1 Depression and Insomnia
An Overview
Insomnia is Important
Sleep is a significant issue for those with major depressive disorder (MDD). Up to 90 percent of those with MDD complain of insomnia (Kupfer, Reynolds, Ulrich, Shaw, & Coble, 1982; Reynolds & Kupfer, 1987). In community samples, just under half of people with MDD meet criteria for an insomnia diagnosis (Breslau, Roth, Rosenthal, & Andreski, 1996; Stewart et al., 2006). In sleep clinics, the most common insomnia patient seen is one with comorbid MDD (Buysse et al., 1994; Coleman et al., 1982; Edinger et al., 1989; Jacobs, Reynolds, Kupfer, Lovin, & Ehrenpreis, 1988). Additionally, there can be complaints of hypersomnia and sometimes an alternation between hypersomnia and insomnia.
Despite the high prevalence, the importance of sleep is under-recognized and as a result undertreated. There are several studies showing that a separate insomnia diagnosis is not considered when MDD is suspected. For example, the best predictor of a MDD diagnosis is the presence of an insomnia complaint (Haponik, Frye, Richards, Wymer, & Hinds, 1996). However, insomnia is not one of the two cardinal symptoms (i.e., depressed mood and/or anhedonia) needed for a MDD diagnosis (American Psychiatric Association, 2013) and thus should not be predictive of this diagnosis. Another potential issue in the underdiagnosis of insomnia is being presumptuous about etiology. Some problems in this area include the presumption that it is important to establish temporal precedence of the insomniaâeven in such cases, some presume that the insomnia is merely the first MDD symptom to appear. There are several problems with this view. One is that patients may not be able to remember which symptoms came first, especially given that those with MDD have autobiographical deficits (Lyubormirsky, Caldwell, & Nolen-Hoeksema, 1998). Second, even in sleep specialists, clinicians exhibit poor reliability in determining whether an insomnia diagnosis is present when there are mood symptoms present (Edinger et al., 2011). There are also assumptions that MDD is more serious and therefore clinical attention should be exclusively focused on the MDD. Although MDD is a very serious disorder, on some quality of life indices, chronic insomnia produces greater impairment than MDD (Foley et al., 1995). Insomnia is associated with large societal costs (Carney et al., 2008; Daley, Morin, LeBlanc, Gregoire, & Savard, 2009; Ozminkowski, Wang, & Walsh, 2007). Indeed, the costs associated with MDD increase by an additional $1K annually in those with untreated insomnia and MDD (Asche, Joish, Camacho, & Drake, 2010). Additionally, insomnia is predictive of developing alcohol and substance abuse (Ford & Kamerow, 1989). Lastly, chronic insomnia is associated with increased suicidal ideation (Agargun, Kara, & Solmaz, 1997; Li, Lam, Yu, Zhang, & Wing, 2010; Woznica, Carney, Kuo, & Moss, 2014), and insomnia is an independent predictor of suicide (Bernert, Joiner, Cukrowicz, Schmidt, & Krakow, 2005); that is, even after controlling for depression, there is an increased risk for suicidality. In those with MDD, suicidal ideation is increased when there is insomnia present and insomnia is a significant predictor of suicide completion (Fawcett et al., 1990).
Inherent in the assumption that MDD is always more serious is perhaps an implicit assumption that treatment of the MDD will likely resolve the (less serious) insomnia problem. There are many studies to confirm that this is a faulty assumption. Across studies using sleep items from depression inventories, the rate of residual insomnia problems after depressive recovery following antidepressant therapy or psychotherapy is a little less than half (Carney, Segal, Edinger, & Krystal, 2007b; Manber et al., 2003; Nierenberg et al., 1999). It is possible that the rate exceeds 50 percent, as a study that utilized a validated sleep questionnaire in lieu of sleep items from a depression measure found a much higher rate (Carney, Harris, Friedman, & Segal, 2011). Additionally, in the same study, although depression cognitions significantly decreased and were in the nonclinical range after depressive recovery, insomniagenic beliefs did not significantly improve with depression recovery and remained in the pathological range (Carney et al., 2011). Insomnia is also a complicating factor for depression treatment because insomnia predicts poorer response to evidence-based psychotherapy or pharma cotherapy depression treatments (Buysse, 1999; Thase, 1996, 1997). Collectively, the data above confirms what was concluded at the National Institutes of Health (NIH) Consensus Conference on Insomnia: Insomnia should be considered a comorbid condition and treated in the presence of MDD. Moreover, after a review of the evidence, the DSM5 Sleep-Wake Disorders Work group concluded that there should be no diagnostic distinction between comorbid insomnia and insomnia alone; the disorder in the fifth edition of the DSM is simply insomnia disorder (American Psychiatric Association, 2013).
Etiological Factors in Insomnia
In considering the relationship between insomnia and depression, it may be helpful to first consider causal factors for insomnia. There are many causes of sleep disturbance and there may be as many precipitating or initial causes as there are clients. Although sleep problems initially can be caused by just about anything, there are three main causes or factors that perpetuate a chronic insomnia: problems with the homeostatic, circadian and/or arousal systems. This idea was first presented in Spielmanâs Three P Model (Spielman, Caruso, & Glovinsky, 1987a). The model postulates that there are predisposing factors that increase vulnerability to insomnia (e.g., a tendency towards rumination), but having a vulnerability factor does not mean that insomnia is inevitable; it simply provides fertile ground for an insomnia disorder in the presence of a stressor. The stressor is the precipitant in the model. As stated above, there are many precipitants, even positive stressors such as having a baby can precipitate sleep disturbance. MDD can be a stressor in this model. Although insomnia is often a precursor to MDD, in some cases, MDD could lead to more protracted insomnia. Sleep disturbances that are associated with a stressor are expected to resolve with the resolution of the precipitant. Thus in the case of MDD precipitating sleep disruption, we would expect insomnia to resolve when the MDD resolves. Unfortunately we know that insomnia frequently does not remit with the resolution of the depressive episode (Carney, Edinger, Meyer, Lindman, & Istre, 2006). Why? Sleep disturbance becomes a chronic insomnia when there are perpetuating factors present. Perpetuating factors are those factors that often arise from coping with the precipitating factor and initial sleep disturbance. The consequence of these coping behaviors can create disturbances in the homeostatic, circadian and/or arousal systems. Below we discuss each of these factors and then return to the situation of MDD and insomnia.
Perpetuating Factor: Homeostatic System Problems
Sleep is regulated by two systems: a homeostatic and a circadian system. We will discuss the circadian system and its role in chronic insomnia in the next section. First, the homeostatic system is a system that balances between wakefulness and sleep. From the moment we are awake and active, we accumulate a chemical in the basal forebrain called adenosine. The build-up of this chemical is associated with increasing sleepiness and pressure for deep sleep; the greater the duration of wakefulness, the greater the buildup of a drive for deep sleep. The greater the amount of time since rising, the greater is the pressure to sleep. This system ensures that we neither sleep too much nor too little. It compensates for sleep loss and lightens sleep if the person was attempting to produce copious, unnecessary amounts of sleep. This means that people neednât do anything during periods of sleep loss except maintain their schedule, because the body will make up for lost sleep with subsequent deep, restorative sleep. However, attempting to make up for lost sleep by spending increased time in bed or at rest, sends a message to the body that less deep sleep is needed; thus the compensatory mechanism is thwarted. Below we include a sample script for CBT-I psychoeducation. Such an explanation is included in the first treatment session of CBT-I. There are other examples of psychoeducation delivery throughout the book, including in Chapter 5 wherein we describe the behavioral components of CBT-I delivered in the first treatment session.
Therapist: From the moment you get up and are active, you begin to build a drive for deep sleep. You build it all day and into the evening until so much has built up that when you go to sleep, you produce some deep sleep and it keeps you asleep throughout the night.
Client: Well, that never happens to me anymore.
Therapist: It may well be that you have a problem with this system. Letâs continue and you can tell me what you think. This system determines how much deep sleep you get and it is based on how many hours you have been awake and active. So if you get up later, go to bed earlier, attempt to nap or rest throughout the day or you are less active, less deep sleep drive is accumulated and the result is light, broken sleep and maybe difficulty in falling asleep too.
Client: I definitely donât get deep sleep anymore but itâs not like I am totally inactive âŚ
Therapist: Let me ask you this, when you feel tired, or youâve had a poor nightâs sleep, or your mood is really low, how much do you feel like keeping up with your regular activities?
Client: Iâm not sure what you mean. I feel really tired so I try to do my normal activities but I canât always do what I want.
Therapist: Can you tell me more about that? Are you able to get right out of bed when your alarm sounds? Are you always able to go to work? Do you keep up with all your social engagements?
Client: Sort of. Not everything. Like I said, I feel exhausted so itâs not always possible.
Therapist: This is very common. Most people do an excellent job trying to do all the things they used to but when the fatigue sets in, they find it more and more difficult and they find themselves spending a little more time in bed and a little more time inactive than before they had their sleeping problems âŚ
Client: I wouldnât say I spend more time in bed.
Therapist: Ok. I was making that assumption based on what you told me was your routine two years ago, before all this trouble started. You had said that you went to bed around 11 PM and got up at 6 AM each morning, you never took naps, you had a weekly card game with friends, lunch on Fridays with coworkers, and you worked out 4 days per week.
Client: Well itâs true that I donât work out anymore, and guess I donât go to lunch or the card game. I donât really take naps now because I often canât sleep. I just try to sleep. I still go to bed at 11 and get up at 6 AM.
Therapist: I see. So some of your activities have decreased and you spend more time resting but not always napping?
Client: Right.
Therapist: Can we take a look at your sleep diary? [See Figure 10.2 in Chapter 10]
Client: Sure. See how I go to bed around 11 PM most nights? Except for Tuesday and Wednesday.
Therapist: Yes, I see. Most nights were around 11 PM and Tuesday you went to bed an hour earlier and Wednesday you went to bed about 2 hours earlier, around 9ish, right?
Client: Thatâs right.
Therapist: And I see that your final awakening during the work week was 6:30 AM and on the weekend it was closer to 8 AM correct?
Client: Thatâs right.
Therapist: The item below your final awakening is the time that you actually got out of bed, what do you notice about the time at which you physically get out of bed?
Client: Itâs later than 6:30 AM. Itâs because I am tired.
Therapist: Right. Because you are tired, you have difficulty getting up at the time you used to and it is even later on weekends. You used to spend 7 hours in bed each night. How many hours were you in bed on Wednesday?
Client: Almost 10 hours. Wow. I never knew that. But I am not sleeping during this time.
Therapist: Right, you are not sleeping, but you are also not building a drive for deep sleep. You also told me that you attempted to nap for 90 minutes that afternoon. If you spent 11.5 hours inactive in bed that day, how much time were you building sleep drive?
Client: I donât know [pauses] I think, 12.5 hours?
Therapist: Yes. So if there were two people and one spent 7 hours in bed so they had 17 hours of deep sleep drive build-up, and the other had 12.5 hours of build-up, who is more likely to have deep, continuous sleep?
Client: Ok, I get it. The person who builds 17 hours has a better chance at better sleep.
Therapist: And donât forget that the person with 17 hours of build-up also has much more activity to add to the build-up. The person with only 12.5 hours also has a lower amount of physical activity to contribute to the build-up.
Client: Ok, I get it.
Therapist: So we will discuss ways to work with this system to produce more deep sleep for you. But first, I had said there is another system that works with your homeostatic system. I think itâs important to talk about this system too.
Perpetuating Factor: Circadian System Considerations
In addition to the homeostatic system that balances sleep and wakefulness, there is a body clock that regulates many systems in the body, including the timing of the sleep and alerting systems. The circadian system is slightly longer than a 24 hour day and thus is highly responsive to cues in the environment, such as the light, for entrainment purposes. The light provides input via the eye into the brain about what time it is. When blue spectrum light is present (i.e., in sunlight) it signals that it is day and this situation is associated with alertness. When red spectrum light is present (i.e., following sunset) it signals night and is associated with melatonin release; a sedative hormone. Improperly timed cues can create sleepiness or alertness at undesirable times. Thus decreased exposure to light can be associated with drift in the circadian system, and ill-timed light (blue light exposure at night) can be associated with ill-timed alertness.
Although light is the most powerful cue for the clock, keeping a regular schedule of activities including rise and bedtimes, and perhaps meal times and other activities can help set the clock. Each of these activities is typically associated with light too, i.e., we typically eat under lighted conditions, when we travel to work we are often exposed to daylight etc. In those with insomnia, the regularity of daily activities is diminished relative to good sleepers even when overall levels of activity are the same between those with insomnia and good sleepers (Moss, Carney, Haynes, & Harris, 2014). When there is irregular environmental input (e.g., light or activities) to the clock, the system drifts, because it is more than 24 hours, and symptoms such as difficulty in sleeping, cognitive difficulties, fatigue, and mood disturbance can occur. These are the symptoms experienced during jetlag. Thatâs because jetlag is the result of the mismatch between the internal time and the time in the environment. Even one hour is enough to produce these symptoms; most people can relate to this because daylight savings is only one hour and it typically produces at least mild symptoms. The reason this is important is that if the rise time is varied by an hour or more then the client will experience jetlag symptoms. When people suffer from sleep or mood disturbance they often struggle at getting up at their regular time. They may continue to set the alarm but will remain in bed longer because they feel tired.
The circadian system regulates a variety of systems in the body including sleep, alertness, and mood. There are regular predictable patterns for the rise and fall of these activities across a 24 hour period but this system is also largely responsive to environmental output. One way to envisage this system is to visualize a curve that rises in the morning, continues to rise all day, and then begins to fall in the evening and through...