CATR: Let’s start with a refresher of normal sleep architecture.
Dr. Morgan: Terminology has changed, so the terms here may differ from what you learned in school. At its most basic, sleep is divided into stages, commonly thought of as “light” and “deep,” though several distinct stages serve different purposes. Today we classify sleep as N1, N2, N3, and REM. N1 is the lightest, representing the transition from wakefulness. N2 is somewhat deeper and makes up a large proportion of total sleep. N3, the deepest stage (previously stages 3 and 4), is also called slow-wave sleep for its large, slow brain-wave oscillations. Normal sleep progresses from N1 to N2 to N3. Most N3 occurs in the first two to three hours of the night. After N3, sleep lightens and cycles into REM; for the rest of the night, most people alternate between N2 and REM. REM sleep involves vivid dreaming and rapid eye movements visible through closed eyelids. Early cycles contain mostly N2 with brief REM, while later cycles contain more REM, concentrating it in the second half of the night.

CATR: What questions should we be asking our patients who report sleep problems?
Dr. Morgan: Start with the basic definitions of insomnia: Are they having trouble falling asleep, staying asleep, or both? Asking about daytime consequences is especially important. We want to know how sleep is affecting the patient’s life. Are they fatigued? Less attentive? Struggling with mood regulation? People may worry about their sleep, but not all sleep-related anxiety reflects a true sleep disorder. We all go through periods of poor sleep if we’re preparing for an exam, dealing with a major project, or facing a stressful life event. The key question is whether the sleep problem persists and develops a life of its own after the stressor resolves. One of the most useful tools is a sleep diary. Have patients record when they went to bed, when they woke up, how long it took to fall asleep, how many times they awakened during the night, and how rested they felt during the day. Approximate answers are fine. A week of data is helpful; two weeks is even better.

CATR: These symptoms can come from a number of different causes.
Dr. Morgan: That’s true. And we should not necessarily jump to a diagnosis of primary insomnia just because someone reports poor sleep. One of the most common causes is obstructive sleep apnea (OSA). Patients reporting sleep issues should be screened for OSA, particularly since it’s treatable and can interact with other issues to worsen sleep even further. OSA can present as daytime sleepiness, non-restorative sleep, frequent awakenings, middle-of-the-night insomnia, or waking up gasping. Sometimes a bed partner will report pauses in breathing or excessive snoring. Patients with high BMI or a large neck circumference are more likely to have sleep apnea as well. If you suspect it, there are easy standardized screeners like the STOP-Bang (www.tinyurl.com/2s35cvfb) or the NoSAS (Costa JC et al, Pulmonology 2019;25(5):263–270). A definitive OSA diagnosis is made with a sleep study, so I set a low bar to make a sleep study referral.

CATR: What other standardized instruments do you recommend?
Dr. Morgan: There’s the Insomnia Severity Index (ISI), which is brief and works well for tracking symptoms over time (www.tinyurl.com/3v22ys73), and the Pittsburgh Sleep Quality Index (PSQI), which offers a broader assessment (www.sleep.pitt.edu/psqi). I use these much like a PHQ-9 for depression—repeated measurements show whether sleep is improving, worsening, or stable. Sleep can be tricky because patient perception doesn’t always match objective measures; sometimes anxiety about sleep changes more than sleep itself. Standardized assessments let clinicians anchor the conversation in data.

CATR: How does substance use affect sleep?
Dr. Morgan: It varies by substance, but virtually every psychoactive substance affects sleep, typically for the worse. Some may seem helpful in the short term, but chronic use almost always worsens sleep in the long run. Take caffeine, for example: It works by blocking adenosine, which accumulates while we are awake and contributes to sleepiness. Not surprisingly, caffeine increases sleep latency and reduces total sleep time. It also increases wakefulness during the night and decreases N2 sleep. Many people respond to the resulting fatigue by consuming even more caffeine, creating a self-reinforcing cycle. Another very commonly consumed substance, and one that many don’t think of as affecting sleep, is nicotine. But nicotine leads to poor overall sleep quality, reduced sleep efficiency, and greater difficulty maintaining sleep. It can worsen sleep apnea and disrupt circadian rhythms. Interestingly, some studies suggest that individuals who smoke heavily and maintain a very consistent pattern of use may experience slightly less sleep disruption than intermittent smokers (Riedel BW et al, Behav Sleep Med 2004;2(1):63–78). That is not an argument for smoking more; rather, it illustrates how the brain adapts to repeated exposure.

CATR: What about alcohol?
Dr. Morgan: Alcohol is particularly interesting. While alcohol is generally considered a CNS depressant, it also activates reward pathways and can produce stimulating effects (Kranzler HR and Soyka M, JAMA 2018;320(8):815–824). It helps people fall asleep, but it wears off quickly. People awaken three to five hours after they first fall asleep, then have fragmented, poor-quality sleep for the remainder of the night. Another issue with alcohol is that people can quickly develop a dependence on it for sleep onset (Sharma R et al, Brain Res Bull 2022;182:30–43). We’ve all heard from our patients, “I can’t fall asleep if I don’t have something to drink first.”

CATR: A lot of treaters hear that same refrain when it comes to cannabis, which is increasingly being used as a sleep aid.
Dr. Morgan: Cannabis is frustrating because so many people think it helps them sleep. Like alcohol, THC can make you sleepy, but chronic use worsens sleep over time; heavy, regular use is associated with reduced total sleep time, REM suppression, and poorer sleep quality overall. Many patients interpret their inability to sleep without cannabis as evidence it’s helping, but this usually reflects dependence (Gorelick DA, New Engl J Med 2023;389(24):2267–2275). I sometimes compare this to cannabis hyperemesis syndrome, which most patients now recognize—cannabis may initially reduce nausea, but chronic heavy use can eventually produce severe vomiting. Sleep works similarly: What helps today may worsen the problem tomorrow.

CATR: Finally, you’ve done a lot of work around cocaine and its effects on sleep.
Dr. Morgan: Cocaine is a powerful stimulant, so unsurprisingly it suppresses sleep. Total sleep time and REM both decrease, and sleep onset is delayed. Acute use can increase slow-wave sleep—a pattern we observed in the laboratory, where participants with cocaine use disorder self-administered cocaine and then slept under observation. We consistently found the same result: reduced total sleep time, reduced REM, and increased slow-wave sleep (Angarita GA et al, Drug Alcohol Depend 2014;143:173–180).

CATR: And the “crash” that many patients experience after using a lot of cocaine?
Dr. Morgan: The “crash” is a period of increased sleep following a cocaine “binge.” Many individuals who binge build up physiologic tolerance and can go days without sleeping during the binge. The crash reflects a combination of cocaine withdrawal and profound sleep deprivation. Beyond increased total sleep time, many patients also experience REM rebound (a dramatic increase in REM sleep with shortened REM latency). Some heavy users enter REM almost immediately after sleep onset, an experience often associated with vivid or bizarre dreams.

“I’ll ask, ‘If I could help you sleep just as well without this substance, would you be willing to stop using it?’ Most people say yes, and that shifts the discussion.” - Peter Morgan, MD, PhD

CATR: You’ve described sleep issues not just as a consequence of substance use, but as a treatment target. Can you elaborate?
Dr. Morgan: Sleep and substance use have a bidirectional relationship. We know that chronic substance use impairs sleep, but we also know that sleep problems increase the risk of developing substance use disorders (SUD). Studies have shown that adolescents with sleep disturbances are more likely to develop substance use problems later in life (Wong MM et al, Alcohol Clin Exp Res 2010;34(6):1033–1044). And there is a growing body of evidence that treating sleep problems may lead to improved substance use outcomes as well (Miller MB et al, JAMA Psychiatry 2023;80(9):905–913).

CATR: What should we know about using sleep medications to treat insomnia associated with substance use?
Dr. Morgan: It’s important to understand what different sleep medications do. Benzodiazepines (BZDs) and Z-drugs reliably decrease sleep latency. Patients generally perceive this as a major benefit because difficulty falling asleep is a common complaint. However, these medications change the underlying sleep architecture by increasing lighter N2 sleep while reducing slow-wave and REM sleep. Patients may fall asleep faster, but the sleep they obtain is not necessarily equivalent to natural sleep and therefore may not have the same effects on learning and memory processing (de Mendonca FMR et al, CNS Neurol Disord Drug Targets 2023;22(2):172–179). In contrast, medications such as gabapentin, pregabalin, and tiagabine tend to increase slow-wave sleep (Yeh WC et al, Sleep Med 2021;81:319–326). We conducted studies of tiagabine in people with cocaine use disorder and found substantially increased slow-wave sleep, but surprisingly, participants disliked it. Subjectively, they preferred BZDs even though it worsened aspects of overall sleep architecture (Morgan PT and Malison RT, Am J Drug Alcohol Abuse 2008;34(6):692–702). This highlights an important theme that we’ve been alluding to all along: Patients’ subjective experience and objective sleep measures do not always align.

CATR: With that caveat, what guidance would you offer clinicians regarding sleep medications?
Dr. Morgan: Don’t be afraid of sleep medications, but use them thoughtfully. Many of our patients are suffering significantly, and these medications can help. Don’t discount their experience; even though sleep architecture may not be optimal with BZDs or a Z-drug, they can still provide meaningful subjective relief. Ultimately, we want to establish healthy sleep patterns and architecture. Medications should be a tool to get you there but should be paired with behavioral interventions, like cognitive behavioral therapy for insomnia (CBT-i). I’ve found many patients are skeptical of behavioral interventions at first, but are more willing to try them once they experience some immediate relief from medication (Editor’s note: For more on CBT-i, see our interview with Dr. Arnedt on page 5).

CATR: Any other tips about discussing medication with your patients?
Dr. Morgan: Again, don’t discount medication out of hand, but start with basic sleep hygiene. The most common cause of insomnia is that people do not give themselves enough time to sleep. They don’t allow sufficient time to wind down, relax, and not look at a screen—which is not a problem to solve with medication. That’s probably the highest-yield piece of advice I can give.

CATR: Many patients insist they can’t sleep without alcohol or cannabis. How do you approach that conversation?
Dr. Morgan: First, I try to understand what role the substance is playing. Sometimes the complaint reflects genuine physiological dependence, usually with more consistent heavy use; sometimes it reflects psychological attachment, in which case patients express ambivalence about their use or briefly stop altogether; sometimes it’s both. Next, I work on engagement. I’ll ask, “If I could help you sleep just as well without this substance, would you be willing to stop using it?” Most people say yes, and that shifts the discussion: Now we’re working together rather than me trying to convince the patient to stop a substance that, to them, is useful.

CATR: Any other strategies?
Dr. Morgan: I’ll work with patients to taper their substance use if possible; in my experience, this approach is often more helpful than stopping cold turkey. I might ask them to try sleeping at 80% of their current dose. These patterns are usually built up over years, so there’s no rush, and gradual reductions tend to be more acceptable and allow for careful monitoring. Many patients with SUDs, however, may not be able to adhere to a careful taper. In that case, treating the substance use becomes paramount. These patients may be willing to cede control that they cannot yet exert for themselves—for example, receiving frequent limited supplies of taper medication, or having the medication held by a loved one or professional, steps that can eventually help the patient toward more self-reliance. The key is showing that sleep matters to you. Patients need to know you’re not asking them to suffer through weeks of insomnia, but that you’re committing to help them sleep while also addressing substance use. Sleep can be both a consequence of substance use and a contributor to it. Understanding sleep architecture and addressing sleep problems directly can improve recovery outcomes and overall well-being.

CATR: Thank you for your time, Dr. Morgan.