.
Speaker 3 (13:08):
Even if your LDL is perfect.
Poor metabolic health driven bydiet can be Okay, but here's
the crucial part then, the goodnews that is absolutely the most
(13:28):
hopeful part of this wholeshift in understanding yes,
chronic inflammation isreversible.
By targeting these root causesthe diet, the gut health, the
insulin resistance, the stressyou can significantly improve
your vascular function.
You can help stabilize existingplaques, make them less
dangerous and lower your overallrisk for a heart attack or
(13:49):
stroke.
Speaker 2 (13:49):
So where do we start?
What's the most impactful thing?
Speaker 3 (13:52):
One of the biggest levers you can pull is
definitely anti-inflammatorynutrition.
Focusing your diet on whole,unprocessed, anti-inflammatory
foods can make a massivedifference.
Different approaches work fordifferent people.
Things like low-carbohydrate oreven ketogenic diets have
strong data showing they lowerinsulin, reduce blood sugar
spikes and decrease inflammatorymarkers like HSCRP.
(14:13):
The Mediterranean diet isanother great one, rich in those
healthy fats like olive oil,omega-3s from fish, lots of
colorful plants, full ofpolyphenols and fiber.
It's consistently shown toimprove endothelial function and
reduce heart events.
But maybe the most criticalfirst step for many people
getting rid of theultra-processed stuff,
especially anything high inadded sugars, those refined seed
(14:36):
oils like soybean or corn oiland refined starches.
Just cutting those out can makea huge difference.
And then, yeah, adding certainsupplements can help too, Things
like high-quality omega-3s,magnesium.
They can further help calm downthat inflammatory cascade.
Speaker 2 (14:52):
So it's about taking out the bad stuff, but also
strategically putting in thegood stuff Makes sense.
What about beyond diet,lifestyle stuff?
Speaker 3 (15:00):
Lifestyle factors are just as crucial, absolutely.
For example, poor sleep, notgetting enough quality sleep,
consistently that cansignificantly raise your CRP,
your TNF-alpha, your cortisollevels, all driving inflammation
.
Speaker 2 (15:14):
Sleep matters.
Speaker 3 (15:15):
Big time and chronic, unmanaged stress.
Same thing.
It activates your fight orflight nervous system, promotes
vasoconstriction, tightening ofblood vessels and messes with
your immune regulation.
And, of course, regularphysical activity.
Moderate exercise is key.
It's proven to reduce CRP,improve insulin sensitivity and
boost nitric oxide production.
Speaker 2 (15:33):
Nitric oxide.
That helps keep vesselsflexible right.
Speaker 3 (15:35):
Exactly Essential for good vessel health and
flexibility.
So movement is medicine too.
Speaker 2 (15:40):
And for anyone who's really serious about tackling
this, tracking progress withthose advanced labs seems
critical.
It sounds like QuickLab Mobileis making that part easier.
Speaker 3 (15:48):
It really is.
Monitoring your inflammationshouldn't be guesswork, right,
it should be data-driven.
You can use tests like HSCRPand oxidized LDL to actually
track your vascular inflammationlevels over time, see if your
changes are working.
Fasting insulin, hniot, glucosethose are essential for
tracking your metabolic health,your insulin sensitivity, and
(16:10):
then for that reallypersonalized deep dive into risk
, you'd look at things likelipid particle size and number,
lpa, homocysteine and yeah,services like QuickLab Mobile
are helping people access manyof these advanced labs more
easily.
They offer convenient, oftenat-home, blood collection.
It makes it much more feasibleto test for that silent
inflammation, the insulinresistance, the oxidized
(16:30):
cholesterol, the endothelialdamage.
It really gives individuals,gives you the beta and the
visibility to understand what'struly driving your heart health
and make informed changes.
Speaker 2 (16:40):
OK, so let's recap this deep dive then.
For gosh decades really,cholesterol was kind of painted
as the main villain, theundisputed bad guy behind heart
disease.
But the science, now it'sgiving us a much clearer picture
and, honestly, a more hopefulone.
The big aha moment here.
The key takeaway is thatatherosclerosis isn't just a
(17:01):
cholesterol problem.
It's primarily an inflammationproblem.
Speaker 3 (17:04):
Precisely that chronic inflammation is what
damages the blood vessel lining,it's what oxidizes the LDL, it
recruits the immune cells and itbuilds up those dangerous
unstable plaques that can leadto heart attacks and strokes.
And if we connect this to thebigger picture that inflammation
usually stems from factors thatare, you know, not only
measurable but cruciallymodifiable Right Things we can
(17:27):
actually change Exactly.
We're talking about things likeinsulin resistance, a
pro-inflammatory diet, maybe gutdysfunction, unmanaged chronic
stress.
So by shifting your focus fromjust I need to lower my LDL
number to actively loweringinflammation, well, you unlock a
much more powerful, much morepersonalized approach to
protecting your cardiovascularhealth.
(17:47):
And that's why these advancedinflammation and metabolic tests
are so vital and why serviceslike QuickLab Mobile, making
at-home testing easier, are sohelpful.
They give you the results, thedata that can drive real,
meaningful lifestyle change.
Speaker 2 (18:01):
You know, heart disease is often talked about
like it's just bad luck orinevitable with aging.
But this deep dive really showsit's largely preventable if you
know what to actually look forand you know which levers to
pull.
So here's a final thought toleave you with Consider how your
daily choices what you eat, howyou sleep, how you manage
stress, how you move, how arethose choices constantly sending
signals to your body'sincredibly complex systems?
(18:22):
Are they fueling that fire ofinflammation or are they helping
to calm it, protecting yourcardiovascular health for the
long haul?
Something to think about.
Speaker 1 (18:37):
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.
Speaker 2 (00:26):
Welcome to the Deep Dive.
We're your shortcut to beingtruly well-informed.
Today we're diving intosomething pretty fundamental
about heart health, Somethingthat might just change how you
think about it.
Get this stat from the AmericanHeart Association Nearly half
the people who have a heartattack they actually have
cholesterol levels considerednormal.
Speaker 3 (00:47):
Yeah, it's a statistic that really stops you
in your tracks, doesn't it?
It challenges well decades ofthinking.
For so long, the story was allabout cholesterol, specifically
LDL, you know the bad one.
But the science, the newerresearch, it's giving us a much
more complete picture and,honestly, a more hopeful one too
.
It's giving us a much morecomplete picture and, honestly,
a more hopeful one too.
It's really pointing towardsinflammation as the actual
underlying driver behindatherosclerosis.
Speaker 2 (01:09):
Atherosclerosis.
Ok, that's the plaque buildupinside your arteries.
Speaker 3 (01:12):
Exactly that slow, progressive buildup and
inflammation seems to be thereal spark.
Speaker 2 (01:17):
So if it's not just about cholesterol, what's
actually happening?
This is already making merethink things.
Speaker 3 (01:23):
Right, it's not simply about high LDL numbers
floating around causing troubleon their own.
Atherosclerosis really seems tostart when inflammation damages
that delicate inner lining ofyour blood vessels.
It's called the endothelium,and that damage it sort of
creates the sticky surface,almost like Velcro.
It lets cholesterol particles,yeah, but also immune cells and
(01:44):
other debris latch on, and thatkicks off a whole cascade of
immune reactions.
It lets cholesterol particles,yeah, but also immune cells and
other debris latch on, and thatkicks off a whole cascade of
immune reactions.
It's like starting a fireinside your arteries.
The result is those hardened,narrowed vessels, and that
explains why someone can havesignificant heart risk, even
with normal cholesterol.
Speaker 2 (01:58):
Okay, right, let's really dig into this then.
This deep dive is all aboutgiving you the insights to
understand what really drivesheart disease.
So we're going to explore whatatherosclerosis truly is, how
inflammation sparks it and whatmakes it worse, which lab
markers you might need to gobeyond just the standard
cholesterol test and, maybe mostimportantly, how you can start
(02:20):
addressing the root cause, notjust chasing a symptom like high
cholesterol, because if you'veonly been focusing on
cholesterol numbers, you'reprobably missing a huge part of
the picture.
We want to help you see itclearly.
Speaker 3 (02:30):
Absolutely.
Let's start with that basicidea.
Atherosclerosis it's just themedical term for that plaque
buildup inside arteries.
Think of your arteries like Idon't know clean, flexible pipes
that carry oxygen-rich bloodeverywhere in your body.
But over time this plaquebuilds up, it narrows those
pipes, restricts the blood flowand that dramatically increases
(02:50):
the risk for things like a heartattack or a stroke.
And it's not just a simple blobof fat either.
It's this complex sticky mixcholesterol, sure, but also
calcium, dead immune cells, fats, other cellular junk, all sort
of sticking together.
And you know this doesn'thappen overnight.
It's a slow burn.
It can start silently, maybeyears, even decades, before you
(03:11):
feel anything.
Speaker 2 (03:12):
And for so long the old view was pretty
straightforward LDL cholesterolthe bad stuff was the enemy.
Just lower it, maybe withmedication, and you reduce your
risk.
Simple Seems simple, but here'swhere it gets tricky and, like
you said, maybe more interesting.
Up to half of people havingheart attacks have LDL levels
that are technically normal oreven optimal.
Clearly, that old view justdoesn't capture everything.
Speaker 3 (03:33):
Exactly, and what's really fascinating is how the
modern view has shifted.
It's quite different Now.
Atherosclerosis isn't reallyseen as starting with
cholesterol.
It starts with damage to thatinner lining, the endothelium,
and that damage it's oftencaused by things like chronic
inflammation, yeah, but alsohigh blood pressure, toxins from
the environment, even justfrequent blood sugar spikes.
Speaker 2 (03:56):
Ah, okay, so the lining gets damaged first.
Speaker 3 (03:59):
Right.
And once that barrier iscompromised, then LDL particles
can slip into the artery wall,but it's in the wall that they
become oxidized.
Think of it like they rust.
They rust.
Yeah, essentially.
And that oxidation that's whattriggers the big alarm for your
immune system.
It calls in immune cells.
Think of them like tiny cleanupcrews, macrophages mainly.
(04:19):
These cells then gorgethemselves on this damaged,
oxidized LDL and they becomethese bloated things called foam
cells.
Speaker 2 (04:26):
Foam cells I've heard that term.
Speaker 3 (04:28):
And those foam cells.
They're basically the firstbuilding blocks of plaque.
That's why atherosclerosis isreally being recognized more and
more as an inflammatory diseaseat its very core, not just a
simple cholesterol storageproblem.
Speaker 2 (04:41):
So, wow, it's less about just having cholesterol
around and way more about how itgets changed or transformed by
inflammation.
That feels like a criticalturning point.
It's like, ah, cholesterol ismaybe the bricks, but
inflammation is the architect,the construction crew and maybe
even the fire that hardens thestructure.
(05:01):
Is that a fair way to thinkabout it?
Speaker 3 (05:03):
That's actually a great analogy, a really powerful
one.
Modern cardiology, you know thethinking now widely accepts
atherosclerosis as thisimmune-driven inflammatory
process.
Every time that endothelium,that lining, gets hit with high
blood sugar, oxidative stress,toxins, high pressure, it gets
injured, it gets inflamed.
Speaker 4 (05:40):
And this triggers the release of inflammatory signals
.
Things we can actually measurelike high sensitivity C-reactive
protein or HSCRP.
Speaker 3 (05:46):
Also specific cytotimes like IL-6 and and over
time the whole process leads tothicker artery walls, less
blood flow, higher risk of clotsforming and eventually a higher
chance of that plaque rupturingand causing a heart attack.
So it sounds like we reallyneed.
That is a crucial distinction.
(06:07):
Yes, not all LDL is inherentlybad or created equal.
The real troublemaker isn'tjust the LDL molecule itself.
It's what happens when it getsoxidized and that oxidation
process.
It's heavily fueled byinflammation, often from a poor
diet and general oxidativestress in the body.
This oxidized LDL is highlyatherogenic, meaning it's very
(06:28):
good at causing atherosclerosis,and you almost always find it
in those unstable plaques, thekind most likely to break open
and trigger a heart attack.
Speaker 2 (06:35):
That makes so much sense now.
Speaker 3 (06:36):
Yeah, and it explains why you can see patients with
perfectly normal LDL numbers,but if their inflammation is
high, they still develop seriousheart disease.
Just focusing on totalcholesterol or even just
standard LDL, it completelymisses this root issue and it
raises a really importantquestion, right?
If atherosclerosis isessentially a chronic immune
disorder you know where theimmune system is constantly
(06:56):
reacting to what it sees as aninjury inside the arteries well
then, our prevention strategiesneed a fundamental shift.
Speaker 2 (07:03):
That is a huge shift, wow.
So, instead of just lowercholesterol, lower cholesterol,
it sounds like we need to bethinking about calming the
immune system down, reducingthat inflammation, protecting
that vascular lining, and Iguess, for those wanting to
track our own risk, the standardcholesterol tests just aren't
going to cut it, are they?
Speaker 3 (07:20):
You're absolutely right.
If you're only testing totalcholesterol and maybe LDL, hdl,
you're really only seeing a tinypiece of the whole
cardiovascular puzzle.
So many people with normallipids still develop heart
disease precisely because theirinflammation markers are high,
and those markers are what trulydrive the process.
Functional and preventativemedicine labs offer a much
deeper look under the hood, soto speak.
(07:41):
For instance, hs-crp, highsensitivity C-reactive protein.
It's a well-known marker ofjust general systemic
inflammation, and elevatedlevels correlate really strongly
with heart risk, even in peoplewho have normal LDL.
Speaker 2 (07:55):
OK, so HS-CRP, what level should people aim for?
Speaker 3 (07:59):
Ideally you want that below 1.0 milligel.
Lower is generally better.
Speaker 2 (08:03):
Got it Below 1.0.
What else Beyond HS-CRP, whatgives us that fuller picture?
Speaker 4 (08:07):
Well, we can actually measure oxidized LDL directly,
which, as we've been saying, isthat more dangerous form,
strongly linked to those on thestable plaques.
Then there's LPA, lipoprotein.
It's kind of a tricky one.
It's not so genetic, it's anLDL-like particle, but it not
only promotes inflammation, italso makes your blood more
likely to clot.
Oh wow.
Speaker 2 (08:27):
A real double whammy then.
Speaker 4 (08:33):
Exactly, it's a real double whammy for heart risk.
Speaker 3 (08:34):
And guess what?
It's not even included instandard cholesterol panels, but
having high LPA significantlybumps up the risk of early heart
disease, especially if you alsohave high CRP or high oxidized
LDL.
Speaker 2 (08:44):
Okay, lpa, that feels really important to know about,
especially if it's genetic.
Speaker 4 (09:08):
Stay even lower, maybe seven or eight.
Speaker 3 (09:11):
Then there's fibrinogen.
That's a clotting factor.
High levels can indicateincreased risk of thrombosis,
blood clots, but also coinstowards inflammation.
And you know, for digging evendeeper into metabolic health,
which is often driving theinflammation, we look at markers
like fasting insulin andcalculate home AIR.
These directly measure insulinresistance.
Speaker 2 (09:32):
Ah, okay, because insulin resistance is a big
driver of inflammation itself.
Speaker 3 (09:36):
A major driver.
Yes, and for the most advancedpicture, you can even measure
the direct signals of immuneactivation specific cytokines
like IL-6 and TNF-alpha.
These basically tell us howloud those inflammatory distress
calls are inside the body.
Speaker 2 (09:51):
Wow.
So these labs, they go waybeyond just seeing if
cholesterol is building up.
They help show why it might bebuilding up and like how active
that whole inflammatory fire is.
It really changes theperspective.
And this all comes back to well, our daily lives, doesn't it?
Our choices, especially diet, Iimagine.
Speaker 3 (10:07):
Oh, absolutely.
Atherosclerosis doesn't justhappen in a vacuum, and one of
the most powerful drivers maybeone we underestimate is diet,
specifically a diet heavy inrefined carbs, added sugars and
certain processed seed oils.
These foods directly fuelinsulin resistance, oxidative
stress and immune dysfunction.
They basically create theperfect storm for inflammation
(10:29):
inside your arteries.
Speaker 2 (10:31):
So OK, those sugary drinks, the white bread, the
pastries, the processed snacks,they're not just about weight,
they're actively fuelinginflammation in our blood
vessels.
Speaker 3 (10:39):
That's exactly it.
Think about it Meals high insugars and refined starches
cause these big blood sugarspikes.
Your body pumps out insulin tohandle it, but over time, doing
that again and again leads toinsulin resistance.
Your cells just stop listeningproperly to insulin, so you end
up with high, fasting insulinlevels, chronic, low-grade
inflammation.
Your body starts producing moreinflammatory cytokines like
(11:02):
IL-6 and CRP, and it leads tomore oxidation of those LDL
particles we talked about.
In fact, studies clearly showthat people who are insulin
resistant tend to have moreinflamed arterial plaques, even
if their LDL levels are exactlythe same as someone who isn't
insulin resistant.
Speaker 2 (11:18):
That's huge.
That insulin resistance pieceseems absolutely critical.
Speaker 3 (11:22):
It's a massive piece of the puzzle.
Speaker 2 (11:23):
Yes, and I keep hearing more and more about gut
health being connected toeverything.
Does the gut play a role heretoo?
Speaker 3 (11:30):
It absolutely does.
It's a critical connection.
Your diet doesn't just messwith blood sugar, it profoundly
shapes your gut microbiome andyour gut bacteria are major
players in your cardiovascularhealth.
Speaker 2 (11:41):
How so.
Speaker 3 (11:42):
Well, when your gut gets out of balance maybe from
too much sugar, alcohol, stress,processed foods, antibiotics
that protective gut barrier canweaken.
It gets leaky and this allowsbacterial toxins, things like
lipopolysaccharides or LPS, toleak from the gut into your
bloodstream.
Speaker 2 (11:58):
Leaking from the gut into the blood.
That sounds bad.
Speaker 4 (12:01):
It is.
The process is called metabolicendotoxemia.
Think of it like a slow,constant loop of inflammatory
triggers coming from your gutand circulating throughout your
body, including your arteries.
This is now recognized as areally significant contributor
to atherosclerosis, especiallyin people who aren't
metabolically healthy.
That LPS triggers immuneactivation, ramps up vascular
(12:24):
inflammation and can even makeexisting plaque more unstable,
more likely to rupture.
Speaker 2 (12:28):
Wow, it really is all connected, isn't it?
You've got health directlyimpacting your heart risk.
Yeah, who knew?
And I guess if we're eating alot of those highly processed
foods, we're probably notgetting enough of the good stuff
either.
Speaker 4 (12:40):
That's spot on.
Diets high in processed carbsand sugars are almost always low
in key anti-inflammatorynutrients, Things like omega-3
fatty acids, magnesium, vitaminD, antioxidants like CoQ10,
glutathione.
These nutrients are vital.
They help reduce oxidativestress.
They improve insulinsensitivity.
They protect that delicateendothelial lining.
So yeah, the bottom line ispretty clear you really can't
(13:03):
separate your diet frominflammation and you can't
separate inflammation from yourcardiovascular risk.
Speaker 3 (13:08):
Even if your LDL is perfect.
Poor metabolic health driven bydiet can be Okay, but here's
the crucial part then, the goodnews that is absolutely the most
(13:28):
hopeful part of this wholeshift in understanding yes,
chronic inflammation isreversible.
By targeting these root causesthe diet, the gut health, the
insulin resistance, the stressyou can significantly improve
your vascular function.
You can help stabilize existingplaques, make them less
dangerous and lower your overallrisk for a heart attack or
(13:49):
stroke.
Speaker 2 (13:49):
So where do we start?
What's the most impactful thing?
Speaker 3 (13:52):
One of the biggest levers you can pull is
definitely anti-inflammatorynutrition.
Focusing your diet on whole,unprocessed, anti-inflammatory
foods can make a massivedifference.
Different approaches work fordifferent people.
Things like low-carbohydrate oreven ketogenic diets have
strong data showing they lowerinsulin, reduce blood sugar
spikes and decrease inflammatorymarkers like HSCRP.
(14:13):
The Mediterranean diet isanother great one, rich in those
healthy fats like olive oil,omega-3s from fish, lots of
colorful plants, full ofpolyphenols and fiber.
It's consistently shown toimprove endothelial function and
reduce heart events.
But maybe the most criticalfirst step for many people
getting rid of theultra-processed stuff,
especially anything high inadded sugars, those refined seed
(14:36):
oils like soybean or corn oiland refined starches.
Just cutting those out can makea huge difference.
And then, yeah, adding certainsupplements can help too, Things
like high-quality omega-3s,magnesium.
They can further help calm downthat inflammatory cascade.
Speaker 2 (14:52):
So it's about taking out the bad stuff, but also
strategically putting in thegood stuff Makes sense.
What about beyond diet,lifestyle stuff?
Speaker 3 (15:00):
Lifestyle factors are just as crucial, absolutely.
For example, poor sleep, notgetting enough quality sleep,
consistently that cansignificantly raise your CRP,
your TNF-alpha, your cortisollevels, all driving inflammation
.
Speaker 2 (15:14):
Sleep matters.
Speaker 3 (15:15):
Big time and chronic, unmanaged stress.
Same thing.
It activates your fight orflight nervous system, promotes
vasoconstriction, tightening ofblood vessels and messes with
your immune regulation.
And, of course, regularphysical activity.
Moderate exercise is key.
It's proven to reduce CRP,improve insulin sensitivity and
boost nitric oxide production.
Speaker 2 (15:33):
Nitric oxide.
That helps keep vesselsflexible right.
Speaker 3 (15:35):
Exactly Essential for good vessel health and
flexibility.
So movement is medicine too.
Speaker 2 (15:40):
And for anyone who's really serious about tackling
this, tracking progress withthose advanced labs seems
critical.
It sounds like QuickLab Mobileis making that part easier.
Speaker 3 (15:48):
It really is.
Monitoring your inflammationshouldn't be guesswork, right,
it should be data-driven.
You can use tests like HSCRPand oxidized LDL to actually
track your vascular inflammationlevels over time, see if your
changes are working.
Fasting insulin, hniot, glucosethose are essential for
tracking your metabolic health,your insulin sensitivity, and
(16:10):
then for that reallypersonalized deep dive into risk
, you'd look at things likelipid particle size and number,
lpa, homocysteine and yeah,services like QuickLab Mobile
are helping people access manyof these advanced labs more
easily.
They offer convenient, oftenat-home, blood collection.
It makes it much more feasibleto test for that silent
inflammation, the insulinresistance, the oxidized
(16:30):
cholesterol, the endothelialdamage.
It really gives individuals,gives you the beta and the
visibility to understand what'struly driving your heart health
and make informed changes.
Speaker 2 (16:40):
OK, so let's recap this deep dive then.
For gosh decades really,cholesterol was kind of painted
as the main villain, theundisputed bad guy behind heart
disease.
But the science, now it'sgiving us a much clearer picture
and, honestly, a more hopefulone.
The big aha moment here.
The key takeaway is thatatherosclerosis isn't just a
(17:01):
cholesterol problem.
It's primarily an inflammationproblem.
Speaker 3 (17:04):
Precisely that chronic inflammation is what
damages the blood vessel lining,it's what oxidizes the LDL, it
recruits the immune cells and itbuilds up those dangerous
unstable plaques that can leadto heart attacks and strokes.
And if we connect this to thebigger picture that inflammation
usually stems from factors thatare, you know, not only
measurable but cruciallymodifiable Right Things we can
(17:27):
actually change Exactly.
We're talking about things likeinsulin resistance, a
pro-inflammatory diet, maybe gutdysfunction, unmanaged chronic
stress.
So by shifting your focus fromjust I need to lower my LDL
number to actively loweringinflammation, well, you unlock a
much more powerful, much morepersonalized approach to
protecting your cardiovascularhealth.
(17:47):
And that's why these advancedinflammation and metabolic tests
are so vital and why serviceslike QuickLab Mobile, making
at-home testing easier, are sohelpful.
They give you the results, thedata that can drive real,
meaningful lifestyle change.
Speaker 2 (18:01):
You know, heart disease is often talked about
like it's just bad luck orinevitable with aging.
But this deep dive really showsit's largely preventable if you
know what to actually look forand you know which levers to
pull.
So here's a final thought toleave you with Consider how your
daily choices what you eat, howyou sleep, how you manage
stress, how you move, how arethose choices constantly sending
signals to your body'sincredibly complex systems?
(18:22):
Are they fueling that fire ofinflammation or are they helping
to calm it, protecting yourcardiovascular health for the
long haul?
Something to think about.
Speaker 1 (18:37):
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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