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November 2, 2024 25 mins

Over 30 years ago, I help set up the first CT heart scan device in Wisconsin, one of the first in the entire midwest. This was so long ago that it was really an electron beam tomogrraphy, or EBT, device that predated the more recently developed CT devices. The point is that these devices acquired images quickly, about 1/10th of a second. This is important because the heart is perpetually in motion through various cycles of its beating rhythm, with motion also provided by breathing. But these devices allowed us to precisely quantify calcium in the coronary arteries of the heart, the arteries that close and cause heart attacks. My friend, Dr. John Rumberger while at the Mayo Clinic, performed studies demonstrating that calcium consistently occupies 20% of total atherosclerotic plaque volume in the coronary arteries. In other words, quantifying calcium in the coronary arteries served as a gauge or dipstick for total atherosclerotic plaque in the heart’s arteries.

Some years later, cardiologist Dr. Arthur Agatston, whose name you may recognize from his popular South Beach Diet books, developed a scoring system for coronary calcium, yielding something that came to be called an “Agatston score”: the higher the Agatston or calcium score, the more atherosclerotic plaque was present in the coronary arteries. Subsequent research has shown that the Agatston or calcium score is, by a long stretch, the best predictor of future cardiovascular events, far better than crude measures like cholesterol and these scores, in the 30+ years since my team and I started doing these scans, have become well-established as predictors of cardiovascular events like heart attack.

But what to do with the score—can it be stopped? Can it be reduced? That is the topic for this episode of the Defiant Health podcast, highlighting what my colleagues call, even to this day, “optimal medical therapy” that has repeatedly been shown to NOT work and the answers lie elsewhere, answers that I shall discuss. 
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Episode Transcript

Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:07):
Over 30 years ago I helped set up the first CT heart
scan device in Wisconsin, oneof the first in the entire
Midwest.
This was so long ago that itwas really an electron beam
tomography or EBT device thatpredated the more recently
developed CT devices.
The point is that these devicesacquired images quickly about a

(00:28):
tenth of a second.
This is important because theheart is perpetually in motion
through various cycles of itsbeating rhythm, with motion also
provided by breathing.
But these devices allowed us toprecisely quantify calcium in
the coronary arteries of theheart, the arteries that close
and cause heart attacks.
My friend, dr John Rumberger,while at the Mayo Clinic,

(00:51):
performed studies demonstratingthat calcium consistently
occupies 20% of totalatherosclerotic plaque volume in
the coronary arteries.
In other words, quantifyingcalcium in the coronary arteries
served as a gauge or dipstickfor total atherosclerotic plaque
volume in the heart's arteries.

(01:12):
Some years later, cardiologistDr Arthur Agatston, whose name
you may recognize from hispopular South Beach diet books,
developed a scoring system forcoronary calcium, yielding
something that came to be calledan Agatston score.
The higher the Agatston orcalcium score, the more
atherosclerotic plaque waspresent in the coronary arteries

(01:34):
.
Subsequent research has shownthat the Agatston or calcium
score is, by a long stretch, thebest predictor of future
cardiovascular events, farbetter than crude measures like
cholesterol.
And these scores, in the 30years since my team and I
started doing these scans, havebecome well-established as
predictors of cardiovascularevents like heart attack.

(01:55):
But what to do with this score?
Can it be stopped?
Can it be reduced?
That's the topic for thisepisode of the Defiant Health
Podcast, highlighting what mycolleagues call, even to this
day, optimal medical therapy.
That has repeatedly been shownto not work.
And the answers lie elsewhere,answers that I shall discuss

(02:17):
Later in the podcast.
Let's talk about DefiantHealth's sponsors Paleo Valley,
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(02:39):
favorite microbe, lactobacillusroteri, and a skin formulation I
designed that improves skinfrom the inside out.
As I mentioned in the openingcomments, about 30 some years
ago I helped set up the firstheart scan device in Wisconsin
one of the first in the Midwestand we started scanning people.

(03:00):
These are people without heartdisease symptoms.
They don't have chest pain,they're not in an emergency room
.
They're not having heartattacks.
They're going about theirbusiness, riding bikes, going
for walks, etc.
With no limiting symptoms.
They'd come in because of someconcern over having heart
disease Perhaps theircholesterol was high or perhaps
a family member had heartdisease early in life, maybe in

(03:20):
their 50s, and they'd come in towant to know were they headed
in the same direction.
They'd have a scan and they'dhave a positive score.
So a normal score is zero,meaning no calcium.
Recall that calcium occupies 20%of total atherosclerotic plaque
volume, so it serves as anindirect measuring stick or
dipstick for how much totalplaque you have.

(03:41):
So, for instance, if someonehad two cubic millimeters of
calcium, they'd have 10 cubicmillimeters of total
atherosclerotic plaque.
And the more plaque you have,the greater the volume of plaque
, the more likely it is torupture.
That's what a heart attack is.
People often wrongly think thata heart attack is when an
artery progressively narrows,and that does happen.

(04:03):
But it's much more common for aminor plaque, maybe blocking
only 30% of the diameter of theartery, to rupture like a little
volcano.
And when that happens, some ofthe internal components of that
plaque are exposed to flowingblood and that is a trigger for
blood clot formation.
So that's why it's verydifficult to predict heart

(04:24):
attack, because if you looked atblockages only you'd see a
bunch of 10%, 20%, 30%, 40%blockages and you can't tell
which one's going to rupture.
That's why it's so difficult tomanage this disease with
procedures.
So instead we're measuringcalcium as an indirect way to
quantify the totalatherosclerotic plaque volume

(04:47):
lining all three coronaryarteries.
So a score of zero is normal andthe more plaque you have, the
higher the score.
And your score is compared toother people of your same sex
and age.
So, for instance, a score of300 in a 55-year-old woman would
be a very bad, very high score.
A score of 300 in a 75-year-oldmale would be only a moderate

(05:12):
score.
So they should tell you how youcompare to other people and it
gives you a kind of sense howbad it is.
But know that when you get to ascore of about a thousand, the
risk for dying, having a heartattack, sudden cardiac death or
a need for a procedure likestent implantation or bypass
surgery is about 15% per year,meaning that those things are

(05:34):
inevitable in about six to sevenyears.
In other words, you're givenkind of a crystal ball for the
future of whether you're goingto have heart problems with your
heart or not.
So what happens if you donothing?
Let's say you have a score of400 at age let's just say 60.
If you do nothing, that scoreand this is well worked out, we

(05:55):
helped contribute some of thesedata that score will increase
25% per year.
So a year later it would be 500.
Another year later, 625 and soon, and with each increase in
score you're a step closer toheart attack and other events.
Well, this goes back now 30-someyears.
What do you do about this?
Well, back then all we had wasbaby aspirin, a high dose of a

(06:19):
statin cholesterol drug, alow-fat, low-saturated fat,
low-cholesterol diet and anexercise program what my
colleagues back then calledoptimal medical therapy, and to
this day they still call it that.
Well, we help publish thesedata.
If you do that optimal medicaltherapy baby aspirin, statin
cholesterol drug, low-fat diet,exercise how fast does that

(06:42):
coronary calcium score andthereby coronary atherosclerotic
plaque grow?
25% per year, maybe more so.
Several studies even showedthat it accelerates, that
optimal medical therapyaccelerates the increase in
score to 27% or so per year.
It became clear that what mycolleagues were calling optimal

(07:03):
medical theory was uselessmedical therapy.
It did virtually nothing.
That program may reduce some ofthe soft elements of plaque,
but it does not put a stop tothe disease, not even close.
So you can imagine.
I had many panicked peoplecoming in who saw their scores
going up.
Unfortunately, when theyconsulted with my colleagues,

(07:25):
all too often they were toldthat even though they had no
symptoms, they were told toundergo what my colleagues
called the real test, a heartcatheterization, to see if they
needed a preventive stentimplant or bypass operation.
Well, it's well establishedthat doing such procedures on
people with no symptoms, that is, no chest pain, no

(07:45):
breathlessness etc.
Provides no benefit Because youcan't bypass or stent
everything and you don't knowwhich plaque is going to rupture
and cause a heart attack.
So it's been clear preventiveprocedures we call them
revascularization procedures donot benefit people without
symptoms, do not benefit peoplewithout symptoms.

(08:07):
So what do you do if the bestthey have in conventional
healthcare, so-called optimalmedical therapy, does virtually
nothing for the progression ofcoronary atherosclerosis?
What can you do?
Well, it took some years, sometrial and error and logic and
consulting science.
We had to come up with aprogram.
It led to insights like addingvitamin D and achieving a
25-hydroxyvitamin D blood levelof 60 to 70 nanograms per

(08:31):
milliliter was a major factor inachieving regression Not a
slowing but a regression ofcarnic calcium progression.
In other words, we went from25% per year progression to
drops of a score, say from 400to 240, something like that.
Now, when you do that, when youstop the progression let's say
0% change your risk for acardiac event like heart attack

(08:54):
is virtually zero.
If you reduce the score, yourrisk for a heart attack or other
events is also zero and youdon't have to get back to a
heart scan score of zero to besafe.
In other words, if you didreduce your score from 400, say,
to 290, 290 sounds like a badscore but because it was

(09:14):
achieved via reversal of plaque,your risk for heart attack,
provided you stay in the program, is virtually zero.
It's highly unusual to have anykind of heart event when you've
had regression of carotidplaque.
So by having this means oftracking the growth or
regression of carotidatherosclerotic plaque, it
taught us that vitamin D, as Imentioned, was very important.

(09:36):
It was the first time we sawactual drops in calcium scores.
Omega-3 fatty acids veryimportant Iodine, because people
have forgotten that iodinedeficiency was a major public
health problem up until 1924,when the FDA advised salt
manufacturers to add iodine andthen urged everybody to use lots
of salt to prevent goiters.

(09:57):
Well, you know what happenedsince then?
Right, the use of salt and theother advice to cut fat and
increase consumption of grainsled to insulin resistance, which
in turn leads to sodiumretention.
The problem was not the salt,the problem was the insulin
resistance from diet.
So the FDA wrongly advisedAmericans to cut back on salt

(10:19):
and what do you think is comingback?
Thyroid dysfunction and goiters.
And so we add back iodine andof course we take steps in the
program to reverse insulinresistance so that you do not
retain sodium.
We also add magnesium becausewe drink filtered water, we have
to.
Water in streams and rivers hassewage and farm runoff and

(10:39):
other things, and so we filterour water by necessity, and
water filtration removes allmagnesium, so we have to
supplement magnesium.
Then we take steps to addressthe modern disrupted
gastrointestinal microbiome,because all of us have been
exposed to antibiotics off inmany courses over a lifetime, to
glyphosate and other herbicidesin food preservatives that are

(11:03):
antimicrobial in your food butalso in our GI tracts, other
food additives like emulsifyingagents like polysorbate 80,
carboxymethylcellulose andcarrageenan that disrupt the
intestinal mucus barrier andchange the microbiome
composition and many otherfactors.
So we address that.
We do so by making sure we addback fermented foods, lots of

(11:25):
fermented foods like kimchi,kefir, sauerkraut, fermented
vegetables.
We re-implant keystonemicrobial species that colonize
the small intestine, likeLactobacillus roteri and
Lactobacillus gasseri, and we doso by fermenting them in
something that looks and smellslike yogurt.
It's not yogurt, don't befooled by that.
It's nothing like the stuff youbuy in a store which will not

(11:47):
accomplish this.
But we make the yogurts orother fermented foods with those
microbes and re-implant them atvery high numbers and that
starts the process ofreacquiring beneficial species.
We also include lots of fibers,prebiotic fibers from foods
like asparagus, brussels sprouts, legumes like black beans,
white beans, chickpeas, hummus,other foods rich in fibers that

(12:08):
nourish microbes.
And because reducing cholesterolwith statin drugs was proven to
be a useless and perhaps evenharmful practice, I resorted to
using a better, a superiormethod of testing to identify
the particles in the bloodstreamthat cause coronary disease.
There are various methods, butthe one method that has become
kind of the gold standard is NMRnuclear magnetic resonance,

(12:32):
lipoprotein analysis, and itbecame crystal clear that people
who had coronary disease andcontinued to progress their
coronary calcium scores had anexcess of small LDL particles.
So we knew that a low-fat dietactually worsened small LDL
particles.
So we knew that a low-fat dietactually worsened small LDL
particles.
So we also knew with goodscience science performed at

(12:53):
University of California,Berkeley Hopkins and other
places that the only foods thatprovoke formation of small LDL
particles very dangerousparticles were wheat, grains and
sugars, the amylopectin Aunique to wheat and grains, and
then all forms of sugar, whetherit's sucrose, fructose or
glucose.
Because the conventionalmethods of stopping the

(13:14):
progression of plaque of calciumsugars did not work, I asked
patients to try this insteadeliminate wheat, grains and
sugars.
And that's when I saw small LDLmeasures.
A typical measure in someonewith coronary disease would be
something like 1,800 nanomolesper liter.
That's part of a count pervolume.
They would go wheat, grain andsugar-free and it would drop to

(13:37):
zero or some other very lowvalue.
In other words, it wasn't justbetter by 10% or 30%, it was
eliminated in the vast majorityof cases.
And this is also where it ledto all the lessons I talked
about in my wheat belly books,and that is, people would
decimate small LDL particles.
But they'd also say why did Ilose 47 pounds and why did my

(13:57):
waist shrink by eight inches?
Why is my rheumatoid arthritisbetter?
Why is my blood pressure nownormal?
I had to stop my blood pressuremedication.
Why am I no longer a type 2diabetic or pre-diabetic?
So it led to huge successes inregaining control over health,
including a reversal of thefactors that led to an increased
carnic calcium score andcarneric atherosclerotic plaque.

(14:20):
By following this program, we'veachieved reversal or reduction
in cardiac calcium scores timeand time again, and it became
clear that statin drugs aresimply not necessary.
It's also not necessary tocontrol cholesterol.
We do control lipoproteins, sowe don't rely on cholesterol
testing.
We use NMR lipoprotein testingto quantify VLDL particles and

(14:42):
small LDL particles.
Those are the real drivers,along with insulin resistance
and inflammation, ofcardiovascular risk, and so we
focus on the real causes ofheart disease.
That also includes endotoxemia,by the way.
That is when you have theinfestation of the small
intestine by fecal microbes.
Because of our exposure toantibiotics and those other
things, there's been anoverproliferation of fecal

(15:03):
microbial species like E coliand salmonella and Campylobacter
and Pseudomonas that haveinfested the small intestine the
24 feet of small intestine.
Now those microbes only livefor a few hours and when they
die they release some of theircomponents, especially something
called lipopolysaccharideendotoxin.
That gains entry into thebloodstream and that's called

(15:23):
endotoxemia.
That is a major driver ofincreasing and growth of
atherosclerotic plaque,increasing carnic calcium score.
So we address that and you dothat, starting with the
reimplantation of lactobacillusroteri, lactobacillus gasteri
and those other efforts we maketo restore a healthy
gastrointestinal microbiome.
Now let's pause for a moment tohear something about Defiant

(15:45):
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we come back let's discuss somenew findings from some recent
clinical trials that shed lighton how to achieve regression of
plaque.
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.
So for years we've been seeingthat this combination of the
diet where we eliminate wheat,grains and sugars the foods that
provoke formation of small LDLparticles.

(19:19):
And, by the way, the reason whysmall LDL particles are so
harmful is because they're veryprone to oxidation.
They're prone to glycation,which makes them much more
dangerous.
They are better able to enterthe walls of arteries and start
the process of formingatherosclerotic plaque when
they're in arteries.
They're very adherent to thestructural proteins in the walls

(19:41):
of arteries.
They're more likely to provokean inflammatory response,
because it's inflammation in thewall of arteries in
atherosclerotic plaque that is amajor driver of those plaque
ruptures that cause heart attack, and small LDL particles, after
being formed from yourconsumption of wheat, grains and
sugars, persists in thebloodstream for five to seven
days, as compared to only 24hours of a large LDL particle

(20:06):
formed from consumption of fatsand oils.
So it's the amylopectin A ofgrains and all those sugars that
trigger formation of small LDLparticles.
That are exceptionally bad.
But you can get rid of them byjust following a diet and then
also our nutritional supplementprogram.
Now the nutritional supplementsvery simple Omega-3 fatty acids
, magnesium, iodine and vitaminD, when combined, minimize

(20:31):
insulin resistance andinflammation, because it's those
two processes, insulinresistance and inflammation,
that serve as an amplifyingeffect on the production of
small LDL.
So those supplements contributeto a marked reduction in small
LDL particles.
Then we go even further.
We address all those factors inyour gastrointestinal

(20:51):
microbiome to minimize orreverse SIBO small intestinal
bacterial overgrowth and theendotoxemia it causes, because
the endotoxemia is a majorcontributor to, once again,
insulin resistance andinflammation.
So you'll be given anextraordinary panel of powerful
tools to gain control overcoronary atherosclerotic plaque

(21:14):
and putting a stop to theprogressive rise of your
coronary calcium score.
And we have done this time andagain without having to
introduce statin cholesteroldrugs or other efforts to reduce
LDL cholesterol.
Instead, we're focusing onsmall LDL insulin resistance,
inflammation, endotoxemia.
Now there's been a recentseveral trials.
You know there's always been adebate about just how helpful

(21:37):
fish oil is for reducingcardiovascular events, and
that's because in 1999, theGissi-Pravenzione trial, that's
an Italian study of thousands ofpeople who took 1,000
milligrams of EPA and DHA fromfish oil and there was a 10%
reduction in cardiovascularevents.
So that sparked a lot moreinterest in fish oil.

(21:57):
But a number of smaller studies, often using lower dose or low
doses of omega-3s, did not showbenefit.
And then more recently in thelast few years, there have been
a series of very large studiesinvolving 10,000 to 25,000
people, each given higher dosesof omega-3 fatty acids, and
those studies have consistentlyshown decreased cardiovascular

(22:20):
events.
For instance, the JEALIS trial,j-e-l-i-s In Japan, that is, a
fish-consuming population weregiven 1,800 milligrams of EPA
alone only EPA, not the DHA andthere was a 19% reduction in
cardiovascular events.
There was the REDUCE-IT trialthat showed that 4,000
milligrams of the EPA alonereduced cardiovascular events by

(22:43):
25% over three years.
And there's the vital study of25,000 participants who took
1,000 milligrams of EPA and DHAand experienced a 25% reduction
in cardiovascular events overfive years.
Now the clincher in this are twostudies using CT coronary
angiography, and all that meansis the CT heart scan device, but

(23:06):
participants were given anintravenous bolus of a die, a
radiographic die, so they cansee the arteries.
This yields exquisitethree-dimensional pictures.
But in both of these studies,fish oil was given.
In the EVAPORATE trial, 4,000milligrams of EPA alone over 18
months, and in the HEARTS trial,3,360 milligrams of EPA and DHA

(23:31):
were given over three years.
And in both trials, and withuse of coronary CT angiography,
it was shown that both thefibrous and soft elements of
plaque were reduced.
And these were both trials.
Everybody took a statin drug,because my colleagues feel that
it's unethical to not givesomebody with heart disease a
statin drug.
We could argue about that, butnonetheless everybody in both

(23:53):
those trials were on statindrugs and the people who got
placebo had progression ofdisease on a statin drug.
And the people who got fish oileither EPA 4,000 milligrams or
EPA and DHA 3,360 milligramsshowed regression of fibrous
plaque and of soft elements ofplaque, that's, the soft

(24:14):
elements that are more prone torupture.
And one of the studies alsoshowed regression of the
coronary calcification measure.
We now have good evidence thatomega-3 fatty acids not only
reduce the likelihood ofcardiovascular events, they also
facilitate regression orreversal of coronary disease.
And these studies also showthat statin drugs are

(24:35):
insufficient.
They allow progression.
It's the fish oil that is theactive component, at least in
these trials that achieveregression.
So there you have it the diet,wheat, grain, sugar, elimination
, supplements combined thatsynergize to minimize insulin
resistance and inflammation, thefactors that amplify the
production of small LDLparticles.

(24:55):
And then we address SIBO andendotoxemia by our program of
fermented foods, re-implantationof keystone microbes and
ingesting lots and lots ofprobiotic fibers to nourish
beneficial microbes.
Now, if you've learnedsomething from this episode of
the Defiant Health Podcast, Iinvite you to subscribe to your
favorite podcast directory.
Post a review, post a comment.

(25:17):
Let's help build this movementof self-empowerment and health.
Thanks for listening.
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