April 24, 2025 • 55 mins
Metabolic Endotoxemia: The Gut–Gut-Inflammation Link You Can’t Ignore!
Could chronic, low-grade inflammation be rooted in your patient’s gut? In this compelling episode, naturopath Steven Judge unpacks the emerging science of metabolic endotoxemia—where bacterial endotoxins (LPS) escape a compromised gut barrier and trigger systemic immune responses linked to cardiovascular disease, insulin resistance, endometriosis, and more.
You'll gain a deeper understanding of intestinal hyperpermeability, toll-like receptor activation, and how to identify root causes like stress, toxin exposure, and circadian disruption.
Steven also shares evidence-based tools—including omega-3s, polyphenols, PEA, and bovine immunoglobulins—to help reduce the inflammatory load and support long-term gut healing.
This episode is a must-listen for practitioners wanting to connect ancient gut wisdom with today’s cutting-edge clinical practice.
Connect with Steven: Steven Judge Clinical Naturopathy
Shownotes and references are available on the Designs for Health website
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DISCLAIMER: The Information provided in the Wellness by Designs podcast is for educational purposes only; the information presented is not intended to be used as medical advice; please seek the advice of a qualified healthcare professional if what you have heard here today raises questions or concerns relating to your health
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:19):
Music.
This is Wellness by Designs,and I'm your host, andrew
Whitfield-Cook.
This is Wellness by Designs,and I'm your host, andrew
Whitfield-Cook.
And joining us again today isStephen Judge, a naturopath and
nutritionist who specialises incomplex, chronic gut issues.
Today, we're going to bespeaking about metabolic
endotoxemia.
All diseases have a gutcomponent.
(00:40):
Welcome back to Wellness byDesigns, stephen.
How are you?
Speaker 2 (00:44):
thanks, angela.
Speaker 1 (00:44):
I'm great thanks for having me again absolute
pleasure and thank you so muchfor joining us today.
So I think we start off withwhat is in metabolic endotoxemia
and where is it applicable yeah, sure.
Speaker 2 (00:59):
So before defining that, I guess to provide the
context as a reminder, you knowwhat is this concept of
so-called leaky gut orintestinal hyperpermeability?
Right, so the intestinalbarrier wall is a gatekeeper,
right, physiologically healthygut.
(01:21):
This barrier should selectivelybe allowing macro and
micronutrients and water throughthe gut wall and into our
bloodstreams so that thesecomponents can be sent to the
organs and tissues that needthem.
So we could say that the liningof our gut wall should be
selectively permeable, right, soit should only be letting
(01:42):
through what needs to go throughand it should not be letting
anything through that shouldn'tbe found in circulation, so
microbial toxins, bacteria,metabolic waste, et cetera.
And the structure of theintestinal barrier wall is like
this three-layered membrane.
So the first layer is thesingle-celled semi-permeable
(02:06):
layer of epithelial cells heldtogether by tight junctions.
On top of this is a doublelayer of mucus on top of these
cells and the gut bacteriareside on top of that mucus
layer.
Due to various factors, whatcan happen is the tight
junctions between thoseepithelial cells on the first
layer can degrade, gaps can formin the lining of this wall,
(02:28):
subsequently increase thebarrier's permeability, leading
to what we call intestinalhyperpermeability, aka leaky gut
.
So the loss of integrity in thehealth of this barrier, aka
leaky gut, has been suggestedfor decades, you know, if not
longer, um to supposedly lead toor be a contributing factor to
(02:53):
a variety of symptoms andconditions like not just
digestive, but metabolic andneurological and autoimmune.
And all these things, and whatthe research on this area called
metabolic endotoxemia ishighlighting is that it appears
that, okay, it looks likeeverything really does start in
the gut, or is driven by a leakygut, so to speak, and the
(03:16):
mechanisms of metabolicendotoxemia explains this very
well at a very specific kind ofbiochemical level.
And, yeah, the research isconfirming there's a lot of
truth to the concept ofso-called leaky gut, which is
(03:39):
amazing because, consideringthat, considering the wisdom of
ancient traditions have heldthis perspective for centuries.
Right In Ayurvedaveda, you know, they've always taught that the
agni, or digestifies, the keyto optimal health in tcm, spleen
and stomach, qi are fundamentalto overall health and they are
a fundamental component of thedigestive system, and
Hippocrates said that death sitsin our bowels and Henry Lindlar
(04:02):
said that, you know, um, theaccumulated, accumulated morbid
matter and systemic poisons thatare reabsorbed are what drives
disease.
So, yeah, it's kind of coolthat this field of research on
metabolic endotoxemia isstarting to confirm all this
right.
So, with all that right so withendotoxemia, the the simple
(04:27):
definition of it, which I'llexpand upon, is a condition
where there are excessive levelsof something called lps, short
for lipopolysaccharide, in thebloodstream.
And so the term endotoxin,which is what lps is referred to
.
It comes from the greek wordendo, meaning within, because
(04:51):
lps is a molecule found withinthe outer membrane of
specifically gram negativebacteria.
It's what differentiates gramnegative bacteria from
gram-positive bacteria.
It is this LPS that is housedwithin the outer membrane.
And you know, lps inherentlyshouldn't be an issue.
(05:13):
And you know, while a healthygut wall can handle a small
amount of LPS getting intocirculation and be appropriately
handled by the liver to becleared from the body, it
shouldn't, this LPS, endotoxinshould not be getting through
that gut wall in large amounts.
If excessive levels of LPS doget into systemic circulation
(05:35):
due to the gut being toopermeable, this essentially
triggers the innate immunesystem, leading to this chronic,
low-grade subclinicalinflammation.
And, as we know, you know, thechronic inflammatory state is
increasingly recognized as a keydriver of most chronic diseases
.
(05:55):
Um, so we have to step back andgo, okay.
Well what's driving chronicinflammation in all of these
chronic diseases, and we arerepeatedly being brought back to
the gut, and specifically thisendotoxemic mechanism is a very
common explanation linking allthese conditions together.
(06:16):
So you know, we're essentiallylooking at the downstream effect
of specific types of dysbiosisor bacterial imbalances and a
hyperpermeable gut wall.
So if someone has LPS producingbacteria dominating their
microbiome and their gut wallbecomes too permeable, this is
essentially going to lead tometabolic endotoxemia and so the
(06:41):
excessive LPS endotoxin in thebloodstream.
It triggers the innate immunesystem in some very specific
ways, which we'll get into,because the immune and kind of
subsequent inflammatorychemicals that are triggered as
a result of this can interactwith and impact such a wide
(07:04):
variety of tissues and organs inthe body, which is why so many
conditions are being linked backto endotoxemia, which is so
interesting, and so the termmetabolic endotoxemia is simply
a term researchers came up withto describe when this successive
LPS in the bloodstream wasobserved to directly kind of be
(07:28):
the beginnings of metabolicdisorders such as insulin
resistance and obesity and thatkind of thing.
Speaker 1 (07:36):
So just, there's so many questions floating around
about LPS.
Firstly, let's talk about thatquote-unquote leaky gut.
So first things first.
It was Brad Leach who basicallyhelped to dismantle that
syndrome issue.
There's no leaky gut syndrome.
(07:56):
It's not a syndrome.
That's kind of like sayingthere's a pain syndrome or a
breathing syndrome but there isleaky gut and there is excessive
leaky gut, yeah, but it's not adefined syndrome, if you like.
So thank you, brad, for doingthat, and I've watched Vlad's
(08:16):
career blossom over the years,which is great to see.
One of my questions, though, isthat kids and the elderly have
naturally more leaky guts, evenleaky brains.
How does this tie into functionversus dysfunction?
Speaker 2 (08:39):
Yes, love your work, brad.
And I agree.
You know like I'm very carefulwhen with clients, when
discussing these topics of leakygut, gut dysbiosis, sibo, et
cetera.
I don't like to refer to themas conditions or diseases, so to
(08:59):
speak, even though when youread about things like metabolic
endotoxemia in the research itgets referred to as like a
condition, um, so to speak, um.
But you know the danger therewith um, particularly with
clients who, um are desperatelylooking for a, um, a reason for
why they're so unwell and what'skind of the quote-unquote root
(09:21):
cause of their illness.
I'm very careful with mylanguage these days to make sure
people understand that leakygut is certainly not a syndrome
or a condition.
It's just something, that it isthe downstream effect of a
variety of upstream contributingroot causes.
I'm very careful to say look,leaky gut, sure it's become a
(09:45):
contributing factor to um,perpetuating a disease related
to chronic inflammation, butit's that I wouldn't say it's
the root cause, because what canhappen is people can become a
bit too reductionist about itand they're just looking for the
next antimicrobial protocol andthe next probiotic and it's not
to say those interventions arenot useful and helpful, but it's
(10:08):
like one-tenth of the picture,you know.
So while it is helpful to getreductionist about it and get
into the mechanics of it, at theend of the day to address all
this you kind of actually justhave to zoom out and address
someone's overall health.
Really, you know.
Speaker 1 (10:25):
Yeah, I totally agree with you.
I think it was Dr McLion whosaliently pointed it out about
this kill-kill mentality and hesaid what happens, particularly
with extremely sick peoplechronic fatigue people, multiple
chemical sensitivity, et ceterais you kill everything off in
the gut and they've got nothing.
(10:46):
So they become what's calledthe mashed potato and peas
brigade and they end up cyclingat a lower ebb.
They never revitalise theirsystem.
So I love what you say aboutwe've got to dig down, or you
know, to the root causes.
So let's start with thosecauses.
Speaker 2 (11:02):
Stress, anyone, yeah, yeah, and to your point, like,
for example, just recently, youknow very recently, in the past
number of years, you knowthere's a lot of awareness
around.
You know, one of the conditionsit's a new study came out, a
few weeks ago I think, on an lpsproducing bacterial overgrowth
(11:26):
being commonly associated inwomen with endometriosis.
Um, okay, cool, it's anotherstudy looking at this lps
endotoxemic link withendometriosis.
But then what I see and youknow this is just in the online
world, but like what I see fromthe general public and even some
practitioners, you know,following from that, which is
(11:47):
like cool, this, there's thisresearch here confirming this
link with endotoxemia.
But then what can happen ispeople go, okay, cool, the
solution, therefore, is going tobe how do we kill this bacteria
?
Um, what are all the things toget this bacteria Like?
It becomes this almost likeconventional medical germ theory
(12:08):
kind of discussion.
It's like, look, it'sabsolutely wonderful, there's
another link to proving thiswhole and its relationship to
perpetual endometriosis.
But I guess, like, the dealingwith the bacterial overgrowth is
just one piece of this puzzle.
You know, it's almost like adamage control kind of style of
(12:29):
treatment.
Cool, we want to get on top ofthat.
But, like, in the longer term,to get on top of this and
educate people about how, to youknow, truly reverse LPS kind of
endotoxemia and leaky gut wehave to zoom out and go and go,
cool.
But what led to that type ofbacterial overgrowth, right and
to your point?
Yes, stress, nervous systemdysregulation, circadian rhythm
(12:51):
disruption and poor sleep it washuge, like um a bit more longer
term to consider and address.
But, like toxicant exposures,the amount of environmental
toxicants, um, and medicationspeople being exposed to which
you know are perpetuating thison a deeper level, long term, is
huge.
Um, yeah, we've got there's somuch to consider, so to speak,
(13:15):
um but that doesn't mean in theshort term we can get very hyper
focused on the gut environmentand begin to reduce that lps
load.
That's still important it like,particularly at the beginning.
Just start getting that chronicinflammation down just just a
point.
Speaker 1 (13:33):
You made that um dysbiosis and endometriosis
paper, was that that wouldn'thave been written by justin
sinkley, would it, I think?
he's on a paper I think he has,and and and I also take your
point there was a, an author,one of my favorite, uh,
(13:53):
microbiota authors, katherinelozapone, who years ago now, and
she used the analogy of agarden and things like that,
which you know some people don't, but in there she spoke about
now she mentioned the Americanspelling, acetaminophen, which
in Australia is paracetamol, andparacetamol overuse, leading to
(14:14):
increased amounts of P-cresol,which is a metabolic byproduct,
which is one of the byproductswhich can affect heart function,
particularly in those peoplewith kidney disease, when they
can't get rid of it.
It's just amazing.
So you're talking about thiswhole.
It's not just there in the gut,it's the gut things that affect
(14:38):
the gut and then the gutobviously flows out into the
rest of the body, has to behandled by other tissues, not
just the liver, but the kidneys,et cetera.
Speaker 2 (14:46):
has to be handled by other tissues, not just the
liver, but the kidneys, etc.
So you really have to treat the,the patient, in a holistic
manner yeah, and like, I love toexplain to clients that if you
look at the etymology of theword dysbiosis, it's a greek
word that means it's a greekword that means wrong living.
So it's like yes, it's.
You know, dysbiosis.
(15:08):
Um is the manifestation, oragain, the downstream effect, of
many different things that doan accumulation of those things
over a lifetime.
Right, I know some people havethis kind of um.
There's typically like a umcatalyst of an event that you
know started everything, so tospeak, like an antibiotic or
(15:28):
gastro or something.
But I don't know, I think Ikind of feel like that's usually
the straw in the camel's back,so to speak.
Um, but yeah, you know, again,it's just, I really, really it
can take.
If people have never thoughtabout it like this, it can take
them a while to kind of get it.
But it's just cause and effectlike, yeah, dysbiosis is
perpetuating and has now beenleft untreated for so long.
(15:51):
It's led to a state of apermeable gut and endotoxemia,
but there were thingscontributing to that dysbiosis
over time I, I, you.
Speaker 1 (16:00):
You are so insightful , steven, I've got to say even
the word dysbiosis, wrong living.
We think wrong living of thebacteria within us.
Speaker 2 (16:08):
It's our wrong living that's caused this yeah, you
know, and so poignant, yeah, Imean, when I first heard that I
went wow, but that wasn't evenexplained to me in my training.
I just said, oh well, bacteriabecome imbalanced and it's just
something that happens andwhatever.
When you look more deeply andbecause you know again, like the
(16:30):
medical, conventional medicalmodel is very, um, germ phobic,
let's say like um, very hardcoregerm phobic.
And you know, the opposite ofdysbiosis is symbiosis.
So we should be living withthese organisms, um, we should
not be afraid of them and phobicof them.
And they're always, you know,even if they're quote unquote,
(16:52):
um, imbalanced.
They're always trying to serveus.
So, you know, I think againthere's this kind of in terms of
supporting people who've gotintense degrees of a permeable
gut and lps getting into theirbloodstream and driving
endotoxemia, like, yes, we, wewant to as quickly as possible
reduce that endotoxic load andheal and seal that gut and
(17:12):
reduce the populations ofcertain organisms in the gut
that are perpetuating that.
But not in this, you know, kindof black and white warfare
mentality of, oh, we've just gotto destroy all the bacteria.
We have to really step back andtry and get people to say cool,
but like, why did this happenin the first place, and that's
(17:33):
you know.
There's a lot to unpack thereover time.
Yeah.
Speaker 1 (17:39):
So I guess much of your treatment phase, if you
like, must be psychologyteaching people how to address
the psychology that's affectingtheir stress, that's affecting
their physical aspects.
Speaker 2 (17:57):
Yeah, that has become pretty huge for me, like you
know, people booking inpredominantly for help with the
gut issue and I don't't know.
But I think a lot of people areexpecting a prescription of all
this kind of what I would callgut centric supplements,
probiotics and robotics, and youknow all the supplements for
(18:18):
their gut, quote unquote.
But I rarely actually do likewhen I first meet people, um,
and you usually send them offfor some testing in the meantime
.
Oh look, I'll usually whackthem on some PHGG.
But outside of that, I'm prettymuch just supporting their
nervous system and their stressand their sleep, because that is
(18:40):
one of the major contributingfactors to dysbiosis and leaky
gut and why these imbalances areshowing up in the first place.
And you know, the gut justwon't heal, so to speak, in a
state of nervous systemdysregulation.
So I am, you know, hugelyfocused on that from the get-go.
Speaker 1 (19:00):
Can I ask, steven, what sort of assessments do you
favor to check leaky gut?
And I've got a second part tothis question, sort of and that
is what you mentioned beforeabout working first on these
areas that affect theendotoxemia or the leaky gut
yeah, and yet people very oftenwant a quick, not bang for buck,
(19:23):
but a quick effect, yeah, sohow do you balance the longer
term issues with getting themfeeling a little bit different?
And and you know, I think thatthe term is different not
necessarily all well, um, aslong as they can feel a change,
is that?
Do you find that?
Or do they need to feel wellnow?
Speaker 2 (19:46):
yeah, look, I guess that's as a clinician.
Like you know, we obviouslyhave this overarching theme if
we want to treat the underlyingcauses, right.
But you know, some people arein significant pain and distress
and we absolutely want to givethem symptom relief too, right,
it's a bit of a um.
So you know, when I first meetpeople and you know we're
(20:12):
discussing testing, if we aregetting testing.
While we're waiting for thattesting, you know, like I said,
we do want some symptom reliefand so, if appropriate, I try
not to impose strict eliminationdiets on people unless they're
pretty debilitated with symptoms, you know, and I see a need for
them to establish a bit of abaseline.
(20:34):
Like we need to calm all ofyour symptoms down, to establish
a baseline of you know what itcan feel like, like how is your
body functioning when you removethe variable of all these foods
coming in and perpetuating yoursymptoms, so that people aren't
just chasing the nextsupplement when you know,
(20:56):
because of their state ofchronic inflammation and leaky
gut, their diet is unfortunatelymaking them very systematic.
So, look, I will get into theelimination style diet area if
appropriate, but some people,just based on what else might be
going on, I may not see a needto take them that far and I will
just, you know, give them somesupplements to improve their
(21:17):
sleep and support their nervoussystem or some, you know, just
some herbal medicines to improvetheir gut function, like
bitters or liver support.
Yeah, it's kind of dependent onthe person, um, but while I'm
trying to get them some symptomrelief and give them some
foundational support at thebeginning, um, with test, with
(21:41):
the testing question, um, look,on paper, so there's two areas
to this.
Right, it's like if you have adysbiotic gut with a dominance
of lps producing bacteria,combined with a very leaky gut
wall, that is going to lead tosignificant endotoxemia.
So you know, on paper it's likeokay, well, to see if someone
truly does have a leaky gut, I'dgo to the lactulose monotone
(22:02):
test now in clinical realityjust to save people some time
and money.
If we need to prioritize testing, I will go with microbiome
testing as a big priority, justbecause I say to them look,
whether or not it turns out, youtruly have a very permeable gut
wall.
All the style of treatments weneed to do anyway are going to
(22:23):
treat a leaky gut.
It's going to improve that.
So I'm happy to safely assumebecause it's not going to treat
a leaky gut.
It's going to improve that.
So I'm happy to safely assumebecause it's not going to change
what I need to do for you.
To begin with, if you want tocheck, cool, we can check.
But at a minimum let's checkthat in six months, make sure
it's, you know, actually gone,so to speak.
And so the reason I want toprioritize the microbiome
testing is like, cool, if ourtreatment's going to take care
(22:44):
of a leaky gut anyway, I'drather see what the entire
microbial environment looks likeand what your type of dysbiosis
is, so to speak.
You know, are there significantLPS bacterial overgrowths and
or hydrogen sulfide overgrowths?
I'd rather have the informationthat will help direct their
treatment, if that makes sense.
But if people want all the data, cool, we'll get it all.
(23:06):
If that makes sense.
But if people want all the data, cool, we'll get it all.
Um, and you know I'm always,yeah, outside of gut testing,
I'm again zooming out andlooking at someone's overall
health.
So I'm always getting theappropriate pathology done, so
to speak.
And you know because, again,well, what contribute?
What contributes to dysbiosisand leaky gut?
Well, nutritional deficienciesand, you know, maybe some
(23:28):
undiagnosed conditions thathaven't been found, like gilbert
syndrome and all that kind ofthing, but that, yeah, that's
generally my approach withtesting yeah, um, you've just
turned what I used to do on ated.
Speaker 1 (23:42):
I used to favor the lactulose mannitol test and I
totally get you.
Yeah, I totally get you.
So I used to favour thelactulose mannitol test because
it's relatively inexpensiveversus the microbiome testing.
But I totally understand whatyou're saying, so thank you for
that.
That's great.
(24:02):
That's actually really good.
It gives you a lot moreinformation about what's going
on, because the other stuff isgoing to improve the lactulose
management test anyway.
Speaker 2 (24:10):
so it's like yeah, yeah, because some I know it's
like tests, don't guess, quote,unquote, it's like, but again
it's not going to.
It's not going to change mytreatment too dramatically, at
least to be, yeah, let's justget into it yeah you know, yeah,
love it, love it.
Speaker 1 (24:26):
Um.
So can we dive into a fewconditions at all?
You mentioned, for instance,you know your metabolic, neuro,
autoimmune.
Can we start with those?
I know that this is, this ismore than a broad brushstroke,
but um, can we start with maybethose sorts of types of
(24:46):
conditions?
Speaker 2 (24:51):
patients that come and see you with those For sure.
So I guess to preface that,what I'll just briefly explain
is like what happens once theLPS endotoxin is in circulation
in excessive amounts, becausethis is honestly when you
understand this.
It's like okay, well, how doesendo endo, how does pcos, how
does insulin resistance relateto metabolic endotoxemia?
It's like the same pathway,it's the same chain of events
(25:14):
and then will just manifest in adifferent way depending on the
person.
So if lps endotoxin is in thecirculation in excessive amounts
, there's this very specificcascade of events where and this
can get super dry andcomplicated.
But if people want to um, thisis awesome paper 2021 paper in
(25:36):
frontiers of immunology, calledthe role of metabolic
endotoxemia in systemicinflammation.
Um, you know, that's the paperyou'd give to anyone, especially
like a health care, especiallya health care practitioner,
who's like still living under arock and is skeptical about all
this.
Um, that explains it so well.
But essentially, um, you know,lps gets in the bloodstream and
(26:00):
binds to something called lbp.
There's this lps lbp complex.
It attracts the attention ofCD14, so protein made of
macrophages.
It's part of the innate immuneresponse and so the LPS-LBP
complex gets transferred by CD14to something called toll-like
(26:20):
receptor 4.
So when you start looking at allthe research on metabolic
endotoxemia and oh, what's goingon with endotoxemia and endo
and endoxemia and parkinson's,it's talks about many things,
but particularly particularlythis tlr4.
So, um, with toll-likereceptors.
(26:41):
They are the principal inducersof innate immunity, and it's
why sometimes you'll see what isendotoxemia.
They define it as a chronicstate of innate immune
activation due to toll receptoractivation, because the job of
toll receptors is to detect thepresence of microbes in
circulation or their components,and so different types of TLR
(27:04):
receptors are responsible fordetecting specific types of
microbes and components.
Tlr4's job is to recognize lps,and so when it finds lps in
circulation, it binds to thisand there is this subsequent
release of a myriad ofinflammatory cytokines, um.
So tlr4 activation activatesnfcaptop, nfkb, which then leads
(27:30):
to production of, you know,tnfa and toluquin one and
toluquin six, etc.
Um.
So you know a cool way to thinkabout it is like tlr4 detection
of microbial components isconsidered the first line of
defense against bacteria, themost extreme example of this
(27:52):
being sepsis.
Right, it's the same thing.
It's just a much more end stageversion of endotoxemia, if it
gets bad enough.
So when bacteria translocateinto the gut and it overwhelms
our immune system to the pointthat the inflammatory cytokines
triggered by TLR4 lead to tissuedamage and organ failure, right
(28:17):
?
So I think I was reading inthat paper.
The LPS levels observed insepsis are about 15 times higher
than those seen in individualswith what we call metabolic
endotoxemia.
This lower-grade endotoxemia,but it's the same thing
happening on a lower-grade,subclinical level, but obviously
people aren't, you know, havingorgan failure.
Speaker 1 (28:39):
But it's the same mechanism in the heart, gland.
That's huge what you're sayingthere, stephen, because with
sepsis it gallops along.
You know, the early signs areso weird like they're more
delirium and things like thatthat you would not associate
with quote-unquote an infection.
(29:00):
Yes, and yet just imagine,forgive me, sorry and their
treatments for sepsis are not,let's say, optimal.
You know, there was PaulMarrick trying to use his tap
therapy.
That's the.
What is it?
Thiamine, ascorbic acid andprednisolone, or prednisone,
(29:23):
knocked on the head, if you like, by Monash University or
poo-pooed by it.
But nobody is looking,certainly in the orthodox world,
about changing or treating thegut.
Imagine, just imagine, ifpeople presenting early enough
(29:48):
with sepsis were treated withquite innocuous things given
orally, like, I'm going to say,this serum bovine immunoglobulin
complex, which I love, orprobiotics like Saccharomyces
boulardii or, you know,lactobacillus coagulans,
(30:08):
whatever, rhamnosus LGG,whatever.
Yeah, imagine if orthodoxtherapists started to embrace
this in a hospital situation.
Yeah, oh my God.
Speaker 2 (30:25):
Yeah, and you know, and again, to the lay person, or
maybe even practitioners andpeople in healthcare, again,
it's just a subtle use oflanguage.
For me I think it's important.
But it's like, you know, sepsisisn't just an overnight random
event of a bacterial invasion.
It's like there was a sequenceof events leading up to that.
(30:48):
You know it's um, yes, oncethey got in in that to that
degree, cool, you're going toneed the damage control level of
, you know, acute emergencytreatment.
Um, but, yeah, it's, this ishuge in between gap.
And but you know, even like Iwas reading a paper 2024 paper
this year, august in onco target, a cancer journal, talking
(31:13):
about how, in post-operativepatients treated for colorectal
cancer, it discussed theimportance of gut barrier
integrity in preventingbacterial lps endotoxin
translocation into circulationafter surgery.
Because they're acknowledgingthat, due to the damage to the
(31:33):
gut barrier post-surgery, ifthat gut wall is still quite
permeable, it's thetranslocation of LPS compounds
which increases their risk oflocal bowel and systemic cancers
post-surgically in the future.
So I thought that was reallycool to read that they're
(31:54):
looking at that and to note LPStrans because of this TLR4
activation pathway and thesubsequent immune and
inflammatory events.
I mean, if you just pop google,pop med, a type of cancer, lps,
endotoxemia all of them arebeing connected to this, like
it's starting to be acknowledged.
(32:16):
Um, you know, whether it'sprostate or colorectal, um, you
know, like helicobacter, and therisk of gastric tumors is a
classic example as well.
But, yeah, so once weunderstand that pathway, it's
like, okay, cool.
(32:36):
How does this relate tometabolic issues?
You know, with atherosclerosis,obesity, type 2 diabetes, you
know, the atherosclerosis one isa really interesting one
because you know when LPS isessentially transported from the
(32:56):
lumen into circulation viahyalomicrons, right?
So, and there are differentsizes of all these lipoproteins,
right, you've got LDL, vldl,small, dense LDL, and LPS can
bind to all of them, and youknow.
So the ability of thelipoproteins to bind to LPS,
(33:20):
it's again, the body doeseverything very intentionally
that binding of LDL to LPS isconsidered protective.
You know the ldls are trying toprevent sepsis.
They're like, oh shit, there'slps in the system.
Bind to that, get it, recycleit through the liver and get it
out.
Um, the issue, and you know, instudies, this is partly how
(33:42):
statins appear to work too um,because statins increase LDL
receptors, which increasesrecycling of LDL and LPS from
circulation.
The issue, though, is that, youknow, not all lipoproteins get
recycled.
The smaller, denser LDLparticles don't get recycled, so
(34:03):
LPS remains in circulation, andso it's like well, what happens
then?
Again?
We go back to this kind of tlrfor activation, so the lps
triggers the innate immunesystem, um, and that forms a
foam cell like soft plaque atthe endophilium, and that is the
beginning of atherosclerosis.
This is so interesting.
Speaker 1 (34:26):
Oh, it's a.
Look, there's a huge topic,look, it's a massive topic.
Can I ask, though, at somestage we're talking about
interventions, right?
So when do you intervene with?
You mentioned it partiallyhydrogenated guar gum, phtg,
(34:48):
probiotics.
We've spoken about the bovineserum.
Immunoglobulins yes, when doyou institute those things that
heal the gut versus other things, like you know, nac, calcium
deglucorate, other detox regregimens, liver, gallbladder,
(35:08):
herbs that might clear toxins?
Do you work on, obviously,stress and psychology in that
first diet and then what comesin Soothe the gut?
When do you start clearing?
Speaker 2 (35:32):
Yeah, look, I do begin immediately.
Um, the main, I mean prettymuch these days, assuming
against this, safely, assumingthere's a degree of this
permeability to deal with.
And everyone's got a bit ofdespise is going on the end,
from all the testing I do,everyone gets a very high dose
of a, you know, purified thirdparty um tested omega-3.
(35:55):
That's really important.
Um, there's research on theomega-3 for, you know, reducing
LPS translocation and adampening of TLR4 signaling and
it's, you know, crucial to thenervous system.
So the omega 3 is up there.
The?
Um, the bovine derivedimmunoglobulins is a really nice
one I'll use at the beginningfor some people and or once that
(36:18):
results, about confirmingthings, it's really nice to
again come in with that.
You know, initial damagecontrol, like okay, we've got to
get this inflammatory load downas soon as possible by trying
to neutralize and clear lps,like to start that process.
So the immunoglobulins arereally good for that, as is the
fish oil.
Um, as is, um, you know,prebiotics, you know prebiotics
(36:53):
right, particularly um, thepolyphenol variety, let's call
it right.
Oh, so I mean, yeah, they actas prebiotics, so to speak.
So, um, yes, you know, likedietary, all our kind of like
rich colored plants, so to speak.
Um, pomegranate is a prettyincredible one.
Um, may sneak that into someoneinitially, but if not always
like pretty much everyone getspomegranate for a variety of
(37:15):
reasons.
But in the context of um lpsendotoxemia, um, you know there
was, for example, there is areally cool human trial.
It's a randomized trialpomegranate polyphenols given to
overweight and obese peoplewith hyperlipidemia over three
weeks and it showed asignificant decrease in plasma
(37:35):
LPS binding protein, crp, whileincreasing butyrate-producing
bacteria and decreasingpro-inflammatory organisms like
methanobrevibacter.
Decreasing pro-inflammatoryorganisms like
methanobrevibacter.
So polyphenols, particularlypomegranate, are kind of like
the ultimate intervention forreducing LPS load, likely via
(37:55):
feeding bacteria that reduce gutinflammation and heal a leaky
gut and decreasing the bacteriathat are perpetuating that issue
.
Yeah, honey oil, theimmunoglobulins, um look some
people, I will get them straightonto a curcumin just because
it's um.
The research on that forreducing gut inflammation and
(38:17):
for permeable gut is just um,yeah, pretty awesome too yeah,
cool and sorry.
Speaker 1 (38:24):
I mentioned things like you know, your calcium
decalucrates, your nacs, yourclearers, your phase yes yes um,
can you give us a doseguesstimate, a dosing range that
you might use and perhaps, ifyou might um you know, start off
a little bit sheepishly in somepeople?
Speaker 2 (38:44):
yeah, yeah.
So yeah, to your point there.
Like something I haven'tmentioned I should have is when
we're getting a bunch of testingdone.
I make everyone do um anat-home transit test, right.
So they consume um corn orsesame seeds first thing in the
morning.
Write down what time they didthat and what time they first
see it in their toilet bowl,because bowel movements this
(39:06):
observation of bowel movementsare notoriously not reliable to
tell for someone to say whetheror not they're constipated, so
to speak.
And having optimal transit timebetween 16 and 24 hours um is
crucial because otherwise you'rereabsorbing compounds right and
that dramatically perpetuatesand worsens a leaky gut lps
(39:28):
issue um.
So in that context hence it'skind of another win for phgg.
But in that context,particularly in a female who has
super obvious relative estrogenexcess issues, I will very
regularly put them on calciumdeglucorate um to help the liver
and the gut along um.
(39:49):
That I'm usually doing likeit's about a thousand milligram
dose, kind of higher end dose,but that works so well.
Um and nac does have some verycool um research on reducing
kind of lps endotoxin load umand helping with um tight
junction protein regulation.
(40:12):
That, and we know it has.
Again that what I might pullout, particularly if, on top of
the gut issues, um, I've got aclient who has got some pretty
intense nervous systemdysregulation and, you know,
anxiousness and because of itskind of glutamate modulating
kind of properties, um, you onlyneed about 600 milligrams a day
(40:33):
of that, I find.
Um, it seems to do the job andit's super cheap.
Um, yeah, so so many options,options to support all this.
Speaker 1 (40:43):
Right, this really depends on the person oh yeah,
um diabetes, let's move on tothat.
Disorders, um, I mean, diabetesis so huge.
You, you were talking aboutsomebody, um I think with, was
it?
You were talking about somebodywith polycystic ovarian
syndrome.
I know you were talking aboutwomen with estrogen problems.
That was it.
(41:03):
That was oh wording yeah, socan.
Can we talk about that hormonalregulation then?
Speaker 2 (41:11):
yeah, so um with um.
You know, addressing insulinresistance, I mean, like
anything, there's many factorsto consider, right, like sleep,
diet, macronutrient, stressdeficiencies, etc.
Um, but you know I do see a lotof women with pcos and people
on a weight loss journey andmany things um, and you know,
(41:35):
typically I wouldn't say most ofthose people have a chronic gut
issue at the same time.
So they're not thinking aboutlinking up.
But the research is pretty umstrong on this point that you
know, metabolic endotoxemia mayactually be the primary insult,
beginning the pathogenesis ofsomething like type 2 diabetes
due to its effects on insulinresistance, right, wow.
(41:58):
So I think it's like theAmerican Diabetic Association
have been researching this sincelike 2007.
American Diabetic Associationhave been researching this since
like 2007.
And you know, in this paper,you know, first of all they
showed if you took that CD14innate immune system protein out
(42:19):
mice with it, you know,injected with LPS didn't have
any immune activation, right.
So just kind of clarifies oneof the mechanisms.
But again, this um tlr4activation occurs due to
excessive lps.
There's there's so manymechanisms to back up that lps
may be the primary insult.
Like you know, the tl of tlr4activation um reduces insulin
(42:42):
sensitivity um by inhibitinginsulin receptor activities and
the inflammatory cytokinesincrease liver glucose
production and subsequentchronic inflammation.
It decreases glut4translocation which prevents
proper glucose uptake um.
So this idea that the metabolicendotoxemia piece is what
(43:04):
begins to make someone not soresistant sorry, not so
sensitive to insulin iscompelling, you know, because
there's this big question whenwe talk about all this, like
well, was it chicken or the egg?
Right, who knows, maybe it'sdifferent depending on the
person.
But I think at the end of theday, because of the tlr4
(43:28):
activation induced by lpsendotoxicity um, it needs to be
considered.
I think it's a really smartapproach to say reducing insulin
sensitivity um in people who,whether it's pcos or obesity and
or right um, it does.
You know it's not really goingto change my approach and you
(43:48):
know, with obesity as well, youknow there's interesting
research on that.
You know Many people I knowassociation isn't causation but
in studies they do observepeople with obesity have much,
significantly higher populationsof the LPS producing bacteria,
gram-negative bacteria.
(44:11):
And once there is, what theresearch shows, like,
particularly on, like theeffects of diet on LPS
endotoxemia, is that if you givea quote-unquote normal weight
versus an overweight individuala very endotoxic meal.
It's a very high in, say,processed saturated fats and
(44:34):
refined sugars.
They both have a very similarendotoxic response but if you
give that same meal to an obeseperson, their endotoxic response
is significantly more toxic.
Their endotoxic response issignificantly more toxic.
So it's kind of like oncesomeone is obese and because the
TLR4 activation that's onoverdrives, kind of perpetuates
(44:58):
fat storage and increasesinflammatory cytokines, an obese
person's endotoxic response tofood is a lot stronger.
Obese person's endotoxicresponse to food is a lot
stronger.
So taking an approach ofinvestigating and addressing
metabolic endotoxemia in thatpatient group is really
important.
And yeah, like really educatingpeople on how to reduce and you
(45:23):
know a strong endotoxicresponse in their diet.
And again there's this questionof what came first.
You know a strong endotoxicresponse in their diet.
And again there's this questionof what came first.
You know a higher endotoxicresponse to food due to being
obese, or was it?
You know weight gain due tohigh metabolic endotoxic
responses to food, and you know,I mean you could argue on both
(45:45):
sides.
But there's some interestingresearch suggesting the
metabolic metabolic endotoxemiapreceded the obesity um, just
based on studies showing thatpeople who had more potent
endotoxic responses to food umhad a significantly increased
risk of developing diabetes andobesity down the track.
(46:08):
So you know, are someindividuals pre-programmed with
a certain microbiome to havemore significantly endotoxic
responses to food and thereforebe at higher risk of developing
metabolic issues?
Is the argument?
Speaker 1 (46:24):
Stephen, can I ask just to give us an overview of I
mean, this would be an overviewof your mind, obviously, but
give us an overview of what sortof journey these patients have.
You know, if you can just tryand think about a few patients
that you've treated recently,recently around this concept of
(46:45):
metabolic endotoxemia, can yougive us a an example of of how
they improve over time, whatsort of conditions you've
treated?
Speaker 2 (46:56):
yeah, look, I do see a lot of endometriosis, um, and
so, for example, if I can thinkof some people recently and you
know these clients particularlythey're not well, you know,
they're in a lot of pain anddistress.
They're desperately seekingsolutions, right, and so they're
(47:16):
absolutely a group who, whileI'm begging on about treating
the cause, I want to get themsome symptom relief ASAP.
Right, that's right.
With these people, I love mesome PEA and yeah, I guess,
similar to the story what I wastrying to say earlier, it's like
(47:37):
, because people are so unwelland really want a solution and
find out about this link withthe gut.
You know, again, a lot of theseclients come in very focused on
the gut and it, you know, Imake sure I explain to people
really well, yes, we're going totreat your gut, but, um,
requiring that actually sorry,treating that actually requires
(48:00):
us to zoom out and reallysupport your overall health too.
It's not just going to be a gutprotocol of probiotics and it's
a mix.
You know some people thatreally hits home and they get it
, um, and they're they're up forit.
I'm looking at their overallkind of life and health and the
sleep and the stress and all thethings um, and others not so
(48:24):
much Um, but I'd say theoverwhelming majority of people,
once you get that point across,they get it and you know their
treatments are similar in someways and different in others,
just depending.
But yeah, look, endo, I havereally good results.
I don't know why.
It's just once you and they all.
(48:46):
For example, endo has this biglink with histamine as well,
right, they're all.
It's like cool, he's lowhistamine diet, it'll give you
some relief, but it's not asolution.
Um, so with the histamineconversation, everyone's like oh
, I want to find it if I've gothistamine bacteria in my gut.
Honestly, 90% of them don't um,but 90 of them do have, like in
(49:10):
my experience, significantovergrowth of e-coli, right,
kind of classic lps, um,producing microorganisms.
So I, I don't know, with endo,I find if you really get on top
of that endotoxemia and you know, get gut centric and cool,
reducing coli populations andall that kind of thing like they
get significantly better um canI ask what dose of pea do you?
Speaker 1 (49:37):
what do you use?
Speaker 2 (49:39):
I'll go pretty high for the first month, like about
600 milligrams twice a day for amonth, and then ideally reduce
that back to a three to sixhundred maintenance dose.
But awesome, awesome for painrelief, right, because right,
and when someone's in thatdegree of pain, it's like they
don't care about the multiplevariables of dysbiosis that they
(50:01):
need to address over you knowyears.
Just like, yes, but we need toget people symptom relief.
So the the PEA is prettyincredible for that, like yeah
and and do you take?
Speaker 1 (50:13):
do they take the PEA every day through their cycle or
just when they're experiencingpain?
Speaker 2 (50:19):
no, I get them every day, every day, yeah, yeah, most
people, it's such a huge issue,so under treated, poorly
managed, poorly diagnosed.
Yeah, it's a travesty, yeah, Imean you know when we talk about
medications and okay, whatcontributes to leaky gut,
(50:40):
dysphosis and lps?
Okay, what medications?
If the anti-inflammatories areshocking, you know they are very
well known to perpetuate okay,well, what actually leads to
these bacterial population?
Um balances and yet some peopleare surviving on those meds and
it's like cool, yes, that'ssome good alternatives.
Speaker 1 (51:03):
Um yeah, in in desperation.
I've seen one woman, uh, takingthe high dose ibuprofen, that's
the 400 milligram tablets, justpopping them, yeah, all day,
trying to get relief becausethere was.
She couldn't get relief from,uh, a doctor who was hesitant
(51:24):
about using opioids and um, andso she was popping these
ibuprofen during the day and hada gastric bleed.
Yeah, so she was done eitherway.
Speaker 2 (51:35):
She, you know, yeah yeah, yeah, and you know again,
a lot of this comes down tolifestyle and diet.
And you know what's the sayingOutcomes are generated by habits
, but most you know people inchronic pain.
They know what they need to do,but they can't deal with it you
(51:56):
know.
So the symptom relief is reallyimportant at the beginning.
Right, that's what's thechallenge about being a
clinician.
It's like cool, we want totreat the cause, but we also
want to get you feeling betteras soon as possible, without
ignoring the root cause, youknow.
Speaker 1 (52:09):
So pea is just a total winner for that and also I
have to ask about omega-3 fishoil.
You said that you you know youput a decent dose in.
What dose do you use?
Speaker 2 (52:23):
uh usually about.
I mean, I'm using uh fish oilwith a very high ratio of EPA to
DHA.
So if someone's pretty inflamed, some pretty serious gut
nervous system issues, I'll goabout two to three grams total
omega-3 with about a three toone ratio of EPA DHA.
(52:48):
Yeah, I go pretty high dosewith that.
They may not need to take thatmuch forever but again just to
get as much impact on thatinflammation and endotoxic stuff
ASAP.
Yeah, really high dose fish oilto begin with is very helpful
Beautiful.
Speaker 1 (53:05):
We've learned so much from you, stephen.
Just one last quick questionwhere can we learn more now?
You've?
You've given us some greatpapers throughout this.
I hope we're going to beputting these up on the website,
um, and in the show notes, um.
We'll definitely do that.
Not, I hope, anything else.
Any other seminal works?
Have you got any courses, forinstance?
Speaker 2 (53:26):
no, they're in the works.
Um, you know, because I've beentalking a lot um in this chat
about, you know, symptom reliefand damage control treatments
for lps, and but there's a muchbigger picture to um consider,
right?
Um, that's kind of what I'm inthe process of developing a
(53:49):
course on, because it's justit's not sustainable for me or
clients like legit time or moneyto get through all of like,
okay, what are the things I haveto consider to get figure that
all out in appointments.
It's just not sustainable foranyone.
Um, so and I'm a bit all ornothing, like I don't want to I
(54:11):
well, I'm gonna make somethingwhich kind of covers everything,
all these variables, and youknow, here's the phases to go
through and that isn't the work,so it'll be out eventually I
look forward to that mind map.
Oh my gosh.
Yeah, it's been a process, butyeah.
(54:32):
So until that is out, you canjust find me rambling on my
Instagram.
Speaker 1 (54:39):
Stephen Dutch, that's your path on my website.
Yeah, I love your work, Stephen.
I love your mind and I lovethat you don't just focus on the
problem at hand but look atwhat's causing the problem.
You can see it's pretty evidentthat you've got a lot of love
and care that you give to yourpatients and it's not just in
(55:01):
about a little bit of poking itwith a symptom relief.
You really want to get themwell, you want to get them vital
.
I really applaud you and whatyou do.
Thank you so much for your work.
Speaker 2 (55:12):
No worries, andrew, it's a really cool chat.
Speaker 1 (55:14):
Thank you everyone for joining us today.
We're going to be putting up aheap of information for you in
the show notes and remember youcan catch up on all the other
podcasts on the Designs forHealth website.
I'm Andrew Whitfield-Cook.
This is Wellness by Designs.
Music.
This is Wellness by Designs,and I'm your host, andrew
Whitfield-Cook.
This is Wellness by Designs,and I'm your host, andrew
Whitfield-Cook.
And joining us again today isStephen Judge, a naturopath and
nutritionist who specialises incomplex, chronic gut issues.
Today, we're going to bespeaking about metabolic
endotoxemia.
All diseases have a gutcomponent.
(00:40):
Welcome back to Wellness byDesigns, stephen.
How are you?
Speaker 2 (00:44):
thanks, angela.
Speaker 1 (00:44):
I'm great thanks for having me again absolute
pleasure and thank you so muchfor joining us today.
So I think we start off withwhat is in metabolic endotoxemia
and where is it applicable yeah, sure.
Speaker 2 (00:59):
So before defining that, I guess to provide the
context as a reminder, you knowwhat is this concept of
so-called leaky gut orintestinal hyperpermeability?
Right, so the intestinalbarrier wall is a gatekeeper,
right, physiologically healthygut.
(01:21):
This barrier should selectivelybe allowing macro and
micronutrients and water throughthe gut wall and into our
bloodstreams so that thesecomponents can be sent to the
organs and tissues that needthem.
So we could say that the liningof our gut wall should be
selectively permeable, right, soit should only be letting
(01:42):
through what needs to go throughand it should not be letting
anything through that shouldn'tbe found in circulation, so
microbial toxins, bacteria,metabolic waste, et cetera.
And the structure of theintestinal barrier wall is like
this three-layered membrane.
So the first layer is thesingle-celled semi-permeable
(02:06):
layer of epithelial cells heldtogether by tight junctions.
On top of this is a doublelayer of mucus on top of these
cells and the gut bacteriareside on top of that mucus
layer.
Due to various factors, whatcan happen is the tight
junctions between thoseepithelial cells on the first
layer can degrade, gaps can formin the lining of this wall,
(02:28):
subsequently increase thebarrier's permeability, leading
to what we call intestinalhyperpermeability, aka leaky gut
.
So the loss of integrity in thehealth of this barrier, aka
leaky gut, has been suggestedfor decades, you know, if not
longer, um to supposedly lead toor be a contributing factor to
(02:53):
a variety of symptoms andconditions like not just
digestive, but metabolic andneurological and autoimmune.
And all these things, and whatthe research on this area called
metabolic endotoxemia ishighlighting is that it appears
that, okay, it looks likeeverything really does start in
the gut, or is driven by a leakygut, so to speak, and the
(03:16):
mechanisms of metabolicendotoxemia explains this very
well at a very specific kind ofbiochemical level.
And, yeah, the research isconfirming there's a lot of
truth to the concept ofso-called leaky gut, which is
(03:39):
amazing because, consideringthat, considering the wisdom of
ancient traditions have heldthis perspective for centuries.
Right In Ayurvedaveda, you know, they've always taught that the
agni, or digestifies, the keyto optimal health in tcm, spleen
and stomach, qi are fundamentalto overall health and they are
a fundamental component of thedigestive system, and
Hippocrates said that death sitsin our bowels and Henry Lindlar
(04:02):
said that, you know, um, theaccumulated, accumulated morbid
matter and systemic poisons thatare reabsorbed are what drives
disease.
So, yeah, it's kind of coolthat this field of research on
metabolic endotoxemia isstarting to confirm all this
right.
So, with all that right so withendotoxemia, the the simple
(04:27):
definition of it, which I'llexpand upon, is a condition
where there are excessive levelsof something called lps, short
for lipopolysaccharide, in thebloodstream.
And so the term endotoxin,which is what lps is referred to
.
It comes from the greek wordendo, meaning within, because
(04:51):
lps is a molecule found withinthe outer membrane of
specifically gram negativebacteria.
It's what differentiates gramnegative bacteria from
gram-positive bacteria.
It is this LPS that is housedwithin the outer membrane.
And you know, lps inherentlyshouldn't be an issue.
(05:13):
And you know, while a healthygut wall can handle a small
amount of LPS getting intocirculation and be appropriately
handled by the liver to becleared from the body, it
shouldn't, this LPS, endotoxinshould not be getting through
that gut wall in large amounts.
If excessive levels of LPS doget into systemic circulation
(05:35):
due to the gut being toopermeable, this essentially
triggers the innate immunesystem, leading to this chronic,
low-grade subclinicalinflammation.
And, as we know, you know, thechronic inflammatory state is
increasingly recognized as a keydriver of most chronic diseases
.
(05:55):
Um, so we have to step back andgo, okay.
Well what's driving chronicinflammation in all of these
chronic diseases, and we arerepeatedly being brought back to
the gut, and specifically thisendotoxemic mechanism is a very
common explanation linking allthese conditions together.
(06:16):
So you know, we're essentiallylooking at the downstream effect
of specific types of dysbiosisor bacterial imbalances and a
hyperpermeable gut wall.
So if someone has LPS producingbacteria dominating their
microbiome and their gut wallbecomes too permeable, this is
essentially going to lead tometabolic endotoxemia and so the
(06:41):
excessive LPS endotoxin in thebloodstream.
It triggers the innate immunesystem in some very specific
ways, which we'll get into,because the immune and kind of
subsequent inflammatorychemicals that are triggered as
a result of this can interactwith and impact such a wide
(07:04):
variety of tissues and organs inthe body, which is why so many
conditions are being linked backto endotoxemia, which is so
interesting, and so the termmetabolic endotoxemia is simply
a term researchers came up withto describe when this successive
LPS in the bloodstream wasobserved to directly kind of be
(07:28):
the beginnings of metabolicdisorders such as insulin
resistance and obesity and thatkind of thing.
Speaker 1 (07:36):
So just, there's so many questions floating around
about LPS.
Firstly, let's talk about thatquote-unquote leaky gut.
So first things first.
It was Brad Leach who basicallyhelped to dismantle that
syndrome issue.
There's no leaky gut syndrome.
(07:56):
It's not a syndrome.
That's kind of like sayingthere's a pain syndrome or a
breathing syndrome but there isleaky gut and there is excessive
leaky gut, yeah, but it's not adefined syndrome, if you like.
So thank you, brad, for doingthat, and I've watched Vlad's
(08:16):
career blossom over the years,which is great to see.
One of my questions, though, isthat kids and the elderly have
naturally more leaky guts, evenleaky brains.
How does this tie into functionversus dysfunction?
Speaker 2 (08:39):
Yes, love your work, brad.
And I agree.
You know like I'm very carefulwhen with clients, when
discussing these topics of leakygut, gut dysbiosis, sibo, et
cetera.
I don't like to refer to themas conditions or diseases, so to
(08:59):
speak, even though when youread about things like metabolic
endotoxemia in the research itgets referred to as like a
condition, um, so to speak, um.
But you know the danger therewith um, particularly with
clients who, um are desperatelylooking for a, um, a reason for
why they're so unwell and what'skind of the quote-unquote root
(09:21):
cause of their illness.
I'm very careful with mylanguage these days to make sure
people understand that leakygut is certainly not a syndrome
or a condition.
It's just something, that it isthe downstream effect of a
variety of upstream contributingroot causes.
I'm very careful to say look,leaky gut, sure it's become a
(09:45):
contributing factor to um,perpetuating a disease related
to chronic inflammation, butit's that I wouldn't say it's
the root cause, because what canhappen is people can become a
bit too reductionist about itand they're just looking for the
next antimicrobial protocol andthe next probiotic and it's not
to say those interventions arenot useful and helpful, but it's
(10:08):
like one-tenth of the picture,you know.
So while it is helpful to getreductionist about it and get
into the mechanics of it, at theend of the day to address all
this you kind of actually justhave to zoom out and address
someone's overall health.
Really, you know.
Speaker 1 (10:25):
Yeah, I totally agree with you.
I think it was Dr McLion whosaliently pointed it out about
this kill-kill mentality and hesaid what happens, particularly
with extremely sick peoplechronic fatigue people, multiple
chemical sensitivity, et ceterais you kill everything off in
the gut and they've got nothing.
(10:46):
So they become what's calledthe mashed potato and peas
brigade and they end up cyclingat a lower ebb.
They never revitalise theirsystem.
So I love what you say aboutwe've got to dig down, or you
know, to the root causes.
So let's start with thosecauses.
Speaker 2 (11:02):
Stress, anyone, yeah, yeah, and to your point, like,
for example, just recently, youknow very recently, in the past
number of years, you knowthere's a lot of awareness
around.
You know, one of the conditionsit's a new study came out, a
few weeks ago I think, on an lpsproducing bacterial overgrowth
(11:26):
being commonly associated inwomen with endometriosis.
Um, okay, cool, it's anotherstudy looking at this lps
endotoxemic link withendometriosis.
But then what I see and youknow this is just in the online
world, but like what I see fromthe general public and even some
practitioners, you know,following from that, which is
(11:47):
like cool, this, there's thisresearch here confirming this
link with endotoxemia.
But then what can happen ispeople go, okay, cool, the
solution, therefore, is going tobe how do we kill this bacteria
?
Um, what are all the things toget this bacteria Like?
It becomes this almost likeconventional medical germ theory
(12:08):
kind of discussion.
It's like, look, it'sabsolutely wonderful, there's
another link to proving thiswhole and its relationship to
perpetual endometriosis.
But I guess, like, the dealingwith the bacterial overgrowth is
just one piece of this puzzle.
You know, it's almost like adamage control kind of style of
(12:29):
treatment.
Cool, we want to get on top ofthat.
But, like, in the longer term,to get on top of this and
educate people about how, to youknow, truly reverse LPS kind of
endotoxemia and leaky gut wehave to zoom out and go and go,
cool.
But what led to that type ofbacterial overgrowth, right and
to your point?
Yes, stress, nervous systemdysregulation, circadian rhythm
(12:51):
disruption and poor sleep it washuge, like um a bit more longer
term to consider and address.
But, like toxicant exposures,the amount of environmental
toxicants, um, and medicationspeople being exposed to which
you know are perpetuating thison a deeper level, long term, is
huge.
Um, yeah, we've got there's somuch to consider, so to speak,
(13:15):
um but that doesn't mean in theshort term we can get very hyper
focused on the gut environmentand begin to reduce that lps
load.
That's still important it like,particularly at the beginning.
Just start getting that chronicinflammation down just just a
point.
Speaker 1 (13:33):
You made that um dysbiosis and endometriosis
paper, was that that wouldn'thave been written by justin
sinkley, would it, I think?
he's on a paper I think he has,and and and I also take your
point there was a, an author,one of my favorite, uh,
(13:53):
microbiota authors, katherinelozapone, who years ago now, and
she used the analogy of agarden and things like that,
which you know some people don't, but in there she spoke about
now she mentioned the Americanspelling, acetaminophen, which
in Australia is paracetamol, andparacetamol overuse, leading to
(14:14):
increased amounts of P-cresol,which is a metabolic byproduct,
which is one of the byproductswhich can affect heart function,
particularly in those peoplewith kidney disease, when they
can't get rid of it.
It's just amazing.
So you're talking about thiswhole.
It's not just there in the gut,it's the gut things that affect
(14:38):
the gut and then the gutobviously flows out into the
rest of the body, has to behandled by other tissues, not
just the liver, but the kidneys,et cetera.
Speaker 2 (14:46):
has to be handled by other tissues, not just the
liver, but the kidneys, etc.
So you really have to treat the,the patient, in a holistic
manner yeah, and like, I love toexplain to clients that if you
look at the etymology of theword dysbiosis, it's a greek
word that means it's a greekword that means wrong living.
So it's like yes, it's.
You know, dysbiosis.
(15:08):
Um is the manifestation, oragain, the downstream effect, of
many different things that doan accumulation of those things
over a lifetime.
Right, I know some people havethis kind of um.
There's typically like a umcatalyst of an event that you
know started everything, so tospeak, like an antibiotic or
(15:28):
gastro or something.
But I don't know, I think Ikind of feel like that's usually
the straw in the camel's back,so to speak.
Um, but yeah, you know, again,it's just, I really, really it
can take.
If people have never thoughtabout it like this, it can take
them a while to kind of get it.
But it's just cause and effectlike, yeah, dysbiosis is
perpetuating and has now beenleft untreated for so long.
(15:51):
It's led to a state of apermeable gut and endotoxemia,
but there were thingscontributing to that dysbiosis
over time I, I, you.
Speaker 1 (16:00):
You are so insightful , steven, I've got to say even
the word dysbiosis, wrong living.
We think wrong living of thebacteria within us.
Speaker 2 (16:08):
It's our wrong living that's caused this yeah, you
know, and so poignant, yeah, Imean, when I first heard that I
went wow, but that wasn't evenexplained to me in my training.
I just said, oh well, bacteriabecome imbalanced and it's just
something that happens andwhatever.
When you look more deeply andbecause you know again, like the
(16:30):
medical, conventional medicalmodel is very, um, germ phobic,
let's say like um, very hardcoregerm phobic.
And you know, the opposite ofdysbiosis is symbiosis.
So we should be living withthese organisms, um, we should
not be afraid of them and phobicof them.
And they're always, you know,even if they're quote unquote,
(16:52):
um, imbalanced.
They're always trying to serveus.
So, you know, I think againthere's this kind of in terms of
supporting people who've gotintense degrees of a permeable
gut and lps getting into theirbloodstream and driving
endotoxemia, like, yes, we, wewant to as quickly as possible
reduce that endotoxic load andheal and seal that gut and
(17:12):
reduce the populations ofcertain organisms in the gut
that are perpetuating that.
But not in this, you know, kindof black and white warfare
mentality of, oh, we've just gotto destroy all the bacteria.
We have to really step back andtry and get people to say cool,
but like, why did this happenin the first place, and that's
(17:33):
you know.
There's a lot to unpack thereover time.
Yeah.
Speaker 1 (17:39):
So I guess much of your treatment phase, if you
like, must be psychologyteaching people how to address
the psychology that's affectingtheir stress, that's affecting
their physical aspects.
Speaker 2 (17:57):
Yeah, that has become pretty huge for me, like you
know, people booking inpredominantly for help with the
gut issue and I don't't know.
But I think a lot of people areexpecting a prescription of all
this kind of what I would callgut centric supplements,
probiotics and robotics, and youknow all the supplements for
(18:18):
their gut, quote unquote.
But I rarely actually do likewhen I first meet people, um,
and you usually send them offfor some testing in the meantime
.
Oh look, I'll usually whackthem on some PHGG.
But outside of that, I'm prettymuch just supporting their
nervous system and their stressand their sleep, because that is
(18:40):
one of the major contributingfactors to dysbiosis and leaky
gut and why these imbalances areshowing up in the first place.
And you know, the gut justwon't heal, so to speak, in a
state of nervous systemdysregulation.
So I am, you know, hugelyfocused on that from the get-go.
Speaker 1 (19:00):
Can I ask, steven, what sort of assessments do you
favor to check leaky gut?
And I've got a second part tothis question, sort of and that
is what you mentioned beforeabout working first on these
areas that affect theendotoxemia or the leaky gut
yeah, and yet people very oftenwant a quick, not bang for buck,
(19:23):
but a quick effect, yeah, sohow do you balance the longer
term issues with getting themfeeling a little bit different?
And and you know, I think thatthe term is different not
necessarily all well, um, aslong as they can feel a change,
is that?
Do you find that?
Or do they need to feel wellnow?
Speaker 2 (19:46):
yeah, look, I guess that's as a clinician.
Like you know, we obviouslyhave this overarching theme if
we want to treat the underlyingcauses, right.
But you know, some people arein significant pain and distress
and we absolutely want to givethem symptom relief too, right,
it's a bit of a um.
So you know, when I first meetpeople and you know we're
(20:12):
discussing testing, if we aregetting testing.
While we're waiting for thattesting, you know, like I said,
we do want some symptom reliefand so, if appropriate, I try
not to impose strict eliminationdiets on people unless they're
pretty debilitated with symptoms, you know, and I see a need for
them to establish a bit of abaseline.
(20:34):
Like we need to calm all ofyour symptoms down, to establish
a baseline of you know what itcan feel like, like how is your
body functioning when you removethe variable of all these foods
coming in and perpetuating yoursymptoms, so that people aren't
just chasing the nextsupplement when you know,
(20:56):
because of their state ofchronic inflammation and leaky
gut, their diet is unfortunatelymaking them very systematic.
So, look, I will get into theelimination style diet area if
appropriate, but some people,just based on what else might be
going on, I may not see a needto take them that far and I will
just, you know, give them somesupplements to improve their
(21:17):
sleep and support their nervoussystem or some, you know, just
some herbal medicines to improvetheir gut function, like
bitters or liver support.
Yeah, it's kind of dependent onthe person, um, but while I'm
trying to get them some symptomrelief and give them some
foundational support at thebeginning, um, with test, with
(21:41):
the testing question, um, look,on paper, so there's two areas
to this.
Right, it's like if you have adysbiotic gut with a dominance
of lps producing bacteria,combined with a very leaky gut
wall, that is going to lead tosignificant endotoxemia.
So you know, on paper it's likeokay, well, to see if someone
truly does have a leaky gut, I'dgo to the lactulose monotone
(22:02):
test now in clinical realityjust to save people some time
and money.
If we need to prioritize testing, I will go with microbiome
testing as a big priority, justbecause I say to them look,
whether or not it turns out, youtruly have a very permeable gut
wall.
All the style of treatments weneed to do anyway are going to
(22:23):
treat a leaky gut.
It's going to improve that.
So I'm happy to safely assumebecause it's not going to treat
a leaky gut.
It's going to improve that.
So I'm happy to safely assumebecause it's not going to change
what I need to do for you.
To begin with, if you want tocheck, cool, we can check.
But at a minimum let's checkthat in six months, make sure
it's, you know, actually gone,so to speak.
And so the reason I want toprioritize the microbiome
testing is like, cool, if ourtreatment's going to take care
(22:44):
of a leaky gut anyway, I'drather see what the entire
microbial environment looks likeand what your type of dysbiosis
is, so to speak.
You know, are there significantLPS bacterial overgrowths and
or hydrogen sulfide overgrowths?
I'd rather have the informationthat will help direct their
treatment, if that makes sense.
But if people want all the data, cool, we'll get it all.
(23:06):
If that makes sense.
But if people want all the data, cool, we'll get it all.
Um, and you know I'm always,yeah, outside of gut testing,
I'm again zooming out andlooking at someone's overall
health.
So I'm always getting theappropriate pathology done, so
to speak.
And you know because, again,well, what contribute?
What contributes to dysbiosisand leaky gut?
Well, nutritional deficienciesand, you know, maybe some
(23:28):
undiagnosed conditions thathaven't been found, like gilbert
syndrome and all that kind ofthing, but that, yeah, that's
generally my approach withtesting yeah, um, you've just
turned what I used to do on ated.
Speaker 1 (23:42):
I used to favor the lactulose mannitol test and I
totally get you.
Yeah, I totally get you.
So I used to favour thelactulose mannitol test because
it's relatively inexpensiveversus the microbiome testing.
But I totally understand whatyou're saying, so thank you for
that.
That's great.
(24:02):
That's actually really good.
It gives you a lot moreinformation about what's going
on, because the other stuff isgoing to improve the lactulose
management test anyway.
Speaker 2 (24:10):
so it's like yeah, yeah, because some I know it's
like tests, don't guess, quote,unquote, it's like, but again
it's not going to.
It's not going to change mytreatment too dramatically, at
least to be, yeah, let's justget into it yeah you know, yeah,
love it, love it.
Speaker 1 (24:26):
Um.
So can we dive into a fewconditions at all?
You mentioned, for instance,you know your metabolic, neuro,
autoimmune.
Can we start with those?
I know that this is, this ismore than a broad brushstroke,
but um, can we start with maybethose sorts of types of
(24:46):
conditions?
Speaker 2 (24:51):
patients that come and see you with those For sure.
So I guess to preface that,what I'll just briefly explain
is like what happens once theLPS endotoxin is in circulation
in excessive amounts, becausethis is honestly when you
understand this.
It's like okay, well, how doesendo endo, how does pcos, how
does insulin resistance relateto metabolic endotoxemia?
It's like the same pathway,it's the same chain of events
(25:14):
and then will just manifest in adifferent way depending on the
person.
So if lps endotoxin is in thecirculation in excessive amounts
, there's this very specificcascade of events where and this
can get super dry andcomplicated.
But if people want to um, thisis awesome paper 2021 paper in
(25:36):
frontiers of immunology, calledthe role of metabolic
endotoxemia in systemicinflammation.
Um, you know, that's the paperyou'd give to anyone, especially
like a health care, especiallya health care practitioner,
who's like still living under arock and is skeptical about all
this.
Um, that explains it so well.
But essentially, um, you know,lps gets in the bloodstream and
(26:00):
binds to something called lbp.
There's this lps lbp complex.
It attracts the attention ofCD14, so protein made of
macrophages.
It's part of the innate immuneresponse and so the LPS-LBP
complex gets transferred by CD14to something called toll-like
(26:20):
receptor 4.
So when you start looking at allthe research on metabolic
endotoxemia and oh, what's goingon with endotoxemia and endo
and endoxemia and parkinson's,it's talks about many things,
but particularly particularlythis tlr4.
So, um, with toll-likereceptors.
(26:41):
They are the principal inducersof innate immunity, and it's
why sometimes you'll see what isendotoxemia.
They define it as a chronicstate of innate immune
activation due to toll receptoractivation, because the job of
toll receptors is to detect thepresence of microbes in
circulation or their components,and so different types of TLR
(27:04):
receptors are responsible fordetecting specific types of
microbes and components.
Tlr4's job is to recognize lps,and so when it finds lps in
circulation, it binds to thisand there is this subsequent
release of a myriad ofinflammatory cytokines, um.
So tlr4 activation activatesnfcaptop, nfkb, which then leads
(27:30):
to production of, you know,tnfa and toluquin one and
toluquin six, etc.
Um.
So you know a cool way to thinkabout it is like tlr4 detection
of microbial components isconsidered the first line of
defense against bacteria, themost extreme example of this
(27:52):
being sepsis.
Right, it's the same thing.
It's just a much more end stageversion of endotoxemia, if it
gets bad enough.
So when bacteria translocateinto the gut and it overwhelms
our immune system to the pointthat the inflammatory cytokines
triggered by TLR4 lead to tissuedamage and organ failure, right
(28:17):
?
So I think I was reading inthat paper.
The LPS levels observed insepsis are about 15 times higher
than those seen in individualswith what we call metabolic
endotoxemia.
This lower-grade endotoxemia,but it's the same thing
happening on a lower-grade,subclinical level, but obviously
people aren't, you know, havingorgan failure.
Speaker 1 (28:39):
But it's the same mechanism in the heart, gland.
That's huge what you're sayingthere, stephen, because with
sepsis it gallops along.
You know, the early signs areso weird like they're more
delirium and things like thatthat you would not associate
with quote-unquote an infection.
(29:00):
Yes, and yet just imagine,forgive me, sorry and their
treatments for sepsis are not,let's say, optimal.
You know, there was PaulMarrick trying to use his tap
therapy.
That's the.
What is it?
Thiamine, ascorbic acid andprednisolone, or prednisone,
(29:23):
knocked on the head, if you like, by Monash University or
poo-pooed by it.
But nobody is looking,certainly in the orthodox world,
about changing or treating thegut.
Imagine, just imagine, ifpeople presenting early enough
(29:48):
with sepsis were treated withquite innocuous things given
orally, like, I'm going to say,this serum bovine immunoglobulin
complex, which I love, orprobiotics like Saccharomyces
boulardii or, you know,lactobacillus coagulans,
(30:08):
whatever, rhamnosus LGG,whatever.
Yeah, imagine if orthodoxtherapists started to embrace
this in a hospital situation.
Yeah, oh my God.
Speaker 2 (30:25):
Yeah, and you know, and again, to the lay person, or
maybe even practitioners andpeople in healthcare, again,
it's just a subtle use oflanguage.
For me I think it's important.
But it's like, you know, sepsisisn't just an overnight random
event of a bacterial invasion.
It's like there was a sequenceof events leading up to that.
(30:48):
You know it's um, yes, oncethey got in in that to that
degree, cool, you're going toneed the damage control level of
, you know, acute emergencytreatment.
Um, but, yeah, it's, this ishuge in between gap.
And but you know, even like Iwas reading a paper 2024 paper
this year, august in onco target, a cancer journal, talking
(31:13):
about how, in post-operativepatients treated for colorectal
cancer, it discussed theimportance of gut barrier
integrity in preventingbacterial lps endotoxin
translocation into circulationafter surgery.
Because they're acknowledgingthat, due to the damage to the
(31:33):
gut barrier post-surgery, ifthat gut wall is still quite
permeable, it's thetranslocation of LPS compounds
which increases their risk oflocal bowel and systemic cancers
post-surgically in the future.
So I thought that was reallycool to read that they're
(31:54):
looking at that and to note LPStrans because of this TLR4
activation pathway and thesubsequent immune and
inflammatory events.
I mean, if you just pop google,pop med, a type of cancer, lps,
endotoxemia all of them arebeing connected to this, like
it's starting to be acknowledged.
(32:16):
Um, you know, whether it'sprostate or colorectal, um, you
know, like helicobacter, and therisk of gastric tumors is a
classic example as well.
But, yeah, so once weunderstand that pathway, it's
like, okay, cool.
(32:36):
How does this relate tometabolic issues?
You know, with atherosclerosis,obesity, type 2 diabetes, you
know, the atherosclerosis one isa really interesting one
because you know when LPS isessentially transported from the
(32:56):
lumen into circulation viahyalomicrons, right?
So, and there are differentsizes of all these lipoproteins,
right, you've got LDL, vldl,small, dense LDL, and LPS can
bind to all of them, and youknow.
So the ability of thelipoproteins to bind to LPS,
(33:20):
it's again, the body doeseverything very intentionally
that binding of LDL to LPS isconsidered protective.
You know the ldls are trying toprevent sepsis.
They're like, oh shit, there'slps in the system.
Bind to that, get it, recycleit through the liver and get it
out.
Um, the issue, and you know, instudies, this is partly how
(33:42):
statins appear to work too um,because statins increase LDL
receptors, which increasesrecycling of LDL and LPS from
circulation.
The issue, though, is that, youknow, not all lipoproteins get
recycled.
The smaller, denser LDLparticles don't get recycled, so
(34:03):
LPS remains in circulation, andso it's like well, what happens
then?
Again?
We go back to this kind of tlrfor activation, so the lps
triggers the innate immunesystem, um, and that forms a
foam cell like soft plaque atthe endophilium, and that is the
beginning of atherosclerosis.
This is so interesting.
Speaker 1 (34:26):
Oh, it's a.
Look, there's a huge topic,look, it's a massive topic.
Can I ask, though, at somestage we're talking about
interventions, right?
So when do you intervene with?
You mentioned it partiallyhydrogenated guar gum, phtg,
(34:48):
probiotics.
We've spoken about the bovineserum.
Immunoglobulins yes, when doyou institute those things that
heal the gut versus other things, like you know, nac, calcium
deglucorate, other detox regregimens, liver, gallbladder,
(35:08):
herbs that might clear toxins?
Do you work on, obviously,stress and psychology in that
first diet and then what comesin Soothe the gut?
When do you start clearing?
Speaker 2 (35:32):
Yeah, look, I do begin immediately.
Um, the main, I mean prettymuch these days, assuming
against this, safely, assumingthere's a degree of this
permeability to deal with.
And everyone's got a bit ofdespise is going on the end,
from all the testing I do,everyone gets a very high dose
of a, you know, purified thirdparty um tested omega-3.
(35:55):
That's really important.
Um, there's research on theomega-3 for, you know, reducing
LPS translocation and adampening of TLR4 signaling and
it's, you know, crucial to thenervous system.
So the omega 3 is up there.
The?
Um, the bovine derivedimmunoglobulins is a really nice
one I'll use at the beginningfor some people and or once that
(36:18):
results, about confirmingthings, it's really nice to
again come in with that.
You know, initial damagecontrol, like okay, we've got to
get this inflammatory load downas soon as possible by trying
to neutralize and clear lps,like to start that process.
So the immunoglobulins arereally good for that, as is the
fish oil.
Um, as is, um, you know,prebiotics, you know prebiotics
(36:53):
right, particularly um, thepolyphenol variety, let's call
it right.
Oh, so I mean, yeah, they actas prebiotics, so to speak.
So, um, yes, you know, likedietary, all our kind of like
rich colored plants, so to speak.
Um, pomegranate is a prettyincredible one.
Um, may sneak that into someoneinitially, but if not always
like pretty much everyone getspomegranate for a variety of
(37:15):
reasons.
But in the context of um lpsendotoxemia, um, you know there
was, for example, there is areally cool human trial.
It's a randomized trialpomegranate polyphenols given to
overweight and obese peoplewith hyperlipidemia over three
weeks and it showed asignificant decrease in plasma
(37:35):
LPS binding protein, crp, whileincreasing butyrate-producing
bacteria and decreasingpro-inflammatory organisms like
methanobrevibacter.
Decreasing pro-inflammatoryorganisms like
methanobrevibacter.
So polyphenols, particularlypomegranate, are kind of like
the ultimate intervention forreducing LPS load, likely via
(37:55):
feeding bacteria that reduce gutinflammation and heal a leaky
gut and decreasing the bacteriathat are perpetuating that issue
.
Yeah, honey oil, theimmunoglobulins, um look some
people, I will get them straightonto a curcumin just because
it's um.
The research on that forreducing gut inflammation and
(38:17):
for permeable gut is just um,yeah, pretty awesome too yeah,
cool and sorry.
Speaker 1 (38:24):
I mentioned things like you know, your calcium
decalucrates, your nacs, yourclearers, your phase yes yes um,
can you give us a doseguesstimate, a dosing range that
you might use and perhaps, ifyou might um you know, start off
a little bit sheepishly in somepeople?
Speaker 2 (38:44):
yeah, yeah.
So yeah, to your point there.
Like something I haven'tmentioned I should have is when
we're getting a bunch of testingdone.
I make everyone do um anat-home transit test, right.
So they consume um corn orsesame seeds first thing in the
morning.
Write down what time they didthat and what time they first
see it in their toilet bowl,because bowel movements this
(39:06):
observation of bowel movementsare notoriously not reliable to
tell for someone to say whetheror not they're constipated, so
to speak.
And having optimal transit timebetween 16 and 24 hours um is
crucial because otherwise you'rereabsorbing compounds right and
that dramatically perpetuatesand worsens a leaky gut lps
(39:28):
issue um.
So in that context hence it'skind of another win for phgg.
But in that context,particularly in a female who has
super obvious relative estrogenexcess issues, I will very
regularly put them on calciumdeglucorate um to help the liver
and the gut along um.
(39:49):
That I'm usually doing likeit's about a thousand milligram
dose, kind of higher end dose,but that works so well.
Um and nac does have some verycool um research on reducing
kind of lps endotoxin load umand helping with um tight
junction protein regulation.
(40:12):
That, and we know it has.
Again that what I might pullout, particularly if, on top of
the gut issues, um, I've got aclient who has got some pretty
intense nervous systemdysregulation and, you know,
anxiousness and because of itskind of glutamate modulating
kind of properties, um, you onlyneed about 600 milligrams a day
(40:33):
of that, I find.
Um, it seems to do the job andit's super cheap.
Um, yeah, so so many options,options to support all this.
Speaker 1 (40:43):
Right, this really depends on the person oh yeah,
um diabetes, let's move on tothat.
Disorders, um, I mean, diabetesis so huge.
You, you were talking aboutsomebody, um I think with, was
it?
You were talking about somebodywith polycystic ovarian
syndrome.
I know you were talking aboutwomen with estrogen problems.
That was it.
(41:03):
That was oh wording yeah, socan.
Can we talk about that hormonalregulation then?
Speaker 2 (41:11):
yeah, so um with um.
You know, addressing insulinresistance, I mean, like
anything, there's many factorsto consider, right, like sleep,
diet, macronutrient, stressdeficiencies, etc.
Um, but you know I do see a lotof women with pcos and people
on a weight loss journey andmany things um, and you know,
(41:35):
typically I wouldn't say most ofthose people have a chronic gut
issue at the same time.
So they're not thinking aboutlinking up.
But the research is pretty umstrong on this point that you
know, metabolic endotoxemia mayactually be the primary insult,
beginning the pathogenesis ofsomething like type 2 diabetes
due to its effects on insulinresistance, right, wow.
(41:58):
So I think it's like theAmerican Diabetic Association
have been researching this sincelike 2007.
American Diabetic Associationhave been researching this since
like 2007.
And you know, in this paper,you know, first of all they
showed if you took that CD14innate immune system protein out
(42:19):
mice with it, you know,injected with LPS didn't have
any immune activation, right.
So just kind of clarifies oneof the mechanisms.
But again, this um tlr4activation occurs due to
excessive lps.
There's there's so manymechanisms to back up that lps
may be the primary insult.
Like you know, the tl of tlr4activation um reduces insulin
(42:42):
sensitivity um by inhibitinginsulin receptor activities and
the inflammatory cytokinesincrease liver glucose
production and subsequentchronic inflammation.
It decreases glut4translocation which prevents
proper glucose uptake um.
So this idea that the metabolicendotoxemia piece is what
(43:04):
begins to make someone not soresistant sorry, not so
sensitive to insulin iscompelling, you know, because
there's this big question whenwe talk about all this, like
well, was it chicken or the egg?
Right, who knows, maybe it'sdifferent depending on the
person.
But I think at the end of theday, because of the tlr4
(43:28):
activation induced by lpsendotoxicity um, it needs to be
considered.
I think it's a really smartapproach to say reducing insulin
sensitivity um in people who,whether it's pcos or obesity and
or right um, it does.
You know it's not really goingto change my approach and you
(43:48):
know, with obesity as well, youknow there's interesting
research on that.
You know Many people I knowassociation isn't causation but
in studies they do observepeople with obesity have much,
significantly higher populationsof the LPS producing bacteria,
gram-negative bacteria.
(44:11):
And once there is, what theresearch shows, like,
particularly on, like theeffects of diet on LPS
endotoxemia, is that if you givea quote-unquote normal weight
versus an overweight individuala very endotoxic meal.
It's a very high in, say,processed saturated fats and
(44:34):
refined sugars.
They both have a very similarendotoxic response but if you
give that same meal to an obeseperson, their endotoxic response
is significantly more toxic.
Their endotoxic response issignificantly more toxic.
So it's kind of like oncesomeone is obese and because the
TLR4 activation that's onoverdrives, kind of perpetuates
(44:58):
fat storage and increasesinflammatory cytokines, an obese
person's endotoxic response tofood is a lot stronger.
Obese person's endotoxicresponse to food is a lot
stronger.
So taking an approach ofinvestigating and addressing
metabolic endotoxemia in thatpatient group is really
important.
And yeah, like really educatingpeople on how to reduce and you
(45:23):
know a strong endotoxicresponse in their diet.
And again there's this questionof what came first.
You know a strong endotoxicresponse in their diet.
And again there's this questionof what came first.
You know a higher endotoxicresponse to food due to being
obese, or was it?
You know weight gain due tohigh metabolic endotoxic
responses to food, and you know,I mean you could argue on both
(45:45):
sides.
But there's some interestingresearch suggesting the
metabolic metabolic endotoxemiapreceded the obesity um, just
based on studies showing thatpeople who had more potent
endotoxic responses to food umhad a significantly increased
risk of developing diabetes andobesity down the track.
(46:08):
So you know, are someindividuals pre-programmed with
a certain microbiome to havemore significantly endotoxic
responses to food and thereforebe at higher risk of developing
metabolic issues?
Is the argument?
Speaker 1 (46:24):
Stephen, can I ask just to give us an overview of I
mean, this would be an overviewof your mind, obviously, but
give us an overview of what sortof journey these patients have.
You know, if you can just tryand think about a few patients
that you've treated recently,recently around this concept of
(46:45):
metabolic endotoxemia, can yougive us a an example of of how
they improve over time, whatsort of conditions you've
treated?
Speaker 2 (46:56):
yeah, look, I do see a lot of endometriosis, um, and
so, for example, if I can thinkof some people recently and you
know these clients particularlythey're not well, you know,
they're in a lot of pain anddistress.
They're desperately seekingsolutions, right, and so they're
(47:16):
absolutely a group who, whileI'm begging on about treating
the cause, I want to get themsome symptom relief ASAP.
Right, that's right.
With these people, I love mesome PEA and yeah, I guess,
similar to the story what I wastrying to say earlier, it's like
(47:37):
, because people are so unwelland really want a solution and
find out about this link withthe gut.
You know, again, a lot of theseclients come in very focused on
the gut and it, you know, Imake sure I explain to people
really well, yes, we're going totreat your gut, but, um,
requiring that actually sorry,treating that actually requires
(48:00):
us to zoom out and reallysupport your overall health too.
It's not just going to be a gutprotocol of probiotics and it's
a mix.
You know some people thatreally hits home and they get it
, um, and they're they're up forit.
I'm looking at their overallkind of life and health and the
sleep and the stress and all thethings um, and others not so
(48:24):
much Um, but I'd say theoverwhelming majority of people,
once you get that point across,they get it and you know their
treatments are similar in someways and different in others,
just depending.
But yeah, look, endo, I havereally good results.
I don't know why.
It's just once you and they all.
(48:46):
For example, endo has this biglink with histamine as well,
right, they're all.
It's like cool, he's lowhistamine diet, it'll give you
some relief, but it's not asolution.
Um, so with the histamineconversation, everyone's like oh
, I want to find it if I've gothistamine bacteria in my gut.
Honestly, 90% of them don't um,but 90 of them do have, like in
(49:10):
my experience, significantovergrowth of e-coli, right,
kind of classic lps, um,producing microorganisms.
So I, I don't know, with endo,I find if you really get on top
of that endotoxemia and you know, get gut centric and cool,
reducing coli populations andall that kind of thing like they
get significantly better um canI ask what dose of pea do you?
Speaker 1 (49:37):
what do you use?
Speaker 2 (49:39):
I'll go pretty high for the first month, like about
600 milligrams twice a day for amonth, and then ideally reduce
that back to a three to sixhundred maintenance dose.
But awesome, awesome for painrelief, right, because right,
and when someone's in thatdegree of pain, it's like they
don't care about the multiplevariables of dysbiosis that they
(50:01):
need to address over you knowyears.
Just like, yes, but we need toget people symptom relief.
So the the PEA is prettyincredible for that, like yeah
and and do you take?
Speaker 1 (50:13):
do they take the PEA every day through their cycle or
just when they're experiencingpain?
Speaker 2 (50:19):
no, I get them every day, every day, yeah, yeah, most
people, it's such a huge issue,so under treated, poorly
managed, poorly diagnosed.
Yeah, it's a travesty, yeah, Imean you know when we talk about
medications and okay, whatcontributes to leaky gut,
(50:40):
dysphosis and lps?
Okay, what medications?
If the anti-inflammatories areshocking, you know they are very
well known to perpetuate okay,well, what actually leads to
these bacterial population?
Um balances and yet some peopleare surviving on those meds and
it's like cool, yes, that'ssome good alternatives.
Speaker 1 (51:03):
Um yeah, in in desperation.
I've seen one woman, uh, takingthe high dose ibuprofen, that's
the 400 milligram tablets, justpopping them, yeah, all day,
trying to get relief becausethere was.
She couldn't get relief from,uh, a doctor who was hesitant
(51:24):
about using opioids and um, andso she was popping these
ibuprofen during the day and hada gastric bleed.
Yeah, so she was done eitherway.
Speaker 2 (51:35):
She, you know, yeah yeah, yeah, and you know again,
a lot of this comes down tolifestyle and diet.
And you know what's the sayingOutcomes are generated by habits
, but most you know people inchronic pain.
They know what they need to do,but they can't deal with it you
(51:56):
know.
So the symptom relief is reallyimportant at the beginning.
Right, that's what's thechallenge about being a
clinician.
It's like cool, we want totreat the cause, but we also
want to get you feeling betteras soon as possible, without
ignoring the root cause, youknow.
Speaker 1 (52:09):
So pea is just a total winner for that and also I
have to ask about omega-3 fishoil.
You said that you you know youput a decent dose in.
What dose do you use?
Speaker 2 (52:23):
uh usually about.
I mean, I'm using uh fish oilwith a very high ratio of EPA to
DHA.
So if someone's pretty inflamed, some pretty serious gut
nervous system issues, I'll goabout two to three grams total
omega-3 with about a three toone ratio of EPA DHA.
(52:48):
Yeah, I go pretty high dosewith that.
They may not need to take thatmuch forever but again just to
get as much impact on thatinflammation and endotoxic stuff
ASAP.
Yeah, really high dose fish oilto begin with is very helpful
Beautiful.
Speaker 1 (53:05):
We've learned so much from you, stephen.
Just one last quick questionwhere can we learn more now?
You've?
You've given us some greatpapers throughout this.
I hope we're going to beputting these up on the website,
um, and in the show notes, um.
We'll definitely do that.
Not, I hope, anything else.
Any other seminal works?
Have you got any courses, forinstance?
Speaker 2 (53:26):
no, they're in the works.
Um, you know, because I've beentalking a lot um in this chat
about, you know, symptom reliefand damage control treatments
for lps, and but there's a muchbigger picture to um consider,
right?
Um, that's kind of what I'm inthe process of developing a
(53:49):
course on, because it's justit's not sustainable for me or
clients like legit time or moneyto get through all of like,
okay, what are the things I haveto consider to get figure that
all out in appointments.
It's just not sustainable foranyone.
Um, so and I'm a bit all ornothing, like I don't want to I
(54:11):
well, I'm gonna make somethingwhich kind of covers everything,
all these variables, and youknow, here's the phases to go
through and that isn't the work,so it'll be out eventually I
look forward to that mind map.
Oh my gosh.
Yeah, it's been a process, butyeah.
(54:32):
So until that is out, you canjust find me rambling on my
Instagram.
Speaker 1 (54:39):
Stephen Dutch, that's your path on my website.
Yeah, I love your work, Stephen.
I love your mind and I lovethat you don't just focus on the
problem at hand but look atwhat's causing the problem.
You can see it's pretty evidentthat you've got a lot of love
and care that you give to yourpatients and it's not just in
(55:01):
about a little bit of poking itwith a symptom relief.
You really want to get themwell, you want to get them vital
.
I really applaud you and whatyou do.
Thank you so much for your work.
Speaker 2 (55:12):
No worries, andrew, it's a really cool chat.
Speaker 1 (55:14):
Thank you everyone for joining us today.
We're going to be putting up aheap of information for you in
the show notes and remember youcan catch up on all the other
podcasts on the Designs forHealth website.
I'm Andrew Whitfield-Cook.
This is Wellness by Designs.
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