July 31, 2025 • 33 mins
Jess Tran was 24, thriving in her career, and training as a powerlifter when a mysterious rash changed everything. It turned out to be guttate psoriasis—and it forced her to rethink everything from ambition to self-image. In this episode, Jess shares how she learned to listen to her body, why visibility can be both empowering and exhausting, and what she wants to change about the wellness industry. Plus, a scientific journey into the immune system—and the breakthrough that changed how we treat psoriasis today.
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Episode Transcript
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Speaker 1 (00:09):
I'm Holly Fry and this is season two of Our Skin,
a personal discovery podcast. Today we are honored to welcome
Jesstrand to our Skin. Jess is many things, a model,
an entrepreneur, and a passionate psoriasis advocate whose voice has
become a very powerful force in redefining what it means
(00:29):
to live and thrive with a visible chronic condition. Jess
develops psoriasis at twenty four, navigating flare ups and the
emotional toll of a skin condition while coming of age
in environments that often valued perfection over authenticity. But over time,
Jess started to reclaim her story. She challenges traditional beauty
(00:50):
standards by showing her skin exactly as it is, and
through entrepreneurship and online storytelling, she has built a platform
grounded in transparency, vulnerability, and cultural nuance. Today, Jess continues
to break barriers, helping others find beauty in their own
skin and pushing the wellness industry to be more inclusive.
(01:11):
Her advocacy centers on body neutrality, mental health, and creating
spaces where people with chronic illnesses truly feel seen. Jess,
Welcome to Our Skin. We are so thrilled to have
you with us.
Speaker 2 (01:25):
Thank you for having me. I'm excited to be here.
Speaker 1 (01:27):
I want to know your whole story. So starting off,
can you take us back to that first diagnosis of
psoriasis because you were only twenty four, and I'm sure
this was a very intense time, both emotionally and physically,
so talk us through it. Yeah.
Speaker 2 (01:44):
So, when I was twenty four, I was on the
back of a job that was extremely toxic. So there
were a series of events that happened with some old
bosses of mine that were kind of doing a number
on my immune system and my mental health. So right
after one of these major events, so I think it
was actually a performance review, I broke out in this
rash across my chest, which I had never seen before.
(02:07):
It kind of spread all over my chest and my shoulders.
There were big, fread, angry welds. I'd never seen anything
like it, and they lasted for about a month. So
it kicked off this series of dermatology appointments with about
eight to ten different dermatologists. A lot of them couldn't
tell me what it was. I don't know really why
that was the case, but it went from everything from
(02:28):
we think it might be lupus to you might have
to go to a different specialist, And on the eighth
visit they finally diagnosed it assiasis and gut tapedsoriasis specifically.
So there was a long period of time where I
was doing allergy test and nothing was showing up. I
did a holistic course of treatment, which included like twenty
vials of my blood being taken and being tested for
(02:50):
everything under the sun. And to this day, outside of
having an official diagnosis, I don't think anyone's actually ever
been helpful in any sense in the traditional medical establishment
on how to treat it or how to contain it.
Speaker 1 (03:04):
Your story makes me wonder about something because you talked
about this flare up happened after a stressful event, and
we know that stress can impact the body in a
lot of ways. But I hadn't really thought about it
until just now as you were talking having all of
these maybe diagnoses like it might be this, it might
be this is its own stress cycle. Do you think
(03:24):
that was a factor in how it was developing as
you were trying to figure it out.
Speaker 2 (03:30):
Yeah, I think the idea that I didn't know what
it was and that there was something seriously wrong with
my body, and that traditional doctors could not tell me
what it was was incredibly destabilizing for me. The amount
of time it took to even diagnose it was a
really really stressful year of my life because it was
navigating by myself different avenues and different doctors and the
(03:51):
same type of doctor to give me different results and diagnoses,
which was really confusing for me.
Speaker 1 (03:58):
You were training as a weight list at this point
in time, right, is that correct?
Speaker 2 (04:02):
Yes? As a powerlifter.
Speaker 1 (04:03):
The intensity of that surely was also hard on your body. Right.
Speaker 2 (04:08):
What I ended up figuring out was that I had
been living at a level of intensity, like you say, physically,
with my career, emotionally, with the background that I come from,
that I think all coalesced into this condition. I think
my personality is geared towards pushing myself to the absolute limit,
and zoriasis was the result of that. It was genetic
(04:30):
as well, I'm sure, but living this way for such
a long time, it doesn't matter if it's seriasis or
another type of chronic condition, it's just the one that
was handed to me.
Speaker 1 (04:40):
Was there a particular moment or a slow shift when
you really started to challenge that instinct of being embarrassed
or ashamed and start to realize that you could share
your skin and your story more openly.
Speaker 2 (04:55):
So I've always been a really open person, like you
can say hi to me, and I'll tell you my
whole life star sorry. So I've never really been embarrassed
about the soriasis. I've been very open and candid about
the entire experience, from diagnosing it to treating it. I
think personally, within me there's been a process of accepting
what psyriasis is, which I think with everyone with chronic illness,
(05:16):
you go through a period where you deny that it's
happening to you. And it took me about a few
years to get over that mentality of this is not fair.
I'm a powerlifter, I eat while I take care of myself.
I'm excelling in all these parts of my life. Why
would this be happening to me to a place where
I do genuinely think that the psiasis is a gift
that was given by my body to understand and to
(05:37):
help regulate how I process and how I move through
the world, because without it, I'm very prone to running
at a million miles an hour, and with it, I
can't do that. I really have to listen to my body.
It's such a physical symptom of pushing yourself too hard.
So I would say that it came with just growing
up and becoming like a turning thirty, getting out of
(05:58):
my twenties. I think everybody goes through a period of
accepting themselves whatever, whether that's chronic illness or not, and
just a lot of years of therapy and thinking through
it and living with it, and then also committing to
different treatments and changing my lifestyle to accommodate it. It
just took a long time to adjust that that is
the way that I'm built, and there's no other way
that I can choose.
Speaker 1 (06:18):
As I was looking at your social media and there
was a picture that you posted in twenty twenty, and
it's you, and you're in like a kind of goldish
pumpkinny colored bikini in it. Just as I have finally accepted,
I'm paraphrasing because I'm going from memory that psoriasis will
always be part of my body. And it was one
of those things where it's so obvious as a reader,
as someone perceiving that post, that's almost like the late
(06:42):
light bulb moment where like full acceptance happens. Yeah, how
do you get there? From the early part, a lot.
Speaker 2 (06:49):
Of complaining, of a lot of why Me'm my ex
and current boyfriends are probably so sick of me talking
about it, and all my friends as well. But I
think that was just after maybe five cycles of flare
ups where I'd get rid of it and then it
would come back, and I'd get rid of it and
would come back, and then it just stopped feeling like
a temporary thing, and I started getting sick of going
(07:13):
through the same cycle, because if you have the same
mentality with something over and over and over again without
changing it, it starts to just grate on yourself and
everyone around you. So at some point, I think I
just realized that if I was going to fight against acceptance,
this was going to be a bigger deal than it was,
because fighting against it makes it worse.
Speaker 1 (07:33):
It sounds like the shift is the difference between looking
at it as a problem to solve and the situation
to manage.
Speaker 2 (07:41):
Yeah, And I think that like, as a daughter of
refugees and someone who's always strived to fix everything in
my life with hard work ethic, I cannot apply that
same logic to my chronic illness. My chronic illness requires
me to slow down, It requires me to emotionally regulate,
It requires me to eat well, to sleep well. Especially thirties,
I can't do the same things I was doing in
(08:01):
my twenties. It makes my sorices flow up even more now.
So it's an almost inverse response to how I was
conditioned to treat every problem in my life, which was
to apply myself one hundred percent to it.
Speaker 1 (08:15):
You also model, which of course involves a lot of
varieties of visibility literal visibility, but also a degree of
emotional visibility, et cetera. Tell me about getting into modeling.
How did you get your start there.
Speaker 2 (08:29):
I was approached online by an agency who asked to
sign me, and I'm five foot one, which is something
you don't get to see on a podcast. So the
context of being five foot one Asian woman with tattoos,
with the way I grew up in Sydney, there was
no representation of Asian women modeling at that height. I
just assumed that would never be going to be something
that I could do, And when you add the skin
(08:51):
to it, it just didn't seem like that's what people
are looking for in the modeling industry. So I was
approached by an agency and I started doing a bunch
of commercial modeling work. And the ciasis has been an
interesting factor because in the modeling industry they distill you
into physical traits, Like they even talk about hands modeling
as parts modeling, right right. You get like defined by
(09:13):
these features of yours. So at times I've been casted
for mysoriasis, which is an interesting thing to be casted
for because I'm not in control of my flare ups.
So if a skin brand comes knocking and they're like,
we want people with psoriasis, I may not have a
flare up. So I functionally don't have czoriasis at that moment,
and I'm not helpful to them. And then they got
(09:34):
back to me and they said, Okay, that's great, but like,
do you have any on your face? And I kind
of was like, I can't really control if it goes
on my face. And then they said, well, we can't
find anyone with csoriasis on their face as a model,
And like, I don't think a lot of people get
crisis on their face.
Speaker 1 (09:51):
I'm still a little bit gobsmacked at that. You have
described visibility as something of a double edged sword before
it's both empowered, worrying and exhausting. So I'm wondering, how
do you decide when you want to show up publicly
versus when you want to prioritize your own piece and
get a little bit of rejuvenation.
Speaker 2 (10:11):
It just goes through cycles and whatever's going on with
the rest of my life and my mental landscape. But
during flare ups lately, they've been more severe. So when
they become more severe, it just takes over my life
a little bit more, and I'm more prone to speaking
about it because it's so present for me. But there
are times two where I'm thirty two now, so I've
(10:31):
been living in with it for eight years. It's just
such a part of my everyday life that I don't
think to share about it because it becomes a ritual
and a routine, the hair care thing with the Dandroff
on my head or whatever it is. But I think
in periods of particular insecurity, my response is to talk
to other people about it and to be public about it,
because I think the thing with being a creator online
(10:53):
too and having a visibility with the public online is
that you have a platform to share when things don't
feel amazing. There's always something going on in the background.
So in some way for me, if were a called
to share when I'm experiencing challenge, so when it's worse,
I'll share how to and be more public about it.
Speaker 1 (11:11):
You have also talked about, you know, how you focus
on what soriasis doesn't like, like gluten stress, et cetera.
But you have also thought about what it does like.
So I want to know what does your soiasis like.
Speaker 2 (11:26):
It likes when I'm living like a monk on a beach,
That's what it likes. It likes when I'm in Costa Rica,
not doing anything on vacation. It loves the ocean, It
loves sunshine. It loves eight hours of sleep and eating
only an only vegetable diet and not having any toxicity
in my life, which is unfortunately very far from the
reality of living in New York. So yeah, I would
(11:49):
say the main thing it loves is the ocean and
salt water.
Speaker 1 (11:52):
What changes would you like to see in the way
that the wellness industry talks about healing and health.
Speaker 2 (11:59):
I think this is a really big conversation that ties
into my opinions on the American healthcare system in general,
and it starts with food, and it starts with the
pollution in the air, in the water, in the way
that we grow our food. And I think there are
so many systems tied into it and what the wellness
industry is in America. So I would like for the
(12:19):
wellness industry to move away from you know, vitamins and
quick fixes and just all these like very broad solutions
that don't address what is at its root, which is
that the way that you take care of people here
through what we are fed and the way that we
go to the doctor needs to fundamentally change.
Speaker 1 (12:39):
You have also built this very impressive, thoughtful, and really
welcoming online presence. I'm wondering how that relationship between you
and the chronic illness community has impacted your own journey
and what you've learned from other people.
Speaker 2 (12:55):
For me, I don't have anyone in my life who
has a chronic skin condition that I know personally, so
I feel very alone in that sense in my day
to day life. So sharing online and being a member
of this larger online community it makes me feel a
little bit more stable. I think understanding that there are
other people who are like me who have the same
(13:17):
issues who struggle in the same ways, instead of what
I am physically reminded of every day in my normal life,
which is just gorgeous, gorgeous people. I love my friends,
They're beautiful, but they don't make me feel good about
my skin sometimes. And then on the other side, I
think there's an interesting aspect to this community, which is
that a lot of us might have siasis or exama
or whatever it is, but every condition is so specific
(13:38):
to the person. So when I post videos about my crisis,
I'll get a whole bunch of people offering that they
think I should do this. It must be a fungus,
I should do this, And whatever applies to you does
not necessarily apply to someone else. So this kind of
like spraying diagnoses to people online is something that I
think is problematic. When I try to talk about what's
worked for me, I try to have the caveat that
(14:00):
this has worked for me and that's specific to me
and like eight years of research and trial and error,
But it doesn't mean that this might work exactly for you.
But that's also the beauty of having psoriasis is that
it teaches you that you have to figure out your
own path and your own set of solutions and treatment
and management, and you can't really just rely on somebody
else's solution what they've learned from their condition.
Speaker 1 (14:22):
You have already accomplished so much at thirty two, but
I am wondering what is next for you, whether that's
in your advocacy or your creative work or something that
we don't even know you have going on yet. What
do you have in your future?
Speaker 2 (14:35):
So at the moment, I have about five jobs, so
I'm consulting for Planned Parenthood, which is my main client
with Vocal Media, so hopefully continuing with that work and
making sure they're not defunded. I'm also writing a fiction
book right now which I'm hoping will be released the
next year. And then finally I'm working on a photographic
series documenting the Vietnamese diaspora, which will be an exhibition
(14:57):
and an art book in a few years as well.
Speaker 1 (15:00):
So when you said you were a high achiever, you
were not exaggerating a tiny amount. Jess, thank you so
much for telling us your story. As we hear often
in these interviews, treatment for psoriasis and for a lot
of chronic illnesses very rarely a straight line. Coming up
when we step back through a little bit of skin history,
we're going to learn how a few very groundbreaking scientists
(15:21):
solved a medical mystery. Why do perfectly effective medications sometimes
just stop working on psoriasis. We're going to come back
after this and talk all about it. In the early
(15:47):
two thousands, dermatology was experiencing a revolution. The arrival of
TNF alpha blockers had completely transformed the management of psoriasis
and other chronic inflammatory diseases. These new biologic medications, drugs
that targeted tumor necrosis factor alpha, were helping patients achieve
(16:07):
clearer skin than many had seen in decades. For patients
with severe psoriasis, that change was dramatic. Prior to these
breaks through treatments, options were limited topical treatments requiring meticulous
daily application, oral medications with serious side effects, or light
therapy demanding frequent clinic visits. The most effective systemic treatments,
(16:29):
like methotrex eight, required careful monitoring for liver damage and
other complications. I'm curious just the side effect thing is
always in any medication. I'm going to take the first
thing I'm looking at. How much have you been thinking
about that? As you've been presented with options.
Speaker 2 (16:46):
It's the only thing I think about. I think about
what's the long term side effects? With the short term
side effects are not telling me what it is forah person.
Speaker 1 (16:53):
So when patients started on these TNF alpha inhibitors, the
results often seemed really miraculous. Within months, severe plaques would
fade dramatically. Many people achieved about seventy five percent improvement
in their symptoms. That was a life changing transformation. It
allowed them to feel comfortable wearing short sleeves and to
(17:14):
feel confident in social situations. Often for the first time
in years. You've mentioned that you're very transparent. Did you
ever have that sort of like I don't want to
go out My skin is misbehaving right now.
Speaker 2 (17:25):
Every day I'm someone who has thong bikinis to the beach,
and it affects my ability to wear my thong bikinis,
which is not fun.
Speaker 1 (17:32):
Right, But the thing is, even as dermatology celebrated these
revolutionary treatments, there was this nagging question lingering in the
minds of scientists, which was why didn't these treatments work
for everyone? And why did some patients who initially responded
beautifully suddenly stop improving. Have you had one of these
(17:53):
drop off situations where something is working for you and
then it's not anymore.
Speaker 2 (17:57):
Yeah, steroid cream specifically.
Speaker 1 (17:59):
That's got to be heartening when you think you have
found the solution and then well you.
Speaker 2 (18:03):
Start to enter the territory were you're mixing six different
staroid creams to see if there's any result, which is
not fun.
Speaker 1 (18:09):
And also hard to have like a control in terms
of like how it's all going wow, can't Yeah. And
here's the thing. The logic behind TNF blockers seemed completely sound.
TNF alpha, a protein that signals inflammation throughout the body,
was clearly elevated in sooriatic skin, so block TNF alpha
reduce inflammation cleared the skin. That all makes perfect sense,
(18:33):
and it did work, sometimes spectacularly. But as these medications
moved into widespread use, there were patterns emerging that puzzled
researchers because while TNF alpha blockers were undeniably effective, they
had limitations that suggested that psoriasis inflammation was more complex
than previously understood. So some patients would show partial improvement
(18:57):
and then kind of plateau. Other had a better response
but lost responsiveness over time. And then a small but
significant number experienced paradoxical psoriasis. So that's an unexpected onset
of psoriasis following the use of TNF inhibitors to treat
inflammation related to another condition. So sometimes a person would
(19:21):
have a flare up that had not had it before.
Oh wow. Listen. Bodies are a fascinating mechanism, and the
way the bodies solve problems isn't always how they should
go on paper. Have you ever had any of those
like this did not go how I expected?
Speaker 2 (19:35):
I mean every time I think that's when I was like,
I should stop eating dairy and it did nothing, So
I was, I guess I can keep eating ice cream.
At least that's a win.
Speaker 1 (19:43):
The thing that was finally realized is that solving these
mysteries of why these variant responses would happen would come
not from studying the success stories, but from examining the
cases where the medications fell short. What researchers discovered would
fundamentally change how we understand seriasis and lead to an
(20:04):
entirely new generation of therapies. As scientists started dissecting the
immune pathways involved in psoriasis more carefully, a protein called
INTERLUCN seventeen or IL seventeen, kept appearing in places where
it could not be ignored. Ile seventeen had actually been
discovered in the nineteen nineties, but its role in human
(20:24):
disease remained unclear until a new class of immune cells
was identified. Interluken is a type of protein secreted by
a lot of different types of cells, and these assists
the cells in our body in communicating with one another. Specifically,
interlukens stimulate immune response, so you can see why they
would be tied to psoriasis. So in a healthy immune system,
(20:48):
your inter lukens act like traffic controllers. So when a
pathogen shows up, like if you have a fungus on
your skin, certain immune cells called THH seventeen cells release
IL seventeen A and IL seventeen F that rallies the
immune system. The area gets inflamed, and that inflammation is
what kills the invader. But then once the thread is gone,
(21:09):
anti inflammatory signals turn off the response. Ideally, to give
a little more context to the IL seventeen family, because
we're putting these letters on the end, the IL seventeen
family actually has six members. IL seventeen ABC, ET, cetera
all the way to F. A is the most active
(21:30):
in the body. It is also the most studied. It
triggers inflammation. It's the most influential gas pedal of the group.
IL seventeen F is very similar to A in its
structure and function, and they can even pair up to
form a hybrid molecule. And their similarity is why these
two cytokines targeted together can be such a useful treatment
(21:52):
for people with psoriasis and other autoimmunity. So just so
we get the other letters out of the way. D
is a little less well understood. It's primarily active in
the gut and nervous system. C is produced by epithelial cells,
which make up a lot of the outer layer of
our skin, but also the gut, so they're implicated in storiasis,
(22:14):
but also in conditions like inflammatory bowel disease. D is
actually the most mysterious of this group. It may have
a role in our bodies natural monitoring for cancer, but
we need more research in that area. And then E
is kind of a player. It also goes by the
name IL twenty five, so it steps out on the
rest of the group. It's got multiple identities it actually
(22:36):
inhibits IL seventeen a, a natural break to ALE seventeen A
and f's gas pedal function that we talked about. I
know this is a ton of science, but this idea
that we have these things in our bodies that are
telling it what to do, and that if those communications
get disrupted, the whole system kind of falls apart is
(22:56):
very fascinating to me. Have you ever heard about it
talked about that way or talk to your any medical
professionals that explained it that way. No, absolutely not. It's
really interesting. So in psoriasis, these danger signals like ILE
seventeen A and ILE seventeen F get turned on, but
the problem is that they never fully turn off. They
(23:17):
act like there's a fire alarm going off in your
body when there is no fire, and that is what
causes things like overproduction of skin cells, so thickened areas
of skin that you would call a plaque redness which
is just blood vessel dilation, scaling, which indicates rapid skin turnover,
and chronic inflammation which is caused by those immune cells
(23:39):
staying active and ready all the time. So this whole
mechanism was discovered and presented in a landmark article in
the journal Nature in two thousand and six, working together
out of Harvard Medical School and Brigham Women's Hospital in Boston.
Two researchers on this paper, doctor V. J. Cushru and
doctor Estelle Batelli, along with their team, played a completely
(24:01):
key role in describing THH seventeen and how it works,
because before this paper came out and you may have
gotten this version, the immune system was thought to have
a basic binary going on. THH one cells are pro inflammatory,
they ramp up the immune system. THH two cells are
anti inflammatory, and they calm the immune system down and
turn off those alarm bells. But that's not accurate. It's
(24:23):
more complicated, just like life and treatment. So Kutru and
Beatelli introduced a third axis. THCH seventeen is uniquely pathogenic,
produces IL seventeen and is distinct from those other two
TH one and THH two, So there was like a
third whole situation going on. They essentially in this paper
(24:45):
identified the immune cell type responsible for chronic IL seventeen signaling, which,
in the years following their paper was finally directly linked
to psoriasis, soriatic arthritis, and other autoimmune diseases, and then
later other researchers applied these findings to skin and joint diseases,
and all of this work ultimately reinforced the findings of
(25:09):
that two thousand and six paper. Around the same time
that IL seventeen A was taking center stage, there was
another closely related cytokine that's ILE seventeen F, and it
was quietly being characterized by another leading researcher. That was
doctor J. Coles, who at the time was at the
University of Pittsburgh, and Coles had been studying IL seventeen
(25:30):
family cytokines in the early two thousands, focusing specifically on
their roles in mucosal immunity and inflammation, so kind of
working in tandem and separately. In two thousand and one,
Coles and his team published one of the first detailed
papers on IL seventeen F, identifying it as a distinct
cytokine co expressed with IL seventeen A by THH seventeen cells,
(25:54):
so just meaning that it gets put into the system
at the same time as ILE seventeen A by the
TCH seventeen cells. So his lab was able to demonstrate
that ASLE seventeen F could independently induce inflammation and was
prettylarly active in lung and epithelial tissues, which make up
ninety five percent of the outer layer of our skin,
(26:16):
So that of course had special relevance to psoriasis research.
So Cole's work opened the door to a deeper understanding
of how dual signaling pathways could operate in tandem and
compound inflammation in chronic diseases like psoriasis. So even if
you're addressing one, its buddy can come to the party
and still make a mess. So we're going to step
(26:37):
back to the beginning of this story. We started with
TNF blockers. TNF alpha is a general purpose inflammatory amplifier.
Like a police siren. You don't know what the issue is,
You just know that you hear the alarm somewhere. With
the discovery of th seventeen cells and how they work,
researchers were able to single out immune responses that specifically
(26:59):
affected the skin as well as other things. It's kind
of like getting an alert on your phone with a
weather warning. You hear the alarm and you get information
about the problem rather than it just being a general
alarm and you going, hey, I wonder what's up, So
they were able to develop treatments that had more specific
and precise applications. And as that picture clarified, so did
(27:21):
the clinical ones. Because patients who had plateaued on TNF
inhibitors or even medications that had blocked ILE seventeen A
often still had lingering symptoms, and dermatologists and rheumatologists started
to suspect that blocking ile seventeen F Ile seventeen a's
messy friend was actually the missing link, that there was
(27:44):
an aspect to it that had not been addressed at
that point. So with treatments that block both IL seventeen
A and ile seventeen F, studies showed not only faster
improvement of psoriasis symptoms, but also far more complete skin clearance.
So patients that were previously kind of plateaued or stuck
at a seventy five percent improvement rate, we're now reaching
(28:05):
ninety percent clearance and even in some cases one hundred
percent clearance. One of the biggest risks when treatment involves
our immune system, and if you are looking at side
effects as I know you are, is infection. So one
way these discoveries make patient lives better is that their
suppression of the immune system is highly targeted, so you
(28:27):
can treat the mechanisms that cause psoriasis flare ups, but
leave the rest of the immune system free to proceed
accordingly handling any other pathogens or issues that require an
immune response, Like if you get the flu, your body
is still ready. Yeah, this is so incredibly cool and important.
Looking back, it's of course clear that the major breakthroughs
(28:47):
that led to dual targeting of AISLE seventeen A ANDISLE
seventeen F did not come from a single lab or
a Eureka moment. They emerged from two decades of methodical research,
which was often driven by a desig to understand just
why some patients didn't improve when they were supposed to.
When I was initially reading this information and looking at
(29:08):
your story, this to me seemed like an odd but
interesting parallel to the way a lot of people come
to a point of acceptance in their psoriasis, which is
also very gradual. Right. It's not as though you just
decide one day I'm going to accept it. There's a
lot of other work that you put in mentally and emotionally,
just the way this was a very slow progression of
(29:29):
people going. I think we have part of it. No,
we have another.
Speaker 2 (29:32):
YEA, let's speed it up, let's keep it crying.
Speaker 1 (29:36):
Doctor J. Coles helped identify the biological relevance of Aisle
seventeen F, showing that it mattered independently, and doctors VJ.
Kushru and Estelle Batelli helped define the origin of these
cytokines the th seventeen cells that produce them in a
regulated cascade. So without these insights together, the rationale for
(29:56):
dual targeting would never have reached the clinic. So the
lesson in complex diseases is that you often need more
than one key to unlock the door, and there's still
a range. I want to be clear, like, it's not
as though this works for everybody. You, yourself, and all
of our guests have talked about every path is different
and what helps you is not necessarily going to be
(30:17):
the solution for someone else.
Speaker 2 (30:18):
Has this been reflected in prescribe medication today or are
they still trialing and testing?
Speaker 1 (30:24):
This is reflected in the medications that we're using today.
So if someone had been receiving medication in like two
thousand and two, it would be potentially very different from
what they would be prescribed today. So thanks to the
vision and perseverance of researchers across multiple institutions and disciplines,
patients now have access to treatments that offer not just improvement,
(30:45):
but the possibility of complete skin clearance and with it
a new kind of freedom. Cool.
Speaker 2 (30:51):
That's so great.
Speaker 1 (30:52):
Support our scientists and researchers people, we need them. This
is all so incredible to me, and we see this
all the time on the show, how science build upon
each other's work and it's that combination of insights that
brings us these amazing breakthroughs, And it feels so hopeful
to me, and I suspect you as well.
Speaker 2 (31:11):
Yeah, I mean, I definitely want to learn more about
it now.
Speaker 1 (31:14):
I do want to ask you two quick questions Jess,
before we let you go. First, I want suggestions from
you that you may have for people that perhaps don't
have psoriasis themselves, but they love someone who does. They
have someone in their lives that they want to support.
What is the advice you give.
Speaker 2 (31:32):
Them compliment them on every other thing that's going on
if they're going through a particularly insecure period, like something
that my friends tell me a lot, which actually does
help when I'm down about it is one of my friends,
Jeremy says, if you didn't have psoriasis, you would be
too perfect, and nobody thinks perfect is interesting and I
actually that really helps me every time I'm like, I
(31:52):
can't be too perfect, because then it would be unfair
to everybody else.
Speaker 1 (31:56):
Jeremy with the Life Insight, if j just didn't have
says we couldn't handle it. And last, but not least,
I know you have a platform that you do this,
but for our listeners, if you could send one message
to anyone who may be grappling with their own diagnoses,
what would that be.
Speaker 2 (32:14):
I think I would say that everything is given to
you for a reason, and you're never given something that
you're not able to handle. So I think searching for
what it's meant to teach you, rather than resisting it
is always going to be helpful.
Speaker 1 (32:26):
AH, beautiful approach, Jess. Thank you so much for spending
this time with us today. Thank you for having me.
This was so fun, just a delight for us. We
are so grateful and cannot wait to see what you
do next. Our Skin is hosted by myself, Holly Frye
and executive produced and engineered by Ryan Martz. Our executive
(32:50):
producer and writer is Meredith Barnes. If you enjoy the show,
share it with your friends. You can also listen and
follow on the iHeartRadio app, Apple Podcasts, or wherever you
get your podcasts.
I'm Holly Fry and this is season two of Our Skin,
a personal discovery podcast. Today we are honored to welcome
Jesstrand to our Skin. Jess is many things, a model,
an entrepreneur, and a passionate psoriasis advocate whose voice has
become a very powerful force in redefining what it means
(00:29):
to live and thrive with a visible chronic condition. Jess
develops psoriasis at twenty four, navigating flare ups and the
emotional toll of a skin condition while coming of age
in environments that often valued perfection over authenticity. But over time,
Jess started to reclaim her story. She challenges traditional beauty
(00:50):
standards by showing her skin exactly as it is, and
through entrepreneurship and online storytelling, she has built a platform
grounded in transparency, vulnerability, and cultural nuance. Today, Jess continues
to break barriers, helping others find beauty in their own
skin and pushing the wellness industry to be more inclusive.
(01:11):
Her advocacy centers on body neutrality, mental health, and creating
spaces where people with chronic illnesses truly feel seen. Jess,
Welcome to Our Skin. We are so thrilled to have
you with us.
Speaker 2 (01:25):
Thank you for having me. I'm excited to be here.
Speaker 1 (01:27):
I want to know your whole story. So starting off,
can you take us back to that first diagnosis of
psoriasis because you were only twenty four, and I'm sure
this was a very intense time, both emotionally and physically,
so talk us through it. Yeah.
Speaker 2 (01:44):
So, when I was twenty four, I was on the
back of a job that was extremely toxic. So there
were a series of events that happened with some old
bosses of mine that were kind of doing a number
on my immune system and my mental health. So right
after one of these major events, so I think it
was actually a performance review, I broke out in this
rash across my chest, which I had never seen before.
(02:07):
It kind of spread all over my chest and my shoulders.
There were big, fread, angry welds. I'd never seen anything
like it, and they lasted for about a month. So
it kicked off this series of dermatology appointments with about
eight to ten different dermatologists. A lot of them couldn't
tell me what it was. I don't know really why
that was the case, but it went from everything from
(02:28):
we think it might be lupus to you might have
to go to a different specialist, And on the eighth
visit they finally diagnosed it assiasis and gut tapedsoriasis specifically.
So there was a long period of time where I
was doing allergy test and nothing was showing up. I
did a holistic course of treatment, which included like twenty
vials of my blood being taken and being tested for
(02:50):
everything under the sun. And to this day, outside of
having an official diagnosis, I don't think anyone's actually ever
been helpful in any sense in the traditional medical establishment
on how to treat it or how to contain it.
Speaker 1 (03:04):
Your story makes me wonder about something because you talked
about this flare up happened after a stressful event, and
we know that stress can impact the body in a
lot of ways. But I hadn't really thought about it
until just now as you were talking having all of
these maybe diagnoses like it might be this, it might
be this is its own stress cycle. Do you think
(03:24):
that was a factor in how it was developing as
you were trying to figure it out.
Speaker 2 (03:30):
Yeah, I think the idea that I didn't know what
it was and that there was something seriously wrong with
my body, and that traditional doctors could not tell me
what it was was incredibly destabilizing for me. The amount
of time it took to even diagnose it was a
really really stressful year of my life because it was
navigating by myself different avenues and different doctors and the
(03:51):
same type of doctor to give me different results and diagnoses,
which was really confusing for me.
Speaker 1 (03:58):
You were training as a weight list at this point
in time, right, is that correct?
Speaker 2 (04:02):
Yes? As a powerlifter.
Speaker 1 (04:03):
The intensity of that surely was also hard on your body. Right.
Speaker 2 (04:08):
What I ended up figuring out was that I had
been living at a level of intensity, like you say, physically,
with my career, emotionally, with the background that I come from,
that I think all coalesced into this condition. I think
my personality is geared towards pushing myself to the absolute limit,
and zoriasis was the result of that. It was genetic
(04:30):
as well, I'm sure, but living this way for such
a long time, it doesn't matter if it's seriasis or
another type of chronic condition, it's just the one that
was handed to me.
Speaker 1 (04:40):
Was there a particular moment or a slow shift when
you really started to challenge that instinct of being embarrassed
or ashamed and start to realize that you could share
your skin and your story more openly.
Speaker 2 (04:55):
So I've always been a really open person, like you
can say hi to me, and I'll tell you my
whole life star sorry. So I've never really been embarrassed
about the soriasis. I've been very open and candid about
the entire experience, from diagnosing it to treating it. I
think personally, within me there's been a process of accepting
what psyriasis is, which I think with everyone with chronic illness,
(05:16):
you go through a period where you deny that it's
happening to you. And it took me about a few
years to get over that mentality of this is not fair.
I'm a powerlifter, I eat while I take care of myself.
I'm excelling in all these parts of my life. Why
would this be happening to me to a place where
I do genuinely think that the psiasis is a gift
that was given by my body to understand and to
(05:37):
help regulate how I process and how I move through
the world, because without it, I'm very prone to running
at a million miles an hour, and with it, I
can't do that. I really have to listen to my body.
It's such a physical symptom of pushing yourself too hard.
So I would say that it came with just growing
up and becoming like a turning thirty, getting out of
(05:58):
my twenties. I think everybody goes through a period of
accepting themselves whatever, whether that's chronic illness or not, and
just a lot of years of therapy and thinking through
it and living with it, and then also committing to
different treatments and changing my lifestyle to accommodate it. It
just took a long time to adjust that that is
the way that I'm built, and there's no other way
that I can choose.
Speaker 1 (06:18):
As I was looking at your social media and there
was a picture that you posted in twenty twenty, and
it's you, and you're in like a kind of goldish
pumpkinny colored bikini in it. Just as I have finally accepted,
I'm paraphrasing because I'm going from memory that psoriasis will
always be part of my body. And it was one
of those things where it's so obvious as a reader,
as someone perceiving that post, that's almost like the late
(06:42):
light bulb moment where like full acceptance happens. Yeah, how
do you get there? From the early part, a lot.
Speaker 2 (06:49):
Of complaining, of a lot of why Me'm my ex
and current boyfriends are probably so sick of me talking
about it, and all my friends as well. But I
think that was just after maybe five cycles of flare
ups where I'd get rid of it and then it
would come back, and I'd get rid of it and
would come back, and then it just stopped feeling like
a temporary thing, and I started getting sick of going
(07:13):
through the same cycle, because if you have the same
mentality with something over and over and over again without
changing it, it starts to just grate on yourself and
everyone around you. So at some point, I think I
just realized that if I was going to fight against acceptance,
this was going to be a bigger deal than it was,
because fighting against it makes it worse.
Speaker 1 (07:33):
It sounds like the shift is the difference between looking
at it as a problem to solve and the situation
to manage.
Speaker 2 (07:41):
Yeah, And I think that like, as a daughter of
refugees and someone who's always strived to fix everything in
my life with hard work ethic, I cannot apply that
same logic to my chronic illness. My chronic illness requires
me to slow down, It requires me to emotionally regulate,
It requires me to eat well, to sleep well. Especially thirties,
I can't do the same things I was doing in
(08:01):
my twenties. It makes my sorices flow up even more now.
So it's an almost inverse response to how I was
conditioned to treat every problem in my life, which was
to apply myself one hundred percent to it.
Speaker 1 (08:15):
You also model, which of course involves a lot of
varieties of visibility literal visibility, but also a degree of
emotional visibility, et cetera. Tell me about getting into modeling.
How did you get your start there.
Speaker 2 (08:29):
I was approached online by an agency who asked to
sign me, and I'm five foot one, which is something
you don't get to see on a podcast. So the
context of being five foot one Asian woman with tattoos,
with the way I grew up in Sydney, there was
no representation of Asian women modeling at that height. I
just assumed that would never be going to be something
that I could do, And when you add the skin
(08:51):
to it, it just didn't seem like that's what people
are looking for in the modeling industry. So I was
approached by an agency and I started doing a bunch
of commercial modeling work. And the ciasis has been an
interesting factor because in the modeling industry they distill you
into physical traits, Like they even talk about hands modeling
as parts modeling, right right. You get like defined by
(09:13):
these features of yours. So at times I've been casted
for mysoriasis, which is an interesting thing to be casted
for because I'm not in control of my flare ups.
So if a skin brand comes knocking and they're like,
we want people with psoriasis, I may not have a
flare up. So I functionally don't have czoriasis at that moment,
and I'm not helpful to them. And then they got
(09:34):
back to me and they said, Okay, that's great, but like,
do you have any on your face? And I kind
of was like, I can't really control if it goes
on my face. And then they said, well, we can't
find anyone with csoriasis on their face as a model,
And like, I don't think a lot of people get
crisis on their face.
Speaker 1 (09:51):
I'm still a little bit gobsmacked at that. You have
described visibility as something of a double edged sword before
it's both empowered, worrying and exhausting. So I'm wondering, how
do you decide when you want to show up publicly
versus when you want to prioritize your own piece and
get a little bit of rejuvenation.
Speaker 2 (10:11):
It just goes through cycles and whatever's going on with
the rest of my life and my mental landscape. But
during flare ups lately, they've been more severe. So when
they become more severe, it just takes over my life
a little bit more, and I'm more prone to speaking
about it because it's so present for me. But there
are times two where I'm thirty two now, so I've
(10:31):
been living in with it for eight years. It's just
such a part of my everyday life that I don't
think to share about it because it becomes a ritual
and a routine, the hair care thing with the Dandroff
on my head or whatever it is. But I think
in periods of particular insecurity, my response is to talk
to other people about it and to be public about it,
because I think the thing with being a creator online
(10:53):
too and having a visibility with the public online is
that you have a platform to share when things don't
feel amazing. There's always something going on in the background.
So in some way for me, if were a called
to share when I'm experiencing challenge, so when it's worse,
I'll share how to and be more public about it.
Speaker 1 (11:11):
You have also talked about, you know, how you focus
on what soriasis doesn't like, like gluten stress, et cetera.
But you have also thought about what it does like.
So I want to know what does your soiasis like.
Speaker 2 (11:26):
It likes when I'm living like a monk on a beach,
That's what it likes. It likes when I'm in Costa Rica,
not doing anything on vacation. It loves the ocean, It
loves sunshine. It loves eight hours of sleep and eating
only an only vegetable diet and not having any toxicity
in my life, which is unfortunately very far from the
reality of living in New York. So yeah, I would
(11:49):
say the main thing it loves is the ocean and
salt water.
Speaker 1 (11:52):
What changes would you like to see in the way
that the wellness industry talks about healing and health.
Speaker 2 (11:59):
I think this is a really big conversation that ties
into my opinions on the American healthcare system in general,
and it starts with food, and it starts with the
pollution in the air, in the water, in the way
that we grow our food. And I think there are
so many systems tied into it and what the wellness
industry is in America. So I would like for the
(12:19):
wellness industry to move away from you know, vitamins and
quick fixes and just all these like very broad solutions
that don't address what is at its root, which is
that the way that you take care of people here
through what we are fed and the way that we
go to the doctor needs to fundamentally change.
Speaker 1 (12:39):
You have also built this very impressive, thoughtful, and really
welcoming online presence. I'm wondering how that relationship between you
and the chronic illness community has impacted your own journey
and what you've learned from other people.
Speaker 2 (12:55):
For me, I don't have anyone in my life who
has a chronic skin condition that I know personally, so
I feel very alone in that sense in my day
to day life. So sharing online and being a member
of this larger online community it makes me feel a
little bit more stable. I think understanding that there are
other people who are like me who have the same
(13:17):
issues who struggle in the same ways, instead of what
I am physically reminded of every day in my normal life,
which is just gorgeous, gorgeous people. I love my friends,
They're beautiful, but they don't make me feel good about
my skin sometimes. And then on the other side, I
think there's an interesting aspect to this community, which is
that a lot of us might have siasis or exama
or whatever it is, but every condition is so specific
(13:38):
to the person. So when I post videos about my crisis,
I'll get a whole bunch of people offering that they
think I should do this. It must be a fungus,
I should do this, And whatever applies to you does
not necessarily apply to someone else. So this kind of
like spraying diagnoses to people online is something that I
think is problematic. When I try to talk about what's
worked for me, I try to have the caveat that
(14:00):
this has worked for me and that's specific to me
and like eight years of research and trial and error,
But it doesn't mean that this might work exactly for you.
But that's also the beauty of having psoriasis is that
it teaches you that you have to figure out your
own path and your own set of solutions and treatment
and management, and you can't really just rely on somebody
else's solution what they've learned from their condition.
Speaker 1 (14:22):
You have already accomplished so much at thirty two, but
I am wondering what is next for you, whether that's
in your advocacy or your creative work or something that
we don't even know you have going on yet. What
do you have in your future?
Speaker 2 (14:35):
So at the moment, I have about five jobs, so
I'm consulting for Planned Parenthood, which is my main client
with Vocal Media, so hopefully continuing with that work and
making sure they're not defunded. I'm also writing a fiction
book right now which I'm hoping will be released the
next year. And then finally I'm working on a photographic
series documenting the Vietnamese diaspora, which will be an exhibition
(14:57):
and an art book in a few years as well.
Speaker 1 (15:00):
So when you said you were a high achiever, you
were not exaggerating a tiny amount. Jess, thank you so
much for telling us your story. As we hear often
in these interviews, treatment for psoriasis and for a lot
of chronic illnesses very rarely a straight line. Coming up
when we step back through a little bit of skin history,
we're going to learn how a few very groundbreaking scientists
(15:21):
solved a medical mystery. Why do perfectly effective medications sometimes
just stop working on psoriasis. We're going to come back
after this and talk all about it. In the early
(15:47):
two thousands, dermatology was experiencing a revolution. The arrival of
TNF alpha blockers had completely transformed the management of psoriasis
and other chronic inflammatory diseases. These new biologic medications, drugs
that targeted tumor necrosis factor alpha, were helping patients achieve
(16:07):
clearer skin than many had seen in decades. For patients
with severe psoriasis, that change was dramatic. Prior to these
breaks through treatments, options were limited topical treatments requiring meticulous
daily application, oral medications with serious side effects, or light
therapy demanding frequent clinic visits. The most effective systemic treatments,
(16:29):
like methotrex eight, required careful monitoring for liver damage and
other complications. I'm curious just the side effect thing is
always in any medication. I'm going to take the first
thing I'm looking at. How much have you been thinking
about that? As you've been presented with options.
Speaker 2 (16:46):
It's the only thing I think about. I think about
what's the long term side effects? With the short term
side effects are not telling me what it is forah person.
Speaker 1 (16:53):
So when patients started on these TNF alpha inhibitors, the
results often seemed really miraculous. Within months, severe plaques would
fade dramatically. Many people achieved about seventy five percent improvement
in their symptoms. That was a life changing transformation. It
allowed them to feel comfortable wearing short sleeves and to
(17:14):
feel confident in social situations. Often for the first time
in years. You've mentioned that you're very transparent. Did you
ever have that sort of like I don't want to
go out My skin is misbehaving right now.
Speaker 2 (17:25):
Every day I'm someone who has thong bikinis to the beach,
and it affects my ability to wear my thong bikinis,
which is not fun.
Speaker 1 (17:32):
Right, But the thing is, even as dermatology celebrated these
revolutionary treatments, there was this nagging question lingering in the
minds of scientists, which was why didn't these treatments work
for everyone? And why did some patients who initially responded
beautifully suddenly stop improving. Have you had one of these
(17:53):
drop off situations where something is working for you and
then it's not anymore.
Speaker 2 (17:57):
Yeah, steroid cream specifically.
Speaker 1 (17:59):
That's got to be heartening when you think you have
found the solution and then well you.
Speaker 2 (18:03):
Start to enter the territory were you're mixing six different
staroid creams to see if there's any result, which is
not fun.
Speaker 1 (18:09):
And also hard to have like a control in terms
of like how it's all going wow, can't Yeah. And
here's the thing. The logic behind TNF blockers seemed completely sound.
TNF alpha, a protein that signals inflammation throughout the body,
was clearly elevated in sooriatic skin, so block TNF alpha
reduce inflammation cleared the skin. That all makes perfect sense,
(18:33):
and it did work, sometimes spectacularly. But as these medications
moved into widespread use, there were patterns emerging that puzzled
researchers because while TNF alpha blockers were undeniably effective, they
had limitations that suggested that psoriasis inflammation was more complex
than previously understood. So some patients would show partial improvement
(18:57):
and then kind of plateau. Other had a better response
but lost responsiveness over time. And then a small but
significant number experienced paradoxical psoriasis. So that's an unexpected onset
of psoriasis following the use of TNF inhibitors to treat
inflammation related to another condition. So sometimes a person would
(19:21):
have a flare up that had not had it before.
Oh wow. Listen. Bodies are a fascinating mechanism, and the
way the bodies solve problems isn't always how they should
go on paper. Have you ever had any of those
like this did not go how I expected?
Speaker 2 (19:35):
I mean every time I think that's when I was like,
I should stop eating dairy and it did nothing, So
I was, I guess I can keep eating ice cream.
At least that's a win.
Speaker 1 (19:43):
The thing that was finally realized is that solving these
mysteries of why these variant responses would happen would come
not from studying the success stories, but from examining the
cases where the medications fell short. What researchers discovered would
fundamentally change how we understand seriasis and lead to an
(20:04):
entirely new generation of therapies. As scientists started dissecting the
immune pathways involved in psoriasis more carefully, a protein called
INTERLUCN seventeen or IL seventeen, kept appearing in places where
it could not be ignored. Ile seventeen had actually been
discovered in the nineteen nineties, but its role in human
(20:24):
disease remained unclear until a new class of immune cells
was identified. Interluken is a type of protein secreted by
a lot of different types of cells, and these assists
the cells in our body in communicating with one another. Specifically,
interlukens stimulate immune response, so you can see why they
would be tied to psoriasis. So in a healthy immune system,
(20:48):
your inter lukens act like traffic controllers. So when a
pathogen shows up, like if you have a fungus on
your skin, certain immune cells called THH seventeen cells release
IL seventeen A and IL seventeen F that rallies the
immune system. The area gets inflamed, and that inflammation is
what kills the invader. But then once the thread is gone,
(21:09):
anti inflammatory signals turn off the response. Ideally, to give
a little more context to the IL seventeen family, because
we're putting these letters on the end, the IL seventeen
family actually has six members. IL seventeen ABC, ET, cetera
all the way to F. A is the most active
(21:30):
in the body. It is also the most studied. It
triggers inflammation. It's the most influential gas pedal of the group.
IL seventeen F is very similar to A in its
structure and function, and they can even pair up to
form a hybrid molecule. And their similarity is why these
two cytokines targeted together can be such a useful treatment
(21:52):
for people with psoriasis and other autoimmunity. So just so
we get the other letters out of the way. D
is a little less well understood. It's primarily active in
the gut and nervous system. C is produced by epithelial cells,
which make up a lot of the outer layer of
our skin, but also the gut, so they're implicated in storiasis,
(22:14):
but also in conditions like inflammatory bowel disease. D is
actually the most mysterious of this group. It may have
a role in our bodies natural monitoring for cancer, but
we need more research in that area. And then E
is kind of a player. It also goes by the
name IL twenty five, so it steps out on the
rest of the group. It's got multiple identities it actually
(22:36):
inhibits IL seventeen a, a natural break to ALE seventeen A
and f's gas pedal function that we talked about. I
know this is a ton of science, but this idea
that we have these things in our bodies that are
telling it what to do, and that if those communications
get disrupted, the whole system kind of falls apart is
(22:56):
very fascinating to me. Have you ever heard about it
talked about that way or talk to your any medical
professionals that explained it that way. No, absolutely not. It's
really interesting. So in psoriasis, these danger signals like ILE
seventeen A and ILE seventeen F get turned on, but
the problem is that they never fully turn off. They
(23:17):
act like there's a fire alarm going off in your
body when there is no fire, and that is what
causes things like overproduction of skin cells, so thickened areas
of skin that you would call a plaque redness which
is just blood vessel dilation, scaling, which indicates rapid skin turnover,
and chronic inflammation which is caused by those immune cells
(23:39):
staying active and ready all the time. So this whole
mechanism was discovered and presented in a landmark article in
the journal Nature in two thousand and six, working together
out of Harvard Medical School and Brigham Women's Hospital in Boston.
Two researchers on this paper, doctor V. J. Cushru and
doctor Estelle Batelli, along with their team, played a completely
(24:01):
key role in describing THH seventeen and how it works,
because before this paper came out and you may have
gotten this version, the immune system was thought to have
a basic binary going on. THH one cells are pro inflammatory,
they ramp up the immune system. THH two cells are
anti inflammatory, and they calm the immune system down and
turn off those alarm bells. But that's not accurate. It's
(24:23):
more complicated, just like life and treatment. So Kutru and
Beatelli introduced a third axis. THCH seventeen is uniquely pathogenic,
produces IL seventeen and is distinct from those other two
TH one and THH two, So there was like a
third whole situation going on. They essentially in this paper
(24:45):
identified the immune cell type responsible for chronic IL seventeen signaling, which,
in the years following their paper was finally directly linked
to psoriasis, soriatic arthritis, and other autoimmune diseases, and then
later other researchers applied these findings to skin and joint diseases,
and all of this work ultimately reinforced the findings of
(25:09):
that two thousand and six paper. Around the same time
that IL seventeen A was taking center stage, there was
another closely related cytokine that's ILE seventeen F, and it
was quietly being characterized by another leading researcher. That was
doctor J. Coles, who at the time was at the
University of Pittsburgh, and Coles had been studying IL seventeen
(25:30):
family cytokines in the early two thousands, focusing specifically on
their roles in mucosal immunity and inflammation, so kind of
working in tandem and separately. In two thousand and one,
Coles and his team published one of the first detailed
papers on IL seventeen F, identifying it as a distinct
cytokine co expressed with IL seventeen A by THH seventeen cells,
(25:54):
so just meaning that it gets put into the system
at the same time as ILE seventeen A by the
TCH seventeen cells. So his lab was able to demonstrate
that ASLE seventeen F could independently induce inflammation and was
prettylarly active in lung and epithelial tissues, which make up
ninety five percent of the outer layer of our skin,
(26:16):
So that of course had special relevance to psoriasis research.
So Cole's work opened the door to a deeper understanding
of how dual signaling pathways could operate in tandem and
compound inflammation in chronic diseases like psoriasis. So even if
you're addressing one, its buddy can come to the party
and still make a mess. So we're going to step
(26:37):
back to the beginning of this story. We started with
TNF blockers. TNF alpha is a general purpose inflammatory amplifier.
Like a police siren. You don't know what the issue is,
You just know that you hear the alarm somewhere. With
the discovery of th seventeen cells and how they work,
researchers were able to single out immune responses that specifically
(26:59):
affected the skin as well as other things. It's kind
of like getting an alert on your phone with a
weather warning. You hear the alarm and you get information
about the problem rather than it just being a general
alarm and you going, hey, I wonder what's up, So
they were able to develop treatments that had more specific
and precise applications. And as that picture clarified, so did
(27:21):
the clinical ones. Because patients who had plateaued on TNF
inhibitors or even medications that had blocked ILE seventeen A
often still had lingering symptoms, and dermatologists and rheumatologists started
to suspect that blocking ile seventeen F Ile seventeen a's
messy friend was actually the missing link, that there was
(27:44):
an aspect to it that had not been addressed at
that point. So with treatments that block both IL seventeen
A and ile seventeen F, studies showed not only faster
improvement of psoriasis symptoms, but also far more complete skin clearance.
So patients that were previously kind of plateaued or stuck
at a seventy five percent improvement rate, we're now reaching
(28:05):
ninety percent clearance and even in some cases one hundred
percent clearance. One of the biggest risks when treatment involves
our immune system, and if you are looking at side
effects as I know you are, is infection. So one
way these discoveries make patient lives better is that their
suppression of the immune system is highly targeted, so you
(28:27):
can treat the mechanisms that cause psoriasis flare ups, but
leave the rest of the immune system free to proceed
accordingly handling any other pathogens or issues that require an
immune response, Like if you get the flu, your body
is still ready. Yeah, this is so incredibly cool and important.
Looking back, it's of course clear that the major breakthroughs
(28:47):
that led to dual targeting of AISLE seventeen A ANDISLE
seventeen F did not come from a single lab or
a Eureka moment. They emerged from two decades of methodical research,
which was often driven by a desig to understand just
why some patients didn't improve when they were supposed to.
When I was initially reading this information and looking at
(29:08):
your story, this to me seemed like an odd but
interesting parallel to the way a lot of people come
to a point of acceptance in their psoriasis, which is
also very gradual. Right. It's not as though you just
decide one day I'm going to accept it. There's a
lot of other work that you put in mentally and emotionally,
just the way this was a very slow progression of
(29:29):
people going. I think we have part of it. No,
we have another.
Speaker 2 (29:32):
YEA, let's speed it up, let's keep it crying.
Speaker 1 (29:36):
Doctor J. Coles helped identify the biological relevance of Aisle
seventeen F, showing that it mattered independently, and doctors VJ.
Kushru and Estelle Batelli helped define the origin of these
cytokines the th seventeen cells that produce them in a
regulated cascade. So without these insights together, the rationale for
(29:56):
dual targeting would never have reached the clinic. So the
lesson in complex diseases is that you often need more
than one key to unlock the door, and there's still
a range. I want to be clear, like, it's not
as though this works for everybody. You, yourself, and all
of our guests have talked about every path is different
and what helps you is not necessarily going to be
(30:17):
the solution for someone else.
Speaker 2 (30:18):
Has this been reflected in prescribe medication today or are
they still trialing and testing?
Speaker 1 (30:24):
This is reflected in the medications that we're using today.
So if someone had been receiving medication in like two
thousand and two, it would be potentially very different from
what they would be prescribed today. So thanks to the
vision and perseverance of researchers across multiple institutions and disciplines,
patients now have access to treatments that offer not just improvement,
(30:45):
but the possibility of complete skin clearance and with it
a new kind of freedom. Cool.
Speaker 2 (30:51):
That's so great.
Speaker 1 (30:52):
Support our scientists and researchers people, we need them. This
is all so incredible to me, and we see this
all the time on the show, how science build upon
each other's work and it's that combination of insights that
brings us these amazing breakthroughs, And it feels so hopeful
to me, and I suspect you as well.
Speaker 2 (31:11):
Yeah, I mean, I definitely want to learn more about
it now.
Speaker 1 (31:14):
I do want to ask you two quick questions Jess,
before we let you go. First, I want suggestions from
you that you may have for people that perhaps don't
have psoriasis themselves, but they love someone who does. They
have someone in their lives that they want to support.
What is the advice you give.
Speaker 2 (31:32):
Them compliment them on every other thing that's going on
if they're going through a particularly insecure period, like something
that my friends tell me a lot, which actually does
help when I'm down about it is one of my friends,
Jeremy says, if you didn't have psoriasis, you would be
too perfect, and nobody thinks perfect is interesting and I
actually that really helps me every time I'm like, I
(31:52):
can't be too perfect, because then it would be unfair
to everybody else.
Speaker 1 (31:56):
Jeremy with the Life Insight, if j just didn't have
says we couldn't handle it. And last, but not least,
I know you have a platform that you do this,
but for our listeners, if you could send one message
to anyone who may be grappling with their own diagnoses,
what would that be.
Speaker 2 (32:14):
I think I would say that everything is given to
you for a reason, and you're never given something that
you're not able to handle. So I think searching for
what it's meant to teach you, rather than resisting it
is always going to be helpful.
Speaker 1 (32:26):
AH, beautiful approach, Jess. Thank you so much for spending
this time with us today. Thank you for having me.
This was so fun, just a delight for us. We
are so grateful and cannot wait to see what you
do next. Our Skin is hosted by myself, Holly Frye
and executive produced and engineered by Ryan Martz. Our executive
(32:50):
producer and writer is Meredith Barnes. If you enjoy the show,
share it with your friends. You can also listen and
follow on the iHeartRadio app, Apple Podcasts, or wherever you
get your podcasts.
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