August 29, 2025 • 25 mins
Your body whispers before it screams—and when it comes to coronary artery disease (CAD), those whispers could mean everything. In this episode of The Health Pulse, we explore how CAD, the leading cause of death in America, develops silently for decades before symptoms appear.
You’ll learn how tiny injuries to the artery lining trigger a cascade that leads to plaque buildup—and why CAD is more than just a cholesterol issue. We unpack the role of insulin resistance, inflammation, and lipid particle number in driving risk, and explain why tests like ApoB, LDL particle counts, and inflammatory markers offer far better insight than cholesterol levels alone.
Most importantly, we reveal how CAD is largely preventable—and even reversible when caught early. From advanced lab testing to personalized nutrition and targeted therapies, you’ll discover actionable strategies to identify risk before it turns into a heart attack.
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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 (00:24):
Have you ever noticed those subtle shifts in your
body, maybe feeling a littlemore tired than usual, perhaps a
bit more winded, going upstairsand you just kind of brush them
off, as, oh, I'm just gettingolder, happens all the time,
right?
But what if those quietwhispers were actually signs of
something well, pretty serious,a condition that, according to
the American Heart Association,impacts nearly one in five
(00:47):
deaths in the US.
Yet it often developscompletely silently.
Today we're diving deep intocoronary artery disease, or CAD.
It's not just common, it's theleading cause of death worldwide
.
So our mission in this deepdive is to cut through the noise
, maybe reveal some surprisingfacts about CAD and really give
you a shortcut to being trulywell informed about your heart
(01:09):
health.
Speaker 3 (01:10):
And what's truly fascinating here and frankly
often quite alarming is that CADusually develops silently.
Speaker 1 (01:16):
Yeah.
Speaker 3 (01:17):
It can progress for years, maybe even decades,
before it causes any symptomsyou'd really notice.
Speaker 2 (01:22):
Decades Wow.
Speaker 3 (01:23):
Yeah, but the really good news and this is why this
deep dive is so critical for youis that if you catch it early
with targeted prevention, youcan significantly slow its
progression or even, in manycases, actively reverse it.
Speaker 2 (01:38):
Okay, that's a powerful word reversed.
Can you give us a quick idea ofwhat reversal actually looks
like, like in practice?
What's the key factor there?
Speaker 3 (01:45):
Well, it's essentially about turning the
tide on that plaque buildupinside the arteries.
Reversal means you're not juststopping it from getting worse,
but you're actually seeing areduction, maybe in the size or
improving the stability ofexisting plaques.
Better blood flow Right and thebiggest factor, it's an
aggressive sort of multi-prongedapproach Lifestyle changes
absolutely, but also, whennecessary, targeted medical help
(02:08):
, and all of that is informed bygetting tested early with
advanced methods.
It really shows how the bodycan heal if you give it the
right support.
Speaker 2 (02:16):
That's incredible, really helpful and to guide us
through this pretty intricatelandscape, we're drawing from
some comprehensive insights onadvanced testing and prevention
strategies.
Our goal here is to shine alight on these hidden risks and
the crucial role advancedtesting plays in finding them
long before symptoms show up,equipping you with some powerful
(02:36):
, actionable knowledge.
Okay, so let's unpack this.
What exactly is coronary arterydisease?
Speaker 3 (02:42):
Right.
So, at its core, cad is whenthe arteries, the specific ones
that supply blood to your heartmuscle, get narrowed or blocked.
Speaker 2 (02:50):
And the main culprit.
Speaker 3 (02:51):
It's a process called atherosclerosis, basically a
buildup of plaque, and thatplaque isn't just one thing.
It's a mix of cholesterol,calcium, inflammatory cells,
other gunk.
Speaker 2 (03:01):
OK, plaque buildup.
So how does that actuallyhappen?
Is it just cholesterol stickingto the walls?
Speaker 3 (03:06):
We connect this to the bigger picture.
It's not quite that simple.
It's not just one factorappearing overnight.
It's actually a fascinating butkind of insidious step-by-step
process.
It often starts with somethingcalled endothelial dysfunction.
Speaker 2 (03:20):
Endothelial dysfunction.
Okay, what's that?
Speaker 3 (03:22):
Think of the endothelium as the super smooth,
nonstick inner lining of yourarteries, like the Teflon on a
frying pan.
Speaker 2 (03:29):
Got it, keeps things flowing.
Speaker 3 (03:31):
Exactly.
Dysfunction means that lininggets damaged.
Things like high blood sugar,smoking, chronic inflammation.
They rough it up, damage it,and that damage makes the artery
walls kind of leaky, morepermeable.
This allows LDL particles, youknow, the bad cholesterol,
especially the small, dense andoxidized kind to wiggle through
(03:51):
that damage lining.
Speaker 2 (03:53):
Ah, so the damage opens the door.
Speaker 3 (03:55):
Precisely, and once those LDL particles are inside
the artery wall, where theyshouldn't be, they trigger an
immune response.
Your white blood cells rush into clean up the mess.
Basically, they gobble up thisoxidized LDL and in doing so
they transform into these thingscalled foam cells.
Speaker 2 (04:11):
Foam cells.
So it's like a tiny, silentwound on the inside of our
artery and our body tries topatch it up, but the patch
itself, made of thesecholesterol-filled foam cells,
actually starts the biggerproblem.
Speaker 3 (04:20):
That's a great way to put it.
Yeah, it really paints apicture of how sneaky this whole
thing is.
Yeah, these foam cells thenpile up.
They form what are called fattystreaks.
Over time these streaks growinto more serious plaque
deposits.
These plaques can hardenBecause of calcium.
They grow bigger, narrowing theartery and reducing that vital
blood flow to the heart muscle.
Speaker 2 (04:41):
And the real danger point.
Speaker 3 (04:42):
The critical point is if one of these plaques
ruptures, breaks open.
If that happens, a blood clotcan form right on top of it,
potentially blocking the arterycompletely, and that's what
causes a myocardial infarctionwhat we commonly call a heart
attack.
Speaker 2 (04:59):
Okay, that's where it gets really interesting, and
this is a key insight from theresearch we looked at.
Cad isn't just about havinghigh cholesterol.
You're saying it'sfundamentally a metabolic and
inflammatory disease.
What does that mean for us,practically speaking?
Speaker 3 (05:10):
It means we can't just look at one number like
your total cholesterol on astandard lab report and think,
ok, I'm fine, it doesn't workthat way.
We have to recognize thatthings like insulin resistance,
chronic inflammation, oxidativestress and the number of certain
particles, like ApoB particles,all play huge interconnected
roles.
They're involved in bothbuilding the plaque and making
(05:32):
it unstable, making it morelikely to rupture.
It's a much more complexpicture.
These factors kind of conspiretogether.
Speaker 2 (05:38):
That brings us to a really crucial question then
what are the true drivers?
We've all heard aboutcholesterol for ages, but what
other forces are really at playhere that the research is
highlighting now?
Speaker 3 (05:51):
Yeah, that's key.
The research really points outthat, while, yes, high
cholesterol is linked, often theprimary forces driving this are
insulin resistance and chronicinflammation.
They're often the root issuesbehind the plaque formation and
the arterial damage we justtalked about.
Speaker 2 (06:04):
Okay, so let's dive into those.
Insulin resistance andinflammation.
Speaker 3 (06:08):
Right.
So first let's talk metabolicdysfunction.
This is a huge root cause.
For many people it often showsup as insulin resistance.
That means your body cellsaren't responding properly to
the hormone insulin, and thatoften leads to hyperinsulinemia,
which is just a fancy term forhaving chronically high levels
of insulin circulating in yourblood.
Speaker 2 (06:27):
High insulin all the time.
What does that do?
Speaker 3 (06:29):
Well, these high insulin levels.
They actually kind of sendsignals to your body to do
things you don't want, like holdon to sodium, which can raise
blood pressure.
It also promotes unhealthychanges in your blood vessels
what we call vascular remodelingand fuels systemic inflammation
.
It's like having a constantlow-grade fire simmering in your
system.
This environment acceleratesthe oxidation of LDL cholesterol
(06:52):
, making it more dangerous, andmakes those plaques in your
arteries really unstable.
You see this really clearly intype 2 diabetes and prediabetes.
The persistent high blood sugardirectly damages those artery
walls, making them even morepermeable to those
ApoB-containing particles likeLDL and VLDL cholesterol.
It's why diabetic patients havelike a two to four times higher
(07:14):
risk of CAD compared tonon-diabetics.
It's a major connection.
Speaker 2 (07:17):
You mentioned, hyperinsulinemia leads to
vascular remodeling.
What does that actually looklike for our arteries?
Are they just getting stifferor that's a great question.
Speaker 3 (07:26):
Think of it like this those high insulin levels are
basically signaling your bloodvessel walls to kind of bulk up,
but in an unhealthy way.
They get thicker, less flexible.
It's almost like the pipes inyour house getting coated and
narrowed from the inside.
It makes it harder for blood toflow smoothly, increases
pressure.
It's not just stiffness, it's astructural change that makes
them less resilient, more proneto damage.
Speaker 2 (07:48):
OK, that makes sense.
So metabolic dysfunction is onehuge piece.
What else?
Speaker 3 (07:52):
Then there were the lipid abnormalities, and what's
really crucial to understandhere is that just looking at
your total LDL cholesterol orLDL-C isn't the whole story.
Yeah, actually, elevated APOBlevels and LDL particle number,
ldlp, are often strongerpredictors of your actual CAD
risk.
Speaker 2 (08:08):
APOB and LDL particle number.
Why are they better predictors?
Speaker 3 (08:13):
Okay.
So think of ApoB as a proteinfound on the surface of all the
potentially plaque-causingparticles LDL, vldl, lpa.
Measuring ApoB basically countsthe total number of these
troublemaker particles.
Ldl-p is similar it directlycounts the LDL particles.
It's like counting the actualnumber of cars on the highway
causing traffic, rather thanjust estimating the total weight
of all the cars.
(08:33):
More particles, even if theyaren't all full of cholesterol,
means more chances to bump intothe artery wall and cause
problems.
Speaker 2 (08:40):
Got it More particles equals more risk, and you
mentioned LPA.
That sounds important too.
What's the story there?
Speaker 3 (08:46):
Absolutely.
Lpa, pronounced L-P-little-A,is a specific type of
lipoprotein particle.
The level you have is largelygenetically determined, passed
down in families.
Speaker 2 (08:54):
So diet doesn't change it much.
Speaker 3 (08:56):
Not significantly no, and that's why knowing your
number is so important.
High LPA is a major independentrisk factor.
It's linked to developingplaque earlier in life and,
importantly, a higher risk ofblood clots forming.
It's a really sticky,aggressive particle.
Speaker 2 (09:13):
A genetic red flag, basically.
Speaker 3 (09:14):
Exactly.
We also look at HDLfunctionality.
Sometimes your HDL cholesterolnumber the good cholesterol
might look okay on a standardtest, but if those HDL particles
aren't actually workingefficiently to remove
cholesterol from arteries andreduce inflammation, then
they're not providing theprotection you think they are.
Function matters, not just theamount.
Speaker 2 (09:33):
Okay, so metabolic issues the type and number of
lipid particles.
What's next?
Speaker 3 (09:38):
The third big piece is chronic inflammation and
oxidative stress.
We touched on this, butspecific markers really
highlight it.
Elevated HSCRP, that's highsensitivity C-reactive protein,
is a general marker ofinflammation anywhere in the
body, but we can also measureLP-PLA2.
It's a mouthfullipoprotein-associated
phospholipase A2, but it's anenzyme that's much more specific
(09:58):
to inflammation happeningwithin the artery wall itself.
Speaker 2 (10:01):
So you can pinpoint inflammation right where the
plaque forms.
Speaker 3 (10:04):
Exactly High levels of these markers tell us there's
active inflammation going on inthe arteries.
Even if someone's standardcholesterol looks totally normal
and remember those oxidized LDLparticles we talked about they
directly fuel this inflammation,trigger the immune system, help
those foam cells form and makeplaques grow.
Speaker 2 (10:23):
Okay, and then there are the lifestyle factors we
always hear about.
Speaker 3 (10:26):
Absolutely.
Lifestyle and environmentalfactors contribute heavily.
Smoking is a huge one.
It basically doubles your CADrisk, partly by dramatically
increasing oxidative stress,like constantly bathing your
arteries in harmful chemicals.
Speaker 2 (10:39):
And diet.
You mentioned refined carbsearlier.
Speaker 3 (10:42):
Yes, a diet that's consistently high in refined
carbohydrates and certain seedoils is a major driver.
Think sugary drinks, whitebread, processed snacks.
They spike your blood sugar,which spikes your insulin,
driving that inflammation andinsulin resistance we discussed.
Speaker 2 (10:58):
What about seed oils?
There's a lot of talk aboutthose.
Speaker 3 (11:01):
Well, the concern often relates to oils high in
omega-6 fatty acids, especiallywhen consumed in excess and when
they're highly processed orrepeatedly heated.
This can potentially shift thebalance in the body towards more
inflammation and oxidativestress, creating an environment
that's less friendly to yourarteries.
It's less about avoiding thementirely, perhaps, and more
(11:22):
about the balance with omega-3sand the overall quality and
processing of the fats you eat.
Speaker 2 (11:26):
So it's the overall pattern of the diet, the
processing, the balance.
Speaker 3 (11:30):
Precisely.
It's about the message yourfood sends to your body systems.
And, of course, a sedentarylifestyle doesn't help.
Being inactive reduces yourmetabolic flexibility, your
body's ability to efficientlyswitch between fuel sources, and
it tends to worsen lipidprofiles and insulin sensitivity
.
Speaker 2 (11:46):
It's just amazing how interconnected it all is
Metabolic health, lipids,inflammation, lifestyle and then
there's the part we can'tcontrol our genes.
Speaker 3 (11:55):
Exactly.
Finally, genetic and familyhistory are undeniable factors.
If you have a strong familyhistory of premature CAD,
meaning a close relative like aparent or sibling, diagnosed
before age 55 if they're male or65 if female, your lifetime
risk is significantly higher.
Speaker 2 (12:12):
Why is?
Speaker 3 (12:12):
that significantly higher.
Why is that?
There's specific geneticvariations that can affect
things like your LPA levels, howyour body metabolizes
ApoB-containing particles oreven your baseline insulin
sensitivity.
And you can't change your genes, obviously, but knowing you
have these geneticpredispositions is incredibly
empowering.
It means you can be much moreproactive, much more aggressive
with prevention strategies.
Speaker 2 (12:32):
So a family history isn't destiny, but it's
definitely a call to action forearlier testing and really
focusing on those lifestylefactors.
Speaker 3 (12:40):
Absolutely.
It's a strong signal to payclose attention.
Speaker 2 (12:43):
Okay, so we've painted this pretty detailed
picture of how CAD develops,often quietly, driven by all
these interconnected factors.
What does this actually meanfor you, the listener?
The really challenging part, itseems, is this silent
progression.
Many people don't know what'shappening until there's a major
event, right.
Speaker 3 (12:59):
That's the scary truth for many.
But there can be subtle warningsigns, those quiet whispers
from your body, even when youthink you feel fine.
Speaker 2 (13:07):
What should people be listening for?
What are those early, subtlesigns?
Speaker 3 (13:11):
Well, these initial signs of early or silent CAD are
often really easy to dismissbecause they can be so
nonspecific.
You might just feel unusualfatigue, like a deep tiredness
that doesn't seem to go awaywith rest.
Speaker 2 (13:23):
Just feeling drained.
Speaker 3 (13:24):
Yeah, or maybe reduced exercise tolerance.
Activities that used to feeleasy now leave you feeling
winded or unusually tired.
Mild shortness of breath duringactivity, maybe occasional
chest discomfort, notnecessarily pain, maybe just out
of shape, or I had a stressfulweek.
Speaker 2 (13:58):
But you're saying a subtle pattern of fatigue or
getting winded could actually beyour body signaling something
critical about your heart.
Speaker 3 (14:05):
Precisely.
It's about noticing changesfrom your normal baseline, and
as those blockages in thearteries worsen and blood flow
becomes more significantlyrestricted, then the classic
symptoms of stable CAD tend tobecome more noticeable,
especially during exertion.
Speaker 2 (14:21):
Okay, what are those classic symptoms?
Speaker 3 (14:23):
This is when you might experience angina.
That's the medical term forchest pain or discomfort, often
described as pressure, tightness, squeezing or burning Crucially
.
It's usually triggered byphysical activity or emotional
stress and typically gets betterwith rest.
Speaker 2 (14:38):
So activity brings it on rest, relieves it.
Speaker 3 (14:42):
Generally, yes, for stable angina.
You might also notice morepronounced shortness of breath
because the heart is strugglingto pump enough blood to meet the
body's oxygen demands duringactivity and persistent fatigue
or weakness can also occurbecause your tissues just aren't
getting the oxygen they need.
Speaker 2 (14:59):
That paints a clearer picture.
But then the big question whendoes it cross the line?
When is it an emergency?
When do you need to dropeverything and get help
immediately?
Speaker 3 (15:10):
This is absolutely critical to know.
You need immediate medicalattention.
Call 911 or your localemergency number if you
experience any of these Suddenintense chest pain or pressure,
especially if it radiates toyour arm, usually the left, neck
, jaw or back.
Shortness of breath, even whenyou're resting, breaking out in
a cold sweat, feeling nauseousor vomiting.
Feeling dizzy, lightheaded oractually fainting.
Speaker 2 (15:32):
Those sound like the heart attack symptoms we see on
TV.
Speaker 3 (15:35):
They are the classic signs of what's called acute
coronary syndrome, whichincludes a heart attack.
It's a true medical emergencywhere time is muscle the faster
you get treatment, the lessdamage to your heart.
And it's precisely because CADcan progress so silently for so
long that relying on symptoms istoo risky.
That's why advanced lab testingis so vital for catching this
(15:55):
early, before any of thesealarming symptoms appear.
Speaker 2 (15:58):
Okay.
So given how sneaky CAD can be,how do we actually catch it
early?
What's the cutting edge here?
Our sources emphasize thatstandard cholesterol tests often
miss the mark right.
Speaker 3 (16:08):
They often do miss significant hidden risk.
Yes, that's where advanced labtesting really becomes the
foundation for a deeper look.
These tests give us a muchclearer picture of your lipid
quality not just quantity, plusinflammation and your metabolic
health status.
For instance, measuring ApoB,as we discussed.
It counts the number ofpotentially harmful particles.
(16:30):
It's generally a betterpredictor of risk than just
LDL-C alone.
Speaker 2 (16:35):
Right Counting the cars, not just weighing them.
Speaker 3 (16:37):
Exactly.
Then there's LPA, that geneticmarker for early and aggressive
plaque.
Knowing your number is crucial.
We can also measure oxidizedLDL, which identifies those
really unstable, damaged LDLparticles that are prone to
triggering inflammation andplaque rupture.
Speaker 2 (16:52):
And the inflammation markers.
Speaker 3 (16:53):
Yes, hscrp, and especially RPPLA2.
They detect that hiddenarterial inflammation.
Even if your standardcholesterol looks perfectly fine
, they tell us if there's firein the vessel walls.
Speaker 2 (17:03):
And the metabolic piece.
Speaker 3 (17:04):
Crucial Testing fasting insulin and calculating
home AIR helps us evaluateinsulin resistance.
Since we know insulinresistance is a key driver of
CAD progression, getting ahandle on that is essential.
Now don't get me wrong.
The standard lipid panel stillgives us useful baseline
information, but for trulycomprehensive risk assessment it
(17:24):
really should be paired withthese advanced markers.
Speaker 2 (17:27):
So the blood tests give us the biochemical picture.
What about actually seeinginside the arteries?
Do imaging tests help too?
Speaker 3 (17:33):
Absolutely.
Imaging and functional testsare fantastic complements of the
lab work.
A coronary artery calcium thatscore is a great example.
It's a quick, non-invasive CTscan that detects and measures
the amount of calcified plaquein your heart's arteries.
Speaker 2 (17:47):
What does the score tell?
Speaker 3 (17:48):
you.
It directly quantifies yourplaque burden.
A score of zero is excellent,meaning no detectable calcified
plaque.
Higher scores indicate moreplaque and a significantly
higher risk of future heartevents.
Even if you have no symptoms,it's a powerful reality check.
There's also carotid intimamedia thickness CIMT.
That's an ultrasound of thecarotid arteries in your neck.
(18:11):
It measures the thickness ofthe inner layers of the artery
wall.
Thickening is an early sign ofatherosclerosis.
Speaker 2 (18:18):
And tests that see how the heart works under
pressure.
Speaker 3 (18:20):
Right Like stress testing, maybe combined with
echocardiography, an ultrasoundof the heart.
These see how your heartfunctions when it has to work
harder, looking for areas thatmight not be getting enough
blood flow due to blockages, andfor a very detailed look.
Coronary CT angiography CCTAuses CT imaging with contrast
dye to create high-resolutionpictures of the coronary
(18:42):
arteries themselves, allowingdoctors to see blockages
directly.
Speaker 2 (18:45):
It really sounds like a combination of advanced labs
and targeted imaging gives theclearest picture.
Speaker 3 (18:51):
It really does.
It moves us beyond justguessing based on cholesterol
alone.
Speaker 2 (18:54):
And the good news is accessing these advanced tests
is getting easier.
Our source material highlightedexamples like services you know
QuickLab Mobile down in Miamithat are actually making this
more convenient.
They offer these advancedcardiovascular panels,
inflammatory marker tests, andthey do it with at-home sample
collection.
You get fast, accurate resultsto help you and your doctor
identify risks way beforesymptoms might ever show up.
(19:17):
It's really bringing thiscrucial early detection closer
to people.
Speaker 3 (19:20):
And that accessibility is key, because
knowledge is really mostvaluable when you can understand
it and then actually apply it.
Preventing CAD fundamentallystarts with identifying those
risks early, and the data we getfrom this kind of advanced
testing allows clinicians,working with you, to design
truly personalized preventionplans.
It's not a one size fits allsituation anymore.
Speaker 2 (19:41):
So how does that personalization work?
How do those test resultstranslate into action?
Speaker 3 (19:46):
Well, it's about personalizing prevention.
The data informs tailoredstrategies.
For example, in nutritionaloptimization, the focus is on
lowering those insulin spikes.
We talked about improving yourmetabolic flexibility, basically
helping your body use energymore efficiently.
This often means shiftingtowards lower glycemic whole
food ways of eating.
Speaker 2 (20:06):
And medications.
Speaker 3 (20:07):
When it comes to targeted medications, the test
results really guide thedecisions.
If ApoB or LDL particle numberis high, maybe statins or PCSK9
inhibitors are considered tolower them.
If LPA is significantlyelevated, treatments like niacin
might be discussed, althoughits use is more nuanced now and
specific anti-inflammatorystrategies can be employed.
(20:28):
If markers like HSCRP or LPPLA2are high, targeting that
underlying inflammation andlifestyle is still huge right.
Crp or LPPLA2 or high targetingthat underlying inflammation.
Speaker 2 (20:34):
And lifestyle is still huge right.
Speaker 3 (20:36):
Oh, paramount.
Lifestyle optimization isfoundational.
First, as we've stressed,lowering insulinic stimuli.
Since high insulin drives somuch of this, reducing those
spikes is key.
This means focusing on thoselow glycemic whole food diets
lots of vegetables, leanproteins, healthy fats, and
actively avoiding excessiverefined carbs and sugars.
(20:56):
Tracking things like yourfasting insulin, hma-ir and
HbA1c helps you see the progress.
Speaker 2 (21:02):
Makes sense.
What about exercise?
Speaker 3 (21:04):
It's essential Exercise and movement.
Regular aerobic activity likebrisk, walking, jogging, cycling
, plus some resistance orstrength training significantly
improves your insulinsensitivity, helps lower
triglycerides and reduces thatoverall inflammatory burden.
It doesn't have to be extreme.
Consistency is key.
Speaker 2 (21:20):
And smoking we mentioned it's bad, but is there
any nuance, like with nicotineitself?
Speaker 3 (21:24):
That's an interesting point someone might bring up
Nicotine, when metabolized,produces nicotinic acid, which
is essentially niacin, andniacin can technically raise HDL
and lower ApoB slightly.
Speaker 2 (21:34):
Ah, so a theoretical, tiny upside.
Speaker 3 (21:36):
Theoretical maybe, but completely overshadowed.
The massive inflammatory loadand oxidative stress caused by
smoking itself, all thethousands of other chemicals in
tobacco smoke, far, faroutweighs any tiny theoretical
niacin-like effect from nicotine.
It's incredibly damaging.
Speaker 2 (21:53):
So the bottom line is unequivocal.
Speaker 3 (21:55):
Absolutely.
Smoking cessation is critical.
Quitting smoking leads to rapidreductions in CAD risk, often
significant improvements withinjust 12 months.
There's no contest.
Speaker 2 (22:05):
Got it.
Lifestyle is non-negotiable,but sometimes, even with the
best efforts, medication isneeded.
Speaker 3 (22:11):
Exactly and when indicated medications play a
vital role.
We have statins and PCSK9inhibitors, which are very
effective at lowering APOB andLDL particle numbers, slowing
plaque growth.
There's azatomide and pembidoicacid, which work differently,
reducing cholesterol absorptionfrom the gut and lowering
circulating APOB.
We mentioned anti-inflammatorytherapies guided by markers and
(22:33):
for patients at higher risk ofclots, perhaps because they've
already had an event,anti-platelet agents like
aspirin or others might beprescribed.
Speaker 2 (22:40):
And if the blockages are already severe.
Speaker 3 (22:41):
Then we move into interventional and advanced
therapies For significantblockages causing symptoms or
high risk.
Procedures like coronaryangioplasty and stenting are
common.
That's where a tiny balloon isused to open the narrowed artery
and then a small mesh tube, astent, is often placed to help
keep it open.
Speaker 2 (22:58):
And for more widespread disease.
Speaker 3 (23:00):
For more extensive blockages involving multiple
arteries, coronary artery bypasssurgery, or CABG, might be
necessary.
That's where surgeons use bloodvessels from elsewhere in the
body to create new pathways forblood to flow around the blocked
sections of the coronaryarteries.
Major surgery, but it can belife-saving.
Speaker 2 (23:18):
Wow, we have really covered a lot of ground today,
digging deep into coronaryartery disease.
It's clear it's a conditionthat often develops silently,
kind of lurking beneath thesurface.
But the really strong messagecoming through from our sources
is that it is largelypreventable, maybe even
reversible in some cases,especially when those risks are
identified and tackled early on.
Speaker 3 (23:38):
That's the key takeaway.
You now understand that byreally focusing on lowering that
insulin load from your diet, bylooking beyond just standard
cholesterol numbers tounderstand your lipid quality
and particle numbers, and byactively working to reduce
systemic inflammation, you coulddramatically lower your
cardiovascular risk.
This kind of information, thisdata, it empowers you and your
(24:00):
healthcare provider to trulypersonalize your heart health
strategy.
It helps you move from justreacting to problems to being
genuinely proactive.
Speaker 2 (24:07):
So, thinking about all this, what does it really
mean for you listening right now, moving forward?
If CAD can creep up silentlyfor years, what other hidden
stories might your own body betrying to tell you, maybe
through those subtle whispersyou've been tempted to brush off
?
How can you start to listenmore closely now, armed with
this knowledge?
How can you engage moreproactively with your own unique
(24:30):
health story?
It's really something toconsider.
What's happening beneath thesurface for you?
And just a reminder as always,this deep dive is intended for
educational and informationalpurposes only.
We're here to help youunderstand the landscape, but
this is definitely not asubstitute for professional
medical advice.
Please always consult with yourown qualified physician or
another healthcare professionalfor personalized guidance
(24:51):
regarding your specific healthsituation and any decisions you
might make.
Speaker 1 (24:59):
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 (00:24):
Have you ever noticed those subtle shifts in your
body, maybe feeling a littlemore tired than usual, perhaps a
bit more winded, going upstairsand you just kind of brush them
off, as, oh, I'm just gettingolder, happens all the time,
right?
But what if those quietwhispers were actually signs of
something well, pretty serious,a condition that, according to
the American Heart Association,impacts nearly one in five
(00:47):
deaths in the US.
Yet it often developscompletely silently.
Today we're diving deep intocoronary artery disease, or CAD.
It's not just common, it's theleading cause of death worldwide
.
So our mission in this deepdive is to cut through the noise
, maybe reveal some surprisingfacts about CAD and really give
you a shortcut to being trulywell informed about your heart
(01:09):
health.
Speaker 3 (01:10):
And what's truly fascinating here and frankly
often quite alarming is that CADusually develops silently.
Speaker 1 (01:16):
Yeah.
Speaker 3 (01:17):
It can progress for years, maybe even decades,
before it causes any symptomsyou'd really notice.
Speaker 2 (01:22):
Decades Wow.
Speaker 3 (01:23):
Yeah, but the really good news and this is why this
deep dive is so critical for youis that if you catch it early
with targeted prevention, youcan significantly slow its
progression or even, in manycases, actively reverse it.
Speaker 2 (01:38):
Okay, that's a powerful word reversed.
Can you give us a quick idea ofwhat reversal actually looks
like, like in practice?
What's the key factor there?
Speaker 3 (01:45):
Well, it's essentially about turning the
tide on that plaque buildupinside the arteries.
Reversal means you're not juststopping it from getting worse,
but you're actually seeing areduction, maybe in the size or
improving the stability ofexisting plaques.
Better blood flow Right and thebiggest factor, it's an
aggressive sort of multi-prongedapproach Lifestyle changes
absolutely, but also, whennecessary, targeted medical help
(02:08):
, and all of that is informed bygetting tested early with
advanced methods.
It really shows how the bodycan heal if you give it the
right support.
Speaker 2 (02:16):
That's incredible, really helpful and to guide us
through this pretty intricatelandscape, we're drawing from
some comprehensive insights onadvanced testing and prevention
strategies.
Our goal here is to shine alight on these hidden risks and
the crucial role advancedtesting plays in finding them
long before symptoms show up,equipping you with some powerful
(02:36):
, actionable knowledge.
Okay, so let's unpack this.
What exactly is coronary arterydisease?
Speaker 3 (02:42):
Right.
So, at its core, cad is whenthe arteries, the specific ones
that supply blood to your heartmuscle, get narrowed or blocked.
Speaker 2 (02:50):
And the main culprit.
Speaker 3 (02:51):
It's a process called atherosclerosis, basically a
buildup of plaque, and thatplaque isn't just one thing.
It's a mix of cholesterol,calcium, inflammatory cells,
other gunk.
Speaker 2 (03:01):
OK, plaque buildup.
So how does that actuallyhappen?
Is it just cholesterol stickingto the walls?
Speaker 3 (03:06):
We connect this to the bigger picture.
It's not quite that simple.
It's not just one factorappearing overnight.
It's actually a fascinating butkind of insidious step-by-step
process.
It often starts with somethingcalled endothelial dysfunction.
Speaker 2 (03:20):
Endothelial dysfunction.
Okay, what's that?
Speaker 3 (03:22):
Think of the endothelium as the super smooth,
nonstick inner lining of yourarteries, like the Teflon on a
frying pan.
Speaker 2 (03:29):
Got it, keeps things flowing.
Speaker 3 (03:31):
Exactly.
Dysfunction means that lininggets damaged.
Things like high blood sugar,smoking, chronic inflammation.
They rough it up, damage it,and that damage makes the artery
walls kind of leaky, morepermeable.
This allows LDL particles, youknow, the bad cholesterol,
especially the small, dense andoxidized kind to wiggle through
(03:51):
that damage lining.
Speaker 2 (03:53):
Ah, so the damage opens the door.
Speaker 3 (03:55):
Precisely, and once those LDL particles are inside
the artery wall, where theyshouldn't be, they trigger an
immune response.
Your white blood cells rush into clean up the mess.
Basically, they gobble up thisoxidized LDL and in doing so
they transform into these thingscalled foam cells.
Speaker 2 (04:11):
Foam cells.
So it's like a tiny, silentwound on the inside of our
artery and our body tries topatch it up, but the patch
itself, made of thesecholesterol-filled foam cells,
actually starts the biggerproblem.
Speaker 3 (04:20):
That's a great way to put it.
Yeah, it really paints apicture of how sneaky this whole
thing is.
Yeah, these foam cells thenpile up.
They form what are called fattystreaks.
Over time these streaks growinto more serious plaque
deposits.
These plaques can hardenBecause of calcium.
They grow bigger, narrowing theartery and reducing that vital
blood flow to the heart muscle.
Speaker 2 (04:41):
And the real danger point.
Speaker 3 (04:42):
The critical point is if one of these plaques
ruptures, breaks open.
If that happens, a blood clotcan form right on top of it,
potentially blocking the arterycompletely, and that's what
causes a myocardial infarctionwhat we commonly call a heart
attack.
Speaker 2 (04:59):
Okay, that's where it gets really interesting, and
this is a key insight from theresearch we looked at.
Cad isn't just about havinghigh cholesterol.
You're saying it'sfundamentally a metabolic and
inflammatory disease.
What does that mean for us,practically speaking?
Speaker 3 (05:10):
It means we can't just look at one number like
your total cholesterol on astandard lab report and think,
ok, I'm fine, it doesn't workthat way.
We have to recognize thatthings like insulin resistance,
chronic inflammation, oxidativestress and the number of certain
particles, like ApoB particles,all play huge interconnected
roles.
They're involved in bothbuilding the plaque and making
(05:32):
it unstable, making it morelikely to rupture.
It's a much more complexpicture.
These factors kind of conspiretogether.
Speaker 2 (05:38):
That brings us to a really crucial question then
what are the true drivers?
We've all heard aboutcholesterol for ages, but what
other forces are really at playhere that the research is
highlighting now?
Speaker 3 (05:51):
Yeah, that's key.
The research really points outthat, while, yes, high
cholesterol is linked, often theprimary forces driving this are
insulin resistance and chronicinflammation.
They're often the root issuesbehind the plaque formation and
the arterial damage we justtalked about.
Speaker 2 (06:04):
Okay, so let's dive into those.
Insulin resistance andinflammation.
Speaker 3 (06:08):
Right.
So first let's talk metabolicdysfunction.
This is a huge root cause.
For many people it often showsup as insulin resistance.
That means your body cellsaren't responding properly to
the hormone insulin, and thatoften leads to hyperinsulinemia,
which is just a fancy term forhaving chronically high levels
of insulin circulating in yourblood.
Speaker 2 (06:27):
High insulin all the time.
What does that do?
Speaker 3 (06:29):
Well, these high insulin levels.
They actually kind of sendsignals to your body to do
things you don't want, like holdon to sodium, which can raise
blood pressure.
It also promotes unhealthychanges in your blood vessels
what we call vascular remodelingand fuels systemic inflammation
.
It's like having a constantlow-grade fire simmering in your
system.
This environment acceleratesthe oxidation of LDL cholesterol
(06:52):
, making it more dangerous, andmakes those plaques in your
arteries really unstable.
You see this really clearly intype 2 diabetes and prediabetes.
The persistent high blood sugardirectly damages those artery
walls, making them even morepermeable to those
ApoB-containing particles likeLDL and VLDL cholesterol.
It's why diabetic patients havelike a two to four times higher
(07:14):
risk of CAD compared tonon-diabetics.
It's a major connection.
Speaker 2 (07:17):
You mentioned, hyperinsulinemia leads to
vascular remodeling.
What does that actually looklike for our arteries?
Are they just getting stifferor that's a great question.
Speaker 3 (07:26):
Think of it like this those high insulin levels are
basically signaling your bloodvessel walls to kind of bulk up,
but in an unhealthy way.
They get thicker, less flexible.
It's almost like the pipes inyour house getting coated and
narrowed from the inside.
It makes it harder for blood toflow smoothly, increases
pressure.
It's not just stiffness, it's astructural change that makes
them less resilient, more proneto damage.
Speaker 2 (07:48):
OK, that makes sense.
So metabolic dysfunction is onehuge piece.
What else?
Speaker 3 (07:52):
Then there were the lipid abnormalities, and what's
really crucial to understandhere is that just looking at
your total LDL cholesterol orLDL-C isn't the whole story.
Yeah, actually, elevated APOBlevels and LDL particle number,
ldlp, are often strongerpredictors of your actual CAD
risk.
Speaker 2 (08:08):
APOB and LDL particle number.
Why are they better predictors?
Speaker 3 (08:13):
Okay.
So think of ApoB as a proteinfound on the surface of all the
potentially plaque-causingparticles LDL, vldl, lpa.
Measuring ApoB basically countsthe total number of these
troublemaker particles.
Ldl-p is similar it directlycounts the LDL particles.
It's like counting the actualnumber of cars on the highway
causing traffic, rather thanjust estimating the total weight
of all the cars.
(08:33):
More particles, even if theyaren't all full of cholesterol,
means more chances to bump intothe artery wall and cause
problems.
Speaker 2 (08:40):
Got it More particles equals more risk, and you
mentioned LPA.
That sounds important too.
What's the story there?
Speaker 3 (08:46):
Absolutely.
Lpa, pronounced L-P-little-A,is a specific type of
lipoprotein particle.
The level you have is largelygenetically determined, passed
down in families.
Speaker 2 (08:54):
So diet doesn't change it much.
Speaker 3 (08:56):
Not significantly no, and that's why knowing your
number is so important.
High LPA is a major independentrisk factor.
It's linked to developingplaque earlier in life and,
importantly, a higher risk ofblood clots forming.
It's a really sticky,aggressive particle.
Speaker 2 (09:13):
A genetic red flag, basically.
Speaker 3 (09:14):
Exactly.
We also look at HDLfunctionality.
Sometimes your HDL cholesterolnumber the good cholesterol
might look okay on a standardtest, but if those HDL particles
aren't actually workingefficiently to remove
cholesterol from arteries andreduce inflammation, then
they're not providing theprotection you think they are.
Function matters, not just theamount.
Speaker 2 (09:33):
Okay, so metabolic issues the type and number of
lipid particles.
What's next?
Speaker 3 (09:38):
The third big piece is chronic inflammation and
oxidative stress.
We touched on this, butspecific markers really
highlight it.
Elevated HSCRP, that's highsensitivity C-reactive protein,
is a general marker ofinflammation anywhere in the
body, but we can also measureLP-PLA2.
It's a mouthfullipoprotein-associated
phospholipase A2, but it's anenzyme that's much more specific
(09:58):
to inflammation happeningwithin the artery wall itself.
Speaker 2 (10:01):
So you can pinpoint inflammation right where the
plaque forms.
Speaker 3 (10:04):
Exactly High levels of these markers tell us there's
active inflammation going on inthe arteries.
Even if someone's standardcholesterol looks totally normal
and remember those oxidized LDLparticles we talked about they
directly fuel this inflammation,trigger the immune system, help
those foam cells form and makeplaques grow.
Speaker 2 (10:23):
Okay, and then there are the lifestyle factors we
always hear about.
Speaker 3 (10:26):
Absolutely.
Lifestyle and environmentalfactors contribute heavily.
Smoking is a huge one.
It basically doubles your CADrisk, partly by dramatically
increasing oxidative stress,like constantly bathing your
arteries in harmful chemicals.
Speaker 2 (10:39):
And diet.
You mentioned refined carbsearlier.
Speaker 3 (10:42):
Yes, a diet that's consistently high in refined
carbohydrates and certain seedoils is a major driver.
Think sugary drinks, whitebread, processed snacks.
They spike your blood sugar,which spikes your insulin,
driving that inflammation andinsulin resistance we discussed.
Speaker 2 (10:58):
What about seed oils?
There's a lot of talk aboutthose.
Speaker 3 (11:01):
Well, the concern often relates to oils high in
omega-6 fatty acids, especiallywhen consumed in excess and when
they're highly processed orrepeatedly heated.
This can potentially shift thebalance in the body towards more
inflammation and oxidativestress, creating an environment
that's less friendly to yourarteries.
It's less about avoiding thementirely, perhaps, and more
(11:22):
about the balance with omega-3sand the overall quality and
processing of the fats you eat.
Speaker 2 (11:26):
So it's the overall pattern of the diet, the
processing, the balance.
Speaker 3 (11:30):
Precisely.
It's about the message yourfood sends to your body systems.
And, of course, a sedentarylifestyle doesn't help.
Being inactive reduces yourmetabolic flexibility, your
body's ability to efficientlyswitch between fuel sources, and
it tends to worsen lipidprofiles and insulin sensitivity
.
Speaker 2 (11:46):
It's just amazing how interconnected it all is
Metabolic health, lipids,inflammation, lifestyle and then
there's the part we can'tcontrol our genes.
Speaker 3 (11:55):
Exactly.
Finally, genetic and familyhistory are undeniable factors.
If you have a strong familyhistory of premature CAD,
meaning a close relative like aparent or sibling, diagnosed
before age 55 if they're male or65 if female, your lifetime
risk is significantly higher.
Speaker 2 (12:12):
Why is?
Speaker 3 (12:12):
that significantly higher.
Why is that?
There's specific geneticvariations that can affect
things like your LPA levels, howyour body metabolizes
ApoB-containing particles oreven your baseline insulin
sensitivity.
And you can't change your genes, obviously, but knowing you
have these geneticpredispositions is incredibly
empowering.
It means you can be much moreproactive, much more aggressive
with prevention strategies.
Speaker 2 (12:32):
So a family history isn't destiny, but it's
definitely a call to action forearlier testing and really
focusing on those lifestylefactors.
Speaker 3 (12:40):
Absolutely.
It's a strong signal to payclose attention.
Speaker 2 (12:43):
Okay, so we've painted this pretty detailed
picture of how CAD develops,often quietly, driven by all
these interconnected factors.
What does this actually meanfor you, the listener?
The really challenging part, itseems, is this silent
progression.
Many people don't know what'shappening until there's a major
event, right.
Speaker 3 (12:59):
That's the scary truth for many.
But there can be subtle warningsigns, those quiet whispers
from your body, even when youthink you feel fine.
Speaker 2 (13:07):
What should people be listening for?
What are those early, subtlesigns?
Speaker 3 (13:11):
Well, these initial signs of early or silent CAD are
often really easy to dismissbecause they can be so
nonspecific.
You might just feel unusualfatigue, like a deep tiredness
that doesn't seem to go awaywith rest.
Speaker 2 (13:23):
Just feeling drained.
Speaker 3 (13:24):
Yeah, or maybe reduced exercise tolerance.
Activities that used to feeleasy now leave you feeling
winded or unusually tired.
Mild shortness of breath duringactivity, maybe occasional
chest discomfort, notnecessarily pain, maybe just out
of shape, or I had a stressfulweek.
Speaker 2 (13:58):
But you're saying a subtle pattern of fatigue or
getting winded could actually beyour body signaling something
critical about your heart.
Speaker 3 (14:05):
Precisely.
It's about noticing changesfrom your normal baseline, and
as those blockages in thearteries worsen and blood flow
becomes more significantlyrestricted, then the classic
symptoms of stable CAD tend tobecome more noticeable,
especially during exertion.
Speaker 2 (14:21):
Okay, what are those classic symptoms?
Speaker 3 (14:23):
This is when you might experience angina.
That's the medical term forchest pain or discomfort, often
described as pressure, tightness, squeezing or burning Crucially
.
It's usually triggered byphysical activity or emotional
stress and typically gets betterwith rest.
Speaker 2 (14:38):
So activity brings it on rest, relieves it.
Speaker 3 (14:42):
Generally, yes, for stable angina.
You might also notice morepronounced shortness of breath
because the heart is strugglingto pump enough blood to meet the
body's oxygen demands duringactivity and persistent fatigue
or weakness can also occurbecause your tissues just aren't
getting the oxygen they need.
Speaker 2 (14:59):
That paints a clearer picture.
But then the big question whendoes it cross the line?
When is it an emergency?
When do you need to dropeverything and get help
immediately?
Speaker 3 (15:10):
This is absolutely critical to know.
You need immediate medicalattention.
Call 911 or your localemergency number if you
experience any of these Suddenintense chest pain or pressure,
especially if it radiates toyour arm, usually the left, neck
, jaw or back.
Shortness of breath, even whenyou're resting, breaking out in
a cold sweat, feeling nauseousor vomiting.
Feeling dizzy, lightheaded oractually fainting.
Speaker 2 (15:32):
Those sound like the heart attack symptoms we see on
TV.
Speaker 3 (15:35):
They are the classic signs of what's called acute
coronary syndrome, whichincludes a heart attack.
It's a true medical emergencywhere time is muscle the faster
you get treatment, the lessdamage to your heart.
And it's precisely because CADcan progress so silently for so
long that relying on symptoms istoo risky.
That's why advanced lab testingis so vital for catching this
(15:55):
early, before any of thesealarming symptoms appear.
Speaker 2 (15:58):
Okay.
So given how sneaky CAD can be,how do we actually catch it
early?
What's the cutting edge here?
Our sources emphasize thatstandard cholesterol tests often
miss the mark right.
Speaker 3 (16:08):
They often do miss significant hidden risk.
Yes, that's where advanced labtesting really becomes the
foundation for a deeper look.
These tests give us a muchclearer picture of your lipid
quality not just quantity, plusinflammation and your metabolic
health status.
For instance, measuring ApoB,as we discussed.
It counts the number ofpotentially harmful particles.
(16:30):
It's generally a betterpredictor of risk than just
LDL-C alone.
Speaker 2 (16:35):
Right Counting the cars, not just weighing them.
Speaker 3 (16:37):
Exactly.
Then there's LPA, that geneticmarker for early and aggressive
plaque.
Knowing your number is crucial.
We can also measure oxidizedLDL, which identifies those
really unstable, damaged LDLparticles that are prone to
triggering inflammation andplaque rupture.
Speaker 2 (16:52):
And the inflammation markers.
Speaker 3 (16:53):
Yes, hscrp, and especially RPPLA2.
They detect that hiddenarterial inflammation.
Even if your standardcholesterol looks perfectly fine
, they tell us if there's firein the vessel walls.
Speaker 2 (17:03):
And the metabolic piece.
Speaker 3 (17:04):
Crucial Testing fasting insulin and calculating
home AIR helps us evaluateinsulin resistance.
Since we know insulinresistance is a key driver of
CAD progression, getting ahandle on that is essential.
Now don't get me wrong.
The standard lipid panel stillgives us useful baseline
information, but for trulycomprehensive risk assessment it
(17:24):
really should be paired withthese advanced markers.
Speaker 2 (17:27):
So the blood tests give us the biochemical picture.
What about actually seeinginside the arteries?
Do imaging tests help too?
Speaker 3 (17:33):
Absolutely.
Imaging and functional testsare fantastic complements of the
lab work.
A coronary artery calcium thatscore is a great example.
It's a quick, non-invasive CTscan that detects and measures
the amount of calcified plaquein your heart's arteries.
Speaker 2 (17:47):
What does the score tell?
Speaker 3 (17:48):
you.
It directly quantifies yourplaque burden.
A score of zero is excellent,meaning no detectable calcified
plaque.
Higher scores indicate moreplaque and a significantly
higher risk of future heartevents.
Even if you have no symptoms,it's a powerful reality check.
There's also carotid intimamedia thickness CIMT.
That's an ultrasound of thecarotid arteries in your neck.
(18:11):
It measures the thickness ofthe inner layers of the artery
wall.
Thickening is an early sign ofatherosclerosis.
Speaker 2 (18:18):
And tests that see how the heart works under
pressure.
Speaker 3 (18:20):
Right Like stress testing, maybe combined with
echocardiography, an ultrasoundof the heart.
These see how your heartfunctions when it has to work
harder, looking for areas thatmight not be getting enough
blood flow due to blockages, andfor a very detailed look.
Coronary CT angiography CCTAuses CT imaging with contrast
dye to create high-resolutionpictures of the coronary
(18:42):
arteries themselves, allowingdoctors to see blockages
directly.
Speaker 2 (18:45):
It really sounds like a combination of advanced labs
and targeted imaging gives theclearest picture.
Speaker 3 (18:51):
It really does.
It moves us beyond justguessing based on cholesterol
alone.
Speaker 2 (18:54):
And the good news is accessing these advanced tests
is getting easier.
Our source material highlightedexamples like services you know
QuickLab Mobile down in Miamithat are actually making this
more convenient.
They offer these advancedcardiovascular panels,
inflammatory marker tests, andthey do it with at-home sample
collection.
You get fast, accurate resultsto help you and your doctor
identify risks way beforesymptoms might ever show up.
(19:17):
It's really bringing thiscrucial early detection closer
to people.
Speaker 3 (19:20):
And that accessibility is key, because
knowledge is really mostvaluable when you can understand
it and then actually apply it.
Preventing CAD fundamentallystarts with identifying those
risks early, and the data we getfrom this kind of advanced
testing allows clinicians,working with you, to design
truly personalized preventionplans.
It's not a one size fits allsituation anymore.
Speaker 2 (19:41):
So how does that personalization work?
How do those test resultstranslate into action?
Speaker 3 (19:46):
Well, it's about personalizing prevention.
The data informs tailoredstrategies.
For example, in nutritionaloptimization, the focus is on
lowering those insulin spikes.
We talked about improving yourmetabolic flexibility, basically
helping your body use energymore efficiently.
This often means shiftingtowards lower glycemic whole
food ways of eating.
Speaker 2 (20:06):
And medications.
Speaker 3 (20:07):
When it comes to targeted medications, the test
results really guide thedecisions.
If ApoB or LDL particle numberis high, maybe statins or PCSK9
inhibitors are considered tolower them.
If LPA is significantlyelevated, treatments like niacin
might be discussed, althoughits use is more nuanced now and
specific anti-inflammatorystrategies can be employed.
(20:28):
If markers like HSCRP or LPPLA2are high, targeting that
underlying inflammation andlifestyle is still huge right.
Crp or LPPLA2 or high targetingthat underlying inflammation.
Speaker 2 (20:34):
And lifestyle is still huge right.
Speaker 3 (20:36):
Oh, paramount.
Lifestyle optimization isfoundational.
First, as we've stressed,lowering insulinic stimuli.
Since high insulin drives somuch of this, reducing those
spikes is key.
This means focusing on thoselow glycemic whole food diets
lots of vegetables, leanproteins, healthy fats, and
actively avoiding excessiverefined carbs and sugars.
(20:56):
Tracking things like yourfasting insulin, hma-ir and
HbA1c helps you see the progress.
Speaker 2 (21:02):
Makes sense.
What about exercise?
Speaker 3 (21:04):
It's essential Exercise and movement.
Regular aerobic activity likebrisk, walking, jogging, cycling
, plus some resistance orstrength training significantly
improves your insulinsensitivity, helps lower
triglycerides and reduces thatoverall inflammatory burden.
It doesn't have to be extreme.
Consistency is key.
Speaker 2 (21:20):
And smoking we mentioned it's bad, but is there
any nuance, like with nicotineitself?
Speaker 3 (21:24):
That's an interesting point someone might bring up
Nicotine, when metabolized,produces nicotinic acid, which
is essentially niacin, andniacin can technically raise HDL
and lower ApoB slightly.
Speaker 2 (21:34):
Ah, so a theoretical, tiny upside.
Speaker 3 (21:36):
Theoretical maybe, but completely overshadowed.
The massive inflammatory loadand oxidative stress caused by
smoking itself, all thethousands of other chemicals in
tobacco smoke, far, faroutweighs any tiny theoretical
niacin-like effect from nicotine.
It's incredibly damaging.
Speaker 2 (21:53):
So the bottom line is unequivocal.
Speaker 3 (21:55):
Absolutely.
Smoking cessation is critical.
Quitting smoking leads to rapidreductions in CAD risk, often
significant improvements withinjust 12 months.
There's no contest.
Speaker 2 (22:05):
Got it.
Lifestyle is non-negotiable,but sometimes, even with the
best efforts, medication isneeded.
Speaker 3 (22:11):
Exactly and when indicated medications play a
vital role.
We have statins and PCSK9inhibitors, which are very
effective at lowering APOB andLDL particle numbers, slowing
plaque growth.
There's azatomide and pembidoicacid, which work differently,
reducing cholesterol absorptionfrom the gut and lowering
circulating APOB.
We mentioned anti-inflammatorytherapies guided by markers and
(22:33):
for patients at higher risk ofclots, perhaps because they've
already had an event,anti-platelet agents like
aspirin or others might beprescribed.
Speaker 2 (22:40):
And if the blockages are already severe.
Speaker 3 (22:41):
Then we move into interventional and advanced
therapies For significantblockages causing symptoms or
high risk.
Procedures like coronaryangioplasty and stenting are
common.
That's where a tiny balloon isused to open the narrowed artery
and then a small mesh tube, astent, is often placed to help
keep it open.
Speaker 2 (22:58):
And for more widespread disease.
Speaker 3 (23:00):
For more extensive blockages involving multiple
arteries, coronary artery bypasssurgery, or CABG, might be
necessary.
That's where surgeons use bloodvessels from elsewhere in the
body to create new pathways forblood to flow around the blocked
sections of the coronaryarteries.
Major surgery, but it can belife-saving.
Speaker 2 (23:18):
Wow, we have really covered a lot of ground today,
digging deep into coronaryartery disease.
It's clear it's a conditionthat often develops silently,
kind of lurking beneath thesurface.
But the really strong messagecoming through from our sources
is that it is largelypreventable, maybe even
reversible in some cases,especially when those risks are
identified and tackled early on.
Speaker 3 (23:38):
That's the key takeaway.
You now understand that byreally focusing on lowering that
insulin load from your diet, bylooking beyond just standard
cholesterol numbers tounderstand your lipid quality
and particle numbers, and byactively working to reduce
systemic inflammation, you coulddramatically lower your
cardiovascular risk.
This kind of information, thisdata, it empowers you and your
(24:00):
healthcare provider to trulypersonalize your heart health
strategy.
It helps you move from justreacting to problems to being
genuinely proactive.
Speaker 2 (24:07):
So, thinking about all this, what does it really
mean for you listening right now, moving forward?
If CAD can creep up silentlyfor years, what other hidden
stories might your own body betrying to tell you, maybe
through those subtle whispersyou've been tempted to brush off
?
How can you start to listenmore closely now, armed with
this knowledge?
How can you engage moreproactively with your own unique
(24:30):
health story?
It's really something toconsider.
What's happening beneath thesurface for you?
And just a reminder as always,this deep dive is intended for
educational and informationalpurposes only.
We're here to help youunderstand the landscape, but
this is definitely not asubstitute for professional
medical advice.
Please always consult with yourown qualified physician or
another healthcare professionalfor personalized guidance
(24:51):
regarding your specific healthsituation and any decisions you
might make.
Speaker 1 (24:59):
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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