Treating Traumatic Brain Injury with Ibogaine | Dr. Nolan Williams ~ ATTMind 188 - Adventures Through The Mind

Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
Hello everyone and welcome back to Adventures Through the Mind.
This is a podcast that explores topics relevant and related to
psychedelic culture, medicine, and research. I'm your host, as
always, James W. Jesso. This episode is going to explore
some of the groundbreaking research that has come out

(00:20):
recently around the use of the psychedelic compound
ibogaine in the treatment of mild traumatic brain injury,
also called concussions. Our guest is Dr. Nolan Williams.
[Music]

(01:04):
Nolan Williams, MD, is an associate professor within the
Department of Psychiatry and Behavioral Science and
director of the Stanford Brain Stimulation Lab. He has a broad
background in clinical neuroscience and is triple
board certified in general neurology, general psychiatry,
and behavioral neurology, and neuropsychiatry. Themes of Dr.

(01:27):
Nolan's work include examining the use of spaced learning
theory in the application of neurostimulation techniques,
development, and mechanistic understanding of rapid acting,
antidepressants, and identifying objective biomarkers that
predict neural modulation responses in treatment-resistant
neuropsychiatric conditions. His work resulted in an FDA

(01:51):
clearance for the world's first non-evasive rapid acting
neuromodulation approach for treatment-resistant depression.
He has published papers in high-impact peer-reviewed
journals including Nature Medicine, Nature Mental Health,
Brain, American Journal of Psychiatry, and the Proceedings
of the National Academy of Science. Further, Dr. Williams

(02:13):
also has an expertise in psychedelic medicines for
neuropsychiatric illnesses and is the first investigator to
conduct mechanistic clinical trials exploring the
neurobiological effects of ibogaine. Specific to that last
point, Dr. Williams was the head of a study run at the
AmbioLife Sciences Center in Mexico where he evaluated the

(02:35):
effects of ibogaine on veterans with brain injury, particularly
mild traumatic brain injury also called concussion. The first
paper released from these results is titled Magnesium
Ibogaine Therapy in Veterans with Traumatic Brain Injuries
and was published in the journal Nature in 2024. He joins

(02:57):
us on the show today to talk about brain injuries, generally
ibogaine, and the treatment of brain injuries with
ibogaine. We also talk about ibogaine as an anaerogen, the
cardiac risks of ibogaine, and how to mitigate them, how
ibogaine compares to other treatment methods for brain

(03:18):
injuries, including other psychedelic molecules,
microdosing ibogaine for traumatic brain injury,
and that ibogaine can seemingly de-age the brain.
Additionally, we also talk about pharmacology versus context in
the healing benefits of psychedelics, separating high
technology from time, and how and why using the vehicle of

(03:43):
capitalism to fund psychedelic research may be a good thing.
Okay, so that's the interview you're about to hear before we
get into it. Two things. Number one, this interview isn't two
parts. It's one episode, but it's two parts. I had to get on
two separate calls with Dr. Williams in order to get the
entirety of this interview, and you'll notice the bandwidth isn't

(04:05):
super great in the first one, but it's quite clear in the second
one. You might not notice a difference at all, but if you're
watching the video feed, you'll definitely notice a difference, so
a bit of a heads up there. The second thing is that this podcast is
brought to you by listeners like yourself via Patreon.
If it wasn't for my patrons on Patreon and their ongoing
continuous contributions to the production of the show and the

(04:28):
various costs, time-wise and material-wise, in its
production, I wouldn't be able to do it, and I love doing this, and I
love the larger body of work that supports it.
So, thank you patrons. An extra thank you goes to those who have been
giving quite significantly, and in doing so, their names are
presented on the screen here on YouTube or in the description to

(04:50):
this episode, wherever you are checking it out. So, thank you
very much to them. If you are finding value in the show,
and you're not yet a patron, you're not yet financially
contributing to the production of the show, I ask you to please
consider becoming my patron on Patreon. You can do so for as
little as $2 a month, and everything is something, and it all

(05:12):
adds up into the possibility for me to do this thing that I so
deeply care about as my full-time job and get paid a
full-time wage to do it. You can head to patreon.com/jameswjesso
or follow the link in the description to this episode in
order to check out becoming a patron. You can't afford to
become a patron right now, but you'd like to stay up to date

(05:33):
with what I'm putting out on Patreon. You can always become a
free member, and I encourage you to do so, and thank you in
advance. Without much further ado, here is my interview with
Dr. Nolan Williams on Adventures Through the Mind,
episode 188, Treating Traumatic Brain Injury with Ibogaine.
Enjoy. Dr. Nolan Williams, welcome to Adventures Through

(05:54):
the Mind. Yeah, thanks for having me. Appreciate it.
I am interested and excited for this interview because, I mean,
psychedelics generally, psychedelic medicine is a topic
that I'm very curious about, have a lot of excitement for.
Sometimes I've got an edge for the movement of the culture, but
that's an aside. But, specifically, the excitement is

(06:21):
pertaining to where this particular psychedelic medicine
or what it's treating, which is essentially traumatic brain
injury. And what makes me excited about that is that I
found out that you were doing this research. She's from a
friend of mine and also a colleague for many years, Trevor

(06:42):
Miller, who works at Ambio, which is the same center that
you did the research we're going to be talking about today at.
And I've also known Jonathan Dickinson for quite a while as
well, one of the other members of Ambio. In fact, he was, I
think, the third person I ever had on this show, which is back
several years ago. And I got a message from Trevor

(07:04):
explicitly telling me about this research because he had
learned that I had incurred a head injury from a car
accident now a little over two years ago. And he was like,
"Hey, you might find this personally interesting and
professionally interesting." And I was like, "You know what,
Trevor? You are absolutely correct. Fast forward some amount

(07:25):
of time. Your paper has been released and here we are talking
about it." So the paper is about the efficacy of using Ibogaine
in a combination with magnesium in a structured setting, that
structure being Ambio's sort of clinic or center there and the

(07:47):
effects that it had on veterans that had traumatic brain
injuries. Now, I want to explore that piece by piece throughout
the course of the interview and starting with specifically,
maybe seems like an obvious question, but it's quite a
complex question, which is what is a traumatic brain injury?

(08:08):
And you could tackle this and/or the causes, symptoms, prevalent
impact on persons in society, however you want to tackle the
question. Yeah, that's a good question. So whenever the head
gets accelerated and kind of immediately stops, what happens

(08:31):
is that the components that had the brain, the skull, all that
stuff, the cerebral spinal fluid decelerates at different
speeds, and the brain decelerates slower than the skull.
And what that does essentially is it allows for the brain to

(08:54):
impact the skull and effectively hit the skull. And that's
what you see, whether it be football, TBI, or even a blast
injury or whatever, that the brain moves in a different way
than the skull moves, since the brain effectively hits a part of

(09:14):
the skull and causes injury to the brain, because obviously the
brain is less hard and less dense than the skull. And so
there are kind of standard ways in which that happens. And
that's kind of the frame that this kind of falls under.

(09:37):
So in the case of military TBI, a lot of it ends up being blast
injuries and whatnot, where people get thrown back and their
brain actually accelerates quite quicker than their skull.
Their brain effectively smashes into a part of the skull and
causes a dysfunction. And that can produce a whole host of
symptoms that for some people persist ongoing.

(09:59):
Can you give us a sense? I guess any kind of injury can
take a number of forms. If I think about injuring my knee,
I could tweak it a little bit and it hurts for a little while
and I cause minor damage, but it's whatever. Or I could have a
minor strain or I could fully tear my ACL. I could shatter my

(10:25):
part of the bone or something. There's like a wide range of
potential injuries that can occur when I say fall on my
knee. What's the sort of range for the kind of what will
qualify as a traumatic brain injury? You don't have to go
into every single one, but at its least extreme, it might be

(10:46):
like this. At its most extreme, what has happened to the brain
would be diagnosed as this. Just give us a sense of the range.
Yeah, I mean, so there's mild, moderate, and severe traumatic
brain injury. Severe traumatic brain injury is seen on
structural MRI. It usually takes the form of a kind of a

(11:08):
traumatic subarachnoid hemorrhage or a contusion of
the brain. So basically there's some bruising bleeding that
happens alongside structural injury. You can have people get
in car accidents and they can have the orbit fracture backwards
and hit the orbitofrontal cortex and cause contusions and whatnot.

(11:29):
So that's all kind of within the range of possible kind of severe
TBI, whereas mild range of what we think about as a concussion,
really, there's nothing on brain MRI. There's nothing on CT,
standard MRI and structural MRI and CT. So you're really just
seeing a kind of functional impairment and then a headache,

(11:49):
nausea, vomiting, that sort of thing. And so there's a big range
of what you can experience from the severity. And then because
the brain has different functions in the place in which
the brain accelerates and hits has a different function,
you can have a host of symptomatology that presents

(12:09):
as a result of where on the head you were hit or which
direction the blast injury happened.
Yeah, like say theoretically, I could hit my head in a part
that is like that area of the brain is more involved with,
say, emotional regulation or I could have the trauma happen

(12:32):
somewhere that's more involved in sort of like neuro-optical
function. So on one end, I could have a lot of emotional
dysregulation, on another end, it might present as like
difficulties and sort of like managing my I function. Is that
kind of what you're speaking to?
Yeah, yeah. So it's anatomically specific, as is everything with

(12:53):
the brain, right? If you have a stroke in one region, you have
one set of symptoms, you have a stroke in another region, you
have another set of symptoms, you have a, you know, whatever
other, you have a seizure in one part of the brain, you're gonna
have a set of symptoms, you have a seizure in another part of
the brain, you have a different set of symptoms. So that's the
complexity of the heart is that the trauma inflicted has a

(13:15):
gradation of severity, as well as a location specific
symptomatology that coincides. So that's the, does it make
sense?
Yeah. And so like TBI as a term refers to like a possibly quite
a huge range of both sort of like, what's injured, how it's

(13:36):
injured, and are like what part of the brain, but like what's
injured, how it's injured, the severity of that injury, and it's
sort of like, its symptom expression.
Yeah.
And I'm wondering what, like, if you could give us a sense of
what the impact that would have on a person and then maybe

(13:57):
expand that out into society as well. Because, you know, even
if you said, you know, they could have headaches or, you
know, dizziness, etc. But there's a whole range of other
symptoms that people with head injuries tend to have going all
the way into increased sort of anxiety symptoms that present
as post traumatic stress disorder, depression, like

(14:18):
ongoing sort of like energy, crisis, these kinds of things.
What would you describe as the sort of impact a head injury
could have on a person's life?
Yeah.
So, you know, any neuro dysfunction, whether it be head

(14:40):
injury or stroke or whatever it is, can have profound impact
on quality of life and ability to perform activities of daily
living, right? Those are the two things that people think about
as a kind of general metric that's not neuro atomically
specific, right? You know, my ability to get everything done
I need to get done my ability to be happy with my own life,

(15:05):
right? And traumatic brain injury symptoms that are
chronic affect both of those things, right? They reduce your
quality of life and they increase they reduce the, you
know, the amount of activities of daily living that you can be
involved in, that you can perform yourself, right? And, you

(15:27):
know, that's a huge personal cost and it's a huge societal
cost, right? The personal cost is the personal cost is that,
you know, quality of life years are reduced, you know, so it's
not just, you know, you can think about the number of years

(15:49):
you live, you can also think about the number of years that
you live well, right? And you want, from my vantage point, you
want to live a long life and you want to live a healthy life,
right? If not all of it, right? And traumatic brain injury, you

(16:13):
know, at minimum reduces for some people the number of
quality years they have. And then depending upon the
interaction between that and other factors, it can even
reduce, you know, lifespan, you know, if it's associated with
other medical comorbidities. And so I think, I think that coming

(16:35):
up with ways of reversing disability related to anything,
including traumatic brain injury is super important. I think that
the promise of neuroplasticity psychedelics are the ability to

(16:59):
potentially have a restorative effect beyond just a symptomatic
improvement. Symptomatic improvement is great.
Restoration, neuro-restoration is the name of the game, right? If
you can restore function to pre-morbid levels, that's super
important. And just to clarify, because you cut out there for a
second, you were, you had said that the potentials of like

(17:23):
neuroplastic effects of psychedelics can have like
long standing positive effects on like brain injury, not just in
reducing symptoms, but even just like bringing back a more sort
of like functional brain. Is that what you're saying there?
Yeah, I mean, in the like, kind of sci-fi range of the

(17:44):
possibilities of what this is doing, right, if you can, you
know, if you can restore function to pre-morbid levels by
having a neurotrophic effect, having an effect where you're
effectively, at least in kind of mild cases, as we saw in this
study, like, seemingly restoring function, you know, restoring

(18:06):
function is different than symptomatically improving
something, right? I can have heart failure and have a terrible
heart and give drugs that restore my heart's ability to
might that can, can reduce the symptoms of congestive heart
failure, such that while my heart's the same, I'm not having
shortness of breath and water in my lungs and stuff like that.

(18:29):
But my heart's the still the same, right? If you do an
echocardiogram, that drug really hasn't, in some cases, hasn't
changed the nature of my heart. It's just like, change the
physiology such that like my bad heart works okay, you know, for
symptom, you know, symptomatically. That's very
different than saying, you know, I've got a drug that can

(18:52):
effectively reverse congestive heart failure, we don't have
drugs that can totally reverse congestive heart failure to a
point where people don't meet criteria for congestive heart
failure, right? And so even in the heart, which we know a lot
more about, we don't have like, completely restorative
technologies. So the idea that, again, and they're kind of, I

(19:15):
don't, we don't totally know, right, but in the kind of sci-fi
range of what this could do, you know, and what, you know, some
people are hoping it can do, we have a lot more work to do to
figure out if that's true, is that you could have some
restorative function, right? You're bringing the brain back
to some place that it was at pre injury. And that's the part

(19:37):
that I don't know, but it seems to me like, if there is a drug
that could do it right now, that Ibogaine has, you know, is one of
the best candidates for that, given what we've seen. But we
just don't know, we have a lot more work to do to really figure
that out.
I want to dive specifically into Ibogaine, and then the results

(20:02):
that you got out of your study in a minute. But I think I want
to really like double down for listeners who, like even myself
as somebody who is still in the sort of long running effects of
what, you know, post concussion syndrome, the amount of sort of

(20:23):
misunderstanding I had about the, about the condition and
about its impact and the amount of misunderstanding and
misperception that the sort of like, larger society has on on
how this would impact a person, I want to kind of like, really
help accentuate that. It's I've heard it described oftentimes

(20:44):
as like an invisible injury. Like if you see somebody walking
on crutches, you know, right away, oh, they have some sort
of, you know, orthopedic condition that means that they
need to rely on this thing to walk. But you don't generally
see and be like, Oh, that person has a brain injury, you just
perceive their behavior, or they're sort of, you perceive

(21:07):
their behavior in a particular way, and not recognizing that
sometimes both as a consequence of the symptom, and as a direct
symptom, their ability to function cognitively,
emotionally, relationally, socially has all been
compromised to a point that makes it extremely difficult
and sometimes problematic for not just the person, but their

(21:27):
relationships. For example, from what I understand, there's a not
insignificant sort of observation that emotional
destabilization and of course, from that problems in relating
even as far as like intimate partner violence could be a
direct consequence of changes that happen to the brain from

(21:49):
brain injury or repeated concussions. I think I just
want to make that clear for listeners by saying it. But if
you'd like to comment or sort of like expand on any that I
welcome you to do so.
I mean, there's, you know, there's a huge, like I said,

(22:13):
it's much more about the neuroanatomy and the severity
than it is like that it's TBI per se, right? You have the same
symptoms of somebody has a stroke in the same region, right?
It's not a, it's not like, hyper specific to TBI. The problem
with TBI and constructing therapeutics for TBI is that
there's no symptom, there's no good symptom scale, right? If

(22:34):
you have a visual cortex hit, you're going to have a very
different set of symptoms. And if you have a prefrontal cortex
hit, or primary auditory cortex, or whatever it is, right, like
there's, there's just like a whole host of potential
symptomatology that aligns much more with the anatomy than it in

(22:54):
the severity than it does the specifics of TBI per se, but the
idea that brain injured persistent brain injuries can
manifest in a huge range of symptomatology makes sense
because the brain can manifest its behavior in a whole huge
host of potential behaviors that you see for people walking

(23:15):
around in the streets today, you know, and so it just falls
within that same big range.
I want to before I specifically move on to Ibogaine, this is the
last question I have about TBI specifically, which is, you know,
you spoke to like the huge implications this could have on
compromising someone's quality of life and ability to function

(23:38):
in life. I'm wondering what kind of metrics there are with
respect to the amount of TBI that is happening broad scale, say
in the United States, I believe that's where you're located. And
what the sort of proposed impact of this sort of amount of TBI is

(24:00):
is having on society as a whole, as we understand like the
necessities of a person's function within our socio
economic system.
Yeah, I mean, that's probably pretty hard to quantify just
because, you know, we don't even know, a lot of people have had

(24:21):
at least a concussion at some point, right? And we don't even
know the the, the scale of that the implications of that, it's
probably super under diagnosed, because a lot of people just
shake it off. You know, are there persistent symptomatology
related to that? It is some of the risk of what we think about
as idiopathic psychiatric illness. So the things that we

(24:44):
think are just spontaneous or happen as a result of like,
stress within one's life, how much of that is actually
post traumatic mild traumatic brain injury, we just don't even
register that, right? So I think the question is a good one. The
answer is completely unclear, you know, it's it's seemingly very
broad. You know, from from what you can kind of read in the tea

(25:08):
leaves of how many people have had a concussion in their life,
you know, and how many of those percentage of those people have
had, you know, a subsequent psychiatric illness, you know,
it could be a fair amount of those that at least that was a
risk factor for but we don't we don't really we don't really
know, you know, I think what we do know is the folks that have

(25:31):
had a reasonably pretty least reasonably significant, let's
say sports related concussion that everybody on the field
visit, you know, can kind of visualize as it happens, or
people that are in blast injuries in the military that
have some set of symptomatology that their fellow military kind

(25:54):
of acknowledge is a change. But you know, even with, you know,
the sort of thing, the were, were folks have, you know,
ex football players or boxers or whatever, like 20 years later,
start having these cognitive problems. Even in some of those

(26:14):
cases, it's not a direct head injury, right? It's, it's
repeated body injury, like body pressure injuries where people
get hit in their stomach, and then there's a force transmitted
up to the head, for instance, right, and there's repeated
body hits that happen over and over again. And that seems to
have a negative, you know, negative impact on the brain,

(26:37):
because you're transmitting high amounts of force up to the
head, you know, we just don't, we don't have a good handle on
this, because none of it's being measured. You know, nobody's
really going around and kind of measuring other than some of
these, like football helmets that people have made and that
sort of thing. But, you know, there's probably there's, there's a

(26:58):
paucity of kind of brain measurements at, you know, at
large in society that can answer that question. I hope in 20
years, we, we, we have metrics and measurements that are
continuous measurements that can tell us some of this.
But from your, if you were to, if you were to make a sort of

(27:19):
educated guess from the data that you do have, you do feel
like it would be fair to say whatever that effect is, it's
likely substantial?
Yeah, I think so. I mean, it's, you know, anything that crosses
the 1% mark in culture and society has a huge impact,
right? I mean, we know that, you know, and so just by the scale

(27:44):
of things. And so in that way, absolutely.
So let's move in directly into Ibogaine. So I kind of wanted to
structure it like, okay, this is traumatic brain injury, that's
its own little island, you know, this is Ibogaine, that's its own
little island. Now let's, you know, explore the waters around
these two things where that where they sort of meet in the in
the tidal flow. So with that, what what is Ibogaine? Can you

(28:08):
give me a little sense of what this molecule is and how it
affects the brain?
Yeah, it's a it's an alkaloid of the the Iboga root bark, which
is the Iboga tree is a central West African tree. The root bark

(28:32):
is contains a host of alkaloids, including Ibogaine. But there
are others, Ibogalein, Ibogamine, you know, on and on.
So it's not the only alkaloid. The buliti have used Iboga root
bark ceremonially for for millennia. The French discovered

(28:55):
this in 1899. And by 1930, isolated Ibogaine and turned it
into a drug that was used in France until 1966. Then that
went on the Controlled Substances Act in France. And, you know,
as a Controlled Substance Act in the US and other places that
that limited use of these these compounds. Every country, not

(29:20):
Canada, not Mexico, not Australia, not New Zealand. And
so Ibogaine is kind of unique in the sense that it didn't get
kind of worldwide band, it got banned in certain places. And,
you know, it's been used kind of in these underground clinics
since the 70s to try to treat folks with with a variety of

(29:43):
symptomatology, but primarily in the addiction range, you know,
and the kind of opiate use disorder and related addictions
in it. For some reasons, we understand for some reasons, we
don't seems to interrupt addiction. And then, you know,
much more recently, there's, there's been an interest in in

(30:03):
utilizing this as a neuroplastic agent to try to treat people
with brain injury, as you noted earlier.
What do we know about about the direct pharmacological effects
of Ibogaine unrelated to, you know, treating a particular
condition or disability or injury? What do we know about

(30:26):
just broad scale Ibogaine goes in, this seems to happen in the
brain? Yeah. So it upregulates neurotrophic factors like glial
derived neurotrophic factor, brain derived neurotrophic
factor, and produces, you know, a whole host of interactions with

(30:47):
the serotonin receptor with with the opioid receptors with
glutamate receptors. And so it works kind of like ketamine, it
works kind of like MDMA, it works kind of like classic
psychedelics, it has this really broad effect. And the kind of
synthesis of all that is that it produces this very stereotype
psychological phenomenon in which people have a earlier life

(31:12):
reevaluation of memories that primarily were emotionally
salient. And for a lot of people end up being traumatic in which
they reevaluate the memory in a neutral third party stance, and
they're able to re contextualize it and then seemingly reintegrate
the new context into their memory system such that the

(31:36):
traumatic aspects of it change and people have a better
understanding of what it is. And so that's, that's the, you know,
that's the drug both phenomenologically and
pharmacology pharmacologically.
Now I, I did, you did refer to it as a psychedelic, I understand

(31:57):
that to be a very fair characterization, although, and
you'll have to forgive me if I'm kind of like confusing this
because I read a couple of papers on the effect of ibogaine
including including yours to prepare for this interview. So
it might not have been used specifically. But the
referencing ibogaine, not just as a psychedelic, but also as an
onyrogen, which is like a substance or chemical that

(32:22):
generates dreams or dreamlike states. Can you just let me know
if I'm just like misattributing that to you? But if so, can you
outline a little bit why it would sort of fit as an
onyrogen as well as a psychedelic in contrast to say,
no one's calling psilocybin an onyrogen?
Yeah, so the reason why people think about as an onyrogen is

(32:44):
that it produces a dreamlike phenomenon in which that
reevaluation occurs, right? And it's all like, you know,
primarily closed eye reevaluation, it's not an open
eye, kind of visual distortion, visual, you know, hallucination,
visual, perceptual change that happens with say, LSD or

(33:04):
psilocybin, right? And so, you know, it's these things are
imperfect, right? You know, the psychedelic terminology you
talk to, a really strict folks who have this kind of very
a psychedelic, a receptor agonist in order for them to

(33:32):
accept it as a psychedelic and only classic psychedelics like
psilocybin else to really fit into that bucket, you know, and
then that's kind of the splitters and the lumpers will
think about ketamine, even in MDMA is psychedelics, and the
splitters are going to say that, you know, that's the ketamine
is a dissociative anesthetic and MDMA is an intactogen or an

(33:56):
empathogen, right? So it's, these are splitter, lumper
problems, it's not really like, you know, and so, you know, you
can call it an erogen, I think it's totally fair to call it a
psychedelic in the paper, we call it an atypical psychedelic.
I think the nice thing about referring to it as an erogen,
which is how we primarily referred to it in the paper is,

(34:18):
you know, there's there's baggage on LSD, you know, and
that baggage is going to stick around for a while until the
boomers are, you know, until it's 2060 or something, you know,
to be in and so it's one of these things where, you know,
from from that standpoint, you know, there's there's some

(34:38):
baggage around the term psychedelic, there's some baggage
around some of the psychedelics, that's going to take some time
to shake, I think. The nice thing about Ibogaine as a
therapeutic agent is that Ibogaine does it is not, you
know, is not a recreational substance in any form or

(35:00):
fashion, right? You can make an argument and a pretty strong
one that MDMA can be a therapeutic MDMA can be a
recreational substance, you know, as we all know, right,
people were using MDMA and raves, they probably continue to do
so, you know, we're going to see an FDA approval for this
hopefully, in the summer, you know, I don't think that that's

(35:20):
the that's going to be a fair characterization of Ibogaine at
all, right? It's not recreational, people don't
particularly enjoy it, for the most part. And, and because of
that, it's not, you know, it's not something that I think we're
going to have as much of an abuse liability risk on. And in
fact, like people, you know, the stories of Howard Lotsoff and

(35:42):
others were, they ordered this because they wanted to have a
therapeutic, a recreational effect when nobody knew what it
would really do. And they had a therapeutic effect, but not a
recreational one, right? And a lot of what you hear about with
Ibogaine too, is that people are not, if you, if somebody takes

(36:05):
Ibogaine, you have a conversation with me, so it
really helped me, I was like, Oh, when are you gonna do it
again? Like, I don't know. I'm not really sure. I'm gonna do
that again. You know, I don't know if I'm gonna go through
that again. You know, and so it's one of these things where,
you know, and that's not everybody, you know, I'm sure
Trevor and Jonathan have some friends or whatnot that that
I've done it multiple times, but as a generality, it's not, it's

(36:30):
not something that like people are like jumping to do the next
week, right? You got to be really intentional about it. And
it's not a frequent use thing. So it doesn't really fall into
the abuse liability tolerance kind of story. Whereas ketamine
certainly does, you know, and some, for some folks, you know,

(36:50):
MDMA does, you know, and then I think like the classic
psychedelics, it's more, more in the middle, right? People will
take those a burning man or whatever people will not take
them in a, you know, an abuse liability sort of way,
generally, so it's kind of pretty low risk, but but also,

(37:10):
you know, reasonably recreational.
Yeah, it's exciting to see the sort of, you know, medical
potential or like just even the research potential of ibogaine
because of what you just described there with a kind of
like not necessarily having that same baggage and not necessarily
having that same abuse liability, sort of potential. And also

(37:34):
to its, its, its regulatory status makes my assumption is it
makes it perhaps easier to do research on it than it would if
it had no.
No, and that's because of the cardiac risk, right? And so it's
probably the hardest to get through the FDA, because of the
risk of having an arrhythmia, but it's not really the

(37:56):
psychedelic effects as much as it is the cardiac risk and it's
kind of long tail of drug, you know, in system, you know, it
lasts for a while. And so that's really the issue from
regulatory standpoint is that there's been deaths, right?
Primarily in people with opiate use disorder and addiction and

(38:17):
whatnot. But even in the absence of that, there have been, you
know, a couple of cases of people that didn't have that. And so
studying this is very hard. You know, we did this study with
Ambio for that reason. You know, our plan is to, you know, to
look into trying to do a US based trial or trial in, you

(38:38):
know, a country that is accepting to do a trial, you
know, normal healthy control trial in this, but it's now
going to be under a regulatory auspice, you know, under, you
know, kind of the monitored settings that regulatory bodies
would want. And that's not straightforward, it's going to
take some time, it's going to take some work to get that done.

(39:00):
But it's worthwhile to do.
Yeah, I appreciate that clarification. And also it
speaks to another aspect of Ibogaine that is unique under the
the Lumber's categorization of psychedelics, which is that, you
know, you could, you could effectively die as a direct

(39:21):
result of what Ibogaine does when you put it in the body,
like, you could theoretically die under LSD or psilocybin, but
this is usually as a consequence of, you know, with the dose that
you would have to take to directly kill you, the LD50 of
psilocybin is massive. But you could theoretically die as a
consequence of choices that you make when under the influence,

(39:44):
but with Ibogaine, you could directly die as a consequence of
its effect on the heart. And I understand that and I'm going to
ask you about the study, just this next questions about the
study, so don't go too much into it yet. But I understand you
attempted to compensate for this potential risk with an aspect of
variable that you put into your study design. But can you tell us
what that risk is? Like, from what I understand, it's, it has

(40:07):
something to do with the interval between heartbeats,
that in some people, the interval can get so wide that
the heart just stops beating completely.
Yeah, yeah, you're very close. Yeah, that's a great, great
understanding. So essentially, there's a there's a receptor, a
potassium channel receptor in the heart called the HERG Herg

(40:28):
potassium channel. It's very well characterized. There are
drugs that are FDA approved that have an impact on her and so
chemo drugs, actually some anti rhythmics can be anti rhythmic
and pro rhythmic rarely. So they're anti rhythmic, almost
everybody and then pro rhythmic and a small group of people. And
in that group of people where they're pro rhythmic, I mean,

(40:50):
you know, the in this case, tikka send is the drug where it's
pro rhythmic, it can cause a widening of the q t interval,
the interval you're talking about and the q t interval
widening past a certain number of milliseconds increases your
risk of going into another rhythm called torsades de pointe,

(41:12):
which is a an arrhythmia that is not I became specific, again,
it can be induced by a whole host of things. And it's a fatal
arrhythmia, meaning that if you don't get somebody out of that
rhythm, they're going to die. Right. And so, so, you know,
torsades is a is a risk that that, you know, you don't want

(41:36):
to have with any drug, I being has that risk. It's somewhere in
the one in 300 range, the risk with tikka send is closer to one
in 100 range. You know, there are other chemo drugs that have
a risk there too. The way to deal with it is a combination of,
as we see it prophylaxis plus monitoring, right. And the

(42:00):
prophylaxis piece is utilizing a range of compounds that have
been shown to shorten q t interval and reduce, reduce
risk of, of torsades and other arrhythmias and q t
prolongation. And so, you know, like, you know, IV magnesium is

(42:21):
one of those potassium is another calcium is another. So
we know those three, you know, elements can do it. oral
lidocaine can actually do this. So there's a host of cardiac
agents that have been shown in various experimental
manipulations to do this. And so what's novel about this kind of

(42:43):
vantage point is this idea that that essentially we can modulate
this, this risk by, you know, by pre administering it in
everyone. So
the next question I had for you is now that we've talked about

(43:06):
TBI generally and Ibogaine generally, specifically, I want
to go into the study that you ran with Ibogaine. Tell me, tell
us about your study, the design, and I guess, in some sense, what
drew you to investigate the potential of Ibogaine for this
purpose?
Yeah, you know, I guess your last question first, I've, I've

(43:27):
always been very interested in Ibogaine since I came across it,
you know, more than a decade ago. You know, I was in a in the
airport in a pretty much Central American country and, and was in
a books, like a bookstore in that airport. And there was not
a whole lot of English books, but for whatever reason, Breaking

(43:51):
Open the Head was one of the classic Daniel, like, yeah, so I
read that, that book, got it really interesting. And
obviously, he has a part in there where he went and had an
Iboga ceremony and then read a lot about it, you know, from the
experiences that folks had written up around opiate use

(44:15):
disorder. Got pretty convinced that it was a useful compound
for that, but then thought it was reasonably unstudiable,
right, because of the regulatory hurdles, one would have to get
over to do something in the US, given that it's a psychedelic,
which is kind of problem for FDA number one, especially back in

(44:36):
2010 or 2012, or whenever that was. And then on top of that, the
issue of the cardiac risk, right, and the fact that, you
know, folks had a cardiac, there's, you know, one in 300
roughly risk of torsades and death in the opiate use disorder

(45:01):
population, which I think is in part more specific to that opiate
use disorder population, but this is a generality. And so,
you know, you're kind of thinking in those those terms
kept it on the radar, you know, but didn't think it was kind of
immediately actionable, got out to Stanford working on other

(45:23):
things, and then had heard about some early veterans that had
been, you know, treated with with IBM for for PTSD, TBI
related symptomatology depression, and kind of
reengaged into the idea, connected with a number of folks

(45:46):
that you probably aware of, you know, the vets, co founders,
Martin Polanco, others, and talked to everybody and kind of
came out of that conversation with a, you know, conviction
that this was something that would, you know, would be
helpful, you know, to folks and one needed to construct a study

(46:10):
around that. So we went to the Stanford IRB and developed a
trial that would let us, you know, evaluate veterans before
they went to went down to Mexico to participate in this sort of
in this sort of a study where essentially they would be
evaluated by us, they'd go down there, receive treatment and

(46:32):
then come back and be reevaluated at multiple time
points. So
and
the retreats that they were going on, like your study team
wasn't adding anything in particular, or was there
anything specific that your study team was adding to what
otherwise would have been or subtracting, perhaps of what

(46:53):
otherwise would have been the standard sort of retreat
experience for people before and after your testing?
That's a great question. Yeah, you know, I mean, one of the
things that normally happens is there's normally a five m e o
DMT administration that that happens right after the Ibogaine
and we delayed that past our one month follow up very

(47:18):
intentionally to see an Ibogaine only effect, you know, and so in
some ways that was specific to the study, in the sense that
these individuals signed up to know that they weren't going to
get the five m e o. You know, in addition to the Ibogaine, it

(47:38):
really made it for a much more pure Ibogaine question. But you
know, but we didn't, we didn't have an effect on the, you know,
some of the other kind of sweat lodge stuff and that sort of
stuff still happened, but was, you know, limitation in the
right up of the trial.
And what kind of things were you testing? Like what what measures

(48:03):
were you getting before and afterwards that we're allowing
you to track changes?
Yeah, and so, you know, there's multiple layers and levels of,
of kind of assessments, right? But there's like gold standard
FDA level assessments that that, that folks use to get drugs

(48:24):
approved by the FDA, right. And so, you know, there'd been a
couple of studies out there, where folks had used kind of
not FDA compliant sort of measures, and they saw some
effects, and that's great. Mostly patient subjective scales,
which have a lot of, you know, confounds because it's not, it's

(48:47):
not as objective as, as a clinician rated scale, clinician
rated scales aren't completely objective, but they're better
than the self report scales. And so we put together like, like
an FDA, you know, gold standard kind of level of clinician rated
scales that we did with with everybody before after one

(49:08):
month, and then we have followed it out to a year, as well as
neurocognitive evaluations, right. And so the idea of being
able to get a neuro behavioral readout of what various
executive functioning scales read out to look like, as well as

(49:30):
biological measures. So EEG MRI, both functional MRI, structural
MRI. And the goal there was to get, you know, a really, really
complete data set that captured, you know, what is the kind of

(49:51):
the most comprehensive, I began related neurobiology study that's
been conducted, right, nobody's really looked at the effects of
Ibogaine on on the brain, and as well as kind of the most
comprehensive clinical evaluation of what Ibogaine is
doing, from a cognitive psychiatric neurological
standpoint. So pretty exciting to be able to do that.

(50:14):
And you measured things that had to do with their sort of the,
like you said, so objective pictures, MRI, fMRI, EEG, this
kind of thing. But then also, you were measuring their level of
like how they qualify for degree of post traumatic stress
disorder, depression, I'm not sure what else. And then the

(50:38):
neurocognitive testing was because TBI, one of one of its
primary consequences is, you know, compromised, cognitive
function, working memory function, executive function.
And so that's why you included those tests as well.
Yeah, that's right. Yep. And now I understand that you there was

(50:59):
something and I'm not sure if this is normally a part of the
program, that's at Ambio, the center that you that you were
doing this research with. But you added something else, you
added magnesium to the treatment protocol. Can you explain what
that was all about? And why you chose to include that?

(51:19):
Yeah, so magnesium is a is the treatment for torsades to point
the arrhythmia that that can happen with Ibogaine, it can
happen with other drugs, actually. So anything that's a
QT prolonging agent. And we've known for some time, and it's

(51:42):
actually part of the American Heart Association guidelines to
provide Ibogaine, I'm sorry, to provide magnesium in the setting
of torsades. And, and so that's kind of the known treatment for
for torsades. But there hasn't really ever been any

(52:05):
descriptions of using magnesium or any other any other element,
you know, for prevention of a drug induced torsades or QT
prolongation. There's some studies around cardiac surgery
related QT prolongation. And some studies around using

(52:27):
oral lidocaine for for drug induced QT prolongation. But
that's the general idea is that, you know, this, this is one of a
host of potential cardiac protectant sort of drugs that
could could have an effect. And so, so that's, that's the general

(52:48):
idea of why that combination makes sense for that purpose.
And was there a particular particular reason why you
focused on a veteran population for this initial trial, or this
particular trial, rather than sort of larger subset of TBI

(53:12):
people, like why you went specifically to veterans?
That's, you know, that's who's at this stage of the game, who's
going down there, who's willing to go down there, you know, and
so there've been a couple of NFL players. And, you know, there's
some interest, you know, with with professional sports, but
not at the level of the of the military, it makes some level of

(53:35):
sense, like in retrospect, why, why that group would be willing
to do it, right? If you think about it, they're the ones that
are tolerant of one in 300 death risks all the time, right? I
mean, I don't think that's what the risk is here. But that's,
that's the kind of reported risk in the literature with an opiate

(53:55):
used to sort of population. And so, you know, they before the,
you know, before this is at scale, well, there's still, you
know, a handful of folks, every single one of those veterans was
pretty much accepting the assumption that they were
accepting a one in 300 death risk. And it inherent in that,

(54:19):
which is, which is pretty interesting is, you know, the
calculation that maybe their death risk is higher with not
doing it. Because of the suicide risks that these guys encounter
and to my knowledge, there hasn't been a single fatality
from Ibogaine, you know, in these individuals, but there's

(54:40):
plenty of fatalities from suicide of folks that didn't get
it. So I think, on balance, you know, we're gonna have to see how
the data plays out. But, you know, it's, it's probably true
that the risk is higher in the untreated groups than in the
treated groups. But, but that's the thing that's kind of a

(55:04):
speculation at this point, not something that we have any real
super hard data on, we have like 1000, 1000 veterans that have
gone down there, but we need to be able to do this at scale to
really know that but it's an interesting problem, right? That
that's hard to kind of deal with from a regulatory standpoint,

(55:24):
point and like a societal standpoint, when the risk of not
taking a drug is higher than the risk of the drug itself, or an
intervention, it's higher than not having the intervention
itself. And that's certainly where the state of everything is,
right? The oral antidepressants that are out there don't have a

(55:46):
particularly good anti suicide effect, you know, they don't
really seem to have one much at all from from the, you know, the
studies have been done. There are a handful of drugs that do,
you know, it, you know, at scale societal levels, but in
individual studies, don't, it doesn't play out like lithium,
you know, and so it's one of these things where, you know,

(56:08):
it'll be interesting to see is there's more work done in this
space, if we can, you know, have a really substantial reduction
in suicide risk. And if we do, then that's a that's kind of a
big deal for for this group in particular, and then for society
more generally.
So with the group of veterans that you had going down there,

(56:33):
did every one of them qualify as having, like evidence of a TBI
either sort of report it reported evidence or something
visible on a scan somewhere? Or were there was there possibly a
mix? Yeah.
Yeah, mild TBI. So mild TBI and concussion are reasonably

(56:58):
interchangeable terms, you know, in the sense that they both
refer to a traumatic brain injury that does not yield a
structural abnormality on a standard MRI or CT scan. Right.
So when you go and look at their brain, in the kind of normal

(57:19):
scans, you don't see anything. If you look at their brain, you
know, there's this kind of DTI diffusion tensor imaging work
that people have done in various ways of analyzing that, where
you can see that they're what they call pot holing and various
things where there's small tears in the white matter tracts from

(57:41):
the sharing effects of the, you know, this acceleration
deceleration, which is effectively what you're dealing
with, right? You know, with a TBI, I think I said this last
time, too, that your brain is just decelerating at different
rates, so that the, you know, essentially the brain itself is

(58:01):
accelerating and stopping at a different time than the skull.
So if you hit your, if you're, you know, if you're riding your
bike, and you slam your head into a concrete wall, the first
thing that's going to hit is your skull, and it'll stop. But
your brain isn't going to stop quite yet. Right? Your skull
stops, and then, you know, almost, you know, whatever,

(58:24):
milliseconds later, seconds later, whatever it is, the, the
brain will hit the skull and then stop. And so it actually
decelerates on a different time scale. And when that happens,
then you can imagine there's sharing effects on the white
matter tracts that are in the middle of the brain,

(58:45):
particularly around the thalamus. And so, you know,
there are experimental imaging modalities that can show what we
think are abnormalities in mild TBI, but we don't see it with
normal structural scans. There's only one or two people that
actually had abnormalities on a structural scan. Now, the reason

(59:07):
to do that is, you know, you always kind of want to start in
these sorts of studies with a kind of milder folks and see if
you get an effect because if you don't see an effect there, then
it doesn't make sense to go to more severe populations. If you
get an effect there, then you march it up to a more severe
cohort. And that's really, that's really what we did. So

(59:29):
so everyone in your study classified under like a mild TBI
or concussion, you didn't have anyone that had any like obvious
brain damage or or anything like that,
we had like one or two that had had obvious structural scan kind
of moderate TBI. But but the vast majority of people it was it

(59:50):
was, it was mild. Yeah.
Okay, so then what did you what did you observe? Like on the on
the other side, where you've analyzed the data now you've
put out the paper like, with respect to Ibogaine, I guess, in
addition to magnesium, it seems like magnesium was less about
adding to the Ibogaine effect than taking away from the from
the risk.

(01:00:11):
Yeah, that's right. Exactly.
What did you see? Were the like, what did you observe is the
effects Ibogaine had on these veterans with TBI and the
variety of their symptoms?
Yes, so we saw a reversal of traumatic brain injury
disability. We saw a improvement across a broad range of

(01:00:36):
idiopathic psychiatric illness or depression, PTSD, anxiety,
and reduction in suicidal ideation, and that, you know,
reversal of disability on the hudas. And so it's, you know,
that was the particularly robust finding was seeing that, you

(01:00:58):
know, one month, most of these folks had gone into no
disability from mild to moderate disability, which is pretty
striking.
And what about the cognitive function? Like, was there a
notable change in people's cognitive functioning as well?
Yeah, the cognition improved across the board as well. Yeah,

(01:01:19):
so it was pretty great.
How, how significant are these results in the sort of like,
larger field of TBI treatment?
Well, there's no, there's no kind of biological therapeutic
for TBI. And so everybody is always looking for TBI
therapeutics that would be of interest, you know, and this is

(01:01:41):
definitely, you know, one that that's promising, you know,
there was a an editorial that accompanying editorial written by
Dave Brody and Sean Siddiqui or TBI researchers, and they, you
know, they felt that the study was compelling and worthwhile
pursuing more, you know, data on. And that's important, you

(01:02:05):
know, because they've been really the only ones, you know,
that have had recent signals of effect with transcranial
magnetic stimulation, you know, and so they kind of leaned in on
this too. So I think the idea that, you know, more studies
need to be done, we need to do a controlled trial, you know, it
needs to go through the standard, you know, science

(01:02:27):
process to kind of move it forward. So
I guess like, I, I have the question of something like,
because your response was very tempered there, and the sort of
reporting around it, which I don't expect you to take the same
raw raw that sort of reporting on science as a scientist, I

(01:02:50):
imagine you don't want to sound like a science reporter, those
are different roles. But my sense was that, that these
results are, they're really substantial in the sort of in
in the sort of, oh, yeah, we sent people down for this
singular treatment. And it had these these seemingly massive

(01:03:10):
changes in an area of medicine and therapy, that at best is
incremental, and slow over time, if not a lot of the time, almost
entirely ineffective to get people out of a disability
state.
Yeah, you know, there's levels of knowing, right. And the

(01:03:34):
greatest level of knowing in this case would be a multi site
trial that other people conduct that follow, you know, this
protocol and find the same thing with a blind in place. And
you'll see me out saying a bunch of really compelling things that
are definitive. If I if I sit on the show, and I tell you, yeah,

(01:03:56):
this is definitely a treatment. And this is, you know, and my
colleagues that do this sort of work would, would, you know,
would have me at the stake or whatever. Because we don't, we
don't really know, you know, we, I mean, in theory, and that's

(01:04:18):
why nature medicine, you know, had us put all this extra stuff
in there, you know, we, you know, we had to list the sweat
lodges and the this and the that that were going on down there.
Now, we know in isolation, that none of that actually produces
like robust changes in their own right. I think the reason why

(01:04:39):
MBO does that is very good. I'm not trying to detract from that.
But it's, it's likely, it's likely not the primary mechanism
of improvement here. It's likely that the the drug itself was but
without having like a really sterile, non therapeutic
environment with no activities, they're therapeutic, you know,

(01:05:02):
you're, you're basically pulling all that out of it and creating
an environment which everything's neutral other than the
treatment itself, then you, you don't, you can't make the same
level of claims. But on the flip side, you know, nature medicine
was willing to publish it. And so everybody believes the signal

(01:05:24):
is really there. But, you know, to really know, you gotta, you
gotta jump through all the hoops. And it's, you know, the funny
thing about that is that it's, it's just this is a modern day
convention. That's not necessarily how things got into,
you know, into the pharmacist closet forever, right? It's just

(01:05:48):
more of a, you know, modern thing. So, you know, I did a TEDx
talk recently, I may have talked to you about this in the
earlier half of the show, but looking at thinking about how to
really think about these results in the context of history. And
so talked a lot about scurvy and how we knew, you know, that

(01:06:08):
vitamin C and, I mean, eventually vitamin C, what was
vitamin C containing fruits were necessary for treating scurvy.
And, yeah, there was there's levels of knowing, right? And
that's, that's definitely, you know, that's definitely there
embedded in history. But like needing a fully blinded study to

(01:06:31):
know isn't necessarily the way we've always done it. But it's
certainly modern convention. And in order to get things through
and not have people point to something and say, yeah, that's
you don't know, really, you have to do it that way.
Now, it's interesting, like, of course, I can appreciate that. I

(01:06:52):
understand that. And it's also interesting to consider that in
the context of a psychedelic molecule, we'll say, you know,
obviously, Ibogaine doesn't fit the classical group, but it fits
at least loosely into the psychedelic category. Because so
much of because psychedelics are not like an aspirin, right? I

(01:07:12):
take an aspirin, it's got a pretty dedicated result, I take
it, and it's gonna do what it's supposed to do, it's going to
have that pharmacological effect where with psychedelics, the
medicine of the psychedelics, so much of it is influenced by
context, like somebody could take five grams of mushrooms in
one context, and it can heal their depression, maybe they

(01:07:35):
could take it in another context. And they've got depression plus
post traumatic stress disorder from being an absolute terror
for whatever, six hours. And so it I guess I was going to save
this question a bit more for later, but I guess I'll kind of
like weave it in now, which is that, you know, like, how much
do you think the the the benefits that you're seeing, the

(01:07:59):
changes that you're seeing are purely because of the molecule
itself, physical molecule, physical brain, physical change,
and how much of it might be influenced by the sort of like
larger therapeutic container that allows for those changes to
take place, or the larger therapeutic container that

(01:08:19):
allows for these experiences not to be troubling so that they're
more, you know, inclined towards like a like a positive
valence.
Definitely. Yeah, I mean, I think that, you know, we society
and Western culture and kind of the scientific method and kind

(01:08:43):
of how the medical establishment sees how to deal with things.
It's all like centered around certain assumptions about
reality, and about what's therapeutic. And if you're
talking about a knee infection or skin infection, or, you know,

(01:09:06):
osteoarthritis, or whatever it is, you know, I think you can
be reasonably sure that, although some people may disagree
with me on this, but reasonably sure that those assumptions are
are pretty valid, you know, that, you know, you've got this
infection, you take this antibiotic, the antibiotic has

(01:09:28):
an effect on the bacteria that kills the bacteria that ends up
you know, resolving your, your, you know, bacterial infection,
your skin or whatever it is, right? You know, and that's,
there's, there's good evidence that, at minimum, that
particular approach is one effective way of taking care of

(01:09:52):
that problem, right? With, with psychedelics, the problem is, is
that it kind of gets in the way of assumptions and, and
philosophical kind of framework of Western medicine, right?
Because we should just be able to give the pill. And it doesn't

(01:10:15):
matter what the person's thinking or doing that the pill
just kind of works, right? And that's how like, you know, heart
pills work, antibiotics work, and blah, blah, blah. The problem
with, with the psychedelics is that this is, this is something

(01:10:36):
that's a nonspecific enhancer of certain experiences,
particularly MDMA, I would say that one. In particular, it's
important. And I'd argue that classic psychedelics are
somewhere in the middle. And I think I began to is very
important that people feel safe and in a container, but it's not
as much psychedelic assisted psychotherapy, and it's more its

(01:10:59):
own, its own kind of framework. And so that's the, that is the,
the kind of thinking behind that. And because of that, I think
that, you know, we're gonna have to really grapple with this idea
that even more so than the normal with a vulnerable

(01:11:23):
patient, this is kind of an extreme of a vulnerable patient,
and we have to really set a framework up for those extreme,
you know, vulnerabilities that all patients taking these
compounds are in. And, you know, people try to tackle this with a
male and female therapist and in all of these kind of settings

(01:11:44):
to be able to try to safeguard against it. But I think we're
gonna have to really think really deeply about what
interactions and what words are spoken and all of that in a
highly plastic state. You know, the the area where this has been
solved out at some level, which is really interesting, is in

(01:12:06):
therapeutic hypnosis. Right, every word that's spoken by the
hypnotherapist is intentional, the person is in an altered
state, very vulnerable in that altered state. And the
hypnotherapist is very clear about what they're saying and
not saying to the patient, and the setting in which they're

(01:12:26):
producing for the patient. And there's a long, you know, and
that's the first conception of Western psychotherapy, and it's
effectively inducing an altered state. And so that's why I've
been pretty interested. We've done some hypnosis studies,
we've actually been able through neurostimulation to change the

(01:12:46):
trait, make people transiently more hypnotizable. And the goal
of all that is really to understand how do you access
that altered other place, and what's in there? And what are
the the bounds of it? What are the contexts of it? And so in
some ways, that's very similar to what you're talking about.

(01:13:12):
Do you think that it's possible that if in a future study,
people with similar sort of clinical diagnoses and set of
symptoms, etc, are brought into a, you know, very clinical
space, and are just given the Ibogaine with somebody there to

(01:13:36):
just track them from like a pretty standard place, nothing
special, nothing extra therapeutic, just safety
protocol, trying to sort of like, eliminate the humanity as much
as possible to create this kind of objective, drug only measure.
If it turns out that those people aren't getting as much
benefits, you know, according to your study, or in a larger

(01:13:59):
therapeutic container, like was present at the at the Ambio
Center, that that suggests that do you feel like that would be
like a cue to reconsider Ibogaine? Or would that be a cue
to sort of even further consider facilitation context to support
the positive outcomes?
I think the latter, I mean, I think the thing about Ibogaine

(01:14:21):
is really interesting is this life review slideshow that
people talk about seems to happen, irrespective of any
sort of psychotherapeutic interactions, right? And so
Howard Lotsoff, who was a poly substance user, who was, you
know, the first person in the US that really kind of tried to
champion Ibogaine, ordered online for the purposes of

(01:14:43):
recreation, and found quite quickly that this is not a
recreational compound and came out of that, no longer desiring
to use any sort of, you know, substances and to my knowledge
never really did after that point. And, and he, I think he
like ordered it, man order or something and didn't have a,

(01:15:06):
didn't have a container. And so I think, I'm not suggesting that
people do that. But it's, it's, it's probably the case that some
people need more support. It's probably the case that some
people need less support. And the question is, how many people,
what percentage of people need more support? What does that
support look like? Or, you know, vice versa? I have, I'm a

(01:15:31):
scientist, I have no opinions on this. I run a clinic and all,
you know, I don't have any agenda around saying, my way is
the way, you know, I don't have, I don't have any beliefs about
that. I think that, you know, where I sit, there's a signal
there that's really robust, that we have to figure out what's

(01:15:52):
driving it could be all a host of things. I'm totally open to
the idea that the therapeutic environment is mandatory for its
effect. I'm open to the therapeutic environment being
less mandatory for its effect. I don't, I don't have an agenda
there. I, I think it's always best to have a safer

(01:16:15):
environment. And then you scale down the acuity of that safe
environment. And that's what we're going to have to do in
order to be sure that we don't cause harm, which is one of my
like, Hippocratic Oath things is to, to not cause harm, right? So
I have to do that. But the idea that, you know, there's more or

(01:16:37):
less necessity for this, it's just, it's very unclear, because
people haven't done the work to figure that out. I think Robin
Cart Harris, up at UCSF is, is looking at this question as it
relates to psilocybin assisted, you know, psychotherapy, whether
the, you know, the actual psychotherapy, you know, set and

(01:16:57):
setting pieces, important or not, I think he's gonna, he's
gonna help to try to sort that out for psilocybin. But it's one
of these things where you have to almost do that trial. And the
problem is these, I mean, trials gonna be really hard to do, you
know, and so it's gonna be a while till we answer that. So I
think whatever ultimate design comes up from just the base

(01:17:20):
trial, it will be scrutinized, and then we'll have to kind of
figure it out from there.
So let's take a couple steps back to a to the question we were
on there about, you know, how your results compare to other TBI
treatments. I mean, pharmacologically, from what I
understand, we don't have any drugs that that fix the damage

(01:17:44):
that, you know, the symptoms of TBI come from mostly we have
drugs that mask symptoms or support people through their
symptoms long enough that the brain can hopefully heal itself,
various non pharmacological treatments that could support
things.
You have drugs that like treat like, say, you know, spasticity
and things like that from traumatic brain injuries. So

(01:18:05):
there's not nothing but but it's, you know, they're daily
drugs, it's Botox or something. But there's nothing that
certainly is helped with reversing any of the major
cognitive deficits in any robust way, people use stimulants and
stuff like that. But it's not, you know, not at the level that
it's certainly not a single administration that lasts for a

(01:18:25):
long time. That's what's really striking about this. So I think,
you know, it's very compelling, because it looks like it's a
neurotrophic, you know, factor up regulator, it's, it's, it's not
like you have to keep taking this every day, it's like you do
it, and then it persists for, you know, we have day, you know,

(01:18:46):
your one year data, it's persist forever.
Really, one year, it's still persisting the benefits people
had in your wow. Yeah, that's very promising. Or like, I feel
it feels very promising, because I myself am living with post
concussion syndrome. And I felt the sort of yo yo of trying to
find the right treatments and so on and so forth. So yeah.

(01:19:07):
Yeah, it's, it's, it is, it is very compelling. And you know,
placebo degrades quite quickly, right? And so you can have a in
treatment naive people, you can have a pretty robust placebo
effect, but the placebo effect generally degrades quickly over
time. And so the idea that this didn't degrade over time makes

(01:19:31):
it more probable that there's something real about it. While
it's not a controlled trial, at least, you know, that's, that's
a compelling feature. So that's, yeah, we're trying to, we're
trying to, you know, sort a lot of that stuff out and kind of
move forward on some of that. So yeah.
Now, how do you think I began? Okay, so there was a, a paper

(01:19:57):
that came out, I think within the last two or three years,
specifically looking at psychedelics, you know, writ
large as possible agents for treating brain injury, because
of their sort of neuroplastic effects, neutrophic effects,
etc, ranging everything from including MDMA and the classical

(01:20:20):
psychedelics, as well as ketamine, I myself have received
ketamine as a as a TBI treatment. Do you think that the
same principles? Maybe that's not the question. It's more
like, how do you think or what's your thoughts on how your
observations with Ibogaine, do you think that they're also

(01:20:43):
going to apply to other psychedelics as well? Or is there
something special about Ibogaine you think that's having such a
seemingly robust effect?
I mean, it seems to be a longer acting drug, it seems to have a
broader pharmacology. I mean, it doesn't seem it does have a

(01:21:05):
broader pharmacology that affects more neurotransmitter
systems. And so we, you know, we think that's probably a big
piece of what's playing into what's driving that, you know,
that range of effects. So yeah, it's, it's, but it's early days,
you know, the basic science hasn't even been really well

(01:21:26):
worked out on this yet. So
so I think you've maybe alluded to it generally. But is there
like, do you have any sense of or theories as to why the Ibogaine
itself has this effect on participants, sort of like

(01:21:46):
underlying TBI issues and their symptoms? Like you did mention,
it has this neutrophic effect, you mentioned this life review
effect, based on the pharmacology of Ibogaine, do you
have a sense or a theory as to like why it is that it seems to
be having these robust, these robust effects on the brain
specifically?

(01:22:07):
Yeah, I mean, there's, you know, like one way of dealing with
that question, which is to say, Oh, it's just this broad acting
kind of dirty drug. And that's way like most people would, what
most people would say to you. And they say the same thing
about ketamine. Oh, it's just this dirty drug that has these
broad effects or whatever.
And to be clear, dirty just means that it's sort of like,

(01:22:29):
it's it's promiscuous with how much effect it has. Yeah.
Promiscuous. Yeah, it dances with everyone or whatever.
Right. You know, the reality is, is that dirty also implies
random. Random effects, and it just kind of randomly does x, y

(01:22:52):
and z that it does. You know, things in nature aren't that
random. They may seem random. But, you know, evolutionary
pressures create solutions for problems, you know, based off of
the pressure that's exerted being exerted on that plant or

(01:23:15):
animal or whatever it is, right. And in that way, in kind of in
the microwave, that is random, too, in the sense that like, you
know, bird number one is got a yellow or beak because that
helps them, you know, ward off this that or the other. And so
on this island, that's the case, you know, that's kind of random

(01:23:37):
in some sense. But, you know, but in some ways, it's not
random, right? Like, you know, force one exerted pressure on on
on animal or plant to and something happened. So the
question is, how random is these very specific, very interesting,

(01:24:00):
seemingly quite therapeutic, sort of psychological effects of
Ibogaine, you know, is it really, like, just completely random,
that all just played out, you know, or not. And most people
would say yes, I'm just not sure. I think saying yes, and, you

(01:24:21):
know, assumes a level of understanding that we don't
actually have, you know, about what, why that really remarkable
compound sitting in a rainforest shrub in the middle of Central
West Africa and, and why we were drawn to use it and continue to

(01:24:43):
use it, right. I think I think that it's probably not as random
as people would assume.
What about pharmacologically? Like, what do you think there
might? Do you have a sense of what it might be about Ibogaine
as a compound and its effects on the brain that allow it to, like,

(01:25:07):
my assumption is that, is that and maybe this was supported in
your in your fMRI or your your, you know, the scans and
something that you took. But my assumption is that the
resolution of these TBI symptoms after the Ibogaine is likely
correlated with some sort of physical change to the structure

(01:25:29):
of the brain, some repair of the sheared, I can't remember, he's
a dendrites or something, but basically, like repairing some
damage. And that it's not just like, oh, it's not just up in my
mind, I'm thinking differently now, but there was some sort of
structural change to the brain that would allow for the
resolution of these symptoms. Is that correct? And if so, or if

(01:25:51):
not, why do you think that might be the case?
Well, I think that Ibogaine certainly has this neurotrophic
effect that's probably driving some of the biology just
described if that's in fact, we need to do a lot more work to
prove that out. But but, you know, like I said, I mean, I
think the way that I think about Ibogaine, which is really

(01:26:14):
interesting, almost counterintuitive is, you know, we
have this psychopharmacology, psychopharmacological kind of
way of thinking about drugs right now, that's like a 15th
century key, you know, talking about like the single tooth on

(01:26:34):
the metal rod, right? That's right. The modern day key is much
more complicated than that it interdigitates with, you know, a
whole host of pins that ultimately causes for the door to
be unlocked. Right. And, you know, I think the human brain is
a lot more like the modern day key, and a lot less like the

(01:26:56):
15th century key. So we've been trying to jam a 15th century key
into a modern day keyhole. And I think Ibogaine is a lot more
like a modern day key. It it it interdigitates with a whole host
neurotransmitter systems. And it does so in a very sophisticated

(01:27:16):
way. And because we don't have tools to understand the concert
level effects, and we're still stuck on trying to understand
what the violin is doing, we don't really have a way of
answering your question. Right. I hope that's helpful

(01:27:36):
metaphorically.
No, it is very helpful metaphorically. So I appreciate
that. I got two final sort of larger questions and then one
sort of closing question. Now, I've heard some reports. This,
you know, I don't know where it came from. I can't remember if I
read it in your study. I don't think I did. But I've heard

(01:27:57):
other people report on this idea that Ibogaine can de age the
brain. What do you have any knowledge of that of that
proposition and what your thoughts are on it?
Yeah, so Ibogaine can can reverse brain age estimations by AI

(01:28:21):
algorithms per our data. It's unpublished, but everybody and
their brothers talking about this. My talk in Denver, I it
makes me a little bit nervous, because I think we need to do a
lot more before we actually really know that, you know, but
but you know, that's a signal that that's there that may be

(01:28:44):
true. And, and why it does that again is, is kind of unknown to
me. But I think it's important if that's true, because, you
know, people probably would want that to be something that that
we know. So that's that one. And then, yeah, what was your second

(01:29:05):
question? I mean, I think that that was the question around,
oh, like, essentially, like, is, is that the case? And if so,
what your thoughts were around why or how, but I imagine that
the the wire how is goes back to that, that metaphor about the
modern key versus the 15th century key.
Yeah, I mean, if you think about it, like, if we are 15th

(01:29:29):
century key makers, and you give, if you go back to the 15th
century, and you give a key maker, a modern day lock, and
they look at that, their mind's gonna blow up, right? And so
you're asking a 15th century key maker to understand your modern
lock, or your modern key or whatever. And the idea, now, if

(01:29:51):
you gave that to them, and had them take it all apart and take
a look at it, and then go and try to build a new one, would we
have had modern day keys earlier in time? Absolutely. Right? It
would have sped up the key and lock technology, maybe by 100
years or whatever, because they'd have been able to inspect

(01:30:11):
and look at this. And that's the value of psychedelic research,
right? Is this ability to, you know, we've been muddling around
with 15th century keys, we've been trying to optimize a
15th and a half century key or something. And now all of a
sudden, we've got this modern day key and lock in front of us,

(01:30:32):
we're able to use it again. And we're looking at it and going,
well, gosh, you know, that 15th century keys, not very good. And
this one's really good. But God, I don't even know how to begin
to understand how this works. Because it's so many pins, it's
so many interactions of the key with the thing. And we're just
so used to this one tooth with variable heights. And that's it,

(01:30:55):
right? Like, that's really like the simplistic way we've been
dealing with pharmacology. And so to, you know, to, to kind of
go, go into that and try to have any explanation, real
explanation, I mean, give you hand waving, but any real
explanation about what is going on there would be me making up a

(01:31:16):
story for you. And people like to make up these stories and say
things. But I don't, you know, I just acknowledge the fact that
we don't have the tools.
One thing that was interesting when you when you use this, oh,
now we have this new modern day key as 15th century key makers,
I, you know, I couldn't help but think about sort of, well, I'll

(01:31:40):
just leave this as just like a throwaway reference or whatever,
but just kind of like in our modern kind of so much research
is being led by profit agenda, especially in pharmacology, from
what I understand is like, can we make a marketable drug? If not,
like, let's not fund this research, or so on and so forth.
But when I think about it, this very reductionist, like bringing

(01:32:03):
it down to the basic single thing, you know, single pin,
single key, so on and so forth, and when you're talking about
bringing in this advanced modern day key, it's also interesting
because it's you're also saying, well, well, actually, we're
bringing back this other thing that existed for 1000s of years,
in other cultures before we developed the single key and

(01:32:25):
now wondering how to sort of like, up level our whole key
process now that we're sort of analyzing based on the reference
of these like ancient tools. I've again, obviously being used
for a very long time, from what I understand, or the plant
Ebola likely longer than, you know, we're making keys.
Yeah, you have to separate high technology from time. That that

(01:32:49):
TED talk that I just gave the whole like, essentially set of
assumptions that was in there was that it's about separating
time from technology and that we have linked the future with high

(01:33:10):
technology. And in the pharmacological space is not true,
in my view, right? And some I mean, some drugs that we made
that are outside of the CNS, that's, it's probably true, some
new chemo drugs or whatever. But, but as far as like, what do
you do with somebody with depression? You know, I think
the SSR eyes that humans have made are very impressive, right?

(01:33:33):
They're kind of like old tech in many ways. And psychedelics are
more high tech, you know, and so this idea that you can separate
time, linear time from technological sophistication.
Right. And I think that that's where people get really stuck.

(01:33:56):
The idea of getting drug companies to get, you know,
psychedelics through and having a profitable drug to me is
unrelated, relate, right? Like, you know, let them do that.
Because that's the only way you're going to get this out to
people, you know, people have this, especially the

(01:34:17):
psychedelics, basically, well, that shouldn't happen. And all
this reality is those people live in Northern California,
have the financial means to go buy their psychedelics from
wherever and get to go on an ayahuasca retreat, because they
have the money to go down to Peru. The, you know, what these

(01:34:37):
companies are doing is they're really getting access for people
to get this through Medicare that are on disability that
don't have access. Right? Like, in some ways, I find it'd be
kind of counterproductive to think about things like that.
So I think that's that, which I think is really just about
getting psychedelics to the masses when you threw a vehicle

(01:35:00):
of capitalism, right? You can have a view of that or not have
a view of that. And then there's a separate agenda around using
and understanding these drugs to either make new drugs, or to
refine how the drug is administered, or what it's doing,
or to understand something about the brain. And I think they're,

(01:35:22):
they touch each other. But they're, they're, they're
really separate issues, you know, and they're probably gonna
be companies that do the second thing too, which is going to be
ultimately more important, but to get this thing done to
normalize this whole space, and to be able to say this is
actually a treatment, you know, that's actually a policy

(01:35:44):
importance.
Yeah, and the policy follows. Well, hopefully it follows
research, usually, a decade behind from what I understand.
But yeah, this is good. I'd like to I'd like your comments there.
I, I've heard Dennis McKenna talk often around like trying to

(01:36:04):
nudge big pharma companies and big otherwise, like massive
thing, massive corporations, or just basically like economic
super forces to be like, hey, you should save the rainforest
because your next billion dollar drug might be in there. And if
you plow it down, you're never going to find it.
And I think he's spot on with that. Right? I think he's 100%

(01:36:29):
that is 100% true. And that's absolutely what they should be
doing. You know, and I think that's 100% right. And I think
that's the value of those entities, right? It's, you know,
if Pfizer could go in and buy, you know, 5000 acres of the
rainforest and preserve, you know, all that vegetation and

(01:36:51):
study it, it would it would behoove them to do that. That's
1000% true. And it's the right thing to do for the world, you
know, and I think I think he's he's spot on about that. So yeah,
it's, if there was some big, you know, some big pharma company

(01:37:12):
that grew out of doing psychedelic, you know, approvals
and that one went in and was able to, you know, preserve,
preserve the rainforest or preserve Gabon's, you know, I
boga tree supply and give back to the people or something like
that. I think that's a huge win. You know, I think that you know
what I mean? I think, but it's got to be that right. It's, it's

(01:37:35):
got to be this kind of hand in hand dance between how do you
give? How do you get everybody access? How do you give back?
And I think if we can figure out a good way of doing that, then
you can use capitalism as a vehicle for good.
Giving back and hopefully over time taking less, but that taps

(01:37:56):
into the larger sort of force of the consumption machine that
capitalism is presently sort of, you know, banking on. But that
was kind of intended as a throwaway reference. I really
appreciate that you brought your mind to it. I want to ask you
this, this sort of final larger question before I kind of ask

(01:38:17):
you what's next and yada, yada. So based on what you so I'm going
to ask you to speculate something based on what you know
now about Ibogaine, what you know and don't know about Ibogaine,
Ibogaine treatment, TBI, etc. Could you speculate on what the

(01:38:37):
potential efficacy might be for smaller long duration
administration of Ibogaine for TBI? Of course, I'm talking about
micro dosing here. But I do understand that there's a, there's
some relationship to the neurotrophic effects between the
immediate action of Ibogaine and the longer, you know, impact of

(01:38:58):
nor Ibogaine is one of its metabolites and so on and so
forth. Maybe that's a part of it, maybe not. But yeah, anything
that you'd be able to offer on that.
Yeah, but we just don't I mean, the big thing is we just don't
know, because we know even less about that. But I would say that
you know, the French were using low doses of Ibogaine from 1930

(01:39:18):
to 1966. And while there's not really the, you know, the data
back then is, you know, very scant is like a, is like a, you
know, a positive spin on, you know, maybe non existent on
what, you know, what that was. I think it's important to kind of
understand that, you know, that that that drug was was around at

(01:39:43):
micro dose levels for a time. And the reality is, is that if
people didn't didn't have benefit for doing that, then it
wouldn't have been a product, right? And so, you know, there
are plenty of things that that were offered up as potential
cures for various things, and probably had a similar sort of

(01:40:05):
placebo effect possibility and didn't stick around for 36
years. You know, but low doses of Ibogaine did. And so as a base
case, I'd argue that just the sheer fact that it was around
for multiple decades and utilized, you know, suggest
there was something there. Now what, beyond that, I can't

(01:40:28):
really talk much about the data. But I but my, my suspicion is
that that's going to be an area that's going to be really
studied over the course of the next couple of years, the decade
to really sort that out.
Yeah, it is it is very, it's very interesting to me, I think
explicitly because, you know, if I consume psilocybin, it

(01:40:49):
metabolizes and is like out of my system in a very short amount
of time, the metabolize from what I understand have little to
no sort of ongoing effect. But with Ibogaine, nor Ibogaine has
several other like clinically relevant effects, and it will
build over time because it's fast soluble, it can build up in

(01:41:09):
your neural tissue over time where you take small amounts
every day, eventually you get to the place that you've built up
enough nor Ibogaine in your system that might mimic what
would have been there after a single flood dose. Now, that's
based on what I understand, which is, excuse me, you know,
clearly, clearly less than the data set that you're working

(01:41:30):
with. But I do find it something as something uniquely
something unique in the micro dosing space that it might have
to offer. Mind you, and maybe you could answer this is, you
know, Ibogaine still has this cardiac risk. And my assumption
is that perhaps, you know, micro dosing it over a month long

(01:41:54):
might introduce that risk, it might not. I don't know. Again,
I assume we don't have this data.
Yeah, I mean, we, we don't have a sense that I mean, it's scant.
So you don't know, we don't really know this. But I didn't
get the sense that the really low dose Ibogaine in the French
population, you know, had any, there's, there's nothing in the

(01:42:15):
literature to suggest that that had, you know, a cardiac risk
that was, that was written down, you know, and so, you know,
whether it did or not, I bet, I bet you couldn't really know
that. But it, I would think that you'd have some sense that that
could have been present, really, a lot of this stuff ends up

(01:42:36):
being, you know, dose related anyways, that was several
orders of magnitude less than a flood dose. And so, so my
suspicion is, is that I'm not gonna sit here and tell you
there's no risk. But my suspicion is that there's less
risk, if you look at the information that we have
available to us. But still, again, a lot of work to be done.

(01:42:57):
You know, you don't, you're not gonna really know that until you
do the trials.
Okay, this has been excellent two part, two part interview.
Before we close out, and I get sort of whatever final
information you want to share us with, what's, what's next for
you? What are you working on now? Like, what has you excited as a
scientist right now?

(01:43:18):
Okay, yeah, yes, we're developing. We're working on a
drug delivery system with a guy who kind of invented this in
radiology here at Stanford, Rage, Iran. It's this idea of
that we can package drug and nanoparticles, and use ultrasound
to release it into specific brain regions and deliver drug just
to that brain region. So it'll help us to understand kind of

(01:43:40):
brain behavior relationships.
Cool. And, and what's, what's next for, for people who are
interested in your, your stuff with Ibogaine here? Should they
be waiting expecting follow up reports at any time or follow up
papers?
Yeah, we have a ton of papers coming out on the neuroimaging in
the EEG and the long term follow up and then looking into other

(01:44:02):
ways to do this in the US. So a lot of Ibogaine work, you know, is
coming that paper was just the first one. Yeah, excellent. So
obviously, you're a scientist, not a social media influencer.
But if you have any sort of social media channels or
somewhere that you would suggest people that they would follow
you to stay up to date on your research, or, or, or, or, or

(01:44:26):
or, or you know, get in contact with you in some way. Yeah, the
X, Twitter, whatever, handles Nolan, RY, Williams. And, and
so people can see me there, Nolan R Williams.com is the website.
Happy for anybody to kind of check in with us around studies

(01:44:49):
and papers and all that good stuff. So thank you, sir.
Appreciate the time.
Thank you so much, Dr. Nolan Williams, been a excellent
conversation, and I appreciate you offering your time today.
Thanks, man. Take it easy. Goodbye.
Okay, thank you so much for tuning into this episode,
listening all the way to the end. If you're like me, you're

(01:45:09):
probably really excited about the work that Dr. Williams is
achieving here with Ibogaine with traumatic brain injury in
connection with MBO. And you want to really stay up to date
with what's coming out with respect to that. And so
definitely follow Dr. Williams at his X handle, the platform

(01:45:31):
formerly known as Twitter. And in order to, in order to stay up
to date with what he's doing, if you'd like to stay up to date
with what I'm doing, you become, you could become a free member
of Patreon to follow my posts there, or you could become a
pledged member of Patreon, which would help contribute to the
resources that are required to produce the show both time and

(01:45:54):
material. Or you could sign up for my newsletter, I send a
newsletter once a month or so. Or you could follow my, my
telegram. Links to all of that are in the description to this
episode, wherever you're checking out. I appreciate that
very much. If you're interested in psychedelic mushrooms, I have

(01:46:14):
a couple of books that I've written on them. I'm in
production on the third. My second book, it's a storytelling
narrative, the true light of darkness, my first one, more
academic scholarly style, decomposing the shadow, both of
which are available on Amazon, or, you know, somewhere that
isn't Amazon if supporting Jeff Bezos is not your highest

(01:46:36):
highest desire. And they're also available at ebook, or you could
get signed copies from me directly from my site. And yeah,
that's it for this episode. Thank you so much for tuning in
all the way to the end. And until the next one, take care.

All Episodes

Treating Traumatic Brain Injury with Ibogaine | Dr. Nolan Williams ~ ATTMind 188

Episode Transcript

Popular Podcasts

United States of Kennedy

Stuff You Should Know

Dateline NBC

.css-15opob5{left:0;position:absolute;top:0.8rem;} All Episodes

.css-14f5ked{margin:0;word-break:break-word;display:-webkit-box;-webkit-box-orient:vertical;box-orient:vertical;-webkit-line-clamp:2;overflow:hidden;}Treating Traumatic Brain Injury with Ibogaine | Dr. Nolan Williams ~ ATTMind 188