Eric Hermes, MD
Assistant Professor, Department of Psychiatry, Yale School of Medicine, New Haven, CT
Dr. Hermes has disclosed that he has no relevant financial or other interests in any commercial companies pertaining to this educational activity.
CATR: With substance use disorders (SUDs) that are comorbid with chronic insomnia, what would you say are some of the main treatment challenges? Dr. Hermes: The first thing I’d say is that chronic insomnia has a high comorbidity rate with SUDs as well as general psychiatric conditions and medical conditions, including chronic pain, COPD, heart disease, and diabetes to an extent. These comorbidities often take precedence, and treating insomnia becomes sort of a sideshow. Clinicians have limited time, and getting into the ins and outs of treatment options for insomnia usually doesn’t happen. For instance, SUD clinicians don’t usually receive special training about managing insomnia, and sleep disorders may not be high on their list. So, I think insomnia ends up being a secondary issue, and that means the focus may be more on the easier treatment regimens, like psychopharmacology—sometimes to the detriment of behavioral treatment options.
CATR: And then it becomes a potential issue for the patient? Dr. Hermes: Exactly. For the patient, chronic insomnia is often primarily a behavioral disorder. Chronic insomnia is technically defined as having affected the patient for at least 3 months. But if you’ve had trouble sleeping for a couple of weeks or even days, cognitive and behavioral issues can start to reinforce the problem, where you have negative thoughts that drive behaviors and thereby perpetuate the insomnia. Pharmacologic treatment is really good at putting people to sleep, but it doesn’t address these cognitive and behavioral issues that are part and parcel with chronic insomnia.
CATR: The theme of this month’s issue is sleep and addiction, but we also know that chronic insomnia can be comorbid with many additional mental health disorders we see in our patients. How can treating the insomnia help there? Dr. Hermes: First, we know that there are strong associations between insomnia and many mental health disorders. Most critically, we know that independent of all other comorbidities, insomnia increases the risk of suicidal ideation and attempts. We also know that treating insomnia reduces risk when it comes to some of the other comorbid disorders. For instance, the treatment of comorbid insomnia will improve depression and reduce posttraumatic stress disorder scores (Krakow B et al, Am J Psychiatry 2001;158(12):2043–2047; Manber R et al, Sleep 2008;31(4):489–495). Treating insomnia will also likely reduce the risk of relapse in patients with SUDs.
CATR: So, let’s talk about behavioral interventions. What’s your approach? Does cognitive behavioral therapy for insomnia (CBTi) really work? Dr. Hermes: There have been multiple systematic reviews showing that CBTi has an incredibly strong evidence base. It’s a very powerful treatment, with treatment effects at 3, 6, and 12 months after a course of therapy has been completed (Smith MT et al, Amer J Psychiatry 2002;159(1):5–11). According to the American Academy of Sleep Medicine, CBTi is a recommended first-line treatment for chronic insomnia.
CATR: If CBTi is so effective, then why are clinicians quick to prescribe medication? Dr. Hermes: Some clinicians may not be aware of what CBTi is or that it has such a strong evidence base. There are not a lot of providers out there who are trained to deliver CBTi. Also, it is a time-consuming process for both the provider and the patient—it involves showing up for therapy once a week for 6 weeks, and often as many as 9 to 12 weeks. Then the patient has to go home and actually do the CBTi activities. These are sometimes difficult, as with any therapy. So, there are these barriers, but in the end—if it’s available—providers should really try to use CBTi as a first-line treatment.
CATR: Has CBTi been validated for patients with SUDs? Dr. Hermes: Yes, there have been some studies that have validated CBTi in substance-using populations. I think most of those populations were for alcohol use disorder (AUD) and sorted in terms of what stage of treatment a patient was in, whether it was early sobriety or after years of sobriety (Currie SR et al, Addiction 2004;99(9):1121–1132).
CATR: For those who aren’t trained in CBTi, can you give us some basics? Dr. Hermes: CBTi is sort of a mish-mash of different behavioral and cognitive activities. One of those is sleep hygiene, and that’s really the bare bones of learning practices that promote good sleep habits. But sleep hygiene education as a stand-alone intervention does not have a particularly strong evidence base—it’s necessary, but not sufficient by itself. The most powerful component of CBTi seems to be “sleep restriction,” which involves getting patients to stay up late to ensure they are indeed tired when they hit the bed, and then locking down consistent wakeup times in the morning. Doing that basically allows them to reset their sleep cycle. This can take as little time as a couple of days (Edinger JD and Means MK, Clinical Psychol Review 2005;25(5):539–558).
CATR: I’ve heard that fixing the wakeup time is the most vital component when using sleep restriction. Do you agree? Dr. Hermes: Yes, I think locking down wakeup time is also quite beneficial. Many practitioners I talk to will work on sleep hygiene practices first, which serves as preparation for getting patients to set up a wakeup time as part of sleep restriction activities. But as we’ve learned, it’s not always easy having people stay up late to ensure they’re ready for sleep and then getting them to wake up at a consistent time. It’ll take constant reminders and working with patients to troubleshoot difficulties.
CATR: Considering the challenges of dealing with patients who are new to recovery—maybe they’re just coming off detox—would it be a good idea to delay CBTi until they stabilize, using a non-benzodiazepine drug to help them sleep in the interim? Dr. Hermes: Yes, I don’t know if CBTi would be appropriate for most people in early sobriety. Obviously, during early sobriety, patients are most focused on their recovery activities. It might be difficult for these patients to also focus on CBTi activities. So, helping them initially—at least for a few weeks—with a pharmacological solution makes sense.
CATR: Let’s talk about pharmacological solutions, either as an interim step before beginning CBTi for chronic insomnia or for simply treating acute, short-term insomnia. What do you recommend for patients who have a comorbid SUD? Dr. Hermes: First, I think the key is talking clearly with patients up front about the benefits and especially the risks of pharmacologic insomnia treatment. Make that the first conversation. Talk about what the plan would be if, in a few weeks, the prescription isn’t working, and explain what the probabilities are around that. Then, talk about side effects and the short-term risks, which are pretty minimal. Most of the sedative-hypnotic medications are well-tolerated. The risks in my mind are more long-term involving how patients come off these medications.
CATR: Should they still need medication in a few weeks, do you then tell them what the plan would be next? Dr. Hermes: Yes, at that initial talk, you want to at least introduce the idea of starting CBTi. I actually don’t use the word “therapy,” though. I tend to use the term “training,” such as, “We should begin that training soon.” I don’t even use the term “CBTi.” I’ll tell patients, “If you feel you still need the drugs for your insomnia in 2 or 3 weeks, we can try an effective training regimen instead. It will be more of a commitment, but it really works, and it doesn’t involve medication.”
CATR: What medications do you usually consider: benzodiazepines, the Z drugs, or another medication? Dr. Hermes: Well, I put them all in a group of sedative-hypnotics, and within that group I personally define them as the benzos, the non-benzo GABA-agonists [Z drugs (eg, zolpidem)], antihistamines, and “others,” such as sedating antidepressants. In substance-using populations, I’ll usually start with a sedating antidepressant such as trazodone. I’ll do that because in most of the populations I treat, the risk of going from acute pharmacologic treatment to chronic pharmacologic treatment in substance-using populations is high. After the sedating antidepressants or the antihistamines, I would go to the Z drugs and then—if necessary—the benzos. With antihistamines, I will use a drug like Benadryl with patients that have more of a middle insomnia picture after something like trazodone has failed. This is usually not very well-tolerated because of the morning grogginess, so I will mainly use it short-term—say, a week—as I am trying to get the patients into CBT. I will use hydroxyzine for more early insomnia.
CATR: Since many patients are familiar with Ambien (zolpidem), is that typically what they ask for first? Dr. Hermes: Yes, it’s a household name at this point and the most commonly prescribed sleep drug, so usually patients will know it if not request it. When they ask, I will start a conversation to educate them about how there are less risky drugs that we should consider first. But it can be a challenging conversation, since most people know Ambien, and many patients have been on it and like its effectiveness.
CATR: So, how do you have that conversation with the patient? Dr. Hermes: I’ll start the discussion with, “Where do you want to be in 3 months? A year? Do you still want to be taking this medication? Most of these drugs will work very well, especially in the short term, but for some people they are difficult to stop.” This allows me to discuss drugs that are less likely to evolve into chronic use, and then dovetail that into introducing the idea of an “effective training regimen” with CBTi.
CATR: Can you tell us more about why you mention benzodiazepines as a last-line option for an SUD patient? Dr. Hermes: Simply put, it’s because of the much higher risk of benzo use disorder in the SUD population, particularly with those who have AUD. I think that’s the worry. It’s less of a question that benzo use will throw a patient with an AUD into relapse. It’s more about the high potential for a new SUD involving the benzo.
CATR: But isn’t that also the case with those who have an AUD and are also taking zolpidem? Dr. Hermes: I think the risk of relapse is lower with zolpidem, but it does happen. As I remember, there are some early studies showing that those in AUD recovery didn’t risk zolpidem misuse, but the bulk of the evidence shows that there is a connection (Griffiths RR and Johnson MW, J Clinical Psych 2005;66(9):31–41). I see many patients with an AUD who find it very, very difficult to quit the zolpidem.
CATR: How about the use of melatonin? Dr. Hermes: Most people I see are already on melatonin, usually at a lower dose than is recommended. I have never really seen melatonin work, but this may just be the population I see. I generally don’t even increase the dose and will just start another agent and try to get them to stop the melatonin in order to simplify the medication regimen. Interestingly, patients will usually stay on it of their own accord. I think this is more about it being a “natural substance” than its efficacy for insomnia.