- Welcome to "The Minor Consult," where I speak with leaders shaping our world in diverse ways. I'm your host, Dr. Lloyd Minor, Dean of the Stanford School of Medicine and Vice President for Medical Affairs at Stanford University. Today, I'm excited to launch "The Big Idea," a special series of episodes spotlighting some of society's most critical issues and transformative solutions that promise to lead us into the future. In this episode, we're asking a bold question. What if we could precisely map and modulate the brain circuitry to better understand and ultimately treat mental illness? Our guest is Dr. Karl Deisseroth, a Stanford neuroscientist and psychiatrist, whose pioneering work has changed how we study the brain. Karl helped develop optogenetics, a revolutionary technique that uses light to control the activity of specific brain cells. His latest work goes even further, using cutting-edge imaging and behavioral science to decode the neural pathways behind our most complex emotions. Karl's big idea is this: by illuminating the brain circuits with unprecedented precision, we can unlock new ways to diagnose and treat psychiatric disorders and gain precious insights into how the brain functions as a system. It's a vision that could transform the future of mental health. Welcome to "The Minor Consult," Karl.

- Thank you, Lloyd. It's a real pleasure to be here, and thank you for organizing this. It's very important.

- Well, it's great to have a conversation. And you became interested in science and very talented in science at an early age. Can you start by telling us your pathway from, you know, a very talented young person to the mature and highly impactful research program and career that you have today?

- Well, I was a reader. I loved books. I loved literature. I loved understanding how feelings could be stirred in people by a few letters on a page. That was an amazing thing for me, and I was introspective enough to think about that and be curious about how it worked. And I was interested in how the physical systems, biological systems, also work, really stemming from that, what bridges from matter to feeling? And I was always curious about that. I loved experimenting with that on my own, creating words and putting them together. And when I went to college, I explored creative writing, but I also got very interested in biology, and that led to the MD-PhD route as a way of, you know, both working with the human brain and the human mind and human feelings and health and disease. But getting down to the science of it, to the cells that were involved, and seeing if that was a bridge even that could be built, because who knows? Who knows how hard that would be? But I came here to Stanford for my MD-PhD program and became a neuroscientist, and used biochemical methods and optical methods to probe how neurons work in circuits. And then starting after my psychiatry residency, which gave me even further understanding of how these feelings and perceptions can go wrong, also at Stanford, I then started my faculty position here in bioengineering and psychiatry. And those two departments, helping bring them together, it was what was needed. But that's a stretch, right? Bioengineering and psychiatry is not the typical dyad of departments, let's just say. But it's been thrilling to work at this interface and to help build this interface. And optogenetics was part of this approach, using engineering methods to create ways of turning cells on or off during behavior, during affect, during emotion, feeling, perception, aggression, nurturing, you know, all these very powerful, primal processes that happen in the mammalian brain. And then, you know, all along the way, seeing patients in psychiatry. But then in the last five years, really, we've been so lucky at Stanford to be able to bridge clinical opportunities with the basic science. And that has been just thrilling. And leading up to the present day, using very advanced computational and electrical recording methods in human beings and explicitly bridging that to cells and circuits in mice and seeing what's shared, what's ancestral for what it means to be a mammal feeling an emotion has been our latest work. And the whole trajectory, you know, I think, out of this, you know, I'm just so grateful to have been surrounded by wonderful environments and wonderful students that have helped us, you know, achieve these goals.

- Can we maybe walk through optogenetics a little bit because it was a really pioneering advance? It was entirely a new paradigm; wasn't something that was out there written or even thought about. Can you tell us how you used a study of bacteria and some special properties of bacteria and then reasoned that this could be an extraordinarily valuable tool to understand the nervous system? Can you walk us through that process?

- Yeah. The story of what optogenetics really, I think, is a classic example of fundamental basic science having unexpected dividends to help understand the human condition and human health. And the essence of these tools, as you mentioned, what allowed optogenetics to happen, it required genes that come from microbes, single-celled organisms: bacteria, single-celled algae. And they don't have a lot of space to work with in what they do, so they do things very efficiently, much more efficiently than we do. And they make single genes that encode single proteins that both receive photons of light and move ions across the membrane, electricity. And this they do for their own reasons. But, you know, one amazing potential would be: what if we could take these genes from these microbes and put these into brains and use this light-induced creation of electricity to turn cells, electrically active cells like neurons, on and off? And the irony was these proteins, opsin genes, they're called, microbial opsins, that encode these proteins, they had been known for decades, studied for decades, you know, thousands of papers published on them over the years. But it was such a leap to think that this would even work: to put a gene from a microbe into a mammalian brain during behavior. There were so many reasons it could have failed and not worked. And I could list them here, but I won't bore you. But indeed, that's the striking thing, is you do have to just try things. And so I remember, you know, in 2004 was that first experiment, so, you know, 21 years ago, almost exactly. And it was not even the most likely thing to work. It was part of a broader screen I was doing; I was trying different genes that might turn on or off neural activity. And so I did try a microbial opsin gene, but in parallel, I tried some mammalian potassium channel genes. Those were much more likely to work, by the way, 'cause they were coming from mammals. These were genes that mammalian cells know what to do with, right? And so the channelrhodopsin experiment, this particular microbial opsin that I selected, I put it in there as one of the things to try. But you know what worked was that one. The least likely thing to work was the one that worked beautifully. And the mammalian genes didn't work at all. They turned out to be toxic to the cells. So, a lot of lessons I learned from that. Of course, once I saw those very first bits of evidence that it was working, of course, that was thrilling, but it was also clear how much work we still had to do. That was all in culture, in a Petri dish, effectively. And we had to develop the methods, fiber optics, to get light into the brain. We had to develop genetic targeting tools to get the genes just into one cell type, but not another cell type, to really meet the promise of the method. And all that took at least another five years to sort out. But yeah, it taught me a lot about not being too confident in what is likely to work.

- Indeed. And optogenetics has been used to understand, to study, and now leading in to treat a variety of different conditions. Can you talk about some of those from Parkinson's disease to some of the more complex mental health-related diseases and disorders?

- Yes. So there are really two phases to this. One is the discovery phase, which I think will continue to grow. It will never stop. There's been more than 10,000 papers now published using optogenetics to just discover things about how biological systems work, you know? Which cells really matter for making things happen. And not even just brain cells, by the way; heart cells and other cells across the body. So that discovery process, though, of course, it's fundamental exploration of the natural world. But then, along the way, you discover, "Oh, these, when we turn up or down, these cells or these connections, that can cause or suppress a symptom-like effect. So, whether it's anxiety, whether it's Parkinsonian behaviors, memory, and social interaction, all these things that we, and now many others, have discovered along the way gave us clues, knowing that some cells are causal, that actually matter. As you well know, for the brain, this is a big step because most psychiatric treatments, for sure, have been serendipitously discovered by chance. We discover, oh, you know, an anti-infection agent turns out to have some benefit for a psychiatric disorder. That's been the history of psychiatric medication. And the reason is that we just haven't known which cells are actually important for doing specific things. And the nice thing about optogenetics in this regard is that now we know that these cells actually matter, they're well-defined, and then that opens the door to so much. You can design medications targeting those cells, once you know what's causal. You could help guide brain stimulation treatments, whether these could be electrical or magnetic. And it's helping already to guide Parkinson's treatments, as you mentioned. There are multiple companies developing medications, drugs using this sort of causal insight from optogenetics. And then finally, there's direct optogenetics. This is where you actually put the gene from these microbes straight into the human body of a person suffering from a disorder and deliver light. And that's already been shown to work in the case of a degenerative central nervous system disorder, retinitis pigmentosa, and this was published a couple of years ago. One of my colleagues, Botond Roska, and Jose Sahel in Switzerland, they used a channelrhodopsin in a human being with degeneration of the retina who couldn't see anything. If you had them in front of a table with objects on it, he couldn't see objects, couldn't reach for them. And then after they put in a channelrhodopsin into his retina and goggles to amplify the light from the environment and project it onto the retina, he was able to see and reach for objects on the table perfectly well. And this was published in Nature Medicine a few years ago.

- That's great. That's great. You mentioned in your introductory remarks that you have been and continue to be a physician-scientist. You still see patients with psychiatric disorders. In your books, your publications that are addressed for general audiences, you've written a lot about what you've learned from your patients and how they have informed your science in the past and even today. Can you tell us more about that? This has clearly been a conscious decision. Someone like yourself, a very, very distinguished basic scientist, could have easily made the decision to focus exclusively on the science you're doing and also on the early stage development of treatments, but letting others, you know, really pursue those after they're out of the lab and after they're beyond the concept phase. But you've instead stayed very focused on maintaining a clinical practice throughout your career.

- Yeah, as you say, it's a conscious decision. It's one that matters and has to be considered. People in the MD-PhD realm, as you know, they often have many opportunities that come from being able to walk in both worlds. But also, they can feel pulled in different directions. If the lab work is going well, it can seem like seeing patients, you know, pulls you away from the lab. And likewise, of course, patients are always the top priority if you're their physician. And then that can pull you away from the lab work. And for me, my solution to this has been trying to make sure that these two are working together, that they're pulling me together in the same direction, that I can push these realms also in the same direction. And for psychiatry, of course, I've always been... From the very beginning, the reason I chose psychiatry was I was so struck by the suffering and the mystery of psychiatry. And I wrote about this, as you said, in my book "Projections." But also in the papers that we write from the lab, we try to capture the need from psychiatry that's coupled to, frankly, the ignorance. You know, we don't know what's really happening in the brain that is leading to this suffering. And so for me, it's been not difficult to keep that at the forefront of my mind and to realize that actually helps the science. I can talk to my students. They don't have to read a dry list of symptoms and try to understand the disorder; I can tell them. I can express to them what an autistic person is really like, what actually matters to them, when the symptoms are causing problems for them with eye contact, with social interaction. I can talk to my students in the lab who are doing experiments, and I can say, "This is what matters to them. This is what's really important." And that means so much more than what you can get from going to the textbook and reading the list of symptoms.

- Sure.

- And there've been many examples of this over the years. You know, being able to... That I've had actually concrete, you know, impact on guiding experiments. I remember I had a patient with a severe depression who told me in a very vivid description, he said, "When I'm depressed, when I'm at the depths of my depression, I can see something neutral. Like, I can see a piece of paper on the floor or the table, and I can feel bad about that piece of paper. That makes me feel terrible inside, a negative feeling from seeing a piece of paper." And I thought about that; I was struck by that. And that helped us guide experiments in the lab where we can explore, are there cells that can make a mammal like us, in this case a mouse, avoid something neutral, something that has no value, positive or negative, at all. Like, if it has a choice between two neutral rooms that are equivalent, are there cells that will make it avoid one in favor the other, even though they're both neutral? And that helped us guide experiments and identify particular kinds of cells that did indeed govern that sort of process. So that's one example. There are many. And now, you know, not only has the clinic then helped the lab, but now the lab is helping our clinical explorations as well.

- That's wonderful. I think it was about four years ago that you called me and said that you wanted to talk about an idea, and you mentioned it in your opening remarks, an idea about how we can study the human brain. And that led, of course, to the Human Neurocircuitry Research Program. You know, how did you come up with that idea? And from very first conversation that we had about it, you knew exactly what needed to happen and what was needed in order to establish this program. And it involved a number of collaborations. It involved some real hardware needs, like running dedicated fiber to a room in our hospital so that these patients could be studied. But can you walk me through why you wanted to do this? And of course, it's been phenomenally successful, some of the things that you're learning from the program, and what was essential to make it successful.

- Yeah, well, I remember that conversation very well, and thank you. It was clear to me what we needed, what the opportunity was. And kudos to you for appreciating that as well, because these things are not necessarily always so clear. And it takes, I think, courage to take the steps needed to meet the opportunity of the moment. But what we had, it came from the lab. So we'd been exploring altered mental states. As a psychiatrist, I'm so interested in the diversity of ways that the brain can start to operate differently. And we've talked a little bit about depression, we've mentioned anxiety. One very interesting disorder, or rather a symptom that can appear across multiple disorders, is dissociation. This shows up in PTSD and epilepsy, in some drug intoxication states, and certain personality disorders. But it's also a common theme in human life; two-thirds of people who have trauma will experience dissociation. And what this is, it's a separation of parts of the brain that normally are tightly together. One of these is the sense of self and the sense of the body. We think of those normally as the same. Myself and my body, they're the same. At least they overlap.

- Sure!

- But in dissociation, there can be a separation of those two. And so people can be fully aware of their body, but not feel as if it is their self. And this is very important. This happens. Probably it has some adaptive significance; it helps people deal with pain, severe pain, severe trauma-related issues. But it also can be problematic if people no longer are protecting their body, their self appropriately. People with certain drug intoxication states, like PTSD or certain personality disorders, will allow damaging things to happen to their body because they don't attribute it to their self. And what a fascinating thing when you think about that. It's almost hard to believe when you describe it. But of course, there's no question what the patients are experiencing, and what happens to them. And the consistency of these symptoms across these different causes, whether, you know, PTSD or trauma, you know, or intoxication, this discrete symptom appears. And so it's tractable, it's reproducible, it's consistent. And as a scientist, then you think, "Okay, how can we study this?" And so we did experiments first in mice, where we gave dissociative medications to mice, imaging across the brain using some of our optical methods. And we found that dissociative drugs caused a rhythm, a particular pattern in one part of the brain called the retrosplenial cortex. And then we used optogenetics to test what if we gave that rhythm, what if we made that rhythm happen, and we saw dissociative behaviors in the mice. That they no longer engaged in self-protective behaviors, even though they were perfectly aware of what was going on around them. And so we wrote that up as a paper. And then we were presenting the results to some of our neurosurgery colleagues here at Stanford. I organized a little lunch group where people get together and just share what's happening, bridging the clinic and the lab, just bringing the doctors and the scientists together. And we described this, and one of the neurosurgeons, Jaimie Henderson, said, "Hey, we've got a patient on the Epilepsy Monitoring Unit who is dissociating as the aura, the period of time right before his seizure." And we thought, "Oh, that's interesting." And he said, "Yeah." And all the electrodes are in place to do seizure mapping. This is the Stereo-EEG method, where many deep electrodes are placed across the brain. And so it was like an unbiased global screen in a human being. So we went and looked at the data, and what did we see? We saw a rhythm that was the same frequency as what we'd seen in the mice and in the homologous region, the same retrosplenial cortex region in the human beings, as we'd seen in the animals. And so we published that paper in the depths of the pandemic in 2020. And then we thought, "Well, we got really lucky there." It was, you know, a chance conversation. I mean, not completely chance, but pretty chance, right? If Jaimie hadn't been there that day, if we hadn't presented it that day, never would've happened. And so the thought was, "Okay, let's operationalize this. Let's use all the amazing opportunities that we have and create new ones, and work with every patient coming through. And let's not wait to be lucky, let's build what we need to make this part of Stanford's infrastructure and the discovery effort, bridging psychiatry and engineering in general." This could be a paradigm that other institutions carry forward, and people we train here could go forward and bring it elsewhere. What would we need for that? We'd need ways of dealing with the vast amount of data coming out of all these patients. You know, we have many electrodes. They're very fast, huge amount of data. Huge. Literally astronomical. The cosmologists and astronomers here are impressed with how much data that we generate to give you some scale. And so right away, there had to be storage, there had to be transmission of the data, and then infrastructure in the hospital itself, you know, in and around the patient rooms, always keeping safety and privacy at the forefront. But you know, thanks to your help, we got it done. And what followed then we called this the Human Neural Circuitry Program, with the idea being that we could study all the patients coming through and all the symptoms they might have, whether it's children with autism who come through the Pediatric Epilepsy Monitoring Unit or adults with depression, and get to the inner workings of the brain during the symptoms, what's actually happening during a symptom, at the moment of a symptom, and ideas coming from that can then feed back to the laboratory. Then we can go and test those using optogenetics and other methods to see what's actually important. And it's going very well, thanks to the opportunities of the environment.

- And of course, not only are you studying the electrical activity in the brain, the neural discharge, but also when those electrodes are removed, which they are removed either before, at the time of surgery, but inevitably removing an electrode, there are some cells that are attached to the electrode, and you're also studying those as well, right? And what are you learning from that, and how is it correlating, you know, with the electrical activity that you've studied in advance?

- Yes, this was another opportunity, again, that came from realizing just what could be done without changing too much about what happens with patients, our normal workflow.

- Sure.

- But what are we missing? What's right there in front of us?

- Yeah.

- Like the microbial opsins, like these patterns of activity just before the seizure. And what was right in front of us was that after these electrodes get taken out, after seizure mapping, they're normally discarded. You're done with the recording. The neurosurgeons and neurologists have established what they need to know, and they can work to treat the patients with epilepsy after that. But we thought, well, now these electrodes have been sitting there in the brain for a number of days. What if there are cells? What if there are neurons attached to them? And the beauty of exploring this was that we didn't have to change anything about the clinical process.

- Right.

- We don't change the electrodes. We don't change how they're put in, we don't change how they're removed. It's only at the moment of when they're out and they're about to be discarded; in those few seconds, we then take the electrodes. And you know, they're electrodes. They have a number of little contacts along them where a different recording happens. And by the way, we know from imaging exactly where each contact was in the human being's brain, and those electrical contacts we've also been recording from during symptoms, not just during seizures, but we can be giving them depression tests. We can be giving them dissociative experiences. And so we have recordings happening. And now what we found is when we take out these electrodes, they're coated with cells, and we have cells stuck to the electrodes at each of these spots that we've been recording from in the human being during behavior and during expression of subjective experiences. So used, you know, modern single-cell transcriptomic methods looking at all the genes that are in these cells that are expressed. And all the main cell types of the brain and the immune system are present in these preparations. We can see neurons, we can see astroglia, we can see T cells and B cells, and oligodendrocytes, and things make sense. So we can see, for example, on a contact that we know was in the hippocampus, we can see it has hippocampal seizure-related genes expressed in it. So everything lines up as we expect. And the pediatric cases we've worked with are also very interesting. There are developmental questions that we can explore. Some of the kids coming through the epilepsy program can be quite young, and so they could be quite early in their development. So there are fundamental questions about human brain development that are accessible now. And we can work with these cells within seconds of the removal from the brain. So it's probably the highest quality that we know of understanding of cells that are living in the human brain-

- Right.

- That has been accessible. So early stages; we're analyzing the data now. But it's just an example of opportunity that, once you look at what's already going on clinically in a different way, and if you can capitalize on the opportunity, there are amazing possibilities that can be lying right in front of you.

- Karl, you know, as you've mentioned, psychiatric diseases, mental health conditions are difficult. They're difficult to understand. They're horribly debilitating for patients and families. We are making progress thanks to your work, the work of other colleagues, for example, transcranial magnetic stimulation, other types of novel modalities. Using your crystal ball, if we look, for example, back over the past 10 years, we have enormous progress in cancer. Still a lot of work to do, but the whole development of checkpoint inhibitors, cell-based therapies, cardiovascular diseases, both for pharmacotherapy as well as interventional therapies, we have made enormous progress. I have the sense that we're on the cusp of a decade like that in both psychiatric diseases and in degenerative neurological diseases, which, of course, have in many cases enormous psychiatric manifestations and behavioral health manifestations. Can you sort of predict for us what you think the trajectory will be? And just as in cancer, for example, the development of checkpoint inhibitors really reopened the field of modulating the human immune system to treat cancer, which people have been trying to do but had been really, really difficult. And yet after checkpoint inhibitors, we had a host of related therapies, both pharmacotherapies as well as cell-based therapies that have followed on, and I think still have the sense that we're in the early days of the impact of all of those. Do you think that there's gonna be a signatory sort of turning point in our work on psychiatric diseases, degenerative neurological diseases that will open up a whole new realm of therapies just as checkpoint inhibitors did in the cancer world?

- Yeah. Well, I think the analogy with cancer is very apt for many reasons. And this was one of the bits of understanding that helped guide me very early on down this career path. I read deeply. I started from the chemical and biochemical level in my entrance to biology. Not from neuroscience or psychology. I really started as a biochemist, and I learned about the cancer, you know, story.

- Sure.

- And how, of course, the stigma is another parallel. You know, cancer had a much greater stigma comparable, you know, in many ways, to the psychiatric stigma. So there was difficulty in talking about it, but also in establishing rigorous preparations that let you make precise interventions to understand what actually mattered. And the answers came, as with the checkpoint inhibitors, it came from biochemical, it came from cellular studies. And then the impact, of course, required ultimately intact animal multi-system integration work, but it started from cells and molecules. And I found that very powerful. And I do think the same flow is going to happen with neuropsychiatry. And by the way, of course, in cancers, getting to that molecular understanding, not only helped the patients, but it helped with the stigma, too. It helped the general public understand these are molecules, this is something that people have, you know, no longer any mystery about. Yes, it's hard. Yes, it's difficult, but it's something we can work with as doctors. It's something we can treat. You don't need to feel differently about someone with cancer. I think we're headed in that direction for psychiatry. And I think very similarly. The initial, you know, tipping points will come from molecular and cellular, particularly cellular, understanding. Knowing which cells matter, that's something that can be communicated to people in the world. The lay public will understand that. If you can finally say to them, "You know, the symptoms of autism are related to cells doing something in a particular way that they don't do in some without autism," the lay public will understand that, and it'll matter to them, and it'll help everybody understand. And so the cellular understanding is gonna be critical. And I also found the analogy apt with the immune system and cancer; the leverage came from this multi-system understanding. I think that's gonna be the case as well in neuropsychiatric disorders, is that you won't be able to make headway just with the cells, though, just with a cellular-molecular understanding. You have to transpose that into the brain-wide and body-wide context. And this is why we've put so much effort into these brain-wide recordings, 'cause we don't know where the answer's gonna be.

- Sure.

- And it's probably not gonna be something that you can understand by looking in one spot and one set of cells. It's gonna be an interacting system answer. But now we're doing that; now we're collecting these brain-wide data streams at the moment of psychiatric symptom expression. We have cellular resolution measures and interventions. And I think it's exactly that. It's the bridging from the cell to the system that made things happen in cancer, and it'll happen in psychiatry as well.

- Karl, your work and so much of progress in biological sciences is driven by the convergence of biology, the study of living systems, with technological advances, and now increasingly with data science, artificial intelligence, and, of course, we're living today in a world where that convergence continues to grow every minute of every day. What's important to make sure that you're able to continue to do your work, that institutions like Stanford, for example, where we have the benefit. You, for example, are a professor of bioengineering. You have a laboratory in, surrounded... One of your laboratories is surrounded by other engineers as well as other basic scientists. What's important in making sure that we leverage that convergence? Because a lot of the progress I think you're talking about is gonna be increasingly dependent upon that convergence.

- One thing I've noticed about what makes things work well here is the low barriers to communication and interaction across fields, across disciplines. And what makes that happen here? I've been paying attention to this, for many years because I've been very curious about it. I was an undergrad at a school on the East Coast, and it's a wonderful place, but things are a little more siloed there. And one thing I noticed about Stanford is the students feel completely uninhibited, wandering into other labs, other departments, exchanging information. And really fostering that freedom, that sense of no barriers and no hierarchies, is a very important thing about Stanford. I really do think that's allowed us to break down the barriers we have already, and we're perfectly set up for exactly in the domains that you're talking about.

- Well, this has been a wonderful conversation, Karl. I'd like to end with two questions that I ask all my guests, but with a little twist on the first question. Which the first question typically is about leadership and the most important qualities for a leader today. Maybe we could put a twist on that and focus on innovation, and what are the most important qualities for an innovator today? And I can't think of a better example of an innovative scientist and physician than you. So what's important, and what do you try to instill in those with whom you work in your lab, those that work with you in the clinic, to make sure that we're nurturing an environment of innovation?

- Well, I think humility is very important, both for leadership and for innovation, I would say. So the answer might be the same for both. I think the best leaders are the most humble. They know what they don't know. They know where they can go wrong, and they know how to take advice from people who are likely to be able to help them. It's the same for innovation, I think. And my very first experiment 21 years ago with, you know, testing the different optogenetic methods, I had no idea what was gonna work, and I knew I didn't know. And so I knew I had to try a number of different things. But if I'd been, you know, more dogmatic, I would've been steered the wrong way. And to this day, I'm in awe at the mysteries that face us. And I feel very small in front of them. And I think that's very helpful to keep for innovation, to realize the magnitude of what's before us.

- And finally, what gives you hope for the future?

- Oh, it's the students and their energy and their brilliance. You know, I see that in their faces. I think I see that in... You know, even when times are hard, the fire is there, and it gives me hope every day. So my hope and my goal is to nurture that spirit. I think as a society, we have great strengths. Our institutions are strong, and we have to make sure we don't steer things wrong and make sure the institutions don't change in their support for the young people who will build the future.

- Well said. Karl, thank you very much. This has been a delightful conversation. And thank you for listening to "The Minor Consult," with me, Stanford School of Medicine Dean Lloyd Minor. I hope you enjoyed today's discussion with Karl Deisseroth, Stanford neuroscientist and psychiatrist. Please send your questions by email to theminorconsult@theminorconsult.com and check out our website, TheMinorConsult.com, for updates, episodes, and more. To get the latest episodes of "The Minor Consult," subscribe on Apple Podcasts, Spotify, or wherever you listen. Thank you so much for joining me today. I look forward to our next episode. Until then, stay safe, stay well, and be kind.