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Freakonomics Radio: How Are Psychedelics and Other Party Drugs Changing Psychiatry?
    #26963608 - 10/01/20 10:33 AM (3 years, 5 months ago)

How Are Psychedelics and Other Party Drugs Changing Psychiatry? (Ep. 433)

September 30, 2020 @ 11:00pm

by Stephen J. Dubner

Produced by Mary Diduch


The program podcast page lets you read the transcript, download audio, or watch it on youtube.
Obviously, if you search for "Freakonomics Radio" on any podcatcher software, you'll find it.
It's on Apple iTunes, RSS, Stichter and others.



Three leading researchers from the Mount Sinai Health System discuss how
ketamine, cannabis, and ecstasy are being used (or studied) to treat
everything from severe depression to addiction to PTSD. We discuss the
upsides, downsides, and regulatory puzzles.


We gathered three medical researchers to talk about how a variety of drugs often used for recreational purposes are increasingly being used in medical settings. It is a topic of great interest these days — one example being Michael Pollan’s best-selling book How to Change Your Mind: What the New Science of Psychedelics Teaches Us About Consciousness, Dying, Addiction, Depression, and Transcendence. The substances we’ll be discussing today are ketamine, MDMA, and CBD. The entire Zoom conversation lasted 90 minutes; and you can watch it above. This episode was edited down to podcast length.

Quote:

Stephen DUBNER: Good evening, and thanks for tuning in. As you likely know, there are many natural and synthetic psychedelic substances. They have been used by countless cultures for centuries, perhaps millennia, for many purposes — medicinal, religious, social, recreational and so on. The first synthetic hallucinogenic molecule, LSD, was discovered by the Swiss chemist Albert Hofmann in 1938. And it came to be considered a “wonder drug,” helpful not only in expanding consciousness, but potentially treating mental illness. Before long, there were thousands of medical studies underway on LSD and other psychedelic drugs.

But of course, drugs are susceptible to abuse. And the U.S. government, as part of its wider war on drugs, effectively killed off that research, and those drugs and many others were made illegal. For the most part, European and other governments followed. Economists think of the war on drugs as a failure, for the most part. Much of the law enforcement community does as well. For the medical community, in particular, the war on drugs produced widespread collateral damage in the form of treatments undiscovered, in the form of human suffering unalleviated, in the form of scientific knowledge unattained. Today, that is changing.

Cultural attitudes have shifted, public policy has started to move as well — albeit haltingly and inconsistently — and scientists around the world are once again looking at these and a variety of unorthodox drugs in the hopes of finding new treatments for mental illness, addiction, PTSD, and other maladies. Tonight, we have gathered a trio of medical researchers at the forefront of this work, all three from the Mount Sinai Health System right here in New York City. They are James Murrough, Rachel Yehuda, and Yasmin Hurd. James, Rachel, and Yasmin, good evening and thank you so much for being here.

MULTIPLE: Good evening.

DUBNER: So, here’s the plan: I would like to ask each of you to introduce yourselves briefly, and then we’ll open up the conversation more broadly. So, let’s start with James Murrough. Would you tell us quickly about your research specialty and how that feeds into your clinical practice?

James MURROUGH: Sure, Stephen. I’m a psychiatrist at Mount Sinai and I did my residency there — started in 2005 — went on to do a research fellowship, and currently I direct a clinical research program focused on finding causes and treatments for depression and related conditions, such as anxiety. When I was just a trainee, Dennis Charney had started what was a very early research program in looking at whether ketamine could have rapid antidepressant effects. And as a resident, hanging around looking to get involved in something, I got involved in that. 

DUBNER: Dennis Charney, we should say, is now dean of the Mount Sinai medical school; and before that, he did ketamine research at both Yale and the National Institute of Mental Health. So, James, you came to Sinai as a resident — and now fast forward for us.

MURROUGH: And fast forward more than 10 years, we and others are still doing research to understand how ketamine works, who it works for, and what it can tell us about depression, and point the way towards even other treatments maybe we haven’t even thought of yet.

DUBNER: And ketamine, it is, as I understand, a very popular surgical anesthetic, correct?

MURROUGH: Yeah, ketamine is a medicine that was synthesized and approved as an anesthetic.

DUBNER: But also a big party drug in some points in its history, yes? In the ’80s and ’90s? Maybe now?

MURROUGH: It’s still used recreationally. It’s actually classified as what’s called a “dissociative anesthetic.” And apparently that’s the only drug sort of approved by the F.D.A. that’s a “dissociative anesthetic.” It causes a unique, altered state of mind when taken at certain doses, and sort of a hallucinogenic state almost, and it got famous for folks taking it at raves and things like that.

DUBNER: Okay. So, for those of you keeping score at home, that was James and he’s your ketamine guy. Now, let’s move on to Rachel Yehuda. Rachel, would you tell us quickly about your research specialty and again, how it feeds into the treatment?

Rachel YEHUDA: Well, I’ve been studying post-traumatic stress disorder since the late 1980s, and I’ve been at Mount Sinai since 1991. I think we were among the very first medical schools to establish a center for the study of traumatic stress and PTSD. And for the last 30 years, we’ve been investigating the biology of post-traumatic stress disorder, the epigenetics, looking at resilience. And in the course of that work, we’ve tried a lot of treatments and done a lot of treatment trials on PTSD. And those studies haven’t really provided great outcomes. And I heard about MDMA a few years ago—.

DUBNER: You have to tell us how you heard about it. Because, like a lot of people, you first discovered MDMA at the Burning Man festival, I understand, yes?

YEHUDA: That is true. But my mentor in all things MDMA was Rick Doblin, who really encouraged me to go to the MAPS training.

DUBNER: MAPS stands for what, please?

YEHUDA: The Multidisciplinary Association for Psychedelic Studies.

DUBNER: Okay.

YEHUDA: And they’re largely responsible for sponsoring all of the work that’s been done on MDMA in the last 30 years or so.

DUBNER: And just to clarify, MDMA is also known as ecstasy and molly and has been widely used recreationally. And Rachel, as I understand, MAPS offers a training program for medical practitioners who may want to use MDMA to facilitate therapy.

YEHUDA: Yes, And after I did the training and had some other experiences talking to people, I was very eager to bring it to Mount Sinai. There are so many questions about how it works, why it works, for whom it works. And it’s a whole frontier out there.

DUBNER: Okay. Let’s keep circling on and cover the basics. Yasmin Hurd, would you tell us a little bit about your research specialty, and especially in your case, the somewhat circuitous route of your drug of choice and how it’s used and in what kind of treatment?

Yasmin HURD: I am the director of the Addiction Institute at Mount Sinai and my drug of choice — actually, there are multiple. We actually have one of the largest clinical-addiction services in the country, treating over 6,000 people with opiate-use disorder. And I look at addiction from the perspective of what increases risk. And also I’m a neurobiologist, looking at what happens in the brains of people who have a substance-use disorder, and can we start thinking about novel treatments? And when we looked at risk factors — you know, early cannabis use — we see strongly increased risk for substance-use disorders later in life, as well as certain psychiatric disorders. And our animal models confirm that.

DUBNER: When you say your animal models confirm that, that suggests that the correlation between early use and later problems is not behavioral. It’s chemical, yes?

HURD: Correct. So, these rats, for example, their mothers tell them to stay away from certain other kids. But they still develop certain sensitivities to opioids, for example, later in life. But in our animal models, we study THC, which is the part of the cannabis plant that creates the high. And one day I said, “Let’s at least look at another cannabinoid in the cannabis plant.” And we started looking at cannabidiol, CBD. And there we actually saw an opposite effect. We saw that it actually reduced heroin-seeking behavior in the rat model. And then we started thinking, “Wow! Could this potentially work for our human subjects?” And started doing clinical trials. That was actually over 10 years ago, before CBD became so popular.

DUBNER: Okay, very good. So, I’d love to go around one more time. And I’d like to get from you a little bit of the background or history on the drug or drugs that you study. Because the story of how these drugs are invented or discovered, and then what they’re used for initially, and how they get repurposed a hundred times is fascinating. But I’m also curious to know how each of your drugs is unique. And by that I mean, not just in terms of chemical composition, but how they help a clinician achieve your goal. Okay, so James, we’ll start with you again and ketamine, please?

MURROUGH: Absolutely. So, ketamine has been known to the medical community for decades. It was actually initially synthesized to be an anesthetic and is used for that reason today widely. In terms of what this molecule is, it’s unique in terms of anesthetics and certainly it’s very unique in terms of antidepressants. There’s no antidepressant drug which acts like it does in the brain. This interferes with signaling in a specific type of receptor in the brain called the N.M.D.A. receptor that’s very important for learning and memory and what’s called neuroplasticity.

It seems to help brain circuits adapt to the environment. It’s part of the glutamate system, and glutamate is the primary transmitter in the brain, which excites neurons and makes them fire more, and that’s basically how information is transmitted in the brain. It looks like — jumping ahead a little bit, from brain-imaging studies and things like that — that if you give ketamine, it sort of somehow disrupts or scrambles temporarily the function of circuits in the brain, which ultimately give rise to consciousness. That’s actually why, at high-enough doses, you block consciousness in people, you can operate on them. And they don’t actually have a memory, even though they don’t go to sleep in a standard sense, like if you were to receive something else, like Propofol.

So, people don’t go to sleep. They enter some kind of what’s called “disconnection state,” and they have a profound alteration of consciousness at high doses. And initially a very small study, with I think eight people at Yale that was published in 2000, show that if you give an intravenous infusion of this powerful anesthetic drug, but at a low dose — a quarter of the dose you would need to actually have an anesthetic state — they got altered temporarily. And then the next day, they reported a lifting of their depression.

DUBNER: And how long does that last typically?

MURROUGH: It only lasted a few days. And since then, it looks like it’s variable. For some people, it could last more than a week. But it’s certainly temporary.

DUBNER: Now we should say, there is one ketamine — or ketamine-derived drug — on the market now, a prescription nasal spray, correct?

MURROUGH: That’s right. A form of ketamine, if you will, a so-called enantiomer called esketamine, was approved last year as an antidepressant. And it was the first antidepressant approved which, from a chemical perspective, was not like the rest. The only drug that worked on this system of glutamate — rather than something like, for example, Prozac affects things like serotonin as does all the other dozens of antidepressants on the market. But this one is different.

DUBNER: As I understand it — correct me if I’m wrong, please — this is called Spravato?

MURROUGH: Exactly.

DUBNER: Distributed or sold by Janssen. And I also understand that, just for the record, Mount Sinai, with whom you’re all affiliated, does have a financial interest in that drug? Some of the research is licensed from there, correct?

MURROUGH: Yeah, that’s exactly right.

DUBNER: Okay. I understand you treat what’s called “treatment-resistant depression.” I want to know a little bit about the population for whom this ketamine-derived drug is most successful. But then I also want to know, it sounds like it’s a medicine I take twice a week, and it is a medicinal treatment of depression. There is no psychotherapy attached to the administration of that drug, correct?

MURROUGH: That’s exactly right. So, “treatment-resistant depression” — and sometimes my patients remind me that that might not be the best term — because as psychiatrists, or so-called psychopharmacologists — which is basically just a fancy word for a psychiatrist that focuses on using medicine instead of psychotherapy, I fall into that camp — we do a lot of cheerleading with our patients, right? So, depression for many people, they respond beautifully to psychotherapy or an antidepressant, a standard what we call conventional antidepressant. And that’s great. And we never see those patients, right? Because they’re treated in primary care or maybe they don’t even go to their doctor and it eventually resolves.

But unfortunately for some patients, there’s a more severe course and they just don’t respond. Whether it’s their brain chemistry is different, giving more serotonin in the brain is not doing the trick for them. They tell you, “I went to my doctor and they said, ‘Okay, Prozac didn’t work.’ And then I tried another drug and then another,” and this is sort of trial-and-error. The problem was, if you have a trial-and-error approach, but every medicine works the same in the brain, what are you going to get? So, that’s why this was sort of a big deal.

DUBNER: Now, Rachel, MDMA, I’d like you to describe again a little bit of the back story of the drug. But then I’m really curious to know not just how chemically MDMA or the MDMA derivation differs from the ketamine derivation, but also how the application differs, including psychotherapy.

YEHUDA: Yeah, MDMA was first synthesized by Merck in 1912, and it was originally supposed to be an intermediary compound towards making a drug that stops bleeding. The drug basically stayed dormant for a while. The patent ran out. And in the ’50s and ’60s, of course, the C.I.A. and the Department of Defense were very, very interested in all psychedelics — LSD, all of them — because they wanted to better understand their mind-altering properties or whether they could be used to kind of get secrets from people. We don’t know anything about what the outcome of that research was. But what we do know is that in the ’60s and ’70s, MDMA surfaced as a drug that was used clinically by therapists. It wasn’t illegal to use MDMA then, and—.

DUBNER: Was there F.D.A. approval or was that not necessary?

YEHUDA: No, there wasn’t F.D.A. approval, but it wasn’t—. 

DUBNER: Meaning it was just used off-label?

YEHUDA: It was used. And no randomized clinical trials like we’re used to, but kind of word-of-mouth on it spread. And actually, it was called “Adam” because people felt it restored patients to their innocence state. It was actually called “Empathy.” It’s a drug that increases empathy and connectedness and prosocial behavior, for yourself and others.

DUBNER: As James said, the treatment with ketamine is medicinal. The treatment with MDMA is, as I understand it, to open the doors of perception slightly to allow psychotherapy to get at the depression. Is that about right?

YEHUDA: Yes. If you’re put in the exact right state where you’re not afraid of your emotional reactions or your memories, you have maximum interpersonal trust, a minimum self-blame or guilt or any of those things. This is the state that is a perfect place to be to start processing very difficult, traumatic memories and really catalyzing a therapeutic process. So, unlike ketamine — and James told you how it works in the brain — I could tell you similarly about the molecule of MDMA and I could tell you about how it works in the brain. But I’m not sure that those short-term pharmacologic effects really explain what happens.

And you might ask, “Why do you need a drug to catalyze a therapeutic process?” And the metaphor that’s often used is that psychedelics to the mind are what the telescope is to astronomy and what the microscope is to biology. It’s not that all of a sudden you see things, you’re hallucinating things that didn’t exist or that aren’t real. You’re actually allowing yourself to have a tool so that you can really see things that actually are there, things that are really important that aren’t that obvious or cannot be looked at in any other way. And so once they started to understand that that was the purpose of MDMA, it really clicked into place as something that is very necessary.

Because trauma survivors with PTSD, they don’t want to look at their traumatic experiences. They don’t want to look at the reasons that they’re kind of stuck where they are. Because it’s very, very painful. Trauma survivors also have a lot of shame and guilt and self-blame. And it’s just very, very hard. Almost brutal to try to think about doing that kind of honest reflection and in usually a short period of time. Most sessions in psychotherapy are about an hour or an hour-and-a-half. But with MDMA, you have an eight-hour session where you’ve got a lot of time to process the events.

DUBNER: Wait. And if you’re the therapist, you’re the therapist for the entire eight hours?

YEHUDA: You have a co-therapist. So, there are two therapists, usually a male and a female. And they’re with the patient through the three sessions of preparation, the eight-hour MDMA session, the three sessions of integration, and then you do it again a few times.

DUBNER: Wow.

YEHUDA: So, it’s not a quick fix at all. But there’s something about being able to do this in an eight-hour period that’s not interrupted and a session where you don’t say, “Okay, our time is up,” just when you’re getting to the good stuff. And the metaphor that I like to use for this is like pregnancy. It’s like labor. So, when you’re in labor, right—.

DUBNER: Again, just as “treatment-resistant depression” is not the greatest sell, I don’t know if labor is also—. 

YEHUDA:Well, but hear me out. Hear me out. Because if you are in labor to have a baby, the last thing that anyone is going to do is tell you after the first or second contraction, “Well, our time is up for today.” They’re going to be sitting by your side until you keep going with the process and the contractions get closer and closer together.

DUBNER: All right, Rachel.

YEHUDA: And finally, at the end of the day—.

DUBNER: You saved it.

YEHUDA: You got something.

DUBNER: All right, you saved that one.

YEHUDA: You’ve really got something important.

DUBNER: I do have one more quick question for Rachel before we move on from MDMA. You, Rachel, are a scholar of and have researched, for years, PTSD. You are using MDMA to treat PTSD, first medicinally as a means to get there therapeutically. Is the MDMA treatment that you propose particularly useful for PTSD? Or is that the avenue you’ve pursued because PTSD is a particular specialty? Do you have any ideas about how useful MDMA would be for other maladies?

YEHUDA: We have just gotten our F.D.A. approval so that we can begin a study. So, we haven’t actually treated anybody yet. But we’re very close now. That was a very big hurdle. The F.D.A. has designated MDMA-assisted psychotherapy “breakthrough treatment for PTSD.” But I don’t think that this is going to be restricted to PTSD. I think that this is a very powerful way to foster psychotherapy for almost any condition in which life experience contributes to the symptoms. And I don’t know of any in which it doesn’t.

DUBNER: Right. Other conditions may not require eight-hour sessions necessarily?

YEHUDA: Well, no. That’s how long the journey lasts. So, it’s the kind of thing where once you take off, you can’t get off until the plane lands, you know?

DUBNER: So, bring a book. Yasmin, most people listening — I would say everybody listening — is familiar to some degree with marijuana, and its history and uses. Many people are familiar with THC Probably more people now are familiar with CBD. So, just give us a quick taxonomic lesson. What’s what, what does what, and why are you working with CBD?

HURD: So, the cannabis plant has over 500 chemicals. Over about 140 of them are cannabinoids. As I said before, THC, that’s the cannabinoid that induces the high, the rewarding effects. And THC is known to also induce psychosis. And depending on the dose of THC, people say can reduce their anxiety, but it often exacerbates their—.

DUBNER: There’s a lot of variance in the population, correct?

HURD: Absolutely. But it’s often dose-dependent. And THC is the most concentrated cannabinoid in the cannabis plant. Unfortunately, over the decades, the cannabis on the street, the THC concentrations have increased tremendously. At the same time, CBD, cannabidiol, was the second-most concentrated in the normal cannabis plant. And the concentration of cannabidiol on the regular cannabis that’s smoked recreationally has gone down over the years. So, you have a much stronger THC-to-CBD ratio.

DUBNER: I assume the THC was increased by selective breeding for the purpose of making people — right, making it more concentrated.

HURD: Exactly. Improving the high.

DUBNER: What about the CBD decrease, though? Is that just a side effect of increasing the THC?

HURD: That was an initial side effect. However, as people started to become more interested in CBD — so CBD does not induce the high. Sometimes people say, “Oh, we’ve been, you know, taking this really great CBD that makes us high.” You know, you’re not. Because CBD doesn’t make you high. One of the things that initial studies showed is that it’s even had this anti-anxiety effect. And then they started to even look at it for psychosis, so they could see that it seemed to have antipsychotic properties.

For our studies, it was a bit serendipitous because we just wanted to study another cannabinoid, when we were making all these conclusions about, “cannabis.” But we were really studying THC. And so, when we saw this, you could say the yin to yang of how THC and CBD tended to do not opposite things, but for the rewarding effects, they had opposite things — for the anxiety, for the psychosis effects. So, we wondered about, in regard to addiction, when looking at opioids, and there CBD tended to reduce craving, reduce anxiety, in our first clinical studies.

DUBNER: When were your first clinical studies of using CBD to treat opioid addiction?

HURD: So, we first did safety studies. So, cannabis, as everybody knows, we’ve gone in this country from prohibition to now, many states legalizing the use of cannabis. So, when we first started to look at cannabidiol it was still considered under the cannabis and was a Schedule I drug, meaning there are a lot of hoops that you have to jump through as a researcher to work with a Schedule I drug, even if everybody on the street has access to it.

DUBNER: And supply, I understand, is limited, right? Isn’t there one farm in Mississippi that grows all the research-grade marijuana? I may be wrong on that.

HURD: Right, for the cannabis. And that’s changing a little bit — but yes, for cannabis. But for cannabidiol, there were also very few companies back then making cannabidiol. Last year, we finished a little larger study — and still not large, but we replicated the results where we showed that CBD reduced cue-induced craving and cue-induced anxiety in people who have a heroin-use disorder. And we focus on cues because, people don’t realize, in addiction, it’s not the reward that drives addiction. It’s a lot of the negative states and the craving and anxiety. And the cues in your environment trigger a lot of the craving. And this is one of the things where — often for treatments of addiction — we either go for harm reduction where we try for substitution therapies.

DUBNER: Buprenorphine, for instance?

HURD: Exactly. Methadone. And they’ve saved millions of lives. But they come with their own problems because they themselves are a scheduled drug. They themselves can have addictive properties. And they have to be monitored clinically, very carefully. So, we’re looking at trying to find non-addictive new therapies for addiction, and CBD fell within that.





The rest of the transcript is on the URL posted above. It also contains links to resources at MAPS and other institutions.

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Offlinezaros
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Registered: 01/14/18
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Re: Freakonomics Radio: How Are Psychedelics and Other Party Drugs Changing Psychiatry? [Re: sonoramo]
    #26963891 - 10/01/20 01:34 PM (3 years, 5 months ago)

well i listened to half of it only talking about mdma and cannabis not really describing psilocybin topics.

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