Psychiatry & Psychotherapy Podcast - Commonly Prescribed Sleep Medications and Treatment for Insomnia

Episode Date: September 15, 2021

Insomnia is a fairly common problem; it is likely that almost all individuals suffer from at least transient insomnia. In this episode, Michael Cummings, M.D., Shizuka Tomatsu, M.D., and Shilpa Krishnan, D.O. join the discussion on psychopharmacological treatments, lifestyle, and therapy recommendations for insomnia.  By listening to this episode, you can earn 1.5 Psychiatry CME Credits. Link to blog. Link to YouTube video.

Hello and welcome to the Psychiatry and Psychotherapy Podcast. I'm here to talk about getting rid of burnout, increasing job satisfaction, and feeling like an expert in what you do. One thing that created a lot of burnout and angst for me was trying to get continued medical education right at the last minute. So why not join the CME membership and do CMEE while listening to this podcast? Go to Psychiatrypodcast.com, sign up, sign in, take the test, and the certification is emailed to you in seconds. Today we'll be discussing the various psychopharmological treatments for insomnia, some of the lifestyle and therapy recommendations as well with Dr. Cummings and two second-year psychiatry resident physicians from Atrium Health in Charlotte, North Carolina.

I got connected with them from Dr. April Schindler, a former medical student and someone who I have connected with since she graduated and done some coaching with her. She's an awesome psychiatrist in Charlotte, North Carolina, if you need one. So Dr. Tomatsu is interested in the biopsychosocial connection between mental health and sleep, and Dr. Krishnan is interested in providing care for the LGBTQ community and trauma therapy. They have prepared a comprehensive 35-page handout about sleep medications, often used in practice with my mentorship, and Dr. Cummings' recommendations on articles to include. I have enjoyed their incredible work ethic, responsiveness, and professionalism.

So if you know them, give them a big hug for me. There is no conflict of interests to report for any of us for doing this episode. And in this episode, we will start with an overview of insomnia, go over some treatments, that we may not think about very often, such as screens before bed, and talk about it with some nuance that hopefully you learn something. I know I did. And then we discuss medications. We go over the major classes of medications, you know, which ones are better for some situations. I had about 300 questions that came in. For those of you who are part of the free resource library, I sent out an email and got questions for this episode, and it was about 300. So we try to

include as many answers as we could. Obviously, we couldn't get to everything, so I apologize. Hopefully you take away a lot of really good nuggets of clinical pearls that you can just immediately put into your practice. That's really the goal of this podcast to give you things that you can translate directly into those you see. As always, I would like to thank those who continue to get CME for this podcast. I am blocking off more time to get these episodes flowing and your support is allowing this to happen. If you don't already support this podcast, this can be done by going to Psychiatrypodcast.com and signing up. I have tried to make this process super straightforward and I think that it will be an easy way to get your CME needs met,

your self-assessment needs met, while enjoying listening to this podcast. If you're listening right now, you're already listening. And so why not sign up for seeing me? All right, here we go with the episode. Welcome back to the podcast. I am joined with Dr. Cummings, a veteran of this podcast. I am here also with Dr. Tumatsu, Dr. Tumatsu, they are psychiatry residents, second years. Dr. Tumatsu is going into sleep medicine. Dr. Krishna, interested in trauma. Helped out quite a bit. Both of them creating the handout. It's about 44 pages at this point. And today we are going to be talking about. about commonly prescribed sleep medications. We'll talk about CBTI just a little bit, insomnia. I asked for your questions if you are a member of the psychiatry and psychotherapy podcast email

list, which if you've gotten any of the resources you are a part of that list, and I got three, four hundred questions. So I was not expecting that many questions. It shows a lot of interest in this. We'll get to as many questions, responses as we can, but then maybe we'll have to do a Q and a follow-up to just kind of see what else we can flesh out. So Dr. Cummings and colleagues, thank you so much for joining us. Yes, glad to be back. Dr. Christian and I are very excited to be here. Yeah, thank you so much for being here. It's good to having you guys. And this handout is pretty amazing at this point. It goes through pretty much every sleeping medication. We looked at effect sizes, side effects. So Dr. Covings, why don't you start us off and tell us a little bit about

the big picture of insomnia and then we'll get into the medications. Okay, insomnia is a fairly common problem. In fact, surveys in most countries, including the U.S., suggests that at some point, almost all individuals suffer from at least transient insomnia. The American account, of sleep medicine defines transient insomnia as lasting a week or less, acute insomnia, a month or less, and chronic or recurring insomnia as lasting more than a month. The other thing that's interesting about the broad population statistics is that primary sleep disorders are relatively rare compared to secondary sleep disorders. some 90% of sleep disorders appear to be caused either by other psychiatric disorders such as depression or anxiety or psychosis

or by associated comorbid medical illnesses about 5% are primary chronobiologic disorders and about 5% are primary insomnia of various types Yeah, I can relate to that. I recently had COVID and probably the worst insomnia I've ever had. And the sort of the fear of the future, you know, what's going to happen also. Kind of made that worse. We were talking about COVID before we came on here. And I don't know.

Have you seen that with COVID at all, Dr. Cummings? Quite a bit. There's both insomnia as a common component during the actual acute phases. of COVID-19 infection. And there also have been several studies looking at either what's come to be called a long-haul COVID, those people who were unfortunate enough to have ongoing symptoms for three months or more. Insomnia is a common component of that.

And even in people who don't have long-term COVID symptoms per se, post-infection, anxiety, cognitive deficits, and sleep disturbance are very common, at least for six months following the infection. Yeah, I've had a number of cases like that. Okay, so getting back to this overview, what would you consider terminal insomnia? Some people ask some questions about terminal insomnia. Okay, in terms of the structure of insomnia, sleep scientists have largely described it in three phases. People can have initial insomnia, which essentially is difficulty going to sleep. Middle insomnia, which is characterized by waking up during the middle of the night, in particular around the time of the inflection point for low body temperature,

and what should be maximum melatonin plasma concentration, and then terminal insomnia is early awakening, in essence, that is waking up early in the morning before the person should be waking up. So when you think about just general treatment and you're taking your history of insomnia, are you trying to delineate like when this happened, what started it, what coincided with it, what time of the evening, it is like what are some of the general yes and indeed i think one of the one of the core elements when somebody presents with a complaint of insomnia as in all of medicine the first step is not

to reach for the prescription pad the first step is to ask them about the insomnia indeed when did it start were there associated factors illness injury acute stressors change in job demands, change in habits around bedtime. Do they wake up early, middle, late, or they wake all night? Because essentially what the clinician should be attempting to do is discover if there are identifiable causes of the insomnia, because indeed the treatment needs, of course, to follow the cause. if, for example, the person's insomnia is caused by a pain disorder, then treatment of the pain

may be the focus of treatment. If it's being caused by a central or obstructive apnea, that needs attention. If it's being caused by a comorbid psychiatric disorder, often treatment of the comorbid disorder rather than the insomnia itself becomes the focus of treatment, which is a roundabout way of saying that we, as in all things in medicine, we need to look for what's causing the insomnia before leaping forward to choosing a treatment. Yeah, and Dr. Tomatsu and Dr. Tumatsu and Dr. Krishnan, you can jump in whatever you want if you have any questions for them as well.

Yeah, I definitely agree with Dr. Cumming. With medication, you know, it could physically knock you out and put you to sleep, sure, but it may not enhance the quality of sleep and it's masking the underlying cause of insomnia. And CBTI is really the gold standard recommendation from American Academy of Sleep Medicine. But why is it that we don't do a lot of CBTI? It primarily has to do with the fact that, you know, it's a time intensive therapy course. And, you know, if someone cannot afford it, insurance. So all those barriers are there, which causes.

this patients to not prefer CBTI as the first line of treatment. And that kind of puts us in a position where, you know, if the patient is saying, I want to sleep tonight, we look at the medications that could potentially help them fall asleep, but we're not really treating the insomnia. Yeah. And indeed, sometimes there are very simple environmental interventions. I have seen patients, for example, where when you ask, them about their sleep, you begin to discover things such as they're drinking a stimulant just before

bedtime, tea or coffee. They may be engaging in activities such as late night reading on a brightly lit screen, which is a great way to cause circadian disturbance, or engaging in vigorous exercise just before bedtime, another way to wake yourself up. Or they follow an erratic sleep pattern because they're doing shift work or other such things. Many things in the environment can also cause difficulty with insomnia. Yeah, we had some questions about adolescent sleep, and one of the studies that I found showed that a lot of adolescents are on their phones in the middle of the night.

And I've done all of those things that you listed, by the way, Dr. Covings. I think I had coffee last night, which was like a bad decision. And unfortunately, especially with, you know, now that we live so much of our lives on screens, unfortunately, the screens we're using often emit light in the part of the spectrum that human beings are most sensitive to in terms of resetting the super-chaismatic nucleus, the internal clock. Humans are relatively insensitive to light at the red end of the spectrum above 680s. 80 nanometers as you get down closer to the blue green end of the spectrum, our sensitivity peaks at right around 210 nanometers. And unfortunately, a lot of our phones and computer screens emit a lot of light toward the blue

green end of the spectrum. And that's a great way to suppress melatonin and essentially make your brain think that, oh, it's morning, I need to wake up. What time do you recommend, like, some people wear like these glasses that stop the blue light coming through, or you can have your iPhone or phone often stop showing these colors? Yes. What time of day do you recommend how many hours before sleep? Like, let's say someone's going to sleep at 10 o'clock. What do you recommend?

They should stop probably exposure to light by around 8 p.m. This isn't light as in lights on the ceiling, is it? No. In fact, it wasn't until 1980, and a researcher at the University of Oregon, Al-Louis, discovered that human beings actually were sensitive to light. Prior to that, it was thought that humans didn't respond in terms of their chronobiology to light exposure, because compared to nocturnal animals, were way less sensitive.

But he demonstrated that if you get the light bright enough, we do respond. For white light, a human being requires exposure to about 2,000 lux, which is about what you'd get if you were standing close to a sunny window on a sunny day. In contrast to that, most of the lights in people's homes, bedside lamps, ceiling lamps, the average lighting is right around 500 lights. which is below the level that human beings will respond to. Okay, but there's something about the screen being up close to your face and the brightness of it.

Yes, it's close, it's bright, and unfortunately, these settings tend to be toward the blue end of the spectrum, which we're more sensitive to. Okay. I had a question, Dr. Cumming. So I looked into the blue light walking glasses a couple years ago. And at least at that time, I couldn't find any actual evidence of those glasses being helpful because they're not harmful. It's one of those, well, if you think it helps you, great. But there really was no concrete evidence as to those pair of glasses helping. Indeed. There is not great data to support the glasses.

In part, I think, because people still tend to expose themselves to more like, than they should when they're using glasses that block part of the blue-green spectrum. The other issue has been that there's been a huge amount of variability and the quality of the glasses that people buy. I think probably the better advice for our patients is to stop looking at screens that emit bright light at least by 8 o'clock in the evening. The onset for most people with a fairly average. sleep wake cycle for onset of melatonin secretion is right around 9 p.m. So if you're exposing yourself to bright light at 9 p.m. 10 p.m. 11 p.m.

You're going to be causing a suppression of melatonin secretion. And the consequence will be that you will phase delay your sleep wake cycle because your brain doesn't yet know that it's dusk, that it should be time to go to bed. Essentially, melatonin is the neurohormonal reflection of dusk or, you know, sun's gone down, it's getting dark. Yeah, I could improve my own patterns here. One thing that I've realized is like sleep associations, as I'm thinking about this, I'm thinking probably most people who are listening to this have a sleep association of being on their phone before bed,

or having the TV on, or a lot of people have that, at least that I talk to. And so the sleep association may take a couple days to break, you know, because we're so used to that which we sleep around. Yes. So, like, I've had a couple clients who, like, TV is their sleep association. So I said, either you have to have the TV on all night or you have to completely remove the TV. Because when you wake up in those lighter cycles of sleep, you want that sleep associated. and that's why you're waking up, you know, every two to three hours throughout the night.

I don't know if you have any thoughts on that. I would certainly encourage people to migrate away from things that emit light at night and move more toward, you know, if they need a sleep association, pick something relaxing like background white noise. There are plenty of options such as babbling brook sounds, rain, you know, other sounds that people may find soothing and may actually help keep them awake, or a sleep rather. You know, so certainly a place that all of us, I think, can improve our sleep is by improving

sleep hygiene. You know, one of the mantras during the sleep research that I did was that people should not, you know, take work projects, other things to bed with them. They should use the bed for sleep, essentially, rather than all sorts of other things. Sleep and sex. No arguments in bed is one thing that I say to clients as well. Don't argue in the bedroom because then that will be associated with like sleep, right? Or sleep will, it's kind of like this.

Yes. Yes. I had a patient that was pretty interesting. So she would have Western Cowboy movies playing before she would go to bed. And obviously the first thing we thought of was, well, let's turn off that TV in the bedroom. But when we really got to the bottom of why she was watching specifically Western Cowboy movies before bed, it turned out that when she was little, she used to crawl into her parents' bed and they would always watch cowboy movies before bedtime and it would soothe her to fall asleep. And so when we heard this, we realized that for this patient in particular, even though, you know, TV is not really recommended for most people before bedtime, for her, it was actually acting as a way to calm her brain down and calm herself down at the end of the day to fall asleep.

So I just thought that was really interesting that, you know, even the majority, TV is bad. People can do something like that. I do make a couple of suggestions in those cases. is one, they should set a timer on the TV so that the TV will turn itself off after they go to sleep. You know, because there's nothing like going to sleep with a soothing Western and then waking up at one in the morning when the infomercial comes on. And the other thing they can do is be sure that the TV screen is not overwhelmingly bright. most TVs have some capacity either by placing it further away or by angling it or in some cases, depending on the TV type, you can actually change the brightness of the screen so that it's dimmer.

So if it's dimmer and it's soothing and then it turns itself off after you go to sleep, that's not so bad. What you really don't want is something bright and glaring that might initially be soothing, but then at 1 o'clock in the morning, the guy who's trying to sell, you know, ginsu knives or whatever comes on and is yelling at you. Yeah. Oh, man. Wow.

I mean, there's so much here, like, that's behavioral. And one thing you mentioned, Dr. Cummings, is don't exercise before bed. I used to exercise at 8 o'clock every night just because that's when the kids were sleeping and I could exercise. And then, like, once I started deadlifting heavy. heavy, I noticed it was hard to sleep. But I do think that exercise in general does help with sleep as well, and that's one of the recommendations I make. Yes, exercise is very helpful with sleep, especially aerobic exercise, but it shouldn't

occur just before bedtime, because if you're exercising, you're intentionally increasing sympathetic activity and tone, and that will keep you awake. I have a question for you, Dr. Cummings and Dr. Puter, about how to improve sleep overall in the inpatient setting. I know we have a lot of non-pharmaceutical options kind of on a day-to-day basis that we can manage with patients on an outpatient setting. But acutely, you know, we use a lot of pharmaceutical options, but what can we do otherwise to just stay away from using the drugs? There are things in hospitals, by the way, in general, are terrible places to sleep. in part because, you know, in many hospital settings, especially medical wards, the nurse is going to come wake you up in the middle of the night to take vitals, etc. And cases where people don't really

need their vitals taking that often, one thing physicians can do is actually do away with the nocturnal measurement of things like vitals. You know, if somebody's not being treated for something that involves disturbance of their vital signs, that particular medical habit is not something we actually have to do. We can also be sure that medications are scheduled so that if the person is somebody who goes to bed earlier in the evening, we don't necessarily want to wake them up after they go to sleep and say, here, I have a medication for you to take, that sort of thing. So doing those sorts of things in the environment and certainly working with, the hospital administration and nursing staff,

hospital units can be looked at in terms of changing the lighting in the evening, changing the noise level. Now, there's some areas in hospitals where that's very difficult to do ICU's, for example, often actually induce delirium because of all of the alarms and machinery and the activity. You know, the person is in an environment that doesn't have good time cues and which is, in many cases, determined to keep them awake 24-7. Those are all good things.

I would say, you know, there are situations where meds are going to be very important, I think especially about, like, bipolar patients. I can't imagine treating them without sleeping medications almost. I don't know, Dr. Cummys, if you have similar thoughts. Yeah, there are situations in which sleep medications are useful. we should always, when we can, be attempting to use them for as short a period as feasible, in part that's because there are a number of studies that have shown that chronically taking sedatives or anxiolyics

is associated with an increased mortality rate, usually with a hazard ratio of between three and four. So these are not inherently innocuous medications. Are we talking about benzodiazepines or? Benzodiazepines or the selective Z drugs. Both have been associated with increased mortality rates when taken chronically. Now, is that because these people are sicker and these people have lots of other problems and that's why they get on these drugs? Or is that because, you know, the drug itself and the risks that the drug puts them at?

It may likely be because of the drug itself. One of the studies I included that I sent to you for inclusion along with the information to go with this podcast was a very large United Kingdom study in which they looked at literally thousands of patients in primary care and found an association with a hazard ratio above three for treatment with anxiolyics. or sedatives. The people who were being treated with the anxiolyics and sedatives were compared in a two-to-one ratio with people who were not taking sedatives and anxiolyics, but they were all being treated in a primary care setting, which would suggest they were all suffering with a variety of medical problems. You know, the rate of mortality, all-cause mortality, was higher in the people who were taking sedatives or anxiolytics for a long period of time. They specifically did avoid looking at people who were severely ill, terminally ill,

so that one of the things included in their model is people had to survive for at least 12 months after entry into the study in order for their data to be included. So these were not people who were receiving massive amounts. of sedatives or anxiolyics because they were at the end of life. Yeah, Dr. Cummings, I took a look at that study. I found it to be really interesting. I mean, they were able to kind of control for a range of psychiatric and physical comorbidities and match, like, you know, so that they could get as close of an approximation as possible

with, you know, the impact of benzodiazepines and the Z drugs. Yes. And that, you know, and absolutely, like a three to four. you know, three times to four times more with the Z drugs and the benzodiazepines compared to people of similar backgrounds. And, yeah. Well, indeed, that was one of the reasons that one of the things that prompted them to pursue this very large-scale study was that smaller, shorter studies had, frankly, produced mixed data in part because of the

problem of comparing oranges and apples, people who, had different types of illness that were on drugs for varying lengths of time. So they didn't have good direct comparison. So this study was unique and was very beneficial in terms of helping to isolate those people taking sedatives and anxiolytics versus those people who were not. You know, so there's data in the U.S. that like 12.6% of adults reported past year, benzodiazepine use and misuse accounted for nearly 20% of overall use highest in the range of 18 to 25 and lowest in the elderly, which is 0.6%. So mostly the elderly are not misusing these

drugs. But it's just like, it's like one in 10 people is on one of these meds. And if you look at that data from the, you know, that was taken, I think from the national survey on drug use and health in 2015 and 2016, misuse was the highest in the younger population, but in terms of use as prescribed, you know, the highest number of prescriptions was actually in adults over 50 years old. Yes, which brings us back in some ways to where we started with, we should be looking for underlying causes of insomnia rather than committing the individual to chronic insomnia treatment. And although the other thing about the benzodiazepines that as a pharmacologist I always bring

up is that for treatment of insomnia, the benzodiazepines are useful as very short-term medication, somebody who has transient or acute insomnia, but people become very tolerant of the benzodiazepines in terms of sedation very quickly. By the time somebody has taken a fixed dose of benzodiazepine for four diseases, you know, six weeks every night, it no longer has a sedative effect. When I was at UC San Diego, we did that study in which we looked at people, put them on a fixed dose of tamazepam, and indeed their sleep duration, their sleep efficiency improved during the first week of treatment.

Then it began to deteriorate. And by the time they were out four to five weeks, their polysumogram looked just like it did the first two nights when they were only taking placebo. Yeah, there was a study we found on CBTI versus Tamazepam in 2006. It was a randomized controlled trial. And what we found was that after three to eight months of follow-up, it seemed like the CBTI was considerably better. Do you want to speak to this study in particular? Who looked at this one? Yeah, that was me, Dr. Krishna. Yeah, so it was a 2006 randomized control trial. It compared CBTI with a combination of CBTI and Tamazepam and then Tamazepam alone, as well as the placebo. And they looked at outcomes of sleep latency, efficacy, and total sleep time. And initially, kind of within the eight weeks of the treatment duration, the Tamazepam alone group actually did better than the CBTI. But in terms of the

of the sustained, you know, improvements with at three months and eight months, that was really only observed with the CBTI group. Yeah. Yeah. You know, as a provider, what I got through the emails was a lot of people are frustrated on how difficult it is to get patients into CBTI. So one of the episodes I want to do in the future is just like teaching CBTI to the providers, giving them a handout that where they can get started doing that on their own. But I'm wondering, Dr. Cummings, like, with this knowledge that CBTI is so effective and it's so difficult to get patients this treatment, what do we do as providers, you know, when we get hit with someone with insomnia and we want to help them? Well, I think, you know, I think indeed short-term use of sedatives, particularly the Z drugs, can be useful. They do not disturb sleep architecture nearly as much as the benzodiazepines or the antihistamines do. So they can be useful, particularly in people whose insomnia is not chronic. And indeed the vast majority of people who have a difficulty with insomnia have it for a shorter period of time. They either have transient insomnia or acute insomnia, but not chronic primary insomnia, although there are such people.

The Z-drugs, at least Zopa clone outside the U.S. and S-Zopaclone inside the U.S. has been used to treat chronic insomnia successfully, albeit it comes with that risk of an increased hazard ratio for all-cause mortality. I think the other thing that we can do, the other primary type of insomnia, the circadian disturbance is we do have good interventions for that if people can find a reliable source of melatonin, that is useful as chronic treatment does not appear to have

much of a downside for circadian disturbances. And we also have Ramealtion and Tasameltion, which are synthetic analogs of melatonin, which can be used to treat people with phase disturbance or shift work or jet lag types of insomnia. successfully without a lot of downside or risk. Okay, so a couple things people asked about. One is, can you take melatonin long term? What dose is the best? What dose is the best for children, specifically, is 20 milligrams too much?

In terms of the studies, which have looked at modulation of circadian rhythms, have found that the peak efficacy, occurs between three and five milligrams a day, usually taken in the early evening, about an hour before the natural synthesis and release of melatonin would begin. So we're talking about taking the melatonin dose around eight in the evening for most individuals, or about an hour before they would like to start to become sleepy. Now, if you raise the dose, at least the studies I've looked at haven't found anything catastrophic that occurs. At doses above five milligrams, the melatonin

begins to become directly sedative. And by the time you're up to around 15 to 20 milligrams, people then do have some impairment of alertness and cognition, at least in the early part of the following day. So my guess is for most people, you're probably looking at a dose range between three and five milligrams. As in most things, melatonin has not been as well studied in children as in adults, although there is no evidence of toxicity in children. I have a question.

I read somewhere that the melatonin receptors in our brain are saturated. at one milligram or less of oral melatonin. Yes. And so I guess my question is, you know, everything you see over the counter really starts at three milligrams plus. That's largely because when you're taking the medication exogenously, melatonin and the two synthetic analogs all have fairly limited bioavailability when ingested. The other issue with melatonin is that melatonin, remeltion and tasimeltyon also are very short half-life drugs,

which of course is different than melatonin being supplied by the pineal gland, because it's engaging in synthesis, particularly during slow wave sleep throughout the night, so that it doesn't go away quickly. the pill the person takes, if they were to take one milligram, their melatonin receptors would be saturated, but it would be a very brief saturation because it falls off so rapidly. Half-life ranges from a little less than an hour to about an hour and a half. So the oral medication goes away quickly, unlike what occurs in the pineal gland where synthesis begins once darkness, occurs and then continues throughout the night beginning to fall about two or three in the

morning and then being truncated by sunrise the next day. So the other thing I wanted to ask you was about Rameldean. Oftentimes, a lot of insurance don't cover Ramellion for the patients at least I've encountered, and so I definitely don't have a lot of experience with it. But when I looked into the literature, it looks like there is a study that showed if you take romeltyon compared to placebo, people may fall asleep about 19 minutes faster if you take 16 milligrams of remeltion. But in the big picture of things, you know, is that really clinically significant? For most people, no. You know, the dose range for Rameltyon is 8 to 16 milligrams.

Its bioavailability is 1.6%. So truly awful bioavailability. It does improve sleep onset and very early stage sleep. So if that's the person's problem, it works very well. If they're having more difficulty with middle and terminal insomnia, frankly, taking an oral dose of Rameleon is not going to. to do much for them as a direct sedative. The other area where Ramealtion or Tasameltian or Melatonin actually is better than being a direct

sedative is when the person has issues with, for example, phase advance of their sleep wake cycle. A good example of that are in older people, elderly people who want to go to bed at 6 p.m. and then get up at 2 in the morning and they're not very happy because that doesn't fit their social obligations very well. If they take even a modest dose of one of these chronobiology drugs in the early evening and they can retrain their clock so that at phase delays, they can start going to sleep more at 10 and getting up at 6. Now if you reverse that and you take one of these drugs in the early morning, say you set your clock and you take a dose at five or six in the morning, you'll actually cause your brain to think that it's staying darker or longer,

so you'll phase delay your sleep. In the middle of the day or in the middle of the night, the response to melatonin or the analogs is fairly negligible. Okay. So you're saying, in general, good for sleep onset issues? Good for regulating your clock, but not so good as they direct overall sedative. Okay. I want to jump back to Benzos real quick because there was a question in a previous episode on if it increased the risk of dementia. And when I asked you about this, Dr. Cummings, you know, we looked at a paper and you said that was never really a big concern for you. And that was actually really helpful. The concerns are for short-term memory issues, working memory, process. processing speed, are those issues, because they're taking this at night before bed, are all of the benzos affecting people during the day? I guess would be one of my questions. And any comment you have on the dementia risk?

Taking benzodiazepines chronically is statistically associated with an increased rate of dementia. It's not clear that the benzodiazepine is causing the dementia. It may well be that people who suffer from chronic anxiety, insomnia, and other issues for which they're taking the benzodiazepine. Because they're an association, those people also have a greater burden of general physical illness and so forth. All of those things can be risk factors for dementia. The degree of impairment caused acutely by the benzodiazepines during the daytime depends on the, half-life of the benzodiazepine. For example, if the person is taking a long half-life benzodiazepine like clonazepam or diazepam, yes, it's clearly present at bioactive concentrations throughout the day.

If they're taking a very short half-life benzodiazepine at night, it may be having minimal effects during the daytime because it's largely washed out. But then again, you have the issue that the benzodiazepines rapidly become ineffective as a sedative. So, you know, my own view, as I've expressed before, is that benzodiazepines are good, short-term rescue medications, either for sleep or for anxiety. They are generally dangerous long-term medications because of the increased mortality risk and increased cognitive impairment that cause. So I do have, I want to comment on that as well. So there was a 2020 study that we found that was done in Denmark,

which they looked at the prescription registry data for benzodiazepines and Z drugs in patients with affective disorders. And it was a large study. They did it from 1969 to 2016 looking at the data. And they looked for a diagnosis of dementia or prescriptions for dementia during six-year follow-up period. They didn't really find any association between use of benzodiazepines or Z drugs with the diagnosis of dementia. And I wanted to hear your take on this possible protective effect. The study concluded that, you know, continued and new users of benzodiazepines had lower rates of dementia compared to those with no lifetime use or patients with former use. And one of the hypotheses was that the calming effect of benzodiazepines kind of reduced the

pathological effects of stress on the brain. So I would like to hear your take on that as well. It's an interesting hypothesis. It seems to run counter to other data that's out there in terms of long-term risks of benzodiazepines, even if it were true that it decreases the risk of dementia, the increased rates of depression, increased mortality risks, I think it might be often. setting effects. Okay, this, I think we've demonstrated that, ideally, someone who's elderly would not be on chronic benzodiazepines for sleep. If we get inherent, if we, you know, end up with a client who's on a benzodiazepine and

sleeping well, and we want to taper them off and the patient's willing to be tapered off, how fast do you do that? Very gradually. One of the chief problems that physicians who practice in this area have is they underappreciate that if a person has been taking a benzodiazepine for a long, long time, that taper needs to be incredibly slow. We're talking about for a therapeutic amount of sedative, taking as long as six months to a year to taper the person off of the medication. because going faster will very likely cause the person to have a relapse of insomnia or anxiety. And if it's very fast, it may actually cause withdrawal signs and symptoms. So it's prudent to go very slowly in terms of tapering a benzodiazepine.

And frankly, you may find in some people that there is underlying pathology that will prevent you from taking the person all the way off For example, I had a patient who, years before it had catatonia and association with depression, came in with two milligrams every night of clonazepam. Was able to get that patient down to a quarter milligram of clonazepam at night, anything below that, and the person began to become catatonic. Yeah, yeah. So they stayed on a quarter milligram. Yep. You know, I think that's actually worth reiterating something we talked about in our catatonia episode is it's so important to go down super slow. Like we're talking about if they, let's say if they get discharged to you as their outpatient provider and they're on 20 milligrams of Ativan, going down one milligram a month would be appropriate and then watching for signs of relapse into Catatonia. Yes. I had one of these patients as well, drop them down to two, from two to one and a half, that's when they develop the catatonia again.

So I don't think that that's common practice, so I think that's good to talk about again and again. Yeah, a physician sometimes to be, tend to be too much in a hurry. Yeah. You know, the brain in general, no matter what we're talking about, is far more tolerant of gradual change. Yeah, in my IOP, it's common for me to make a med change and then wait for a month or six weeks. And in the meantime, you know, once a week I'm talking about exercise, diet, lifestyle, sleep hygiene. You know, I'm using that time for other things and I'm monitoring side effects and stuff. So, so important.

So, okay, decreased taper, very slow, six months to 12 months. Very good. any other comments on benzodiazepines? In the handout, we have individual ones listed, effect sizes, unique risk factors, but I want to get kind of an overview from you. I think, again, my own, if I'm the person who's deciding whether to use a benzodiazepine or not, I'm looking for short-term use essentially as a rescue medication, recognizing that there may be clinical circumstances where the person will need to take it chronically, but I try to avoid those whenever I can. In some ways, I think of the benzodiazepines as being similar to the

high potency steroids. Excellent for rescue, miserable long-term medications. And the same thing with sedative medications in general, in this case, the direct sedatives, the Z-drugs, the orexin antagonists. I'm looking for short-term use, not long-term use, although the orexin medications appear to be safer long-term than the Z-drugs, provided they don't cause narcoleptic symptoms. They're now two of them. You have suvorexent and limb vorexent. They're very similar to each other. They're both orexone 1 and orexin 2 antagonists. limborexin is a little more potent with the dose range of five to ten, whereas the suvorexin's 10 to 20. So those are useful. By and large, for sedatives, true sedatives about all I order are

the Z drugs and the orexin antagonists. In psychiatry, it's also very common to use a variety of things for sedation. You'll see people use trazodone, low-dose quatyapine, diphenhydramine. In all of those, essentially what you're giving the person is an antihistamine as a sedative. My own favorite, if I'm going to use an antihistamine, is hydroxazine because it is not anticholinergic, so it doesn't disturb REM sleep. And it doesn't come with other effects other than, histamine blockade. You know, I think, what do you think about doxapin? Because I think that's at low doses, it's highly histaminergic.

And it seems to, you know, I'm talking about like 5, 10 milligrams. Yeah, can be, can be, yeah, doxapin and very low doses can be useful. You know, it was remarketed at 6 milligrams as a sedative. frankly, there's no reason to pay the extra money giving the generic at 5 to 10 milligrams is essentially biologically equivalent. And again, though, what you're really giving the person is an antihistamine. Yeah. I was a little bit disappointed by the Trazidone data that I saw. It didn't seem like it was that much more effective for sleep. Yet often I hear from patients it's helpful for sleep. Any thoughts on that? So I actually looked into tracidone, and the history was so fascinating.

It turns out that, you know, there's this concern of tolerance and dependency with benzodiazepy. And so physicians decided, hey, let's prescribe these antidepressants off label, especially trazodone. And so when they looked at these office-based surveys from practices, between 1987 to 1996, there was a 50% decline in benzoprescriptions that coincided with 150% increase in tracadone prescriptions. And then like you said, Dr. Peter, the data that I found, you know, it really showed that trazodone may help someone fall asleep 10 minutes earlier than placebo, which, again, you know, is that clinically significant.

And if someone were to wake up in the middle of the night, they were able to go back to sleep seven minutes quicker than placebo. So that's not really strong evidence that Trazadone is really helping. But Dr. Cummings, what do you think? I haven't found Trazidone to be all that useful. The other concern I have with it is that people tend to forget that

Trasadone is an antidepressant. And I've seen people make the mistake of giving somebody who is bipolar and hypomanic or manic, tracadone as a sedative, thereby helping to drive their hypomania or mania. Yeah. I see that often, and they'll crank it up to 300, not realizing like, hey, this person is not doing well because of that high dose of the tracidone. The other, the biggest issue that I see with it outpatient, Dr. Cummings, is sedation during the day. It seems to have a second dip. It has like the initial dip that gets them to sleep, they'll wake up at two to three in the morning,

and then they'll have the second dip that hits them right at 6 a.m. It's so miserable. Yeah, and it's a case of, well, if I'm going to choose nanostamine, the reason for my preference for hydroxazine is that it lacks all of the undesirable side effect. You know, Kotyapine is now antagonists fairly robustly. So is Trasidone. Diphonhydramine is very highly anticholinergic. Hydroxazine is not anticholinergic. It has no affinity for alpha receptors. So if you want to give somebody an antihistamine, why give them something that will do all sorts of things that you're not looking for? Okay. And what about dose for hydroxazine? What do you look at? 25 to 50 milligrams at bedtime. Now, the other caveat with using an antihistamine as a sedative is the

site of action for an anihistamine is primarily cortical, particularly prefrontal cortical. So you do an effective job of turning the cortex off, but you're not having much of an effect on the subcortical systems. So in a few people, particularly the elderly and children, you may get idiosyncratic activation because essentially you've you've turned off the person that's cortex but not the rest of the brain and they're and behaviorally they may run amok on you yeah what do you think about mertazepine i know that's commonly used i've it's been effective for some of my patients where trazinone hasn't been effective or dachsapin hasn't been effective um metazepine also is acting primarily as an antihistamine at low doses you know this is a drug that as you include

increase the dose becomes less sedating because it's effect that the alpha-2 receptor causes an increase in norapinephrine release as the dose goes up. So that by the time people are taking more than 30 milligrams a day, the drug is not very sedating at all, whereas at 7.5 to 15 milligrams is pretty sedating because the antihistamine effect is present long before the increase in norapinephrine secretion. One thing that I read with mertasapine is one of the major side effects is the discontinuation syndromes and having this almost withdrawal-like experience, but does that happen with low dose? It is less likely with low dose, as you'd expect. However, it is not zero. If the person has been on

or tasapine for a long time, I generally recommend that people taper the drug rather than stop it abruptly. And basically explaining to the patient that there is a risk of a withdrawal syndrome should they go from a dose that's effective for treatment of acathesia or depression to nothing. whereas they can go from whatever dose they're on gradually down to seven and a half and then stop at that point. What do you think about magnesium? I got a couple people, one that said that it worked for them, a couple people asking about if there was evidence behind it. Any thoughts on that? magnesium does decrease brain excitability largely by blocking calcium influx at both AMPA and NMDA receptors. So there is a possible theoretical mechanism for it causing calming.

It is not reported by most people to be directly sedating. And I haven't frankly seen any good, well-controlled studies where it was compared to placebo specifically in groups that were suffering from primary insomnia. That's really interesting because when I looked into L. Fanning, it was something very similar where the thought process is that, you know, there's an action on this AMPA and MDA receptor and it blocks the re-uptake of glutamine and glutamate. But in terms of efficacy, I think there's only one rat model that I could find where they should. showed maybe some effect on sleep onset latency.

Yeah. So I think the data on magnesium is basically at this point still out. I think with like L-theonine, part of the problem is we don't have big studies being done on this because there's no money behind it. Yes. And the same thing would be true of magnesium. there is no pharmaceutical firm who is going to be investing a large amounts of money and studying the effects of magnesium on sleep. Yep.

Interestingly, if you look at some of the sleeping medications over-the-counter, a lot of them will have al-thianine in the combination of the sleeping meds. It'll be like a cocktail of stuff. Any other comment Dr. Cummings on over-the-counter sleeping medication? Most of the over-the-counter sleeping medications are indeed mixtures with at least one component typically being a drug that has antihistaminic properties. I do think people need to be careful in those when they choose an antihistamine, they often choose the cheapest they can get, which by and large is diphenhydramine benadryl. and the problem with Benadryl is not that it's a bad antihistamine, it was the very first one developed. It's that it's also highly anticholonergic, which can cause all of the anticholinergic side effects that people deal with,

including memory impairment, blurred vision, dry mouth, constipation, urinary retention. So people can run into all sorts of difficulties because of that component of the drug. Dr. Cummings, what are your thoughts on Valerian? When I looked into it, the mechanism of action was very vague, and all I could find was that it binds to the GABAA receptor and, quote, allosterically modulates the receptor. Have you found it to be helpful? It is a sedative, both in purified form and as the nutritional product, Valerian root. of course, as with most nutraceuticals, frankly, the control over manufacturing quality is not very tight. And consequently, the quality of products that are out there is highly variable.

Valerian is sedating. It's been used for traditional cultures for literally millennia as a sedative. We use a modern variant of it as a mood stabilizer, valproic acid. is a derivative of valeric acid and has some in some ways some similar effects. I frankly wouldn't prescribe it. I don't typically recommend nutraceuticals very often because of the poor control and lack of good testing and study.

We haven't talked about a commonly used one, Syracquil, which is often used inpatient from what I've seen for sleep. I think they're using it for the antihistamine effects, but I think it's worrisome because of some of the side effects. Do you have any thoughts on this, Dr. Cummings? Yeah, I tend not to suggest

Cerequil quatapine as a sedative. It has, of course, it's an antipsychotic, albeit it's a fairly weak antipsychotic. It's dissociation from dopamine receptors, limits its effectiveness as an antipsychotic medication. It's also a very potent antihistamine, which provides sedative effect. It's also a very potent alpha adrenergic antagonist, which can cause difficulties with problems people can have in terms of hypotension, etc. But, you know, it's, I think psychiatrists reached for it just because it has antihistinic properties.

I'm a little uncomfortable with using drugs off-label that haven't been well studied and which do things other than what I'm looking for. Yeah, that's good. Okay, so one of the common questions was any advice for people with sleep apnea who are not responding to a CPAP or who have difficulty with the sleep apnea machine? Yeah, a lot of people have difficulty tolerating CPAP. Many of the machines are noisy. There are a variety of machines produced,

so they can try to look for a better machine. There are also surgical revisions of the palate that can be considered and may be effective in some individuals. Probably the principal thing, albeit it is not easily accomplished, is weight loss. will in many people cure their apnea. Yeah. Yeah.

So one of the studies, I think Dr. Cummings, you had email to us, was on obstructive sleep apnea and drugs. So I read through that study. It was really interesting because they looked at the respiratory arousal threshold. And the idea is that people with obstructive sleep apnea have low levels of respiratory effort, which leads to frequent awakening and a greater ease of arousal. And say they look to see if isopiclone and zolpidem, which are two Z-drugs, specifically have any impact at all in sort of raising this level to, you know, impact and help with sleep, but they actually didn't really find any evidence.

So I was wondering if you could comment on that. Yeah, the Z drugs have not been found to be very useful in apnea. And, of course, the benzodiazepines are overtly dangerous, in sleep apnea because they may indeed make the person not respond to rising CO2 levels and consequently they may artificially produce a combination of

obstructive and central apnea which can be fatal of course for the person. I think it's important for the listeners to understand the reason people are so tired when they have obstructive sleep apnea

is that they spend most of their night waking up several times an hour in order to breathe. When they are asleep, they often stop breathing for periods of time. Their CO2 level begins to climb, and eventually it causes them to gasp, snore, strangle, and essentially they're having to wake up over and over and over again. And of course, that's exhausting. That's not exactly conducive to a restful night's sleep. the point of the CPAP machines is to maintain positive airway pressure so that the person's airway doesn't obstruct, doesn't close down when they go to sleep and the muscles relax. Unfortunately, those machines are not entirely comfortable, and in some cases, depending on manufacturer, they're also somewhat noisy. We should do a full dive on this.

I've had so many patients who have such issues, so much resistance using these machines, that it's something I often will ask patients, I'll often get studies, sleep studies. That sometimes takes a lot of convincing as well. And then when they have an issue with them, I'll sometimes have them bringing the mask and we'll do some relaxation stuff with them having the mask on with me in the room, and that can sometimes help. Any other like tips or tricks that you have Dr. Cummings on how to get people to do this study to wear their CPAP?

100%, right? Because often as well, you should be asking if the patient has CPAPNIA, what percentage do you use? You know, most patients don't use it all the time. They'll be like, oh, yeah, I only use it like about half the time. or oh, it comes off in the middle of the night and I don't know how, you know. So any other thoughts, pearls? It's important to indeed do the kind of analysis where you have the person bring in the mask and,

one, be sure it fits them and is comfortable. People can, of course, if the machine is keeping them awake because of noise, earplugs can help. basically the person who is using a CPAP machine needs to be sure that their sleeping arrangements are otherwise as comfortable as they can make them because unfortunately introducing a CPAP machine introduces an element that inherently makes it I think somewhat more difficult to relax and go to sleep yep any medications that you might give to someone that won't mess with their sleep apnea if they have a machine that could help them sleep or at least get to sleep?

I think melatonin has been shown to be safe. Does not have any direct respiratory suppressant properties, does not alter sensitivity to CO2. The benzodiazepines are at the other end of the spectrum. They're definitely a no. The Z drugs are not as dangerous, but they're also, as was noted, don't have much data to support efficacy.

The low-dose antihistamine, like hydroxazine, may help with going to sleep. I've not seen as much benefit in her helping to keep the person asleep, but sometimes it is a problem of going to sleep while wearing a CPAP machine. So I have used hydroxazine for that reason. Okay. The other element, although I've not seen great studies so far as the orexon antagonists, don't appear to have a direct respiratory suppressant effect either. So they may be safe, but they haven't been widely enough used in part

because they are still proprietary and therefore expensive. Another big category of questions was with the treatment of bipolar, let's say acute treatment, they're in the hospital. What might you use to help them sleep? What would be like your first line, second line? Usually first line for them is esopaclone. And sometimes that, you know, the approved dose range for esopaclone is one to three milligrams. Frankly, for our acutely manic patients that sometimes gets pushed up to as much as eight milligrams,

because maintenance of sleep during acute mania is very important. Whoa, whoa, eight milligrams? Yes. Okay. that's new for me. Wow. And it works. It works fairly well without much in the way of adverse effects. Now they don't stay at that dose because, frankly, when they're not manic,

they don't need that kind of dose to sleep, and they may not need anything at all. So this is during acute treatment of mania. And so far, we've been doing that for about the last decade in the state hospital, and it has worked well in those cases where the person is hypomanic or manic. Because, of course, the issue with insomnia and somebody who's bipolar is that sleep deprivation, especially in the latter half of the night, acts as an antidepressant and will actually derive the person's hypomania or mania. You know, I was going to, I just asked, you know, when I was looking through the literature on a Zopa clone, I was actually kind of surprised as to how very little side effects I could find that were consistent across the studies.

I mean, dry mouth, unpleasant tastes were like the ones that kept popping up, but, you know, it doesn't really seem to impair next day performance as far as I could see. No, it doesn't. And that tends to be true even at higher doses. In fact, in Europe, to give credit, where credit is due, we did not invent the higher dose usage. that actually came out of France, which has had access to Zopaclone and S. Zopaclone for decades and in circumstances where the insomnia is refractory or in context of things like mania, they've used it at higher doses for a long, long time without much in the way of adverse effects. What about the difference between S. Zopulone and Ambien, Zopidem?

Do you see a difference between specifically sleep walking, sleep eating activities where they're not remembering them? Yes. Zolpidem is much more prone to inducing dissociative episodes. In fact, when Zolpidem was first marketed, one hotel chain in the UK took to instructing their staff to keep large bath towels at the front desk because they kept having naked guests. wander down to the lobby in a disoriented state. And they would have to wrap them up and take them back to the room, basically. Now to be fair, many of these people had inadvisedly decided to have a nightcap to wash down their zolpidum, thereby dramatically increasing the probability of a dissociative state. Ooh, that brings up a really good point.

which of these medications, if you were to drink alcohol, would you not use? Benzodiazepines and Z drugs, because they are acting via gabbergic systems. The orexinant antagonists and the chronobiological drugs don't seem to have much of a direct interaction with ethel alcohol. What about cannabis? If, like, if you had a patient who was unwilling, willing to quit their cannabis, would any of these drugs interact with cannabis in a negative way? There have been very small, well, usually anecdotal case reports. Zolpidim, again, in particular, combined with cannabis, seems to be, again, prone to cause a dissociative mental state. You know, there are very good reasons why in the package, answer for Zolpidum, it basically says,

take the drug and go immediately to bed. Do not pass go, don't do anything else. Because if the person is doing anything else that alters the drug like drinking alcohol or taking cannabis, it appears to be then dramatically more prone to causing dissociation. Nice. Okay. So you talked about different phases of sleep. Let's say it's terminal insombole. is there a specific strategy, let's say they have depression with terminal insomnia, which seems to be sometimes more of the melancholic type of insomnia or melancholic type of depression. Is there any treatment for that specifically or does that need to be treated in your mind?

Certainly the principal treatment is treatment of the depression itself. giving the person melatonin or one of the melatonin analogs when they wake up too early may help them by tending to phase delay their clock i tend to stay away from other sedatives in that context because most of the sedatives we give don't have half lives that are long enough to be effective for terminal insomnia. And that's especially true in the Z-drugs. Zaloplon has a one-hour half-life. Zolpidem has about a two-to-three-hour half-life.

Asopaclone comes the closest having a four-to-six-hour half-life, but even it is waning quite a bit by the time you get to the point where the person with terminal insomnia would benefit. And, of course, if they take a dose when they wake up in the wee hours, they then are prone to having essentially hangover symptoms when they actually should then be awake. So this doesn't apply to terminal insomnia, but I do, just because we're talking about a Zopa clone, want to bring up a study that was done in 2006 where they looked at patients that met criteria for major depressive disorder and persistent insomnia. and they look to see whether fluoxetine, you know, treating the depression with fluoxetine in the morning,

and then these patients were randomized to either placebo or isopac clone at bedtime. And the duration was for about eight weeks. And they actually found greater reduction in both depressive symptoms, which they identified through like the Ham D and the CGI scores, greater significant reduction in depressive symptoms in the group that took both azopic clone and fluoxetine. as well as greater reductions in sleep latency, wake after sleep onset, and greater increases in total sleep time. Yeah. Yeah, esopaclone has been, again, the one drug in this context that has produced benefit. The other Z drugs, albeit I haven't seen a good study of Zolpidim controlled release,

which is really like taking two doses. Zolpidem, though, and Xalloplon in particular have half-lidim. that are too short to have much effect on terminal insomnia. Asopaclone is much closer to the mark. Okay, so let's say you had a patient with dizziness. Now, there could be three different types of dizziness. Could be vertigo. It could be orthostatic hypotension.

It could be like dizziness. First of all, like, would any of these meds worsen dizziness during the day? and if you were to have a patient who was very dizzy, which meds would probably be the best bet. Certainly if the person had dizziness related to orthostasis, I would want to stay away from any drug that had alpha adrenergic antagonist properties because that will do a wonderful job of making them more orthostatic.

Vertigo is not typically adversely affected by most of the sedative drugs. What I've seen in some people is an exquisite sensitiveness to what amounts really to mild ataxia. And for them, almost all of the sedative drugs can cause worsening. So I would be looking for either use of, of a chronobiologic drug like melatonin, or with a sedative drug like a Z drug, I'd be choosing the ones with the shortest half-life, so that essentially the drug would be gone

by the time they got up the next day. And which of the Z drugs has the shortest half-life? Zaloplan is the shortest with a one-hour half-life. So it peaks at about 45 to the same. 60 minutes after you swallow the pill, and then from there, five hours later, it's gone. Okay. That's helpful. Okay. I think we are kind of nearing saturation probably for the audience for this session. Are you suggesting we may have put them to sleep? It's funny. I've heard, I have a couple people who have emailed me that have told me that

for some reason our episodes, Dr. Cummings, put them to sleep, and they like to listen to it on repeat. Maybe instead of looking at a screen, they should listen to this episode before going to bed. Well, I don't have any objection to helping people relax. Yeah. I warn them about driving and listening to us, if that's the case. Yes, yes, yes, do not operate heavy machinery until you know how these podcasts will affect you. Yeah, yeah. Okay, so if you are the serious, curious, go to our resource library, download this handout,

go on thepsychiatrypodcast.com. It's there. It's free. You've enjoyed the mailing list by signing up for it. And Dr. Cummings, any final kind of thoughts, pearls of wisdom that you want to throw out there before we kind of bring this to a close. I think the one thing I would repeat for the providers and psychiatrists is when somebody says, I can't sleep, ask more questions before choosing an intervention.

Yeah. I think I would repeat, think about the things that are not broadcasted by drug companies that are going to make a lot of money from broadcasting it or people come in your office as well. You know, think about exercise, think about the lifestyle. changes. Notice that we started with about a half an hour of that. And I think as prescribers and as psychiatrists, we want to help our clients. And so, you know, not feeling guilty when we do prescribe medications if it's necessary, but thinking long term we're going to continue to work on

some of these lifestyle factors that make a big difference. That would be one of my closing thoughts. Any closing thoughts, Dr. Tomatsu? Yeah, I agree with everything you both have said. I definitely am a huge proponent of CBTI. I wish that it wasn't so expensive for people and it was more affordable. But one thing that I do like to keep in mind when I do see patients with insomnia is that not everybody is the same. And so kind of going back to that story with the patient who would watch that cowboy TV, you know, in general, TV is not good to watch before bedtime, but in her particularly. case, this was something that was soothing. But like Dr. Cummings said, you know, then you would have to put a timer on the TV and sort of modify therapy according to who the patient is. Good. Excellent thought. Excellent thought. Any final thoughts, Dr. Krishnan? I would just, you know, exactly like Dr. Tamatsu and Dr. Cummings had said, it's always really important to, you know, personalize the care to each patient. And, you know, always just kind of look at the

big picture, like never forget that in terms of, you know, what are the other causes that may be attributing, or maybe contributing to the insomnia. Yeah, and Dr. Krishnan is an interest in trauma, and I've had a lot of clients who have had something traumatic happen and then the insomnia started afterwards. And so sometimes it's about doing the deeper work and going back to when this started and what led to this start. Exactly. I have this belief that trauma really underlies like pretty much everything. Yeah. Well, it's been a pleasure. I'm really glad to put this stuff out there for free for people. And if you want CME, of course, you can sign it for the CME. That helps fund the staff to develop the audio.

And we will leave it there for today. Okay. Thank you. Thank you. Thank you. All right, guys. Take care. I just want to give a special thanks to Dr. Tomatsu and Dr. Krishnan. They did an amazing job preparing for this episode. And also, I'm very thankful for my continued mentorship with Dr. Cummings. What a resource. I get emails thanking Dr. Cummings and I forward them to him. And so if you have any thoughtful words that you want me to pass on, I would love to.

I'm going to have him on for a future episode actually on a book that he released on psychotic disorders, treatment-resistant psychotic disorders. So if you want to pre-read that book with me, that would be awesome. I am looking forward to that. Once again, if you want to sign up for CME, just go to Psychiatrypodcast.com. It's super easy and straightforward to sign up. and it does help move things along in terms of getting episodes out, blocking off time to mentor and to guide the formation of these episodes.

So I will leave it there for today. Have a great day.