All right, let's talk about insomnia slash sleep. Why did you want to talk about sleep today? Well, we were talking about sleep medications, and I feel like it comes up. I get a lot of people requesting sleep medications, and I thought it would be a nice overview for us to talk about, one, how we view insomnia, two, how we prescribe meds, and three, which medications we prescribe.
Well, it's certainly very clinically relevant. I feel like sleep is a weird area in psychiatry. You know, the people who are labeled as sleep specialists who have the sleep committees and the publications are not psychiatrists. But the people who are treating the broad umbrella of sleep problems, by and large, must be primary care and psychiatry.
Mm-hmm. And what impact do you think that has in that there's a disparity between who's talking about treating sleep and the people who are actually treating sleep?
I think the main issue I have with how people think about sleep and treat sleep in the field is not what most people have. I think most people are just worried about inappropriate medication of sleep. I'm worried that the existing evidence is not translatable to the majority of patients who present with a sleep problem, but I'm also going to be a little, I don't know actually how controversial this is.
I don't know if primary insomnia actually exists and I'm not a sleep expert, but does primary insomnia actually exist?
Well, I think we can have an interesting conversation because I do think that there is... I have some thoughts on that that I think it does. And I can describe what it is that I think exists. And we can go back and forth on that.
Oh, yeah. I'd like to hear that. So I guess we should probably define primary insomnia. Yeah. Maybe we can pull up a textbook definition so we can kind of agree on that. I can read the DSM criteria.
So the DSM criteria is complaint of dissatisfaction with sleep quantity or quality with one or more of the following. First one is difficulty initiating sleep. Second one is maintaining sleep. And the third one is early morning awakenings. The second criteria is distress and impairment surrounding these issues. Then it's for three nights per week for three months. And the difficulty occurs despite adequate opportunity for sleep. And it's not explained by another sleep-wake disorder.
Here we're thinking narcolepsy, breathing disorders, circadian rhythm, or parasomnia. And it's not a substance. Not as a result of a substance.
They don't have exclusion criteria in the DSM for psychiatric causes. uh yeah i think i just didn't write it out because i thought it was obvious i mean i i want to emphasize that um if it's not i think that's a huge oversight but think about this it's essentially a diagnosis of exclusion isn't it yeah that's why i
mean you can call like a wastebasket diagnosis um now i'm i'm okay with there being
diagnoses where We don't have direct markers. Obviously we have to be, we're psychiatrists. I'm okay with diagnoses of exclusion. What I'm not okay with is when there's an implicit belief or feeling in professional field, that something is a thing in itself. Yet the way it's defined is that it's, we haven't been able to find a primary cause for this symptom. Therefore it's a primary issue, right? That's what I'm concerned about.
And now, so what is your concern? Like, can you go into more detail about why that's?
Well, it's not describing an entity, is it? It's describing a symptom. And it's saying that if you can't find the cause for this symptom, it's primary insomnia, which is meaningless. It's meaningless, right? That's like, again, the problem of saying a headache disorder. Well, you have a headache disorder. We've tried to find a cause for it. We haven't. So we think it's its own thing, right? We don't, well, at least we shouldn't, assume that anyone with psychotic hallucinations has the exact same syndrome underlying it.
I mean, unfortunately, we sort of treat it the same way because that's all we have. But I think when it comes to insomnia, it's such a condition that can be caused by so many different things, medically speaking, biological, psychological. It's pretty irresponsible to describe primary insomnia, locate it in the population, and then do tests, research, and then to say, I have some treatments that aren't indicated for primary insomnia.
Because we have no idea what it is, right?
I have a differing – I do see where you're coming from. I have a differing – I think that there's a good parallel with depression where it is both potentially a symptom of something else and its own discrete condition. I think – I don't think that insomnia is just a symptom. I think it also is a condition. Based on what? Well, I could talk about my formulation of it, which might be helpful.
Yeah, that's what I want to hear. Well, so I think I guess I'll probably talk for too long and it probably won't make a lot of sense, but let's give it a shot. So I guess let me talk about how insomnia develops and maybe that'll help answer the question. Maybe it won't. And I think a lot of this is true for depression, but basically how I conceptualize it is I think that having a night or two of insomnia is a normal, inevitable part of life.
So almost inevitably, you're going to have something stressful occur, death of a loved one, divorce, family issues, being hospitalized, and you're not going to be able to sleep as a result of it. Now, this happens with 95% of people. And not sleeping during these periods is adaptive. So the thought is that when you're stressed, you're mulling things over, you get extra time kind of ruminating about these things, you're trying to cope with these issues.
This short-term insomnia is normal, and it lasts a few days, and the normal person returns back to normal and gets back to sleeping after a few days. Okay. Now, I think chronic insomnia is the people that have this short-term insomnia and then start to develop beliefs and behaviors that create a feedback loop that worsens the insomnia. So the cycle that turns short-term insomnia to chronic insomnia, which the fundamental part is, the fundamental issues is the beliefs and behaviors as a result of the cycle.
Okay. Essentially, you have this acute insomnia, which is normal and an adaptive part of being a human being. Then you try to fix it with things that are not helpful, like napping, spending extra time in bed, sleeping later, trying to sleep later on the weekends. This, because these don't help, develop more sleep problems. And you develop negative thoughts surrounding sleep. And I think the negative thoughts are really core to it.
Then because of the negative thoughts as a result of not sleeping, you get anxiety around going to sleep and around bedtime, which worsens sleep and restarts the cycle. So you try more things, you develop more sleep problems, you develop more anxiety. And essentially, you develop a ton of belief systems that are very damaging for sleep. And the reason why they're damaging for sleep is because if you have negative sleep thoughts while you're trying to sleep, these thoughts make you more anxious.
They increase your stress response. They make it so you can't actually fall asleep. And then you stay awake.
Dr. Malzberg, I have to interrupt. I think you've described very nicely a very real clinical entity and very common clinical entity. But what you're describing is not primary insomnia as defined. in the textbooks and research, you're describing insomnia habits due to a psychological and behavioral cause, right? If you're able to find that cause, then definitionally, it's not primary insomnia. Primary insomnia supposedly is its own thing. My understanding of it, from what I've read, that is what they're theorizing.
If you cannot find a cause to it, then it's primary, right? But I guess what I'm saying is trying to say all primary insomnia that has been captured or should be captured in research studies is due to this mechanism, then I think we're talking about different things.
I'm not sure because when I'm saying primary, like the problem is the negative thoughts surrounding about sleep that perpetuate the behavior. Yes, there's an identifiable factor, but that identifiable thing is not the underlying, it's not a secondary insomnia.
It is a secondary insomnia. It's secondary to the psychiatric or the psychological mechanism of behaviors. So it would be some kind of an anxiety component, right? Or it would be some kind of a sleep-wake cycle delay, right? You identify the cause. I think that when they talk about and write about and research primary insomnia, they are theorizing insomnia that has no identifiable biological or psychological component that is causing it.
You know what we really need here is we need one of those sleep experts from the society to clarify this.
Yeah, I guess I'm not saying that there's necessarily underlying anxiety or mood disorder. I'm saying that the insomnia is... I didn't mean anxiety or mood disorder.
Subclinal. And if that's the case, if that's uniformly the cause of a primary insomnia, this cycle, as you say, then... Why are the treatment studies not therefore focused entirely on treating that and discussing that and psychoeducating the patients about that? Now, some do kind of do that CBTI, right? Sort of targets that. But I don't think that's how the field approaches primary insomnia in the research and the treatment.
And I'll give a counter anecdote. Oh, go on.
Okay. I think that this cycle is describing what occurs in the DSM criteria.
I don't think the DSM is actually giving an etiology. And I don't think that there is a uniform etiology. And I think that the moment you create a uniform etiology for a primary insomnia, it ceases to be primary insomnia. I think that... Well, okay. I would... suspect at least that a lot of people agree with you. And then I would say, well, then that's not primary insomnia.
What you're describing is subclinical psychological factors, creating a perpetuating set of behaviors. Okay. If we all agree, that's what it is. Why are we calling it that? Why are we saying primary insomnia, which philosophically says there's no cause it comes on its own when we know the cause and the mechanism. Let's call it psycho-behavioral insomnia and create treatment guidelines for it that center around that mechanism. We don't do that.
We sort of do that with some of the treatment, talking about sleep hygiene, CPDI, but here comes my counter anecdote. I know of a patient who was treated for a decade with Z-drugs for primary insomnia. Okay. Until, uh, finally see she seized. Okay. She had new onset seizures. Okay. After 10 years of treatment for primary insomnia, first brain scan ever occurred as a result of that. And there was a lesion in the frontal lobe.
Okay. This is the problem with primary insomnia. It's defined based on our ability to assess rather than being defined on shared characteristics, family history, genetic studies, psychopathology, not psychopathology, clinical signs and symptoms and constellations that always come together. Do you see what I mean? It just says, look at the insomnia, work it up. If you haven't found a cause, then it's primary insomnia. I don't like that.
So you're taking, I feel like Dr. Gamey talks a lot about this in terms of like- I guess so.
Yeah. I mean, I just wonder if there's anyone that's applied the Robbins and Goose style analysis to primary insomnia the way we have at least tried to do for a lot of psychiatric illnesses. Because to me, primary insomnia is probably psychiatric.
Can you describe that analysis to our listeners?
Yeah. Basically, they want five phases. You have to create a first a clinical description, you know, describe the syndrome. Next, you should take that clinical syndrome, find a body of patients that everyone agrees matches that clinical syndrome and begin to do laboratory studies, anatomical, physiological, everything that we have possible. then we have to say how is this actually in itself different from other disorders that are similar and then based on that we can identify a core group of patients and we can do studies okay we can do studies that include looking at family we can uh look at the course of illness and then we can essentially try our best to refine and be certain that we are looking at a medical thing in itself diagnosis rather than a medical symptom categorization diagnosis.
It's about diagnostic validity.
What diagnoses do you feel like fit this?
Which diagnoses have we made better efforts in for this? Schizophrenia since 1980. Bipolar disorders. Major, no, I'm not going to say major depression disorder. So basically, bipolar disorder is schizophrenia. We've succeeded. I think that the American approach.
I think you can add melancholic depression.
Yeah, I don't know if we have enough research on it, actually. I don't know if there's been enough efforts. I would say that American PTSD approach, not in the clinic, but in the research realm, does try to do this better than the rest of the world. it would be, I would consider a failed, um, a failed approach for things like intermittent explosive disorder or ADHD and autism.
So now with that said, how do you approach patients who come in and say, doc, I have insomnia.
Okay. So let's get to the meat then. Um, as psychiatrists, I'm actually extremely, uh, I'm an extreme advocate for treating the sleep medically with medications. I mean, why? And it does relate to my gripes about primary insomnia. All the research out there on primary insomnia, in my opinion, does not apply to 9% of the patients that are presenting to a psychiatric clinic because these are psychiatric patients and psychiatric patients usually get excluded from those studies.
Why? Because simply, They don't have a primary insomnia. Most of the time, the vast majority of the time, the sleep problems in somebody that is seeking psychiatry's help is coming from the psychiatric condition. And so I'm going to challenge you, which categories of the DSM do not include sleep disruption? And I don't mean the diagnostic criteria. I mean the diagnostic categories from what we know about those typical illness courses, how many of them do not come automatically with sleep disruption?
Is it a trick question? Is it any?
No, it's not a trick question. I mean, this is not something that we've necessarily had formal studies for. But if you can look into... I mean, in terms of DSM ones, you got bipolar, depression... Those are the ones that have it right. I think it's just very few that don't come automatically with some sleep disruption. The ones I think do come with sleep disruption automatically neurodevelopmental disorders, okay, like autism, schizophrenia and psychosis.
Definitely. We have research to support that bipolar and depression mood disorders, obviously, right. Anxiety disorders, obviously. Trauma disorders, obviously. The majority of the primary chief complaints that come into our offices as psychiatrists, they have a sleep state problem wrapped up within the core psychiatric illness.
And you were saying that you treat, I think you said treat pretty aggressively acute insomnia.
What I mean by that is I try to treat the sleep first. Now, obviously, I don't just throw a medication at it. I do some counseling. But I try to treat the sleep first. And I don't mean with what the sleep societies recommend based on their evidence, because I find that their evidence favors habit-forming medications, that there's incentives to do studies for so that you can sell medications on patents.
I mean the basic sleep mechanism medications that we have access to as psychiatrists that can help support sleep without being overly habit forming.
Now, I guess before I dive into your algorithm, I can talk about like the algorithm that you're kind of describing. This is like general guidelines, up-to-date guidelines, and I think based off of like the American sleep medicine guidelines. So the meds that have regulatory approval are benzos and non-benzos, something like Z-drugs, the Doras, the dual orexin receptor antagonists, low-dose doxepin, and ramelteon. In terms of their general algorithm, for sleep onset insomnia, they typically recommend the Z-drugs, Dora's, or Meltheon.
And for sleep maintenance, they usually recommend the Z-drugs with a longer duration of action, the Dora's, or low-dose doxepin.
Mm-hmm.
So now that's what's recommended. And as you said, leans heavily. When I say the Z drugs, I'm referring to controlled substance. You said why you think that's wrong. So tell me how your approach is.
Well, again, I think because those studies that got the regulatory approval and that the Sleep Society uses to say there's evidence for this over that, are not based on psychiatric patients, number one. And number two, are very much focused on treating the symptoms of primary insomnia, which to me are never a core condition, so much as a manifestation of some other cause that we are not adequately describing or detecting, right?
So my approach is different. Well, first of all, my approach is somewhat tailored to the cause of the sleep disruption. I try to isolate determine the causes of sleep disruption? Is it really psychological? Is it from a primary anxiety disorder like ruminations? Is it what comes with a melancholic or more, let's call it biological depressive disorder? where you might have early awakening, right? Is it from a bipolar disorder where it's episodic or mixed episodes of unusual decreased need for sleep with preserved or increased energy?
Is it paranoia and hallucinations that intensify in the evening? Is it Trauma nightmares and recurrence and then sleep fear related to that. I want to find out what's going on to sleep specifically, whether it's linked to a psychiatric condition. And then I try to tailor at least education about it, even if I use a lot of medications the same way.
I'm going to give you a tough time and we're going to go through each one and go through how you tailor it. I don't know if that's going to be interesting, but let's do it. I think so. So I'll just go through each one you mentioned. So you mentioned psychological. Is it primarily psychological?
Yeah. So I see that the least. There's always a psychological component that accompanies any psychiatric illness of any ideology, right? It's interacting with the psychology. But to me, that one requires that there is no more than mild axis one condition that can be identified. Then I will be more willing to say this is likely psychological. For that, the, in my opinion, appropriate intervention is CBTI and sleep hygiene.
So just going through the specifics about avoiding blue light, screens, and also just checking for ruminations, mild ones that may not qualify under a specific anxiety disorder. Again, seen the least, but everyone knows about how to treat that.
I respectfully disagree with your opinion on how prevalent this is, but I will save...
No need for the respect, but again, probably a difference in clinical population, right?
Yes. I think that plays a big part in it. I will save my perception of how to treat it and what a big part of it for later because it's such a big topic that it would destroy the topic we're on. Okay. So we must remember to go to that. I do want to hear about that. But we must remember, the listener must know that I disagree.
Now, the next one is anxiety.
Okay, anxiety, I'm still willing and I think it's important to support the sleep. I think that a lot of the effects that we see in terms of improvement of both symptoms and functioning in psychiatric medication studies is a lot of time from sleep support. We're going to go off from anxiety here and talk about, for example, the effects they saw in Abilfi when they're trying to get approved, they were actually managing to do that by combining it with benzodiazepines, you know, which work.
So I'm not talking about that right now, but poor anxiety. I feel like as you've described in the sub. The more the more mild version, the quote unquote primary insomnia, stress related version, I think that's basically the same thing at work, but just much more severe in people with anxiety disorders. And I don't think they're going to be able to engage appropriately with the psychological and behavioral changes in their lives to treat that anxiety disorder if they're just not sleeping right.
So I give a sleeper. And if that's not working enough, I'm not going to necessarily push those too high. I want to visit their level of rumination and what they're doing about it. And we do now have protocols for... treating ruminations with behavioral therapies, cognitive behavioral therapies. But if you don't have a practitioner for that, you can at least give the basic psychoeducation and make some recommendations.
Now, you said a sleeper, which is incredibly nonspecific. Can you talk about your sleeping, sleep drug algorithm for anxiety?
Yeah, I have medications that I think are more applicable broadly, and I have medications that are more applicable per disorder. So talking about just the broad ones, you can think of sleep medications as acting in four quadrants. This is how I was trained by a sleep doctor who did lectures for the psychiatry residency. But you can think of GABA mechanism, generally speaking. You can think of the melatonin mechanism, orexin area, you can think of the cholinergic system, and you can think of the histamine system.
Four major categories. Unfortunately, one of my favorites does not actually work in the GABA category. It's just called GABA, gabapentin. Technically, it's more like working, as far as I'm aware, more like a mood stabilizer in terms of sodium channel stuff. But those are the four major categories.
I personally try to avoid... You got to split up melatonin and adoras. They're not similar enough to group together.
No, it's the same system. It doesn't work the same way, but it's the same system. uh no it's not i'm pretty sure it is i could be wrong uh orexin is the wakefulness
system and melatonin is the circadian system it just has like broader effects well
yeah there are broader effects but melatonin promotes sleep by inhibiting orexin
and gaba promotes sleep by inhibiting all the other ones you can't well that's what
i mean gaba is a broader inhibitor of all neurons
But I guess if you were to group, you could group cholinergic in there. You can group histamine in there if you wanted to apply your logic.
Again, we're not actually differentiating so much. This is all in the same system, right? All is working in the reticular activating system and the sleep-wake cycle. um but this also is encompassing how we think about medications and different medication actions so yes um why but well i guess i've seen different systems
because orexin is wakefulness and melatonin is both the wakefulness and sleep system so i think it's it's worth differentiating i just don't find it worth differentiating anyway so they have such massive doors versus melatonin have such massively different effects
Maybe. Unfortunately, since I work in a community level, I don't get to use the doors very much. So I can't speak to that. I'm just talking about a way to conceptualize it. A lot of the medications, even within the same category, do have massively different effects. So you have to account for that when you're prescribing anyway. So anyway, based on that, I try not to do cholinergic, obviously, for the side effect profile and the sneaky, not sure if it's true, higher risk of dementias long-term.
I just try to avoid it. So why am I left it? Well, it's histamine agents, right? And it's gabapentin, not as habit-forming as the benzos and Z drugs. And there's melatonin. which I actually try not to rely on. I think it's a problem with our regulation of melatonin in the United States. And then there's actually a mechanism I haven't described, which is agents which seem to have a profile similar to a low-dose Seroquel, meaning agents that have mixed effects on histamine, serotonin receptors, and alpha receptors.
So what's like that? Well, you have your mirtazapine, right? And you have your trazodone are the most commonly available ones. Now, I don't like to make patients gain weight. So what am I left with? The broadly applicable medications for sleep in most to all disorders are therefore hydroxyzine, trazodone, and gabapentin. And melatonin is a runner-up because it's not regulated and it kind of depends on which one you buy.
Okay, so I'm going to try to recap everything you said. You said initially four mechanisms, but then kind of expanded on more.
Yeah, that's just a categorization to think about.
There's GABA, so we're thinking about the benzos and the Z-drugs. There's melatonin slash orexin, which I slightly disagree with combining them, but regardless, melatonin is going to be working on sleep circadian rhythm more so than the sleep or wake cycle. There's cholinergic, which we like to avoid because of problems. uh there's histaminergic um then there's a mixed thing which are the low dose sedating antidepressants some of them so you're talking about mirtazapine and trazodone and then gabapentin's kind of its own class um now you were saying that you prefer the ones that don't have any problems don't cause that much weight gain uh so you tend to lean towards trazodone hydroxyzine seems like the more and gabapentin and gabapentin um i
think you are sorely missing doxepin in there i am um why doxepin counts but i don't like it because it is a tca okay there is a higher risk compared to the other agents and um the low dose is not covered most of the time for my patients um unfortunate if it was i'd probably use it more
I am going to disagree incredibly. I think Doxepin is great. I don't think the fact that it's a TCA causes a lot of problems. I got a pro tip for you. Big pro tip. Liquid Doxepin.
Oh, liquid docs.
Um, yeah, it's incredibly cheap. Um, you tell the patient to get just a little tiny syringe that is one milliliter. And then each little cutoff is a milligram and three milligrams. You just suck up the little liquid and it's covered.
I also think that is brilliant. Okay. I have not thought of that. I'm definitely gonna start doing that.
I also, for some reason, uh, My girlfriend's an MP, and I think she said she was able to prescribe one of the three to six milligrams with no for super cheap.
It just depends on insurance. Some different insurances will negotiate certain formularies. It can even change year to year. So it's very local in terms of what you can get covered and what you can't.
Gotcha, because I get very confused by that. But regardless, the liquid is wonderful.
Yeah, that's a really good tip. Doxepin is, within the category, by the way, a really good antihistamine. It's the purest antihistamine under 8 milligrams.
And yeah, I think talking about, so it is a TCA, but at the lower doses, it's an incredibly, probably the most selective antihistaminergic that we have. That's right. So, you know, we're using it at tiny, tiny doses. Now, I'm curious. And so a lot of the medications you mentioned are just antihistamines, or at least that's a primary mechanism. Yes. So how do they differ?
Well, I would say that hydroxyzine is more of a regular ole antihistamine. But we have to be careful of hydroxyzine because it definitely has anticholinergic properties, especially the higher you go. So from a standpoint of treatment of sleep, I mean, that's helpful. You get dual mechanism, but also side effects, right? So it's definitely not my favorite one. Antihistamine agents are also much more sedating for some patients than others.
This can go based on race as well. So really, I don't like to give hydroxyzine actually as a anti-anxiety medication. I think it's overly sedating for most people during the daytime. So I almost exclusively use it for nighttime dosing, but it's not the first one I reached for. The first one I reached for is Trazodone because it's got a lot of additional effects. In my opinion, it's effective also for things like nightmare suppression and trauma disorders and anxiety to some extent.
It's very sedating. It helps promote the maintenance of sleep, not just the onset, but it's tricky because you have to know that it's very long lasting. And people can be either insensitive to it or very sensitive. So I actually start incredibly low. I start at half a tablet of the 50 milligrams most of the time and have people try that. And I tell them to take it one or two hours before their desired bedtime.
And I do give instructions that they should find the timing that works for them.
Yeah. So can you continue? I'll probably add some commentary afterwards, but can you continue with the differences between the different antihistamines?
So that's Trazodone. The difference. Well, and then there's Benadryl, which is just way too anticholinergic in my opinion. So I don't like to use that unless I'm looking for anticholinergic in conjunction with a antipsychotic that's being used for a primary treatment of something like a schizophrenia or bipolar one disorder.
And so now what about mirtazapine, Seroquel, all these antihistamine is a huge component of it.
I mean, people go like, oh, mirtazapine, Seroquel, you know, it's a low dose. It shouldn't be bad. I find that even at low doses, there's considerable appetite increase in weight gain for both of those medications. So I avoid them. Interestingly, I don't really see that with trazodone or hydroxyzine. At least if it's happening, it's more mild. It doesn't mean I don't use serequil or mirtazapine. No, I still use them, but I use it sparingly.
I try to exhaust the other possibilities first. And I find that most of the time I don't need to go to serequil or mirtazapine. Now, if there's someone that has no concerns about weight gain or if they're even underweight and they want to be gaining some weight and they want help with that, then, yeah, I'm perfectly happy to give those medications.
Sure, and I'm going to give my own little summaries about how I think they differ. So, trazodone, as you kind of mentioned, has other mechanisms of action. So, even at low doses, you're hitting H1. You're also probably hitting a little bit of serotonin, like 5-HT2A, and a little bit of alpha-1. In my experience, I do see a small proportion of patients have like a paradoxical reaction. where it, I think you mentioned that, like where it makes it more difficult to sleep.
It's not quite clear if it's psychological or not.
It could be like the alpha one thing.
I don't know.
I don't know. I mean, my money is psychological, but I've also seen it happen in people that have either a bipolar disorder or something close to it. So I do wonder about some kind of a unusual mechanism based on someone's individual biology that we just don't really understand. But yeah, I see that occasionally. But that's why I give all these instructions, of course, with sleepers for people to discontinue if it's not helping or if it's overly sedating.
Yeah, and then I also see a little bit like stuffy nose. I think that's also probably the alpha one. For mirtazapine, we're talking about lower doses, you know, 15 and below. Usually, you're getting other mechanisms. You're getting like alpha two, a little 5-HT2, 5-HT3. There, it's got a really long half-life, and you do see weight gain, even at the lower doses, absolutely.
Oh, yeah, big time.
Doxepin, there, it's got a longer half-life. We're talking about probably about 20 hours. So that's why it's pretty good for sleep maintenance. It's one of the only ones that the Sleep Association recommends for sleep maintenance. That's probably because of the long half-life. Super selective at histamine. Seroquel, as you're going to mention, there is definite weight gain even at the low doses. Probably less risk of EPS and TD that we'd be worried about with antipsychotics.
But with the weight gain, to me, it's way too low on the algorithm to ever get there. Benadryl, we're concerned about the anticholinergic effect, so I prefer antihistamines that don't have the cholinergic. Similar for hydrooxygen, but not as much of a concern.
Mm-hmm.
I think that covers it for most of the commonly available antihistamines. I mean, I'm not going to talk about, isn't there a doxalamine that is an antihistamine? It's an over-the-counter, I don't prescribe it.
Yeah, I think there's a few other OTCs that I don't know as well.
Yeah.
All right, so that covered anxiety-based. So that was your broad base for- Yeah,
which applies to anxiety-based because the anxiety-based is kind of biopsychological. And the ultimate treatment is to manage the psychological component and whatever biological driver of it is. And so I give the sleep support, but I tell them what the primary treatments are, which are, of course, psychotherapy and usually a serotonin-based medication.
Okay. Now, any differences in your algorithm with, say, a depressed patient?
With a depressed patient? I really emphasize, well, first of all, depression, as you know, changes sleep in at least two possible ways, right? And it's oversimplifying, but we'll say there's sleep initiation problems or early awakening versus oversleeping. So we're going to leave aside oversleeping at this point because that would be sleeping too much and we're not going to give medication for that. But it's either early awakening, problems falling asleep, or both.
And often it's both, which is why I prefer to go to Trasnone first. Again, for the maintenance issue and its efficacy for onset and Additionally, if they're not very sensitive to trazodone, they can take a very high dose. I can take it up to 200 plus, and now it's an antidepressant too. So it's got a nice uniform avoids polypharmacy or too much polypharmacy benefit there. But doxepin is very similar, actually.
And if I think a patient is appropriate for doxepin, then that's a very similar choice in my mind.
Yeah, and I guess just to recap, when you're using trazodone at the lower doses, don't think of it as a mild antidepressant. Like at 50 milligrams, it's not reuptaking serotonin, which is its antidepressant mechanism. But what you're saying is you like its profile, even at the low doses, independent of the depression. And then at the higher doses, it also treats the depression. It's kind of a whole whammy.
Which Doxepin does the same thing, right? It's a TCA. But I expect Doxepin to cause more weight gain at higher doses. So I don't reach for that first.
Yeah. And the TCA just has more, more problems, just different receptors and whatnot. Um, yeah. And I guess, you know, when people are depressed, I guess just some, some sleep facts in regards to how it changes sleep. People are depressed. They get decreased deep sleep, uh, increased light sleep, increased REM percentage. So they enter, they have the REM latency, which is like the time from when you start sleeping to when you hit REM is basically hit REM earlier when they do sleep.
Um, It seems like there's a big problem with their circadian rhythm, and it seems bi-directional in that depression causes problems with circadian rhythms. Circadian rhythm problems causes depression. An interesting thing, which is very weird to me, a lot of antidepressants suppress REM. Yeah. Isn't that funny? Some of the MAOIs entirely repress REM. Mm-hmm. where people don't get REM at all, which is crazy. I didn't know that was consistent with life.
I don't know if that's true. The studies are older. It doesn't make any sense to me.
I'm sure it's not absolute, but we definitely have that demonstrated mechanism. If you think about dream theory, it's kind of interesting, right? If we don't imagine dreams to be some coincidence of the brain, then why are people dreaming more in depression? Are they trying to process something and they're failing to?
Right.
And then when you suppress it, are you just short circuiting the processing and treating the symptoms? This is all nearly pseudoscience, by the way. It's just something that I think is a little bit fun to think about, because in my opinion, most dreams actually have quite a lot of meaning. But I wouldn't avoid the antidepressant for that reason.
that's good stuff some you know psychoanalytic uh theory is heavily founded on dreams um yeah and i guess another to continue with the weird rem stuff um rem deprivation can treat depression which is very bizarre to me yeah if you just wake people up before they hit rem which if you do that to an average person they'll hate you and be miserable um it can help treat depression not in everyone but uh it's very odd
Yeah, it makes me think my little fan theory, not going to be studied, I don't think, is that what's happening in REM sleep for people who are in a major depressive state is what's happening with their mind in the awake state. They're stuck. They're ruminating. They're cycling instead of appropriately emotionally processing, even within the dreams, even the unconscious. And that by sort of breaking them out of that cycle, they're able to do new things during the daytime.
rewire themselves, if you will, and get out of that. And that is part of the treatment approach that I have for doing sleep in depression. I don't just want them sleeping more. I want them starting to get into a habit of sleeping at night and being active during the day. I try to build that into the behavioral activation component and making sure that they're well-rested. If you're not well-rested, I think it is actually unreasonable for us to expect people to start doing the exercise and daytime activities and sunlight exposure socialization so let's get the rest of the first i i that seems
like a really wonderful i would love to hear your uh my favorite things are probably your non-scientific theories because that's when you're kind of going into combining different um all right so that we we're touching about depression in regards to your treatment algorithm for sleep um let's move to bipolar
So bipolar is easier in a sense, right? In that the primary thing that you're trying to do is achieve mood stabilization. So obviously you want to try a mood stabilizer first. That being said, there's a directional effect where if you disrupt the sleep of someone with a bipolar disorder, they're more likely to cycle, right? So if that's the case, then I also want to stabilize the sleep.
For example, lithium might take up to two weeks to really start kicking in, right? I'm not going to rely on that. So I definitely give sleepers. And for a severe bipolar disorder, it's one of the few conditions where I personally might consider a benzo earlier or even as a long-term agent. I try to avoid that because, again, they do have their own side effects and problems and they have the dependency issue.
But some people with a primary bipolar disorder can only really be maintained well with a benzo long-term. It's still a minority. But what I do is then I will use the Moon Stabilizer in conjunction with one of these sleep agents. But I'm much more likely to reach for Gabapentin. And some of you may know that Gabapentin enjoyed more enthusiasm earlier in... the 2000s, as an agent for bipolar disorders.
And why not? It's an anti-epileptic drug at sufficient doses, right? There's got to be something going on. It's got a mechanism that makes you kind of wonder about that as well. And it's pretty well tolerated and not a lot of side effects. You don't have to do blood draws. So I tend to reach for it. And I find it pretty effective as well. Some people need a very high dose to get effect from it.
But it seems to work well and it's well tolerated.
Yeah, I will say I don't think gabapentin has good evidence.
No, the Cochrane reviews have concluded there's no evidence. I would say that based on the mechanism and clinical practice, it's a hit and miss medication, but worth using because of the considerations of risk compared to other agents.
So I would say the logic there is not that you're using another mood stabilizer, but rather you're not thinking it's helping, but that it's not hurting.
Well, personally, I do think it helps. I just don't think. Well,
I guess I guess based on the evidence, you wouldn't you wouldn't like you shouldn't say like, oh, I'm using another mood stabilizer. I don't think exactly.
Exactly. It's always at best a adjunctive treatment. Right. And it's adjunctive treatment only for things like anxiety and insomnia. in the bipolar disorder. It's not the primary treatment. You should not be confused for the primary treatment.
Now, talk to me about medications that you would avoid for sleep with bipolar.
Well, I wouldn't give peroxidine. A lot of people like to use Paxil kind of for sleep, but this is an SSRI. This is a potent SSRI with a lot of withdrawal effects. I don't want to give anything that can worsen the bipolar disorder. is the approach that I take with bipolar disorders. And that includes stimulants, you know, even methylphenid they'll avoid. But, um, yeah, antidepressant class medications.
Um, I generally don't avoid second generation as a rule, but obviously I would second generation antipsychotics. I'd prefer to maintain someone with bipolar disorder on mood stabilizers alone. If I can, obviously that's not feasible a lot of the time. And you're going to see, uh, depressive episodes sometimes, even if you're not going for an effective second-generation antipsychotic for some patients. It's just a matter of the side effect profile, the level of risk that you're giving the patient based on the medication.
I think it's worth mentioning that I would recommend avoiding trazodone or tazapine.
I would not say that. I don't find that trazodone in most people with bipolar disorders is a problem. Keep in mind, we have Psychiatrists out there who are still routinely prescribing antidepressants to people with bipolar disorders, the full-on ones. I do get wary and careful if we're going to TRASM above 150 in bipolar disorder or if we're doing mirtazapine above 15 or 20-ish. But yeah, they don't seem to be as agitating.
It's interesting to see that they used to give TCAs for mixed depression states. That's a little unusual, isn't it? It does seem like if there's sufficient sleep stabilization in some people with bipolar disorder, you're more safe giving an antidepressant class action.
Yeah, I had a mentor who felt that trazodone and mirtazapine could increase the risk of
switching to mania.
So I would typically just avoid them just because I think there's better options.
Well, I may be a cowboy. I find they're pretty good as long as you keep below a certain level.
All right. So I guess you mentioned you probably gabapentin goes way higher on your algorithm. Anything else that kind of moves up or down based off of broad algorithms?
Again, based on those concerns about the ones that can acquire antidepressant action, hydroxyzine, not a bad choice as well. But the attention really goes off that sleep support in the bipolar disorder and onto the mood stabilization, as you can expect.
Moving on, you mentioned paranoia and hallucinations that intensify in the evening.
Yeah. I mean, that's a simple algorithm. For the psychosis, you treat the psychosis. And as long as you're dosing the medication appropriately at the right time, you will help both the psychosis and the sleeve. I find that earlier career psychiatrists and residents sometimes will maintain their habits from inpatient and do things like give Risperdal BIDs. You know, giving it both in the morning and the nighttime or doing that with Haldol.
Not necessary, right? You can dose it all at night. That's fine. And you're going to help them stay active and less sedated during the daytime and more sleeping better during the night. Now, obviously, that's patient to patient. Some patients do do better on twice a day dosing. It just kind of depends. But I find that to be the exception.
Yeah, that's helpful because I was never explicitly taught that you can almost all meds, you can just move to all at bedtime. And that, you know, you come off inpatient, you're seeing meds TID or BID and simplify regimens for patients because it makes a
big difference. It's the shift to the outpatient that doesn't necessarily always get communicated in residency. I can only think of a few exceptions. Geodon, if you need a high enough dose, you're not going to absorb enough. in one meal, so you might have to go to BID. Saffiris, similarly, we don't have testing about how much is going to be absorbed if you exceed a certain amount. But if the patient wants to do this trouble, they can do two doses separated by about 30 minutes at night.
You know, you could do that. There's nothing technically wrong with that. There's another one that I'm thinking of. Oh, Seroquel, technically, all the FDA testing, at least, was with twice-a-day dosing, which is why they created Seracol XR if you wanted to do once-a-night dosing. But I expect that you can probably maintain a lot of people, even with primary psychotic disorder, that are being treated by Seracol with once-a-night dosing.
You may need to increase the dose. It's probably better just to use XR.
I think you can get away with the IR.
Yeah, I mean, I agree.
All right, now moving on to the next category is trauma and fear-related issues.
Yeah. I mean, in the trauma disorder, you do have what seems to be the neurobiological disruption of the sleep process. You kind of wonder about the dream mechanism getting dysregulated nor problematic, just like in major depression, because why are people having recurrent nightmares of a trauma? How does that help you? Well, that seems... pretty unusual compared to you know what we'd like for people anyway and it's extremely distressing right people become afraid to go to sleep in this condition because of how bad the nightmares can be and uh if your sleep's messed up well your mood's going to be messed up and you're not going to be able to make the necessary changes to recover from the trauma disorder in your day-to-day life uh you know returning slowly to safe places and um acquiring new safe experiences with people and environments is what you need in a trauma disorder.
So you really, really need to treat the sleep first, in my opinion, for the trauma disorder. And now you could wait several weeks sometimes or longer and try to rely solely on your SSRI. I think that's less effective and you don't need to do that. So trazodone is one of my big picks because, again, can be a little helpful for nightmare stuff. Prazosin, as you know, even with this mixed evidence, I see a lot of clinical efficacy.
Just watch that blood pressure. It's nice when the patient has hypertension. And then you can just give prazosin at the same time. You could think about things like clonidine. I don't use it myself. I find that its effects on blood pressure are a little too strong and it's not necessarily that effective. I have found gabapentin actually to be more efficacious in some people for nightmares related to traumas and sleep disruptions related to traumas than you might expect.
But that's very case to case. Some people don't respond to it at all. So just switch agents and pick one that works. You can, of course, use your hydroxyzine, your serequils, your mirtazapine. Theoretically, high-dose mirtazapine has more noradrenergic effect could potentially worsen nightmares, but that's theoretical.
Yeah, I'm surprised you don't have... quality a little bit higher.
Yeah, I don't. Okay. I mean, it's kind of based on your patients, right? When you have patients that are less willing to come in for blood pressure, I'm not going to use the things that may alter blood pressure too much.
Yeah, and I think another, you know, in terms of non-medication related things, image rehearsal therapy works really well for nightmares, you know, for high functioning patients, which, you know, can be difficult. But DBT has a nice nightmare protocol. I also made a little PDF that can help walk through someone. If I remember, I'll link it in the description or something. You should, yeah. Those can be helpful, but of course challenging because, you know, with anything that's fear related,
thinking about it can be very distressing yeah I mean you gotta remember the well I tell all the patients with trauma disorders that the medication is supporting their treatment but that the primary treatment is the things that they're doing in their lives and the psychotherapy if they're willing to engage with it right I think that's the key you have to be clear about what we have that has an effect you know you can help someone regress to the mean faster with just the SSRI but really the treatment is the psychotherapy and What's the first stage in the Jeanne model for trauma treatment is safety, right?
And you can offer skills, but if you don't specifically address their sense of safety and the safety of their environment and the safety or trust that they have with you in the treatment, just giving a handout is not going to go very far, right? So you got to have attention to that first.
Yeah. And what modalities of therapy do you refer to when you see a big trauma component?
You know, you got to go with what is local. Therapy is very local. You can probably get, you know, you see the studies. There's a lot of different therapies now that have been shown to be effective in trauma disorders. But anything that is a named and specific psychotherapy for trauma, I would generally recommend. That includes the IP, you know, the CPTs, right? the CBT traumas, even EMDR.
I don't have a problem with that as long as it's focused on trauma and kind of protocolized around trauma.
All right. Now moving on a category that you didn't mention, but I think is an important one. Medication induced insomnia. See a lot of patients who start SSRI and develop insomnia. What's your algorithm there?
Well, Personally, being sensitive to bipolar disorders and mixed states, if you are developing considerable insomnia on the SSRI and it's not that anxiety reaction that you sometimes see, it's pretty common for people of GAD to develop a transient insomnia that's actually their psychological anxiety getting worse, understandably, about trying this new medication. If I'm seeing more insomnia lasting than that from an SSRI, I'm pulling them off of the SSRI.
Okay. Again, I want the sleep to be stable first. Uh, so I'm going to try them on an alternative, um, medication at that point.
Would you try another SSR? Like when you say an alternative, let's say, you know, Lexapro caused it bad. What's your next step?
It kind of depends on how bad the sleep disruption is. You know, um, if the sleep disruption is bad enough, I won't try them on another mainstream SSRI at all. I'll probably go to something like a mirtazapine or a trazodone, um, or I'll at least try to add a gabapentin. I don't have a specific algorithm for that. It really just depends on the patient and what they're interested in trying.
Well, and what would you do? Because I do see patients who report a very effective SSRI that hurts their sleep, and the sleep problems did start. Like, I guess I'm not worried about a bipolar component.
Well, tell me about what happened to the sleep in a case like that, hypothetically.
I don't have, I'm not picking a particular example right now.
Well, that's okay. So, yeah, I mean, if it's sufficiently mild and I'm not concerned that it's some kind of a mixed state, then I just add any of my standard all-covered sleepers, basically. And I have them move the SSRI to the daytime, which is pretty obvious to you, probably. But if you look at the studies for how people tend to respond to different SSRIs, you can't really predict if someone's going to feel activated or they're sleeping on it.
And so I tell patients that and say, as long as you're taking it around the same time every day, that's fine. Find the time that works for you, morning or night.
Anything else that we didn't cover in regards to categories and different treatment of the symptom of insomnia?
I mean, there probably is. We have to understand that personality disorders can come with a lot of maladaptive coping or emotional dysregulation that will then disrupt sleep considerably. Right. And we have to be wary of that and wary of medicalizing that, of course, can be hard to differentiate between that and some trauma disorders. Right. We want to be careful about being overly aggressive in treating sleep, but I just feel like the field right now is maybe under-aggressive.
It always changes depending on the year that you're practicing.
Now, what do you rule out if someone is reporting bad sleep before starting a sleep med?
What do I rule out? Well, I do have concerns about sleep apnea. It's something I keep in mind. I go off the clinical history, though. I'm not sending everyone to a sleep study. If I hear something that sounds at least suspicious for sleep apnea, like multiple nighttime awakenings, trauma disorders can mimic this, but I still consider it, you know, gasping, choking, snoring, if they have the risk factors.
if they have excessive daytime sleepiness on top of that, then I'll do a little stop bang or I'll just tell them to talk to their primary care doctor about sleep study. Since I get a detailed sleep history, I listen for anything that suggests there may be a primary sleep disorder and I'll refer as appropriate.
Yeah, in that area, there's a cool website, com. You can do it with the patient or have the patient do it themselves. It basically, it's nothing too fancy, but it screens for insomnia disorders, circadian disorders, obstructive sleep apnea, restless leg syndrome, narcolepsy, or parasomnias. Basically, it just asks the very basic screening questions. I think it's helpful just for ruling out things this way. You're not treating insomnia.
You're not trying to treat insomnia when you're actually missing something else that's important. You should never treat... It's dangerous to treat insomnia with... Or treat what would be like a sleep apnea when... Yeah,
you're not supposed to give sleep medications to untreated sleep apnea. It's not good, right? You're just going to be suppressing their respiratory drive that they need. This is a big challenge for me, for my patients that have the sleep apnea, but don't like the CPAP. And, you know, not having worn a CPAP myself, I don't know what it's like, but based on their reports, it sounds like some people find it extremely uncomfortable, you know, and it's tough because that's one of the big issues for them.
That's impacting their sleep quality, which is therefore secondarily impacting their mental health.
I recommend before starting a sleep med, I think it's worth doing com. I think some other things you want to make sure that you're not treating with a sleep med for patients that easily sleep super late at night or easily sleep early but aren't able to do that because of their work schedule is You're dealing with a circadian disorder rather than an insomnia. Not that we have insomnia defined well.
There, you should be going more for melatonin and bright light regimen. Because there you're dealing... You want to adjust their circadian rhythm.
Yeah, great point. That is definitely my approach as well. If you're seeing it's a sleep cycle offset issue, you have to really examine the behavioral... or psychological components that are contributing to that. Maybe it's something they're not willing to change at all, right? Maybe it's something to do with their work schedule that they can't change. But if they can change it, I try to get people on a better track.
And melatonin, in that case, you got to remember, has double effect, right? It has an effect on sort of regulating the sleep clock and also has a sedative effect. You may want to be using it earlier than you'd think several hours before the intended bedtime in order to try to pull someone's sleep clock back a little bit.
Yeah. It's very, there's also massive, or I might be wrong, but it, you know, some people call melatonin sedating to me, Tic Tacs are more sedating. Um, it's very, there's like, yeah, everyone's different on that one.
Some people find it very sedating, but yeah, because of its weird deal effect and the unregulated quality on the American market, I don't tend to go for melatonin, um, very often, but, uh,
you know,
some people find that they like it or they're already using it over the counter. I'll definitely keep track of it. And, um, time it and give instructions around it and other medications.
Other things I would avoid using a sleep medication. If someone's drinking a lot of coffee or stimulants, even if it's super early in the day, I see it all the time where physiologically it doesn't make sense because it should be out of their system. But if the person cuts back on those things, you do see improvement in sleep. Of course, within reason, I'm not saying if they're drinking one cup of coffee, don't have them cut it out.
But If someone's drinking four cups of coffee at 8 , it could have an impact, even if it doesn't make sense that it should be out of their system. I see all the time.
Well, if I recall, the amount of cruciferous vegetables, broccoli, cauliflower, Brussels sprouts that you eat can affect your caffeine metabolism. There are certain racial trends in caffeine metabolism as well. So, yeah, totally plausible that one person's caffeine metabolism may be rather different. And yeah, you definitely want to examine what kinds of herbs, supplements, natural remedies, drinks that people are taking before you jump straight to sleeping medications.
Other things, alcohol and marijuana massively negatively impact sleep architecture. It's worth telling patients, why don't you try going off of it for a little bit? Now, with marijuana, you're going to see massive REM rebounds. I hear people have crazy, crazy dreams when they come off of it, so they don't want to. That's telling you how much REM is being suppressed because they're trying to make up for it.
You know, if someone says, you know, if you ask them to stop for a period and they say like, oh, I'm not able to stop for a period, you're probably having a substance use disorder there.
Yeah, it's a tough one because it's so easily available now. And we're now on to decades of unfounded assumptions that it's harmless. Now that we are on several years of legalization now, we're seeing a lot more evidence of harm, right? and even brain structural changes with heavy use. Be careful, folks. I tend to reach for gabapentin when it comes to helping patients who are motivated at least reduce the cannabis use.
Often, if it's not purely recreational, there's definitely a component that they're using it to help regulate their sleep, secondary to the issues they're having from the XS1 condition. Gabapentin, at least a little evidence for it, but you can use anything to help with that.
How do you dose gabapentin?
It kind of depends on the person. Some people find 300 milligrams to be nothing. Some people find it to be overly sedating. At least for my clinical population, I'll start with 300 and I'll say, if it's not enough, go to 600 and call me. And if it's way too much, call me and I'll send you 100s. So basically starting on 300 and then titrating to effect. If they use daytime cannabis, I will give them additional doses to take PRN during the daytime, but specifically in place of using the cannabis.
I'm saying I'm giving you to use this when you have a craving for cannabis, try using this instead, and let's see how you do.
Right. Next thing that I don't think is insomnia and should not have a sleep med, people who stay up doing exciting things. So people who are on their phone till 3 , people who are on their computer till 3 m. will come in and say, I can't sleep. You know, I can't sleep. I need a sleep pill to fall asleep. The if you're on your phone, you can't be asleep.
So, yes, they might report request a sleep med. You need to. I mean, realistically, we're talking about potential like cell phone addiction. I don't want to, you know, people who are going to use addiction just say using their cell phone too much, using their computer too much. A lot of people wait till, you know, no one else is up and they can use the phone one on one.
Their psychoeducation is important.
Yeah. It all depends on the reason, though, right? Some people do that doom scrolling or go into the bar or the club as a way to avoid certain memories, thoughts, ruminations. And if you give enough, if you give the medication with instructions to take it every night at the right time, it may just sedate them out of doing that regularly. You know, that's, by the way, why I think we even have a signal from that study with mirtazapine for meth use disorder.
I think we were just sedating people keeping them asleep overnight and out of trouble um yeah and that
that brings me to i do want to talk a little bit about sleep hygiene um and i think that you know this is related one thing that's interesting is when they do studies handing someone a sleep hygiene sheet does not work oh what a surprise um yeah and you'll see online saying that like you know there's low quality evidence for sleep hygiene what i do agree with is telling someone uh you need to work on your sleep hygiene does not work um handing someone a generic sheet with a bunch of sleep hygiene rules doesn't work um but that doesn't mean that the things that are on it don't work
Correct. Yeah, the things are on our key, right? And the question is, how do you get someone to appreciate that something that they're used to doing is a problem enough that they should put in the effort and face the anxiety of change to do it? Well, I think it's best to just get a good sense of what they're actually going through and doing at night and then asking them what they're willing to change by the next visit.
Small steps, even if it's one small thing, even if they're going to try it once. The goal is to have a goal and to try it more so than to reach some change. I think that's a little bit more effective than raring to go on big clinical changes.
So I guess what would be examples of like questions you would ask and things you would try, you know?
Tell me what you do at night. Tell me about your, what time are you going to sleep? When you go to bed, what are you doing? And then what happens? What's going on in your body and your mind? Are you waking up after that, et cetera, et cetera, right? And let's say, well, I honestly, I do have a tendency to doom scroll. Okay. Well, are you using a blue light filter?
Okay. Well, is there something that you're willing to do to change the amount of phone use that you're having at bedtime. What about you just set a timer on it? What if you say that I'm going to stop using it after a certain time? It's just, you know, any of the basic sleep hygiene stuff, making small changes, whatever they're willing to do. And of course, impressing upon them how it is impacting their life.
That's important, right?
Mm hmm. Yeah, absolutely. And I've seen, you know, saying, even though handing a sheet of sleep hygiene doesn't work, I have seen patients that the only recommendation, the only recommendation that occurred after kind of a similar conversation was, take your phone and keep it. I mean, this is a big one, just charge your phone outside your bedroom, like your, your phone should not be on your bed, bed, nightside bed table, and you should not be using it, putting it down before you go to sleep.
that one recommendation alone for people who are kind of in that cycle of doom scrolling can be the thing that fixes problems.
Yeah. Small changes can be underrated.
Yeah. And I think I could talk, uh, I do want to do more of a deeper dive into the, the psychological aspects of insomnia, but I think I'll save that for a solo thing just because it'll be a, yeah. Any other topics you want to talk about things that we haven't touched on?
No, I mean, I think that's it. To me, sleep's like pretty bread and butter, even though I think it's under-emphasized in training programs, you know, almost an afterthought. Again, because I think the field has framed it as something that isn't psychiatry, even though we treat it all the time. And I think we just need to have a lot of attention to it as a core component of psychiatric conditions, sleep dysregulations, and the treatment.
Yeah, it's funny you say it's bread and butter because... If you actually go out and look for an algorithm for sleep, there's none guiding psychiatrists. Exactly. The American Sleep ASAM recommends against all the medications we use for insomnia. That's right. They basically say CBTI or Doxepin or nothing. Yeah. And I think they do like the Z drugs and whatnot. But that's not what you see at all in terms of how people see it.
Yeah, because we're seeing different patients. And I guess we just don't conceptualize it as sleep treatment we conceptualize as psychiatric treatment yeah and i you know i
it's weird i do because you were talking about you feel like it's under medicated i think it's under medicated in some areas and over medicated in some that's because
i do see a lot of private practice psychiatry is probably being over medicated by addictive drugs
Yeah, and in New York City, I see it. Everyone's on it even. Yeah. People who were probably handed a sleep hygiene PDF, and then that failed, and they started a sleep med.
So let's say you can simultaneously undertreat and over-medicate a sleep problem. Maybe that's what's happening.
Ooh, undertreat, over-medicate.
Yeah.
Yeah, and I agree. I think it's undertreated and over-medicated.
Well, that's probably a good point to stop. It's about that.
Do you have anything else? Any other burning thoughts?
Like and subscribe, I guess, when you have nothing else to say. Like and subscribe. All right. What did you learn? What did I learn? Oh, liquid doxepin. That was great. Yeah. That's a banger, as the kids say.
um yeah i like like the doc spin um what did i learn i learned a lot i liked the breaking it down uh like i said i this kind of stemmed from the fact that i was looking for site like you know nice guidelines and they don't exist so hearing you know pretty helpful rules of thumb is is very helpful All right. Are we signing off? Signing off.
See you next time.