Psychiatry & Psychotherapy Podcast - Psychotic Disorders: Comorbidity Detection Improves Diagnosis, Treatment and Outcome with Expert Jeffrey Paul Kahn, MD.

Episode Date: June 7, 2021

In this podcast episode, we will interview Jeffrey Paul Kahn, MD, a psychiatrist who recently co-edited a book called Psychotic Disorders: Comorbidity Detection Promotes Improved Diagnosis and Treatment. Our focus will be on different presentations of psychosis and how through a good history you can better treat the underlying issue and choose optimal treatments. By listening to this episode, you can earn 1.5 Psychiatry CME Credits. Link to blog. Link to YouTube video.

Hello and welcome to the psychiatry and psychotherapy podcast. I'm here to talk about getting rid of burnout, increasing job satisfaction, and feeling like an expert in what you do. One thing that created a lot of burnout and angst for me was trying to get continued medical education right at the last minute. So why not join the CME membership and do CMEE while listening to this podcast? Go to Psychiatrypodcast.com, sign up, sign in, take the test, and the certification is emailed to you in seconds. All right, welcome back to the podcast. I am joined today with an expert Jeffrey Paul Kahn. He is an author of a recent book that he edited and put together called Psychotic Disorders. Comorbidity Detection promotes improved diagnosis and treatment. This book focuses on different presentations of psychosis and how through good history and good treatment you can uniquely,

look at and think through how to properly diagnose and then treat these different psychotic comorbidities. Dr. Kahn completed medical school, psychiatry residency, and fellowship at Columbia University. Other than this recent book on psychosis, he has done extensive work, including books, book chapters, and publications in occupational psychiatry, anxiety, heart disease, and one book on an evolutionary theory that anxiety and depressive disorders evolved from an altruistic instinct, which I'm going to have to have you explain what that means. He has no conflicts of interest. I'm also joined with Catherine Wu, who is a psychiatry resident, who has done an amazing job helping us write this material up into a article that you can check out on my website, psychiatrypodcast.com.

So, yeah, thank you guys for coming on. Well, thank you, David, for the nice introduction, and it's wonderful to be here. Yeah, I'm happy to be here as well. Yeah, so let's talk a little bit about the five different types in general, and then maybe we'll go specifically one by one. So in general, how did you come to sort of this idea that there's these five different types of, you know, psychosis, comorbidities? How did you start to think through that yourself? What was your process? Well, the process of defining five psychotic subtypes started with the previous book on evolutionary psychopathology.

And in thinking about my own practice and my training in anxiety disorders in particular and research that I'd done in anxiety and depression, it occurred to me that the diagnoses I see most often in my own practice, are two subtypes of depression, melancholic depression and atypical depression. Both of them are in DSM, atypical depression, may be a little less well known to some psychiatrists. And within depressive disorders, within anxiety disorders, the most commonplace ones are social anxiety and panic anxiety. And then there's OCD, which may be an anxieties. disorder and then again maybe not dependent on who you ask. And in thinking that through, it occurred to me that there must be a reason why we humans have

these conditions because they're not things that we want or like. They cause pain for us and interfere with our function. So if you're thinking about it from an evolutionary standpoint, maybe at one point in primeval times, they served a purpose. To tell you the truth, I was thinking about that as I was reading a book about beer and wondered why beer was so important to ancient men. And it occurred to me as I woke up that maybe it served the same purpose then that it serves now. For example, people have a drink to loosen up when they go to a party or go to a bar and to feel that they have more of a level playing field. and it's easier to get along.

This resulted actually this excerpt in an op-ed in the New York Times, which the Times editors had the wisdom to publish on St. Patrick's Day, how beer gave us civilization, and it was wildly popular online for the New York Times. But it also led to thoughts of what kinds of purpose these might have had in primeval times. The easiest one to describe, they're all easy to describe, but the simplest one is social anxiety. People who have social anxiety are shy people. We can, those of us with social anxiety, can take the lead. We can give a speech in front of an audience. We can perform on stage.

but if you have social anxiety, you tend to be uncomfortable, and something inside you tells you, you're not supposed to be here. You're supposed to be hiding in the back where no one can see you. That tends to be how people with social anxiety feel. And if you think about ancient groups of humans, I call them herds in the evolution book, social harmony was important for the herd to survive. So there were a spectrum of degrees of confidence on one end and social anxiety on the other.

The advantage of having some people who had varying degrees of social anxiety is that there was less competition for hierarchy and rank within the group, and so the group as a whole did better. And people were at the low end were constrained by their social anxiety, which they probably didn't like even back then, but at least there was more peace within the community. It later occurred to me that I had previously done work on panic and schizophrenia, and it occurred to me and panic was one of these five diagnoses.

And so the thought occurred that, well, maybe there are psychotic versions of each of these five. And it turns out that there had been research on all five of them in varying degrees, not to the degree that we like to have, but enough research to put it together and support the idea that each five of those core diagnoses had a psychotic version. And as we'll talk about later, collectively, they may account for much of the psychotic disorders that we see today. Yeah. I think about my two cats. I have twin cats. One is very socially anxious, and the other is more of a warrior. The warrior wants to be outside all day. The anxious one wants to be kind of like hidden in the house. And I think inevitably one will survive better, right? If the coyotes are out one night,

probably the warrior will pass away and the shy one will remain, right? Well, that depends on whether or not the coyotes break into the house. Right. Right. Do you see these, do you see these anxiety types of issues, this evolutionary wiring going back before humans, or do you see it being uniquely human? Well, we shouldn't spend too much talking about the prior book, but I suspect that it goes way back in human evolution, and it's been present for a long time, including now in many species, not just humans. You know, as you talked about with your cats, there are alpha cats and alpha dogs and not so alpha cats and dogs. And in experiments with a captive monkey troop, for example, for safety reasons, they removed

the alpha male monkey from the troop, and then they identified the lowest ranked male monkey in the troop and gave him Prozac. And sure enough, he became the new Alpha male, and he was in charge of the troop, Prozac, as your listeners know, is a commonly used treatment for social anxiety. And when they stopped the Prozac, he dropped right back down to the bottom again. So even in monkeys, it's not purely biological what determines social rank, but it's part of it. Other things like age or experience or size can play a role too.

But biology like this, and we may have something similar in humans. Social anxiety, for example, is if you look at the prevalence by socioeconomic status, it's more common in people with lower socioeconomic status. So even today, when our conscious minds and our culture tell us that we can achieve anything we want to, we still have something in us that tells us, well, maybe that's not such a great idea. Yeah, and with good treatment, I've seen a lot of patients who then climb up and do better in different jobs, make more money. It's not uncommon for, I've had patients tripled their salary in five years. And I think that's a combination of therapy, of course, and medications, but I see it.

Absolutely, but this is one specific aspect of it. And it applies to some of the other diagnoses, too. Here in New York, tripling your income, for some people, would be a minor thing because we have Wall Street. Yeah, they would want a 10-X-it. So, okay, let's jump into this content of this book and the five different types of psychosis. But before we jump into the different ones, let's talk about, like, in general, What is psychosis and how do you sort of define it? Well, psychosis is a disorder in humans where people have fixed false beliefs and they fall into two main categories. One of them is hallucinations, which is a perceptual sensation which seems real. And unless I'm mistaken, there's evidence that, in fact, for example, auditory sites light up in the brain, when people are hearing voices, because from their perspective, they actually are hearing the voices, even though there's no voices around them. There are other kinds of perceptual hallucinations,

including visual and olfactory and others, but they play a relatively small part in common psychotic disorders. The other major category is delusions. The most common one, of course, is paranoid delusions of various kinds. There are ideas of reference, which are also, you could call them paranoid, but they're slightly different than thinking that the authorities are out to get you. So there are different flavors of delusions, although most of them, not all of them, most of them are about the idea that somebody in power doesn't like you and might do something about it. But there are other ones too.

Yeah, what do we say the common theories for psychosis are at this point? You talk about the dopamine dysfunction theory. Maybe we could start there. Well, a growing theory, not yet accepted by everyone, is that there's a common thread among the various psychotic disorders, that all of them are an overlay on top of a susceptibility to psychosis, sometimes called psychogenesis. Some people have factors, aspects about them that make them more likely to become psychotic, a variety of different psychoses, but more susceptible to the psychotization of them, if I might invent a word.

And there are many factors that have been proposed, ranging from early childhood loss of a parent, for example, to various specific genetic abnormalities. But I think the two that are perhaps not speaking as an expert, but as someone who has met experts, I think the two that play the most prominent role are a variety of of factors that do one of two things. One of them is our frontal lobes are where we do our conscious thinking. And one of the things that our thinking does is it modulates certain instinctive fears and behaviors that we have and puts them in more rational terms for us. Some people, for a variety of reasons, have frontal lobes that don't function as well. Either they are smaller or they have a different neuronal structure or fewer neurons. There's a variety of things that have been proposed. So one possibility is that people have what's

called hypofrontality, a low level of frontal lobe functioning. That doesn't make people psychotic in itself. Another possibility that's likely, as most people listening know, dopamine is a neurotransmitter that's involved in psychosis. And when people are psychotic, the main way that all existing antipsychotics work is by reducing dopamine activity. Too much dopamine is associated, too much dopamine activity is associated with psychosis and drugs like the original drugs like thorezine and haloperidol and more modern atypical antipsychotics all have a dopamine blocking effect so some people have a genetic variation there are genetic variations one in particular that cause hyperfrontality and likewise with dopamine activities there are genetic variations there are

genetic variations, one in particular, that increased dopamine function. And what effect might this have? Well, dopamine is a neurochemical. People think of it as a pleasure chemical, but it's not exactly that. What it does is if we sense something pleasurable or desirable in our surroundings, our brain releases dopamine by a way of encouraging us to seek whatever it is that we've already sensed. If you have too much dopamine activity, you may get all wired up about trying to find some good things around you, which can have effects of a variety of kind on instincts, on other neurochemicals and on other diagnoses. So the two primary but not only factors contributing to susceptibility to psychosis or hyperfrontality and increased dopamine activity. Then when people have certain other common anxiety or depressive disorder subty and certain difficult circumstances roll around, they might combine. to produce a psychotic disorder.

Yeah. Yeah, so you were talking about with this hypofrontality theory, this idea that you have with that impaired conscious thought, reduced attention span, impeding processing of social cues. And with that, I was curious if you had any thoughts about these micro-expression studies, there's one Russell 2006, which I've looked at, which they've trained people with schizophrenia on how to read micro-expressions better, and it actually improved their emotion mask, a matching task, back up to the normal control level,

not superior than control, but back up to the normal control level they were impaired before. Is this kind of an example of, you know, how with that hypofontality you might have impeded processing of social cues? Any thoughts on that in particular? Well, people who... have psychotic disorders often have reduced ability to recognize social cues, and there are other things that can do that too. And one possibility is that the frontal lobe serves as a center for viewing social cues and determining on a conscious or unconscious level what emotions are being seen. Another possibility is that with hyperfrontality, the frontal lobes can't filter inborn

perceptions of emotion, and therefore people have to learn to balance the inborn perceptions with the observed things. As a side note, there is literature that suggests that the way we determine emotions is kind of indirect through something called mirror neurons so that if you look at someone and they're smiling, that's not sufficient for you determine that they're happy. In a subtle way, one part of your brain detects the smile, mimics it, and then your brain notices that you're smiling, and in that indirect way, it determines that someone else is smiling. And you can actually block this with Botox, which would paralyze the relevant muscles.

And if you do that, people's ability to detect other people's emotions goes down. Yeah, I've wondered about that with Botox specifically because they usually block the middle of the forehead where people have anger, disgust, fear, and sadness. And they block that area. and how that influences their ability to potentially interact with other people as well and other people to read what they're feeling. Well, you know, the research suggests that if they block that part, they have less wrinkles, which they're happy about. But it means also that their anger and disgust are less likely to show. It also means, by the mirror neuron theory, that they're less able to perceive other people's anger and disgust. So they're walking around in, oh, a partial emotional vacuum as a result.

But I think what happens in psychotic disorders is that people can become so overwhelmed by emotion and by cognitive dysfunction that it's hard for them consciously or unconsciously to focus on other people's emotions and perceive what they're doing. So they have kind of a sort of flat quality to them, at least some of them, and they don't interact well socially because they don't pick up on social cues very well or express them very well themselves. But that varies from one to another, and the story of that study you mentioned is fascinating. It suggests that people with schizophrenia, can learn to do better job of picking up on social cues. But the next question is, do those abilities persist?

And are those abilities socially useful to them? Or are they just something that they're able to learn and use, but it doesn't have a social value? Yeah, I would say for myself, it took me probably a lot longer than the study said it took them so many hours. for me it probably took a couple hundred hours to figure out how to use that information accurately that's one of my my interests so to speak i'm just launching a training program online for that so yeah i would say probably it didn't persist for them very long because it does it does take

some repetition and some practice and then how to integrate that knowledge in a meaningful way is another question which is more difficult to teach okay let's jump into um that the different types. The first one being, you know, what is obsessive, compulsive schizophrenia? Well, by way of brief introduction, to me, and it's fascinating that maybe psychotic disorders or psychotic versions of common anxiety and depressive disorders that we know about, and that we can, if we can overcome the obstacles to diagnosis, we can treat the comorbidities that go with those psychoses and help people get a whole lot better, which is what you see in clinical practice. And in addition, maybe these associated diagnoses can help define the nature of the psychotic disorders as well.

In one case, that's well established, and that's further down the list, but that's the association of melancholic depression with psychotic depression. and it's long been recognized that psychotic depression is preceded by melancholia and that treating both is essential for people getting better. OCD is one of the ones on the list. It's probably the one that I've seen the least frequently of those there, but I've certainly seen it. And our chapter author for that were two of the leading experts on O.C. schizophrenia, Michael Wang, and his colleague. So what you see is people, if you are able to get the history,

is people who have a prior history of OCD, which may or may not have been noticed or treated. And then at some point they start developing psychotic symptoms. Those psychotic symptoms might include delusions. They might include hallucinations, auditory hallucinations, but that might also include things that resemble a psychotic version of OCD symptoms. For example, one woman dressed only in white clothing and lived in a room assisted by her husband

for decades with the windows painted black and the door always closed and she was immaculate careful with how clean she kept her room. The white clothing had a number of reasons it symbolized purity to her, but it was also for cleanliness. She would not drink tap water because of the certainty that it was contaminated. New York City tap water is actually among the purest in the country. And she had other eccentricities as well, which resemble rituals, for example, that resemble things you might see in someone with non-psychotic OCD, but in her case it took on a psychotic form. And she was treated with a combination of an antipsychotic, of course,

as well as with an SSRI fluoxetine for her. And gradually over time, she had an additional comorbidity as well, but between the two comorbidities and the psychosis itself, it took six or eight months for her to get better. She was already 60 years old and had never been treated, and she was able to return to a level of functioning that was mildly eccentric, but no more. She cleaned the paint off the windows on her room. She and her husband celebrated her feeling better by drinking the glass of tap water together. And they started going out of the apartment every day. They were retired, but every day they'd go to a restaurant or a store or a park.

And so it made a huge change. Wonderful. Matt, maybe I want to draw you in here a little bit. Anything jump out when you were reading this, when you were reading the book chapter, anything jump out to you as something new for you that you didn't know before? I mean, so I guess Dr. Kahn, so with patients who come in, you know, with OCD, how do you kind of interview the patients to differentiate if the patient maybe has an underlying primary psychotic disorder versus just an OCD? like how do you differentiate or do you just treat, you know, how is your strategy in terms of interviewing patients, I guess? Well, that's an overall question about how do you assess somebody who's psychotic, which is a great

question. And sometimes you can get some hint of what some of the comorbidities are by two ways. If people are known to have a prior history of the comorbidity, with the exception of melancholia, the other four comorbidities we're talking about are all chronic syndromes. So if they have them during a psychosis, they also had them before the psychosis. That might be known to family, for example, but you may or may not get that history when they're actively psychotic. Sometimes you can. The next thing is that sometimes people have certain symptoms that are characteristic, not

perfectly, but are much more common in association with certain comorbidities than with others. Things like rituals and obsessions with cleanliness naturally would hint at the possibility of OCD. Things like auditory hallucinations hint at the possibility of panic disorder. We did two different studies, small samples, looking at, at whether auditory hallucinations are actually psychotic panic attacks and whether ordinary panic attacks preceded the onset of psychosis. And we found that in virtually all of our subjects, but it's a small sample. One of the samples was a double-blind controlled study. The other one was not. But it's enough to suggest that it's something worth thinking about.

To reiterate that real quick, so you're saying that the panics, for panic disorder with associated auditory hallucinations, the panic attacks preceded the psychotic auditory hallucinations? Is that what you're saying? In psychotic patients who have auditory hallucinations or voices, as we call them, there's some suggestion that the voices are actually psychotic panic attacks. And we developed a semi-structured interview, which is in our book and is also available, that is the structured way of looking at this with patients to help them identify that sudden moment when voices begin, and then to explore whether at the same moment that the voices begin, there are symptoms sufficient to meet criteria for panic.

and in all the patients that we studied, including in a double-blind controlled study, this seemed to be virtually always the case. When these patients become non-psychotic, for example on antipsychotics alone, the voices disappear, but the panic attacks come back. And there's an expression that I try out with these patients, which universally works. And that is, are you having voices without voices now? And they know exactly what I mean. And they say yes. And they proceed to describe a panic attack. And, of course, if you get a careful history, you learn that the panic attacks began,

and in all of our studies, always begins before the psychosis. And to answer another part of Katz's question, the best way to get the full, history and the most accurate history of all the comorbidities that might be present, is to wait until the patient is stabilized and then do a more thorough and careful interview when the patient is more interactive, less cognitively impaired, and more cooperative. And then you can get further information. Once patients get better still, anecdotally, they can often get back to baseline, sometimes better than that, and then you can get even more history.

But in the book, we try to describe some of the ways of learning about which comorbidities might be involved as you go along so that you can get started on treating people for the comorbidities, which helps them indirectly helps the psychosis as well. I have one question. So, you know, from my understanding, patients with schizophrenia, they, most of them usually always have auditory hallucinations. It never truly goes away with treatment. So how could, do they have insight into their, you know, conditions like comorbid conditions, like OCD, for example, if the hallucinations are constantly there?

I know a lot of them, they know that the voices aren't real. Some patients' voices will go away with antipsychotics alone. That doesn't make them functional. but it means they're not hearing voices. Later on, often after a long time, they can understand that the voices seem real but are not real. But it remains a bit confusing to them. Early on, they're not able to make that distinction. Does that answer the question?

Yeah, yeah. Great. Okay, so interestingly, there's a citation that in this one, one study of 3,000 participants, over 3,000 participants, there was an estimated 12.1% prevalence of OCD in schizophrenia. So this is something that actually happens. I've had a couple patients, one that comes to my mind in particular. It wasn't until we got him on both Cyprexa and anaphernal that he did better. You know, he had both, and it was a little bit puzzling to me that someone could have two very serious issues at the same time as a resident.

And he went on to, you know, get a job, have a family, which he had, you know, he was basically living alone prior. So, yeah, let's move to treatment a little bit. Well, what you observed is what some of us think that we've observed, that people can, if the comorbidities are treated, and in certain specific ways are treated well, and the psychosis is also treated well, that people can get back to basically a normal life. Not all of them, but many of them. Yeah.

Yeah, so for this population, you're treating with SSRIs, anti-psychotics, but you also mention that sometimes antipsychotics can be serotonin blockers, so you can run into some issues. any clinical pearls on treatment of people with both OCD and schizophrenia? Well, one thing that's impeded some of the studies, there are studies that suggest that SSRIs added to antipsychotics can be of significant benefit to people who have schizophrenia and might fall into the group that some have called schizoobsessive disorder.

But one of the problems is that the doses of, say, Prozac for depression might typically be 20 milligrams. And the dose for schizophrenia, it varies, but it's commonly 80 milligrams. And some people go higher than that. In people who are psychotic, it seems that they often have difficulty tolerating higher doses of a vaccine. SSRIs so that most of them, if you put them on 80 milligrams of Prozac, many or most, might have an exacerbation of psychosis or might get agitated. So that leads us to a clinical pearl that's purely anecdotal, and that in a couple of cases with these patients, I've put them on fixed doses every 12 hours of Klinazepam, and that's a couple of,

seems to allow them to tolerate a higher dose of SSRI, which is then more likely to help them get better. But it's anecdotal, a small number of cases. It's definitely not proven that that works, but, you know, a couple of cases makes you start thinking. That's about the stage where that is. Yeah. Yeah. So with the treatment of OCD, you know, often you'll give much higher doses of SSRIs, like you said, like up to 80, but you're saying that sometimes when they have schizophrenia on top of that, it's harder to push that up, but maybe something like the clenazepam allows for you to push that up. Well, if it turns out to be the case, it would be wonderful. Yeah. Well, you know, maybe there's a little bit of acesia underneath that you might

be treating as well with that clenazepam. I don't know. Um, anything is possible. You are correct. something I'm on the look for. Yeah, you also mentioned in this chapter was that CBT may actually stress them out and may cause a relapse. I had never thought about that before. But intuitively, most of these patients that I treat have responded the best to just focusing on the therapeutic alliance, focusing on empathy, because sometimes even getting them to take the medications is tough.

Oh, absolutely. And developing, there's a short section of the book that talks about psychotherapy for these patients, for all psychotic patients. And what we suggest in the book is not so much CBT as a sort of gradual and graded interpersonal therapy, which starts in a very nominal way. When they're acutely psychotic, you just spend a little bit of time sitting with them so that you're a non-threatening presence. And that's basically all that it is. And that, as they get better, then you move to supportive therapy, helping them with things, encouraging compliance. And as you get better, you can do more involved supportive therapy and discuss relationships. And in a small number of patients, you can even get into some dynamic psychotherapy, which would actually be contraindicated earlier on because if you tried that, it probably would exacerbate the psychosis. When I was a resident, I was taught with most patients, you want to help them get it out. With psychotic patients, you want to help them push it back in.

Interesting. Yeah, that's good. We talked a little bit about the mixture of panic disorder and psychosis. that's the number two sort of comorbid psychotic illness you look at in this book. Any other things that you really jump out that help you understand that this is someone who also has panic disorder in the midst of schizophrenia? Well, panic and schizophrenia is how I started out in this area of research back in the 1980s working under a fellow named Donald Klein, who was probably the preeminent researcher of his time

and my mentor back then. And there had been some studies that came out suggesting that Xanax, given to unselected psychotic patients, seemed to make some of them better, a lot better, in positive symptoms, negative symptoms, and cognitive symptoms. But they couldn't, figure out which ones. So I figured, well, this is worth trying out. And at the time, I was teaching part-time at a state hospital. And working with one of the attendings there and with the residency director there, we, and with Donna Klein, we found some patients on the wards who had schizophrenia and who had current panic attacks. And we added, um, um, we added, um, I think Xanax every six hours, Xanax is a short-acting drug.

And we just rated how they were doing, and they did better. They did better in positive symptoms and negative symptoms. We did not rate cognitive symptoms at that time. But these were, although they were clearly better, and it was statistically significant, it wasn't a blind study. and these were backwards patients who had been in the hospital for a very long time, many years, and their function improved in that instead of hiding in their rooms or behind a couch, they would sit in the couch and watch TV and sometimes talk to staff.

And if you think about it, that's quite an improvement. Some of their psychotic symptoms also improved. their delusions, their panic attacks, their remnant voices, most of them had reduced voices at that time. But with the addition of the Xanax, which is not what I use today, they got significantly better. And I've treated many more patients since then, and that's fairly routine for them to show that kind of improvement. A word about clonazepam and benzos. Not all benzos are alike. There are only two benzos that are not only FDA approved for panic disorder,

but that clearly have a strong anti-panic effect. One is Xanax, which is too short acting and more subject to abuse, and the other is clonazepam, which is longer acting, so you can give it every 12 hours in order to prevent panic attacks from happening. And that seems to work much better. And there's more in the book about how to do that. You have to raise the dose gradually and carefully, mostly because it can cause some initial drowsiness,

which usually goes away fairly quickly. But if you raise the dose too fast or too high, people will fall asleep, which is not what you're trying to do. There's a lot of concerns that people have about chnazepam. I think the concerns are overblown. There are, some of them are real, but you do need to be careful in who you give chlonezapam to. You need to be attentive to that they're not taking more or less than prescribed. And with that in mind, many of the concerns that have been examined carefully don't hold up.

And there have been a series of articles lately, including a recent editorial in the British Journal of Psychiatry that Chlonezapam in particular and benzos in general are not as bad as some people think That's like that's interesting because where I train Benzos are very I mean we learn that Benzos are just like a no-no

and even with psychotic patients or patients with panic I feel like we abstain from prescribing benzos Well you know Your mission should you decide to accept it okay you know as uh dr conn i saw a micro expression of anger as she said that on the face how do you feel about that you know honestly i've been hesitant in a lot of cases but there's certain cases

panic disorder being one of them that i feel a little bit more liberal aceshesia another catatonia obviously a third and i think that initially when starting SSRIs sometimes it can be helpful I'd be curious for panic disorder in these patients like, do you lean into SSRIs as long-term treatment, Dr. Kahn, or do you sort of see? My experience has been that SSRIs and tricyclics both have anti-panic benefits, but do not help with the overall psychotic disorder in the way that Klonazepam does. There are not good studies on this. there should be, but I've seen many patients come through who are already on SSRIs, but their psychosis continued, and with clonopin added, then it works better. In ordinary panic patients, the two drugs that are most likely to cause complete cessation

of panic are the tricyclics, nortripylene in particular, and chlonesopam given as a fixed dose every 12 hours, titrated up to a fully effective dose as drowsiness goes away. And people do much better if panics are completely treated. SSRIs are often effective, but they don't necessarily stop panics completely. They make them statistically significantly better, but the panics often continue to some degree. And over time, there's a partial reduction in the anti-panic benefit. So I often start people with panic disorder on SSRIs, and most of the time, sooner or later, the panics are still a problem, and then I'll add some clonesopam, and that works better. I suppose you weren't expecting heresy on your show.

No, I think for those who really listen, because I have a bunch of episodes on like Sensorium, working memory. And so my caveat would be like, you know, if you have someone who's higher functioning, you want to check for ongoing working memory, cognitive function, and make sure the benzos aren't messing with it too much. And sometimes when I see like a medical student, it's like they need to be on something that stops the panic.

This is like it's going to be, you know, tough to not completely preserve their cognitive function? I have not seen problems with cognitive function. I don't use benzos. Virtually never, except for

clonapin, only for panic, and long-acting Al-Prasalam also only for panic, and in elderly people who get too sedated by

clonipin, Al-Praselam is slightly less sedating. and where the short half-life of the Alprazlam is an advantage because they've got reduced metabolism. And in them, Clonopin would have too long a half-life. And I've had people come out of nursing homes because they were started on medication for their panic and their mental function in return closer to normal. Okay. there's a whole

there's a whole lot of controversy there it gets back to the issue we talked about a couple of minutes ago well you know and this is where I think you know looking and identifying that panic

and those discrete panic episodes is so important well you know I'm not sure we fully answered a question you asked before how do you know when someone has panic with psychosis and you need to explore it, not take it on faith.

But my experience has been is if they hear voices, they're having panic attacks. And the voices are the panic attacks. We've published some pilot studies on that, but large-scale control studies would be important to do. But meanwhile, that approach works, and it works when you add clonupin to the antipsychotic. And then also treat, and there are other studies, too. Clonopin in the ER will reduce agitation and allow lower doses of antipsychotics in the ER. Other studies that say Clonin will allow lower doses of antipsychotics in the long run as well. What would you say to someone who would say, okay, you know, one of your theories is hypoprontality as causing the psychotic events, you know, doesn't benzodiazepines lower frontal lovel?

function to some degree? Not that I've seen. I mean, there's like studies where it's like, you know, they have an effect size of lowering, you know, different cognitive neuropsych tests, right? I'd be interested in seeing those studies and learning which benz-o they were on at what dose and for what length of time.

Initially, when you start someone on clonazepam, they may feel a little drowsy, which is why you start low. but I have treated plenty of people who do technical work of all sorts and when their panics get better their level of cognition and concentration always goes up and they're much more able to focus on their work. I think that that's the testament to, if they're in a panicked state,

they're so stressed out that their brain is not functioning well at all. That's right. So it's like maybe in a normal person in some of these studies, you know, maybe it would reduce some cognitive function. But if you have someone who's already a stressed out brain, it's like reducing them out of panic might actually make their brain function better. Well, that's an interesting thought. That's another study that should be done.

So, you know, what about patients with schizophrenia and panic disorder? You know, you mentioned that quinopin reduces positive, negative symptoms and hallucinations, have you seen those in schizophrenics without panic disorder? Would Benzos help there with their symptoms? That gets back to the definition of what is schizophrenia. And what we're positing in our book is that the functional psychotic disorders, functional means there's no known organic cause. So in the functional psychotic disorders, which includes schizophrenia,

schizophrenia, that they can be divided up into these five categories related to these five specific comorbidities. And there's a other people have proposed for, from different perspectives, the notion that once we get a real handle on it, schizophrenia will no longer exist because it will be other things. Most notable for saying that directly among prominent schizophrenia researches is a named Jim Van Osse in Holland. And he wrote a well-known paper called Does Schizophrenia Exist? And obviously his view is that it doesn't, and I tend to wonder about it myself. So if they're my view of classic paranoid schizophrenia is that it contains voices and delusions and cognitive dysfunction,

and because from this new way of thinking, because of the voices, it always contains panic disorder. If you're looking at the same patient with no voices, or what comes closest to that, you have something called persecutory delusional disorder, which is commonly misdiagnosis schizophrenia, but it's not. It's a different diagnosis. people with prescatory delusional disorder have strong paranoid beliefs generally that some powerful figure is out to get them, but they appear to be fairly normal if they don't talk about it and if they don't deteriorate seriously. But they may act to protect themselves if they are overwhelmed by these thoughts. They don't hear voices. and I'm sure that David was planning to get to this shortly.

We've published studies suggesting that persecutory delusional disorder is a psychotic form of social anxiety. If you imagine yourself who has someone at social anxiety whose biology tells you you're supposed to be at the bottom of the heap, submissive to all the authority figures, imagine the psychotic version of that, and you have someone who firmly believes that the CIA is out to get them. And they're often able to function at least adequately, if not well, at jobs. Their social interactions are not as close as they had been, but sometimes they appear to be okay on the surface. And those people, with that kind of problem, get better with a combination of an antipsychotic and an SSRI.

which treats social anxiety, and they tend to stay better. But in case conferences and teaching, I can't tell you how many patients I've seen in a high-quality hospital that were called schizophrenic when actually they had persecutory delusional disorder. I've also been sent articles to review where people, evaluated psychotic patients in a hospital population and concluded that there were two kinds of schizophrenia, one with voices and one without, and the group without had a higher level of functioning. And as a referee, you know, I commented, well, you know, maybe that's because they don't have schizophrenia. You know, could it be that some or all of that group have

persecutory delusional disorder? It's a disorder that people don't often think about. was certainly underestimated, under-discussed in my own training a long time ago, although it was well known back then. Okay, I want to pick your brain on this article here. This is the one that I go off of. So chronic, it's a meta-analysis, cognitive effects of long-term benzodiazepine use. And in this study, they found the effect size around 0.74 for reducing different types of cognitive function. I'll take you down to this main table here.

What journal was this in? Oh, this is from 2004. 2004, CNS drugs. And we'll put in our article, the final of the debate. I'll let him write if he has any other thoughts. But yeah, any, this is the kind of stuff where I'm like a little bit concerned for some people. I mean, this is compared to normal control. So it's not like this is, this is long-term use of benzodiazepines in an elderly population showing a reduction in various cognitive function, correct? Let's see here. This is a meta-analysis.

This is a meta-analysis, yep. Okay. Well, there are a lot of studies like that, and more published since 2004. You have to be very careful about correlation and causality. Correlation doesn't show causality. And if benzodiazepine use is associated with reduced mental functioning, there are a number of possibilities. The one that concerns people, of course, is that benzodiazepines, you know, gee, what if they caused reduced mental functioning or dementia?

As a side note, clonazepam is not separated out in those studies. In fact, in one study, it was excluded for reasons that were obscure from the analysis. Who is it that takes benzodiazepine? people people who are more sick right and more needing them people people with anxiety with anxiety disorders or insomnia that would be the bulk of them i would think so it raises uh you know puts in another factor um there was a study that was published i think uh in june of last year in the american journal of psychiatry, along with an accompanying editorial. And what they did was they did yet another one of these studies, but they broke down those people who used benzodiazepines into people who used higher doses and people who used lower doses. And they looked at the incidence of dimension in the

two groups. And what they found was that if you thought that benzos were caused, and all benzos were lumped together, of course. If you thought that benzos were causing dementia, you would expect more of it in the high-dose group and less of it in the low-dose group. If you thought that untreated anxiety was causing dementia, you would expect more of it in the low-dose group and less of it in the high-dose group. And actually, that's what they found in this study. They reported that among benzodia users, the more they took, the less likely they were to have dementia compared to those who were benzodia users and taking less of it. And it was support for the speculative possibility that maybe it's the anxiety disorders that are causing the dementia. And there was an editorial

in the American Journal that supported this, you know, acknowledged that the anxiety relationship is speculative, but clinically, when you see people who are getting demented, the ones that I've seen, many of them, if not most of them, have a prior history of a significant anxiety disorder, which tends to get worse at the initial phases of the dementia. So that in particular, people are likely to get benzos as the dementia is starting and may have been on them before. So the evidence, it depends on how you look at the causality. The data aren't all in, but, you know.

I appreciate your, I appreciate the back and forth here. Most of my patients recognize me. I think it's, well, I think that's good. Well, and you know, it's not that I haven't used them and don't use them. It's just that I'm cautious with the use. And maybe I should reassess this. So maybe I'll have to do a deep dive with CAT or something and we'll look at this. Yeah, I think it's very interesting.

Yeah. I honestly, like, we never prescribe benzos at our institution. I never prescribed benzos either. Only clenazepam, which happens to be a benzone, and rarely Xanax, and only for panic disorder, not for other things. Okay. Well, I don't want to belabor this point too much. And we'll look at, we'll put those articles in this. in the article will produce so that if you're listening to this and you're curious,

you can go and you can read more until our sort of deep dive on this specific topic. But I do, I like my brain being stretched. So I'm going to take the challenge and read some of these things and rethink this. Okay, yeah, anything else that you want to talk about social anxiety and the overlay of psychosis? I was a little, like, when we talk about this, are we talking about like a spectrum? And it seems like the further you go into the social anxiety, the more, potential you have for some psychotic process, or is it a continuum, or how do you see this? I think that social anxiety in the non-psychotic population is a spectrum. At one end, you have

the severely shy, and at the other end you have the genuinely confident, not falsely confident people. And there are people all along the line in between. It's a spectrum of severity corresponding to the biological component, but not the other. other parts of a social hierarchy. So I think one of the questions that you implied was, if you have more social anxiety, does that make you more likely to be developed persecutory delusional disorder than someone who is a quietly confident person with no social anxiety? That's a great question. I hadn't thought about that. I don't know anybody who has. And assuming that, you know, the psychotogenic factors that underlie psychosis are there,

I could only speculate. My speculation is that the more social anxiety you have, the more at risk you are for a persecutory delusional disorder, if that connection is true. And if you're confident enough, not false confidence, but true confidence, then maybe, you know, you're not going to get psychotic in that way. So when you're assessing someone who may look psychotic, how do you assess for if they also have social anxiety on top of that? Well, you ask them same questions you would for anybody with ordinary social anxiety.

And since it's a chronic syndrome, if they had social anxiety beforehand, that means that it's still there because never goes away, although it may vary. So you would ask questions like, you know, were you a very shy child? Do you, you know, how comfortable are you with public speaking? Or do you try desperately to avoid public speaking? And if you go, do you get anxious? Do you worry in particular that you'll somehow embarrass yourself?

make yourself look like a second-class citizen to the people in the audience. And the last point is something that people with social anxiety identify with. Yeah, that's exactly what I'm afraid of. They'll think that I'm an imposter, only pretending to know what I'm talking about. And you can ask about people in during situations they're being evaluated, formally evaluated like in a college interview or in a job assessment or job application or informally evaluated like where they're going into a room of strangers that they will be working with and they know that these strangers are going to be giving them the once over

and forming a first impression. And what you'll find is a pattern of these situations and a few others where people are afraid that they'll make a mistake or they'll have the wrong clothing or something will happen that will leave them having embarrassed themselves with the result of people, less of them. There are other people who have underlying social anxiety and who deal with it in a different way. And this is true for many of these syndromes. instead of avoiding those settings, they'll dive into them, and they'll do extra speeches when they get the chance to try and conquer their fear.

And that's something we humans do, but, you know, that bottom-rank monkey probably wouldn't do. He wouldn't try to take over unless he had help from Prozac. But what you get then is people who are counterphobic. They still are nervous, they still might be sweating, they might get flushed, their heart might go fast, but they're able to give the speech and give it well and then worry about it afterwards. There was an article recently in the paper. There are many articles about actors and performers who were socially anxious who go into the field partly to overcome their field as a, their fears, and they're able to do so, but they're never quite comfortable with it. And as a rule, they never want to listen to the finished product if they do a recording, they don't want to listen to it because they know that even if everybody loves it,

they'll only hear what they think are their mistakes. Are you talking about yourself right now or me? I don't know. We're going to have to ask Kat. I can never, I have a really hard time listening to, listening to finished episodes. So I do usually. I think that's everyone. I hate hearing my own voice too.

That's everyone. But you said you used to be like on radio, right? So were you trying to conquer your fear of it or were you since really enjoying that? Not the my analyst ever told me. But what do you think? I don't think that social phobia is something that I suffer from, but I certainly know people who do, and I've treated performers of all kinds, some of them are quite severe social phobia. And having social phobia is an advantage if you go there, if you go the counterphobic route,

because you work extra hard to develop your skills because you're so afraid of embarrassing yourself and you're also much more than usually attuned to audience reaction, which is very important for performers of all kinds, particularly if they're in front of a live audience. And so it's a career advantage. So another study that could be done.

My speculation would be, my question, is whether there's more social, anxiety in the more talented performers than in the less talented performers. Interesting. Yeah. Okay, let's get on to, let's see, what's our last one? Oh, okay, we're talking about depression, like a melancholic depression. And so we know that, you know, as the depression progresses, they may have psychotic symptoms later on. I think it's, I really like how you differentiate between the atypical and the melancholic depression. So maybe we'll talk about those both at the same time, because that's exactly how I split my depressed people into,

like, are they this category or this category, right? I couldn't agree with you more. They have specific patterns, and I look for those patterns. And if they don't have them, then I wonder if they're really depressed, or whether they're having a grief reaction, if they're hypothyroid, or in the case of one person who didn't believe that he didn't have a biological depression with a capital D, he turned out to have both a vitamin B-12 deficiency and hypothyroidism and didn't have a psychiatric depression at all. It's not rare, but it's not uncommon to see that, something we psychiatrists need to think about. So when we're thinking about melancholic depression, we're thinking about psychomotory

retardation. We're thinking about what are the other symptoms that really jump out of you, pessimism, anadonia, hopelessness. Loss of appetite, hopelessness, guilt, psychomotor, retardation, an unreactive affect. People can't smile, no matter how good it is, something that might happen. They often have suicidal thoughts, although they're more likely to act on them as they're getting better than during the melancholia. And in addition, there are two characteristic symptoms. One of them is early morning awakening. If their normal waking hour is 7 a.m., they wake up at 4.30 and can't fall back to sleep, even though they're tired. And do they wake up anxious? And the other is a diurnal variation. Melancholic depression is typically worse in the morning when people get up, and it gradually

gets a little bit better as they get more energized during the day. Not a lot better, but enough that people notice a small improvement. And those are characteristic symptoms as well. It's the classically described form of depression when psychiatrists of old talked about depression in the formal sense that that's what they were referring to. Yeah. And you know, you talk about TCA's better than SSRIs, potentially ECRs, potentially ECEs. a short-term course of benzodiazepines for initial reduction of anxiety? The, you know, Andre Veris and I were the editors of this book. We didn't write all of the chapters.

But the person who wrote that chapter is a good friend, a wise clinician, and so if he thought that short course of benzos were useful, we weren't going to argue with them. Yeah. You talk about doing a thoroughhouse. thorough history, head imaging, assessment of delirium, laboratory tests, and really trying to be direct with questions rather than open-ended questions. I think that's a good history taking Pearl. Well, when you're taking a diagnostic history, that's generally true, although some open-ended questions are useful, but in the case of a melancholic depression, people's thinking is

slowed. So open-ended questions might stump them and might not get you useful information. So it's better to ask more direct and clear questions so that they can try to give direct and clear answers, which is hard for them to do in that state. And so when you think about a typical depression, what symptoms are you looking for in particular? And why do you consider this also a psychotic type of comorbidity? First things first. Atypical depression got its name at the same hospital where I was working on anxiety with Donald Klein. He had a depression group, which did much of the early work on atypical depression. They used the name atypical to contrast it with melancholic depression, which is what had

generally been considered typical depression. And some of them later on, decided they made a big mistake. It's far more common than melancholia, and they should have called it typical depression. It's different because people tend to oversleep or want to, schedule permitting. Their energy level goes down. They often feel lethargic or leaden. Their appetites typically increase, not decrease, although in young people, that might not be so. And in all ages with atypical depression, when people are more depressed, they often have cravings, particularly for sweets, chocolates, and carbohydrates. And maybe some people for greasy food. I think that, you know, people with atypical depression like junk food, basically, or they may avoid it, but they have a craving for it. They can cheer up, and they can share up in your office if you tell them a joke. I generally tell bad jokes. They will laugh, and then they will go back to feeling depressed as soon as they've stopped laughing.

But they will genuinely cheer up, but only briefly. And they will describe having a nice conversation with a friend or even seeing a movie and being able to cheer up and then going right back to being depressed again. But probably the core cognitive symptom of atypical depression is something that's called rejection, sensitivity. People who are more than usually sensitive to minor social slights and rejections. If they have a group of buddies who are going out to lunch and they know for a fact that they hadn't been invited by accident, they'll be terribly hurt, you know, even if they know the reason why the accident happened, an actual rejection can be.

be crushing for them, breaking up with a romantic partner, for example. And rejection sensitivity is one of the core symptoms of atypical depression. And, you know, touching briefly on evolution, that has advantages too for a primeval group of humans. If you are rejection sensitive, you're likely to try and avoid giving offense. So that also, helps perverse, preserve social harmony and the emotional and reproductive health of an ancient group of humans or other species. That's basically what atypical depression is. That's really interesting to think about how the rejection sensitivity is adaptive for that culture, but you don't think it's adaptive for this culture that we're in? Well, I think it is.

but you know here again because of our human consciousness and culture we can learn to you know carry on even if we feel rejected and even if we feel hurt and some people will respond instead of with being inoffensive they'll adopt the attitude semi-consciously of well if they're going to treat me like that you know just wait until you see how I treat them and they'll respond by by being angry and socially assertive in a way that doesn't actually get them close to people, but makes them feel like they're, you know, pushing back against rejection. And they might turn up at a party to which they weren't invited precisely because they weren't invited, just to give one minor example. A party that they might have skipped had they been invited. So important to note that melancholic depression is the one of our five comorbidities that's an acute illness. If you have one melancholic depression, it lasts a discrete length of time, and you're at risk for another episode of melancholic depression at a later time.

But each illness is separate. It's not an ongoing process. Atypical depression is chronic. It varies in severity. It comes and goes. It's certainly influenced by social factors and other factors, but it never goes away completely and forever without treatment. Do you think of atypical depression differently than maybe like personality disorders? Like is it, in your mind you mentioned, or in this chapter it was mentioned that atypical depression is associated with personality disorders, specifically avoidant, borderline, history. but at the same time different? Personality disorders, to some extent,

are a different way of looking at similar phenomenology. Probably the closest concordance is between social anxiety and avoidant personality disorder. If you think about it, shyness can be thought of a social anxiety, if it's sufficient and of the right type, and that's what avoiding personality is. It's shyness.

And there are other personality disorders that have correlates among anxiety and depressive disorders. It hasn't been looked at well enough, and some of the personality disorder criteria have been rethought and are continuing to be rethought, such as narcissism has reverted to its original concept from Otto Kernberg, not as the specific type of personality disorder, but rather as a severity of personality disorder, so that there are narcissistic people with obsessional traits and narcissistic people with paranoid traits, and narcissism in that context refers to a deeper level of those personality disorders, which adds an additional level of symptomatology. similarly for borderline personality.

In addition, some people have wondered whether narcissism might be associated with social anxiety in some ways. They've wondered whether a borderline personality is associated with panic disorder. And of course, all of the anxiety and depressive disorders that we've talked about, all five of them are common. In non-psychotic people, if you have one, you usually, you usually, have more than one, so there's a lot of comormidity within that group, comorbidity, and that would be true in personality disorders and psychosis as well, that you often see

multiple diagnoses to look at. That's in the book, but it's kind of hidden. Kat, do you have any questions that are jumping into your mind that you want to make sure we hit on these two topics? So do you think atypical depression is associated with bipolar disorder? I think I read that in the book. Do you see it more often? Well, the way DSM is written is to have bipolar one disorder, you have to have an episode of mania, and you probably have a history of depression, but you don't have to. I think if you look more closely, and studies have done this, the predominant kind of depression found in bipolar disorder, consistent, but in a small number of studies, is atypical depression, not melancholia.

Major depression is more of a catch-all diagnosis, which encompasses both of those and more. And so many people think that atypical depression is the most common kind of depression associated with bipolar one disorder. Do you feel like, because from my training, I feel like we just clump all the depression types into one. We don't really talk about atypical or, I mean, atypical, yes, but not melancholic. Do you think that they should be separate disorders? Many people do. They used to be separate.

They're now both listed as subtypes of major depression in DSM. But many depression researchers think that they're distinctly different. forms of depression. They're not subtypes of some overarching disorder. And there was actually a great deal of debate about it. A guy named Max Fink up in, I think he's up in Toronto. He wrote a book on Melancholia. It's a wonderful book, if you like reading long books about a specific disorder. It's very well written. But he describes how major depression came into DSM to displace melancholia and atypical depression is separate diagnoses. And it was partly political. Somebody said, you know, we can't have this debate go on forever. We're just going to say everything's major depression.

Now, that's one person's point of view, but it's certainly plausible that something like that happened. Clinically, they're very different in the way they present. There are some similarities and medications you can use to treat them. But basically, all antidepressants will treat melancholia, but only some will treat atypical depression, something that Donald Klein called pharmacologic dissection, the response to different psychoactive drugs, is one part of what helps differentiate different conditions.

So just give me a brief, kind of like, which ones would you go to for atypical depression first? Well, in atypical depression, the best drugs are, some people say the MAAO inhibitors, but MEO inhibitors have a lot of side effects and a special diet. There is a new one that's given as a patch, which is easier to use and safer. But even so, I think the easiest route for most people is an SSR, And SSRIs often usually work nicely for atypical depression, but not well enough. So you can add a booster that makes them work better for atypical depression and as it happens,

also for social anxiety. The boosters that I commonly use are buzperone in low dose, which was originally marketed for anxiety. but that's not the reason for using it here. The boosters all seem to be 5HT agonists, which have a synergistic effect with the serotonary uptake inhibition of the SSRIs. So it's basically a two-pronged approach to increasing serotonin activity.

Lithium and low doses also works. Trazidone and low doses also works, particularly if somebody wants a sleeping pill, because you can take it at bedtime. The doses in each of these, cases is much lower than what's used when you use these drugs for other purposes. Other drugs that work are aeropipypersol and Rixalti. I forget the generic name, it's new. They're produced by the same company and some of you may have seen television ads that say

if your antidepressant isn't working well enough, ask your doctor about these two drugs. They seem to work, but they are antipsychotics. in terms of class and their dopamine blockers. And if people stay on them long enough, as they might for chronic syndrome, they might develop long-term neurologic side effects, such as Tart of Dyskinesia. And they have a warning for that, but I don't think people fully appreciate it. So I prefer to use drugs that are long ago off-patent are less expensive and safer, even though they don't have marketing budgets.

Are you ever scared of those patients? Let's say you put them on an SSRI or ever scared of them, you know, going into like a manic episode if they do maybe have a comorbid bipolar disorder? Great question. Great question. There's a great deal of concern about whether antidepressants can cause trigger mania in bipolar one disorder or alternately. if not trigger it, then at least whether they can shorten the time until the next manic episode happens. Both possibilities have been mentioned. The literature makes you wonder about tricyclics and some of the others,

but the literature on SSRIs suggests that they have the least risk and may be relatively little risk at all. I've often done this. People do better. I do wait until mania is completely resolved before starting an SSRI, and I've not seen any problems. That doesn't mean it can't happen, and there's room for more research, but the alternative is to leave it inadequately treated, and that, you know, so you're weighing a trade-off of a known problem, untreated depression, versus a potential risk. of triggering an episode of mania. It also helps that people that, if the people you treat are on adequate doses of solid anti-manic drugs, the two best still appear to be lithium and depocode, although there are some newer drugs as well.

But that's a great question. A group called, I think it was the International Society for the Study of Bipolar Disorder, within the last year did a meta-analysis and review, and basically concluded that the risk is lowest with SSRIs and maybe quite little. All right. Well, this time has escaped us. We've gone really long, and I think it's been a great conversation. And so thank you for your time, Dr. Khan.

I really appreciate it. Thank you. It's been delightful. You've had wonderful questions. You've hit on all the right points, including the ones where some clarification was useful. And I hope people will help their patients get more better than has been possible in the past. That's the hope of this podcast.

You know, if we can multiply our effect, you know, teach people a little bit about mental health and have them take care of their patients a little bit better, and that makes a big impact in the world, I think. If you are listening to this and you want to read this book, if you go to the resource library on the psychiatrypodcast.com. I will give the the discount code and the link so that you can get it for a discounted price. I've asked the publisher has offered to give that to me. I do not make any money off of this

book. Obviously, hopefully Dr. Khan does. At best, very little. I know these things go. It's been a pleasure. And man, there's so many things that I feel like I would like to dive into your mind and your experience more, and so maybe I'll have you back on in the future. Oh, that would be wonderful. You two have been great to talk to, and it was wonderful feeling your questions. And if I got carried away with myself at some point, I apologize, but at least I didn't tell any jokes. Oh, man. Okay, well, we will leave it there,

and I really appreciate it. And so there we go.