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Let’s go into daridorexant a little more deeply, and let’s take in the data from the phase 3 trials. Can you get into some of those? Starting with the randomized, double-blind, placebo-controlled international trials of patients 18 and older, can you start there?

Sure, there were 2 studies. One is called Study 1 on the product label, and it looked at doses of daridorexant at 50 or 25 mg vs placebo, and that included close to 1000 people. That is supported by Study 2, which looked at a lower dose of 25 mg and included a 10 mg dose arm as well compared to placebo, also in close to 1000 people. The bottom line is that 50 mg appears to be the best dose in terms of the effect in helping patients fall asleep faster and stay asleep longer, as well as scores on the IDSIQ [Insomnia Daytime Symptoms and Impacts Questionnaire] sleepiness domain. The 25 mg a night dose still works, numerically it also shows improvements over placebo, but did not separate from placebo statistically on the IDSIQ sleepiness domain score the next day. So putting all the data into perspective here, and if I had to choose a starting dose, I would select 50 mg. However, 25 mg is available, and there may be instances where that may be preferred by the patient under certain circumstances.

So there’s a 25 and 50 mg dose, but there’s no mandate to start with the 25 mg and titrate upward, is that correct?

That’s correct. You can start at 50 mg, you can start at 25 mg, you can give 25 mg and then 50 mg, you can give 50 mg and then give 25 mg. You can do whatever you like with those 2 doses. I look at the clinical trial data, and I ask myself where is the effect size the most robust, and where would I increase my chances of success? It would be with the 50-mg dose.

Now you’ve already said that the 25 and 50 mg both increase the latency to persistent sleep, how long it took patients to get to sleep. It also improved wake after sleep onset, they both did. They both also increased the total sleep time, and you’ve also said that with the IDSIQ score, the next day effects were only improved by the 50 mg. Does that make us want to consider the 50 mg more, and to prescribe that more often because it was the one compared to 25 mg that improved the daytime sleepiness?

I would think so. Some of these measures [such as] the latency to persistent sleep, LPS, and wake after sleep onset, or WASO, they’re polysomnography measures. It may be difficult to wrap our heads around it. I do pay a lot of attention to subjective measures because that’s what I would expect patients to report to me in treatment. So subjective total sleep time is really important. We saw that improvement after 1 week in the clinical trials, and it continues to improve over time, so I pay special attention to that. With the idea of the IDSIQ sleepiness domain score showing a statistically significant degree of improvement over placebo at the 50-mg dose, but not statistically significant at the 25-mg dose, it tells me I probably will be better off with 50 mg. But although it was not statistically significantly different for the 25-mg dose, it was still numerically better, so I wouldn’t completely dismiss the 25 mg dose. There may be instances where a patient may be skittish about trying a new medicine and worried about dosing. They may tell you, “I’m very sensitive to medicine, doctor, and I really don’t want to take too much of it.” The last thing you want is for them to have a complaint when you force a dose they’re not comfortable with. So in those circumstances I would think about a 25-mg dose, but I would also say that the clinical studies tell us that 50 mg is a better dose.

You’ve already said that some of these data that came out were at month 1 and month 3, but I’m aware that the clinical studies showed also weekly increments about how things went with patients over a 3-month period. It seemed like when you looked at the total sleep time and at the IDSIQ that it seemed to build over time. That means that as the patient took the medication, it seemed to do better. Maybe you’re reaching maximum effect at around 5, 6, or 7 weeks. Does this translate into telling our patients that when they take this medication, “Start taking the medicine, but don’t judge it let’s say after the first week or two. Give it longer than that because it seems from the clinical trials that the benefits of it seem to improve over time,” at least when we look at the total sleep time and at the IDSIQ. Is that fair to say?

I’d be a little cautious there because you would expect something like this to start to work right away. A phase 2 clinical trial was done, and it demonstrates that daridorexant does work right away. But the first time point that was measured in the phase 3 clinical trial program for the polysomnography measures was at the end of the first month. And the first time point where subjective total sleep time was assessed was at the end of the first week. But I would expect something like a DORA [dual orexin receptor antagonist] to work right away. I’m glad to see that there is continued improvement over time as someone persists in taking it. That’s good. That’ll be self-reinforcing for the patient to continue that medicine.

I tell patients it should work, it should work pretty quickly, but you do have to give it about a week or so before making any judgment here. I say this particularly for patients who are used to taking other medicines like Z-drugs or benzodiazepine, when they’re used to being knocked out with a sledgehammer. This does not do that, but it does help patients fall asleep faster and stay asleep longer, and that’s definitely true. That’s seen in polysomnography as well as in subjective measures. Patients need to be told it works differently and it will feel different to them. They won’t get that same kind of sensation that they may have gotten with a benzodiazepine, but it’ll still work with their sleep.

This medication as you said earlier has the shortest half-life of all the DORAs; I think you said it was 8 hours or so. Does that translate into next morning residual effects?

If you look at the rate of adverse events, of somnolence or sedation, they are low, and they are comparable to what was observed with placebo, so I wouldn’t expect it to be an obstacle to its use.

Are there any safety data and maybe even dose discontinuation data with daridorexant?

I tell patients that with the DORAs including daridorexant, you can stop it at any time, and there is no rebound insomnia as they may have experienced in the past when they tried to stop their zolpidem abruptly, for example, and it was a disaster for them. They may be very leery about a new sleeping medicine. They may be worried about being physically dependent on it, hooked on it. They don’t want to experience that again. So I have encountered that from time to time in patients who are no longer on a sleeping medicine, and somehow they did manage to wean off it, and they’re very hesitant to start again with something that they worry may be difficult to stop. I can tell them it can be stopped abruptly. There were no withdrawal symptoms, there was no rebound insomnia, and the effects don’t wear off as you continue taking this medicine like it did the last time they were on a hypnotic.

I do run into some patients, and this is quite common in clinical practice, who are continuing to take something like zolpidem every night, and they’ve been taking it for 10 years, and every time they tried to stop it they’d run into problems. They’re not sleeping well. The medicine no longer works for them. I want to offer them a DORA, and I’ll give them the DORA, and then I’ll proceed to wean them off the other hypnotic very slowly, over many weeks. That way I ensure a better experience. If I too abruptly discontinue their prior medicine that they have been taking every night for years, they might experience rebound insomnia. Then they tell me, “This new medicine you gave me doesn’t work at all.” In fact, it’s not the new medicine; it’s the withdrawal effects from their old medicine.

So, one way of going from a present sleeping medication to another is to have an overlap period with a discontinuation gradually of the first medication.

Experts discuss daridorexant efficacy and safety data, and dosing considerations and what to communicate with patients when using daridorexant for insomnia.

Daridorexant Trials for Insomnia Treatment

Let’s talk about the dual orexin receptor antagonists, or DORAs. How do they impact sleep and wakefulness cycles?

Just a quick recap of these orexin neurons; their cell bodies are in the hypothalamus, we only have about 50,000 of them, they project to various parts in the brain, and they keep us awake. Now, people with insomnia, they’re working overtime. The dual orexin receptor antagonists block those receptors in the brain and help someone fall asleep and remain asleep. It’s very different than knocking someone over the head with a sledgehammer with a Z-drug or a benzodiazepine.

: What advantage, if any, would a DORA offer compared to other treatments that you said are like using a hammer to put them out? What advantage would a DORA necessarily offer?

In addition to not deleteriously affecting sleep architecture, long-term use of DORAs is not associated with tolerance. That’s huge. It’s not associated with withdrawal or rebound insomnia when abruptly stopped, so that’s huge too. It continues to work, in fact they are tested. There are 3 of them in the marketplace here in the United States, and they’ve been tested as daily, once a night treatment for insomnia disorder. They’re not PRNs taken as needed, they weren’t studied like that, and they’re not middle of the night drugs. They were all designed to be taken 30 minutes or so before falling asleep when you have about 7 hours ahead of you to be asleep, and taken every night. This is a very different approach than in the past where you’d take something to knock yourself out, and maybe at 2 in the morning repeat again. A very different approach. This is much more thoughtful in terms of saying you have insomnia disorder, here’s how to treat it, here’s a medicine, you take it every night, and your sleep is better regulated.

So you’re targeting the hypervigilance and hyperactivity that’s keeping somebody awake as opposed to doing what you’ve been doing with the benzodiazepines. Now many DORAs have been studied in insomnia, and 3 are FDA approved. The first one that came out was suvorexant, the second lemborexant, and the third daridorexant. Can you tell us how these are different in their pharmacologic and pharmacodynamic properties?

The 3 drugs—suvorexant, lemborexant, and daridorexant—share in common affinity toward the 2 orexin receptors. They’re called No. 1 and No. 2; I guess there was a lack of imagination among those who called them those names. Basically they are dual orexin receptor antagonists, and they have somewhat different affinities to 1 or 2. I don’t think that’s the major difference between these 3. The drugs are very different in terms of their pharmacokinetic profiles, some have longer half-lives, for example. The most recently approved DORA, daridorexant, has a half-life of about 8 hours or so. It’s the shortest, and when you look at the pharmacokinetic curve, the concentration curve over time, you reach a maximum concentration in about an hour or two, and then the concentration drops off. The exposure is primarily when someone is in bed, when they’re supposed to be sleeping, and there are no carry over effects the next day, and there’s no accumulation. That in itself is very attractive, the pharmacokinetic profile itself.

As far as suvorexant and lemborexant go, they have longer half-lives, which may spill over into the next day, so that may have some bearing on some of the adverse effects. Is that possible?

It is possible. I’m not sure how relevant clinically that would be for most people, but the rates of somnolence the next day are somewhat higher for lemborexant than they are for daridorexant.

Drs Paul Doghramji and Leslie Citrome provide an overview of dual orexin receptor antagonists (DORAs), suvorexant, lemborexant, and daridorexant, in treatment of insomnia disorder.

Dual Orexin Receptor Antagonists (DORAs) in Treatment of Insomnia

Research increasingly is finding a heavy mental health burden among 

+. Now, new data indicates gender-affirming therapy may help address an increased risk of sleep disturbances among this patient population.

Ronald R. Gavidia Romero, MD, MS, clinical assistant professor of neurology at the University of Michigan Medical School, and colleagues conducted a retrospective cross-sectional study utilizing a large US-based administrative claims database. Participants included 1,216,044 youth aged 12 to 25 years, of which 2603 (0.2%) identified as 

(TGNC). About half (1387) pursued gender affirming therapy (GAT); 868 and 519 were identified as transmasculine and transfeminine, respectively.

In comparison with cisgender youth, TGNC youth had higher odds ratios (OR) of insomnia (OR = 5.4, 95% confidence interval 4.7, 6.2), sleep apnea (OR = 3.0, 95% confidence interval 2.3, 4.0), and other sleep disorders (OR = 3.1, 95% confidence interval 2.5, 3.9). However, data indicated that GAT had a positive impact on reported sleep disorders. Romero and colleagues found a decreased risk of 

 for TGNC youth who were receiving GAT as opposed to those who were not receiving GAT (OR = 0.5, 95% confidence interval 0.4, 0.7).

“This study demonstrated a high burden of sleep disorders in TGNC youth in comparison to cisgender,” Romero and colleagues concluded. “However, GAT may confer a protective effect on sleep disorders among TGNC youth. Longitudinal assessments of sleep disorders prior to and post-GAT are needed to uncover their temporal relationships.”

1. Gavidia R, Whitney DG, Hershner S, Selkie EM, Tauman R, Dunietz GL. 

Gender identity and transition: relationships with sleep disorders in US youth

New research explores the impact of GAT on TGNC youth. 

 Leveraging GAT to Address Sleep Burden in Youth

Give us an overview of the commonly used pharmacologic agents for insomnia, like the benzodiazepines, the nonbenzodiazepines, etc. Can you go into them please?

I think in order to fully understand the options available, you have to understand how people sleep. Basically there are 2 competing circuits in the brain. One of them I’ll call the sleep circuit, the other one is the wake circuit. Either the sleep circuit is stronger than the wake circuit and you’re asleep, or the wake circuit is stronger than the sleep circuit and you’re awake. It’s basically a flip-flop switch. You can’t be both asleep and awake at the same time. So once that’s understood, and I explain this to patients, I say, “In the past the medicines you’ve received have been pressing on that sleep switch, making you feel tired and overcoming your wake drive, and you fall asleep. Actually, your brain may be working overtime.” There’s research to support that assertion, that people with insomnia disorder have an overactive or excess wake signal. Probably a more physiological approach would be dialing down that wake signal so that someone could fall asleep at night faster, remain asleep throughout the night, and wake up at a reasonable hour in the morning. By dialing down the wake signal, that’s a whole new approach.

This is where the new drugs come in. The Z-drugs and the benzodiazepine pressed on that sleep switch. The dual orexin receptor antagonists dial down the wake signal. They work by antagonizing orexin receptors. Orexin receptors and orexin, the neurotransmitter, is relatively new. I didn’t learn about it in medical school. I learned about at the turn of the century. That’s around the time they discovered this; they discovered orexin as the neurotransmitter whose job it is to keep us wake. The orexin signaling is strong during the day and is a little less so at night when we’re asleep, but people with insomnia disorder may have an increased wake drive. One way of [dealing with] it is antagonizing the orexin receptors and helping patients fall asleep faster and remain asleep longer.

So our understanding of insomnia is that there’s nothing wrong with our ability to get to sleep in a sense, but rather that we’re having trouble taking away that part of our brain that’s keeping us awake, too much wakefulness. Isn’t that what’s going on basically, is that correct?

I think so, for many people that’s the problem. If you measure their brain waves when they’re supposed to be sleeping or falling asleep, they’re more active than someone who is falling asleep normally. Their metabolic indices, if you measure all that, they are very similar to someone who’s awake rather than asleep. All this is supporting the idea that people with insomnia disorder need to dial down their wake signal, and that may be more physiological. Also, the dual orexin receptor antagonists don’t alter the sleep architecture in a deleterious way, so this may be a more normalizing way of addressing insomnia disorder.

A novel way of treating insomnia where we’re not basically working on the majority of the brain with benzodiazepines and GABA [gamma-aminobutyric acid] receptors but rather only targeting a very small area of the brain that is involved in orexin.

Drs Paul Doghramji and Leslie Citrome discuss the sleep and wakefulness signals and pathways that contribute to insomnia.

Sleep and Wakefulness Signals in Insomnia

A lot of clinical studies have been done, especially with the sleeping medications that have come out in the last 20 years or so, and there are a lot of patient-reported outcomes in assessing treatment efficacy. Are they important?

I think so. For depression, we’ve learned to use the PHQ-9 [Patient Health Questionnaire-9], haven’t we? PHQ-9 is a way of a patient telling us how they feel in terms of their mood as well as other symptoms associated with major depressive disorder, and it provides an educational resource for the patient to learn about their illness. In a similar vein, having patient-reported outcomes will get the patient involved in assessing how they’re doing in terms of improvement in their insomnia and associated impairments.

Excellent. There’s something new that’s come out, Leslie. I’d like you to review this. It’s called the Insomnia Daytime Symptoms and Impact Questionnaire, IDSIQ. Can you discuss what this tool is and how it’s used?

The IDSIG is derived from an older scale and places it in the modern age, so to speak. It was intended to support the development program of a specific orexin receptor antagonist that was approved this year. It looks at different domains of daytime functioning, looking at issues such as sleepiness, mood, and cognition. It has these 3 domains of sleepiness, mood, and alertness or cognition. It helps us get a full understanding of a person’s ability to perform during the daytime with the presumption that they’ve had a good night’s sleep the night before.

It’s a way of assessing next-day functioning. As far as I know, this is the first time that this has ever been done with sleeping medication. Is that correct?

The IDSIQ is unique in that regard with the development of this particular dual orexin receptor antagonist. Various other patient-reported outcomes have been used in the past, but not ones as finely tuned as this. We’ve had, for example, the Patient Global Impression of Change and various questions being asked about the speed of falling asleep and remaining asleep and the satisfaction with one’s sleep. That information has been collected for a very long time, but there has not been the same degree of attention on next-day functioning.

That’s a very important thing because, as we said earlier with insomnia, patients report not only trouble getting to sleep and staying asleep and that sort of stuff but also that they don’t function very well during the day. You even talked about presenteeism and sleepiness during the day. Here’s a tool that’s developed to specifically assess how well or how sleepy somebody is during the day.

Drs Paul Doghramji and Leslie Citrome review the use of the Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ) to assess treatment efficacy.

Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ) and Patient Reported Outcomes

Let’s go on to pharmacological therapy. When a patient comes in with insomnia and we decide—hopefully with some shared decision-making—that a medication is a wise idea, what considerations are there in choosing a medication?

For 1 thing, I’d want to ask my patient exactly what they’ve tried to help themselves sleep better because more often than not, they’ve already tried. Before seeing you, they’ve already gone to the drugstore and bought something over the counter. Whether it was successful or not, we need to find out. I wouldn’t be surprised at all if someone had already gotten diphenhydramine over the counter or tried other supplements with a combination of ingredients. I need to get that history. I also need to find out if they’ve received any prescription medicines in the past. Basically, they fall into 2 categories: those that are FDA approved for insomnia and those that are not and are used off-label. I want a complete history of what they’ve already gone through.

Do you have a particular opinion that you give to your patients about some of these over-the-counter remedies? There are so many of them. If you research on the internet, as far as insomnia goes, you’re going to see all these things, including herbal supplements and maybe nonprescription medications that you can get over the counter. Do you have an opinion that you share with your patients? What can we tell our patients about that?

I tell my patients that a lot of over-the-counter remedies have been tested and found to be ineffective or are potentially dangerous. The most common 1, diphenhydramine, can cause next-day drowsiness. That’s particularly a problem. Insomnia disorder is associated with daytime tiredness because you’re not sleeping well. If you’re going to use a medication approach that makes you fall asleep but still leaves you tired the next day, that’s not going to get at the next-day functioning that has to be improved. I emphasize the need to be alert the next day and that we can’t use anything with carryover effects. Many of the over-the-counter remedies have that or are simply ineffective.

Next, I have a discussion about what the FDA has approved in terms of insomnia disorder. In the old days we had benzodiazepines, which were used a lot, and then the Z-drugs, which are the nonbenzodiazepine receptor agonists that help people sleep. They replaced the benzodiazepines for many people, but they come with some baggage. The baggage with both benzodiazepines and the Z-drugs is the development of tolerance. When patients try to stop taking these medicines, they experience rebound insomnia—much worse than when it started. These are problematic. I also describe how melatonin receptor agonists have also been developed. There’s 1 in the marketplace, however, it takes a bit of time before it starts to work and is not for everyone. I mention low-dose doxepin because it’s out there, but that’s basically a repurposing of a tricyclic antidepressant at a lower dose and leveraging its adverse effect profile to help someone sleep. Lastly, I talk about the latest medicines available, the orexin receptor antagonists, as offering probably a superior approach to the treatment of insomnia disorder.

Drs Paul Doghramji and Leslie Citrome review prescription drugs and over-the-counter remedies for treating insomnia.

Pharmacological Treatment Options for Insomnia

For most patients with insomnia comorbidities, whether they’re medical or psychiatric—some psychiatric disorders may even be addiction—do you recommend when you’re treating somebody with insomnia to first treat their comorbidity? Or do you suggest using or treating the insomnia at the same time that you treat a comorbidity?

This often comes up for the treatment of not only insomnia disorder but also, believe it or not, depression and psychosis. People say, “They’re using street drugs, and we can’t treat them unless they become clean.” I don’t think that’s the right approach. You need to treat the psychosis, you need to treat the mood disorder, you need to treat the insomnia; otherwise, you’re never going to be able to address anything else in that person’s life.

It’s really important, a lot of times, to treat the insomnia and the comorbidity at the same time. An antidepressant and an insomnia medication together would not be a bad idea. Is that correct?

I do that all the time. In the old days, all I had were traditional hypnotics, but I used them with some trepidation. I didn’t want them to use it every night because that could be problematic. They stop working if they’re taken nightly. The development of tolerance is very real, and ultimately patients take more than what they originally started to take, and it still doesn’t work after a little while. When it’s time to stop, it takes a long time, gradually decreasing the dose over weeks.

Experts discuss treatment for patients experiencing insomnia in conjunction with other health conditions.

Treatment of Insomnia and Comorbidities

Let’s talk about some treatment considerations and also some monitoring. Let’s highlight some factors that impact the treatment selection of insomnia and choosing between, let’s say, nonpharmacologic and pharmacologic options. Are there nonpharmacologic options that we have to treat insomnia?

Absolutely. There’s CBTI, cognitive behavioral therapy for insomnia, which is a preferred treatment when you have access to it. It may take a little longer than a pharmacologic intervention to start to work, but its effects can be enduring. The problem I have in my community is that there aren’t enough skilled practitioners of CBTI, so access may be limited in that regard. There are some CBTI apps available, so that can be helpful as an adjunct to performing CBTI. That’s called CBT-i Coach. It’s a smartphone app that was developed by the US Department of Veterans Affairs, released about a decade ago, and people do like it. That is available out there but needs a little extra help from the clinician in terms of navigating it. So there’s certainly that.

Sometimes people ask me, what about sleep hygiene? Well, sleep hygiene is not a treatment, sleep hygiene is a way of managing a healthy lifestyle. But once you have insomnia disorder, sleep hygiene is not going to be effective alone, and you’re going to need to do something else. Sleep hygiene is number 1 in terms of the advice I give my patients about keeping a regular sleep/wake schedule. Reducing noise in the bedroom, blocking out light, removing electronic devices from the bedroom as well, avoiding daytime napping, and avoiding alcohol, nicotine, and caffeine before sleeping. Avoiding eating dinner late is also an important point to make. Although sometimes people like to eat dinner late and then they feel kind of tired after eating. It’s a terrible idea, especially as one gets older when you also have reflux coming into the picture. Then regular exercise is important, and stress management is also part of sleep hygiene. But sleep hygiene alone is not going to treat insomnia disorder.

As far as cognitive behavioral therapy, I think this is going to be pretty foreign to a lot of primary care providers. Are there any tips on how one can get a therapist who does CBTI, or is this something that a patient has to look for and get themselves? Can you give some options there?

I find it very helpful to know what sleep centers are in your community. Sleep centers, in their heyday, were the only place you could get a sleep study done. Now we have home sleep studies that are primarily used, but these organizations still exist. You have specialists in many communities that have a full array of different specialty areas that are offered at that sleep center. That may include psychologists skilled in CBTI. So, I wouldn’t give up, you just have to do a little homework.

Experts highlight cognitive behavioral therapy for insomnia (CBTI) and sleep hygiene as nonpharmacological approaches to the treatment of insomnia.

Non-pharmacological Treatment Options for Insomnia:  

We’ve talked about the poor symptoms of nighttime, but we also hinted earlier, Leslie, about daytime symptoms. How does insomnia impact the quality of life, especially in patients with comorbidities? What is happening to these people during the daytime?

Well, it sounds kind of obvious. If you don’t sleep well at night, you’re going to be tired during the day, and when you’re tired during the day, you’re not going to function very well. You can have problems with your concentration and level of alertness; the need to nap during the day, that can be a problem. You have something called presenteeism. It’s not like you’re not going to work, but when you’re at work, you’re just not all there and you’re not very productive, so it is a substantial problem. It’s also a risk for those in public safety kind of situations where someone needs to really remain alert during the day.

Before we talk about treatment considerations, there is one other thing I want to pass on to my primary care colleagues. Most patients with insomnia—and we’ve already said about 50% of patients who come into your office may qualify for the diagnosis of insomnia—most of them won’t tell you that they have insomnia. So be on the lookout for that. When you see your patients with the risk factors that Leslie talked about, patients who have these comorbidities, ask them about their sleep because they’re probably not going to tell you about it.

It’s interesting, they won’t tell you about it because they may think you’re not interested, or they have so many other pressing issues on their mind to resolve. If they’re coming to see you for a very specific problem, they may think that the sleep is kind of incidental to this, and they have to be encouraged from the get-go about telling us about their sleep. I use it as part of my mental status examination, and part of the overall evaluation is I need some idea of how well they’re sleeping, their appetite, and their level of concentration, for example.

Very important. If we’re interested in their sleep, they’re going to be interested in their sleep. Ask those questions proactively because most of the time they’re not going to ask about it.

Drs Paul Doghramji and Leslie Citrome discuss daytime sleepiness and other symptoms of insomnia and their impact on quality of life.

Quality of Life for Patients with Insomnia

Interestingly, insomnia when it occurs, at least I know in primary care, but also you’ll share with me as well, Leslie, about your practice, insomnia rarely occurs by itself. It seems to have co-occurrences with medical conditions and psychiatric conditions. I know that 30%, 40% of patients with insomnia have psychiatric disorders, and a lot of them also have medical conditions. Isn’t that correct?

Absolutely. We can take a look at research that’s been done looking at, for example, the odds ratio of having heart disease, cancer, high blood pressure, and so on, and insomnia. Basically, people with chronic health conditions also have insomnia disorder, and they’re more likely to have insomnia disorder than the general population. If we look at the psychiatric population, it’s really interesting because insomnia or difficulty with sleep is part of the diagnostic criteria for many conditions. But people can actually meet the full diagnostic criteria for insomnia disorder in addition to meeting the criteria for, let’s say, major depressive disorder, schizophrenia, bipolar disorder, or some anxiety disorder. There was an interesting cross-sectional study done of outpatients in Singapore where they calculated the percentage of people with major mental disorders, who also had DSM-5 [Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition] insomnia disorder. It’s basically 1 out of 2 people with major depressive disorder also meet the full criteria for insomnia disorder. It’s 1 out of 4 of those with schizophrenia, and 1 out of 3 for those with an anxiety disorder. So it is a very common comorbidity.

Let’s also not forget that it’s common also in medical comorbidities like COPD [chronic obstructive pulmonary disease], obstructive sleep apnea, chronic pain, coronary artery disease, stroke, and neurologic conditions. A lot of insomnia is occurring in a lot of medical conditions.

Let’s talk about the triggers and risk factors for insomnia. Who gets insomnia? Who is at highest risk, Leslie, of getting insomnia?

The older you are, the higher the risk. If we look at the whole population, the prevalence of insomnia disorder is higher for older people. It’s also higher in women than in men. We know that much. If you have a medical or psychiatric condition, as we mentioned, that also increases your risk. I’d like to address this issue of sleep and psychiatric conditions because I find as a practicing psychiatrist, it’s very helpful to know if someone has a problem with their sleep. I use it as the canary in the coal mine, so to speak. If someone who’s doing reasonably well all of a sudden has trouble sleeping, I think that maybe this is a sign of things to come, and I need to be prepared for addressing a potential recurrence of their, let’s say, depressive disorder.

So sleep is a problem, and it can also be used diagnostically to help prognosticate how someone is going to do in the future. We know there’s this bidirectionality. I know we’ll talk a bit more about this later, but it’s incredibly important for me as a psychiatrist to acknowledge that and know that insomnia is associated with, let’s say, a 4-fold relative risk of new-onset major depressive disorder. It’s a robust predictor of depression relapse, as I mentioned before. Unfortunately, insomnia often persists once the acute depressive episode has essentially resolved itself. I can help patients along with their mood, their concentration; sometimes though the sleep problem persists, and I have to think of something beyond the treatment that I had used to treat their depressive symptoms.

As far as medical problems go, we all know that insomnia, poor sleep, not sleeping well for a long period of time, increases the probability of medical problems, whether it’s weight gain, diabetes, or cardiovascular disease. There’s a lot of evidence suggesting that when you don’t get a good night’s sleep and for a long enough period of time, that bad things can also happen medically.

Experts review the co-occurrence of insomnia with other medical conditions and discuss risks and triggers that lead to insomnia, such as age and psychiatric conditions.

Sleep Disorders