TCPR: How do you assess sleep in mood disorders?
Dr. Chopra: I focus on three variables. Total time asleep is also useful. The first is sleep onset latency—how long it takes to fall asleep after lights out, which should ideally be under 30 minutes. The second is wake after sleep onset, or WASO, the total time awake during the night after first falling asleep. WASO reflects disrupted, fragmented sleep, and is ideally under 30 minutes. The third is sleep efficiency, which is the percentage of time spent in bed asleep (divide total sleep time by total time spent in bed over a 24-hour period, then multiply by 100). Ideally, patients’ sleep efficiency is above 85%, meaning they spend 85% of their time in bed asleep. I compare this week’s sleep efficiency to the prior week using the subjective report. These numbers give you a practical baseline and something concrete to track over time.

TCPR: What are some common pitfalls in gathering that data?
Dr. Chopra: There is a tendency for recall bias. Things can blur together in a depressive episode, and patients may overestimate how severe their sleep problems are. What they describe as hypersomnia often reflects low energy, low motivation, or anhedonia—they’re in bed because the world feels too heavy, not because they are oversleeping.

TCPR: What are the main diagnostic possibilities you’re sorting through for insomnia in depression?
Dr. Chopra: I keep three differentials at the top of my list. The first is circadian rhythm disturbance, specifically delayed sleep phase (“night owls”). To get at that, I’ll ask about their sleep patterns on weeknights versus weekends. These patients naturally fall asleep late, like 2 am, so they struggle with sleep during the workweek but then sleep fine when left to their natural schedule on weekends. The second is restless leg syndrome, which patients often describe as “feeling antsy” or as classic creepy-crawly sensations, accompanied by an urge to move their legs. Consider both circadian rhythm disturbance and restless leg syndrome in the differential diagnosis of sleep initiation insomnia. After that, I look for obstructive sleep apnea as a potential trigger for sleep maintenance insomnia. All three sleep disorders are prevalent in patients with major depressive disorder.

TCPR: A lot of anxious patients fixate on whether they can fall asleep. How do you get them to look at the big picture, viewing sleep as a 24-hour process?
Dr. Chopra: I explain that sleep is driven by two forces. There’s the homeostatic drive, which is linear. It increases the longer a person stays awake and is driven in part by adenosine, which caffeine blocks. The other is the circadian drive, which is cyclical, driven by light, darkness, and daily routines. That brings us to what patients do during the day: oversleeping, napping, staying in bed, using substances, or blocking melatonin production with screens and lights at night. Alcohol can help with sleep onset, but it fragments sleep during the night. Sleeping in on weekends, even by an hour or two, erodes the circadian anchor that stabilizes the whole system. When I explain the two-process model—homeostatic drive and circadian drive—patients often connect the dots themselves. It shifts the conversation from saying, “Give me something to knock me out” to “Here’s what is undermining my sleep and how I can address it.”

TCPR: That sounds like a good start to cognitive behavioral therapy for insomnia (CBT-i).
Dr. Chopra: Yes, that’s the backbone of interventions for insomnia. CBT-i has about 60%–70% efficacy for insomnia, and those gains can last three or more years—outcomes that outperform hypnotics for durability (Morin CM and Buysse DJ, N Engl J Med 2024;391(3):247–258). It starts with education on the homeostatic and circadian drives. Next, stimulus control is probably the highest-yield component you can teach in 10 minutes. If the patient hasn’t fallen asleep within 15–20 minutes, they should leave the bed, go to a dimly lit room, and do something monotonous until they feel genuinely sleepy. The goal is to reassociate the bed with sleep, rather than wakefulness and frustration. Consistent wake time matters more than bedtime. I tell patients to get up at the same time every day, no matter how the night went, because sleeping in compounds the problem by depleting the next night’s sleep drive. Relaxation techniques aimed at reducing hyperarousal can often be helpful. Other parts of CBT-i are best done with a specialist in CBT-i, such as identifying and restructuring unhelpful thoughts about sleep, and using sleep restriction, where patients limit time in bed and gradually expand it as their sleep efficiency improves.

“When I see someone on multiple sleep agents, my first instinct is to ask what’s missing and address any underlying disorders.” - Amit Chopra, MD

TCPR: What if a CBT-I therapist isn’t available?
Dr. Chopra: There are apps for digital CBT-I. Two are cleared by the FDA (Sleepio and Somryst), and another is free (Insomnia Coach, sponsored by the VA; Forma F et al, Curr Med Res Opin 2022;38(10):1727–1738). My caveat is that patients with depression may not engage well with an app, so I’ll refer to a CBT-i therapist there. I also use therapist-led CBT-i when tapering hypnotics.

TCPR: We have a lot of hypnotics. Where do you begin?
Dr. Chopra: I organize them by the type of insomnia they address and the risks for that patient. For trouble falling asleep, my primary options are ramelteon (8 mg), a melatonin receptor agonist, and zaleplon (10–20 mg), which also has a unique role in middle-of-the-night awakenings, as it can be taken safely if 4 or more hours of sleep remain. For trouble staying asleep (sleep maintenance), I reach for low-dose doxepin (3–6 mg) or a dual orexin receptor antagonist (the DORAs): suvorexant (5–20 mg), lemborexant (5–10 mg), and daridorexant (25–50 mg). For patients who have difficulty falling and staying asleep, eszopiclone covers both problems. However, these Z-hypnotics carry risks of complex sleep behaviors—sleepwalking, sleep eating, sexsomnia—that the DORAs do not. In patients with substance use disorders, respiratory compromise, or age-related fall risks, I strongly favor DORAs or low-dose doxepin over Z-hypnotics (Editor’s note: For more information, see “A Quick Guide to Sleep Medications” below).

TCPR: Let’s talk about DORAs. Are there differences among suvorexant, lemborexant, and daridorexant?
Dr. Chopra: They share the same mechanism—blocking orexin signaling to reduce wake drive—and all three address both initiation and maintenance. They have a favorable safety profile in sleep apnea because, unlike benzodiazepines and Z-drugs, they don’t suppress respiratory drive. There’s less addiction potential, less tolerance, and fewer falls compared to older agents. The comparative head-to-head data between the DORAs is limited, so I tend to choose based on formulary access and individual patient response. The next-day residual sedation data is broadly similar, though the longer half-life of lemborexant may make that worse for some patients. I’ve found all three useful in bipolar disorder, where I want to avoid doxepin given its antidepressant activity.

TCPR: What do you use if the insomnia is driven by phase delay (“night owls”)?
Dr. Chopra: For pure circadian delay—the patient who can’t fall asleep by midnight but sleeps beautifully on their own schedule—melatonin 1–3 mg taken around 8 pm is my first move (Meyer N et al, Lancet 2022;400(10357):1061–1078). Low-dose immediate-release formulations are more effective for phase shifting than higher doses, and timing earlier in the evening is essential. Taking melatonin at bedtime doesn’t achieve the circadian effect. But if the patient has circadian delay and initiation insomnia, ramelteon is stronger than melatonin. Both work through the melatonin system, and both have similar circadian-correcting properties. They are generally well tolerated, but both can cause vivid dreams and nightmares.

TCPR: How do SSRIs and SNRIs affect sleep?
Dr. Chopra: Around 16%–17% of patients who start an SSRI or SNRI will develop insomnia as a side effect, and a similar percentage of patients develop hypersomnia. The insomnia may not be obvious, particularly if it only disrupts sleep quality. The key is to establish a baseline before starting the medication, so you can recognize when the drug is the culprit rather than attributing it to undertreated depression. SSRIs and SNRIs are potent REM suppressants, as are most antidepressants. REM suppression was once considered a core mechanism of antidepressant action, but that theory has weakened. There are effective antidepressants that don’t suppress REM, like bupropion (Szynkarek A et al, CNS Drugs 2026;40(6):787–801). REM has important functions in emotional processing, and whether suppression is a net benefit in depression is still an open question.

TCPR: Are there antidepressants that improve sleep quality?
Dr. Chopra: Yes. Mirtazapine increases slow-wave sleep, which is reduced in depression. Quetiapine does that as well. Trazodone works primarily through 5-HT2A receptor blockade, which produces sedation and also tends to improve sleep quality. It’s widely used off label for insomnia and doesn’t suppress REM at the hypnotic doses.

From the Expert Q&A
“Sleep and Depression”
by Amit Chopra, MD
The Carlat Psychiatry Report, Volume 24, Number 11 & 12
Nov/Dec 2026
www.thecarlatreport.com

TCPR: How do mood stabilizers affect sleep?
Dr. Chopra: Lithium has the strongest data for correcting circadian rhythm disturbances—which is relevant in bipolar disorder, where circadian and seasonal changes often disrupt mood. Lamotrigine can cause vivid dreams or nightmares in some patients.

TCPR: What about gabapentin and pregabalin?
Dr. Chopra: They act on alpha-2-delta subunits of calcium channels, which reduces excitatory neurotransmission, including glutamate activity. They’re not acting on GABA receptors directly, despite what the names suggest. They treat restless legs, and their sedative mechanism may improve sleep in some patients, though sedation can be problematic at higher doses.

TCPR: What sleep disorders should we watch out for in mood disorders?
Dr. Chopra: Sleep apnea and restless leg syndrome are often missed, and parasomnias are also common. I screen for sleep apnea with the STOP-BANG questionnaire. In major depressive disorder, roughly one in five patients has undiagnosed, untreated sleep apnea. These are often patients with treatment-resistant depression, or they may be taking multiple hypnotics without much effect. No amount of sleep medication will give someone with untreated sleep apnea restorative sleep.

TCPR: And if they don’t have sleep apnea, what’s your take on hypnotic polypharmacy?
Dr. Chopra: When I see someone on multiple sleep agents, my first instinct is to ask what’s missing. They may have undiagnosed sleep apnea, restless legs, parasomnia, or an untreated psychiatric disorder. Once I’ve addressed underlying disorders, I refer for CBT-i, which has intrinsic efficacy and also facilitates medication tapering.

TCPR: How do you switch from one hypnotic to another?
Dr. Chopra: I’ll cross-taper over one week. That’s usually enough time to minimize the rebound from discontinuing the old medication. Benzodiazepines are an exception and require a much slower taper. The DORAs, doxepin, and ramelteon can usually be introduced and titrated to an effective dose within that one-week window, which helps make them practical transition agents.

TCPR: Final words of advice?
Dr. Chopra: Sleep is critical to nearly every disorder we treat. Ask about sleep onset latency: “How long does it take you to fall asleep?” Then ask about WASO and sleep efficiency. Think about sleep as a 24-hour system, not just a nocturnal event. Look beyond insomnia to circadian disorders, sleep apnea, and restless leg syndrome—they are common, underdiagnosed, and highly treatable. And try to refer for CBT-i early, before adding a second or third medication.

TCPR: Thank you for your time, Dr. Chopra.