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January 4, 2025 41 mins

I’ve touched on the topic of endotoxemia in past episodes of the Defiant Health podcast. In this episode, let’s dive deeper into this topic that is absolutely crucial to understanding and managing SO many aspects of health, from subduing anxiety and panic, to depressive, to joint pain and skin rashes, to gastrointestinal conditions, even weight management. 

What is endotoxemia? Fecal microbes, so-called Gram-negative species because of the way these microbes take up stain for examination under a microscope, species such as E. coli and Salmonella, have something called lipopolysaccharide endotoxin in their cells walls. Other species, so-called Gram positive species such as Enterococcus, Staphylococcus, and Streptococcus, that stain in a different manner, have something called lipoteichoic acid in their cell walls. When these microbes die, both Gram-negative and Gram-positive, these toxic factors are released into the intestines. If these fecal microbes are confined to the colon, where they belong, a section of GI tract adapted to their presence, the entry of these toxic components are limited and current evidence is unclear in how importat this process is. The real trouble occurs, however, when fecal microbes have invaded the 24-feet of small intestine, a process we label small intetinal bacterial overgrowth, or SIBO, because the small intestine—the stomach, duodenum, jejunum, and ileum are not well-adapted to the invasion of fecal species. Here, they die, release their toxic components, which then enter the bloodstream, the process labeled endotoxemia. People with SIBO therefore have high blood levels of endotoxin. This is how microbes in the GI Tract export their effects to other parts of the body. Let’s discuss this process and how you can take control over your emotions, mood, sleep, energy, weight, and numerous other aspects of health. _______________________________________________________________________________
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Transcript

Episode Transcript

Available transcripts are automatically generated. Complete accuracy is not guaranteed.
William Davis, MD (00:05):
I've touched on the topic of endotoxemia in
past episodes of the DefiantHealth podcast.
In this episode, let's divedeeper into this topic that is
absolutely crucial tounderstanding and managing so
many aspects of health, fromsubduing anxiety and panic to
depression.
Aspects of health from subduinganxiety and panic to depression

(00:27):
, to joint pain and skin rashes,to gastrointestinal conditions,
even weight management.
What is endotoxemia?
Fecal microbes, so-calledgram-negative species.
Because of the way thesemicrobes take up stain for
examination under a microscope,species such as E coli and
Salmonella have something calledlipopolysaccharide endotoxin in

(00:49):
their cell walls.
Other species, so-calledgram-positive species, such as
enterococcus, staphylococcus andstreptococcus, that stain in a
different way, have somethingcalled lipotychoic acid in their
cell walls.
When these microbes die, eithergram-positive or gram-negative,
these toxic factors arereleased into the intestines.

(01:12):
If these fecal microbes areconfined to the colon, where
they belong, a section of the GItract adapted to their presence
, the entry of these toxiccomponents are limited and
current evidence is unclear onhow important this process is.
The real trouble occurs,however, when fecal microbes
have invaded the 24 feet ofsmall intestine, a process we

(01:36):
label small intestinal bacterialovergrowth or SIBO, s-i-b-o,
because the small intestine, thestomach duodenum, jejunum and
ileum are not well adapted tothe invasion by fecal species.
Here they die, release theirtoxic components, which then
enter the bloodstream, a processlabeled endotoxemia.

(01:59):
People with SIBO therefore havehigh blood levels, typically
200 to 400% higher levels ofendotoxin in their bloodstream.
This is how microbes in the GItract export their effects to
all other parts of the body.
So let's discuss this processand how you can take control
over it, to be better able totake control over your emotions,

(02:22):
mood, sleep, energy, weight andnumerous other aspects of
health.
And let me tell you aboutDefine Health's sponsors Paleo
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(02:42):
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So endotoxemia is thisbacterial process in which fecal

(03:06):
microbes microbes thatoriginated in the colon have
overproliferated and when theydie they release their toxic
compounds, such as thatlipopolysaccharide and the
lipoticoic acid I mentioned.
Now it's not entirely clearjust how bad endotoxemia can be
if those fecal microbes remainwhere they're supposed to be Now

(03:28):
.
An overproliferation of some ofthese microbial species in the
colon does have implications,such as increased risk for colon
cancer, diverticular diseaseand some other conditions unique
to the colon.
But it appears to be thebiggest problem is when those
fecal microbes over, proliferateand then ascend into the 24

(03:49):
feet of small intestine, andthis can be quite bad.
For instance, people who are intheir beyond age 65, it's not
uncommon for them to have severestomach dysbiosis with fecal
microbes.
It's not uncommon to have fecalmicrobes recovered from
gallstones.
The gallbladder and the biliarytract that empties into the

(04:09):
duodenum is 24 feet up from thecolon.
24 feet, that is three timesthe height of your ceiling, of
the room you're probably sittingin right now.
Yet those fecal microbes havemanaged to colonize the
gallstones 24 feet higher, wherethey don't belong.
Another example of how bad thisprocess of small intestinal

(04:31):
bacterial overgrowth can be.
It's not uncommon for someoneto have pancreatic cancer For
that cancer to be examined.
It's once again like thosegallstones filled with fecal
microbes.
Well, how'd they get there?
The pancreas, likewise, is 24feet up from the colon.
Well, once again, thefootprints of small intestinal

(04:53):
bacterial overgrowth, and thisis incredibly common.
We're not talking aboutsomething that happens to other
people only.
We're talking about at least atleast conservatively estimated
one half the US population,something on the order of 160
million people, have it.
I was skeptical that this couldbe true, even though the
evidence tells us it is.

(05:14):
Until the consumer device, theAIR device remember that A-I-R-E
made by the Food Marble Companythat tests for hydrogen gas gas
as well, as now the currentdevice measures methane also,
but it's hydrogen gas we'remostly interested in and we use
it as a mapping device to tellus where these fecal microbes

(05:35):
are living in the gi tract.
Are they living in the colon,where they're supposed to be, or
had they ascended into the 24feet of stomach, duodenum,
jejunum and ilium?
Now, if you don't know what I'mtalking about, refer to prior
episodes of the Fine HealthPodcast, my blog
WilliamDavisMDcom, as well as mySuper Gut book, and it tells

(05:55):
you how and why to use the airdevice.
It's a consumer device.
You do not need theparticipation of the doctor, you
don't need to get the airdevice to do all these things,
but it's just one of the thingsto be aware of.
So it's this process of smallintestinal bacterial overgrowth
that we're mostly interested in,where trillions, trillions of

(06:15):
bacteria, fecal species, areliving in the 24 feet of small
intestine and when they die theyrelease their toxic compounds
of small intestine.
And when they die they releasetheir toxic compounds,
especially endotoxin,lipopolysaccharide, endotoxin
and lipoticoic acid, that enterthe bloodstream.
And this is how a disruption ofthe gastrointestinal microbiome

(06:36):
enters the bloodstream andexports the effects to all other
parts of the body.
So, yes, a disruption of thegastrointestinal microbiome can
affect your brain or yourthyroid gland or your airway or
your oral cavity or your skin oryour prostate or your uterus or

(06:58):
just any other organ.
A lot of this is driven notentirely other processes that
microbes can participate in thatcause disease, but a big part
of this is driven not entirelyother processes that microbes
can participate in that causedisease.
But a big part of this is thisendotoxemia of the two kinds of
toxins.
Can we measure it?
How do you measure whether youhave an increased level of
lipopolysaccharide orlipoptychoic acid?

(07:18):
Well, unfortunately theseremain research tools not
clinically available.
You can't go to LabCourse, say,or Quest Diagnostics and get
these things measured, perhapsin the future.
But the reluctance is that theyare not the best methods
because the lipopolysaccharidemeasurement, for instance, only
measures the we say LPS, the LPSof only selected species.

(07:41):
So for instance, if we measurethe LPS of E coli and Klebsiella
it might miss the LPS of otherspecies and it underestimates
the severity of the endotoxemia.
But existing evidence tells usthat in people with endotoxemia
typically have 200 to 400%increase in blood levels of LPS

(08:05):
endotoxin.
My personal view is even thatflawed or underestimated
measurement could still behelpful.
So I'm hoping at some point wecan make these measurements
outside of research and do themclinically, because of this
difficulty in trying to quantifythe severity of endotoxemia.
A second best is to measurehydrogen gas on the breath, as I

(08:27):
mentioned, because microbesproduce hydrogen gas when fed
properly, that is, fed aprebiotic fiber or sugar.
You cannot on your own producehydrogen gas.
So we can use the timing of howquickly hydrogen gas is
released when you ingestsomething.
We use inulin, the fiber inulin, and depending on how fast

(08:48):
hydrogen gas is produced fromthe conversion of inulin to
hydrogen gas, we can use that tomap where microbes are living.
So that whole protocol is in myblog, is in my Super Gut book,
if you're interested.
Now endoscopy can be used butit's not very public because it
requires an invasive procedureand when they do an endoscopy
upper endoscopy they canretrieve some of the liquid in

(09:11):
your duodenum or your jejunumand they can look at it.
Unfortunately, most clinics andhospitals don't have DNA
testing for this specificpurpose available and they
culture that liquid.
Well, that's a flawed methodbecause the vast majority of
species that invade the smallintestine that is SIBO cannot be

(09:31):
cultured, and so if theyculture it, it's only of limited
usefulness.
But if it's positive for a lotof fecal microbes, you know
you've got SIBO.
But don't rely on this methodbecause it underestimates the
severity of SIBO.
It's only helpful when it'spositive when a culture is done.
How about stool testing?
Well, stool testing is useful,but think of stool testing as a

(09:55):
rectal test, that is, a testingof a sample of rectal stool.
It does not necessarily reflectthe microbiome composition, say
, of the ileum about five feetup from the rectum or the
jejunum or the duodenum.
So it can be helpful, but itreally can't be used to diagnose
SIBO specifically, because youreally need to know where those

(10:20):
fecal microbes are living.
So stool testing can't tell youthat.
The best stool testing can dois if you submit a sample and
you see lots of thosegram-negative species like E
coli, klebsiella, salmonella ora lot of those gram-positive
species, especiallyStreptococcus, staphylococcus
and Enterococcus.
It hints at the presence ofSIBO, even though it's taken

(10:44):
from a rectal test or at thevery least you have colonic
dysbiosis.
So it still can be very useful.
And you know what?
The methods, the strategies tocorrect rectal or colonic
dysbiosis are not that differentfrom the strategies to correct
SIBO.
So even though you really can'tdiagnose SIBO from stool

(11:04):
testing, you can at least safelypresume that SIBO is present if
you see these kinds of patternsof excessive quantities of
gram-negative or gram-positivemicrobes in the fecal sample
obtained from the rectum.
Now there are numerous otherlaboratory measures that can
hint at the presence ofendotoxemia, but they're not

(11:25):
specific for endotoxemia.
But they're not specific forendotoxemia.
They can suggest to you thatsomething is continuing to drive
metabolic distortions fromendotoxemia.
These mostly drive factors suchas insulin resistance and
inflammation.
Recall that insulin resistanceis the process in which your
body's organs liver, muscle,brain do not respond normally to

(11:48):
insulin.
So your pancreas compensates byoverproducing huge quantities
of insulin and that leads to itsown collection of problems,
including an expansion ofabdominal fat, increased
likelihood of high bloodpressure, high blood sugar,
fatty liver, coronary disease,atrial fibrillation, cognitive
impairment, breast cancer risk,etc.

(12:09):
So these two processes insulinresistance and inflammation are
very important in driving riskfor many diseases.
So these measures that cansuggest that endotoxemia is at
work, making these measuresworse, includes triglycerides.
A higher triglyceride suggestsendotoxemia.
Low HDL, higher blood glucose,higher fasting insulin,

(12:33):
especially above four microunits, and increased measures of
inflammation, such as C-reactiveprotein or interleukin-6.
Now here's another twist to allthis.
If you're on my programs inwhich we address diet no wheat,
no grains, no sugars we addresscommon nutrient deficiencies
that drive insulin resistanceand inflammation, like omega-3

(12:54):
fatty acids, magnesium, iodine,vitamin D, and then we take
basic steps to address thedisrupted gastrointestinal
microbiome.
And then we take basic steps toaddress the disrupted
gastrointestinal microbiome.
Well, if you've done all thesethings, you've lost weight and
now your weight has plateaued.
Maybe you lost 40 pounds doingthese kinds of things, but your
weight has plateaued for thelast four weeks or more If

(13:15):
you're left with any of thosemeasures I mentioned high-ish
triglycerides anything above 60milligrams per deciliter.
Low HDL anything below 60milligrams per deciliter.
Blood glucose higher than 100milligrams per deciliter.
Low HDL anything below 60milligrams per deciliter.
Blood glucose higher than 100milligrams per deciliter, higher
blood insulin above 4 microunits or any C-reactive protein
above 1.0 milligrams perdeciliter.

(13:36):
Those are all suggestions thatendotoxemia is still ongoing and
that specific efforts need tobe made.
In other words, those measuresare not perfect.
Those measures should beperfect on my programs
Triglycerides less than 60.
Hdl greater than 60.
Blood glucose 60 to 90.
Insulin almost zero, c-reactiveprotein almost zero.

(13:59):
They should all be near perfecton the program, but if they're
not, they can serve as atherapeutic test, a red flag
that there's some level ofendotoxemia, sibo and therefore
endotoxemia driving theseabnormal factors.
How common is this?
How common is it to have SIBOand thereby endotoxemia in some

(14:24):
form?
Extremely common.
All we have to do is look atthe several dozen studies done
in humans that ask this question.
Now, if you've read my superguide, you already know these
arguments.
But nonetheless, for review, ifwe ask, for instance, in
condition blank, what proportionof people test positive for

(14:45):
SIBO, usually using hydrogen gasor some variation.
So how about irritable bowelsyndrome, IBS?
Well, there's 60 to 70 millionAmericans with IBS and while the
results vary from study tostudy, about 31% will test
positive for SIBO.
So that's 31% of 60 to 70million?

(15:07):
Well, that's 18 to 20 millionor so people right there.
How about the 110 or so millionpeople in the US who are obese?
How many test positive?
What percentage test positivefor SIBO?
50%, well, that's another 50,some million people to add to
the list.
How about type 2 diabetes?
37 million people.

(15:29):
50% would test positive.
Add another 18 million.
Now add on fibromyalgia,restless leg syndrome, sleep
apnea, various forms ofinflammatory bowel disease like
ulcer of colitis and crohn'sdisease, neurodegenerative
disorders like Alzheimer's orParkinson's disease.
How about autoimmune diseases?

(15:50):
Add those all.
There's going to be someoverlap.
Right, an obese type 2 diabeticwith fatty liver, but you can
see that we rapidly exceed 150million people.
We don't have a precise number,but we don't need to.
You know that this isexceptionally common.
Look to your left, look to yourright.
You're going to see at leastone, if not two, people with

(16:12):
SIBO, who often are not aware ofit, that this is driving their
diseases.
And without specificallyaddressing the SIBO and
endotoxemia you can never hopeto have Now let's pause for a
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(16:36):
conditions in which SIBO andendotoxemia are major driving
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(19:55):
Now let's get back to ourdiscussion.
Let's first consider overweight, obesity and the expansion of
abdominal fat.
For the sake of illustration,let's assume you start this
process without SIBO and you'reslender and don't have a lot of
abdominal fat.
Of course that's not.
You start this process withoutSIBO and you're slender and
don't have a lot of abdominalfat.
Of course that's not the casefor many people.

(20:17):
They've got abdominal fat andare overweight because of
overconsumption of sugars,grains and other junk foods,
ultra-processed foods.
But for the sake ofillustration, for the sake of
argument, let's assume you startin good health with only
minimal abdominal fat and you'renot overweight.
Start in good health with onlyminimal abdominal fat and you're
not overweight.
Well, you develop SIBO forwhatever reason.

(20:37):
Maybe you took a course ofantibiotics, maybe you've been
overexposed to the glyphosate ingrain products, maybe you eat
too many processed foods withadditives like emulsifying
agents or preservatives that areantimicrobial.
For whatever reason, youdevelop SIBO and thereby
endotoxemia.
Recall that endotoxemia drivesinsulin resistance and

(21:00):
inflammation that causes theexpansion of abdominal fat.
Abdominal fat, of course, isthe form of fat that is
inflammatory and makes insulinresistance worse.
So you can appreciate what isgetting started.
Here is a vicious cycle, rightSIBO, endotoxemia, resulting in
insulin resistance andinflammation, which causes

(21:21):
expansion of abdominal fat, andweight gain, which in turn,
worsens insulin resistance andinflammation, which causes
further expansion of abdominalfat.
That, in turn, amplifies theinsulin resistance and
inflammation around and aroundand around in this awful vicious
cycle that is very difficult tobreak if all you do is change

(21:42):
your diet.
So, while changing diet is veryimportant, addressing those
common nutrient deficiencieslike vitamin D and magnesium
that help regulate insulinresponses you also have to
address the SIBO and endotoxemiathat is driving these processes
.
In a similar way, type 2diabetes high blood glucose from

(22:05):
excessive levels of insulinresistance and inflammation is
driven by SIBO and endotoxemia.
Inflammation is driven by SIBOand endotoxemia.
So while, yes, you can dothings like cut your carb
content, get vitamin D those areall very important you can also
go farther by addressing theSIBO and endotoxemia.

(22:26):
I would like you to ignore thepeople, many of them the
American Diabetes Association.
Most doctors, includingendocrinologists, say that once
you have type 2 diabetes, youcan never not have type 2.
This is patent nonsense.
There's more than ampleevidence to tell us that type 2
diabetes in most not all, but inmost cases.

(22:47):
There are some exceptions inmost cases is completely
reversible or at the very least,you can further.
You can reduce measures likehemoglobin a1c to the very
lowest possible range.
I, for instance, was a type 2diabetic about 40 years ago.
It lasted maybe six monthsuntil I understood what was
going on and, by the way, thatdeveloped in me when I follow a

(23:10):
strict low-fat vegetarian diet,even though I was jogging
several miles a week.
I was riding my bicycle playingtennis.
I was in my 30s, so a long,long time ago.
Yet I developed type 2 diabetes.
I stopped eating badly that is,eating a low-fat vegetarian
diet added back oils, fats andstarted limiting carbohydrates

(23:31):
instead and became confidentlynon-diabetic, and have remained
so for the last 40 years.
So don't listen to the peoplewho say you cannot undo it.
The rare exceptions are peoplewho've done irreversible damage
to their pancreases, and you'llknow that if you do everything
right, you've lost the weight,you've addressed endotoxemia,

(23:51):
you've restored vitamin D,magnesium, omega-3 fatty acids
and iodine, your thyroid's ingood shape, yet you still have
some measure of insulinresistance or type 2 diabetes
that tells you you've damagedyour pancreas.
Thankfully, that's less than 5%of people who are currently
type 2 diabetic, meaning thegreat majority over 90% have the

(24:12):
capacity, if given the righttools, to undo completely,
reverse type 2 diabetes.
Coronary disease Coronarydisease or coronary
atherosclerosis is the process,of course, that leads to heart
attack.
Sudden cardiac death leads toprocedures like stent
implantation and bypass surgerywhich, becoming clear, if you

(24:35):
have coronary disease meaningyou had a heart attack or you
had a procedure like a stentimplantation or you had a
positive coronary calcium score,say, of 200 or 700 or whatever
you have endotoxemia, sibo andendotoxemia driving the
expansion of coronaryatherosclerotic plaque.
Even worse, endotoxemia seemsto drive events that is, the

(25:00):
rupture of so-called soft plaque, the fatty elements in
atherosclerotic plaque.
That rupture and that's whatcauses the internal contents of
that plaque to be exposed tocirculating blood rushing past
and that provokes blood clot.
And so, while blood clot is notthe primary process, it's a

(25:22):
consequence.
It's the coronary diseasethat's being driven by
endotoxemia.
Inflammation in theatherosclerotic plaque leads to
plaque rupture.
So seabone endotoxemia, majorplayers in all the various ways
that coronary disease can showitself.
Atrial fibrillation is verycommon.
Abnormal heart rhythm in whichthe top little sacs of the heart

(25:43):
ordinarily low pressure andyou're not even aware that these
things are contracting in yourheart.
When you feel your heart beatby the way, that's the major
pumping chamber, the leftventricles you don't really feel
the atria on top, the right andleft atria.
You don't feel them, butthey're contracting and
contributing to the output ofyour blood flow from your heart.

(26:03):
When the atria are exposed toendotoxemia, they gradually
develop fibrosis or fibroustissue deposition into the walls
of the atrial muscle and thatcauses chaotic rhythms, chaotic
electrical rhythms that resultin this rhythm called atrial
fibrillation.

(26:23):
Typical experience Someone'sjust sitting minding their own
business, maybe watching TV, andthey all of a sudden are
breathless, lightheaded.
They check their pulse Ratherthan a normal 70 or so beats per
minute, it's 150 or 160 orsomething like that, and you
feel breathless.
You go to the ER.
They thin your blood with ananticoagulant to prevent the
stroke that can come from thisrhythm.

(26:45):
They slow the rhythm down sothat you can catch your breath
and then over time they do otherthings like try to convert the
rhythm with medications verydangerous by the way, or what's
called cardioversion, where theygive you a shock to the chest
to break the rhythm and someother methods.
It's something you don't want.
Atrial fibrillation once youdevelop it tends to rule your

(27:05):
life.
You're back and forth to theemergency room having
recurrences.
They sometimes then tell you tohave it ablated, where they
take catheters and they burn outthe source of the rhythm.
Sometimes it's effective,sometimes it's not.
Bottom line here, major driverof both the development of
atrial fibrillation and the veryfrequent recurrences is

(27:25):
endotoxemia.
Sadly, once you've developedatrial fibrosis that is, fibrous
replacement of atrial muscletissue with fibers it becomes
harder and harder to control therecurrences of this rhythm,
even if you address endotoxemia.
So the key is to addressendotoxemia as early as possible

(27:46):
, before irreversible changesdevelop, such as atrial fibrosis
, skin rashes.
It's become clear that some ofthe more complex skin rashes,
especially rosacea and psoriasis, are driven largely by seabone
endotoxemia.
So once again, an example ofhow body part skin far away from

(28:09):
the gastrointestinal tract isinfluenced by what goes on in
the gastrointestinal tract.
Now there's more to skin rashthan this.
There's also disruption in theskin microbiome, such as the
provocation of the pathogenStaphylococcus aureus instead of
the beneficial microbesStaphylococcus epidermidis.
Please see my other DefineHealth podcast episodes and my

(28:31):
blog for a conversation aboutthat.
But know that a drivinginitiating factor is endotoxemia
from your GI tract and if youwant control you can take those
biologics that blocks one partof a pathway that leads to skin
inflammation.
But why not go to the rootsource, endotoxemia that
initiated that inflammation inthe first place?

(28:55):
Cognitive impairment, all thephases and degrees of cognitive
impairment, early cognitiveimpairment, early dementia,
well-established alzheimer'sdementia.
A big player is SIBO andendotoxemia.
That's why if you ask anybodywho's got cognitive impairment,
ask them about theirgastrointestinal health, they'll
say well, I'm eitherconstipated or have intermittent

(29:16):
diarrhea or abdominal pain.
They have other problems,gastrointestinal problems,
because a driving force hereonce again is SIBO and endotoxin
or, at the very least, colonicdysbiosis.
So you can imagine you can takethose silly drugs for cognitive
impairment, the so-calledacetylcholinesterase inhibitor
drugs, very expensive, that doalmost nothing for improving

(29:40):
memory and certainly do not doanything in slowing the
progression of the disease.
So you need to get at the rootcause, in this case the thing
driving endotoxemia, and that'swhere you start to regain
control over cognitive health.
Cancers it's becoming clear thatnumerous forms of cancer are
driven by SIBO and endotoxinGastrointestinal cancers like

(30:04):
pancreatic cancer or coloncancer or small intestinal
cancers or gallbladder cancer orliver cancer, but also cancers
outside the gastrointestinaltract Breast cancer, prostate
cancer, other cancers.
In fact, I call endotoxemia theuber risk factor for cancer,

(30:25):
that is, it's responsible for somany forms of cancer.
Maybe there's more to do toprevent cancer beyond addressing
endotoxemia, but knowing thatendotoxemia is a major driver
gives you the key to reducecancer risk dramatically across
numerous organs.
Female health, the two ends offemale health, reproductive age

(30:48):
when you're having children andmenopausal and postmenopausal
the microbiome plays a huge role.
A disrupted vaginal so we'retalking about vaginal and
gastrointestinal microbiomeleads to unhealthy things like
eclampsia and preeclampsia inpregnancy that can lead to
seizures in the mother and thechild and threaten the survival

(31:10):
of either or both Endometriosisvery painful condition driven by
endotoxemia.
Premature labor and miscarriagedriven by both a disrupted
vaginal microbiome and agastrointestinal microbiome.
Even difficult or turbulentmenstrual cycles with a lot of
pain and cramping or excessbleeding, also driven by the

(31:34):
vaginal and the gastrointestinalmicrobiome.
Now, this is one area I won'tfully cover in this episode of
the podcast.
I'll cover this separately, orsee my Super Gut book or my blog
, williamdavismdcom.
You'll see severalconversations about the unique
features of a disrupted femalemicrobiome and what steps you

(31:55):
can take both for thegastrointestinal and the very
important vaginal strategies youcan adopt to reduce the risk
for all those health conditions.
How about mental or emotionaleffects?
What's become clear?
That the gastrointestinalmicrobiome, via endotoxemia, is
a major driving force.
A major driving force innumerous aspects of mental

(32:19):
health depression, anxiety,panic attacks, uncertainty, that
feeling of you don't reallyknow what you're doing, hatred,
violence, social anxiety,anxiety in social settings and
numerous others.
These are, to an astoundingdegree, phenomena driven by a

(32:40):
disrupted gastrointestinalmicrobiome via blood-borne
endotoxemia.
For similar reasons, disruptionof sleep and nightmare dream
content, largely influenced bywhat's going on in your
gastrointestinal system and yourbloodstream.
So if you're struggling withsleep frequent interruptions,
early morning awakenings,nightmares, unhealthy dream

(33:03):
content think about endotoxin asa driver of those phenomena.
Now here's a twist it's shockinghow many people have no
symptoms.
So people often say I have nosymptoms of diarrhea or bloating
or abdominal discomfort, I musttherefore not have SIBO.
Not true?

(33:23):
Remarkably, this fact is oftenoverlooked.
If we looked at all thosestudies we talked about, in
which we asked, in conditionblank, what proportion tests
positive for SIBO?
Well, those people, let's say,with irritable bowel syndrome or
ulcerative colitis or obesityor type 2 diabetes, are compared

(33:44):
to so-called healthy controls.
These are people chosen forcomparison in these studies
because they lack thoseconditions and lack any symptoms
of gastrointestinal disease.
They don't have bloating, theydon't have diarrhea, they don't
have constipation.
They have no symptoms.
What proportion of those peoplepurported healthy control

(34:05):
people test positive?
Well, it varies widely fromstudy to study, but typically 20
to 30% or so test positive forSIBO.
In other words, you can takewhat appear to be healthy
control people with nogastrointestinal symptoms, no
coronary disease, no atrialfibrillation, no rosacea,
nothing.
Yet they still test positive.

(34:25):
About a fifth to a quarter oreven a third of those people
test positive.
And accepting that the methodsof testing likely underestimate
how many people do test positive, but recognize that the lack of
symptoms does not necessarilymean you're not heading to a
level of endotoxin that couldtrigger such things as atrial

(34:47):
fibrillation or fibromyalgia orweight gain.
Now let's talk about how tocorrect this.
Now, if the solution wassomething drastic, like surgical
removal of your small intestine, well, we better be absolutely
certain, as certain as we can be, that this situation applies to
you and that a surgicalsolution is necessary.

(35:08):
But what if the solution issomething that looks and smells
like yogurt?
It's not yogurt, but it looksand smells like yogurt that you
can make in your kitchen, andthat's what I call SIBO yogurt.
This is a recipe or formulationI created by asking this simple
set of questions.
If you have SIBO right 24 feetof small intestine, bacterial

(35:31):
overgrowth, thereby endotoxin,but driving all those processes
we talked about, what if youjust took a commercial probiotic
off the shelf from the healthfood store or the big box store?
Will this process go away?
No, those studies tell us youcannot take a probiotic and
expect SIBO to recede completely.
It might be reduced slightly,you might experience a little

(35:53):
reduction bloating, for instance, or some phenomenon associated
with SIBO like a skin rash butit will not get rid of the SIBO.
So I asked a different set ofquestions.
I asked what if we specificallychose microbial species that
are known to colonize the smallintestine?
That's where SIBO occurs, right, that's where the increased

(36:15):
permeability that allowsendotoxins to enter the
bloodstream.
So what if we chose speciesthat colonize the small
intestine where all this occurs,and also produce bacteriocins?
These are natural antibioticseffective in killing fecal

(36:35):
microbial species, bothgram-negative and gram-positive.
I chose three.
I chose a strain oflactobacillus reuteri, a strain
of lactobacillus gasseri and thespore-forming microbe bacillus
coagulans, because all threewill take up residence or will
germinate in the small intestineand produce bacteriocins.

(36:57):
So I call this SIBO yogurt.
We're going to use my method ofextended or prolonged
fermentation because microbesdon't have sex right.
There's no male and femalemicrobes, they just double
themselves.
Well, lactobacillus rhodori,which is probably the most
important of the three, we usedoubles every three hours at
human body temperature, everythree hours at human body

(37:17):
temperature.
So let's ferment it for 36hours, or 12 doublings.
We count the microbes usingsomething called flow cytometry
and we get 300 billion microbesper half cup or 120 milliliter
serving.
We do that for four weeks andso far this has exceeded my
expectations.

(37:38):
By the way, I initiallyformulated this I didn't think
it would get rid of SIBO.
I thought it might help peopleget some relief from some of the
symptoms of SIBO, like bloatingand diarrhea.
To my great surprise, with theavailability of the air device
that tests and maps wheremicrobes are living fecal
microbes in the GI tract, lo andbehold, we're seeing about a

(37:58):
90% success rate when this SIBOyogurt is consumed every day for
four weeks.
Now some people an occasionalperson has SIBO so bad that they
have to do it for months.
These are people who say thingslike I've taken an antibiotic
for the last three years forthis or that process, like acne
or something like that.
Those people have SIBO to suchan extreme degree that a

(38:20):
prolonged course of the SIBOyogurt is required.
But no, it's just somethingthat looks and smells like
yogurt and so far it hasexceeded expectations.
In normalizing breath hydrogengas, the only caution is that
lactobacillus reuteri itself cancause release of hydrogen gas.
Hydrogen gas is not per seharmful.
It's just a reflection of fecalmicrobes in the small intestine

(38:44):
.
But oddly, lactobacillusroterite shares that capacity to
convert inulin that we use toprovoke this to hydrogen gas.
So if you're going to test atthe end of your SIBO yogurt
course, you have to stop theSIBO yogurt for two weeks, then
test and you can see whetheryou're positive or negative.
Or you can watch some symptomLike is your food intolerance

(39:05):
better?
If that's true, you got rid ofSIBO.
Is the fat malabsorption?
Fat drops in the toilet.
Has that stopped?
That means you reversed SIBO?
Is your sleep disruption muchimproved?
You've likely reversed SIBO, soyou always use one of those
signs to tell you whether or notyour SIBO has been corrected or
not.
But you know what?
I kind of regret calling itSIBO yogurt, because it makes it

(39:26):
sound as if it's only usefulfor management of SIBO, which is
not true.
Especially, rotaroy has benefitsfar beyond just reduction of
SIBO and endotoxemia.
Recall that Rotarot can do allkinds of things via its capacity
to provoke release of oxytocinfrom your brain, as well as
colonizing the GI tract, theentire length of the GI tract,

(39:47):
and producing bactericids.
So you can expect all kinds ofother effects an increase in
empathy and generosity, a returnof youthful musculature, an
increase in libido, reduction inwaist circumference, abdominal
fat, so many other things.
So for that reason and becauseSIBO recurs, the rule is
recurrence.
You may have had a successfuleradication and then it comes

(40:11):
back in three, four, five or sixmonths.
So while we use the SIBO yokefor four or more weeks, it's
also a good idea to continue toget it two or three times per
week for the rest of your lifeor until we figure out how to
make rhodorite and those othermicrobes take up permanent
resins.
No one has figured that out yet.
So until then we continually oroccasionally re-implant those

(40:34):
species to keep SIBO fromrecurring and to make sure you
continue to enjoy all thewonderful benefits of those
microbes, but know that you haveextraordinary control over what
goes on in yourgastrointestinal tract and
thereby endotoxemia, and youthereby can address risk for all
those conditions we talkedabout obesity, type 2 diabetes,

(40:57):
atrial fibrillation, skin rashes, cognitive impairment all
starting with restoring thiscollection of microbes that we
call SIBO yogurt.
Now, if you've learnedsomething from this episode of
the Defiant Health Podcast, Iinvite you to post a review,
post a comment, subscribe toyour favorite podcast directory.
Let's help build this movementof self-empowerment and health

(41:18):
that you can accomplish on yourown, without the interference of
the doctor.
Thanks for listening.
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