In the second part of our interview with Melissa Arbuckle, MD, she continues to discuss active learning methods. What makes interaction in a learning environment difficult for people? She then summarizes the use of quantitative measurement in psychiatric care, including in therapy. She details its effectiveness as a tool for self-monitoring in patients and whether it can predict relapse and to quantify a "baseline." She further mentions the use of the Working Alliance Inventory as not only an outcome measure but also a teaching tool. Can doctors learn to tolerate that not every patient likes them?
Dr. Arbuckle is Vice Chair for Education and Director of Resident Education in the department of psychiatry at Columbia University and the New York Psychiatric Institute,
Intro: Welcome to Psyched!, a podcast about psychiatry, that covers everything from the foundational to the cutting edge, from the popular to the weird. Thanks for tuning in.
Arbuckle: I remember the first grand rounds I did, where I decided I wasn't going to do a lecture, and I think it kind of shocked people in the audience, that no, we're actually going to do something different, and yet they walked away saying, "This was fun. Wow."
David Carreon: Tell that story. Where were you, who invited you, and did they know what was coming?
Arbuckle: The first time I did it, it was for a quality improvement curriculum that I teach, and the idea ... I asked everybody to come up with something they want to change in their own life and use that as a prompt for walking through the steps of quality improvement and how you set aims, how you measure outcomes.
For example, if you're going to set a goal for yourself ... My favorite goal that residents always say when I say, "Oh, let's set some goals," it's always read more. That translates into, probably nothing's going to happen. So if you think about it in the context of a quality improvement paradigm, then you're going to think about, what exactly am I going to read, how much am I going to read, what's my goal, what's my timeline for doing that, and it's far more likely to happen.
So we use that framework, I use that framework for teaching about quality improvement. So I did that exercise in a grand rounds and people played. I said, "You're going to pair up with a neighbor, and I want you to talk to your neighbor and report back," and it was fun.
David Carreon: Where was it? What was the room like? Tell us more about that picture.
Arbuckle: It was a traditional auditorium, so people were sitting in seats in an auditorium and kind of scattered about the room. I think the one thing that I sometimes have to do is get people to sit next to each other. So sometimes I say, "Okay, you're going to have to move, to sit next to somebody, because we're going to do something interactive." I think it takes people off guard. I think people are still a little uncomfortable about it. I did some interactive stuff, here at the APA, and a couple of people snuck out of the room rapidly.
Jessi Gold: I noticed that, too. Not in yours, but I was noticing that it was like as soon as the workshop part started, everyone was like ... some people just snuck out.
Jessi Gold: Yeah.
Jessi Gold: I wonder what ... I mean, I guess it's scary to have to actively do something. I don't know.
Arbuckle: Well, I think there's a piece of this thing that we're all afraid of being found out as a fraud, that we don't really know something, and perhaps, if you have to do something with someone else as part of an exercise, you're going to feel stupid or people are going to realize you're not the expert you're supposed to be. I think there's some performance anxiety that comes with that.
Jessi Gold: Probably scary for all levels of whatever for different reasons.
Arbuckle: Absolutely, yeah.
Jessi Gold: Yeah.
David Carreon: I mean, if somebody find out that we're not all omniscient, how are we going to be able to keep our jobs?
David Carreon: Another thing we wanted to talk to you about was the ... In psychiatry, I mean, medicine in general, but particularly psychiatry, we like to not measure things. We prefer to just sort of go along without measuring things and particularly in psychotherapy training. There's a lot of thought, particularly in psychodynamic or those sorts of approaches, that it really isn't science, and so you really can't measure things. I know that some of your work has involved trying to measure that and trying to improve that.
David Carreon: How would you even approach ... ? I mean, with all of the squishiness of the psychodynamic approach, how do you nail that down into something that is quantitative?
Arbuckle: Well, I think it depends on, with any treatment, what your goals are. Many patients that come to us for treatment have depression, anxiety, and there are standard rating scales available that you can use to measure those things, and to track them over time.
One of the classes I've taught is measurement based-care, and we literally talk about, how do you integrate this into a weekly treatment? Like, how often would you want to do measurement based care and how would you integrate it into a psychodynamic treatment, and it's not really any different than any other treatment. They fill out the scale at the beginning of the session, you look at the scale, you can a conversation about the scale, and then you can talk about their mother or whatever.
Jessi Gold: That's usually where I go, from scale to mother.
Jessi Gold: Yeah.
Arbuckle: But I think it's actually incredibly valuable to measure outcomes with patients and actually not just your own subjective impression about how a patient's doing. It provides you with more objective data about how a patient is progressing over time through treatment, but it's also incredibly tool for self monitoring for patients. They can see when they start to relapse, what are the first things on the scale that they struggle with?
One of my patients who has bipolar, we know it's sleep, so we're tracking that item really, really closely. One of my patients who has OCD ... I mean, I think the challenge was, for her, was, even though we both would have a subjective impression of how she was doing, the numbers were far more useful for the both of us. She would say, "Oh, ... " We would talk about, should we make a medication change, in terms of her treatment, and she'd say "No, I actually think this is probably my baseline. This is probably as good as I get." We pushed the medication, she got better. So for both of us, it was useful to say, "Oh, no, that wasn't your baseline.
This is your baseline. This is as good as you get, so let's keep this as our marker and our goal in your treatment."
I think no matter what kind of treatment you're doing, you want your patients to improve, and having real data for you and your patient to track that over time is helpful.
Jessi Gold: I know that also, there's ways to measure whether the patient likes the doctor, or feels like they're doing a good job, and you've been trying to integrate that some, as well.
David Carreon: Yeah, and that's challenging to our idea that we're always good doctors to all of our patients.
Arbuckle: Right. Right.
Jessi Gold: Right, or as a trainee, that we're never good doctors to any of our patients.
Arbuckle: Yeah, right. Yeah, so the Working Alliance Inventory is one particular tool where you can track how that's going, and I think that's particularly useful for trainees, in terms of ... And that's probably one of the most useful indicators of outcomes, is how good of an alliance, working alliance you have. I think that probably translates into treatment adherence and lots of positive contributions in terms of outcome. So having that kind of feedback early on could be really helpful. Yeah.
Jessi Gold: Also, could kind of kick your ego down a little bit.
Arbuckle: It could.
Jessi Gold: Yeah.
Arbuckle: So a couple of years ago, our residents did a quality improvement project, where they did patient feedback surveys. Patients filled out the surveys anonymously, and then residents got a graphic report back about how their feedback was, relative to their peers. But what was interesting is that some people got feedback from only one patient and some people got feedback from 20 patients, and actually the more positive feedback was usually from people who got feedback from lots of patients. So I think the challenge with that kind of data is, if you have one data point, not to overestimate the value of that data, whether it's positive or negative. For me, the take home point was really that the more data you have, the more accurate of a representation it's going to be.
And as a psychiatrist, I think we also ... you have to learn how to tolerate that every patient is not going to love you and make a connection with you, for all hosts of reasons. Maybe it's complicated, so we're talking about counter-transference, or maybe it's that they haven't come to terms with the illness they have and they're ambivalent about treatment altogether, so I think learning how to work with patients who are ambivalent about treatment is also a very useful skill to develop.
David Carreon: Well, we're coming toward the end of our time, and we like to ask a few rapid fire questions at the end.
David Carreon: And so we will ask you to keep your answers to one to two sentences, and this is very hard for psychiatrists and affiliated people-
David Carreon: ... so if we can try to keep it to two sentences, that'd be spectacular, so ...
David Carreon: First question is, what is something that psychiatry as a field can improve in, or an area that we, as a field, kind of get wrong?
Arbuckle: Wow. One or two sentences, huh?
Jessi Gold: If you want to talk longer, it's okay.
Arbuckle: No, it's okay.
Jessi Gold: Does that mean you have too much to say?
Arbuckle: No, I think that ... I wouldn't say that we get it wrong, I just think there's all these things on the horizon, that's coming down the pike, that we need to be paying attention to, so whether it's neuroscience training and the impact of neuroscience on our field, whether it's thinking about new healthcare delivery models and integrated care, or thinking about resource manager, these are all things we could do better and we need to do better.
Jessi Gold: What's your favorite book?
Arbuckle: Wow. I'm probably not ... I'm not a good person to ask that. You know what it is? It's Better.
Jessi Gold: By Atul Gawande?
Arbuckle: Yes. I love that book.
Jessi Gold: It sort of goes with quality improvement.
Arbuckle: It does. I quote his stuff in my presentations all the time.
Jessi Gold: Yeah.
David Carreon: What's advice you would give to a trainee?
Arbuckle: I think it would be about setting a framework for lifelong learning. I think they think ... you think, "Oh, I've got four years and I've got all this stuff to learn," and it's true, I think your learning during medical school and during residency is really exponential, in terms of all the things you learn, but there are going to be extraordinary advances in the field in your lifetime, and you need to be prepared to adapt to those changes. So I would recommend approaching learning in a way that really embraces a lifelong effort.
Jessi Gold: And who is a person, either living or dead, or fiction, non-fiction, whatever, who you consider a hero? Or someone you look up to?
Arbuckle: Wow. Well, there's a couple of different people that came to mind when you said that. I mean, I look up to my mother as a hero. She was a single mom for much of my childhood, raising four kids, and really struggled financially. I think that she was ... still maintained her compassion, and so I look up to her.
I would say I also really have been so fortunate to have Maria Oquendo as a mentor. She, just so selflessly, has been invested in my career and supporting me in a way that, I think ... She's just an amazing, busy person with all these other things she's doing, and the fact that she always set aside time to mentor me, I think that was incredibly special, so people like that.
David Carreon: You'd mentioned having fun is important. What's something fun that you've done, either as a child, or as an adult?
Jessi Gold: Just one thing.
Arbuckle: Just one fun thing ... Well, I have a seven-year old and an eight-year old, and ... I don't know, just spending time with them is super fun. My seven-year old just learned how to ride a bike a couple of weeks ago and seeing his excitement at figuring it out finally, that was really fun.
David Carreon: Great. Thank you for joining us.
Jessi Gold: Yeah, thank you.
Arbuckle: All right. Thanks. Bye.
Neuroscience Education: Relevant, Stigma Reducing, and Fun to Learn (with Dr. Arbuckle, part 1 of 2)
In the first part of this interview, Dr. Melissa Arbuckle, Vice Chair for Education and Director of Resident Education in the department of psychiatry at Columbia University and the New York Psychiatric Institute, discusses neuroscience education for psychiatrists and the general public. She focuses on an innovative teaching curriculum that she co-developed called the National Neuroscience Curriculum Initiative and the ways in which this curriculum makes neuroscience accessible, clinically relevant, and interesting.
She describes how understanding and teaching neuroscience can actually reduce stigma towards psychiatric illness (eg, addiction) for patients and decrease countertransference in psychiatrists. Additionally, she broadens the scope to discuss active teaching methods and adult learning principles in general. In rejecting lecture as a good teaching method, she also discusses what is so "scary" about teaching and "making" participants interact with each other.
David Carreon: Hey, everybody. This is David Carreon.
Jessi Gold: This is Jessi Gold.
David Carreon: And this is Psyched! Today we have Melissa Arbuckle with us, the Co-director of Resident Education in the Department of Psychiatry at Columbia and the New York State Psychiatric Institute. She went to medical school at the University of Oklahoma and did a residency at Columbia. She served as a New York State Office of Mental Health policy scholar, 2009 to 2012, exploring the implementation of standardized patient assessments and measurement based care in the clinical practice of residents in training. She directs the quality improvement curriculum for the residency training program. Thank you for joining us.
Arbuckle: My pleasure.
Jessi Gold: You have a correction?
Jessi Gold: What is it? It's okay.
Arbuckle: I'm now the Director of Residency Training and I'm the Vice Chair for Education, so, yeah, that hasn't been updated.
Jessi Gold: So a promotion?
Arbuckle: Yes, a promotion.
Jessi Gold: That's always good.
David Carreon: Congratulations.
Arbuckle: Thank you.
Jessi Gold: Congratulations.
David Carreon: So, well, thank you for joining us, and we've got a lot of ... I'm excited to talk to you about a number of things, but particularly the role of neuroscience in the psychiatry curriculum.
David Carreon: What are your thoughts on why that's a good idea or not?
Arbuckle: Well, I think our knowledge, in terms of neuroscience and its relevance to the clinical practice of psychiatry, is increasing daily. The research in neuroscience and psychiatry is really exploding, and if that research is going to reach patients, it's going to require a clinician workforce that understands that work and can speak that kind of language.
David Carreon: So, say more about what are some of the ways that neuroscience can be integrated into a curriculum. I mean, what would that look like?
Arbuckle: In terms of medical training?
David Carreon: Yeah.
Arbuckle: I think that, as part of the National Neuroscience Curriculum Initiative, we've been developing teaching resources, and that started in terms of thinking about how we teach neuroscience in the classroom, and particularly how we make sure that neuroscience for a medical audience feels clinically relevant, that it's taught in a way that capitalizes on adult learning, and that it's experience near to trainees and their role with patients.
When we first started, we were really thinking about how to do that in the classroom, but most of your training is in clinical settings, so more recently we've moved towards developing short videos, in terms of teaching core neuroscience topics, that can be used in clinical settings with both the teacher and the trainee together.
I think we have this model for education where the teacher is supposed to be the expert, teaching something to a student, and for neuroscience, the field is exploding and most clinicians are not neuroscience experts and feel uncomfortable teaching. So we've developed really short educational videos that teachers or faculty and trainees can watch together and learn together. So it's really a different way of teaching.
David Carreon: Yeah, no, I think that's definitely ... The old model, or at least the traditional model of expert trainee is ... that kind of turns it on its head. I mean, are these videos that are available online or what's-
David Carreon: What is the project?
Arbuckle: Yes. In 2014, I joined with Mike Travis and David Ross to develop the National Neuroscience Curriculum Initiative, and in that project we put all of these open resource videos, papers online. Anyone can log in, create a login to access the materials, and the idea was to really disseminate neuroscience education in a way that was accessible and clinically relevant and all of those things.
Jessi Gold: Do you feel like neuroscience has the potential for people that are in psychiatry to feel like it's boring?
Arbuckle: In terms of the way it's currently taught?
Jessi Gold: Yeah.
Arbuckle: Yeah, so I think that's one of the major challenges in teaching neuroscience, is that the way it has been historically taught is, in our traditional models, that the expert will come in and do a lecture, because scientists are used to teaching to a scientific community, and that's usually ... that dissemination is usually a PowerPoint slide set. So they come in with their talk from their latest meeting, ready to engage medical students or residents, and I think they miss the mark a lot of times.
They don't really realize the lack of foundational knowledge that medical trainees have, so they make a lot of assumptions about what clinical trainees know and don't know, and within a few minutes, trainees are often lost and it doesn't feel clinically relevant. It's about their latest rat study and they don't make that effort to say, "This is how this matters to the patient that's going to be in front of you tomorrow." I think that's been a huge challenge and partly why neuroscience in education has not been so great, up until now.
David Carreon: Is this something that ... ? You said these modules are online, is this ... ? Some of our listeners are psychiatrists, but some of them are not. Some of them might be patients or family members. Is this something that you're hoping everybody can use?
Arbuckle: Absolutely. When we first started, we had this idea that we would create different modules for different learners. So we would have some basic stuff that was more for the lay public, we'd have some intermediate stuff that might be for medical students and residents, and then perhaps expert level content. What we found is, really, everyone's kind of at the lay public level, that we don't know anything about neuroscience, and so all of these resources are incredibly accessible to anybody.
One of our modules that I think is particularly great is called Talking Pathways to Patients, and in these sessions a ... in one, it's a trainee, in another it's a faculty member, role play what they would say to a patient. One is about the neuroscience underlying addiction, and the idea is that they're demonstrating what you could say to a patient, but there's no reason why those videos couldn't be directly useful to the patient population that they're targeting.
David Carreon: Now, have you gotten any feedback from non-doctors or non-trainees about the modules? Do you know of anybody who's used these or who's gone through these modules, that's not a medical affiliate?
Arbuckle: So, I don't know ... Our main outcome measure we've been looking so far is just uptake and we don't really know who's using the modules so far, but certainly the people who have been using them have been incredibly enthusiastic. We also have several resources that we've shared over Facebook and when we're getting the highest hits, in terms of the things we disseminate, my suspicion is that it's the lay public that's really doing the uptake, as opposed to faculty and trainees.
I think it's a huge potential target for the work we're doing, and a lot of interest ... I think patients really want to understand what's going on, and to have a medical model that explains addiction in the context of the reward circuit, I think, can really decrease stigma, self stigma, and can be a really powerful treatment tool.
Jessi Gold: It probably does patients a bit of a disservice to really, really dumb it down because we don't understand it ourselves.
Arbuckle: That's right.
Jessi Gold: Yeah.
Jessi Gold: Wow.
David Carreon: With that, the stigma piece, from one perspective they could say, well, the dopamine sort of ... there's too much dopamine, simplistic 30-year old story. How would the neuroscience version of that, or the circuit based model of the past, you know, updating things, how could that reduce stigma even further than what's already been done, say with the more simplistic dopamine model?
Arbuckle: Well, the current session that we have posted online really talks about the neurocircuit and different areas of the brain, and with happens with a heroin addiction. So what is the normal reward circuit, and then what happens and how heroin can hijack that circuit, and how different areas of the brain are upregulated and different control mechanisms are downregulated. I think that it explains why patients can find themselves with a lack of control over something that they feel they should be able to control. I think having that perspective can take away some of the self blame, the guilt that patients experience. It also provides a really robust model for thinking about how we can target each area of that circuit with different treatments, whether it's medication or psychotherapy. I think it's a model that brings together a lot of different treatment modalities in a unifying model.
David Carreon: This is sort of a story that's more compelling, say, then a more simplistic biological version from the past, or a moralizing version from maybe the present.
Arbuckle: Yeah. I think it's also helpful for physicians, in terms of counter-transference, that when you're working with patient populations where there is a lot of relapse, it can be incredibly frustrating, and particularly when it's associated with ineffective behaviors. So for clinicians to reframe what's happening with your patients, that your patient who is, quote, unquote, "drug seeking" isn't in your office to torture you, but there's something going on at a biological basis in their brain, I think it just reframes your own empathy for that person and could be really helpful in that way, as well.
David Carreon: So there's a few ways to approach the counter-transference relationship and I think that, certainly, there's been some evidence to suggest that a neuroscience understanding, or a biological understanding, can sometimes increase stigma, that if you say, "I am this way because of stuff that happened to me in childhood," rather than, "I am this way because I have a brain disorder," there are some studies suggesting that there's even more stigma ...
Arbuckle: Right. I think it's important to keep it balanced so that, you know, neuroscience isn't just about underlying genetics, but epigenetic changes, so it really is ... When we say that neuroscience and biology is a part of that, experience shapes biology, so these are not one or other.
The other thing is that there's been some really interesting research looking at stigma and what shapes stigma, and some of the data suggests that if you pair psychiatric illness with a message of hope that there is treatment available, that that can be incredibly powerful in decreasing stigma. I think that when we start talking about these biological models, one of the things we've done in the sessions we've developed is really talk about how that biological perspective can inform treatment, and so pairing it with this message of hope and there's something we can do about it, and this how this transforms into treatment options for you and how we can frame treatment options within the context of the neuroscience, I think that could be very powerful.
David Carreon: So sort of trying to take the fatalism out of biology.
Arbuckle: Exactly. Exactly. Yeah.
Jessi Gold: I noticed, also, that you've done some work with teaching trainees how to explain drugs and the side effects of medications to patients as well, and I'd assume that this falls into the same realm for you.
Arbuckle: I think the things that they have in common is really thinking about active teaching approaches. I think medical education, in general ... I probably unfairly targeted the neuroscientists, coming in with their slide deck. This is actually what all of our professors do, right. They come in ... for psychopharmacology, let's say, they come in with their slide deck and they're going to run through, "These are the drugs, these are the starting doses, these are the side effects," and I can't imagine a more boring way to spend an hour, than having someone lecture on something I could look up in a book.
So for teaching, in terms of talking to patients about psychopharm, it's really about using active teaching modules. So residents role play talking to each other, one playing the role of the physician, one playing the role of the patient, and saying, literally, what would you say to a patient when you're going to start a certain medication, in terms of informed consent? What do they need to know about the starting doses, the side effects? How do you talk about really scary side effects in a way that's not going to contribute to medication non-compliance? And that just transforms what was previously a passive learning experience into something incredibly active and incredibly applicable to clinical work. I think that's what's in common, is really thinking about different ways of teaching.
David Carreon: Yeah, and I guess that gets into something that goes far beyond psychiatry, but you've mentioned a few times adult learning and ways that we, just as people, as human beings, remember things better. What are some principles that you've come to appreciate from your work in adult education?
Arbuckle: Well, I think that learners have to be actively manipulating information. So being a passive recipient and not doing anything to actively manipulate information ... The data suggests that if you're sitting in an hour-long lecture, you might remember 5 to 10 minutes' worth of content. When we're pressed to teach so many thing in training, we can't afford to have wasted time, so it's really about getting trainees thinking and coming up with solutions themselves. If you can come up with a solution yourself rather than someone telling you the answer, that's more likely to stick. If you can learn something in an experiential way, that's more likely to stick.
For example, in the neuroscience education, one of the modules is on the fear circuit, and prior to a conversation about the fear circuit, and how we understand the fear circuit, everyone watches a short horror film. Once you've had your own fear circuit activated then talking about what just happened in your brain, that's a very different experience than passively having someone lecture to you.
Jessi Gold: And probably more fun.
Arbuckle: Well, that's the thing. I don't know what happened in education, that somewhere between kindergarten and medical education we decided that learning shouldn't be fun. I'm a big fan of learning being fun, so as part of the NNCI we have trainees make brains out of play dough and it's fun. It's really fun.
David Carreon: So let me get this straight, you have people with advanced degrees making play dough brains?
Jessi Gold: I think we did that.
Arbuckle: You did it. I'm sure you did.
David Carreon: Yeah, it was spectacular.
Arbuckle: But, you know, it's funny, because I originally thought ... My anxiety about doing play dough brain and having people make a brain out of play dough was not that they would think it was too hokey and be unwilling to do it, but they just wouldn't know how to do it. When Dave Ross suggested we were going to do this, and we were going to create brains out of play dough, I said, "Well, I wouldn't even know how to start." He said, "No, no. We're going to make a video. We're going to show people how to make a brain out of play dough," and it was not only fun, it was incredibly useful.
Usually, when you're sitting in a grand rounds, you're looking at some two dimensional image and you're trying to orient yourself, "Okay, they're pointing at something. What is that?" And actually, in this exercise, I discovered I'm a kinetic learner. I really learned in this way of manipulating objects in space was really a useful learning tool for me, so ...
Jessi Gold: I think it's interesting, too, you mentioned kindergarten to college, like if you never tried any of these methods of learning, you wouldn't know that you were a kinetic learner, right?
Jessi Gold: But you just kind of go with whatever the people do.
Arbuckle: Yeah, right. Right.
Jessi Gold: Yeah.
David Carreon: So you're saying that most people are not dry, boring-slides-from-a-PowerPoint-deck-that-are-presented-monotone learners?
Arbuckle: That's right. That's right, most people are not. That's probably the least effective way to teach, and yet we do it everywhere.
Here: Part 3 of 3 with Emeran Mayer, MD, PhD on the mind-gut connection. Dr Mayer talks about the role of the gut in psychiatric illnesses and mood-from a history of forced colectomy in psychiatric patients to an inflammatory diet influencing mood. He answers the question: are we happier when we don’t eat sugar or gluten and should we all be gluten-free? Dr. Mayer is a pioneer of medical research into brain-gut interactions and author of The Mind-Gut Connection: How the Hidden Conversation Within Our Bodies Impacts Our Mood, Our Choices, and Our Overall Health.
David Carreon: Let's also talk about nutrition and diet and microbiology of psychiatric conditions. I know there's been some discussion and some work that you've ended up with around depression and probiotics or depression in the microbiome. How good is this evidence, or what is the relationship between something that we would consider a psychiatric illness and the gut?
Emeran Mayer: As you know, some 100, 150 years ago, there were psychiatrists who are actually obsessed with the role of the colon and fermentation and it led to this unfortunate situation that many psychiatric inpatients in hospitals had to forcefully undergo colectomy and many died because ... There was a phase where psychiatry was actually very much interested in the microbes playing a major role in the psychiatric disease. That obviously has completely disappeared. Today, there's something new that's sort of come up, and that's the role of diet in influencing the nervous system. Felice Jacka in Australia has recently published the SMILE Study. She and her colleagues found that in a randomized study, if they compared the outcomes of patients, I think it was with major depressive disorder, who underwent conventional therapy and their regular diet vs with conventional therapy with a Mediterranean-type diet, there was a significant difference. She has written about this topic.
One explanation of that is related to this concept of an inflammatory diet. We know that high fat, high sugar diets change the microbiota in a way that there's a whole series of events. Increased permeability of the gut is the result of that, increased access of micropolysaccharides or other pro-inflammatory molecules, the gut-associated immune system, which then creates a ... It's not full-blown inflammation, like in inflammatory bowel disease, but a low-grade inflammatory state which then often becomes systemic, so you have circulating LPS levels. My opinion, that's most plausible explanation. As you know, neuroinflammation has been so implicated for depression and other psychiatric diseases as well, so it could well be that diet plays a role in exacerbating it. Certainly not diet is the cause of psychiatric disease, but it's a significant modifier.
Jessi Gold: I've heard people say that when they went on sugar-free diets, or when they went on gluten-free diets that their mood improved. Do you think that's true with what you're seeing in research? Is it totally subjective and they just believe in the diet?
Emeran Mayer: There's certainly, with anything diet, a huge psychological dimension. I think there's few things that have such a placebo effect as diet has. The high-sugar phenomenon, I do believe, because we know a lot about this. High sugar, high fat, it's sort of like opiates. It makes you feel better right away. That's why people almost self-medicate when they're stressed out you crave for something like that. In the long-term, it has these detrimental effects and leads to this low-grade inflammatory state. I think when people say that when they switch their diet to a healthy diet that they feel better, I certainly believe that. In terms of the gluten, that's a whole other story.
As a gastroenterologist, I'm obviously fully aware of the seriousness of celiac disease. It does appear now probably also related to the microbes and the early interaction with the immune system that people develop more and more hypersensitivities and even allergies to food items that 20 years ago nobody ... Like the peanuts and wheat ... If you have that condition, if you eliminate any agent, most likely you will feel better as well, but then you have, it's like 40% of the US population now, who thinks gluten is toxic for them. That's really unsubstantiated. There's nothing that's been found, sort of like IBS, you can take biopsies, you don't find any possible pathological or pathophysiological mechanism.
There was an interesting phenomenon. This really started with a book that came out by a person, an author, won't mention the name, that before was really on the candida connections. This was an early phase that people say all your symptoms, including IBS and fibromyalgia and everything was related to candida and it was due to the high sugar. The same group of people that promoted that like some 20 years ago, are now promoting this gluten-free diet. All the things before there was sugar across all these orders, now it's gluten. That single book, called The Grain Brain, I personally think is responsible for most of that worldwide, I like to call it hysteria, really, which is centered in the US, which is interesting. You go to any other part of the world, people love bread, couldn't live without bread. Whenever I go to France, I ask people, "Have you heard of a gluten sensitivity?" They just laugh at you.
Like many things in science, there may be a certain truth to it. Give you this example about the candida connection, so now that we not just measure the microbiomes, as people have started to look at the virome and the fungi, there is now scientific evidence that people have increased levels of certain fungi, including candida. It would be sort of an amazing thing that 25 years after this non-scientific theories came out that we would support this. That could happen with gluten as well. I have a personal opinion, but as a scientist, I like to say nothing is impossible.
Jessi Gold: Yeah, it's crazy to think one person could write a book and then everyone stops eating bread.
Emeran Mayer: Yeah, it's amazing. An amazing phenomenon.
David Carreon: Yeah. We are running low on time, so we'll have a few more rapid-fire questions and if you can answer in one or two sentences max, we'll go through these questions. Before we do, I also wanted to ask you to say a little bit about the book that you just published. What's it about and who should read it?
Emeran Mayer: It's called The Mind-Gut Connection. It's written for the lay public and I would say it's not just for the lay public, it's also the lay public, but also for a lot of professionals who are not microbiome experts and have not been aware of the science that has involved brain-gut connections and brain-gut microbiome connections. It has a lot of different things in it, different topics in it, from neurobiology of gut feelings, emotional regulation, early life events and influence to diet and optimal health, which is the final conclusion. I think everybody should read it. Even for experts in the area, there's parts in it, including patient anecdotes. Interesting thing to me, now a lot of patients come to me that have heard about the book or read the book and they say, "I am so-and-so in your book. I don't have to tell you much about my symptoms. I'm so-and-so in your book." I think it must have resonated a lot with patients.
Jessi Gold: As a psychiatrist, which sort of patient in my clinic should I recommend would read your book? Is it any illness, anything?
Emeran Mayer: I would certainly say patients with depression, anxiety, particularly if they also have experienced GI symptoms. Autism spectrum disorders, those would be the three main that ... There's also a lot of evidence, Parkinson's disease playing a role. I would say you could probably recommend it to every patient.
David Carreon: Good. I think that sounds like a fascinating book and I'm looking forward to reading it myself.
Jessi Gold: Me too.
David Carreon: First rapid-fire question is, in a sentence or two, what does the field of psychiatry and mental health, where is it that we go most wrong? What is the biggest oversight or mistake that we make?
Emeran Mayer: I don't see patients in a psychiatric clinic. I would say to kind of stop at the neck or not go into the body is, in my opinion, a big flaw. I'm sure there's some psychiatrists who do that. I see the same patients from the opposite end. Most of them have anxiety and depression and compulsive disorders, but I start at the body. I always see the symptoms at the body. They're clearly both there, and I think with psychiatrists, that would be an important lesson.
Jessi Gold: What is your favorite book?
Emeran Mayer: My favorite book, I would say The Black Swan by Taleb. Realizing the complexity of the world and the more complexity, the more interconnectedness and the more unpredictable it becomes. I think our brain functions, also discusses in the book, is a prediction machine that tries constantly to make predictions and if that's done in a linear way, they will almost certainly go wrong. In a complex world as today, it's no longer possible to do that.
David Carreon: What advice would you give to a young doctor, a trainee?
Emeran Mayer: I would say listen to your patient. Most things that the patient will tell you can be explained in a holistic model of brain and body. I would say listen to the patient and don't reject things that don't fit your textbook description. Most textbooks will become obsolete in 10, 15 years. What the patients say, I've experienced this in ideas, research, has stayed the same, and now we're finding so many answers.
Jessi Gold: What is your favorite food and what is your favorite food to recommend to patients to feel better?
Emeran Mayer: While writing my book, I've become a big fan of the Mediterranean diet for various reasons. Since then, since I pay a lot more attention now to dietary factors, it seems there's almost universal agreement that a Mediterranean-style diet, it doesn't have to come from Italy or Spain, many traditional Asian diets have the same composition of 75% plant-based foods and small amount of meat, protein. I would recommend, even in psychiatry now I think it's the same that's in the study showing the slowing of Alzheimer's progression, depression seems to be universal truth to that. It's tasty, you don't have to eat strange things or elimination diets. It's a tasty diet and it's probably one of the best documented health benefits of anything.
David Carreon: What is your favorite species of bacteria?
Emeran Mayer: That's a tough one. There's one, one out of several, that's called Akkermansia muciniphila, funny name. The second name, you can hear the recent connections. They are a bacteria that stimulate especially the cells in intestines that put mucin, mucous, and that's a very healthy thing because the thicker the mucous layer is, the more we're protected from a leaky gut and Akkermansia goes up with a high plant-based diet. It's the food that nourishes these organisms.
David Carreon: Excellent.
Jessi Gold: The last question is, is there a person that you would consider a hero, either living or dead or fiction, somebody that you would consider a hero?
Emeran Mayer: In the microbiome field?
Jessi Gold: Or in anything, really.
Emeran Mayer: That's a tough one. I would say, let's limit it to the microbiome field, Martin Blaser from NYU, who has sort of been the main driving force behind revealing the detrimental effect of antibiotic use, inappropriate antibiotic use on microbial diversity. He's written a phenomenal book, Missing Microbes, which I would recommend to anybody because you will change your antibiotic prescribing behavior dramatically once you've read this book.
David Carreon: Excellent. Thank you for joining us on the show.
Jessi Gold: Yeah, thank you.
Emeran Mayer: It was a pleasure.
Part 2 of a 3 part interview, with Emeran Mayer, MD, PhD on the mind-gut connection. Dr Mayer talks about irritable bowel syndrome (IBS) as an example of a known brain-gut disorder, focusing on the research on dysbiosis—alteration of the gut microbe from healthy individuals—and what it means for the 15% of world population suffering from IBS. He answers the question: is it all in patients' heads? He also discusses the development of the gut microbiome in infants and the influence of prenatal events, breastfeeding, and antibiotics on gut content.
David Carreon: This is the fascinating idea that neural hacking, that the bacteria are hacking into our nervous system to get what they want. That's such a cool idea and I’m certainly excited to see what the science shows as this field develops. Would you talk a little bit about maybe an area where the communication relationship is more well established. You mentioned IBS a little bit earlier. Could you explain what is IBS and what is the gut microbiome have to do with it?
Emeran Mayer: IBS is the acronym for Irritable Bowel Syndrome, a very common disorder, about 15% of the world population are affected. It's a syndrome defined by symptoms because we don't really have a biomarker for it. It's a combination of chronic, recurrent abdominal pain and discomfort and altered bowel habits. It seems like a very loose definition, but it's pretty accurate, with a pretty high sensitivity and specificity, if you can rule out other causes for these symptoms.
David Carreon: I think just to pause and emphasize there's something that I don't think everybody is aware of, but 15% of population and you put an endoscope in, do a colonoscopy and there's nothing there, there's nothing that you can see or take tissue. It's not something that you can diagnose with objective, at least thus far, signs. That's a huge burden. I think the emphasizing the importance of figuring out what it is, what's going on, trying to better characterize this thing that's rather common and underdiagnosed.
Emeran Mayer: What has happened this area, because it's recognized as a brain-gut disorder, so when the microbiome science started, immediately people jumped on it, including ourselves. There's a series of studies that they all can be criticized based on small sample size, mixing males and females, not controlling for diet. Then, not unexpected, several labs found different abnormalities. These abnormalities are called dysbiosis; that means an alteration of the gut microbial composition from a healthy control population. Most of the studies have found evidence for dysbiosis even though the type of dysbiosis, what taxa are altered, if there's increased or decreased diversity and abundance has varied from study to study. The latest evolving concept is that there are several subtypes of IBS based on their microbial signature, as many want to call it. One that's indistinguishable from healthy controls and one that has significant dysbiosis. Interestingly, these two do not correlate with the typical clinical parameters that we use, like bowel habits, subtype, or pain versus discomfort. Seems to have a different function.
You may ask yourself, if half of the patients have a normal microbial composition, the others have an abnormal, but they have the same symptoms, do these microbes really have a causative role, or is this something that's a consequence of something else? My personal feeling about this is that, and that's often forgotten now in this fascination that the microbes can talk to us, that our brain can really effect the microbes, both their environment in which they live, meaning the transit rate through the intestine and the stomach, which is regionally regulated, slow versus fast transit, the secretion.
Many things are being secreted, which the brain sort of modulates, like the defensins from Paneth cells, there are many endocrine cells, serotonin cells in the gut, enterochromaffin cells, which are under autonomic control, so that we now know that serotonin, as well as norepinephrine, can, under stress for example, increase in the lumen of the gut. Since these microbes have receptor or analogs for those substances, can influence their behavior. What I think, and I've had sort of this bias for a long time and seen a lot of those patients, that this is something that really starts at the brain level, possibly, most likely early in life. Could be stress, hyper-responsiveness, or increased emotionality, which sends chronic signals to the gut and its microbes and changes their development. The first three years of life, the microbes, the community is actually shaped, so if during that time there's an imbalance of the autonomic influence on these microbes, they will assemble in a different way. That may happen in some patients and not in others. That's why I personally think you now find a subgroup of IBS patients that have a normal gut microbiota. There's other people that disagree with that, but I think, we'll see.
IBS has been an interesting research area, interesting in quotation marks. So many hypothesis, just during my career, have been proposed to explain it, and most of them have come and gone. Right now it's the microbiome. We'll see if this is the final answer.
Jessi Gold: I've heard people say that IBS is all in people's heads and it's all anxiety and there's nothing else besides anxiety and the idea that it's a separate disease entity is wrong.
Emeran Mayer: That's the thing. When people say it's all in the head, this got a bad name and a very bad impression for patients because what the physicians meant, it's not a neurobiological process, but it's a neuroticism. I still am, in my early parts of my career I sort of taped these talks of the leaders in the field that would say it's a disease of neurotic housewives, middle-aged neurotic housewives. I think now, when we know so much more about the brain and how intricately it is connected and wired with the gut and back to the brain, I think this has a different connotation. I would never use that term to a patient, "It's all in your heard," but surprisingly, if you explain to them with the concept of the brain-gut axis, they all agree, they'll all tell you, "Oh, yeah, I've always known that it's connected to my emotional state or to the stress." It's very few patients, if you give them the right model, that would not accept that.
David Carreon: One of the things you said just a few minutes ago was that the gut microbiome is established around the ages of zero to three, which, as a psychiatrist, is very interesting. We talk about how critically important the first few years of life are for the psychological development, but you're saying that those years are especially important for the microbiological development as well.
Emeran Mayer: Yeah. The microbiome has added another dimension to the importance of developmental diseases. We also know that it predates delivery as well, so prenatal influences. Very interesting studies that, for example, nutrition of the mother, the pregnant mother, stress of the pregnant mother have an influence on the development of the microbial composition and abundance and diversity, and there's even an animal experiment that shows some very intriguing mechanism that stress of pregnant mother changes the microbial composition of the vaginal microbiome and when the baby goes through the birth canal, one initial seeding of the infant's gut microbiome comes from the vagina. In these animal experiments, it's been shown that stressed mother, different vaginal microbiome, the gut microbiome of the newborn is different because of that different priming. Again, in animals, that was associated with a change in brain development in the first few months of life. If that happens also in humans, it just illustrates the importance of prenatal events on the development and the architecture of the gut microbiome of the infant.
After three months, it seems to be fairly stable. It's also very important concept. Regardless what you do later, if you become a vegetarian or become gluten-free or whatever, your microbes will change and the metabolites that they produce will change, but if you go back to the default diet, you'll go back to that same architecture that you had after three years. You don't change that basic ... You can modify it in a certain bandwidth, but you can not really reverse it. There's very few exceptions.
Treatment with antibiotics could do that and also there's this one infection, this C. difficile colitis, which can basically knock out most of your microbes and lead to this overgrowth of the C. difficile organism. Antibiotics, I should mention that they also now have gotten a very new meaning because an extensive amount of antibiotics given to babies, the mother during pregnancy, treatment of the vaginal area with antiseptics, prophylactic antibiotics to the mother to prevent sepsis, this is a huge field. The amount, I forgot the number, that infants by the age of three have received an antibiotic dose is just phenomenal. That clearly interferes with that establishment of the gut microbiome.
Jessi Gold: You're saying that before age three, there's stress, there's antibiotics, there's whatever else the mother went through, there's just natural stress to the infant, how does then from three on can you regain that, are you just now at a disadvantage as a kid because you have this altered microbiome for life?
Emeran Mayer: As I said before, it doesn't stay exactly the same, but I think the current thinking, and you always have to realize that we're just at the very beginning of this microbiome science. This is like, let's say the first decade of neuroscience 150 years ago. I think a lot of things we're talking about today will be thrown out. Yes, pretty much the basic structure, it's like the operating system is established. You don't change during life the operating system of your gut microbiome. You can add new software to modulate it, but the operating system stays the same.
David Carreon: Interesting. That's an interesting analogy. What is the heritability of it? Where do the microbes that are in my gut, where do they come from? You mentioned the birth canal is one source.
Emeran Mayer: Yeah, there are a lot of influences. I should have also mentioned breast feeding during the first three years of life. One very interesting mechanism of how they're programmed. One is clearly the genetic make-up of the infant's GI tract that attracts certain parts of the gut, different communities of microbes. The microbes are not, the microbiomes are not a homogeneous population from the stomach to the end of the colon. In each of those areas, we have to assume there's different communities that are attracted to these regions by genetic influences of the person.
In addition, during programming, in the breast milk of the mother there are these so-called human milk oligosaccharides, or HMOs. These are large molecular substances that cannot be absorbed by the infant's GI tract, so they evolved to the evolution exclusively as food for the microbes of the infants. They play a major role in establishing this community early on. Does a large number of these HMOs that are contained in mother's milk, they're influenced by the genetics of the mother and they're also influenced by the diet of the mother. Two major genetic influences. One is through this early nutrition of the microbes comes exclusively from the mother, then the GI tract of the infant it comes only from genes of the father and mother. There are examples. Genetics don't dominate the population. They play an part. I think there is some mouse models, where genetics play a much bigger role, but in humans, I think influences other than genetics have a major influence, including early nutrition.
The mind-gut connection: What is it and how did it evolve? That is the question posed for this short podcast (the first in a series of three on the topic) to gastroenterologist Emeran Mayer, MD, PhD, a pioneer of medical research into brain-gut interactions and author of The Mind-Gut Connection: How the Hidden Conversation Within Our Bodies Impacts Our Mood, Our Choices, and Our Overall Health. Here, Dr. Mayer talks about his interest in the mind’s relationship to the GI tract, some basics of what bacterial gut/brain communication is, and the evolutionary biology theories behind it. He even discusses the hypothesis that bacteria actually tells our bodies what to eat—like to crave sugary foods in obesity. Dr. Mayer's website is http://emeranmayer.com. Twitter: @emeranmayer.
David Carreon: Hey everybody this is David Carreon.
Jessi Gold: And this is Jessi Gold.
David Carreon: And this is Psyched, a psychiatry podcast. Today we have Emeran Mayer on with us. He was born in a small town in Bavaria, where his family ran a confectionary business since 1873. After deciding against taking over the family business he finished medical school at Ludwig Maximilian’s University in Munich, completed his residency training at Vancouver General Hospital in Vancouver, before moving to Los Angeles. Dr. Mayer is a professor in the department of medicine, physiology and psychiatry at the David Geffen School of Medicine at UCLA, and Executive Director of the G. Oppenheimer Center for Neurobiology of Stress and Resilience. And Co-director of the CURE: Digestive Diseases Research Center at UCLA. Dr. Mayer, thank you for joining us.
Emeran Mayer: It's a pleasure to be on the show.
David Carreon: So, you've done a fascinatingly broad set of work over your career, looking at your research interests from traditional healing, to hypnosis, to gut microbiology. How did you get such diverse research interests?
Emeran Mayer: Well, there was one common thread that goes through all of this from the very beginning and that is really I've always been interested in the interaction between the mind, the brain, and the body. And just have pursued this from really from college on, and so there's certainly a red line going, a straight line going through all of my visits to different topics in this area. I think right now ... so I was looking at the mind, brain, gut, micro environment interaction so that integrating all of these elements into one, and that's in some ways really been my interest from the very beginning.
David Carreon: Say more about that with the mind-gut connection. How do you conceive of the gut and how is there a connection?
Emeran Mayer: Well, I mean I've been interested in brain, gut interaction for the better part of my career. That topic was in some ways relegated to studying a disease called Irritable Bowl Syndrome, because that was sort of a classic entity where you had psychological commodity, GI symptoms, psychological interventions were beneficial. And then only about I would say seven years ago I developed this interest in including the gut microbes in this communication, so I think right now people are getting so excited about the microbes themselves. I mean there's always been this very intricate by directional communication between the brain and the gut. There's many interesting cells in the gut, but the microbes now play a role in using these various communication channels from the gut to the brain to be included in this dialogue.
Interestingly, and it was never been really great interest of people outside very narrow area of Neurogastroenterologists, until the microbiome arrived. Now, it's almost like everybody has become a gut microbiome expert of brain, gut microbiome expert. As you know there's many books written on this topic, the lay media loves it. And for me it's nice because at this stage in my career I get invited to all kinds of meetings outside of gastroenterology, including the APA meeting.
David Carreon: So, you said something that was rather astonishing I think to most people, that there's a dialogue between the microbes and the person, or the brain. Are there really like signals sent back and forth? How do you justify saying that this is communication?
Emeran Mayer: If you go back in evolution you'll find that microbes were obviously the dominant life form on planet Earth for billions of years, four and a half billion, a billion years, and then at some point there was a decision made by some algae in the ocean to settle inside the digestive system of a primitive marine animal, the Hydra. That animal itself was a floating digestive tube with a nerve net around it. Very similar actually to our GI tract, so our GI tract started ... like the earliest forms of life were GI tracts with an attached nervous system around it.
The microbes started living inside that system, and used their own communication signals that they had developed over four and a half billion years in the oceans to start communicating with the nerve cells of these floating digestive tubes. That actually explains a lot why the gut and the brain are so closely connected. And it also explains why the microbes have developed this ability, not just to communicate with the host but also to most likely exchange genes with this process lateral gene transfer, to the host. You can almost assume that the similarity of some neuro active substances that the microbes can produce, that we know today like GABA and tryptophan metabolites, where actually transferred then to the entire nervous system of these marine animals, and were really the origin of our own neurotransmitters ultimately. So, it's a very interesting story, which I think is quite convincing in terms of why that is happening.
David Carreon: Wait, so the thought is that there was the bacteria are sending their own genes into the host organism, and the host organism is incorporating those and then producing those things that the bacteria want?
Emeran Mayer: Yes. So, that's the assumption and that probably explains why the host has common language, it's common biological language, which goes from the microbes to various cells and receptors in the gut, including nerve cells. And also, since a lot of microbes live on plants, many plants have again, very homologous structures that sort of resemble some of our neurotransmitters. So, this clearly is a certain universality in terms of these signals, and the origin of all this is most likely the microbes that four and a half billion years to develop that language, had 400 times more genes than we humans have. And they have the ability, this ongoing evolution, I mean this is not a static system, so there's constant selection and that may be one of the advantages of having these microbes inside of us, because you can adapt to many things much better than our human system could adapt.
Jessi Gold: So, what you're saying is, there's things that the microbes signal for in us? Like, what kind of things would a microbe want our brain to be thinking, or doing, or can you explain that a little bit more?
Emeran Mayer: Yeah, so that's a very good question. I think right now it's more speculative, the answers, so somebody has suggested that the microbes may actually be able to hack into our reward system, and get us to do things, particularly to eat things that is beneficial for their own growth. And that is not been proven yet, I mean there's a recent study in fruit flies where it's been shown that microbes are able to change the behavior of these fruit flies. I mean obviously in humans and even in rodents we don't have this yet, but there's an interesting possibility for example in obesity where people develop this craving for high fat, high sugary foods. The normal composition of our microbes changes in a way that certain strains start dominating that then send signals to our brain, into the reward system, that makes us crave for these particular food items. Almost then it becomes like a parasitic relationship. It's no longer the symbiosis that exists normally, that everything is beneficial for both players. In this case the microbes then would take over in terms. It's really speculation. You know.
Jessi Gold: Yeah.
Emeran Mayer: But it's intriguing because we don't have the clear answer as what they would like to tell our nervous system, so I guess that's still really a mystery.
Here: Part 3 of a 3-part interview with Richard Bermudes, MD on transcranial magnetic stimulation (TMS). Dr. Bermudes is founder and medical director of TMS Health Solutions and founding member of the Clinical TMS Society. Part 1 can be found here: Transcranial Magnetic Stimulation: A Look Under the Hood. Part 2 can be found here: Transcranial Magnetic Stimulation: The Procedure.
Some say antidepressants work from the bottom up. and cognitive therapy and TMS, from the top down. In this final of three podcasts on TMS, Dr. Richard Bermudes highlights why magnetic stimulation might be an effective treatment for depression, particularly for symptoms that are resistant to pharmacotherapy.
He addresses these questions and more:
. What are the major cortical networks we are trying to change with TMS?
. Where will TMS fit into psychiatry in the next decade?
. What is psychiatry gettimg wrong right now?
Although TMS gives us a third pillar of treatment along with medications and psychotherapy, we don't always know what's going with each individual patient. We need some way to measure a biomarker to measure efficacy, whether we're doing psychotherapy, medication, or some sort of neuromodulation.
Psyched! Episode 2 - Part 3 of 3
Bermudes: Although TMS has improved and give us this sort of third pillar of treatment to have along with medications and psychotherapy, in a way we still don't really know what's going on, with each individual patient, what's going on under the hood. We need some way to measure a biomarker. I think that will help us sort patients and monitor what's going on with our patients, whether we're doing psychotherapy, medication, or some sort of neuromodulation.
Jessi Gold: What sort of symptom differences would mean that you move like, two spaces to the right, or two spaces to the left?
Bermudes: There's a lot of debate about that. You know, I would just say the clinical trials really haven't ... There's sort of this initially FDA approved protocol, stimulation protocol, that targeted at the left front part of the head, or the left dorsolateral prefrontal cortex. There are other stimulation protocols that are emerging, but we don't really have a superior. They all seem to be about the same. Some of the doctors we ... If one's not working, we'll change to another stimulation protocol, because I think we want to do something. When the patient gets better, we assume it's because of that change.
It's much like working with anti-depressants. This person needs some activation, I'm going to add a little Wellbutrin.
Jessi Gold: Prozac didn't work, but we'll try Zoloft because they're so different.
Bermudes: Yeah, or they've only been on Prozac for three weeks. Yeah, they still need a little more active ... You know, they could use like a little more than a cup of coffee. You add that touch of Wellbutrin, and then they come back three weeks later like, "Oh, that's great." It's like, "See?" Somehow my measurement of their symptoms, in this change ... With head-to-head trials, we know that, yeah, they all sort of end up at the same place. That's where we're at with the stimulation protocols, unfortunately.
David Carreon: I know that we can't go into ultimate depth on the neuroscience of it, I mean in the same sort of cartoonish way that anti-depressants ... The story was that there's low serotonin, and so we need to increase the serotonin, but of course there's a lot of problems with that as a theory. We've made adjustments in anti-depressants, and the SSRIs do work, but maybe not by that initial cartoon version. What is, I guess, an equivalent TMS circuit cartoon? What are the major networks that you're trying to change?
Bermudes: Without getting too much into the details, the way I describe it to patients and colleagues is there's sort of this top down approach to some of our psychiatric treatments. There's cortical and sub-cortical loops, or circuits, and generally with depressed patients, they have a lack of cortical control, or sort of decreased top down functioning, if you will, between these areas of the brain. Generally, when you stimulate or modulate the dorsolateral prefrontal cortex, there's sort of this window into this cortical control circuit. What you see in time is increased blood flow, increased metabolism, and downward sort of top down control of maybe hyperactive or hyper-functioning circuits.
It kind of works in the opposite. Anti-depressants seem to, what they say, work from the bottom up. Where cognitive therapy and TMS seem to work from the top down. Where anti-depressants would sort of down regulate limbic systems, and then you'd get more cortical control that way. That's kind of how I try to keep it, sort of at these upper circuits and lower circuits. I got to point to my forehead and then…
Jessi Gold: I imagine it's not the easiest thing in the world to explain.
Bermudes: You know, I think when you keep it kind of, you kind of have these two ... There's obviously more than one network, but when you kind of keep it simple. I tend to be, I'm basically a general psychiatrist. I'm not a neuroscientist. I like to conceptualize things rather simply myself, and then sort of add to the model as I learn more and more about the neuroscience.
David Carreon: Where do you see TMS fitting into psychiatry, say in 10 or 20 years? What do you think this looks like when it's mature and developed?
Bermudes: I think that there's a few ways that our field can develop as a whole, and I think that TMS hopefully will be a part of that development. We talked about some sort of biomarker. I think there's a very big appetite with our field to find a biomarker that will help us sort patients into the right diagnostic categories. I think when we can get that, then hopefully that will help us get people to the right treatments quicker. There's really a big need for a biomarker to provide feedback into the treatments we're rendering. That's with TMS, [inaudible] therapy, as well as psychotherapy.
In terms of TMS specifically, I think one of the things that would be helpful is really finding other target, other, I call them cortical windows or windows into these networks. There are some emerging targets, depending on what's going on with the patient. We might want to move the coil over the supplementary motor area, for example. There's some indications that stimulating in that area of the brain helps people with a lot of obsessional symptoms. In terms of coil navigation, there's a lot of room for us to grow in terms of stimulation protocols, there's a whole variety that are being developed.
Targeting stimulation biomarkers, any of those three variables, that would change, I think the field, as well as TMS would improve.
Jessi Gold: TMS is just for depression, in your mind, or do you think that in 10 years, we'll be using TMS for other illnesses?
Bermudes: There's definitely a number of phase three trails that have been completed and are sort of going to the FDA in the next couple years. I think there will be an indication expansion. Both within psychiatric conditions as well as neurological conditions.
David Carreon: We're coming to the end of our time, and we like to ask our guests a few questions at the end about sort of, rapid fire. A question or two, a sentence or two, and then we'll cut you off after two sentences.
Bermudes: Yeah, sure.
David Carreon: We'll ask some of these questions. First off, what is something that psychiatry is getting wrong, or a major misconception in psychiatry right now?
Jessi Gold: Plain and simple, diagnosis.
David Carreon: There we go.
Jessi Gold: There we go.
David Carreon: I love it.
Jessi Gold: What's your favorite book?
Bermudes: Rapid fire, right?
David Carreon: We're doing it.
Jessi Gold: Yep, exactly. What's your favorite book?
Bermudes: What is it called, The Brain That Changes Itself.
David Carreon: Doidge.
David Carreon: Fascinating book. Alright. Advice for a trainee?
Jessi Gold: Anything? Everything?
David Carreon: You're killing it. This is amazing. Most of our guests incapable of short answers.
Jessi Gold: Yeah, is it because you're a procedural person?
Bermudes: No, no. I really believe there's two things. Reading thirty minutes a day. It doesn't matter what you read. If you have a regular habit, you will change your brain. You will continually learn. It's about idea making. Reading, to me, is the way I keep up. It's not just about psychiatry, it's outside of that.
Jessi Gold: Would there be a person living or dead that you would consider a hero? It could also be a fictional character.
Bermudes: My father, actually. He was a teacher. He was an artist. He had his own construction company. He moved us to ten acres of land, without a well, without heat, electricity. Put a generator, single-wide trailer. It's a wonderful piece of property in northern California. He's passed, but just a really creative individual. He's someone who always told my brother and I that we could do anything.
David Carreon: Last, but not least. What's your favorite color?
David Carreon: Green. Thank you for joining us.
Jessi Gold: Thank you.
Bermudes: Thank you.
Dr. Richard Bermudes (Part 2 of 3): Dr. Bermudes talks about the experience of TMS (including his own) as well as the future of neuromodulation as it transitions from research to practice. He is founder and medical director of TMS Health Solutions and founding member of the Clinical TMS Society. Part 1 can be found here: Transcranial Magnetic Stimulation: A Look Under the Hood.
David Carreon: Have you ever gone under the coil yourself?
Bermudes: Yes, I have. Several times. I think it's a procedure that is ... It's an interesting experience. Certainly I've sat through several treatments, in different systems, some of the coil types are different. I think it's a good thing to do. It's an interesting experience, and certainly, we all have our subjective sort of experience about what it felt like and what it did to our thinking, or mood, or whatnot.
David Carreon: No, I'm a big believer in that and especially done that myself within my own experience. It is really interesting, sort of the subjective effects and how it feels. What was your experience of, what does it feel like during the stimulation? What [crosstalk] the coil itself, when it goes off? What does it, what did you feel?
Bermudes: Yeah, you know, some of the descriptors that we use and that I would use, it's a tapping sensation. For me, underneath the coil, there's a lot of prickly, kind of pins and needles sort of sensation. I think at first, it's a bit like, oh, there is some sensitivity there. It's a sensation that seems to, at least my scalp, I was able to accommodate to pretty quickly. I was able to get up to a fairly high tolerance, even in the first couple of treatments that I did. There are times when we are on the sort of the trigeminal nerve, and there's sort of this optile [inaudible]. You can get some eye movement sometimes, some tearing. I experienced that as well during my couple sessions that I've sampled.
Jessi Gold: Is sampling just something that all people that do TMS do to themselves?
Bermudes: Yeah, I mean, I think experiencing that, sitting through actually complete treatment, I think is important. We actually have our doctors do it, unless there's of course, a medical contraindication. I think it's important the providers and the technicians ... We tend to have them do that.
Jessi Gold: Does it make you happier?
Bermudes: You know, for me, the way that my sort of subjective experience is ... I'm a big time trail runner, and I run basically every day about four to five miles. I get this sort of level of optimism after I run. Clarity of thinking, and I have a lot of ideas that I have during my runs. The four or five times that I've sat through a treatment, sort of randomly, they're not in a row, I have a similar sensation actually. Like I just went out for a nice four to five mile run, and sort of have this level of optimism about the day and clarity of thinking. That's been my experience. Not everybody has those sorts of immediate, sort of experiences with TMS. It can really vary.
David Carreon: I guess it depends on the day and the location. There's so many variables, and I think that the subjective effects of TMS are something that I think you need a lot more work. Because the standard story is, "No, you don't feel anything. It's just sort of the neuro-plastic effects over months," but I don't know. For some of my research subjects, and even myself and lab mates that have done it, there are some pretty significant subjective effects if you're at least either mindful enough or paying attention. It's pretty interesting. One of the times was this feeling of, for me it was more or less of a euphoria and more of a confidence, more of a mastery or control feeling.
Bermudes: Yeah, I would say it was that way for me as well. I tend to feel that way after I run. It's sometimes euphoric, but yeah, definitely a sense of here's what I'm going to do today and I can do it. Clarity of thinking.
Jessi Gold: Do you feel like if everybody felt like that, then they just wouldn't go for a run and would just put a magnet to their head?
David Carreon: What about recreational TMS?
Bermudes: I actually have thought about that. I'm kind of glad I get that, because it provides a lot of positive reinforcement for me to run. There are times when I start out in the day not wanting to, and I just sort of tap into that feeling. I'm getting this done, because I know I'm going to feel this way. Yeah, I'm glad there's not like a little device in my closet that I can kind of access, because I certainly know that I would slide on the exercise.
Jessi Gold: I think everybody would.
David Carreon: Any lab break-ins or clinic break-ins to TMS stimulation?
Bermudes: Not that I know of or will admit to.
David Carreon: This does raise the question of, I mean I know that with antidepressants, some of the probably more fringe opinions, but you know, everybody would be better if they were on an antidepressant. That antidepressants make anybody happier. Would you say something like that might be true of TMS, in a different world with different laws? What do you think it's doing to you or to me, to make us feel good, and is that a good idea?
Bermudes: I actually have some reservations about that, because I think that from a data point of view, we know that there are certain patients with clusters of symptoms. We can take patients with a certain score on the PHQ-9 or the [inaudible], and we know they have elevated depressive symptoms. We do a history, and we diagnose them with major depression. We know a certain part of them will have, basically network problems, so to speak. Broadly spoken, so there's sort of network disconnect. If we utilize TMS, we know that that network function improves, essentially. I'm trying to speak broadly, because without getting in to the specifics of the different networks that have been named and claimed, so to speak.
I don't know that if we modulate sort of, healthy networks, that are in a homeostatic balance and functioning the way they "should be," that that is necessarily a safe thing to do. I think it's one thing to sit through one or two random treatments, and it's another thing to get stimulated four to five days a week. I wouldn't put myself through that sort of protocol unless there was really clear evidence that I needed a particular network modulated. There was a point when people talked about how, what would the world be like if everyone were on Prozac. I think we're past that. In fact, I've even read some editorials about, is there an increased level of treatment resistance that we haven't seen before? Could the prolific use of antidepressants maybe contribute to that? I don't know. I don't know enough about antidepressants to be able to speculate on that, but-
Jessi Gold: Like antibiotic resistance somehow?
Bermudes: Maybe, I don't know. I know that sort of, there is an editorial by [Inaudible] recently in brain stimulation, where there's pretty clear evidence that the chronic resistant depression that we're seeing today is definitely less responsive to medication than what they were seeing in the late 90's, for example.
David Carreon: That brings up, I think this is also something that is a new idea for me at least of recent years in psychiatry, of sort of ... There's some sort of a story of psychiatry where we have these diseases, and they're fixed. The prevalence is fixed, and they're just sort of, you drew the unlucky genetic hand. Things don't really change, and there's no real cultural influences. It's just sort of this fixed lump of a field. We come up with treatments and the diseases don't move. You're sort of describing psychiatry almost like the world of infectious disease, where sometimes new things come up and resistances develop.
It's just sort of this, much more dynamic process, that brain stimulation now is a possible way to treat something that is now no longer responsive to antidepressants. I guess that's a different world than the sort of fixed universe that people maybe described before.
Bermudes: Yeah. I think we're all very, I think psychiatry, I hope is moving sort of ... I don't know what the word is. Kind of trans-diagnostically beyond the DSM-5. There's some usefulness to the DSM-5 or DSM-4, but I've started to think more in terms of network connectivity. I think that's what TMS has taught me, is that some of these older models. The serotonin, the [inaudible] hypothesis. I'm a cognitive therapist, so there's sort of this cognitive model of the mind. Before that, there was the more psycho-dynamic, sort of models. Those were useful at the time because they drove treatment at that time.
I think TMS and other modalities that involve neuromodulation, DBS, DNS, TDCS. It's really about the network, and can you associate a network or a dysfunctional network with dysfunctional behavior, emotions, [inaudible], et cetera? Can we then develop stimulation protocols, patterns, frequencies, that can sort of bring those networks more into balance? I think it is dynamic. I don't know if there's a cure out there. The brain is incredibly dynamic. We're in a dynamic environment, and one environment for one person can produce sort of illness, where another person can have the same environmental stressor and only take something like abuse, or divorce, or bankruptcy.
These are big environmental stressors that a lot of us will encounter at some point during our lives. They don't all produce the same problem with the brain. I think it is very dynamic, if you will.
Jessi Gold: Then if someone comes into your office, is there a depression space in the brain that you're just putting a magnet, or how does that work?
Bermudes: Yeah, so I'm talking about this new, sort of way to think of the brain, but in a way, I don't have biomarkers to tell me what's going with each person who comes into our office. We're sort of stuck with this diagnostics symptom-based, we measure very carefully the symptoms, and then we make assumptions of where on the cortex the magnet needs to be. What sort of modulatory pulse sequence needs to be prescribed. Then what we do, is we have people go through treatment, but there's no biomarker feedback with that. We do more measurement with symptoms, and then we make assumptions about what's going on in the brain based on that.
Transcranial magnetic stimulation: an exciting FDA approved technology in psychiatry. But exactly what is TMS, and why should psychiatrists—and perhaps even the general—public be aware of it?
That's the key question the hosts of this short podcast (the first in a series of three on the topic) put to Richard Bermudes, MD, founder and medical director of TMS Health Solutions and founding member of the clinical TMS society, Inc. Here, Dr. Bermudes talks about some basics: what these devices look like, how they work, and about the patient experience.
David Carreon: Welcome to Psyched, a podcast about psychiatry that covers everything from the foundational to the cutting edge, from the popular to the weird. Thanks for tuning in. This is David Carreon.
Jessi Gold: This is Jessi Gold.
David Carreon: This is Psyched. We have with us today, Dr. Richard Bermudes, the founder and medical director of TMS Health Solutions. He earned his medical degree from the University of California San Diego in 1997. He served as chief resident for the family medicine and psychiatry combined program at the University of Cincinnati, then completed a fellowship at the Beck Institute for Cognitive Therapy and Research in Philadelphia. He's the founding member of a clinical TMS society, and he chaired the first annual meeting in 2013. Now was elected president of the society in 2015. Dr. Bermudes, thank you for joining us.
Bermudes: Thank you.
David Carreon: I wanted to talk to you a little bit about TMS. This is something that is a new and exciting technology in psychiatry, and just wanted to give you the chance to talk about ... What is TMS, and why should psychiatrists and maybe even the general public be aware of it?
Bermudes: That's a great question, and actually, it's a question I think about a lot. Probably too much. In its simplest form, TMS is transcranial magnetic stimulation. It's an FDA approved treatment for adult patients who have not responded to one or more anti-depressants, medications. In its basic form, we're using high powered magnetic coil to generate energy across the cortex. We're using that to modulate populations of neurons, so to speak.
David Carreon: You're taking this device, and walk us through, what does the device look like? If you're a patient walking into the office, what happens to you?
Bermudes: Well, the devices are pretty ... Each device essentially has a few components, but there's generally a stimulator with a bank of capacitors. This basically is a way for energy to store up and be discharged quite quickly, in milliseconds. This current then goes through a coil. There are various shapes of coils, the most common being, there's kind of two shapes that are pretty common. I won't digress yet, but basically, this current gets discharged into a coil, and then perpendicular to that coil, a fairly high powered magnetic field abruptly is on and then off.
This happens, it's a fluctuating current, which produces a fluctuating field. It's because it's not static, because it's fluctuating in milliseconds that it actually affects [inaudible] channels essentially. The discovery of this in the 80's by Mark George and others, that really kind of took our initial offering of, basically we've been waving magnets around the brain for quite a bit of time trying to change it. It's sort of this notion that it's a fluctuating current with a fluctuating magnetic field that makes it pretty powerful for the brain.
Patients would see, generally there's sort of a cart, or some sort of bank, or stimulator. Then there's some sort of arm that holds these coils. There's usually a user interface for the technician or physician to sort of navigate that coil around the person's head. There's generally some sort of medical looking chair to these systems as well.
Jessi Gold: I'd imagine patients don't get exposed to magnets in their brains very often. Probably the only thing they know from magnets would either be like, the little kid toys or maybe an MRI or something like that. Does that come up? Are people nervous about the idea of a magnet on their brain?
Bermudes: We get a lot of responses when we talk to patients about this procedure. I think it really depends on the patient, how they're conceptualizing their depression, or how they've been taught to think about their depression. Certainly, the experience of treatments and then, what treatments they're also being offered. For example, if I'm talking to a patient who's been on five, six, ten antidepressants and has suffered a lot of side effects, maybe have had an MRI in their life. The fact that it's a magnetic field, you know, they've had the MRI before, they know that's tolerable. Had side effects from the antidepressants, it's generally not a big deal to think about. Particularly for patients with moderate or moderately high or severe depression. They've been suffering for years.
It's not a first line of treatment. It's generally third, fourth, fifth line treatment. For the right patient population, it's actually pretty acceptable. Sometimes we have to clarify that it's not ECT. Patients will ask, "Are you going to shock my brain?" We're not generating a seizure. This is sub-seizure threshold. TMS actually introduced the idea that we could do neuro-modulation without generating a seizure and improve mood.
Jessi Gold: Since you brought up ECT, is there a reason why TMS doesn't get the reaction that ECT has? You know, right outside there were protestors. People tend to be pretty scared of ECT. The press has kind of destroyed it at one point and it's come back into fruition. They don't necessarily know it's better. Is there a reason TMS hasn't had that same reaction?
Bermudes: I'm a big believer in ECT. I used to do ECT. It's a very powerful treatment, very effective treatment. We don't have to overcome the kind of stigma that I used to have with patients who were getting consultated for ECT. I think some of the reasons, you know, not having to go under general anesthesia. It's a treatment that is accessible for patients who aren't as severely ill as those who are getting ECT. It's an outpatient setting. There's been no cognitive side effects associated with this procedure. All the modern day stimulation protocols for ECT, the cognitive side effects are pretty mild to non-existent.
You know, you started battling that legacy with ECT. I think people have been able to differentiate the two treatments.
David Carreon: You say it's not shocking the brain, but come on, it's a pretty powerful magnet you're putting out. 1.5 Teslas for a lot of these guys. That's a pretty hefty stimulation, isn't it?
Bermudes: Yeah, so it's kind of an interesting dynamic when we're demonstrating this with patients, because on the one hand, I'm saying, "Yeah, it's a fairly benign procedure. The seizure is rare. It's a benign procedure. The seizure is rare. It's not what we're trying to induce. Here I'm going to place this over your meta-cortex, and I'm going to get your thumb to move." That's a pretty powerful demonstration of how we can do non-invasive neuro-modulation at this point in time. It is powerful, but it doesn't have that stigma.
Our discussion this month was with Dr. Paul Appelbaum. It ranged from the history of current settled ethical positions to hot issues in ethics and law in psychiatry today. We discuss the history of involuntary hospitalization, genetics, human freedom, and responsibility and how these issues impact practitioners, patients, the legal system, and the general view of psychiatry in the public.
Also, in the context of recent political events, we discuss the Goldwater Rule, which prohibits psychiatrists from commenting on the mental health of public figures and really try to understand its origins and purposes to the field of psychiatry.
About Paul Appelbaum
Paul S. Appelbaum, MD, is the Elizabeth K. Dollard Professor of Psychiatry, Medicine and Law, and Director, Division of Law, Ethics and Psychiatry at Columbia. Dr. Appelbaum went to Harvard Medical School and his residency at Massachusetts mental health center. Dr. Appelbaum is Past President of the American Psychiatric Association, the American Academy of Psychiatry and the Law, and the Massachusetts Psychiatric Society, and has twice served as Chair of the Council on Psychiatry and Law and of the Committee on Judicial Action for the American Psychiatric Association (APA). Dr. Appelbaum is currently Chair of the DSM Steering Committee for APA, and of the Standing Committee on Ethics of the World Psychiatric Association. Dr. Appelbaum performs forensic evaluations in civil and criminal cases, and treats patients with a broad variety of problems, including depression, anxiety, and adjustment problems. Twitter: @appelbap