Latest / The Biological Psychiatry Podcast / Trauma Exposure and the Visual Cortex
Transcript
- Elvisha Dhamala: And then just get uploaded. So even if it starts to freeze during the episode, that shouldn't be an issue until unless if the whole thing crashes out, which we have happened before. Alright. ⁓ Can you just start by saying your name and title exactly as you'd want it to appear in the episode? Nate: Mm-hmm. Mm-hmm. Yeah. ⁓ God, I wish I I I knew that was the one question I wasn't gonna prepare for. ⁓ so Elvisha Dhamala: Or it could just be the affiliations that you want mentioned. It doesn't have to be the actual titles. Cause I have just McLean at l hospital and Harvard Medical School, but I don't know if you have others that need to be in there. Okay. Nate: Okay, perfect. ⁓ no, that's perfect. So Nate Harnett, assistant professor at McLean Hospital in Harvard Medical School. Elvisha Dhamala: Okay, perfect. Thank you. Alright, so to start things off, what do we know about how PTSD affects brain structure and why is the visual cortex in particular an area of interest? Nate: It's a really question. So, you know, we have been looking at the neurocorrelates of PTSD for the better part of almost three decades now. And we've learned a lot in terms of how chronic PTSD is associated with brain structure, brain function, all these different aspects of neurobiology. One of the things that we see pretty often are changes in what we typically consider threat neurocircuitry. So this is regions like the prefrontal cortex, hippocampus, and amygdala, regions that are really involved in emotional processing, threat learning, and threat responses. And what we often see across the prefrontal and hippocampal regions are these reductions in grade minor volume, in cortical thickness that we think is related to the emotional deficits that we see in PTSD. One of the things that my lab and many other labs now across the country have been looking at is how do we use brain structure to predict who's going to go on to develop PTSD? So shortly after someone experiences a trauma, how can we image the brain? What regions come out as most predictive for if they go on to develop the disorder? And something that we've seen across several data sets now is that this structural organization really of the visual cortex. What I tend to lean towards looks a lot like the ventral visual stream is seems to be uniquely predictive of PTSD. So in recent trauma survivors and a couple different data sets, we've shown that there are these positive associations between this thickening volume sort of covariance in PTSD symptoms. And then later on, as we look at chronic individuals with PTSD, ⁓ we see this sort of flip in this association, really suggesting that something is happening with visual cortex. That might be really related to ⁓ intrusion symptoms or the development of negative alterations in cognition and mood. Perhaps this flip from acute to chronic might be related to changes in how these symptoms express over time. Elvisha Dhamala: Great, so as you mentioned, PTSD research often focuses on the threat neuroscircuitry, including the regions that you described, like the amygdala hippocampus, but here you were talking more about sensory processing. Can you give us an overview of what that circuit overall looks like and why it might matter? Nate: Give me one second, Alicia. I know I have the answer for this, but of course we start recording and my brain goes, ⁓ my God, do I know anything about these brain regions? Don't put that in. Don't put that in as like a little a fun little social media clip. So I'll give a very honest answer that's that seems a little bit less canned, hopefully. But the way in which we approach When we think about how the brain is processing information in PTSD, we think about, as you just mentioned, in terms of that threat neuroscircuit, but we often think about it in terms of, well, people are just learning incorrect associations, right? Like there was something dangerous, and now that's being attributed to something that's safe. But there's this sort of implicit assumption that information that gets to these threat neuroscircuits. has already sort of valence neutral, right? Like that it doesn't really have any effective properties. And I don't think that's entirely true. The way in which visual stimuli gets into these different brain regions through a couple different pathways. The one that we focus really on goes from the retina through the algal nuclei and then through hierarchical processing through these early visual regions, visual areas one through four, that then move on through the ventral visual stream, this sort of canonical what pathway, this object recognition pathway. And what might be happening, what we think about in my lab and a couple of ⁓ other groups now are starting to think about is is it that there is information that as it is hierarchically processed, something is happening, some dysfunction of how that stimulus is appreciated as it moves through this stream might be then making its way to these quote unquote higher order, threat-involved brain regions, and that is sort of compounding. the emotional difficulties that you might expect. And so we really think about these sensorial circuits as being important, not just for, okay, can you see the thing in front of you, but how are you actually processing and working with these other higher order brain regions to understand the meaning of what you're looking at? Elvisha Dhamala: Great, so essentially these sensory areas need to take in that information of the stimuli before it can then get passed on to the threat neuroscircuit and have a downstream effect. Is that correct? Nate: That's such a much more succinct way of what I said. Thank you. Yeah. Elvisha Dhamala: So overall, a central goal of this study is to distinguish brain changes related to trauma itself from those that are tied to PTSD stims ⁓ from those that are tied to PTSD symptoms. Why is that distinction in particular important and what are the implications of that distinction? Nate: So PTSD is a very unique psychiatric disorder because it is one of the few disorders in which we know what the cause is. Definitionally, for someone to be diagnosed with PTSD, they have to have experienced trauma. And that offers us a really unique opportunity to time lock when their symptoms simply must start. And so if we can look at what's happening in the brain as close to trauma as possible, we want to develop. Biomarkers that help us understand who's susceptible, who's going to go on to develop the disorder, but also biomarkers of treatment, who's going to be most responsive and most receptive to different types of interventions so that we can prevent the development of the disorder. The problem that we run into though is that if you only look at associations between you know, what the brain looks like soon after trauma and PTSD symptoms two weeks, six months, twelve months after ⁓ the event, you're really only understanding if there are these sort of associations, right? Like things that might be sort of predictive. What you might be missing though are sort of unique adaptive potentially responses or even maladaptive responses that are due to the trauma itself. And if you want to have biomarkers, they're gonna be really functional. They're gonna actually predict what you want to predict. You need to be able to differentiate between is this an impact of trauma, in which case it could lead to PTSD or it could not lead to PTSD, depending on individuals' individual variability in susceptibility or resilience, or is this really a biomarker of the psychiatric disorder that you care about? Elvisha Dhamala: That was a great explanation. Thank you. so you mentioned the visual areas V one through V four. For listeners who aren't familiar with the anatomy and that visual processing ⁓ pathway, can you tell us what the regions do and how they work together? Nate: I can. Do vision scientists listen to this podcast? Because they're gonna yell at me, ⁓ which is perfectly fine. They're allowed to do that. ⁓ so I I think as everyone knows, ⁓ or I think as as some people might be aware, the the the visual cortex has long been a study in imaging research. It's a long study in neurophysiology research, because so much of what we do every single day involves taking in visual information. And so There's a lot of work that's been done on trying to understand very specific things that these regions do. In a very broad sense, you know, information that hits our retina and that passes through the lateral genic nucleus to get to the visual cortex is first processed in V1 and it builds hierarchically. So V1 is processing very, very basic stimulus information like lines or edges or spatial orientation. V2 builds on this to ⁓ help. discern boundaries of different stimuli to help understand contours of those stimuli. V3 can build on that further to understand a little bit more about what objects you might be looking at and whether or not they're moving. And then V4 builds even further to understand sort of more complex geometric features. And then all that information is then spread if we're thinking about the ventral visual stream as opposed to the dorsal visual stream, to the inferior temporal gyrus, to V5, to MT, to other regions that again subsequently build. One thing that's very interesting about these circuitry, or that the about this circuit in particular, is that a lot of times we think about them as like it just builds in one direction, but it's actually a recurrent processing and feedback loop. And so information that passes from V1 to V2 and V3 and so on actually can go back for certain regions. And so you can have this very interesting relationship between regions where yes, they're feeding information forward, but they're also feeding information backward. And you think about that in regards to say the threat neuroscircuit. where information has this sort of affective or emotional valence to it, this emotional tone, how then might that sort of feed backward into these other regions? And does that impact the way in which you process these sort of visual information? So ⁓ you know, getting back to your earlier question, understanding how these regions in particular might be important for BTSD and trauma has been really important for us. Elvisha Dhamala: So let's talk about your study design. You have a discovery sample and a replication sample, and they differ in very and they differ in important ways. So they have different demographics, different scanners, different clinical assessments, and even slightly different control groups. Why use two different samples to begin with and how does this actually strengthen your findings? Nate: Yeah. So the first reason to use two different samples is it's always nice to be able to show that you can replicate an effect. When we initially started doing this research in the discovery sample, we said we were we thought that we were gonna see some difference in visual cortex thickness that was related to trauma and probably related to PTSD too. And we did see something related to PTSD, but the thing that came out strongest was this. difference in cortical thickness between individuals who've been recently exposed to traumatic event and individuals who had not recently been exposed to traumatic events, about 30-day window, and V1, where these recently trauma-exposed individuals showed greater thickness in visual area one. Which I think that sort of as a heuristic is sort of hard to wrap your head around at first, if only because a a lot of the way in which we treat you know brain thickness or brain volume is that That is a measure of brain health. So more thickness or more volume, that's that's better. And stress is bad. So it should lead to less brain health. So why is it that individuals who just experience something really stressful, really traumatic, might actually show what we want to infer is greater brain health, but really let's think about it as just cortical thickness. And so that is already sort of an uphill battle in terms of like, well, did we do something wrong? Did our is our sample just weigh like very, you know, idiosyncratic, esoteric in some way. ⁓ and very luckily we knew of a data set that had some of this very similar data, had a very similar design ⁓ from my original dissertation mentor at the University of Alabama at Birmingham, Dave Knight, ⁓ and ⁓ his collaborator Amory Knight. And so we thought if we found this here, we should at least test it and see if we find it again. And if we find it again, we want to report it. If we don't find it again, maybe just bury it. No, we wouldn't do that. But like it was really important to us to say, like, is this real or did we do something wrong? And so when we found it in the replication data set, that was really sort of a moment for us to say, okay, we think this is a real thing, that there's something biologically happening right in area V one that has to do with trauma exposure. Doesn't seem to be related to PTSD, but it's at least related to trauma exposure. And so let's try to figure out what that might be. Elvisha Dhamala: So that is a great segue into my next question, which what does this greater thickness actually mean biologically? And what are the potential mechanisms that might be driving that increase in thickness? Nate: Yeah. I think that's a great question and it's the response to it is my favorite answer, which is I don't fully know. So there there are a couple caveats to why we could or couldn't know, but one of the things that we thought about was that maybe, just maybe, you know, throwing things out there, maybe that maybe trauma exposure would be associated with not sort of neuronal atrophy, but maybe some sort aspect of neural genesis. Is it that ⁓ right after trauma exposure, individuals have this like proliferation of neurons within a month. That doesn't sound very plausible, but you know, we thought that might be an idea. So we actually, in addition to looking at cortical thickness, also looked at cortical volume. These are sort of distinct metrics in how they're calculated. Thickness looks at the distance between the white matter and the peel boundary, volume looks at sort of the amount of gray matter itself within individuals' voxels, and we might use that as a proxy in. Other sort of prior animal research has shown this is a good correlation for the amount of neuronal bodies. When we looked at gray matter volume in these samples in both the discovery and replication sample, we didn't see any differences between recent trauma and non-recent trauma individuals. And so that really suggests that it's not it might not be really sort of neural changes. It might be something else. And so maybe there is sort of neuroimmune responses, neuroinflammatory responses as a result of. experiencing that traumatic event and that's in leading to some sort of like micro edema, like a little bit of fluid building up because of that immune response. That is sort of the the end of where we came. But you know biologically I think we're leaning towards at least for this acute phase after the traumatic event, maybe there's some sort of immune response that's driving this increased thickness. And maybe you might expect it to among individuals who don't develop PTSD to go down over time. Elvisha Dhamala: So as you mentioned, this change in V1 thickness that you observed was related to trauma exposure, but not symptom severity overall for PTSD. What exactly does that tell us in terms of the acute versus chronic effects of trauma on these brain regions? Nate: Yeah. We can glean quite a bit, I think, about the acute effects, right? Because all of these imaging data, at least for our recent trauma exposed individuals, ⁓ across both samples, was collected within about 30 days after the traumatic event. So at least acutely, we're we're pretty confident in inferring that trauma may, and I want to be careful about my wording here, may lead to an increase in cortical thickness, at least in the short term. One of the interesting differences between the discovery and replication sample data set is that in the discovery sample, our non-recent trauma survivors were just non-recent trauma, and the replication sample, they were non-trauma exposed. And so the fact that we don't see differences in both groups or both data sets really suggests that over time this sort of difference in V1 thickness may dissipate. ⁓ And again, might not be related to PTSD. This might just be sort of the body's natural response for whatever reason to experiencing ⁓ an acutely traumatic event. It's difficult to know without subsequent imaging data. Like if we had image people both at that sort of initial one month, three months, six months, maybe twelve months, ⁓ maybe one day we can get the funding to do that sort of study. it'd be a lot easier, I think, to know like, okay, is there s what what is the sort of time course of that thickness and does it really subside over time? ⁓ and part of the reason I'm trying to be careful is I I had it drilled into me very early on that it's it's a bit of a faux pas to say change when you're doing a cross-sectional study. ⁓ these are all individuals collected after the traumatic event. ⁓ and so we don't really know what their ⁓ brains look like right before. Although I think, you know, I I I lean towards that it's probably change. Elvisha Dhamala: So going a little bit further up the visual pathway, you also looked at V4 and saw that it was negatively associated with PTSD symptoms, but this was only in the discovery sample. So what might V4's role in the visual processing overall have to do with symptoms like intrusions and flashbacks, and why might your results not have replicated for that specific analysis? Nate: Mm-hmm. Can you give me like literally one second? Because I realized as you were asking that, I was like, I forgot to read my own paper and make sure I know what I say before ⁓ before the last thing I want to do is come up with a brand new inference and all my co authors are like, excuse me? What are you talking about? ⁓ Elvisha Dhamala: Of course. Totally fine. I've definitely done that. I'm like, I wrote this a year ago. I don't know what I said. Like Yeah. Of course. Nate: I can't remember. All my ideas changed like the week after we published these things. ⁓ I'm sorry, one more time. It doesn't have to be super great. What was the question again? Elvisha Dhamala: And it's okay. So in contrast to what you saw with V1 thickness, V4 thickness was negatively associated with PTSD symptoms, but only in the discovery sample. So what might V4's role overall in visual processing ⁓ have to do with that? And why might those results not have replicated? Nate: Yeah, it's a good question. I I think that in comparison maybe to the V one findings, the the ventral V four findings fit a little bit more of our heuristic that stress would be associated with that sort of aspect of lower brain health, right? If we wanted to really simplify it. And if we're gonna do, I think, a little bit of reverse inference, we we really know that V four is very involved in object recognition, especially for complex geometric ⁓ shapes and things like that, that it's really involved in selective feature extraction. And one of the things that we think about in PTSD is this sort of over-generalization of acquired threat to new safe threat. So this idea that when you learn that a cue predicts an aversive outcome, you start to generalize that association to other cues that don't necessarily predict that aversive outcome. Because you're trying to maintain the sense of safety. And part of what we might think is that maybe there is the disruption in this brain region that's really important for recognizing what exactly it is we're looking at and for having that understanding of the complex shapes that can help differentiate these objects. And maybe that helps contribute to fear overgeneralization in some way, right? There's sort of this inability in some cases, or perhaps to really differentiate. between these different objects, at least at like a very basic neural level, maybe not at a conscious level. ⁓ One thing though that I that you brought up is that we didn't see this in both data sets. We really only saw this in the discovery data set. And it's really unclear to us if that is a function of the type of measure we used or the type of sample that we included. ⁓ You know, the discovery sample I think had greater PTSD symptom severity overall compared to the replication sample. But it's unclear again if that's because in one we used a PCL and one we used a PDS, right? Different measure, different ways of measuring these PTSD symptoms. And so the jury, I think, is still out in terms of whether or not that is going to be a generalizable finding, but that's sort of where we're sort of landing with what we think, what we might hypothesize is going on. Elvisha Dhamala: Another interesting thing you found is that the trauma related thickness differences were specific to the visual cortex. So you didn't see them in terms of global cortical thickness or in other regions like the prefrontal cortex. What does that tell us? Nate: So interesting. I forgot that we did that. Elvisha Dhamala: I love educating you on your own work. Nate: I keep I feel like I keep I feel like we keep getting distracted because I don't even know what I did. ⁓ Yeah. Yeah. Yeah yeah yeah wait wait wait. It's all coming back to me now. All coming back. Yeah, the fact that we only saw these findings in visual cortex and it was robust to a number of different covariates, including just using, you know, global or average cortical thickness, ⁓ in some ways was a nice confirmation that this is sort of V1 specific, and other ways adds to our confusion about what these sort of threat neuroscircuit regions that you know other large-scale analysis have shown in PTSD ⁓ might be doing or if the thickness and volume and just general neural structure differences might be something that builds up over time, right? So we can imagine that what may happen, one sort of speculative hypothesis, is that for individuals that are susceptible to PTSD that show this sort of ⁓ well what I'll effectually use is change in V4 ⁓ thickness, ⁓ that that leads to subsequent Alterations and processing of stimuli exacerbates PTSD symptoms and that chronic stress of then having those symptoms, having that disorder, then contributes to greater atrophy in these threat neurosurcular regions, right? So it's question of you know, which is the sort of trauma acquired ⁓ brain. Okay, let me try that again. You know, which brain region is sort of impacted by trauma versus which is sort of impacted or which are sort of impacted by the experience of PTSD itself. ⁓ I don't think we totally know the answer to that, but I I think that, you know, to to directly answer your question, I think what this tells us is that something else has to be happening for these threat neuroscircuit regions that we know are important for PTSD. And maybe it is simply just the case that. as time goes on, as these individuals live with this stress, that's when we start to see ⁓ what we might call breakdowns in the underlying structure of those regions. Elvisha Dhamala: So I guess given that you saw that the V1 was thicker in both samples, but they differed in terms of their control groups. So one was recent trauma or not recent trauma, whereas the other one was no trauma. Does that have any implications on how these differences or sorry, let me start again. ⁓ I'm trying to relate that to what you just said, but it's like tricky because I feel like there's a lot in there. Nate: That's that's a c that's a nice way of saying that. Thank you. Elvisha Dhamala: ⁓ so your control group in the discovery sample included people with prior trauma histories but no recent trauma, and V one was still thicker in the recently exposed group. Does that suggest that the changes that you see or the differences that you see are transient, where thickness actually increases acutely after trauma and then might normalize over time? Nate: Good thing you can edit out long pauses. Yeah, I think that's exactly where we end up in our inference, right? That based on the study design, based on what we have, based on when our imaging was done, we really think these are sort of acute changes. Again, it's hard to know without the longitudinal data if, you know, among some individuals it stays elevated over time. Among ⁓ maybe for those that are most susceptible to PTSD, it drops more precipitously back, you know, below baseline. ⁓ But I I think you're you're exactly where we are in that these V1 trauma-related changes we think are most likely transient. They probably have some other sort of importance that we just weren't able to gleam here. Again, maybe it's this neuroimmune thing. Maybe it is how this brain region is talking to other brain regions. It's really hard to tell with just the structural data. ⁓ but we think that thickness is probably gonna be transient. It's just something else that we didn't get. that might be related to the psychiatric disorder itself. Elvisha Dhamala: So in the paper you acknowledge several limitations, including small sample sizes and as you mentioned earlier, the absence of pre-trauma imaging. What does that shape how and what we can what we can and can can't conclude from this study? Nate: So in my very ⁓ So based on my behavioral neuroscience training, what I would say is we can conclude exactly what we put in the title of paper, that thickness is associated with ⁓ differences in in in ⁓ V1 thickness. What what I would say sort of more broadly is that what our design allows us to say is that something about trauma is associated with both the the the let me try this again. Trauma seems to be associated with V1 thickness independent of PTSD symptoms, and ventral V4 thickness seems to be associated with PTSD symptoms, which may or may not be independent of trauma, given definitionally how we define PTSD. I think that our limitations are really that in an ideal world, we would be able not just to look at individuals who've recently experienced a traumatic event, but people before they experienced trauma to know what their individual profiles of susceptibility to the disorder would be. And without that pre-trauma baseline, even in the case where we have ⁓ you know discovery and replication data set and we think it has to be related to change, even even with that, in the absence of this pre-trauma baseline, it's really hard to know for certain, as much as we need to be, what those brain profiles would look like and whether or not trauma is inducing this change. Or if the fact that they're experiencing trauma might be hiding some other associ some pre-traumatic association with PTSD. You can imagine that V1 thickness among individuals who have not been exposed to trauma and are about to be might be different in some way. Maybe there's some brain you know thing that leads people to be exposed to trauma. I don't necessarily think that, but as scientists, we have to be open to alternative explanations. ⁓ until we have evidence that disproves that. So it it would just be nice to have some sort of pre brain imaging to be able to devise new biomarkers, really. Elvisha Dhamala: Would you say that there might be something in the pre-trauma imaging that would that could indicate susceptibility to PTSD? Nate: I think that is a lot of people's hope. I think that a number of us really want something that helps us understand, you know, if the worst were to come to pass, right? If the worst happens, can we get them, can we get individuals help even sooner? And ideally having that pre-trauma profile, that pre trauma neural signature would say, okay. N now they don't need to get brain imaging right after they've fallen and broken their leg or right after they've been in a twelve car pileup. We can just ⁓ immediately know that they need the the most amount of treatment or they need the specific treatment. and then from again, from a from a basic science standpoint, it would just be nice to know of like, is this really a change as a function of trauma, or is this just something that, you know, is a spontaneous recording that might not be related. Not to not to not to drill all of my hard work down into ⁓ maybe it doesn't matter. But you know, again. Nah, keep it. It's good. Just add my just add the little caveat at the end, please. I swear it's real. I promise. I work so hard it still matters. Elvisha Dhamala: Great. I can always edit that out later if you want. My last question is if there's one key message you'd want clinicians, researchers, and the broader public to take away from your work, what would it be? Nate: ⁓ man, I almost just like took our tagline from the Center for Developing Child. They have like this great tagline now that's like what surrounds us shapes us. It's so it's so good. I wish I could steal it, but Lindsay would kill me. ⁓ But I will borrow it actually, I think. ⁓ Elvisha Dhamala: Ooh, th that is a good one. That's such a good one. Nate: Let me figure out how I want to say it briefly so that it's not getting an email. It's like, did you just steal? ⁓ very weird sidebar, but they just had that happen with like a podcaster who like literally took some of their work and then like started talking about it without even like once once acknowledging all the years of work and then decided it was it was wild. I I think that the key message that Elvisha Dhamala: Of course. No of course. Mm. That's crazy. Nate: I'd want everyone to take away is that the things that happen to us are embedded in us. That some things that we experience have to go someplace. And what I really think, despite the limitations, is that what we've shown is trauma has some very acute impacts on the brain. It's associated with PTSD through visual neurobiology. And as much time as we've spent on prefrontal cortex, hippocampus, and amygdala, because they are our favorite brain regions, I think if we want to tackle the issue of PTSD susceptibility, we really need to zoom out and expand the circuits that we're looking at so we can devise the best types of biomarkers to help those who are gonna be most in need. Elvisha Dhamala: That was amazing. Nate: Thank you. I you don't you'd never think that I'd talk about this like in my office by myself all day. Elvisha Dhamala: No, that was great. Is there anything else ⁓ you'd want to add or anything ⁓ specific that you'd like to change how you phrased it or anything? Okay. Thank you. Nate: I don't think so. Good job. Like these are really good questions. And it's like a actual like when I saw that you were using Riverside, I like, wow, this is professional. This is really good. Elvisha Dhamala: Well it's also this makes it so much easier than like using Zoom recordings or everything because they have all the tools. Yeah. Whereas like if it was Zoom, I would just then be on like Adobe trying to edit it myself. Now I still have to edit it myself, but it does a lot of the work for me, so Nate: Yeah. ⁓ yeah, yeah, yeah, yeah. Okay. That all works out then. ⁓ Yeah. Are you going to S Fn, S O V P, A C ⁓ P ⁓ Elvisha Dhamala: Yeah. But thank you so much for your time. This was great. I will I will be at SOVP. I am not planning on going to S FN or A CNP. A CNP's in San Diego, right? Yeah, no. It's not a strong enough draw. Nate: Okay. It's in San Diego this year, yeah. I think it'll be back in the Bahamas the year after. Okay, yes. You've you've you've already done the work. You know when you're going Elvisha Dhamala: It is next year. Yeah. Yeah, that one'll be at. But so the the crazy thing is, ⁓ next year's twenty twenty seven, right? Yeah, so January twenty twenty eight it's in the Bahamas. And then December twenty twenty eight, it's in Vegas. Nate: That's wild. Okay. All right. I I think my associate member is like three more years, so I think I get to go to all of these. I'm very excited. Elvisha Dhamala: Yeah. Vegas is a weird one and like crazy that both of them are like I guess they're going back to December. I don't know. Nate: Yeah, I I have no clue what that choice is. ADAA was in Vegas a few years ago. ⁓ I did not go, but I think people had a bad time 'cause it was just like it's I don't think so. I think like if you like to gamble I think what it is is like I think people like gambling at the Bahamas and so now they're like now we need to do like more gambling. That's exactly what we need. Elvisha Dhamala: I've heard Vegas isn't like great. Right. So they're like, they must like Vegas. Right. Of course. Nate: Great. Elvisha Dhamala: Great. All right. Well, thank you so much. ⁓ I will send you everything once I have it. ⁓ and then if there's anything else that comes up, ⁓ just let me know. Awesome, great. Thank you. You too, bye. Nate: Sure, sounds good. All right. Good to see you. Talk to you later. Bye.