B (9:19)

I am so, so excited to be here with you and to have this conversation.

A (9:24)

So before we get started, I know I just did an intro. Is it actually, like, let me go off on a tangent right off the bat. Is it actually called neurobiology? Is that what you do? And what does that mean?

B (9:38)

That's such a great question because the term neuroscience really is such a broad term and it means, right, the science of the brain. But there's so many levels of inquiry by which we can look at the brain. And for me, neurobiology is looking at the biological substrates, the biological underpinnings, what is going on on a cellular systems level, on a molecular level, what's, what's driving this. But you know, you can look at it more broadly and it transitions and translates to cognitive concepts and psychological concepts. And I think more broadly it speaks to the point that people sometimes look at the brain versus the mind as two different things. And there's a lot of debate about that. But in my view, in the view of most people who do this work with me, they're the same thing. The brain is driving what we consider the mind. So long story short, with neurobiology, we are looking at biologically, what is going on. But that speaks to the broader way of looking at science and all the different levels of how they interrelate to come up with ultimately what we're experiencing and how to do anything about it.

A (10:39)

It's literally mind blowing. That sentence you just said blows my mind. So let's just go straight to it, shall we? What is going on in the brain of someone with ocd? Maybe even let's say as you explain it, like comparative to someone who doesn't have ocd. Can you share? I know that might be like a 24 hour training, but like, can you give us a little bit of an understanding? And I want you if you can like speak to my level where I, I know a little, but let's pretend I know nothing.

B (11:15)

That's my favorite thing to do, like to make these things accessible and understandable because that's what science should be. And I promise it won't be with so much jargon other than maybe naming things so people can google those different brain structures and stuff. But it will be understandable. That is my goal and that's what I do as a science communicator. So thank you for opening like that.

A (11:34)

And the reason I say that is like, you can get into the research and I have. And before you know it. You're reading words that you're like, I am in another language. Right. So, okay, what is going on? Like, literally what's going on.

B (11:48)

Yeah. So as we were talking about, there's different levels of looking at things. I'll start from the brain structure level, the different parts of our brain, and on a high level, how they're communicating with each other, both in, let's call them healthy people, healthy controls, and people with ocd. And I'll say up front, this is what we think we know in the world of research. We don't claim to fully know anything because there's always so much more to learn. And we can always, with new technology and new findings, reconceptualize what's going on. So this is what we think we know from decades of evidence, and yet there's also so much more to know. And that's usually not a fun answer for people. They want a straightforward 100% certainty in both in OCD and also in science. There's no such thing.

A (12:36)

Yes, it's a good lesson really, isn't it?

B (12:38)

Yeah, it's funny that I've chosen this career of absolute no certainty ever.

A (12:44)

Well, wait, wait. Actually, before we even go there, tell me about why you do this work.

B (12:51)

I do this work because I live with. I have lived with severe debilitating OCD for my whole life. Before doing this work, before being labeled as a scientist doing this research, I had a completely different life. I was completely and utterly debilitated by OCD and other disorders as well. Ptsd, Major depressive disorder, that was treatment resistant, generalized anxiety. It's really fun being me, but I was born into a family that had no understanding of mental illness and I had no access to treatment and it was extremely stigmatized. And I also had no idea that there was anything wrong. I just believed that that was life. And from the earliest parts of my life, my intrusive thoughts governed everything about me. Everything from harm thoughts, perfectionism. Early on, before my brain had a lot more to latch onto, it was about making sure people were safe and just doing physical and mental compulsions to manage my entire life. And I just thought that was life. And as I progressed through life and many other things happened to me, traumatic incidences, almost dying from cancer, many other things. I truly just believed that I was a monster and I wouldn't be able to live. I ended up dropping out of college after two years because I was that dysfunctional with the 1.87 GPA. At my very worst, I was fully Housebound, I could not communicate with other people. And I attempted to end my life many times. And I'm very grateful that I didn't succeed at that. Because finally, at age 25, at the brink of all death, even going through cancer treatment and wishing I would die through cancer treatment, which is a very strange experience to have, I finally came across what real OCD actually is. I was also under the myth of OCD being an adjective and something to describe being neat and quirky. And I never had any idea that that was what I was experiencing and what had governed my entire life. I had been at that point misdiagnosed and mistreated by 22 different clinicians. I had been admitted to inpatient facilities, I had been on suicide watch. I, you know, from the time I was onward. And I just never received evidence based or effective treatment. And I had always internalized that as this is really just evidence that I'm a monster and I should die and this is all my fault. Not that I'm just not being treated correctly by proper clinicians. So from the Internet, from people like you, who have been so open and generous with their education online, that's how I ended up learning about what OCD really was, through the Gateway of Anxiety, Anxiety advocacy, I guess. And I learned for the first time what ERP exposure and response prevention treatment was. It was extremely difficult to buy into that when I had been mistreated with psychodynamic therapy, traditional cognitive behavioral therapy, emdr, so many other things for so long, and I'd been told that all of my thoughts were caused by something in my childhood or something about me that was actually based on things I wanted. So it was really hard to believe that there was a treatment out there this whole time that could have helped me that I just never got from 22 different professionals that were psychiatrists, licensed therapists, psychologists. But with the last shred of willpower I had before I fully ended my life, I ended up starting to engage with erp. And it was such a transformative experience for me. It wasn't linear. I'm still in it three years or four years later because I have comorbid ptsd, which I know that you've been really open about with your own journey too. And that's made treatment a little bit more complicated. But even with the gains I have made in my life, it's fully turned my entire life around. I've been able to go back to college, earn my bachelor's, earn my master's in neuroscience, I'm doing my PhD in neuroscience right now. And the reason that I study OCD is because I want to understand what's going on in my brain and in the brain of people who I love. OCD is one of the most understudied and underfunded conditions out there because of such a lack of correct understanding in our field about what it is and the fact that it deserves more awareness and attention and funding to further the way we understand. We're so behind in OCD compared to other conditions. So, you know, there's just been a light under my ass. Am I allowed to cuss on this? Yeah, there's been a light under my ass since I started experiencing what recovery looks like of, you know, this is unacceptable, that we don't understand this and people seem to not care to understand it. So I have shoved my way into academia and I'm not someone who is the typical trope of someone in academia. I'm, like I said, I'm a non traditional student. I had previously failed out of college. Most of us don't end up making it to a PhD program. People who are open about their lived experience, especially with taboo and harm themes that I've been open about for so long, we end up not being allowed into these systems because there's so much discrimination and stigma against researchers who disclose lived experience. And I've just been trying to move forward as much as I can.

A (17:49)

And you've succeeded. You've just told me like a short story that made me feel every single emotion I could feel, like devastation, anger, sadness, grief, absolute shock and joy and pride. And that was a roller coaster story that you just told us.

B (18:08)

Yeah. It's been such a small amount of time relative to the decades I spent, like completely dysfunctional, that I've now been in recovery and living a life that completely feels like a, like a third lease on life. And I still cannot wrap my head around the fact that I'm here alive, let alone doing this, let alone having this conversation with you. So thank you for letting me share that and I appreciate that too, because it's really important to me as I talk about neuroscience and neurobiology and all the research, that it's centered and rooted in my lived experience and the fact that I understand deeply the pain. There's often such a disconnect between people doing this work and the people who have the condition. And that's, that's a failure of science communication and inclusion. And when I'm talking about this, it's from a place of understanding truly what these symptoms are and it's informed the way I can do this work and the projects that I'm building because of my very deep understanding of the condition and looking at things people haven't looked at. So I just appreciate getting to center everything we're going to talk about today in my own lived experience and being able to use real life examples.

A (19:12)

Right. Well, number one, I just. I'm so sorry you went through all that. I, I have heard your story before, but I don't think I really grasped the depth of it. It's just, first of all, you just must be so proud of yourself. Are you?

B (19:30)

No, I'm working on it. That's.

A (19:33)

Yeah. That is like the best story ever. It's like a movie right there.

B (19:40)

I, my, I'm working through treatment on allowing kind words like that to actually permeate through and to cultivate self compassion. The thing that I told you about a few years ago, I just makes me cringe. But I appreciate that so much and maybe one day I'll get there.

A (19:56)

Yep. Well, I think that's it.

B (19:58)

Right.

A (19:59)

And I think, true, we won't get into this too much today, but I'm sure that the brain of PTSD is also a very hot topic for people to understand because that too. Am I right? There are differences in the brain of someone with PTSD as well, which makes this more complicated. And that was a big shock for.

B (20:18)

Me to understand absolutely, 100%. And my ultimate goal, long term with research is to understand the overlaps and things that distinguish OCD from PTSD because they are two distinct disorders. But there's so much overlap and so much predisposition on both ends to develop the other if one has one. So 100%. Yes. So there's a lot going on in my head and I have to develop compassion for that. But given the stark difference from where I was to where I am now, it's hard for me to still remember that. I'm still, you know, I still clinically score moderate to severe for ocd. I'm still in treatment. I still need to give myself grace and compassion and, you know, I don't need to be a hundred percent, but it's, it's a work in progress. And everything I do, including this podcast, including every single time I step in the lab or every single time I open my mouth about research is an exposure and to my, My fears of saying the wrong thing about my memory, about my integrity. So it's very full circle.

A (21:16)

Yeah. Well, I'm just so grateful you're here. Truly, I am I'm so grateful for the work you're doing because as a clinician, we can talk about tools and strategies and treatment all day long. But I've had so many clients who have said, oh, understanding the brain helped me come to grips with the fact that it. That this is not made up, that I didn't just. This isn't a story. It's not because I'm weak. It's not because that I'm broken. There's actually something just like if it was diabetes or another condition that's so validating and helpful.

B (21:52)

It's so helpful for the people experiencing it. It's also so helpful to dispel the. The myths that go on in the world of OCD not being a real condition or just like an exaggerated form of anxiety or it being just a quirk or myth. Like, no, it's a neurobiologically driven condition that's extremely obvious, and we have so much data on that. But to your point, before we get into the science of it, I do think it's interesting that some people appreciate the biological perspective because then it helps them interact with treatment, but they tend to prefer more medication, like pharmacological treatment, because they conceptualize a brain disorder, quote, unquote, as something that can be treated by drugs. And then there's some people who prefer to look at it more like a psychological condition because then it makes therapy make more sense. But circling back to what I said at the beginning, there's all the same thing, and all of our experiences and therapy changes the brain in the same way. Maybe not the same mechanisms, but the same way as medication. So it's all the same and both there. It's not either or, it's both. And at the end of the day, it's all. It's all biological. We all experience it as something beyond biological, but it is driven by this organ in our brain, and all treatments are working on the same thing. So I just wanted to add that to that.

A (23:11)

Okay, so this is a perfect segue. Somebody walks into the office of an OCD clinic. Let's tell the story. So they went. The day they walk in, what is going on with their brain? And then we'll talk about what happens as they walk out and they've completed treatment, and maybe even contrast what happens if they're on meds. Can we sort of take that structure and story?

B (23:35)

Totally.

A (23:36)

Okay, so someone's coming in, or let's say they've learned about OCD for the first time because they've listened to this Podcast or yours or social media, what's going on in their brain.

B (23:47)

We'll start talking from the vantage point of brain regions, and we can narrow down, we can go more broad from that. But starting from brain regions, we have our cortex, which I'm sure people have heard, prefrontal cortex or frontal cortex, there's different parts of that. So we have the orbitofrontal cortex, the ofc, which is right behind your forehead. It's sort of the brain's what's important center. And it decides something that we call salience, which is how important this stimulus or this thought or the thing we see is what to pay attention to or what to worry about or what to just feel discomfort around. In ocd, this region seems to over detect or exaggerate potential threats, which can look like anything, right? The more classic examples in the world are things like contamination, which are extremely valid and important in the same way. Also, if we have a random intrusive thought about harming a child, our OFC is going to take that and make it more important, because we're having it, because it scares us, because it's something that we don't actually identify with versus someone with. Without ocd, we always say everyone has intrusive thoughts, but not everyone's intrusive thoughts end up being sticky. It's because people are able to filter that out more. We also have something called the anterior cingulate cortex, which is near more of the midline of your brain's frontal region. And the ACC is typically monitoring conflict and error to where when it's hyperactive, when it's doing too much, it can constantly signal to us like something's off, something's wrong, you know, and offs may be a better word because there's also just right ocd, and whatever the case is, it's telling us something's strange or off. And that can fuel more anxiety or disgust or distress or shame or whatever emotion is going on. Because as we know, OCD is not just anxiety. There are many other emotions that can be in that cycle, and many people have all of them, like me. And then ultimately the ACC and the OFC are driving this urgent need to address whatever that intrusive thought is. Then from there, the cortical regions, the ofc, the acc, they project to something called the striatum, which is part of the basal ganglia. Some people might have heard the basal ganglia in terms of basal ganglia, encephalitis, which is a whole other conversation. But this part of our brain is buried deeper and there's different parts of the striatum. There's the caudate, putamen, and the nucleus accumbens. We don't need to get into the details of that. But essentially, the striatum influences habit formation. It's telling us both what to do and what not to do. And then there's this constant balance of go and no go and what. What movements, what behaviors, mental and physical, should we engage in versus what should we not? And those are, it's not either or, it's both all the time. And that balance is what's modulating how we're existing in the world at all times. In ocd, because of that overactivity of the frontal regions that we talked about, it's telling the striatum what to do. And in ocd, the striatum can get sort of stuck in gear and ultimately drive repetitive mental or physical behaviors. So once the OFC is calling something highly important or salient, like in a very clear cut case, like a doorknob being contaminated or an intrusive thought about harming a child, something terrifying and scary to someone, the striatum is going to compel someone to do the same behavior or ritual over and over again. And the balance of go versus no go is imbalanced, which then projects to a part of the brain called the thalamus. The thalamus sort of acts as a relay station, and it funnels a lot of our sensory and our cognitive information back upward to the cortex. So it's a loop, the cortical, striatal, thalamic, cortical loop, which is way more complex than it sounds. But overall, just look at it like a circle. And in this case, when the thalamus, which is really deep in our brain, it's taking all this sensory information, everything that just went on with how important we thought our thoughts were and all the behaviors that we did. And then over activation of the thalamus and poor gating of what's important versus not important here then means that intrusive thoughts can keep passing through back to our conscious attention, and it reinforces the cycle. We've heard often in OCD treatment that by doing compulsions, we're reinforcing the cycle, where that's how it's happening. And the thalamus is also influencing our physiological arousal and responses. So, like the panic or the, you know, our body freezing or sweating or our heartbeat or whatever, which, when that happens in our body, whether we have OCD or not, that's supposed to tell us that perhaps something is going on that we should pay attention to. Oftentimes, in many conditions, this is not working well, and it's giving us these signals way more than we need. But nonetheless, if you don't interrupt this pattern cycle, it's going to reinforce everything we just did and tell us to do it more and more and more. So that's a high level of the circuit that drives ocd, and at least the one that we're most focused on. I do want to add really quickly here, because people always talk about the amygdala, the fear center, and they implicate that as the main part of ocd. It's not. We're not saying it's not involved. The brain is the most complex organ in our body. It's so fascinating. I mean, that's why I've dedicated my life to trying to understand this organ. Right. And there are so many structures in our brain that are communicating to each other with, like, billions of cells all the time. So it's definitely not as easy as saying that. It's just these four things that I describe, like, even between or even within the cortical regions, there's so many cortical regions, and I talked about, like, two of them that are doing things, but they're doing so much more. Even, like, to talk to different parts of the striatum. I didn't want to go into all that detail, but I say that because there are so many other regions, like the limbic regions, like the amygdala, our memory center, the hippocampus. Like, everything's involved, and it's involved because these regions are talking to all those other regions at the same time, but they're not reliably involved. Where everybody who has ocd, for example, like, has an overactive amygdala. If that were the case, one, this would be an anxiety disorder, and it's not. It involves so many other emotions. And not everybody has anxiety when they have ocd. Right. Two, like, there's downstream effects of the corticosteroidal thalamic loop being overactive, such as in some people, the amygdala being more hyperactive. Some people have memory issues. Some people have, you know, more just. Right. Symptoms that can involve the insula. There's so many other structures that then get talked to differently by that first circuit. But I just want to say that upfront, because there's a lot of misinformation that goes around about neuroscience, period. People are trying to talk about it when they're not trained, and it's it sucks. But, like, one of the biggest ones is like, OCD's and amygdala disorder. Not true. And some of the most fascinating, funny data to me to dispel that is in deep brain stimulation surgery, when people are having, you know, things implanted in their brain to stimulate certain areas, the amygdala isn't one of them. It doesn't work. So. Right. Not part of what we're talking about.

A (31:03)

Okay, I have so many questions. You mentioned the amygdala. Is that a big part of general anxiety disorders?

B (31:11)

Yes.

A (31:12)

And so those other pieces that these, these four parts with OCD are less. Are less a part of, let's say, generalized anxiety disorder than they are OCD?

B (31:22)

Yes. To the point that the DSM 4, I'm sure, you know, like, had anxiety and OCD in the same category and the DSM 5 split them. And yeah, the DSM is not perfect. And we can have like an existential conversation about our diagnoses, even real. But in the world where we're talking about diagnoses, the. One of the main reasons that OCD was moved to its own category was because it does not share the same neurobiological substrates as anxiety. And if they were looped or if they were lumped together in the dsm, most companies that are trying to develop treatments or researchers developing treatments would be lumping them in the same category to like, this drug will treat anxiety and ocd, and that's not true. So in order to help spin off and encourage OCD specific treatments, they had to put it in its own category because they don't share the same neurobiology. It doesn't mean that, like, you know, I know ERP can be helpful in both conditions and many clinicians do use it. That. That doesn't change that. It's just that what's driving the disorder and how are we intervening, especially on a biological level, it's really important to parse out the two.

A (32:26)

Oh, so good to know. Okay, next question. I've got. I could go for hours here, but what you're also saying is this cycle for OCD isn't the same for all subtypes that some people with more discussed obsessions. It looks different to some who have just right OCD or more just like Homo cd. You know, is that true?

B (32:54)

I would say that as far as we understand and the way we conceptualize it, this could change in the future. So I'll always add that caveat. Yes. This. The circuit that I described, the corticostriatothalamic cortical loop tends to be how we reconcile like OCD as a whole. And it probably is the case that most people with OCD have that general dysfunction. More so in terms of different subtypes, different themes, different experiences is more like how that loop then downstream affects other brain regions, might look different in different ways people are experiencing or getting treated for ocd. And that's been shown in some translational literature too with like disgust based OCD being maybe treated slightly differently. Yes, this is for more of an advanced audience. Everyone do first line evidence based treatment for sure. But like when you're with a clinician who specializes in disgust based, maybe there's some other ways of handling it versus more, you know, even rooted in ptsd, for example, like that's something that I've been going through for years and how I treat my OCD and PTSD with a trained clinician, it's slightly different or has more considerations and probably has something more to do with my hippocampus and my memory center. So it's more that, yeah, the circuit is probably generalizable across ocd, but how that circuit and all the bazillions of different connections between these regions and how they implicate everything that they talk to might look different in other people.

A (34:20)

So interesting that I did not know and that is so interesting. Okay, all right, so you're walking into therapy. That's what's going on with your brain as you start to engage in ERP or some type of behavioral change. What shifts in that process in the brain? Is there any shift and what does that look like?

B (34:47)

I would overlay the shift to what treatment looks like and interrupting the cycle because we talk about the OCD cycle all the time. We can also look in parallel and really the same thing, but in the brain to this circuit, this cycle where I just described all this over salience, these intrusive thoughts, then going to our motor center and telling us what to do and us feeling like we don't have control over behavior. So then the physiological sort of reinforcers of all that that then tell our brain to do it more and more and more in treatment. We're interrupting that and it's, it's pretty difficult to say exactly like where in that cycle we're intervening. And I'll also say that we're also trying to understand in the population like where does this start? Because we're. I did start talking about the circuit like it's the ofc, but like I said, it's a circle and it's like.

A (35:38)

It'S chicken and the egg.

B (35:40)

Exactly. So it's like where, like perhaps was the. In some people, maybe the striatum started being super overactive with repetitive behaviors to some random ass thought that, like, if we'd interrupted there, then it would interrupt the cycle, versus for some people, interrupting more at the ofc's part of it versus the thou. You know, there's. There's so many. We. We don't know exactly where to interrupt in general, but specifically with erp. But ERP seems to interrupt at all parts of that in that we. Some people say that through treatment, their intrusive thoughts in general go down, and some people it doesn't, but then they're able to not do those behaviors. So either way, you're getting that benefit. But getting back to your original question, when we're going through exposure and response prevention therapy, what we're doing is we're experiencing those intrusive thoughts. And instead of doing that behavior to then reinforce that cycle and tell our brain that that thought or that fear, whatever mattered, we're just not doing that compulsion, which is extremely difficult. It sounds so simple. Say it for 10 seconds and it's done. Is taking me years to do so. I understand how hard it is, but in principle, when we're doing that, that projection from the cortical areas to the motor areas, we're interrupting that by, hey, we have that thought. But we're not automatically just doing this behavior anymore. And by doing that, we're experiencing that whole peak of what that intrusive thought can look like and all of the emotions that come with that. And we're allowing that to happen without doing that behavior. And then ultimately that experience from the intrusive thought ends, which is wild to experience when you've done compulsions your whole life. I know that's been the case for me. And when we show ourselves that we can tolerate that intrusive thought and that behavior doesn't need to be. Need to happen, then our physiological response to said behavior isn't happening anymore. And it's not reinforcing that cycle, that repetition, that. That association. We talk a lot in neuroscience about this phrase called Hebbian learning, where neurons that fire together wire together. You're literally interrupting that cycle. And it's a lot more complicated than that. But in sum, you're changing your brain by doing therapy.

A (37:53)

And is that the definition of neuroplasticity? I know a lot of people ask, I think what happens with the term neuroplastic is we think of plastic as A hard thing that doesn't break down. But can you give us a definition of what neuroplasticity is?

B (38:09)

I'm glad you asked because I appreciate that the word neuroplasticity has made it into the zeitgeist. And as something that means that our brain can change. And that's absolutely true. It's so much deeper than that. As someone who literally studies on a cellular level how synaptic plasticity happens, how the actual structure of a cell can change in response to stimuli, in response to drugs, in response to literally changing anything about the cell environment. Like I'm looking at the actual cell and the synapses on the cell change and grow and the spines change and grow. So like on a very, very micro level, your brain is able to change for better and for worse. And I think that's really evident. That can sound scary, but it's also really empowering in that, you know, we, we, we grow through our life and we're constantly changing. We're constantly meeting new people, we're learning their names, we're going outside, we realize like, oh, that's a busy road, like, I'm going to drive on a different road now. Like, we're always changing. Obviously we can change negatively where if we experience an extremely terrifying life threatening trauma, some people can develop ptsd like it's. Our brain can change all the time. And in the same way we're also, you know, learning and change is essentially the same thing with learning and memory. We're learning positively, we're, we're learning negatively. And in the case of treatment, we are able to learn different habits, different ways of thinking, different ways of, of responding to something that we've automatically responded to for so long. And yeah, it can be really difficult and it can take a long time, but we can do it. So it's an empowering concept and we can just call it neuroplasticity. But I just want to make so clear, like it's not just this effervescent cool concept that, oh my gosh, we can change these people, like literally everything, like in our brain, like we can change the way our cells look and interact with each other and then the way our brain regions interact with each other and perhaps the way even our brain regions look now. It's not like a magic cure. And I wish I could wave a wand and I could change my brain so much that I don't have OCD at all. One day we can get there, hopefully if we all work on it. But for now we can Change enough to be functional in the world again.

A (40:18)

Okay, pause for a second. My curiosity is killing me here, so I'm laughing at myself. So you're telling me you walk into an office and you're like, looking in a brain. Like, what does that mean?

B (40:34)

Oh, I would love to talk about this. I walk into a lab, which is close to an office, but it doesn't look like this. It's exactly what you imagine. It's like a scientist. Yeah.

A (40:46)

And do you have a cap on and a gown and the whole thing?

B (40:50)

I have a lab coat sometimes. And sometimes if I'm just not working with live animals or brains anymore, it's more tissue that's been processed. I'm not going to wear a lab coat. They're really hot and annoying, but they look cool. But I'm wearing gloves. I'm wearing gloves. I'm wearing, like, all the required things. And I particularly, like, literally work with brains and cells and. And I'm like, actually taking brains out of living creatures and most of the case, most of the time animals. And we can talk about why animal models matter. I also work with human brain tissue as well. And then I'm like, literally, yeah, postmortem human brain tissue from people who've donated their brains. And I will be one of those.

A (41:30)

I donated my brain.

B (41:32)

Literally. Like, we. This is a sidebar, but we're ordering. This sounds really weird to say out loud. We're ordering brains of OCD patients. And unfortunately, like, in the United States, from the National Institutes of Health, across all the universities, there's like 40 something brains. As compared to other psychiatric conditions, there's thousands. So that's another reason why OCD advocacy and awareness is so important, because there's such a downstream lack of, like, we don't even have enough brains to look at because people don't know they have the condition to know that they should donate their brain or that even if they did that they could label it with OCD on top of like, whatever they have. So that's. Sorry, that's such a side tangent.

A (42:09)

How do we order an OCD brain? Is it like you go on to like an Amazon inventory? Like, what does this even mean? My brain is like, so excited right now.

B (42:19)

I. I was gonna say I wish, but I don't wish that it was that easy. There's a. There's something called a neuro brain bank, which is more broadly, like, when we donate our brains, they're put into banks of, you know, all of our organs and stuff. And this neuro brain bank, at least in the United States, is run by the National Institutes of Health. And they have different. They have six different brain banks at different institutions, including Harvard, University of Miami, whatever. And wherever we are closest to. And we're. When we die and our brain is going to be donated to, will go to one of those. And then I go on this website, actually me and my boss, because I'm. Luckily I'm not qualified enough to get it all on my own. I need like, there's like so many. Yeah, we have to make sure, like this is such precious tissue. Like, we have to make sure the most legitimate researchers are getting it who have the best rationale for what they're doing. But yeah, basically it ends up looking kind of like a menu where you, where you go and you put in obsessive compulsive disorder. You can put in different, like you can choose the sex if you need to, or different age groups and whatnot. And then you have just like a list of de identified people without their names but all of their information. And then you just click all the samples you want. You also pick the brain regions that you want and how you want the tissue prepared. And then they send it to you.

A (43:29)

And then you don't have a whole brain. You could just get a prefrontal cortex if you wanted.

B (43:33)

Yeah, and ideally we aren't getting the whole brain because, like, we're not experts in how to harvest brains. So like, that would be so much pressure on us. Like, we're just getting the, like that tissue homogenate is what we're using. So it's like they take the. Not even just the pfc. You can subcategorize all of these brain regions into really small parts. So, for example, the amygdala, we always talk about that. First of all, in our field, we don't even have a general consensus of how many parts of the amygdala are. But the highest number I've thought is, I've heard is 12. So literally our brain is that subdividable into different regions. Right. Anyway, so we pick whatever we want that's relevant to our research and we have to provide rationale. And then they send us these tiny little homogenous. And from there we have to be really strategic about how we use it to its maximal efficiency. And so, you know, mostly with human brains, we're not able to look at too much in that state other than like protein levels. And that can be correlated to or reverse translated back to animal models. And like, what genes are driving that protein Expression and is it different in different brain regions? And I can. That's what my thesis research is.

A (44:36)

So does it come in, like, a cooler?

B (44:41)

Yeah, it's in. It's in dry ice. It has to be, like, negative 80.

A (44:46)

You're way off track.

B (44:48)

No, I love this. I know people. I love when people want to know this process, because it's my whole life, and people just. I think people, like, they talk. They think I'm working in some office, and I'm just, like, looking at cool pictures of, like, human brains. Like, no. I'm literally, like, pipetting brain tissue with my hands. And, you know, with animals, like, Like, I'm doing brain surgery, putting viruses in them to look at different conditions. And I'm taking these brains out, and I. With, like, all day long. And then I'm harvesting them, and I'm cutting them to thin slices, and I'm visualizing them on a micro level. Like, it's. That it's. It's literal, like, science.

A (45:20)

With our hands, you, like, jump up and down with excitement. I would be, like, clapping. No.

B (45:25)

Thank you for saying that. Because people think it's disgusting. And I'm like. And I. Funnily enough, an example of my ocd. Like, I. I feel such, like, joy and euphoria and excitement when I can do an experiment. Well. Or when I got, you know, the results I was looking for. Or when I master a technique which can take years, because this is a very grueling, long, thankless process to become a scientist. And my OCD used to. And sometimes still latches onto that. Like, wow, you're so excited that you successfully, like, ended an animal's life and you, like, did something with their brain. Like, you're such a bad person. It's like, both can be true. But, like, no.

A (45:58)

I'm so excited. Maybe I'm a bad person, too. Let's just be. Let's just allow that.

B (46:03)

Oh, my gosh. If you're a bad person, I'm happily gonna do that.

A (46:06)

I'm like, does it come in. Does it come in a cooler?

B (46:09)

Like, no, literally. And I'm walking around with, like, dry ice and these, like, brain samples just happily, like, walking around the building to put it away.

A (46:19)

Totally get that. Okay, so I'm sorry I took this off, but I'm so. That was my favorite part of my week. That little. Little or offset. Okay. All right, so then let's say somebody starts medication. Is it the same process in that the medication reduces them from doing those behaviors, which stops the behavior, the cycle, or does the medication do something different to stop that cycle?

B (46:44)

So medications, as it currently stands, we're mostly talking about ssri, serotonin, selective serotonin, reuptake inhibitors, right? Sometimes there's also secondary medications that involve dopamine. But the thing with medications as they stand is that you're taking them and they're affecting the same system across the entire brain. There's no way that we have at this moment to specify where this medication is going in the brain to interrupt a particular part of our brain or circuit or whatnot that's in development and is really. It blows my mind. Like, science is magic. Like, people, science is the coolest thing on earth anyway. So that's currently being developed, but that's not what we have right now. So in that way, medication is very different in that it's going everywhere and we're kind of just modulating whatever neurochemical that we're working with in the case of SSRI is, it's serotonin primarily everywhere. And we aren't necessarily able to figure out where in the brain we're targeting. And so, one, that's the case. Two, we're not, with current medications targeting what we think is wrong with OCD in the brain. Like, there's, you know, a specific serotonin deficiency. So we're using SSRIs, like, that's not what's happening. SSRIs were found by accident to help depression as well as OCD and other things. Interestingly, other antidepressants that don't involve serotonin don't seem to have the same effect in ocd. So it's like a happy coincidence that we found that SSRIs can help with OCD, but it's not targeting the pathophysiology of, like, what is wrong ocd. I'm not saying either that there's not like a serotonin issue with ocd. It's way more complicated than that. But overall, this medication is being used to harness capabilities in the brain to do different things, as opposed to, like, there's something wrong in ocd, we're taking a medication to fix that thing. So with that, serotonin works sort of as something that can turn up and down the dial of activity. It's. It's found all throughout the brain, but it's actually by far not the most, like, commonly found chemical. That's glutamate. And that's also something that's being looked at for OCD, too. But overall, SSRIs are changing the way the brain is communicating overall, and that seems to help with OCD and also SSRIs or serotonin medications in general, or rather serotonin helps with the brain to be able to change itself. So getting back to that point, if we're administering a medication, we can take advantage of enhanced synaptic plasticity for the brain to change itself in response to erp, in response to treatment. And I also find really, really interesting that in the current literature of putting ERP versus SSRIs against each other, like, which one works better, alone or together? ERP has been shown to outdo SSRIs, and SSRIs can amplify that effect. Not for everybody it can, but on their own. Yeah, there are some people that have reported benefit, but most of the time that isn't what works for people. And that's because you're enhancing the ability's brain to change itself. But to do what?

A (49:48)

Yes. Okay, There are some people who have an onset of OCD when they have some hormonal changes, either teenagers or even, you know, perinatal cases. Is it just simply that hormonal changes can, like, turn the switch on that cycle?

B (50:09)

So in terms of different average ages of onset, there are a few ideas of, like, why things may be happening. Then when we look at more of the childhood side, it's, you know, our brains are developing and that circuit is maturing more, and so it can come on more easily there. If people are predisposed in that way, based on genetics, which we can also talk about genes after this if we, if we want. That's also something I'm very, very interested in sharing information on. But in terms of later onset, either in adolescence or puberty, there are hormones that are modulating the way these neurochemicals, like serotonin and dopamine and other ones, especially neuromodulators, are acting. So with. That's sort of maybe the second spike that people see in terms of age of onset and then in terms of stressful life events, but especially things that involve hormones like perinatal ocd, postpartum during menopause. These events and the hormonal changes can definitely influence the activation of circuits and can. It's like pouring gasoline on a fire that already exists. Which people also ask, like, why are there flares in OCD sometimes? Like, why isn't it just linear, especially if you do treatment? Or why are there relapses? Well, we are working on interrupting that circuit, but we're not breaking it. We're not, unfortunately. We're not curing it. So there are many things that can cause that circuit to work on overdrive again or to pour, you know, fire, or pour gasoline on that fire that is kind of simmering all the time.

A (51:34)

Right. We might need to do a part two here eventually. But I noticed for me that my OCD can be really well managed. And then one night of not getting enough sleep sets me back so far. What's that about?

B (51:53)

Same thing in that it's all. These are all stressors to our brain and our body. And if our brain isn't working correctly, it can cause compensatory changes where our brain is trying to overcompensate for what we're lacking. And that often includes the brain structures I talked about that are involved in every single part of our existence. So it's really nuanced, it's really complicated. And at the same time it's pretty simple in that if you throw something off course or if there's some lack or, you know, you get sick or whatever the case is, that can influence overactivity and under activity again and again. Of course, the good news is we can also intervene after and we can get things back on track and we can practice our skills. And that's something I want to share in terms of hope for people in that no matter, I have to stick to this because my OCD is very strong and it's. It's worse sometimes than others. And I haven't quite gotten it to a point of subclinical yet, but I always have to remember that I am always working from an upward spiral, that I'm always facing OCD with all the skills and techniques and experience that I've now had. So no matter how bad it feels or how strongly can come back, you are facing it with everything you've already experienced. You're not facing it anew like you did at the very beginning, which is so hard as much as it feels that way, because logic doesn't permeate ocd, reason doesn't permeate it, it's our experience. But just remember, you've dealt with it and you can again.

A (53:17)

Okay, let's say you've done your treatment, you are at a subclinical or you no longer reach criteria for ocd, you start to get booster sessions, you're coming out of treatment. What does your brain look like then?

B (53:30)

That's interesting question because there's some data that have done brain scans on people with ocd, which I want to quickly say that brain scans are not the end all be all of us understanding anything in the brain. I just talked about using animal models. Brain scans are extremely. They're a great tool, but they're very behind in their capability. And that's why we do not use brain scans to diagnose individuals with OCD or any other condition. If anyone's telling you that it's misinformation and run. But we do use scans to look at the differences between groups of people using statistical power. So, like hundreds of people who have OCD versus hundreds of power who don't have ocd. And we're comparing very subtle differences between the two too, because brains are really complicated. Right. But we can see subtle differences. So I say that tangent to answer your question, in that there have been some studies that have shown less hyperactivity in those frontal regions and to the circuit becoming more balanced. And even the morphology of our brain, like the thickness of certain areas changing as a response to treatment. That's not the case for everyone. And also there are so many variables that can go into that because are they medicated, are they not? Where in their treatment are they. How long did they have it to begin with? Did they have. Have those changes before treatment? Like, we don't know. But we have seen some changes in the brain and how it's communicating and what it looks like in that circuit for certain people, not for everyone.

A (54:55)

Yep. So good to know. In fact, as I think I mentioned to you, I'm redoing all of my OCD courses for the clinician and the sufferer, and I actually included those images because I feel like it gives people so much hope. But it's so good to know that it's. That's actually not the full picture. Right. Those brain scans isn't like, oh, look, your brain's fine now. Like. Right, yeah, exactly.

B (55:17)

Because that's. Because we can't whether someone's in the thick of OCD or after or before. We can't look at anyone's scans and decide if they have the condition to begin with or not. Sometimes it's like it's an outlier and it's. You would guess with way more confidence. Yes, but. But no, in terms of structure and function. And also, like, there's just such variability amongst people in general. Like, many people who don't have OCD might still have some part of that looking that way for a whole host of reasons. So it's just. It's also just so nonspecific in that when we're looking at functional imaging and we're looking at how active a certain part of the brain is. Like, we don't know why. We don't know, like, what chemicals are involved, what cell types, what's talking to what to make that happen. Like, that's why we have to go outside of human models to go into animals who have similar brains to us to be able to directly manipulate. I think you'll think this is cool. We use lights. Like, literally blue lights. Like, we do these tiny little surgeries and we're doing blue lights and we're turning on and off cells and seeing if we do that, how does their behavior change and what. How does the cell change from there? Like, we have to get that specific. And unfortunately, we can't do that in human brains. It would. I don't think anyone would want that. So, yeah, it's.

A (56:27)

Yeah, don't set me up for that.

B (56:29)

But I just want to give you.

A (56:30)

My brain when I'm dead. But I don't want you to do that to my brain.

B (56:33)

And unfortunately, unfortunately, when you're dead, we, at this time, we can't really do anything about how it's functioning. We can just look at what it look like when you're dead. So there's. That's why there's limitations to every single model. And that's why human imaging studies are the very beginning of giving us hints to what we should look at more mechanistically and preclinically. But we can't do that with human brains right now. And I just. I have to drill that into anyone listening because there's such a misconception about that.

A (56:55)

Right. Okay. I have one more question before I let you go, because I want to be respectful of your time.

B (57:00)

So genes, Genesis.

A (57:01)

I know. That's what I'm gonna ask. I got diagnosed with OCD in my 40s. I have had an eating disorder. I have had generalized anxiety my whole life. I don't think my parents or my grandparents had OCD that I am aware of that I can honestly get in information. So what is going on with the genetics? Is it. We know that there is a genetic component. We can use me as an example of. Like, okay, so it makes sense that if my grandmother or my dad or somebody had it, it would make sense that genetically I would have more likely to have that. So tell me about the genetic component.

B (57:43)

Yeah, that's one of the biggest questions I get. Genes are so complicated. Just like everything else I said in that there's not one single gene for many mental illnesses that anyone has ever found to cause a disorder or even a few, it ends up being, you know, hundreds of them. And in the case of ocd, just to put numbers to it, it's determined to be around 40% genetic. But we, and we think they're going to be probably 4 to 500ish genes found. And we until last year literally had zero of those. And the reason for that is not because it's not there, it's because we have to do something called genome wide association studies where we're looking at people who have OCD and people who don't. And we're looking for those very subtle differences in their. It's not even, it's not necessarily different genes, it's different expression of those genes, different single nucleotide polymorphisms or different alleles. And we need millions of people for those studies. So similarly to the whole issue of we don't have enough postmortem brains of people with ocd, we also have nowhere near enough people in these genome wide association studies because again, there's such a lack of understanding and outreach and the fact that what is even OCD for people to know, to enroll in these studies. So for other comparable conditions with the same amount of incidents like schizophrenia, bipolar disorder, we have, you know, hundreds of thousands, millions of people. Last year we had finally one paper come out for OCD that had like, I think 30 to 40,000 people, which was more than ever, but still hardly anything compared to what we need. We need millions and millions of people to definitively find these differences. And so that's going to be a long time and a lot amount, a lot of work. And hopefully conversations like these inspire people to donate, you know, tissue samples or spit samples to these. It's so easy to do, but we just need more people to do it. All that to say, how do we do that?

A (59:34)

Is there a place we donate aspit to?

B (59:37)

Yeah.

A (59:37)

Can I ship it to somebody?

B (59:39)

No, actually, literally, yes. There are different studies going on. You know, Eric Storch, like his lab and working with, he works with different genetic researchers to have. They're actually expanding it for beyond white people because like so much of the other issue is these samples were predominantly white. There was a Latino project that was looking at people from Latinx communities. They're starting an Asian project that I'll be a part of that I'm really excited about. So all that, but we need also white people and other samples too. You can find all of that on the IOCDF website. They're generally recruiting for these. We need all of us who have platforms, as, you know, especially people with bigger platforms, to post about these, and then more people can donate. But it ends up being very simple where you get sent a kit, you just swab your cheek, or I don't know what, like put it up your nose, some version of getting your data, and then just you send it back and there you've donated to research forever. And it's really, really easy. But. But with that, I like to say that ocd, because of its complexity and just like other psychiatric conditions, it's. It's more like the complexity genetically of. Of height, as opposed to something like Huntington's disease, where there are one or a very few genes that definitively show one has the condition. These psychiatric conditions are so complicated. And what I want to clearly say about genes, like, why do genes matter? Because I think there's a disconnect between genes and what happens in our brain. Genes help dictate the way our brain is shaped and forms and functions and what our cells look like. And so that connection of what genes are doing to our brain, we have hundreds that are going to probably all subtly change the way our brain forms to ultimately lead to ocd. So coming back to your question of why you might have OCD and your parents don't, it's having enough of that genetic predisposition and enough of those risk genes, those risk alleles, like hundreds and hundreds of them, to finally maybe predispose you to having OCD. And that's only 40% of the explanation. You have that whole, you know, pulling, as many people say, like pulling the. I don't know enough about guns, but there's like a gun of like, you. You load the gun, I guess, but then like, pulling the trigger. There's that simple word environment. But that means so much more than just like, what's around us. It's literally age and experience we have of stressful life events, of traumas. Like, there's what's out around us. There's oftentimes like infection triggers or virus triggers. That's the whole Panspanda side of things. There's so many things that can ultimately cause those genes to be expressed. There's also something called de novo mutations where, you know, your parents don't have something, but you're born with it. And why did that change in your. You? We don't know, but we're trying to figure that out. So there's so many factors that lead to genetic components and otherwise ultimately OCD coming out from people. But I do want to say that it is very much a biological disorder in that genes are biological, our brains are biological. And I want to use that to dispel the myth that it's just. Oh, yeah, like, some people just develop ocd, and if they have enough resilience, they won't.

A (62:41)

It's almost like all the stars need to align perfectly, and if they happen to it. Clips on.

B (62:52)

Yep. Would you agree? Exactly.

A (62:56)

Like, you might. You might have the stars. They might be moving around, and. But nothing happens until they all line up perfectly. And it's sort of like it unlocks something.

B (63:07)

Mm. And that's. I mean, that's why we have so much more work to do in figuring out how those stars came to be and how they aligned what line they're in. Does that line look differently for different age groups, different backgrounds, different people? And ultimately, will there be any way to identify risk early on? And I want to say at this time in April of 2025, there isn't. So if anyone's selling you that, don't buy it, because it's not true. I wish we had that. And people try to sell. Sell weird scientific tools to identify things. We don't have it, so.

A (63:38)

Right.

B (63:39)

We need to figure that out. Yeah.

A (63:42)

This has been the most fun conversation I have had in the longest time.

B (63:46)

I love how much you love it, because so many people want to talk about the science, but not about the nitty gritty. And I appreciate you letting me do that. And I will literally come back and talk to you anytime about anything more often. I know we didn't even cover, like. Like, 30% of what we said we would.

A (64:01)

No. But I feel so good about what I know now. I loved this conversation. Thank you so much. If there's ever a specific research that comes out that you want to talk about, let me know, because I feel like. I mean, for me, it just gets me totally geeked out. And you are like, a freaking genius in understanding this stuff. It's so cool.

B (64:25)

Well, thank you for saying that. I don't think it's me being a genius. I think it's the fact that I care so much, and I can and part. And a huge amount of my care is because I have it and because so many people I love like you, like, other people have it. And there's so much. There's such a disconnect of the information and all the amazing work going on by these people, and I'm trying to do it too. And then the people who want to know and they're just not talking to each other. And it's so empowering and exciting, even if we don't have all the answers, to know that so much is going on and that we can contribute to it. So I think that's what you're picking up on and I. That's why I'm invested in communicating it accessibly. So hopefully that happened. Also, if I would love to come on in the future, talk about psychedelic research, because that is what I'm most excited about pharmacologically. And that's dbs, all the things I'd be happy to.

A (65:11)

Okay. Thank you so much. How can people get a hold of you, learn about you, get, you know, hear about your. What you're doing?

B (65:21)

I thank you so much for having me. Thank you for everything you do for the community, first and foremost, people like you or who have kept me going, especially as a scientist who doesn't have enough people around me in my everyday life who understand the real struggle of being someone living with this condition. Thank you for being such an ally and for being so vulnerable and for being just the kindest human. I called you Sunshine two years ago on my podcast and I. You're only more Sunshine now than ever. So thank you for being you and. And for me, I'm. I'm everywhere. I have a podcast called A Chat with Uma where I bridge research and lived experience to talk about my own journey of survivorship and talk to so many people like Kim, who was on my podcast a few years ago, and hopefully I'll bring her on for so many more if she'd be willing. And I also talk to other researchers who are doing this exact work, but I make their work accessible to people like us who want to know what's going on. So you can find me on A Chat with Uma. I'm on social media everywhere at Umar Chatterjee and I'm happy to answer any question ever as best as I can. And mostly I just appreciate everyone's interest in science and research and making it understandable because it should be accessible to everybody and hopefully we can do that together.

A (66:30)

Thank you. So fun. Thank you truly. It's been so much fun.

B (66:34)

Thank you.

A (66:37)

Please note that this podcast or any other resources from CBT cbtschool.com should not replace professional mental health care. If you feel you would benefit, please reach out to a provider in your area. Have a wonderful day and thank you for supporting CBTSchool.com.