20% Discount On Thorne Supplements

Episode Transcript
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Stephen McCain (00:06):
Welcome to another episode of the Stephen
McCain podcast, where I bringyou people making world-class
decisions in the field of humanoptimization and performance so
that you can look, feel andperform your best.
Today, I'm very excited to haveone of my favorite doctors in
the whole world on the podcast,dr Elizabeth Yerth.
She is a double board certifiedphysician in physical medicine

(00:29):
and rehabilitation, andanti-aging and regenerative
medicine.
She has more than 30 years ofclinical experience and
continues to stay at theforefront of orthopedics,
cellular medicine, regenerativemedicine and the future of aging
.
Thanks for having me understandcellular medicine.

(01:07):
The approach becomes far moreefficacious and sophisticated
and we dive into some prettycool topics about how to
properly do NAD supplementation,her thoughts on exosomes,
hormones, new novel way toaddress arthritis so many great
things.
I think you're going to reallyenjoy this podcast, so let's do
this.
Dr Yerth.

(01:28):
Welcome to the Stephen McCainpodcast.

Dr Yurth (01:31):
Good to see you.

Stephen, yeah, I'm so excited for this one.
I just absolutely adore havingany opportunity to chat with you
.
I will never forget the firsttime I ever saw you at the World
Peptide Congress a couple ofyears ago, and it was just a
panel and you up there and youstarted speaking and I said this
woman knows what she's talkingabout.

(01:52):
And it's been that way eversince, every time I've seen you
speak, so you're one of myfavorites and I'm just I'm
excited to share your knowledgewith my audience and just let's
see what comes of it, becauseevery time we talk it seems to
be very interesting.

Dr Yurth (02:07):
Well, I appreciate that so much and I'll give you
back the same kudos, because Ilove listening to you and I love
you coming at this from a verypractical sense, right?
I mean, we as physicianssometimes throw out all these
things and people like you arethe ones who kind of refine it
into well, I did this and thisand this and this and this works
and this doesn't work.
It's really good to hear that,especially from somebody like
you, who comes from this veryhigh performance attitude which

(02:30):
is really fun to work with.
Anyway, those are the kinds ofclients that are always fun to
work with.
So I love to live off yourfeedback on all this stuff,
because those are the peopleyou're like.
Okay, this guy is reallyoptimized, and if this isn't
working in him, you know whatare we doing wrong.
So it's it's.
You know, you and I always havefun talking about that stuff.

Yeah, my, my mutual appreciation for
everything you're doing.
Oh fantastic, you know, I it'snice to for someone like me to
really be so motivated by thisindustry and to be able to fit
in and feel capable of doingthat, because, you know, when

(03:06):
you're surrounded by I talked tomore doctors than any other
type of person now you know I'mconstantly ripping apart their
protocols.
What are you doing, what areyou doing?
And so it's it's nice to beable to fit in.
I mean, I was pre-med at UCLA,so I have.

Dr Yurth (03:20):
I have some of that and then decided to be an
Olympian anyway.

That was a good plan.

Dr Yurth (03:29):
Yeah, yeah, I wish I could have knocked out both, but
I like who I am, so I thinkit's all-.
Well, it's funny because, asmuch as you know, if I look at
what I learned in medical school, it was nothing to do with what
I'm doing now.
And I would say, if anythingkind of distorts your brain a
little bit to be able to learnthese new things because you're
so, start, you know, in theseparadigms of medicine that have
just been going from generationto generation to generation and
not much really ever changes inmedicine.

(03:50):
And it's funny, when I first gotinto this field, you know, I
don't know many, many years agonow, probably 17 years ago, I
started kind of transitioningmore into this kind of work and
you know, and I was like, well,I'm learning from bodybuilders.
I'm actually not learning fromphysicians anymore, I'm learning
from these people who areactually more performance
athletes, who said, okay, youknow, you know, like my first

(04:12):
delve into even back then when,no, you know, a4m was 500 people
and and there wasn't a wholelot of research in this area and
we didn't have the Dr Seeds outthere that you know it was, it
was a lot learning from peoplewho were just sort of using end
of one experiments on themselves, and it was the bodybuilders
and the people like you and welearned a lot from that, right,
we learned a lot from the peoplewere like okay, this is my
optimal performance piece, andso it's very funny that I would

(04:33):
say early on in this world, Ilearned more from that group of
people than I did from themedical world.

Yeah, I mean that's so interesting because I
you know, it seems like doctors.

Dr Yurth (04:57):
You go through this whole 12 year process I don't
know how long it is, I thinkit's 12 years.
But and then your educationdone it this way.
This sucks, this sucks, thissucks.
And you're not going to listento that, right?
You just spent 10 yearsbuilding this gorgeous house
that you think is perfect, andnow when somebody comes in and
says probably not, you're likeblah, blah, blah.
I don't want to hear it.
And so it's really hard tochange physicians.

(05:18):
They are very set in theirparadigms and changing that is
almost impossible.
You know, sometimes isimpossible.
I will tell you like I came fromthe orthopedic worlds, like
Bill seeds and you know, comingfrom orthopedics, which is about
as far a cry from doinganything sort of health focused.
And you know these guys don'twant to ever hear that we should

(05:39):
be doing anything different,because they're, you know
they're making good money andthey're doing well replacing
your joints.
And you know, and why should wechange?
And you know I, you know I didorthopedics, solely orthopedics,
for 17 years before I everstarted studying longevity,
functional health, medicine, andthen I tried to do both and my
partners finally came to me andsaid you know what?

(05:59):
We don't do medicine here.
We do orthopedics.
You need to stop getting labsand stop talking to these people
for 30 minutes and I'm like youknow?
Okay, obviously this isn'tworking, yeah.

Wow, yeah, and it's.
It's also probably compoundedby the fact that these
orthopedic surgeons are I mean,trust me, I've had, I've been
operated on many times as aprofessional athlete.
They're rock stars Like I've.
I've been operated on byliterally rock stars of
orthopedics and they'retremendous at what they do.
But if you don't have to openme up and there's another way to

(06:31):
do it, utilizing cellularmedicine, I'm all in on that, if
possible, or prevent.

Dr Yurth (06:40):
Most orthopedics is not fixing your broken bone.
You had acute injuries, you hadthese things with gymnastics,
but that's not most orthopedics.
Most orthopedics is not fixingyour broken bone, right?
You had acute injuries, youhave these things with
gymnastics, but that's not mostorthopedics, right?
Most orthopedics is your peopledeveloping arthritis.
It's the, you know, nursingalong people who have a worn out
joint and putting steroids intoit until you replace the joint.
That's most orthopedics.
Certainly, we're never going tonot need orthopedics to fix my

(07:00):
broken bone.
Or you know, I a couple monthsago completely tore off my
rotator cuff lifting and neededto be put back together.
That wasn't going to be fixedby cellular medicine.
But I can markedly improve therecovery doing those things and
prevent the outcome ofprogressive arthritis that
occurs when we have, when we dosurgeries on people.
So I think the difference islet's take away that.
You know orthopedists shouldfix your broken bone or put

(07:23):
together a tendon that tore.
You tore your anterior cruciateligament, fix it.
But where we're failing is inall those other people who are
simply you have sore joints andthey're being treated very
poorly, with the ultimateoutcome being replaced the joint
, which is, I mean, does it workSometimes, sometimes not.
So we're doing a lot of thingswrong in that world, and that's

(07:46):
where they're not rock stars,they're rock stars, that.
They're one little piece right.

Yeah, it's a really good point.
A friend of mine he works inmedical sales and makes great
money and his opinion he doesall these joint replacements and
to me that stuff just seemslike medieval medicine in a way
it's like well, are we reallydoing this?
Yeah, I mean, when you look atlike actually what they're doing
, like this is kind of modernmedieval practice.

(08:11):
And his opinion is by the timeyou're 60, you just start
needing this and I'm like no,you don't, and that's the whole
problem.

Dr Yurth (08:20):
That's where I started looking at orthopedics.
We're not wearing out ourjoints.
You don't wear out your jointany more than you wear out your
brain or you wear out your heart.
It's an inflammatory disease,just like all those other
diseases, just like braindiseases or heart diseases.
And so when you go in there andyou're 50 years old and you
tore the meniscus in your kneeand your doc's like, well, let's
just go clean that up and trimit up.

(08:41):
Well, let's just go clean thatup and trim it up, I always tell
people it's a lot like going inwith your demented mother and
the doc going, well, let's justtrim out those bad parts of the
brain, that'll be good, she'llbe fine.
That's exactly the same thing.
So when you look at arthroscopicsurgery, which has been banned
in every other country over theage of 30, nobody else will do

(09:01):
it because the data is socompelling that it worsens
arthritis.
It's the number one surgerydone here in the US for
orthopedics is go up, clean outa joint, trim up a meniscus, and
yet it leads to a rapidlyprogressive arthritis.
British Medical Journal 2019said there is no more data
needed.
There's so much data to supportthat this is a bad surgery,

(09:21):
doing bad things, that they willnot allow it, and yet we are
doing it.
Dime a dozen here and we're.
So we're trying to treat aninflammatory disease process
which we well know now, becausenow we have drugs and things
like that that we know areworking the inflammatory
pathways that halt the arthritisand even reverse it.
We we know that we're dealingwith altered inflammatory
pathways and not just.

(09:41):
You wore out your joint becauseyou were an athlete you know?

yeah, it's so interesting.
I'm definitely all in ontalking about this stuff because
I've had both.
Uh, had two meniscus tears, onein each knee and they just trim
around it and they cut that outand right, and one of them I
can my knees 100 to the left,one I'm starting to.
I'm wondering if I have alittle bit of some muscle

(10:05):
imbalance issues around it or ifit's starting to slightly show
a little bit of maybepre-arthritis or whatever
arthritis.
I mean, it's not bad, I stillfeel pretty amazing.

Dr Yurth (10:18):
You do everything, but you've got a lot of years on it
.
So here's what we know aboutarthritis, but you've got a lot
of years on it.
So here's what we know aboutarthritis, right.
So we know that when you lookat people who are developing
arthritis and it's most of thosepeople who have, you know, who
have painful joints is it's acombination of factors.
There's genetic factors andthen there's injuries.
That can progress things.
But when we get an injury, whatis supposed to happen is our

(10:41):
body comes in and it tries toclean things up right.
So best world to happen is ourbody comes in and it tries to
clean things up right.
So best world.
You get this inflammatoryreaction.
All these cytokines, thesepro-inflammatory enzymes, come
in hard at work and they try andclean stuff.
That should last a few days.
Then those should turn off andwe should turn on some healing
processes, right.
But let's say you don't havethe perfect genetics or you

(11:02):
don't have the perfect lifestyle.
Then what happens is theseinflammatory proteins, things
like tumor necrosis factor alphaand interleukin-1 beta, stay
elevated and, as a result,instead of just cleaning up a
little debris, they just keepcleaning up.
So, for instance, there's thisenzyme called metallomatrix
protease that is elevatedinitially in an injury.
Enzyme called metallomatrixprotease that is elevated

(11:23):
initially in an injury and it'skind of I like to think about
the you know there was a crimein your house.
This is a cleanup crew to kindof get rid of all the signs that
there was a crime there.
But if they keep scrubbing awaythe debris, what happens?
They actually start scrubbingaway the joint.
So these very high levels,these metallomatrix proteases,

(11:47):
are really detrimental to thecartilage of congenital grafts.
Let's say you tear yourcartilage of your knee right and
now somebody goes in the scopesand they trim out that little
torn piece which temporarily isgoing to make you feel better
because the knee is going tofeel more stable, and these
pro-inflammatory enzymes come in.
They start trying to help out.
Then they stick around a littlebit too long.
Now you start actually not justcleaning up what happened but
cleaning up your own cartilage.
So we know very well now thatin joints we have very high
levels of these enzymes, we havevery high levels of these

(12:09):
inflammatory cytokines and thatif we block those that we
actually halt and even reversethe arthritis.
So we need to stop thinking ofthis disease as a wear and tear.
It is completely and utterly aninflammatory disease process.
And so we are using a drug, arepurposed drug, called pentosin
polysulfate.

(12:30):
So pentosin polysulfate, whichhas been approved in Australia
by a company called ParadigmPharmaceuticals it's called
Xylosol.
It's in phase three trials herein the US to cure
osteoarthritis and in fact inAustralia it's done just that.
It's reduced the need for jointemplacements by almost 90%.
One-year follow-up studiesshowed almost 25% improvement in

(12:54):
cartilage space after one yearon this drug 25% improvement in
cartilage space in an arthriticknee, whereas the placebo drug
had a 4% loss in cartilage space.
So not only are we helping pain,but we're actually reversing
the disease process, and that'sall by using a drug that is
blocking these inflammatoryprocesses right.

(13:14):
So we know that we can reverseit by stopping the inflammatory
process.
You don't have to just replacethe knee joint.
We can actually reverse thisprocess.
So this drug's in phase threetrials right now here in the US.
We actually can get itcompounded because it is an
orally available drug here inthe US called Elmiron.
So orally it's for bladderinflammation.

(13:35):
But if you inject a littlesub-Q injection of it a couple
of times a week it actuallyworks systemically and at a much
lower dose, so systemically, toactually stop this arthritic
process, and oftentimes within12 weeks people have reduction
in pain.
It takes longer to start seeingthe changes in cartilage space
and sometimes people take alittle longer.
But it's dramatic, and I've beenon this.

(13:56):
I have horrible arthritis in myknees.
I've torn my ACLs four times,and so anybody who looked at my
knees would say, oh my God, youjust need joints replaced.
But I have zero pain.
I'm totally functional becauseI'm on this medication.
I've been on it for now threeyears.
It's dramatically worsening.
Now.
I have lots of patients who wecan treat for a short period of
time and they get better.
I kind of need it ongoing.

(14:17):
If I don't take it, I startover time.
Over a few months it'll startincreasing a little bit of pain
in my knee.
So I know that, whatever mygenetics are, I need to block
these enzymes.
I need to block these cytokinesthat are doing the damage.
But, Stephen, it's actuallydramatic and it's going to make

(14:37):
a huge shift in how we treatarthritis.
It'll get approval for kneeosteoarthritis.
It's good for any kind ofosteoarthritis and backs.
So it did the same thing in arabbit model using pentosin.
They actually stopped discdegeneration and the drug's all
been around since the 1980s asan oral medication.

(15:00):
So safety profile is good andagain we're using a microdose of
what they have to use orallyfor bladder stuff.
So we're microdosing it.
It also, very interestingly, ata low dose orally.
So we've also had it compoundedas a very low dose orally,
which doesn't work as well forosteoarthritis, but a low dose
orally it's really good for thegut.

(15:22):
So people who have gut issues,it helps the gut and it's a
potent antiviral, anti-cancerand anti-athrosclerotic agent.
So this is because, when youlook, all these diseases have
some overlap.

Yeah right, Exactly.

Dr Yurth (15:36):
Inflammation, inflammatory diseases, yeah.

Fantastic.
I remember I saw yourpresentation on this at the
World Peptide Congress this yearand I was enamored, because
I've put a lot of mileagedynamic, dynamic mileage on my
joints, and I have to takereally good care of myself.
Unfortunately, I have prettyminimal pain, but I just think

(16:00):
this is like a perfect exampleof a repurposed drug doing
something that is a huge need,right, and what was this thing
you were saying, though, in yourspeech about it potentially
causing blindness if you took itfor so long at such a dose?

Dr Yurth (16:17):
So the big thing.
So Elmiron, which is the drug,last 2020, I guess, or 2019,
they put a black box warning onthe drug and a lot of lawsuits
went on.
Because after this again, thisdrug's been around a long time,
right, but they started to seean incidence of people who had a
retinopathy that was associated.
It was very unique retinopathy.
They'd never seen it before,but it was causing damage to the

(16:39):
retina of the eye and, somepeople, some progressive loss of
vision, and what they found wasit was a dose dependent.
That's why it took so long toactually see this, because you
had to be on the drug at a highenough dose for a long enough
period of time.
And those people when theylooked at their eyes.
So then they brought inasymptomatic people, people who
had no problems with theirvision, but they looked at them
and in a small number of peoplethey did see these changes in

(16:59):
the retina.
They said, oh, big black boxwarning, big lawsuits went out
on Elmiron and it got prescribedless and less orally because of
that.
Now, if you look at the trueincidence of that number one,
you have to get to a high enoughcumulative dose over a lifetime
.
So remember we're using a microdose.
That dose is 500 milligramsdone every day.

(17:20):
We're using a micro dose ofthat.
We're using a microgram of thator 25 milligrams, orally and
not on an everyday basis.
So for us to ever hit thecumulative doses that was ever
seen to be associated with thisretinopathy would take you
taking this drug regularly forabout 80 years of your life, and
maybe I'll be on it for 80years, I don't know.
Hopefully then we'll have atreatment for retinopathy.

(17:41):
But so it got kind of overblown, as things do here in the US.
Now xylosol if you look at theFDA or the whole printout on the
pharmaceutical xylosol, theinjectable form of Elmiron or

(18:02):
Pentosyn, they left that offcompletely because we actually
don't think it's going to be arisk factor done as the
injectable.
Now that may be a dosedependent thing and it may be a
difference in how it'smetabolized, but it doesn't
appear that it's going to causethe same problems, at least not
with the animal studies.
They was not supported.
So if you look at the packageinsert on xylosol it doesn't say
that.
And it is funny when you lookat Elmiron even, which is widely

(18:22):
used in other countries as well, they have no black box warning
or no warning about theretinopathy.
So that may be a little bit of athing here, because it's about
0.0001% of people that willdevelop this, but we our lawyers
like that kind of stuff right,that's huge money when you get a
group of enough people who havea disorder and you can make a

(18:44):
whole lot of money off of itfrom a drug company.
So I think we have to take thatwith a little bit of okay.
Yes, keep a cautious eye, butnot abandon this drug because of
that Cautious eye?

no pun intended, and would there be a time where
you'd want to go off of it,like you said, if you're
shutting down some of thesethings that clean up, would you
like, if you, it seems to bereally regulatory, right?

Dr Yurth (19:09):
So it's not going to shut them down completely.
Okay, it's going to helpmodulate the currents of it,
right?
Okay, got it so.
So you can use it more as amodulatory agent than you can
really being a clear, it's goingto shut everything down.
It's probably just not potentenough to do that and you don't
do it every day, so you're doingit on an intermittent basis.
So you're doing it, you know,once or twice a week you're
doing an injection, so we'reprobably not shutting it down

(19:30):
continuously.
Now I do tell people when they,when they have surgery number
one, it's a weak blood thinner,so I tell them stop it, for, you
know, a few days before surgery, and I tell them to wait a few
days till after surgery, pick,pick it back up, just for that
very reason, just in case wewant to, we want to sort of let
that inflammation kind of comeup a little bit more.
Yeah, before, and so I do, I doutilize it that way.

(19:51):
You know, I'll take people offfor a few days around surgeries,
things like that yeah, thatmakes perfect sense.

So that's available.
Someone could literally come toyou and say I'm suffering
massively with arthritis, canyou?

Dr Yurth (20:02):
help me and and and.
Honestly I will tell you it'sbeen life-changing for people,
really life-changing, okay.

Fantastic.
Well, I mean, that's a realpiece of gold right there, and I
would love to dive a littlefurther on it, but you have so
many pearls of wisdom.
I did want to talk about this1-MNA that you-.
Yeah, let's talk about onewhich is 1-methylnicotinic acid
this 1-MNA.

Dr Yurth (20:25):
Let's talk about one which is one methyl nicotinic
acid and one MNA.
So everybody now is very giggedout on NAD, right?
You all have heard about NADand I think there's very little
argument to say that NAD doesnot decline when we age and that
replacing or getting more NADis probably good for us.
I don't think anybody woulddoubt it, and I know you had
James.

(20:45):
What's his name?
The big NMN?

guy.

Dr Yurth (20:47):
Dr she.
Yeah, yeah, I know, you knowyou had him on a podcast
recently and he and I got into abig kind of argument at one of
the conferences and it endedwith he didn't want to hear what
I had to say.
So whatever, but you know, andand so who, who knows?
Because this is a field whereevery, all of us are going to be
a little bit married to some ofour opinions.
But I come from everything andthis is my.

(21:10):
You know you work with BillSeeds, my Bill Seeds training,
coming from everything, from a,looking at pathways, and what
are we doing?
Because you know, Bill Seeds isvery big on this.
You know, you, you you have tokeep things homeostatic and when
we overdo, you take too manyantioxidants, you do things.
You're screwing up your cell,right.
So now what are people doing?
They're like oh, NAD is reallyimportant.

(21:32):
We need a lot of NAD.
As we age, we're going to havemore energy.
If we have more NAD, that's theultimate electron donor.
We make more ATP.
We have more energy.
We know it declines as we age,declines as we age.
We know energy declines as weage.
Let's just give everybody nad.
So people are going in theredoing these massive nad
infusions or the precursors likenmn or nr, which are basically
the same thing, in fact probablya little better, because really

(21:54):
there's no evidence nad caneven get into the cell.
You have to use one of theprecursors to get into the cell.
But the problem is, I tellpeople it's a little bit like
why are our NAD levels declining?
We actually don't make lessNADs.
That's been well proven in micemodels that if you do like
what's called a CD38 knockoutmouse, where they don't have the
enzyme to degrade NAD, theydon't lose NAD.

(22:15):
So it's not that we really makeless, at least not
substantially.
To some degree maybe, yes, butwhat we do is we lose more.
So what happens is we getupregulation of several enzymes.
I think Nicole Conlin in herproduct, which I'm blanking on
the name on, where she usesniacinamide and kind of a
combination of blockers, isprobably the best kind of so far

(22:37):
that we've done with this.
But basically the key is thatif I give you a whole bunch of
NAD and all you're doing isturning on the enzymes that are
degrading it, what have I done?
Have I really increased yourNAD levels?
You've just charged thosepathways right, right, so I
always like to pick this.
It's a big bucket right andyour bucket has got a hole in it
and it's leaking out all overthe floor.

(22:57):
So you're ruining your woodfloor and you just keep.
You're like, oh my God, mybucket is empty.
I'm going to keep filling mybucket and your bucket stays
nice and full, maybe as long asyou keep enough of it going.
But what's happening is yourfloor is now ruined.
So what happens when you givethose NADs is you accelerate
once you've gotten as much asyou need, and we don't know what
that is right, I don't know howmuch you need.

(23:18):
Once you've got as much as youneed, your body's pretty smart,
so it's got to get rid of theexcess.
So it does so by a couple ofenzymes, and one of the main
ones is CD38.
And so people have said, okay,well, let's block CD38.
That's a great thing, and itdoes.
It helps.
So blocking CD38, you can usethings like epigenin to block
CD38.
So you can block that drain alittle bit there.

(23:40):
But body's still pretty smart.
And so now it's like okay, westill got too much.
You block CD38 and it goes downanother pathway and there's an
enzyme called NNMT, and NNMT isreally upregulated in cells that
are not so happy, like yourcancer cells, your senescent
cells, your fat cells.

(24:01):
They have very high levels ofNNMT.
So now your body is.
What your body's doing?
Is it's sensing there's oh,there's a whole bunch of drain
of NAD.
It turns up NNMT and,interestingly, it does so to
actually make another productcalled 1-MNA.
This is all really technicallydifficult.
Sorry, make another product,1-mna.
So you're doing two thingsYou're making 1-MNA, which is

(24:22):
trying to sort of help you, andyou're feeding all these cancer
cells to nascent cells.
So NNMT is being looked at veryactively in the cancer world
Because if you block NNMT youseem to be able to reduce cancer
cell metastasis.
So there's a lot of work goingon in that realm.
So now we're giving people NADand NMN and NR, while the rest

(24:43):
of the cancer world is trying toblock the enzyme that you just
accelerated by doing that Right.
It's a little worrisome thatthe rest of the world who's in
the traditional medicine cancerworld is like ooh, block this
enzyme.
And we're doing things that areturning the enzyme up.

Yeah, cancer world is like.
Ooh block this enzyme and we'redoing things that are turning
the enzyme up yeah, I didn'tmean to cut you off.
If you want to roll here, oh,go ahead.
So you have.
You have CD38 and NNMT, whichare these two enzyme pathways
that are stealing, and they eachhave their own sort of
downstream effects.
Usually, you would do apigeninto kind of tamper CD38 and you

(25:17):
would use maybe 5-amino-1-MQ forNNMT, right?
So does this 1-MNA help forboth of those pathways or just
the NNMT?

Dr Yurth (25:29):
So basically, the feeling is that the CD38 is
probably less important as aregulatory than as you get
downstream to the NNMT.
So 5-amino-1-MQ is great,because 5-amino does block NNMT
and that's why it's so good forcancer and it's so good for
producing more energy and helpswith weight loss, right, the

(25:53):
problem with if I block NNMT, II will build up nad and I block
the cancer cell growth.
But nnmt makes one mna, and onemna is actually a really good
thing.
It actually in and of itselfhelps cardiac function, uh,
helps lung function, helpsenergy and metabolism.
So so now we've yes, we'veblocked all the bad stuff, right

(26:14):
, but we've also blocked one ofthe good things.
So a company in Poland, verysmall company in Poland came up
with a molecule, 1-mna, which isbasically just a food source,
right, 1-mna, 1-methyl nicotinicacid.
And they said, oh, this, sowhen?
1-mna?
So if you picture this pathwaywith NNMT going to 1-MNA or NMT
going to cancer cells, right, ifwe give, once 1MNA gets filled

(26:40):
up, it's going to turn off NNMT.
It's like, oh, I've got enough1MNA, I'm going to turn off NNMT
.
So now I've actually kept thegood thing I need at 1MNA,
because I'm giving it to you.
I've blocked the bad thingbecause I've blocked NNMT right,
and 1MNA is something I cantake orally and so it's 5-amino,

(27:06):
but orally on a regular basis.
Keep that really nice adjusted.
Keep this really activemolecule, the 1-methylnicotinic
acid, which actually hasNAD-like properties, so in and
of itself has really goodproperties.
For that I've blocked cancercell growth and I've got the
best of both worlds and it's aheck of a lot less expensive
than 5.01 MQ.
So the problem with this companywhich was making it in Poland

(27:27):
is they were trying to get it tothe US as a drug because it's
really good for cardiac stuff,it's really good for obesity,
it's really good for cancer.
So they've been trying for thepast few years to bring it to
the US as a drug.
So they were starting sometrials on it for a drug and so
they would not sell it to the USas a supplement.
So when we came across 1MNA,we're like my God, it does exist

(27:50):
, somebody makes it.
But it was this littlepharmaceutical company who would
not sell it to us in the US.
So we're like damn, can't get,it impossible to get.
And so we spent a few yearsflying to Poland and meeting
with this company and finallykind of hit them at the right
point where.
And what we told them waslisten, it's going to take you
15 years to ever get this thingthrough the FDA and then you're
going to have to get physiciansadopted to it, which might not

(28:13):
be that easy to it, which mightnot be that easy.
We'll help you get this here asa supplement, because we had
some work with working with someother international companies
to help people transport stuff,get things to the US.
So we had some expertise inthat realm Not me, but another
company I work with and so theyfinally and I think we kind of,
because we've been in thesediscussions for a while I think

(28:33):
we finally kind of hit them at apoint where probably they
financially were getting likemaybe we need to think about
something else.
I don't know.
We finally got them compelledby saying, okay, let's just keep
this as a supplement.
So it's taken two years.
We finally have it to the US asa supplement.
It should actually be available.
If you guys go to just 1MNAcom,it should be available as a

(28:57):
supplement.
I'm.
I don't know for sure, but Ithink the company says in within
a week it's now, it's now, it'snow.

Is there a way?

Dr Yurth (29:03):
literally waiting to purchase it until I had this
conversation with you because II saw your talk and I and I was
like yeah to to us and you know,and bill seeds he's actually,
as usual, the first one to kindof turn me on to this but but it
is sort of the answer to allthis NAD, because we do need
more NAD, but we need to do itin a safe fashion.

(29:25):
And all you guys who are doingNAD infusions and taking tons of
NR and NMN and, like I said,that's why I got into a big
argument, and his argument was Ifeel better, everything's
better, it's obviously working,and I think the problem is that
you will temporarily potentiallyfeel better.
You're also releasing a lot ofsome inflammatory proteins when
these senescent cells get turnedon, and sometimes that actually

(29:47):
gives you a little bit of arush.
It's when people do an NADinfusion like, oh, I felt all
this rush of energy.
It's actually not necessarily agood thing.
It's because you had this rushof inflammatory stuff that was
released from the senescentcells, because you just fed a
whole bunch of senescent cellsexactly what they wanted to grow
.
So I think you have to bereally aware and cautious and I
think the problem is that we'redoing a lot of things that we

(30:08):
don't know enough about, and Ithink this is a place where
we're doing harm.

And believe me.

Dr Yurth (30:16):
I'm just as guilty.
I was doing a lot of NMN and NRand recommending that stuff.
I always did it with a CD38blocker.
So do you need the CD38 blocker?
I don't know the clear answerto that.
I take both.
So I'm gonna take one MNA and aCD38 epigenin because I feel
like, okay, that's probably mybest way of keeping these stores

(30:36):
really perfect On the upside.
Cd38 doesn't form anything bad,right, although it's draining
some of your NAD, it's notforming anything bad and I am
getting the NAD up by the 1-MNA,so I may not need it.
I don't know for sure.

Yeah, it might be nice to offer an escape route
if it needs it right, that'sexactly right.

Dr Yurth (30:58):
Like is that maybe the escape valve that maybe you
know?
This is I.
I do have too much you know inthat, in that you know reaction,
reaction phase.
Maybe that's a nice little youknow thing.
Because where I get moreconcerned about is this downward
pathway that's feeding thesenescent cells, and cd38
doesn't appear to have that samedownward spiral unless it goes
down from cd38 down to nmt.

(31:19):
So I kind of think thatblocking that downstream will
probably be good enough andmaybe you're right, maybe the
keeping the cd38 turned down ormaybe doing it intermittently
right like doing thingsintermittently yeah, yeah.

And do you know if you get the same muscle
benefits of 1-MNA as you do with5-amino-1-MP?
Because you get this like stemcell activation of muscles.

Dr Yurth (31:45):
It really should do exactly the same thing, in fact
even better.

All right.

Dr Yurth (31:50):
And if you look at the data, so there's a really good
study on long COVID, improvingendurance in long COVID with one
MNA that came out last yearthat was very compelling.
There's a really good study oncardiac output.
But the long COVID study showedsignificant improvement in
muscle strength, at least in thelong COVID group.
Now, in someone like you who'salready optimized, will we see

(32:10):
that?
Not sure we'll see it asmassively, but it should have
the same benefits.
You're doing the same thing,except, I think, better than the
5-amino is.
That's fantastic.

Okay, so we go to 1mnacom.
I was literally just thereyesterday, I think.
Right now you have to buy it,by the case.
Well, I don't think so.

Dr Yurth (32:32):
No, well, either way, it's available and I'm buying it
because you go there I meanphysicians so it will be so it's
going to be.
So there may be.
You may have to go to adifferent site as an individual
person.
So because the 1MNA site may befor practitioners, I think that
you may have to go to what'scalled OHPHealthcom.

(32:54):
If you log in there, then Ithink you can.
That's why I've been sending mypatients to buy an individual
supplement.
The 1-MNA may be for thephysician site.
They are trying to keep itwithin more of a professional
line, but you can, especially ifyou're under physician's care.
So if you log in and you'reunder physician's care, usually
you can buy it through the OHPhealth site.

Okay, Got it.
Yeah, Well, and, and whatever Idig up, I'll put in the show
notes for people that um.

Dr Yurth (33:20):
I can, I can, I can hook you up to the people from
that, from who can answer thosequestions too.

Okay, fantastic.
Well, I, I, I am excited tocause you know.

Dr Yurth (33:30):
I will tell you from my perspective.
So you know, I basicallybrought back a suitcase of it
from Poland when we went there,so I had a supply for a while
and it definitely improved likeenergy levels, muscle strength,
but definitely endurance for me,which is what I find with
5-Amino.
I'm not sure it improves mymuscle strength as much.
It improves my glucose controland it improves my endurance,
and that's what I found with1-MNA.
I didn't find I mean, did youfind with 5-Amino that you

(33:53):
improved muscle mass?
So what?

I have found with it.
I've always kind of recommendedit to people, like when they
first start a new strengthbuilding routine, they're
getting it started, they'regoing to do some weights and I
think it's a nice spark.
Because I have noticed thatsometimes when you start and
you're really rusty and you feellike you have no activation in
your muscles, you're like God,these things aren't even working

(34:18):
.
But I have found with5-amino-1-MQ I just feel like I
get a little bit more neuralactivation in some capacity and
I've also noticed the fatburning effect or whatever it
seems to have this musclebuilding and fat burning.
It definitely has fat burningeffects when you block.

Dr Yurth (34:35):
NMT, this muscle building and fat burning.
It definitely has fat burningeffects.
When you block five and whenyou block in an mt, you
definitely get fat burningeffects because you you're
stabilizing metabolic controland you definitely any of you
guys who have more of a you knowinsulin issues at all, uh or or
are on the heavier side it's itis it can be definitely helpful
for weight loss because it'snormalizing metabolic control so

(34:56):
well.
Yeah.

And it is expensive.
So this one M&A is yeah 5-aminois outrageously pricey.

Dr Yurth (35:04):
Yeah, it is really.
I mean, probably less so fromresearch chemical sites, but
from our compounding pharmacies.
Not cheap?

Yeah, well, I mean this is so yeah, we're
super excited about thishonestly.

Dr Yurth (35:16):
I mean, it's been a long time coming and I think
that it is like 5-minute, likemore of an exercise memetic, so
it does kind of act like you'reexercising for you.
They showed in the long COVIDpeople dramatic improvement in
like their six-minute walk test.
Their quad strength improveddramatically.

(35:39):
And I know a lot of people somepeople are not even aware of it
how much COVID, or sometimesCOVID vaccine, has done in terms
of their quality of life, interms of endurance and strength.
A lot of people have gotten hitby that.
My practice is now full of longCOVID people.

I mean that's been a bad problem, yeah, and
I've seen people complainingthat we're really optimal
individuals, like at first.
I kind of thought it wouldmaybe just be for, like, the
metabolically challenged orpeople that were really out of
shape.

Dr Yurth (36:08):
No, these are really healthy people.

Yeah.

Dr Yurth (36:10):
I've had some really high level athletes who have
just been down and out sinceCOVID, really high level
athletes who have just been downand out, you know, since COVID.
This mitochondrial dysfunctionthat COVID causes is, you know,
the hair loss.
The hair loss clients have gonerampant now because of hair
loss post-COVID.
It's all some.
You know a mitochondrial loss.
You know it's a lot of you know, ongoing damage.

Yeah, it's not funny, you can end up chasing
your tail for a whole year, andso I really think that's when
you got to find someone likeyourself that really knows these
pathways.
And I mean, you just dropped twogolden nuggets of this pentasin
polysulfate, this one MNA, andyou talk about how everyone was
doing these.
You know, it started with thesemassive NAD infusions and it got

(36:52):
into the precursors because ofDavid Sinclair, and then now
there's like the third phase andit.
You know, in the beginning Icame into this thing as a I
guess you would call it abiohacker.
And now, as I've sort ofmatriculated and I've tried my
best to do as much as I can tolearn these pathways or listen
to people that know thesepathways, but I just find that

(37:14):
you, as you matriculate, you goup, you start getting up into
the functional medicine and allthe protocols that all the
doctors like you are doing,because that's really where you
want to play at.
Those are the people that youreally want to learn from,
because you talk about thesecellular pathways and I'd like
for you just to take a moment toexplain that.

(37:36):
So maybe if someone doesn'tunderstand cellular health,
because if you optimize a cell,you optimize the body, right.
So maybe if you could just kindof explain why this is so
important right now.

Dr Yurth (37:46):
To look at the stuff this way yeah, I think that's
really important because so wecall ourselves cellular medicine
providers.
So at Seed Scientific Researchand Performance, which I'm on
faculty with, so disclaimer yes,I'm going to be very pro this
type of medicine because I trulybelieve in it, but where it
lies, different even from whatsort of our functional medicine.

(38:07):
So if you think abouttraditional medicine, it's a
disease focused, right, it'sokay, you have this disease.
These are our protocols we doto treat this disease.
Right, you have this disease.
These are our protocols we doto treat this disease.
Right, you have diabetes.
This is the protocol.
You have, you know, heartdisease.
This is the protocol.
So everything's very protocoldriven.
And then we went.
People went oh, that's not theway we should be.
Let's go to functional medicine, right, let's look more deeper,

(38:28):
what is causing that person tohave diabetes?
And let's treat morefunctionally, right, where did
things go awry?
But if you've looked at, youknow and this is the hardest
thing I think in trainingphysicians or training my
clients is that when you go, youknow a little deeper than that.
What everybody still wants isprotocols.

(38:49):
Okay, so now you have diabetes,here's your protocol, you're
going to take berberine andyou're going to exercise this
and you're like, well, guess, ifthat didn't work for me, why
didn't that work for me, right?
So protocol-driven medicine,which, unfortunately, is what
doctors like, because it'sreally nice to have a cookbook.
Well, okay, now I have this.
So they've got metabolicdysfunction.

(39:09):
Here's my protocols and there'sa lot of and it's one of the
things like A4M teaches a lot ofprotocols and people like
protocols.
I get it, it's easy.
The problem is protocols don'talways work and so what you have
to go back down to is at thecellular level, what pathway
serves you down that road?
And that's where you have torelearn biochemistry, and nobody

(39:29):
wants to relearn biochemistry.
We all hated biochemistry thefirst time, right?
Somebody told me actually theKrebs cycle was important.
I was like, oh God.
And now I literally spend allday long trying to learn new
pathways, because every year wediscover new pathways.
So I can actually look at adisease and say, okay, this
weird pathway, something calledlike the sea gas sting pathway,

(39:51):
these weird ass pathways arewhat actually are starting this
process of you going down thisroad.
So now I have to actually goback to where in this pathway
that's gone awry in you do Ineed to intervene?
So it's really looking at thesepathway driven inside the cell,
these pathway driven responsesthat are causing the underlying

(40:13):
metabolic dysfunction whichcaused the diabetes you know,
and diving down that level.
And there's not protocols totreat that because everybody's
going to be a little bitdifferent.
But I can say, okay, wow, allthese things are going on.
I know it must be a dysfunctionat.
You know, cytochrome two in my,you know, in my mitochondria.
So you have to get down to thatkind of level to really treat

(40:35):
some of these more complexthings and I'll say, not even
complex, but some of the simplethings.
And it's not easy and it's notprotocol driven and it takes
tons and tons of time andresearch and education to do so.
It's not for everybody butultimately it's going to be what
makes us be able to heal hard,to heal people or really truly
prevent disease.
Because if I keep all my cellpathways going the right

(40:58):
direction, if everything'sworking right, then I won't
develop this or this or this.
But it's so incredibly complex,stephen, and I will tell you,
like I said, some of thesepathways, like the C-gas sting
pathway, which honestly, if youlook at it, it's rooted in a
whole bunch of differentdiseases, and yet it was
discovered in 2019.
I mean, so you can't hang yourhat on the things you learned in

(41:20):
medical school 30 years ago,because every year we're
discovering some new pathway,some new mechanism and you have
to keep up on it.
So it takes tons of reading, ittakes tons of time, but it's so
much fun Because then I canlook at okay, this person is
exhibiting all these things.
It must be a defect here in thispathway.
Now, what can I use, Be it apeptide, be it a repurposed drug
, be it a supplement, be it achange in their exercise routine

(41:43):
, that will actually alter thatspecific pathway and cure a
whole host of dysfunction downthat road, right?
So it's super fun to do, butyou know, but you'll go down
these rabbit holes ofresearching things for you know,
eight hours at night, becauseyou're like oh, my god, where
can I make a change here and howdo I change this?
And sometimes it's super simplethings right, like a baby

(42:05):
aspirin and how much you can dowith a baby aspirin a day.

Yeah, I mean it's fascinating.
I've been at the World Pet PetCongress for a couple of years
now.
I sat there and I mean I got tospeak at it this year, but
before I was in the back, justwide eyed and just Jesus, these,
these, these people are you'respeaking a different language.

Dr Yurth (42:30):
I call it.
Do you speak cell?

That's usually what I tell doctors.
You know I'm good friends with,you know, sandra Kaufman, yeah,
so you know she speaks cell andevery time she explains
something she's speaking to.
So, like for me, I'm alwaysstriving, striving to, to, to
learn as much as I can aboutthese pathways, and because I
understand that the people thatunderstand the pathways are the

(42:53):
people that probably understandsome issue, the best, at least
the best snapshot we have rightnow.
We can't look quantumly at theissue yet, but we can look at it
.

Dr Yurth (43:05):
AI is going to make this even better and better.
Right, when we can actually nowfeed a load and say, okay, this
is in that pathway where youneed to intervene, and then I
can say, okay, give me a list ofthe drugs that might
potentially do that and be ableto pull more of those People.
Always I hear this from all mypatients right, oh, I don't want
a pharmaceutical.
Pharmaceuticals are not evil.
I mean, there, there's a lotyou could do with pharmaceutical

(43:26):
drugs.
Yeah, you know that that isgreat.
And and people, you know peopleare willing to take a list this
long of supplements becausethey think they're safer, and
I'm like, actually, I probablyhave one pharmaceutical drug
that may actually address allthose pathways that you just are
trying to treat with your 15different supplements.

So a lot of it's like repurposing drugs.

Dr Yurth (43:42):
I, you know, I love that because a lot of these
drugs have been around.
They are safe, they are good,you know and and you know so.
For instance, there's a drug weuse a lot called Amlexanox, and
Amlexinox is.
It was approved for aphthousulcers, for canker sores, as a
topical.
So it's called Apsol and it wasapproved for canker sores, and

(44:03):
then the little company thatmade it really didn't go very
far with it, so it sort of gotabandoned.
But what it does, the pathwaysit works on and if you look at
it you know there's a greatarticle on is this the, you know
, is this sort of the cure-allfor everything?
Because if you look at thepathways it works on, it's
incredible the number ofdiseases, from autoimmune to
cancer, to hypertension, toobesity, that you can treat with

(44:25):
this drug.
Now, because it's available,the compound's available.
Amlexox is available in the US,so we have a compounding
pharmacist make it into a tabletfor us and people can only take
it and I will tell you it canbe remarkably life-changing for
people from autoimmune diseases,things like that.
It is, frankly, a remarkabledrug.

(44:46):
It's another repurposedmedication, but when you know,
wow, this pathway is reallyimportant.
Here's a drug that actuallyaddressed that pathway, used for
a completely different purpose.
I can now pull that in and do awhole lot of things.
So when you understand thesepathways, now I can search for
things.
I can say, okay, I need thispathway altered at this spot,
give me the drugs that do it.

(45:07):
And technology has allowed usnow to really be able to come up
with a list where I can feedthat into chat, gpt, and it's
going to say, okay, these arethe drugs that have been
discovered that work there andyou know, now I can play with
that.
So so don't close your mind toall the things that really
medicine has and is available ifwe use them in the right way
yeah, yeah, I remember for likeyears ago I kind of went through
this phase.

I was like oh no , I don't do any, I'm not gonna
take a drug and then you know,hey, I take, you know, five
milligrams of sialis every daybecause it improves my blood
open your blood vessels reducesyour risk of dementia.

Dr Yurth (45:36):
Helps prevent stroke right.
Yeah, it's not for yourerections.
It's because, you know, I putalmost all my patients, women
and men, on five milligrams ofCialis because, if you look,
dementia risk is reduced,hypertension risk is reduced,
cardiovascular disease isreduced, all by taking five
milligrams of this simple drug.
Exercise performance is.
You know, as we do this, whyit's banned as a water band drug
right?
Because it actually hassignificant benefits on exercise

(45:58):
performance.
So those are exactly.
You know your patients are likewhat.
I take five milligrams of salisevery day.

Yeah, I mean, I consider that to be an operating
system upgrade because youimprove blood flow to-.

Dr Yurth (46:10):
Right.
Improve blood flow right.

Every organ, everything gets an upgrade,
Exactly Every organ, everythingand your brain being a big one,
right, yeah, so I've completelyopened my mind up to this stuff,
and the beauty about thisoff-label usage is the fact that
it's already gone through allthe rigors.

Dr Yurth (46:25):
It's already gone through the testing.

Yeah.

Dr Yurth (46:26):
Right, exactly, it's like you've already got the
safety data there.

Yeah, more so than a lot of supplements do
right, oh, do Right, oh yeah,well, jesus, yeah, the
supplements that can.
That's like a wild, wild West,you know, I mean right, yeah, I
mean this is fascinating.
We're 46 minutes into it andI'm like, oh God, we haven't
even gotten into like peptidesfor crying out loud.
But I mean, look, I it's.

(46:51):
Let me ask you this what areyour thoughts on hormones?
Cause, a lot of these people,that that cell, these doctors,
they're like well, if youoptimize the cell, you don't
need hormones.
And I'm like, really like, onall cases, you know, like you
know, yeah, I, I will tell you II don't agree with that.

Dr Yurth (47:11):
I mean, we know that our hormones decline.
If I optimize the cell, can canI keep my hormone levels up to
where they were when I was 20?
I will challenge that.
And I know you and I are veryfond of Bill Seeds and he very
much speaks that you don't needto do these things, you can do
everything by cell optimization.
I don't see it.

(47:32):
I think that we were justtalking about that recently
because he said nobody needsthyroid medication.
I'm like there are people whoneed thyroid medication, you
know, you know.
So my belief is that you need totry and keep the body in a
state.
You know, even when our cellswere working great we're 18
years old, right, and everythinggenerally was working well Our
hormones start to decline.
Our hormones start to declineearly, right.

(47:53):
Our hormones start to declinein our early 20s I mean 25, you
start dropping your hormonesdown by 30, you're on the
downward slope, and that's notjust cell health, it's just what
happens in terms of some of ourorgan decline.
Can we maintain that betterwith doing some things?
Yes, we can lengthen it out.
Can we get them back to wherethey were?
I don't think so.

(48:14):
So I'm a little bit of thebelief I'm going to replace
everything that I definitely amlosing right and that's going to
help my cell function better.
So I'm going to go on thereverse, that I can improve
cellular function and cellularpathways if my hormones are
there.
Maybe I can reduce the dose ofthe hormones as the cell
functions better.
But you know, peptides in ourbody decline as we age.

(48:36):
We know that, that bpc, whichis an, you know, endogenous
peptide that our gut makes thatthose levels decline as we age.
Even if I keep myselfself-healthy, those levels
declines we age.
So our thymic peptides?
We don't have thymus glands.
There's nothing thatmaintaining your cell health is
going to do to give you back athymus gland.
It's not.
Your thymus gland is at itsbiggest at puberty and then it

(48:57):
starts shrinking down and youknow, by your time in my age
it's a little fatty nub that'snot making thymic peptides
anymore.
So I'm not getting thymus andbeta-4 which helps with me with
growth and recovery, or thymusand alpha-1 which helps my
immune system, you know, andimproving the cells not going to
also make my thymus glandregenerate or my pineal gland
not calcify.
We can help it, but thosethings.
So, yeah, so my feeling is, youknow, your, your pineal gland

(49:20):
calcifies.
You need to give epitalin.
Your, my, your, your.
Your thymus gland is going away.
You need to give thymicpeptides or thymic bioregulators
.
You know, periodically, to keepthat function that you don't
have anymore.
Because you don't have it, yourovaries are not going to work
as well.
Do I think you need hormones?
Your testicles are not going towork as well.
Yes, I think men, most men, aregoing to benefit from
testosterone and estrogen andprogesterone and, and you know,

(49:44):
and I, you know, and and I I'mgonna have to say I think that's
what's going to help keep mycellular mechanisms going as a
turn, as opposed to vice versa I, I, I couldn't agree with you
more.

and, granted, I'm, I'm not some doctor or
whatever, but I've paidattention and and I've I've paid
attention through the pointwhere I'm about to turn 50 and
and I've.
You know there's these cyclesof being alive, that these
things start to shut down, oryou know, you become resistant
to anabolic signaling.
You don't fold proteins as wellyou, you don't make as much

(50:17):
stuff.
I mean it all starts to cascadeinto something.
And you know, my opinion is youknow, I look at hormones as a
communication system.
I'm like, do you remember whatit was like to be on dial-up?
I don't want to be on dial-up,I want to be on broadband, like
I want you know when the?
I want the muscles to get thesignal hey, let's grow, it's

(50:39):
time.
I just worked out like, let'sdo this, you know.
And but I, I see a lot of thatand it's refreshing to hear your
opinion that kind of feels likeintuitively, like where I'm at.
You know that you have to juststart propping the body up as it
ages with all the things.

Dr Yurth (50:51):
Again, it's the replace what you're losing bit,
right, I'm going to replacethose things that I'm I'm losing
with time and and that I meanyou know, can you keep growth
hormone levels up?
I mean, even you know, if seedsis in that he fixes the cell
and everything gets better, thenwhy do you need growth hormone
secretogogs?
Right, but people need growthhormone secretogogs, or you know
, to keep growth hormone levelsup.

(51:12):
I I think that hormone levelsare going to decline even in the
face itself.
And again, I think that if youlook at a lot of cellular
mechanisms like mitochondria,they function better with
estrogen.
So you need some estrogen formitochondrial function to be
better.
So I think that there's a piecethere of I don't think you're
going to independently fix thecell and all of those hormones

(51:35):
pick back up.
I just don't think that's theway our bodies are designed.

Yeah, yeah, but who knows, maybe we'll learn
more in a few years.

Dr Yurth (51:44):
Yeah, Maybe this is the NAD precursor phase.
That's right.
We just keep learning andchanging our protocols as time
goes on.

But now.

Dr Yurth (51:48):
I'm using hormones.

Yeah, I've used HCG for a monotherapy, for
because I was trying to maintainmy fertility and I started to
see I had this guy on thepodcast.
It hasn't been released yet.
This guy, uh, zach, and and hewas, basically he can he's been
turning menopausal women backand making them fertile by
putting stem cells in their,their ovaries and yeah and he

(52:11):
has some shows.
Gave me some science that showsthat the longer you can
maintain your fertility, thelonger that's the health factor.

Dr Yurth (52:17):
That's exactly right.
Yeah, there's a lot of researchgoing in that realm.
That that's you know, andthat's like rapamycin showed
that too right that that women,that that at least in animal
studies, that rapamycinmaintained fertility at least
started early enough, that itmade fertility much longer, at
least in mice what is youropinion on rapamycin?

because I have it and I'm a, I'm like, I read a
book on it and I've you know, Iwas just about to do it and I
had this little pink eye thingor whatever I'm like.
Well, I'm not going to shutdown my immune system for a day
to do this, but what is youropinion on it?

Dr Yurth (52:48):
So you know, most of the research on rapamycin has
come from Mikhail Blagosklany,who is very well-researched in
this area, and he has somereally good articles out there
to really show that this is notan immune suppressing agent
unless you dose it at animmunosuppressive dose.
So if we're using it for canceror we're using it to keep you
from rejecting your transplantedkidney and you have to use it

(53:09):
at immunosuppressive doses butat a low dose, it is an immune
modulating agent and I think thedata is pretty damn compelling
that it is one of the fewlongevity agents that we've.
We have some pretty goodevidence to support right, at
least in every other animalmodel.
Yeah, unfortunately, like mattcaberlin's you see this today,

(53:32):
matt caberlin's, who was doing abig, huge study on rapamyamycin
in dogs, the dog aging projectand so everybody had their dog
on rapamycin and it's beenreally a compelling project and
doing very well and the FDA forsome reason just shut it down,
who knows why.
Really, their infinite wisdom.

Interesting.
That must mean it works.
That must mean it works.

Dr Yurth (53:53):
But yeah, I mean, I think the data is pretty
convincing.
I think what we don't know iswhat the proper dose is for us
as humans.
Yeah, so most you know, most ofthe longevity docs I know are
taking five, six milligrams oncea week.
But there's people who aredoing it higher.
There's people who are doing it, you know, one week out every

(54:14):
month.
Nobody really knows the answerto how we're dosing.
The five to six milligrams isbased more on sort of our animal
or mouse studies.
Do we need more?
We just don't know.
So I think at this point mostlongevity docs have kind of
jumped on board with rapamycin.
I take it, you know.
I take it once a week.
I think that it makes sensewhen you look at sort of, I want
to just shut off mTORperiodically.

(54:34):
I want to have a sort ofcleanup.
I think that the evidence ispretty convincing, I think.
Are we dosing it enough to doanything?
I don't know the answer to it.
Blagosklany thinks not.
He thinks here in the US we'reprobably not dosing it high
enough.
He doses it much higher inhimself.
So I don't know the answer tothat.
So I'm probably playing it onthe conservative side and we'll

(54:57):
have to see.
You know it's just going totake a lot of time and research
to figure it out At this point.
By what data we have.
It looks good and I think it'svery safe.
I think it's notimmunosuppressive, I you know.
I I don't ever get sick.
I take rapamycin, I you know.
I think that it has good immunemodulating properties.
You will see it bump upcholesterol.

(55:18):
That's probably the biggestnegative.

Oh, really it does.

Dr Yurth (55:21):
So you will see a bump up in cholesterol in some
people.
It's usually not the ApoB thatgets bumped up, it's usually
just the total cholesterol.
So usually ApoB which is thebad player.
Remember all of you guys whoare testing cholesterol don't
look at your cholesterol, lookat your ApoB.
I don't care if yourcholesterol.
Look at your ApoB.

(55:42):
I don't care if yourcholesterol is 300, you want
your ApoB low.
And so you know, look at yourapolipoprotein B.
That's the number you need tofocus on and keep that low.
Keep that at least below 90,you know, but even lower,
probably better.
There's data now that showsthat there's no too low level.
That's good, no-transcript.

So sometimes you know you will see that people
yeah, well, I think if anybody'slearned anything from this and
they, if someone, whoever'slistening this, probably already
kind of knows what I'm about tosay, but in listening to you,
and that there are these doctorsthat understand this cellular
pathways, you know, god, I, ifanybody's listening to this
podcast and they're still in thetraditional medical system, let

(56:27):
this be your notice right nowthat like, hey, there is a much
better way to do things.
And, and you know there's just,I mean you're and it's your
life for crying out loud.
I think that's the hardestthing, I mean, you know they're
just I mean you know, and it'syour life for crying out loud,
right, I think that's thehardest thing.

Dr Yurth (56:39):
I mean, you know you and I spent a lot of money on
this stuff, right?
People, you know, I know you'vetalked to Brian Johnson and you
guys have interacted and youknow, and people are like, oh,
we spend two million a year.
How stupid is that?
I'm like I have patients whospend two million a year on
their stupid horses.
I mean, you know, it's like tome, it's like I, you know, I
have patients all the time whothey come in and see me, who

(57:01):
have plenty of money, believe me, and I recommend these
protocols that are notinexpensive, You're right, and
they drive out in their Lexus,you know, to get their $9
Starbucks coffees and, and Ithink we've got to learn to
prioritize that this money spenton health is the most important
place to put your money.
I mean, it's probably wheremost of my ancillary income goes

(57:22):
.
Unfortunately, probably, I haveno social life or anything.
I just take a lot ofsupplements and peptides, you're
the same person.

I mean, we're all cut from the same cloth.
Who needs friends?

Dr Yurth (57:34):
I've got peptides.
I think that is a place wherepeople are still in this
paradigm of well.
Insurance doesn't cover thatand it's a lot of money.
And you know, and I think ifonce you're sick I mean I've had
cancer patients, stage fourcancer Now they're willing to
put in whatever amount of moneyit takes to stay alive Right,

(57:54):
but what we need to do is put inwhatever money it takes to stay
healthy.
You know, within our means,obviously, whatever money it
takes to stay healthy, startingbefore we get sick, which is a
hard thing to convince people of.

And look, most people are on the financial
investment track that theybelieve in compounded interest.
Right, that they're going toput so much money away every
month and over time they'regoing to benefit from the
compounding interest.
Well, my opinion is okay.
You spend a little bit of moneyup front on all this
pay-as-you-go stuff to be andit's not a ton as you're when

(58:28):
you're 20, as you get older itwill get more, but if you can
get 10 more usable productive,years, Healthy years, where you
feel good and active and youknow that that is going to add
to the compounding interest oftime.
So you can make it up on theback end, but also, at the same

(58:49):
time, I don't ever really wantto retire.
I always want to be doing whatI'm doing and if I can be
totally, that's why everyone'stalking about health span.
You know, like if I can just belike full faculties till I'm,
till the day I, you know, yeah.

Dr Yurth (59:01):
We want to just do this and then die Right.

Yeah.

Dr Yurth (59:03):
This is what most of us do, right.
Yeah, at the end, the last 10years, and any of you have gone
through I've gone through agingparents, my parents lived into
their nineties but it was notknow, not easy, right for
anybody, and that's what wereally want to avoid.

we want to go like this and then boom, fall
off a cliff, right yeah yeah,exactly, I mean, and it's funny
because you look at, likesuzanne summers who died people
were like what, what happened?
You know what happened and Ikind of thought about that.

Dr Yurth (59:30):
I was like huh hellspan, she just you know it
was like, yeah, I mean she wasdoing pretty, I mean she was
really good for you know, really, until her cancer came back.
And you know, she, I think herlast really month wasn't good,
or even a few weeks, honestly,but she was doing podcasts right
up until, like, it was a littleshock to me.
I was like, oh my god, she died.
I just saw her podcast to me.

I was like there's a perfect you know, sort
of I'm not perfect, I mean, butthere's a.
There's sort of like at least a, a semblance of this health.
Yeah she looks good.

Dr Yurth (01:00:00):
She felt good.
She was having sex, she was,you know, exercising, she was
doing podcasts, she wasinteracting with her family yeah
, you know, you know,unfortunately cancer got her and
maybe that could have beendealt with in a different way
but you know but you know thatyou're right that she was.
She was really an epitome.
It's funny, when I first at A4M, she was a guest speaker I

(01:00:21):
don't know a few years ago, itwas a while ago, maybe three,
four years ago and I was like,oh my God, suzanne Somers,
suzanne Somers is a guestspeaker.
She was really compelling.
Right, I don't agree witheverything she does, but she was
very compelling as a speaker of.
You know exactly that that sheis.
You know, and her husband.
You know exactly that that sheis.
You know and her husband.
You know, alan is like like Idon't know, 89 years old and the
guy you know, they're stilltalking about having sex and

(01:00:41):
running around naked, and youknow, you know, and all the
stuff that we all want to bedoing when we're 90 years old,
yeah, and wheelchairs beingpushed around our nursing homes
I went and saw two years ago.

Stephen McCain (01:00:52):
I saw the rolling stones here in vegas and
mick jagger was 78 at the timeand I we me and my friend were
joking before they came out thatthey were going to be wheeled
out.
They were going to be proppedup on all this stuff and be
super geriatric and the wholetime at dinner we're joking
making making as many jokesabout that as it was a running
joke and I know human bodiesWell.

(01:01:14):
I can watch when someone moves.
I can tell if they have hippain, ankle, bad knees.
I've studied people moving foryears.
When you just coach and dogymnastics, nothing Besides his
face, which clearly has aged, Icouldn't see anything.
That was any different than whenhe was in the club Jumping
around I know Metabolicallysuper fit and his movements, he

(01:01:39):
had other mood.
I was, I literally I cried.
My friend was taking socialmedia things and posting all
time and I'm sitting there withtears in my eyes because I'm
like this is so inspiring,because, right that people can
do that right yeah, because likefor me, he didn't even take
care of himself.
So yeah, I mean those guys were,I I remember, doing blood
transfusions because they weredoing so many drugs between

(01:02:00):
concerts, like back in the day.
I mean, Jesus, Well, look,we've covered some good stuff
you are seeing that's kind ofcoming, or is there anything
you've come across that maybeyou haven't necessarily we
haven't spoken about or youhaven't made a lecture about, or

(01:02:23):
maybe it's you know like?
I mean, there's someinteresting things out there and
I'm always curious what, whatpeople maybe are kind of
dabbling in that that no oneknows about.

Dr Yurth (01:02:34):
Yeah, I think that, um , you know the big, the big
place, the big place, like youand I were both at A4M this year
and I kind of went through andI always go through, you know if
I can find one kind of new coolthing, and you know, and there
wasn't anything huge there.
But there's some cool workgoing on with some of the immune
antibody stuff and I think thatthat might be a player like.

(01:02:54):
So this is something calledGlectin-3, and Galectin-3 is
elevating a lot of bad diseases,but particularly in Alzheimer's
, and Galectin-3 may be more theetiology of Alzheimer's.
We keep blaming amyloidprobably not amyloid, it's
probably this Galectin-3.
And so this company is makingthis antibody to Galectin-3.
And we're actually signed up asa research are antibodies to

(01:03:26):
these molecules that we'remaking and doing too much of and
start binding out some of thesebad things and treat diseases.
So I think some of the focuswe're going to start seeing a
little bit is going to be onsome of these immune modulating
things, using antibody therapiesto actually, you know, for
cancers and things like that.
I think that that's probablywhere this focus is.
I mean the results.
Steve, you should have seen someof these videos of these

(01:03:46):
Alzheimer's patients with justlike one or two infusions of
this antibody to bind thescolactin-3.
They went from like one guythey interviewed.
He didn't even know hisdaughter's name sitting next to
him.
Two months later they interviewhim.
He's like yeah, he's talkinglike a normal person.
He's like I'm actually drivinga little bit, driving short
distances to the store.
It was remarkable.
Wow, they had case after caselike this.

(01:04:08):
Nothing have I ever seen thathad those kind of results.
And I think, as we startlooking at things like that,
well, where else can we startusing that same technology?
As time goes on, the biggestthing is so many of these things
are so pricey, so expensive.
That makes it hard.
But I think that's somethingwe're going to start seeing is,

(01:04:28):
where can we start using some ofthese antibodies against bad
things?
So we can do things likelooking at metabolomics and
looking at abnormal proteinsthat are being expressed and now
saying, okay, this person isdoing this very, their body is
doing this very poorly, and nowI can form an antibody that
stops that from having any kindof bad effects and then work
upstream to try and fix why thebad effect occurred.
So, anyway, I'm starting to seea lot more of this
immunotherapies and treating allsorts of diseases cancers,

(01:04:52):
alzheimer's, probably obesity.

And that will be a cool place to keep an eye on.
Yeah, probably obesity, andthat'll be a cool place to keep
an eye on.

Dr Yurth (01:05:00):
yeah, it's almost like a alternative instead of gene
therapy doing it at the source.

You're basically just doing it at the uh the
metabolite like the right alittle further down the road.

Dr Yurth (01:05:07):
And I think gene therapies.
I mean you know I you know, ifI could afford false statin gene
therapy, I think that's prettycool, right you know, do that?
Would you do the false statin?
You know, I don't know if Iwould do it just yet, but I mean
I heard Liz Parrish speak atRadfest.
I mean she did it years ago,right, cause Liz is on the
lineage of all that stuff, butbut you know, it's, it's pretty
compelling.
I mean, you know, I guess thescary thing is, are you doing

(01:05:29):
other things that we're just notquite aware of yet?
Yeah, you know, but you look at, like you look at the results
of some of these people.
It's pretty impressive yeah, butyou know, right now it's 25 000
and it lasts about a year and ahalf and then you got to do it
again and again.
I just am not 100 certain thatthere's not things we're doing
when we're screwing up at thatgene level.

(01:05:50):
Are we doing anything that wejust don't have quite a handle
on?

I just don't know yet.
Yeah, I'm a little uh, you know, like the.
There's the telomerase one lizparis does I'm right, yeah,
right yeah my first podcastguest, paul tozer.
Like a friend of mine, he didfalse statin, the, the
telomerase and and he's done allaround.
Yeah, I was like jesus.
You know that, doesn't let youfeel great.
I mean, yeah, he's, he's a.

(01:06:15):
He was a hard charging guy,worked in, uh like, video game
development.
So he, he basically tested his.
He basically said his telomereswere like gone and so a little
bit of an emergence, you knowright, and he's shown whether or
not these look.
That also brings into questionlike are these?

Dr Yurth (01:06:34):
are these tests right?
How good are these tests right?
Yeah, we could talk all dayabout that one too.

Yeah, because they're.
They're measuring the averageand it's really about which ones
are the shortest you have thesemodalities that people are
doing, like the phallostatin andthe plasma exchange, and they,
you know the plasma change.
Yeah, you know, and and I, I'ma big, I like exosomes.
I mean, maybe that's last thing, if we could have one little
final, you know, get youropinion on exosomes, because I

(01:07:00):
know you guys had exosomes atWorld Pet Pet Congress as one of
the booths and stuff.
So you guys always recommendthe vendors that are there.
What are your opinions on?
What is your opinion onexosomes?

Dr Yurth (01:07:12):
So we look at you know , we I think nobody would deny
that stem cell therapy hassignificant benefits to our
health and I saw you had, youknow I can't remember his name
but the stem regem guy you know,he and I had this big talk
about stem cells a little bit.
Yeah, it was brilliant and youknow, and I love his product and
it certainly has some goodoutcomes.
But you know, one of the thingsI said to don't age, I said

(01:07:41):
there's some data to supportthat.
Actually it's not true.
Some of the Chinese data that'scoming out shows that stem
cells, asian stem cells Uh-oh,are you there?
There I am.
You disappeared for a minute.
Okay, asian stem cells actuallydid have senescent phenotypes
and that they actually do somedamage down the road.
You and I had a discussionabout that.
I don't know if we figured itout, but if you think about
probably the best stem cellsources, it still is probably

(01:08:04):
taking young stem cells, sotaking umbilical stem cells.
The problem is umbilical stemcells contain data you probably
don't always want, right?
They contain information, evenDNA information, that you
probably don't want.
So what exosomes are is they'relittle nanoparticles contained
inside stem cells that containall the micro RNAs and growth
factors to regenerate right.

(01:08:24):
So if I can take, instead ofstem cells, I can take all the
guts of the stem cells that havethe really good things that I
want the mRNAs, the growthfactors that are going to use my
own system to design a new skinor new hair or whatever.
In my mind, that's the safestand best way of regenerating
tissue right Is to use umbilicalstem cell derived exosomes.

(01:08:46):
And now I can also take, let'ssay, if I can fit, you know, a
hundred, obviously a very smallnumber, but a hundred stem cells
and each of those contains athousand exosomes.
What if I take, you know now, awhole lot more exosomes again,
15 trillion exosomes, as opposedto maybe not that kind of
volume if I'm giving stem cells,so you know.
So I think that you can getbetter volume.

(01:09:06):
I think you can get betteroutcomes.
I think the data is certainlytrending towards.
Some of the new data that'scoming out on exosomes is
showing some really amazingthings in terms of regenerating,
even in the face of spinal cordinjuries, things like that.
I think we have a ways to go onunderstanding everything about
it, but in my mind, everything Iknow, and even in my results in

(01:09:27):
my own clinic.
I still think they have themost regenerative potential.
I do think you want goodsources.
I don't know if we know enoughto say, okay, this is the
perfect place to use them, butthe data is awfully compelling
and I think that that that youknow.
My belief is they probably havethe most regenerative potential
of anything that we have in ourarmatarium.

Yeah, I, I I'm leaning in that and I've been
experimenting with them.
this year was like the year ofexosomes for me and tried to
amniotic and placental and andI've used the placental derived
ones uh for pretty consistentlythis year and I'm a huge
advocate of it even doing it ata lower pulse but more kind of

(01:10:07):
frequently to kind of right youknow.
But uh, it's always refreshingto get your opinion on it
because it it just keeps whatyou're saying is echoing exactly
how I think about it.
Man, we covered some good stuffon this one.
We covered some good stuff.
I feel like we did it justicehaving you on.
It is always a delight to justhave a few moments with you, and

(01:10:31):
this was I got to indulge.
So, yeah, I would love tooffline.
I would love to talk to youabout the pentosin polysulfate,
maybe coming on as one of yourguys' clients or something like
that, because I just feel likethat's something.

Dr Yurth (01:10:47):
Yeah for you, probably with all the stuff, and you
know, if you had knee scopes Iwould tell you probably not a
bad thing to actually maybe doat least a course of now and
then.

Yeah, yeah.
I would love to work with youon that and I really appreciate
it.
How can people find what's thebest way for them to find you?
Reach out to you if they wantto work with you.

Dr Yurth (01:11:05):
BoulderLongevitycom is our clinic.
We see patients from all overthe world licensed in most of
the States in the US about 46.
And we see people all over theworld, mostly virtual people,
who want to come here forprocedures, orthopedic
procedures and things.
Obviously they have to fly herefor doing those things, for
doing more regenerativeprocedures, but otherwise we
just work virtually with most ofour clients.
So borderloggevitycom you canjust sort of fill in and want

(01:11:27):
more information piece there andsomebody will contact you or
you can set up an appointmentonline.
Those of you guys who want tolearn more you know I love, like
steven, doing all thiseducation on this stuff.
So we've actually tried to setthis thing called human
optimization academy.
So if you go to bliacademy youcan sign up there we actually
have some free content and thenthere's some, if you can join

(01:11:49):
the academy, really cool stuff.
So we put together coursesthere to try and teach people.
How do you read your own labs?
How do you understand?
You know the stuff your doctordoesn't tell you.
How do you understand?
And we try and teach from awhat doctors should be learning.
Not, you know not and theydon't.
So we're trying to teach youthat way as opposed to trying to
get all your information fromyour instagram.
Influencers, we have toremember, are sometimes trying

(01:12:09):
to sell you things, and so we'retrying to keep it.
You know, it's all.
You know.
Nothing that we do is topromote a product.
It's all all really justeducational.
We also do these really funQ&As.
They're kind of like thisPeople ask really cool questions
and we just rap about it.
So those are really fun everymonth.
So if you go to bliacademy, youcan look at the academy and we
love that and it's growing thecontent on that.
Again, there's courses on how doyou fix things first where you

(01:12:31):
go, how do I look at my CBC andknow whether it's abnormal or
not, or my cardiac panel or myhormones?
So we help you learn how toread your own labs, because you
guys can't rely as Stephen said,you just can't rely on your
traditional doctor to do thisstuff.
You just can't.
You're going to have to becomeyour own health advocate.
So we're trying to help you todo that, Because even good
functional medicine doctorsaren't all that easy to find,

(01:12:53):
honestly.
So you at least be your ownadvocate, find a doctor who you
can work with and talk to.
You know, when you become asmartest, even then you, just
you know, you kind of dictateyour own care a little bit, but
you want to find a doctor whocan help you along that road.
When you want a prescription,they can.
They can say, okay, that's agood idea, All right.

Don't.
So that's what you want to findis somebody who just works as a
team with you, dot com orbliacademy, and and you should
be able to get everything youneed.
Yes, and I will put links toall of that in the show notes.
You can find those atstephenmccaincom backslash earth
y-u-r-t-h.
Anyone who's listening to this,I hope you.
You see that there's a caliberof doctor out there that is on
the cutting edge and when itcomes to your health, I mean
that there's a caliber of doctorout there that is on the
cutting edge and when it comesto your health, I mean that's

(01:13:41):
where we want to be.
That's why I started thispodcast for Cry Out Loud.
Thank you so much for comingand thank you everyone for
listening.

Dr Yurth (01:13:48):
Thank you, I appreciate the time and I always
appreciate talking to you.
Thanks for listening.

We'll see you on the next episode of the Steve
McCain Podcast.
Stay healthy, cheers.

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