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October 20, 2025 70 mins

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Dr. Dan Pardi is the Chief Health Officer at Qualia Life Sciences, where he leads education to advance healthspan and peak performance. He’s the founder of humanOS.me and host of humanOS Radio, the official podcast of the Sleep Research Society. Dan has advised elite military units, Fortune 500 companies, and startups through his consultancy, Vivendi Health. He holds a PhD in Cognitive Neuroscience from Leiden University and Stanford, and speaks regularly at events like TEDx, VC Firms, and the Institute for Human Machine Cognition.

Think of your body’s repair crew as always on call, rarely on stage. Stem cells sit quietly in protective niches until growth factors wake them, chemokines guide them to damaged tissue, and local signals shape them into exactly what’s needed. We invited Dr. Dan Pardi, Chief Health Officer at Qualia Life Sciences, to break down that invisible choreography—why it weakens with age and how to support it without pushing the system into overdrive.

We start by making stem cells simple: potency tiers, key types like hematopoietic and mesenchymal, and what “exhaustion” really means. Dan explains how inflammation, mitochondrial dysfunction, and epigenetic drift—core hallmarks of aging—distort the niche and blunt self-renewal. From there, we map the full life cycle: quiescence, activation, mobilization, migration, and differentiation guided by ancient pathways like Wnt, Notch, and Sonic Hedgehog. Understanding this sequence clarifies the therapy landscape, from evidence-backed marrow transplants to targeted orthopedic injections, and why unproven IV offerings can be risky.

If you care about healthy aging, joint health, recovery, and evidence-based wellness, this conversation offers a grounded roadmap. We keep the science clear, the hype in check, and the focus on balance—protect, pulse, and let biology do its best work. Subscribe, share with a friend who lifts or runs, and leave a review to help others find the show. What would you most want to regenerate first?

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Episode Transcript

Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Sandy Kruse (00:02):
Hi everyone, it's me, Sandy Kruse of Sandy K
Nutrition Health and LifestyleQueen.
For years now, I've beenbringing to you conversations
about wellness from incredibleguests from all over the world.
Discover a fresh take onhealthy living for midlife and

(00:25):
beyond.
One that embraces balance andreason.
Without letting only sciencedictate every aspect of our
wellness.
Join me and my guests as weexplore ways that we can age
gracefully with in-depthconversations about the thyroid,

(00:48):
about hormones, and otheralternative wellness options for
you and your family.
True Wellness Nurtures ahealthy body, mind, spirit, and
soul.
And we cover all of theseessential aspects to help you
live a balanced, joyful life.

(01:11):
Be sure to follow my show, rateit, review it, and share it.
Always remember, my friends,balanced living works.
Hi everyone, welcome to Sandy KNutrition Health and Lifestyle

(01:32):
Queen.
Today with me, I have Dr.
Dan Parde, and he is the ChiefHealth Officer at Qualia Life
Sciences.
I've had numerous recordingswith Qualia Life Sciences, and
they're always so engaging.
If I remember, I'm gonna putall the links to all of my other

(01:54):
recordings with qualia in theshow notes.
There will also be a discountcode Sandy Kay.
I think it's Sandy Kay, is thecode, but the link will be
there.
Now, this is a differentdiscussion on stem cells than
I've had before.
The discussion that I hadbefore was more about stem cell
transplants versus stem cellactivators.

(02:17):
Oh, actually, I did do anothershow about stem cell activators
as well.
I find it really fascinating.
I find the research reallyfascinating.
This show is gonna have a lotof science in it with Dr.
Dan Parde.
So buckle up and put yourthinking caps on so that you can

(02:38):
really, really soak it all inbecause there's so much
information in this episode.
Last week was my first shorterepisode.
I am changing my style a littlebit.
I am having amazing guests likeDr.
Dan, but I'm also doing more ofthe explorative wellness

(02:59):
topics, not to dictate to youwhat is health and what you must
do to be healthy and so on andso forth, but more about how can
you think critically about whatthe health news says for you

(03:20):
and if it's applicable for you.
Because one thing I havenoticed in this space of
wellness is there are a lot ofopinions and a lot of expert
opinions.
And it's great.
We definitely need experts,there's no question.
However, a lot of times itcomes to us in a way that seems

(03:45):
like it is blanket advice foreveryone, which is why I do
these more think about it shortform podcasts.
They also tie in with mySubstack.
So go find me there if you liketo read short explorative
essays.
It's sandykruse.substack.com.

(04:07):
Be sure that you are followingme on Instagram.
I've been a little quieterthere lately, but that's
definitely my most activeplatform.
I'm also on TikTok, I'm onthreads, I'm on Facebook.
I have a private Facebook groupas well as a page.
I am also on Lemonate.

(04:28):
I mean, I'm kind of everywhere,you guys.
Just search for Sandy KNutrition everywhere and follow
me there.
And now let's cut on through tothis amazing interview with Dr.
Dan Parti of Qualia.
Hi, everyone.
Welcome to Sandy K Nutrition,Health and Lifestyle Queen.

(04:49):
Today with me, I have a specialguest.
His name is Dr.
Dan Parde.
He is the chief health officerat qualia life services, where
he leads education to advancehealth span and peak
performance.
He's the founder of humanois.meand the host of Human OS Radio,

(05:13):
the official podcast of SleepResearch Society.
Dan has advised elite militaryunits, Fortune 500 companies and
startups through hisconsultancy, Vivendi Health.
He holds a PhD in cognitiveneuroscience from Leiden.

(05:33):
Leiden University?
Did I say that right?

Dr. Dan Pardi (05:36):
Leiden, yeah.

Sandy Kruse (05:37):
Okay, Leiden, thank you.
He holds a PhD in cognitiveneuroscience from Leiden
University and Stanford andspeaks regularly at events like
TED Talks, VC Firms, and theInstitute for Human Machine
Cognition.
And today our talk is all aboutstem cells and how this

(06:01):
research can change the face ofhealth and wellness as we know
it.
And most of you guys who havebeen following me for a while
know I think this is maybe mythird show on stem cells.
As most of you know, I like toalways have authentic
conversations with integrity.

(06:22):
And also things change.
I mean, I've been around for awhile.
So things change.
And this is new.
I know it's new from Qualia.
I'm excited.
I've started using it.
So I'm really excited to hearabout the newest research on
stem cell activation.
So with that, welcome, Dr.

(06:43):
Dan.
Thank you.

Dr. Dan Pardi (06:45):
Thank you so much for having me, Sandy.
It's great to be here.

Sandy Kruse (06:48):
Yeah.
So one of the things, ofcourse, I always like to start
with is asking my guests, howdid you get here?
How did you get into thisspace?
I think it's always importantto the conversation.

Dr. Dan Pardi (07:01):
Yeah.
Yeah.
I love that as a foundingquestion.
So I've been interested inhealth my whole life.
And I've tried to pinpoint whenthat began.
Probably when I was younger, Iwas into sports.
I cared about performing mybest.
And I unfortunately got acouple of injuries early on.

(07:21):
And I think that might havebeen fortuitous in a way,
because it started me thinkingabout my relationship with my
body at that time.
How do I get back onto theplaying field?
How do I heal?
And from that point on, after Idealt with those injuries, I
almost became like the de factosports performance coach for my

(07:44):
entire team, whether it wassoccer or basketball.
So I was always reading aboutand researching ways to, you
know, improve my performance.
And then that led to a veryauthentic interest in
physiology.
I went on to pursue a master'sin exercise physiology at
Florida State.
And then I did a variety ofthings.

(08:04):
I didn't know what I wanted todo.
I worked in bioinformatics,which is, I was a part of a
company called Double Twist,really exciting company in the
race to sequence the humangenome for before anyone else.
So we had, you know, raised $75million and ended up creating
these products that were wherewe'd work with pharmaceutical

(08:26):
companies to help them usegenomic data in the drug
development process.
So it was very technical, verycool work we were doing.
Then I went into the pharmabusiness for almost a decade.
So I worked in sales for abouta year, but my interest was
really on the science side.
So I ended up becoming thefirst member of Medical Affairs,

(08:48):
which does post-marketingscientific support for products.
And that where I worked was insleep.
And that's where my interest insleep, I knew nothing about
sleep.
And all of a sudden I wasfascinated by it.
And so the condition that wewere working on was narcolepsy,
which is most people think of itas excessive sleepiness, but it
is that plus some othersymptoms as well.

(09:08):
And there wasn't really greatmedications.
And so we were trying to helpimprove their quality of life
and reduce their symptoms.
And so for that company, I rana research grant program.
Um, I started an outsideorganization called ISRA, where
I created an executive committeewith representatives from big
names, and we petitioned the FDAto change um the guidance for

(09:33):
how to employ best practices uhin these types of grants.
And anyway, so that was greatwork that really loved it.
But working in sleep, I thenhad my own questions.
Like uh so I decided to pursuemy PhD.
And it was right at the timewhen quantified
self-technologies were cominginto the market and the

(09:55):
ancestral health movement wastaking off.
So the idea of the paleo diet.
Uh, and so I started my PhD,but I knew that I didn't want to
become a lifelong researcher.
I knew that I wanted to beworking in more of the public
health sphere, doing scientificwellness.
So I finished my PhD.
Um, and by the way, I did itbecause I also was so curious

(10:19):
about like the answering somequestions that I had around
ecological sleep loss.
So if a lot of sleep studies,what they'll do is they'll give
you one full night of sleepdeprivation to then see how
whatever parameter of interestchanges in response to no sleep.
But what I was more interestedin was, well, that's not a
that's interesting because youcan test the capacity here to,

(10:42):
you know, does sleep actuallyaffect this?
But what's more practical iswhat if we just lose a couple of
hours here and there?
Does things like eatingbehavior and decision making, do
those things change in responseto what's much more normal in
society?
So that's those are thequestions that I asked.
Uh, and then all the while Ihad started to create my own
behavior model.
So I dissected well-knownbehavior models in the world.

(11:06):
And I um then rebuilt my owncalled the loop model to adopt
and sustain health behaviors,presented that at Stanford
Medicine X and Health 2.0 andsome other conferences, and that
became the basis by which Itried to operationalize a health
tool called Human OS to thenmake people smarter, more
knowledgeable, wiser about theirown health practices.
And then that sort of did thatfor a long while.

(11:30):
That's where the podcast cameinto play.
Uh, and I started my podcastback in 2014 because at that
time, what I was missing was adirect conversation with the
researchers who did their work.
A lot of times it wasinterpreted through a person who
was a personality who, youknow, um had varying degrees of
knowledge in different areas,but was oftentimes a good

(11:53):
communicator.
And I wanted to go right to thesource.
So that's why I started mypodcast and interviewed over a
hundred professors in the healthsciences.
And it was great.
Um, and then uh I grew up inNorthern California, moved to
Texas in um the early 2020s.
I became the chief healthofficer for a large brand, half
a billion dollar brand calledRestore Hyperwellness.

(12:14):
And we they were democratizingthese ideas of like sauna and
cryo and compression and redlight, all ideas that I think
have a lot of potential.
And so that was great.
Um now, company ended up goingin a direction of performance
medicine, which I think isreally interesting and cool too.
But I am firmly more interestedin what I call scientific

(12:35):
wellness.
So that how lifestyle supportsour health.
Um, and then I joined Qualialess about a month ago, maybe a
little bit more now, maybe two.
Uh and I've been friends withthe company for a long time and
I've really admired how they dotheir job, uh, how they see
their responsibility in thespace, the products that they

(12:57):
make.
And they were looking forsomebody who would be able to
communicate the science aroundall the products that they're
creating and beyond.
And it just felt like a reallygood fit.
So now I'm here and I'm thechance to talk with you.

Sandy Kruse (13:12):
Awesome.
Wow, you've done a lot, Dan.
And, you know, about qualia, Ihave a long-standing
relationship with them and Ilove their products.
And I've been also supportingthem for many years.
I've had many conversationswith other doctors,

(13:33):
practitioners within the qualiaspace.
So wow, you've done a lot.
I mean, and and you know, eventhe sleep, you see so much about
sleep nowadays.
And like almost, you know, ifyou're scrolling through
Instagram, you're seeing allthese like sleep coaches, sleep
coaches.
You can see I've got my deviceson.

(13:54):
Um, you know, I listen, I'm abig believer in not just
tracking, but resolving, right?
Like, so, and obviously I Iknow that you would support
this.
It's so bioindividual.
Like, what works for you maynot work for me.
My like, you know, I'm a55-year-old menopausal woman.

(14:17):
Of course, sleep is gonna be afactor in my life, right?

Dr. Dan Pardi (14:21):
So anyway, I think that applies to just about
everything.
So I really appreciate yourcomment about our individuality.

Sandy Kruse (14:31):
I actually just posted about that today, Dan.
Oh, nice.
Because um, I'm like, I there'sa new document documentary out,
and it's really fascinating.
I started to watch it and I'mlike, oh my god, yes.
You know, the scientificcommunity, uh meaning also MDs,

(14:53):
are catching on to the fact thatnot all pharmaceuticals work
the same for all people, not allsupplements work for this the
same for all people, like it'sjust so bioindividual.
And I think it's never gonna bea one size fits all, but that's
all.
And so um, I love the take thatyou have on wellness, and I

(15:17):
think talking about stem cells,it's it's now a big topic,
right?
You see, and and I've actuallydone an interview a couple years
ago.
It was a live interview aboutstem cell activators.
Um, I've done an interviewabout what was it?

(15:38):
It was I don't even know.
It's like placenta stem cellsor something.
But I think we need to beginwith what are stem cells.

Dr. Dan Pardi (15:49):
Yes, that's a great place to start.
So they are special cells inthe body that can the best way
to think about about it withoutmaking using a ton of jargon is
that they make copies ofthemselves.
And one of those copies is uhjust a duplicate, like a clone
of the original stem cell.
And then the other one be candifferentiate and become uh it's

(16:12):
a part of our repair system,and it could become any type of
tissue in the body.
And so this is how the bodywill regenerate when cells are
die off, right?
Because they don't lastforever, even though we outlive
our cells, right?
We replace them at differentcadences in different tissues,

(16:33):
but we need to be able to rereplace those cells, and the
stem cell system in the bodyenables us to do that.

Sandy Kruse (16:41):
Okay.
Now, different parts of thebody have different stem cells,
don't they?
Yeah.

Dr. Dan Pardi (16:47):
Yes, that's right.
So a term that we use when wetalk about stem cells is
potency.
So we have different types ofstem cells in the body, and they
are based off of their potency.
Now, potency is a word thatdescribes what they can become.
So if you move down the potencycategories, the number of cells

(17:10):
that they can become narrows.
And there's five maincategories of potency.
So you have tody potent orpluripotent.
Those two basically are stemcells that can become any type
of tissue in the body.
Okay.
Uh, and there are someimportant differences between
them.
It's probably more than we needto go into.

(17:31):
But the best way to think aboutthose two is that it's a
one-to-many relationship withtodipotent or pluripotent cells.
And you'll hear pluripotentdiscussed a lot more.
But an example of a totipotentcell stem cell would be like an
zygote.
And of course, that is, youknow, that becomes a full human,
right?
It can become any type oftissue.

(17:52):
Then you have multipotent,oligopotent, and unipotent.
Those are the last three typesof potencies.
And multipotent cells canbecome multiple cell types, but
only within certain lineages.
So, an example would behematopoietic stem cells.
They generate different typesof blood and immune cells across

(18:14):
these the lineages that Imentioned, so myeloid and
lymphoid.
And a myeloid lymph uh lineageproduces red blood cells and
platelets and monocytes, thingsthat you get measured on blood
work, uh, and alsogranulocyte-based blood cells
like neutrophils, osonophils, uhbasophils, things like that.
The lymphoid lineage is makingyour immune cells, B cells, T

(18:39):
cells, natural killer cells.
So those you can see that whatthis multipotent lineage means
is that it can become multiplethings, blood cells or immune
cells, but it can't becomeanything.
All right.
So another example of thatwould be mesenchymal stem cells.
When we talk about stem cellsin the clinic, you hear about

(18:59):
those two the most hematopoieticfrom bone marrow and
mesenchymal stem cells.
And those form different typesof connective tissue.
So bone, cartilage, fat,muscle, things like that.
To continue on the describingpotency, you also then have
oligopotent cells.
They can become only a fewclosely related types.

(19:20):
So an example would be anosteoprogenitor cell that can
only become different types ofbone, so osteoblasts or
osteoclasts.
And then lastly, you haveunipotent stem cells, and they
can only become one type.
Um, but they can stillself-renew.
That is a key feature to stemcells, self-renewal.
Uh, but an example of aunipotent cell would be a muscle

(19:43):
satellite cell.
So, as you can see, you havedifferent types of stem cells,
all of which self-renew anddifferentiate, but some can turn
into anything, and some canonly turn into one thing.
So that, and actually, if you'dlike, we can talk about even
how cells differentiate.
Because for me, when I seethose connections, like, ah, how

(20:05):
does this actually work?
That helps me understand thissort of opaque topic a little
bit differently.
But you tell me.

Sandy Kruse (20:13):
Okay, okay.
So most of the people thatlisten to my podcast, you know,
they're like, I'm certainly nota scientist in nutrition
college.
I took science courses, ofcourse.
However, you know, high level,yeah.
You hear in general the thermthe term stem cell therapy.

(20:38):
I want to break this down sopeople can understand it.

Dr. Dan Pardi (20:42):
Yes.

Sandy Kruse (20:43):
When people go and say, Oh, you know, my knee is
wrecked.
I want to do stem cell therapy.

Dr. Dan Pardi (20:51):
Yeah.

Sandy Kruse (20:52):
Okay.
So that is very different fromlet's say I have a blood cancer,
right?
And and they they use bonemarrow for some sort of therapy.
Like there's different types oftherapies that use stem cells.
Yeah.
So maybe if you could kind ofbreak that down simply so that

(21:18):
people can understand it.
Because we see this all thetime.
Oh, yeah, I'm gonna go for stemcell therapy.
But wait a minute, there'sdifferent types of stem cells
that do different things.
And I need to understand whatthat means.

Dr. Dan Pardi (21:31):
Yeah, yeah.
So stem cells uh in the in theclinic have been used now for a
while.
Um, they're they're eventracking back to the late 1950s
where some stem cell replacementtherapy occurred.
Uh, and so just looking at thethe research history of that to

(21:54):
as a starting place, uh, becausethat is interesting to look at
first, because you can then seehow it evolved.
But in 1958, a Frenchoncologist named George Mathey
performed the first uh stem celltransplant.
So he treated six workers thatwere exposed to high dose
radiation in a nuclear accidentin Yugoslavia, and Mathe

(22:17):
transplanted bone marrow stemcells to restore their blood and
immune system.
So we were just talking abouthematopoietic stem cells and how
they can produce blood cellsand immune cells.
And so that's exactly what hewas trying to do.
And five out of the six endedup surviving long term, and one
did die of complications.

(22:38):
But this was really the firstdemonstration that stem cell
transplants could rebuild humansystems after damage.
And it it marked the really thetrue beginning of modern stem
cell therapy.
Now, from there, we have, youknow, the two groups that
typically get anything new onceit gets into the commercial area

(23:00):
are very wealthy people andathletes.
Right?
Those are like the two groups.
Um, you know, we learn a lotfrom athletics because what
typically happens is that goodscientists in that space start
to use technologies prior to,you know, the the very slow time

(23:21):
course that uh can sometimesoccur with, you know, other
types of therapies where theyhave to go through all these
levels of validation uh prior togetting standardized, which
would mean it's implicateduniformly through our entire
healthcare system.
And that can be reallyfrustrating for a lot of people
because there's a 20-year delay,oftentimes, if not more,

(23:46):
between the science that showspromise in an area.
Um, and I would actually saythe timescale is even beyond
that, like when we really knowthat something is efficacious.
And so athletics will tend tostart using those types of
things much, much earlier thanbeing spread ubiquitously

(24:06):
through a healthcare system.
So, yes.
So then going back to yourquestion, so that was really the
first demonstration of stemcell replacement in the body,
and you saw very positiveoutcomes there because it's
likely that all six of thosefolks who were exposed to that
radiation would have diedotherwise.
Um, but you were able, theywere able to replace the stem
cells, able to restore theimmune system, and that had a

(24:29):
very positive effect.
Nowadays, you might go and getyour own stem cells removed from
your body, and there arevarious ways to do that.
Uh again, they'll either bemesenchymal stem cells from fat
or hematopoietic stem cells frombone marrow, and then they will
be concentrated and put rightback into the body where they
can have a regenerative effect.

(24:50):
So that is uh pretty exciting.
And I've spoken with orthopedicsurgeons who use this, and uh,
the guy who I know here inAustin, who I have conversations
with about this, he's reallyhe's seen great things in the
clinic.
He really likes uh, you know,he's like, yeah, it really,
really work.
Like I've tried, it's not thefirst thing I try.

(25:10):
They're pretty expensive.
It might be four or fivethousand dollars a therapy.
And you've got, you know, let'ssay two sore feet that you need
to have addressed uh forvarious reasons, then you know,
it's getting close to tenthousand dollars.
It's expensive.
Um, and the this can be moreexpensive than that at other
places.
But you know, you areperforming a little surgery.

(25:31):
Um, so if you're trying to takestem cells out of bone, you
usually go to the iliac crest,which is that prominence in the
front of your hip area.
And the reason why is becauseit's a very easy area to get
stem cells, um, because there'snot much distance between, you
know, there's not much tissuebetween the bone and uh the

(25:52):
outside.
So you can aspirate uh the stemcells from your bone marrow.
Again, you can concentrate themand then you can put them right
back into the an area where uhyou know you're you're dealing
with an injury and you need somerestoration.
So, yes, so that is those aresome ways that stem cell
therapies are mostly occur.

(26:14):
And then there has been uh atrend now, a movement towards
injecting them IV and havingstem cells theoretically repair
damage throughout the body.
And now, stem cells do kind ofwork in that way.
And we we should talk aboutlike what is the actual like
life cycle of a stem cell, sopeople understand how they work

(26:36):
naturally.
Um, those types of therapiestypically people have to go
outside of the United States inorder to get them because they
are not approved by the FDA, andthere has been several uh major
uh issues with companies thatwere starting to sell unapproved
stem cell therapies.
And in fact, some some of thefounders have ended up on the

(26:58):
FBI's most wanted list becausethey were just you know not
acting, I would say, ethicallyuh in this regard.
So there is, you know, umworking ahead of the curve.
And then there's also beingsort of grossly um immoral by
making big claims that have noproof about, you know, sort of

(27:20):
playing off of people'svulnerabilities, like saying
that it can cure things wherethere's no evidence at all that
it could cure that.
And so that's you know, that'ssort of the balance of the
industry, uh, the promise, theexcitement, and um maybe some of
the hyperbole.

Sandy Kruse (27:37):
Okay, I have a couple of questions.

Dr. Dan Pardi (27:39):
Yeah.

Sandy Kruse (27:40):
With is it true that you know, people who say,
okay, I'm gonna go and get stemcell therapy, I have severe
arthritis in my knee, I don'twant to have knee replacement,
you go, you have the whatever,it's like a small surgery.
What's the success rate of thatsort of thing?

(28:02):
And aren't can't stem cells gettoo old?
Like, meaning, like if I'm like80, are my stem cells any good
to do that with?

Dr. Dan Pardi (28:12):
Yeah, that's a really that's a really important
question.
Um, and the general thinking isthat younger stem cells uh are
going to be more effectivebecause if your stem cells are
exhausted, which is a term thatis now used uh to describe what

(28:32):
happens to stem cells as we age,and we can of course go into
what that specifically means,then would simply taking out old
stem cells and putting themback into the body really do
much good, right?
The older you get, the more youmight need them for some
osteoarthritic pain in yourknee, as the example you used.
Uh is that going to be helpful?

(28:53):
And um so there areorganizations that are looking
to try to address this problemof can we bank your own stem
cells?
So you're young, you bank yourstem cells, when you get older,
you have a a knee in a kneeissue, and then you use your own

(29:16):
autologous, which means selfstem cells, to then fix so you
you you avoid the risk of immunerejection uh when you're using
uh other people's stem cells.
So that is uh definitelysomething that is of interest.
There's also interest where youcan take your own stem cells

(29:36):
and in a way make them newagain.
So you go through this processwhere you would uh reverse the
there's you can make them umyoung again in a way.
And uh that is some very coolscience that is taking place.
And then there are also uh munew types of cells called mu

(29:59):
cells.
I would say new in that theywere discovered in the last 20
years by a Japanese scientist.
And then they seem to avoidsome of the immune rejection.
So you could actually get stemcells from a different person.
And they also, what you, if youtake one thing that's been
known for a long time, if youtake stem cells and you inject
them into the body, they can betumorogenic.

(30:20):
They can form tumors.
And so that's something that,of course, we would want to
avoid as well.
But the mu cells do not dothat.
And so, yes, there's a lot ofdifferent companies that are
working in this space.
There's a lot of excitementhere.
And the main reason is because,you know, as we get older, our
ability, the the ability toreplace tissue that dies starts

(30:45):
to lose out.
So the damage outpaces uh theability to renew.
And then we really start to seethe signs of aging.
And it can start in the 40swhere you start to notice, it
can start before that, but youstart to notice it more in the
40s.
And by every decade, thatprocess yields signs of aging
that become more visible, morepalpable.

(31:07):
And so the excitement, I wouldsay, high level, is that we
might be able to tilt the scale.
So we we either delay thatcurve, um, and then moonshot, we
actually have a great impact tokeep our bodies renewed well
into the human lifespan and youknow, possibly even extend the
human lifespan too.

Sandy Kruse (31:28):
I think that's an important thing to note here,
Dan, is what are the signs?
Like, are there any specificsigns that, you know, and and do
we is it about losing stemcells, having dead stem cells?
Because I know synolytics cancome into play in this
conversation.
It's all kind of intertwined.

(31:50):
So, you know, what are thesigns?
Number one.
Um, I know I recorded a podcaston the hallmarks of aging, and
that probably connects to this.
So maybe get into some of thatso that people can go, okay.
So, how do I know?
Like I know if I have a badknee, that's one scenario.

(32:12):
If I have a type of bloodcancer, that's another scenario,
right?
So, what about just in general?

Dr. Dan Pardi (32:21):
Yeah.
So maybe we'll start with thestem cells.
Like, what happens to the stemcells?
Um, so looking into the petridish, if you will, and then we
can think about well, what isthe experience?
Okay.
So we'll move in thatdirection.
Uh so the term is called stemcell exhaustion, and it is this

(32:42):
decline in their ability toself-renew and to generate
functioning cells.
So remember, that is what stemcells do, right?
They have ability to copythemselves and then make a clone
of itself.
And then also, that's theself-renewal part, and then also
to generate cells that becomenew tissue.
And just as you mentioned, thisbasically leads to uh reduced

(33:06):
tissue repair.
And that's why it's consideredone of the now 12 hallmarks of
aging.
And uh just for the audience,if they missed your podcast on
this, the hallmarks of aging arebasically the main biological
processes that drive how we age.
And they include things likegenomic instability from DNA
damage, shortened telomeres, um,epigenetic changes uh that

(33:31):
alter how genes are expressed.
There's a variety of thingsthat are occurring reliably that
we can track when a personages, and they can occur at
different rates.
Um, but generally they dohappen.
And a stem cell exhaustion isone of those hallmarks.
And so if we then look at, allright, so what does um what

(33:57):
happens with stem cells inparticular?
I mean, another major hallmarkof aging is chronic
inflammation.
And so this elevation.
Now, I do want to say somethingabout inflammation.
It has, it's sort of thought ofas a dirty word.
Inflammation plays an extremelyimportant role in the body,
right?
It is doing somethingfunctional in the body.

(34:18):
So what we really care about isa dyshomeostasis of
inflammation, which means ourinflammation system, our
inflammation communicationsystem is out of balance.
And the reason why we noticehigher levels of inflammatory
markers is because they'rehaving to try to speak louder to
get their message across.
We're developing resistance uhat cells that are hearing those

(34:41):
signals.
And so the the volume of thosesignals has to rise.
Now, why is this problematic?
Well, you know, for example, inaged muscle satellite stem
cells, which we talked aboutearlier as unipon stem cells,
when you see an increaseelevation in inflammatory
markers like ILL6 or TN alfalfa,then that will cause stem cells

(35:02):
to differentiate into myoblaststoo early.
Now, a myoblast is a precursormuscle cell.
Um, and so they can, it's like,you know, on the way from a
stem cell to a fully functionalmuscle tissue cell, there are
these intermediate steps.
And that precursor cell is oneof those steps along the way.

(35:23):
Um, but what ends up happeningwhen inflammation causes them to
differentiate into that liminalstep too soon is that it
prevents them, the self-renewalprocess.
So they can fuse into fibers,but what it ultimately does is
reduces the stem cell pool andimpairs regeneration.
So that's one issue that isrelated to uh stem cell

(35:46):
exhaustion.
Inflammatory markers causedysregulation and reduce
self-renewal.
Another factor would beincreases in oxidative stress
that can damage DNA.
Another hallmark of aging is uhmitochondrial dysfunction.
So when you have mitochondrialdysfunction, and mitochondria
are the internal organelles inyour cells that make energy.

(36:11):
Um, and when those get impairedthrough a variety of
mechanisms, then that is goingto increase the amount of
oxidative stress, whichincreases the amount of DNA
damage.
And then that too is going toharm self-renewal of stem cells,
and it's also going to impairexisting stem cell survival.
So it makes the ones that arealive not be able to replicate

(36:33):
and not be able to survive.
All right.
So that's another aspect of theexhaustion that we experience.
Another key one is that if yourepeatedly activate stem cells,
then that's going to cause adepletion of your stem cell
reserves over time.
You do not want to beconstantly driving new stem cell
creation because they havetheir own life cycle.

(36:56):
So we're not trying to overridethe natural system.
We're trying to support it.
And I think that actually kindof will come back to how we
formulated our product, right?
Constantly driving theproliferation of stem cells, it
can itself lead to stem cellexhaustion.
All right.
And then there's even thingslike epigenetic drift, which is

(37:18):
these random marks to theepigenome that disrupts the
stable gene programs that willkind of reduce the identity of
stem cells and the regenerativecapacity.
And so I know that there's someterms in there that we haven't
really described yet.
Um, but that's, you know,there's even more things, and I
think more would be too much,but that you can now see lots of

(37:41):
stuff that are occurring,that's occurring during aging,
that is also now aging stemcells themselves, which is a
part of also the experientialeffects of aging too.
So you can see all of thesehallmarks of aging aren't acting
independently, but they'reinfluencing each other as well.
And stem cells is involved inthat mix.

Sandy Kruse (38:02):
Yeah, and it and it does get complicated.
So, you know, that's why forme, I think it's important that
people listening just have thebasic knowledge and
understanding and know how itwould apply to them and where it
would apply.
One thing I and maybe this isjumping around, Dan.

(38:22):
I know we talked about this.
We don't want to jump aroundtoo much, but you said something
that just triggered thisquestion in my mind about like
almost like an overactivation.
Yeah.
So it's almost like too much ofa good thing is too much or can
be.

Dr. Dan Pardi (38:42):
Yeah, that's exactly that's exactly right.
So um, I think this wouldprobably be a good time to just
talk about like what is thenatural life cycle of a stem
cell.
So we under it puts things incontext because if you don't
understand what the naturalprocess looks like, then you
might take out a portion of itand say, we're gonna just drive
this one portion of it, and thatmight seem good in the absence

(39:04):
of a full understanding of howthey really work.

Sandy Kruse (39:07):
Right.
I think this is importantbecause for anybody who's
listening, I'm a big fan ofpulsing things in and out
because I also know what myneeds are.
So go ahead.
Let let's let's talk aboutthis.
This is important.

Dr. Dan Pardi (39:25):
Okay.
So we talked about differenttypes of stem cells, their
potency, which means what youknow that they can become
different things.
Uh, and they also reside indifferent parts in the brain.
You have intestinal stem cells,you have your hematopoietic
bone stem cells, mesenchymalstem cells and fat and tissues.
So, right, they're they're allout neural stem cells, they're
all throughout the body.

(39:46):
So we have these differentpools.
And they usually start in thisprotective environment called a
niche, uh, such as you know,bone marrow in for blood stem
cells.
And in that niche, they'rereceiving signals from
neighboring cells, uh, adhesionmolecules, even the soluble
factors that keep them quietuntil needed, right?

(40:08):
That is part of the naturalstate, is that they are in
quiescence or they are dormant.
They're just they're hangingout and they're ready to be
activated.
So when the body does need newstem cells, it receives growth
factors.
Some of those growth factorsare um basically the different

(40:29):
types of colony stimulatingfactors.
And the colony refers to thestem cell colony, right?
And they are activated by thesethings like GCSF and GMCSF.
And then enzymes and signalingproteins loosen their grip um of
the stem cells in their niche.
So remember, they're they're inthere, imagine like a little

(40:51):
stem cell in bed, sleeping,under the covers and happy.
And now we got to get them outof bed and we got to get them
active, right?
So we're waking them up.
And that that is a the firststep there.
So once they are active, thenthey need to enter into

(41:11):
circulation, right?
That's if they need to go fromsome reserve place in the body
to where they need to fixtissue, they need to get there,
right?
They need to go from point A topoint B.
How do they do that?
Well, they are guided bychemical gradients.
And so they don't just wanderaimlessly, like, oh, I'm just
gonna, you know, circulate untilI land in a particular place.

(41:34):
This is actually anorchestrated activity.
And so what they do is theyfollow a centrail by um
compounds called chemokines.
Um, and there's an axis that'simportant for this.
And it's a it's a technicalterm, but I'll explain it.
So the axis is called CXCR4SDF-1.
Now, SDF1 acts like a beacon.

(41:57):
And I don't know why, but thisimage popped into my head.
So remember that scene in umJurassic Park where I can't
remember who the actor was, buthe was trying to save the child
who was about to get eaten by aT-Rex.
So he grabbed the flare and hestarted to, he got the attention
of the T-Rex and he startedrunning away from it, and then
the T-Rex started to follow him.

Sandy Kruse (42:16):
Yes, I remember that.
Yeah, yeah.

Dr. Dan Pardi (42:18):
Great scene, great visual.
That is SDF one.
Okay.
That is that is a, hey, followme.
Okay.
Then CXCR4 is a receptor onstem cells that helps to follow
that gradient.
Okay.
That's going to help it followthe signal.
And then once it gets, once thestem cell gets close to uh an

(42:43):
area of need, it has to slowdown, right?
It's in the circulation.
So there are then theseadhesion molecules like
L-celeptin and integrins, andthey help them stick to the
vessel walls, where then theycan move into the right tissue.
All right.
So they're in their bed,they're activated, they move
into the bloodstream.
Now you're the T-rex chasingthe beacon, and now it's gotten

(43:05):
to the right place and it slowsdown, and now it has to move
into the right tissue.
And at that point, it starts toreceive local cues like growth
factors, um, factors from theextracellular matrix, uh, all
sorts of things that then starta really interesting process in

(43:25):
my mind.
So they they will, these growthfactors will now signal these
signaling pathways that havevery, they're very ancient.
They came, these pathways havebeen around for 600 to 800
million years, right during whenstem cells first developed um

(43:46):
in evolution.
And those signaling pathwaysnow will affect what's
happening, and they have funnynames like wint, uh, sonic
hedgehog, um, notch.
They will now affect what'shappening inside of a cell, and
they will affect what are thesetranscription factors.
And if you remember, atranscription factor is binding

(44:07):
to our genes and telling itwhich proteins to turn on and
off.
Because every cell has all yourgenes, but you don't want all
your genes to be activated,making all sorts of proteins all
the time.
You want it to make, if you'rea liver tissue, you want those
cells to make livertissue-specific proteins.
If you're a neural cell, youwant it to make those specific

(44:30):
ones.
Muscles, the same.
And so, in this, in thisprocess now, you now have these
transcription factors that aredoing several things.
They are activating the rightgenes and turn and silencing the
wrong ones.
And then that whole processgets locked in.
So it now, all of a sudden,this stem cell that could be

(44:50):
anything, just about, I mean, atleast theoretically, right?
Remember, we it depends on thelineage, right?
Some can only become certainthings, but they now start to
take on characteristics specificto the tissues that we want
them to become.
And then as that happens,epigenetic changes occur at the

(45:10):
same time that lock in thatidentity.
And now that's how you have astem cell that goes from its
niche sleeping in bed, now intoa tissue and turning into a very
specific type of cell and notanother type of cell.
You do not want a muscle tomuscle cell to be created in
your neural stem, in your youknow, neural tissue, right?
And that can be used in allsorts of contexts.

(45:33):
I love, I just love goingthrough those details because
now I understand stem cells alot better.
Like when you sort of like,okay, we see now this is a
process.
There's proliferation, makingmore stem cells, activation,
mobilization, migration,differentiation, all of those
things are occurring.
It's not just about makingmore.
What we really care about isstem cell homeostasis, which is

(45:58):
the balance of that entiresystem that continues to create
healthy tissue and not create,you know, cancerous tissue or
other problematic, you know,things that can occur, right?
We do not want excessiveproliferation.
We want targeted, directed,healthy tissue repair.

Sandy Kruse (46:15):
That was a brilliant explanation.
And by the way, the t-shirtthat I made like over five years
ago, it says it's all about thebalance.
And I have scales.
Because that I'm a big believerin all of that in life, period.
So what you just described isreally fascinating.

(46:35):
So let me ask you thisquestion.

Dr. Dan Pardi (46:37):
Yeah.

Sandy Kruse (46:38):
Because I mean, you I feel like I love your
passion.
We could probably talk for twohours.
But what I want to ask is ifyou're 80 years old, yeah, do
you have more of those stemcells in bed that just don't get
up?

Dr. Dan Pardi (46:58):
Yeah.
So it's a really importantquestion.
Is do we see a major decline instem cells?
Or do we see that there are isthere something else happening?
And Irena Conboy at UC Berkeleyis somebody that I interviewed
in my podcast probably in 2017.

(47:18):
And what her work, she's donework related to this area very
specifically.
So she did these experimentscalled parabioses, and in that
they're they're sort ofhorrific, but they tie, they sew
an old mouse to a young mouse.
And the I know brutal.

(47:38):
Yeah, yeah.
But what ends up happening isthat the the young mouse becomes
older, and the old mousebecomes younger.
Why?
You know, what is the whatexchange is taking place?
And that has led to a line ofinvestigation into what are the

(48:00):
factors that are drivingregeneration or stopping it.
And what she has commented onis that we don't see major
declines in stem cell pools.
Like you might have, there is adecline, but it's not major.
So, you know, by your 50s, youmight have only 90% of what you
had when you were younger.

(48:21):
So still plenty.
So there is a decline, but notdramatic.
What happens with stem cellexhaustion has more to do with
the niche.
Remember, the niche is theenvironment in which they live.
And when you do have a rise ininflammatory factors, you then
will start to see that the stemcells are there.
They just can't differentiateinto new tissue, right?

(48:41):
They can't become the newhealthy tissue that you want.
And the all the things that Ijust talked about, the system
can break down at almost anypoint.
The net I the net effect of itis you're not replacing tissue
at the pace that you once were.
And that pace accelerates.
And that's why we see thesereliable signs of aging as you

(49:03):
get from decade to decade.
And again, we're not, you know,at this point, we're not going
to stop that process entirelybecause remember, it's not just
stem cells.
Like even if we were to fullysolve the stem cell issue, that
actually could have a verypowerful effect on how we age
over time, but it's not the onlyissue.
And so, you know, what we'reinterested in now, the whole

(49:24):
field of geroscience, is whatare all the drivers?
And are there ways that we caninfluence them?
And all of the smartest mindsin this area realize that it's
not going to be a silver bullet.
It's not going to be one pillthat does it all.
But rather, we're going to haveto try to address these one by
one.

(49:44):
And hopefully we can work atthe most consequential uh
hallmarks of aging and influencethem in a positive way.
And we already know we can dothat through lots of things
related to lifestyle.
And that's why we talk about itso much, because it matters.
So what we really care about iscan we then do things that go
beyond that?
Like I'd never want to giveshort shrift.

(50:05):
I mean, even if you recall fromthe beginning, my interest lies
in scientific wellness, likeunderstanding how to use
lifestyle in a way, you know,foundational almost feels like
it's not giving it credit itdeserves.
It's so powerful, and it's, butyet it's hard to do.
And yet at the same time, I'mstill interested in how we can

(50:26):
go beyond that, right?
How can we then take it to thenext level?
And and that's where thescience of this stuff is so
exciting, particularly, youknow, with stem cells.
But I just wanted to make thatcomment that it's going to be a
suite of solutions that get uscloser to where we want to go.

Sandy Kruse (50:44):
So, you know, just to kind of fast forward, I think
most people who listen to mypodcast already got that down in
terms of you want to sleep, youwant to eat whole real foods,
you want to move your body, youwant to limit alcohol and
smoking.
Like we kind of all have thatdown.

(51:05):
So I think it's a really goodtime just to kind of you know
touch on stem cell activatorsbecause that's kind of going
above what you were saying.

Dr. Dan Pardi (51:17):
Yeah, yeah.

Sandy Kruse (51:18):
How they work.
And so for me, you know, Dan,like I I think of it as like,
what?
You know, you can actually takea supplement and you swallow it
like it's like whatever.
So I know that qualia'sformulation is six capsules a
day for only four days, becauseit goes back to what you were

(51:41):
saying about not overstimulatingthat activation, but just
helping it along, maybe helpingthe ones that need to get out of
bed to get out of bed and dotheir thing.
Does that make sense, Dan?

Dr. Dan Pardi (51:58):
Absolutely.
That's how we see it.
So the reason I think it's soimportant to discuss that life
cycle of stem cells is becausewe not only does it help you
avoid overfixating,over-indexing your solution into
just one aspect, which if yourfocus is entirely on you know

(52:20):
improving proliferation andactivity, remember that's one of
the things that can cause stemcell exhaustion, overusage.
You don't want that, right?
That's not how stem cells work,right?
They they have to stay quiet intheir niche.
So again, going back to ourgoal is more about how do we
maintain stem cell homeostasisor health, right?

(52:43):
Now, health is the ability forthe body to maintain an
evolutionarily derived function.
And so this the body knows howto maintain stem cells.
We just lose that ability as weage, right?
In the process ofhomeostenosis, which is this
general decline that we allexperience and we know.
And, you know, some animals, assoon as they reproduce, they

(53:03):
die, like salmon, right?
They live up to a week and thenthey're totally dead.
We have this protracted periodwhere we stay alive after
reproduction window, whether wereproduce or not, but the window
in which is most common thathumans do reproduce, and that is
because we continue to play avital role in the survival of
offspring, even if they're notour you know direct descendants.

(53:24):
It could even be within thetribe.
That's the evolutionarycontext.
And as a result, you know, thisis important to mention the
body doesn't actuallynecessarily it has different
priorities across the commonlife history, which is a life
every animal has its own lifehistory, and a part of life

(53:45):
history is how long we tend tolive.
So, you know, we live around 80years, some people can live
more, some people less, butthat's like the average uh, you
know, approximately maximumhuman lifespan is can thought to
be 125 years old.
So that means that we can'tlive beyond that.
Um, I believe the oldestsurviving person lived up to 122

(54:09):
years, uh, Gene Celmont, whichis amazing.
Uh, but that's well beyond whatmost of us, how most of us
live.
How long?
But you know, a house mouselives a year and a dog lived
maybe like 13, right?
So is it because our biology isso much better?
No, it's because our lifehistory, our lifespan is shaped

(54:32):
by evolution to live aparticular time.
And all of that comes back tothe successful reproduction of
new versions of humans, becauseevolution doesn't want our
bodies to live forever.
That's not a failure ofevolution.
It could if it wanted.
Rather, it's trying to justrenew the cycle of being.
So reproduction is important.

(54:53):
Now, I say that because whetherthat doesn't mean that you have
to have children.
That's just evolution's goals.
Your goals as a human can betotally different, right?
Totally different.
But it's important tounderstand these things because
it does shape what we understandabout like why how we live and
when we age.
Now, aging, yes, these thingsdo decl occur, these declines,

(55:16):
but we still have enormous valueto society by accumulating
wisdom and knowledge.
Our body is just no longerputting that much energy and
resources into maintaining fullhealth, which is really useful
for signaling health forreproduction.
Now it starts to prioritizeother things like accumulation
of knowledge so that we canshare that with younger

(55:38):
generations.
That's a really cool outlook.
And you still have to work hardat it, uh, you know, at being
healthy so that you can do yourjob and take care of society.
So that's a little extracontext there, not exactly
related to your question.
But going back to stem cellsand what we do is that we are
trying to maintain balance.
We're not trying to say we knowbetter than the system and

(56:00):
we're gonna constantly push outstem cells.
And so, yes, there are thingsin our formula that will improve
proliferation, whichproliferation expands the
numbers of stem cells throughdivision.
And then this is gonna maintaina steady pool of stem cells to
meet our ongoing repair needs,of which we have many.
Okay.
Then there is the activationside, and that's gonna wake up

(56:22):
the dormant cells in their nicheand put them into action.
And that means that basicallymore stem cells are ready to
repair tissue after stress andinjury, right?
So there's making more, and nowthere's waking them up, and now
we have to mobilize them.
So there are there's there'senough of them there, they're
ready to go, and now we got toget them to where they need to
go.
And so mobilization moves thestem cells from, let's say, bone

(56:45):
marrow into circulation or fromtheir like resident pool into
the circulation.
Um, and then that means thatthey can have much wider
distribution.
So the repair signals canactually reach the tissues.
Then they migrate into the newarea where it's needed, and then
they differentiate.
We talked about all of that.
And then, of course, there'sprotection, right?

(57:07):
So another thing that weconsidered in the formulation
generation in creating ourformulation is how do we protect
and shield those stem cellsfrom oxidative damage, DNA
damage, cellular senescence,other hallmarks of aging, and
keep them healthy, right?
And the real effect there isbasically longer lasting and
healthier stem cell functionacross the lifespan.

(57:30):
And then, of course, we alsowant to support and promote
self-renewal, which is, if youremember, the two hallmark
characteristics of stem cells istheir ability to make a make a
copy of themselves, and then theother is to differentiate into
tissue.
Well, we also we've alreadytalked about and seen areas
where this step, the stem cell,because of inflammation, can
actually make a newdifferentiated cell.

(57:52):
It can make a tissue cell, butit can no longer self-renew.
That's going to shut down therepair capability of the body.
So those are all of the thingsthat we considered when we
thought about making ourformulation.
And four days a month is atime, you know, like you said,
we don't really want to be doingthis in perpetuity day by day.

(58:12):
We want to have a pulse thatstimulates all of these
functions.
And then we go back and letstem cell homeostasis maintain
itself.
So our vision is that 12 timesover the year, you take this
product and the net result ofwhich is better repair and
renewal.

Sandy Kruse (58:30):
Okay.
So that's that's really the keythere.
So if I'm somebody uh with I'm55, of course, I've got some
things that, you know, littlethings here and there that may
not work as efficiently as theyused to, or some old injuries.

(58:50):
Um, I can take this.
Really, the goal is to take itonce a month, four days a month,
and I should overall feel what?
What should I feel?

Dr. Dan Pardi (59:05):
Yes.
So this is a uh an importantquestion to address because with
I've been thinking aboutcategorizations for our products
since I've been here.
And there's really threecategories that I see.
So there are the first categoryis what I what I call health

(59:25):
perform performance promoters.
And what that means is thatyou're trying to do something
now, and our product is going tohelp you do that thing that
you're trying to do now.
So quality of mind helps youthink today, right?
Quality of night helps yousleep tonight, right?
So that is helping you in thehealth related performance of a

(59:46):
particular activity.
Health span is now looking toaffect more of the longer term
effects of elevating healthlonger into the lifespan.
So that you might say, allright, well, my I have a higher
level of health than I wouldhave if I was not doing these
activities, right?

(01:00:06):
Of which stem cell support canbe one of them.
And what might you feel?
Well, you actually if you'rehaving achy feet or you know,
sore knees or sore joints, youmight feel that they are not
barking at you, you know, thatyou feel um that you feel more

(01:00:28):
youthful in that regard.
Um, you might notice your hair,skin, and nails feeling more
vibrant, youthful, less old.
Um, because what remember, youknow, the the decline in repair
means your body is going to thenstart to wear the signs of
aging.
And if you can bolster repair,you might actually start to see

(01:00:49):
some of these tissues that lookright back at us in the mirror,
start to look younger again.
That is, you know, our our hopeand goal with this.
Now we have done um one thingI'm very proud about uh for my
company is that we uh always tryto do research on products that
we introduce into the market.

(01:01:09):
So instead of just makingclaims, we say, all right, how
can we test this to see if ourideas like the the science
science fills every aspect ofour development process?
So what are the what are theideas upon which the formulation
we make is created?
We talked about that, right?
Do we want to always bestimulating stem cells or do we
want to possibly be like lookappreciating and respecting the

(01:01:33):
full life cycle, right?
That was a part of thescientific process.
Then it's the all right, well,what ingredients can do that and
why we have 15 differentingredients in our product, all
of which, you know, some ofwhich are affecting more, most
of which are affecting multiplestages of the stem cell balance.
Um and so that was a whole, youknow, we screened hundreds of

(01:01:56):
compounds.
And then we have to make it'ssort of the art of formulation,
some determinations that say,okay, I think the this group uh
is really well supported for ourpurposes.
And then with the last stage ofthat is then saying, all right,
well, now we're gonna put thisto the test.
And typically what we do is westart with, like with all

(01:02:18):
research, you start withsomething that is uh easier to
implement, like a survey, andwhich would at this point we
have conducted that, which isreally important.
Get it to the hands of peopleand see what they say about it.
What do they feel?
Did they like it?
Did it cause any untoward sideeffects that we should know
about?
Um, and then we might go into apilot trial, which is like an

(01:02:38):
open label type of a researchstudy where we it has more
controls over it than a survey.
And then we move into adouble-blind placebo control
study where now we are using thegold standard methods to assess
the efficacy of our products.
And that is a process thatbuilds over time.
But I'm very proud that we dothis and we do this for all of

(01:03:00):
our products.
And in fact, Qualia just wonthe Science and Innovation Award
from the National Um NutritionBusiness Journal.
And we feel really proud aboutthat.
Um they gave it us that awardis because of the of the
approach that we take to uhformulating and testing the

(01:03:20):
products that we bring tomarket.

Sandy Kruse (01:03:22):
Yes, and safety too.
Because you know, okay, Dan, Iknow you're extremely, you know,
scientific.
I respect that.
I am very much that person mostpeople who follow me, they know
I'm like, I'm a little bitscience, I'm a little bit woo,
you know.

(01:03:42):
I'm I kind of I I sway and Iactually test, you know, muscle
test for supplements.
I have never ever, I I've hadsituations where I'm like, no,
my body doesn't like that.
And um because I'm such a bigbeliever in bioindividuality,
and I will say I muscle testextremely strong.

(01:04:05):
That's not to say anybody elsewill like I'm I'm just saying
for me, because my audienceknows I'm gonna be honest with
integrity and talk about qualityof supplements.
I have had other situationswhereby I'm like, I will not
touch that, I won't put that inmy body.
I'm very choosy about what Iput into my body.

(01:04:26):
So I trust qualia'sformulations.
I've been connected with youguys for many years.
And you know, we're we we gottawrap up because we're like, I
don't know, an hour and 10 now.
So, and and I am running out ofbattery.
My husband was working in myoffice and I think he unplugged

(01:04:46):
something.

Dr. Dan Pardi (01:04:47):
Uh-oh.

Sandy Kruse (01:04:48):
This is why I don't like people working in my
office.
Um, but I do want to ask you ifthere's uh if there's anything,
because I I just want toquickly touch on the the
synolytic with the stem cell,because I've used both and
people like to stack.

(01:05:08):
Yeah.
How do you stack with the two?
Because I know Cynolytic maybequickly describe what a
Cynolytic cell is.
I don't know if you can do thatquickly though, Dan.

Dr. Dan Pardi (01:05:19):
I will do my best.

Sandy Kruse (01:05:21):
You know, yeah.

Dr. Dan Pardi (01:05:22):
Uh, I think you could tell just how interested I
am in all of this stuff, andsometimes that means I can be a
little wordy, but it's amazing.
I really think as as Imentioned previously, that the
the best effects are likelygoing to become are going to
come from stacking, not likelyare going to become from
stacking different productproducts that target uh

(01:05:45):
different hallmarks of aging.
So I think that thiscombination of our synolytic
followed by our stem cellproduct makes great sense.
Here's why.
Senescent cells are aptlydescribed like zombie cells.

(01:06:07):
They partially die, but notfully.
And that actually has there's abiological cause for that.
So they release a lot ofinflammatory markers into the
surrounding.
Uh, and then that triggers tothe immune system to come clean
them up.
But as we as we get older, weundergo immunosinescence, which
means our immune system is lessgood at doing its job.

(01:06:29):
So now you have what do youthink that leads to?
An increase in senescent cellsthat then rise the state of
inflammation in the body, thatthen suppress stem cell
regeneration.
Okay.
So what we do, what I do everymonth is I take qualia
synolytic.

(01:06:49):
It's you take it two days in arow and then you wait a month.
So I do the first Saturday andSunday of every month.
I take synolytic and then Iwait two days, right?
And that what that does iswithout going into all the
details, that actually is acombination of nine products
that is designed to cause stemcells to be cleared.
A synolytic is a senescent cellkiller.

(01:07:12):
Okay.
And we want that.
So we want to get rid of those,particularly since our immune
system is not doing it as well.
After that, inflammatory, youknow, the because you're killing
them, that's going to releasecontents into their surrounding
space.
That's going to rise yourelevate your inflammation for a
couple of days.
So you let a couple days go by.
So two days later go by, andthen you start stem cells.

(01:07:32):
So you've now lowered yourinflammation overall after
getting rid of those stem cells,or excuse me, the synolytic
cells.
And that's a perfect time tonow boost your senescent cell
regeneration.
And what's a what's a potentialbenefit here that's not been
shown in research, but the uh,you know, conceptually it makes
great sense, is that when youhave better functioning stem

(01:07:54):
cells, that is going to improveyour immune system.
Right.
So you're going to get sick lessoften, but you're also going to
help clear out senescent cellsbetter.
So just like the hallmarks ofaging create this vicious cycle,
counteracting them can create avirtuous cycle, where now
you're promoting betterfunction, which is, of course,

(01:08:15):
extending the higher level ofhealth deeper into how long you
live, which is awesome.
And so during that time, wealso, so NAD is a product that
we have, which is supportingNAD.
NAD levels is this crown jewelof our metabolism.
And we have massive amounts ofthese reactions that are taking

(01:08:37):
place in our body every singleday.
And our those levels decline.
And so our energy levels startto decline.
And when so NAD boostingproducts help to raise those
levels back up.
So what uh Greg Kelly, ourchief product officer, does is
he actually takes double thedose of our NAD product during
the days he takes our stem cellproduct and then goes back to a

(01:08:59):
normal dose for the rest of themonth.
So you can see that some of ourproducts you just take once a
month in varying days, synolytictwo days in a row, uh, stem
cell product four days in a row,and then NAD every day.
And I have those onsubscription, so you don't have
to even think about it.
You just get it in the mail acouple of days before when
you're going to take it.

(01:09:20):
You take it, and then you waitfor the next month.
So that protocol, I think, is avery advanced protocol for
helping us age better.

Sandy Kruse (01:09:29):
I love it.
I love all your wisdom.
Oh my God.
And and passion.
Thank you so, so much forspending time with me today.
I'm really, really honored tohave met you.
You're wonderful.

Dr. Dan Pardi (01:09:44):
Oh, thank you so much, Sandy.
It's been a delight.
I hope this information wasvaluable.
I really care about helpingpeople.
And um, you know, kudos to thelisteners for you know showing
up, paying attention, learning.
Keep doing it.

Sandy Kruse (01:09:58):
Yeah, yeah.
Thanks, Dan.
I hope you enjoyed thisepisode.
Be sure to share it withsomeone you know might benefit.
And always remember when yourate, review, subscribe, you
help to support my content andhelp me to keep going and bring

(01:10:22):
these conversations to you eachand every week.
Join me next week for a newtopic, a new guest, a new
exciting conversation to helpyou live your faster life.
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