B (3:41)

Yeah. Wow. If you don't mind me asking, at what age did you go back to school to study medicine?

C (3:47)

So I had to go back because I never took all the pre med courses in college because it wasn't something I was planning on. So I went back to Columbia University at 28, and I did two years of all the physics and the biology and the organic chemistry. And then I started med school when I was 30. So, you know, where most people were 21, 22. So it definitely started a bit later.

B (4:11)

Yeah. Wow. Awesome. And. And what makes it, you know, so I, I changed my career in my late 20s to become a therapist specifically because I wanted to work with ocd. So similar choice to you, but you chose to do medicine instead of just becoming a therapist. So what was your thinking behind that? And be nice in your.

C (4:31)

No, it's a great question, and I'll tell you exactly what happened. I actually, you know, the. The therapist that was treating my family member, I kind of came into them one day and I said, I think I know what I want to do. I said, I want to do what you do. And they looked at me and he said, not a chance. And I said, why? He said, well, he said, I think you're able to get into medical school, and I think that that will give you more options and more different ways you can treat ocd. And you could always learn the therapy and will always work with you on the therapy. So, you know, my, you know, for me, you know, my kind of treatment schedule, you know, is about 5050, so. Or maybe a third. A third? A third. I would say there's about a third of people that they see a therapist and I just do their meds. About a third of people, you know, I do both. And there's like another portion where I just do therapy because they don't need meds. And so to me, I never thought of it in that way of like, I'm going to be a pharmacologist or a therapist. To me, it was more, I'm going to be an OCD specialist. And therefore, whatever treatments are used to treat ocd, I want to know them and be able to access them all. So I kind of thought of it that way more than being a pharmacologist or, you know, or the therapist in that way.

B (5:55)

Yeah, yeah. And that's a good way to look at it. I don't know if I would have had the stomach to go back and do medical training, but I'm happy with my choices. But, yeah, no, I like that approach. That's a good way of looking at it. And we need more psychiatrists that will do both and understand both. At least a lot of the psychiatrists I deal with in the uk, they're primarily all about pharmacology. Not to say there aren't ones out there that do both, but that just seems to be my experience. So it's great to see someone like yourself.

C (6:25)

And I think it's. And I think it's really, you know, to me, one of the most important things that I can do is remind people that when it comes to ocd, right, you don't have to choose. But if I had it, if I had to choose between using therapy or medicine, it's not even close. Right. It's always going to be therapy. You know, there are some people that can get better from OCD just with exposure, response prevention and therapy. Very few people do that with medicine. And to me, the job of medicine really is to decrease the volume of the symptoms so that they can access the therapy and do a better job. That's always the way I think about medication for ocd, so as a way.

B (7:06)

Of enabling and supporting the therapeutic work.

C (7:09)

Yeah. And I think, you know, it's. And some people can do therapy from the outset and they don't need medicine. And there's other people where they'll come to me or their therapist will send them to me and say, steve, like, the volume is just so high, they can't even. They can't even hear what I'm saying. But to me, that's the real goal of medicine is. To me, it's something that brings down the volume and that really allows people again to engage in therapy, which, as you know, is really, really difficult. Therapy is not easy.

B (7:41)

Yeah, that's a good way of looking at it. So I thought it'd be good to start with what are some. Some common myths and misconceptions about medication for OCD that we could dispel? And I could nudge you in a direction if you want, but you could probably guess.

C (7:57)

Sure. I mean, there's a bunch. I mean, I think. I think there's a few that people worry about with medicine, period. Right. One, which is medicine's going to change my personality. And I think, you know, what I often say to patients is it's actually quite the opposite. Right. That the medicine can help the disease and allow your actual to be who you really are. Right. That it's actually the disease that gets in the way of you being you. You know, and that doesn't mean that some people don't kind of get them. You know, sometimes when you. When you give people an antidepressant or a high dose ssri, there can be things occasionally with people like a little bit of emotional blunting, and we have ways of dealing with that. But, you know, I get a lot of people who are artists especially, and they're terrified because this me is me, and that's how my art comes. And, you know, I found in my experience that they usually feel like they can do their art better. I think there's just some myths that we can talk more about within the world of, like, SSRI treatment for ocd. One of the most common one is probably the drug Luvox. You know, we have multiple SSRIs which we can talk more about, which are the main treatments for ocd. One is a drug called Fluvoxamine or Luvox. And there is this mythology that it's the OCD drug. And that just literally comes from the fact that they couldn't actually get a depression indication to get it into the United States. So they were the first ones to go for an ocd and they were the first ones to get an OCD indication. So then they started marking themselves as like, where the OCD drug, when there's no evidence that any one SSRI works better than any other, not only for ocd, but for anything. But I'd be interested in some myths that you want me to tackle.

B (9:47)

Yeah, yeah, I can answer that. And from my perspective uk, the names I'm familiar with are like Fluoxetine, Sertraline, Sertraline citalopram, they're the kind of key three. So if you could just translate as you name drugs into those English terms as well, that'd be good, because obviously it's us, uk and other countries listen to this. But, yeah, cool. So, I mean, a big one that's been controversial over the years, maybe more so for depression, but I think it gets viewed in the same way for OCD is the serotonin imbalance. So is there any evidence to suggest we have an imbalance in serotonin, or is that a.

C (10:30)

So quite the opposite. Right. That when you look at people with not only ocd, but most of these disorders, there's no evidence, you know, that there's either a serotonin imbalance or low serotonin. Right. And the way I kind of teach this a lot to people is, you know, if you were, you know, you woke up this morning and you were really tired because you didn't sleep much and I gave you some coffee, you'd feel more awake. You can't assume that, oh, if this helped me be more awake, then the reason I was sleepy was because I had low caffeine. No, you had low sleep. But we can fix it through another gateway. And so to automatically assume, Right. Like when you have a headache and you take acetaminophen, which is Tylenol here, and your headache gets better, you can't assume, oh, I must have been low on my Tylenol brain. And so the assumption that just because SSRIs work for something, therefore the disease process must have something to do with that, that's actually not kind of logical thinking. And rarely is that the case in medicine, really. The only times we really see that a lot, it's like hormone stuff where, yes, you don't feel good because you're low in a certain hormone. We give you that hormone and you feel better. But most medical treatments, we're not actually accessing the thing. That's the problem.

B (11:50)

Okay, interesting. So is that how that kind of myth got started, then, was because the drug got invented and because it was working, saying there must be an imbalance?

C (12:00)

Yeah, I think some of it, and I think some people believed in bound. But again, also, this whole thing about imbalances of a certain kind of neurotransmitter is really not the way the brain works. Right. It's such an oversimplification of brain circuitry. All of these things are playing off other neurotransmitters and other neurotransmitters. And so I think, again, I Think this belief that there are imbalances or, or things like that, we're really kind of, you know, we don't really look at it intense of, you know, neurotransmitter imbalances. We tend to look at disease process in terms of circuitry issues. So, you know, in ocd, classically. Right. That, you know, the way we tend to see the circuitry is you have hyperactivity in what are called these kind of corticostriata circuits. And so in particular circuits, there might be some imbalances. But trying to look at it globally, I often say to people, saying somebody has a high amount or a low amount of serotonin is like saying, the United States has a lot of traffic. Well, there's a billion roads in the United States. Some of them have a lot of traffic. Some of them, you don't see a car for miles. And the classic one is when we talk about schizophrenia, right. In schizophrenia, the classic model was that they have too much dopamine in what's called a meso limbic pathway, and that's what causes psychosis. But they have too little dopamine in the mesocortical pathway, which is what makes them kind of dull and cognitively slower. So again, it's just, I think sometimes people are trying to access it to people and make it, simplify it. But sometimes when you try to simplify something, you create more problems than yourself.

B (13:48)

Yeah, yeah, good point. Is there any indication of why SSRIs work for OCD? Can we be sure? Is it still a bit of a mystery?

C (13:57)

It's still a bit of a mystery. Again, you know, we. It seems to be that, you know, so it's interesting, you know, sometimes people talk about serotonin, right? But it's not that all serotonergic drugs work for ocd. It's very particular, Right. It's really drug. The only drugs we have evidence for are things that really powerfully affect the serotonin reuptake pump. Right? Because there are other drugs that increase serotonin that don't seem to do bupkis for ocd. And I think we know they kind of modulate certain circuits. Again, those kind of corticostrateal thalamic circuits. And we know that when we give people SSRIs, we can actually see the hyperactivity in those circuits slow down. Interestingly, when we do therapy and it works well, we can see those things slow down. But exactly what's happening. No, you know, people, we have theories and stuff like that, but no but nobody can tell us for certain exactly how the SSRIs are doing it.

B (14:53)

Interesting. And blanket on my question. So let's talk about medication then for ocd, just for anyone listening that is maybe on it, that wants to know more or maybe not on it, or what are the kind of key SSRIs for OCD?

C (15:12)

So again, you know, the main treatment for OCD are serotonin reuptake inhibitors. You know, the first one, just so historically. Right. The first serotonin reuptake inhibitor we used wasn't an ssri. It was what's called the tricyclic antidepressant, and it was called clomipramine. And you know, clomipramine is a tricyclic, but it was different from the other tricyclics. And by the way, this goes back to what you were asking about, where the serotonin hypothesis comes from. Most of the tricyclics affected norepinephrine and none of them worked for ocd. Some of them worked for depression and anxiety, but not for ocd. And then we had this newer one that affects serotonin reuptake, and that one did work. And so then you say, oh, clomipramine works. What happened is because we knew that clomipramine affected the serotonin reuptake pump, we said, oh, when the SSRIs came out in the, in the 80s, well, maybe these will work too. They do the same thing. And because they have less side effects, we go with the SSRIs. And the SSRIs are again, are Sertraline, Fluoxetine, Fluvoxamine, Citalopram, Escitalopam and Paroxetine. And there's not a shred of evidence to show that one works any better than another. That doesn't mean some don't work better for some people. We don't really know why. And sometimes we choose them based on side effect profiles because while they all work equally well, they have different side effect profiles.

B (16:41)

And what are those names in my American listeners or I'm not sure how Canada does it, but what are the names?

C (16:48)

Yep. So Paroxetine is Paxil, Sertraline is Zoloft, Fluoxetine is Prozac, Fluvoxamine it is Luvox, Citalopram is Lexa, and S. Citalopram is Lexapro.

B (17:02)

So Lexapro, for example, is that just a brand name? Yes. Yeah.

C (17:07)

Well, Lexapro is the name that the developers came up with. And once it goes generic so there's always a brand name and then the generic and then. So those are. Yes, those are the brand names of the brand.

B (17:18)

Okay, cool. So, okay, so are you picking then based on side effect profile? Because if they're all kind of level in terms of outcome, are you kind of just looking at. And how are you then picking side side effect profile? Are you asking them what they want to avoid or how do you know?

C (17:37)

Yeah, well, it's interesting, right? So like for example, I think a good example is Paroxetine Paxil. So I don't use a ton of Paxil. And the reason is because Paxil causes the most somnolence, makes people sleepy, it causes the most weight gain and it causes the most sexual dysfunction, which with SSRIs is mostly what's called anorgasmia, the late orgasm. So most people don't want those things. On the other hand, if I have an OCD patient that can't sleep, that is really depressed, so he's not eating and he's an 18 year old guy, so he ejaculates quicker than he would like, Paxil is the perfect drug for them. Right. So that's why, you know, calling them adverse effects, you know, it's better to call them side effects because one man's adverse effect is another man's great effect. And so, you know, there's, you know, so some of the reasons we'll use different drugs is based on side effects. And yes, definitely, we talk to patients about are you more concerned about sexual side effects, Are you concerned about weight gain and things like that? You know, in other ways, some have more drug interactions. So especially when people are on other medicines, we often go with drugs that have less interactions. And another way, which is kind of a, you know, it's more thinking genetically is if I have somebody who has a family member and says, look, my sister's got OCD and she does amazing on Zoloft. You share some genetics with her. It's not a perfect science, but if all other things are equal, I might say let's try you on Zoloft. So those are kind of the factors we kind of take in.

B (19:15)

Yeah. Okay, fair enough. And how do you like for kids, do you adjust for kids? Are there certain ones for kids that work better kids teams?

C (19:25)

No, no, it's not really. Again, you know, I mostly treat adults, but for children it's all basically kind of the same rules. The general, you know, again, the effectiveness of the drugs does not appear different.

B (19:36)

Okay, cool. And when you let's say your client comes to you and says, you know, I'm doing well in therapy, I've got my skills, my symptoms are down, I'm feeling like I'm in a good place, and I want to consider coming off medication. Now, how do you. What's your recommendation for, like, weaning off of that in terms of timeline?

C (19:57)

So, you know, a few things before I wean anybody off anybody I want to. First of all, you know, I always want to give informed consent, right? I want them to know what the risks are and things like that. One thing I always tell everybody, it is rare, but about 5% of people, when you lower or taper or take them off of medicine, will not regain their response when you restart, most people will, about 95%. But you want people to know that that's a risk, right? I don't want them to assume 100% that if we take them off and it doesn't work out, we'll bring them on again. 95% of the time it works. A couple don't. So I let them know about that. And then to me, the goal is you want to do it really, really slowly. So remember, in the same way that it can take six to eight weeks for a medicine to work, it takes the same amount of time for it to unwork, right? So if I have somebody, let's say on 100 milligrams of fluoxetine Prozac, I might lower them to 90. If they tell me in a couple weeks they still feel good, I'm not lowering them again yet. They still haven't. Their brain hasn't changed back. So I will do it really slowly. I drop from 100 to 90 and I give them like two months. If in two months they're doing really good, I drop it to 80 and I keep going like that. So sometimes, you know, there's. So there are a bunch of possibilities. One is that I lower it, lower it, lower it, get them off of it. They do great, fantastic. Other times it's, I lower it, I lower it, I lower it. And then we go past a certain thing and they go, I don't feel that good anymore. Okay, but now at least we've got you on a lower dosage. But it's just knowing that when we do take people off, you know, there is a high rate of relapse. And again, I think the best way to prevent the possibility of relapse is really, really pushing hard in your therapy, you know. And so again, you know, I've done it A ton of times. For some people it works out and they do great in therapy without medicine. Others don't do. I will tell you that when I start somebody on medicine, I want them doing well, like really well for at least a year before I consider kind of lowering or stopping something. I think the longer your brain is in a good pattern, the less likely you are to kind of stumble backwards. So I usually like to see. It's been a solid year. I talked to your therapist, by the way, which is, I think maybe I don't know how it happens where you are in the States. It's kind of not good. A lot of psychiatrists just don't talk to the therapist. And this is the person that's going to see your patient more frequently than you and not to kind of, you know. And so, you know, at some point, if me and the psychologist, therapist agree, you know, then we might say, okay, this person's been doing really well for a year and now we're both going to really watch carefully and lower slowly.

B (22:44)

Yeah, it's a good point. I mean, in my current caseload, I have one client whose psychiatrist reaches out to me. So whenever he meets the client, he asked me for an update and obviously I give it to him. Um, but not, not a single other one contacts me. Um, I will ask to be connected sometimes. Um, but yeah, that's no criticism of psychiatrists, me just stating the facts of how I see it for my caseload. Um, and I get it, they're super busy, but we all are.

C (23:16)

Yeah, well, but, but I think that's being very nice about it. I think that that's part of what your job is. So if you're super busy and you can't talk to people or get kind of that information from psychologists, then you maybe should be seeing less patients.

B (23:32)

Okay, right.

C (23:33)

Like that's, that, that's part of your job. You know, I don't say I'm super busy, so I'm not going to tell somebody about side effects. Right. Because, well, I got to get. I got to get. Yeah, yeah. This is part, this is part of the job. And to not get collateral information, it's just to me it's. You're not doing your job.

B (23:51)

Yeah, it's a good point. I mean, some, some of my, not everyone's who I work with is on medication, but some of them will have like, you know, our National Health Care Service will have an NHS psychiatrist and they are way overstretched.

C (24:04)

But.

B (24:05)

Yeah, but, but many have private psychiatrists and I don't hear from them either. So. So, yeah, so let me think on that.

C (24:14)

So.

A (24:16)

More, more.

B (24:17)

In recent years I've seen a lot of my clients and a lot of people I've spoken to on the podcast have had SSRIs augmented with anti psychotics. So and I remember maybe interviewing someone like five years ago and maybe them saying something along the lines of there's not a lot of research at the minute for it, but now it seems to be really common that that is. I say common, it happens, I hear it enough. And so I just wanted to get your take on it. Good, bad, depends.

C (24:48)

So. So a couple of things. So actually out of any augmentation strategy, when we add something and that low dose antipsychotics have the most data by far that they work, that they're effective now, what does that mean? It means actually when you look at the data that with people that don't respond to an SSRI alone, if you add a low dose antipsychotic, about a third of people now will respond. So it's again not a perfect drug and it has a lot of side effects. One thing is that it's interesting because I was doing the pharmacological guidelines for the OCD foundation, we were doing the updates for that, we were looking at different algorithms. It's interesting because that usually falls pretty high on the algorithm, right? The SSRIs alone don't work. You switch, you try other things, then you add an antipsychotic. And I think it's remembering that there are other medicines that we can augment with that don't have as much data efficacy wise as the antipsychotics, but are a lot safer and lower on side effects. So sometimes you might say, yeah, I don't have as much evidence for this one, but if I can try it and if it works and I don't have to use the antipsychotics, that would be great. And so, you know, when it comes to the antipsychotics and again, you know, it's tough, you know, I keep trying, hopefully over time we're just going to start calling these dopamine blockers. You know, antipsychotics are, you know, what are called dopamine 2 receptor blockers. The antipsychotics of those that we have the most evidence for in OCD are kind of these couple of the newer atypical drugs. One is Risperidone, which is Risperdal, and the other one is Aripiprazole Abilify. We have some data for others, but those probably are where Our strongest data is. But again, you know, when you're, when you're putting somebody on atypical antipsychotics, you have to worry about things like what's called metabolic syndrome, right. Where people can get elevations in cholesterol and fasting blood sugar, get prediabetes. You have to worry about possible movement issues. And those can be kind of the static reactions of kind of like tightening of the musculature. Those can be what's called tardive dyskinesia, which is a long term effect that some people have that causes kind of these movements of the face and of the mouth. And so, you know, again, these. I think my biggest problem with them is I think people give them out too easily. And I think sometimes maybe that's because they think, well, we're using low doses, so it's not a big deal. And so to me, that, that's my big issue with them is that I think people are a little bit too cavalier with them.

B (27:28)

Okay, okay. Yeah. So they have their uses, but maybe too cavalier at times. So you mentioned other things you can augment with other that have less research. If you can share, what would those be? Sure.

C (27:42)

So probably the biggest area that we've looked at is drugs that modulate the neurotransmitter glutamate. And you know, when I teach this stuff, one of the easiest ways to just kind of describe this to people is, you know, think of your brain as like a car radio. And glutamates, the on switch, and gaba, which is what's called gaba, aminobutyric acid is kind of the off switch. And then all the other ones, serotonin, dopamine, they're all like tuners, right? You can turn the volume down and you can turn it up. And so there's been a lot of thought that maybe that one of the reasons these kind of corticostriatal thalamic circuits are hyperactive is because people have excessive amounts of glutamate in those circuits. And so that those are turning everything on and keeping them going. A lot of people, Chris Pittenger, has done probably the most work in a lot of ways on this at Yale. There are also some other reasons to believe that glutamate is involved in kind of ocd. One is that when you look at the candidate genes that seem to be involved with ocd, several of them are glutamate receptors. The other thing is that if you look at the cerebral spinal fluid of people with ocd, there seem to be more Glutamate breakdown products in there than for people without ocd. And so the question's been, can we lower glutamate? And so a bunch of different drugs have been tried to modulate glutamate. Probably the two most commonly talked about are a drug called reliazole. And riluzole is typically used for amyotrophic lateral sclerosis, or als. In this country. We call it Lou Gehrig's disease. And really is always interesting because it's very interesting in the same way that the serotonin reuptake pump, the SSRIs block it, so it keeps more in the synapse. This makes the pump getting actually glutamate out work better, not worse. And so you're taking more glutamate out of. You take more glutamate out of the synapse. Then the other drug that we kind of hear quite a lot about is a drug called memantine, which is also called Mementa, and that actually blocks glutamate receptors, particular NMDA receptors. And you know, the reality is we've studied them both. You know, it seems like they work in some people, they don't work in other people. The nice thing is they're really side effect friendly. You know, with riluzole, you have to check people's liver enzymes at the beginning and every year because sometimes they can rise a little bit. Typically not an issue. But people tend to tolerate these much better. And they're much safer in many ways than the antipsychotics. You know, the other glutamatergic drug that people talk a lot about is ketamine. You know, some people consider ketamine psychedelic. It doesn't really fall into that category. You know, ketamine is an anesthetic. And ketamine really affects glutamate receptors also. And blocking NMDA glutamate receptors. The research on ketamine has been split. So it's really interesting. Actually, two friends of mine have studied this. Chris Pittenger at Yale and Caroline Rodriguez at Stanford. Caroline Rodriguez had good results. Chris Pittenger didn't have good results. And then they talked to each other because why is that and what it looked like the difference was in Dr. Rodriguez's study, it looked like most of the people weren't. They weren't on any other medicine and they really had primary OCD and not a lot of comorbid conditions. And they tended to do well with the ketamine. People in Dr. Pittenger's group tended to be on multiple. On medicine or multiple medicines. And they tended to also have more comorbid depression and things like that. And so that's also the question, I think, is, you know, whether something works for OCD or not might not be always. The most important question is, does it work for certain profiles of people with ocd, and those are the main. We've also had studies of other blutamatergic drugs, including lamotrigine and topiramate. We have a little less kind of data to support them, but some studies. And that's really kind of the other kind of augmentation thing that we've looked at. Emily Stern at NYU looks a lot into a drug called on Bancetron, which is typically used for nausea and vomiting. It blocks serotonin 3 receptors. And there's also been some studies that when you add on Dansetron, it can be actually helpful for people with ocd. But again, none of these are large studies. None of them are wow studies. And again, my guess is that it probably works for certain subtypes or certain people with OCD and not others, because OCD is a heterogeneous condition. You know, So I think that's also part of why kind of you don't see these things getting knocked out of the park. Doesn't mean it doesn't work. It just might not work for certain types of. You know, the example I give people is, you know, remember in psychology and psychiatry, we basically come up with diagnosis based on symptoms, right? They have these X number of symptoms. But if you did any of that with any other. I mean, imagine you took. So this is perfect for you because you're a little under the weather. Imagine you took somebody who had the symptoms, a syndrome of cough, sore throat, and fever, and you gave all of them antibiotics. You would think antibiotics don't work very well because most of them, the cause is viral. Now, if you could do a strep test and figure out who has strep throat, and you just give the people with those symptoms an antibiotic. Antibiotics look really good. And so the question is, again, are there just some types of ocd? And maybe some people have OCD in those circuits because glutamate's the issue, and those are the ones responding to that. And maybe the third of the people that respond to antipsychotics is, because in that same pathway, dopamine is the issue. So, again, I think sometimes it's hard to judge drugs just by studying for the disease alone, because in psychiatry and psychology, our diseases are so heterogeneous.

B (33:48)

Yeah, that's a really good point. So much more profiling across the different medications to find which one is the best. One for the best profile. Yeah. Okay, interesting. And I've seen a couple other pharmaceutical companies researching glutamate for ocd. So it seems to be some sort of race for the next, like, drug.

C (34:10)

Always.

B (34:11)

Yeah. I mean, if it works, who cares, right? Hopefully. So you mentioned ketamine. Similar but different psychedelics. Like what, what are your. Actually, no. Come back to psychedelics in one second. This is one other more. So I know benzodiazepines aren't prescribed as a treatment for ocd, but they will get prescribed to people with OCD and high levels of anxiety. What are your thoughts on benzodiazepines and when would you prescribe them and when. Yeah, when wouldn't you?

C (34:44)

So. So again, you know, remember, I think, you know, OCD is, you know, not considered an anxiety disorder for a bunch of reasons. And the primary symptoms are obsessions and compulsions. Right. Part of the reason is, you know, it kind of doesn't make sense to call it an anxiety disorder is there's plenty of people with OCD that don't feel anxiety. Right. There's plenty of people with OCD where it's about disgust. There's plenty of people with OCD where it's about guilt. Right. There's plenty of people that just don't feel right. And what we know is that benzodiazepines don't seem to have any effect on obsessions and compulsions. We know benzodiazepines can work for anxiety. I think for me, in general, with benzodiazepines, I don't like using them on an as needed basis. I think it just becomes, as, you know, it just becomes another form of compulsion.

B (35:34)

Right.

C (35:34)

Where teaching people to sit with the discomfort and the anxiety by not doing compulsions. But yet you can go take a Xanax, well, which is alprazolam. So I don't like it for those reasons. Other times there are people where their anxiety levels are really, really high and I don't mind giving them a standing dose so they're not popping it when they feel anxious. They're kind of, you know, with. With clonazepam, Klonopin, I might give it to them twice a day. So it's kind of in their system. It kind of lowers their overall anxiety levels. But even that I don't like to do long term. I don't think it works best for anxiety it's also just remembering benzodiazepines don't work as well as SSRIs for anxiety. Like they don't work as well there, you know. And so, you know, I think, I think I use them sparingly, but I also think like anything, I think the pendulum shifts and I think there was a period of time where people were giving everybody benzodiazepines and I think then there's also been a period of time where there are some clinics in the United States they just won't give anybody benzodiazepines. And I don't think that's right. And I think so, you know, you really do have to look at each case.

B (36:42)

Are you factoring in people with like history of addiction and stuff? When always. Yeah, always.

C (36:48)

So always, you know, whenever you're going to give, you know, a benzodiazepine or any drug that can be addictive or abused. Right. You always want to say like this is somebody with a high abuse potential, past history, you know, and that always, that always comes into your decision making process.

B (37:04)

Yeah. Okay, cool. So yeah, psychedelics, something you're interested in, curious about? Think it's all hype. Where are you?

C (37:16)

Well, I think so, so maybe define, let's define psychedelics.

B (37:19)

Okay. So, so the ones that have been trialed here in the UK and obviously in the States is psilocybin or magic mushrooms for the street name mdmn. Mdma. It's ecstasy.

A (37:33)

Right.

C (37:35)

And so, so yeah, so in general, just for people out there, you know, really a, psychedelics are drugs that really affect drastically consciousness and perception. Right. And, and, and, and mo, when we look at kind of them, they are typically drugs that affect serotonin and particularly serotonin 2a receptors and the big two that we look at a lot are psilocybin, which is what's in magic mushrooms. Lsd, which is a lysergic acid is also one. Things like MDA are kind of like what we call kind of almost psychedelic like drugs. They're really more what we call empathogens or anactogens. Reason being is because they don't tend to affect consciousness and perception as much as they kind of foster connectiveness. And so, you know, what do we know? You know, we've looked at, there's some studies of psilocybin and depression that have been nice studies that show that there looks like there's some benefit right now Chris Pittenger at Yale is currently doing the study on psilocybin for ocd very small study, limited data, not published yet, but they're getting some promising results. You know, as far as mdma, there is no research into ocd. There have been some nice studies of its use in ptsd, and they seem to gotten some good results. But none of these things, including ketamine, should be used to treat patients right now. These are experimental treatments that should be used in a research setting only. You know, unfortunately, especially with ketamine, since people do use it for depression, so they're already giving it to people. They're also treating people for ocd, and we just don't have the data yet to support that. My biggest concern is because psilocybin is something that people can get when they find out it works. They go out and get psilocybin. They don't know how they're dosing it. Where you take psilocybin matters, right? When you take a psychedelic, if you take it in an environment where you feel unsafe. And so there's just so many factors to it. And so that's my only concern. I think these drugs do have a lot of potential to help us with a lot of things, but I think it's going to take time. And that's my big worry, is that people are restless. Obviously, when you're sick, you want to do everything possible and are going to go out and use these drugs on the street. Things like that, which, you know, which obviously I worry about is, you know, most people know you can have really bad experiences, right? What people used to call bad trips, really, really horrifying experiences with these drugs if they're not dosed right in the right environment and even if they are. So, you know, I just always caution people with that, but I think it's an important area of research.

B (40:22)

Yeah, 100% agree, I was going to say. And I think also with psilocybin, it's having, at least in these trials, it's having a therapist there with you the entire time to support you through it. At the end of it, they do integration sessions. What did you learn? What came up? How do we process this?

C (40:41)

And also remembering that in research, these patients are very carefully picked.

B (40:47)

Yeah, right.

C (40:48)

And so we are, you know, they go through a lot of interviews and a lot of overview, you know, to see. You know, obviously we worry if people have a history or potential for psychosis, there's some concerns. We don't know how accurate they are, but that these people, these things, these drugs will push people into psychosis. And so, again, you know, we're very Careful right now. And we always are at the beginning with a drug, we're picking a very kind of low risk, kind of specific population. And that doesn't necessarily apply always to the broader population.

B (41:20)

Yeah, yeah, good point. And I, yeah, so I hope they keep researching it and find out where, you know, where it's useful, where it's not where, how it's safe to do it, and then if it is safe, you know, allow companies to safely administer and help people with it.

C (41:38)

But.

B (41:40)

Okay, so you mentioned Columbia earlier, right? That's where you studied.

C (41:45)

I went, I did my pre med at Columbia and then I went to medical school at Downstate in Brooklyn and then did my resident, my residency at Montefiore and I did my fellowship and obsessive compulsive and related disorders there.

B (41:58)

Okay, cool. Awesome. So I saw a few years ago, Columbia did a study on cannabis for ocd. Is there any evidence to support any use of cannabis for OCD?

C (42:10)

Unfortunately, no @ this time we really have any, any evidence. You know, again, and sometimes they were looking at cannabis like within the four hour period of kind of being high and what that did. But, but there's not that we have no evidence to support right now the use of cannabis for ocd. And I will tell you, in my experience, you know, people that smoke regular cannabis don't tend to do well overall. I often, you know, if somebody's smoking regular cannabis, you know, on a regular basis and smoking multiple times a day, I often won't even try to treat them with medicine until they're kind of cleaned out. You know, they're taking one psychoactive substance. And you know, I think the thing with cannabis that I've, I've noted over time is, you know, I don't, I'm fine with people doing whatever makes them happy, but I think that sometimes people who smoke cannabis will tell me it doesn't negatively impact them and I will ask them like, can we do a one month trial? And they go off of it for a month and they go, oh, I didn't realize my sleep now I'm sleeping through the night now I have more energy and things like that. I think cannabis can be insidious like that. You use it kind of slowly over time and you don't actually notice kind of how it's affecting your functioning, your thinking and things like that.

B (43:27)

Yeah, yeah, interesting. And then of course, you've got the different strands of cannabis.

C (43:35)

Exactly. And so makes that so hard to study. Right, because what are you studying? Yeah, you have this broad thing, cannabis, you have different strains, different strengths. And so it's. It's, again, it's kind of a broad thing to be able to say, like, it doesn't or it does this or that, because we're not talking all. Always about the same thing.

B (43:54)

Yeah, no. Cool. Thank you for that, though. So is there anything else on medication, medicinal things more generally you want to mention?

C (44:05)

Yeah, I mean, I think when it comes to medicine, just we should probably talk about some of the basic reasons why people fail on medicine. And when people come to my office, there's a couple of reasons, right. So the most common thing we see is that someone will come to my office and say, I was on Fluoxetine, Prozac, and then Sertraline, Zoloft, and then they didn't work. So then they added an antipsychotic and then that didn't work. And I will say, well, how much were you on them for how long? And they will say, I was on 20 milligrams of fluoxetine or I was on Sertraline Zoloft that was on 150 milligrams. Well, these aren't dosages that are effective for OCD, right. When we're treating OCD from a pharmacological standpoint, you know, we use SSRIs, which are also used for all the anxiety disorders and depression, but the dosages we use are significantly higher. They're often two to three times, sometimes four times the dosages that we use. And so a lot of people have been tried on these medicines, but not at dosages where they could ever expect anything. And then they come get really down on medicine or think they're treatment refractory. And so I think that's just probably one of the most important things. I think another common reason that people don't succeed on SSRI sometimes is they have another disorder that's not being treated. And, you know, the common example, one of the most common things I see when people aren't responding is often they are people with adhd, Attention hyperactivity deficit disorder. And part of the problem is because, you know, if you can imagine somebody with adhd, right, they often have problems with impulsivity, right? They call out, they can't wait their turn. Well, if you have somebody that's already impulsive, they can't even wait their turn, how in the world would you think they're going to be able to resist doing a compulsion? And when people's brains are already kind of disorganized and things like that from adhd, how well, do you think we're going to be able to kind of disconnect kind of from obsessions? And so a lot of times in those cases, I'll treat the adhd. And not only will you notice the ADHD get better, but the OCD symptoms start to get better. And so that's mostly my job. I very rarely these days, although I'm happy to get them, but I rarely get a person that says, I think I have ocd. I've never been on anything. That's not the nature of my practice. The nature of my practice is I have OCD. I've seen five psychiatrists. I've been on 13 drugs. And it's just, again, there are some basic things that are missed, including, again, high enough doses and for long enough periods of time. Right. That when you're treating somebody for ocd, you know, trials can be, you know, you want them at least 8 to 12 weeks before you're determining whether something works. Usually at least at the highest dose, you're using for at least six weeks. And so some people will try something and two weeks, it doesn't work. Four weeks doesn't work. They assume it doesn't work. They change drugs. And it might be that they didn't wait long enough.

B (47:10)

Yeah, interesting, because. Yeah, because how. I was kind of obviously not a psychiatrist, but we. We studied medication for various mental health things, just briefly. So we had a rough understanding. And. And in SSRIs, they said, you know, two to four weeks, you should see it start to work. And I think that kind of narrative gets pushed. If it's not working in two to four weeks, it's not working.

C (47:35)

And I think that's typically a time period where you see antidepressants work for depression and often anxiety, and they do kind of sometimes work for ocd. You actually do see movement early on. It's just not necessarily perceptible at that point. So if you're asking the patient at that point, do they notice a change? They might not notice a change. Right. And you really do want to give it at least six weeks at a high dose, really, before, again, you kind of judge it. And so, again, it's just realizing that people kind of, I think, think of an anti. An SSRI, and they go, well, these are the rules for SSRIs, but no SSRIs are different in different disorders. The dosages you use, time periods are different. And so, again, that's, you know, something that. Yet it's not just knowing what drug to use, but it's knowing what dosage to use it for a particular illness and what time period. Because they're not, they're not all the same.

B (48:29)

Yeah, good, good points. So let's change direction slightly. You could pick up the phone and call the 20 year old you. What'd you tell him?

C (48:41)

God in general, in life. Wow, this is a broad one. Yeah, I think I would tell him to like, try to learn and don't make learning stressful. Scary thing, I think, I don't know how it is where you are, but I think kind of learning gets beat out of us because it's always learning for a test or an exam. And so you actually learn to not like to learn. And you know, learning if you're just relaxed and you can accept not knowing stuff. And some of the times we get anxiety and things like that about really approaching learning as something fun and realizing you're never going to know kind of everything and that's okay. Being okay, not knowing, which is what we teach all our OCD patients. Right. Being okay, being uncertain. And so I think I would have tried to learn more and kind of memorized less and, you know, if I could go back again.

B (49:40)

Yeah, yeah, good point. And then you've got a billboard in New York. What do you want written on that billboard?

C (49:48)

Oh, God, if I had a billboard in New York, I would probably. One of my famous things I often use is the state motto of the state of New Hampshire in the United States, which is live free or die. And you know, especially with ocd, you know, I really tell people all the time, right. There's no two ways about it. OCD is slavery. Right. You're just a slavery to this thing in your brain that makes. Tells you what you can do, what you have to do here. And while freedom is scary, it's really kind of saying like, I'm gonna live a free life, because otherwise it's just not. It's not really a life. And you know, especially with ocd, again, I just think people get used to kind of you're doing the things that you think you need to do to be safe so that nothing bad happens and you're not free and really trying to kind of get people to want to be free, even though, again, free freedom is scary. The things you have to do to get it are scary, but it's, it's, it's not much of a life without it.

B (50:50)

Yeah, really good point. And I will ask you actually one other question on not medication, but do you ever consider or advise like supplements of any kind like vitamins, omega 3, anything like that.

C (51:03)

So, you know, again, in for when we're looking at ocd, you know, there hasn't been a lot of evidence. Different things have been studied. It's, it's. There's nothing impressive. The one that people use, and I think a little mistakenly, is another glutamate modulating drug, which is N acetylcysteine. Sometimes people call it NAC or nac. The studies, there was a group of studies, they looked promising, but they were reanalyzed. And newer studies really show that for ocd, it doesn't tend to be effective. It is effective and looks like in people with some of the OCD and related disorders that like we call kind of body focus, repetitive behaviors. So it is useful for hair pulling at times and skin picking. But the data for OCD hasn't been, well, obviously being healthy, eating well is always an important thing. I always push eating well ahead of supplements, you know, if we're getting all the things we need. But I think Omega 3s, you know, there's some data with depression and mood, but in general for ocd, nothing has really kind of proven itself as effective. And we've looked at things like inositol, you know, tryptophan, you know, and nothing really has been impressive. So I don't recommend any to my patients, nor do I know anybody that does this. That does.

B (52:23)

Yeah. Okay, cool. Brilliant. Will, thank you so much for coming on. I really appreciate it. It's good to cover medications in more detail.

C (52:33)

Well, thanks so much and thanks for the show that you're doing an unbelievable service. So it's. It's a great thing for the OCD community.

A (52:40)

Thank you for listening to this week's.

B (52:42)

Podcast and thank you to our patrons who helped make this episode possible. And if you would like to find out more about Patreon and the rewards and benefits, then there will be a link in the episode description.

A (52:52)

If you enjoy the OCD Stories podcast and would like to support us, please subscribe and rate the show wherever you listen to the podcast. And thank you to NOCD for supporting our work. If you want to find out more about nocd, you can click the link in the episode description and quick disclaimer. Guys, this podcast is not therapy. It is not a replacement for therapy. Please seek treatment from a trained professional until we speak. Take care.

C (53:25)

Ra.