January 25, 2025 • 54 mins
In this episode of the Next Level Human Podcast, Dr. Jade interviews Alex Martinez, CEO and founder of Intrinsic Medicine, who shares his journey from a corporate attorney to a leader in the field of gut health and immune function. The conversation delves into the significance of human milk oligosaccharides (HMOs) and their role in modulating the immune system and gut microbiome. Alex explains the mechanisms by which HMOs influence health, their potential in treating chronic diseases, and the importance of safety in pharmaceutical development. The discussion highlights the need for innovative approaches in medicine and the promising research surrounding HMOs. In this conversation, Jade and Alex Martinez delve into the world of bioidentical compounds, particularly focusing on human milk oligosaccharides (HMOs) and their clinical implications. They discuss the safety and efficacy of these compounds, the ongoing clinical studies, and the potential impact of 2-FL on pediatric health, especially in relation to inflammatory bowel disease. The conversation also explores the gut-brain connection, particularly in Parkinson's disease, and the challenges faced in functional medicine treatments. Alex shares insights on the future availability of these innovative treatments and emphasizes the importance of dietary fiber in health.
Connect with Intrinsic Medicine: https://www.intrinsicmedicine.com/
Chapters
00:00 Innovative Approach to Gut Health
09:13 Human Milk Oligosaccharides and Immune Health
24:40 Advanced Clinical Studies of Human Oligosaccharides
37:19 Impactful Discussion on Gut Health
45:53 Empowering Self-Care Through Data Sharing
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
All right, welcome to the show everybody.
This is the Next Level HumanPodcast.
I'm your host, dr Jay Tita, andtoday I have with me Alex
Martinez.
He is the CEO and founder ofIntrinsic Medicine and is doing
some really neat things.
I'm going to say a little bitabout why I became interested in
him and really selfishly wantedhim here to educate me on some
(00:23):
of the things that he is doing.
And so, as it normally happens,being a podcast host, you
oftentimes get reached out bypromoters and people who
essentially have an expert thatthey're saying, hey, you might
want to have this particularperson on your show.
And so Alex came across my deskthis way and I went and looked
at what he is doing.
(00:44):
And many of you who follownaturopathic medicine,
functional medicine, know thatone of the mainstays of our work
is really around gut immunefunction, and so we have seen
for a very long time.
Just as a reminder, I graduatedfrom medical school back in
2004, started in 1997.
And back then no one wastalking about the gut and the
(01:06):
immune system, but we got thatas one of our first courses.
We learned before our gutrestoration programs how
integral the gut immuneconnection was, so it's been
really neat to see this,especially over the last 10
years.
Everybody talking about this,influencers even talking about
this, and I think Alex and hiscompany are doing something
(01:28):
really, really cool here.
So, alex, the first question Isort of want to get into as we
begin this discussion isobviously intrinsic medicine is
doing a lot around thisrecognition of gut and immune
function, and you all are comingat it from a different
perspective, and so what I wantmaybe to ask is how you came to
(01:52):
this in general, and then whatis it that intrinsic medicine is
doing that's so different?
Speaker 2 (01:58):
Awesome.
Hey, thanks, jade.
Thanks for having me Excited tospeak to you about this.
So what's?
It's a pretty fascinating storyto some, but it's essentially
is you know, I came to thisafter a pretty different career
path.
You know, studied public health,was actually a corporate
(02:20):
attorney, practiced in SiliconValley doing med device work,
and really the running theme inmy life was I wanted to figure
out a way to help people andwithout becoming a doctor, tried
that early in undergrad and itdidn't work well.
So I took a health policy route, realized a legal education
would be important to that.
Realized that the mere practiceof healthcare law was actually
(02:43):
perpetuating dysfunction in thesystem.
Recognized innovation as anopportunity.
So I actually helped spin out acouple of companies when I was
in law school and then foundmyself at a premier group in
Silicon Valley doing the mostboring work for the most
interesting companies, and sonever one to sit.
Still, I shortly started myfirst company, which was an MIT
(03:04):
spinout, which was digitalhealth.
It was a patient education atthe point of discharge company.
We re-engineered the patientdischarge experience.
This was before digital healthwas even a thing and
paradoxically, I discovered atthat time the CEOs of hospitals
loved what we were doing.
We kept patients, we preventedreadmissions.
Cfos did not.
They said that's actually wherewe make our money from, right,
(03:26):
and so what a striking factpattern to be living so moved on
from that after drafting partof the Affordable Care Act that
actually created the financialpenalties for readmissions.
So that was a parting gift andwas lucky enough to get a very
unique role that I was grosslyunqualified for, so I had to get
(03:48):
it by actually doing a projectfor the company.
But I got to run corporatedevelopment, competitive
intelligence and market researchfor a biotech company called
Ionis that was developing mRNAtargeting therapeutics mRNA
(04:09):
targeting therapeutics and sothat was kind of my infiltration
into biotech and my opportunityto learn.
The business at a keyinflection point Helped to take
Ionis from a small cap companyto over $10 billion company with
four approved drugs, whichreally creating a third new drug
discovery platform.
And it was all about antisensetargeting mRNAs, primarily for
monogenic diseases.
(04:30):
And this is when I learnedsomething very interesting that
sometimes companies look attheir toolkit and they say, oh,
let's apply this to everything,including maybe some GWAS
markers that are not monogenic,that the disorder is more
multifactorial and thenrisk-benefit really changes.
So at that time they were doingsome cardiometabolic diseases
(04:55):
and I was like I don't love thisand it turned out to be the
neurology programs and I got towork very closely on the program
.
That was the first drug everapproved for spinal muscular
atrophy and that drug did haveLazarus effects.
You could give it to babiesearly enough and they would
develop normally versusgenerally dying by the time they
(05:16):
were two years old.
So that was a privilege to workon that.
But sort of right there in mymind the entire time as I worked
at another program that I wouldsay wasn't that great and
actually had some very severeside effects is who's developing
drugs for the rest of us?
Because all of pharma was sayinglet's focus on rare diseases
(05:37):
because there's a wide leniencyin terms of safety.
And then everyone flips aroundand sells these drugs for half a
million dollars a year.
And I'm coming from a healthpolicy, a public health
perspective I'm saying thisdoesn't sit right Not to say
that rare disease patients don'tdeserve attention and efforts.
But we have a chronic diseaseepidemic and what we've learned
(06:02):
from the Human Genome Project isthat genes are not
deterministic.
So myself and my co-founder,who also worked at that company.
He was like me.
Somebody couldn't stick totheir job description.
He was a patent attorney,medicinal chemist turned patent
attorney, turned runningregulatory affairs for that same
company.
We recognized that the ultimatearbitrage opportunity in pharma
would be safety.
(06:22):
Opportunity in pharma would besafety.
What if we could find trulysafe compounds?
And then we said, well, how dowe stop siloing disease?
And this is probably somethingthat you talk about in your
practice.
Let's not silo diseases.
Let's look at the common causaldrivers.
And we said, well, what'swhat's common to all these
(06:43):
chronic diseases?
And we're, it's immune,dysregulation and dysbiosis.
And then you know, so you havethat.
And then you probably have alayer of genetic susceptibility
and a loss of regulatoryfunction from other
environmental factors andlifestyle factors.
Well, we just outlined a prettycompelling profile for
(07:05):
something we'd want to do.
It needs to work through thosemechanisms and be absolutely
safe.
Where are we going to find it?
How are we going to find it?
And that's why I said, well,the only lens we should look at
is evolutionary biology.
Let's look for compounds thatappear at unique junctures in
human development, starting inearly life, compounds that
appear at unique junctures inhuman development starting in
(07:27):
early life.
Let's see if there are anycompounds there that appear sort
of nowhere else.
And we came across a library ofcompounds called human milk
oligosaccharides in an infantnutrition lab and the first
thing I recognized is that, well, these are not nutritional
because they're amylaseresistant.
The body can't break them downfor calories because their
amylase is resistant, the bodycan't break them down for
(07:47):
calories.
So, after fat and lactose, whyis nature having human mothers
produce these at anunprecedented diversity of
structures and concentration?
And furthermore, we also, atthat same time we're looking at
they're not just in milk, theyactually enter maternal
circulation during the firsttrimester.
They actually enter maternalcirculation during the first
(08:10):
trimester and they're in thefetal cord blood and they're in
the amniotic fluid.
So literally from conception toseveral years out, literally
encompassing the entiremother-infant dyad and then
promoting the baby's, I'd saysay, foundational immune and
microbiome programming afterbirth.
(08:30):
So took a look at this and said, well, I don't have to develop
a drug.
Nature already did.
I need to reintroduce it.
Speaker 1 (08:36):
I love this man.
I'm just like.
It's almost like you took theengineering approach in your
career, right, and, like me, youand I are similar in this.
I've traveled an interestingpath.
I mean, it was biochemistry,psychology, functional medicine,
transpersonal psychology,philosophy, and what's
interesting about when you comeat it from this perspective is
you get people who are veryintegrative thinkers right.
(08:57):
So I always like to think aboutwhat is real intelligence?
Well, it's not just gatheringinformation, it's being able to
put different pieces ofinformation together in
interesting and novel ways, andit's interesting how your story
got here.
And then you began to look atthese compounds, so these human,
identical milk oligosaccharidesright, this is what you all do,
(09:21):
and so this came from the humanmilk oligosaccharides and I'm
interested.
You said a couple of thingsthere that I know.
I have a lot of practitionerslistening, so let's just deal
with this just for a minute.
So these things are not beingdigested, right, was what you
hinted at here.
So they're obviously beingtaken in to the infant.
(09:41):
They're also around, as youpointed out, prior to birth, but
they're being taken into theinfant.
They're also around, as youpointed out, prior to birth, but
they're being taken into theinfant.
I assume the name human milkOligosaccharides that they are
very high in quantity in themother's milk, and so the child
is taking these compounds in.
They are not being digested inany way, and I'm assuming, since
(10:03):
you mentioned, they're found inthe blood stream of mothers as
well.
They are going intact into thesystem and having some type of
major impact there.
And, given what you do, itseems that they are having an
impact on the immune system, andwe know that the gut and the
microbiome of the gut is theseat of the immune system.
(10:27):
So this story is starting toget pretty interesting here,
given that we know that theimmune system is highly
regulated and differentiated atthe level of the gut, and now we
have these compounds that seemto be acting right at this
particular, you know sort ofarea, and so you have honed in
(10:47):
on this area.
Now tell us a little bit aboutwhat exactly these things are
doing.
What do we know about?
Speaker 2 (10:55):
Yeah, yeah, great question.
And so what's nice, especiallysince I think a large portion of
your audience probably isfamiliar with kind of
plant-based oligosaccharides,they'll appreciate some of the
nuanced differences in themechanism here.
So, as you alluded to, there'sdefinitely a systemic effect.
One of the fascinating thingsthat this is actually the sort
(11:16):
of inception Sherlock Holmesmoment of the company was
there's been a longstandingobservation that mothers with
autoimmune conditions rheumatoidarthritis, others often during
pregnancy they go into remissioneven though they're off their
drugs, right.
And so if you go back inhistory to the 90s, that
actually was an observation thatresulted in the search for
(11:40):
something called Substance X,and actually the urine of
pregnant women was fractionatedand different compounds were
isolated and tested and one ofthem, substance E, actually
seemed to be effective onrheumatoid arthritis at the time
when really there were notreatments, and that turned out
to be cortisol.
So that was a discovery ofcortisol.
(12:01):
It was synthesized as cortisone.
They won a I think it was a1950 Nobel Prize for that.
But if you actually read theirlaureate speech, they said well,
we actually didn't findsubstance X, we don't believe
cortisone was that, but we foundsomething that worked and it's
still a mainstay, you know, ofcourse it has some chronic side
effects and but you know the thethe the aha moment came was the
(12:24):
same exact year 2018, that I'mlooking at these human milk
oligosaccharides andunderstanding their mechanisms a
little bit better.
That was the same year it wasdiscovered that they enter
maternal circulation, startingthe first trimester, which
corresponds to when thehistorical observations of
remission have been seen.
(12:45):
At the same time, there wasalso a cohort that was an
epidemiology study in Canadalooking at 521 mothers,
including some with existing RA,and they looked at ones that
went into remission versus onesthat did not.
(13:06):
And the ones that did go intoremission had a single had a
unique elevation in a specifichuman milk oligosaccharide in
their milk which corresponds tothe levels in their serum and
the p-value is like 0.001.
And then they and that formed ahypothesis and they said well,
(13:29):
what if we put this in a mousemodel of rheumatoid arthritis?
What does it do?
And lo and behold, it works,disease modifying.
So that's one of the thingsthat's unique is you have a
prebiotic here that's enteringthe colon intact.
It's the preferential substratefor bifidobacterium, right,
right, but these work by verysymbiotically with our symbiotes
(13:52):
.
They upregulate adhesion genesin the bifobacterium so it can
create a biofilm.
They actually can break upexisting biofilms as well, and
then simultaneously these are,they're sugars, and sugars are a
language that mediate a lot ofintracellular responses,
including pathogen-hostinteractions.
Sugars on cells are doorwaysthat are hacked by pathogens to
(14:17):
enter the body.
So some of these HMOs, theyactually serve as soluble
receptor decoys.
So as they're terraforming thatmicrobiome you can have
invasive E coli microbiome.
You can have invasive E coli.
You can have H pylori isbinding to these instead of the
baby's immature gut cells andbeing passed out.
(14:38):
So that's how it disadvantagesand really enables a healthy
foundational microbiome to beformed and then once that
happens as substrates for thecommensal microbes, basically
turns them into little drugfactories and they are just
spewing a whole host of smallmolecules and metabolites,
including, like butyrate, ofcourse, other short-chain fatty
(15:00):
acids and then even neuroneuroprotective, neuro
neurodevelopment compounds aswell.
And then to your point aboutthe sort of direct immune
modulating activities.
Here that's when things getinteresting.
So about like one to 4% ofthese do enter systemic
circulation.
This is essentially thebootcamp for the immune system
(15:31):
and they work on, they balancethe immune responses with Th1,
th2.
And we've actually seen thatindependent of any of the
microbiome effects, so we can doit in completely a clean
environment.
We can change macrophagepolarization from like a M1 to a
regenerative M2.
Phenotype also enhance Tregs aswell, and it makes absolute
(15:55):
sense.
They're helping terraform themicrobiome.
The baby's immune system isbeing trained to recognize self,
non-self as well as friends,not friends, and so that's kind
of how they work.
Speaker 1 (16:10):
Yeah, and now I think the listener can understand why
, when I started looking intothis, I got so excited because
this is one of these things thatworks with the body's immune
system and sort of the thingsthat we have in place, our
microbiome, to do what a healthysystem would be doing anyway.
Right, and so it's one of thesethings that I was just like.
(16:31):
This is a really interestingset of mechanisms, not just one
simple mechanism.
Of course, one of the thingsthat my medical background
taught me right from the get-gois, you know, sort of this
integrated, holistic approach inboth the approach of the
practitioner but in the way thebody works.
So many of these drugs that wetake, they are big guns focused
(16:51):
on one particular area, and thiscan cause downstream effects,
because our physiology is likethat spider's web you touch one
part of the web, everything elsemoves, and so having compounds
like this that influencemultiple aspects of immune
function, from the bacteria tothe actual cell membranes, to
(17:15):
actual immune cells andmodulating those cells, is
really incredibly fascinating.
So I would imagine and this ismy next question that for me,
with knowing nothing else, Iwould be thinking about,
obviously, autoimmune conditions, I would be thinking about
allergic conditions, atopicconditions.
Do we see that these things arehaving an impact on these
(17:40):
conditions, and to what extentare they?
Is the research already there?
Is this emerging research?
But we can begin to guess thatthis could have far-reaching
effects, even in things likecancer and other things like
that.
So I'm curious what have youactually seen these compounds be
able to do in terms of disease?
Speaker 2 (18:04):
Yeah, it's a great question and actually a really
exciting one, because there issubstantial preclinical data and
sort of translational datasuggesting that these can be
disease-modifying in theconditions that you mentioned.
As I told you, the sort ofGenesis story is pretty
fascinating because you havekind of a human epidemiology
(18:25):
with a direct nexus to it.
That was, then, what I likeabout some of these studies is
there's there's always a humanepidemiology component, whether
it's coming from mothers orinfants, right, because we can
also look at infants that areformula fed, right, and and
there's also a human knockoutmodel, for that's actually based
(18:46):
on on on secretor status, bloodgroup, where some moms have a
markably different HMO profilein their milk, including one of
the foundational ones, and whatyou can see is you can see
completely differenttrajectories in terms of health
and it corresponds to adifferent microbiome.
And then you're able to doreverse translational.
You're able to form ahypothesis and do a reverse
(19:08):
translational experiment in mice, which is important for drug
development, of course, and Ithink one of the other things
you know, I like how youappreciate the kind of
meandering path because, you'reright, it enables a different
form of pattern recognition andsort of bias, uh, where you're
(19:32):
like I just it was.
I just want to find the truthbehind something that's
intriguing that no one's foundthe truth for and it's not mine,
I didn't invent it.
Uh, there's a a differentresponsibility associated with
it and, you know, one of thethings that is pretty annoying,
quite frankly, to me is the lackof translation of of studies
(19:53):
that are published in nature.
They're published in science,are published in cell, and they
don't make it.
The biology just seems to peterout, usually after a company
has raised a ton of money andand in the popular science media
has already put out somearticles saying these geniuses
at this, these, you know, eliteinstitutions, may have found the
(20:15):
cure for blank right, creatinghope in patients, and it just
never, never gets there.
Yeah, and that's why, when youlook at, uh, you know the, the
perverse statistics in thepharmaceutical field, they're
saying now the cost to develop adrug is $3 billion.
(20:37):
That tripled in the past decade.
So this rebuts the soloresidual right.
Wait, technology is supposed tomake things cheaper and faster.
Instead, it's longer and moreexpensive and when something
does get across the finish line,it's expensive to the system
line.
It's expensive to the systemand it's really expensive to the
patient and oftentimes it has amediocre profile at best.
(20:58):
So, that rant aside, it wassaying how do I remove that kind
of translational risk?
And there's a lot of reasonsyou can talk about it.
Fraud is actually one of them,but a lot of it's the imperfect
nature of animal models, mousemodels, especially when they're
genetically manipulated.
You're creating somethingthat's essentially so artificial
(21:20):
.
It's designed to give you aconclusion that matches your
hypothesis, so there's asubconscious bias that's been
introduced even in preclinicalproof of concept.
So that's a long way of sayingguess what?
These are not just human milkoligosaccharides, they're
mammalian milk oligosaccharides,and so we've prioritized our
(21:43):
initial candidates that wereally want to kind of prove
this thesis on, based on onesthat are common.
So these are not artificialconstructs.
It's is the biology preservedso we're able to look at, you
know, every single differentrheumatoid arthritis model.
These work disease modifying.
(22:04):
They've been tested againstthings like methotrexate high
dose methotrexate high-dosemethotrexate a human mainstay
disease-modifying effects,reducing the systemic cytokines
you want to see, but evenpromoting cartilage repair and
even like PANIS and bone erosionreductions as well as edema
swelling.
Same thing in atopic dermatitismodels as well, and you see a
(22:46):
reduction in the validatedcytokines IL-4, il-13, where we
do have DMARDs and, importantly,these are same things with
human cells as well, with thecorresponding human cells, the
monocytes and the T cells, andseeing basically the translation
at the cellular level of theeffects that led to the in vivo
(23:11):
did to the in vivo?
Speaker 1 (23:11):
Yeah, and just real quick, alex, let me, for the
listener, for those of you whoare getting a little bit lost
with Alex talking about thescience here, basically what
he's essentially saying is, ascompounds go through sort of the
rigor of seeing if they'regoing to be effective for a
disease or diseases, they gothrough a process, usually in
vitro, meaning in test tubes,petri dishes, that kind of thing
(23:33):
, and then in animal studiesprior to going into, maybe human
cells in petri dishes andthings and then finally into
clinical studies.
And so what Alex is walking usthrough right now is how this is
going in sort of the in vitroanimal world, showing that there
are disease modifying effects.
(23:54):
And the next step is going tobe and that's what's going to be
the next question I was goingto ask Alex is do we yet have
any in vivo or clinical trialsunpublished in humans yet?
And I think, from what I heardyou before, that's not yet the
case, but maybe there is some ofthat going on.
But the interesting thing isthat, you know, obviously these
(24:14):
things have been in human milksince the beginning of humanity.
They're in mammals.
This is what he's talking about,and so we have an interesting
way of looking at this, becausethis translational material, the
in vitro studies, the animalstudies, along with this idea of
evolutionary biology, knowingthat these things are there
makes this incredibly intriguing.
(24:35):
And of course, one day we willget to, hopefully, clinical
trials, if they're not here yet.
But I just wanted to giveeveryone who's not skilled in
the science of this a catch upto understand where Alex is with
this.
And then, alex, do we have andhow far off are we all from sort
of human trials with this?
Is that stuff going on behindthe scenes right now or not, or
(24:56):
can you even tell us?
Speaker 2 (24:58):
Yeah Well, thanks, jade, and first of all, you know
, yeah, thank you and apologiesto the audience.
Sometimes I jump into my nerdhole.
Speaker 1 (25:06):
Yeah, I like, don't worry, I like it man.
Speaker 2 (25:15):
I like it and so.
So thank you for offering thatcontext.
So one of the neat things hereand again my premise was safety
is an arbitrage opportunity,right, and so it was actually
the infant nutrition companiesthat they've spent a lot of time
, they've been working on thisfor decades and part of that
included.
You know understanding, youknow the safety profile of this.
So manufacturers of thesecompounds?
Of course we're not.
We don't have a.
There's no human dairy outthere.
(25:37):
So these are being producedwith synthetic biology and so
that that pioneering work hasoccurred and the manufacturers
have demonstrated thebioequivalency, so it's
equivalent to the natural thingand that they that it's super
safe.
Speaker 1 (25:50):
Yeah, and let me just say something about that,
because you and I know thatpeople are going to ask this
question as well, and just forthose of you who are, again, not
practitioners and concernedwith this kind of stuff,
whenever you hear things likeyou know, built in a lab, or
something like this, what a lotof people don't know is if you
take vitamin C, for instance,and you take it from an orange
right, like that vitamin C, andthen you make vitamin C in the
(26:14):
lab, those two vitamin Cs arecompletely alike, okay, so like
they're basically the exact samething, and a lot of people sort
of get upset about this.
All that's left is vitamin C.
And so when we talk about and Iguess this is my next question
so these are bio-equivalent,they are essentially the same
thing.
Is that what you're saying,alex?
(26:34):
That these are human identicaloligosaccharides, human milk
identical oligosaccharides, sothat while they are made in a
lab, they are the exact samecompound in terms of the way
they look, function in the body,and that's what we're talking
about here.
But we cannot say that they'redirect because, as Alex said, we
(26:54):
don't have a dairy factory forhuman milk and so these are
being engineered in the lab.
In the same way, insulin mightbe sort of made in the lab.
Speaker 2 (27:04):
Yeah, absolutely correct.
Yeah, and they're trulybio-identical.
They're absolutely identical.
And they're truly bio-identical, they're absolutely identical.
And part of this that's ethicalright, because you can isolate
this from donor milk.
But then what you've done isyou've diverted this from babies
that need donor milk.
So it's something that'scertainly important for us.
(27:26):
There are some companies thatare taking it from donor milk
and I disagree with that.
And also that's a pool.
There are actually 200 distinctstructures of these and even
(27:48):
ones that are same exactbuilding blocks, but the bond
angle is different on thestructure, completely different
bioactivity.
So there's a ton of work toreally understand what the
merits of each structure are andwhat the applications are.
And that actually leads to yourquestion about where we are in
terms of clinical studies.
So safety has been establishedin human beings already, not
long-term, but long enough toget into meaningful clinical
studies.
(28:09):
We've met with FDA on that andon the basis of that we've been
even approved in Australia toget into like meaningful
clinical studies.
And we've met with fda on thatand on the basis of that we've
been even approved in australiato get into two different phase
two clinical studies.
And just so everyone knows,phase one is typically the
safety studies, um, and that'susually in a healthy, normal
volunteer population.
And then a phase two is reallykind of where the rubber meets
(28:29):
the road, where for the firsttime you're putting the compound
into a patient situation andseeing if not only is the safety
preserved in that patientpopulation but does it do
something that's clinicallyrelevant to them.
The lead compound that we aredeveloping is the most abundant
(28:51):
of these human milkoligosaccharides, so it's like
30%.
If they're 200 differentstructures, this one is like 30%
of the concentration.
So it's really important forsomething and, as I mentioned,
there is a human knockout model.
What I mean by that is thatsome people have different
genetics so they don't producethis most abundant HMO in their
(29:12):
milk and that also correspondsto they don't produce a similar
oligosaccharide that lines theirmucosal tract, including like
the GI, and it's identical.
The oligosaccharide isidentical between the milk and
the one that lines theirintestines and mucosal tracts.
So those people that aremissing this they have a
(29:39):
different microbiome WestBifidobacterium and they get
inflammatory bowel disease.
So this compound is actuallybeing tested at Cincinnati
Children's Hospital right now inpediatric and young adult
inflammatory bowel disease.
Speaker 1 (29:47):
And is this 2-FL?
Is this the compound?
Yes, yep, okay, yeah, so that's2-FL.
Is this the compound?
Speaker 2 (29:50):
Yes, yep, okay, yeah, so that's 2-FL so this is
fucosyl lactose.
Speaker 1 (29:57):
Yes, yeah, how do you say that?
Yeah, how do you say that?
Speaker 2 (30:00):
Yeah, yeah, two prime fucosyl lactose yeah, yeah, and
yeah, so that's being assessedin that population.
And, interestingly enough, atthat same hospital who's a
partner of Intrinsic Medicinethey had a phase two.
That was a controlled study.
It's actually the firstcontrolled study.
No one really knows about thisstudy so I really want to give
(30:21):
them credit for it.
It was in children and youngadults that received bone marrow
transplants, that gotallergenic bone marrow
transplants, and these arereally sick patients yeah, no
kidding.
And the prognosis for that hasbeen known to be because they're
(30:45):
at risk of, basically, a graftrejection.
You got a transplant withsomeone else's genes in it.
The immune system can rejectthat and kill you basically.
So these transplant patientsare put on tons of
immunosuppressives, but thereare still ones that get what's
called like it's like a steroidresistant acute graft versus
host disease, where their bodybasically attacks the, the
(31:06):
transplant and, unfortunately,like the mortality is extremely
high when you have thatrejection and it's happening
systemically, meaning in your GItract or in your liver, and so
you know the scientists andclinicians taking care of these
kids are saying, like, well,what determines whether someone
gets that or not?
(31:26):
Patients who have dysbiosis.
It makes sense.
They have a dysregulated immunesystem as a result of that
dysbiosis, so it's more primedto attack and cause this really
severe and fatal consequence.
So the hypothesis was hey, weknow 2-FL can rescue dysbiosis,
(31:47):
maybe we can try it in thesechildren and see if we can
change that.
And so they did that in thestudy.
It was a controlled study 25patients received 2-FL, 20
didn't, and not only weremarkers of the dysbiosis
improved, but none of thepatients that received FL had
(32:10):
systemic acute graft versus host, compared to four in the
control group that did notreceive it and the overall
occurrence was very striking.
Only one patient had a skingraft versus host in the 2F,
which is a mild one, whichactually has a good prognosis,
(32:30):
and in the controlled ones thatdidn't, it was five patients had
nine total occurrences.
So you had patients that notonly had systemic ones but they
also had the skin ones, so itwas a full-.
Speaker 1 (32:41):
Yeah, so a small study, but a huge impact.
Huge impact Two prime fucosallactose was having marked effect
on these children.
Speaker 2 (32:52):
Yeah, yeah, and it was, and you know, and I think
it would have seen a bit of awider recognition their p-value
if they were underpowered by acouple of patients yeah, yeah,
that's, yeah, that's what I wasthinking, yeah it was 0.07,
which is like it's pretty darnclose.
Yeah, so they're off by a coupleof patients, but we're still
(33:13):
going to be talking toregulators about, like, what we
can do with that.
No, I think that was animportant study.
And then, you know, going on tothe programs that we're running
, we're actually getting readyto initiate a Parkinson's
disease study in Australia atthe beginning of next year with
Phell.
What's interesting here is thisis really, I think Parkinson's
is almost kind of like theprototypic gut-brain axis
(33:35):
disorder and it's really been inthe past year that that's come
out in a striking way.
I guess last summer there was a25,000 patient that was
published in Gut BMJ and itshowed basically, if you had
constipation, your odds ofgetting Parkinson's are like
400% higher than anyone else.
(33:57):
And then, I think just a couplemonths ago in the JAMA network,
another 10,000 patientspublished same thing
constipation your risk ofParkinson's is, I think, 165.
Speaker 1 (34:11):
Yeah, and you guys are all over this because I
don't the listeners, any of thepractitioners know.
Anyone who's in functionalmedicine knows we've been
talking for at least the lastdecade about, you know, this gut
brain, immune sort of axis andthings like Parkinson's,
especially Alzheimer's is thebig one, even autism, ADHD, so
this is a really big area, ahuge area.
(34:33):
That actually is one of theareas, Alex, that I'm very
excited about, because obviouslythese are huge issues and we
don't have a whole lot oftreatment.
You know things for these.
Speaker 2 (34:43):
Yeah, yeah, and it's amazing that functional
practitioners have been lookingat this for so long.
Right, it's like it's been longrecognized that the
neurologists that seeParkinson's patients they said
like, oh, of course.
Yeah, all of our patients areconstipated.
And then you go into theirhistories and you're like this
has preceded any of their motoror neurological symptoms by
(35:05):
years.
So it represents, now thatwe're looking at this big data
set, all of a sudden, it's likeconstipation is a functional
risk factor for these cognitiveand neurodegenerative diseases
and it's something where youknow, I think so many people
have been trained in.
You know I'm against riskfactor medicine that's based on
(35:25):
biomarkers.
I think you you scare peopleinto doing something and maybe
you're budging a needle on apopulation-wide level.
But that's looking at people asstatistics, when, even with
things like statins, it's likewhat are you doing in terms of
the myalgia, the muscle pain,the insulin resistant stuff?
It's like you're-.
Speaker 1 (35:44):
You and I are on the same page here, man.
I've seen it.
I just went through it with myfather.
Actually, you know, we put himon a statin recently and he
couldn't you know.
I just took him right back offyou know, because it's just so.
Yeah, so we're doing some.
You know, actually, I'll giveyou one of my pet peeves about
my field in functional medicine.
One of the things that we takewe might have been talking about
the gut brain immune and thegut immune balance but we're
(36:06):
doing these treatments anddietary approaches which I know
I'm going to get in trouble withmy fellow colleagues here, but
they don't work most of the timefor the things that we're
really trying to help.
Now, of course, we can make astrong argument they're working
way better than what we weredoing in the traditional realm.
But this is what excites meabout this style of medicine and
(36:27):
this approach to findingsolutions, and so obviously it's
one of the things that excitesme about you and your company
and how you're approaching this,because I do think even the
functional medicine world yes,we may have been talking about
this stuff, but our treatmentsand our gut restoration programs
and just giving probiotics andall the things if we are going
(36:49):
to be honest and I think we haveto be evidence-based we have to
realize that this is not beingthat effective for most people.
Sure, it's more effective thannot looking at this stuff, which
the traditional medical worldis not looking at this stuff at
all, but it's also not thateffective on the functional
medicine sides Just a pet peeveof mine.
I think it's important that wekeep looking and rather than
(37:11):
acting as if people in my fieldhave figured this out just
because we've been talking aboutit.
I think we've been talkingabout it, but I don't think we
figured it out.
Speaker 2 (37:19):
Yeah, yeah, and Jade, what I'd like to add to that is
you know, again, I think it'slike being constantly curious,
having identified the problem,and then I think that's actually
a good thing that there's animperfect solution as well,
because that will sort oftruncate and shorten the
diffusion of maybe a newpractice standard from something
(37:42):
where people can say, yeah,we've actually done, you know, a
probiotic approach.
I mean, if you look at it, ifyou look at the trajectory on
this, it started with the fecalmicrobiota transplants and those
demonstrated that cool, you cantherapeutically intervene at a
systems level on the microbiomein a major way.
(38:03):
You know, we, we look at, Ilook at every single FMT study
as a non-competitive proof ofconcept, because then there's
always going to be a scalingissue and then there's some real
infection issues and alsosometimes you achieve the effect
on the disease but then youchange the phenotype of the
person, right, like it actuallyshows how much that impacts
(38:25):
things.
And so what happened in termsof like microbiome treatments is
again, we're in the currentstate of medicine.
You guys are the ones who arereally breaking loose of it, are
the ones who are reallybreaking loose of it.
But if we say the allopathicapproach is a reductionist,
mechanical approach, not asystems approach.
(38:46):
It's more biochem versusbiology, which is an ecosystem
and a system and bidirectional.
Then it's saying, hey, whatdiscrete components of that FMT
led to that effects?
And then all of a sudden youhave limited consortia
probiotics and they're sayingthey're following the same thing
.
The association study is likeGWAS and say oh, this, this bug
(39:07):
is that one.
And then they say OK, let'sisolate it, let's introduce some
antibiotic resistant genes,because that a completely
different timescale than a humanbeing.
And so it's effectively outsideof the host for geological time
periods it's probably forgottenwhat it's like to be inside
(39:31):
that host.
And then it's reinserted andyou have engraftment liabilities
.
And that's not to sayprobiotics are not without their
merit, but it's probably animmunostimulatory, it's probably
more of a transient, limitedeffect and at the end of the day
, where the field's going is itmatters less about who's in
(39:52):
there and more about whatthey're doing.
Speaker 1 (39:54):
Right and I think what you're saying here, alex,
is so important for us asclinicians who are listening to
this, and even those of you whoare interested in this
conversation, who are or who are, patients.
This, what alex just alluded toin my mind is the reason why
you'll get all this marketingfrom different companies and
different supplements, where thescience is very exciting, but
(40:17):
the translation into the actualproduct doesn't seem to have a
huge effect.
I can't tell you how many timesI've seen new products come to
market where people are like, ohmy God, look at this amazing
study and look at this thing wefound, and then, based on what
Alex is telling us how they comeup with this, in this very
reductionistic approach and notunderstanding how to look at
this in a holistic manner, youend up with a product or a
(40:41):
program that is not thateffective, and so I do think
it's interesting where wecurrently are in medicine.
It's all important, but thissort of reductionistic approach
to this without the moreholistic, systemic approach is
probably not going to get usthere, which is why I get
excited about where we're goinghere.
(41:01):
So let me go ahead and wrap upwith you and ask you I mean the
first question everyone's goingto ask.
You know, this is like OK.
Where do I get this?
How do I take this?
What do I do with this?
Alex?
Speaker 2 (41:15):
Absolutely, and so, yeah, I always, always want to
add something that's of value.
So these are not broadlyavailable yet there are some
companies that do have them.
The quality control, the purity, is certainly not up to our
standards.
So I'd say the announcementthat I can make is, while we are
(41:36):
a pharmaceutical company, whileIntrinsic Medicine is a
pharmaceutical company, I'mcommitted to making earlier
access available for thesecompounds, given that they are
safe, and so I will be startingkind of a parallel wellness
company that offers these on astructure function basis, and
initially we will be launchingin collaboration with a
(41:57):
functional medicine clinic outof Chicago and we'll be putting
together a protocol of use caseon this, based on clinical data,
including some positive data inall different forms of
irritable bowel syndrome, andwe'll be producing this at a
clinical grade spec, and so ifpeople are interested in that,
(42:18):
you can go to our currentwebsite, intrinsicmedicinecom,
and just fill out the contactform and then we'll update you
on that one, and that's going tobe primed for a Q1 launch, but
we'll have material available.
Speaker 1 (42:32):
So we don't have long to wait.
Speaker 2 (42:34):
Yeah, so you don't have long to wait, because and
then the way I envision thingsworking between the companies is
we'll be running like truepharmaceutical gold standard
phase two clinical programs onthe intrinsic medicine side and
on the intrinsic wellness side.
Practitioners within theirscope of practice can actually
look at that, look at thoseprotocols and say, cool, do I
(42:58):
want to do this on acase-by-case basis with my
patients and they'll have accessto a high-quality spec material
as well aspractitioner-developed resources
on the use of that.
And that's kind of the way ofsaying that these compounds are
for everyone and I don't want tocreate excitement without
providing access at the sametime providing access at the
(43:23):
same time, 100%.
Speaker 1 (43:24):
Well, alex, I have to say man, I just want to say
this podcast right, it's calledthe Next Level Human Podcast.
Part of the reason for that isthat I believe that every single
one of us are unique.
There's never been another Jade, there's never been another
Alex, there never will be, andyour unique background and the
way you came to this gives youthe ability to do something that
only you can do in a way thatyou can do it, and I really
(43:44):
appreciate that you are doing it, alex.
I really appreciate youbringing this to the world.
I think it's needed.
I think you're doing, I thinkyou're just a brilliant dude and
you're doing like some reallyamazing stuff here.
So I just want to say thank youfor your work, thank you for
your time.
Is there anything else you wantto leave us with before we part
ways?
Speaker 2 (44:03):
Yeah, yeah.
So thanks, thank you, jade.
It's been my pleasure and thishas been a wonderful discussion.
So I think there's a couple ofthings.
The first and foremost is that95% of Americans are not at
their dietary fiber levels, sothat is a low-hanging
opportunity for everyone to doan audit, for practitioners to
(44:27):
do an audit, and even though theplant-based, the
galactooligosaccharides, thefructooligosaccharides, may not
have the full profile, there'smerit there.
And, of course, there's meritfrom whole foods, right, and so
that's an opportunity for peopleto really profoundly shift
(44:48):
their health and theirmicrobiome.
And so I don't want todisempower anyone and say, hey,
you have to wait for the nextscientific miracle.
There's something that trulyyou can do today.
And then I'd say the secondthing is that I had a vision
when I was starting this companyand said, well, we would have
entirely different drugs ifevery CEO founder was required
(45:08):
to be the first one to taketheirs.
So you know I'm not talkingfrom a soapbox saying, hey,
everyone else has to do this.
I'm actually the I think theperson who has taken these
chronically for the longestperiod of time.
So I'm four years in and it'sconstructively enabled me to
cure my IBSD, which was fairlydebilitating.
(45:31):
So and and same thing, my sonhad very severe atopic
dermatitis.
There was a milk allergy and hewas, you know, zero, and we
were able to get him from anEpiPen with 21 food allergies to
eating peanut butter sandwichesbetween ages two and four.
(45:51):
So we're living it.
And now it's about creating adata set that other people can
use to inform their own use case.
And of course, that's alsowhat's driving me for sort of
novel commercialization tocreate an early access
opportunity, because I dobelieve in practice autonomy and
then personal sovereignty forpeople to direct their own
(46:13):
self-care and health andwellness journey 100%.
So thank you so much everyonefor listening, jade you for
having me and the insightfulconversation.
Speaker 1 (46:23):
Yeah, my pleasure, Alex.
Alex Martinez fromIntrinsicMedicinecom.
We appreciate you very much.
You all go check out thewebsite and do me a favor, Alex,
hang on the line, just so I canmake sure all this uploads.
But for all of you, thank youfor hanging out with Alex and me
and we will see you at the nextshow.
All right, welcome to the show everybody.
This is the Next Level HumanPodcast.
I'm your host, dr Jay Tita, andtoday I have with me Alex
Martinez.
He is the CEO and founder ofIntrinsic Medicine and is doing
some really neat things.
I'm going to say a little bitabout why I became interested in
him and really selfishly wantedhim here to educate me on some
(00:23):
of the things that he is doing.
And so, as it normally happens,being a podcast host, you
oftentimes get reached out bypromoters and people who
essentially have an expert thatthey're saying, hey, you might
want to have this particularperson on your show.
And so Alex came across my deskthis way and I went and looked
at what he is doing.
(00:44):
And many of you who follownaturopathic medicine,
functional medicine, know thatone of the mainstays of our work
is really around gut immunefunction, and so we have seen
for a very long time.
Just as a reminder, I graduatedfrom medical school back in
2004, started in 1997.
And back then no one wastalking about the gut and the
(01:06):
immune system, but we got thatas one of our first courses.
We learned before our gutrestoration programs how
integral the gut immuneconnection was, so it's been
really neat to see this,especially over the last 10
years.
Everybody talking about this,influencers even talking about
this, and I think Alex and hiscompany are doing something
(01:28):
really, really cool here.
So, alex, the first question Isort of want to get into as we
begin this discussion isobviously intrinsic medicine is
doing a lot around thisrecognition of gut and immune
function, and you all are comingat it from a different
perspective, and so what I wantmaybe to ask is how you came to
(01:52):
this in general, and then whatis it that intrinsic medicine is
doing that's so different?
Speaker 2 (01:58):
Awesome.
Hey, thanks, jade.
Thanks for having me Excited tospeak to you about this.
So what's?
It's a pretty fascinating storyto some, but it's essentially
is you know, I came to thisafter a pretty different career
path.
You know, studied public health,was actually a corporate
(02:20):
attorney, practiced in SiliconValley doing med device work,
and really the running theme inmy life was I wanted to figure
out a way to help people andwithout becoming a doctor, tried
that early in undergrad and itdidn't work well.
So I took a health policy route, realized a legal education
would be important to that.
Realized that the mere practiceof healthcare law was actually
(02:43):
perpetuating dysfunction in thesystem.
Recognized innovation as anopportunity.
So I actually helped spin out acouple of companies when I was
in law school and then foundmyself at a premier group in
Silicon Valley doing the mostboring work for the most
interesting companies, and sonever one to sit.
Still, I shortly started myfirst company, which was an MIT
(03:04):
spinout, which was digitalhealth.
It was a patient education atthe point of discharge company.
We re-engineered the patientdischarge experience.
This was before digital healthwas even a thing and
paradoxically, I discovered atthat time the CEOs of hospitals
loved what we were doing.
We kept patients, we preventedreadmissions.
Cfos did not.
They said that's actually wherewe make our money from, right,
(03:26):
and so what a striking factpattern to be living so moved on
from that after drafting partof the Affordable Care Act that
actually created the financialpenalties for readmissions.
So that was a parting gift andwas lucky enough to get a very
unique role that I was grosslyunqualified for, so I had to get
(03:48):
it by actually doing a projectfor the company.
But I got to run corporatedevelopment, competitive
intelligence and market researchfor a biotech company called
Ionis that was developing mRNAtargeting therapeutics mRNA
(04:09):
targeting therapeutics and sothat was kind of my infiltration
into biotech and my opportunityto learn.
The business at a keyinflection point Helped to take
Ionis from a small cap companyto over $10 billion company with
four approved drugs, whichreally creating a third new drug
discovery platform.
And it was all about antisensetargeting mRNAs, primarily for
monogenic diseases.
(04:30):
And this is when I learnedsomething very interesting that
sometimes companies look attheir toolkit and they say, oh,
let's apply this to everything,including maybe some GWAS
markers that are not monogenic,that the disorder is more
multifactorial and thenrisk-benefit really changes.
So at that time they were doingsome cardiometabolic diseases
(04:55):
and I was like I don't love thisand it turned out to be the
neurology programs and I got towork very closely on the program
.
That was the first drug everapproved for spinal muscular
atrophy and that drug did haveLazarus effects.
You could give it to babiesearly enough and they would
develop normally versusgenerally dying by the time they
(05:16):
were two years old.
So that was a privilege to workon that.
But sort of right there in mymind the entire time as I worked
at another program that I wouldsay wasn't that great and
actually had some very severeside effects is who's developing
drugs for the rest of us?
Because all of pharma was sayinglet's focus on rare diseases
(05:37):
because there's a wide leniencyin terms of safety.
And then everyone flips aroundand sells these drugs for half a
million dollars a year.
And I'm coming from a healthpolicy, a public health
perspective I'm saying thisdoesn't sit right Not to say
that rare disease patients don'tdeserve attention and efforts.
But we have a chronic diseaseepidemic and what we've learned
(06:02):
from the Human Genome Project isthat genes are not
deterministic.
So myself and my co-founder,who also worked at that company.
He was like me.
Somebody couldn't stick totheir job description.
He was a patent attorney,medicinal chemist turned patent
attorney, turned runningregulatory affairs for that same
company.
We recognized that the ultimatearbitrage opportunity in pharma
would be safety.
(06:22):
Opportunity in pharma would besafety.
What if we could find trulysafe compounds?
And then we said, well, how dowe stop siloing disease?
And this is probably somethingthat you talk about in your
practice.
Let's not silo diseases.
Let's look at the common causaldrivers.
And we said, well, what'swhat's common to all these
(06:43):
chronic diseases?
And we're, it's immune,dysregulation and dysbiosis.
And then you know, so you havethat.
And then you probably have alayer of genetic susceptibility
and a loss of regulatoryfunction from other
environmental factors andlifestyle factors.
Well, we just outlined a prettycompelling profile for
(07:05):
something we'd want to do.
It needs to work through thosemechanisms and be absolutely
safe.
Where are we going to find it?
How are we going to find it?
And that's why I said, well,the only lens we should look at
is evolutionary biology.
Let's look for compounds thatappear at unique junctures in
human development, starting inearly life, compounds that
appear at unique junctures inhuman development starting in
(07:27):
early life.
Let's see if there are anycompounds there that appear sort
of nowhere else.
And we came across a library ofcompounds called human milk
oligosaccharides in an infantnutrition lab and the first
thing I recognized is that, well, these are not nutritional
because they're amylaseresistant.
The body can't break them downfor calories because their
amylase is resistant, the bodycan't break them down for
(07:47):
calories.
So, after fat and lactose, whyis nature having human mothers
produce these at anunprecedented diversity of
structures and concentration?
And furthermore, we also, atthat same time we're looking at
they're not just in milk, theyactually enter maternal
circulation during the firsttrimester.
They actually enter maternalcirculation during the first
(08:10):
trimester and they're in thefetal cord blood and they're in
the amniotic fluid.
So literally from conception toseveral years out, literally
encompassing the entiremother-infant dyad and then
promoting the baby's, I'd saysay, foundational immune and
microbiome programming afterbirth.
(08:30):
So took a look at this and said, well, I don't have to develop
a drug.
Nature already did.
I need to reintroduce it.
Speaker 1 (08:36):
I love this man.
I'm just like.
It's almost like you took theengineering approach in your
career, right, and, like me, youand I are similar in this.
I've traveled an interestingpath.
I mean, it was biochemistry,psychology, functional medicine,
transpersonal psychology,philosophy, and what's
interesting about when you comeat it from this perspective is
you get people who are veryintegrative thinkers right.
(08:57):
So I always like to think aboutwhat is real intelligence?
Well, it's not just gatheringinformation, it's being able to
put different pieces ofinformation together in
interesting and novel ways, andit's interesting how your story
got here.
And then you began to look atthese compounds, so these human,
identical milk oligosaccharidesright, this is what you all do,
(09:21):
and so this came from the humanmilk oligosaccharides and I'm
interested.
You said a couple of thingsthere that I know.
I have a lot of practitionerslistening, so let's just deal
with this just for a minute.
So these things are not beingdigested, right, was what you
hinted at here.
So they're obviously beingtaken in to the infant.
(09:41):
They're also around, as youpointed out, prior to birth, but
they're being taken into theinfant.
They're also around, as youpointed out, prior to birth, but
they're being taken into theinfant.
I assume the name human milkOligosaccharides that they are
very high in quantity in themother's milk, and so the child
is taking these compounds in.
They are not being digested inany way, and I'm assuming, since
(10:03):
you mentioned, they're found inthe blood stream of mothers as
well.
They are going intact into thesystem and having some type of
major impact there.
And, given what you do, itseems that they are having an
impact on the immune system, andwe know that the gut and the
microbiome of the gut is theseat of the immune system.
(10:27):
So this story is starting toget pretty interesting here,
given that we know that theimmune system is highly
regulated and differentiated atthe level of the gut, and now we
have these compounds that seemto be acting right at this
particular, you know sort ofarea, and so you have honed in
(10:47):
on this area.
Now tell us a little bit aboutwhat exactly these things are
doing.
What do we know about?
Speaker 2 (10:55):
Yeah, yeah, great question.
And so what's nice, especiallysince I think a large portion of
your audience probably isfamiliar with kind of
plant-based oligosaccharides,they'll appreciate some of the
nuanced differences in themechanism here.
So, as you alluded to, there'sdefinitely a systemic effect.
One of the fascinating thingsthat this is actually the sort
(11:16):
of inception Sherlock Holmesmoment of the company was
there's been a longstandingobservation that mothers with
autoimmune conditions rheumatoidarthritis, others often during
pregnancy they go into remissioneven though they're off their
drugs, right.
And so if you go back inhistory to the 90s, that
actually was an observation thatresulted in the search for
(11:40):
something called Substance X,and actually the urine of
pregnant women was fractionatedand different compounds were
isolated and tested and one ofthem, substance E, actually
seemed to be effective onrheumatoid arthritis at the time
when really there were notreatments, and that turned out
to be cortisol.
So that was a discovery ofcortisol.
(12:01):
It was synthesized as cortisone.
They won a I think it was a1950 Nobel Prize for that.
But if you actually read theirlaureate speech, they said well,
we actually didn't findsubstance X, we don't believe
cortisone was that, but we foundsomething that worked and it's
still a mainstay, you know, ofcourse it has some chronic side
effects and but you know the thethe the aha moment came was the
(12:24):
same exact year 2018, that I'mlooking at these human milk
oligosaccharides andunderstanding their mechanisms a
little bit better.
That was the same year it wasdiscovered that they enter
maternal circulation, startingthe first trimester, which
corresponds to when thehistorical observations of
remission have been seen.
(12:45):
At the same time, there wasalso a cohort that was an
epidemiology study in Canadalooking at 521 mothers,
including some with existing RA,and they looked at ones that
went into remission versus onesthat did not.
(13:06):
And the ones that did go intoremission had a single had a
unique elevation in a specifichuman milk oligosaccharide in
their milk which corresponds tothe levels in their serum and
the p-value is like 0.001.
And then they and that formed ahypothesis and they said well,
(13:29):
what if we put this in a mousemodel of rheumatoid arthritis?
What does it do?
And lo and behold, it works,disease modifying.
So that's one of the thingsthat's unique is you have a
prebiotic here that's enteringthe colon intact.
It's the preferential substratefor bifidobacterium, right,
right, but these work by verysymbiotically with our symbiotes
(13:52):
.
They upregulate adhesion genesin the bifobacterium so it can
create a biofilm.
They actually can break upexisting biofilms as well, and
then simultaneously these are,they're sugars, and sugars are a
language that mediate a lot ofintracellular responses,
including pathogen-hostinteractions.
Sugars on cells are doorwaysthat are hacked by pathogens to
(14:17):
enter the body.
So some of these HMOs, theyactually serve as soluble
receptor decoys.
So as they're terraforming thatmicrobiome you can have
invasive E coli microbiome.
You can have invasive E coli.
You can have H pylori isbinding to these instead of the
baby's immature gut cells andbeing passed out.
(14:38):
So that's how it disadvantagesand really enables a healthy
foundational microbiome to beformed and then once that
happens as substrates for thecommensal microbes, basically
turns them into little drugfactories and they are just
spewing a whole host of smallmolecules and metabolites,
including, like butyrate, ofcourse, other short-chain fatty
(15:00):
acids and then even neuroneuroprotective, neuro
neurodevelopment compounds aswell.
And then to your point aboutthe sort of direct immune
modulating activities.
Here that's when things getinteresting.
So about like one to 4% ofthese do enter systemic
circulation.
This is essentially thebootcamp for the immune system
(15:31):
and they work on, they balancethe immune responses with Th1,
th2.
And we've actually seen thatindependent of any of the
microbiome effects, so we can doit in completely a clean
environment.
We can change macrophagepolarization from like a M1 to a
regenerative M2.
Phenotype also enhance Tregs aswell, and it makes absolute
(15:55):
sense.
They're helping terraform themicrobiome.
The baby's immune system isbeing trained to recognize self,
non-self as well as friends,not friends, and so that's kind
of how they work.
Speaker 1 (16:10):
Yeah, and now I think the listener can understand why
, when I started looking intothis, I got so excited because
this is one of these things thatworks with the body's immune
system and sort of the thingsthat we have in place, our
microbiome, to do what a healthysystem would be doing anyway.
Right, and so it's one of thesethings that I was just like.
(16:31):
This is a really interestingset of mechanisms, not just one
simple mechanism.
Of course, one of the thingsthat my medical background
taught me right from the get-gois, you know, sort of this
integrated, holistic approach inboth the approach of the
practitioner but in the way thebody works.
So many of these drugs that wetake, they are big guns focused
(16:51):
on one particular area, and thiscan cause downstream effects,
because our physiology is likethat spider's web you touch one
part of the web, everything elsemoves, and so having compounds
like this that influencemultiple aspects of immune
function, from the bacteria tothe actual cell membranes, to
(17:15):
actual immune cells andmodulating those cells, is
really incredibly fascinating.
So I would imagine and this ismy next question that for me,
with knowing nothing else, Iwould be thinking about,
obviously, autoimmune conditions, I would be thinking about
allergic conditions, atopicconditions.
Do we see that these things arehaving an impact on these
(17:40):
conditions, and to what extentare they?
Is the research already there?
Is this emerging research?
But we can begin to guess thatthis could have far-reaching
effects, even in things likecancer and other things like
that.
So I'm curious what have youactually seen these compounds be
able to do in terms of disease?
Speaker 2 (18:04):
Yeah, it's a great question and actually a really
exciting one, because there issubstantial preclinical data and
sort of translational datasuggesting that these can be
disease-modifying in theconditions that you mentioned.
As I told you, the sort ofGenesis story is pretty
fascinating because you havekind of a human epidemiology
(18:25):
with a direct nexus to it.
That was, then, what I likeabout some of these studies is
there's there's always a humanepidemiology component, whether
it's coming from mothers orinfants, right, because we can
also look at infants that areformula fed, right, and and
there's also a human knockoutmodel, for that's actually based
(18:46):
on on on secretor status, bloodgroup, where some moms have a
markably different HMO profilein their milk, including one of
the foundational ones, and whatyou can see is you can see
completely differenttrajectories in terms of health
and it corresponds to adifferent microbiome.
And then you're able to doreverse translational.
You're able to form ahypothesis and do a reverse
(19:08):
translational experiment in mice, which is important for drug
development, of course, and Ithink one of the other things
you know, I like how youappreciate the kind of
meandering path because, you'reright, it enables a different
form of pattern recognition andsort of bias, uh, where you're
(19:32):
like I just it was.
I just want to find the truthbehind something that's
intriguing that no one's foundthe truth for and it's not mine,
I didn't invent it.
Uh, there's a a differentresponsibility associated with
it and, you know, one of thethings that is pretty annoying,
quite frankly, to me is the lackof translation of of studies
(19:53):
that are published in nature.
They're published in science,are published in cell, and they
don't make it.
The biology just seems to peterout, usually after a company
has raised a ton of money andand in the popular science media
has already put out somearticles saying these geniuses
at this, these, you know, eliteinstitutions, may have found the
(20:15):
cure for blank right, creatinghope in patients, and it just
never, never gets there.
Yeah, and that's why, when youlook at, uh, you know the, the
perverse statistics in thepharmaceutical field, they're
saying now the cost to develop adrug is $3 billion.
(20:37):
That tripled in the past decade.
So this rebuts the soloresidual right.
Wait, technology is supposed tomake things cheaper and faster.
Instead, it's longer and moreexpensive and when something
does get across the finish line,it's expensive to the system
line.
It's expensive to the systemand it's really expensive to the
patient and oftentimes it has amediocre profile at best.
(20:58):
So, that rant aside, it wassaying how do I remove that kind
of translational risk?
And there's a lot of reasonsyou can talk about it.
Fraud is actually one of them,but a lot of it's the imperfect
nature of animal models, mousemodels, especially when they're
genetically manipulated.
You're creating somethingthat's essentially so artificial
(21:20):
.
It's designed to give you aconclusion that matches your
hypothesis, so there's asubconscious bias that's been
introduced even in preclinicalproof of concept.
So that's a long way of sayingguess what?
These are not just human milkoligosaccharides, they're
mammalian milk oligosaccharides,and so we've prioritized our
(21:43):
initial candidates that wereally want to kind of prove
this thesis on, based on onesthat are common.
So these are not artificialconstructs.
It's is the biology preservedso we're able to look at, you
know, every single differentrheumatoid arthritis model.
These work disease modifying.
(22:04):
They've been tested againstthings like methotrexate high
dose methotrexate high-dosemethotrexate a human mainstay
disease-modifying effects,reducing the systemic cytokines
you want to see, but evenpromoting cartilage repair and
even like PANIS and bone erosionreductions as well as edema
swelling.
Same thing in atopic dermatitismodels as well, and you see a
(22:46):
reduction in the validatedcytokines IL-4, il-13, where we
do have DMARDs and, importantly,these are same things with
human cells as well, with thecorresponding human cells, the
monocytes and the T cells, andseeing basically the translation
at the cellular level of theeffects that led to the in vivo
(23:11):
did to the in vivo?
Speaker 1 (23:11):
Yeah, and just real quick, alex, let me, for the
listener, for those of you whoare getting a little bit lost
with Alex talking about thescience here, basically what
he's essentially saying is, ascompounds go through sort of the
rigor of seeing if they'regoing to be effective for a
disease or diseases, they gothrough a process, usually in
vitro, meaning in test tubes,petri dishes, that kind of thing
(23:33):
, and then in animal studiesprior to going into, maybe human
cells in petri dishes andthings and then finally into
clinical studies.
And so what Alex is walking usthrough right now is how this is
going in sort of the in vitroanimal world, showing that there
are disease modifying effects.
(23:54):
And the next step is going tobe and that's what's going to be
the next question I was goingto ask Alex is do we yet have
any in vivo or clinical trialsunpublished in humans yet?
And I think, from what I heardyou before, that's not yet the
case, but maybe there is some ofthat going on.
But the interesting thing isthat, you know, obviously these
(24:14):
things have been in human milksince the beginning of humanity.
They're in mammals.
This is what he's talking about,and so we have an interesting
way of looking at this, becausethis translational material, the
in vitro studies, the animalstudies, along with this idea of
evolutionary biology, knowingthat these things are there
makes this incredibly intriguing.
(24:35):
And of course, one day we willget to, hopefully, clinical
trials, if they're not here yet.
But I just wanted to giveeveryone who's not skilled in
the science of this a catch upto understand where Alex is with
this.
And then, alex, do we have andhow far off are we all from sort
of human trials with this?
Is that stuff going on behindthe scenes right now or not, or
(24:56):
can you even tell us?
Speaker 2 (24:58):
Yeah Well, thanks, jade, and first of all, you know
, yeah, thank you and apologiesto the audience.
Sometimes I jump into my nerdhole.
Speaker 1 (25:06):
Yeah, I like, don't worry, I like it man.
Speaker 2 (25:15):
I like it and so.
So thank you for offering thatcontext.
So one of the neat things hereand again my premise was safety
is an arbitrage opportunity,right, and so it was actually
the infant nutrition companiesthat they've spent a lot of time
, they've been working on thisfor decades and part of that
included.
You know understanding, youknow the safety profile of this.
So manufacturers of thesecompounds?
Of course we're not.
We don't have a.
There's no human dairy outthere.
(25:37):
So these are being producedwith synthetic biology and so
that that pioneering work hasoccurred and the manufacturers
have demonstrated thebioequivalency, so it's
equivalent to the natural thingand that they that it's super
safe.
Speaker 1 (25:50):
Yeah, and let me just say something about that,
because you and I know thatpeople are going to ask this
question as well, and just forthose of you who are, again, not
practitioners and concernedwith this kind of stuff,
whenever you hear things likeyou know, built in a lab, or
something like this, what a lotof people don't know is if you
take vitamin C, for instance,and you take it from an orange
right, like that vitamin C, andthen you make vitamin C in the
(26:14):
lab, those two vitamin Cs arecompletely alike, okay, so like
they're basically the exact samething, and a lot of people sort
of get upset about this.
All that's left is vitamin C.
And so when we talk about and Iguess this is my next question
so these are bio-equivalent,they are essentially the same
thing.
Is that what you're saying,alex?
(26:34):
That these are human identicaloligosaccharides, human milk
identical oligosaccharides, sothat while they are made in a
lab, they are the exact samecompound in terms of the way
they look, function in the body,and that's what we're talking
about here.
But we cannot say that they'redirect because, as Alex said, we
(26:54):
don't have a dairy factory forhuman milk and so these are
being engineered in the lab.
In the same way, insulin mightbe sort of made in the lab.
Speaker 2 (27:04):
Yeah, absolutely correct.
Yeah, and they're trulybio-identical.
They're absolutely identical.
And they're truly bio-identical, they're absolutely identical.
And part of this that's ethicalright, because you can isolate
this from donor milk.
But then what you've done isyou've diverted this from babies
that need donor milk.
So it's something that'scertainly important for us.
(27:26):
There are some companies thatare taking it from donor milk
and I disagree with that.
And also that's a pool.
There are actually 200 distinctstructures of these and even
(27:48):
ones that are same exactbuilding blocks, but the bond
angle is different on thestructure, completely different
bioactivity.
So there's a ton of work toreally understand what the
merits of each structure are andwhat the applications are.
And that actually leads to yourquestion about where we are in
terms of clinical studies.
So safety has been establishedin human beings already, not
long-term, but long enough toget into meaningful clinical
studies.
(28:09):
We've met with FDA on that andon the basis of that we've been
even approved in Australia toget into like meaningful
clinical studies.
And we've met with fda on thatand on the basis of that we've
been even approved in australiato get into two different phase
two clinical studies.
And just so everyone knows,phase one is typically the
safety studies, um, and that'susually in a healthy, normal
volunteer population.
And then a phase two is reallykind of where the rubber meets
(28:29):
the road, where for the firsttime you're putting the compound
into a patient situation andseeing if not only is the safety
preserved in that patientpopulation but does it do
something that's clinicallyrelevant to them.
The lead compound that we aredeveloping is the most abundant
(28:51):
of these human milkoligosaccharides, so it's like
30%.
If they're 200 differentstructures, this one is like 30%
of the concentration.
So it's really important forsomething and, as I mentioned,
there is a human knockout model.
What I mean by that is thatsome people have different
genetics so they don't producethis most abundant HMO in their
(29:12):
milk and that also correspondsto they don't produce a similar
oligosaccharide that lines theirmucosal tract, including like
the GI, and it's identical.
The oligosaccharide isidentical between the milk and
the one that lines theirintestines and mucosal tracts.
So those people that aremissing this they have a
(29:39):
different microbiome WestBifidobacterium and they get
inflammatory bowel disease.
So this compound is actuallybeing tested at Cincinnati
Children's Hospital right now inpediatric and young adult
inflammatory bowel disease.
Speaker 1 (29:47):
And is this 2-FL?
Is this the compound?
Yes, yep, okay, yeah, so that's2-FL.
Is this the compound?
Speaker 2 (29:50):
Yes, yep, okay, yeah, so that's 2-FL so this is
fucosyl lactose.
Speaker 1 (29:57):
Yes, yeah, how do you say that?
Yeah, how do you say that?
Speaker 2 (30:00):
Yeah, yeah, two prime fucosyl lactose yeah, yeah, and
yeah, so that's being assessedin that population.
And, interestingly enough, atthat same hospital who's a
partner of Intrinsic Medicinethey had a phase two.
That was a controlled study.
It's actually the firstcontrolled study.
No one really knows about thisstudy so I really want to give
(30:21):
them credit for it.
It was in children and youngadults that received bone marrow
transplants, that gotallergenic bone marrow
transplants, and these arereally sick patients yeah, no
kidding.
And the prognosis for that hasbeen known to be because they're
(30:45):
at risk of, basically, a graftrejection.
You got a transplant withsomeone else's genes in it.
The immune system can rejectthat and kill you basically.
So these transplant patientsare put on tons of
immunosuppressives, but thereare still ones that get what's
called like it's like a steroidresistant acute graft versus
host disease, where their bodybasically attacks the, the
(31:06):
transplant and, unfortunately,like the mortality is extremely
high when you have thatrejection and it's happening
systemically, meaning in your GItract or in your liver, and so
you know the scientists andclinicians taking care of these
kids are saying, like, well,what determines whether someone
gets that or not?
(31:26):
Patients who have dysbiosis.
It makes sense.
They have a dysregulated immunesystem as a result of that
dysbiosis, so it's more primedto attack and cause this really
severe and fatal consequence.
So the hypothesis was hey, weknow 2-FL can rescue dysbiosis,
(31:47):
maybe we can try it in thesechildren and see if we can
change that.
And so they did that in thestudy.
It was a controlled study 25patients received 2-FL, 20
didn't, and not only weremarkers of the dysbiosis
improved, but none of thepatients that received FL had
(32:10):
systemic acute graft versus host, compared to four in the
control group that did notreceive it and the overall
occurrence was very striking.
Only one patient had a skingraft versus host in the 2F,
which is a mild one, whichactually has a good prognosis,
(32:30):
and in the controlled ones thatdidn't, it was five patients had
nine total occurrences.
So you had patients that notonly had systemic ones but they
also had the skin ones, so itwas a full-.
Speaker 1 (32:41):
Yeah, so a small study, but a huge impact.
Huge impact Two prime fucosallactose was having marked effect
on these children.
Speaker 2 (32:52):
Yeah, yeah, and it was, and you know, and I think
it would have seen a bit of awider recognition their p-value
if they were underpowered by acouple of patients yeah, yeah,
that's, yeah, that's what I wasthinking, yeah it was 0.07,
which is like it's pretty darnclose.
Yeah, so they're off by a coupleof patients, but we're still
(33:13):
going to be talking toregulators about, like, what we
can do with that.
No, I think that was animportant study.
And then, you know, going on tothe programs that we're running
, we're actually getting readyto initiate a Parkinson's
disease study in Australia atthe beginning of next year with
Phell.
What's interesting here is thisis really, I think Parkinson's
is almost kind of like theprototypic gut-brain axis
(33:35):
disorder and it's really been inthe past year that that's come
out in a striking way.
I guess last summer there was a25,000 patient that was
published in Gut BMJ and itshowed basically, if you had
constipation, your odds ofgetting Parkinson's are like
400% higher than anyone else.
(33:57):
And then, I think just a couplemonths ago in the JAMA network,
another 10,000 patientspublished same thing
constipation your risk ofParkinson's is, I think, 165.
Speaker 1 (34:11):
Yeah, and you guys are all over this because I
don't the listeners, any of thepractitioners know.
Anyone who's in functionalmedicine knows we've been
talking for at least the lastdecade about, you know, this gut
brain, immune sort of axis andthings like Parkinson's,
especially Alzheimer's is thebig one, even autism, ADHD, so
this is a really big area, ahuge area.
(34:33):
That actually is one of theareas, Alex, that I'm very
excited about, because obviouslythese are huge issues and we
don't have a whole lot oftreatment.
You know things for these.
Speaker 2 (34:43):
Yeah, yeah, and it's amazing that functional
practitioners have been lookingat this for so long.
Right, it's like it's been longrecognized that the
neurologists that seeParkinson's patients they said
like, oh, of course.
Yeah, all of our patients areconstipated.
And then you go into theirhistories and you're like this
has preceded any of their motoror neurological symptoms by
(35:05):
years.
So it represents, now thatwe're looking at this big data
set, all of a sudden, it's likeconstipation is a functional
risk factor for these cognitiveand neurodegenerative diseases
and it's something where youknow, I think so many people
have been trained in.
You know I'm against riskfactor medicine that's based on
(35:25):
biomarkers.
I think you you scare peopleinto doing something and maybe
you're budging a needle on apopulation-wide level.
But that's looking at people asstatistics, when, even with
things like statins, it's likewhat are you doing in terms of
the myalgia, the muscle pain,the insulin resistant stuff?
It's like you're-.
Speaker 1 (35:44):
You and I are on the same page here, man.
I've seen it.
I just went through it with myfather.
Actually, you know, we put himon a statin recently and he
couldn't you know.
I just took him right back offyou know, because it's just so.
Yeah, so we're doing some.
You know, actually, I'll giveyou one of my pet peeves about
my field in functional medicine.
One of the things that we takewe might have been talking about
the gut brain immune and thegut immune balance but we're
(36:06):
doing these treatments anddietary approaches which I know
I'm going to get in trouble withmy fellow colleagues here, but
they don't work most of the timefor the things that we're
really trying to help.
Now, of course, we can make astrong argument they're working
way better than what we weredoing in the traditional realm.
But this is what excites meabout this style of medicine and
(36:27):
this approach to findingsolutions, and so obviously it's
one of the things that excitesme about you and your company
and how you're approaching this,because I do think even the
functional medicine world yes,we may have been talking about
this stuff, but our treatmentsand our gut restoration programs
and just giving probiotics andall the things if we are going
(36:49):
to be honest and I think we haveto be evidence-based we have to
realize that this is not beingthat effective for most people.
Sure, it's more effective thannot looking at this stuff, which
the traditional medical worldis not looking at this stuff at
all, but it's also not thateffective on the functional
medicine sides Just a pet peeveof mine.
I think it's important that wekeep looking and rather than
(37:11):
acting as if people in my fieldhave figured this out just
because we've been talking aboutit.
I think we've been talkingabout it, but I don't think we
figured it out.
Speaker 2 (37:19):
Yeah, yeah, and Jade, what I'd like to add to that is
you know, again, I think it'slike being constantly curious,
having identified the problem,and then I think that's actually
a good thing that there's animperfect solution as well,
because that will sort oftruncate and shorten the
diffusion of maybe a newpractice standard from something
(37:42):
where people can say, yeah,we've actually done, you know, a
probiotic approach.
I mean, if you look at it, ifyou look at the trajectory on
this, it started with the fecalmicrobiota transplants and those
demonstrated that cool, you cantherapeutically intervene at a
systems level on the microbiomein a major way.
(38:03):
You know, we, we look at, Ilook at every single FMT study
as a non-competitive proof ofconcept, because then there's
always going to be a scalingissue and then there's some real
infection issues and alsosometimes you achieve the effect
on the disease but then youchange the phenotype of the
person, right, like it actuallyshows how much that impacts
(38:25):
things.
And so what happened in termsof like microbiome treatments is
again, we're in the currentstate of medicine.
You guys are the ones who arereally breaking loose of it, are
the ones who are reallybreaking loose of it.
But if we say the allopathicapproach is a reductionist,
mechanical approach, not asystems approach.
(38:46):
It's more biochem versusbiology, which is an ecosystem
and a system and bidirectional.
Then it's saying, hey, whatdiscrete components of that FMT
led to that effects?
And then all of a sudden youhave limited consortia
probiotics and they're sayingthey're following the same thing
.
The association study is likeGWAS and say oh, this, this bug
(39:07):
is that one.
And then they say OK, let'sisolate it, let's introduce some
antibiotic resistant genes,because that a completely
different timescale than a humanbeing.
And so it's effectively outsideof the host for geological time
periods it's probably forgottenwhat it's like to be inside
(39:31):
that host.
And then it's reinserted andyou have engraftment liabilities
.
And that's not to sayprobiotics are not without their
merit, but it's probably animmunostimulatory, it's probably
more of a transient, limitedeffect and at the end of the day
, where the field's going is itmatters less about who's in
(39:52):
there and more about whatthey're doing.
Speaker 1 (39:54):
Right and I think what you're saying here, alex,
is so important for us asclinicians who are listening to
this, and even those of you whoare interested in this
conversation, who are or who are, patients.
This, what alex just alluded toin my mind is the reason why
you'll get all this marketingfrom different companies and
different supplements, where thescience is very exciting, but
(40:17):
the translation into the actualproduct doesn't seem to have a
huge effect.
I can't tell you how many timesI've seen new products come to
market where people are like, ohmy God, look at this amazing
study and look at this thing wefound, and then, based on what
Alex is telling us how they comeup with this, in this very
reductionistic approach and notunderstanding how to look at
this in a holistic manner, youend up with a product or a
(40:41):
program that is not thateffective, and so I do think
it's interesting where wecurrently are in medicine.
It's all important, but thissort of reductionistic approach
to this without the moreholistic, systemic approach is
probably not going to get usthere, which is why I get
excited about where we're goinghere.
(41:01):
So let me go ahead and wrap upwith you and ask you I mean the
first question everyone's goingto ask.
You know, this is like OK.
Where do I get this?
How do I take this?
What do I do with this?
Alex?
Speaker 2 (41:15):
Absolutely, and so, yeah, I always, always want to
add something that's of value.
So these are not broadlyavailable yet there are some
companies that do have them.
The quality control, the purity, is certainly not up to our
standards.
So I'd say the announcementthat I can make is, while we are
(41:36):
a pharmaceutical company, whileIntrinsic Medicine is a
pharmaceutical company, I'mcommitted to making earlier
access available for thesecompounds, given that they are
safe, and so I will be startingkind of a parallel wellness
company that offers these on astructure function basis, and
initially we will be launchingin collaboration with a
(41:57):
functional medicine clinic outof Chicago and we'll be putting
together a protocol of use caseon this, based on clinical data,
including some positive data inall different forms of
irritable bowel syndrome, andwe'll be producing this at a
clinical grade spec, and so ifpeople are interested in that,
(42:18):
you can go to our currentwebsite, intrinsicmedicinecom,
and just fill out the contactform and then we'll update you
on that one, and that's going tobe primed for a Q1 launch, but
we'll have material available.
Speaker 1 (42:32):
So we don't have long to wait.
Speaker 2 (42:34):
Yeah, so you don't have long to wait, because and
then the way I envision thingsworking between the companies is
we'll be running like truepharmaceutical gold standard
phase two clinical programs onthe intrinsic medicine side and
on the intrinsic wellness side.
Practitioners within theirscope of practice can actually
look at that, look at thoseprotocols and say, cool, do I
(42:58):
want to do this on acase-by-case basis with my
patients and they'll have accessto a high-quality spec material
as well aspractitioner-developed resources
on the use of that.
And that's kind of the way ofsaying that these compounds are
for everyone and I don't want tocreate excitement without
providing access at the sametime providing access at the
(43:23):
same time, 100%.
Speaker 1 (43:24):
Well, alex, I have to say man, I just want to say
this podcast right, it's calledthe Next Level Human Podcast.
Part of the reason for that isthat I believe that every single
one of us are unique.
There's never been another Jade, there's never been another
Alex, there never will be, andyour unique background and the
way you came to this gives youthe ability to do something that
only you can do in a way thatyou can do it, and I really
(43:44):
appreciate that you are doing it, alex.
I really appreciate youbringing this to the world.
I think it's needed.
I think you're doing, I thinkyou're just a brilliant dude and
you're doing like some reallyamazing stuff here.
So I just want to say thank youfor your work, thank you for
your time.
Is there anything else you wantto leave us with before we part
ways?
Speaker 2 (44:03):
Yeah, yeah.
So thanks, thank you, jade.
It's been my pleasure and thishas been a wonderful discussion.
So I think there's a couple ofthings.
The first and foremost is that95% of Americans are not at
their dietary fiber levels, sothat is a low-hanging
opportunity for everyone to doan audit, for practitioners to
(44:27):
do an audit, and even though theplant-based, the
galactooligosaccharides, thefructooligosaccharides, may not
have the full profile, there'smerit there.
And, of course, there's meritfrom whole foods, right, and so
that's an opportunity for peopleto really profoundly shift
(44:48):
their health and theirmicrobiome.
And so I don't want todisempower anyone and say, hey,
you have to wait for the nextscientific miracle.
There's something that trulyyou can do today.
And then I'd say the secondthing is that I had a vision
when I was starting this companyand said, well, we would have
entirely different drugs ifevery CEO founder was required
(45:08):
to be the first one to taketheirs.
So you know I'm not talkingfrom a soapbox saying, hey,
everyone else has to do this.
I'm actually the I think theperson who has taken these
chronically for the longestperiod of time.
So I'm four years in and it'sconstructively enabled me to
cure my IBSD, which was fairlydebilitating.
(45:31):
So and and same thing, my sonhad very severe atopic
dermatitis.
There was a milk allergy and hewas, you know, zero, and we
were able to get him from anEpiPen with 21 food allergies to
eating peanut butter sandwichesbetween ages two and four.
(45:51):
So we're living it.
And now it's about creating adata set that other people can
use to inform their own use case.
And of course, that's alsowhat's driving me for sort of
novel commercialization tocreate an early access
opportunity, because I dobelieve in practice autonomy and
then personal sovereignty forpeople to direct their own
(46:13):
self-care and health andwellness journey 100%.
So thank you so much everyonefor listening, jade you for
having me and the insightfulconversation.
Speaker 1 (46:23):
Yeah, my pleasure, Alex.
Alex Martinez fromIntrinsicMedicinecom.
We appreciate you very much.
You all go check out thewebsite and do me a favor, Alex,
hang on the line, just so I canmake sure all this uploads.
But for all of you, thank youfor hanging out with Alex and me
and we will see you at the nextshow.
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