Exploring the Future of Psychiatry with Dr Martijn Arns: From Biomarkers to Brain Stimulation

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Today I sit down with Martijn Arns, a biological psychologist at the forefront of applied neuroscience, to discuss the advancements and challenges in psychiatry. We delve into his pioneering research on brain biomarkers, the promising applications of brain stimulation techniques like Transcranial Magnetic Stimulation (TMS), and how lifestyle factors may influence conditions such as ADHD. Martijn also shares cutting-edge insights into the role of heart-brain coupling and the potential impact of psychedelics in mental health treatment, offering a glimpse into the future of personalised and stratified psychiatry.

What You'll Learn:

1. Understanding Biological vs. Clinical Psychology:   Martijn explains the focus of biological psychology in studying brain activity rather than engaging in traditional talk therapy.
2. The Role of Biomarkers in Psychiatry:
• Discover the challenges of seeking biological signatures for psychiatric conditions.
• Understand why a biomarker-driven psychiatry might be theoretically impossible due to clinical impairment and situational variables.
3. Innovations in Brain Stimulation:
• Explore the mechanisms and applications of TMS for treating depression and other psychiatric disorders.
• Learn about the groundbreaking use of heart rate to optimise TMS targeting, enhancing treatment effectiveness.
4. Lifestyle Factors and ADHD:
• Understand the significant role sleep and sunlight exposure play in ADHD symptoms.
• Consider the implications of lifestyle interventions in managing and reducing ADHD diagnoses.
5. The Exciting Future of Psychiatric Treatments:
• Dive into how psychedelics might transform therapeutic approaches with their profound effects in combination with therapy.
• Reflect on the potential shift from daily medication to periodic brain stimulation treatments.

Key Takeaways:

• Psychiatry is evolving, with innovations in neuroscience paving the way for more personalised and effective treatments.
• There's a growing recognition of the importance of lifestyle factors, like sleep and sunlight exposure, in influencing mental health conditions, especially ADHD.
• Advancements like TMS offer hope, showing potential even where conventional treatments have failed.

Future therapies may focus more on brain stimulation and targeted interventions rather than a one-size-fits-all medication approach.

Resources:

For more insights and updates on cutting-edge neuroscience research, visit Brain Clinics at brainclinics.com.

Connect with Martijn Arns on LinkedIn to follow his latest work in applied neuroscience.

Share this episode with someone who might benefit from these insights—understanding and innovation in psychiatric treatment are vital as we move towards a future of tailored mental health care.

00:40 Biological vs. Clinical Psychology

01:38 Journey Through Academia and Early Career

04:04 Starting Brain Clinics and Translational Research

06:48 Challenges in Psychiatric Diagnosis

16:20 Stratified Psychiatry and Biomarkers

27:26 Transcranial Magnetic Stimulation (TMS)

31:25 Ethical Considerations in TMS Treatment

32:40 Future of Brain Stimulation Treatments

33:34 Personal Experiences with TMS and Psyched

Episode Transcript

Speaker 1 (00:09):
Martain Arnes, Welcome to the podcast.

Speaker 2 (00:11):
Yeah, well thanks a lot for inviting me.

Speaker 3 (00:15):
Look, the reason I invited you is I saw a
post of yours on LinkedIn, and I dove into the
post and end I looked into your background, and as
soon as I look into your background, I'm like, this
is the guy that I want to get in onto
my podcast because of the research that you're doing. But
you describe yourself as a biological psychologist, not a clinical psychologist.

(00:40):
So tell our listeners the difference between that those two things.

Speaker 2 (00:45):
I think. I think that's quite a big difference. I mean,
at the time when I started studying, it was like
from the say three four hundred psychologists students a year,
that would only be like three to four maybe a
handful that would opt for studying physiological psychology or biological
psychology as we name it nowadays. And usually I tell
people I don't talk to people. I just want to

(01:05):
see their brain activity. So biological psychology is more really
the biological side of psychology where we're more interested in
interrelating behavior to brain. So it's not about checking checklists
or just talk therapy. I mean, although it could be
part of the interest when you want to see how
it works at the brain. But the primary viewpoint is

(01:29):
coming from the brain, which is been quite different from psychology,
which is more than a clinical psychology, which is more
the reverse.

Speaker 3 (01:38):
Yeah, and so given our listeners a bit of a
journey through your background and spoke in academia and then
in the work that you do.

Speaker 2 (01:48):
So when I finished my study, which is let me
count a long time ago, there was somewhere ninety ninety eight,
after having spend also some time and down Under and
some other research places. When I started studying, my specialty
was mostly educating people off to mostly get a role
in farmer industry because there was a lot of pre

(02:09):
clinical research going on where behavior of animals was very
important to inform if a drug would be an antidepressant
drug or an anti psychotic rug, etc. So I've worked
there for a very brief bit at that point in
time as well, But over and over again I was like, well,
I want to do more translational research. I want to
better understand how we can benefit from knowledge from the

(02:31):
brain and applying that to humans directly in order to
make a difference from treatment perspectives. So after I spent
doing research at various research institutes. For example, I did
my studies in Name and the Netherlands. Then I had
a tour in Sydney, Australia and the Westmead Hospital. I

(02:51):
joined the group of Evian Gordon and lie and Williams.
I think she joined it later.

Speaker 3 (02:55):
Actually I know Evan Garden and lay Valliums so Avian
with the brilliant Resource Institute. I used to work with
those guys a decade ago.

Speaker 2 (03:06):
Yeah, exactly, I find exactly. I mean that was also
a little bit of the way how I got started
several years later because ninety seven ninety eight I did
a project at the westmin Hospital and the supervision of
Evan Gordon. They really learned about applying collecting EG data
and lots of people. And then I made a bit
of a detour. I also went to the Max Plunk Institute,

(03:26):
which was more like memory research, and then I started
a PhD in Glasgow and in Scotland together with Oreganaude,
which was a farmer company at that time. And that
all results in effect of me realizing like, well, it's
all this fundamental research is too far away of where
we are going. And then after a couple of years

(03:47):
spending time in the it. This was like beginning of
the two thousands, where even a psychologist could get a
job in it and would all be over a good
salary and the car. I spent one and a half
years there, because of course scientists traveling the world doesn't
make you a lot of money, so I needed to
pay back some of my dad's at that time. So
then Evian Gordon indeed went IPO with the Brain Resource

(04:07):
Company and approaching again like if I was interested in
setting up at least in a Netland slash the some
of the European parts of the Brain Resource Company. And
that's how I got started with brain clinics in the
very early days. So I made a business plan at
that time, and the conclusion was like this no money
to be made me. So I thought, well that's a
great business plan, let's start doing it. So I jumped

(04:31):
into it and we started collecting some data for the
Brain Resource Company. But very early on I already realized like, well,
we have this brain scanning technique, we can compare brain
scans to a database and we have more objective information,
and therefore realizing like this could be a very interesting
jumping platform to branch out to other applications. And one

(04:55):
of the ideas I had at that time already is like,
rather than making a diagnosis on the outside based on
behavioral checklist like raiding, depression, etc. We need to look
under the hoods to better marry a patient to their
treatment or their drug of treatment, if you will. And
that's been the primary motivation ever since, and I think

(05:16):
we've come a long way across the journey ever since.
And that's basically how it got started, in starting my
own private research institute at that time, on the one hand,
collaborating with Brain Resource, but also getting to go with
our own research lines and advancing applied neuroscience. So that's

(05:36):
in a.

Speaker 3 (05:37):
Nutshell, yes, very interesting because I actually studied in Glasgow
University as well. I did a master's in nutrition at
Glasgow Uni. Jesus, it's a cold, wet place in the
middle of winter, isn't it. Yeah.

Speaker 2 (05:51):
You know. The funny thing is I've spent quite some
time in all these places, and to be honest, Munich
was my least favorite place, at least at that time
as a student. It's really hard to get integrated in.
Glasgow was the funniest place. Sorry, even above Sydney.

Speaker 1 (06:06):
It's a lot of things.

Speaker 2 (06:07):
It's a lot of people really go good, no matter
how dark and depressing it was outside inside of the
bars in places, they're really friendly, welcoming people. I had
the greatest time in Glasgow, to be honest.

Speaker 3 (06:21):
Yes, yes, Meeter Ashton Lean a bit of time in there.
I'm sure I'm sure you've forquented ashtle Leon once or twice.

Speaker 1 (06:27):
Tell me this before we dig into this.

Speaker 3 (06:28):
Did you ever come across doctor Roy Sugarman in your
time in the Brilliant Resource company?

Speaker 1 (06:33):
He worked with heavy Yeah.

Speaker 2 (06:34):
I know, well exchanges with him. I mean this is
probably like more than twenty twenty five years ago that
that we had so lates.

Speaker 3 (06:42):
Yeah, nah, very cool.

Speaker 2 (06:45):
The name rings the bell for sure.

Speaker 1 (06:48):
So so let's talk.

Speaker 3 (06:50):
You mentioned something there about with psychiatric disorders the checklist.
Now my listeners will have heard me, Steph. Your listeners
say before that that psychiatry is the only branch of
medicine where people are diagnosed with conditions without a biological

(07:10):
signature at all. And are we any closer to biological signatures?
And and and if you could explain what that means
to people, you'll explain it a lot better than me.
And are we getting any closer to biological signatures for
different psychiatric conditions? And then and and how do we

(07:33):
use the brain and the information from the brand to
inform treatment. There's a few questions in there, take them
any order you want.

Speaker 2 (07:41):
Well, it's going to be a longer answer. Yes and no,
it's the short answer, and the longer answer is indeed,
like you're suggesting, the running joke is a little bit
like the psychiatrist. You know, that's the only MD that
doesn't first inspect the organ he's treating. And that's that's
how it is in current medicine, and especially in PSYCHAI.
We take a checklist, we rate specific behaviors, we measure

(08:05):
to the DSM four very important. It's not the set
of behavioral criteria that make a diagnosis of depression or ADHD.
It's the final question. And the final question is clinical impairments.
So someone can have meet a list of criteria and
not being able to concentrate, impulsive, et cetera. But in

(08:26):
the end, if there's no clinical impairment, then the diagnosis
will not be made. And remember this because this is
a very important notion, because let's visualize two people. We
have one person with a CEO and a company, very impulsive,
very inattentive, probably has a PA to cover up for

(08:47):
all that inattentive behavior, et cetera, but this impulsiveness, et
cetera is one of his core strengths. Now let's take,
on the other hand, this other person white collar workers, say,
very inattentive in PILM and well, his job is, his
boss is not really happy with it, and therefore gets
reverred out to an MD or to a psychiatrist. They

(09:08):
do the checklist, and that they will note some clinical
impairment because his complaints are impacting on his job and
therefore this clinical impairment. So therefore that person might receive
a diagnosis of ADHD, of course a bit more complicated
like I'm painting the picture right now. But the CEO
on the other end will not get a diagnosis. And

(09:29):
this automatically will already tell you that a biomarker driven
psychiatry will be impossible because with my biomarker, I might
pick up on the level of inattention impulsivity. I could
pick up on all those complaints, maybe very reliably, but
I will never pick up on the clinical impairment, which
is more situational environmental, and that's why by definition, a

(09:52):
biomarker will never work. And this is the most important reason.
There's multiple other reasons of reliability that even raters could
could vary well in rating, and there's also environmental societal
changes where some behavior is seen more easily as deviating
from the norm than it would be ten twenty years ago.

(10:14):
But apart from that, I think this is the most
crucial reason why a biomark can never be used for
diagnosis as they are today. So we need to develop
ourselves to a new framework now with the other question
you asked, and I think this is a way more
important question, because why would we want to stick a
label to someone's forehead in terms of a diagnosi as well.

(10:38):
According to the DSM for DSM five, the only reason
to have these terminologies of depression, ADHD etc. Is to
foster communication among professionals. So it's only meant as a
language that if you and I talk about depression, that
we both understand what we're talking about. The DSM four

(10:59):
and five never developed to be a diagnostic framework to
be used to develop treatments upon. It was never designed
for insurance companies to exercise upon that was never behind it.
But still there was all industry that started building anti
psychotics and anti depressants, et cetera. Wherever, whereas it was
never intended intended for that purpose. Now it's just there

(11:23):
to foster.

Speaker 1 (11:24):
So it's been so some margins.

Speaker 3 (11:26):
It's my understanding though, that it's kind of it's been
hijacked a little bit by industry for them to develop
specific treatments.

Speaker 2 (11:36):
What you're saying, yeah, I mean that's that's one one
way to look at it. I may not maybe purposely.
I mean, on the other hand, developing a drug. I'm
not saying hijacked in a negative sense. I mean, if
you develop a drug, you would like to ting onto
something to make understandable what it is that drug is doing.
So it's very understandable. But it's also I think has
put us on a trajectory where we are currently are

(12:00):
that the effectiveness of most treatments are very very low.
If we look at depression, and I can paint the
whole landscape from you ranging from psychotherapy, all anti press
and medications, brain stimulation techniques, ketamine psychedelics, et cetera. Overall
the response for mission rates on the group level are
roughly thirty forty forty five percent when you look at

(12:23):
the largest studies around. So if you go to the
casino and you know you're winning chances or a dead low,
I'm not sure that casinos will do good business well.
In psychiatry, that's what we have to deal with, and
that's why we have this stepped care model that we
keep on putting people on new drugs until we have
found a treatment that will benefit the majority, and when
going through four different steps, only two thirds of people

(12:46):
are actually helped. So it's a very excruciating process knowing
that you're dealing with patients that have co morbid suicideality
that are very impaired in their lives. So this is
really the worst discipline I think from an effectiveness point
of view. Maybe in the hall of metasine.

Speaker 3 (13:06):
And yeah, look, I think that's pretty clear from the
data that the interventions in psychiatry are pretty poor compared
to other branches of medicine and unacceptable for some branches
of medicine.

Speaker 1 (13:23):
But how is neuroscience helping?

Speaker 2 (13:27):
Oh, this is I think the topic where we have
to be more optimistic because knowing that on the group level,
a treatment is only effective in thirty to forty percent,
and also knowing that if people that do not respond
to one treatment might be responding to another treatment. That's
where the real hope is and that's really really where

(13:48):
I think we can make a difference and consistently throughout
all the data we have collected in our lives. So
we've been part of the I spot D study that
was this large study that was funded by by Evan
Gordon and Brain Resource, the largest biomarker study to date,
and that study has been confirming what I just said.
If we make correlations between symptom profiles and baseline EG,

(14:12):
we never found something. But if you start making correlations
between brain activity at baseline and behavior in the future,
so like the symptoms in the future, we did find
a significant association. So that's already telling you that your baseline,
the way your brain activity is at this point in time,

(14:33):
is predictive of the trajectory to responding to a drug.
So if you're responding to a drug, you have a
different type of EG then relative to when you're not
responding to a treatment. So in the first quest, we
really started to asking the question can we predict people
that are responding and non responding to treatment? And the

(14:54):
simple answer is yes, and we can do quite some
substantial degree predicted.

Speaker 3 (14:59):
However, when you develop what sort of accuracy, sorry, Mark,
what sort of accuracy are we talking here in terms
of predictive.

Speaker 2 (15:07):
Yeah, that's why I wanted to get to get into
because it was not like in the eighty ninety or
a ninety plus kind of sensitivity, so we would still
be on the lower end of sensitivity and specifict you
have more like sixty seventy percent, which that's what I
wanted to explain as well, which indeed is clinically very
challenging because if you cannot be absolutely accurate that someone

(15:32):
will or will not respond, then you also cannot make
a decision to prescribe or to withhold a treatment. And
to prescribe a treatment can ethically be justified quite easily,
but you cannot very easily tell someone like, well, my
biomarket tells me you're not going to respond to this
treatment with an eighty percent accuracy, that still means that

(15:54):
someone has likely to twenty percent to respond to the treatment. Ethically,
you cannot make that, not until you have an alternative
to offer, and that's where we have also based on
a lot of the studies we conducted based on I SPOT,
based on these ethical and moral decisions we needed to
make as well, and that's why we've shifted to a
different way. Many people talk about precition psychiatry, personalized medicine

(16:18):
that deals with such questions, and we've moved away to
a model that we call stratified psychiatry and in stratified
psychiatry in depression. For example, we take the whole family
of antidepressant treatments and what we'll do will develop a
biomarker that might predict some responsiveness to say, antidepressant A,

(16:39):
and as long as the same biomarker does not predict
impaired response to another one, then we have a winner,
because what we can we can gain with one drug.
But if we have to then tell someone you cannot
use this drug, however we stratify you to the other
drug that at least is equally effective as the group
level response remission, then we still win because we take

(17:03):
away the drugs so of say that people are less
responsive to, and then we will never have to make
the life or death decision of withholding someone from a treatment,
and so it's a slightly different perspective, but clinically very important.

Speaker 3 (17:19):
Yes, yeah, now that that that is important and it's
worthwhile excuse me, it's worthwhile just dubbing clicking on that
in that you can with what you're saying now is
you're moving towards well. Actually this is saying that this
treatment may not be good for you, or you may
not respond well to this treatment, so instead you should

(17:42):
have this one. Now that's important because a you can
potentially increase the effectiveness, but b the patient doesn't go
on to a drug that is not helpful, that often
has very very significant side effects. And I've been you
Professor John Reid on my podcast, who's done large studies

(18:04):
of real people with antidepressants and find that sixty plus
percent of them have a whole host of side effects,
including suicidal ideation. So if we can can basically go
this drug is not useful for you, or or are
our information is saying don't take this drug. Whereas if

(18:25):
they'd just gone to the doctor, the doctor could have say,
well let's try you on this one first, and they
go and they have a bad outcome and then they
have to go on to another treatment, but they could
potentially be worse off than when they started right exactly.

Speaker 2 (18:39):
So, rather than patients coming to a psychiatrist and a
psychiatrist having a whole range of first line choices, have
first line treatments of psychotherapy and SSRIY in ten different
kinds and as NRI in several kinds. And then there's
second line treatments which is more like OURTMS for example,

(19:00):
treatment used for more treatment resistant patients. So rather than
doing a random pick out of one of these, you
take a simple biomarker, which most consistently we've shown with EG,
and you pick the one that someone is most likely
to respond to. And what we've seen is in replicated
studies that we've been publishing out there, and we've seen

(19:21):
that you could enhance based on a cop one or
two very simple biomarkers, enhance your remission rates from say
forty fifty percent to sixty sixty five percent. So we
see about a thirty percent gain in the remission rates
by simply using one biomarker and stratify people between an
evident between two evidence based treatments.

Speaker 3 (19:44):
And that is really significant, right, that's thirty percent uplift.

Speaker 2 (19:48):
And that's also what these studies have shown. If we
look at I spot where people were actually randomized to
three different drugs, two SSRIs, one s and ri I
and one drug with even a completely slightly different working
mechanism on the group level, remission rates were completely identical
for all all three groups. So the psychiatrist could as
well roll the dice and vside on a treatment based

(20:12):
on rolling the dice. And we know it doesn't make
a difference from any studies.

Speaker 3 (20:16):
That's crazy and can you just let the listeners know.
So you mentioned ssrright, selective excuse me, serotonin reoptic inhibitors
and selective neurepinephron tell our listeners how those drugs are
different in terms of their mechanisms of action.

Speaker 2 (20:34):
Well, the drugs usually impact on a specific neurotransmitter, and
a neud transmitter is like a small chemical in the
brain that facilitates communication between between urins, and some of
them are communicating via means of serotonin, other via means
of neu adrenaline. And we have very often heard about
dopamine as well, So some antidepressants have a preference for

(20:56):
more dopaminergic neurotransmitters. So we have multiple, maybe tens more
close to one hundred different antidepressants and they all have
a slight different preference for one of the other neurot
transmitted systems. However, on the group level, people are equally
responsive to one or the other. And that's really sobering

(21:18):
because in the old days we used to think like, well,
maybe we are more dealing with a subgroup of people
that have a more certnergic depression and other people have
a more say no other nergic depression. Well, all the
research in that specific area has not indicated any evidence
for that, and at this point in times, psychiatrists have
no means other than their gut feeling, other than their

(21:42):
experience with patients to prescribe people with a better treatment.
But overall, still you could as well randomize people to
the treatments because on the group level it's not going
to make a difference at all. And even this is
within antidepressants, but even if you would add psychotherapy or
TMS to it as well, we know tms relative to antidepressants,

(22:04):
tms relative to each other. There's multiple tms producols as well.
For the for rights prefrontal or less prefontal cortex, and
on a group level, they have identical results as well.
So it's not only true for for drugs, but for
any antidepressant treatment. We see group level remission rates being

(22:25):
quite identical.

Speaker 1 (22:26):
And that's that's going to be really confusing.

Speaker 3 (22:31):
Me as well for researchers when you're looking at different
drugs with different mechanisms of actions, and then when you
take a thousand people, same effectiveness, and so that that
begs the question as to when they are effective, what

(22:51):
is the mechanism of action. I've heard some people talk
that they think that it's nothing to do with the
serotonin and orap and effort, but it might be that
the these drugs are increasing BDNF and and helping the
brand that way. Any comments on that or have you
got any insights into this?

Speaker 2 (23:10):
Yeah, I mean that's the final common pathway of any
antidepressant treatment, including electro convilsive therapy, psychedelics rTMS. The final
common pathway is b D and F or nerve growth
factors expressed in the hippocampus that supposedly can facilitate neural
growth and functioning of specific networks in the brain. So

(23:34):
they all have that. So it's not true. Serotonin it
was thought to be a final part of what was
explaining depression, and now we know it's not actually has
more specific networks and specific parts of the brain where
these nerve growth factors play play an important role. But

(23:55):
I think that the honor sensor is how do all
these treatments work. I mean, we know there's a final
common part way in BDNF, for example, but still knowing
that some treatments will be very ineffective, they might still
have this downstream effect that maybe you're not strongly enough.
I think the first question I would and that's why
I'm an applied neuro scientist. The first question I would

(24:16):
like to answer, can we first improve the remission rates
by using a stratified psychiatry approach before we start understanding it,
because our understanding will even get way more complicated. Where
we assume the whole family of treatments we have the
same effect. We're now seeing that within that family of treatments,
one drug has a supposedly different working mechanism relative to

(24:39):
another drug, even if it's the same family. So we're
complicating the whole story much more by taking individual variation
into account and that's really where we need to go to.

Speaker 3 (24:49):
Right, I think what you're saying, so you're saying nis like,
let's let's do stratification, find the drug that is working better,
and then explore the mechanisms, rather than as what happened
twenty thirty years ago, propose a serotonin mechanism, make a
drug that has an action on it, and then use

(25:10):
that drug. So it's a kind of bit of reverse
way of doing things, which I get.

Speaker 1 (25:16):
I actually get that.

Speaker 3 (25:18):
But the BDNF story probably at least partly explains why
I would imagine you're a ware of the British Medical
Journal our BMJ studies comparing a whole different type of
exercise interventions to antidepressant therapy and find that every single

(25:38):
form of exercise had a greater effects size than antidepressants.
And we know that exercise is very potent at stimulating BDNF,
particularly more vigorous exercise, so that would kind of seem
to play into BDNF being the ultimate thing that might
make a difference.

Speaker 2 (26:00):
Yeah, I mean, in that sense, it's not really surprising.
One of the most powerful psychological treatments is called behavioral activation.
As you imply any type of activation, especially in depression,
could be very powerful. Even so strongly, and I recall
this from a long time ago. There was the big
professor who was specialized in cogitive behavior therapy, and in

(26:23):
order to do concuaitive behavior therapy it requires a lot
of training, right, and he explained behavioral activation as being
so simple that you can even teach a psychiatrists how
to do it. Then he was a psychiatrist at that time.
As a behavioral activation is much simpler to do, and
they actually have done had to head studies in very
large numbers where behavioral activation is non inferior to CBT,

(26:47):
and so it's much simpler to do. And even there
that's similar to possibly medications, behavioral activation is a very
powerful technique to at least get some initial antidepressant benefit. Again,
if that's just to be f I think we should
also be cautious by just similar to in the past
saying oh, it's a bit of a certain one thing slow,

(27:07):
we're going to increase it. I think we need to
be cautious about it and not oversimplify things. It's probably
more complicated. Let's be humble, let's only start focusing on
all the mechanisms. Once we have identified the various subgroups,
and that makes more sense in my view, and anything
is simplification beforehand.

Speaker 3 (27:25):
Yeah, no, that makes sense. So let's not talk about TMS. So,
because you have done a lot of work in the TMSPS, firstly.

Speaker 1 (27:34):
Explain what it is and high and.

Speaker 3 (27:38):
Actually what's its mechanisms of action? And then what sort
of conditions is it being used for?

Speaker 1 (27:46):
And what the hell does heartbeat have to do with it?

Speaker 2 (27:50):
Interesting question. I'll finish off with a heart rate and
keep the most exciting to the end. I think TMS
is a very exciting technique. And this was so remember
that what with brain clinics, we're onto doing EG research
and with EG we pick up the activity that's projecting
perpendicular to your scope. So at that point in time

(28:13):
two thousand and five, two thousand and six, I thought like, well,
there's this technique TMS, which is a very vocal, strong
magnetic field and it works in exactly the opposite direction
as the EEG that we're picking up. So I very
naively thought like, oh, that's interesting. I can see an
EEG where something is different and maybe I can use
this technique to then specifically in an individualized way modulate

(28:37):
brain activity. And so we bought our first TMS machine
in two thousand and six and we got started and well,
in the end it turned out to be completely different.
So with transcranial magnetic brain stimulation, and we generate a
magnetic fields in the strength of roughly one point five
to two testa that's very strong and very quickly build setting.

(28:59):
And because it's the magnetic or the decay of the
field is in the order of nanoseconds, we have a
very quick change which can elicit a small current in
the brain. And just to illustrate this, if I hold
it above my hand, my right cortex, so they say,
and I'm stimulating the area that's responsible for my left hand,

(29:22):
then I can also elicit a movement in my left hand.
So it's wow, physical stimulation exactly. So it's physical stimulation.
There's no people have done magnet therapies and stuff like that,
there's nothing related to that. This is really like physical
brain stimulation. So on the other hand, that's also the
only outcome we can get. We can stimulate your motor

(29:43):
areas and see motor movement, and that's it. So it's
always been very surprising to me if I move the
stimulation well to my prefrontal cortex where my high higher
order thinking processes that take place, that I can stimulate
whatever I want, but there's no conscious recollection. Get It's
not that I think like, oh my brain is working different,
my cognition is impaired. You really need to do very

(30:05):
very sophisticated behavioral algorithms to get some kind of a
readout from the prefrontal cortex on your Ownand we do
know that if you move your coil five centimeters interior
in the prefront or quartex and stimulate for say twenty
to thirty sessions, we know you get a very strong
and robust antidepressant effect in quite a number of people. Again,

(30:28):
on a group level, you get remission rates to say
forty to fifty percent, which is still meaningful. Also, and
this is a very important distinction taken into account. This
is mainly investigated in treatment resistant people, so people that
have filled all most other treatments before and getting such
a remission rate in that subgroup of patients, I think

(30:51):
it's very very encouraging because for these people the only
thing left will be electroc convulsive therapy or shock therapy,
which is not something you want to be considering too lightly, So.

Speaker 3 (31:02):
Every s sorry, before you go any further, can I
ask why it is used as second line rather than
first line if its effectiveness appears to be as at
least effective as some of the first line drugs, and
these are on treatment resistant people that you're getting the

(31:23):
same effectiveness, So why isn't it used for first line treatment?

Speaker 2 (31:28):
Yeah, very good question. Yeah, this is usually how research
goes have for ethical reasons. You're not going to be
experimenting in people that are feel still very likely to
respond at an early stage of the depression, and that's
why you always start with the toughest cases. But then
automatically the insurance mechanism kicks in again, and the insurance

(31:51):
mechanism then tells us to only start treating people if
they filled a couple of sessions, whereas personally, and again
don't take this as official advice, but personally I would
consider that we might make it available much more quickly
and to maybe first line patients as well. I think
in the Netherlands we have one of the few systems

(32:13):
where people could qualify for it quite early on, and
we require people to have filled two evidence based treatments,
which could be psychotherapy and medication. But if people don't
want to take medication, they could even have tried two
very different types of psychotherapy and then still qualify for
our TMS for example. And there's also based on the

(32:34):
evidence out there that that will really increase the likely
of people to respond to to TMS. But firstly, I
do think the future will be going there as well.
We will be going to a completely different model. Rather
than taking popping a pill every day that's the current model,
people will start moving, in my view, more to brain
stimulation treatments, short intensive treatment and then you're after treatment

(32:58):
for a longer period or maybe with some maintenance treatment
once every six months, people can maintain their remission, and
I think similar to psychedelics, model is probably going that
direction as well, even though the clinical outcomes might not
be blowing all the drugs out of the water. But
the big advantage of psychedelics is you have a one
time psychedelic experience which can keep your remission for at

(33:21):
least three to six months, and then you might redo it,
which is I think at least better than popping a
bill every day, which is all kinds of side effects
and other mechanisms associated it.

Speaker 1 (33:33):
Yeah, yeah, absolutely.

Speaker 3 (33:34):
And look, I actually know somebody who had treatment resistant
depression and did TMS and said, did ten sessions and
was like this is doing nothing. Said after the ten
session bomb complete and other shift and was just completely
blown away by it. And actually I interviewed on my

(33:56):
podcast a guy who's running the first sack of psych
delic lab in Australia and they're getting some really interesting results.
He so they use it with therapy and his words
are that the psychedelic the psychedelics act as a rocket
ship for the therapy. But he says, if you're going
to use a rocket, you need to know how to.

Speaker 1 (34:18):
Steer a rocket.

Speaker 3 (34:19):
That's that's his big thing, because he says they're so potent.
So so, wh is TMS being used we talked about depression.
Is it being used in other psychiatric conditions with any
effectiveness at this stage?

Speaker 2 (34:34):
Yeah, it's for sure. It's being investigated pretty much in
almost any psychiatic disorder. I would say, although the effectiveness
varies quite a bit. We know there's very strong evidence
for a good use of rTMS in the treatment of depression,
in the treatment of obsessive compulsive disorder. Those I think

(34:56):
are the two main indications. Then when we cross over
to neurology, there's some indication in pain, in chronic pain,
But the question there is how sustainable are the effects,
because you can get an acute suppression of pain, but
if you need to do TMS every day, it might
not be as clinically meaningful there, And that's I think

(35:18):
still the jury is still out on that one. And
other than that, I think there's multiple PTSD is also
quite effectives as a treatment with with our TMS, using
quite similar approaches that we use for the treatment of
depression as well. The network seem to overlap to some degree,
but I think that's that's why we have the strongest
evidence at this point.

Speaker 3 (35:40):
Okay, can we shift TAC now and and talk about
what is probably the fastest growing psychiatric condition that that's
just from what I'm observing and hearing, which is ADHD,
And there seems to be.

Speaker 2 (36:00):
They wanted to touch out on a little bit because
I think we've now mainly described TMS, but I just
wanted to give this example because I think it's a
very nice example. Also about I think the field of
applied neuroscience I remember that with TMS we want to
stimulate the prefrontal cortex, but the current way of thinking
is that TMS is more about stimulating specific networks in

(36:23):
the brain, and that by stimulating the prefrontal cortex, the
signal will be carried through the whole network too much
deeper structures that are inaccessible, like the subgenuine interior singlet cortex.
We're also deep brain stimulations being done so in TMS.
When we talk about biomarkers and improving treatment response, the
most often heard way of doing that it's using fMRI,

(36:46):
and fMRI scans are very complicated scans where we can
look at connectivity from the subgeneral to prefrontal cortex. So
although this is the most evidence based at this point
in time and most investigated, we've been looking at the
for a long time and wanted to achieve a similar
kind of outcome, but without using the fMRI because in
my view, for clinical practices, it's not always feasible to

(37:10):
have an fMRI scan on premise and have every patient
goes through in the MRI scan. So this is also
where you alluded to that where the heart rates and
I think I think it's an interesting topic so by
doing a lot of research and also realizing that there's
a lot of overlap between the depression network and what
we call the frontal Viagel network or the network that's

(37:32):
involved in the brain in regulating heart rate, hard rate friability,
we realize there's a lot of overlap. And what we
found actually was that when you apply TMS acutely to
your brain and when you're hitting the right area that
you see in acute heart rate suppression. And that's very
opposite to what you would think because feeling TMS, it's

(37:54):
not painful, but it's also not the most pleasant thing
to undergo because muscle shoe will will be stimulated as well,
so you would expect herd rate to increase, but not decrease.
So we described it a long time ago. It's a
good long story short. We've done a lot of research
now actually validating it against fMRI based acquisitions, and we

(38:16):
found that the overlap by using heart rate as an
acute readout of TMS to identify the right connected areas,
it overlapped with fMRI with between eighty five and ninety percent.
So we have now developed an iPhone app where people
can use a simple polar heart rate strap together with

(38:37):
an iPhone app, do a five or ten minute procedure
with TMS look at the hard rate at the same time,
which we call heart brain coupling and apps called heart
brain connect and we're using that procedure, you can now
indeed target the individualized right brain network and an individual
increase likelihood of response and being as accurate as one

(39:00):
could be with m right. The reason why I wanted
to highlight this because I think this is really the
type of innovation that we need in psychiatry to make
things scalable as well, and we can have all kinds
of advances and over engineering things as we go, which
is happening a lot, to be honest, because over engineering
making more sophisticated stuff will earn companies more money. But

(39:21):
we also have to think in the opposite direction, like
disrupting the field of brain stimulation and making it way
more accessible. I would like to see that every first
line psychology practice would have access at some point in
time over a very simple stimulator, maybe only doing one HURTZ,
and have very simple targeting techniques like using heart rate

(39:43):
to improve the clinical outcomes to a large degree. Already
and therefore making it way more accessible to people. And
I think that's why I wanted to highlight this as
an example of how very sophisticated fMRI based neuroimaging can
also be re engineered if you will, to refrisatile clinical
clinically based utility using heart.

Speaker 3 (40:05):
Rate that comes and the cost of a heart rate
monitor and an app versus an fMRI machine is a
little bit different, isn't it? And so is this is
this process mediated to the vegus nerve and because right
because it often depressed, people have got very suppressed heart

(40:25):
rate variability. Can you just dive into this little a
little bit more, that connection between the heart the heart
rate variability in the Brian and exactly high are you
using heart rate to inform the TMS or guide the tms?
This is fascinating, So just ridiculously fascinating.

Speaker 2 (40:43):
Yes, So when you spend the whole network ranging from
the prefioto cortex that's accessible, you then do a deep
dive so it's between your eyes and then you go
a couple of centimeters to the back of the head.
That's where the subgenuale interior signal that is located. The
sub genuineteriors England is involved in the treatment of depression
because if people do deep brain stimulation, they lower some

(41:06):
electrodes into that area and start stimulating that pretty much
permanently in order to resolve your depression, which is very effective.
And then when we go to the back of the
head basically to the brain stem, there we have the
vagal nerve that will exit the brain and will be
going to your heart but also to the gut as
well as the heartbreak access bas And we also know

(41:29):
that when we take this vagal nerve and we encapsulate
it by an electrode and we start stimulating that called
vague nerve stimulation, that can also be a very powerful
antidepressant treatment. So we know that these three notes ranging
from the cortex to subcortical areas to the brain stem,
that there's the whole network that's being aligned that's functional,

(41:51):
has some functionality in the bet officienology of depression, and
indeed therefore mediates a heart rate heart friability heart with
friability levels. But also there's a big cross start between
cardiovascular disease and depression. People that experienced cardi vascular accidents
are more likely to develop a depression and people with

(42:12):
depression are more likely to develop cardiovascular accidents. So there's
a lot of overlap between those two networks. And that's
basically the network that we utilize. So imagine that the TMS.
We always thought that the TMS we're only stimulating local
focal areas. Not true. We're stimulating a prefont area and

(42:32):
the stimulation pattern that we apply on your prefonted cortex
is a pattern that your vaguel nerve is responding to
with an identical stimulation pattern that we can read out
on your heart rate, So we can even tell by
using one protocol or the other. I can tell by
looking at your heart rate. Only I can tell which

(42:53):
producol you're stimulated with if you hit the right area.
And we've tested this because many colleagues share data with us,
heard great data, and we did not know who we
were dealing with. But by simply looking at the heart rate,
we could unblind clinical trials within ninety percent accuracy, so
we could tell like, this is real, this is faced

(43:13):
and by just looking at heart rates, So that's how
profound these effects are as well. We're not looking at
a small correlation. We're looking about something that you can
individually apply and tell on an individual level as well.

Speaker 3 (43:27):
Is there I mean that that is just unbelievable. Is
there Is there anybody looking at or is there any
intention to then look at whether the gut microbiome is
being affected as well? Because the vegus nerve stimulates the
gut and I know it has an impact on the
gut microbiom. I mean, anybody who has had had arable

(43:49):
bowel syndrome from stress knows that body brain and connection.
And we know that eating a shit do and changing
your microbiome can influence your brain function and drive depression
as well. So is there anybody looking at that or
is there any plans to look at the whether the
gut microbound was playing a role?

Speaker 2 (44:09):
Well, very spot on. I mean two aspects there. I
think looking at the heart, brain, gut access. Some of
our colleagues in at Burn University in Switzerland are currently
running a study where they look at that, where they
look at TMS applied to the cortex, look at hardware changes,
but also looking at the electro gastrogram, which is like

(44:31):
the measuring the very slow electrical activity of the gut.
So that's one group that's the first kind of research
to see if that type of top down stimulation is
also arriving in the gut as the first first step,
but I think also a second step is that there's
a lot of overlap between the vegel system and vegel
integrity on one hand in immune function, and we know

(44:54):
inflammatory marks also highly elevated in subgroups of the PRESS
patients and to get with another group in Germany, they
are also looking at using hardware and coupling to tease
out how that relates to possible anti inflammatory effects or
inflammation in general. So yes, for sure this technique is

(45:15):
getting more widely available. It's very easy to do obviously,
but as multiple people currently diving into.

Speaker 3 (45:21):
This much deeper and Martin, so just to clarify for
our listeners who may have miss missed that the immune system.
The reason why this is important is that about the
eighty percent of your immune system resides in the gut
because basically that barrier between the micoso barrier is the

(45:45):
last barrier between the outside world and the inside world
essentially and is a very easy way for pathogens to
get into our system. Hence, if people have an irritable
bile they can develop or they have leaky got they
can develop.

Speaker 1 (46:00):
All sorts of autoimmune disorders.

Speaker 3 (46:01):
So not only do so, these magnets then are applied
to the head, stimulating brilliant tissue and pathways that then
through the activate the nervous system, have an impact on
the heart also then can impact on the gut and
potentially modulate the immune system just from placing magnets on

(46:24):
the head.

Speaker 1 (46:25):
Who would have known not fifty years ago. It's crazy exactly.

Speaker 2 (46:29):
But this is also a very very new information. And
also I think it testifies to the fact that brain stimulation,
where we saw that was very focal and only one effect.
We now see this a multitudes of potential mechanisms that
might impact and therefore treats various subgroups of people as well,
maybe people with an inflammatory subtype or people with a

(46:51):
brain connectivity issue that can And that's why I stated
before trying to already jump the gun and start thinking
about war working mechanism or what is affecting what is
the final common pathway like BD and F in my
view of jumping again, we first need to split understand
the subgroups much better before we can really talk about

(47:12):
a final common pathway or a working mechanism, et cetera.
Because here, again we had one treatment where we thought
we only had one effect, but we've also already isolated
here a couple of potential mechanisms in how the press
of symptoms could be mediated, whether anti inflammatory, whether from
brain connectivity, et cetera.

Speaker 3 (47:32):
Wow, that is just astounding. Let's not jump and talk
to ADHD. I have often said to people that if
your diet is shit, and you don't sleep well, and
you don't exercise well, and you will probably feel an

(47:55):
IDIOHD example. And what's your view on the lifestyle factors
playing into ADHD and this explosion that we are seeing
in ADHD diagnosis? And I'm not going to ask you
to put a figure on it, but is at least

(48:17):
some of that mediated by poor lifestyle?

Speaker 2 (48:22):
Very good question. Well, lifestyle for sure, although I cannot
cover all aspects of lifestyle. I think there's one important one.
I was trained as in sleep medicine for a while
as well during my studies, and I've always found sleep
very fascinating. And we spent about thirty percent of our
whole life in this state called sleep, so that must

(48:44):
have ripercussions in our daily function, especially I think in
psychiatry where Unfortunately, psychiatry and sleep medicine are to completely
isolated fields and they don't really talk to one another,
whereas in my field. In my view, is very important
because the symptom checklist for depression and for ADHD, there
is questions relating to sleep, asking about it but not

(49:06):
acknowledging it could be an ethological factor in causing such symptoms.
In depression, the most powerful treatment we have is sleep
deprivation treatment. You keep someone up all minds the depression
has gone next morning. Unfortunately, unfortunately, when they fall asleep again,
their depression pops back up. There's a way to mitigate it,

(49:28):
but that's a whole different discussion. So sleep plays a
very very crucial role in my views in psychiatry. So
with ADHD we stumbled on this quite accidentally. We have
been involved in a field called neurofeedback for quite a
long while I will not dwell on it too long.
There has a lot of pros and cons about that field,
and know myself as well, but one of the things

(49:50):
we observed at that time was that when we did
a specific protocol called sensory motorator neuro feedback, which can
also be used in sleep, people sleep problems. That's the
most free wequ report. A side effect people reported was
improving sleep, and we were treating a lot of people
with ADHD, and after a while we started using actigraphy

(50:11):
similar to Apple watches and all the devices we have
to quantify sleep these days, and we started actually putting
a magnifying glass and did saying like, well, what's happening
with sleep? And when we started doing it, we found
that many people with ADHD actually were presenting with what
we call sleep onset insomnia, having difficulty falling asleep or

(50:33):
falling asleep at a time way too late for someone's
age group bedtime, so to say, but also disrupted sleep
in very short sleep in the second half of night. Well,
to cut a long story short, there's actually quite a
lot of research available right now, also out of Australia,
there's some some groups looking at it. But I think

(50:54):
what we now know is that when you look at
the population of ADHD, about seventy to eighty percent eight
zero of people with ADHD suffer from something called sleep
onset insomnia, which means that they take longer to fall asleep.
And we also know that's pretty much related to melatonin
because Melatonin is a sleep hormone that starts slowly to

(51:15):
be released in your brain to make you fall asleep
more likely to fall asleep, and that rhythm is often
delayed in ADHD. So not only do we have the
behavioral symptom of difficulty falling asleep, we also know that
the sleep hormone is significantly delayed for a couple of
hours in people with ADHD. So what we're seeing is

(51:36):
that these many people with ADHD. Basically, especially if we
focus on children, school times are the same for everyone,
but if you fall asleep two hours later, you are
chronically missing out on two hours of sleep per night.
So how can we link that to behavior? Well, that's
very simple. A lot of research has been done in

(51:57):
the United States, for example, with very simple question, if
we send our people out to a war zone, can
they do well with less sleep? And so they've done
a lot of sleep restrictions, that is, chronically sleep restricting
completely healthy people and measuring the consequences. Well, the very
simple answer is no, they cannot do with less sleep.
So they've taken healthy people and if you measure something

(52:19):
called the PVT lapses, which is like a neuside test,
you then observe how often they have lapse of attention.
Then people were submitted to sleeping eight hours for two weeks,
six hours or four hours, and there was also a
group of people that were not allowed to sleep at
all for two nights because you can't extend that much longer.

(52:40):
So after two weeks of sleep restricting people to let's
take the six hour example, and I think many people
listening to your show will say like, well, that's me.
Some people are proud of it. Personally, I would not
be too proud of it. And basically after two weeks,
their concentration would be as that after two weeks as

(53:02):
the people that did not sleep at all for two nights,
with the very big difference. If you ask them like,
how are you performing? How are you functioning, they would
say I'm doing fine. So sleep restriction is really a
silent killer because without you being aware of it, without
you knowing it, your cognitive performance, your working memory, your

(53:23):
concentration will significantly deteriorate after two weeks to a level
quite similar to someone being sleep deprived for two nights
you are not aware of it, and also recovering from
sleep debts, you can go to a bank and borrow money.
But your body is even worse than a bank. If

(53:43):
you build up a sleep debt, you need to pay
back your sleep debt. If you don't pay it back
in time, you will be suffering in terms of cognition,
et cetera. So the sleep debt that has been gradually
building up over two weeks, you need to pay it off,
and it takes often the same amount of time before
you have paid back the sleep debt. So it's not

(54:04):
true that sleeping in on the weekend for one or
two nights, which really is not like the same quality
of sleep that you've been lacking off. But that's not enough.
You need to have a consistent amount of sleep, which
is really between seven to nine hours for the majority
of people. So with this model, we now understand that

(54:24):
if people are missing out in two, one or two
hours of sleep every night, their concentration in school will
be disadvantage will be at a lower level. We also
understand that if you and I would have that night
of bad sleep for multiple times we're driving a car,
we know the likelihood of an accident increase. So what
do we do. We take a red bull? So what

(54:45):
are we doing with the kids we're prescribing psycho stimulant
medication like metal vanidades, which we know will improve their
neuropsych function at that time, but it's not a cure
for their symptoms. The cure you will need to seek
into the sleep promote moting effects and sleep enhancement effects.

(55:06):
And this is really I think complementing the whole circle
in how we understand how one lifestyle effactor. Imagine if
we focus on all the other ones, but things like
sleep can explain the behavior. And also the high peractivity
is very easily explained as well because people you probably
have observed small children and when they need when they're

(55:26):
approaching that a bad time, they're running around like crazy,
which is a compensateory behavior to keep yourself awake, and
so it's an utter regulatory behavior. And therefore the whole
symptom domain of ADHD can be for a maturity of people,
not for everyone, but for many people can be explained
by not getting enough sleep. So remember then, a small

(55:50):
rewind we came from the biological clock, this melotone in
transcription being coming up too late, So how can we
understand that, Well, there's many environmental influences these days, like
blue lights, iPads, big screens very close to your eyes
that are emitting a lot of blue light, and we

(56:12):
know that this blue light can acutely suppressure melatonin. On
the other hand, the biggest source of blue light is sunlight,
and when you have a jet leg, the best way
to beat your jet leg is get out and get
enough sunlight so you resynchronize again. So we know that
there's like a balance between blue leg exposure in the

(56:33):
evening on one hand, but especially getting enough sunlight in
the morning that will resink your brain. So we've published
one study and I think there might be a couple
of graphs online about it, where we've looked at the
prevalence rate of ADHD in the United States and the
amount of sunlight you get throughout the US as so

(56:54):
basically a map where do I need to put my
solar panels. So we merit these two maps. Could find
that the amount of sunlight in California, for example, relative
to New York, would explain twenty five percent of the
prevalence rates in ADHD. So this is way more than
the current geogenetic influences we have found. And we've replicated

(57:16):
this now about three to four times, and it still
holds for mainland Europe in the US. It does not
hold for Nordic countries like Scandinavia. That's a whole different story.
Probably has to do with genetic differences in people being
more protected against low levels of sunlight because they're close
to the north.

Speaker 1 (57:38):
They're adapted in some way.

Speaker 2 (57:41):
So again the conclusion should not be takeaway all these iPads,
et cetera. Prohibition is something that I'm not a big
fan of as a Dutch Dutchman. But get people, get
people out in the sunlight. If you have your child
and you have a dog, well ask your child to
walk the dog in the morning. And you know the
story about where often they would say in classrooms like

(58:02):
well that hyperactificate kids, don't put it close to the
window because you will get distracted. Now we need to
invert it and say, well, yes, put that kid near
to the window, because they will get more sunlight catching
their eye and they will normalize. They're more lightly to
normalize their sleep in the morning. So more in the
early morning sunlight I think is a very important thing.

(58:23):
It's not going to cost the thing, it doesn't have
any side effect, it's not going to work for everyone,
but it might at least have some improvements. And if
at least twenty to forty percent of the people will
sink below the clinical threshold and not have a diagnose
of ADC, then I think we've won a lot already.
And also, I'm not advocating against medication. It's the most

(58:44):
powerful psychiatric treatment we have available, but I do think
that for many people we need to zoom in more
on sleep. Psychiatrists need to do their work better and
ask more questions about sleep, and maybe wearables use some
sleep red questionnaires to see if there's an other explanation

(59:07):
they can find for the symptoms, which is according to
the deism, they need to ask those questions. But most
people are simply too unfamiliar with sleep medicine to do
it an objective fashion.

Speaker 3 (59:18):
That is unbelievable that it explains twenty five percent. And
to your point, you're not saying we shouldn't be medicating,
but if a chunk of these people don't actually need
to be on the medication, if we can prevent them
going into that, that is clearly the way ahead. And
you know, I'm sure nobody's done the study yet, but

(59:41):
I would be willing to bet my house, my business,
and pawn my children on the idea that if you
also improve people's diet and getting them exercising, especially outdoors,
we would see a significant drop in those symptoms, particularly
when we we see some of the data coming out

(01:00:01):
that American and Australian kids are spending ninety percent of
their time indoors, right. And you know, we have these
circadian rhythms for a reason, and most people don't realize, Martin,
lots of your hormones run off circadian biology as well.
So it's not just the sleep, it's the widespread effect

(01:00:25):
throughout that biological system that is the human being that
is hugely important. So this has been absolutely fascinating. I
could talk for hours about this, but before I do,
let you go. I know you're involved in a number
of spinoff ventures where you're actually taking this research technology

(01:00:45):
and applying it. Tell me about some of the stuff
that you're doing that you're finding quite exciting now for
the future.

Speaker 2 (01:00:54):
Well, A Currently, we've had a couple of spin offlight like,
for example, the Whole Clinic where we by any it's
the TM since says what spun out as newer care group.
I think they also have clinics in Melbourne, Sydney, across
Europe and across the US as well, which I think
was quite exciting. Recently we also span out the EG

(01:01:15):
Prognostics department to Shineida where we do the stratification to
treatments using EG actually, so that also has basically, yeah,
given me a lot of time and then to think
about new things. I'm currently we see where the new
science is going to bring me some doing a sabbatical
currently at Stanford University on one end, wanting to learn

(01:01:37):
more about psychedelics, which I think is a really fascinating field,
and on the other hand, still pushing the research at
brain Clean's Foundation and collaboration with many partners on the
heart brain coupling. I think there's heart brain coupling to
form TMS is a very fascinating field. So that's mostly
the stuff that we're trying to focus on at this
point in time.

Speaker 1 (01:01:59):
That is some very cool stuff right there. I'll tell
you what.

Speaker 3 (01:02:03):
When I was a kid, I always admired explorers, and
there's not much exploration left to do in terms of
geographical exploration.

Speaker 1 (01:02:13):
But oh my god, are you in an area where there's.

Speaker 3 (01:02:16):
A lot of exploration to be done, and you're doing
some very very cool stuff. So so Martin, I tip
my hat to you, sir, and I love everything that
you've talked about here, the stuff that you're doing, it
is super exciting and hopefully that time in your sabbatical

(01:02:37):
spike some new neuronal connections and you'll be off onto
your next venture.

Speaker 2 (01:02:43):
Looking forward to that.

Speaker 3 (01:02:45):
And where can people find out more about you? If
they want to just look at your work words the
beggst place to send them.

Speaker 2 (01:02:58):
The best place to look at this our website, which
is brain clinics dot com so brain Clinics plural. Also
on LinkedIn, you can find my profile and connect me
via LinkedIn or reach out via email whenever people prefer. Now,
for those of those people that have an interest in TMS,
we have an upcoming TMS masterclass end of September beginning

(01:03:20):
of October where we invited some of the world leading
experts with very new insights on TMS. Some people are
doing TMS in one day rather than spreading out across
multiple days. Many new innovations will be shared. So for
those interested to do real deep dive, we have this
master glass coming.

Speaker 3 (01:03:39):
Up excellent Martin, thank you for your time. This has
been awesome.