December 9, 2025 • 15 mins
We trace the life cycle of atherosclerosis from quiet plaque buildup to sudden artery-closing clots that cause heart attacks, strokes, bowel infarction, and limb ischemia. We share clear warning signs, risk checks, imaging options, lifestyle moves, and modern therapies that change outcomes.
• why plaque forms and why it ruptures
• how one mechanism drives four major diseases
• cardiac, brain, gut, and leg warning signs
• transient ischaemic attack as an urgent red flag
• physical clues including pulses, bruits, and ABI
• key labs LDL, HDL, triglycerides, HbA1c, hsCRP, Lp(a)
• imaging with coronary calcium scoring and carotid ultrasound
• prevention through smoking cessation, diet, and weight control
• medications statins, ezetimibe, bempedoic acid, PCSK9 inhibitors
• antiplatelet risks and benefits
• when and how procedures restore blood flow
• the role of ultra-processed foods in rising risk
If you experience chest pain, stroke-like symptoms, severe abdominal pain after meals, or leg pain at rest with cold toes, contact a doctor immediately
This podcast is created by Ai for educational and entertainment purposes only and does not constitute professional medical or health advice. Please talk to your healthcare team for medical advice.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
SPEAKER_00 (00:00):
You know, if you're looking for the uh the single
biggest driver of modernmortality, the one chronic
condition that quietly defineshow long and how well we live
well, you've found it.
SPEAKER_02 (00:11):
It really is.
It's the root of the problem forso many things that seem
disconnected.
We're talking heart attacks,strokes.
SPEAKER_00 (00:16):
And today we are diving deep into that root,
atherosclerosis.
The silent, simmering diseasethat is, without a doubt, the
number one cause of death anddisability across the
industrialized world.
SPEAKER_02 (00:28):
It's a systemic issue and understanding the um
the core mechanics of how itstarts is really the first step
toward managing your own healthlong term.
SPEAKER_00 (00:37):
Absolutely.
And to guide us through this,we've got some truly
authoritative sources today,straight from Harvard Health.
The materials reviewed by Dr.
Christopher P.
Cannon, who's theeditor-in-chief of the Harvard
Heart Letter.
SPEAKER_02 (00:47):
So we're getting the definitive roadmap here.
SPEAKER_00 (00:49):
We are.
Okay, so let's unpack this.
Our mission is to strip away thecomplex jargon and really
understand the story ofatherosclerosis.
What is it exactly?
Why does it strike in so manydifferent parts of the body?
SPEAKER_02 (01:00):
And what new tools do we have right now to prevent
it and to treat it?
SPEAKER_00 (01:04):
Exactly.
We want you to walk away fromthis understanding the invisible
forces at play inside your owncirculatory system.
SPEAKER_02 (01:11):
Okay, so to start at the very beginning, let's just
define the term.
Atherosclerosis is fundamentallythis chronic, slow process of
plaque building up inside thewalls of your artery.
SPEAKER_00 (01:24):
Your body's plumbing.
SPEAKER_02 (01:25):
Your body's plumbing, yeah.
The critical pipes carryingoxygen-rich blood everywhere it
needs to go.
Plaque is the gunk that buildsup on the inside of those pipes
day after day, year after year.
SPEAKER_00 (01:35):
And when we say plaque, this isn't just some
kind of you know generic sludge.
What are the main ingredients inthis highly dangerous cocktail?
SPEAKER_02 (01:43):
Well, the primary ingredient is cholesterol,
specifically the kind that comesfrom low density lipoproteins,
the dreaded LDL cholesterol.
SPEAKER_00 (01:50):
The bad one.
SPEAKER_02 (01:50):
The bad one.
But it's not just fat.
These claques are actuallycomplex mixtures.
They include smooth musclecells, fibrous tissue, and often
calcium.
It gets hard and sticky.
SPEAKER_00 (02:00):
And it narrows the artery.
SPEAKER_02 (02:02):
It narrows the artery, choking off blood supply
to essential organs.
We're talking the heart, thebrain, even your digestive
system.
SPEAKER_00 (02:08):
Aaron Powell Okay, so that narrowing, that sort of
chronic starvation of tissue,that's bad enough.
It causes long-term issues.
But that's usually not thesudden catastrophic event,
right?
SPEAKER_02 (02:19):
No, not at all.
The narrowing is the slow-movingchronic phase.
The real risk is the acutecrisis.
SPEAKER_00 (02:27):
And this work gets, I think, really interesting.
The source material makes it soclear that this plaque, it's not
just sitting there.
It's not a static obstruction.
SPEAKER_02 (02:35):
It's a ticking volatile time bomb.
That is the crucial insight.
SPEAKER_00 (02:39):
So what's the trigger?
SPEAKER_02 (02:40):
The most dangerous step in the whole process is
when that fatty fibrous plaqueruptures or cracks.
Think of it like breaking open avolval capsule inside the artery
wall.
SPEAKER_00 (02:50):
And the body's response.
SPEAKER_02 (02:51):
The body panics.
It activates its emergencyresponse, the clotting cascade,
right there at the site of thedamage.
SPEAKER_00 (02:56):
Which is designed to stop bleeding.
But in this case, it forms ablood clot, a thrombus, inside
the artery itself.
SPEAKER_02 (03:04):
Precisely.
And while the plaque may haveonly narrowed the pipe by, say,
70%, that thrombus that formscan completely block the
remaining 30% in a matter ofminutes.
SPEAKER_00 (03:15):
Total blockage.
And that means the organsupplied by that artery suddenly
starves for blood and oxygen.
SPEAKER_02 (03:22):
That's it.
That rapid tissue death orsevere injury, whether it's in
the heart causing a heart attackor in the brain causing a
stroke, it's fundamentally thesame mechanism.
SPEAKER_00 (03:31):
It's just about the location of the ruptured plaque.
SPEAKER_02 (03:34):
It's staggering, really.
One underlying pathology canmanifest in such a huge range of
massive health problems.
The sheer scope of diseasescoming from atherosclerosis is
immense.
SPEAKER_00 (03:45):
So let's break down those four primary disease
pathways, the material outlines.
Let's start with the oneeveryone thinks of the heart.
SPEAKER_02 (03:52):
Right.
Coronary artery disease, or CAD.
This is when the arteriesfeeding the heart muscle itself
get narrowed.
At first, it leads to chest painor angina, especially when you
exert yourself.
But if that plaque ruptures andfully blocks one of those
coronary arteries, that's aheart attack.
SPEAKER_00 (04:07):
Okay.
Then we shift dramatically tothe brain.
We hear about different kinds ofstrokes, but atherosclerosis is
the villain behind the mostcommon kind.
SPEAKER_02 (04:18):
It is.
About 75% of strokes inindustrialized countries are
what we call thrombotic strokes.
And again, it's the exact samepattern.
A thrombus forms inside a brainartery that was already damaged
and narrowed by plaque.
SPEAKER_00 (04:31):
Cutting off that vital blood supply.
SPEAKER_02 (04:32):
And that rapid oxygen loss causes the specific
neurological damage that wedefine as a stroke.
SPEAKER_00 (04:38):
What's truly counterintuitive to me is the
link to the digestive system.
Most people just don't thinkabout clogged arteries causing
stomach pain.
SPEAKER_02 (04:46):
It's a huge, often missed piece of the puzzle.
When the arteries that supplyyour intestines narrow, it
creates pain because yourdigestive system needs a massive
surge of blood to process ameal.
SPEAKER_00 (04:57):
So if the flow is restricted.
SPEAKER_02 (04:58):
The symptoms are very particular, a dull or
cramping pain that usuallystarts 15 to 30 minutes after
you finish eating.
SPEAKER_00 (05:05):
And if that blockage is sudden and total?
SPEAKER_02 (05:07):
Then you're looking at a bowel infarction, which is
as severe as it sounds.
The source material calls iteffectively a heart attack, but
in your intestines.
Severe pain, vomiting.
It's a crisis.
SPEAKER_00 (05:19):
Finally, let's go to the legs, the furthest extent of
the circulatory system.
This is where the conditioncauses peripheral artery
disease, or PA.
SPEAKER_02 (05:28):
Right, and PA is often misunderstood.
People just dismiss it asgetting old, but it's severe
atherosclerosis.
It's usually narrowing the majorarteries of the legs, like the
femoral and popocheal arteries.
SPEAKER_00 (05:39):
And the main symptom.
SPEAKER_02 (05:40):
The Hallmark symptom is something called intermittent
claudication.
It's a crampy, painful feelingin your calf or thigh muscles
that starts when you walk orexercise, but, and this is key,
it eases immediately when yourest.
SPEAKER_00 (05:54):
So we have this silent process happening for
decades, and its impact is feltacross every major organ system,
which explains why it's so hardto catch, because it often flies
completely under the radar.
SPEAKER_02 (06:05):
That's right.
This disease can be developingfor years with no noticeable
symptoms at all.
It's only when the blood supplydrops to a critical level that
the body starts sending outdistress signals.
SPEAKER_00 (06:15):
Okay, so let's break down those signals.
What does it actually feel likewhen the heart is screaming for
more oxygen?
SPEAKER_02 (06:20):
For the heart, you know, beyond that classic chest
pain or angina, the body canreact with a whole cluster of
serious symptoms.
We're talking shortness ofbreath, unusual sweating, a
sudden wave of nausea, feelingdizzy or lightheaded, even
palpitations.
SPEAKER_00 (06:35):
Aaron Powell All signs the heart muscle is under
severe duress.
SPEAKER_02 (06:38):
Exactly.
Due to not getting enough blood.
SPEAKER_00 (06:41):
And when the brain is the organ being choked off,
the symptoms becomeneurological.
SPEAKER_02 (06:46):
They do.
You see sudden functionaldeficits, dizziness or
confusion, weakness or evenparalysis that strikes one side
of the body, sudden severenumbness.
SPEAKER_00 (06:54):
Vision problems, too, right?
SPEAKER_02 (06:56):
Yes, visual disturbances, even abrupt loss
of vision, or problems withcoordination difficulty,
walking, staggering, slurredspeech.
SPEAKER_00 (07:03):
And the source material highlights a critical
warning sign that you absolutelycannot ignore, even if it goes
away on its own.
SPEAKER_02 (07:09):
That would be the transient ischemic attack or
TIA.
This is when those exactstroke-like symptoms appear, the
slurred speech, the numbness,but then they disappear
completely within an hour or so.
SPEAKER_00 (07:20):
It's temporary.
The physical damage istemporary, but the event itself
is an enormous warning sign.
It means a clot formed andluckily dissolved, but that
unstable underlying plaque isstill there.
It's a five-alarm fire.
SPEAKER_01 (07:34):
Let's go back to those unusual abdominal
symptoms.
What kind of pain are welistening for?
SPEAKER_00 (07:39):
It's described as dull or cramping, and the timing
is the key.
15 to 30 minutes after eating,usually in the middle of the
abdomen.
If it's severe, acute pain withvomiting or swelling, you have
to think about that suddenblockage, the bowel infarction.
SPEAKER_02 (07:54):
And in the legs, what does it look like when it
goes beyond just cramping whenyou walk?
SPEAKER_00 (07:59):
If the narrowing gets really extreme, the pain
will start happening even atrest, often at night, and you'll
see visible signs of tissuestarvation.
The feet and toes get cold, theskin might look pale or even
bluish, and you often see hairloss on the legs because the
follicles aren't getting enoughcirculation.
SPEAKER_02 (08:15):
Those are all major alarm bells.
SPEAKER_00 (08:17):
Profoundly reduced blood flow.
That gives us a really clearpicture.
But the good news is we havesophisticated ways of detecting
this long before a crisis hits.
So let's pivot to how doctorslook for this and how you can
identify your own personal riskprofile.
SPEAKER_02 (08:33):
It always starts with a thorough medical review.
Doctors were looking for familyhistory.
Did a parent or sibling haveheart disease at a young age, a
history of high cholesterol, andthen of course the lifestyle
factors smoking, diet, exercise.
SPEAKER_00 (08:46):
Aaron Powell And the physical exam itself goes much
deeper than just the standardvitals.
SPEAKER_02 (08:50):
Oh, absolutely.
Beyond blood pressure and heartrate, doctors are manually
checking pulses in your neck,wrists, groin, and feet to
assess the strength of the bloodflow.
But crucially, they use astethoscope to listen for uh
brutes.
SPEAKER_00 (09:04):
Brutes, okay, that's a term we don't hear every day.
What does that sound actuallysignify?
SPEAKER_02 (09:09):
Think back to our plumbing analogy.
Brutes are the rough, whooshingsound of turbulent blood flow.
It's like a hiss.
It's the sound of blood tryingto rush past a serious
obstruction in the artery.
SPEAKER_00 (09:18):
So if a doctor hears that, it's a major red flag.
SPEAKER_02 (09:20):
It's a key clinical sign that plaque is causing
major interference.
They also compare the bloodpressure in your legs to the
pressure in your arms.
SPEAKER_00 (09:28):
And that comparison brings us to a really powerful,
simple diagnostic tool, theankle brachial index or ABI.
SPEAKER_02 (09:36):
The ABI is fantastic.
It's non-invasive and it givesyou a hard number.
It's just the ratio of the bloodpressure at your ankle to the
pressure at your elbow.
In a healthy person, thepressure should be about the
same or even a little higher inthe angle.
SPEAKER_00 (09:49):
So if that ratio is off.
SPEAKER_02 (09:51):
If the pressure in your ankle is significantly
lower than your arm,specifically an ABI of 0.9 or
lower, it's a clear,quantifiable sign of impaired
circulation.
It means the plumbing below thewaist is clogged.
SPEAKER_00 (10:04):
Beyond the physical exam, blood markers give us a
huge snapshot of what's brewingsilently.
What are the key things to trackon our annual blood work?
SPEAKER_02 (10:12):
Well, the standard lipid panel is first total LDL
and HDL cholesterol plustriglycerides.
We also tracked fasting bloodsugar and HBA1C for diabetes
risk, which is a massiveaccelerant for atherosclerosis.
SPEAKER_00 (10:24):
But the source material also highlights a few
more specific tests.
SPEAKER_02 (10:28):
It does.
Things you might want to askyour doctor about, like HSCRP,
which is a marker for generalinflammation in your body, and
another one is LPA orlipoprotein.
It's a particularly sticky,fatty particle that's
independently linked to a higherrisk of heart attack.
SPEAKER_00 (10:45):
Okay, so we have the history, the physical findings,
the blood markers.
If those start to lookconcerning, the next step is to
get a visual confirmation.
SPEAKER_02 (10:53):
That's where imaging comes in.
The calcium score test is a CTscan of the heart that measures
calcium buildup in the coronaryarteries.
Calcium is a definitive sign oflong-term atherosclerosis.
For the brain, a carotidultrasound can look for plaque
in the arteries supplying thehead.
SPEAKER_00 (11:10):
This all brings us to the proactive side.
So what does this mean forcontrolling this condition?
Let's start with prevention,because the material really
stresses that its progressioncan be delayed and even halted.
SPEAKER_02 (11:20):
Prevention starts and ends with lifestyle.
It sounds obvious, but the mostessential step is simple.
Avoid smoking entirely, or ifyou do smoke, you must quit.
Smoking just directly damagesthe arterial lining and
accelerates everything.
SPEAKER_00 (11:34):
And then we move to diet and weight, which seems so
directly linked to theingredients in that arterial
gunk.
SPEAKER_02 (11:40):
It is.
Maintaining a healthy weight isvital, especially avoiding fat
around the waist.
Diet-wise, the focus should beon fruits and vegetables and a
strict avoidance of saturatedand trans fats.
SPEAKER_00 (11:52):
What about cooking oils?
SPEAKER_02 (11:53):
The recommendation is clear.
Stick to monounsaturated oilslike olive oil and
polyunsaturated oils, likesunflower or canola.
And your protein should mostlycome from fish and plant sources
like soy, beans, and legumes.
SPEAKER_00 (12:07):
The source also provides some really actionable
timelines for checkups, which Ifind incredibly useful.
SPEAKER_02 (12:13):
They do.
If you have no existingproblems, get your cholesterol
checked every five yearsstarting at age 20, blood
pressure checked every twoyears.
And if you're overweight or havehigh blood pressure, start
getting fasting blood sugarchecked every few years starting
at age 45.
SPEAKER_00 (12:29):
The goal is to catch the risk factors while there's
still just risk factors.
SPEAKER_02 (12:33):
Before they become advanced plaque.
SPEAKER_00 (12:34):
Exactly.
If lifestyle isn't quite enough,that's when medicine comes in.
And treatment, the materialconfirms, can effectively slow
or halt the worsening of thedisease.
The cornerstone is lowering thatdangerous LDL cholesterol.
SPEAKER_02 (12:48):
And that means statins.
Drugs like a torvostatin orsymvostatin, they're the
workhorses.
Their mechanism is ingenious.
They block the H and G CoAreductase enzyme, which is
basically the control switch forcholesterol production in the
liver.
SPEAKER_00 (13:04):
Aaron Ross Powell So the liver just produces less
cholesterol.
SPEAKER_02 (13:06):
Simple as that.
SPEAKER_00 (13:07):
But what's fascinating is that science has
moved beyond just statins.
We now have treatments thatattack the problem from
completely different angles.
SPEAKER_02 (13:14):
That's what's so promising.
We have non-statin drugs withvaried mechanisms.
For example, isidema works inyour gut.
It blocks cholesterol absorptionfrom food.
Then there's bempadoic acid,which tells the liver to make
less cholesterol, but through adifferent pathway than statins.
SPEAKER_00 (13:28):
And finally, the most advanced class.
The PCS-Canine inhibitors.
SPEAKER_02 (13:32):
Yes, the PCS-Canine inhibitors.
These are revolutionary.
They dramatically increase thenumber of LDL receptors on the
surface of your liver cells.
Think of those receptors aslittle vacuum cleaners.
SPEAKER_00 (13:42):
More vacuums, more cleaning.
SPEAKER_02 (13:44):
More vacuums means the liver can grab that
circulating bad cholesterol outof the bloodstream much, much
faster.
It's incredibly effective.
SPEAKER_00 (13:51):
Beyond cholesterol, we also have to think about the
risk of the clod, that acutetrigger.
SPEAKER_02 (13:56):
Right, which brings in anti-clotting medications
like aspirin and otherantiplatelet drugs.
These reduce the likelihood of athrombus forming, but there's a
vital warning here.
Because they inhibit clotting,they increase the risk of
bleeding.
So that requires a very carefulmedical assessment.
SPEAKER_00 (14:13):
And finally, for the most severe cases where an organ
is already compromised, we havethe physical interventions.
SPEAKER_02 (14:19):
These are procedures to immediately restore blood
flow.
For the heart, we haveangioplasty, often with a stent
to keep the artery open, orbypass surgery.
The same techniques are used forblocked abdominal or leg
arteries.
SPEAKER_00 (14:32):
And for the brain.
SPEAKER_02 (14:33):
If the critical carotid arteries are dangerously
narrowed, a procedure can bedone to physically clear or open
that artery to prevent a stroke.
SPEAKER_00 (14:40):
That really brings together the entire life cycle
of this condition, from themolecules to the high-tech
solutions.
SPEAKER_02 (14:46):
The key takeaway is that while there is no cure, the
prognosis is better than ever.
People are living significantlylonger with better quality of
life because we can delay thebeginning and worsening of the
disease, even for those with astrong genetic predisposition.
SPEAKER_00 (15:01):
So, what does this all mean for you?
The disease operates silentlyfor years, but when those
distress signals finally appear,that crampy leg pain, chest
discomfort, sudden vision loss,you have to act.
SPEAKER_02 (15:14):
The instruction is immediate.
If you experience thesesymptoms, contact a doctor
immediately.
Waiting even a few hours whensymptoms are acute is what turns
a manageable chronic probleminto a life-threatening crisis.
SPEAKER_00 (15:26):
And this leads us to a final thought for you to
consider, pulled directly fromthe recent research accompanying
our source material.
The dramatic rise inatherosclerosis over the last
century perfectly aligns with adramatic shift in our global
diet.
SPEAKER_02 (15:38):
Specifically ultra processed foods.
SPEAKER_00 (15:40):
Exactly.
And given that these foods haverecently been linked directly to
claque buildup in neck arteries,what does that imply for the
future prevalence of thischronic disease in rapidly
industrializing nations that arejust now enthusiastically
adopting this same Westerndietary model?
SPEAKER_02 (15:57):
Something to chew on.
You know, if you're looking for the uh the single
biggest driver of modernmortality, the one chronic
condition that quietly defineshow long and how well we live
well, you've found it.
SPEAKER_02 (00:11):
It really is.
It's the root of the problem forso many things that seem
disconnected.
We're talking heart attacks,strokes.
SPEAKER_00 (00:16):
And today we are diving deep into that root,
atherosclerosis.
The silent, simmering diseasethat is, without a doubt, the
number one cause of death anddisability across the
industrialized world.
SPEAKER_02 (00:28):
It's a systemic issue and understanding the um
the core mechanics of how itstarts is really the first step
toward managing your own healthlong term.
SPEAKER_00 (00:37):
Absolutely.
And to guide us through this,we've got some truly
authoritative sources today,straight from Harvard Health.
The materials reviewed by Dr.
Christopher P.
Cannon, who's theeditor-in-chief of the Harvard
Heart Letter.
SPEAKER_02 (00:47):
So we're getting the definitive roadmap here.
SPEAKER_00 (00:49):
We are.
Okay, so let's unpack this.
Our mission is to strip away thecomplex jargon and really
understand the story ofatherosclerosis.
What is it exactly?
Why does it strike in so manydifferent parts of the body?
SPEAKER_02 (01:00):
And what new tools do we have right now to prevent
it and to treat it?
SPEAKER_00 (01:04):
Exactly.
We want you to walk away fromthis understanding the invisible
forces at play inside your owncirculatory system.
SPEAKER_02 (01:11):
Okay, so to start at the very beginning, let's just
define the term.
Atherosclerosis is fundamentallythis chronic, slow process of
plaque building up inside thewalls of your artery.
SPEAKER_00 (01:24):
Your body's plumbing.
SPEAKER_02 (01:25):
Your body's plumbing, yeah.
The critical pipes carryingoxygen-rich blood everywhere it
needs to go.
Plaque is the gunk that buildsup on the inside of those pipes
day after day, year after year.
SPEAKER_00 (01:35):
And when we say plaque, this isn't just some
kind of you know generic sludge.
What are the main ingredients inthis highly dangerous cocktail?
SPEAKER_02 (01:43):
Well, the primary ingredient is cholesterol,
specifically the kind that comesfrom low density lipoproteins,
the dreaded LDL cholesterol.
SPEAKER_00 (01:50):
The bad one.
SPEAKER_02 (01:50):
The bad one.
But it's not just fat.
These claques are actuallycomplex mixtures.
They include smooth musclecells, fibrous tissue, and often
calcium.
It gets hard and sticky.
SPEAKER_00 (02:00):
And it narrows the artery.
SPEAKER_02 (02:02):
It narrows the artery, choking off blood supply
to essential organs.
We're talking the heart, thebrain, even your digestive
system.
SPEAKER_00 (02:08):
Aaron Powell Okay, so that narrowing, that sort of
chronic starvation of tissue,that's bad enough.
It causes long-term issues.
But that's usually not thesudden catastrophic event,
right?
SPEAKER_02 (02:19):
No, not at all.
The narrowing is the slow-movingchronic phase.
The real risk is the acutecrisis.
SPEAKER_00 (02:27):
And this work gets, I think, really interesting.
The source material makes it soclear that this plaque, it's not
just sitting there.
It's not a static obstruction.
SPEAKER_02 (02:35):
It's a ticking volatile time bomb.
That is the crucial insight.
SPEAKER_00 (02:39):
So what's the trigger?
SPEAKER_02 (02:40):
The most dangerous step in the whole process is
when that fatty fibrous plaqueruptures or cracks.
Think of it like breaking open avolval capsule inside the artery
wall.
SPEAKER_00 (02:50):
And the body's response.
SPEAKER_02 (02:51):
The body panics.
It activates its emergencyresponse, the clotting cascade,
right there at the site of thedamage.
SPEAKER_00 (02:56):
Which is designed to stop bleeding.
But in this case, it forms ablood clot, a thrombus, inside
the artery itself.
SPEAKER_02 (03:04):
Precisely.
And while the plaque may haveonly narrowed the pipe by, say,
70%, that thrombus that formscan completely block the
remaining 30% in a matter ofminutes.
SPEAKER_00 (03:15):
Total blockage.
And that means the organsupplied by that artery suddenly
starves for blood and oxygen.
SPEAKER_02 (03:22):
That's it.
That rapid tissue death orsevere injury, whether it's in
the heart causing a heart attackor in the brain causing a
stroke, it's fundamentally thesame mechanism.
SPEAKER_00 (03:31):
It's just about the location of the ruptured plaque.
SPEAKER_02 (03:34):
It's staggering, really.
One underlying pathology canmanifest in such a huge range of
massive health problems.
The sheer scope of diseasescoming from atherosclerosis is
immense.
SPEAKER_00 (03:45):
So let's break down those four primary disease
pathways, the material outlines.
Let's start with the oneeveryone thinks of the heart.
SPEAKER_02 (03:52):
Right.
Coronary artery disease, or CAD.
This is when the arteriesfeeding the heart muscle itself
get narrowed.
At first, it leads to chest painor angina, especially when you
exert yourself.
But if that plaque ruptures andfully blocks one of those
coronary arteries, that's aheart attack.
SPEAKER_00 (04:07):
Okay.
Then we shift dramatically tothe brain.
We hear about different kinds ofstrokes, but atherosclerosis is
the villain behind the mostcommon kind.
SPEAKER_02 (04:18):
It is.
About 75% of strokes inindustrialized countries are
what we call thrombotic strokes.
And again, it's the exact samepattern.
A thrombus forms inside a brainartery that was already damaged
and narrowed by plaque.
SPEAKER_00 (04:31):
Cutting off that vital blood supply.
SPEAKER_02 (04:32):
And that rapid oxygen loss causes the specific
neurological damage that wedefine as a stroke.
SPEAKER_00 (04:38):
What's truly counterintuitive to me is the
link to the digestive system.
Most people just don't thinkabout clogged arteries causing
stomach pain.
SPEAKER_02 (04:46):
It's a huge, often missed piece of the puzzle.
When the arteries that supplyyour intestines narrow, it
creates pain because yourdigestive system needs a massive
surge of blood to process ameal.
SPEAKER_00 (04:57):
So if the flow is restricted.
SPEAKER_02 (04:58):
The symptoms are very particular, a dull or
cramping pain that usuallystarts 15 to 30 minutes after
you finish eating.
SPEAKER_00 (05:05):
And if that blockage is sudden and total?
SPEAKER_02 (05:07):
Then you're looking at a bowel infarction, which is
as severe as it sounds.
The source material calls iteffectively a heart attack, but
in your intestines.
Severe pain, vomiting.
It's a crisis.
SPEAKER_00 (05:19):
Finally, let's go to the legs, the furthest extent of
the circulatory system.
This is where the conditioncauses peripheral artery
disease, or PA.
SPEAKER_02 (05:28):
Right, and PA is often misunderstood.
People just dismiss it asgetting old, but it's severe
atherosclerosis.
It's usually narrowing the majorarteries of the legs, like the
femoral and popocheal arteries.
SPEAKER_00 (05:39):
And the main symptom.
SPEAKER_02 (05:40):
The Hallmark symptom is something called intermittent
claudication.
It's a crampy, painful feelingin your calf or thigh muscles
that starts when you walk orexercise, but, and this is key,
it eases immediately when yourest.
SPEAKER_00 (05:54):
So we have this silent process happening for
decades, and its impact is feltacross every major organ system,
which explains why it's so hardto catch, because it often flies
completely under the radar.
SPEAKER_02 (06:05):
That's right.
This disease can be developingfor years with no noticeable
symptoms at all.
It's only when the blood supplydrops to a critical level that
the body starts sending outdistress signals.
SPEAKER_00 (06:15):
Okay, so let's break down those signals.
What does it actually feel likewhen the heart is screaming for
more oxygen?
SPEAKER_02 (06:20):
For the heart, you know, beyond that classic chest
pain or angina, the body canreact with a whole cluster of
serious symptoms.
We're talking shortness ofbreath, unusual sweating, a
sudden wave of nausea, feelingdizzy or lightheaded, even
palpitations.
SPEAKER_00 (06:35):
Aaron Powell All signs the heart muscle is under
severe duress.
SPEAKER_02 (06:38):
Exactly.
Due to not getting enough blood.
SPEAKER_00 (06:41):
And when the brain is the organ being choked off,
the symptoms becomeneurological.
SPEAKER_02 (06:46):
They do.
You see sudden functionaldeficits, dizziness or
confusion, weakness or evenparalysis that strikes one side
of the body, sudden severenumbness.
SPEAKER_00 (06:54):
Vision problems, too, right?
SPEAKER_02 (06:56):
Yes, visual disturbances, even abrupt loss
of vision, or problems withcoordination difficulty,
walking, staggering, slurredspeech.
SPEAKER_00 (07:03):
And the source material highlights a critical
warning sign that you absolutelycannot ignore, even if it goes
away on its own.
SPEAKER_02 (07:09):
That would be the transient ischemic attack or
TIA.
This is when those exactstroke-like symptoms appear, the
slurred speech, the numbness,but then they disappear
completely within an hour or so.
SPEAKER_00 (07:20):
It's temporary.
The physical damage istemporary, but the event itself
is an enormous warning sign.
It means a clot formed andluckily dissolved, but that
unstable underlying plaque isstill there.
It's a five-alarm fire.
SPEAKER_01 (07:34):
Let's go back to those unusual abdominal
symptoms.
What kind of pain are welistening for?
SPEAKER_00 (07:39):
It's described as dull or cramping, and the timing
is the key.
15 to 30 minutes after eating,usually in the middle of the
abdomen.
If it's severe, acute pain withvomiting or swelling, you have
to think about that suddenblockage, the bowel infarction.
SPEAKER_02 (07:54):
And in the legs, what does it look like when it
goes beyond just cramping whenyou walk?
SPEAKER_00 (07:59):
If the narrowing gets really extreme, the pain
will start happening even atrest, often at night, and you'll
see visible signs of tissuestarvation.
The feet and toes get cold, theskin might look pale or even
bluish, and you often see hairloss on the legs because the
follicles aren't getting enoughcirculation.
SPEAKER_02 (08:15):
Those are all major alarm bells.
SPEAKER_00 (08:17):
Profoundly reduced blood flow.
That gives us a really clearpicture.
But the good news is we havesophisticated ways of detecting
this long before a crisis hits.
So let's pivot to how doctorslook for this and how you can
identify your own personal riskprofile.
SPEAKER_02 (08:33):
It always starts with a thorough medical review.
Doctors were looking for familyhistory.
Did a parent or sibling haveheart disease at a young age, a
history of high cholesterol, andthen of course the lifestyle
factors smoking, diet, exercise.
SPEAKER_00 (08:46):
Aaron Powell And the physical exam itself goes much
deeper than just the standardvitals.
SPEAKER_02 (08:50):
Oh, absolutely.
Beyond blood pressure and heartrate, doctors are manually
checking pulses in your neck,wrists, groin, and feet to
assess the strength of the bloodflow.
But crucially, they use astethoscope to listen for uh
brutes.
SPEAKER_00 (09:04):
Brutes, okay, that's a term we don't hear every day.
What does that sound actuallysignify?
SPEAKER_02 (09:09):
Think back to our plumbing analogy.
Brutes are the rough, whooshingsound of turbulent blood flow.
It's like a hiss.
It's the sound of blood tryingto rush past a serious
obstruction in the artery.
SPEAKER_00 (09:18):
So if a doctor hears that, it's a major red flag.
SPEAKER_02 (09:20):
It's a key clinical sign that plaque is causing
major interference.
They also compare the bloodpressure in your legs to the
pressure in your arms.
SPEAKER_00 (09:28):
And that comparison brings us to a really powerful,
simple diagnostic tool, theankle brachial index or ABI.
SPEAKER_02 (09:36):
The ABI is fantastic.
It's non-invasive and it givesyou a hard number.
It's just the ratio of the bloodpressure at your ankle to the
pressure at your elbow.
In a healthy person, thepressure should be about the
same or even a little higher inthe angle.
SPEAKER_00 (09:49):
So if that ratio is off.
SPEAKER_02 (09:51):
If the pressure in your ankle is significantly
lower than your arm,specifically an ABI of 0.9 or
lower, it's a clear,quantifiable sign of impaired
circulation.
It means the plumbing below thewaist is clogged.
SPEAKER_00 (10:04):
Beyond the physical exam, blood markers give us a
huge snapshot of what's brewingsilently.
What are the key things to trackon our annual blood work?
SPEAKER_02 (10:12):
Well, the standard lipid panel is first total LDL
and HDL cholesterol plustriglycerides.
We also tracked fasting bloodsugar and HBA1C for diabetes
risk, which is a massiveaccelerant for atherosclerosis.
SPEAKER_00 (10:24):
But the source material also highlights a few
more specific tests.
SPEAKER_02 (10:28):
It does.
Things you might want to askyour doctor about, like HSCRP,
which is a marker for generalinflammation in your body, and
another one is LPA orlipoprotein.
It's a particularly sticky,fatty particle that's
independently linked to a higherrisk of heart attack.
SPEAKER_00 (10:45):
Okay, so we have the history, the physical findings,
the blood markers.
If those start to lookconcerning, the next step is to
get a visual confirmation.
SPEAKER_02 (10:53):
That's where imaging comes in.
The calcium score test is a CTscan of the heart that measures
calcium buildup in the coronaryarteries.
Calcium is a definitive sign oflong-term atherosclerosis.
For the brain, a carotidultrasound can look for plaque
in the arteries supplying thehead.
SPEAKER_00 (11:10):
This all brings us to the proactive side.
So what does this mean forcontrolling this condition?
Let's start with prevention,because the material really
stresses that its progressioncan be delayed and even halted.
SPEAKER_02 (11:20):
Prevention starts and ends with lifestyle.
It sounds obvious, but the mostessential step is simple.
Avoid smoking entirely, or ifyou do smoke, you must quit.
Smoking just directly damagesthe arterial lining and
accelerates everything.
SPEAKER_00 (11:34):
And then we move to diet and weight, which seems so
directly linked to theingredients in that arterial
gunk.
SPEAKER_02 (11:40):
It is.
Maintaining a healthy weight isvital, especially avoiding fat
around the waist.
Diet-wise, the focus should beon fruits and vegetables and a
strict avoidance of saturatedand trans fats.
SPEAKER_00 (11:52):
What about cooking oils?
SPEAKER_02 (11:53):
The recommendation is clear.
Stick to monounsaturated oilslike olive oil and
polyunsaturated oils, likesunflower or canola.
And your protein should mostlycome from fish and plant sources
like soy, beans, and legumes.
SPEAKER_00 (12:07):
The source also provides some really actionable
timelines for checkups, which Ifind incredibly useful.
SPEAKER_02 (12:13):
They do.
If you have no existingproblems, get your cholesterol
checked every five yearsstarting at age 20, blood
pressure checked every twoyears.
And if you're overweight or havehigh blood pressure, start
getting fasting blood sugarchecked every few years starting
at age 45.
SPEAKER_00 (12:29):
The goal is to catch the risk factors while there's
still just risk factors.
SPEAKER_02 (12:33):
Before they become advanced plaque.
SPEAKER_00 (12:34):
Exactly.
If lifestyle isn't quite enough,that's when medicine comes in.
And treatment, the materialconfirms, can effectively slow
or halt the worsening of thedisease.
The cornerstone is lowering thatdangerous LDL cholesterol.
SPEAKER_02 (12:48):
And that means statins.
Drugs like a torvostatin orsymvostatin, they're the
workhorses.
Their mechanism is ingenious.
They block the H and G CoAreductase enzyme, which is
basically the control switch forcholesterol production in the
liver.
SPEAKER_00 (13:04):
Aaron Ross Powell So the liver just produces less
cholesterol.
SPEAKER_02 (13:06):
Simple as that.
SPEAKER_00 (13:07):
But what's fascinating is that science has
moved beyond just statins.
We now have treatments thatattack the problem from
completely different angles.
SPEAKER_02 (13:14):
That's what's so promising.
We have non-statin drugs withvaried mechanisms.
For example, isidema works inyour gut.
It blocks cholesterol absorptionfrom food.
Then there's bempadoic acid,which tells the liver to make
less cholesterol, but through adifferent pathway than statins.
SPEAKER_00 (13:28):
And finally, the most advanced class.
The PCS-Canine inhibitors.
SPEAKER_02 (13:32):
Yes, the PCS-Canine inhibitors.
These are revolutionary.
They dramatically increase thenumber of LDL receptors on the
surface of your liver cells.
Think of those receptors aslittle vacuum cleaners.
SPEAKER_00 (13:42):
More vacuums, more cleaning.
SPEAKER_02 (13:44):
More vacuums means the liver can grab that
circulating bad cholesterol outof the bloodstream much, much
faster.
It's incredibly effective.
SPEAKER_00 (13:51):
Beyond cholesterol, we also have to think about the
risk of the clod, that acutetrigger.
SPEAKER_02 (13:56):
Right, which brings in anti-clotting medications
like aspirin and otherantiplatelet drugs.
These reduce the likelihood of athrombus forming, but there's a
vital warning here.
Because they inhibit clotting,they increase the risk of
bleeding.
So that requires a very carefulmedical assessment.
SPEAKER_00 (14:13):
And finally, for the most severe cases where an organ
is already compromised, we havethe physical interventions.
SPEAKER_02 (14:19):
These are procedures to immediately restore blood
flow.
For the heart, we haveangioplasty, often with a stent
to keep the artery open, orbypass surgery.
The same techniques are used forblocked abdominal or leg
arteries.
SPEAKER_00 (14:32):
And for the brain.
SPEAKER_02 (14:33):
If the critical carotid arteries are dangerously
narrowed, a procedure can bedone to physically clear or open
that artery to prevent a stroke.
SPEAKER_00 (14:40):
That really brings together the entire life cycle
of this condition, from themolecules to the high-tech
solutions.
SPEAKER_02 (14:46):
The key takeaway is that while there is no cure, the
prognosis is better than ever.
People are living significantlylonger with better quality of
life because we can delay thebeginning and worsening of the
disease, even for those with astrong genetic predisposition.
SPEAKER_00 (15:01):
So, what does this all mean for you?
The disease operates silentlyfor years, but when those
distress signals finally appear,that crampy leg pain, chest
discomfort, sudden vision loss,you have to act.
SPEAKER_02 (15:14):
The instruction is immediate.
If you experience thesesymptoms, contact a doctor
immediately.
Waiting even a few hours whensymptoms are acute is what turns
a manageable chronic probleminto a life-threatening crisis.
SPEAKER_00 (15:26):
And this leads us to a final thought for you to
consider, pulled directly fromthe recent research accompanying
our source material.
The dramatic rise inatherosclerosis over the last
century perfectly aligns with adramatic shift in our global
diet.
SPEAKER_02 (15:38):
Specifically ultra processed foods.
SPEAKER_00 (15:40):
Exactly.
And given that these foods haverecently been linked directly to
claque buildup in neck arteries,what does that imply for the
future prevalence of thischronic disease in rapidly
industrializing nations that arejust now enthusiastically
adopting this same Westerndietary model?
SPEAKER_02 (15:57):
Something to chew on.
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