September 29, 2025 • 15 mins
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
SPEAKER_01 (00:00):
Inflammation, which is really how our body fights
infection, how our body dealswith foreign objects, things
that aren't supposed to bethere, and how you mount a
response to that is reallyimportant for ultimate survival.
So I'm gonna try to avoidgetting jargony on you here, but
(00:21):
we take back about 30,000 years.
Imagine you're living in a cavesomewhere, um, and you just want
to survive.
I still live in a man cave, bythe way.
Yes, I can tell.
But 30,000 years ago, childhoodinfection would kill the vast
majority of people who wereborn.
(00:42):
Measles, malaria, mumps,schistosomiasis, you name it.
You need a pretty good innateimmune system to survive that.
The second thing that killed alot of our forebearers was um a
saber-toothed tiger, if youlike.
You had to have a coagulationsystem that would survive
bleeding.
Very important for women whoused to die so commonly in
(01:03):
childbirth because ofhemorrhage.
And the third piece that peoplemay not think about is in a
pre-agriculture universe, uh,starvation.
So starvation would kill a lotof people.
And what do those three thingshave in common?
Well, it's a insulin resistant,that's how you get by the
starvation, pro-coagulant,that's how you get past the
saber-tooth tiger.
(01:25):
Uh, and pro-inflammatory, that'show you get past these
infections.
So our immune system is designedto help us survive these
challenges of life when humansbegan.
But you know, I live in Boston.
Uh we don't have a lot ofsaber-tooth tigers.
Uh women now survive childbirthbecause we have fantastic
(01:47):
medical care.
Uh, and childhood infections arelargely dealt with with uh
immunizations and vaccines.
But that survival benefit ofhaving this activated immune
system in midlife becomes ahindrance.
From a strictly evolutionarybiology perspective, all we're
really supposed to do is livelong enough to reproduce, have
(02:10):
kids, get our children launched,and then, as I laughingly
sometimes say, everything elseis extra genetic debris.
But it's it's it's debris we allwant in midlife and later.
So the question is, how do wedampen down this inflammation
that was so useful to surviveearly life that's coming back to
haunt us in later life?
(02:32):
And the reality, Mike, is thatalmost all the diseases of
chronic aging, and in particularas cardiologists, we focus on
heart attack and stroke, butit's equally true of cancer and
other things, they all turn outto be driven, at least in part,
by this chronic inflammatoryresponse.
We had recently shown that thesestatin drugs, not only do they
(02:53):
lower cholesterol, they alsolower a biomarker of
inflammation.
This is a mouthful.
It's called high sensitivity Creactive protein or HSCRP.
That's gonna be importantbecause that's the thing that we
actually measure in clinic tosay, aha, my patient has a
little bit of inflammation, amoderate amount of inflammation,
a lot of inflammation.
So that HSCRP test, we're gonnacome back to it, I'm sure, is
(03:16):
gonna be quite important.
But the point is we had shownthat statin drugs actually lower
this inflammatory marker, theHSCRP.
And we had tantalizing evidencethat maybe people with a high
CRP would benefit from being ona statin, even if their
cholesterol levels were low whenthey didn't even qualify for a
statin.
Anyway, fast forward, wepublished these data in 2008.
(03:39):
It's a nearly 18,000 patientmultinational global trial,
critically of people who wereprimary prevention, so no prior
heart attack or stroke, healthymen and women, middle-aged
folks, who would never qualifyto be on a statin because their
cholesterol levels were actuallypretty low.
But they all were selectedbecause they had this marker of
(04:01):
inflammation, they all had anelevated HSCRP, a level greater
than two, uh, to qualify for thetrial.
And what's so remarkable is thatin this study where nobody would
have gotten a statin, becauseagain, the whole idea from the
guidelines was to lower thecholesterol uh and only given a
high cholesterol, uh, in thisgroup of people with high
(04:22):
inflammation and lowcholesterol, we had a 44%
reduction in heart attacks andstrokes, a 63% reduction in
heart attacks itself, and quiteremarkably a 20% drop in
all-cause mortality.
Right.
It's crazy.
And it was really a realrevelation.
SPEAKER_00 (04:40):
Yeah.
So again, to kind of fastforward again, between the years
of say 1980 and 2010,cardiologists were making huge
strides in reducingcardiovascular morbidity
mortality.
And that curve has flattened.
In fact, maybe hasn't changed atall in the last 10 years, which
is of great concern.
(05:00):
So it leads to the idea thatmaybe we should be looking at
other things.
And this gets into some researchthat you and I are working on
together as we speak.
SPEAKER_01 (05:09):
Well, that's right.
So uh we learned during COVIDthat sometimes rates can
actually go up.
And that was a little scary.
Uh but I think you're right,Mike.
The the constant decline of thelast 35, 40 years has really
flattened out, telling us we nowneed to focus on some of these
newer biologies.
So, what's been a lot of fun,and again, working with you has
been great.
Um, we're trying to figure outcan we target this inflammation
(05:33):
directly?
I must be a little carefulthere.
That Jupiter trial we talkedabout was giving a statin.
It's a drug that lowerscholesterol and has
anti-inflammatory properties.
Could we give a pureanti-inflammatory drug to lower
risk?
We actually did a clinical trialuh called Cantose, which used a
very specific kind ofinflammation inhibitor, and it
(05:56):
really worked really well.
But that drug's not available,unfortunately, for our patients
for some complicated reasonsthat actually had to do with
cancer prevention.
SPEAKER_00 (06:04):
So that's a molecule called canicinemab.
Is that still used for certainpediatric arthritic conditions?
I know it's briefly on themarket for that.
SPEAKER_01 (06:13):
Well, it's still on the market for that.
So kinikiniumab, which isanother mouthful, uh, these are
drugs that are called monoclonalantibodies.
Um, they target a very specificpiece of this inflammation
pathway.
And we showed it could lower therisk of a heart attack or stroke
by about 15 or 20 percent, whichis great.
But uh the drug also has somegreat benefits in cancer.
(06:35):
So it's being repurposed intothe oncology community.
Um, and so we need to findanother way of targeting this.
SPEAKER_00 (06:42):
Sorry for that aside.
Uh just for our audience, one ofthe little tricks of the trade
is if you hear a molecule or achemical that ends with MAB,
it's a monoclonal antibody.
So you can surprise your friendsuh at a dinner conversation that
you know the nature of theirparticular medicine.
So sorry, sorry about that.
SPEAKER_01 (07:00):
No, that's a that's that's a great pearl even for
those of us who live in thisworld uh on a daily basis.
Um so the question was (07:06):
could we find another one of these MABs
uh that hits a different part ofthis particular immune system?
Um and actually anothermouthful, that drug turns out to
be called Ziltaveca Mab.
It starts with a Z.
Um and we designed a series ofclinical trials which are
ongoing right now using thisparticular kind of inflammation
(07:29):
inhibitor, which, by the way, isalready commonly used.
It's in a class of drugs thatare commonly used to treat
rheumatoid arthritis.
Uh, some patients take it totreat inflammatory bowel disease
like Crohn's disease orulceritis.
So the class of drugs has beenaround for 20, 25 years.
We know it's pretty safe, butit's been used to treat
(07:50):
classical autoimmuneanti-inflammatory disorders.
The trick is, can we use it toactually improve outcomes for
patients with heart disease?
We're going to focus a bit onHermes, which is, again, it's a
heart failure trial.
That's a particular kind ofheart failure.
It's something that we call,cardiologists call HEF-PEF,
(08:11):
which is heart failure withpreserved ejection fraction.
What's that really mean?
That means that uh your heart'spumping and it looks pretty good
on a standard echocardiogram,but it doesn't work really all
that well.
And you get the symptoms ofheart failure, shortness of
breath, a feeling of congestion,a feeling of not being able to
(08:34):
walk as far as you used to beable to, even though the heart
seems to pump okay, but theheart's actually too stiff.
I think that's the easiest wayto understand what this is.
When we talk about inflammation,we're not talking about a
sprained ankle.
We're not talking about drugslike Advil or ibuprofen or even
aspirin.
We're talking about the kind ofinflammation that classically
(08:58):
would lead to things likerheumatoid arthritis or um
inflammatory bowel disease orpsoriasis, more severe disorders
that go under the rubric ofauto-inflammatory or um uh, you
know, things like that.
And there's certain specificpathways of this immune system
(09:19):
that impact on some of thesedisorders more than others.
And we're going to get veryjargony very fast, but I think
actually it makes sense.
There's one particular pathwaythat all of us have.
Understand, everybody has thisbecause I said at the beginning,
you need these things to survivechildhood and get into early
adulthood, but it kind of comesback to haunt us later in life.
(09:42):
One of these pathwaysupregulates a certain cytokine.
Now, a cytokine is a chemicalmolecule that tells cell A to
talk to cell B.
It's a communication system.
That's all it is.
It says, hello out there, thiscell is doing this, you better
do that.
I see something over therethat's not good.
Let's go attack that.
That's right.
SPEAKER_00 (10:01):
Yeah, kine means means to move.
So cytokine means move cells.
It's a chemical that moves cellsin one direction or another.
That's exactly right.
SPEAKER_01 (10:09):
It's just telling them move over here because
there's something over there wegot to deal with.
It's just an infection, it's abug, it's a virus, whatever.
One of these cytokines has aname, interleukin 1.
It's the first one that was everdiscovered.
It's at the top of the chain.
The drug you mentioned before,kennakinumab, remember that MAB,
that blocks the function ofinterleukin 1.
(10:33):
Actually, it's even moretechnical than that.
It blocks the function ofinterleukin 1 beta, but let's
skip over that.
Um, and that turns out to lowerthe risk of heart attack and
stroke without changingcholesterol.
In fact, that's the proof ofprinciple that this whole thing
actually works, came out of thatcannokidomab trial.
Now, the study with Hermes, aswell as the Zeus study and the
(10:55):
Artemis study, remember that'sthe chronic kidney disease
study, the heart failure study,and the acute cornea ischemia
studies.
They're all using this drug,another MAB, Ziltefeca MAB.
It targets a downstreamcytokine.
So again, a cell-moving moleculecalled intraleucin 6.
(11:16):
Intraleukin 6 is the centralcytokine.
It's it's it's the biggestplayer.
It's the one that we think ismost involved in this process.
And what's really interesting isthere's several drugs on the
market that block IL-6 thatalready work for several of
those more serious inflammatorydiseases that patients actually
(11:36):
know they have because they havesymptoms.
The question being asked,particularly in the Hermes
study, the heart failure studywe're talking about, is can we
use this inter-leucin 6 blockerto improve the outcomes in heart
failure patients where theydon't feel their inflammation?
Mike, I think that's probablythe most important thing we're
talking about today.
This is silent inflammation.
(11:59):
If a patient hasrheumatoarthritis, their hands
and joints hurt.
If they have lupus, their skinhurts.
If they have psoriasis, theyhave issues, they know about.
The inflammation we're talkingabout for all of these heart
disease conditions, it's silent.
You don't know what's there.
And that's why running thisblood test, the high sensitivity
C-reactive protein, the HSCRP isso important because this is
(12:22):
just like cholesterol.
I can't feel my cholesterol.
I can't really feel my bloodpressure either.
I need my physician to measuremy blood pressure, to measure my
cholesterol, to measure myinflammation, my HSCRP.
So I now have information aboutthe silent things that might
well be big problems for me.
And it's that silentinflammation we're trying to
(12:44):
reduce to see if we can benefitour patients.
SPEAKER_00 (12:46):
Yeah, that's an incredibly helpful description.
Thank you for that.
I'm going to ask you one morequestion that is sometimes a
source of controversy andconfusion about HSCRP, which
historically was something thatwas originally discovered
related to streptococcalinfections, particularly
pneumococcal pneumonia.
(13:07):
And what happens and whatconfuses people is sometimes
they have extremely high levelsthat are not related to vascular
disease.
And people get very confusedabout this when we talk about,
quote, HSCRP as a risk factor.
You gave a brilliant discussionabout this at a recent meeting.
I think it'd be extremelyhelpful if you can break that
down for folks.
SPEAKER_01 (13:28):
Sure.
So, Mike, your your memory isvery good on this.
Many physicians, unfortunately,only knew about C-reactive
protein uh as something calledan acute phase reactant, which
is again a fancy word for itgoes up when you're sick.
And that has been a problembecause physicians, again, don't
always get as much new educationas they probably should.
(13:50):
And people remember that.
Um we recently published a verybig study.
It was actually 28,000 initiallyhealthy American women that
we've tracked since 1993.
So in 1993, we took a randomblood drop and we measured this
HSCRP.
(14:12):
And 30 years later, that value,that random value, is a stronger
predictor over 30 years of who'sgoing to develop a heart attack,
a stroke, or die from acardiovascular event than was
LDL cholesterol, the thing weall measure all the time.
Now, what's really interesting,Mike, is that when there's a
biomarker like the CRP that intheory has some extra
(14:37):
variability built into it, uhthe epidemiologist would say,
well, variability is what wecall a bias towards the null.
It actually makes it harder tosee a true effect, not easier.
So if CRP is alreadyoutperforming our standard go-to
LDL cholesterol, that meanswe're underestimating the true
(14:59):
impact of inflammation longterm.
Uh, I've said this before, I'llrepeat it here.
Many of your listeners today,their physicians may not
actually know this.
Uh, I've told a lot of people goto the New England Journal of
Medicine website.
It's free, it's on the internet.
You can download this recentmanuscript and take it to your
doctor's office.
(15:20):
They may need to actually readit and think about it.
Because part of the educationfor physicians honestly comes
from family members and caring,you know, people who just want
to do the right thing.
Um, all of us need lifelongeducation.
Inflammation, which is really how our body fights
infection, how our body dealswith foreign objects, things
that aren't supposed to bethere, and how you mount a
response to that is reallyimportant for ultimate survival.
So I'm gonna try to avoidgetting jargony on you here, but
(00:21):
we take back about 30,000 years.
Imagine you're living in a cavesomewhere, um, and you just want
to survive.
I still live in a man cave, bythe way.
Yes, I can tell.
But 30,000 years ago, childhoodinfection would kill the vast
majority of people who wereborn.
(00:42):
Measles, malaria, mumps,schistosomiasis, you name it.
You need a pretty good innateimmune system to survive that.
The second thing that killed alot of our forebearers was um a
saber-toothed tiger, if youlike.
You had to have a coagulationsystem that would survive
bleeding.
Very important for women whoused to die so commonly in
(01:03):
childbirth because ofhemorrhage.
And the third piece that peoplemay not think about is in a
pre-agriculture universe, uh,starvation.
So starvation would kill a lotof people.
And what do those three thingshave in common?
Well, it's a insulin resistant,that's how you get by the
starvation, pro-coagulant,that's how you get past the
saber-tooth tiger.
(01:25):
Uh, and pro-inflammatory, that'show you get past these
infections.
So our immune system is designedto help us survive these
challenges of life when humansbegan.
But you know, I live in Boston.
Uh we don't have a lot ofsaber-tooth tigers.
Uh women now survive childbirthbecause we have fantastic
(01:47):
medical care.
Uh, and childhood infections arelargely dealt with with uh
immunizations and vaccines.
But that survival benefit ofhaving this activated immune
system in midlife becomes ahindrance.
From a strictly evolutionarybiology perspective, all we're
really supposed to do is livelong enough to reproduce, have
(02:10):
kids, get our children launched,and then, as I laughingly
sometimes say, everything elseis extra genetic debris.
But it's it's it's debris we allwant in midlife and later.
So the question is, how do wedampen down this inflammation
that was so useful to surviveearly life that's coming back to
haunt us in later life?
(02:32):
And the reality, Mike, is thatalmost all the diseases of
chronic aging, and in particularas cardiologists, we focus on
heart attack and stroke, butit's equally true of cancer and
other things, they all turn outto be driven, at least in part,
by this chronic inflammatoryresponse.
We had recently shown that thesestatin drugs, not only do they
(02:53):
lower cholesterol, they alsolower a biomarker of
inflammation.
This is a mouthful.
It's called high sensitivity Creactive protein or HSCRP.
That's gonna be importantbecause that's the thing that we
actually measure in clinic tosay, aha, my patient has a
little bit of inflammation, amoderate amount of inflammation,
a lot of inflammation.
So that HSCRP test, we're gonnacome back to it, I'm sure, is
(03:16):
gonna be quite important.
But the point is we had shownthat statin drugs actually lower
this inflammatory marker, theHSCRP.
And we had tantalizing evidencethat maybe people with a high
CRP would benefit from being ona statin, even if their
cholesterol levels were low whenthey didn't even qualify for a
statin.
Anyway, fast forward, wepublished these data in 2008.
(03:39):
It's a nearly 18,000 patientmultinational global trial,
critically of people who wereprimary prevention, so no prior
heart attack or stroke, healthymen and women, middle-aged
folks, who would never qualifyto be on a statin because their
cholesterol levels were actuallypretty low.
But they all were selectedbecause they had this marker of
(04:01):
inflammation, they all had anelevated HSCRP, a level greater
than two, uh, to qualify for thetrial.
And what's so remarkable is thatin this study where nobody would
have gotten a statin, becauseagain, the whole idea from the
guidelines was to lower thecholesterol uh and only given a
high cholesterol, uh, in thisgroup of people with high
(04:22):
inflammation and lowcholesterol, we had a 44%
reduction in heart attacks andstrokes, a 63% reduction in
heart attacks itself, and quiteremarkably a 20% drop in
all-cause mortality.
Right.
It's crazy.
And it was really a realrevelation.
SPEAKER_00 (04:40):
Yeah.
So again, to kind of fastforward again, between the years
of say 1980 and 2010,cardiologists were making huge
strides in reducingcardiovascular morbidity
mortality.
And that curve has flattened.
In fact, maybe hasn't changed atall in the last 10 years, which
is of great concern.
(05:00):
So it leads to the idea thatmaybe we should be looking at
other things.
And this gets into some researchthat you and I are working on
together as we speak.
SPEAKER_01 (05:09):
Well, that's right.
So uh we learned during COVIDthat sometimes rates can
actually go up.
And that was a little scary.
Uh but I think you're right,Mike.
The the constant decline of thelast 35, 40 years has really
flattened out, telling us we nowneed to focus on some of these
newer biologies.
So, what's been a lot of fun,and again, working with you has
been great.
Um, we're trying to figure outcan we target this inflammation
(05:33):
directly?
I must be a little carefulthere.
That Jupiter trial we talkedabout was giving a statin.
It's a drug that lowerscholesterol and has
anti-inflammatory properties.
Could we give a pureanti-inflammatory drug to lower
risk?
We actually did a clinical trialuh called Cantose, which used a
very specific kind ofinflammation inhibitor, and it
(05:56):
really worked really well.
But that drug's not available,unfortunately, for our patients
for some complicated reasonsthat actually had to do with
cancer prevention.
SPEAKER_00 (06:04):
So that's a molecule called canicinemab.
Is that still used for certainpediatric arthritic conditions?
I know it's briefly on themarket for that.
SPEAKER_01 (06:13):
Well, it's still on the market for that.
So kinikiniumab, which isanother mouthful, uh, these are
drugs that are called monoclonalantibodies.
Um, they target a very specificpiece of this inflammation
pathway.
And we showed it could lower therisk of a heart attack or stroke
by about 15 or 20 percent, whichis great.
But uh the drug also has somegreat benefits in cancer.
(06:35):
So it's being repurposed intothe oncology community.
Um, and so we need to findanother way of targeting this.
SPEAKER_00 (06:42):
Sorry for that aside.
Uh just for our audience, one ofthe little tricks of the trade
is if you hear a molecule or achemical that ends with MAB,
it's a monoclonal antibody.
So you can surprise your friendsuh at a dinner conversation that
you know the nature of theirparticular medicine.
So sorry, sorry about that.
SPEAKER_01 (07:00):
No, that's a that's that's a great pearl even for
those of us who live in thisworld uh on a daily basis.
Um so the question was (07:06):
could we find another one of these MABs
uh that hits a different part ofthis particular immune system?
Um and actually anothermouthful, that drug turns out to
be called Ziltaveca Mab.
It starts with a Z.
Um and we designed a series ofclinical trials which are
ongoing right now using thisparticular kind of inflammation
(07:29):
inhibitor, which, by the way, isalready commonly used.
It's in a class of drugs thatare commonly used to treat
rheumatoid arthritis.
Uh, some patients take it totreat inflammatory bowel disease
like Crohn's disease orulceritis.
So the class of drugs has beenaround for 20, 25 years.
We know it's pretty safe, butit's been used to treat
(07:50):
classical autoimmuneanti-inflammatory disorders.
The trick is, can we use it toactually improve outcomes for
patients with heart disease?
We're going to focus a bit onHermes, which is, again, it's a
heart failure trial.
That's a particular kind ofheart failure.
It's something that we call,cardiologists call HEF-PEF,
(08:11):
which is heart failure withpreserved ejection fraction.
What's that really mean?
That means that uh your heart'spumping and it looks pretty good
on a standard echocardiogram,but it doesn't work really all
that well.
And you get the symptoms ofheart failure, shortness of
breath, a feeling of congestion,a feeling of not being able to
(08:34):
walk as far as you used to beable to, even though the heart
seems to pump okay, but theheart's actually too stiff.
I think that's the easiest wayto understand what this is.
When we talk about inflammation,we're not talking about a
sprained ankle.
We're not talking about drugslike Advil or ibuprofen or even
aspirin.
We're talking about the kind ofinflammation that classically
(08:58):
would lead to things likerheumatoid arthritis or um
inflammatory bowel disease orpsoriasis, more severe disorders
that go under the rubric ofauto-inflammatory or um uh, you
know, things like that.
And there's certain specificpathways of this immune system
(09:19):
that impact on some of thesedisorders more than others.
And we're going to get veryjargony very fast, but I think
actually it makes sense.
There's one particular pathwaythat all of us have.
Understand, everybody has thisbecause I said at the beginning,
you need these things to survivechildhood and get into early
adulthood, but it kind of comesback to haunt us later in life.
(09:42):
One of these pathwaysupregulates a certain cytokine.
Now, a cytokine is a chemicalmolecule that tells cell A to
talk to cell B.
It's a communication system.
That's all it is.
It says, hello out there, thiscell is doing this, you better
do that.
I see something over therethat's not good.
Let's go attack that.
That's right.
SPEAKER_00 (10:01):
Yeah, kine means means to move.
So cytokine means move cells.
It's a chemical that moves cellsin one direction or another.
That's exactly right.
SPEAKER_01 (10:09):
It's just telling them move over here because
there's something over there wegot to deal with.
It's just an infection, it's abug, it's a virus, whatever.
One of these cytokines has aname, interleukin 1.
It's the first one that was everdiscovered.
It's at the top of the chain.
The drug you mentioned before,kennakinumab, remember that MAB,
that blocks the function ofinterleukin 1.
(10:33):
Actually, it's even moretechnical than that.
It blocks the function ofinterleukin 1 beta, but let's
skip over that.
Um, and that turns out to lowerthe risk of heart attack and
stroke without changingcholesterol.
In fact, that's the proof ofprinciple that this whole thing
actually works, came out of thatcannokidomab trial.
Now, the study with Hermes, aswell as the Zeus study and the
(10:55):
Artemis study, remember that'sthe chronic kidney disease
study, the heart failure study,and the acute cornea ischemia
studies.
They're all using this drug,another MAB, Ziltefeca MAB.
It targets a downstreamcytokine.
So again, a cell-moving moleculecalled intraleucin 6.
(11:16):
Intraleukin 6 is the centralcytokine.
It's it's it's the biggestplayer.
It's the one that we think ismost involved in this process.
And what's really interesting isthere's several drugs on the
market that block IL-6 thatalready work for several of
those more serious inflammatorydiseases that patients actually
(11:36):
know they have because they havesymptoms.
The question being asked,particularly in the Hermes
study, the heart failure studywe're talking about, is can we
use this inter-leucin 6 blockerto improve the outcomes in heart
failure patients where theydon't feel their inflammation?
Mike, I think that's probablythe most important thing we're
talking about today.
This is silent inflammation.
(11:59):
If a patient hasrheumatoarthritis, their hands
and joints hurt.
If they have lupus, their skinhurts.
If they have psoriasis, theyhave issues, they know about.
The inflammation we're talkingabout for all of these heart
disease conditions, it's silent.
You don't know what's there.
And that's why running thisblood test, the high sensitivity
C-reactive protein, the HSCRP isso important because this is
(12:22):
just like cholesterol.
I can't feel my cholesterol.
I can't really feel my bloodpressure either.
I need my physician to measuremy blood pressure, to measure my
cholesterol, to measure myinflammation, my HSCRP.
So I now have information aboutthe silent things that might
well be big problems for me.
And it's that silentinflammation we're trying to
(12:44):
reduce to see if we can benefitour patients.
SPEAKER_00 (12:46):
Yeah, that's an incredibly helpful description.
Thank you for that.
I'm going to ask you one morequestion that is sometimes a
source of controversy andconfusion about HSCRP, which
historically was something thatwas originally discovered
related to streptococcalinfections, particularly
pneumococcal pneumonia.
(13:07):
And what happens and whatconfuses people is sometimes
they have extremely high levelsthat are not related to vascular
disease.
And people get very confusedabout this when we talk about,
quote, HSCRP as a risk factor.
You gave a brilliant discussionabout this at a recent meeting.
I think it'd be extremelyhelpful if you can break that
down for folks.
SPEAKER_01 (13:28):
Sure.
So, Mike, your your memory isvery good on this.
Many physicians, unfortunately,only knew about C-reactive
protein uh as something calledan acute phase reactant, which
is again a fancy word for itgoes up when you're sick.
And that has been a problembecause physicians, again, don't
always get as much new educationas they probably should.
(13:50):
And people remember that.
Um we recently published a verybig study.
It was actually 28,000 initiallyhealthy American women that
we've tracked since 1993.
So in 1993, we took a randomblood drop and we measured this
HSCRP.
(14:12):
And 30 years later, that value,that random value, is a stronger
predictor over 30 years of who'sgoing to develop a heart attack,
a stroke, or die from acardiovascular event than was
LDL cholesterol, the thing weall measure all the time.
Now, what's really interesting,Mike, is that when there's a
biomarker like the CRP that intheory has some extra
(14:37):
variability built into it, uhthe epidemiologist would say,
well, variability is what wecall a bias towards the null.
It actually makes it harder tosee a true effect, not easier.
So if CRP is alreadyoutperforming our standard go-to
LDL cholesterol, that meanswe're underestimating the true
(14:59):
impact of inflammation longterm.
Uh, I've said this before, I'llrepeat it here.
Many of your listeners today,their physicians may not
actually know this.
Uh, I've told a lot of people goto the New England Journal of
Medicine website.
It's free, it's on the internet.
You can download this recentmanuscript and take it to your
doctor's office.
(15:20):
They may need to actually readit and think about it.
Because part of the educationfor physicians honestly comes
from family members and caring,you know, people who just want
to do the right thing.
Um, all of us need lifelongeducation.
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