E185 | How Psychiatry Became Fixated on Chemical Imbalance (w/ Prof. Justin Garson)

What if one of psychiatry’s most influential ideas began with LSD, amphetamines and a handful of experiments that would be difficult to imagine today?

In this episode, Dr. Alex speaks with philosophy Professor Justin Garson about his new book, The Madness Pill: One Doctor’s Quest to Understand Schizophrenia. They explore the remarkable story of neuroscientist Solomon Snyder, whose work helped establish the dopamine hypothesis of schizophrenia and contributed to psychiatry’s shift towards a more biomedical understanding of mental illness.

The conversation also asks a broader question: if mental illness is more complex than one faulty brain mechanism, what would a genuinely holistic model of psychiatric care look like?

Interviewed by Dr. Alex Curmi. Dr. Alex is a consultant psychiatrist and a UKCP registered psychotherapist. Website: alexcurmitherapy.com

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Transcript

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SPEAKER_00 0:00

Today we're going to be discussing the madness pill, one doctor's quest to understand schizophrenia, the very important story in psychiatry's history.

SPEAKER_01 0:08

Burton Angrist, who is fascinated with the power of amphetamines to induce a schizophrenia-like state. And he actually got together uh a number of volunteers and he literally gave them amphetamines until they became psychotic.

SPEAKER_00 0:22

Would you say that's fundamentally where the dopamine hypothesis for schizophrenia comes from?

SPEAKER_01 0:27

You know, a lot of our biomedical conception of psychiatry was not based on groundbreaking evidence. It was not based on any scientific smoking gun.

SPEAKER_00 0:37

The tragedy was that then psychiatrists kind of discarded psychological knowledge, you know, an interest in human nature, an interest in the humanities, which made us much more well-rounded professionals. Today I'm joined by Professor Justin Garsons. Justin is a professor of philosophy at Hunter College and the Graduate Center, City University of New York. He's a regular contributor for psycholytoday.com, Aon and MadinAmerica.com. He writes on the philosophy of madness, the evolution of mind and purpose in nature. Justin, thanks so much for joining me today.

SPEAKER_01 1:17

Yeah, thank you for having me here, Alex. I appreciate it.

SPEAKER_00 1:21

Just a quick word if you're watching or listening on YouTube, do like, comment, and subscribe. If you're not watching on YouTube, do consider watching us here. We want to become a YouTube first podcast, and we are directing all feedback, comments, and discussion about our episodes to our YouTube comments section. Today we're going to be discussing Justin's new book, The Madness Pill, One Doctor's Quest to Understand Schizophrenia. Although I think this is a very important story in psychiatry's history. It's a story I was totally unfamiliar with. It follows Dr. Solomon Snyder, whose experiments with mind-altering drugs helped change the way we think about the causes and treatments of schizophrenia. Firstly, Justin, it would be great to start. Who was Solomon Snyder?

SPEAKER_01 2:07

Yeah, absolutely. I mean, he was really, I mean, he's alive uh now. He's about 87. I had a chance to talk with him uh for this project. But he's really one of the most influential neuroscientists and psychiatrists in the world, even though I had never heard of him until about 10 years ago when I started doing this research into this chapter of Psychiatry's History. Um but he was really uh a pioneer in neuroreceptor technology in the 1970s. He was a psychiatrist fascinated with how drugs interact with the brain, fascinated by how antipsychotic drugs work. And one of his major innovations uh that I was interested in was coming up with the dopamine hypothesis of schizophrenia, this idea that schizophrenia could ultimately be understood in terms of, you know, uh excess levels of dopamine in the brain. And so even though I don't, I don't think this was his intention, I do think that he was largely responsible, uh you know, partly responsible for pushing psychiatry into this more kind of somewhat narrow biomedical direction.

SPEAKER_00 3:27

And my understanding is he was quite precocious, like started medic medical school at the age of 19, something like that. So quite uh unusually gifted personality.

SPEAKER_01 3:37

Yeah, he it was very uh one of the words that comes up again and again when I talked with uh his colleagues and his friends and family members is genius. He really was one of these very annoying, you know, child prodigies, was playing piano and clarinet and mandolin almost at a professional level uh by the time he was a teenager, uh, you know, graduated high school at 16, started medical school at 19, by 21, he was writing uh theoretical papers about schizophrenia. And then at age 30, in 1970, I believe, he became the youngest full professor in Johns Hopkins history. So he was really one of these just brilliant uh kids. Uh and what was fascinating though, one thing that was fascinating is that he didn't start off with an interest in medicine or even an interest in science. He wanted to be, first, he wanted to be a musician, uh, and then he thought, I want to be a philosopher. You know, he loved reading Nietzsche. Uh, but then he started reading Freud, got fascinated with Freud, and he thought, you know, I could be a psychiatrist because psychiatry is about as close as I can get to philosophy while having a medical degree, while enjoying the prestige of medicine. So it was uh that that's how he ended up in psychiatry. Only later on did he kind of develop this fascination with the biological underpinnings of mental illness.

SPEAKER_00 5:11

Yeah, that's I kind of feel the same about psychiatry. You know, of all the medical specialties I could choose, this seems to be, I kind of want your job, Justin. I kind of wanted to be a philosopher on some level. But this is the closest I can get in a medical specialty, so I can definitely resonate with that. Maybe to like set the scene a bit. So, what was how was schizophrenia viewed before the discoveries that were made in this book? How was schizophrenia viewed by the psychiatric community?

SPEAKER_01 5:40

Yeah, well, he uh I think he graduated high school in 1955. So that would be a nice kind of reference point. Well, really, let's go to 1950, because 1955 you already were having antipsychotic drugs in this kind of pharmacological revolution that was still very new. So go back to 1950. As you know, you have effectively these two camps in psychiatry. You have the asylum doctors who are very much into experimenting on patients' bodies, obviously, a lot of times not getting informed consent, a lot of times with very kind of shallow theories. So uh, you know, there is this idea that people, when they're having epileptic fits, they don't experience psychosis. So they thought, uh-huh, well, maybe if we induce uh seizures, uh, then that will be a cure for psychosis. So we know about the asylum doctors and these sometimes rather cruel experiments. On the other hand, you had the Freudians, which in the United States was the dominant movement in psychiatry. Uh, and of course, the the psychoanalysts at the time generally believed that almost all psychological distress, whether we're talking about depression or bipolar disorder or schizophrenia, personality problems, whatever it was, ultimately was rooted in these unconscious uh conflicts, childhood uh conflicts, and that the key was to unearth these deep-seated uh conflicts. So at the time, psychiatry was really treated with disdain by other medical specialists. They thought, okay, on the one hand, you have these kind of barbaric experiments. Uh, on the other hand, you have this psychoanalytic approach that doesn't seem to be really helping the people who are most in need of uh help. And so a lot of doctors just didn't really consider it a valid medical specialty. Pills started to change that a little bit, but not initially, not by that much. So by 1954, you have these new uh antipsychotic drugs. They're helpful. They're allowing some patients to go home and live on maintenance doses. They're at least playing some role in helping to empty out uh uh the asylums. But at the time, we didn't really have any theory about why these drugs worked or how these drugs worked. Uh, there was this wonderful uh quote by a Canadian uh psychiatrist named Heinz Lehmann, and he said, it's just like giving a patient a chemical lobotomy. That was what he thought these drugs do. It's kind of like giving a lobotomy, but not quite as uh invasive. So it the advent of drugs definitely started helping people in some ways, but it didn't immediately kind of change the perception of psychiatry. Well, now that we have drugs, we're a legitimate branch of medicine. So it was in pretty rough shape when Solomon Snyder uh decided to devote his life to it.

SPEAKER_00 9:01

And my understanding was at that time they just didn't understand the right doses as well. So even though the drugs may have been helpful, they were using really, really high doses, getting like heavy sedation as a side effect, hence getting that sort of chemical lobotomy type of effect.

SPEAKER_01 9:17

Yeah, absolutely. Very high doses, high enough to, you know, start inducing uh some of the things that now we consider undesirable uh side effects, like uh tremors, and of course, lithium. Uh I I believe it was tested in the late 40s, seemed to have some benefit, um, but it was so toxic and they didn't know about correct doses, uh, dosage. So I think it was pretty much uh not really considered in a serious way until the 60s.

SPEAKER_00 9:48

Was there any particular catalyst that got Solomon Snyder involved? Any kind of epiphany or moment where he decided to start to pursue this track of trying to understand the biology of schizophrenia?

SPEAKER_01 10:00

Yeah, that happened quite by accident. When he was 19, he was starting uh uh medical school at George Washington University in Washington, D.C. And he was living pretty close to National Institute of Mental Health, massive campus in Bethesda, Maryland, at the time that NIMH was really uh spearheading this biological approach. They were looking for some kind of defective uh enzyme problems or neurotransmitter problems or something like that underlying uh schizophrenia. So he he had initially had no interest in that approach, but he, through his uh passion for music, actually met a young psychiatrist who was working at an NIMH. They bonded over their interest in music and psychiatry, uh, guy whose name was Don Brown. And Don said, Hey, Saul, why don't you come work for me as a lab tech at NIMH? And suddenly he's you know 19 years old and he's studying uh how hormones work and how enzymes are broken down in the body, and he's learning about these biological theories of schizophrenia, and he really almost immediately develops this love for science, this passion for science. He still has these psychoanalytic views, so he hasn't completely embraced this narrow biological um perspective, but that's when he fell in love with the brain.

SPEAKER_00 11:34

And then what what happens next?

SPEAKER_01 11:37

What's funny is he he was doing uh some interesting research trying to synthesize this emerging biological perspective on schizophrenia with psychoanalysis and looking, taking a very broad, you know, holistic biological, psychological, um, social perspective. His earliest writings on schizophrenia had this very holistic uh point of view. Uh, and here's another thing that happened quite by accident. In the early 1960s, he went on an LSD trip. He was finishing his medical research, he was finishing his medical residency uh in San Francisco. This was uh 1963, so the Beatnik era, a lot of casual uh pot speed LSD. And so him and his friends decided to take LSD. They got a hold of some uh from a neighboring lab. Uh, psychiatrists were fascinated with this drug for a number of reasons. And he took this drug and he took too much of it. Uh uh, it he has kind of a funny story about how he had uh come up with the doses. He had weighed out each dose very carefully, 500 micrograms or whatever it was. Him and his friends take a first dose, they wait half an hour, nothing's really happening. So they're like, well, it clearly didn't work, we need more. And that's uh that was the funny story he shared with me about why he had such a mind-blowing LSD trip. But after he reflected on the trip over the weeks and months afterward, and he started to become convinced that he had experienced schizophrenia, that he had experienced uh not exactly what his patients with schizophrenia were experiencing, but some there was some essential kind of experience of this complete and total disappearance of selfhood. And he thought, you know, this may be the key to understanding schizophrenia. And that's what led him to this idea that, you know, if I can just understand what LSD is doing to the brain, I might understand schizophrenia itself. So think about his kind of world view. The idea is that in schizophrenia, you have some kind of broken brain mechanism, some kind of dysfunction in your brain. His job is to figure out where it is. After his LSD trip, he thinks, aha, LSD must somehow work by activating that under temporarily activating the underlying mechanism of schizophrenia. And so that's what led him to this idea that if I just understand what LSD does to the brain, I would understand uh schizophrenia uh itself. And there had been a precedent for that kind of research. So in the night, early 1950s, there were some psychiatrists who were very interested in LSD because they thought it might induce a schizophrenia-like experience. And so they thought, okay, if we just understand what LSD does to the brain, perhaps that will somehow illuminate the underlying mechanism of LSD. But by the early 1960s, that project really waned. Uh, psychiatrists started losing interest in it. Enough psychiatrists had tried LSD uh or supervised LSD research that they thought, yeah, this isn't really that much like schizophrenia. So it's probably not a useful model for exploring schizophrenia. So, in a sense, when Solomon Snyder went on his LSD trip in uh 1963, he really wanted to kind of revitalize uh this dying tradition. No, understanding LSD is exactly the key to understanding schizophrenia.

SPEAKER_00 15:46

Which makes sense. I mean, I guess there are for listeners, there are important similarities and differences between a psychedelic experience and a psychosis. I suppose the biggest similarity which jumps to mind is you just understand that your perceptual systems are more malleable than you might expect. You know, you can hear things, you can hallucinate visually on LSD, you can have very like disturbances of how you experience yourself. Sometimes that's very positive in the sense that the sense of like a loss of ego. Sometimes that same loss of ego can be experienced very negatively and very destructively. Um, I suppose the main differences are that with a psychosis, you'd expect kind of a disruption of thought that's much more profound and a disruption of your ability to act in the world. And of course, psychosis lasts a lot longer, it can last in episodes of weeks, months, sometimes years at the extreme. But it makes sense to me, you know, that that at that time it would feel that's these kinds of compounds could be a really useful gateway to understand a psychosis. And so did Dr. Snyder's initial experiments. Did they focus on LSD primarily?

SPEAKER_01 16:56

Yeah, so the first um from about 1964 to 1966, he devoted himself to trying to figure out what LSD does to the brain. He was uh went back to NIMH and got a research uh assistant, uh like a research associate position. So something more than a lab tech where he was given a lot of freedom to do what he wanted. Uh he was injecting monkeys with radioactive LSD to figure out where it was going in their brain. He was coming up with these very elaborate mathematical models of the LSD molecule and how it interacts with brain cells and using quantum chemistry to try to think about that. And um he also went through hundreds of uh case studies of patients uh that had come through Johns Hopkins psychiatric clinic to see whether he could find evidence of psychedelic uh experiences. And you're absolutely right. I I think it was a logical connection to make. Of course, and this is how he reasoned about it, of course, there are differences between an LSD trip and schizophrenia. But those differences are usually based on the fact that the person who's on LSD, they know they're on LSD. And so they're not panicking. And the same, they're not that they have some narrative to make sense of what's going on. And also, uh, unlike LSD, psychosis can go on for weeks or months at a time. But he thought that those differences were somewhat superficial. So it did make sense that he pursued this route. Uh, unfortunately, what happened was that 1966 came along. Uh, 1966 research with LSD became almost impossible in the United States. It was outlawed in all 50 states. The LSD use was outlawed in all 50 states. LSD research was not impossible, but it was very, very difficult to get uh approval to do that kind of research. You certainly couldn't inject monkeys with radioactive LSD just to just to kind of because you were curious about where it went in the brain. And so he he tried to find indirect ways to keep working on LSD. He took up an interest in other psychedelic drugs, some of the psychedelic drugs that were legal at the time. He tested uh there was this uh uh psychedelic drug uh that was uh circulating in San Francisco called STP, and it was said to give uh experience very much like LSD, but it had not been uh legally banned yet. And so, yeah, so he tried it on his students at Johns Hopkins to see whether he could induce any schizophrenia-like uh um responses. But by 1969, uh he had largely given up on LSD because he uh decided that amphetamines, speed, was a much more interesting key to thinking about schizophrenia.

SPEAKER_00 20:06

And what did he discover with with his experiments using amphetamines?

SPEAKER_01 20:12

Well, what had happened uh is that I mean, we've always known that there was a connection between amphetamine use and psychosis. So in the 1930s, 1940s, a lot of people were using uh uh amphetamines, and some people, a very small minority, were having psychotic episodes that looked almost exactly like schizophrenia, like auditory hallucinations, paranoid uh delusions. But doctors were pretty much able to kind of brush that under the carpet, again, because it was rare, and they thought, well, it's probably mainly drug addicts who are uh experiencing psychosis, not people who are just using amphetamines uh at their prescribed uh doses for appropriate clinical purposes. But by 19 uh the 1960s, uh what happened is that you had a whole uh drug subculture in the United States that was built around injecting speed directly. And so they were uh drug subculture was known as the speed freaks. I don't know if they called themselves speed freaks or other people called them uh speed freaks, but they were taking far, far greater quantities of amphetamines uh than any of the artists and writers of the 1940s, uh 1950s, like Andy Warhol or Jack Kerouac. You know, they liked taking amphetamines, but they they that was like child's play compared to the levels that the that the what they called the speed freaks were taking. Uh but what would often happen is that after somebody was injecting speed, usually over. You know, two to three to four days uh at a time, they would often enough develop uh an episode that was almost identical to paranoid schizophrenia. They were routinely misdiagnosed with doctors as having uh paranoid schizophrenia. And so coming back around to uh Snyder, there was another psych, there was a psychiatrist in New York, Burton Angrist, who is fascinated with the power of amphetamines to induce a schizophrenia-like state. And he, in order to demonstrate that amphetamines could do this, he actually got together uh a number of volunteers. Uh then they were all recreational speed users from New York. He brought them to Bellevue Psychiatric Hospital, and he literally gave them amphetamines until they became psychotic. So he would give them, you know, 10 milligrams an hour later, another 10 milligrams an hour later, another 10 milligrams, and he found that within about 20 hours he could induce auditory hallucinations, delusions, sometimes thought disorder, this kind of complete fragmentation of logic. And so when Solomon Snyder encountered Burton Angrist's work and saw that you could reproduce something that was so similar to schizophrenia using amphetamines, uh, that's what he decided he wanted to study, that he was wrong about LSD and amphetamines. Uh, this was the tool that he needed. And so you asked what he discovered. What he was interested in this uh uh in was this how exactly do amphetamines bring about psychosis? So he knew that amphetamines uh impact a number of different neurotransmitter systems like dopamine and noradrenaline. And he wanted to know, okay, which one of those neurotransmitter systems is primarily connected with uh psychosis. So in uh, I believe in 1970, he did some pretty ingenious research with rats. I mean, debatable what he what conclusions he could draw, but it was fairly ingenious research. And it convinced him that amphetamines induce psychosis by flooding the brain with dopamine. And that in 1970 is what really woke him up to the dopamine hypothesis of schizophrenia, or at least an early version of that. Namely, uh, what if schizophrenia itself is just a disease of excessive uh dopamine? And then he spent the next five or six years pursuing that trail, and that's how he got the dopamine hypothesis.

SPEAKER_00 24:55

And I would add, just from my own clinical experience, I totally agree. And a psychosis that's kind of a more typical schizophrenia without drugs, is in my experience clinically indistinguishable from a psychosis that someone gets from heavy cannabis use, heavy amphetamine use. We have had I've seen many cases of patients, for example, uh coming to a psychiatric ward with like a full-on psychotic episode, and then they stay off, for example, cannabis for three days and they go completely back to baseline. So totally makes sense that then he would follow the path to studying amphetamines. What was, how did he figure out in rats that dopamine was implicated that it was a flooding of dopamine? Was it kind of radioactive uh isotopes?

SPEAKER_01 25:43

Well, it's a little bit complicated, but he he he he knew that amphetamines come in these two slightly different forms or what they call isomers. There's the levoamphetamine and there's the dextroamphetamine. And he knew that dextroamphetamine, that's the one that really associated with central nervous system stimulation, getting focused, getting, you know, energized, uh, having a lot of ideas and a lot of uh uh projects. And so he knew that the dextroamphetamine was more closely connected with the central nervous system stimulation and less closely connected with the psychosis or the behavior in rats that he thought resembled psychosis, namely the stereotyped uh behavior. Whereas he realized that uh levoamphetamine seemed to be much more closely associated with this psychosis-like behavior and less associated with the central nervous system stimulation. So through a fairly indirect uh path of reasoning, he thought, okay, uh what neurotransmitter system is levoamphetamine uh interacting with that the dexteroamphetamine is not so much, and that's what led him to uh uh dopamine. And so it's you know, I mean, even at the time it was contested a bit, um, partly because is this a valid animal model of psychosis, stereotyped behavior in rats? But that's how he he he got to that conclusion.

SPEAKER_00 27:21

And then was that did he could then continue his research onto human subjects after that?

SPEAKER_01 27:26

He did not. Uh though Burton Angrist did, he was inspired by um Solomon Snyder's research, and so he decided to do a similar uh kind of experiment with humans, where he divided up his volunteers into two groups, and I think he gave some levoamphetamine and he gave others dextroamphetamine, and he found uh, I mean, he really had a very small population, so I don't know what we can really draw from that. But he did find that the levoamphetamine seemed to be more closely associated with uh uh psychosis. No, for Solomon Snyder, his main question, once he had come to this conclusion that uh amphetamines could trigger psychosis by flooding the brain with dopamine, uh, that led him to his next question, which was okay, how do antipsychotic drugs work? Because he had this picture in his mind, something like this. Suppose that anti-psychotic drugs like chloropromazine and Haldol, suppose they work by blocking dopamine receptors. Then I have this simple, beautiful picture where if I flood your brain with dopamine, I can induce uh schizophrenia or a schizophrenic uh schizophrenia-like state. If I block dopamine activity, I can alleviate uh this schizophrenia state. And so by turning dopamine on and off, it's almost as if I can turn psychosis uh on and off. And so after the amphetamine research, uh all of a lot of his research was focused on understanding exactly what antipsychotic drugs did to the brain, which interestingly enough, even in 1970, was not entirely known. People did theorize that there was some connection between drugs like chloropromazine and uh dopamine. Many people uh suspected that these drugs worked by blocking dopamine receptors, but there was some mixed evidence. There was some evidence that while perhaps chloropromazine was a dopamine blocker, maybe haloperidol had some completely different mechanism uh uh of action. So it really wasn't settled until some of the research that he did in the in the early 70s.

SPEAKER_00 29:51

So he conclusively proved it. And then would you say that's fundamentally where the dopamine hypothesis for schizophrenia comes from, primarily from his work, would you say?

SPEAKER_01 30:02

I I believe it does. I I well I think that the dopamine hypothesis of schizophrenia is really based on these two main pillars of evidence. It certainly uh was in the in the 1970s, in the mid-1970s. The one pillar of evidence is that was that amphetamines seem to trigger psychosis by flooding the brain with dopamine. And the other pillar of evidence being that it seems that we can alleviate symptoms of schizophrenia by blocking your dopamine. Again, giving rise to this simple intuitive picture that by turning dopamine on and off, I can turn uh psychosis on and off. There were other people at the so he wrote this paper, the dopamine hypothesis of schizophrenia, in 1976. Uh, it was very influential. A few other people were writing papers that were similar on the role of dopamine in schizophrenia, but a lot of the research they were relying on was Solomon Snyder's research with amphetamines, and certainly his research uh proving conclusively that these uh early antipsychotic drugs worked by blocking dopamine. So even the the other people writing about it were were inspired and motivated by his research.

SPEAKER_00 31:20

And I'm imagining this must be a huge deal for the psychiatric community at the time because this is finally giving some biological credence to a major cause of mental illness, giving doctors, you know, doctors love tangible things, giving doctors tangible mechanisms, explaining how and why the medications work. So, what was the reaction of the psychiatric community at the time to these revelations?

SPEAKER_01 31:46

I think you're exactly right. It was a simple, beautiful picture that a lot of psychiatrists just latched onto. And, you know, as you know, there were biological psychiatrists uh before the 1970s in the 1950s and 1960s, with the idea that schizophrenia or depression or bipolar disorder probably has its roots in a neurotransmitter imbalance. But that remained kind of theoretical, hypothetical, and it and it um they didn't really have compelling evidence on their side. So one way I read the dopamine hypothesis of schizophrenia paper is finally giving psychiatry what seemed to be strong evidence that schizophrenia could be explained in terms of a single uh neurotransmitter imbalance. Solomon Snyder was very clear, incidentally, uh, right at the outset of the paper. He said, look, all of this evidence is ultimately indirect. We don't have evidence uh that there are actual dopamine abnormalities in patients who have been diagnosed with schizophrenia and particularly diagnosed with schizophrenia uh and who have not been on these antipsychotic uh drugs. But he put together the indirect evidence into such a compelling picture that I think a lot of psychiatrists considered it to be almost as if he had given them smoking gun evidence. And I love the way that the historian Ann Harrington, she has a wonderful book called Mind Fixers. And I think she puts it like this the dopamine hypothesis helped schizophrenia become the poster child disorder for the new biological orthodoxy in psychiatry. So it really was, I think it functioned as a poster child in that way. It got a lot of uh uh researchers very interested in using the emerging neuroimaging technologies to try to locate the actual uh dopamine dysfunction in the brains of uh patients. I think it also gave rise in the 1980s and 1990s to a lot of like copycat chemical imbalance theories. It was like, well, the dopamine hypothesis was so successful, now we're going to promote the serotonin hypothesis of depression, or now we're gonna promote the noradrenaline hypothesis of ADHD. So I think it really helped to um solidify this much larger paradigm that sees mental disorders in terms of uh neurotransmitter imbalances.

SPEAKER_00 34:40

Yes, and I think I mean we do know that so our attempts to understand the neuroscientific, you know, basis of different mental health conditions, you know, depression, schizophrenia, have been uh largely not as fruitful as we would have hoped. You know, there was a real sense of optimism in the 90s and the 2000s, and you know, new new interesting studies do come out from time to time, but certainly it isn't the sense of optimism that there once was that we're gonna figure out the exact neuroscientific mechanisms and underlying mental health conditions. But in my view, like the bigger tragedy wasn't that we focused on that, because I think that's a legitimate thing to focus on. In my view, the tragedy was that then psychiatrists kind of discarded psychological knowledge, you know, an interest in human nature, and interested in the humanities, which I think up until that point, you know, 50s, 60s, 70s, psychiatrists would generally functioned as therapists as well and had a good understanding of like human nature and psychology. And that made us much more well-rounded professionals. And something I noticed in my training, and I trained in psychiatry from you know, 2016 to around 2022. That was my training, my residency. You know, I noticed this intense preoccupation with biological forces at the expense of understanding of human nature. So I see that as a huge loss, really, to the field.

SPEAKER_01 36:05

Yeah, and that's I mean, one reason I wanted to write this book was because I've always been fascinated with that question. Okay, you might not agree with everything going on in the 50s and 60s, and maybe the psychoanalysts were overextending themselves and were kind of arrogant. Uh, but even in the early 1970s, there was a more pluralistic outlook. You could, you know, get medication for a serious mental illness, you could talk with a uh consult with a talk therapist, you could do other kinds of uh psychological treatment. And so I do see it as it was more pluralistic, more eclectic. And it seems to me that by the mid-1980s, psychiatry had really narrowed down to this uh kind of single-minded focus on mental disorders can be understood in terms of chemical imbalances that can be managed with uh uh pills. So part of my motivation was okay, what what happened in the 1970s and 1980s that really led to this biomedical reorientation? And I think you're absolutely right. That's the big project now is how do we how do we create a more genuinely holistic and genuinely uh pluralistic model? I I just wanted to say one thing. I I loved uh how you put this is that there was a time when psychiatry was much more optimistic about the idea that schizophrenia would turn out to be very simple. Uh, depression would turn out to be very simple. And I think that's one thing that's happened in the last 20 years or so. We we no longer have that kind of optimism. But one of the things I found fascinating talking with Solomon Snyder, I was uh fortunately able to talk with Burton Angrist. Uh, I interviewed him before he died. He was the one at Bellevue Hospital giving speed to uh volunteers. One of the things that I found fascinating is that certainly in the 60s and 70s, and I think you're right, even in the 80s and 90s, there was this profound optimism. You know, what if schizophrenia turns out to be something very simple? What if depression turns out to be something very simple, and we can create this magic bullet drug, and within three to four weeks, we could uh cure people. Uh, that was absolutely the idea that people had. And that was one of the reasons that they were willing to do these experiments, which in retrospect, we think that seems kind of unethical.

SPEAKER_00 38:49

It's a different time.

SPEAKER_01 38:54

Uh yeah, very different then.

SPEAKER_00 38:57

And to be fair, uh, there are many cases of psychosis where medication is useful, can be used temporarily, can relieve an acute psychotic episode quickly, and then they might never an individual might never have another episode, and then there's plenty of cases where they might continue to take a small or moderate dose of an antipsychotic medication that helps them, you know, function well day to day. So it's not like there's there isn't a there there. But the other tragedy is that while the causes and the exact brain mechanics remain uh mysterious, what it takes to make someone more mentally healthy isn't a mystery, in my view. It's just hard to achieve. Like, for example, we know that for someone to be more likely to be mentally healthy, they need to have a group of people around them to support them. They need to have uh some sort of meaningful task or work to engage in. Their bodies and their nutrition needs to be okay. They need to do a reasonable amount of physical activity, uh, they need to have an understanding maybe of their internal conflicts, if that's a huge issue. There's a whole I could go on and on, but it's actually not that much of a mystery what people need to be mentally healthy. It's just very, very difficult to achieve and often much harder than prescribing a medication, which can be obviously quite simple.

SPEAKER_01 40:16

Yeah, that I mean, and that to me is so exciting. And it was something I I was not aware of in the 1980s and 19 uh 90s. I mean, my dad was hospitalized for a time with uh uh in the 70s with schizophrenia and then the 80s bipolar disorder. I was briefly hospitalized in the uh early 90s with with depression. Um and one thing I I didn't I I really bought into this idea that, oh, okay, mental health problems or chemical imbalances to be rectified with pills. That was really the only conception I I had. And it wasn't until more recently uh, you know, that I've been encountering this research saying it's actually a lot of the most effective interventions are fairly common sense interventions, a sense of purpose, a social community, a sense that you're contributing in a in a meaningful way. Um how is your sleep doing? How's your diet doing? How's your exercise doing? I mean, there are a lot of obviously that's not everything, and that's not gonna be the cure all. And I absolutely agree that there's a role for medication. Um but it's it's it's striking to me that it's in some ways though those basic truths and these kinds of common sense beliefs about intervention, I think, really got obscured by this, by this biomedical view.

SPEAKER_00 41:49

Yeah. And I I guess from observing your father's experience and your own experience, how would you have wanted the sort of, I guess, inpatient and outpatient potentially, psychiatric care to be different to what it was?

SPEAKER_01 42:04

I mean, uh, that's a uh uh obviously I've thought about that a lot. Um my dad was a a different uh case because he was, you know, diagnosed with uh schizophrenia in the 1970s. He heard voices. In the early 70s, he was able to uh get that under control with talk therapy. Uh but by the mid-1980s, he started having similar problems. He thought God was talking to him. He thought the French actress uh Catherine Deneuve was talking to him. But by the mid-80s, everything was based on your diagnosis, you know, we're putting you in the hospital and trying to figure out the right combination of drugs to get you on. And again, not that there was anything wrong with medications, but that that eclipsed uh everything else.

SPEAKER_00 42:53

And you know, what was going on in his life at the time, perhaps his stresses, his psychological dynamics.

SPEAKER_01 42:59

Absolutely. I I think he did see a talk therapist for a while, but it was really believed in the mid-80s that it was the medication that was going to really be the um the central thing. So I mean, I think it wasn't until he died in 2005. I think it wasn't until about 2007 or 2008 that support groups like the Hearing Voices Network made it to the United States. And I remember reading about that and reading about, okay, here are some people, at least, who, through groups like uh Hearing Voices Network, have come to make peace with their voices or have come to befriend their voices, or have come to learn that, okay, I can navigate life with voices. This is a kind of neurodiversity. I don't necessarily need medication, or I don't need so much medication that I never hear these voices. And yeah, I I really, you know, regret that he was not, he would not have. Have had access to those kinds of opportunities, to that kind of messaging. Like, hey, maybe this will work for you. What if we think of your voices as a kind of neurodiversity that, in the best of cases, uh could help you, could stimulate your creativity. And I think for me in the in the early 90s, I mean, this was, I was hospitalized at 16 for depression. And this was shortly after Prozac came out. And so the message that I got was your depression is a chemical imbalance in your brain, and Prozac works by correcting that imbalance. Uh, and you don't need to be on it forever. You know, you give it about six months and then we'll see how it uh goes. So fortunately, I was not, I was never on Prozac um uh long uh term. But at the time, I wish, you know, I was a 16-year-old going through a lot of life problems. We, you know, my dad was in and out of hospitals. I was moving schools a lot, really struggling to find a social uh community and a social uh connectedness. And I would have loved if if uh somebody said, you know, one way of thinking about depression, it's not the only way or the exclusively, but a way, but one way of thinking about depression is that it's it's your brain trying to tell you that there's something really not going well in your life and that deserves some reevaluation. It's it's a functional signal, part of your brain trying to tell you that there's something out there that's not working for you, and we need to correct. So I do wish that I had been exposed to what I see as this more kind of um, I don't know, humanistic messaging about mental health. And I wish my dad had been exposed to that. And maybe it wouldn't have worked, and and that's fine if it wouldn't have worked, but we would have tried it out.

SPEAKER_00 45:55

I mean, two things that come to mind for me in terms of improving, particularly inpatient psychiatric care, but obviously outpatient as well, and from different conversations I've had, I would say firstly, that it's surprising how many inpatient staff, you know, psychiatric nurses, of course, psychiatrists, um, don't have an actual uh training, enough psychological training to understand, you know, verbal de-escalation, how to create a really psychologically safe, containing environment versus a actually more sort of conflict uh-laden environment, often quite an adversarial environment, which you think of something like paranoia, the milder end, and then psychosis, often it is a response to a feeling of a lack of safety. Often people feel paranoid, for example, when they emigrate, go to different countries, are socially isolated when they're poorer socioeconomically, so they feel more under threat. And I think this is where you can understand something like psychosis or schizophrenia adaptively, at least at the milder end, people become paranoid when they're by themselves and they feel unsafe. Now, that could then become a positive feedback loop, I think, which could become something like psychosis. But whether you're dealing with someone um paranoid or someone with full-blown psychosis, a safe, very psychologically safe environment is very helpful. And I think um often because psychiatric staff just don't have that training, they're just not as good as they could be at creating that sense of safety. And then the second thing which I learned talking to someone who is responsible for the way they work in Treste, Italy. So Trester Italy is focused for having a very effective mental health system which relies on sort of less mandatory medication, less sectioning, stuff like that, is the integration of mental health and social services, which I think is a super good idea, something we should be thinking about because what that allows you to do is to integrate people who have mental health difficulties more into society. So if you have a mental health problem interested, they say, How can we get you in the community? How can we get you working? How can we get you feeling valuable to others? Uh, how can we get you feel being connected to others? And that is so central because human beings are so sort of related, such relational creatures. Our mental health is so closely tied to how relevant we feel to a community. I think those two things, like psychological safety and integration with social services, will be so useful to have when we're treating people, even with severe mental um illness, I think.

SPEAKER_01 48:30

Yeah, absolutely. And and it's I I mean, I certainly hope I think in the UK you're probably farther along toward that path than in the United States, where I I think in the US we we just we still have this very simplistic idea, and more so, I mean, in the Western world as a whole, but I think in the UK, you're probably further down that path of really thinking about, you know, how do we create these environments where people feel safe and we're not just re-traumatizing people or uh triggering uh uh paranoia again through these adversarial relationships. And then B, how do we plug people into a community where they feel that they have a social role and they feel that they have a purpose and they feel that they're making uh a contribution? And yeah, I certainly would love to see those insights incorporated more broadly.

SPEAKER_00 49:28

I'd be really interested to hear your uh philosophical point of view on madness and perhaps the mild ends of madness like paranoia as well. How do you think about phenomena like schizophrenia philosophically?

SPEAKER_01 49:43

Yeah, I mean, that's a huge uh question. Um it's a great question. So I wrote a book uh about four years ago uh called Madness of Philosophical Exploration that really dives into exactly okay, what is my big philosophical outlook on madness? Because the madness pill was written as a more straightforward history of science. Hey, here's how we got into this kind of somewhat narrow uh biomedical view. I mean, I'm trying to think of how to convey that in a in a f in a few minutes. Um, but the but well, let me just start with my own uh experience. So, you know, 90 or 91, I'm I'm hospitalized for uh uh depression for six weeks. I was given this idea that depression is a dysfunction. Something inside of me is not working the way that it's uh supposed to. And it was only, you know, maybe 20 years later that I came across this alternative view of depression, uh, but associated with psychoanalysis and associated with uh evolutionary uh psychiatry. And it's the idea that no, depression isn't a dysfunction at all. Your brain is not broken at all. It's actually uh your brain's functional signal that something in your life is not going well and needs more uh attention. And so I started getting really fascinated with this distinction between what you might call dysfunction-centered frameworks and function-centered frameworks. This idea when somebody's having a mental health crisis, do I immediately revert to the notion that something inside of them is not working the way it should? And we have to figure out what's wrong and go in there and fix it? Or can we be open to these function-centered frameworks where we see, okay, maybe this person's depression, nothing is going wrong. Their brain is working exactly as it's supposed to, given the kind of situation. They're supposed to shut down a little bit when life is feels uh completely uh overwhelming and hopeless. And then I started thinking about, okay, what would shifting from a dysfunction-centered framework to a function-centered framework mean for other kinds of problems, like uh, you know, person, so-called personality disorders, or even uh, you know, symptoms of schizophrenia, like delusions. And I came across uh the this uh fascinating body of research on the nature of delusions, where some people will say, okay, delusion that's clearly something's gone seriously wrong with your brain, if you think that, you know, uh the president of the United States has put you on some secretive special mission, or you think that some famous actress is in love with you. Whereas this there is this alternate point of view which says, okay, there might be something going wrong in your brain, but let's look at the function that this belief might be performing for you. And when you look at that, suddenly you see, okay, for some people, these what we call delusional beliefs may have the function of giving them exactly that sense of significance and purpose that everybody needs, or giving them a sense that they're not isolated, misunderstood, that somebody out there really understands them. So I I part of the goal of my earlier book on madness was really what would it look like on this more abstract philosophical level to take this shift from a dysfunction-centered point of view to a function-centered point of view, or at least to take a shift where we focus single-mindedly on uh dysfunction style explanations to one where we have a truly pluralistic outlook where we can look both at dysfunction and at function and purpose.

SPEAKER_00 53:55

Yes, I think I think that's interesting. And I I I feel like there are ways you can bridge the dysfunction and the function-centered view. Uh so for example, taking and and I I would do this using an evolutionary point of view. So I think depression is a great example. It's normal to be sad, we all feel sad and we can understand that sadness serves a purpose. Sadness tends to make us retreat a bit, make us more introspective, more introverted. What we can do now in the modern, uh, you know in a modern society, which we could never do really as hunter-gatherers, is we can spend really, really long periods of time by ourselves. So if a person could hold themselves up now in their apartment for three months, you know, or the take out delivery and watch Netflix for three months. That could never happen in a hunter-gatherer society. And what that isolation can do is then promote a positive feedback loop where you get more and more sad and more and more depressed. And then I think potentially that's where things can go wrong neurobiologically. I think that's potentially where things can become much more dysfunctional, and that's how you can potentially end up with the kind of depression where someone doesn't speak or they don't eat or they don't drink. So it's not purely the brain going wrong per se, but the brain being allowed to go wrong because it's under such extraordinary circumstances that you would rarely expect in nature, in a hunter-gatherer society, someone would pay attention to you at some point because the second you're out of the child functionally, you're kind of dead in those times, you know. Whereas now we can be in these really, very strange circumstances.

SPEAKER_01 55:30

Yeah. I I think that's a great point of view. I mean, I think it's a great perspective to adopt, not just this evolutionary perspective, but also asking that question okay, to what extent do some of our modern ailments uh reflect a kind of mismatch between the environments in which human beings have spent the vast majority of their of their existence as a species and these very recent kinds of environments. And there's uh some other research I got exactly this kind of evolutionary mismatch research that I'm fascinated by with ADHD. And one point of view is that actually, in uh a more nomadic community, people with ADHD-like traits, people with very novelty-seeking, kind of very fluid uh attention uh patterns often get bored easily if they're asked to do the same uh thing. The theory is that in those kinds of communities, ADHD is really a boon to the community as a whole, because these are folks who are the natural explorers. They're the ones who are, you know, because of the fact that they get bored easily and they need stimulation, they're the ones going out and finding new water sources or finding new food sources, or coming up with these new uh uh inventions. And some people think, you know, it's only this uh ADHD only becomes a kind of mental health crisis because of these modern environments where we don't give kids those kinds of opportunities to be the natural explorers and and adventurers, but we expect them uh uh to just sit for hours at a time learning in this kind of abstract uh uh way. There is actually some research that was done uh about 15 years ago, and there's a uh a group of people in uh Kenya, I think they call uh the REL. And about half of them have a nomadic uh hunter-gatherer structure, and about half of them have a market economy where they, you know, they they're done with the nomadic thing and they they have a cash-based uh economy. And there was a researcher who did a lot of work out there, and what he found, or what he claimed, uh, was that people in the nomadic parts of the Ariel society who have these ADHD traits tend to be healthier and wealthier than the people in the market-based society who have these ADHD traits. And the point that he was getting at is that this isn't, you know, this kind of evolutionary mismatch view isn't just a theory. There's some actually solid evidence that ADHD is just an alternative cognitive style that our society no longer has has the same use for.

SPEAKER_00 58:34

And I guess in an increasing sliding scale, like it's a slow progression, like as a society, we have slowly but surely progressed to a state where we value slower work, work delayed across months and years, work that's more abstract, less, less hands-on. Even with ADHD, you can find there are there's a spectrum, there's like the milder and moderate end, and then there's like really severe ADHD, where you really see that come on, someone can't sit still for like basically any length of time, can't stay on a topic of conversation. And then you wonder, now are we perhaps in the disorder realm? I'd encourage everyone to go read your new book, The Madness Spill. Maybe before we finish, what do you think is like the key lesson that what was the key lesson you learned when you read about the events that that you wrote about in this book?

SPEAKER_01 59:22

I I guess two kind of big uh takeaway points. Uh one lesson is that, you know, we're we're tempted to see the biomedical paradigm, this kind of mental disorders or brain disorders to be managed with pills. I think certainly by the 90s, we saw that as kind of the apex of scientific progress. Like people just thought, oh, there must be all of this scientific support for this uh biomedical view. And so one of the lessons from my book, I think, is you know, a lot of our biomedical conception of psychiatry was not based on groundbreaking evidence. It was not based on any scientific smoking gun. It was based on these outsized personalities. It was based on these experiments where in retrospect they they really have dubious value, like giving a handful of volunteers speed until they become psychotic or thinking that there's a connection between stereotyped behavior and rats and psychosis. And so once you start to see that this biomedical perspective was really not the outcome of a, you know, the cold march of scientific progress, but it was the outcome of these political, economic, even personalities, uh, then I think that that helps demystify it. And that helps to helps us to see, okay, this was one particular perspective that really uh gained a foothold, but probably did not deserve that. And I think once you see that, it it becomes easier to start thinking in a more open-minded way about alternatives to this biomedical view, or at least it makes it easier to start constructing a genuinely holistic and pluralistic viewpoint.

SPEAKER_00 1:01:17

And lastly, are there any books you would recommend, books that have been particularly influential for you when you started learning about mental health or perhaps the philosophy of mental health?

SPEAKER_01 1:01:28

I think probably the book that was most helpful to me uh was uh Ann Harrington's book, uh The Mind Fixers. She just does uh such a great job of walking us through what was going on in the 1960s, um and showing how a lot of the developments that were taking place and that were shifting us toward this biomedical perspective were really more based on politics. They were based on economics, they were based on these outsized personalities. So I think she does a great job uh kind of demystifying uh this biomedical shift.

SPEAKER_00 1:02:11

Professor Justin Garsons, he's a professor of philosophy at Hunter College and the Graduate Center, City University of New York. Justin, thanks so much for joining me.

SPEAKER_01 1:02:19

Yeah, thank you for having me, Alex. This has been a lot of fun.