October 28, 2023 • 30 mins
Cholesterol testing is among the most common blood tests run in conventional healthcare, yet it is a perennial source of confusion and, to be honest, abuse by doctors who don’t appreciate the full implications of the values. It may surprise you to know that doctors focus on the least helpful values such as total or LDL cholesterol while often ignoring the two genuinely helpful values, HDL cholesterol and triglycerides. HDL for instance is packed with useful insights into your health, as it is a reliable index of metabolic health. Low HDL, that I would define as less than 60 mg/dl, is a reflection of multiple health distortions such as insulin resistance, inflammation, excessive intra-abdominal fat, small LDL particles and VLDL that cause heart disease.
You might also be surprised to learn that consuming fats only spikes triglyceride levels for a few hours, whereas the process of your liver converting carbohydrates to triglycerides can cause a much larger increase after six to eight hours or more. Discover the factors that can amplify this process, including insulin resistance, inflammation, excessive intra-abdominal fat, and even dysbiosis and small intestine bacterial overgrowth.
The road to cardiovascular health doesn't have to be paved with cholesterol. We'll reveal how VLDL particles and triglyceride levels are intricately linked, why it's essential to keep your triglycerides below 60 milligrams per deciliter, and how higher triglycerides can result in lower HDL levels. Discover how simple dietary changes can lead to lower triglycerides and higher HDL levels, and why measuring LDL particles using NMR lipoprotein analysis offers a more accurate picture than the commonly used LDL cholesterol. Join us as we dispel the myths around cholesterol and empower you to take control of your cardiovascular health.
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A 15% discount is available for Defiant Health podcast listeners by entering discount code UNDOC15 (case-sensitive) at checkout.*
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Episode Transcript
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William Davis, MD (00:06):
Cholesterol testing is among the most common
blood tests run in conventionalhealthcare, yet it is a
perennial source of confusionand, to be honest, abuse by
doctors who don't fullyappreciate the full implications
of values.
It may surprise you to knowthat doctors focus on the least
helpful values, such as total orLDL cholesterol, while often
(00:30):
ignoring the two genuinelyhelpful values HDL cholesterol
and triglycerides.
Hdl, for instance, is packedwith useful insights into your
health, as it is a reliableindex of metabolic health.
Low HDL that I would define asless than 60 mg per deciliter is
a reflection of multiple healthdistortions, such as insulin
(00:54):
resistance, inflammation,excessive intra-abdominal fat,
small LDL particles and VLDLparticles that cause heart
disease.
Likewise, your triglyceridevalue also indicates similar
processes.
The higher your triglycerides,the lower HDL tends to be, as
triglycerides cause the body todegrade and discard HDL
(01:17):
particles.
Higher triglycerides that Iwould also define as any level
greater than 60 mg per deciliteralso indicates insulin
resistance, inflammation,greater intra-abdominal fat and
increased small LDL particlesand VLDL particles.
In other words, while focusingon the least helpful values of
(01:38):
total and LDL cholesterol, yourdoctor nearly always ignores the
values with the greatesthelpfulness.
So in this episode of DefiantHealth, let's dive into these
values that virtually everybodyhas had measured to uncover what
they mean.
Later in the podcast, let'stalk about Defiant Health's
sponsors that include Paleovalley, who provides fermented
(02:00):
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There are four values on everycholesterol or lipid panel
there's total cholesterol,there's triglycerides, hdl
cholesterol and LDL cholesterol.
(02:43):
To understand what these valuesmean, it helps to recall just
how this all got started.
So a lot of this work was donein the 1950s and 1960s by two
scientists at the NationalInstitutes of Health, nih
doctors, william Friedewald andWilliam Fredrickson.
They were trying to figure outa way to quantify, to count, the
(03:05):
number of particles in thebloodstream that cause heart
disease.
So they would take blood,remove the red blood cells and
you'd have a clear plasmaremaining that was filled with
lipoproteins or fat-carryingproteins.
You see, fat can occur freelyin the bloodstream because if it
did, fat would coalesce andwould actually block capillaries
(03:27):
and other vessels and you'dhave tissue death.
So fats cast a ride on a proteinto make it soluble in an
aqueous or water-basedenvironment.
Blood is an aqueous orwater-based environment, so fats
ride on proteins.
When they do that, that'scalled a lipoprotein, refring to
the fat on the protein.
(03:47):
So when they spun orcentrifuged plasma they would
see layers "from At the very top.
They called that very lowdensity lipoproteins.
At the very bottom was thehighest density, just like a
stone falls to the bottom of alake Low density lipoproteins at
the bottom and low densitylipoproteins in the middle.
(04:08):
How do you go about countingthese particles in the various
layers?
Well, they chose a workaroundand that was to choose one
component shared by theseparticles.
They could have chosen, forinstance, a protein like
ApoProtein B, they could havechosen triglycerides, but they
chose cholesterol.
Cholesterol was a fat fractionin all these layers of
(04:30):
lipoproteins and they measuredthe amount of cholesterol in
each fraction.
They could measure thecholesterol in the very low
density fraction at the top,cholesterol in the high density
fraction at the bottom, etc.
They used that as a crude andindirect way to quantify how
many particles there were ineach layer.
(04:50):
Now they are also mindful thatin the 1950s and 1960s, they
wanted to make sure this wasaccessible in community
hospitals that often did nothave sophisticated laboratory
equipment.
So they devised anotherworkaround, and that is they
would measure the cholesterol inthe entire sample that would be
total cholesterol.
Then they'd measure thecholesterol in the high density
lipoprotein fraction at thebottom that would be HDL
(05:14):
cholesterol.
And rather than measuring thecholesterol in the very low
density fraction at the top,they could estimate it by simply
measuring triglycerides anddividing by 5, because there's 5
times more triglycerides thancholesterol in the VLDL fraction
.
So that triglycerides dividedby 5 was a quick and easy
workaround.
Now they also wanted to avoidhaving to measure that tricky
(05:36):
middle level in communityhospitals and other poorly
equipped labs.
So they chose to develop anequation that they could
calculate the LDL cholesterolfrom the other measures.
So they reasoned that LDLcholesterol could be calculated
not measured but calculated bytaking the total cholesterol
value, subtracting the HDLcholesterol value and then
(05:59):
subtracting triglycerides,divided by 5.
And that equation is called theFriedewald equation, or
Friedewald calculation, tocalculate LDL cholesterol.
Now this is what's called aregression equation, that is, it
falls apart when things change,when circumstances change.
So if triglycerides are alittle high, let's say 160, it
(06:19):
invalidates the measurement.
If you change your diet, youinvalidate the measurement, the
equation.
If you cut fat or you cut carbsor make a change in diet,
you've invalidated the equation.
If you're diabetic, either oneor two, type one or type two,
you invalidate the equation.
In other words, there's lots ofassumptions built in.
So LDL cholesterol is wildlyinaccurate when you compare it
(06:43):
to the actual measurement of LDLparticles, which you can
measure.
Now.
It was believed that LDLparticles were the primary
contributor to heart disease.
In real life it's actually LDLparticles, and the LDL particles
are the particles that actuallycontribute to growing or
expanding coronaryatherosclerotic plaque.
That's the stuff that causesheart attack, sudden cardiac
(07:06):
death, or gets stented orbypassed with heart procedures.
In the ensuing years, sincedoctors Friedew ald and
Fredericksen, early work, becameclear that total cholesterol
was a virtually worthlessmeasure.
It was a very poor predictor ofheart disease events like heart
attacks.
Part of the reason is because,let's say, you had an HDL
(07:26):
cholesterol.
Remember, hdl cholesterol is acomponent within total
cholesterol, along with LDLcholesterol and triglycerides
divided by five, or VLDLcholesterol.
So what if you did something bad?
You gained a bunch of weightand your abdomen, your blood
sugar went up, you haveinflammation and, let's say,
your HDL dropped, say, from 60to 30.
(07:46):
30 milligrams for an HDL isvery bad.
It's a high risk marker.
So you dropped HDL 30.
That means total cholesterolvalue also drops 30.
And many doctors say, oh, thisis a good change, not
recognizing that it was a dropin HDL that led to a drop in
total cholesterol.
Conversely, let's say youstarted with an HDL cholesterol
of 30 milligrams and you didgood things.
(08:09):
Maybe you added exerciseprogram, you lost some abdominal
fat and inflammation went downand HDL goes from 30 to 60.
Well, your total cholesterolalso goes up 30 milligrams and
your doctor says, oh no, yourcholesterol is higher, we need
to treat it with a statincholesterol drug or other drug.
In other words, totalcholesterol is misleading.
It's a composite measure ofboth good and bad things and so
(08:32):
total cholesterol is worthless.
I tell people to take a blackmagic marker and cross it out
and pay no attention to totalcholesterol.
Now, what about this calculatedLDL cholesterol, calculated by
the Friedewald equation?
Well, we know with confidencethat LDL cholesterol is not only
wildly inaccurate andunreliable when you make those
(08:53):
changes like dietary changes, orchange triglycerides or blood
sugars.
We know that LDL cholesterol isa very poor predictor.
For instance, the LDLcholesterol of the average
person without heart disease is133 milligrams per deciliter.
What's the LDL cholesterol ofsomeone who had sudden cardiac
death or needs a bypassoperation or had a heart attack?
(09:15):
133 milligrams per deciliter.
It is indistinguishable.
So LDL cholesterol is anexceptionally poor predictor of
heart disease events.
So, total cholesterol worthless.
Ldl cholesterol very poorpredictive power.
Yet these are the two valuesmost practicing physicians focus
on to assess your risk and thenintervene, typically with a
(09:39):
statin cholesterol drug or nowsome other drugs.
But the truth of it is thereare, even though total
cholesterol and LDL cholesterolare nearly useless values,
despite all that attention.
The other two values,triglycerides and HDL
cholesterol, actually do tellyou a lot about your risk for
heart disease and what yourlipoproteins might look like if
(09:59):
you were to examine them, notjust rely on lipids or
cholesterol testing.
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Health listeners.
All right, let's considertriglycerides.
So triglycerides are fats.
If you have, for instance, abottle of extra virgin olive oil
, that is a bottle of fat, abottle of triglycerides.
Likewise, butter, fats on meatsare all triglycerides.
So if you consume a meal thatcontains fats and oils let's say
(13:23):
a piece of a pork chop with fator butter on your green beans
your levels of triglycerideswill go up.
Now you're actually increasinglevels of something called
chylomicrons that aretriglyceride rich.
But that occurs in the firstfew hours, about the first five
to six hours after afat-containing meal.
So there's a modest rise intriglycerides after consuming
(13:46):
fats.
So at a typical level, let'ssay you started at 100
milligrams per deciliter oftriglycerides and you eat a
fatty meal, maybe it goes to 180or 200, something like that,
transiently for a few hours.
That's from fat consumption.
Now there's a delayed processcalled de novo lipogenesis.
All that means is in the liver.
The liver has the capacity toconvert carbs and sugars to
(14:10):
triglycerides.
De novo lipogenesis, making newfats.
That's all that means.
And so you had that meal.
You had that initial rise intriglycerides from chylomicrons
in the first few hours and thenmore than six to eight or so or
longer hours, there's asecondary rise that's much
larger.
So triglycerides can go up to300 or something like that.
(14:32):
And that's because it takes.
There's a delay in the liver'sconversion of those
carbohydrates to triglycerides.
Now the triglycerides onceagain cannot occur as
triglycerides in the bloodstream.
They are packaged into VLDLparticles, very low density,
lipoprotein particles.
So once again, initial rise oftriglycerides from fat
(14:53):
consumption.
Secondary, much larger risefrom the liver process of
converting carbohydrates intotriglycerides.
The liver has a great capacityfor this process of de novo
lipogenesis and it can producehuge quantities of triglycerides
.
That process is amplified inthe presence of insulin
(15:13):
resistance, inflammation and thepresence of excessive
intra-abdominal fat, and in thepresence of dysbiosis or
especially SIBO, small intestinebacterial overgrowth and
endotoxin.
Let's consider each of those.
So when you have insulinresistance, it means your body
is unresponsive to insulin.
Muscle, brain, liver don'trespond properly to insulin and
(15:37):
your pancreas compensates byproducing huge quantities more
insulin 30 times more, 50 timesmore, 100 times more.
A person who's insulinsensitive let's say a slender
athletic person may have afasting insulin level of one or
two micro units per liter.
A person who, with insulinresistance, may have a level of
50, 90, 130 or more micro units,in other words, many times
(16:03):
higher.
And that high level of insulincauses abdominal fat to grow,
which makes insulin resistanceworse, which causes abdominal
fat to grow, and so it's avicious cycle that makes it
worse and worse over time.
But the presence of insulinresistance is a major amplifying
effect on liver, de novolipogenesis, so it causes your
(16:24):
liver to churn out more and moretriglycerides as VLDO particles
Now when you have inflammationfrom that same abdominal fat.
So abdominal fat, that is fat,and certainly the abdominal
organs like the intestines andliver and pancreas is itself
very inflamed.
If you biopsied abdominalvisceral fat surrounding organs,
(16:45):
you'd see white blood cellsinfiltrating the fat and flaming
it, and that fat producesinflammatory mediators that pour
into the bloodstream and thatalso recall that the
gastrointestinal tract isdrained by a venous system to
the liver it's called the portalvenous system.
And so the liver takes abeating of inflammation from
(17:08):
abdominal visceral fat, whichfurther amplifies the process of
liver de novo lipogenesis.
It also adds insulin resistance, so it's feeding upon itself.
These processes feed upon eachother Now that intra-abdominal
fat, abdominal visceral fat, istherefore a major amplifier of
liver de novo lipogenesis andthe production of triglycerides
(17:28):
into the bloodstream.
So while triglycerides areinitially from fat consumption,
that secondary, much larger riseis fueled hugely by these
processes.
And then another process fuelingde novo lipogenesis is
dysbiosis, but especially if itenters the small intestine, that
is, small intestinal bacterialovergrowth or SIBO.
(17:49):
So what's happened to manypeople by my estimation at least
half the country is thatbecause of our exposure to
antibiotics and other factorslike glyphosate the herbicide
that's also an antibioticpreservatives, emulsifying
agents, et cetera, we've lostnumerous beneficial species in
the colon microbiome.
Well, they were suppressingfecal microbes like E coli and
(18:12):
salmonella and campylobacter, sowe lose healthy microbes.
It allows the excessiveproliferation of fecal microbial
species which in turn can climbup into the small intestine.
And the small intestine, youmay recall, is by design very
permeable.
That's where we absorbnutrients like amino acids,
fatty acids, vitamins andminerals.
(18:33):
Well, when fecal microbes cometo occupy the 24 feet of small
intestine, they live and dierapidly Trillions of microbes
living and dying rapidly.
When they die, they releasesome of their toxins, such as
the so-called endotoxin that isable to penetrate the intestinal
wall because the small bowel isso permeable, and that's when
endotoxin gets in thebloodstream.
(18:54):
That's called endotoxemia.
Endotoxemia in the portal veinsystem hugely amplifies liver de
novo lipogenesis and when itenters the main systemic
circulation it makes insulinresistance worse.
So you can see that while, yes,fats ingested and diet do raise
(19:14):
triglycerides, a much worsesituation comes from liver de
novo lipogenesis amplified,fueled by these other processes.
And that is the problem withtriglycerides.
Now, recall that when you haveyour cholesterol panel drawn,
it's typically fasting.
So if triglycerides are abovethe ideal of 60 milligrams per
(19:35):
deciliter, you know it came fromcarbohydrates, because if you
ate, let's say dinner, at 6pm,you have triglycerides raised
but cleared by midnight.
Right, that is from the fat,but then it's after midnight
where you have that secondaryrise from de novo lipogenesis,
fueled by those other processes.
And when you get to thelaboratory, say at 8am, they
(19:56):
draw your blood and yourtriglycerides are 253, that's
from carbohydrates right, it'stoo late to be from fat
consumption.
It's from carbohydrateconsumption further fueled by
insulin resistance, inflammation, intra-abdominal fat and
metabolic endotoxemia from SIBOor dysbiosis.
One of the reasons why this isso important to recognize is
(20:18):
that when you have excesstriglycerides and thereby VLDL
particles, very low densitylipoproteins rich in
triglycerides, when you have anexcess VLDL particles, are both
a direct cause of coronaryatherosclerosis and thereby
cardiac events like heart attack.
But VLDL particles alsointeract with LDL particles, not
(20:40):
LDL cholesterol, that markerLDL particles and VLDL particles
rich in triglycerides transfertriglycerides to LDL particles
and these LDL particles gothrough a series of remodeling
reactions by enzymes such ashepatic lipase, which converts
them to small LDL particles.
Small LDL particles, you mayrecall, are smaller of course,
(21:04):
and thereby more readily able topenetrate into the walls of
arteries to initiate the processof forming atherosclerotic
plaque.
Small LDL particles are alsomore prone to oxidation, which
makes the much more dangerous,also more prone to glycation,
and they are much more adherentto the structural tissues in the
artery wall and more likely toincite an inflammatory response
(21:26):
in the arterial wall.
That's the process that leadsto atherosclerosis and heart
attacks.
Not cholesterol, but LDLparticles, especially small
glycoxidized LDL particles thatare adherent and able to
initiate an inflammatoryresponse in the arterial wall.
So we'd like to minimize thisprocess.
Because VLDL particles trackvery well with triglyceride
(21:50):
levels, you can still rely, eventhough lipoproteins are, in
general, advanced lipoproteinanalysis is a better way to
assess cardiovascular risk.
You can still rely on thesimple triglyceride level of a
standard four component lipid orcholesterol panel.
Because the triglyceride leveldoes track very well with VLDL
particles and I aim to keeptriglycerides no higher than 60
(22:13):
milligrams per deciliter.
Why?
Well, that's the level at whichyou have almost no VLDL
particles to interact with LDLparticles to make them small.
So when you get yourtriglycerides to 60 milligrams
per deciliter or less, youusually have little to no small
LDL particles.
Now, there are exceptions.
There are some genetic variants.
There are some people with SIBOso bad it still drives
(22:36):
persistent small LDL, but ingeneral most people can know
that they have little to nosmall LDL particles if
triglyceride levels, and therebyVLDL but triglyceride levels
are 60 milligrams per deciliteror less.
Now let's shift over to HDLcholesterol.
So HDL particles are protective.
They're responsible, orbelieved to be responsible, for
something called reversecholesterol transport.
(22:57):
That's an inaccurate name, butthink of HDL particles as a
cleanup crew cleaning uparteries.
So the higher the HDL, the moreprotected you are.
Now there's a funny interactionbetween triglyceride particles,
vldl and HDL particles, andthat is when you have lots and
lots of VLDL particles andthereby triglycerides, they
cause accelerated degradation ofHDL particles and they're
(23:20):
cleared from the kidneys.
So when you have highertriglycerides meaning anytime
above 60, right, you tend to beclearing or metabolizing your
HDL particles and HDL levels godown.
So it's very common to have anincreased triglyceride level of,
say, 250 and a low HDL level of, say, 32, 34, 27, something
(23:41):
like that.
So just as we wanttriglycerides be no higher than
60 milligrams per deciliter, wewant HDL cholesterol to be a
minimum of 60 milligrams perdeciliter or more.
Now what you'll find in doing myprograms, in which we eliminate
wheat, grains and sugars, weaddress common nutrient
deficiencies that plague modernpeople because of modern
lifestyles vitamin D, magnesium,iodine and omega-3 fatty acids.
(24:03):
Then we address dysbiosis inthe colon, as well as SIBO in
the small intestine and theaccompanying endotoxemia.
We address all those things andit's very common to have a
triglyceride level in the 40range 43, 47 milligrams,
something like that.
It's very common to have HDLcholesterol levels of 70, 80, 90
, or 100, well above 60.
(24:24):
And we don't care about totalcholesterol, right, or LDL
cholesterol, because we madedramatic changes in diet
Equation.
Free world equation wasinaccurate to begin with and
unreliable, but we've madechanges that invalidate the free
to world calculation.
So if you want to know what theLDL particles are doing, you
can't tell that.
You can kind of make indirectjudgments right by looking at
the triglycerides and HDL, butyou're not actually measuring
(24:46):
the LDL particle.
You can measure it Now.
My preferred method is calledNMR, nuclear magnetic resonance.
There used to be other methodslike ultracentrification and gel
electrophoresis, but those arekind of hard to get or not
unavailable anymore.
So we're all using NMR, nuclearmagnetic resonance.
Lipoprotein analysis and many ofthe big labs like Quest and
(25:07):
those big companies will do thisfor you.
You just have to have itspecified by your doctor.
If your doctor says somethinglike, oh, we don't do that test
or oh, there's no proof thatworks or helps, provides
additional information, or it'snot covered by insurance.
Those are all lies.
That's nonsense.
I've been doing this for 30years and almost all insurers,
including Medicare, cover NMRlipoprotein analysis.
(25:29):
Why would the doctor lie andsay such things?
I'll translate I can't bebothered going the extra mile of
education to understand thismore advanced form of testing
and I can't be bothered toreading the 55 clinical studies
human clinical studies, forinstance that validate that
small LDL particles aredramatically superior predict of
coronary disease.
(25:50):
It's not that they're notunavailable or not covered by
insurance.
That's nonsense.
They are covered by insurance,they're readily available and
one of the things you'll findwhen you do an NMR lipoprotein
panel.
The two really necessary numbersto look at are LDL particle
number, but especially small LDLparticle number.
So let's say your LDL particlenumber total is 2000 and the
(26:13):
small LDL particle number is1000.
That means 1000 of thoseparticles in the total particle
number of 2000 is small.
That tells you this is going torespond dramatically to
elimination of the foods thatprovoke formation of small LDL
wheat, grains and sugars,because of the amyl, pectin A,
wheat and grains.
And then the sugars, thenutrients we address that
(26:34):
synergize to minimize or reduceinflammation and insulin
resistance.
Vitamin D, magnesium, iodine,omega 3 fatty acids and then we
address dysbiosis, sibo andendotoxemia and what you get is
a dramatic reduction, usuallyelimination, of small LDL If you
start at 1000 or 2000,.
Most commonly drops to zero.
(26:54):
It's not a percentage better,it's gone, and that's because
you're no longer engaging in denovo lipogenesis right from
consumption of carbs and sugars.
You've reversed insulinresistance, you've minimized
inflammation and you'veaddressed endotoxemia.
One of the confusing outcomes ofall this is that it's not
uncommon for LDL cholesterol,and thereby total cholesterol,
(27:17):
to go up.
But you know the equation isinvalid when we've made these
changes in our diet and someother of the basic assumptions
that are used to justify thefree to all calculation.
So even if your LDL cholesterolsays 236 and your doctor's
alarm, think you're going to dieof a heart attack.
It's not a real number.
So what you have to do is getNMR lipoprotein panel to get
(27:39):
that small LDL particle numberNow one of the things we do not
know.
Let's say you get rid of all thesmall LDL out of a total LDL
particle number of 2000.
That means your LDL total LDLparticle number typically drops
to about 1000, right, becauseyou eliminated all the small LDL
particles?
At what level of total LDLparticle number that are all
large and no small.
What is allowable before itcauses coronary disease or adds
(28:02):
to coronary atheroscleroticplaque?
Nobody knows.
Despite the billions andbillions of dollars spent on
cholesterol research, no one hassettled that basic question.
I think, though, that somewherebetween 1400 and 1800 nanomoles
per liter part of the count pervolume of pure large LDL is
probably safe, and above thatmaybe, maybe, adds to risk.
(28:25):
But we don't know that for afact.
But know that by addressing thesmall LDL particle number,
which you've done with all thethings we've talked about,
you've addressed by far the mostvicious cause of coronary
disease.
So, in summary, totalcholesterol worthless,
calculated LDL cholesterolnearly worthless, very limited
in its ability to predict heartdisease and very misleading
(28:47):
information, especially when wechange our diets as we do here.
But there is information intriglycerides and HDL, because
they're inverse to each otherthe higher the triglycerides,
the lower the HDL.
So we're going to turn off yourliver's capacity to manufacture
triglycerides and VLDL particlesby eliminating the foods that
initiate liver de novolipogenesis wheat, grains and
(29:07):
sugars, by minimizing insulinresistance and inflammation that
would have amplified liver denovo lipogenesis, and we're
going to address the unhealthychanges that have occurred in
most people's gastrointestinalmicrobiomes, especially
endotoxemia, and we do so byreintroducing keystone microbes
like lactobacillus rhodii,lactobacillus gastri and perhaps
(29:29):
bacillus coagulants.
These are microbes, especiallyrhodii and gastri, that take up
residence in the small intestinewhere they produce bacteria,
that is, natural antibioticseffective against the species of
sepo, and this reducesendotoxemia.
And there's some additionalthings you can do to reduce
endotoxemia that we can talkabout another time.
But know that you havemagnificent control over
(29:52):
cardiovascular risk and it hasnothing to do with cholesterol.
Now, if you learned somethingfrom this episode of the Defiant
Health Podcast, I invite you topost a review, share a comment,
subscribe to your favoritepodcast directory and help us
build this movement ofself-empowerment in health.
Thanks for listening.
Cholesterol testing is among the most common
blood tests run in conventionalhealthcare, yet it is a
perennial source of confusionand, to be honest, abuse by
doctors who don't fullyappreciate the full implications
of values.
It may surprise you to knowthat doctors focus on the least
helpful values, such as total orLDL cholesterol, while often
(00:30):
ignoring the two genuinelyhelpful values HDL cholesterol
and triglycerides.
Hdl, for instance, is packedwith useful insights into your
health, as it is a reliableindex of metabolic health.
Low HDL that I would define asless than 60 mg per deciliter is
a reflection of multiple healthdistortions, such as insulin
(00:54):
resistance, inflammation,excessive intra-abdominal fat,
small LDL particles and VLDLparticles that cause heart
disease.
Likewise, your triglyceridevalue also indicates similar
processes.
The higher your triglycerides,the lower HDL tends to be, as
triglycerides cause the body todegrade and discard HDL
(01:17):
particles.
Higher triglycerides that Iwould also define as any level
greater than 60 mg per deciliteralso indicates insulin
resistance, inflammation,greater intra-abdominal fat and
increased small LDL particlesand VLDL particles.
In other words, while focusingon the least helpful values of
(01:38):
total and LDL cholesterol, yourdoctor nearly always ignores the
values with the greatesthelpfulness.
So in this episode of DefiantHealth, let's dive into these
values that virtually everybodyhas had measured to uncover what
they mean.
Later in the podcast, let'stalk about Defiant Health's
sponsors that include Paleovalley, who provides fermented
(02:00):
grass-fed beef sticks, bonebroth, protein rich in collagen,
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There are four values on everycholesterol or lipid panel
there's total cholesterol,there's triglycerides, hdl
cholesterol and LDL cholesterol.
(02:43):
To understand what these valuesmean, it helps to recall just
how this all got started.
So a lot of this work was donein the 1950s and 1960s by two
scientists at the NationalInstitutes of Health, nih
doctors, william Friedewald andWilliam Fredrickson.
They were trying to figure outa way to quantify, to count, the
(03:05):
number of particles in thebloodstream that cause heart
disease.
So they would take blood,remove the red blood cells and
you'd have a clear plasmaremaining that was filled with
lipoproteins or fat-carryingproteins.
You see, fat can occur freelyin the bloodstream because if it
did, fat would coalesce andwould actually block capillaries
(03:27):
and other vessels and you'dhave tissue death.
So fats cast a ride on a proteinto make it soluble in an
aqueous or water-basedenvironment.
Blood is an aqueous orwater-based environment, so fats
ride on proteins.
When they do that, that'scalled a lipoprotein, refring to
the fat on the protein.
(03:47):
So when they spun orcentrifuged plasma they would
see layers "from At the very top.
They called that very lowdensity lipoproteins.
At the very bottom was thehighest density, just like a
stone falls to the bottom of alake Low density lipoproteins at
the bottom and low densitylipoproteins in the middle.
(04:08):
How do you go about countingthese particles in the various
layers?
Well, they chose a workaroundand that was to choose one
component shared by theseparticles.
They could have chosen, forinstance, a protein like
ApoProtein B, they could havechosen triglycerides, but they
chose cholesterol.
Cholesterol was a fat fractionin all these layers of
(04:30):
lipoproteins and they measuredthe amount of cholesterol in
each fraction.
They could measure thecholesterol in the very low
density fraction at the top,cholesterol in the high density
fraction at the bottom, etc.
They used that as a crude andindirect way to quantify how
many particles there were ineach layer.
(04:50):
Now they are also mindful thatin the 1950s and 1960s, they
wanted to make sure this wasaccessible in community
hospitals that often did nothave sophisticated laboratory
equipment.
So they devised anotherworkaround, and that is they
would measure the cholesterol inthe entire sample that would be
total cholesterol.
Then they'd measure thecholesterol in the high density
lipoprotein fraction at thebottom that would be HDL
(05:14):
cholesterol.
And rather than measuring thecholesterol in the very low
density fraction at the top,they could estimate it by simply
measuring triglycerides anddividing by 5, because there's 5
times more triglycerides thancholesterol in the VLDL fraction
.
So that triglycerides dividedby 5 was a quick and easy
workaround.
Now they also wanted to avoidhaving to measure that tricky
(05:36):
middle level in communityhospitals and other poorly
equipped labs.
So they chose to develop anequation that they could
calculate the LDL cholesterolfrom the other measures.
So they reasoned that LDLcholesterol could be calculated
not measured but calculated bytaking the total cholesterol
value, subtracting the HDLcholesterol value and then
(05:59):
subtracting triglycerides,divided by 5.
And that equation is called theFriedewald equation, or
Friedewald calculation, tocalculate LDL cholesterol.
Now this is what's called aregression equation, that is, it
falls apart when things change,when circumstances change.
So if triglycerides are alittle high, let's say 160, it
(06:19):
invalidates the measurement.
If you change your diet, youinvalidate the measurement, the
equation.
If you cut fat or you cut carbsor make a change in diet,
you've invalidated the equation.
If you're diabetic, either oneor two, type one or type two,
you invalidate the equation.
In other words, there's lots ofassumptions built in.
So LDL cholesterol is wildlyinaccurate when you compare it
(06:43):
to the actual measurement of LDLparticles, which you can
measure.
Now.
It was believed that LDLparticles were the primary
contributor to heart disease.
In real life it's actually LDLparticles, and the LDL particles
are the particles that actuallycontribute to growing or
expanding coronaryatherosclerotic plaque.
That's the stuff that causesheart attack, sudden cardiac
(07:06):
death, or gets stented orbypassed with heart procedures.
In the ensuing years, sincedoctors Friedew ald and
Fredericksen, early work, becameclear that total cholesterol
was a virtually worthlessmeasure.
It was a very poor predictor ofheart disease events like heart
attacks.
Part of the reason is because,let's say, you had an HDL
(07:26):
cholesterol.
Remember, hdl cholesterol is acomponent within total
cholesterol, along with LDLcholesterol and triglycerides
divided by five, or VLDLcholesterol.
So what if you did something bad?
You gained a bunch of weightand your abdomen, your blood
sugar went up, you haveinflammation and, let's say,
your HDL dropped, say, from 60to 30.
(07:46):
30 milligrams for an HDL isvery bad.
It's a high risk marker.
So you dropped HDL 30.
That means total cholesterolvalue also drops 30.
And many doctors say, oh, thisis a good change, not
recognizing that it was a dropin HDL that led to a drop in
total cholesterol.
Conversely, let's say youstarted with an HDL cholesterol
of 30 milligrams and you didgood things.
(08:09):
Maybe you added exerciseprogram, you lost some abdominal
fat and inflammation went downand HDL goes from 30 to 60.
Well, your total cholesterolalso goes up 30 milligrams and
your doctor says, oh no, yourcholesterol is higher, we need
to treat it with a statincholesterol drug or other drug.
In other words, totalcholesterol is misleading.
It's a composite measure ofboth good and bad things and so
(08:32):
total cholesterol is worthless.
I tell people to take a blackmagic marker and cross it out
and pay no attention to totalcholesterol.
Now, what about this calculatedLDL cholesterol, calculated by
the Friedewald equation?
Well, we know with confidencethat LDL cholesterol is not only
wildly inaccurate andunreliable when you make those
(08:53):
changes like dietary changes, orchange triglycerides or blood
sugars.
We know that LDL cholesterol isa very poor predictor.
For instance, the LDLcholesterol of the average
person without heart disease is133 milligrams per deciliter.
What's the LDL cholesterol ofsomeone who had sudden cardiac
death or needs a bypassoperation or had a heart attack?
(09:15):
133 milligrams per deciliter.
It is indistinguishable.
So LDL cholesterol is anexceptionally poor predictor of
heart disease events.
So, total cholesterol worthless.
Ldl cholesterol very poorpredictive power.
Yet these are the two valuesmost practicing physicians focus
on to assess your risk and thenintervene, typically with a
(09:39):
statin cholesterol drug or nowsome other drugs.
But the truth of it is thereare, even though total
cholesterol and LDL cholesterolare nearly useless values,
despite all that attention.
The other two values,triglycerides and HDL
cholesterol, actually do tellyou a lot about your risk for
heart disease and what yourlipoproteins might look like if
(09:59):
you were to examine them, notjust rely on lipids or
cholesterol testing.
Let's resume with that topicafter I tell you a little about
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Health listeners.
All right, let's considertriglycerides.
So triglycerides are fats.
If you have, for instance, abottle of extra virgin olive oil
, that is a bottle of fat, abottle of triglycerides.
Likewise, butter, fats on meatsare all triglycerides.
So if you consume a meal thatcontains fats and oils let's say
(13:23):
a piece of a pork chop with fator butter on your green beans
your levels of triglycerideswill go up.
Now you're actually increasinglevels of something called
chylomicrons that aretriglyceride rich.
But that occurs in the firstfew hours, about the first five
to six hours after afat-containing meal.
So there's a modest rise intriglycerides after consuming
(13:46):
fats.
So at a typical level, let'ssay you started at 100
milligrams per deciliter oftriglycerides and you eat a
fatty meal, maybe it goes to 180or 200, something like that,
transiently for a few hours.
That's from fat consumption.
Now there's a delayed processcalled de novo lipogenesis.
All that means is in the liver.
The liver has the capacity toconvert carbs and sugars to
(14:10):
triglycerides.
De novo lipogenesis, making newfats.
That's all that means.
And so you had that meal.
You had that initial rise intriglycerides from chylomicrons
in the first few hours and thenmore than six to eight or so or
longer hours, there's asecondary rise that's much
larger.
So triglycerides can go up to300 or something like that.
(14:32):
And that's because it takes.
There's a delay in the liver'sconversion of those
carbohydrates to triglycerides.
Now the triglycerides onceagain cannot occur as
triglycerides in the bloodstream.
They are packaged into VLDLparticles, very low density,
lipoprotein particles.
So once again, initial rise oftriglycerides from fat
(14:53):
consumption.
Secondary, much larger risefrom the liver process of
converting carbohydrates intotriglycerides.
The liver has a great capacityfor this process of de novo
lipogenesis and it can producehuge quantities of triglycerides
.
That process is amplified inthe presence of insulin
(15:13):
resistance, inflammation and thepresence of excessive
intra-abdominal fat, and in thepresence of dysbiosis or
especially SIBO, small intestinebacterial overgrowth and
endotoxin.
Let's consider each of those.
So when you have insulinresistance, it means your body
is unresponsive to insulin.
Muscle, brain, liver don'trespond properly to insulin and
(15:37):
your pancreas compensates byproducing huge quantities more
insulin 30 times more, 50 timesmore, 100 times more.
A person who's insulinsensitive let's say a slender
athletic person may have afasting insulin level of one or
two micro units per liter.
A person who, with insulinresistance, may have a level of
50, 90, 130 or more micro units,in other words, many times
(16:03):
higher.
And that high level of insulincauses abdominal fat to grow,
which makes insulin resistanceworse, which causes abdominal
fat to grow, and so it's avicious cycle that makes it
worse and worse over time.
But the presence of insulinresistance is a major amplifying
effect on liver, de novolipogenesis, so it causes your
(16:24):
liver to churn out more and moretriglycerides as VLDO particles
Now when you have inflammationfrom that same abdominal fat.
So abdominal fat, that is fat,and certainly the abdominal
organs like the intestines andliver and pancreas is itself
very inflamed.
If you biopsied abdominalvisceral fat surrounding organs,
(16:45):
you'd see white blood cellsinfiltrating the fat and flaming
it, and that fat producesinflammatory mediators that pour
into the bloodstream and thatalso recall that the
gastrointestinal tract isdrained by a venous system to
the liver it's called the portalvenous system.
And so the liver takes abeating of inflammation from
(17:08):
abdominal visceral fat, whichfurther amplifies the process of
liver de novo lipogenesis.
It also adds insulin resistance, so it's feeding upon itself.
These processes feed upon eachother Now that intra-abdominal
fat, abdominal visceral fat, istherefore a major amplifier of
liver de novo lipogenesis andthe production of triglycerides
(17:28):
into the bloodstream.
So while triglycerides areinitially from fat consumption,
that secondary, much larger riseis fueled hugely by these
processes.
And then another process fuelingde novo lipogenesis is
dysbiosis, but especially if itenters the small intestine, that
is, small intestinal bacterialovergrowth or SIBO.
(17:49):
So what's happened to manypeople by my estimation at least
half the country is thatbecause of our exposure to
antibiotics and other factorslike glyphosate the herbicide
that's also an antibioticpreservatives, emulsifying
agents, et cetera, we've lostnumerous beneficial species in
the colon microbiome.
Well, they were suppressingfecal microbes like E coli and
(18:12):
salmonella and campylobacter, sowe lose healthy microbes.
It allows the excessiveproliferation of fecal microbial
species which in turn can climbup into the small intestine.
And the small intestine, youmay recall, is by design very
permeable.
That's where we absorbnutrients like amino acids,
fatty acids, vitamins andminerals.
(18:33):
Well, when fecal microbes cometo occupy the 24 feet of small
intestine, they live and dierapidly Trillions of microbes
living and dying rapidly.
When they die, they releasesome of their toxins, such as
the so-called endotoxin that isable to penetrate the intestinal
wall because the small bowel isso permeable, and that's when
endotoxin gets in thebloodstream.
(18:54):
That's called endotoxemia.
Endotoxemia in the portal veinsystem hugely amplifies liver de
novo lipogenesis and when itenters the main systemic
circulation it makes insulinresistance worse.
So you can see that while, yes,fats ingested and diet do raise
(19:14):
triglycerides, a much worsesituation comes from liver de
novo lipogenesis amplified,fueled by these other processes.
And that is the problem withtriglycerides.
Now, recall that when you haveyour cholesterol panel drawn,
it's typically fasting.
So if triglycerides are abovethe ideal of 60 milligrams per
(19:35):
deciliter, you know it came fromcarbohydrates, because if you
ate, let's say dinner, at 6pm,you have triglycerides raised
but cleared by midnight.
Right, that is from the fat,but then it's after midnight
where you have that secondaryrise from de novo lipogenesis,
fueled by those other processes.
And when you get to thelaboratory, say at 8am, they
(19:56):
draw your blood and yourtriglycerides are 253, that's
from carbohydrates right, it'stoo late to be from fat
consumption.
It's from carbohydrateconsumption further fueled by
insulin resistance, inflammation, intra-abdominal fat and
metabolic endotoxemia from SIBOor dysbiosis.
One of the reasons why this isso important to recognize is
(20:18):
that when you have excesstriglycerides and thereby VLDL
particles, very low densitylipoproteins rich in
triglycerides, when you have anexcess VLDL particles, are both
a direct cause of coronaryatherosclerosis and thereby
cardiac events like heart attack.
But VLDL particles alsointeract with LDL particles, not
(20:40):
LDL cholesterol, that markerLDL particles and VLDL particles
rich in triglycerides transfertriglycerides to LDL particles
and these LDL particles gothrough a series of remodeling
reactions by enzymes such ashepatic lipase, which converts
them to small LDL particles.
Small LDL particles, you mayrecall, are smaller of course,
(21:04):
and thereby more readily able topenetrate into the walls of
arteries to initiate the processof forming atherosclerotic
plaque.
Small LDL particles are alsomore prone to oxidation, which
makes the much more dangerous,also more prone to glycation,
and they are much more adherentto the structural tissues in the
artery wall and more likely toincite an inflammatory response
(21:26):
in the arterial wall.
That's the process that leadsto atherosclerosis and heart
attacks.
Not cholesterol, but LDLparticles, especially small
glycoxidized LDL particles thatare adherent and able to
initiate an inflammatoryresponse in the arterial wall.
So we'd like to minimize thisprocess.
Because VLDL particles trackvery well with triglyceride
(21:50):
levels, you can still rely, eventhough lipoproteins are, in
general, advanced lipoproteinanalysis is a better way to
assess cardiovascular risk.
You can still rely on thesimple triglyceride level of a
standard four component lipid orcholesterol panel.
Because the triglyceride leveldoes track very well with VLDL
particles and I aim to keeptriglycerides no higher than 60
(22:13):
milligrams per deciliter.
Why?
Well, that's the level at whichyou have almost no VLDL
particles to interact with LDLparticles to make them small.
So when you get yourtriglycerides to 60 milligrams
per deciliter or less, youusually have little to no small
LDL particles.
Now, there are exceptions.
There are some genetic variants.
There are some people with SIBOso bad it still drives
(22:36):
persistent small LDL, but ingeneral most people can know
that they have little to nosmall LDL particles if
triglyceride levels, and therebyVLDL but triglyceride levels
are 60 milligrams per deciliteror less.
Now let's shift over to HDLcholesterol.
So HDL particles are protective.
They're responsible, orbelieved to be responsible, for
something called reversecholesterol transport.
(22:57):
That's an inaccurate name, butthink of HDL particles as a
cleanup crew cleaning uparteries.
So the higher the HDL, the moreprotected you are.
Now there's a funny interactionbetween triglyceride particles,
vldl and HDL particles, andthat is when you have lots and
lots of VLDL particles andthereby triglycerides, they
cause accelerated degradation ofHDL particles and they're
(23:20):
cleared from the kidneys.
So when you have highertriglycerides meaning anytime
above 60, right, you tend to beclearing or metabolizing your
HDL particles and HDL levels godown.
So it's very common to have anincreased triglyceride level of,
say, 250 and a low HDL level of, say, 32, 34, 27, something
(23:41):
like that.
So just as we wanttriglycerides be no higher than
60 milligrams per deciliter, wewant HDL cholesterol to be a
minimum of 60 milligrams perdeciliter or more.
Now what you'll find in doing myprograms, in which we eliminate
wheat, grains and sugars, weaddress common nutrient
deficiencies that plague modernpeople because of modern
lifestyles vitamin D, magnesium,iodine and omega-3 fatty acids.
(24:03):
Then we address dysbiosis inthe colon, as well as SIBO in
the small intestine and theaccompanying endotoxemia.
We address all those things andit's very common to have a
triglyceride level in the 40range 43, 47 milligrams,
something like that.
It's very common to have HDLcholesterol levels of 70, 80, 90
, or 100, well above 60.
(24:24):
And we don't care about totalcholesterol, right, or LDL
cholesterol, because we madedramatic changes in diet
Equation.
Free world equation wasinaccurate to begin with and
unreliable, but we've madechanges that invalidate the free
to world calculation.
So if you want to know what theLDL particles are doing, you
can't tell that.
You can kind of make indirectjudgments right by looking at
the triglycerides and HDL, butyou're not actually measuring
(24:46):
the LDL particle.
You can measure it Now.
My preferred method is calledNMR, nuclear magnetic resonance.
There used to be other methodslike ultracentrification and gel
electrophoresis, but those arekind of hard to get or not
unavailable anymore.
So we're all using NMR, nuclearmagnetic resonance.
Lipoprotein analysis and many ofthe big labs like Quest and
(25:07):
those big companies will do thisfor you.
You just have to have itspecified by your doctor.
If your doctor says somethinglike, oh, we don't do that test
or oh, there's no proof thatworks or helps, provides
additional information, or it'snot covered by insurance.
Those are all lies.
That's nonsense.
I've been doing this for 30years and almost all insurers,
including Medicare, cover NMRlipoprotein analysis.
(25:29):
Why would the doctor lie andsay such things?
I'll translate I can't bebothered going the extra mile of
education to understand thismore advanced form of testing
and I can't be bothered toreading the 55 clinical studies
human clinical studies, forinstance that validate that
small LDL particles aredramatically superior predict of
coronary disease.
(25:50):
It's not that they're notunavailable or not covered by
insurance.
That's nonsense.
They are covered by insurance,they're readily available and
one of the things you'll findwhen you do an NMR lipoprotein
panel.
The two really necessary numbersto look at are LDL particle
number, but especially small LDLparticle number.
So let's say your LDL particlenumber total is 2000 and the
(26:13):
small LDL particle number is1000.
That means 1000 of thoseparticles in the total particle
number of 2000 is small.
That tells you this is going torespond dramatically to
elimination of the foods thatprovoke formation of small LDL
wheat, grains and sugars,because of the amyl, pectin A,
wheat and grains.
And then the sugars, thenutrients we address that
(26:34):
synergize to minimize or reduceinflammation and insulin
resistance.
Vitamin D, magnesium, iodine,omega 3 fatty acids and then we
address dysbiosis, sibo andendotoxemia and what you get is
a dramatic reduction, usuallyelimination, of small LDL If you
start at 1000 or 2000,.
Most commonly drops to zero.
(26:54):
It's not a percentage better,it's gone, and that's because
you're no longer engaging in denovo lipogenesis right from
consumption of carbs and sugars.
You've reversed insulinresistance, you've minimized
inflammation and you'veaddressed endotoxemia.
One of the confusing outcomes ofall this is that it's not
uncommon for LDL cholesterol,and thereby total cholesterol,
(27:17):
to go up.
But you know the equation isinvalid when we've made these
changes in our diet and someother of the basic assumptions
that are used to justify thefree to all calculation.
So even if your LDL cholesterolsays 236 and your doctor's
alarm, think you're going to dieof a heart attack.
It's not a real number.
So what you have to do is getNMR lipoprotein panel to get
(27:39):
that small LDL particle numberNow one of the things we do not
know.
Let's say you get rid of all thesmall LDL out of a total LDL
particle number of 2000.
That means your LDL total LDLparticle number typically drops
to about 1000, right, becauseyou eliminated all the small LDL
particles?
At what level of total LDLparticle number that are all
large and no small.
What is allowable before itcauses coronary disease or adds
(28:02):
to coronary atheroscleroticplaque?
Nobody knows.
Despite the billions andbillions of dollars spent on
cholesterol research, no one hassettled that basic question.
I think, though, that somewherebetween 1400 and 1800 nanomoles
per liter part of the count pervolume of pure large LDL is
probably safe, and above thatmaybe, maybe, adds to risk.
(28:25):
But we don't know that for afact.
But know that by addressing thesmall LDL particle number,
which you've done with all thethings we've talked about,
you've addressed by far the mostvicious cause of coronary
disease.
So, in summary, totalcholesterol worthless,
calculated LDL cholesterolnearly worthless, very limited
in its ability to predict heartdisease and very misleading
(28:47):
information, especially when wechange our diets as we do here.
But there is information intriglycerides and HDL, because
they're inverse to each otherthe higher the triglycerides,
the lower the HDL.
So we're going to turn off yourliver's capacity to manufacture
triglycerides and VLDL particlesby eliminating the foods that
initiate liver de novolipogenesis wheat, grains and
(29:07):
sugars, by minimizing insulinresistance and inflammation that
would have amplified liver denovo lipogenesis, and we're
going to address the unhealthychanges that have occurred in
most people's gastrointestinalmicrobiomes, especially
endotoxemia, and we do so byreintroducing keystone microbes
like lactobacillus rhodii,lactobacillus gastri and perhaps
(29:29):
bacillus coagulants.
These are microbes, especiallyrhodii and gastri, that take up
residence in the small intestinewhere they produce bacteria,
that is, natural antibioticseffective against the species of
sepo, and this reducesendotoxemia.
And there's some additionalthings you can do to reduce
endotoxemia that we can talkabout another time.
But know that you havemagnificent control over
(29:52):
cardiovascular risk and it hasnothing to do with cholesterol.
Now, if you learned somethingfrom this episode of the Defiant
Health Podcast, I invite you topost a review, share a comment,
subscribe to your favoritepodcast directory and help us
build this movement ofself-empowerment in health.
Thanks for listening.
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Current and classic episodes, featuring compelling true-crime mysteries, powerful documentaries and in-depth investigations.
Stuff You Should Know
If you've ever wanted to know about champagne, satanism, the Stonewall Uprising, chaos theory, LSD, El Nino, true crime and Rosa Parks, then look no further. Josh and Chuck have you covered.
The Nikki Glaser Podcast
Every week comedian and infamous roaster Nikki Glaser provides a fun, fast-paced, and brutally honest look into current pop-culture and her own personal life.