Meet Dr. Charlie Lees!

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Discover the cutting-edge world of inflammatory bowel disease (IBD) research and management with Dr. Charlie Lees, a leading gastroenterologist and professor at the University of Edinburgh. In this episode, Dr. Lees guides us through his groundbreaking initiatives, including the Atomic IBD series and the insightful PREDICT study. Learn how innovative predictive health tools, such as sweat sensors, are shaping the future of IBD care and how the series has become a beacon of hope and knowledge for both patients and professionals.

Dr. Lees provides a deep dive into the findings from his PREdiCCT study, including finding on how mental health testing and diet may help indicate a possible flare. He also sheds light on the role of calprotectin levels in indicating inflammation and how patients can understand these levels and how to use them to track their health. This episode also emphasizes the importance of holistic patient care by addressing psychological factors like depression and inactivity, offering actionable strategies to enhance patient well-being.

Explore technological advancements in non-invasive health monitoring, from wearable tech to smart toilets, and their potential in revolutionizing IBD management. Dr. Lees also shares insights on the successful adoption of biosimilars across Europe, highlighting their cost-effectiveness and efficacy in improving patient outcomes. This episode is a must-listen for anyone interested in the future of sustainable healthcare, as it advocates for clear communication and collaboration between healthcare providers and patients to harness the full potential of these innovations globally.

Links: 

• Dr. Lees' Substack
• Dr. Lees' YouTube Channel
• Dr. Lees' patient video on Fecal Calprotectin
• Dr. Lees' video on biosimilars

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Episode Transcript

Speaker 1 (00:00):
Hi, I'm Alicia and I'm Robin and you're listening
to Bowel Moments, the podcastsharing real talk about the
realities of IBD Serve on therocks.
This week we talked to DrCharlie Lees.
Dr Lees is a professor ofgastroenterology at the
University of Edinburgh and aconsultant gastroenterologist at

(00:20):
the Western General HospitalInspire Shawfare Park Hospitals
in Edinburgh.
Dr Lees has a passion forinflammatory bowel disease
education, both patient andprofessional, and this led him
to develop his very informativeand popular sub-stack and
YouTube series called Atomic IBD.
We talked to him about how hechooses the topics for this
series and the response thathe's gotten.
We also talked to him aboutsome of the videos that he

(00:41):
created, including a reallyinformative one on fecal
calprotectin that helps patientsunderstand how this indicates
inflammation that may behappening within their gut.
We talked to him about hisPREDICT study that looked at a
large population of peopleliving with inflammatory bowel
disease in Scotland that aimedto discover the causes of
disease flares.
We talked to him aboutpredictive health tools,
including sweat sensors andother wearables and or things

(01:04):
that you may be able to use thatwould be able to help indicate
your health without any invasiveprocedures.
And finally, we talked to himabout biosimilars and how widely
and long they've been used inEurope and how that may be
helpful for people living withinflammatory bowel disease here
in the United States.
That may be moved to abiosimilar Cheers.

Speaker 2 (01:24):
Hi everybody, Welcome to Bowel Moments.
This is.

Speaker 1 (01:26):
Robin.
Hey guys, this is Alicia and weare so, so excited to be joined
by Dr Charlie Lees.
Dr Lees, welcome to the show.

Speaker 3 (01:34):
Oh, hello, hi both, thanks for having me along.

Speaker 1 (01:37):
Well, we are so excited for everybody to get to
know you and to get to know yourstory, but our first very
unprofessional question for youis what are you drinking?

Speaker 3 (01:48):
Well, it's currently just after 5pm here in Edinburgh
and I've just finished clinic,so I have made myself a mug of
tea, and there was only a singletea bag left in my closet, so
it's actually a moment of calmherbal tea.
So there we are.
That seems like an appropriateway for the day, nothing too
hard.

Speaker 1 (02:01):
I do feel like that.
That is perhaps the universegiving you a little bit of a
gift there.

Speaker 3 (02:05):
Yeah, right, okay, we'll go with that.

Speaker 1 (02:07):
That sounds good, Robin.
What about you?

Speaker 2 (02:10):
I am on my sparkling water kick.
I am drinking Topo Chico.
Shout out to Topo Chico withlime and mint With ice.

Speaker 3 (02:19):
No, it's just a Right from the can.
That's hard water, just a breakfrom the can.

Speaker 1 (02:23):
That's hard water.
Yes, well, it's still sort ofmorning for us here, and so I'm
still drinking my latte, andit's my first latte of the day,
which is never a good sign, at11, 17 in the morning, for me to
be on my first one.
It means I've been on too manymeetings, so hopefully I'll get
to my second one soon.
But, dr Lise, we are so, soexcited for everybody to get to

(02:43):
know you and for us to get toknow you more as well, so I'm
going to jump.
Oh wait, no, cheers everybody.
Sorry, apologies, we cheers nowCheers Again.
Dr Lise, we are so excited toget to know you and for
everybody to get to know you aswell.
That has not already becomefamiliar with you, because I
think they probably have.

Speaker 3 (03:05):
But so I'm going to jump straight to our second
question what is your IBD story?
What brought you into ourcommunity?
So I'm a gastroenterologist, soI look after people living with
IBD, and my IBD journey goesback to August of 2003.
So we're a little over 20 yearsnow.
I'm from London originally.
I went to medical school inLondon.
I came up to Edinburgh in 2001to do my medical rotation as a

(03:26):
junior doctor then and do mymembership exams for the Royal
College of Physicians, and thenI started working as a research
fellow in gastroenterology inthe Edinburgh IBD unit, where I
have been ever since in August2003.
And so I've been here eversince doing research, looking
after patients, learning mycraft as a clinician from

(03:50):
everybody here and then movingalong the way via completing my
training to a clinicallectureship, to completing my
PhD in the genetics ofinflammatory bowel disease, and
then moving all the way to 10plus years as a full-time
consultant gastroenterologist,building a very busy clinic full

(04:11):
of IBD patients.
In fact, I think I set up thefirst dedicated IBD clinic in
Scotland, if not one of thefirst in the UK, where there was
no other gastro patients.
It was purely IBD, which Imaintained to now, and then in
the end of 2019, I wanted to domore of the research that I was

(04:35):
already doing, and so at thatpoint I was awarded a big
personal fellowship a UKResearch and Innovation Future
Leaders Fellowship and thatenabled me to transition to a
more full-time academic role tobecome a professor of
gastroenterology at theUniversity of Edinburgh.
So I run my research group here, whilst maintaining my busy IBD
clinic and scoping practice,and at the same time, do a lot

(04:58):
of outreach and communicationwork, trying to educate people,
with really the key goal overall, which is to improve the lives
of people living withinflammatory bowel disease
wherever they live in the world,and to me, the sort of global
part of this is a huge, hugelyimportant part of that, and so

(05:19):
I've gone from learning thecraft and learning the needs of
our patients to doing a lot ofresearch in genetics and
treatment and, more recently, inenvironment and the microbiota,
as well as increasingly intousing digital tools, and the
overriding thrust of my researchgroup is in terms of predicting

(05:41):
outcomes using a variety ofdifferent measures in people
with established IBD.
So that's sort of the briefoverarching thing.
I've been working in the IBDspace now for just over 20 years
, and that's a really veryinteresting timeframe to see
very big shift.
From the early days when, youknow, I was literally taught

(06:02):
that our patients with Crohn'sdisease had to earn their right
onto a biologic, we would saveour best drugs to the last, we
had no idea how to use themproperly, really how to manage
patients in any kind oftarget-driven way.
The targets that we had thenwere fairly meaningless and
actually that was probably not aproblem because we didn't
really have drugs that couldachieve meaningful targets

(06:24):
anyway.
And I've lived and breathedthrough the introduction and
implementation of not just aseries of highly effective
therapies that have become veryaffordable, but also treatment
strategies and modes to enableus to improve outcomes Such that
, as we start 2025, I am veryoptimistic that for the vast

(06:47):
majority of newly diagnosedpeople with inflammatory bowel
disease, be it Crohn's diseaseor osteocolitis, the vast, vast,
vast majority can expect tohave, with treatment, for the
most part, deep, prolonged andsustained remission that
modifies the natural history ofthe disease, so they're not
getting the complications thatwe see otherwise.
That's not quite there yet withall those bits, and the reality

(07:12):
is that actually most of ourpatients are the prevalent
patients who've lived with IBDfor many, many years and
accumulated lots of damage overtime.
But for the most part, I'm in amuch more optimistic place than
I was 20 years ago and, with thework that we're doing and my
finger across the pulse ofwhat's happening in terms of

(07:33):
research globally, acrossclinicians, academia and
industry, where we really havegreat interest and attention,
the next five, 10 years they'regoing to see really tremendous
advances.
So it's a very, very interestingspace and there's a whole
number of those different thingsthat we can pick up.
But to come back to yourquestion, what's my journey?
Well, my journey is just thatIBD is what I live and breathe

(07:56):
and I do that now in Edinburghas a clinician, as an academic,
as professor of gastroenterology, looking after patients.
As a clinician, as an academic,as professor of
gastroenterology, looking afterpatients, doing research that is
directed all towards improvingoutcomes for people living with
IBD and, along the way, reallypassionate about educating the

(08:20):
whole community about how we cando things better.
Because if all we do isimplement what we know works now
more across the field, acrossthe whole of Scotland, the whole
of the UK, across the whole ofAmerica, across the whole of the
world, then the standards forevery IBD patient across the
world goes up dramatically.
And if we can improve thingsfrom the ground up and get
things even better, fantastic.

Speaker 1 (08:40):
That is a very hopeful way of starting this, so
thank you for that, because Iknow sometimes this doesn't
always feel like a hopefuldisease.
I am curious how did you chooseIBD to be the source of your
passion?
Is there a personal connection,or what was it that brought you
into this specific community?

Speaker 3 (09:05):
early on.
My father was professor ofradiology at the Middlesex
Hospital University CollegeLondon and heavily involved with
gastrointestinal imaging andinterventional imaging and that
I'm sure had an influence aswell as inspirational teachers
when I was a medical student inLondon.
So I knew that I wanted to be agastroenterologist from halfway
through medical school and then, when it came to the time after
my membership to start doingsome research and moving forward

(09:26):
within that journey, the bestopportunity that was available
was in the IBD space and that'swhere I've been and no regrets
since I've not diverted acrossotherwise, but I've kept all
those interests aligned from thestart, from a young age in my
career.
So, yeah, some inspiration andserendipity and then great
mentors and inspiration alongthe way.

Speaker 1 (09:45):
Yeah, we hear that from a lot of our healthcare
providers that if it wasn't apersonal connection, that it was
somebody that they hadencountered along the way in
their you know, in theirtraining journey, that really
kind of got them to beparticularly invested in the
inflammatory bowel diseasecommunity and inflammatory bowel
disease, what was it that droveyou to invest more of your time
and resources into research atthat particular time?

(10:07):
Because you'd already builtyour clinic and then so what was
it that suddenly made you go?
You know what?
I need to spend more time inthe research side.

Speaker 3 (10:12):
So this now is the pivot I made six, seven, eight
years ago and really what hadbeen happening was that we'd
been doing a lot of bigcollaborative research products
in the genetics field, which hasbeen hugely successful in IBD.
I mean just briefly we've nowmapped out over 650 regions of
the genome that we know areassociated with IBD
susceptibility.

(10:33):
These overlap massively withour current drug targets.
Gives us great hope that youknow the future drugs that will
work even better for IBD are ina lot of the rest of that.
We understand the biology ofthe disease much better as a
result and certainly themolecular architecture of
Crohn's disease and ulcerativecolitis really well.
But I was moving in a slightlydifferent direction from about

(10:56):
2013.
So I'd already been a full-timeconsultant three, four years at
this point.
I was heavily involved in ECHOfrom 2007, 2008.
This is the European Crohn'sand Colitis Organization.
I went into there as a juniormember of the EDUCOM, the
Educational Committee.
I spent many years on EDUCOM.
I totally revamped and ran foryears the course for young

(11:20):
gastroenterologists where wetaught them the nuts and bolts
of IBD.
That became the really.
It was really the sort ofcenterpiece, the flagship of
echo education and then intoscientific committee for a while
.
But at the end of my tenure atEducom I went with in fact, with
Simon Travis from Oxford andJanneke van der Voelde, at the
very start of 2013 to China andwe went and we ran the first

(11:42):
proper collaborative educationalprogram over four days between
the China Internal MedicalFoundation and with ECHO and I'd
done a lot of travel andteaching and already developed a
passion for that at that point.
But that trip back then itwasn't seen that long ago, but
actually in the context ofepidemiology of IBD and the

(12:03):
environment of IBD and ourlearnings of that, it's quite a
long time ago and it reallyopened my mind to the shifting
environment, the dynamic natureof what was happening with IBD
epidemiology where we'veseen this massive increase in
Western populations a fewdecades ago.
That stabilized over the last20, 30, 40 years.

(12:25):
The incidence levels are stable.
We're seeing more and morepatients because of compounding
prevalence, but the incidence ofIBD across North America,
across Europe, is stable, but inthe Far East, in South America,
latin America, the Middle Eastand now in Africa, ibd has been
emerging and then accelerating,and going to China in 2013 was

(12:48):
the start of that accelerationin incidents and you could see
it everywhere you went.
I was in Guangzhou, the slightlystrange Chinese city which was
modernizing in front of youreyes.
I literally remember going andseeing on the one side, the old
market with, you know, peoplebringing back fresh produce from
the field, and over the otherside of the road, the McDonald's

(13:10):
that had been open a month, thePizza Hut next door and these
multiple other chains.
And you would go to the buffetin the morning for breakfast and
you would see, you know, thisconstellation of traditional
dishes and then you know thisincreasingly large Western
buffet and you would see theolder chinese people eating
traditional and the youngerpeople eating the western food
and all the rest of it.
I was thinking, well, hang on,there's something.

(13:31):
This isn't just genetics,there's something different
going on here, there's somethingexplaining all of this.
So that really stimulated me tostart thinking beyond just
genetics, to think about theenvironment, the impact of diet
and other environmental factorson the microbiome and how that
might take place.
And so, having got involved witha couple of big collaborative

(13:52):
international projects, I thenset up from about 2015 and 2016,
the end of that year and westarted our big PREDICT study
where what we were doing wastrying to look, not necessarily
the cause of IBD, because that'sa really really difficult thing
to look at and we didn't havevery much money but to try and
look at later on how genetics,environment and the microbiota

(14:15):
was influencing disease flare.
So we posited that actually ifyou took patients who were in
remission, where there was lessinterference from inflammation
in the gut, that you could maybeget a cleaner signal, looking
at dietary patterns and otherlifestyle and psychological
factors and their influence onthe microbiome and then to see

(14:38):
how that would influence diseasecourse over time.
And so from that point, myinterest has been in really, how
do you predict disease course?
And in this particular study itwas predicting disease flare,
and I'll come back and tell youa bit more about predict in a
minute, but just to finish yourquestion.
So what was then happening wasthat we were recruiting all
these patients, that werecruited two and a half

(14:58):
thousand patients across the UKon the Antipredict, and it was
evident to me that the researchthat I was wanting to do and to
continue to do was demandingmore of my time and energy than
I was able to give if I wasgoing to continue to be so
full-time in the clinic as I was.
And the opportunity throughthis UK Research and Innovation

(15:20):
Future Leaders Fellowship, whichwas running over eight years,
gave me to pivot and free upsome of my time whilst
maintaining my IBD clinic, butto free up some of my time from
doing some of my othergastroenterology clinical
commitments would enable me tohelp more patients in a more
meaningful way than I was doingbefore.

Speaker 1 (15:42):
That makes a lot of sense and, yeah, I think it's
understanding those pieces of italso, just, you know, helps the
community at large and is goingto make you a better provider
as well.
So there's certainly that.
But, yeah, I would love for youto tell us more about your
predict study and what exactlyyou were looking at and then
what were your findings, becausethat's a very that's a big
number of people and myunderstanding is they were all
in clinical remission or no?

(16:03):
Tell me, I did.

Speaker 3 (16:04):
We recruited people in self-reported clinical
remission to make the findingsas generalizable as possible and
then we would follow them toFlair and so we recruited 2,629
patients.
In fact, we were planning to goover 3,000, but we got to March
2020 and we all know whathappens in the world then.
But we got to March 2020, andwe all know what happens in the

(16:29):
world then and we, like allresearch studies, had to close
for a period and actually wedecided at that point to stop
recruitment and to focus on thefollow-up and most of those
patients.
We followed all those patientsfor two years through monthly or
semi-regular patientquestionnaires that they filled
in online, but we did a detailedpost-doc phenotyping from the

(16:50):
electronic medical record ofpatients at the end of the four
years of follow-up.
Actually, so, 2,500 patientswith four years of follow-up.
Interestingly and perhaps notunsurprisingly, because we know
as clinicians and we tell ourpatients this that one of the
huge challenges we havemonitoring is this disconnect
between inflammation andsymptoms.

(17:11):
So, on the one hand, you can bea person living with Crohn's or
you see and feel well, but youhave a lot of inflammation in
the gut and we know that we needto find that and treat it,
because it's inflammation that'sthe damaging signal moving
forwards.
But on the other hand, we canhave people that have a lot of
symptoms but not anyinflammation, and there's a

(17:34):
number of different reasons forthat, from structural damage,
from strictures, to irritablebowel syndrome, to bile acid
malabsorption, to smallintestinal bacterial overgrowth,
to name just a few things.
But in those cases, what youdon't want to do is necessarily
increase the anti-inflammationmedicine, which all of our IBD
meds basically are.

(17:54):
So we found that roughly one infive people just under one in
five people had meaningfullevels of inflammation measured
by calprotectin at a level ofgreater than 250 micrograms per
gram.
And we might come back tocalprotectin because it's
something that we've been doingin Europe much longer than in

(18:15):
America and in fact in Edinburghwe've been doing in routine
clinical practice very regularlyfor 15 years.
So we have a very, verypowerful data set there, and
actually my team of datascientists now are doing some
very cool work modelinginflammatory patterns over time
in our routine collected datafrom the clinic as well as in

(18:37):
our big predict study.
But what it's enabled us to do,what calprotectin does enable us
to do is to see gutinflammation on a poo test that
you won't detect on a blood testand that saves the need for an
invasive procedure like acolonoscopy or an MRI scan or a
CT scan or intestinal ultrasound, for example.

(18:59):
So all of the patients at entryinto PREDICT were in clinical
remission, self-reported, buthad calprotectin tests where we
saw that one in five hadcalprotectin levels that were
higher than the baseline.
And then there's another numberthat had a very low grumbling
level and then the majority thathad no inflammation at all.
We also looked at stool samplesto do a microbiome analysis

(19:23):
through metagenomic sequencing.
We looked at a very detaileddietary survey done by both
self-reported food frequencyquestionnaires based on recall
and a four-day weighed fooddiary, and then a suite of
psychological questionnaireslooking at sleep, exercise,

(19:46):
anxiety and depression,somatization, compliance, as
well as the standard clinicalvariables that you extract from
the EHR.
So we found that about 18% ofthe patients had a high
calprotectin.
We followed all of the patientsuntil disease flare.
We looked at both self-reportedflares, symptomatic flares, as

(20:10):
well as harder flares, where wesaw both inflammation rise and a
change in treatment, and whatwe found is very interesting.
So we can see the predictivenature of calprotectin.
We can see how inflammationdrives those sort of harder
flares over time, and we can getsome very granular data from
the study about how intermediatelevels of inflammation are

(20:32):
damaging over time, which isuseful information for
clinicians in terms of how muchis the target, what's the target
?
How low do you drive theinflammation over time?
And then, really interestingly,we've been looking at things
like diet and psychologicalvariables and some of the key
things that we found actuallydiet's been really interesting,
slightly surprising and in a waya little bit disappointing,

(20:53):
because we thought we were goingto find loads of interesting
things and actually most of thedietary analyses didn't show
anything, which is interestingbecause it suggests that diet's
probably important.
We think it's very importantfor general health, certainly,
and there's lots of good reasonsto promote good dietary health.
But in terms of causing diseaseflares in patients with

(21:16):
established IBD, we didn't seevery much.
The main signal we saw was, inpatients with ulcerative colitis
, an increased risk of flarewith increased meat intake
compared to not, and it lookedlike increased red meat intake
was increasing the risk of hardflares in ulcerative colitis.
Interestingly, we didn't see asignal with ultra-processed

(21:37):
foods that we thought we might.
And we've gone back and we'vechecked it, double-checked it,
analyzed it in three differentways, because we were convinced
there must be something inCrohn's patients but actually in
our data set there isn't.
That may be because patients inScotland have such high levels
of background UPF intake anywaythat the signal is harder to

(21:58):
pick out, or it may be a realfinding.
And then, looking at thepsychological variables, the
really interesting things thatwe found are that patients who
have high depression scores havean increased risk of heart
failure and ulcerative colitis,and that's independent of
previous history and it'sindependent of inflammation

(22:20):
levels and everything else aswell.
And the second thing that wesaw, which is partly correlated,
is lack of physical activity.
So depression levels and lackof physical activity seem to
predict hard flares in patientswith ulcerative colitis.
So to me these are quiteactionable in patients with
ulcerative colitis.
So to me these are quiteactionable takeaways.

(22:41):
In ulcerative colitis.
We can perhaps suggest topeople to decrease their red
meat intake, to do more physicalactivity it doesn't need to be
a lot, evidently, but more thanthe recommended amount and that
we should be screening peoplefor depression, not only because
it's good practice and we knowthe rates are higher in
osteoarthritis patients, butbecause it looks like it
increases the risk of flare, andso that would make good sense

(23:02):
to screen and treat based onthat.
So an interesting series offindings, and we've got lots
more coming out from this.
But these depression andexercise findings we're
presenting as a plenary abstractat the big echo meeting in
berlin next month that is really, really interesting and it does
make sense.

Speaker 1 (23:19):
It feels a little chicken or egg, though, too,
because it's one of those where,like, in order to, in order for
people to be less depressed anddo more physical activity they
also can't be in a flare, youknow.
So, like, their disease has tobe, like, fairly managed in
order for you to like, you know,if you want to want to go
running, and you're verysymptomatic, it does make it
more challenging to go runningif you're having to go to the

(23:40):
bathroom every five minutes.
Right, you know so it's.
It feels a little like gosh.
We really like all of it goestogether.
How do you make sure you'regetting somebody to a place
where they can do more activityand they can, you know they're
not as affected.

Speaker 3 (23:58):
But at any one time, most of our patients are in
remission and remember, theseare the patients.
These patients were coming intothe study in remission and so
it suggests that you know whenyou're doing your housekeeping
things with patients, whenthey're coming in, when they're
well, you know.
We ask about these thingsanyway what certainly I do and
we're trying to encourage peopleto think holistically not just
asking people about how manytimes they poo a day is there
blood, do they have pain?

(24:19):
But asking them you know, howtheir appetite is and what their
diet's like and looking forways to improve that.
Asking them about their sleepand their energy levels, asking
them about their mood andexploring that in more detail.
Them about their mood andexploring that in more detail.
And I think we should be askingabout exercise, doing life
counseling with patients, wherewe're talking about you know,

(24:41):
okay, so your sleep's not sogood.
Let's have a think about this.
What might this be in terms ofbehavioral lifestyle things?
Might this be an IBD thing?
Other ways that we can thinkabout, other ways to boost your
mood, including exercise, etcetera, and all the rest of it.
So, yeah, we need to thinkholistically.
And to me the holistic piece iscontrolling the gut inflammation
, because that's the bit thatreally makes a difference.

(25:04):
But it's not forgetting theseother things, and I think the
key insight here is that theseother things are not just nice
to have, because we want ourpatients to feel well as well as
have healed guts, but thatactually this, if we deal with
it, may also properly influencetheir disease history moving
forward.
So that, to me, is the keyinsight.

(25:25):
It's not quite the killer bitof information, it doesn't quite
show causality, but I think itlines up with lots of other
things that we're learning.
But I think it lines up withlots of other things that we're
learning that you know, thebrain and the gut, the body,
overall it's all interrelatedand it's not just about feeling
good, it's about hardinflammatory signals as well.

Speaker 2 (26:00):
This might be a little bit of a curveball,
because what you just said kindof takes me back to one of your
more recent videos that youposted on YouTube, where you're
talking about, like, what'shappening in 2025, what's coming
up, what's excited about what'shappening in research and I
might be remembering this wrong,so please correct me but
talking about other ways thatpatients like, maybe through
wearables, we can measure otherbodily functions, fluids or
whatever, to help predict when aflare is coming.
I'm very interested in thatbecause, as a patient who's been
living with it for 25 years, Ioften say jokingly that my body
is a liar where I'm feelingsymptomatic, but my labs and

(26:25):
tests don't show signs ofinflammation yet.
And then it's one of thosethings where I'm symptomatic I'm
symptomatic, doesn't showanything, doesn't show anything,
and then the bottom falls outright, and so then it's like oh
wait, how did you go fromnothing to high levels of
inflammation?
So do you think that what'scoming down the pipeline as far
as patients having a little bitmore control through wearables,

(26:48):
of other breathing, sweat,whatever that looks like do you
think that is going to help insituations?
I hear this all the time fromother patients too.
I'm not the only person whosebody is a liar.
So I'm just wondering is thatthe direction we're going, and
did we feel like that will helpin situations where the labs
don't necessarily match thesymptoms?

Speaker 3 (27:08):
Okay, robin, so that's great.
This is a perfect curve ball.
It taps into one of my othermajor interests and and really
is important and it's difficult.
It's a hard problem, right, andit's one that I hope we will
get a good answer to soon enoughand at least a workable, a
semi-workable solution to in inthe near future and, in fact,

(27:29):
cut to the chase from my end.
This is something I've beenthinking about for a good number
of years.
I've not felt like there's beenanything enough to make it
worth properly rolling out atool until now, whereas I'm
bullish enough to be going fullon to build a prototype this
year to move forward with that,and I'll talk about the

(27:50):
different components here.
Now, if you have diabetes, thedifferent components here, now,
if you have diabetes this is nowa relatively easy problem.
There is technology that helpsus solve this problem, because
in diabetes, the importantmetric, the important thing you
measure, is a blood glucose, andyou can measure a blood glucose
continuously through a wearablesensor, a patch, a cheap patch

(28:13):
that you slap on your arm or onyour belly that then
communicates to your phone.
That then allows you toseamlessly measure your glucose
levels.
That then will communicate toan insulin pump that you wear on
your belly that will thendeliver the right amount of
insulin that you need.
Now the problem in IBD is thatwe miss these key parts, and

(28:33):
critical to this is that wedon't have a blood sugar.
We don't have a glucose measure.
The closest I think we get tothat actually is faecal
calprotectin, but we can't verywell have people walking around
with rectal catheters in thatare continuously measuring their
faecal calprotectin level.
There has to be a better way ofdoing this and ultimately,

(28:57):
actually, I think the solutionto this will be some kind of
smart or precision toilet thattakes our daily effluent that
contains the calprotectinmeasure, that contains a variety
of other different metabolitesthat can measure your microbiome
, that you can go for your firstablution of the day and they
can play you a happy song andsay Charlie, your chiropractic

(29:19):
is undetectable, your microbiomeis looking royally beautiful,
go off and have a great day.
Everything is super.
Now there are quite a lot ofcompanies working on this.
The technology is in its realinfancy and it's future leaning,
but I think if we go five, 10years down the line, there'll be
some really interesting thingsthere.

(29:41):
So what can we do in themeantime.
And what else is there?
Well, you know I do a lot ofendurance sport and I'm a big
data nerd.
So I have a GPS watch that Iwear when I'm out in the
mountains my garment thatcollects everything.
But I also wear a whoop.
Lots of people will have anOura ring, lots of people will
have an Apple watch, and throughthat I collect a lot of data

(30:01):
that tells me if I drink alcohol, I sleep badly.
If I work too hard, my heartrate variability is low.
If I'm stressed, if I'mtraveling a lot, if I'm jet
lagged, I'm stressed if I'mtraveling a lot.
If I'm jet lagged, sleepterribly.
It nags at me.
But actually it's a usefulthing to have.

(30:27):
The data is really really nice.
Does it help us if we have IBD?
Tell us anything beyond how ourwellness is generally?
And right now the answer tothat is no.
So I think it's a really niceadjunct to any monitoring system
because it will tell us how ourgeneral wellness, fitnesses,
our sleep, all those holisticthings that are really nice to
have.
But if you're detecting yourflare because your resting heart

(30:49):
rate is 10 beats per minutehigher, you are very likely
already knowing that becauseyou're going to the toilet five
to ten times a day with bloodand you've got pain and all the
rest of it.
It's unlikely currently to besensitive enough to do what we
want.
And what do we want?
We want a digital monitoringtool that is passive and
frictionless, that sits in thebackground so that we can just

(31:11):
very happily get on with ourdays, forget that we have
Crohn's cysts or osteocolitisthat will flag a bing to us
somewhere that says ah, Robin,doesn't look quite right At this
point.
we need you to do apoint-of-care count protecting
at home, or a finger prick bloodtest or whatever it is, and or
phone your IBD team, phone yourIBD nurse, log a formal consult.

(31:36):
Let's do a proper assessmentand see what's going on.
Can we get there?
Well, there's an interestingwork that's going on looking at
heart rate variability.
Day-to-day heart ratevariability, I think, is too
heavily influenced byenvironmental factors like poor
sleep, like alcohol, likeexercise, like stress.
I mean, if I even have, I don'tdrink a lot, but if I even have
just one beer or a glass ofwine or two, that knocks it off

(31:58):
massively, much more than itwould do, I think.
But it's very interesting interms of lifestyle behaviors.
But there was an American groupthis year that reported some
initial findings where they'vegot an algorithm that smooths it
out.
It looks at trends over a fewdays and possibly can show when
people are entering a flarestate.
So I think that's interesting.
The patch data that's out therewhere people are looking to try

(32:23):
and measure in sweat not crazy,dissimilar to the glucose thing
, but looking at inflammatorymarkers like TNF, interleukins,
even Calpro and Sweat, that datais really not fit for primetime
.
At the moment, the technologydoesn't work well enough.
It's interesting something tokeep an eye on, but it's not

(32:44):
ready for a tool for sure yet.
So for now I think, and thereason why I'm quite bullish on
this is that we can start to puttogether something that is more
than just a patient IBD app forlogging symptoms.
That is something that doesthis whilst also capturing the
routinely collected laboratorydata.

(33:06):
So the work that we're doingmodeling CRP on blood and
calprotectin on poo trends overtime looks to have great
predictive utility, and sothat's something that I'm very
excited about.
To add in the wearable data forpeople that can help us bring
in their holistic piece andstart to look at things like

(33:26):
heart rate variability when thatbecomes more available, but to
think also about depression andexercise and a few of those
other parameters.
Will it yet be thatfrictionless, passive early
warning system for IBD flares?
Maybe not, but it will give usthe nuts and bolts so that when
we've got that, we can get itworking.

(33:47):
There's one other thing,actually, just going back to my
rather flippant comment that wecan't very well all go walking
around with, you know, wirescoming hanging out our asses
that measure ourchiroprotectants.
There is some interestingtechnology looking ingestible
sensors, and if we can get thattechnology scaled high enough
and cheap enough, you couldpotentially take a tiny pill

(34:09):
every one or two days.
That would just be keeping aneye from the inside permanently,
sort of beeping out to areceiver on your phone or you
know, at your home, and then wejust ping out the toilet
disposable, throw it away, youknow that and a smart toilet in
five to 10 years.
But you asked me about myjourney and I said it's 20 years
and it feels like both nothingand a long time at the same time

(34:32):
.
And if I'm saying now five to10 years, I'm like well holy
moly, it could be incredible bythen.
So yeah, you remembered it well, robin, it's a great curve ball
.
It's something I'm deeplypassionate about, and we'd love
to hear from people who areinterested in this space,
because I hope to have somethingready for beta testing and some
direct consumer testing comingpretty soon.

Speaker 1 (34:50):
Yeah, I love that.
It's so exciting to think thatthere's ways of measuring these
things without you know, withoutactually having to do invasive
procedures.
I am curious is the only way tomeasure fecal calprotectin in
actual poo?
Because my thought was, ifwe're talking about sort of
wearable sensors, is there a wayto measure calprotectin?

Speaker 3 (35:10):
so people have tried to measure calprotectin in
saliva, um, and in blood sweat.
I mean, the thing about fecalcalprotectin is it's measuring
calprotectin in feces and whatare you measuring right?
Remember what it is.
So calprotectin is a proteinthat is very highly present in
the cytoplasm cells ofneutrophils, the, the white

(35:32):
blood cells that are mostpresent in the gut when it's
inflamed, and it's a very stableprotein.
So when you have inflammationin the gut, you have lots of
neutrophils.
As these are expelled, excretedinto the gut lumen, the
calprotectin is released, andit's stable enough to be
homogeneously evenly distributedin a poo sample.

(35:52):
It's then stable for a few days.
You can measure it and get thatlevel, that good measurement of
it.
So it's kind of getting rightto the action.
So everything else is a furtherproxy if you measure it in
blood or whatever else.
There has been, though, someinterest in inhaled gashes, not
just fumes, the gases.
How do you measure it?

(36:13):
Can it be helpful, same sort ofway that dogs can sniff out
illnesses and things as well asbombs some interest that you
know, maybe that sort of?
Can you develop a diagnosticnose for ibd flares and things?
So there's been work done onthis, been done for quite a
while.
Nothing yet that translates tothe clinic.
I think it's probably justdoesn't work well enough.

(36:35):
But you know, it's one of thosethings that we might just see
someone develop somethingbrilliant in the next five years
.
It's like, oh, that seems towork after all.
Very good, I'd like cowprotecting wipes.
If we can't get the toilet to dothe job and part of the problem
here actually is.
So we do it in the lab here inthe hospital.
So we have a system.

(36:55):
It's worth just explaining topeople what we do, because it's
robust, it works really well,and we don't use the point of
care test because they justdon't do the job good enough.
So everybody knows in ourhospital set up from the
consultants to the trainees, tothe clinical nurses, to the
research nurses, to even thesurgeons, but to all the
administrators as well about theimportance of calprotectin.

(37:18):
So patients go away from everyclinical interaction with a
brown paper bag, with acollection dish and a pot and a
scoop.
They then provide the samplefrom home and they drop it into
their GP, their primary carephysician, which then has a van
that drives it into the lab here.
It's stable enough for thatwhole process to work and then
we run the test, which is anELISA, simple ELISA, which costs

(37:42):
between $10 and $15 a go.
It's a really, really cheaptest.
Now the complexity of the testand the bit that takes the time
in the lab is not doing theELISA, it's diluting the sample
down so that you can measure thecalprotectin.
The problem with calprotectinis there is so much of it when

(38:02):
it goes up with inflammationthat you have to do these
dilution steps Because otherwiseyou could do these kind of
point of care tests that we hadfor COVID and things where you
could just do on a cartridge andget a thing working.
Actually it's really difficultto do that accurately because
there is so much calprotecting,because ideally you want a 50

(38:24):
cents or a $1 wipe or somethingwhere you could do first wipe of
the day, dispose of flushablewipe it's green, flush it
away're happy it's blue, youknow.
Then you know that you need togo and do the proper test and
then the points care caliprotest you do at home.
They do work, they're a bitfiddly but they're two or three

(38:44):
times as expensive for a testthat actually you would like to
do more frequently.

Speaker 1 (38:49):
So it quickly becomes economically not very viable
and it's still pooing into a potto do a test, so yeah, I guess
my concern with the toilet wouldbe like okay, so my initial
thought was all the water, thendiluting the sample, whatever,
but it sounds like that's notnecessarily a bad thing.
But also, you know, I know, forinstance, I have lead in my
water, I think you know.

(39:10):
Or what cleaners are you usingfor your toilet that then
potentially change somethingabout it?
Like you know, if you're usinga bleach cleaner for your toilet
, is that then changing?
What's going to potentiallyhappen with your sample?
So I guess there's like there'ssort of those things that are
in the back of my mind.

Speaker 3 (39:23):
Yeah, the chemistry is not trivial at all and maybe,
but I think it's possible.
I mean there's a lot ofinteresting work done on
wastewater analysis throughsurveillance, right.
So yeah, that's, that'sactually in sewage.
So you know you can do allsorts of things.
You know people measure, youknow the amounts of narcotics in

(39:43):
the sewage to keep an eye onthat misuse in in big cities.
But also looking forsurveillance of you know uh,
sars-cov-2 and other viruses andthings.
So there is technology, theremight be ways to cross-purpose
it.
I bet you we will have afunctioning smart toilet within
10 years.
It just might be that it's$10,000 a go.

(40:06):
I was in Japan just beforeChristmas lecturing about IBD,
and it's the same in South Koreaand in different parts of the
region.
But every toilet you go,wherever you go, is some kind of
smart toilet.
I mean, all it does is warm theseat, raise the lid when you
don't want it to and then squirtall manner of different jets in
places that you didn't evenknow it was possible to have

(40:29):
water.
And you know it's moderatelyamusing amusing if frankly
terrifying, as a tourist has noidea what the instructions mean.
But they've been doing that forthe donkey, so it's scalable,
right it was about to say.

Speaker 1 (40:42):
I did watch that talk that you gave in japan and I
did love that you, like you,gave that problem to them
because, you're right, theirtoilets are pretty remarkable.
Singing toilets, spray,scragrance it does any number of
things.
Maybe it can help with this too.
So I think you've given it tothe right folks to potentially
work on.
So I think that's smart.

Speaker 3 (40:59):
Do you watch it in English or Japanese?

Speaker 1 (41:01):
I watch it in English .
Unfortunately, I don't knowJapanese well at all.
I know a few things, but that'sit.

Speaker 3 (41:07):
If you're watching and you're a Japanese person
with IBD or know someone withIBD, go to my YouTube channel.
There is an hour-long lectureon IBD by me, beautifully
translated into Japanese, boththe audio and all the slides.
So there you go.

Speaker 1 (41:23):
I appreciate that you gave a shout-out to your
translators as well, for thatone.

Speaker 3 (41:26):
They were amazing.

Speaker 1 (41:27):
That actually brings me to the next topic I have for
you, though, is your YouTubechannel.
I mean, that's the reason Ifound you is your atomic IBD
series that you do, of youtalking at your phone while
walking around in beautifulplaces and educating people
about aspects of inflammatorybowel disease.
It's very understandable, Infact.
Somebody on YouTube shouted youout when somebody was like I

(41:49):
need content.
I'm newly diagnosed.
How did you start doing this,and what's been the response?

Speaker 3 (41:54):
How did you start doing this and what's been the
response?
So I have been talking aboutIBD since I started working.
We talked about my journey inat least 15 years.
In some form or other, I'vebeen lecturing.
That's why I got involved withEducom at such an early age with
Echo, and I realized that Ihave this real passion for

(42:16):
communicating, for storytelling,for presenting, for crafting
slide presentations and thingsthat catch people's attention in
a way that they can retain thekey information that allows us
to improve patient outcomes, beit you teaching patients about
their disease, or be it youteaching medical students how to
look after IB patients, or beit which is what a lot of what I
do teaching othergastroenterologists how they can

(42:38):
do better with what they do,and doing that across the world.
When the pandemic hit, I wasdoing a lot of this still, but,
like everything, suddenlyeverything was online rather
than traveling around and doingit.
And I was like hang on, I'mdoing all these different talks,
I might as well just recordthem and stick them up onto
YouTube.
So I got heavily.

(42:59):
I'm a big geek and I lovecameras and I love recording
stuff.
I love the editing, which kindof stems from my passion as a
photographer before that, and soit kind of all sort of fit
together.
So I spent many hours andalmost certainly way more money
than I needed to buying, youknow, setting up a studio at
home and making this all workand at the same time actually

(43:21):
doing quite a lot of verydeliberate outreach work for the
pandemic.
So that sort of triggered.
It kept going with that.
A couple of years ago, two orthree years ago, I started
atomic ibd as a sub stack, as anewsletter, which I have used a
lot at times and at times it's abit dormant and that's a 2025

(43:44):
thing.
There's lots of good things2025.
That's coming back, but youknow it comes and goes, but it's
only ever been me.
But then last year I was likethere was.
I was increasingly aware of alack of authenticity online
People, just very polished stuff, people talking nonsense, lots
of the same stuff, so muchformulaic BS everywhere, just

(44:05):
with particularly a medicaleducation which drives me nuts.
It's like, come on, dosomething a bit different.
And then actually I boughtmyself a new gadget.
Totally, that's how it startedand because actually I don't
walk around talking into myphone, I've got myself this dji
osmo which is amazing this notparticularly expensive, and I
was doing them at home andstable, and I was like, oh, I'm

(44:27):
just gonna.
And I just started walkingaround, people said they like
the ones walking around.
So I kept doing that and what Itypically do is go for a run,
think about something I want totalk about, and then just that
they're all uncut, so it comesfrom it.
Then there's all one take andgoes up and it's low.
It's not low effort, but it'sthe.
It's low in terms of thepost-processing stuff that is

(44:50):
otherwise a barrier to do it.
So there's going to be a lotmore of that coming this year.
But I'm really excited actuallybecause I managed to secure a
bit of money to work with againwith my digital animator that's
done a lot of the work thatwe've done in the past, but also
with a friend we did some workwith a couple of years ago on a
big IBD conference to do someproper production to bring to

(45:15):
life what will be the Atomic IBDshow.
We're going to do a couple ofpilots for that, as well as
having a bit more structure anda bit more finesse around the
uncut pieces, and I'm going todo conversations at conferences
or something like that, becausethe mic set the camera set comes
with two mics so I can go andtalk to people uncut about their

(45:38):
presentations, what's happeningand things as well.
I think we need to do more tobring the information that's
there to the community and it'sthe community as a whole,
because we live in a world ofinformation.
There's so much information andif you just look at ibD, there
is way more published literaturethat any one person can keep up

(45:58):
with.
A whole heap of it's just triterubbish stuff that no one needs
to read, but there have beensome amazing big publications in
the last month, last year, lastfive years, and a lot of it
just ends up just gettingreported on.
Initially there's a bit of hype, bit of chat on twitter or
whatever, and then a few peoplemight be working on it.
A few people might not be, andbut it's the same.
With all the differentconversations that are happening

(46:20):
, we need to bring them in a waythat makes it accessible to us
in terms of the stuff that hasalready got to the clinic and
things, but actually also tobring these conversations around
, interesting ideas and how wecan bring the information to
life in an easy way.
So yeah, a few ideas there andhopefully some of them will

(46:40):
stick and will be cool this year.
But yeah, there's a lot's goingto happen.
So if you're not yet subscribedto the atomic ibd, you should
subscribe to the substaxnewsletter and then you'll get
everything via there, butyoutube is the other place to go
.
Links in the descriptions belowright it's.

Speaker 1 (46:55):
It will be linked in the show notes.
Yes, you are absolutely correct.
One of the things I do findparticularly helpful is you do
explain stuff in a way that Ithink is really approachable to
patients, and including theCalprotectin.
You did a whole video onCalprotectin.
That was really helpful.
I watched that one and so youknow.
After that I really did have abetter understanding of like

(47:18):
what is this and why do theymeasure this, why are they
looking at this?
The other one is you've talkeda lot about biosimilars and I
mentioned to you this is aparticularly fraught topic for
Americans because of how oftenthis is being sort of what feels
like inflicted upon people andsome misunderstanding, I think
about just in general.
So will you mind?
I asked you to just do kind ofyour take?
Europe has been doing a lotmore research and using
biosimilars a lot more than theUnited States, so can you give

(47:39):
us kind of your brief version?

Speaker 3 (47:42):
So it brings a small smile to my face, I have to say,
because you know we've beendoing this biosimilars for IBD
for 10 whole years, right, andit's only just coming to America
, but we've been doing it inEurope for 10 years.
We've had biosimilar infliximabsince the very start of 2015.

(48:06):
We've had biosimilar adalimabsince 2018, when Humira's
European patent expired.
We've been using them in placeof the originators since 2015,
when we started using CTP13instead of Remicade, and 2018,
when we started using actuallythere were a number of different

(48:27):
biosimilar adenomabs thenalready using it for new
patients, switching patients,multiple switching patients,
reverse switching patients, andwe have collected data at every
single step along the way.
Me and my team in Edinburghwe've collected every single
data, point on all of this.

(48:47):
We've published on all of it.
Many, many, many other groupshave published on all of this.
We've seen large randomizedcontrolled trials published on
all of this, and at every singlepoint it's been fine.
We see that biosimilars havethe same effectiveness, the same

(49:09):
safety and the sameimmunogenicity and the same
tolerability as the originators,and they are vastly cheaper.
And so if we want to be able tohave sustainable healthcare
that is delivered to IBDpatients across the world so
that all the patients that needdrugs can get them, whether or

(49:31):
by similar versions available,we should absolutely be using
them.
So if you are an Americanpatient with Crohn's disease or
osteoclitis or indeed any otherimmune-mediated inflammatory
disorder today worried aboutbeing switched from an
originator biologic onto abiosimilar, I have a really

(49:52):
super clear message for you,which is it will be just fine.
We've done it.
We've done it to all of ourpatients in Edinburgh, all in
the UK, all in Europe, all ineverywhere in the rest of the
world.
In fact, the only other placethat has been behind, like
America, is Japan.
It's one of the things I wastalking about when I was there

(50:13):
in December.
If the conversation is had inthe right way, it's absolutely
fine.
There is this phenomenon knownas the nocebo effect, which I
think you see quite a lot of inNorth America, which is where,
if the conversation is donewrong, if patients are told in

(50:33):
the wrong way, then problems canarise.
So, for example, what we'vedone throughout is we've agreed
a policy as a group every time.
We've clearly documented ourpathways and our process.
We've written and communicatedwith our patients and we've
talked to them where they wantmore than a written
communication.
And we said this is what we'redoing.

(50:55):
We're changing our patientsfrom this version of the drug to
this version of the drug.
This is something we've donemultiple times before.
We know that the effectiveness,the safety and the
immunogenicity is the same.
We're doing it because it's acheaper version and that allows
us to be cost-sensitive in aneconomic world, and it's

(51:15):
important for all of us, nomatter what health care system
you work in, to be aware of it.
And where patients have comealong.
We've said look, you know,we've all agreed this, it'll be
fine and we'll be monitoringeverything as usual.
Now contrast that to thebelligerent physician or nurse
or whoever else or administratorthat speaks to a person that

(51:35):
says, well, yeah, I have to havethis conversation with you.
Unfortunately, they're makingus do it.
We're going to have to switchyou from the drug that you love.
I don't know why they're doingthis, but we're going to have to
switch you to this other drug.
Either you're going to have todo it or not.
Whatever, I mean, just imaginehow that sets up the
conversation, and I'mdeliberately giving extreme

(51:58):
examples, but that's where thenocebo comes from.
So, um, and I would reallyencourage anyone that has a
voice in the community to speaksensibly about this.
There are certain patientvoices out there online that
have not been constructive tothis conversation, that others

(52:18):
in the community listen to, butreally, the wealth of data and
patient experience is amazing.
Now, I do just want to add oneother thing, which is that for
us in Europe and across a lot ofthe world, this has not just
been about switching frombiologic originators to
biosimilars.
This has been around thedramatic cost reduction in

(52:41):
therapy that has enabled us touse the drugs that work with the
people that need them, at thetimes that they need them, at
the doses that they need.
And we have seen we've got lotsof data in Edinburgh that show
this a reduction in surgicalrates for Crohn's disease, a
reduction in colectomy rates forulcerative colitis,
dramatically so fewerhospitalizations for IBD players

(53:05):
and our patients in betterdisease control over time and so
globally.
It's been absolutely phenomenalas an innovation and it will
continue to come.

Speaker 1 (53:16):
I think one of the issues with the nocebo effect
here in the United States,though, is that at times, people
are being switched withouttheir doctor's knowledge, and so
they don't have the opportunityto have the conversation with
them either, and that theinsurance company is making the
decision of the change informulary, and they show up to
an infusion center and suddenlyhave something different, which

(53:36):
happened to a friend of the show.
She sat down in the infusionchair and they hung her bag of
the biosimilar, and nobody hadtold anybody that this had
happened, and so she went wait asecond hang on.
I didn't know this was happening, and so I think that's a bit of
the issue too, where it's maybenot just the doctor not having

(53:57):
the conversation in the rightway, it's how it is approached
in general with our patients.
Here is just this like you'regoing to do this, you don't have
a choice, whereas that, likeyou said, having a conversation
that enters into a slightlydifferent like puts it in a
different feel, I think would behelpful for every part of our
healthcare system.

Speaker 3 (54:14):
It's about getting the conversation right, isn't it
?
And we were very proactive withthis process the whole way, so
that meant that we were able tokeep the conversation on our
terms and have that with ourpatients.
So maybe I could encourage mycolleagues in the US to maybe be
more proactive in theconversation and say if this

(54:35):
does happen, it'll be fine.
But also, you know, it'sdifficult when you've got
different stakeholders involvedand if people are doing things
without anyone's knowledge.
But there probably are ways tomake sure that conversation is
joined up.
But I do.
I don't envy my colleagues overthe pond with the constant
navigation of the insurancesagas that seem to be.

Speaker 2 (54:59):
Saga is a good word for it.

Speaker 1 (55:02):
Oh, charlie, yeah, that's just a whole different
can of worms.
Yeah, thank you.
Thank you for that.
I think that's going to bereally reassuring to patients.
Robin, quickly, before we wrapup, because I know we need to,
charlie, I want you to give me aone word answer, maybe three at
the most to this.
You have said in a previousvideo that 2023 was the year of
jack inhibitors, 2024 was theyear of il-1223s.

(55:24):
What is 2025 the year of?

Speaker 3 (55:26):
we've got the tools now and we have the data.
So if it's one word, it's hopeI love that it's not so
obviously a new class of drugs.
In any case, we have the toolsthat are there.
The pipeline is rich, it's deep.
We've got we've got lots ofthings happening, but I I want
to bring and what I will do thisyear with the atomic ibd brand

(55:47):
is we will bring together theinformation to help to show this
, because, you know, we've got a.
We've got a good toolkit thatworks and we've got a rich
pipeline.
We've got strategies that weknow how to implement.
Now.
We've done a really good job, Ithink, with education of the
medical workforce in the lastdecade.
There's still work to do there,so more and more clinicians

(56:14):
know what to do, and theresearch output that is there
already that will translate intonew monitoring tools and newer
therapies and strategies isamazing.
There are other things I couldsay, of course prediction
prediction of disease course,which is a bit I'm really
interested in.
There's a huge interest inprediction of disease onset in
the first place and prevention.
That's something that it'sgreat that we've got a roadmap

(56:35):
towards now.
These are long journeys, butit's great that we're having
those conversations now.
But yeah, that would be hopewould be my word for 2025.

Speaker 2 (56:44):
I'm going to make it my word for 2025 now, shu, but I
am very sad to say that it'stime for us to wrap.
I feel like I could ask you, Idon't know, 100 more questions,
but I'm going to ask you ourvery last question.
And what is the one thing thatyou want the IBD community to
know?

Speaker 3 (57:00):
I want my colleagues to know that they can really
make life better for theirpatients if they just get on and
implement what we know worksnow.
Well, and in particular, to notsave their best drug till the
last.
To not save their best drugtill the last, not make patients
earn their rounds of therapyjust to get them on to effective
therapy early, particularly inCrohn's disease, but also in the

(57:22):
flowing UC patient.
And if there's one thing I wantslightly left field maybe,
there's one thing I want mypatient, all the patients with
IBD, to know.
It's get your count, protectand checked and know what the
number is.
Watch my video if you want moredetail.
But if you get your calprotectinchecked and it's greater than
250, no matter what the scalewell, with most scales broadly.

(57:47):
But if it's greater than 250,someone needs to give you an
answer somewhere about what'sgoing to be done about it.
And if you can get yourinflammation under better
control by doing that, then thatwill make a difference.
Despite all these amazingthings about holistic care and
all the rest of it, it'sinflammation that is the danger
to IBD patients and it'sinflammation that we can now

(58:07):
treat the vast majority of thetime with our great toolkit of
anti-inflammation drugs.
So if you're a patient with IBD, get your calprotectin checked,
know what the number is, and ifyou're a physician treating
patients with IBD, get theinflammation under control.

Speaker 2 (58:24):
I love that so much I'm going to go back and check
all of my calprotectin testspreviously.
I actually have a collectionkit sitting in my other room
right now that I have to dostool samples to send into my
doctor, so I I feel like I needto go do that now.
Now that you've like said it,go get it done.

Speaker 1 (58:43):
Dr Lise, this has been so, so much fun to talk to
you.
It is very evident that you areincredibly passionate about
this topic, and it shows verymuch in this conversation, but
also in your videos, and so Idefinitely encourage people to
go learn from you there, whereyou can find the link in the
show notes.
By the way, thank you so muchfor coming and spending some of
your Friday evening with us.
I know we probably should sendyou home to go run, but we

(59:04):
really really appreciate it andwe hope we get you back on
someday because this was a lotof fun to talk to you.
So thank you so much.
Thank you everybody else forlistening, and cheers everybody,
cheers everybody.
If you liked this episode,please rate, review, subscribe
and, even better, share it withyour friends.
Cheers.