The Dr. Hyman Show - One Dose That Heals Addiction, PTSD, and Brain Injury? Dr. Nolan Williams on The Science of Ibogaine

Episode Date: September 3, 2025

For decades, psychiatry has relied on treatments that are slow and often ineffective. But what if one intervention could reset the brain, break the grip of addiction, and open the door to an entirely new model of care? On this episode of The Dr. Hyman Show, I sit down with Dr. Nolan Williams, a Stanford neuropsychiatrist pioneering new therapies for substance use disorders, depression, PTSD, and traumatic brain injury. We dive into these fascinating topics and more; watch the full conversation on YouTube or listen wherever you get your podcasts. You’ll learn: • Why ibogaine is unlike any other psychedelic—and how it could reset the brain • Its promise for treating substance abuse disorders and breaking cycles of addiction • The safety step that makes ibogaine treatment possible for real patients • Why psychiatry is shifting from trial-and-error to targeted brain circuits Talks like this remind me just how close we are to real breakthroughs in mental health. Dr. Williams calls it psychiatry 3.0. It’s a new era of treatments that actually heal the brain, and it gives me great hope for the future of medicine. View Show Notes From This Episode Get Free Weekly Health Tips from Dr. Hyman https://drhyman.com/pages/picks?utm_campaign=shownotes&utm_medium=banner&utm_source=podcast Sign Up for Dr. Hyman’s Weekly Longevity Journal https://drhyman.com/pages/longevity?utm_campaign=shownotes&utm_medium=banner&utm_source=podcast Join the 10-Day Detox to Reset Your Health https://drhyman.com/pages/10-day-detox Join the Hyman Hive for Expert Support and Real Results https://drhyman.com/pages/hyman-hive This episode is brought to you by Seed, Sunlighten, Function Health,Timeline, AirDoctor and Pique. Visit seed.com/hyman and use code 25HYMAN for 25% off your first month of Seed's DS-01® Daily Synbiotic. Visit sunlighten.com and save up to $1400 on your purchase with code HYMAN. Join today at FunctionHealth.com/Mark and use code HYMAN100 to get $100 toward your membership. Support essential mitochondrial health and save 10% on Mitopure. Visit timeline.com/drhyman to get 10% off today. Get cleaner air. Right now, you can get up to $300 off at airdoctorpro.com/drhyman. Receive 20% off FOR LIFE + a free Starter Kit with a rechargeable frother and glass beaker at Piquelife com/Hyman.

Coming up on this episode of the Dr. Hyman Show. What you said blew my mind, which is that there's this compound out there that can abruptly interrupt and withdrawal from addiction that can help treat PTSD, depression, traumatic brain injury, better than anything else we have out there on the market. And orders of magnitude more. Dr. Nolan Williams is a triple board-certified neuropsychiatrist and founder of Stanford's Brain Stimulation Lab. He's redefining how we treat depression, PTSD, and addiction.

using brain stimulation, psychedelics, and neuroscience instead of meds. I mean, there was a WHO statistic that really struck me, which is one out of two people will have a DSM diagnosis at some point in their lifetime. I think this is just like a really paradigm shifting moment where work like yours have really started to push the envelope and say, hey, wait a minute, like we're thinking about mental illness all wrong. We're talking about like one dose, one day, having an effect of reverse your brain age by a year and a half and a month.

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The solo system is a portable far infrared sauna that's perfect if you're short on space, but still want the benefits of regular infrared therapy. Backed by third-party studies, decades of innovation, and multiple U.S. patents, Sunlighten is a trusted name in infrared therapy. It's a key part of my own wellness routine and one I truly believe in. Visit sunlighten.com and use code Heimann to save up to $1,400 higher on your purchase. That's sunlighten.com, code H-Y-M-A-N. All right, Nolan, great to have you on the podcast.

Thanks for being here. Yeah, thanks for having me. You know, I followed your work. I first heard you talk about three or four years ago, what you said blew my mind, which is that there's this compound out there that can abruptly interrupt withdrawal from addiction that can help treat PTSD, depression, traumatic brain injury, better than anything else we have out there on the market and orders of magnitude more. And I became very interested in following this conversation about this incredible compound called Ibigan.

that we're going to learn more about today. And it comes from a bark of a tree in Gabon in West Africa. It's used in ritual ceremony there for different kinds of ritual transitions through life. It's got a fascinating history. Maybe I would love to start by helping us understand, you know, what is it exactly? And when was it first sort of discovered to be useful in mental health, which is really the focus of your work at Stanford? and a lot of the published trials you've done

and the exciting work to actually scale this up and make it more affordable and accessible and usable to many, many people who suffer. Because, you know, the truth is, one and four people have had sexual abuse, which is crazy. Trauma is a real thing, whether it's micro traumas because your parents neglected you or big traumas, a guy over Monte dachs about big tea,

little T trauma. They can register in your nervous system and have lifelong effects on your mental health, on your functioning, on your perceptual worldview, And all that influences your ability to be happy and function in the world and have a filled life. And, you know, psychiatric medicine is just very antiquated. It's very crude. It's tremendous side effects of the drugs we use.

Many of them don't work very well. And we're kind of in this unfortunate situation where mental health crisis is bigger than ever. We have fewer things that really work. And this seems to hold a promise of something really quite different. Yeah, thanks for the intro there. Yeah, it's, you know, it's an interesting compound. It's been around for a long time. It's an African root bark psychedelic, as you suggested, from Gabon and Central West Africa,

so kind of neighboring areas. And the group of people that use it are called the Buitti, and Bueti just means that you've taken Iboga in ritual ceremony, right? And so folks have been doing this for quite a lot. long time and they've been doing it because it has a it produces this kind of what people would call a transformative psychological experience so people will go into this they'll have kind of a massive change in consciousness over the course of you know 24 to 36 hours and during that time they'll have a psychological experience of re-evaluating earlier life emotionally salient memories and

And for maybe all of us, for a lot of us, those are, you know, trauma at various scales, you know, and people will take a look at those earlier life kind of emotionally salient events, but they'll do it from a position, kind of a third-party position of seeing it from neutrality. So unlike MDMA, where people will take that and they'll need to, while taking that kind of be led into a memory, and then they have this kind of positive emotion about it. IBM, you know, from the subjective sense, people will report seems to produce kind of a neutrality, and it kind of automatically puts people in that space.

So you're not being guided or guided, or there's no therapist. The drug just automatically puts your brain into this mode, it seems. And then people have what they call this life review or slideshow where they're looking at these emotionally salient memories over time. And when they do that, they're able to see, they're able to see the, you know, the memories from a different lens. And, you know, it looks like they reconsolate the memories and then they're able to, with that reconsolidation, really be able to kind of tolerate them or see them in a different way or accept them. And that's pretty powerful. To your point, you know, psychiatric medicine has created tools that look a lot like, you know, medieval or 15,000.

century, whatever keys, right? Like we've thought about the brain like a single tooth key that you put the key into the lock and you turn it and then the key unlocks the door. But the brain is probably much more like a modern day key with a lot of different pins and a lot of different interactions. So when you put the key into the lock, it really needs to interact with a lot of different systems. The problem with, in my view, with kind of current psychopharmacology in the way that we see it is that we still think that it's a single neurotransmitter or single receptor problem. Serotonin's low, so take serotonin riptick inhibitors like Prozac or your dopamine's low, so take basically speed, otherwise it was Adderall or riddle in it.

If you look at the pharmacology of Ibigen, it's very broad acting, right? So it actually interacts with a lot of, I mean, essentially all the neurotransmitter systems in a unique way. And it's probably, you know, if this were to, you know, ultimately be as therapeutic as the initial signals are and we're able to see in big multi-site trials the sort of data that we're seeing now in our studies and studies coming out of that are going to be completed soon out of Texas, then it tells us something about the way we're thinking about pharmacology and that this kind of idea of a dirty drug or a kind of a multi-receptor drug system is probably. correct. And this idea of a single neurotransmitter system, low serotonin or whatever, where we're simplifying things down is probably oversimplified. You know, and those tools are too coarse. You know, in medicine we call the sort of multiple effect phenomenon pleatropic effects, which means they work on many, many different pathways and systems. You know, I want to get into sort of more of the applications of it and what you found. But the mechanism of action is really

interesting because we're sort of still deciphering that. But it works on both the structure and the function of the brain. So it doesn't just change it in the moment. It seems to have lasting changes, which is why, and I think we're still trying to figure out, you know, why, why if you take it once, if you're a heroin addict, that your addiction cravings go away and your withdrawal symptoms don't happen, which is something you, is a physiological response. It's not like they're psychologically suppressing the withdrawal symptoms, they just don't have them. And that's really fascinating. And I think, you know, for PTSD, you've got the NMDA receptors, which are the sort of

excitatory receptors that get calmed down, which get overexcited with trauma, does affect somehow the serotonin system. It affects brain factors like PDNF, which is otherwise known as brain-derived neurotrophic fact that helps stimulate brain growth and connectivity, neurogenesis, neuroplasticity, more brain cells, more connections between brain cells. So they do all these really interesting things that repair the brain, heal the brain, even in traumatic brain injury, which is where you get banged on the head from something where you're in a war zone and you get some kind of dramatic brain injury. It seems to work on that too. So it seems to have all these varying effects.

And they also sort of inhibit what we call the default mode network, which is what a lot of other psychedelics do. It's sort of the ego and the self-protection part of your brain, which is, you know, makes us feel separate and disconnected. And when that is suppressed, whether you meditate for 40 years or you take psilocybin or LSD, MDMA, or Ibegaine, that quiets down quickly. And your sense of disconnection and separateness is suspended for a moment. And it allows you to sort of see how you're actually part of a greater whole.

And so I kind of would love me to unpack some of the mechanisms and how they work in these different disease states. Because it seems like one size fits all. You know, you've got PTSD. got depression, you got anxiety, you got trauma, you got brain injury. Can you kind of unpack those for us and talk about, you know, how they affect across these various pathways in the brain? Yeah, that's a great question. So the other mechanism that we've thought a lot about that's unique type again is glial-derived neurotrophic factor, right? So glial-derived

neurotrophic factor is a neurotrophic factor that's involved a dopamine neuron kind of health Right. And so it upregulates dopamine neuron health. And so it was a study, you know, 20 years ago or something where they took mice and mice or rats and they train them to self-administer, meaning that they basically, you know, it's a mouse, you know, rat model of addiction, you know, where they're drinking alcohol out of a, out of a tube. And if you take a mouse and you do that. A little rat bartender there. Something like that. Yeah, yeah. They pull up to the. bar. They'll drink until eventually they die, right? And if you take a mouse like that and you give them IBM, you can actually reverse it. They'll stop self-administering alcohol, which is cool. If you take a mouse and you inject glial-derived neurotrophic factor into the ventral tegmental area, which is the dopamine-producing area that's involved with more of the reward system, you can also produce the

same effect. They will stop self-administering. Inject just Ibegain just into that area, you can recapitulate the effect, right? And people have also shown that you can produce this effect by directly stimulating into those areas, right? And so it's probably that at least the anti-addiction mechanism of Ibegain is that it's restoring dopamine function within that, um, that ventral tegmental area in a way that resets the reward system. The next piece of data that we have, we published in Nature Mental Health, I don't know, a week ago or something, which is a really interesting study where people that in our trial that received Ibogaine had EEG like brainwave tests before, after, and one month after

they received ibogaine. And what we saw is this kind of general slowing of all of the kind of different power spectra of the EEG, right? So people had a general kind of physiologic slowing of their brain after. And the slowing actually was correlated with the strength of the trip, like the amount that they had a psychological effect. But also interestingly, the reduction in. PTSD symptoms and the improvement in cognition. And so, you know, that's, it's a, it's a first step study, you know, that it was pretty good, I think, in the sense we got in nature mental health, but, you know, we need to do

some more work on this. So I'm not claiming that this is definitive, but it's likely that if you, you have an EEG, you may be able to tune the dose to the physiology of the brain instead of getting a subjective readout, you just, you increase the dose. And then that may also allow for you to tune the PTSD effects, which is really cool, right? So you're kind of, you know, flipping it. Some people need more or something to need less. And you can tell by the EEG, who needs what?

And they can upper. That would be the promise, right? That would be, you know, if it plays out, that would be. And we do this already in medicine, as you know. We use biz monitors and anesthesia to kind of measure the level of anesthesia. or if somebody is, you know, being fully anesthetized with, like, propofal, you can actually, you can actually burst suppress them. And, you know, you're using an EEG to help you dose a drug, you know.

So that's not a new concept in neurology. It's just a new concept within kind of psychiatry, right? Right. And so being able to figure that out, I think, is useful. Well, that's the deal of joke is neurologists pay no attention to the mind and psychiatrists pay no attention to the brain. And here you are, you know, looking at psychiatry through the lens of the brain, not just the mind. And, you know, Freud kind of took us down the path of mind-only psychiatry and talk therapy and psychoanalysis. And it's sort of striking because, you know, you hear,

oh, well, yeah, I heard psychoanalysis say, well, you can come to psychoanalysis five days a week for the next 20 years and then you'll maybe see some improvement. And I hear you're like, well, you can go you know, New Mexico and do one Ibegain journey and like that takes care of like 20 years of psychotherapy. I mean, it's kind of crazy. Yeah, I mean, you know, there's a lot of work to do to to kind of totally prove that. I mean, that's what, that's certainly what people will say. That's what Claudio Naranjo said, I think, and, you know, the Argentinian psychiatrist many, many decades ago about ibegaine it's just one of these things where we're going to have to do do the good work to figure it out but i think that the problem in the kind of common theme of what

we've been working on the problem in psychiatry that's kind of out there right now is this problem of things taking too long to your point you know people can have an entire you know tragic life problem over the course of the time it would take, you know, for many of our treatments to work. I mean, psychotherapy, psychoanalysis for 10 years is one, just normal oral antidepressants, you know. I mean, we've seen, you know, people start out in oral antidepressant and lose their job by the time it starts to have any effect, right? And so you end up being in this situation where we're not really matching the speed of the illness and the speed of the disability from the illness with the speed of the treatment.

It's kind of an exciting moment in psychiatry because we were in a very reductionist phenomenologically driven framework for psychiatry where psychiatric illnesses were described by their symptoms, not by their causes or their mechanisms. And what's really exciting to me in psychiatry, because I've been thinking about this for decades, I wrote a book almost 20 years ago called The Ultra Mind Solution, which details how the brain is influenced by everything happening in your body, and you can actually use those physiological levers to change psychiatric symptoms. So if we need to treat inflammation or mitochondrial function or the microbiome or, you know, with psychedelics, you're altering some kind of structure

function of your brain, that you can kind of change things that seem fairly fixed and permanent in somebody that we, and we ascribe all kinds of meaning, and we have all these stigmas against these things and you know if someone's limping because their meniscus is torn in their knee we don't go oh you're you're you're a fuck up you know like but when someone has a mental illness is a stigma of oh there's something wrong with you like it's it's kind of you're crazy it's your fault but actually there's literally physiological and structural things happening within the brain that make it not work just like if your knee doesn't work or you're limping because you've got a meniscus tear but now we're able to start to image

those things, to see those changes in patterns, and to actually treat the structure and function of the brain through a multi-pronging approach. Most psychiatric illnesses are inflammatory problems in the brain. So if you have inflammation, your knee, it hurts, but if your brain doesn't hurt, it just creates all these crazy psychiatric symptoms. I think it's just like a really paradigm shifting moment where work like yours have really started to push the envelope and say, hey, wait a minute, like we're thinking about mental illness all wrong. And looking at the wrong end of the stick. And to me, that's exciting because so many people are suffering,

but it's not happening fast enough. You're involved in the whole field, but I think there is, and there is funding now going into research, and I think in Texas there's $50 million allocated for a research effort on Ibegain, which I was sort of shocked to see. Your work has kind of taken it to a new level.

And the thing that I think, you know, we're in now is this both metabolic, nutritional psychiatry evolution and this psychedelic psychiatry revolution. They're too, I think, synergistic. I'd like to see them work together more. When it comes to your health, knowledge is power because most of us are flying blind. We're getting basic labs once a year and hope and everything's fine.

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your body build new, more efficient ones. That means better energy, better muscle function, better brain health, all the things that start to slow down as we age. And now Timeline has made it even easier to take with sugar-free strawberry gummies. Two a day gives you the full, clinically effective dose. They taste great and they're part of my daily routine. Timeline is offering my listeners a special discount. Just go to Timeline.com slash DR Hyman and give yourselves the support they deserve. The question, you know, psychedelics is there's a lot of them out there. And people, I think, maybe are confused.

There's MDMA, there's psilocybin, there's LSD, there's ketamine, you know, and now there's ibegene, and probably people are less familiar with ibegain. But it seems to be significantly different in its effects than many of these other psychedelics, which have a lot of benefit. So how is it different? from other psychedelics mechanistically and even experientially for people. To your point, there's a wide range of psychedelics to, you know, right now, there's not really an approval for any classic psychedelics.

You know, there's no, and that, you know, there is some interest at the level of the current administration in the Health and Human Services Secretary and all of that as far as kind of getting that done. But as of now, you know, there's not, there's not an approval. And so there's, you know, there's a lot of trials around MDMA for PTSD, psilocybin primarily for depression. People are trying LSD for generalized anxiety disorder, other things. And Ibegain is probably the latest person to the party or, you know, whatever, to the party in the sense that the... But it's plants of the party.

Yeah, the latest, the last plant to the party. the reason for that is because ibegaine has the most complexity to it and the most inherent risk to it. And so the problem with ibegaine as an inherent risk problem is that it has this cardiac risk, right? So it actually will prolong the QT interval for people that don't know. It's kind of a part of the physiology of the heart. Lots of drugs do that. antipsychotics do that right the geodon for in particular does that at a great degree so it's not a unique you know within psychiatry lots of drugs that do that within medicine as you know there's

lots of drugs that do that but you know it prolongs the QT quite a bit for a very short period of time and there have been there have been a couple of deaths you know because people are going to administered Ibegain in unmonitored or minimally monitored settings. And so the problem with doing Ibogaine research is that, you know, it's been a problem of how do you do a study with a drug that you don't have any human data on because everybody's scared to do the study because of the kind of case reports of risk. So we started, you know, the work that we did actually studying people that were already going to Mexico to take Ibegain, right? So they were already headed down there.

They were already kind of consented to go down there. And then our job was, you know, simply to kind of do an observational study around that phenomenon that was already happening. And that allowed us to get some data and enough public visibility to then be able to justify what's going on now, which is to try to get an I&D to do this in the United States and all that stuff. And so, you know, people have a varying degree. And I&D is just for people listening as investigational new drug applications.

So how do we go to the FDA and ask for permission to study something? You need an application for that. You need an application. And there's a chicken and egg problem of like how do you take such a complicated drug and get an I&D? And so there's a lot of that that goes on. And so people have had a hard time doing this. And you could say, well, you know, this is a drug with risk. you know, should we be doing this or not?

The reality is that, you know, there are drugs that are more risky from a heart standpoint that are already approved by the FDA than Ibegain. And so Ticocin is a cardiac drug. And if you ask the electrophysiologist, you know, cardiac electrophysiologist, and you show them the Ibegian data, they say, well, this is a risk, but Tickason is just as much of a risk, and we've gotten approval for Ticcacin. And so what ends up happening, which is really interesting, is I think what has happened with Ibegain is because of the stigmatization of mental illness

and the issue of how to think about it, people end up being in a scenario where they're looking at this and they're saying, is this problem that you have worth the risk? And Tickason's used for like atrial fibrillation and for other kinds of arrhythmias. And so people say, well, this has a one in 100 risk of a torsades event. But like if we don't do it, then somebody's going to die from a stroke from a fib so we can justify this risk with that risk, right? And we know in an opiate use disorder that there's a huge overdose risk in a person that's untreated. And so the problem at a fundamental level is we're saying, well, by not allowing you to study IBM, you're saying, well, this risk isn't actually real or its personality or

whatever it is, whatever kind of justification that we come up with, and that justification allows us to say, no, actually, we're not going to study this. Instead of understanding how many years of quality of life are lost, which is a real metric, quality of years. Yeah, absolutely. Or real death risk from overdose. Yeah, it is a bit of a double standard because it's, I think it's part of the bias in segmentization and mental illness.

It's not a real thing. You know, your heart arrhythmia is a real thing, but your depression is not a real thing. Your PTSD is not a real thing. But yeah, it's amazing. And so you work not just differently in terms of the effect on this risk, which is why it's different, but it has profoundly different effects on the brain that are very different than many other psychedelic.

I mean, the first story I heard about it was, you know, maybe 50 years ago there was some drug addict who was in Amsterdam and somebody said, hey, try these cool pills, man. he did and the next day his addiction was gone his cravings were gone so that was sort of the beginning of the understanding of its effect in addiction medicine but but it's just got all these broader effects so um it's different than then then seems to be longer lasting and more powerful in terms of resetting the brain and the then the sort of like almost a neurochemical reset than many of these other compounds which work but don't have these persistent lasting effects as much. Yeah, so Howard Lotzoff was the first. So just in the history of all this, you know,

we know that we were using this for at least 300 years, you know, probably, you know, most likely much longer than that. The French started, discovered this in the Western world in about 1900. It was on the French, French formulary from 1930 to 1966. And it was actually a A lower dose is called Labyrinth and was like a daily microdose, essentially. And so there's 36 years for attention problems and depression and things like that. Wow. And so for 36 years, it's used by the French and then placed on the French version of the Controlled Substances Act in 66. And it, you know, and it was put on the U.S. Controlled Substances Act, even though it doesn't really meet criteria for the controlled substance, for the description of a controlled substance.

It is neither, people don't self-administer it. There's no, there's no animal data to suggest that there's a self-administration. In fact, it reverses self-administration of other addictive compounds. It's not a party drug. It's not a party drug. So it stops self-administration and, you know, it has this profound, you know, kind of psychological effect that doesn't really, it's not really reinforcing, right? And so it doesn't really meet controlled substances description, but it was lumped in to the U.S. Controlled Substance Act to Schedule 1 substance, which is where it stayed, you know, since then, and really prevented folks from using it. And so Howard Lotzoff had the story that you're describing, had this resolution of his addiction and spent his entire life trying to get this, you know, kind of out of the off the controlled substances list.

and as a therapeutic. And it's a very complicated timeline for folks to kind of get through. And I think we're getting a signal now that finally we may be able to see that happen in our lifetimes that, you know, it could be that we could actually study this thing and make a real decision of whether or not it's useful. And even if it doesn't work, like let's say all of this is just a bunch of psychological effects and it doesn't really do any of the things that people think it does and all that stuff. that's an important study to do anyways from a public health standpoint, right?

Like the idea that we make plants illegal and then make them inaccessible for science is like, in 300 years, we're going to look at that and think that's just the craziest thing, I think. And we have to study these things. And, you know, if the initial data that you've done and others have done actually bear out to be true, It's revolutionary in psychiatry. I hope so. I mean, I think it could really, you know, impact this incredible degree of trauma and PTSD and depression, anxiety, traumatic brain injury.

That's even fascinating to me, the brain injury stuff. But the pathways that it works on are a lot of different pathways that reduce inflammation, oxidative stress, that increase neural protection, resilience of your cells. And, you know, it just, it almost seems too good to be true of how this works. But it does have to be administering in a way that's safe because it is risk of cardiac arrhythmias is high. And then you have to monitor that. But with the magnesium therapy, which is, you know, what we use. It's funny to me that, you know, I used to work in the emergence room and we had this thing called the crash cart.

If someone comes in with cardiac arrest, you give them all these drugs, you get epinephrine, and you give them this drug, you get that drug. And then finally, like, if every other drug fails and they're still in this terrible arrhythmia, you give them IV magnesium. That's right. That's right. That's like the last draw. I'm like, why don't we start out with that?

You know? That's right. You know, I've given a lot of IV magnesium in my life. It's very safe. We use it all the time of medicine for preeclampsia, hypertension and pregnancy for preterm labor. And doctors don't somehow think of it as a, you know, as a compound that we should be using,

except in these extreme situations. but it's actually one of the most important minerals. And many of us are low in it or insufficient in it. And I think stress causes it to be low. It brings also caffeine, alcohol. A lot of things that we do actually cause us to deplete magnesium. A lot of people are on anti-hypertensive drugs that cause you to lose magnesium, diuretic. So you basically can mitigate a lot of these effects by tanking people up on magnesium

if it's done in a controlled way. And that's mitigated all those. potential risk. You've never had a case in the magnesium administering patients that you've used I began with, right? I mean, I, you know, I, uh, I personally don't, um, administer it. I just talk to, talk to folks in, uh, in places that do. And what they, what they tell me is that, uh, for instance, one clinic wasn't really using it until a couple of years ago, you know, and they'd had a, you know, a bad outcome and then they, you know, started using it. And they hadn't had any cases since then. And the rationale is, you know, as you point out, that magnesium is actually

the treatment and the American Heart Association guidelines treatment for Torsads, the fatal arrhythmia that's the result of Ibegain. If you give magnesium, you can get some people out of torsads. And so the view here is if you're prophylactically administering magnesium before you give ibogaine, then maybe what you're doing, and this is such a low, risk drug, if you want to even call it that, is that you're bathing the heart in this kind of stabilizing agent so that when the ibegaine interacts with the potassium channels that are involved in the herd potassium channels that are involved in this arrhythmia, that they won't throw the heart into the rhythm. And that's the idea because the drug, you know, comes and goes and then nobody has a

risk of like post-treatment arrhythmia. It's only during kind of the kind of the peak levels of the drug. And so if you can give magnesium and stabilize the heart, you can prevent this from happening. Right now, you know, there's, it seems to me, we're just sort of at this beginning of the sort of a phase of research, which is going to help us unpack the underlying benefits, the mechanisms, safety, and that'll lead to a path to potentially approval as a pill

that you can take. But the question is, you know, do you still think people are going to need to be in a moderate setting with ib magnesium in order to actually safely take it because it sounds like it's not something you can just sort of like prescribe people right a bunch of different answers for that but you know the kind of short answer is yes I can't foresee a time when I began isn't going to be a monitored drug now I began at the current doses that people use the kind of what we call flood doses now the the deal is is that there's a bunch of companies that are trying to modify the ibegaine molecule to make it not have the cardiac effects if they're successful

in doing that then you're in a situation where the one of these ibegain analogs may be the solution maybe you could take that at home or whatever and a lot of them aren't particularly psychedelic right and so there's this as you know a big open question of do you need to have the trip do you need to have this experience or can you just have an agent that just changes brain plasticity and that's it And so that's a TBD sort of question. But that may be a way to do it. There are other, you know, ibogaine alkaloid, I'm sorry, iboga alkaloids that have, you know, more or less cardio toxicity.

So that's a question. And then we haven't really studied the dose ranges of ibegain well at all, you know. And so it may be, and there's some, you know, very early kind of anecdotal data around this that people with, with Parkinson's and that sort of. thing, taking micro doses actually show improvements. And so it's one of these things where the Texas effort is going to be important to really hashing out what this is. You know, these effects of dopamine and other things are powerful.

The ability for us to sort of navigate different mental illnesses with these drugs is fascinating to me because we never really had these drugs that are, or compounds that are so diverse than their effects and affect so many different conditions and have such a magnitude effect greater than what we have. So maybe you could spend a minute sort of talking about your more recent study in magnesium and I began in the veterans and what you found in terms of the orders of magnitude improvement compared to conventional therapies around depression, TBI, brain injury, PTSD, and what you found in terms of the connectivity in the brain, what you found in terms of the sort of physiological

changes that you saw with looking at functional MRIs and the EEGs and other other assessment techniques because you're now looking at what's happening in the brain in the ways that we couldn't really do before and that nobody really looked at. So ibegain is is a compound that that like I said produces that physiologic kind of EEG-based change that we just published on. We have more data that's kind of in review now, where we actually took, we took the MRI brain scans and fed them into an analysis pipeline around AI guessing the brain age. So as Mark, you probably already know, you can take a brain MRI and you can have AI guess a brain age. You can scan them the second time, and it'll be very close to the first one. You scan them a third time.

It's going to be very close. So three different scans fed into the algorithm guesses within a very close range of each other, but not necessarily of your chronological age, right? And so, you know, you're a young guy in the sense you look very young, right? And I would suspect your brain looks very young. And I would suspect that it's younger than your chronological age. You're talking about me specifically? Yeah.

Yeah, I'm 65. I hope it's younger than that. That's what I'm saying, right? So let's say we scan your brain and maybe your brain is 55. And that's what AI. And so it's not very good at predicting what the chronological age is because that has much more to do with your lifestyle choices. But it's very good at being consistent about what that brain age is and mapping it on to other folks' brain age, right? And so, and, you know, as an alternative, right, there are some people at your age, they're already developing.

Alzheimer's or you know MCI or whatever it is and their brain age is 75 and if you scan them three times you're going to see that at 75 and what this what this is showing is as a group average people have about a year and a half younger looking brain at one month wow is a compound if you keep doing it this is what everybody keeps asking me I have no idea about that question but it's a It's a good question, right, is can you lock the brain into an age if you just keep re-exposing it? You know, it's a much further along the road question, but it's an intriguing one. Like I didn't, you know, my postdoc who's kind of obsessed with brain age did, you know, ran all these analyses and came to me and said, hey, you know, we're seeing this and we're seeing it de-age the brain. But what we don't see is any real, I mean, there's a little bit of change right after, but it takes a month before you really start to see the brain.

age change. I wonder if it's like affecting epigenetic expression or gene expression in some way because it seems like that's a pretty profound effect. Yeah. And it may actually make sense. We're talking about like one dose, one day having an effect to reverse your brain age by a year and a half at a month. That's pretty remarkable. Yeah. I mean, it's a, you know, it's an open question in the sense that, you know, you need to, you know, we need to do the work. But what you don't see is much of a change right after. And so whereas you do see that with PTSD and depression and everything else, you see it really quickly.

But with traumatic brain injury disability and with the brain age, it takes the month. And it makes sense. Like if these are more hard neurological issues, you're not going to be able to change the brain in five days or whatever. It's going to take some time. One of the things that I heard is that there's a metabolite of Ibegene called Nore. ibegene that lasts longer and i'm wondering if that explains some of the the tail of these effects of the addiction and inhibition withdrawal inhibition and maybe some of these other deeper neurological

effects and and that and i don't know if that neuro ibrahimine has the same cardiac risks or if anybody's looking at studying that so the nor ibegene does have a similar cardiac profile ibegene is metabolized into nor ibegene normally through 2d6 and so you see people with getting ibegain and they they metabolize to nor ibegain in roughly 12 hours eight to 12 hours or something like that and so you know there's lots of folks deboramash is the biggest proponent but lots of folks saying well why don't we give nor ibegain as a treatment and that's an open question you know and that work needs to be done the the issue i think with nor ibegain if you think about PTSD is that The Ibegain seems to be the thing that produces the earlier life re-remembering stuff,

not the nor Ibegain part. Interesting. So the life review, watching move your life, seeing what happened, re-metabolizing it in a way that allows you to be at peace with it and kind of move on from that, doesn't happen with the nor Ibegain. It happens with the... That's based off of the subjective effects and the timeline of the drug, that's what it looks like, right? So if you want to have the, you know, if the goal is to have the experience drive some of the therapeutic effect,

then it probably requires the IBM. And what we found with the EEG stuff that I published a week ago is the degree of that subjective effect is correlated with the degree of the PTSD improvement. So if you take that out, you may be taking out at least some of the benefit, at least the PTSD benefit. I have this theory, and I wanted to know if you've ever thought of this, which is when you look at the global population and you look at the obesity epidemic, it's staggering. There's over 2.5 billion people overweight in the world. Obesies exploding across the planet and in America where, you know, 75% of us were overweight, 42% are obese. The Yale food addiction scale is a way of measuring food addiction. And Kelly Brunano, others developed it.

and 14% of the global population is addicted to food, including 14% of kids. Yeah. You know, that's about the same as alcohol. Alcohol addiction is about 14%. And I wonder if, you know, everybody's talking about OZempic and jumpy ones, but could this be like an unlock for people with food addiction

who are addicted to sugar who are struggling, who may have underlying dopamine receptor issues? When you look at genetics, there's genetics involved in people who tend to move towards more addiction. They don't benefit as much from this dopamine simulation. They need more to feel the same pleasure. And so, you know, how does somebody eat a, you know, a whole sheet cake? I couldn't never do that, but people do. And I think that, you know, is an application. It seems to be a multi-billion dollar application. So our data, we also collected alcohol use. And what we found was, and we're going to publish this soon that people's alcohol use really precipitously dropped almost close to zero.

And so just almost everybody, just really dramatic improvements in alcohol and maintained it. And so, and we also have some biology around that that we're looking at. And so, you know, all those guys, if you ask them, are you going down there to stop drinking? they would have told you no. I'm trying to deal with my like TBI or whatever. And then, you know, nearly everybody came back and reported they really didn't want to drink coffee anymore. They really didn't. And so I always think that, so placebo is expectancy, right?

And the degree of the expectation that you have about how a drug is going to work drives a lot of the effect. So like, I know, you probably have seen this New England Journal of Medicine, total knee replacements. placement study where they did a total, they either did an incision and did nothing or did a total knee. And the total knee patients in the kind of the fake surgery incision folks had no difference in outcomes. It looks like it was driven primarily by by expectancy. And so if the person's being told in medicine, I'm going to do this thing. And when I do this thing, that thing that I'm going to do is going to drive this outcome, then the person has this expectation of that outcome. And that's hard, right?

Like, that's, somebody's going down there and they think this is a TBI treatment or whatever it is, then it's hard to feel good about the data, you know, related to that, not placebo. But what I like to see is when you have off-target effects. Like, we intended to look at TBI disability in this study, but now everybody stopped drink coffee or now everybody stopped drinking alcohol and if you asked them their pre-treatment kind of pre-test probability of any of that was going to happen they'd tell you no like they'd say i didn't know that was going to happen yeah they all just came back fascinated with this thing that happened that they didn't have any expectancy for yeah you know we don't know for sure but the signal is certainly

there that this this appears to be you know if if you kind of read the the the limited data that we we have, this appears to be kind of a global dopamine reward system reorg and that we've just seen it work in opiate use disorder because those are the kinds of folks that are in many ways desperate enough to have taken Ibegaine in the last several decades. So there's all kinds of effects we're just sort of learning about. And I think with obesity, nobody's probably looking at that is my guess, right? With I being? Yeah, I mean, yeah, nobody that I know of. Yeah. I think it could be an interesting offshoot study, like, does it, does their food behavior change? Does their cravings for sugar change?

Does their cravings for, you know, like, because I think it's like that, that, I mean, you're talking about opioid addiction killing 70,000 people a year, but the food addiction part, you know, kills a lot, a lot more, you know, chronic disease related food is, you know, killing a million plus people a year. 100%. In America. So, like, to be, I think it'd be an interesting little kind of side hustle to kind of look at that in your data and see what happens and people change their diets and they change their weight

loss. Like there's other things you can look at. So I encourage you to check that out because I had this theory. But if it, because if it works, it's a, it's a big unlock, you know, and it's probably a lot, a lot better than taking Ozimic. So I want to sort of help people understand that this is not just like an incremental therapy because, you know, as we sort of started out talking about, a lot of the psychiatric treatments we have, don't really work well or have marginal benefits or have a lot of side effects. And with Ibogaine and some of these other psychedelic therapies, we're talking about, you know, 80 to 90 percent reductions in symptoms and things that you just don't see. So can you talk about the magnitude of the effects and how it's different than traditional

psychiatric treatments? Yeah, I mean, so the degree of the effects that we observed were quite striking. The, you know, the data is limited, you know, so that needs to get replicated. And I've heard, you know, that there's another group out of Texas that they're seeing various similar effects to us. And so if that holds, that's really the case, then, you know, that's going to be helpful. In this hypothetical future scenario where, you know, you're right and this is, these are the degrees in which people change compared to conventional treatments, it's a huge difference. I mean, if you look at oral antidepressant differences between active and placebo for some of the pivotal trials that led to approval for something like Prozac, you're talking about a

two to three point difference on a 60 point scale and the inner raider reliability on that scale is two points. Yeah, so basically it's like nothing. So the noise between raiders is the same amount of change as the change observed. Now, on average, they're seeing the change greater in the active group than in the placebo group. I'm not arguing that, but like it's the, yeah, the observer, you know, different. are that level. So it's very hard to discern if you've got totally skilled raiders and they have that problem, how effective these drugs really can be. You wouldn't drink dirty water,

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rating scale, that scale doesn't have a, if you're above 30, 35, you're in really bad shape. You know, you need to go to the hospital or something like that. And so we're seeing a, you know, 20-point change and a lot of people on that scale. The use case for this, drug is across like a whole bunch of different issues that that seem not necessarily related like what does brain injury have to do with PTSD have to do with depression and how do you think that we sort of start to apply these compounds to these conditions in a more systematic way where deliberately working on different pathways that these drugs work on it's an open question you know I think we've got to spend the time to understand what the different alkaloids do and then

use those. It's kind of like where GW pharmaceuticals was as it relates to cannabinoids, you know, and so there's an approval, I don't know if it's like a full approval or an orphan approval, but there's an approval for CBD cannibalial for pediatric epilepsy syndrome. So Lennox Gasto and Dravet syndrome, right? And so those two epilepsy syndromes in kids are really devastating. Sometimes kids have two to three hundred seizures a day. You have to put them on potassium bromide, which is like what we give dogs for epilepsy, you know, and you end up being in a situation where, you know, kids still seizing. And so the kind of interesting story there, which is another story like the veteran story, where there are all these families that

figured out that if they could give their kid lots of CBD, the kid would, the kid would would stop seizing, right? And so they were administering on their own. At the time, moving to Denver. This was, you know, Sanjay Gupta did like a special on this 15 or 20 years ago. So all these families that with Linux guesto kids moving to Denver and then figuring out on their own buying cannabis and then extracting it, extracting CBD. So they called it Charlotte's Web, which is this pure CBD cannabis and they extract that out.

And so GW Pharmaceuticals says, well, let's, you know, let's, in the UK farm, you know, and this is like not, doesn't make people, like, CBD doesn't really make people high. Maybe it's a little anxiolytic, but it doesn't make people high. You know, the kids were actually waking up and they were less encephalopathic when they would take it. Yeah, yeah. And, you know, you give this to a kid and they come out of an epilepsy fit, you know, and so all these families were seeing this. kids, potassium bromide and all this stuff, and then you give them high-dose CBD, and they wake up, you know, for the first time. And so what GW did is they said, okay, we're going to make a pure CBD drug, and we're

going to get that through, and they're going to make a whole host of other cannabinoid drugs to try to really discern, to your point, what's driving what, with variable actions on different neurotransmitter systems and all of that. And I think that's what's going to happen with these iboga alcohol. alkaloids, right? Is that we have to... You don't think it's just the whole plant and you need to take the whole thing as opposed to breaking it down, which is what we do in medicine and break things down on

their component parts and then it doesn't necessarily have the benefit of the whole plant. That is the open question. So there's going to be an experiment on this. You know, Colorado is going to, um, is basically going to allow for whole plant derived iboga alkaloids to be used for people, um, you know, out inside of Colorado. And so the question ends up being, is that the road? Is it isolating ibogaine? Is it isolating other alkaloids?

I'm a pragmatist. Like I don't have a, I don't have like a philosophical view on this other than, you know, somebody's going to die. And you give them this thing and their probability of dying goes way down. We should probably be doing that. And I think that's like, so if that's what happens in Colorado, then that would be good. I mean, I have some open concerns about it because of the car. cardiac, you know, risk, and I'm pretty public about that, but they're going to do it no matter

what I think. And so it's one of these things where that's going to happen. And then there's going to be a kind of a more pure Western medicine pharma play that's going to happen, several. And then there's this kind of organic chemistry thing where they're changing the molecule thing, too. Maybe that's not even psychoactive. And I think we'll get in totality the answer over the next 10 years. And the reality is that if it all works, that's amazing. If one of them works, we know a lot more about how the brain works. I mean, hopefully we're not in a situation where none of them work, but that's possible too. But at least we gave it a college try for sure. But it's the beauty is I think that's all happening and we're going to be able to really actually sort it out and fingers crossed. Yeah, pretty

amazing. Yeah, this is sort of an interesting moment where we have these new compounds we never had before where we're looking at them. But the MDMA stuff is interesting because, you know, that's undergoing phacy trials and other sort of data that's looking at the effectiveness of this. But it's usually combined with psychotherapy. Yep. But what you're talking about, I began not needing the psychotherapy component.

Do people need follow-up, support, treatment, integration? Yes. Is it have to be done in a psychiatric context where there's more continuity of care? It's just like go in and take it, close your eyes, wake up 12 hours later. and that's it. So there is a, there's a pre-post therapy requirement. There's a within dosing therapy non-requirement, it appears, right? Although like nobody's really, you know, could be very helpful.

We don't know. But what happens with MDMA is, you know, I think you've, you've studied is if you, if you give somebody MDMA, they have a positively valence experience. Yeah. Right? They feel good. They feel good and they feel good about, you know, the people around them. And they feel good about the memories they've had. And so if they look at traumatic, memories are going to see those memories from kind of an alternative perspective because they're seeing the world through a lens. And I think that's very useful as a tool. I think it's also very tricky as a tool. There's an analysis of the, you know, events that happened in Israel with the rave. Right. And in that situation, there was a certain percentage of those people that were actually on MDMA. I don't know if you know about it. Yeah.

They actually saw a statistically significantly lower PTSD onset in individuals that were on MDMA compared to people that weren't for that experience, for that kind of traumatic. The mosque came in and terrorized the Noma Festival in Israel on October 7th. And the people who took the MDMA were less traumatized after than the ones who didn't. Correct. Yeah. And so, you know, what it's a terrible story, obviously, what's interesting about that data is that it tells you something about it being protective, right? And those folks, you know, I'm sure it was clearly still traumatizing to them, but for some reason it didn't lock them into, you know, as many people into a permanently traumatized state because they were seeing things from a positively valence place.

but you know it's probably true that you need to you know have a guide to guide people with that drug with ibegaine what's really interesting about it is you can prepare people you tell them what's going to happen or tell them what you think could happen or a variety of things that could happen and then they take it and they have this long experience and then they come out of it and they have to unpack all of the stuff that they saw right they have to unpack all of the earlier life, you know, in many cases, traumatic memories that they have to kind of get through. And in that situation, it's driven by the drug. It's not driven by a therapist telling him, hey, go look at this memory. It's like the drug is doing that. But then the person has to

come out of it and really actually sort it out for themselves mentally. Yeah. Me need help with generally. And they, yeah, basically all need help with. Yeah. I'm fascinated because, you know, there's effects on disease states are, you know, things that are problematic for people like PTSD, traumatic injury, depression, etc. But then there's the brain enhancement component. And I know a number of people have gone down there into Mexico and didn't have these problems, but used it as a way to sort of create neurocognitive and neuropsychiatric enhancement. And you mentioned briefly about the reversal of the brain age as sort of a hint at that. Can you talk more about how it might be used as a as a sort of an enhancement drug in other words that it doesn't

just treat disease that it may actually improve your overall cognitive function memory mood neuroplasticity or neurogenesis and things that you know we all would like to have better brains right yeah so what we observed in the veterans was that they had a improvement in cognitive statistically significant improvement in some aspects of cognition particularly around frontal control you know it's an open question as to whether or not in a non-TBI, non-PTSD individual, you're going to see that, too. But, you know, at least you can see in a diseased population and improvement there. Whereas, like, with a lot of the oral antidepressants and whatnot, you're not really seeing an improvement in cognition.

There's not really a good drug in psychiatry that's approved for depression that improves cognition. And so at least we're getting signals of it with Ibogaine, but it's, you know, it's got to be studied. Yeah, it would be interesting as it just is more of like a longevity and histamid drug. And we don't really think much about those things in medicine at all. We think about things that suppress or inhibit or block some pathway rather than things that optimize enhance and improve the functioning of human physiology, right? Probotics, for example, of something that can optimize health as opposed to an antibiotic.

And in functional medicine, that's a lot we think about is one of the ways to enhance function, one of the pro-drugs as opposed to anti-drugs, right? And it seems like it has that kind of potential. What we really need to understand, I think, is why were the Buiti taking this for hundreds of years, you know, and why did the French think this was helpful for 36? Yeah.

You know, and I think that could give us a signal about what it could do for that, right? because it seems to me that you have a, even in the 30s to 66, you know, which is kind of a different era, obviously, to have a drug on the formulary for 36 years that, you know, it wasn't doing anything for the French, it seems unlikely, it's possible, but unlikely that that would have stuck around and been sold for 36 years. And so my suspicion is, is that there were some disease treatment effects, but maybe a, maybe these effects too, who knows. Yeah, I wonder if there's any people around who took it back then

who were in their 90s probably now from what the effect on them. I think this is such an exciting moment in psychiatry and medicine and I think, you know, a lot of people are stuck in mental health issues and we live in increasingly stressful society and there's just such a limited set of tools for people. Therapy can help a little bit and some of the medication can help a little bit, but there's really, this is like a whole revolution. And I, you know, I wonder if you've, if you've thought about, you know, combining the things that you're doing with other kind of metabolic psychiatry stuff that your colleagues doing at Stanford around nutritional psychiatry and metabolic psychiatry and combining both modalities

as a way of even improving health outcomes and mental health outcomes. A hundred percent, yeah. I mean, I think we, I've taken the stance that if you look at like, MI, Carol, like people having a heart attack. What do we do now? We throw an aspirin. We throw statin. We, you know, we, we do a heart cath. We do all these things in summation that all independently were shown in isolation to benefit. Right. We hit a cocktail therapy as opposed to single therapy, right? The challenge right now is to, we're in cardiology 1950s, right? So we're having to, we maybe have a pacemaker, we have, you know, a couple of drugs or whatever it is, and we need to now figure out

what to do with all the limited tool set to make more tools and improve those tools and do the trials in each one of the tools. Now, or my kids or, you know, whatever the folks that are going to end up, or my students, or your students, the folks that end up combining all of these therapeutics together because there have been trials to show synergy, I think absolutely. You know, I think that's going to be the way we deal with things in the future as we say, okay, well, we're going to, you know, and you're doing a lot of this already. We're going to measure all of these things. We're going to modify your diet, your metabolic, you know, all of that good stuff.

We're going to do brain-based things. I think the interesting question ultimately is if we're in such a disease society that we end up being so far off of like the normal range metabolically stress all that stuff and people end up being way over here do you need multiple therapies to get you back on track but then if we just had the right dietary interventions to begin with that maybe we don't need to do all this other stuff to me that's one of the big questions that you know yourself and others are trying to tackle which is you know a lot of folks now in government is this question of if we can just have kids eat healthy? Is there a world where we have less mental illness? And it's an important question.

And one that we have to ask. You know, we have increasing rates. We don't know why. And so maybe it is because of diet. Oh, yeah. I mean, it's huge. I mean, but I don't think that the dietary change alone or nutritional metabolic changes alone can can do the kinds of things that these psychedelic compounds do. And what's fascinating is we've sort of And it's always fascinating to me I don't know if you have a theory about this But how is it that all these plants

Have compounds that interact with our biology In these profound ways that change us And I wonder if somehow we co-evolve with these plants And if you look across all indigenous societies They all have some sort of psychedelic something That they play with With it's ayahuasca and you know Should be Indian in South America

Or peyote in North America whatever. If you look at the thinking that the 1700s physicians had about vitamin C containing fruits like citrus fruit and the way they thought about it as it relates to scurvy, you kind of understand where we're at today. Many of them thought these were, you know, there weren't that many limes and lemons in Europe at the time, right? This was considered a South American or an African exotic plant. And so most of the physicians the day actually rejected citrus fruit as a treatment for scurvy. And so as you know, the story of anti-fruiter's, right? There are lots of people in the British Royal Society that said that the limes and lemons

may actually be making scurvy worse. And I think that's the situation that we maybe find ourselves in now or used to find ourselves in where somehow we've conflated the solution with the problem in this very weird way and that we blame a plant because man didn't make it. And I think it actually has a greater philosophical problem with the way that we have, you know, that we see the world in our hubris, that for some reason we have this view that SSRI, that's totally fine because man made that and we understand it, plant, not so sure about that, you know? And I think that's the way we've been looking, looking at plant-based psychedelics for a long time, and hopefully that changes.

Pretty amazing. And this, and the sort of, I keep kind of doubling down on the magnitude of size of the effect, and I want to sort of double down on them because I think when you look at the 30 special ops, you know, special forces veterans who had brain injury, you know, you found really large effect sizes, you know, like the disability ratings drop. dramatically from modern disability to like no disability had PTSD drop by 88% depression drop by 87% anxiety by 81% improved cognition seems like too good to be true right when my postdoc showed me the data I didn't believe them and I told them to go back and

reanalyze it yeah you know and so we you know we that's why I don't I don't make claims about it you know because I think that we have to at least be replicated by another group in order to justify. So we need to be replicated by another group in order to justify it. Now I'm hearing from my colleagues out of Texas that they are seeing very similar effects, right? And so I want them to formally see that if that's what it is and publish that. And then we can say it wasn't, you know, our site or whatever, that at least in an open label way, this is what this looks like. And then the next step is to do the big trials. But it would be unusual to have have that level of an effect for, for this sort of level of expectancy.

I mean, they didn't expect that big of a change. So they would, you would less likely to see it. Yeah. The veterans had, have, you followed them ongoingly? Are they still have the lasting effects? So we have data out a year. It isn't published yet. It's kind of in review now, actually. And that looks really good. Most people hold it. And you're talking now more about this idea of circuit-based psychiatry, which helps explain some of the things you're seeing. Can you kind of unpack what that is and how it differs from our current view of psychiatry. If you think about psychiatry and epochs, you know, the first one being talk therapy. And we learned something important there that spoken word can have effects on, you know, mental states and, you know, and now more recently data suggesting that it's having effect on the brain itself.

And that's, that was useful. Psychiatry 2.0, this idea that, uh, pharmacology. can have an effect at the level of synapse. And that was also very useful, right? I got a lot of people that say schizophrenia out of asylums and that sort of thing. I mean like Thorazine. Yeah, like Thorazine, yeah. Chemical straight jackets, we call them.

And then psychiatry 3.0, this idea that you can actually look at the psychiatry 1.0 and 2.0 innovations from the frame of the circuit. and improve upon them, right? Because at the end of the day, lots of the psychiatric treatments that we have are suboptimal for patients' desires, right? ECT is a great example of that. Electric shock therapy.

Can you use insights from before and make things much safer and better and much more tolerated with patients? And that's really been, I think, the emphasis for our work. And so when we look at IBM, we're looking at it from the lens of the circuit, when we're looking at, say, stimulation of the brain, we're looking at it from the lens of the circuit.

And that's helpful because, you know, the whole brain doesn't need, necessarily need to be exposed to things, really, at least in depression, it looks like from our OCD data, that you can get big effects from just isolating one brain circuit and modifying it. Amazing. Well, we're in a kind of revolutionary time in psychiatry, which is exciting to me because I remember first working, in a psych hospital in residency.

And I was like, I spent a month there. I was like, this is just nuts. And I don't mean that as a pun. I just mean the way we treated people, the amount of suffering that's going on, the lack of really good treatments. It feels really hopeful. It feels like a hopeful moment. But it doesn't feel like we're going fast enough to me.

It feels like we're still in this sort of glacial pace of change. And science proceeds that way, unfortunately. but I think many people listening going, wow, you know, can I try it? What do I do? What if I want to go do it? I have this addiction issue. I've got PTSD. I've got trauma. There's a few places people go, like in Mexico, beyond, or Ambio and also in Mexico. There's a few places out there. What do you say to people who want to go sort of explore this? Yeah, I mean, the good news is that we, you know, it looks like there's actually going to be some U.S. trials soon, you know. And so being able to do this from inside of the U.S. is, is kind of the ultimate goal. You know, folks go to these places and, you know, these other countries. But the ultimate goal is really to see that folks can do this safely in the U.S. And so I think, you know, five, ten years ago, I wouldn't be able to say anything right now with you asking me this.

But now, at least, we have the ability. And the hope is, is if everything goes to the FDA, there'll be a normal healthy control study. the FDA will have that IND, that new investigational new drug application through, and you'd be able to actually give people ibign that are normal, healthy controls, right? And so that's... Let's see what happens. And so it is coming soon. You know, we'll have to see what happens with the FDA.

But, yeah, I think that's an exciting moment for folks and, you know, being able to have access to an experimental therapeutic like this. And if people want to go down and try this in Mexico, do you advise against it? You say it's your own risk. It's definitely a people's own risk. I mean, look, it's one of these things where we still don't know that much about this. Like in our Stanford study, we're really clear with people that they had to have already signed up to have anything to do with... Couldn't encourage them to do it, yeah.

Yeah, we couldn't encourage them to do it. we didn't really participate in any of the processes for them to do it. We simply just studied people that were already going down there. I want to ask you a question about a particular flavor of mental illness that is incredibly difficult to treat that is really generally from a lot of trauma, which is personality disorders. Yeah. Borderline personality, narcissistic personality. It gets so effective as all these personality disorders, which are more like fixed personality traits that are hard to,

change. And I'm curious if this kind of life review, the sort of narrative unfolding of your life like a movie during an I-Begaine experience has any impact on these more embedded, like deep-seated traumas that are harder to undo. It's a great question. I mean, the, you know, the Hopkins group demonstrated this profound personality change that they observed out to a year, I think, early on with their trials of psilocybin. And so there's definitely data that there's personality change, you know, in and around psilocybin use. It's an open question.

And the other thing that's interesting, which is data that isn't published yet, but was collected, was around folks that will say they're, you know, they're religious or not. And so actually people that, I think it was like 16% of people were not religious prior to taking ibegain and there's a increased kind of sense of of a higher power or whatever after like almost you know two-thirds of people and so this question of how do people see the world that they live in is really interesting but yeah you know nobody's done a personality inventory study with ibegain so it's still open question is it dangerous for these people to do anything

It's certainly dangerous for people with a psychotic history, you know. I think people with bipolar disorder, that's going to be dangerous. Maybe somebody with severe borderline, maybe, you know, it just depends, it depends on a kind of individual basis. The problem at a fundamental level is we just haven't studied this enough to really know. I don't have enough data sets to know what's going on with these people. Yeah, interesting. So where do you see in closing, where do you see this in five to ten years in terms of psychiatry, psychedelic therapy in general and I begin specifically.

We have to do, we have a lot of work to do to kind of get this to the next step, a lot of studies to do. But, you know, if somehow this is able to get all the way to the finish line, I think that, you know, society will be in a much better place from a mental health standpoint if all the data continues to look like it does just because of, you know, the profound suffering that's out there. I mean, there was a WHO statistic that really struck me, which is one out of two people will have a DSM diagnosis at some point in their lifetime. That's a psychiatric. Purely psychiatric or dementia.

One out of two. One out of two. That's a lot. Half of the population of the world is going to have some mental illness at some point in their life. It's a scaling problem. Think about it. I mean, at the end of the day, we would never be able to actually effectively deal with that. Definitely not through therapy.

Definitely not through therapy. You'd have to have half the world become therapy. I mean, maybe with AI, you know, all of us are trying to figure out. Right, AI therapists are pretty damn good. This psychedelic revolution to me is very promising. And then combined with the metabolic psychiatry revolution, which we're going to do a podcast about soon, that also is another unlock, I think, in terms of mental health. It's harder for people to do that because it requires a lot of lifestyle change,

whereas this is just sort of a brain reset that then seems like it would facilitate behavior in lifestyle change. It's almost like this could set the stage and then you can have an easier time doing that other hard work. What studies are on the horizon for you that you're looking at doing? We're looking forward to seeing what happens, this Texas effort, and hopefully there's some funding for Texas-based universities to do this, you know, and to do these treatments.

But, yeah, it's an open question about what's going to happen with the FDA. And I think if the FDA comes through and lets us do the studies, there'll be a normal, healthy control study. We're hoping to add some biology to that. and then subsequently, hopefully, some traumatic brain injury studies. What do you mean biomarkers, blood tests? What would be the things you're looking at in addition to the functional MRIs and the EEGs, which are brain imaging and brain electrical studies?

We hope to do some of that, at least the EEG side of things. But yeah, it's a great question. Maybe something interesting to talk about later, but, you know, around, is there blood, you know, any kind of blood-based biomarkers that would be of interest to, because we'll have IVs in everybody, you know? Fascinating work. Incredible what you're doing. you're definitely going out of limb in the psychiatric world.

I think, you know, you're brave and, you know, but you're at Stanford and respected institution and they seem to be in support of you doing this work, which is amazing. And, you know, we need a hell Mary in psychiatry because we are in a bad state as a world. We're all divided and disconnected and isolated and struggling with various forms of just anxiety

of living in the 21st century to more serious mental illness and the unlock that you and your colleagues are trying to get with this work and the whole psychedelic field is just amazing. So thanks for doing what you do. Yeah, thanks for having me. Yeah, good to see you. If you love this podcast, please share it with someone else you think would also enjoy it. You can find me on all social media channels at Dr. Mark Hyman. Please reach out.

I'd love to hear your comments and questions. Don't forget to rate, review, and subscribe to the Dr. Heimann Show wherever you get your podcasts. And don't forget to check out my YouTube channel at Dr. Mark Hyman for video versions of this podcast and more. Thank you so much again for tuning in. We'll see you next time on the Dr. Hyman Show. This podcast is separate from my clinical practice at the Ultra Wellness Center, my work at Cleveland Clinic and Function Health, where I am chief medical officer. This podcast represents my opinions and my guest's opinions. Neither myself nor the podcast endorses the views or statements of my guests. This podcast is for educational purposes only and is not a substitute for professional

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