332: Resiliency Radio with Dr. Jill: Infections & the Brain: Inflammation Drivers - Nikki Schultek
Watch on YouTubeVideo summary
Nikki Schultek, the Executive Director of the Alzheimer's Pathobion Initiative (ALZPI), shares her journey from being misdiagnosed with multiple sclerosis to recovering from Lyme disease and co-infections under the care of Dr. Charles W. Stratton. Her experience revealed that many autoimmune conditions are actually driven by persistent intracellular infections rather than primary autoimmunity, a concept central to her work as a "collaboration architect" who bridges gaps between researchers, clinicians, and patients. Pathogens such as *Chlamydia pneumoniae* and *Mycoplasma pneumoniae* can infiltrate cells, steal mitochondrial energy, and prevent programmed cell death, creating "zombie" immune cells that trigger neuroinflammation through heat shock proteins. This process mimics the plaques and tangles seen in Alzheimer's disease, representing the body's failed antimicrobial response to these ubiquitous infections often missed by standard IgG titer tests that only indicate past exposure.
Schultek introduces the concept of the "pathobiome," describing it as a pathological ecosystem where pathogens, toxins, and immune dysfunction interact within the body's terrain, disproportionately affecting women. Through the ALZPI global consortium, researchers utilize unbiased sequencing technologies to map pathogen loads and immune responses in infection-associated brain diseases, including Alzheimer's, Parkinson's, ALS, epilepsy, and PANS/PANDAS. Her work highlights that infections like the Epstein-Barr virus are causally linked to conditions such as multiple sclerosis, urging the scientific community to integrate clinical observations with data to accelerate effective therapies for these complex chronic illnesses. By focusing on direct detection tests for chronic respiratory infections linked to asthma and long COVID, the initiative aims to shift medical understanding away from treating symptoms alone toward addressing the underlying infectious drivers.
Dr. Jill concludes the discussion by encouraging clinicians to explore Nikki Schultek's research and visit her website to understand how this consortium is advancing medical discoveries and transforming clinical practice. She urges patients to educate themselves, ask informed questions, and seek out providers capable of assisting with complex chronic infections, particularly those manifesting as neurodegenerative diseases. The host emphasizes that Resiliency Radio seeks to highlight field researchers who drive foundational change without seeking personal glory, inviting listeners to engage by commenting, sharing the episode with interested individuals or their doctors, and tuning in next week for a new installment of the show.
Read the full video transcript
Hey everybody, welcome to Resiliency
Radio. Your go-to podcast for the most
cutting-edge insights in integrative and
functional medicine. I'm your host, Dr.
Jill, and with each episode we dive into
the healing heart of functional
medicine. I bring you innovators,
medical experts, and today a researcher
that you may have not heard about but
who is doing great work with
collaborations on infections and chronic
illness, especially as to do with the
brain. If you or a loved one has been
diagnosed with dementia or you're
concerned about your brain health, uh
look no further. You are going to love
this episode with Nikki and all of her
collaborations. Um she talks about
herself as a collaborative architect,
bringing people together to do the
research to give us as clinicians
foundation. So stay tuned, you're going
to love this interview. Before we jump
into the interview, I want to remind you
that you can find products and services
for your brain health, for your gut
health, and all things in between at
drjillhealth.com.
Some of my favorite brain products are
the BDNF Essentials and the CogniCare.
Um I also love the Brain Mag, which is
part of our pink drink, uh Dr. Jill's
pink drink, the thing I drink every
single morning. Check those out at
drjillhealth.com.
And if you haven't yet seen the
documentary, you can check that out at
doctorpatientmovie.com.
It's now also streaming if you have
Amazon Prime, which who doesn't
nowadays, you can catch that Dr. Patient
Movie there um with your subscription to
Amazon Prime.
And finally, if you are looking for a
functional medicine provider for complex
uh complex chronic illness or mystery
symptoms, you can uh call our clinic. We
are accepting new patients. Our number
is 303-993-7910,
or you can uh email
info@flatironfunctionalmedicine.com.
Okay, let me introduce Nikki, who is
executive director director of the
Alzheimer's Pathobion Initiative, ALZPL.
Um she's also principal founder of
Intercellular Research Group and
founding director of the PathoBiome
Research Center at the Philadelphia
College of Osteopathic Medicine. She
earned a BS in Business Administration
and began her career with Pfizer and
Genentech. Following her own recovery
from Lyme disease, which you'll hear
about in this episode, Nikki dedicated
her work to advancing research into
infection-associated chronic illness,
including Alzheimer's disease, PANS and
PANDAS, and asthma. Um, you're going to
love this interview. Um, let's jump
right in with Nikki and join the show.
Nikki, I am so excited to have you on
Resiliency Radio. We talked just briefly
before we started this interview and
what I love about you is you're bringing
this whole other area. I deal with a lot
of medical doctors and experts on the
brain and Alzheimer's, but we're all in
this field seeing these clinical
manifestations
and um, trying to make sense of it with
the current research. You're out here
making a difference in the world of
research, giving us data, and actually
validating what we're observing in
clinical science, which is the brain is
so much more complex than we thought.
Plaques are not the whole answer, and
there's a whole brain microbiome that's
affecting our brain health and many
other things that you'll talk about
today. I couldn't be more excited to
have you on to talk about your research
and I get especially excited to talk to
researchers because again, I'm in my
clinic doing patients one-on-one, but
you're out here paving the way for what
we see in clinical practice. And one of
the things you talked about that I love
to start with is how you're really this
hub of bringing together people who
might not otherwise talk to one another.
How did you get into this field? Give us
a little bit of your journey.
>> First of all, thank you, Dr. Jill, for
having me. I'm thrilled to be here. Um,
I absolutely love your energy and I love
the way that you just anchored the start
of our conversation. So, you're seeing
patients, right? You're you are a
practitioner, clinician, boots on the
ground dealing with the type of patients
that our team, our global consortium is
studying, right? But in fact, how I got
here is I'm a patient. So, I was
extraordinarily sick and um was
misdiagnosed for about a year. I ended
up finding out that I had multiple
chronic infections including one that
people commonly know as Lyme disease.
Um a bacterial infection transmitted by
tick bites and other means um that I
contracted along with co-infections. I
also uh ended up learning in this crazy
journey of a year of horrible one after
the next autoimmune diagnoses that I
also had a chronic respiratory tract
infection uh that I had never heard of
called Chlamydia pneumoniae and that's
really that one bacterial infection is
sort of how I arrived on the scene and
decided to start bridging silos and it
all began uh of course figuring out that
I was sick with these infections, right?
Finding a doctor that could accurately
test and diagnosed me, treated me um
using antimicrobial therapies in a
manner which frankly at the time
initially made me very uncomfortable. Uh
the idea of aggressive antimicrobial
therapy. I had a background uh working
for Pfizer and Genentech and at one time
I worked in an anti-infective space
calling on microbiology labs in
hospitals. So, I a lot of people hear
the word resistance, right? Which
antimicrobial drugs not working any
longer because the germs figure out a
way around it because they've been
exposed to it.
So, I had these concerns, yet I was
being faced with life-threatening
symptoms. And my kids were three and
five, right? I'm a mom.
I was completely incapacitated. One of
the things in my diagnosis that uh was
disturbing, the differential diagnosis,
was they feared I had multiple sclerosis
based on my symptoms.
>> Yes.
>> Now, I do not have MS. I didn't have
lesions on the MRI, but the neurologist
at the time in Connecticut said, "This
doesn't mean you won't get it. I see
patients like you all the time where you
smolder and you have these symptoms and
the symptomatology leads to lesions."
And so, I left just like absolutely
terrified, anxious.
And I had developed cognitive symptoms,
too. Now, I was in my early 30s. So,
what I decided once I got on treatment
by an infectious disease specialist and
medical microbiologist at Vanderbilt
named Charles W. Stratton, who
specialized in this chronic bacterial
infection of the lung called Chlamydia
pneumoniae, not the sexually transmitted
Chlamydia, but a cousin
>> Yep.
>> of that germ that you get when someone
coughs and you inhale it,
you know, he had looked at that germ
from the vantage point of, "No, not just
an acute infection, but chronicity." So,
the idea that it could take up residence
and now you have in an area of the body,
whether it's the lung or the bladder or
the brain,
>> Mhm.
>> that it could be creating inflammation.
And we all know inflammation is bad,
right? Most diseases go back to
inflammation that are chronic.
So, I got treated by Dr. Stratton.
And it was funny, as soon as I started
to feel better, I said to him, um he
asked me to call him Chuck. I was
reluctant at first. I'm like, "Okay,
fine, if I must." He's like, "Please
call me Chuck. Um don't call me Dr.
Stratton." So, I was like, "Okay,
Chuck."
He said, um you know,
I I right, what I basically said was,
"What are we going to do about this? You
know, like this is major. Like I had had
multiple devastating conditions,
including this severe and refractory
asthma, go into remission with
antimicrobial drugs." And it turned my
perception of autoimmunity on its head.
And I said to him, "Don't you just want
to scream from the mountaintops with all
these publications you have and other
people? Autoimmunity is is under, you
know, under poorly understood, poorly
characterized. We have chronic
infections, right? Not a hit and run,
it's a continual hit. It's an accident
over and over. So, he said, "Yes, but he
said, "Take it easy. You're not all the
way better yet. This treatment is going
to be a long road." So, he he
you know, encouraged was encouraged by
the fact that I wanted to help. And as
soon as
I was well enough, I decided I needed to
just start contacting these people
studying infection and chronic disease
and introduce them to each other cuz
they reference each other in their
papers. You know, they'll write a
scientific paper.
And so, I said to Chuck, "Have you ever
had a meeting with Dr. David Hahn who
studies asthma in the same bacteria?"
"No, we never sat down for a meeting."
"What about John Carter in Florida?"
"No, we haven't." Um you know, it's
like, "Yeah, I did meet Dr. Brian Balin
once who studies the role of that
bacteria in Alzheimer's." So, we started
getting together the main cast of
characters studying that one bacteria
and chronic disease. And from there, I
start, of course, becoming tangential in
the reading.
And I myself knew that I had been
diagnosed with Borrelia burgdorferi
which can also cause some of the same
disorders that Chlamydia was linked to.
Yes.
>> Yes. Yes.
>> You know, including bladder pain. I had
a diagnosis of interstitial cystitis
that was brutal, but it went into
remission. I remain in remission. I
don't have it anymore. So, that's how
this all sort of began. And the idea to
be a collaboration architect, to bring
scientists together and physician
scientists that have patients, and
people in the lab, and data scientists,
and all different types of domains.
People studying fungus, bacteria,
viruses, parasites,
animals, you know, veterinarians. We
work with Dr. Ed Breitschwerdt at NC
State. The idea behind it was that
everything is so siloed, and the body is
not. It's an ecosystem, right? And we
are very much the brain, especially, has
been thought of as this sort of like
off-limits area, right? And this blood
brain barrier is this impervious shield.
Nothing can get through it. It's
not really the case. And the brain is
interacting with the gut.
>> Mhm.
>> And the brain is also subject to insult
from infections.
>> Yes.
>> And not just things that create a
cytokine storm and hurt the brain from
the outside, but things that can
actually, like a Trojan horse, inside
the very cells that are made to protect
us, our immune cells, it can enter some
of these pathogens and then go right
through like they're just crossing the
George Washington Bridge into Manhattan.
So,
um
So, the idea of bringing these different
people together was really like, okay,
no one's listening.
>> Mhm.
>> You know, decades, you know, there have
been
so many different research teams
publishing papers. Let's just take the
example of Alzheimer's and infection.
Since literally the 1980s.
And even actually before then, Dr.
Alzheimer himself, you know, the
gentleman from which the disease is
named,
published a paper in the very same year
as another scientist named Oscar
Fischer, 1907.
Most people don't realize that this
could have very easily been called
Fischer's disease because their results
were neck and neck in publication.
They both were
living in a time when syphilis, sexually
transmitted infection, in the same
family as Lyme disease. These are
spirochetes,
literally
you know, like a corkscrew.
Um everyone knew that if you got
syphilis and it advanced to tertiary
syphilis or severe infection, it could
get in the brain and cause a dementia.
>> Mhm.
>> Well,
it was really interesting because Dr.
Oscar Fischer, and even Alzheimer
himself, acknowledged the possibility
that there was an infectious component
when they went ahead and saw the brain
of someone that died with the disease
and saw plaques.
>> Yes.
>> These tangles, they said, "These almost
resemble bacterial colonies." And isn't
it's very ironic because today, on my
team, you know, we have this Alzheimer's
Pathobion Initiative Consortium, a
global, multi-disciplinary team,
purposely as diverse as it can be, with
backgrounds even patients, you know,
like myself, people that have lived
experience and also expertise in these
fields.
What some of our teammates have
discovered is that the bad guys, the
plaques, the amyloid plaques,
or, you know, the kindling of a and then
the tau tangles, these these tangles in
the brain,
uh
you know, that have been referred to as
flames, like kindling and flames, right?
These one-two punch uh in the people
that we lost to this devastating
neurodegenerative disease, may actually
be antimicrobial responses that are your
body's way of fighting something that
hasn't been appreciated. And the
research demonstrating that has now been
repeated.
>> Hey guys, just a quick interruption of
this episode to remind you, if you have
not yet got my book Unexpected, I dive
into the healing journey that I went
through with cancer and Crohn's disease,
complex chronic illness, mold-related
illness, Lyme disease, and more. Um be
sure and check it out at unexpected.com.
You can get it anywhere books are sold.
It's right behind me here on the shelf.
Um if you want a signed copy, hop on
over to drjillhealth.com and order it
there. Just put in the memo who you want
it signed to, and I will personally sign
and send you a copy of the book
Unexpected. Okay, let's get back to our
show. Now, Niki, it's so great because a
Promutter and any colleague of mine that
are really in the weeds like you are, we
know those are just bearers of what's
happening underneath and we know that
any drug that targets that is not even
effective because we're dealing with
these underlying inflammatory issues
like infection and toxin. It makes so
much sense and again, we have a lot of
providers here that listen to they're
going to love this episode with what
you've already said because so often in
my complex chronic patients that many of
them neurodegenerative cancer autoimmune
are the top three things we see.
Infection is always in toxin are these
these things that that play into the
immune system and create these
autoimmune responses and inflammatory
responses. And I love that you started
your journey with chlamydia pneumonia. I
check every single patient I suspect
with infection for mycoplasma and
chlamydia pneumonia because these
co-infections, they're actually more
common than Borrelia burgdorferi and
they are insidious. They've been
associated with chronic fatigue,
autoimmune and all those things. You can
keep going but I wanted to just
interrupt and kind of validate what
you're saying from a clinical
perspective. Uh, because every day in my
practice I'm seeing that and when I see
that chlamydia pneumonia, I know we have
to be treating it.
>> Yeah, uh, I really so appreciate that
because like you said Dr. Jill, it's so
prevalent. So by the time people reach
middle age, like 50 to 80 years old, the
prevalence, like if you do population
wide studies of blood indicates that
it's
similar to herpes viruses which are
ubiquitous meaning everybody nearly
everyone has them upwards 80% and then
as old the older you get um, you know,
one of my colleagues cracked a joke and
said, "Yeah, you get old and we each are
becoming a germ bucket year over year."
So it's kind of funny [laughter] but
I'm like and I certainly feel that way
with my own experience with mycoplasma
pneumoniae.
>> Yep.
>> Like lifelong asthma that was way out of
control and you know, these um
it's so key to look for these infections
but yet it's it's not something that the
average practitioner even thinks about.
Um, they're not testing for titers to
chlamydia and mycoplasma. We really need
um, better direct detection tests for C.
pneumoniae.
Um, and then, you know, the the thing
that that's wild about that bacteria as
an example is just how it really lines
up with Alzheimer's specifically in
terms of its behavior. So, to kind of
geek out on that bug
it goes inside the building blocks of
the body, which are the cells,
regardless of essentially any cell type
can be vulnerable to this particular
pathogen. It preferentially infects um,
the lining of your veins and vessels and
arteries like endothelial cells. Yes.
And it uh, absolutely loves immune cells
like monocytes. And and it once it's in
there, it like you know, steals energy.
It's like it plugs its little plug into
your mitochondria, your powerhouse of
your cell, and takes the very fuel that
we rely on for survival, cell division,
and for your immune cells themselves to
work properly. And then it does
something else nasty. Once your cells
are supposed to die so that new ones can
take over and they can divide and we
have a fresh set of cells, it delays
that programmed death because now it's
sort of like I cracked the joke like
that show The Walking Dead with the
zombies.
>> Yep.
>> You now have like a zombie immune cell
that should have died 72 hours ago, but
it's got a
passenger aboard that wasn't welcome in
the first place that's taking energy.
And a lot of the things we see with
Alzheimer's are mitochondrial
dysfunction,
>> Yes.
>> depletion.
Well, you have a mitochondrial parasite,
right? And other organisms can do this.
You have uh, dyshomeostasis with certain
metals, you know, like the findings of
like aluminum for example, calcium. This
pathogen can do that. Dyshomeostasis of
iron, it does that.
And then you start saying, "Hmm, you
know, uh neuroinflammation."
So, Chlamydia releases um something
called a heat shock protein number 60.
And when it does that, it's really bad
because we have that in our cells in our
brain.
And we begin to release our own Well,
it's like a matching campaign in a bad
way. Instead of like fundraising, it's
like a nasty toxic soup. And so,
when people talk about these things,
these infections, that their job is to
become chronic because they can't live
outside a human cell, it literally can't
survive without us.
You know, the idea that the pathogen has
been cleared when we know that it's as
persistent as it is, and the assumption
that it's gone from a short course of,
let's say, a Z-Pak is really a fool's
errand. And so, um
you know, it's it's been something that
our team one of the pathogens, and it's
not the only one that we're focused on
because
there's definitely a pathobiome.
And
>> lot of research too just to validate
your point on ME/CFS with these
intracellular pathogens as a primary.
So, and just to clarify, a lot of people
out there, a lot of docs, a lot of
patients know about Lyme disease. That's
very real, very prevalent. But I often
see these co-infections being just as
big of a deal, kind of like the case
where you presented your own journey.
And if they're missed, I mean, literally
docs should be checking. Let's just talk
briefly about if you know any of the
research around Right now, we do titers,
and the best that we have are some PCR.
There are some other specialty labs. But
the the general Quest, LabCorp, whatever
we have IgG and IgM. And typically, if
it's an older infection, you're not
going to see that IgM. Although,
sometimes you see that reactivate and
pop up. Um but if I see both of those
really high levels and a whole
infectious burden, I start to suspect is
there any more research on better ways
of diagnosing versus just seeing those
high IgG titers? Is that the
>> Yeah, so it just depends on the
pathogen, right? So, in the tick-borne
illness space, you have some fabulous
labs, I'm sure that you use. You know,
you
>> I'm talking just mycoplasma chlamydia
because the tick-borne, yeah, we've got
that PCR, we've got Yeah.
>> [laughter]
>> No, and we've we've had um honestly, Dr.
Jill, like I've had numerous meetings
with different um you know, diagnostic
companies
highlighting the importance and um you
know, chlamydia and mycoplasma would
make a phenomenal respiratory panel for
chronicity because they've both been
strongly associated with asthma. And
asthma is now second to long COVID, the
most common pediatric autoimmune
diagnosis and thus, I think if we caught
kiddos early in life before their lungs
remodel and get filled with mucus and
end up with lung damage like what I have
um from years of untreated asthma and
mucus and inflammation and infection,
then you know, we would have if we had a
better direct detection test, we we
don't have something like that. Now,
there are hospitals if someone has
pneumonia, so this is important. As you
know,
you can get a a bad pneumonia which
requires hospitalization from a
And if you are
fortunate enough, you know, in the sense
to be in the hospital, they can do
direct detection. Like they can look for
those organisms, okay? And so, that
would really be the only context in
which a patient would access it is if
it's going to be like your average
laboratory testing with Quest and
LabCorp, it's going to be chlamydia and
mycoplasma immunoglobulin G and
immunoglobulin M.
And a lot of times if providers like so,
let's say I'm talking to a patient that
has concerns and I say, well, that's
kind of suspicious for these certain
infections and then they go to their
primary care doctor and ask for the
test.
The test comes back with extraordinarily
high levels of immunoglobulin G for
mycoplasma. That practitioner is likely
to say this is a historical infection.
You fought this infection at one time.
It does not indicate active infection or
chronic infection and people that study
those organisms might disagree.
>> I would agree with you 100% cuz I'm
checking these and I obviously
well first thing is in my clinical
experience anyone with Borrelia I bet 90
to 95% of them have these co-infections
one or both of them so it's super
common.
But I think many practitioners are
focused on the Lyme and Bartonella and
Babesia and they're forgetting that
these also are huge players like in your
case. And if I'm seeing that there's
this piece that's not because really
right now we are a little limited with
the science. So if I see these really
high like four times normal titers I
suspect and the clinical
you know symptomology and the responding
to either intracellular antimicrobials
or sometimes natural agents. All that
together puts a clinical picture even
though all I really have is a really
high IGG, right?
>> Yeah.
>> And you're not and you're not doing
something wild or heretical. You mean
it's it's patient-centered care, right?
Because if we go back to a time before
we were so sophisticated I'm going to
put that word in quotes and we had all
of these fancy tests to rely upon.
Practitioners did have to use in some
way shape or form a little bit more
leaning on that clinical picture. You
know, hearing that patient's story
listening to the etiology of like the
onset of it. For example, with asthma a
lot of patients will say, "You know, doc
my asthma began I got a respiratory
infection. I got like a cold. I got a
nasty bronchitis and I never got better.
Now I have wheezing and and you wouldn't
believe how many people's asthma starts
that way." So
we you know, myself and my coworker Dr.
David Hahn, who's an absolute pioneer in
the infectious asthma space,
you know, we publish on that and we we
call it an easily identifiable syndrome,
infectious asthma syndrome, where if the
patient story lines up with this,
and those patients,
many of them, most of them will respond
to azithromycin therapy, um, longer
term, you know, um, in in the dosing
regimen that Dr. Hahn and others have
used in their studies is like anywhere
from 250 mg, uh, Monday, Wednesday,
Friday to 500 mg Monday, Wednesday,
Friday, three times a week cuz the drug
builds up in your system and remains
steady.
Um, but it just if infections are are
treated early,
it's so important. And then in the
future, obviously we know that
broad-spectrum antimicrobial drugs have
impact, too, that may not be positive on
constituents of the gut microbiome and
otherwise. You know, may leave people
vulnerable to certain fungal infections
like Candida. So, we do need better
solutions. And that's part of like what
we do in our team is with basic
research, right? Showing how do these
infections work together to lead to a
disease? Well, we can figure out how to
intercept. And, uh, in the future,
targeted therapies will be amazing. And
I really believe we'll get there or
therapies that are, uh, supporting the
immune system. You know, there are
different angles and ways of going about
this that we don't have yet. And, uh,
unless somebody really underscores this
problem,
um,
you know, we we won't have those
solutions.
>> I love that you mentioned that cuz I've
always talked about with like Borrelia,
I believe I would just go out on the
street and test 10,000 people for
Borrelia burgdorferi. I might find 20 to
30% of them walking around with Lyme, a
true infection, and yet they're not
super symptomatic. They may not know
they have it, maybe they feel really
good. Um, and what I've observed is it's
not a combination of just the infection
that they've been exposed to, a tick
bite when they were 12, but it's that
plus a weakened immune system and like
these sentinel cells that aren't, you
know, doing their job that have
inflammaging or um, or immune um, you
know, resilience, all of this thing. But
what happens is just like you said, you
have this antibiotic or antimicrobial
therapy, absolutely core, but at the
same time, sometimes IVIG, sometimes
beta glucan, sometimes astragalus these
other things that are actually
supporting that natural function of T
cells and B cells to help you. I find
that's kind of the perfect combo of of
really getting someone off the
antibiotics and onto a optimal life, you
know, without that infection weighing
them down.
>> Absolutely. And um, you know, and again,
to bring it back to like, you know,
vulnerable point of vulnerability for
me, I've been playing whack-a-mole with
this thing for 10 years. And I've had
um, you know, it's been such an
incredible journey of not only learning,
you know, and becoming
uh, a member of the scientific community
and you know,
going from being a patient to studying
for like a decade and diving in and, you
know, now writing grants and papers and
and getting research project projects
funded for teams all over the place.
But also going through this journey,
aging with these infections. And how,
you know, for example, perimenopause and
and has affected, you know, some of the
things that never were addressed
properly. So, for example, Dr. Jilly,
you've probably heard this before, I
initially, when I got sick, I had this
air hunger and I kept describing it to
the asthma allergy doctor and I was
like, this isn't like asthma, this is
different. This is new. I've had asthma
forever, this is not, you know, quacking
like a duck, barking like a dog, this is
something else. And
I had rib pain.
And uh,
then I had this this bout of dizziness
that was disturbing and I was like, oh
my gosh, am I having a stroke?"
And I had all these other symptoms.
Well, fast forward to now, I'm a part of
an IRB study at North Carolina State
University,
and with newer detection methods, blood
that I gave in 2021 revealed that I have
Babesia microti.
>> I knew it. I was going to say Babesia.
>> [laughter]
>> So, yeah, and you know, and then so I
never like, you know, to my community of
chronic illness patients that and people
that might be listening that you know,
relate to a story like mine in some
ways,
you know, as a patient, is that I'm
still learning and the science is
catching up and you know, I started
working with an I LADS doctor in
December, or I'm sorry, last August, in
December initiated treatment for
Babesiosis very slowly because when
you're treating for this red blood cell
parasite, you can actually lose too many
red blood cells, right? Because like the
Chlamydia organism, this is living
inside a red blood cell. Yuck. I don't
want anyone hanging out there. Thank you
very much.
So, I had some of these symptoms that
Dr. Jill, because I think of
perimenopause and the reduction in
estrogen and the changes my body is
going through,
plus a
term I want to throw out there that we
think is really important and you
alluded to it, but immunosenescence,
which is my immune system's getting
older.
>> Right.
>> Everybody does, by the day. So,
you know,
my husband and I joke, you know, he's
healthy as a horse, doesn't take, you
know, participate in any of my vitamins
that I'm suggesting, no pills,
runs these races, uh
has likely been in contact with just as
many tick bites as I was in Connecticut,
and
may have Borrelia on board. We haven't
tested him. Some people tolerate
infections, and we know this already,
right? So, it's just like, you know,
there are certain individuals who
got COVID, I guess the most modern
example or poignant one now is people
that got COVID, barely got a sniffle,
got better, moved on with their life, no
problem, fine.
>> Yeah.
>> Some people got COVID and are
debilitated still. They're in bed.
They're in a dark room with a new
diagnosis of ME/CFS or,
you know, some horrible chronic disease.
And, you know, many of the practitioners
have noted that these people have
co-infections. And so, with COVID, it
appears that there's uh a level of
immune suppression.
>> Yes.
>> And, you know, when you bring the immune
system down just that much, and let's
say you were somebody tolerating your
Bartonella, your Babesia, your, you
know, Chlamydia, you were coexisting
with it at one point in time. And that's
why we're called the Pathobiome
Initiative, by the way.
>> I
>> So, love that, Niki. And I want to speak
to if you don't know Amy Proal, she's
got a research um
I'll leave um uh
>> Allie Bio.
>> Yes, yes. I was like, I bet you you
either know each other or should know
each other. I've interviewed her on the
podcast, but what I loved is she was
bringing um validity to what we were
again just like you are to overseeing
the clinical practice. And one of the
things we saw post-COVID was I call kind
of call it the triad. Um we would have
decreased in uh cortisol and adrenal
dysfunction. So, often a fatigue
specifically associated with
the thyroid axis, like hormonal axis.
But, T cells, kind of like this
inflammaging, would retain spike
protein, and these macrophages would
hang around. They should be dead and and
dysfunctional, but they're just hanging
around like those zombies and
dysfunctional. So, this T cell ability
to fight the innate immune system, these
infections keep them down, was really
impaired post-COVID. And then, B cells
would get overactivated, start the
autoimmune chain. So, it was real
common. And then, Amy brought to um to
the forefront with her research that
typically, there was this reactivation
of Epstein-Barr or Bartonella or Babesia
or Borrelia, all the big Bs, right? The
triad that we see so often. And so
often, when I'm seeing this long COVID,
I'm like, "Okay, do you have retained
dysfunctional macrophages where your T
cells aren't working? Do you have
reactivation of Bartonella, do you have
And when we find that or even these
atypicals like Mycoplasma Chlamydia,
those are some of you. And so very
frequently, I'd guess 80% of these long
COVID patients are this combination of
exactly what we're talking about.
Someone who was functioning over here
and then dropped below the way radar and
then it started hit doing the
whack-a-mole that you described of
infections popping up and their immune
system has just been kind of trashed.
And so then we try to figure out, okay,
do we need to treat those infections or
restore immunity or both? But it's so
relevant.
>> And yeah, I'm super familiar with their
work. I think what Polybionics you're
doing is phenomenal. We're thrilled to
have them out in the ether with us. You
know, we have
very synergistic work and you know, it's
just it's like an incredible time.
Honestly, like I in 10 years have never
had
more genuine hope that we are sitting on
the verge of a tipping point of things
changing. But you know, the the
pathobiome concept that we talk about,
people will be like, well, what's the
pathobiome? And it's a great question
because it's a relatively new word.
Hasn't been around forever.
>> describe that and talk cuz we talked
about biofilm stuff. We've talked about
all this stuff that is so fascinating,
but let's kind of focus the last, you
know, 10 minutes or so. This I want to
know what is the Alzheimer's pathobiome
initiative and then also help us link
this to the brain cuz I know a lot of
people are wondering
could I get Alzheimer's? Could I get
dementia? Is there an infection
involved? I'll let you go with it.
>> Yeah, so this Alzheimer's pathobiome
initiative global consortium, it's
multidisciplinary and we actually don't
just study Alzheimer's disease. So
Alzheimer's is a very it it's it's a
catch-all for a lot of different things,
right? It's a
description of a form of dementia. So
the dementia is the umbrella underneath
it. Alzheimer's is the most common form,
but then there are others that people
have heard of like frontotemporal
dementia, vascular dementia. Um then
there is Parkinson's disease that has
some overlap. Um like in the brains of
patients with Alzheimer's, you may also
find some of the Parkinson's disease
uh bad guy pathology, alpha-synuclein,
which may also be a response to
infections, by the way.
Um and then you have other brain
diseases that have similarities, and we
study those, too. So, we look at We're
studying PANS/PANDAS, which are the
pediatric autoimmune neuropsychiatric
disorders associated with infections. Um
PANDAS refers to specifically strep
infection, whereas PANS refers to kind
of like dementia's the umbrella. PANS
refers to that this can be from long
COVID, can be Lyme, it can be
mycoplasma, chlamydia, cytomegalovirus,
a whole lot of other things can trigger
these um symptoms in kids.
But we also are looking at uh ALS. We're
studying epilepsy. So, our team is
looking at infection-associated brain
diseases.
And studying them in a
uh holistic and integrated fashion,
sharing specimens among different labs,
studying the same cases, the same people
that we lost to one disease, uh being
looked at using multiple different
sophisticated technologies, and we're
looking for a few things.
We're looking for uh infections.
And we're doing so in
using very specific approaches, also
unbiased approaches that look for
everything that's there,
um using technologies like uh something
called sequencing that will map out DNA,
uh which is the genetic material from
pathogens or germs. And then we also are
looking at the immune response.
>> Mhm.
>> We are also in women, because many of
these diseases target women
disproportionately, 2/3 of Alzheimer's
and 2/3 of multiple sclerosis. Two
infection associated brain diseases that
target women.
We are looking at what happens in the
context of hormonal shifts. What happens
to the immune system? What happens to
pathogen load to the pathobiome, which
the word pathobiome just to step back
for a second is really key. We chose
that very intentionally even though we
knew people might not know what it means
yet. Because okay, the microbiome is a
word a lot of people have heard of,
right? And when I hear that word, I
think like Kumbaya. Like it's all the
the gut bacteria are happy. I have a
healthy microbiome. The word microbiome
I feel like has like a positive
connotation
for me. I don't know if that's true for
you, too. Um
and pathobiome has the word pathological
woven into it, meaning troublesome.
>> Yes.
>> And it doesn't just refer to the germs.
So yes, I can I call it, you know,
organized crime. You get to a certain
point where the immune system is
malfunctioning either due to an
infection or due to some other
element of aging, hormonal shifts,
exposure to mycotoxins, you name it. Any
of the insults that can We call that the
exposome, the things that you're exposed
to in your life. Um chemicals at work,
you name it. Something brings you down
and now all of a sudden you have
disproportionate numbers of bad guys in
the community.
You have uh like a mafia or a mob type
situation. And we even know that certain
of these bad pathogens collaborate with
each other
>> just like my team collaborates.
>> Yeah.
>> And we don't want that. Um so the
pathobiome takes into account not only
the community,
but the terrain.
And it it refers to also the health of
the immune system. So our team feels um
you know, and we're not the only thing
that we should be looking at. Like the
stuff that we're interested in I I mean
that's this is what we are studying, the
role of infection and the immune
response to infection in the diseases
that target the brain that are
neurodegenerative, neuropsychiatric,
and otherwise, but we also think that
other ideas should be welcomed at the
table because
let's take Alzheimer's for example.
Billions and billions of dollars have
gone into developing therapeutics and we
still don't have something that is truly
effective, affordable, safe,
uh accessible to most patients. So, we
just essentially feel that we know
enough already that infections have been
strongly linked with a variety of
neurodegenerative diseases and the
linkage between MS and Epstein-Barr
virus is so powerful
>> Yeah.
>> that it's
you know,
now when you read the literature on it,
the word causation is used.
>> Yes.
>> You know, people used to say often
association, right? It's It means it's
in the ballpark, it may not be causing
it,
but now the the research is just so
compelling
that Epstein-Barr gets involved, you
know, this huge military database study
revealed that essentially if you did not
get Epstein-Barr, you didn't get MS. And
that's wild. So, it's
>> You know, we have to start using common
sense, right? Where
you know, like a lot of what you
probably do every day with your
patients, which is you look at the
person, you listen to their story,
you're leveraging quite a bit of common
sense and experience, right? On top of
data that you get from lab tests. And we
feel that we should be doing this as a
scientific community also.
>> Wow, this is such a great It's just so
exciting to me because here you are
bringing people together and this
multi-collaborative group, um what do
you call it? Architectural
collaboration? You have some really cool
words in there, but it's just
>> call it collaboration architecture
because
>> [laughter]
>> I couldn't think of a way to describe
what I do, um you know, um
and and I was hoping that it could
become a thing, you know, that other
people that are adept at, you know,
reading broadly and enjoy tangential
learning and science and then can also
socialize with a lot of different people
and build bridges, you know, and and
form alliances that that people could do
this. And there are other people that
like myself, you know, patients with
lived experience that leverage business
skills or other acumen that they have
and and get involved. So, thank you for
saying that, I mean, it's
>> Yeah, it's so exciting because it's
what's needed for even clinicians. We
need to start really collaborating
because there's so much that we're
seeing and as we share stories and share
what's working and talk to So, to me
it's a super exciting cuz on this level
you're bringing the information down
trickling down to us in the clinic, you
know, seeing the patients and and giving
validation to some of the things because
truly the average research back in my
medical school days, you know, say
something was started to be seen as a
pattern, it'd take 20 or 30 years for
that to get into clinical practice. We
can't wait that long. So, you're really
accelerating the pace with your work. If
you want to find out more about you, the
the lab, the work, the all the different
things, what is the best place where
they could come
and maybe even donate money to the to
the cause? I mean, by all means I would
love to see that happen.
>> Yeah, so we have So, my research center
at the Philadelphia College of
Osteopathic Medicine, a medical school,
is called the Pathobiology Research
Center and it's www.pcom.edu
back back splash PBRC. So, like
Pathobiology
>> in the links, guys. If you're driving or
whatever, or you all include that, but
yes, [laughter] I will.
>> Um, so the university center, you know,
uh, PCOM is my collaboration hub and it
is a nonprofit, so donations can be
made. Um, there's like a giving page for
PCOM. Inquiries can be sent directly to
me and then I can send people, you know,
along to a place where they could
donate. We also uh have a website for
the consortium, so that's alzpi.org.
So, it's alz like Alzheimer's, p like
pathobiome, i like initiative.org.
And there, there's a whole collection of
education podcasts, symposia,
publications from our team, and um
really that website is definitely geared
toward clinicians and researchers and
and life sciences professionals. Um but
I do get a ton of emails from patients
all the time cuz I've shared my story so
widely, and I'm always happy to provide
resources. I'm not a practicing
clinician, I'm not a doctor, um but I do
frequently recommend that people that
suspect they have infection-associated
chronic illness find a doctor like you,
Dr. Jill. Um you know, that I often
offer people the ILADS, the
International Lyme Associated Diseases
Society, or for pediatric cases, uh the
MAPS.
>> Yeah.
>> And um you know, which both have
provider searches. And then, of course,
there are, you know, the Dr. Bredesens
and uh Dean Ornish, uh
Dr. Per- Perlmutter. I feel like I
always mispronounce that, and I feel so
badly.
>> Yeah.
>> It's a tongue twister for me, but I'm so
grateful. Thank you so much for for
hosting this and for having
conversations, you know, that are that
are really getting people thinking.
>> You are so welcome, Nikki, and thank you
for taking your uh difficult journey,
but also taking it and transforming and
really this ability for you to be a
connector and bring all these people
together is really extraordinary. Like I
I am just amazed, and again, like I
said, you are doing something that we in
the clinic can't do. So, keep up the
great work. I am so happy to support
you. I hope you guys listening out there
have enjoyed this and will also go to
those websites. If you're a doc, go to
the research, uh do some reading,
educate yourself. Um and Nikki, good
luck with the rest of the journey
because I think this work is super
impactful and super important.
>> Thank you, Dr. Jill. I appreciate it.
Thanks for all you do.
>> Hey guys, as you can tell, I get super
excited when we talk to another um type
of provider. This in this case, Nikki
takes her personal story and has started
the consortium for all of this great
research and work that helps pave the
way for new discoveries and ability for
us as clinicians to actually change the
way we practice medicine.
So, I hope you will go out if you're a
clinician, read her research. Um the
website she gave there will be in the
links below. Um if you are a patient, I
hope you'll educate yourself and ask the
right questions to your doctor and make
sure you find someone to really help
you. And hopefully, you'll find every
week on Resiliency Radio, we are
bringing you great, incredible
interviews with these kinds of people
that are doing the work out there on the
field, um not looking for glory, but
just uh really changing the way we view
medicine and giving us that foundation
of research in order to take things to
the next level. Um hope you enjoyed this
interview as much as I did. If you do,
please leave a comment, share with
someone who you might um think would be
interested. Or if it's your doctor, why
don't you share this episode with your
doctor so that we can educate the
providers out there to start to be
looking for these complex chronic
infections, especially in the realm of
neurodegenerative diseases. Anyway,
guys, I'll see you again next week for a
new episode of Resiliency Radio. And
until then, be well.